✅ URI / UTI / STD / SEPSIS / TB Flashcards

1
Q

💨 UPPER RESPIRATORY INFECTION

A

Usually viral syndrome that is benign and self-limited, lasting <strong>3 to 10 days</strong>. Viruses (eg, rhinovirus, coronavirus, respiratory syncytial virus, metapneumovirus) cause infection by gaining entrance to epithelial cells of the upper respiratory tract, leading to host inflammatory responses, cholinergic stimulation, vasodilation, and increased vascular permeability.

<strong>Tx:</strong> Inhaling heated vapor, such as steam from a hot shower, may decrease nasal symptoms. Other symptomatic measures include increasing fluid intake, gargling with salt water or using saline nasal spray, sucking on throat lozenges, and ensuring adequate rest. Although these measures lack good evidence of effectiveness, they are safe and inexpensive. For relief of nasal congestion, oral decongestants (eg, pseudoephedrine) or short-term (<3 days) use of topical nasal decongestants (eg, phenylephrine) is beneficial.

<strong>Rx:</strong> In patients with rhinorrhea and sneezing, a short course of a <strong>first-generation antihistamine diphenhydramine (Benadryl)​ </strong>or<strong> intranasal ipratropium</strong> may be considered. In patients with a productive cough and wheezing, an <strong>inhaled β-agonist </strong>may reduce the duration of cough. Acetaminophen or an nonsteroidal anti-inflammatory drugs (eg, naproxen, ibuprofen) may be used for headache, myalgia, and malaise.

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2
Q

🦠 Pneumonia

A

A space occupying lesion without volume loss; caused by bacteria, viruses, mycoplasmae and fungi.

Ddx: Airspace filling not distinguishable radiographically: fluid (inflammatory), cells (cancer), protein (alveolar proteinosis) and blood (pulmonary hemorrhage).

Dx: The x-ray findings of pneumonia are airspace opacity, lobar consolidation, or interstitial opacities. There is usually considerable overlap.

Lobar - classically Pneumococcal pneumonia, entire lobe consolidated and air bronchograms common. Abrupt in onset, with fever, pleuritic chest pain, and purulent sputum production.

An “Air bronchogram” is a tubular outline of an airway made visible by filling of the surrounding alveoli by fluid or inflammatory exudates.

Ddx: air bronchograms: Lung consolidation (PNA), pulmonary edema, nonobstructive pulmonary atelectasis, severe interstitial disease, neoplasm, and normal expiration.

Lobular - often Staphlococcus, multifocal, patchy, sometimes without air bronchograms

Interstitial - Viral or Mycoplasma; latter starts perihilar and can become confluent and/or patchy as disease progresses, no air bronchograms. “Ground Glass” is a radiology descriptive term (used in both chest radiographs and CT imaging) to indicate that blood vessels are not obscured as would be the case in alveolar lung opacities. Both atypical bacterial and viral organisms may produce pneumonias that differ radiographically from more common bacteria such as pneumococcus. They may produce a ground glass appearance and increased interstitial markings. The CXR appearance of Pneumocystis pneumonia is typically bilateral, diffuse interstitial (“reticular”) or ground glass opacities.

Hx: “Atypical pneumonia” due to C pneumoniae or 🏒M. pneumoniae: Patients often complain of a sore throat at the beginning of the illness and a protracted course of symptoms. Physical examination is often unimpressive compared to radiograph findings and the diagnosis is often not made as the course is often indistinguishable from other lower respiratory infections.

💨Aspiration - follows gravitational flow of aspirated contents; impaired consciousness, post anesthesia, common in alcoholics, debilitated, demented patients; anaerobic (Bacteroides and Fusobacterium). In a supine patient who has aspirated, the common locations of pneumonia are the posterior segment of the upper lobe and superior segment of the lower lobe. The superior segment of the right lower lobe is the segment most likely to develop aspiration pneumonia.

Diffuse pulmonary infections - Community acquired (Mycoplasma, resolves spontaneoulsy) nosocomial immunocompromised host (bacterial, fungal, PCP)

🏥 Nosocomial by definition occur 3 days after admission. Patients in the ICU are often relatively immunocompromised secondary to their primary disease and are subject to iatrogenic factors which increase their sucseptabilty to pneumonia-causing pathogens. These include the following: endotracheal tubes, which defeat many patient defense mechanisms; medications used to reduce gastric acid, which may promote bacterial growth in the stomach; and the use of antibiotics, which may selectively encourage the growth of some pathogenic bacteria. Nosocomial pneumonias are often polymicrobial and caused by 🔮gram-negative enteric pathogens. The offending organisms often include Pseudomonas species, E-coli, Klebsiella species, and Proteus species (Pseudomonas, debilitated, mechanical vent pts, high mortality rate, patchy opacities, cavitation, ill-defined nodular).

Ventilator-associated pneumonia (VAP) is a type of nosocomial pneumonia that usually develops >48 hours after endotracheal intubation. It is most commonly caused by aerobic gram-negative bacilli (eg, Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae) and gram-positive cocci (eg, methicillin-resistant Staphylococcus aureus, Streptococcus). Patients usually have fever, purulent secretions, difficulty with ventilation (eg, increased respiratory rate, decreased tidal volume), and leukocytosis. Those with an abnormal chest x-ray (eg, alveolar infiltrates, air bronchograms, silhouetting of adjacent solid organs) require lower respiratory tract sampling (ie, tracheobronchial aspiration) for microscopic analysis (Gram stain) and culture

🌆 Community-acquired pneumonias, which usually are caused by 🏮 gram-positive species

Dx:

The radiographic appearance of pneumonia may be difficult to differentiate from atelectasis or early ARDS. Classically, pneumonia first appears as patchy opacifications or ill-defined nodules. It is often multifocal and bilateral, occurring most often in the gravity dependent areas of the lung. This feature makes it difficult to distinguish from atelectasis or pulmonary edem. E-coli and pseudomonas species can rapidly involve the entire lung. Their symmetric pattern often simulates pulmonary edema. The presence of patchy air space opacities, air bronchograms, ill-defined segmental consolidation or associated pleural effusion support the diagnosis of pneumonia. Occassionally, in gram-negative pneumonias small luciencies may be found within consolidated lung which may represent unaffected acini or areas of air trapping. This is particularly likely to occur in patients with underlying COPD. However, these must be distinguished from lucencies created by cavitation and abscess formation.

Cx: Complications of nosocomial pneumonias can have severe consequences and require immediate attention. Unlike community acquired pneumonia, pleural effusions caused by gram-negative organisms are more likely to represent empyema and therefore require drainage. Other complications of nosocomial pneumonias include lung abscess formation and bronchopleural fistulas.

In consolidative pneumonia, the alveoli become filled with inflammatory exudate, leading to marked impairment of alveolar ventilation in that portion of the lung. The result is right-to-left intrapulmonary shunting, which describes perfusion of lung tissue in the absence of alveolar ventilation, an extreme form of ventilation/perfusion (V/Q) mismatch (V≈0). A characteristic of intrapulmonary shunting is inability to correct hypoxemia with increased concentration of inspired oxygen (FiO2). Other causes of V/Q mismatch (eg, emphysema, interstitial lung disease, pulmonary embolism) allow for correction of hypoxemia with an increase in FiO2 because V > 0. In practice, increased FiO2 typically leads to some improvement in hypoxemia in patients with pneumonia because only a portion of the lung is being affected by intrapulmonary shunting.

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3
Q

🏇🏿 Pneumococcal Pneumonia

A

α-Hemolytic streptococci

🏇🏿Streptococcus Pneumonia

💪🏿PR/MDR Pneumococcal Pneumonia​

Hx: Age >65 y, β-lactam therapy (in previous 3 mo), alcoholism, immunosuppression (illness, glucocorticoids), multiple medical comorbidities, exposure to a child in a day care center.

Dx: CA-MRSA or compatible sputum Gram stain

Tx: Add vancomycin or linezolid to β-lactamb plus either azithromycin or a fluoroquinolone.

Patients with bacteremic pneumococcal pneumonia should be discharged on oral amoxicillin to complete 7 days of therapy.

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4
Q

Organizing pneumonia

A

Subacute illness (4-6 wk) with fever and alveolar infiltrates (often peripheral). Diagnosis is based on biopsy (transbronchial or open lung) or characteristic clinical picture and response to glucocorticoids.

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5
Q

Pneumocystis pneumonia (PCP)

A

Clinical

  • Indolent (HIV) or acute respiratory failure (immunocompromised)
  • Fever, dry cough, ↓ oxygen levels

HIV infection with a low CD4 count is the biggest risk factor; however, patients taking 🌚chronic glucocorticoids (especially in combination with other immunosuppressant medications) are at significant risk.

Workup

  • ↑ LDH level
  • Diffuse reticular infiltrates on imaging
  • Induced sputum or BAL (stain)

Treatment

  • TMP-SMX
  • Prednisone if ↓ oxygen levels

Prevention

  • TMP-SMX
  • Antiretrovirals (in HIV)

Hx: Subacute onset of dyspnea on exertion, hypoxia, nonproductive cough; diffuse interstitial infiltrates on chest radiograph

Dx: Chest x-ray usually shows bilateral interstitial infiltrates. Hypoxia out of proportion to the radiographic findings is also suggestive. Serum lactate dehydrogenase levels are frequently elevated. The diagnosis is confirmed by demonstration of the organism in sputum or bronchoalveolar lavage aspirate.

Tx: Trimethoprim-sulfamethoxazole (TMP-SMX) is the initial drug of choice for the treatment of PCP regardless of pneumonia severity. Treatment typically lasts for 21 days. Adjunctive corticosteroids have been shown to decrease mortality in cases of severe PCP (possibly by reducing inflammation due to dying organisms). Indications for corticosteroid use include partial pressure of oxygen (PaO2) <70 mm Hg or an alveolar-arterial (A-a) gradient >35 mm Hg on room air. This patient has a PaO2 of 54 mm Hg on room air, indicating the need for corticosteroid use.

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6
Q

🌆 Community Acquired Pneumonia (CAP)

A

🏇🏽Streptococcus pneumoniae causes the majority of cases, likely due to increased rates of colonization and impaired immunity against encapsulated bacteria.

Dx: Sputum gram stain and Culture. A Gram stain that shows gram-positive lancet-shaped diplococci intracellularly is good evidence for pneumococcal infection.“Rusty sputum” is classic for pneumococcal pneumonia but may not always be present.

Severe CAP, defined as CAP in a patient who requires admission to an intensive care unit or transfer to an intensive care unit within 24 hours of admission. Blood cultures, Legionella and Streptococcus pneumoniae urine antigen assays, and endotracheal aspirate for Gram stain and culture are recommended for hospitalized patients with severe CAP.

IDSA/ATS Minor Criteria for Severe Community-Acquired Pneumonia

Clinical Criteria

  • Confusion (new-onset disorientation to person, place, or time)
  • Hypothermia (core temperature <36.0°C [96.8°F])
  • Respiration rate ≥30 breaths/mina
  • Hypotension necessitating aggressive fluid resuscitation
  • Multilobar pulmonary infiltrates

Px: When a portion of the lung is consolidated (eg, lobar pneumonia), the density of tissue/fluid increases and dullness to percussion is detected. In addition, sound conducts more rapidly through the consolidated lung, resulting in increased intensity of breath sounds and a more prominent expiratory component. More rapid sound conduction also results in increased tactile fremitus as well as egophony (sounds like the letter “A” when the patient says the letter “E”) in areas of lung consolidation. Crackles are also often heard.

Laboratory Criteria

  • Arterial PO 2/FIO 2 ratio ≤250a
  • Leukopenia (<4000 cells/µL )
  • Thrombocytopenia (<100,000 platelets /µL)
  • Blood urea nitrogen >20 mg/dL

CURB-65 Identifies ❗high-risk patients and to predict a complicated course. Patients who meet at least two criteria are usually admitted to the hospital (mortality rate 8.3%), and those with at least three criteria are considered for intensive care unit (ICU) admission (mortality rate 20%).

Confusion, blood Urea nitrogen >20 mg/dL, Respiration rate ≥30 breaths/min, systolic Blood pressure <90 mm Hg OR diastolic blood pressure <60 mm Hg, and age ≥65 years)

Tx: Pneumococcal 💉vaccination is recommended for all patients with HIV to reduce the risk of invasive S pneumoniae disease. Empirical antibiotic therapy becomes more difficult in community-acquired pneumonia as more pathogens a re recognized and as the pneumococcus develops resistance to penicillin, macrolides, and even quinolones.

(Outpatient): 🐦Macrolide (azithromycin, clarithromycin, or erythromycin) or doxycycline

Risk factor(s) for drug-resistant S. pneumoniae or underlying comorbidities

Respiratory fluoroquinolone (moxifloxacin, gemifloxacin, or levofloxacin) or β-lactam plus a macrolide or doxycycline

Tx: (Inpatient):

Medical ward

β-lactam plus a macrolide or doxycycline; or respiratory fluoroquinolone (eg, moxifloxacin, gemifloxacin or levofloxacin)

Intensive care unit

β-lactam plus either azithromycin or a fluoroquinolone; if penicillin allergic, a respiratory fluoroquinolone plus aztreonam

Modifying Factors That Increase the Risk of Infection With Specific Pathogens

Age >65 y, β-lactam therapy (in previous 3 mo), alcoholism, immunosuppression (illness, glucocorticoids), multiple medical comorbidities, exposure to a child in a day care center

Penicillin-resistant and drug-resistant pneumococci

Residence in an extended care facility, underlying cardiopulmonary disease, multiple medical comorbidities, recent antibiotic therapy

Enteric gram-negative bacteria

Pseudomonas aeruginosa 🛀🏿

Structural lung disease (bronchiectasis), glucocorticoids therapy, broad-spectrum antibiotic therapy for >7 d; malnutrition

Dx: 🧞‍♀️Pseudomonas aeruginosa or 🏮gram-negative rods on sputum Gram stain

Tx: Antipseudomonal β-lactam with pneumococcal coverage (eg, cefepime, imipenem, meropenem, or piperacillin-tazobactam) ➕ ciprofloxacin or levofloxacin (750 mg) OR antipseudomonal β-lactam with pneumococcal coverage plus an aminoglycoside plus azithromycin; or antipseudomonale β-lactam with pneumococcal coverage plus an aminoglycoside plus a respiratory fluoroquinolone

Endobronchial obstruction (tumor)

Anaerobes, Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus

💉Intravenous drug use

Anaerobes, S. aureus, Mycobacterium tuberculosis, S. pneumoniae

Influenza epidemic in the community

Influenza virus, S. pneumoniae, S. aureus, H. influenzae

COPD, 🚬 smoking history

S. pneumoniae, H. influenzae, Moraxella catarrhalis, P. aeruginosa, Legionella species, Chlamydophila

Poor 🦷dental hygiene, aspiration, lung abscess

Oral anaerobes

Animal exposure

Coxiella burnetii (farm animals); Chlamydophila psittaci, Cryptococcus (birds); Histoplasma (birds, bats)

PR/MDR 💪🏿Pneumococcal Pneumonia

Hx: Age >65 y, β-lactam therapy (in previous 3 mo), alcoholism, immunosuppression (illness, glucocorticoids), multiple medical comorbidities, exposure to a child in a day care center.

Dx: CA-MRSA or compatible sputum Gram stain

Tx: Add 🚐vancomycin OR 🚧 linezolid to β-lactamb ➕ either 🐦azithromycin or a fluoroquinolone.

Patients with bacteremic pneumococcal pneumonia should be discharged on oral amoxicillin to complete 7 days of therapy.

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7
Q

Sinusitis

Rhitnitis

A

Hx: Facial pain, headache, pressure that incresaes when bending forward, purulent nasal discharge, pus in the nasal cavity, unilateral sinus pain or tenderness, maxillary toothache.

Allergic rhinitis is present in at least 60% of people with recurrent sinusitis.

Dx: sinus CT is rarely necessary (12 weeks)

Tx: Largely symptomatc;

First-generation antihistamine (diphenhydramine)[Benadryl]

Intranasal antihistamine (azelastine, olopatidine)

Intranasal glucocorticoids (Fluticasone [Flonase],

Topical decongestants (Afrin; oxymetazolam) have all been shown to be helpful. Topical decongestants should be limited to a few days of use to avoid rebound rhinitis (rhinitis medicamentosa).

Also try: sinus rinses, inhalation oh humidified air, and adequate hydration.

Criteria for Abx:

  • symptoms for 10-14 days
  • colored discharge
  • sinus pain

Purulent rhinorrhea, purulent secretions in the nasal cavity, tooth pain, and a biphasic history (worsening of symptoms after an initial period of improvement) have been found to be associated with bacterial sinusitis.

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8
Q

Acute bacterial rhinosinusitis

A

Clinical features

  • Cough, nasal discharge
  • Fever
  • Face pain/headache

Diagnostic criteria (1 of 3)

  • Persistent symptoms ≥10 days without improvement
  • Severe onset (fever ≥39 C [102.2 F] + drainage) ≥3 days
  • Worsening symptoms following initial improvement

Treatment

  • Amoxicillin ± clavulanate

Viral URI symptoms typically self-resolve in 7-10 days. In contrast, ABRS is diagnosed by any 1 of the following 3 criteria:

  • Symptoms (eg, cough, congestion) persist for ≥10 days without improvement.

OR

  • Symptoms severe in onset (fever ≥39 C [102.2 F] + drainage) for ≥3 days.

OR

  • Symptoms worsen following initial improvement (ie, biphasic illness). Fever may be absent.

Most cases are due to nontypeable Haemophilus influenzae or Streptococcus pneumoniae. Worsening symptoms (eg, progressive cough ± fever), as seen in this patient, are treated with oral antibiotics (eg, amoxicillin ± clavulanate) at the time of diagnosis. In contrast, in patients with persistent but not worsening symptoms and a milder course, oral antibiotics or a 3-day period of observation for clinical improvement are both acceptable treatment options.

Cx:

Untreated ABRS can lead to life-threatening complications such as periorbital/orbital cellulitis due to orbital extension as well as meningitis or brain abscess due to intracranial extension.

Intracranial complications should be suspected in patients with persistent headache and early-morning vomiting, which occurs due to increased intracranial pressure in the recumbent position. Other findings may include altered mental status (eg, drowsiness), neck pain (suggestive of meningeal irritation), and focal neurologic deficits.

The next step in management is urgent imaging of the brain, orbits, and sinuses. Although MRI is more sensitive, CT scan is faster and can detect early cerebritis; a ring-enhancing lesion confirms the diagnosis. Treatment is intravenous antibiotics and surgical drainage.

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9
Q

Influenza

A

Influenza virus is largely a winter infection that attacks the epithelium of the upper and lower respiratory tract. Approximately 1-5 days after exposure, patients abruptly develop systemic (fever, malaise, myalgias, headache) and upper/lower respiratory (rhinorrhea, sore throat, nonproductive cough) symptoms. Physical and laboratory examinations are often normal but may show pharyngeal erythema (without exudates) and mild alterations in leukocyte count (low early, high later). Most patients recover spontaneously and completely within 1 week of symptom onset. However, patients with advanced age (>65) and chronic medical illness (eg, coronary artery disease, diabetes mellitus) are far more likely to develop complications.

Sudden onset of high fever (body temperature >39°C [102°F]), severe myalgia, and headache.

Coryza, body temperature up to 41.0°C (105.8°F), myalgia, headache, and sore throat.

Severity of symptoms associated with high fever and myalgia suggest influenza.

Outbreak: In institutional settings such as nursing homes, outbreaks are likely to be particularly severe. Thus, prophylaxis is extremely important in this setting. All residents should receive the influenza vaccine unless they have known egg allergy (patients can choose to decline the vaccine). Since protective antibodies to the vaccine will not develop for 2 weeks, oseltamivir can be used for protection against influenza A during the interim 2-week period. Because of increasing resistance, amantadine is no longer recommended for prophylaxis. The best way to prevent influenza-associated pneumonia is to prevent the outbreak in the first place.

Cx: Pneumonia is the most common complication of influenza and is the result of either secondary bacterial infection (eg, Streptococcus pneumoniae) or direct viral attack (influenza pneumonia). Patients with primary influenza pneumonia typically have an acute worsening of symptoms (dyspnea, cough), leukocytosis (although <15,000/mm3), hypoxia, and bilateral, diffuse interstitial infiltrates on chest x-ray.

Tx: Hospitalization with supplemental oxygen support and antiviral (eg, oseltamivir) treatment is usually required. Influenza may also cause complications in the muscle (myositis, rhabdomyolysis), heart (myocarditis, pericarditis), and central nervous system (encephalitis, transverse myelitis).

Adults at high risk for influenza complications

  • Age >65
  • Women who are pregnant & up to 2 weeks postpartum
  • Underlying chronic medical illness (eg, chronic pulmonary, cardiovascular, renal, hepatic)
  • Immunosuppression
  • Morbid obesity
  • Native Americans
  • Nursing home or chronic care facility residents
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10
Q

Actinomycosis

A

Characterized by cough, hemoptysis, and (eventually) draining sinuses. Has an indolent course; patients may have respiratory symptoms for up to 5 mo before diagnosis. Sulphur granules are seen in stained specimens from draining sinuses.

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11
Q

Blastomycosis

A

Blastomycosis is a fungal infection that occurs most often in the vicinity of the Great Lakes, 🗺 Mississippi river and Ohio River basins (Wisconsin has the highest infection rate). The pulmonary symptoms and chest x-ray findings of

Blastomycosis presents with signs and symptoms of chronic respiratory infection.

Systemic Blastomycosis may cause characteristic raised, ulcerated skin lesions and lytic bone lesions. The skin lesions in exposed areas become crusted, ulcerated, or verrucous.

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12
Q

Aspergillus

A

A ubiquitous fungus that most people encounter daily. Conidia are inhaled into the lung and convert to potentially pathogenic hyphae. Patients with immunocompetency rapidly clear the organism and rarely develop infection; however, a subset of immunocompetent patients with a history of pulmonary disease (eg, cavitary tuberculosis) may develop chronic pulmonary aspergillosis (CPA) at sites of lung damage. Diagnosis is made by the presence of all 3 of the following:

>3 months of symptoms - fever, weight loss, fatigue, cough, hemoptysis, and/or dyspnea

Cavitary lesion(s) containing debris, fluid, or an aspergilloma (fungus ball)

Positive Aspergillus IgG serology

Tx: Therapy depends on symptoms and severity of disease; antifungal medication (eg, itraconazole, voriconazole), surgery (to prevent hemoptysis), and bronchial artery embolization (for hemoptysis with extensive disease) may be used together or separately.

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13
Q

Histoplasmosis

A

Histoplasmosis is an endemic mycosis of the central and midwestern United States that rarely causes illness in immunocompetent individuals but may occasionally cause subacute pulmonary symptoms (<5%).

Histoplasma capsulatum (present as mold in soil and in bird and bat droppings) is endemic to the Mississippi and Ohio River basins. In an appropriate epidemiologic setting, pulmonary histoplasmosis should be considered when pulmonary symptoms are accompanied by mediastinal or hilar lymph nodes (or masses) or by arthralgias and erythema nodosum.

Cx: ❗ Disseminated histoplasmosis in immunocompromised patients can present with lymphadenopathy, pancytopenia, and hepatosplenomegaly as the organism targets histiocytes and the reticuloendothelial system.

Caseating granulomas are most common, but non-caseating granulomas may be the only finding. Careful fungal tissue stains and culture, along with Histoplasmaurinary antigen testing, are used for diagnosis.

Small dose inoculation is rarely symptomatic (<5% become ill); patients who inhale larger doses (eg, exposure in enclosed areas such as a cave) are at higher risk for symptomatic infection. Symptoms usually present 2-4 weeks after exposure with subacute fever, chills, malaise, headache, myalgias, and dry cough.

Chest x-ray typically reveals mediastinal or hilar lymphadenopathy (LAD) with focal, reticulonodular, or miliary infiltrates (depending on the degree of exposure).

Diagnosis is usually made with Histoplasma antigen testing of the urine or blood, plus serology. Some patients may require tissue diagnosis, which often reveals granulomas with narrow-based budding yeasts. Most cases resolve completely (over weeks) without intervention. For patients with moderate or severe disease, oral itraconazole or intravenous liposomal amphotericin B can be used.

Dx: Chest radiography may show a miliary (eg, histoplasmosis) or cavitary lesion.

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14
Q

Coccidioides

A

Coccidioides is an endemic mold of the desert southwest whose spores are easily aerosolized in the dry months after a rainy season. Inhalation of a single arthroconidium is sufficient to cause infection (usually 7-14 days after inoculation). Symptoms may be subclinical, but many patients (>50%) develop community-acquired pneumonia (CAP) (fever, chest pain, productive cough, lobar infiltrate) often accompanied by arthralgias, erythema nodosum, or erythema multiforme. This clinical syndrome is also called Valley Fever, and symptoms frequently last weeks or months.

Diagnosis should be suspected in any patient living in or traveling to an endemic region (particularly Arizona or California) who has a lower respiratory illness lasting >1 week. Confirmation primarily relies on serologic testing, but cultures are often sent.

Tx: Most patients who are otherwise healthy and have mild or moderate disease do not need antifungal treatment and can have regular follow-up to ensure resolution. However, patients with severe disease or certain risk factors (eg, HIV, immunosuppressive medications, diabetes mellitus) are much more likely to develop dissemination (bones, central nervous system, skin); these patients require antifungal treatment (eg, ketoconazole, fluconazole).

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15
Q

👩🏿‍🚒Adrenal crisis

A
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16
Q

Allergic rhinitis

A

Seasonal nasal symptoms, including clear rhinorrhea and watery, itchy eyes. Patients may have a history of asthma.

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17
Q

Behçet disease

A

Behçet disease is an uncommon systemic disease with genital ulcers as one component; the ulcers are often painful. Other features include recurrent oral aphthous ulcers, uveitis, pathergy, arthritis, gastrointestinal manifestations, and central nervous system disease. In Behçet disease, serologic tests for syphilis will be negative.

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18
Q

Campylobacter spp.

A

Poultry, raw milk, travel history

Reactive arthritis can occur after Shigella, Salmonella, and Campylobacter infections.

Guillain-Barré syndrome is associated with Campylobacter and Yersinia infections.

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19
Q

💊 Cephalosporins

A

First generation Active against most gram-positive cocci (including penicillinase-producing staphylococci).

Cefazolin (Ancef, Kefzol) IV

Cephalexin (Keflex, Biocef, Keftab) PO

Second generation greater activity against certain gram-negative bacilli; specifically, one subgroup of second-generation cephalosporins has enhanced activity against H. influenzae

Cefuroxime (Kefurox, Zinacef)

Cefotetan (Cefotan)

Cefoxitin (Mefoxin)

Third generation​ The third-generation cephalosporins are less active against most gram-positive organisms than the first-generation cephalosporins. Highly active against Enterobacteriaceae (E. coli, Proteus mirabilis, indole-positive Proteus, Klebsiella, Enterobacter, Serratia, Citrobacter), Neisseria, and H. influenzae. They are the therapy of choice for gram-negative meningitis due to susceptible Enterobacteriaceae.

Ceftriaxone (Rocephin) has the longest serum half-life of this group (6.4 hours) and can be administered once or twice a day.

Cefotaxime (Claforan)

Ceftazidime (Fortaz) 🧞‍♀️

Fourth generation

Cefepime (Maxipime) 🧞‍♀️

Advanced generation and combination agents

Ceftaroline (Teflaro) improved gram-positive activity. activity against MRSA,

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20
Q

Fluoroquinolones

A

Fluoroquinolones upregulate cell matrix metalloproteases, leading to increased collagen degradation; this mechanism is likely responsible for several associated adverse effects, including Achilles tendon rupture, retinal detachment, and aortic aneurysm rupture.

The increased risk of aortic aneurysm rupture with fluoroquinolones is small overall, but it warrants serious consideration due to the high morbidity and mortality of rupture. Hence, when possible, these drugs should be avoided in patients with known aortic aneurysm or substantial risk factors for aortic aneurysm (eg, Marfan syndrome, Ehlers-Danlos syndrome, advanced atherosclerotic disease, uncontrolled hypertension).

Other adverse effects of fluoroquinolones that are likely unrelated to collagen degradation include encephalopathy, peripheral neuropathy, and QT-interval prolongation.

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21
Q

🦠 Chlamydia / Gonorrhea

A

Acute cervicitis is most commonly caused by Chlamydia trachomatis and Neisseria gonorrhoeae. Infection by these pathogens is most prevalent in women age <25. Acute cervicitis is diagnosed clinically by a pelvic examination that shows a mucopurulent discharge and a friable cervix (eg, bleeds easily on contact). Treatment is empiric with azithromycin and ceftriaxone, but nucleic acid amplification testing should also be performed for infection confirmation.

Risk factors

  • Age <25
  • High-risk sexual behavior

Manifestations

  • Asymptomatic (most common)
  • Cervicitis
  • Urethritis
  • Perihepatitis (Fitz-Hugh-Curtis syndrome)

Mucopurulent cervicitis with exacerbation during and after menstruation is classic gonorrhea.

Diagnosis

  • Nucleic acid amplification testing

Treatment

  • Empiric: 🐦Azithromycin + 🔨ceftriaxone (Rocephin)
  • Confirmed Gonorrhea: 🐦Azithromycin + 🔨ceftriaxone OR 🌼 floroquinolone
  • Confirmed Chlamydia: 🐦Azithromycin OR 🎡Doxycycline (Ceftriaxone is NOT for Chlamydia)
    • Azithromycin 1 g orally, given in a single dose or doxycycline 100 mg orally twice daily for 7 d

👓 Spectinomycin is the treatment of choice for pregnant women who have asymptomatic N. gonorrhoeae infections and who are allergic to penicillin. 🐓 Erythromycin is another drug that is effective.

Complications

  • Pelvic inflammatory disease
  • Ectopic pregnancy
  • Infertility
  • Pharyngitis

Tx:

Gonorrhea would be described as a ⚪ clearer cervical discharge (“not so mucopurulent”) and excluded by a gram stain with culture.

Chlamydia generates a mucopurulent 💛 yellow cervical discharge

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22
Q

Disseminated gonococcal infection

A

Disseminated gonococcal infection

  • Purulent monoarthritis OR Triad of tenosynovitis, dermatitis, migratory polyarthralgia

Diagnosis

  • Detection of Neisseria gonorrhoeaein urine, cervical, or urethral sample
  • Culture of blood, synovial fluid (less sensitive)

Treatment

  • 3rd-generation cephalosporin IV AND oral azithromyci

Migratory joint symptoms and often have involvement of several joints with tenosynovitis.

Skin lesions are found in more than 75% of patients with DGI but may be few in number; consequently. Lesions are most likely to be found on the extremities. The classic lesion is characterized by a small number of necrotic vesicopustules on an erythematous base.

Dx: Nucleic acid amplification urine test (NAAT) for Neisseria gonorrhoeae is a noninvasive, sensitive test for diagnosing gonorrhea in men. This test provides rapid results (within hours) and can help to guide therapy pending return of blood and synovial fluid culture results.

Mucosal cultures, including of the throat, anus, urethra, or cervix (in women), may also be helpful in establishing the diagnosis.

Tx: Infection of cervix, urethra, or rectum:

Ceftriaxone 125 mg IM, given in a single dose, PLUS either azithromycin 1 g orally in a single dose or doxycycline 100 mg orally twice daily for 7 days

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23
Q

Trachoma

A

Trachoma is due to Chlamydia trachomatis serotypes A, B, and C and is the leading cause of blindness worldwide. C trachomatis spreads effectively in crowded or unsanitary conditions. The active phase is most common in children and is characterized by follicular conjunctivitis and pannus (neovascularization) formation in the cornea. There is often a concomitant nasopharyngeal infection (eg, rhinorrhea, pharyngitis). Repeated or chronic infection leads to scarring of the eyelids and inversion of the eyelashes (trichiasis). Over time, the lashes rub on the eye and cause ulcerations and blindness (cicatricial trachoma).

The diagnosis can be made clinically by examination of the tarsal conjunctivae. C trachomatis may be visible by Giemsa stain examination of conjunctival scrapings. Oral azithromycin is effective against C trachomatis; in general, the entire region (eg, village, refugee camp) should be treated simultaneously. For individuals with trichiasis, eyelid surgery is needed to preserve vision.

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24
Q

Reactive arthritis

A

Reactive arthritis is a type of seronegative spondyloarthropathy. Reactive arthritis occurs in both men and women, and enthesitis and oligoarthritis are common.

Classic reactive arthritis consists of a triad of nongonococcal urethritis, asymmetric oligoarthritis and conjunctivitis. The arthritis often involves the knee and sacroiliac spine.

Hx: The classic triad of arthritis, urethritis, and conjunctivitis occurs in only about one third of patients.

Manifests within 2 months of an episode of bacterial gastroenteritis or n_ongonococcal urethritis_ or cervicitis in a genetically predisposed patient.

Reactive arthritis was previously called Reiter syndrome, which referred to the coincidence of arthritis, conjunctivitis, and urethritis (or cervicitis). However, only about one third of patients have all three symptoms.

Reactive arthritis usually affects the peripheral joints, often in the lower extremities, although inflammatory back pain also may be present.

Patients may also present with heel pain with enthesitis; keratoderma blennorrhagicum on the palms or soles; or circinate balanitis on the penis.

Differs from rheumatoid arthritis in that it is oligoarticular and asymmetric?

Presents as symmetric? inflammatory oligoarthritis, most often involving weight-bearing joints; may include tendon insertion inflammation (enthesitis).

Extra-articular manifestations include conjunctivitis, urethritis, stomatitis, and psoriaform skin changes (hyperkeratotic lesions on the palms and soles). Infection with Salmonella, Shigella, Yersinia, Campylobacter, or Chlamydia species within 3 wk prior to onset of initial attack.

Synovial fluid analysis is usually sterile. 🧯 Nonsteroidal anti-inflammatory agents (NSAIDs) are the first line therapy during the acute phase of this condition.

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25
Q

🐱 Congenital Toxoplasmosis

A

Toxoplasmosis, a protozoal infection caused by T. gondii

Risk factors

  • Undercooked (or cured) meat (particularly common in Europeans)
  • Unwashed produce
  • Unprotected handling of cat feces (hosts the protozoan oocytes).

Ultrasound findings

  • Bilateral ventriculomegaly
  • Diffuse intracranial calcifications

Clinical features

  • Chorioretinitis
  • Hydrocephalus
  • Seizures
  • Intellectual disability
  • Sensorineural hearing loss

Maternal infection can be asymptomatic, but those with symptoms typically have mild fever and a diffuse, nonpruritic, maculopapular rash that resolves spontaneously in a few days. Although the infection is mild in mothers, transplacental (vertical) transmission can occur and result in devastating fetal infection. T gondii preferentially destroys fetal neural tissue, which results in the ultrasound findings of bilateral ventriculomegaly and intracranial calcifications (particularly within the basal ganglia). Additional ultrasound findings may include low birth weight, hepatosplenomegaly, jaundice, anemia, neurological disease
with seizures, intracranial calcifications, and mental retardation.

Diagnosis

  • Maternal: Serology
  • Fetal: Amniotic fluid PCR

Fetal patients with the above clinical findings undergo amniocentesis for T gondii polymerase chain reaction testing of amniotic fluid.

Treatment

  • Spiramycin

Prenatal antitoxoplasma therapy (eg, spiramycin, pyrimethamine/sulfadiazine/folinic acid) may decrease the risk of neurologic sequelae (eg, chorioretinitis, seizures, intellectual disability).

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26
Q

Coxsackievirus

A

Coxsackievirus
can produce a morbilliform vesiculopustular rash, often with a hemorrhagic component and with lesions of the throat, palms, and soles.

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27
Q

Cryptococcus neoformans

A

Cryptococcus neoformans, an encapsulated yeast. Most cases are seen in patients with AIDS who have CD4 counts <100/mm2.

C neoformans replicates in the central nervous system and clogs the arachnoid villi with yeast components and capsular polysaccharides, leading to CSF outflow obstruction and increased intracranial pressure (ICP). Therefore, patients often develop progressive headaches, nausea/vomiting, and confusion.

Cx: In approximately 25% of cases, elevated ICP compresses the 6th cranial nerve (abducens nerve), leading to lateral gaze palsy and diplopia. Patients also frequently have fever, malaise, and umbilicated skin lesions that resemble molluscum contagiosum (due to hematogenous dissemination to the skin).

Brain imaging is usually normal but may show signs of increased ICP such as enlarged ventricles. The diagnosis is generally made with lumbar puncture (LP), measurement of CSF pressure, analysis of CSF, and capsular polysaccharide antigen testing or India ink stain. Management is with antifungal therapy. In addition, although caution should be exercised when performing an LP in the setting of increased ICP, patients with cryptococcal meningitis often require frequent (eg, daily) LPs and sometimes ventricular drains to decrease ICP.

Diagnosis is established through cryptococcal antigen testing of cerebrospinal fluid (CSF). CSF India Ink stain or culture on Sabouraud agar may also identify the organism. Other features include an elevated opening pressure, low glucose, high protein, and a lymphocytic pleocytosis (although white cells may be reduced in HIV patients). Increased intracranial pressure develops due to the occlusion of CSF flow by the organism. Neuroimaging is performed to exclude mass lesions, although C neoformans infection rarely causes mass lesions in patients with HIV. If no such lesion is found, a lumbar puncture can be performed; it both provides diagnostic confirmation and offers therapeutic value in the relief of elevated intracranial pressure. Some patients require serial lumbar punctures in addition to antifungal therapy to control intracranial pressure.

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28
Q

Cryptosporidiosis

A

Acute or chronic watery diarrhea in an immunocompromised patient; outbreak in a nursing home or day care center or on a cruise ship

1–8 d

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29
Q

Dengue fever

A

Dengue fever is characterized by fever, severe frontal headache, retro-orbital pain, and severe musculo-skeletal and lumbar back pain. A macular or scarlatiniform rash develops within 3 to 4 days of the illness. Virtually all cases respond to conservative measures with bleeding, hepatitis, and myositis reported as potential
rare complications.

Symptoms typically develop 4-7 days (and almost never >2 weeks) following the mosquito bite.

Dengue hemorrhagic fever is a more severe form of the disease. It is more common among infants and elderly people. It is characterized by increased
vascular permeability with hypovolemic shock and thrombocytopenia with spontaneous ecchymoses and mucosal bleeding. Dengue is a mosquito-borne illness.

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30
Q

Chikungunya

A

Chikungunya virus infection is more likely to cause high fever, severe arthralgia, arthritis, rash, and lymphopenia, whereas dengue virus infection is more likely to cause neutropenia, thrombocytopenia, hemorrhage, shock, and death. The diagnosis of dengue fever is established via polymerase chain reaction (PCR) or serology.

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31
Q

💩💩💩💦Diarrhea

Infectious (Acute) Diarrhea:

The most common cause of acute diarrhea is an infectious agent (>90% of cases).

Dx: Stool culture: Used selectively because of low yield (<3%);detects Salmonella, Shigella, and Campylobacter spp.; specify if needed to test for Escherichia coli O157:H7 (if visible or occult blood)

Stool ova and parasites: Microscopic examination for Giardia, Entamoeba, Cryptosporidium, Cyclospora, and Isospora spp. and microsporidia if suspected

Stool enzyme immunoassays: Detect Shiga toxins 1 and 2 and antigens for Giardia, Entamoeba, Campylobacter, Cryptosporidium spp. if suspected

Tx: For acute viral diarrhea, adults should be encouraged to eat potatoes, rice, wheat, noodles, crackers, bananas, yogurt, boiled vegetables, and soup. Dairy products, alcohol, and caffeine should be avoided.

Oral rehydrating solutions can be used if vomiting is a problem, and fasting is not indicated. Some fruit juices can exacerbate diarrhea.

A

Diarrhea is defined as more than three loose stools per day.

Diarrhea can be divided into 3 main categories: watery, fatty, and inflammatory.

Watery diarrhea can be further broken down into osmotic, secretory, and functional.

Secretory diarrhea include larger daily stool volumes (>1 L/day) and diarrhea that occurs even during fasting or sleep. Secretory diarrhea most commonly occurs when luminal ion channels are disrupted in the gastrointestinal tract, resulting in a state of active secretion.

Many patients confuse true diarrhea with three other conditions: pseudodiarrhea (the frequent passage of small volumes of stool), fecal incontinence, and overflow diarrhea caused by fecal impaction.

Acute diarrhea is present for less than 14 days, persistent diarrhea has been present for at least 14 days but 4 weeks or less, and diarrhea is considered to be chronic if it has been present for more than 4 weeks.

Although the vast majority of episodes of acute diarrhea are caused by viruses and are self-limited, further clinical evaluation is indicated in those who have bloody stools, body temperature greater than 38.5°C (>101.3°F), significant abdominal pain, severe diarrhea causing symptomatic dehydration, recent antibiotic use, a history of inflammatory bowel disease, or immunocompromised states; food handlers; the elderly; or pregnant women.

Because most episodes of diarrhea are self-limited, diagnostic testing generally is reserved for patients with severe diarrheal illness characterized by fever, blood in the stool, or signs of dehydration (weakness, thirst, decreased urine output, orthostasis) or patients with diarrhea lasting >7 days.

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32
Q

Echinococcus granulosus

A

Humans contract the infection from close and intimate contact with 🐶 dogs, which are the definitive host in the tapeworm’s lifecycle. E granulosus typically causes unilocular cystic lesions that can occur in any organ (eg, liver, lung, muscle, bone); smaller daughter cysts may be present. Multiple lesions are usually associated with E multilocularis (rather than E granulosus) infection.

Most hydatid cysts are diagnosed incidentally when patients are being evaluated for other problems (eg, fatty food intolerance likely from cholelithiasis). However, these cysts can cause symptoms due to compression on surrounding tissues. Imaging techniques and serologic testing can be used for diagnosis. “Eggshell” calcification of a hepatic cyst on CT scan is highly suggestive of a hydatid cyst.

Many patients remain asymptomatic for years and develop clinical illness only due to large cyst size (>10 cm) or rupture. Manifestations include right upper quadrant pain, nausea, vomiting, and hepatomegaly. Rupture may result in fever. Ultrasound has excellent sensitivity (~95%) and typically shows a large, smooth hepatic cyst often with daughter cysts (internal septations). Positive serology for E granulosusIgG corroborates the diagnosis (sensitivity ~95%) and usually obviates the need for percutaneous biopsy. Small cysts (<5 cm) are typically treated with albendazole; larger or complex cysts usually also require percutaneous therapy or surgery.

Treatment is generally surgical resection under the cover of albendazole. In some situations, aspiration can be performed, although there is a risk of anaphylactic shock due to cyst content spillage.

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33
Q

Entamoeba histolytica

A

Entamoeba histolytica is a protozoan common in developing countries and is transmitted through consumption of contaminated food and water. Approximately 10% of patients have clinical manifestations of colitis or extraintestinal (liver, pleura, brain) disease. Amebic liver abscess develops when E histolyticaspreads from the colonic mucosa to the liver via the portal vein.

Risk factors

  • Developing nations (travel/residence)
  • Contaminated food/water
  • Fecal-oral sexual transmission (rare)

Manifestations

  • 90% of patients asymptomatic
  • Colitis (diarrhea, bloody stool with mucus, abdominal pain)
  • Liver abscess (RUQ pain, fever)
    • Complications - rupture to pleura/peritoneum

Symptoms usually occur 2 to 5 months after travel to an endemic area. Diarrhea usually occurs first but has usually resolved before the hepatic symptoms develop. The most common presentation for an amebic liver abscess is abdominal pain, usually RUQ.

Diagnosis

  • Stool ova & parasites, stool antigen testing (colitis)
  • E. histolytica serology (liver abscess)
  • An indirect hemagglutination test is a sensitive assay and will be positive in 90% to 100% of patients.
  • 🔊 Ultrasound has 75% to 85% sensitivity and shows abscess with well-defined margins.

Treatment

  • Metronidazole & intraluminal antibiotic (eg, paromomycin)

Symptoms are subacute and include right upper quadrant (RUQ) pain and fever, sometimes with recent or concurrent bloody diarrhea (colitis). The pain is often dull and can be referred to the right chest wall or shoulder. Systemic symptoms (eg, anorexia, weight loss, cough) can occur, and hepatomegaly and elevations in leukocyte count, alkaline phosphatase, and transaminases are common. As with other protozoal infections (eg, giardiasis), peripheral eosinophilia is not a frequent finding (in contrast to many helminthic infections, which can stimulate IL-5 production). A characteristic imaging finding is a single, subcapsular, low-density lesion in the right lobe of the liver (due to greater portal blood supply compared with the left). Diagnosis is made with serology; needle aspiration is generally unnecessary.

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34
Q

Enteroadherent:

A

(Infecting organisms adhere to the gastrointestinal mucosa and compete with normal bowel flora)

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35
Q

Enterohemorrhagic E. coli

A

Ground beef, raw vegetables

12–72 h

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36
Q

Enteroinvasive (Bacterial Enteritis)

A

(Infecting organisms invade and destroy intestinal mucosa, resulting in bloody diarrhea)

Minimal Inflammation

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37
Q

Enteroinvasive E. coli

A

Routine stool culture cannot distinguish pathogenic E. coli from normal fecal flora. Therefore, in the setting of blood in the stool, test specifically for E. coli O157:H7

If symptoms have persisted beyond 7 days, stool should be examined for ova and parasites.

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38
Q

Enterotoxigenic Escherichia coli

A

Hx: Salads, cheese, meats

8–72 h

Tx: Although prophylactic antibiotics are not recommended for traveler’s diarrhea, empiric antibiotics (quinolones) may be appropriate for patients with symptoms. Untreated traveler’s diarrhea usually resolves in 3 to 5 days, but treatment can improve symptoms and shorten the course.

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39
Q

Enterotoxin

A

(Toxins produced by intestinal microbes that act directly on secretory mechanisms in the intestinal mucosa, causing watery diarrhea).

Approximately one-third of travelers to underdeveloped countries will develop travelers’ diarrhea. Of those, 40% will
alter their plans because of the symptoms, 20% will be bed-bound for at least 1 day, and 1% will require hospitalization. Most cases of travelers’ diarrhea are due to
enterotoxigenic E coli.

Tx: The antibiotic of choice for travelers’ diarrhea is a fluoroquinolone (ciprofloxacin, ofloxacin, or norfloxacin) with trimethoprim/sulfamethoxazole
or azithromycin being acceptable alternatives.

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40
Q

Epiglottitis

A

Epiglottitis is a rare, potentially fatal infection that presents with acute onset of fever, sore throat, and signs of upper airway obstruction (eg, stridor, drooling).

Severe sore throat with a benign-appearing oropharynx. Adults may have dyspnea, drooling, and stridor. Obtain urgent otolaryngology consultation, and do not attempt to examine the throat. A lateral neck film may show an enlarged epiglottis (“thumbprint sign”). Because of
the possibility of impending airway obstruction, the patient should be admitted to an intensive care unit for close monitoring. The most likely organism causing this infection is H influenzae.

X-ray is not required for diagnosis if clinical suspicion is high, but lateral view shows an enlarged epiglottis, suggestive of edema. Diagnosis is confirmed via direct visualization of an edematous epiglottis. However, detailed oropharyngeal examination is often deferred in children due to risk of laryngospasm from provoked aggravation. Direct laryngoscopy during intubation (a controlled setting to secure the airway) is often preferred for diagnosis and management.

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41
Q

Fever of unknown origin (FUO)

A

Fever of unknown origin (FUO) is applied when significant fever (usually defined as > 38.3°C or > 101°F) persists without a known cause after an adequate evaluation.

Systemic Inflammatory Disorders

One of the more common vasculitides is temporal arteritis, which can present as FUO in adults aged >50 years, even in the absence of the classic symptoms of headache, jaw claudication, or polymyalgia rheumatica. Other vasculitides (eg, granulomatosis with polyangiitis [Wegener granulomatosis]) and systemic inflammatory disorders (eg, systemic lupus erythematosus, adult-onset Still disease) should also be considered.

Malignancy

The most common FUO-associated malignancy is non-Hodgkin lymphoma. Renal cell carcinoma, any malignancy that metastasizes to the liver, and leukemia are other common causes.

Drug fever: Antibiotics can cause or prolong fever, creating confusion for the clinician. A common cause of drug fever is sulfonamide and β-lactam antibiotics and nitrofurantoin.

Dx:

Complete blood cell count with differential, peripheral blood smear

Comprehensive metabolic panel

Urinalysis and microscopy

Chest radiography

Blood and urine cultures

Antinuclear antibody and rheumatoid factor testing; ESR and total CRP

HIV antibody testing

For selected patients:

Viral serology in patients with mononucleosis-like syndrome (cytomegalovirus, heterophil)

Q fever serology (if exposure to farm animals)

Hepatitis serology (if abnormal liver enzyme levels)

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42
Q

Food Poisoning

A

Nausea and vomiting within 1 to 6 hours of consumption of food are caused by preformed toxins of B cereus and S aureus or heavy metals like copper or zinc.
Abdominal cramps and diarrhea that develop more than 8 hours after a meal are caused by C jejuni, E coli, Salmonella, Shigella, and Vibrio parahaemolyticus. It takes more than 8 hours for the bacteria to proliferate in the gut and initiate the infection. Watery diarrhea can also be caused by enterotoxigenic E coli, V cholerae, and Norovirus. Yersinia enterocolitica can cause fever and abdominal cramps without diarrhea—a presentation closely resembling acute appendicitis. Cryptosporidiosis, cyclosporiasis, and giardiasis cause diarrhea that can persist for 1 to 3 weeks.

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43
Q

Gastroenteritis

A

The Norwalk virus, reoviruses, and adenoviruses are common causes.

Generally, these illnesses are self-limited, and will resolve within 5 days.

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44
Q

Genital Herpes

A

Both HSV-1 and HSV-2 can cause primary genital infection, and the incidence of primary infection from HSV-1 has increased in recent years. HSV-1 genital infections are less likely to be associated with recurrences and subclinical viral shedding.

Dx: Confirmed by viral culture or polymerase chain reaction testing.

Tx: First clinical episode of genital herpes:

Acyclovir 400 mg orally three times daily for 7-10 d OR

Acyclovir 200 mg orally 5 times daily for 7-10 d OR

famciclovir 250 mg orally three times daily for 7-10 d OR

valacyclovir 1 g orally twice daily for 7-10 d

In recurrent HSV outbreaks, antiviral therapy is ideally started within 24 hours of onset and continued for 5 days.

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45
Q

🍑🍆 Genital Lesion

A

Genital warts and genital herpes are more common in
heterosexuals, with bacterial vaginosis being more common in lesbians. There is a mistaken belief that lesbians are not at risk for acquiring HIV. However, it has been shown that sexually active lesbians have a higher prevalence of HIV than women who have sex exclusively with men.

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46
Q

Giardia lamblia

A

Giardia duodenalis (sometimes noted as G lamblia or G intestinalis) is common in rural areas and developing countries, and has an incubation period of 1-2 weeks. It is most commonly transmitted by contaminated water but can be foodborne or transmitted person-to-person via a fecal-oral route.

Most patients are asymptomatic; however, a significant minority of those who do develop clinical illness may go on to develop chronic giardiasis characterized by malabsorption, weight loss, or persistent gastrointestinal distress.

Dx: The preferred confirmatory test for giardiasis is a stool antigen assay (direct immunofluorescence or ELISA). Stool microscopy for oocysts and trophozoites can also identify the organism and is useful in resource-poor settings or if other parasitic organisms are suspected. Some facilities also offer a nucleic acid amplification assay.

Tx: Metronidazole is the preferred treatment. Asymptomatic carriers do not usually need treatment. Patients who are not treated are at high risk for chronic malabsorption. 🍼 Lactose intolerance (due to brush border disruption) and fatty acid malabsorption (which causes the oily, malodorous stools) are the most common sequelae. Chronic malabsorption can lead to profound weight loss and vitamin deficiencies.

Cx: During the acute phase, giardiasis causes histologic changes in the small intestine (eg, disruption of the microvilli on enterocytes). This results in malabsorption and subsequent loose, oily stools; weight loss; and flatulence.

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47
Q

Heat Stroke

A

The first sign of serious heat stroke is the absence of sweating and warm, dry skin. Fans, cooling blankets, ice packs, cold intravenous fluids, and oxygen are used; for severe hyperthermia, cold gastric and peritoneal lavage is also used.

The findings of acute confusion, hyperthermia, tachycardia, and persistent epistaxis after exertion under direct sunlight are suggestive of exertional heat stroke. Heat stroke is defined by core temperature >40 C (104 F) and central nervous system dysfunction (eg, altered mental status).

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48
Q

Helminths

A

1–8 d

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49
Q

Herpes Zoster / Varicella

A

💥 Pain

Acute herpetic neuralgia

  • Persists ≤30 days from rash onset
  • NSAIDs, analgesics

Subacute herpetic neuralgia

  • Persists >30 days but resolves within 4 months of rash onset
  • NSAIDs, analgesics

Postherpetic neuralgia

  • Persists >4 months from rash onset
  • Tricyclic antidepressants, gabapentin, pregabalin

Acute zoster (shingles) is due to reactivation of the varicella zoster virus (VZV) and causes transient pain due to hemorrhagic inflammation of the sensory nerve. As viral replication diminishes, the skin lesions resolve and the pain typically fades; however, persistent pain for >4 months indicates PHN.

PHN occurs in approximately 5% of patients with shingles. The risk is greatest in those with advanced age, severe initial pain, or severe rash. The pain may be constant or intermittent and is typically associated with allodynia (pain elicited by nonpainful stimuli [eg, light touch]). Physical examination often reveals sensory abnormalities (eg, anesthesia, hyperesthesia) in the affected dermatome.

PHN often improves over time, but resolution may take years and the severity of pain usually warrants pharmacologic treatment. Anticonvulsants (primarily gabapentin and pregabalin) and tricyclic antidepressants (eg, amitriptyline) are the best-established drugs. Topical capsaicin and lidocaine are options for patients with mild to moderate pain. Opioids (eg, oxycodone) are also effective but are not preferred due to the expected duration of treatment and potential for dependence and abuse.

Cx: Varicella pneumonia develops in about 20% of adults with chickenpox. It occurs 3 to 7 days after the onset of the rash. The hallmarks of the chickenpox rash are papules, vesicles, and scabs in various stages of development. Fever, malaise, and itching are usually part of the clinical picture.

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50
Q

HIV

A

Hx: Symptoms of immunologic dysfunction, weight loss, generalized lymphadenopathy, fever and night sweats of >2 weeks’ duration, oral thrush, severe aphthous ulcers, severe seborrheic dermatitis, or oral hairy leukoplakia. Herpes zoster in a younger person, recurrent pneumonia, chronic diarrhea, or unexplained hematologic abnormalities (eg, anemia, leukopenia, thrombocytopenia, polyclonal gammopathy) should also prompt consideration of HIV infection.

In most cases, when HIV infection develops, an acute symptomatic illness occurs within 2 to 4 weeks of infection. Symptoms typically last for a few weeks and range from a simple febrile illness to a full-blown mononucleosis-like syndrome.

Dx:

HIV antibody antibody enzyme immunoassay (EIA)[ELISA] is the appropriate first test when screening for HIV infection.

Western blot assay if the EIA result is positive, this test has 99% sensitivity and specificity for the diagnosis of HIV infection. May occur and may diagnose HIV as early as 2 weeks after infection occurs. If negative, no further testing is indicated. If positive, supplemental testing is performed to determine virus type present (HIV-1 or HIV-2). If this follow-up testing is equivocal, HIV-1 nucleic acid testing is indicated.

Patients who present with symptomatic acute HIV infection (acute retroviral syndrome) are usually in the “window period,” which may extend for 3 to 6 weeks. During this time, seroconversion of the disease has not yet occurred and results of HIV antibody testing are negative.

Nucleic acid (NAAT)[HIV RNA][Viral specific test] are usually positive at quite high levels during this time frame and can be used to establish the diagnosis.

Dx: Routine monitoring of HIV-RNA and CD4 cell counts can be performed every 3 to 6 months in clinically stable patients with suppressed viral load.

Tx: Suppression of HIV viral load to less than 50 copies/mL should occur by 24 weeks of effective therapy. Virologic failure is suspected when suppression of viral replication to < 200 copies/mL cannot be achieved or maintained.

Cx:

Mucocutaneous candidiasis: Involves primarily the oropharynx and esophagus 200

Cryptococcosis: Cryptococcus neoformans is an invasive fungus acquired by the inhalation of spores that primarily causes pulmonary disease. Immunocompromised patients can develop central nervous system infection leading to meningoencephalitis. The classic presentation is indolent (eg, progressing over days to weeks), and neck stiffness and photophobia are absent in the majority of patients. Causes subacute ⛑ meningitis; often associated with cryptococcemia 100. Diagnosis is established through cryptococcal antigen testing of cerebrospinal fluid (CSF). CSF India Ink stain or culture on Sabouraud agar may also identify the organism.

Cryptosporidiosis: Persistent watery diarrhea

Cytomegalovirus is a common opportunistic pathogen in patients with AIDS who have very low CD4 counts (<50/mm3). It typically attacks the retina and the neurologic and gastrointestinal systems. Gastrointestinal CMV presents with fatigue, low-grade fever, weight loss, and frequent, low-volume stools that are often bloody. The diagnostic test of choice is a colonoscopy with biopsy (eosinophilic intranuclear and basophilic intracytoplasmic inclusions). Active CMV infection is treated with ganciclovir, although improvement and cure is unlikely if the patient does not also receive antiretroviral therapy. In all patients with active CMV, an ocular examination is required to rule out concurrent retinitis.

Kaposi sarcoma: Nontender, raised discrete purplish lesions, often on the lower extremities or intraoral; primarily in homosexual men coinfected with human herpesvirus 8. The color changes from light brown, to pink, to dark violet.

Lymphoma: Burkitt, large B-cell NHL, or primary CNS lymphoma

Mycobacterium tuberculosis: Pulmonary infection. Extrapulmonary manifestations more common if CD4 count <200 (0.20). Plx: Isoniazid and pyridoxine. Alternative: Weekly isoniazid and rifapentine direct observed therapy if not on ART when Induration of ≥5 mm on purified protein-derivative skin test or a positive interferon-γ release assay.

M. avium complex: Disseminated infection, often with liver and bone marrow involvement and diffuse adenopathy. Plx: Weekly 🐦azithromycin when CD4 count <50/µL

Pneumocystis pneumonia: Subacute onset of dyspnea on exertion, hypoxia, nonproductive cough; diffuse interstitial infiltrates on chest radiograph

Dx: Chest x-ray usually shows bilateral interstitial infiltrates. Hypoxia out of proportion to the radiographic findings is also suggestive. Serum lactate dehydrogenase levels are frequently elevated. The diagnosis is confirmed by demonstration of the organism in sputum or bronchoalveolar lavage aspirate.

Tx: Trimethoprim-sulfamethoxazole (TMP-SMX) is the initial drug of choice for the treatment of PCP regardless of pneumonia severity. Treatment typically lasts for 21 days. Adjunctive corticosteroids have been shown to decrease mortality in cases of severe PCP (possibly by reducing inflammation due to dying organisms). Indications for corticosteroid use include partial pressure of oxygen (PaO2) <70 mm Hg or an alveolar-arterial (A-a) gradient >35 mm Hg on room air. This patient has a PaO2 of 54 mm Hg on room air, indicating the need for corticosteroid use. Plx: Daily trimethoprim-sulfamethoxazole DS when CD4 count <200/µL (0.20 x 109/L).

Progressive multifocal leukoencephalopathy: Caused by JC virus (a human polyomavirus); white matter lesions seen on imaging; patient presents with focal neurologic defects including altered mental status

Toxoplasmosis: Fever, headache, focal neurologic deficits; multiple ring-enhancing lesions on CNS imaging; positive toxoplasma serology

Dx: All patients newly diagnosed with HIV should be tested for latent infection with serology for T gondii IgG antibody. If serology is positive and CD4 count is <100/mm3, primary prophylaxis with trimethoprim-sulfamethoxazole (TMP-SMX) reduces the risk of toxoplasmosis dramatically (to 0%-2%).

Tx: Plx: Daily trimethoprim-sulfamethoxazole DS when CD4 count <100/µL (0.10 x 109/L) and toxoplasma seropositive. Patients on antiretroviral treatment can discontinue TMP-SMX when CD4 count is >200/mm3 for 3 months (and there is adequate viral suppression). TMP-SMX is also used for primary prophylaxis against Pneumocystis pneumonia.

Acyclovir or valacyclovir can be used to prevent herpes simplex virus recurrences. It is used for patients with severe or frequent recurrences (secondary prophylaxis) regardless of CD4 count. This patient is not experiencing recurrences. Fluconazole is effective therapy for candidiasis.

Bacillary angiomatosis is caused by Bartonella, a Gram-negative bacillus. Bright red, firm, friable, exophytic nodules in an HIV infected patient are most likely bacillary angiomatosis. Tx: Oral erythromycin is the antibiotic of choice.

Tx: Preferred initial combination therapy for treatment-naïve patients usually involves a “backbone” that consists of two nucleoside/nucleotide reverse transcriptase inhibitors. (The fixed combination of emtricitabine/tenofovir is often a first choice.) The backbone is combined with a “base” that consists of either a nonnucleoside reverse transcriptase inhibitor (typically efavirenz), an integrase strand transfer inhibitor (typically raltegravir), or one of two “boosted” protease inhibitors (typically atazanavir or darunavir combined with a second protease inhibitor ritonavir, which boosts the levels of the first by inhibiting the cytochrome P-450 system).

Side effect profile:

Nucleoside/nucleotide reverse transcriptase inhibitors: Lactic acidosis, hepatic toxicity, lipoatrophy, pancreatitis, peripheral neuropathy

Abacavir (preferred drug): Life-threatening hypersensitivity reaction, increased risk of myocardial infarction. Screen for HLA-B*5701 to reduce risk of hypersensitivity reaction.

Emtricitabine (preferred drug): Lactic acidosis, severe hepatic steatosis

Tenofovir (preferred drug): Nephrotoxicity: renal injury, Fanconi syndrome; osteopenia/osteoporosis

Nonnucleoside reverse transcriptase inhibitors: Hepatotoxicity, skin rash

Efavirenz (preferred drug): Sleep disturbance, depression, vivid dreams or hallucinations, possible teratogenicity

Rilpivirine: Rare rash

Protease inhibitors: GI upset (diarrhea), lipodystrophy, hepatotoxicity, dyslipidemia

Atazanavir (preferred drug): Jaundice (indirect hyperbilirubinemia), cholelithiasis, nephrolithiasis

Darunavir (preferred drug): Hypersensitivity reaction (especially those with sulfa allergy)

Fusion inhibitors: Enfuvirtide: Injection site reactions (itching/swelling/erythema), severe reactions, (sometimes with eosinophilia and signs of allergy)

Coreceptor antagonists: Maraviroc

Cough, fever, upper respiratory infections, rash, hepatotoxicity, musculoskeletal symptoms. Perform co-receptor tropism assay prior to use.

Integrase inhibitors: Raltegravir (preferred drug): Generally well tolerated. Commonly: headache, nausea, diarrhea. Rarely: rhabomyolysis, hypersensitivity reaction, depression

Dolutegravir: Headache, insomnia, hypersensitivity reaction

💉 All patients with HIV should receive the inactivated vaccines (influenza, tetanus-diphtheria-pertussis) recommended for the general population as well as those recommended specifically for people with HIV (pneumococcal, hepatitis B).

Patients with HIV should receive the following additional vaccines due to elevated risk:

  • Vaccination for hepatitis A is recommended for adults who are at increased risk of contracting the virus such as men who have sex with men and travelers to countries where hepatitis A is prevalent (eg, contaminated food or water consumption). It is also recommended for adults who have conditions (eg, chronic liver disease) that increase the risk for severe complications. In the United States, the hepatitis A vaccine became part of routine childhood vaccinations in 2006
  • They should receive vaccination for hepatitis B unless they have documented immunity.
  • They also should receive vaccination for Streptococcus pneumoniae with the 13-valent pneumococcal conjugate vaccine (PCV13), followed by the 23-valent pneumococcal polysaccharide vaccine (PPSV23) 8 weeks later and again in 5 years and at age 65.
  • Many experts also recommend varicella (ie, chickenpox) vaccine for adults with HIV born after 1979 who do not have evidence of immunity, provided that their CD4+ count is >200/mm3.
    • ❗ Patients with HIV with CD4 counts <200/mm3 should NOT receive live attenuated vaccinations (varicella, zoster, measles-mumps-rubella [MMR]).
  • The meningococcal vaccine, including boosters every 5 years, is recommended for all patients with HIV.

Cx: HIV-associated dementia usually affects deep gray matter structures and causes subacute cognitive, behavioral, and motor deficits. Imaging reveals cerebral atrophy with ventricular enlargement.

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51
Q

Progressive multifocal leukoencephalopathy

A

Epidemiology

  • JC virus reactivation
  • Severe immunosuppression (eg, untreated AIDS)

Manifestations

  • Slowly progressive
  • Confusion, paresis, ataxia, seizure

Diagnosis

  • CT brain – white matter lesions with no enhancement/edema
  • Lumbar puncture - CSF PCR for JC virus
  • Brain biopsy (rarely needed)

Treatment

  • Often fatal
  • If HIV – antiretroviral therapy

PML is a life-threatening neurologic disease that is caused by the reactivation of JC virus. JC virus is usually acquired in childhood and lies dormant in the kidneys and lymphoid tissue; most individuals remain asymptomatic, but those with severe immunocompromise (eg, HIV with CD4 count <200/mm3) are at risk for reactivation. Reactivated virus spreads to the central nervous system (CNS) and lyses oligodendrocytes, causing white matter demyelination.

Symptoms include altered mental status, motor deficits, ataxia, and vision abnormalities (eg, diplopia). CT of the brain with contrast usually reveals nonenhancing, hypodense white matter lesions with no surrounding edema. Diagnosis requires lumbar puncture with cerebral spinal fluid evidence of JC virus (by PCR). Brain biopsy is occasionally required. Patients with AIDS are treated with antiretroviral therapy; this may prevent death, but significant neurologic impairment often remains.

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52
Q

HIV during pregnancy

A

HIV management during pregnancy

Antepartum

  • HIV RNA viral load at initial visit, every 2-4 weeks after initiation or change of therapy, monthly until undetectable, then every 3 months
  • CD4 cell count every 3-6 months
  • Resistance testing if not previously performed
  • ART initiation as early as possible
  • Avoid amniocentesis unless viral load ≤1,000 copies/mL

Intrapartum

  • Avoid artificial ROM, fetal scalp electrode, operative vaginal delivery
  • Viral load ≤1,000 copies/mL: ART + vaginal delivery
  • Viral load >1,000 copies/mL: ART + zidovudine + cesarean delivery

Postpartum

  • Mother: Continue ART
  • Infant (maternal viral load ≤1,000 copies/mL): Zidovudine
  • Infant (maternal viral load >1,000 copies/mL): Multi-drug ART

The most important intervention for preventing the spread of HIV from mother to child is administration of combination antiretroviral therapy to the mother throughout pregnancy. Antiviral therapy should be initiated as soon as possible during pregnancy (even during the first trimester), regardless of maternal CD4 count or viral load. Antenatal combination therapy is the best way to suppress maternal HIV and prevent transplacental or perinatal acquisition by the infant. Mothers with undetectable viral loads at delivery have <1% risk of transmitting the infection to their infants. The 3-drug regimen should consist of 2 nucleoside reverse transcriptase inhibitors (NRTIs) plus a non-nucleoside reverse transcriptase inhibitor or a protease inhibitor. An NRTI with good placental transfer (eg, zidovudine, tenofovir) should be administered. Zidovudine should be administered to the neonate for >6 weeks.

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53
Q

Hypersensitivity pneumonitis

A

Recurrent episodes of fever and dyspnea, with rapid resolution of infiltrates; chronic infiltrates after multiple episodes. Diagnose with precipitating antibodies to the antigen (molds etc.), characteristic history, or open lung biopsy.

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54
Q

Infective Endocarditis

A

Hx: Injection drug use, recent procedures associated with risk of transient bacteremia, presence of a prosthetic valve, and certain cardiac abnormalities. Rheumatic fever

Symptoms suggesting septic emboli in patients with tricuspid valve endocarditis include shortness of breath, chest pain, and cough. Blindness, focal weakness, localized back or flank pain, hematuria, and gangrenous skin lesions may be embolic manifestations of left-sided infective endocarditis.

Px: New cardiac murmur, new-onset heart failure, focal neurologic signs, splenomegaly, and cutaneous manifestations (eg, petechiae, splinter hemorrhages). The presence of Osler nodes (violaceous, circumscribed, painful nodules found in the pulp of the fingers and toes) or Janeway lesions (painless, erythematous, macular lesions found on the soles and palms.

Dx: Leukocytosis, normocytic normochromic anemia, electrocardiographic conduction defects (atrioventricular block from extension of infection into the conduction system), hematuria, and low serum complement levels (eg, glomerulonephritis). CRX suggesting heart failure or septic emboli from right-sided endocarditis (eg, multiple bilateral small nodules on chest radiograph) raise suspicion for infective endocarditis.

Laboratory data include an elevated erythrocyte sedimentation rate. The ECG shows evidence of first-degree AV block. An antistreptolysin O antibody is necessary to document prior streptococcal infection.

Evidence of recent streptococcal infection plus two major manifestations or one major and two minor manifestations satisfy the Jones criteria for diagnosis of acute rheumatic fever.

Major criteria include ❤ carditis, polyarthritis, s. chorea, erythema marginatum, and subcutaneous nodules.

Minor manifestations include fever, polyarthralgia (Joints) elevated erythrocyte sedimentation rate, and PR prolongation on ECG.

💙 DUKE

Definite endocarditis = 2 MAJOR criteria OR 1 major + 3 minor criteria OR 5 minor criteria

Possible endocarditis = 1 major + 1 minor criterion or 3 minor criteria

DUKE MAJOR Criteria for Dx:

  1. Microbiologic (Bacteremia) - any of the following:

Typical microorganisms grown from 2/2 blood cultures

Staphylococcus aureus - Prosthetic valves, Intravascular catheters, Implanted devices (eg, pacemaker/defibrillator), Intravenous drug users.

Staphylococcus epidermidis - Prosthetic valves, Intravascular catheters, Implanted devices

Viridans group streptococci - 👄Gingival manipulation, Respiratory tract incision or biopsy

Streptococcus gallolyticus (S bovis) - Colon carcinoma 🦀, Inflammatory bowel disease 💩

Enterococci - Nosocomial urinary tract infections (UTI) 🚽

Fungi (eg, Candida species) - Immunocompromised host, Intravascular catheters, Prolonged antibiotic therapy

Positive serologic test or single positive blood culture for Coxiella burnetii (Q fever) and for Bartonella, Legionella, Brucella, Mycoplasma, and Chlamydophila.

Additional causes of culture-negative endocarditis include a group of gram-negative pathogens constituting the HACEK group: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella species, nutritionally variant streptococci (eg, Abiotrophiaspecies, Trophermyma whippelii), and fungi (eg, Aspergillus species, Histoplasma capsulatum).

  1. Evidence of endocardial involvement (either of the following):

Transthoracic echocardiogram (TTE):oscillating intracardiac mass, abscess, or new partial dehiscence of a prosthetic valve(vegetation). *Transesophageal echocardiography (TEE) is the[initial test of choice]when there is a moderate or high pretest probability of endocarditis (eg, in patients with staphylococcal bacteremia or fungemia, a prosthetic heart valve, or an intracardiac device).TEE is the initial imaging test in some clinical situations, such as detection of left atrial thrombus, evaluation of prosthetic mitral valve dysfunction, and evaluation of suspected aortic dissection, as well as in patients with a moderate to high pretest probability of endocarditis.

Physical examination: new valve regurgitation (change in pre-existing murmur is not sufficient). The vegetations of IE usually cause regurgitant murmurs.

DUKE MINOR Criteria:

  1. Predisposing heart condition (RF, IVDA, endo, prosthetics) or 💉injection drug user
  2. Fever: Body temperature >38.0°C (100.4°F)
  3. Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage, or Janeway lesions
  4. Immunologic phenomena (Rheumatologic): glomerulonephritis, Osler nodes, Roth spots, positive rheumatoid factor
  5. Microbiologic: serologic evidence of infection or positive blood cultures not meeting the major criteria (a single blood culture for coagulase-negative staphylococci is not sufficient)

Rx: Consider antibiotic prophylaxis only in patients with: High-risk cardiac conditions include the presence of a prosthetic cardiac valve, unrepaired cyanotic congenital heart disease, congenital heart disease repair with prosthetic material or device within the last 6 months, presence of palliative shunts and conduits, cardiac valvulopathy in cardiac transplant recipients, and a history of infective endocarditis. High-risk surgical procedures include dental procedures involving manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa as well as respiratory tract procedures that involve perforation of the respiratory mucosa (tonsillectomy, adenoidectomy).

Amoxicillin and cephalosporins, such as cephalexin, are frequently prescribed. Clindamycin, azithromycin, or clarithromycin are appropriate alternatives in patients with penicillin allergy.

Tx: Empiric therapy for early prosthetic valve infective endocarditis includes vancomycin, gentamicin, and rifampin for multidrug-resistant bacteria, particularly coagulase-negative staphylococci.

The Infectious Diseases Society of America Clinical has practice guidelines that recommend intravenous vancomycin (or daptomycin) for the treatment of methicillin-resistant Staphylococcus aureus (MRSA) infective endocarditis. The recommended duration of treatment for S. aureus-associated native valve infective endocarditis is 6 weeks.

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55
Q

Klebsiella pneumonia

A

8–72 h

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56
Q

Laryngitis

A

Laryngitis with pharyngitis is generally associated with a viral infection.

Tx: Supportive care

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57
Q

Legionella Pneumonia

A

Hx: Suspect in patients with risk factors (eg, age ≥50 years, smoking history, immunocompromising condition) who present with severe pneumonia and extrapulmonary symptoms (eg, headache, confusion, diarrhea, kidney failure).

Dx: Hyponatremia (< 136mEq/L); The urine antigen test detects only Legionella serogroup 1.

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58
Q

◼ SPIROCHETES

A
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59
Q

Lyme disease

A

A few weeks after a camping trip and presumptive exposure to the Ixodes tick.

Stage 1: Early localized (days–1 month)

  • Rash (Erythema migrans)
  • Fatigue, headache
  • Myalgias, arthralgias

Stage 2: Early disseminated (weeks–months)

  • Multiple erythema migrans
  • Unilateral/bilateral CN palsy (eg, CN VII)[facial]
  • Meningitis
  • 💗Carditis (eg, AV block)
  • 🗺 Migratory arthralgias 💥

Facial nerve palsy is one of the more common signs; it may be unilateral or bilateral.

Stage 3: Late (months–years)

  • Arthritis
  • Encephalitis
  • Peripheral neuropathy

Synovial fluid shows an inflammatory profile with an average leukocyte count of 25,000/mm3; Gram stain and culture are usually negative, although polymerase chain reaction (done for investigative purposes) may demonstrate B burgdorferi DNA.The diagnosis can be confirmed with serum ELISA and Western blot testing.

Occurs months to years later and is characterized by recurrent and sometimes destructive oligoarticular arthritis.

The causative agent is the spirochete Borrelia burgdorferi, which is spread to humans by the bite of an infected Ixodes tick. Diagnosis of early localized Lyme disease is based solely on the presence of the trademark rash in the context of recent travel to Lyme-endemic areas.

Tx: Clinical trials have shown that oral doxycycline, amoxicillin, and cefuroxime have equivalent efficacy for treating early localized Lyme disease.

👶🏽 Doxycycline should preferably be avoided in children age <8 years and pregnant women. It can slow bone growth in exposed fetuses and, in young children, is associated with risk of enamel hypoplasia and permanent teeth stains during tooth development (although the risk is likely small with a short course of doxycycline). Therefore, oral amoxicillin or cefuroxime is the treatment of choice for children age <8 years and pregnant women.

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60
Q

🌑 Syphilis

A

Primary syphilis: patients present with a painless ulcer (eg, chancre) with a clean base and raised indurated edges as well as painless regional lymphadenopathy.

Secondary syphilis: typically occurs weeks to months after the onset of primary disease and is characterized by a generalized mucocutaneous rash that involves the palms and soles, generalized lymphadenopathy, and constitutional symptoms. Inflammation may develop in other organs, resulting in hepatitis, glomerulonephritis, aseptic meningitis, patchy alopecia, and mucous patches. The hypertrophic, wartlike lesions around the anal area, called condyloma lata, are specific for secondary syphilis.

Dx: primary and secondary-stage mucocutaneous lesions can be established by darkfield microscopy visualization of motile Treponema pallidum in exudative fluid from the lesions. In a patient with suggestive clinical findings, a presumptive diagnosis can be based on reactive syphilis serology, which entails the use of a nontreponemal serologic test (eg, rapid plasma reagin [RPR] or VDRL test) followed by a more specific treponemal serologic test (eg, fluorescent treponemal antibody absorption test or T. pallidum particle agglutination assay ). Treponemal serologies typically remain positive for life, whereas nontreponemal serology titers regress after appropriate treatment and are used to assess disease activity.

Tertiary syphilis, which occurs years to decades after the initial infection, is characterized by neurologic findings (eg, meningitis, tabes dorsalis, Argyll Robertson pupil, mental status changes), cardiac abnormalities (eg, thoracic aortic aneurysm), or gummatous disease.

Latent syphilis is characterized by positive serology without symptoms.

Patients with neurosyphilis require cerebrospinal fluid examination for diagnosis (LP).

Late Latent:

Tx: Penicillin G benzathine 7.2 MU total, given as three doses of 2.4 MU IM at 1-wk intervals

❗ Patients with severe penicillin allergies should recieve doxycycline.

Desensitization is costly and time consuming and reserved primarily for situations in which alternate treatments are either ineffective (eg, central nervous system syphilis, multiple treatment failures) or contraindicated (eg, pregnancy).

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61
Q

🌑 Syphilis / Chancroid / LGV

Incubation: 9-90 d.

Primary lesion: papule Dx: Darkfield

Number of lesions: usually one.

Pain: none

Size of lesion: 5-15 mm.

Edges: indurated.

Base: clean.

Depth: moderate.

Lymph nodes: enlarged, nontender.

U.S. epidemiology: Southeast, urban areas.

Secondary: Fever, targetoid rash on palms and soles Dx: RPR -> FTA-Abs

Early Latent

Late Latent

Tertiary: Neurosyphilis (Tabes dorsalis, argyll-robertson) Dx: LP -> CSF-RPR -> CSF FTA-Abs

A

Painless genital ulcer and bilateral inguinal lymphadenopathy. Initial syphilis screening serology with rapid plasma reagin (RPR). Two types of serologic tests are used in combination to diagnose syphilis:

  • Nontreponemal (eg, RPR, VDRL)
  • Treponemal (eg, fluorescent treponemal antibody absorption)

Although either type may be used to screen for syphilis, nontreponemal tests may have higher false-negative rates (20%-30%) in patients with primary syphilis.

Patients with negative screening serology and strong clinical evidence of primary syphilis (eg, chancre) should be treated empirically with intramuscular benzathine penicillin G as this reduces the risk of transmission. In these patients, repeat nontreponemal serology should be done in 2-4 weeks to establish baseline titers; a 4-fold titer decrease at 6-12 months would confirm adequate treatment.

Primary syphilis

Syphilitic chancres form at the site of direct inoculation with Treponema pallidum. After exposure (3-60 days), patients develop a single papule that turns into a shallow, painless, nonexudative ulcer with indurated edges. Chancres are exceedingly infectious, with rates of T pallidum transmission as high as 30%. Most chancres resolve spontaneously in 6-8 weeks (if untreated), but the systemic spread of T pallidum results in continued infection.

Secondary syphilis: typically occurs weeks to months after the onset of primary disease and is characterized by a generalized mucocutaneous rash that involves the palms and soles, generalized lymphadenopathy, and constitutional symptoms. Inflammation may develop in other organs, resulting in hepatitis, glomerulonephritis, aseptic meningitis, patchy alopecia, and mucous patches.

Dx: primary and secondary-stage mucocutaneous lesions can be established by darkfield microscopy visualization of motile Treponema pallidum in exudative fluid from the lesions. In a patient with suggestive clinical findings, a presumptive diagnosis can be based on reactive syphilis serology, which entails the use of a nontreponemal serologic test (eg, rapid plasma reagin [RPR] or VDRL test) followed by a more specific treponemal serologic test (eg, fluorescent treponemal antibody absorption test or T. pallidum particle agglutination assay ). Treponemal serologies typically remain positive for life, whereas nontreponemal serology titers regress after appropriate treatment and are used to assess disease activity.

Tertiary syphilis, which occurs years to decades after the initial infection, is characterized by neurologic findings (eg, meningitis, tabes dorsalis, Argyll Robertson pupil, mental status changes), cardiac abnormalities (eg, thoracic aortic aneurysm), or 🌑 gummatous disease.

Latent syphilis is characterized by positive serology without symptoms.

Patients with neurosyphilis require cerebrospinal fluid examination for diagnosis (LP). Tx: Aqueous crystalline penicillin G 18-24 MU/d, given as 3-4 MU IV every 4 h or continuous infusion, for 10-14 d

Ddx:

Granuloma inguinale is caused by Klebsiella granulomatis and is marked by the formation of extensive, progressive, and painless genital ulcers, usually without lymphadenopathy. Granuloma inguinale is seen primarily in India, Guyana, and New Guinea. In the United States, <100 infections occur annually, most in patients who have traveled to these countries. Donovan bodies are present in these patients.

Granuloma inguinale (Donovanosis) is extremely rare in the United States. Ulcers most commonly are large, nontender, and beefy red and bleed easily when touched. The lesions differ from the syphilitic chancre in that they are larger, may be multiple in number, and usually have a very beefy red base. The ulcers do not heal spontaneously and can be present chronically.

Chancroid, caused by Haemophilus ducreyi, is most commonly found in developing regions but is rare in the United States and produces a painful, tender ulceration of the vulva. Chancroid is successfully treated with either azithromycin or ceftriaxone.

Incubation: 1-14 d. Primary lesion: pustule. Number of lesions: one or many.

Pain: exquisite. Size of lesion: 5-25 mm. Edges: ragged, undermined. Base: friable, purulent exudate. Depth: deep, excavated.

Lymph nodes: tender, may suppurate/form buboes.

U.S. epidemiology: rare, occasionally seen in warmer climates (many of these cases are imported from Mexico or the Caribbean).

Lymphogranuloma venereum (LGV) is a chronic infection produced by C. trachomatis. It is most commonly found in the tropics. The primary infection begins as a painless ulcer on the labia or vaginal vestibule; the patient usually consults the physician several weeks after the development of painful adenopathy in the inguinal and perirectal areas. Diagnosis can be established by culture or by demonstrating the presence of serum antibodies to C. trachomatis. Therapy for both granuloma inguinale and LGV is administration of 🎡tetracycline.

LGV is extremely rare in the U.S. The infection can begin as a small papule, erosion, or ulcer in the genital or perineal region; the lesion usually is asymptomatic and heals quickly without scarring. Patients with LGV rarely, if ever, present in this early ulcerative stage. Subsequently, patients develop the painful lymphadenopathy and buboes. During this stage, patients may have fever and other constitutional symptoms and develop draining fistulae. The early ulcerative lesions of LGV differ from those of primary syphilis in that they are smaller and less destructive and heal promptly. Dx: NAAT Tx: Doxy

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62
Q

Babesiosis

A

Babesiosis is a tick-borne protozoal illness endemic to the northeastern United States. Human transmission occurs via Ixodes scapularis approximately 48-72 hours after attachment. I scapularis also may transmit Borrelia burgdorferi (Lyme disease) and Anaplasma phagocytophilum (human granulocytic anaplasmosis); therefore, coinfection with multiple organisms is possible. Peak prevalence is in July and August, when tick populations are at their highest.

Infection is often asymptomatic or mild, but patients with immunocompromise, age >50, or a history of splenectomy are at higher risk for severe illness. Symptoms typically include the gradual onset of fatigue, malaise, weakness, chills, and fever. The organism multiplies in red blood cells, so patients may develop anemia with signs of intravascular hemolysis (jaundice, dark urine, indirect hyperbilirubinemia, reticulocytosis, elevations of aminotransferases and lactate dehydrogenase). Thrombocytopenia is common and mild hepatosplenomegaly may occur. Diagnosis is made by identifying organisms on peripheral blood smear (“Maltese cross”). Treatment includes 7-10 days of atovaquone plus azithromycin or quinine plus clindamycin (for severe illness). Symptoms may take up to 3 months to fully resolve.

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63
Q

🌴 Tabes dorsalis

A

Epidemiology

  • Increased incidence of syphilis in men who have sex with men & HIV-infected patients
  • HIV-positive patients develop neurosyphilis more rapidly

Pathogenesis

  • Treponema pallidum spirochetes directly damage the dorsal sensory roots
  • Secondary degeneration of the dorsal columns

Clinical findings

  • Sensory ataxia
  • Lancinating pains
  • Neurogenic urinary incontinence
  • Associated with Argyll Robertson pupils

Tabes dorsalis is a neurodegenerative condition that involves the posterior spinal columns and nerve roots. Posterior column involvement results in impaired vibration/proprioception, sensory ataxia, and instability during the Romberg test. Nerve root involvement can contribute to diminished pain/temperature sensation and reduced/absent deep tendon reflexes. Patients might complain of lancinating pains, described as brief shooting or burning pain in the face, back, or extremities. Tabes dorsalis can also be associated with Argyll Robertson pupils, which are typically miotic and irregular and characterized by normal pupillary constriction with accommodation but not with light.

The treatment of choice for neurosyphilis is intravenous (IV) penicillin for 10-14 days due to its adequate cerebrospinal fluid penetration and efficacy.

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64
Q

Leptospirosis

A

A spirochetal disease that has two phases. The bacteremic phase is characterized by sudden onset fevers, rigors, headache, photophobia, and severe myalgias. Four to 30 days
later, the immunologic phase ensues and is characterized by conjunctivitis, photophobia, retrobulbar pain, neck stiffness, diffuse lymphadenopathy, hepatosplenomegaly, and
aseptic meningitis. The most severe form is called Weil disease; it is associated with up to 40% mortality and is characterized by high direct bilirubin and mild elevation in
alkaline phosphatase and transaminase values, combined with a high creatine phosphokinase.

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65
Q

Leprosy

A

Leprosy is a chronic granulomatous disease of the skin and peripheral nerves caused by the acid-fast bacillus Mycobacterium leprae. Transmission is thought to occur via respiratory droplets, although cases are occasionally linked to close contact with a nine-banded armadillo. Infections are rare in the United States and occur primarily in immigrants or travelers to endemic regions (eg, Asia, Africa, South America).

Manifestations include >1 chronic, anesthetic, macular (often hypopigmented) ⚪ skin lesions with raised, well-demarcated borders. Nearby nerves often become nodular and tender, and segmental demyelination may result in loss of sensation and motor function. Diagnosis is clinical in endemic regions, but in the United States patients usually require a full-thickness biopsy of the skin lesion edge (as M leprae is not culturable).

Patients with minimal lesions (“paucibacillary”) are treated with dapsone and rifampin; those with extensive lesions (“multibacillary”) require the addition of clofazimine. Lesions often take months or years to heal completely.

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66
Q

Lung abscess

A

Frequently involves the posterior upper segments of the upper lobes; may be acute or indolent; causes indolent symptoms of fever, cough, dyspnea, weight loss and CT scan findings of an infiltrate with a cavity.

  • *Hx:** Patients usually have foul-smelling sputum.
  • *Dx:** Usually have necrotic tissue with air fluid levels
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67
Q

Malaria

A

A protozoal disease caused by Plasmodium (red blood cell [RBC] parasite transmitted by Anopheles mosquitoes). The hallmark is cyclical fever, coinciding with Plasmodium-induced RBC lysis.

Patients present with influenza-like symptoms, jaundice, and in its most severe forms with obtundation and confusion.

Fever in the setting of malaria is often intermittent. The diagnosis of malaria is established by visualization of parasites on peripheral smear.

The typical cycle (uncommon) consists of a cold phase (chills, shivering), then a hot phase (high-grade fevers), then a sweating stage (diaphoresis, fever resolution). Headache, malaise, myalgias, vomiting, and diarrhea are often seen. Anemia andthrombocytopenia are classic. Blood smears are the diagnostic gold standard.

Prophylaxis: Should begin 2 days to 2 weeks before departure in order to have adequate levels of drug on arrival and to identify potential side effects before leaving.

Whether or not to use drugs such as atovaquone-proguanil, mefloquine, or primaquine for resistant P falciparum will depend on knowledge of specific local patterns of drug sensitivity of plasmodia.

Tx: Long-sleeved clothing, insect repellent, and insecticide-treated bed nets can be somewhat protective; however, most returning travelers who have malaria did not adhere to chemoprophylaxis. Treatment regimens depend on the species and severity of infection.

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68
Q

Malignant Hyperthermia

A

Malignant hyperthermia is an inherited skeletal muscle disorder characterized by a hypermetabolic state precipitated by exposure to volatile inhalation anesthetics (eg, halothane, isoflurane, enflurane, desflurane, sevoflurane) and depolarizing muscle relaxants (eg, succinylcholine, decamethonium). Malignant hyperthermia usually occurs on exposure to the drug. Increased intracellular calcium leads to sustained muscle contractions, with resultant skeletal muscle rigidity and masseter spasm, tachycardia, hypercarbia, hypertension, hyperthermia, tachypnea, and cardiac arrhythmias. Rhabdomyolysis and acute kidney failure can develop. Malignant hyperthermia is life threatening if not treated immediately.

Tx: Includes discontinuing the offending drug and providing supportive care (eg, hydration, oxygen, cooling measures). Dantrolene sodium, a skeletal muscle relaxant, is the treatment of choice.

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69
Q

Meningococcal infection

A

Meningococcal infection may be associated with meningitis and hemorrhagic rash. The diagnosis is established based on cerebrospinal fluid examination.

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70
Q

Metastatic malignancy to the bone

A

Usually associated with a primary lesion (eg, breast, prostate, lung). Metastasis is usually multifocal and tends to remain isolated to one vertebral body, whereas osteomyelitis often crosses the end plate.

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71
Q

Modifying Factors That Increase the Risk of Infection With Specific Pathogens

A

Age >65 y, β-lactam therapy (in previous 3 mo), alcoholism, immunosuppression (illness, glucocorticoids), multiple medical comorbidities, exposure to a child in a day care center

Penicillin-resistant and drug-resistant pneumococci

Residence in an extended care facility, underlying cardiopulmonary disease, multiple medical comorbidities, recent antibiotic therapy

Enteric gram-negative bacteria

Structural lung disease (bronchiectasis), glucocorticoids therapy, broad-spectrum antibiotic therapy for >7 d; malnutrition

Pseudomonas aeruginosa

Endobronchial obstruction (tumor)

Anaerobes, Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus

Intravenous drug use

Anaerobes, S. aureus, Mycobacterium tuberculosis, S. pneumoniae

Influenza epidemic in the community

Influenza virus, S. pneumoniae, S. aureus, H. influenzae

COPD, smoking history

S. pneumoniae, H. influenzae, Moraxella catarrhalis, P. aeruginosa, Legionella species, Chlamydophila

Poor dental hygiene, aspiration, lung abscess

Oral anaerobes

Animal exposure

Coxiella burnetii (farm animals); Chlamydophila psittaci, Cryptococcus (birds); Histoplasma (birds, bats)

72
Q

VIRUSES

A
73
Q

Human Papilloma Virus (HPV)

A

Human papillomavirus (HPV) is the most common sexually transmitted infection and has been linked to multiple diseases, including condylomata acuminata as well as vulvar, vaginal, anal, oropharyngeal, and cervical cancer.

Warts (cutaneous verrucae), which are the most common cutaneous manifestation of human papillomavirus (HPV) infection. HPV can cause warts in various locations including the plantar, palmar, or genital areas. Plantar warts occur most commonly in young adults and patients with decreased cellular immunity (eg, AIDS, organ transplant patients).

The virus usually enters through tiny cuts or skin abrasions after direct contact with an HPV-infected individual. Patients can develop lesions weeks to months later; these appear as hyperkeratotic papules on the sole of the foot (sometimes with thrombosed capillaries and visible skin lines) that can be painful with walking or standing. Diagnosis is made clinically based on the appearance and location of the lesions.

Persistent HPV infection (particularly with types 16 and 18) results in cellular dysplasia as the incorporation of viral DNA creates increased pro-oncogenic protein expression and inhibits normal cellular regulation. The HPV vaccination induces an antibody response that decreases the risk of future HPV infection and subsequent related diseases.

Disease associations

  • Cervical cancer
  • Vulvar & vaginal cancers
  • Anal cancer
  • Penile cancer
  • Oropharyngeal cancer
  • Genital warts

💉 Vaccine indications

  • All girls & women age 11-26
  • Boys & men age 9-21 (9-26 for men
  • who have sex with men; individuals with HIV)

The quadrivalent HPV vaccination has been shown to be highly immunogenic, safe, and well-tolerated in females aged 9 to 26. To be most effective, the vaccine should be given before a female becomes sexually active. It can be administered when a patient has an abnormal Pap test or when a woman is breast-feeding. It can also be given when a patient is immunocompromised because of a disease or medication. It is not recommended for use during pregnancy. The vaccine was recently approved for use in males aged 9 to 26 to reduce the likelihood of genital warts. As in women, it is most effective if administered before exposure to HPV through sexual contact.

Both vaccines protect against high-risk HPV subtypes (HPV-16 and HPV-18), and the quadrivalent additionally protects against subtypes that cause genital warts (HPV-6 and HPV-11). Either vaccine is recommended for use in women. Both vaccines are administered in three doses: time zero and then 1 to 2 months later, with the third dose being given 6 months after the initial dose. Pregnant women should not receive the vaccine because there is a lack of safety data in this population.

The ACIP also recommends that boys and men age 11 to 21 years receive the quadrivalent vaccine, although the vaccine may be given to boys as young as 9 years of age.

HPV 6 & 11​: Anogenital warts (condylomata acuminata)[benign]

Caused by human papillomavirus (HPV), a common sexually transmitted infection. Condyloma acuminata occur due to persistent infection with low-risk HPV strains 6 and 11, and patients with chronic tobacco use or immunosuppression (eg, HIV) have an elevated risk.

  • Sexual abuse in 👶🏽 children
  • Autoinoculation from other sites
  • Prenatal or perinatal

Clinical features

  • Multiple pink or skin-colored lesions
  • Lesions ranging from smooth, flattened papules to exophytic/cauliflower-like growths
  • Pink/flesh-colored, verrucous papules & plaques
  • Asymptomatic (most common)
  • Pruritic, friable lesions

Anogenital warts typically appear as clusters of soft, pink or skin-colored (fleshy) lesions in the internal or external vaginal, vulvar, and anal regions in women. Most lesions are exophytic, dry-appearing, and verrucous (ie, cauliflower-like), although some may appear sessile and flat. Genital warts are typically asymptomatic and nontender, although pruritic, friable lesions (eg, those that bleed with manipulation) may occur.

Irregular, exophytic growths in clusters on the surfaces of his vocal cords likely has laryngeal papillomas due to recurrent respiratory papillomatosis (RRP). These lesions are often warty or grapelike and, as with skin papillomas, have dark-red punctate areas corresponding to blood vessels. Although benign, RRP is associated with significant morbidity (eg, voice problems, airway obstruction, repeated operative interventions). In addition, the clinical course is variable and unpredictable with fluctuations in severity. In rare instances, it can spread beyond the vocal cords to involve the lower respiratory tract. Medical therapy (eg, interferon, cidofovir) has limited efficacy; therefore, the mainstay of treatment remains surgical debridement, and patients often require many procedures. The incidence of RRP in children is decreasing, likely due to increased rates of maternal HPV vaccination.

HPV can be transmitted via nonsexual contact such as vertical transmission during delivery, autoinfection from other areas of the body, or heteroinoculation from a caregiver (eg, diaper changes). However, because of the association with transmission via direct genital contact, an assessment for sexual abuse is required in all children, particularly those age ≥4.

Diagnosis is primarily clinical, based on the characteristic appearance of the lesions. Small anogenital warts are treated with topical agents that either chemically injure the lesion (eg, trichloroacetic acid, podophyllin resin) or stimulate an immune response to it (eg, imiquimod).

Treatment

  • Chemical: Podophyllin resin, 🔱trichloroacetic acid
  • Immunologic: Imiquimod
  • Surgical: Cryotherapy, laser therapy, excision (large bleeding lesions)

Anogenital warts in children are often self-resolving; therefore, asymptomatic patients typically require only observation. For those with symptomatic or unresolved disease, management options include topical treatments (eg, podophyllotoxin) and surgical removal. Although podophyllum is not recommended for extensive disease because of toxicity (peripheral neuropathy). Medical treatment with podophyllum, imiquimod, trichloroacetic acid, and 5-fluorouricil requires weeks or months of therapy to be effective.

HPV, in particular types 16, 18, and 31, have been linked to 🎒 cervical neoplasia 🦀.

74
Q

Rotavirus (Reovirus)

A

Moderate Inflammation.

75
Q

*Norovirus

A

Minimal inflammation

Outbreaks of diarrhea in families; on cruise ships and airplanes; and in day care centers, extended care facilities, or schools are commonly associated with norovirus.

Acute diarrhea for 1–3 d

For most patients, this finding represents a self-limited gastroenteritis.

Features or clinical characteristics that require additional evaluation for acute diarrhea include fever; bloody stools; diarrhea in pregnant, elderly, or immunocompromised patients; hospitalization; employment as a food handler; recent antibiotic use; volume depletion; or significant abdominal pain.

76
Q

Mononucleosis (EBV infection)

A

Infectious mononucleosis, most commonly due to Epstein-Barr virus (EBV) infection, presents with prolonged fever, malaise, and sore throat. Physical findings include enlarged, erythematous tonsils with exudates; splenomegaly; and lymphadenopathy (commonly posterior cervical but may be generalized). Laboratory findings can include reactive leukocytosis, positive serum heterophile antibodies (Monospot test), and atypical lymphocytes on blood smear. Elevated transaminases are also seen in most patients due to mild, transient hepatitis.

In addition, some patients develop autoimmune hemolytic anemia and thrombocytopenia, rare complications of infectious mononucleosis due to cross-reactivity of EBV-induced antibodies against red blood cells and platelets. In particular, IgM cold agglutinin antibodies cause complement-mediated destruction of red blood cells. This hemolysis, which can occur 2-3 weeks after the onset of EBV symptoms, may lead to jaundice, elevated bilirubin, and increased reticulocyte count, as seen in this patient.

Clinical features

  • Fever
  • Tonsillitis/pharyngitis ± (white) exudates
  • Posterior OR diffuse cervical lymphadenopathy
  • Significant fatigue
  • ± Hepatosplenomegaly
  • ± Rash after amoxicillin

IM is classically characterized by a prolonged course (up to 1 month) of fever, exudative pharyngitis, and tender lymphadenopathy; the adenopathy is commonly located in the posterior cervical region but may be generalized.

Diagnostic findings

  • Positive heterophile antibody (Monospot) test (25% false-negative rate during 1st week of illness)
  • Atypical lymphocytosis
  • Transient hepatitis

Management

  • Avoid sports for ≥3 weeks (contact sports ≥4 weeks) due to the risk of splenic rupture

Complications

  • Acute airway obstruction
  • Autoimmune hemolytic anemia & thrombocytopenia
  • Splenic rupture

A 1- to 2-wk prodrome of fatigue, malaise, and myalgia followed by adenopathy (particularly of posterior cervical nodes), sore throat, fever, splenomegaly, hepatomegaly, and lymphocytosis (atypical lymphocytes).

Palatal petechiae suggest either a group A streptococcal infection or infectious mononucleosis.

Dx:

Peripheral blood smear should be evaluated for atypical lymphocytes.

🎯 A heterophile antibody test should be performed.

If patients with mononucleosis are given ampicillin (and other penicillin derivatives), up to 100% may develop rash sometimes confused as an allergic reaction to penicillin.

Cx: ​Nasopharyngeal carcinoma (NPC) is a tumor associated with Epstein-Barr virus reactivation that is rare in the United States but endemic in southern China. Risk is likely increased in this region due to a nitrosamine-rich diet (eg, salt-cured food, early exposure to salted fish) and genetic predisposition.

The nasopharynx links the nasal cavity and the oropharynx. NPC tumors obstruct this passage and invade adjacent tissues, often resulting in nasal congestion with epistaxis, headache, facial numbness (para-cavernous sinus tumor invasion), and/or serous otitis media (eustachian tube obstruction). Early metastasis to the bilateral cervical lymph nodes is common. Diagnosis is made with endoscope-guided biopsy of the primary tumor, and treatment usually involves a combination of radiation therapy and chemotherapy. Survival is excellent if the neoplasm is discovered early, but most patients present with advanced disease.

77
Q

Parvovirus B19 infectionParvovirus

A

Signs & symptoms

  • Most patients are asymptomatic or have flulike symptoms
  • Erythema infectiosum (fifth disease): Fever, nausea & “slapped cheek” rash (more common in children)
  • Acute, symmetric arthralgia/arthritis: Hands, wrists, knees & feet (resembles RA)
  • Transient pure red cell aplasia; aplastic crisis in patients with underlying hematologic disease (eg, sickle cell)

Diagnosis

  • Acute infection
    • B19 IgM antibodies in immunocompetent patients
    • NAAT for B19 DNA in immunocompromised patients
  • Previous infection: B19 IgG antibodies (documents immunity)
  • Reactivation of previous infection: NAAT for B19 DNA

Parvovirus is among the most common causes of acute viral arthritis (others include hepatitis B and C, HIV, and rubella). Parvovirus infection most commonly affects adults who have frequent contact with children (eg, school teachers, daycare workers). Children with parvovirus infection often develop a “slapped cheek” rash as part of erythema infectiosum. Nearly 75% of adults with parvovirus infection develop a nonspecific rash, but <20% have the characteristic erythema infectiosum rash.

Adults most commonly develop a polyarticular, symmetric arthritis (60% of cases) involving peripheral joints, including the hands (metacarpophalangeal [MCP], proximal interphalangeal [PIP], and wrist), knees, and ankles. Arthritis due to parvovirus B19 typically does not cause joint destruction or chronic arthritis. Other possible nonspecific findings include fever, fatigue, and diarrhea. Parvovirus B19 infection is diagnosed by detecting anti-B19 IgM antibodies in the serum, which develop within 10-15 days of infection and usually remain positive for 1-6 months. The symptoms typically resolve spontaneously in 2-3 weeks without the need for specific treatment.

78
Q

Zika virus

A

Symptoms and signs of Zika virus infection include fever, rash, headache, arthralgia, myalgia, and conjunctivitis.

79
Q

Neisseria meningitidis

A

is a gram-negative diplococcus that causes life-threatening meningitis, particularly in young children and adolescents. N meningitidis accounts for approximately 12% of community acquired bacterial meningitis, trailing only Streptococcus pneumoniae (~70%) in prevalence.

Patients develop sudden symptoms, and rapid, severe progression is the norm. Manifestations often begin with fever, headache, vomiting, and severe myalgias. Within 12-15 hours, most patients develop nuchal rigidity, altered mental status, and petechial rash. Shock often follows shortly thereafter. The mortality rate is >15% (even with appropriate treatment).

Diagnosis requires blood cultures and lumbar puncture. Cerebral spinal fluid (CSF) typically shows low glucose (<45 mg/dL), high protein (often >500 mg/dL), and neutrophilic leukocytosis (>1000/mm3). Gram stain is often able to identify diplococci. The empiric treatment of choice is a third-generation cephalosporin (eg, ceftriaxone) and vancomycin. Dexamethasone is not beneficial in meningococcal meningitis but is often administered prior to organism isolation (once isolated, dexamethasone can be discontinued).

  • Symptoms: Headache, nausea/vomiting, severe myalgias
  • Signs: Neck stiffness, altered mental status, petechial/purpuric rash, meningeal (Kernig & Brudzinski) signs
  • Complications: Multiorgan failure, DIC, adrenal hemorrhage, shock

Treatment

Third-generation cephalosporin + vancomycin

Glucocorticoids not helpful

Chemoprophylaxis (eg, rifampin, ciprofloxacin, ceftriaxone) of all respiratory contacts

80
Q

Neuroleptic Malignant Syndrome (NMS)

A

The neuroleptic malignant syndrome is a life-threatening disorder caused by an idiosyncratic reaction to neuroleptic tranquilizers and some antipsychotic agents. The most common offending neuroleptic agents are haloperidol and fluphenazine. The syndrome can occur with all drugs that cause central dopamine receptor blockade and usually occurs soon after starting a new drug or with dose escalation. Most patients with the syndrome develop muscle rigidity, hyperthermia, cognitive changes, autonomic instability, diaphoresis, sialorrhea, seizures, arrhythmias, and rhabdomyolysis within 2 weeks after initiating the drug. Death may occur from respiratory or cardiac failure, disseminated intravascular coagulation, or acute kidney failure.

Tx: Drug therapy with dantrolene sodium and/or bromocriptine decreases mortality and symptom duration.

81
Q

Nocardia

A

Nocardia is an aerobic bacteria found in soil that may inoculate humans via inhalation (most common) or cutaneous penetration (often while gardening). Branching, filamentous growth helps the organism prevent phagocytosis, making host defense largely dependent on cell-mediated immunity. Therefore, patients who are severely immunocompromised (eg, immunosuppressive medications, HIV) are much more likely to develop active disease.

Pulmonary nocardiosis is the most common manifestation and may present alone or with disseminated disease (eg, skin, central nervous system). Symptoms arise with varying chronicity but often include fever, weight loss, malaise, dyspnea, cough, and pleurisy. Imaging typically reveals nodular or cavitary lesionsin the upper lobes, which may be confused with malignancy or tuberculosis. Sputum culture is often negative, but bronchoscopy with bronchoalveolar lavage can usually provide an adequate sample for diagnosis (sensitivity >85%). Gram stain shows filamentous gram-positive rods that are weakly acid-fast (unlike Mycobacterium tuberculosis, which is strongly acid-fast). Cultures often require >4 weeks of incubation.

Susceptibility testing is needed for all isolates as many strains are antibiotic resistant. Trimethoprim-sulfamethoxazole is usually the treatment of choice and may be combined with additional antibiotics (eg, amikacin) in severe disease. Several months of antibiotics are usually required, and relapse is common despite adequate treatment.

82
Q

Otalgia

A

Temporomandibular joint dysfunction is a common cause of referred otalgia.

Tx: First-line therapies include treatment with NSAIDs, heat, a mechanical soft diet, and referral to the dentist if there is no improvement in 3 to 4 weeks.

83
Q

👂🏽Otitis Externa

A

Hx: otalgia, itching or fullness with or without hearing loss, and pain intensified by jaw motion.

Px: Internal tenderness when the tragus or pinna is pushed or pulled and diffuse ear canal edema, purulent debris, and erythema, with or without otorrhea.

Dx: Pneumatic otoscopy shows good tympanic membrane mobility.

Tx: Ototopical agent containing neomycin, polymyxin B, and hydrocortisone.

Necrotizing (malignant) otitis externa (NOE), a life-threatening infection of the external auditory canal extending to the skull base (osteomyelitis). Most patients are elderly and have diabetes mellitus. The most common manifestation is severe, unrelenting ear pain, especially at night; pain exacerbated by chewing may indicate spread of infection to the temporomandibular joint (TMJ). Other findings may include otorrhea and lower cranial nerve deficits (eg, facial [CN VII]). Otoscopy characteristically shows granulation tissue at the bony cartilaginous junction and an edematous external auditory canal, often with purulent drainage. As in other cases of osteomyelitis, an elevated erythrocyte sedimentation rate is often seen, although leukocyte count may be normal.

Pseudomonas aeruginosa is the most common cause of NOE. Prior to the advent of antipseudomonal antibiotics (eg, fluoroquinolones), mortality was >50%. Intravenous ciprofloxacin is the drug of choice, even with the increased risk of tendon rupture in elderly patients. Surgical debridement (of necrotic bone) is reserved for patients not responding to medical therapy.

84
Q

Otitis media

A

Possible etiologies include strep pneumo, moraxella, and haemophilus.

Hx: Fever >101.4 (38C). Px: Erythema, edema, otorrhea, effusions, TM immobility, buldging TM; Ear pain, decreased hearing acuity. More common in children than in adults.

*A reddened tympanic membrane, by itself, is not a sufficient finding to diagnose acute otitis media. It may be due to increased intravascular pressure associated with crying.

*Purulent discharge in the ear canal may indicate a tympanic membrane perforation, and in the face of an otherwise normal canal is more indicative of acute otitis media than otitis externa.

Dx: Tympanic membrane that is red, opaque, bulging, or retracted.

Tx: Amoxicillin 80-90 mg/kg/d (split into 2 doses)

F/u ENT

*In patients with severe illness (moderate to severe otalgia and/or fever >102°F), therapy should be initiated with high-dose amoxicillin-clavulanate (90 mg/kg/d of amoxicillin in 2 divided doses)

Effusions may take up to 3 months to resolve. Effusions persisting beyond 3 months require evaluation by an otolaryngologist.

Cx: Serous otitis media is the most common middle ear pathology in patients with acquired immunodeficiency syndrome (HIV). It is due to the auditory tube dysfunction arising from HIV lymphadenopathy or obstructing lymphomas. Serous otitis media is characterized by the presence of a middle ear effusion without evidence of an acute infection. Conductive hearing loss is the most common symptom experienced by patients with serous otitis media, and examination typically reveals a dull tympanic membrane that is hypomobile on pneumatic otoscopy.

85
Q

Pseudomonas

A

Pneumonia

Hx: Structural lung disease (bronchiectasis), glucocorticoids therapy, broad-spectrum antibiotic therapy for >7 d; malnutrition

Dx: Pseudomonas aeruginosa or gram-negative rods on sputum Gram stain

Tx: Antipseudomonal β-lactam with pneumococcal coverage (eg, cefepime, imipenem, meropenem, or piperacillin-tazobactam) plus ciprofloxacin or levofloxacin (750 mg); or antipseudomonal β-lactam with pneumococcal coverage plus an aminoglycoside plus azithromycin; or antipseudomonale β-lactam with pneumococcal coverage plus an aminoglycoside plus a respiratory fluoroquinolone

Neutropenic fever is a medical emergency. Infections, most commonly gram-negative bacteria such as P aeruginosa, are responsible for most cases.

Prompt empiric antibiotic therapy with two antibiotics from two different antibiotic classes (double coverage) that have anti-pseudomonal activity is most appropriate. Adding an antibiotic with anti–methicillin-resistant Staphylococcus aureus (MRSA) activity to the initial antibiotic regimen is indicated if the patient was on antibiotic prophylaxis before the onset of the neutropenic fever or if he has any of the following conditions: skin infection, moderate to severe mucositis, central venous catheter, or shock.

86
Q

Pyelonephritis

A

Hx: Fever, malaise, sweats, headache; anorexia, nausea, vomiting, abdominal pain; back, flank or loin pain; ± voiding symptoms.

Px: Fever, tachycardia; costovertebral angle tenderness; possibly abdominal tenderness.

Dx: Elevated leukocyte count, ESR, and/or C-reactive protein; urinalysis with PMNs and bacteria (as in cystitis), ± leukocyte casts;

Urine culture with >104 CFU/mL of a typical uropathogen.

Imaging studies (not routinely indicated for uncomplicated pyelonephritis; may be indicated in specific circumstances (ultrasound, intravenous pyelogram, enhanced CT [looking for obstruction, stone]).

Tx: Fluoroquinolones (Ciprofloxacin) are used as first-line empiric oral therapy (except in pregnancy) because of the higher urine drug concentrations achieved compared with trimethoprim-sulfamethoxazole (TMP-SMX).

Urine culture prior to therapy

87
Q

Rocky Mountain spotted fever (RMSF)

A

Rocky Mountain spotted fever (RMSF) occurs about 5 days into an illness characterized by fever, malaise, and headache. T he rash may be macular or petechial, but almost always spreads from the ankles and wrists to the trunk. T he rash indicates endothelial infection, which in severe cases can lead to capillary leak and shock. North Carolina and East Tennessee have a relatively high incidence of disease. RMSF is a rickettsial disease with the tick as the
vector, and the disease is more common in warm months when ticks are active. About 80% of patients will give a history of tick exposure. Doxycycline is considered the drug of choice,

88
Q

Salmonella spp.

A

Beef, poultry, eggs, dairy, travel history

12 h–11 d

89
Q

Sarcoidosis (see Diffuse Parenchymal Lung Diseases)

A

Patients have dyspnea and cough. Chest radiography shows diffuse infiltrative lung disease with bilateral hilar adenopathy. Biopsy reveals noncaseating granulomas. Diagnosis is made after exclusion of other possibilities.

90
Q

❗💦SEPSIS

A

Sepsis

Severe Sepsis

Septic (Distributibe) shock

Toxic shock syndrome

Cardiogenic shock

Hypovolemic shock

Anaphylactic shock

Neurogenic (spinal) shock

Adrenal crisis

Obstructive shock

91
Q

Sepsis

A

Must meet the criteria for SIRS plus have suspected or confirmed infection (positive cultures not required).

Definition of Systemic Inflammatory Response Syndrome (SIRS): Presence of two or more of the following in the absence of other known causes:

  • Temperature >38.0°C (100.4°F) or <36.0°C (96.8°F)
  • Heart rate >90 bpm
  • Respiration rate >20 breaths/min or arterial PCO 2 <32 mm Hg (4.3 kPa)
  • Leukocyte count >12,000/µL (12 × 109/L) or <4000/µL (4 × 109/L) with 10% bands
92
Q

Severe Sepsis

A

Severe sepsis is associated with systemic effects, including hypotension, confusion, decreased urine output, and metabolic acidosis.

Sepsis with any evidence of organ dysfunction or tissue hypoperfusion, or hypotension (ie, lactic acidosis, oliguria, altered mental status).

The qSOFA is a bedside prompt that may identify patients with suspected infection who are at greater risk for a poor outcome outside the intensive care unit (ICU). It uses three criteria:

Low blood pressure (SBP≤100 mmHg),

High respiratory rate (≥22 breaths per min), or

Altered mentation (Glasgow coma scale<15).

Tx:

Crystalloid (normal saline or lactated Ringer solution)

Restores intravascular volume, which is depleted in patients with severe sepsis. Improves cardiac output, organ perfusion, and mortality in patients with severe sepsis. Fluid challenge infusion of at least 30 mL/kg should be given and repeated until the patient shows a beneficial response without major adverse effects. Most patients need 4 to 6 L of fluid in the first 6 hours.

Achieve central venous pressure of 8 to 12 mm Hg. Repetitive fluid challenges are performed by giving 500- to 1000-mL boluses of crystalloid solution over short intervals while assessing the response to target central venous pressure. If mean arterial pressure ([2 × diastolic blood pressure] + systolic blood pressure)/3 is less than 65 mm Hg despite fluid challenge and adequate preload, treatment with vasoactive agents should be started and titrated as needed.

Antibiotics (fourth-generation cephalosporin, extended-spectrum [antipseudomonal] penicillin, carbapenem)

Early appropriate antibiotic therapy (within 1 hour of recognition) is associated with improved outcomes. Appropriate empiric therapy should be initiated rapidly, even if the source of infection is unknown. A more appropriate, source-directed antibiotic selection should be initiated if the source is known or becomes known (eg, add vancomycin if MRSA is suspected, add double coverage with an intravenous fluoroquinolone or aminoglycoside if a highly resistant gram-negative pathogen is suspected, or add clindamycin if toxic shock syndrome is suspected); consider additional agents (eg, fluoroquinolones, macrolides, tetracyclines, antifungal agents, antiviral agents) depending on the clinical presentation.

Vasopressors: norepinephrine, epinephrine, dobutamine, dopamine, vasopressin phenylephrine

Improves blood pressure and cardiac output. Norepinephrine is associated with less tachycardia than other vasopressor agents with β-effects and is more effective than dopamine in refractory septic shock. Vasopressin works on receptors other than adrenergic receptors and may be useful in refractory septic shock treated with high-dose adrenergic vasopressors. Dobutamine may be used in combination with a vasopressor to increase cardiac output if it is inappropriately low.

93
Q

Septic (Distributive) shock

A

Sepsis-induced hypotension refractory to adequate fluid resuscitation

Hx:

  • Persistent hypotension refractory to fluid resuscitation in the presence of severe sepsis.
  • Patients with septic shock develop hypotension from peripheral vasodilation (which leads to decreased systemic vascular resistance) and capillary leak with loss of intravascular volume into the surrounding tissues (which leads to borderline-low right atrial pressure and pulmonary capillary wedge pressure [PCWP]). To compensate for intravascular hypovolemia, the cardiac index and stroke volume increase, leading to an increased pulse pressure (systolic minus diastolic pressure), which can manifest as bounding peripheral pulses.

The finding of bounding peripheral pulses is seen in the early phase of sepsis, known as the hyperdynamic phase. Cx: Without treatment, this can progress to the more severe hypodynamic phase, with patients developing cool and clammy extremities due to decreased blood supply as blood is preferentially shunted to the vital organs

Fever, leukocytosis, and source of infection are characteristically present.

Dx: Serum lactate levels and blood cultures, as well as a blood count with differential, serum electrolyte and creatinine levels, urinalysis, liver chemistry tests, and coagulation parameters.

Serum lactate level indicating inadequate tissue perfusion: >4 mmol/L (36 mg/dL)

Tx: Surviving Sepsis Campaign Care Bundles

To be completed within 3 hours:

Measure serum lactate level

Obtain blood cultures before administering antibiotics.

Administer broad-spectrum antibiotics.

Administer 30 mL/kg crystalloid for hypotension or lactate ≥4 mmol/L.

To be completed within 6 hours:

Apply vasopressors (for hypotension not responding to initial fluid resuscitation) to maintain an MAP ≥65 mm Hg.

In the event of persistent arterial hypotension despite volume resuscitation (septic shock) or initial lactate ≥4 mmol/L (36 mg/dL):

Measure CVP (target of 8-12 mm Hg).

Measure ScvO2 (target ≥70%).

Remeasure lactate if original level was elevated.

94
Q

Treatment of Sepsis:

A

Crystalloid

Restores intravascular volume, which is depleted in patients with severe sepsis. Improves cardiac output, organ perfusion, and mortality in patients with severe sepsis. Fluid challenge infusion of at least 30 mL/kg should be given and repeated until the patient shows a beneficial response without major adverse effects. Patients may require 4-6 L during initial stabilization.

Antibiotics (fourth-generation cephalosporin, extended-spectrum [antipseudomonal] penicillin, carbapenem)

Early appropriate antibiotic therapy is associated with improved outcomes. Appropriate empiric therapy should be initiated rapidly, even if the source of infection is unknown. A more appropriate, source-directed antibiotic selection should be initiated if the source is known or becomes known (eg, add vancomycin if MRSA is suspected, add double coverage with an intravenous fluoroquinolone or aminoglycoside if a highly resistant gram-negative pathogen is suspected, or add clindamycin if toxic shock syndrome is suspected); consider additional agents (eg, fluoroquinolones, macrolides, tetracyclines, antifungal agents, antiviral agents) depending on the clinical presentation.

Vasopressors: norepinephrine, epinephrine, dobutamine, dopamine, vasopressin phenylephrine

Improves blood pressure and cardiac output. Norepinephrine is associated with less tachycardia than other vasopressor agents with β-effects and is more effective than dopamine in refractory septic shock. Vasopressin works on receptors other than adrenergic receptors and may be useful in refractory septic shock treated with high-dose adrenergic vasopressors. Dobutamine may be used in combination with a vasopressor to increase cardiac output if it is inappropriately low.

95
Q

Shigella spp.

A

Routine stool culture cannot distinguish pathogenic E. coli from normal fecal flora. Therefore, in the setting of blood in the stool, test specifically for shiga toxin.

If symptoms have persisted beyond 7 days, stool should be examined for ova and parasites.

Travel history

12 h–8 d

Hemolytic uremic syndrome (hemolytic anemia, thrombocytopenia, acute kidney injury) can occur with Shiga toxin–producing E. coli or Shigella infection.

96
Q

Staphylococcus aureus

A

Potato salad, mayonnaise, ham

1–8 h

97
Q

Streptococcal pharyngitis

A

Hx: Fever, tonsillar exudates, and tender anterior cervical adenopathy; cough is absent.

The Centor criteria (fever >38.1°C [100.5°F], tonsillar exudates, and tender cervical lymphadenopathy, absence of cough) predict the likelihood of streptococcal pharyngitis.

Patients with all four criteria have a 40% or greater chance of having group A β-hemolytic streptococcal (GABHS) pharyngitis; patients with zero or one criterion have a low (<3%) probability of having GABHS pharyngitis

Patients with two or three criteria have an intermediate probability of having GABHS pharyngitis.

The most cost effective approach to patients who have all four criteria is to treat with antibiotics without performing laboratory testing. If someone has three criteria, the chance of having a strep infection drops to 40% to 60%, and a person with only two of the criteria has a 1% to 5% chance.

Dx: Some guidelines recommend throat culture and others recommend rapid antigen detection test (RADT) with confirmation of negative results.

Tx: Penicillin

Approximately 20% of school age children are carriers of group A β-hemolytic Streptococcus.

Recent studies have shown that these carriers do not need to be identified or treated, as they do not develop complications
from infection and have not been found to be important in the spread of group A β-hemolytic Streptococcus to others.

Cx:

Peritonsilar abscess

Trismus (reduced ability to open the jaw due to muscle spasm), unilateral tonsillar swelling, and deviation of the uvula suggest peritonsillar abscess. This condition can be fatal secondary to either airway obstruction or spread of the infection into the parapharyngeal space, which may lead to involvement of the carotid sheath. Initial treatment consists of aspiration of the peritonsillar abscess and initiation of intravenous antibiotics. Surgical intervention may be necessary if the purulent material cannot be removed with aspiration alone.

98
Q

Eating contaminated pork may result in a Taenia solium gastrointestinal tapeworm infection.

A

Humans can transmit tapeworm eggs to others, causing cysticercosis. Cysticercosis usually affects the brain (seizures) or cerebral ventricular system (intracranial hypertension).

99
Q

💜Tubercuosis

A

Hx: Weight loss, cough, incarceration and homelessness

Dx:

Nearly one third of the worldwide population has latent tuberculosis (TB). The risk of reactivation is fairly low in patients without HIV (lifetime risk ~10%); however, those with HIVare 30-100 times more likely to develop active disease. As such, all patients newly diagnosed with HIV should receive latent TB testing with the tuberculin skin test (PPD) OR interferon-gamma release assay.

A PPD test is considered positive in an HIV-infected individual when induration is ≥5 mm at 48-72 hours. Active TB must then be ruled out with a chest x-ray (infiltrate, lymphadenopathy) and symptom review (night sweats, fevers, cough).

💀 CRX: The classic appearance of reactivation TB is lesions in the apical posterior segments of the upper lung and superior segments of the lower lobe. Chest radiograph results may be normal in patients with endobronchial disease or in symptomatic HIV-infected patients with active TB. In disseminated disease, 50%-90% have a miliary pattern on chest x-ray.

TST: A positive test result may indicate latent TB. False-positive results can occur with exposure to nontuberculous mycobacteria and BCG vaccine. False-negative results occur in anergic patients and in up to 25% of patients with active TB.

IGRA: IGRA is more specific than, and at least as sensitive as TST. It is preferred to TST in the setting of previous BCG vaccination and in individuals who are unlikely to return to have the test interpreted. Like TST, IGRA cannot distinguish between LTBI and active infection.

Sputum “smear” for acid-fast bacilli: At least 5000 to 10,000 organisms should be present for a smear to be positive. The more acid-fast bacilli seen, the more infectious is the patient. Induced sputum or gastric washings may be obtained if a patient does not have a productive cough. Nontuberculous mycobacteria may produce positive smears.

Sputum “culture” for acid-fast bacilli: Solid media cultures in conjunction with liquid media are often the 🥇gold standard used for diagnosis. The only false-positive results that occur are as a result of laboratory error or contamination of the specimen. False-negative results do occur and are often due to nontuberculous mycobacterial overgrowth and antibiotic treatment.

Nucleic acid amplification of smear-positive sputum: Results are available in a few hours. False-positive results occur only with laboratory contamination, although the test does not indicate if bacteria are alive or dead (ie, may remain positive for some time after treatment).

Tx:

Respiratory isolation precautions in a negative pressure room, not contact precautions.

Active tuberculosis is at least 6 months of RIPE a four-drug regimen usually consisting of isoniazid, rifampin, pyrazinamide, and ethambutol (RIPE).

Latent TB: Isoniazid daily for 9 months (Pyridoxine is added to prevent isoniazid-induced peripheral neuropathy) OR rifampin daily for 4 months OR rifapentine AND isoniazid once weekly for 3 months via directly observed therapy.

Ddx:

Presence of multiple nodules with bronchiectasis on lung CT is highly specific for Mycobacterium avium complex.​

≥5 mm

  • HIV-positive patients
  • Recent contacts of known TB case
  • Nodular or fibrotic changes on chest x-ray consistent with previously healed TB
  • Organ transplant recipients & other immunosuppressed patients

≥10 mm

  • Recent immigrants (<5 years) from TB-endemic areas
  • Injection drug users
  • Residents & employees of high-risk settings (eg, prisons, nursing homes, hospitals, homeless shelters)
  • Mycobacteriology laboratory personnel
  • Higher risk for TB reactivation (eg, diabetes, leukemia, end-stage renal disease, chronic malabsorption syndromes)
  • Children age <4, or those exposed to adults in high-risk categories

≥15 mm

  • All of the above plus healthy individuals

Cx: Adrenal Insufficiency: TB is a common cause of chronic primary adrenal insufficiency in endemic areas. Patients typically develop gradual fatigue, weakness, borderline hypotension, and electrolyte abnormalities.

100
Q

Vibrio vulnificus

A

Epidemiology

  • Gram-negative, free-living in marine environments
  • Ingestion (oysters) or wound infection
  • ↑ Risk in those with liver disease* (cirrhosis, hepatitis)
    • Hereditary hemochromatosis is particularly high risk as iron acts as a growth catalyst.

Manifestations

  • Rapidly progressive (often <12 hours)
  • Septicemia - septic shock, bullous lesions
  • Cellulitis - hemorrhagic bullae, necrotizing fasciitis

Diagnosis

  • Blood & wound cultures

Treatment

  • Empiric in those with likely illness as highly fatal
  • Intravenous ceftriaxone + doxycycline

Vibrio vulnificus is a free-living, gram-negative bacterium that grows in brackish coastal water and marine environments. Levels are greatest in the summer months, reaching as high as 8% of total bacteria in some areas. Infections are primarily acquired through the consumption of raw oysters (which concentrate the bacteria) or through wound contamination during recreational activities (eg, sailing) or raw seafood handling. Most patients who become ill have liver disease (eg, alcoholic cirrhosis, viral hepatitis); those with hemochromatosis are at particularly great risk as free iron acts as an exponential growth catalyst.

Patients with wound contamination typically develop a mild cellulitis, but those with liver disease or certain comorbidities (eg, diabetes mellitus) are at risk for necrotizing fasciitis with hemorrhagic bullous lesions and septic shock. Diagnosis is made by blood and wound cultures, but treatment (intravenous antibiotics) should not be delayed due to the high risk of death.

101
Q

Vibrio cholerae

A

Disruption of intestinal mucosal ion transport and subsequent water secretion (eg, cholera)

Hx: Shellfish

8–72 h

102
Q

🐄 Viral hepatitis

A

At least five distinct causes. Determined by serologic testing for hepatitis A, B, C, D, and E and confirmation of viral replication of hepatitis B and C. RIBA for HCV infection may also be used for confirmation.

Hepatitis 🅰:

History of travel to Mexico, work as a teacher. Incubation period of about 1 month.

Typically is associated with an abrupt onset of constitutional symptoms, such as fatigue, anorexia, malaise, nausea, and vomiting. Low-grade fever and right upper quadrant pain often are present as well.

Dx: Confirm the diagnosis with serologic testing, specifically IgM antibody to HAV. In most patients, IgM antibody is detectable by the time a person is symptomatic and becomes undetectable by 6 months. The IgG antibody indicates prior infection and immunity; there is no chronic state of hepatitis A.

Serum AST and ALT > 500 U/L, often greater than 1000 U/L; ALT > AST

Hepatitis 🅱 Drug abuse or blood transfusion

Inactive carrier state there would be no evidence of active viral replication with circulating viral DNA)

🕰 Chronic HBV infection:

Immune-tolerant is identified by the presence of a circulating viral level in the absence of markers of liver inflammation. This pattern typically occurs in patients born in hepatitis B–endemic areas such as Southeast Asia or Africa in whom HBV was likely acquired perinatally. As long as patients maintain normal serum aminotransferase levels, they are at low risk for progression of liver disease.

Resolved hepatitis B virus (HBV) infection: Individuals who are immune to HBV due to natural infection are positive for anti-HBs and negative for HBsAg. They are also positive for IgG anti-HBc because they form antibodies directed against the HBV core antigen.

Dx:

  • HBsAg: The first serologic marker detected in the serum after inoculation. It precedes the onset of clinical symptoms and elevation of serum aminotransferases. It also remains detectable during the entire symptomatic phase of acute hepatitis B and suggests infectivity.
  • Anti-HBs: Appears in the serum after either successful HBV vaccination or clearance of HBsAg, and remains detectable for life in most patients. It indicates non-infectivity and immunity.
    • However, there is a time lag between the disappearance of HBsAg and the appearance of anti-HBs; this is termed the “window period.”
  • HBcAg: This marker is not detectable in serum as it is normally sequestered within the HBsAg coat.
  • Anti-HBc: IgM appears shortly after the emergence of HBsAg and may be the only diagnostic marker for acute HBV infection during the “window period.” IgG remains detectable during recovery from acute HBV infection or progression to chronic infection.
  • HBeAg: This antigen is detectable shortly after the appearance of HBsAg and indicates active viral replication/infectivity. It is associated with the presence of HBV DNA. HBeAg tends to disappear shortly after aminotransferase levels peak and before HBsAg is eliminated; it is followed by the appearance of anti-HBe.
  • Anti-HBe: This marker suggests cessation of active viral replication and low infectivity.

A “window period” exists when HBsAg levels have fallen but antibody to HBsAg (anti-HBs) has not yet become detectable; diagnosis is then based on the presence of antibody to hepatitis B core antigen (anti-HBc [IgM]).

The first serologic marker to appear in the serum with acute hepatitis B is HBsAg, which appears usually 4-8 weeks after infection. IgM anti-HBc appears shortly thereafter, which is around the time clinical symptoms occur and patients develop elevations in hepatic aminotransferase levels (often >25 times the normal limit).

Test patients with evidence of chronic liver disease for chronic hepatitis B. Also test patients with glomerulonephritis, polyarteritis nodosa, or cryoglobulinemia because these are extrahepatic manifestations of chronic hepatitis B.

Tx: Patients with chronic hepatitis B and a circulating viral level may show evidence of liver inflammation, evidenced by persistently elevated serum aminotransferase levels indicating active hepatitis. In these patients, liver biopsy should be considered and treatment should be initiated if significant inflammation or progressive liver injury is seen.

Hepatitis C infection is often progressive and may result in cirrhosis and hepatocellular carcinoma. Hx: Usually manifests as chronic liver disease because the acute infection is usually asymptomatic. Dx: Test patients with chronic liver disease for anti-HCV antibody. Consider testing patients with extrahepatic complications of hepatitis C, including mixed cryoglobulinemia syndrome (eg, palpable purpura, arthralgias, glomerulonephritis, low complement levels), lichen planus, and porphyria cutanea tarda (PCT).

Porphyria cutanea tarda (PCT) presents with fragile, photosensitive skin that develops vesicles and bullae with trauma or sun exposure (eg, dorsa of the hands). Healed lesions typically scar and can form both hypo- and hyperpigmented areas. HCV is strongly associated with PCT, and all patients with PCT should be screened. Dx: Diagnosis of PCT is supported by increased plasma and urine porphyrins. A positive antibody test indicates only exposure, not immunity; therefore, HCV RNA must be measured to confirm ongoing infection. Tx: involves either serial phlebotomy or hydroxychloroquine along with management of underlying causes (eg, HCV).

Tx: Previous treatments were based on pegylated interferon and ribavirin, the introduction of protease inhibitors effective against HCV (eg, boceprevir, simeprevir, telepravir) and direct-acting antiviral agents (eg, sofosbuvir) has markedly changed HCV therapy. Antiviral therapy for HCV infection is associated with significant morbidity; therefore, which patients are candidates for antiviral therapy should be carefully considered.

103
Q

Yersinia spp.

A

Raw milk

Severe inflammation

104
Q

🦠 BACTERIA

A
105
Q

β-hemolytic streptococci

A

Group A Streptococcus 🥧 infection include fever, myalgia, cutaneous manifestations (cellulitis, fasciitis), pharyngitis, and shock.

🥊 Cellulitis is an infection of the deep dermis and subcutaneous fat caused by S pyogenes (group A β-hemolytic streptococci). There is often a preceding event such as a cut in the skin, dermatitis, or superficial fungal infection that precedes this rapidly spreading cellulitis. Patients are usually febrile and may appear toxic. Flat edges

Erysipelas is a skin infection of the upper dermis and superficial lymphatic system most commonly caused by group A Streptococcus. Infections take hold in areas of skin disruption, often due to minor trauma, inflammation, concurrent infection, or edema. Patients rapidly develop systemic symptoms (fever, chills), regional lymphadenitis, and a warm, tender, erythematous rash notable for raised, sharply demarcated borders. Involvement of the 👂🏽 external ear is particularly suggestive of erysipelas as this skin lacks a lower dermis level.

Impetigo is a cellulitis caused by group A β-hemolytic streptococci. Predisposing factors include a warm and humid climate, poverty/crowding, poor personal hygiene, and pre-existing skin trauma/inflammation (eg, insect bite, eczema). Colonization with staphylococci or streptococci is also a risk factor. This superficial skin infection manifests with multiple painful pustules on the exposed areas of the face and extremities. Over the course of a week, the pustules rupture and harden into a characteristic golden-yellow (“honey”) crust. Local lymphadenopathy can be present, but fever is unusual. Antibiotics are indicated to reduce transmission and recovery time. Topical antibiotics (eg, mupirocin) are preferred for localized infection due to fewer side effects and less antibiotic resistance risk compared to oral therapy. Oral antibiotics (eg, cephalexin, dicloxacillin, clindamycin) (Choice B)are indicated when topical therapy is impractical for widespread non-bullous impetigo. Extensive bullous impetigo (ie, flaccid bullae containing yellow fluid) caused by S aureus is an additional indication for oral antibiotics. Thorough handwashing is also important to prevent the spread of this contagious infection.

Toxic shock syndrome: A form of septic shock caused by SA OR GABHS. Diagnosis of staphylococcal TSS requires the presence of fever >38.9°C, systolic BP < 90 mm Hg, characteristic rash with desquamation, and involvement of any three organ systems (GI, muscular, mucous membranes, kidney, liver, blood, CNS) in the presence of positive SA cultures. Streptococcal TSS is diagnosed by the presence of GABHS from sterile sites (definite) or nonsterile site (probable), hypotension, and the presence of organ dysfunction in any two of the following systems: kidney, liver, skin, blood, and pulmonary.

Necrotizing fasciitis is a rapidly spreading deep soft tissue infection. S pyogenes, reaches the deep fascia from the site of penetrating trauma. Necrotic tissue is Gram stained and cultured—streptococci, staphylococci, mixed anaerobic infection, or clostridia are all possible pathogens. Tx: Prompt surgical exploration down to fascia or muscle may be lifesaving. Antibiotics to cover these organisms are important but not as important as prompt surgical debridement.

Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score: White cell count, hemoglobin, sodium, glucose, creatinine, and C-reactive protein.

🌠 Staphylococcus aureus

Can cause cellulitis that is difficult to distinguish from erysipelas, but it is usually more focal and likely to produce furuncles, or abscesses.

Community onset skin infection is often caused by community-acquired methicillin-resistant S aureus (CA-MRSA). Over 63% of S. aureus isolates from the community were methicillin-resistant in one study. However, these isolates are different from the methicillin-resistant S aureus seen in the
hospital setting. Tx: Sensitive to linezolid and trimethoprim-sulfamethoxazole and to a lesser degree to clindamycin and tetracyclines.

Septic arthritis caused by bacteria that form gram-positive cocci in clusters is an orthopedic emergency requiring prompt management. Involvement in a contact sport puts the patient at risk for infections caused by
community acquired methicillin-resistant S aureus (CA-MRSA). Consulting orthopedic surgery and starting an antibiotic with activity against MRSA while awaiting culture results is the most appropriate course of action. Antibiotics with activity against MRSA include vancomycin, linezolid, daptomycin, and telavancin.

Desquamation of the skin usually occurs during or after recovery from /toxic shock syndrome (associated with a toxin produced by S aureus).

Ludwig angina is a rapidly progressive cellulitis of the submandibular and sublingual spaces. Most cases arise from contiguous (rather than lymphatic) spread of polymicrobial dental infections in the mandibular molars. This contiguous spread results in bilateral edema of the submandibular and sublingual spaces. As the submandibular area becomes tender and indurated, the floor of the mouth becomes elevated and displaces the tongue posteriorly, which may lead to acute airway obstruction. Additional clinical features of Ludwig angina include a neck that is often described as “woody” or “brawny” but has no associated lymphadenopathy. As with other lesions that threaten the airway, patients with examination findings concerning for impending airway obstruction (eg, drooling, inability to lay flat, tripod positioning) should have their airway secured, regardless of current oxygen saturation. This is because oxygen saturation is often maintained until very rapid decompensation (within minutes). Therefore, these patients require continued assessment and, if needed, intervention to secure the airway (eg, nasotracheal intubation, awake tracheostomy).

106
Q

☠ Osteomyelitis

<strong>Acute osteomyelitis </strong>typically presents with local pain, erythema, and fever over a few days or weeks.

<strong>Chronic Osteomyelitis: </strong>Indolent infection (ie, chronic osteomyelitis) with necrosis and fragmentation (sequestrum) of the bone.

A

‘Chronic’ osteomyelitis

Mechanisms

  • Hematogenous seeding
  • Extension from infection in adjacent structure
  • Direct inoculation (eg, compound fracture, bite wound)

Pathogens

  • Staphylococcus aureus (most common)
  • Coagulase-negative staphylococci
  • Polymicrobial

Risk factors

  • Surgical hardware/instrumentation
  • Diabetes
  • Impaired circulation or sensation in the limb

Clinical features

  • Persistent pain, swelling, chronic wound
  • Sinus tract with a persistently draining wound
  • Nonunion of fracture

Diagnosis

  • Positive probe-to-bone test
  • Imaging: lytic lesion with loss of cortical & trabecular bone, surrounding sclerosis, periosteal thickening
  • Bone biopsy for culture

Management

  • Surgical debridement
  • Antibiotics (prolonged course)

Hx:

Contiguous infection (eg, diabetic foot, wound): Polymicrobial infection; most commonly Staphylococcus aureus and coagulase-negative staphylococci. May also include streptococci, enterococci, gram-negative bacilli (eg, Pseudomonas sp., Enterobacter sp., Escherichia coli, Serratia sp.) and anaerobes (eg, Peptostreptococcus, Clostridium sp., Bacteroides fragilis)

Contaminated open fracture: Staphylococcus sp., aerobic gram-negative bacilli (eg, Pseudomonas sp., Enterobacter sp., E. coli, Serratia sp.)

Dog bite, cat bite: Pasteurella multocida

Foot puncture wound (wearing sneakers): Pseudomonas aeruginosa

Hematogenous (eg, bacteremia): S. aureus

Illicit intravenous drug use: Varies in different communities but typically includes S. aureus and Pseudomonas aeruginosa.

Sickle cell disease: Salmonella sp.

Hemodialysis: Staphylococcus sp., P. aeruginosa

Dx: Laboratory values typically include a normal leukocyte count. Markers of inflammation, such as an elevated erythrocyte sedimentation (>70mm/hr) rate and C-reactive protein level, but it can be increased by any significant inflammatory process and therefore is nonspecific. It can however be helpful in supporting the diagnosis and monitoring the response to therapy.

Leukocyte count: Absence of leukocytosis cannot be used as evidence against the diagnosis of infection (sensitivity 26%).

Erythrocyte sedimentation rate and C-reactive protein level: Most sensitive in patients with acute hematogenous osteomyelitis but often normal in early disease (sensitivity 50%-90%).

Sinus tract culture: Correlation is best for Staphylococcus aureus (sensitivity 80%). The association is poor for other microorganisms (sensitivity <40%).

Blood culture: Obtain in patients with fever or systemic signs of sepsis. Less sensitive in patients with chronic osteomyelitis and orthopedic implant–associated osteomyelitis (sensitivity <20%).

Blood cultures are obtained when signs and symptoms of infection are present. Superficial cultures obtained from drainage sites are often contaminated with skin flora and correlate poorly with deep cultures.

Plain bone radiography: Obtain in all patients. Soft tissue swelling earliest abnormality. Periosteal reaction and focal bony lysis may not be seen for 2 to 6 weeks (sensitivity 62%). Sclerotic changes with periosteal new bone formation suggest chronic infection. Plain radiographs also useful for identifying other causes of bone pain.

Radionuclide bone scan: High sensitivity (>90%). Specificity variable (38%-82%) because conditions with inflammation or increased bone turnover (eg, trauma, degenerative joint disease, surgery, malignancy) yield positive results. Specificity can be improved by pairing with a plain radiograph.

🥇 MRI: Excellent in distinguishing soft tissue infection from osteomyelitis. MRI can show changes of acute osteomyelitis within days of infection and are superior to and more sensitive (90%) and specific (80%) than plain films and computed tomography. They can also detect soft tissue abscesses and epidural, paravertebral, or psoas abscesses that may require surgical drainage. They can also be used to delineate anatomy before surgery. MRI is sensitive and specific for the diagnosis of vertebral osteomyelitis and is the diagnostic procedure of choice.

CT: Show excellent anatomic detail, and CT is the imaging study of choice for patients with osteomyelitis when MRI cannot be obtained (pacemaker or metal hardware).

Percutaneous bone biopsy: Not as invasive as an open biopsy. Mainly used in disc space infection or diabetic foot infection. Sensitivity 43%-87% varies and is lower with administrating antibiotics before biopsy.

Surgical bone biopsy: 🥇The gold standard for diagnosing osteomyelitis (sensitivity 100%, specificity 100%).

Tx:

6 to 8 weeks of antibiotics, but surgery is rarely required for cure.

🔪 Surgical debridement is usually warranted in cases of chronic osteomyelitis, contiguous osteomyelitis, and orthopedic implant–associated osteomyelitis. Complete drainage and debridement of all necrotic soft tissue and resection of dead and infected bone is required. Failure to remove an infected orthopedic implant allows the offending microorganisms to form a biofilm and, therefore, escape the effect of antimicrobial agents. In patients with peripheral vascular disease, revascularization is extremely important to allow adequate oxygenation of soft tissues, promote bone healing, and increase access of antibiotics and the host humoral response to the infected area. The application of vacuum-assisted closure devices and use of hyperbaric oxygen exposure are adjunctive therapies, which may offer benefit for a selective group of patients.

Hematogenous vertebral osteomyelitis can often be successfully treated with antibiotics alone, with relapse rates of less than 10% at 6 to 12 months of follow-up.

107
Q

♨ Fever

A

Defined as a body temperature ≥37.2°C (99.0°F) in the morning or ≥37.7°C (100.0°F) in the afternoon

Viral Illness

Most cases of fever seen in the outpatient setting are due to viral illness and will resolve in <2 weeks.

Leukopenia is most often due to viral illness but may also be seen in patients with autoimmune or marrow infiltrative disorders.

Bacterial infection

Is more likely if the patient is seriously ill (eg, pale, dyspneic, cool, clammy, hypotensive, tachycardic, cyanotic, confused or with an otherwise altered mental state).

Immature neutrophils (band forms), toxic granulations, or Döhle bodies on a blood smear may indicate a bacterial cause of fever.

Inpatient with source

Intravascular catheters (bacteremia), urinary catheters (urinary tract infection), nasogastric tubes (sinusitis), foreign bodies (infected prosthetic joint, vascular graft, or pacemaker), and blood transfusions (febrile transfusion reaction).

Check all invasive sites for signs of infection, inspect dependent parts of the body for skin breakdown (redness, warmth, tenderness, swelling, discharge), examine the legs for swelling, and look for medications associated with hyperthermia or fever.

Infectious Disease

The most common infectious cause is tuberculosis; intra-abdominal or pelvic abscess is another common cause. Vertebral osteomyelitis is occasionally characterized by FUO without localizing back pain or symptoms.

❤ Endocarditis - usually associated with culture-negative organisms, such as Coxiella burnetii, Bartonella quintana, or the HACEK organisms (Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae).

Febrile illnesses are often associated with rash. The distribution of the rash (eg, extremities [Rocky Mountain spotted fever], trunk [eg, infectious mononucleosis, typhoid fever], or palms and soles [eg, syphilis]), the chronicity of the rash relative to fever, and the character of the rash (eg, vesicular [eg, smallpox, chickenpox] or petechial [eg, vasculitis]) are important in determining a potential cause. Some fever-associated skin lesions suggest serious underlying illnesses, such as Janeway lesions, Osler nodes, or subconjunctival petechiae, which occur in patients with infective endocarditis.

108
Q

⛑ Bacterial meningitis

A

Age 2-50

  • Streptococcus pneumoniae, Neisseria meningitidis
  • Vancomycin + 3rd-generation cephalosporin

Age >50

  • S pneumoniae, N meningitidis, Listeria
  • Vancomycin + ampicillin + 3rd-generation cephalosporin

Immunocompromised

  • S pneumoniae, N meningitidis, Listeria, gram-negative rods
  • Vancomycin + ampicillin + cefepime

Neurosurgery/penetrating skull trauma

  • Gram-negative rods, MRSA, coagulase-negative staphylococci
  • Vancomycin + cefepime

3rd-generation cephalosporins: ceftriaxone or cefotaxime

Alternatives to cefepime: ceftazidime or meropenem

Alternative to ampicillin: trimethoprim-sulfamethizole for Listeria

Cefepime is a fourth-generation cephalosporin that covers most of the major organisms of bacterial meningitis (eg, Streptococcus pneumoniae, Neisseria meningitidis, group B streptococci, Haemophilus influenzae) as well as Pseudomonas aeruginosa. Vancomycin provides coverage against cephalosporin-resistant pneumococci, and ampicillin covers Listeria monocytogenes.

109
Q

🚽 URINARY TRACT INFECTION

A

The most likely responsible organism of UTI is E.coli

🍢Dipsticks are commercially available kits that detect the presence of leukocyte esterase and nitrites in the urine of patients with suspected UTI.

Leukocyte esterase in the urine indicates significant pyuria

Nitrites signify the presence of 🦖Enterobacteriaceae, which converts urinary nitrates to nitrites.

The advent of dipstick testing has significantly reduced the cost associated with urine culture; however, dipsticks are associated with a high false positive rate and high false negative rate. For this reason, a negative dipstick test in a patient with symptoms of UTI should still have urine cultures done.

E coli

Staphylococcus saprophyticus colonizes the rectum or the urogenital tract of approximately 5% to 10% of women and is second only to E coli as the causative agent of uncomplicated urinary tract infections

🧞‍♀️Pseudomonas aeruginosa is most common among non-lactose fermenting oxidase-positive gram negative bacteria. Antibiotics with anti-pseudomonal activity include certain penicillins (piperacillin/tazobactam and ticarcillin/clavulanate), cephalosporins (ceftazidime and cefepime), carbapenems (imipenem, meropenem, and doripenem), fluoroquinolones (ciprofloxacin and levofloxacin), and aminoglycosides (gentamicin, tobramycin, and amikacin).

Tx: Ceftriaxone, doripenem (antipseudamonal activity) , and trimethoprim-sulfamethoxazole can be used to treat urinary tract infections

Recurrent UTI

In 85% of women with recurrent UTIs, symptoms develop within 24 hours of sexual intercourse.

Tx:

Voiding after intercourse, acidification of the urine, and discontinuing diaphragm use.

Prophylactic antibiotics are indicated for women with frequent infections who are unresponsive to to other measures. Single-dose 👙postcoital antibiotic use is often helpful. If that does not decrease infections, daily single-dose antibiotic prophylaxis may be appropriate for 3 to 6 months 📆. If symptoms reoccur after discontinuation of daily prophylaxis, it may need to continue for 1 to 2 years.

110
Q

Cystitis

A

Hx: Dysuria, frequency, urgency, suprapubic pain, and sometimes without systemic symptoms (eg, fever, chills, nausea, vomiting).

Px: Suprapubic and/or lower abdominal discomfort. Laboratory: PMNs on urinalysis;

Urine culture with >104 CFU/mL of a typical uropathogen (in the setting of classic symptoms but a negative dipstick or microscopic evaluation, a culture will confirm the diagnosis).

Rx: Treat nonpregnant women who have uncomplicated cystitis empirically with:

Trimethoprim-sulfamethoxazole (TMP-SMZ) for 3 days.

Nitrofurantoin for 5 days if patient has a reported sulfa allergy

Fosfomycin single dose

Complicated cystitis refers to infections associated with factors that increase the risk of antibiotic resistance or treatment failure. Such factors include diabetes, chronic kidney disease, pregnancy, immunocompromised state, or urinary tract obstruction; hospital-acquired infection; or infection associated with a procedure (eg, cystoscopy) or indwelling foreign body (eg, catheter, stent). These patients should have urine culture prior to therapy.

⚡Painful bladder syndrome/interstitial cystitis

Epidemiology

  • More common in women
  • Associated with psychiatric & pain disorders (eg, fibromyalgia)

Clinical presentation

  • Bladder pain with filling, 🚽 relief with voiding
  • ↑ Urinary frequency, urgency
  • Dyspareunia

Diagnosis

  • Bladder pain with no other cause for ≥6 weeks
  • Normal urinalysis

The diagnosis of IC is largely clinical; however, additional laboratory testing—including a urinalysis, postvoid residual, and sexually transmitted infection screening—is performed to exclude other conditions (eg, cystitis, urinary obstruction, malignancy). Management includes bladder training, fluid management, analgesics, and avoidance of any precipitating agents (eg, caffeine, alcohol, artificial sweeteners).

Treatment

  • Not curative, focus is on improving quality of life
  • Behavioral modification, avoidance of triggers, physical therapy
  • Amitriptyline, pentosan polysulfate sodium
  • Analgesics for acute exacerbations

Hx: Chronic bladder pain associated with bladder filling and/or emptying; urinary frequency, urgency, and nocturia.

Px: Diffuse tenderness in lower abdomen and pelvis.

Dx: Based on characteristic symptoms and exclusion of other conditions.

111
Q

Vaginitis, cervicitis, or genital herpes

A

Hx: Vaginal discharge, no urinary frequency or urgency, possibly new sexual partner or unprotected sexual activity; history of previous STDs, recurrent genital HSV, or vaginitis; gradual onset of symptoms (Chlamydia). Dysuria can result from urine coming into contact with inflamed and irritated vulvar epithelial surfaces in the absence of a bacterial UTI. Women may be able to differentiate between “internal” (UTI associated) and “external” (vulvovaginal) dysuria, which helps to guide evaluation.

Px (Pelvic Exam): Vulvovaginal or cervical erythema, exudate, or ulcers; cervical discharge; adnexal tenderness or mass; cervical motion tenderness.

Dx: Abnormal vaginal fluid findings; viral test from vulvovaginal ulcers positive for HSV; cervical swab with PMNs (± gram-negative diplococci) on Gram stain (if done), and positive by culture (or other test) for Chlamydia and/or Neisseria gonorrhoeae (if indicated); urinalysis with PMNs but no bacteria; urine culture negative or with low counts of nonpathogens.

Tx: The recommended prophylaxis against recurrent UTIs is liberal fluid intake and postcoital voiding. Although these are not evidenced-based recommendations, they are unlikely to be harmful. If UTIs continue to occur despite these measures, prophylaxis with a postcoital antibiotic, such as ciprofloxacin, is appropriate.

112
Q

Urethritis

A

History: New sexual partner, unprotected sexual activity, gradual symptom onset (Chlamydia); history of previous STDs or recurrent genital HSV, ± vaginal discharge; ± urinary frequency or urgency. Inflammation of urethra from sexually transmitted pathogens can mimic bacterial cystitis. Sexual history can suggest the diagnosis. Chlamydia trachomatis is a common cause of urethritis in men.

Dx: Can be made with nucleic acid amplification testing of a first-catch urine sample without pre-cleaning the genital area; urine or urethral swab positive (by culture or other specific test) for Chlamydia or HSV (or Mycoplasma genitalium or Ureaplasma urealyticum). Urinalysis with PMNs but no bacteriuria; urine culture negative or low counts of nonpathogens;

Pelvic exam: Possibly normal, or evidence of coexistent vulvovaginitis or cervicitis/salpingitis.

Tx: Azithromycin or doxycycline.

113
Q

Acute prostatitis

A

In men with urinary symptoms and a normal urinary tract, cystitis and pyelonephritis are uncommon.

Acute prostatitis is most commonly seen in 30- to 50-year-old men. Causative organisms of acute prostatitis are usually gram-negative bacteria, with 🍔 Escherichia coli being the most common. Proteus also

Hx: Spiking fever, chills, dysuria, pelvic or perineal pain, and cloudy urine; possible obstructive symptoms (dribbling, hesitancy, and anuria).

Px: Prostate exam showing an edematous (boggy) and tender prostate.

Dx: Pyuria, positive urine culture

Tx: 🌼 Fluoroquinolones and trimethoprim-sulfamethoxazole have a broad spectrum of antibacterial activity against gram-negative pathogens, have excellent prostate penetration, and are usually well tolerated. Urine culture helps define the underlying organism, but prolonged treatment (6 weeks) with a fluoroquinolone (eg, levofloxacin) or trimethoprim-sulfamethoxazole is generally required to ensure eradication. These agents have excellent coverage against enteric pathogens and achieve high prostatic tissue levels.

Chronic Protstatitis

Hx: Dysuria and frequency in the absence of the signs of acute prostatitis; recurrent urinary tract infections. Prostate tenderness and edema, but is frequently normal. Cultures of urine or expressed prostatic secretions are almost always positive.

Cx: Prostatic swelling can sometimes impinge the urethra and cause difficulty voiding or acute urinary retention (with renal insufficiency). A suprapubic catheter is generally required for decompression because passage of urethral catheters can lead to sepsis (dislodging of bacteria from infected prostate) or prostatic rupture

114
Q

Epididymitis

Orchitis

A

Acute epididymitis in sexually active men younger than 35 years of age is most frequently caused by Chlamydia trachomatis. Neisseria gonorrhoeae also causes epididymitis in this age group. In older men, most infections occur in conjunction with urinary tract infection caused by enteric gram-negative organisms.

Hx: Unilateral pain and tenderness in the epididymis and testis (epididymitis-orchitis). The spermatic cord is enlarged and tender on palpation. Some patients may find relief with elevation of the testicle, whereas elevation usually exacerbates the pain of testicular torsion.

Dx: Leukocytes on urine microscopic examination or positive leukocyte esterase on urine dipstick is supportive of the diagnosis.

Tx: Ceftriaxone and doxycycline

115
Q

TOXIN

A
116
Q

Clostridium botulinum

A

Spores contaminate a puncture wound (eg, injection drug use), germinate in the anaerobic environment, and generate botulinum toxin in vivo. Botulism can also occur when spores (infant botulism) or preformed botulinum toxin (foodborne botulism) are ingested.

Exposure to botulinum toxin, which impairs the presynaptic release of acetylcholine at the neuromuscular junction, generally results in:

  • Symmetric, descending motor paresis beginning with the CNs; this often includes CN III, CN IV, and CN VI (diplopia, ptosis, mydriasis) and CN IX and CN X (dysphagia, suppressed gag)
  • Progressive respiratory compromise due to diaphragmatic paralysis
  • Autonomic dysfunction (eg, ileus, orthostatic hypotension, urinary retention)

Because botulinum toxin targets the motor synapse, sensory abnormalities and confusion are rare(although lethargy from respiratory failure can occur). In contrast to infant or foodborne botulism, wound botulism is often associated with fever and leukocytosis and generally presents ~10 days (rather than within hours) after transmission.

Confirmation requires the isolation of C botulinum in culture or identification of toxin in serum. However, urgent treatment with equine botulinum antitoxin is required to prevent progression and should not be delayed for testing in suspected cases. Respiratory support and wound debridement are also often required.

117
Q

Clostridium tetani

A

Clostridium tetani is an anaerobic, spore-forming, gram-positive bacillus that is found in soil. Following traumatic tissue inoculation, it can release a neurotoxin (tetanus toxin), leading to symptomatic tetanus.

Typical symptoms include tonic contraction and spasm of skeletal muscle (eg, neck stiffness, masseter spasm), which can last up to 4-6 weeks. The risk for tetanus is greatest in wounds that are deep (eg, puncture wounds) or contain devitalized tissue (eg, burns, crush injuries). Risk is increased in those who use intravenous drugs.

Tetanus is a vaccine-preventable illness, and symptomatic cases are uncommon in developed countries. Current recommendations are for children to receive a primary 3-dose vaccine series at ages 2, 4, and 6 months, with additional doses recommended at 15-18 months and 4-6 years. Adults should receive a single dose of tetanus-diphtheria-acellular pertussis (Tdap), followed by revaccination (booster) for tetanus and diphtheria (Td) every 10 years thereafter.

Patients with significant or dirty puncture wounds who have received >3 tetanus toxoid doses but have not received revaccination for tetanus within 5 years should be vaccinated.

Tetanus immune globulin (TIG) provides immediate passive (but temporary) immunity, is used to treat symptomatic tetanus. It is also recommended (in addition to tetanus vaccination) for prophylaxis following severe or contaminated wounds in patients who have NOT received at least 3 doses of tetanus vaccine or whose vaccine status is uncertain. TIG is never administered without tetanus vaccination.

118
Q

😷 Clostridioides (formerly Clostridium) difficile

A

C. difficile infection is an inflammatory condition of the colon caused by the ingestion of the spore-forming, anaerobic, gram-positive bacillus. The inflammatory response is secondary to toxin-induced cytokines (toxins A and B) in the colon. Findings can range from watery diarrhea to ileus and life-threatening conditions (toxic megacolon, perforation, sepsis).

Disruption in the mucosal barrier secondary to infection or inflammation.

Hx: Health care facility or antibiotic exposure; typically have diarrhea up to 10 to 15 times daily, lower abdominal pain, cramping, fever, and leukocytosis that often exceeds 15,000/µL (15 × 109/L)

Dx:

C. difficile toxin enzyme immunoassay should be performed if recent antibiotic use or hospitalization; sensitivity 70%–80% and specificity >97% for toxins A and B. Fecal specimens collected after 3 days of hospitalization have a very low yield for standard bacterial pathogens, and routine stool culture is not indicated for inpatients with diarrhea unless there is evidence of a specific outbreak.

Clostridium difficile polymerase chain reaction (PCR) and stool culture should be considered in patients with any features that require additional evaluation

Tx:

Oral vancomycin and IV metronidazole.

Recommended treatment of severe disease is oral vancomycin

Antidiarrheal agents should be avoided in patients with suspected inflammatory diarrhea (eg, diarrhea due to ulcerative colitis, C. difficile infection, or Shiga toxin–producing E. coli) because of the association with toxic megacolon.

Cx: Toxic megacolon is characterized by nonobstructive colonic dilation. It generally presents with the following:

  • Severe systemic toxicity (eg, fever, hypotension, tachycardia, lethargy)
  • Abdominal distension and pain (diarrhea may cease due to lack of colonic motility)
  • Leukocytosis (usually >15,000/mm3)
  • Radiographic evidence of large bowel dilation (eg, >6 cm in colon, >9 cm [90 mm] in cecum)

Tx: Treatment of toxic megacolon includes bowel rest, nasogastric tube, and aggressive antibiotic therapy against C difficile (eg, oral vancomycin plus intravenous metronidazole). Any agent that contributes to a lack of gastrointestinal motility (eg, opiates, anticholinergics, antimotility medications) should be discontinued. Lack of response or clinical deterioration often necessitates further imaging (eg, CT of the abdomen) and, sometimes, surgical intervention (eg, subtotal colectomy).

119
Q

Coxsackie virus

A

Herpangina is caused by Coxsackie virus and typically affects young children in the late summer or early fall. Patients have gray vesicles that progress to fibrin-coated ulcers. The oral enanthem is located in the oropharynx on the posterior soft palate, anterior palatine pillars, tonsils, and uvula. Unlike hand-foot-and-mouth disease, another condition caused by Coxsackie virus, herpangina is not associated with a rash.

120
Q

Ehrlichiosis

A

Ehrlichiosis is characterized by an acute febrile illness with malaise and altered mental status. Ehrlichiosis is not often associated with a rash (<30% in adults) and is described as “Rocky Mountain spotted fever (RMSF) without the spots.” Neurologic symptoms may include confusion, mental status changes, clonus, and neck stiffness. Laboratory studies often show leukopenia and/or thrombocytopenia, along with elevated aminotransferases and lactate dehydrogenase.

The diagnosis is often clinical, although definitive diagnosis can be made through visualization of intracytoplasmic morulae in white blood cells or through polymerase chain reaction testing. Doxycycline is the appropriate treatment and is often initiated empirically when the diagnosis is suspected while confirmatory testing is pending.

121
Q

🐖 Trichinellosis

A

A parasitic infection caused by the roundworm Trichinella. The organism is prevalent worldwide, but the infection is more common in Mexico, China, Thailand, parts of central Europe, and Argentina. Infection usually occurs after eating undercooked or raw meat (usually pork) containing encysted Trichinella larvae.

Within the first week of ingestion, gastric acid releases the encysted larvae. The larvae invade the small intestine and develop into worms (intestinal stage). Female worms can release new larvae (up to 4 weeks later) that migrate and encyst into striated muscle (muscle stage).

During the intestinal stage, patients can be asymptomatic or develop abdominal pain, nausea, vomiting, and diarrhea. During the muscle stage, patients may develop local or systemic findings due to larval migration, including fever, subungual splinter hemorrhages, conjunctival and retinal hemorrhages, periorbital edema, and chemosis. Larvae entering the muscle can cause pain, tenderness, swelling, and weakness (eg, neck, arms, shoulders).

Laboratory studies show eosinophilia (usually >20%), the hallmark of the disease. Other findings include possible elevated creatine kinase and leukocytosis. Diagnosis is suspected clinically with the characteristic triad of periorbital edema, myositis, and eosinophilia. Severe disease can involve the heart, lungs, and central nervous system.

Tx: Mild infections are typically self-limited; severe infections require antiparasitic therapy (eg, mebendazole, albendazole) with corticosteroids.

122
Q

Mycoplasma pneumonia

A

Epidemiology

  • Respiratory droplets
  • Close quarters/young (eg, school, military)
  • Fall or winter

Clinical

  • Indolent headache, malaise, fever, persistent dry cough
  • Pharyngitis (nonexudative)
  • Macular/vesicular rash

Diagnostic

  • Normal leukocyte count
  • Subclinical hemolytic anemia (cold agglutinins)
  • Interstitial infiltrate (chest x-ray)

Treatment

  • Usually empiric
  • Macrolide or respiratory fluoroquinolone

Mycoplasma pneumoniae is a highly infectious, low-virulence bacterium that is spread by direct contact with respiratory droplets. Outbreaks are common among young individuals who share close quarters (eg, school children, college students, military recruits), with peak prevalence in the fall and winter. Many infections are subclinical, but patients may develop illness in the upper or lower respiratory tract.

M pneumoniae is the most common cause of atypical pneumonia. Symptoms are indolent and include headache, malaise, fever, and incessant dry cough. Nonpurulent pharyngitis, macular skin rash, and subclinical hemolytic anemia (due to cold agglutinins) may occur. White blood cell count is usually normal. Chest x-ray typically reveals interstitial infiltrates; a serous pleural effusion may be present in approximately 25% of patients. Diagnosis is usually made with clinical and radiographic findings; laboratory testing is not generally needed in the outpatient setting. Empiric treatment with oral antibiotics (eg, azithromycin) is almost universally effective.

123
Q

☢ INFECTIOUS DISEASE

A
124
Q

Allergic conjunctivitis (AC)

A

Allergic conjunctivitis (AC) is caused by IgE-mediated acute hypersensitivity to environmental allergens. Episodes may be acute if due to a transient exposure (eg, pet dander) but more commonly are seasonal (pollen) or perennial (mold, dust). Symptoms include bilateral ocular pruritus, conjunctival injection, and eyelid edema. Patients often have clear discharge and mild crusting, but AC does not cause purulent discharge, visual changes, or pain.

The diagnosis is clinical and more common in those who have other atopic diseases (eg, asthma, allergic rhinitis). Treatment includes allergen avoidance when possible. AC can be treated topically with antihistamines, mast cell stabilizers, and artificial tears. Oral antihistamines can be helpful for patients with concomitant allergic rhinitis but may have systemic adverse effects (eg, sedation).

125
Q

Conjunctivitis

A

Gonococcal

  • 2-5 days
  • Marked eyelid swelling
  • Profuse purulent discharge
  • Corneal edema/ulceration
  • Tx: Single IM dose of 3rd- generation cephalosporin

Infants acquire gonococcal conjunctivitisthrough contact with infected genital secretions. Symptoms usually begin at age 2-5 days and include significant purulent discharge, eyelid swelling, and chemosis (conjunctival edema). If not treated promptly, gonococcal conjunctivitis leads to corneal ulceration, scarring, and blindness.

N gonorrhoeae may be visible as gram-negative intracellular diplococci. Culture of gonococci on Thayer-Martin agar is the gold standard for diagnosis. Treatment for the infant is one dose of intramuscular third-generation cephalosporin (eg, cefotaxime).

Gonococcal conjunctivitis in neonates can be prevented by screening pregnant women (age <25 or with risk factors) and treating their infections. However, the majority of infants with gonococcal conjunctivitis are born to mothers who:

  • Were not screened during pregnancy
  • Had negative screening early in pregnancy but were infected later
  • Had positive screening and were either not treated or treated and reinfected
  • Had home delivery or refused postpartum prophylaxis with topical erythromycin

All infants, regardless of maternal screening results, should receive topical erythromycin prophylaxis shortly after birth to prevent gonococcal disease.

Chlamydial

  • 5-14 days
  • Mild eyelid swelling
  • Watery, serosanguineous, or mucopurulent eye discharge
  • Tx: PO macrolide

C trachomatis cannot be seen on Gram stain and does not grow in routine culture; polymerase chain reaction testing is needed for confirming the diagnosis. Infected infants should receive oral macrolide therapy (azithromycin or erythromycin); systemic treatment is needed because topical erythromycin therapy alone has high failure rates. Patients should be monitored for pyloric stenosis, a potential adverse effect of oral macrolides in infants. Azithromycin is often used preferentially in infants <1 month given lower rates of pyloric stenosis when compared with erythromycin.

Bacterial conjunctivitis

  • Erythromycin ointment
  • Polymyxin-trimethoprim drops
  • Azithromycin drops
  • Preferred agent in contact lens wearers: fluoroquinolone drops

Viral conjunctivitis

  • Warm or cold compresses
  • ± Antihistamine/decongestant drops

Allergic conjunctivitis

  • Over-the-counter antihistamine/decongestant drops for intermittent symptoms
  • Mast cell stabilizer/antihistamine drops for frequent episodes
126
Q

CMV

A

Pulmonary symptoms (dyspnea on exertion, dry cough), gastrointestinal symptoms (abdominal pain, diarrhea, hematochezia), pancytopenia, mild hepatitis, and interstitial infiltrates on chest x-ray. This combination of findings strongly suggests tissue-invasive CMV disease (causing pneumonitis, gastroenteritis, and hepatitis). Diagnosis is confirmed by detecting CMV DNA in the blood using polymerase chain reaction (PCR); tissue biopsy is rarely required. Treatment involves discontinuing antimetabolite immunosuppression (eg, mycophenolate) and initiating antiviral therapy. Intravenous ganciclovir is used for patients with severe disease (eg, pneumonitis, meningoencephalitis, high viral loads, significant gastrointestinal disease). Patients with minimal signs and symptoms can take oral valganciclovir.

127
Q

Rabies

A

Rabies is a fatal, neurotropic, viral disease transmitted to humans by exposure to saliva from an infected animal through a bite. Hydrophobia and aerophobia are pathognomonic features of encephalitic rabies; the feeling of water or air triggers involuntary pharyngeal muscle spasms. Many patients are disoriented and agitated, with fluctuating mental status. The incubation period is 1-3 months, and almost all patients die within weeks of developing symptoms.

The majority of rabies transmissions in the United States are caused by bat bites. Other high-risk reservoirs of rabies in the United States include raccoons, foxes, and skunks. In contrast to the bites of these other animals, bat bites are small and relatively painless; they often go unnoticed initially and may occur during sleep. Therefore, all patients with direct exposure to bats require rabies prophylaxis unless they were aware of the bat at all times and are certain they were not bitten.

Known bites from bats or other high-risk animals require thorough wound cleansing with soap and water and urgent postexposure prophylaxis, which includes both rabies immune globulin and rabies vaccine. Prophylaxis can prevent progression to life-threatening encephalitic or paralytic rabies disease.

128
Q

Otitis externa

A

Risk factors

  • Water exposure
  • Trauma (eg, cotton swabs, ear candling)
  • Foreign material (eg, hearing aid, headphones)
  • Dermatologic conditions (eg, eczema, contact dermatitis)

Microbiology

  • Pseudomonas aeruginosa
  • Staphylococcus aureus

Clinical manifestations

  • Otalgia, pruritis, discharge, hearing loss
  • Pain with auricle manipulation
  • Ear canal erythema, edema, debris
  • Tympanic membrane spared (clear, not inflamed, no middle ear fluid)

Treatment

  • Topical antibiotic (eg, fluoroquinolone) ± topical glucocorticoid
  • Consider wick placement to facilitate medication delivery

Also called “swimmer’s ear” due to the most common risk factor: water exposure.

Water exposure facilitates development of OE through several mechanisms. Cerumen typically coats the external auditory canal but can be displaced when exposed to flowing water. Cerumen has antibacterial properties; therefore, its loss can lead to increased bacterial growth. In addition, the ear canal is typically acidic, which inhibits bacterial growth, but significant water exposure can raise the pH. Frequent or excessive water exposure can also cause maceration of the skin of the canal, which disrupts the skin’s protective barrier. Finally, water exposure introduces pathogenic bacteria into the external canal.

Pseudomonas aeruginosa, which grows in water, is the most common pathogenic organism implicated in OE. Topical antipseudomonal antibiotics (eg, fluoroquinolones) are appropriate first-line therapy and would also cover Staphylococcus aureus (the second most common cause). Patients should be instructed to keep the ear dry until the infection resolves.

129
Q

dog bites

A

Most experts suggest a short course of antibiotics should be started for cat, human, or monkey bites. Only 4% of dog bites become infected (and therefore do not necessarily need antibiotic prophylaxis), compared with 35% of cat bites and 50% of monkey bites (which require antibiotics in most cases). Cat bites are usually deep punctures. Human bites almost invariably become infected.

130
Q

Cyclospora cayetanensis

A

can cause prolonged diarrhea after an incubation period of about 7 days. Exposure is through contaminated foods. Diagnosis is confirmed by identifying oocysts in the stool. Trimethoprim/sulfamethoxazole is the treatment of choice; ciprofloxacin is an alternative.

131
Q

Diphyllobothrium latum

A

is the longest tapeworm affecting humans. It is frequently asymptomatic but can present with megaloblastic anemia as the worm will use vitamin B12 for its own growth. Praziquantel is currently the treatment of choice.

132
Q

Infant botulism

A

Pathogenesis

  • Ingestion of Clostridium botulinum spores (eg, environmental dust/soil, honey)
  • Spores colonize GI tract & produce toxin
  • Toxin inhibits presynaptic acetylcholine release

Clinical presentation

  • Age <12 months
  • Constipation, poor feeding, hypotonia
  • Oculobulbar palsies (eg, absent gag reflex, ptosis)
  • Symmetric, descending paralysis
  • Autonomic dysfunction (eg, decreased salivation, fluctuating HR/BP)

Diagnosis

  • Clinical
  • Confirmation by stool C botulinum spores or toxins

Treatment

  • Botulism immune globulin

Infant botulism is a neurologic condition occurring in children age <1 often following ingestion of honey contaminated with Clostridium botulinum spores. Whereas ingestion of preformed botulinum toxin results in foodborne botulism, infant botulism is caused by intestinal colonization of C botulinum spores that produce the toxin in situ. Infants are particularly vulnerable due to an immature digestive system lacking protective microbiota. C botulinum neurotoxin inhibits presynaptic acetylcholine release into the neuromuscular junction (NMJ), affecting the somatic nervous system (eg, skeletal muscles) and the autonomic nervous system (eg, smooth muscles).

Autonomic signaling is impaired first, and constipation from hypoactive bowel, along with poor feeding and irritability, is often the earliest sign of disease. Muscles innervated by cranial nerves are typically affected, causing oculobulbar weakness; absent gag reflex, ptosis, ophthalmoplegia, and impaired pupil constriction are common. Muscular weakness may progress to a descending paralysis and respiratory failure. Symmetric findings of diminished or absent deep tendon reflexes, decreased strength, and hypotonia are present on examination, but sensory function remains intact.

Infant botulism is diagnosed by identifying C botulinum spores or toxin in stool.

Treatment is intravenous botulism immunoglobulin and supportive care.

133
Q

Congenital syphilis

A

The clinical presentation of congenital syphilis is varied. Many newborns appear normal at birth and continue to be asymptomatic for the first few weeks or months of life. Most untreated infants will develop skin lesions, typically an infiltrative, maculopapular peeling rash that is most prominent on the face, palms, and soles. Involvement of the nasal mucous membranes causes rhinitis with a resultant serous, and occasionally purulent, blood-tinged discharge (snuffles). This, as well as scrapings from the skin lesions, contains abundant viable treponemes. Hepatosplenomegaly and lymphadenopathy are common, and early jaundice is a manifestation of syphilitic hepatitis. Liver function tests are elevated; hemolytic anemia and thrombocytopenia are common. Infants may have a saddle nose, a result of destruction of bone from syphilitic rhinitis. Among the later manifestations, or stigmata, of congenital syphilis is interstitial keratitis, which is an acute inflammation of the cornea that begins in early childhood (most commonly between 6 and 14 years of age). Interstitial keratitis represents the response of the tissue to earlier sensitization. Findings include marked photophobia, lacrimation, corneal haziness, and eventual scarring. Hutchinson teeth (peg or barrel-shaped upper central incisors), abnormal enamel, and mulberry molars (first lower molars with an abnormal number of cusps) are dental manifestations of syphilis.

134
Q

HSV

A

Transmission of HSV from mother to newborn can happen in utero, intrapartum, and postnatally. Intrapartum transmission is most common. Infants born vaginally to a mother with a primary genital herpes infection are at highest risk for disease, with up to a 50% possibility of perinatal transmission; the risk to a baby born to a mother with a recurrent HSV infection is much lower. About half the infants of congenital HSV are born to mothers who are unaware of their infection. Infants can display isolated CNS involvement, isolated cutaneous infection, or systemic generalized infection. Treatment usually is with acyclovir; even with therapy, morbidity is high in infants with CNS involvement.

Herpetic gingivostomatitis is a herpes simplex virus infection characterized by clusters of vesicles that generally localize to the anterior oral cavity (buccal mucosa, tongue, gingiva, hard palate) and lips

135
Q

Toxoplasmosis

A

can cause symptoms similar to other congenital infections, but the combination of hydrocephalus, chorioretinitis, and intracranial calcifications is considered the “classic triad” of toxoplasma infection in a neonate. Infection usually occurs during primary infection of the mother or as a reactivation of infection in an immune-compromised host. These infants may also display symptoms similar to other congenital infections, such as anemia, a petechial rash, organomegaly, jaundice, and seizures.

136
Q

Congenital cytomegalovirus (CMV)

A

Epidemiology

  • Most common congenital infection
  • Transmission: bodily fluids (eg, urine, saliva)
  • Main risk factor: caring for young children

Clinical features

  • Growth restriction & microcephaly
  • Periventricular calcifications
  • Hepatosplenomegaly
  • Thrombocytopenia

Diagnosis

  • PCR testing
  • Viral culture of urine/saliva

Treatment

  • Valganciclovir

Cytomegalovirus (CMV) infection is common among children age 1-4, and transmission in the day careor preschool setting is a major risk factor for infection of pregnant women. Most cases of infected children and adults are asymptomatic, but a minority may present with nonspecific symptoms (eg, pharyngitis, fatigue). Transmission of CMV among healthy children and adults occurs through contact with infected bodily fluids (eg, saliva, urine). Standard precautions (eg, hand hygiene, glove use) are an important step in prevention.

Vertical transmission from mother to infant occurs via placental transfer. Clinical features of congenital CMV infection include microcephaly with periventricular calcifications, which are the most specific findings for congenital CMV infection, as well as intrauterine growth restriction, hepatosplenomegaly, jaundice, and thrombocytopenia.

Many cases are asymptomatic; others may develop cytomegalic inclusion disease, a multiorgan manifestation of disease including intrauterine growth restriction (IUGR), hepatosplenomegaly, jaundice, petechiae or purpura, microcephaly, chorioretinitis, and intracranial calcifications. More than half of infants with this congenital infection develop sensorineural hearing loss.

137
Q

Epiglottitis

A

Microbiology

  • Haemophilus influenzae type b (Hib)

Clinical features

  • Distress (tripod position, sniffing position, stridor)
  • Dysphagia, dysphonia
  • Drooling
  • High fever

X-ray

  • “Thumb sign” (enlarged epiglottis)

Management

  • Endotracheal intubation
  • Antibiotics

Prevention

  • Immunization against Hib

Epiglottitis is an uncommon, potentially fatal infection of the epiglottis that can lead to complete upper airway obstruction. Isolated pathogens are usually nasopharyngeal bacteria, most commonly Haemophilus influenzae type b (Hib). Due to widespread vaccination against Hib, the incidence of epiglottitis has diminished. However, the proportion of epiglottitis caused by other pathogens, such as other strains of H influenzae, Streptococcus species (S pneumoniae, S pyogenes), and Staphylococcus aureus, has increased.

Symptoms include the rapid onset of respiratory distress (eg, stridor, retractions), dysphagia, and drooling due to impending airway occlusion from the swelling epiglottis. Therefore, the first step in management of epiglottitis is to secure the airway, usually via endotracheal intubation. Once the airway is secured, broad-spectrum antibiotic therapy with ceftriaxone (targeting H influenzae and Streptococcus species) and vancomycin (targeting S aureus, including methicillin-resistant strains) should be initiated promptly.

138
Q

Bacterial sinusitis

A

Signs and symptoms of someone with bacterial infection: a cold that improved, then became superinfected with bacteria (thus the initial improvement). There is purulent discharge. The illness has been going on for more than 7 days. There is a high fever and maxillary tenderness. All of these signs point to bacterial infection. When you have a bacterial infection on clinical suspicion, all you need do is treat with antibiotics. Amoxicillin-clavulanate (they will not make you choose between this and just amoxicillin) is the antibiotic of choice.

139
Q

HIV

A

In certain situations, such as in an infant born to an HIV-positive mother, prophylaxis against P jiroveci (formerly known as P carinii) infection is instituted. While awaiting final determination of this infant’s HIV status, which can take several months, prophylaxis with trimethoprim-sulfamethoxazole starting at 6 weeks is usually appropriate.

140
Q

Reye syndrome

A

Reye syndrome is an acquired mitochondrial hepatopathy that results from the interaction of an influenza (or varicella) infection and aspirin use. While prevalence has decreased over the last few decades and it is now a rare disease, mortality remains the same at more than 40% of cases. Liver enzymes and ammonia are elevated, but total bilirubin is not. Patients initially present toward the end of a viral infection with sleepiness, emesis, and abnormal liver functions. As the disease progresses, the patient may develop seizures, coma, hyperventilation, and decorticate posturing. Ultimately they may develop respiratory arrest, loss of deep tendon reflexes (DTRs), and fixed and dilated pupils. Death is usually from cerebral edema and subsequent herniation. While aspirin is no longer routinely used in children as an antipyretic or pain reliever, the increase in the use of aspirin in adults with heart disease requires specific counseling for parents of children with influenza and varicella to avoid aspirin use. In addition, both of these infections are preventable with proper immunization. N-acetylcysteine is protective of hepatocytes in acetaminophen overdose.

141
Q

Kawasaki disease

A

Epidemiology

  • 90% age <5
  • Increased incidence in East Asian ethnicity

Diagnostic criteria

  • Fever ≥5 days plus ≥4 of the following findings:
    • Conjunctivitis: bilateral, nonexudative
    • Mucositis: injected/fissured lips or pharynx, “strawberry tongue”
    • Cervical lymphadenopathy: ≥1 lymph node >1.5 cm in diameter
    • Rash: erythematous, polymorphous, generalized; perineal erythema & desquamation; morbilliform (trunk, extremities)
    • Erythema & edema of hands/feet

Treatment

  • Aspirin plus intravenous immunoglobulin

Complications

  • Coronary artery aneurysms
  • Myocardial infarction & ischemia

Scarlatiniform rash, desquamation, erythema of the mucous membranes that produces an injected pharynx and strawberry tongue, and cervical lymphadenopathy are prominent findings in both.

Although KD is self-limited, untreated patients are at risk for developing life-threatening cardiovascular sequelae, particularly coronary artery aneurysms. The dilated arteries are prone to thrombosis, potentially leading to myocardial ischemia and death. Left ventricular (LV) dysfunction due to systemic or myocardial inflammation may occur and, in young children, manifests as tiredness, poor feeding, and diaphoresis during feeds. Lower extremity edema and hepatomegaly occur with progressive LV overload. Tachypnea, tachycardia, and an S3 gallop on auscultation are characteristic.

Prolonged fevers (>10 days), delayed treatment with intravenous immunoglobulin (IVIG), and age <1 are risk factors for cardiac complications. Most aneurysms regress over time, and LV dysfunction typically improves with intravenous immunoglobulin administration.

142
Q

Leptospirosis

A

Leptospirosis is the most common zoonotic infection worldwide, and is often a mild or subacute illness, frequently escaping detection. Usually a history of exposure to dogs, cats, livestock, rats, or other wild animals is obtained. Two distinct courses of infection are described: “anicteric” leptospirosis and “icteric” leptospirosis (also called Weil syndrome). Both courses start with similar symptoms, as described in the case vignette, termed the “septicemic” phase. The majority of cases are anicteric, and after a few days of symptom resolution, patients go on to the “immune” phase in which meningitic symptoms return and can last up to a month. Between 50% and 90% of cases have meningeal involvement. Less than 10% of leptospirosis cases are “icteric,” but these patients go on to have more severe symptoms involving liver and kidney dysfunction. Penicillin and tetracycline (in children 10 years and older) are appropriate treatments, and seem to shorten the duration of the illness if started in the first week of symptoms. Some recommend prophylaxis with weekly doxycycline in endemic areas of the world. IVIG and aspirin are appropriate treatments for Kawasaki disease, but not leptospirosis.

143
Q

Measles (Rubeola) 🔼

A

Transmission

  • Airborne

Clinical presentation

  • Prodrome (eg, cough, coryza, conjunctivitis, fever, Koplik spots)
  • Maculopapular exanthem
    • Cephalocaudal & centrifugal spread
    • Spares palms/soles

Prevention

  • Live-attenuated measles vaccine

Treatment

  • Supportive
  • Vitamin A for hospitalized patients

Measles (rubeola) is an uncommon disease in areas where immunization rates are high, but sporadic outbreaks do occur.

Measles causes a blanching, maculopapular rash that spreads cephalocaudally and, after a few days, coalesces and appears darker (eg, reddish-brown) and nonblanching. Patients are ill-appearing with high fevers up to 40 C (104 F), coryza, cough, and conjunctivitis. The rash typically lasts 6 days. Koplik spots on the buccal mucosa are diagnostic.

The World Health Organization (WHO) recommends that, in communities where vitamin A deficiency is prevalent, vitamin A be given to all children with measles. Compliance with this recommendation has resulted in a definite reduction in measles-related morbidity and mortality. In the United States, vitamin A supplements should be considered for use in measles patients with immunodeficiency, impaired intestinal absorption, and malnutrition. Recent immigrants from areas with a high mortality from measles and who show ophthalmologic evidence of vitamin A deficiency (blindness, Bitot spots, or xerophthalmia) should also be included in that group.

144
Q

Mumps

A

Although mumps is usually thought of as a parotitis, it is a generalized infection and, as such, can have widespread effects and a variety of clinical presentations. Many infections with the mumps virus are unrecognized because of the substantial rate of subclinical attacks. Meningitis, pancreatitis, and renal involvement can occur as part of the disease. Many patients with mumps have some WBCs in their spinal fluid. The meningitis that occurs with mumps can occur at the same time as the parotitis, or following the parotitis by about 10 days. Orchitis, seen most frequently in postpubertal males, has been reported in young children as well. All of these problems can be prevented by prior immunization with live attenuated virus vaccine; widespread use of this vaccine has reduced the number of cases in the United States to less than 500 per year. Arthritis is rare in children. Subendocardial fibroelastosis in a newborn was once thought to be associated with prenatal infection with mumps, but this does not appear to be true.

145
Q

Stevens-Johnson syndrome

A

The combination of erythema multiforme and vesicular, ulcerated lesions of the mucous membranes of the eyes, mouth, anus, and urethra defines the Stevens-Johnson syndrome (erythema multiforme major). Fever is common, and even pulmonary involvement occasionally is noted; the mortality rate can approach 10%. Common complications include corneal ulceration; dehydration due to severe stomatitis, and, subsequently, poor fluid intake; and urinary retention caused by dysuria. Among the known causes of the Stevens-Johnson syndrome are allergy to various drugs (including phenytoin, barbiturates, sulfonamides, and penicillin) and infection with a variety of organisms including Mycoplasma pneumoniae or herpes type 1.

146
Q

Shigella gastroenteritis

A

Transmission

  • Fecal-oral
  • Food or waterborne

Clinical presentation

  • Rapid-onset, high fever
  • Abdominal pain, watery diarrhea with mucus, +/- blood
  • +/- Seizures in children

Management

  • Fluid & electrolyte replacement
  • Antibiotics if immunocompromised, bacteremic or severely ill

Bacterial gastroenteritis (rapid onset of symptoms, high fever, profuse diarrhea with mucus), can be caused by multiple organisms; however, in children, seizures in the setting of an acute bacterial gastroenteritis are most closely associated with Shigella. Possible mechanisms include febrile seizure resulting from infection or toxins produced by the organism itself. Shigella gastroenteritis usually causes mucoid diarrhea (~80%) that is often but not always bloody.

147
Q

HSV infection

A

Herpes viruses (eg, herpes simplex, varicella, Epstein-Barr) most commonly cause encephalitis in immunocompetent adults. HSV-1 most often presents as temporal lobe encephalitis; HSV-2 causes aseptic meningitis. HSV meningitis is often associated with primary genital infection.

Hx: Patients typically present with fever, altered mental status, agitation, headaches, and seizures that can rapidly progress to complete Clinical signs of meningeal irritation (eg, photophobia, nuchal rigidity) are usually absent in patients with pure encephalitis. unresponsiveness or coma.

Px: can show neurologic abnormalities, including hemiparesis, cranial nerve palsies, and exaggerated deep-tendon reflexes.

Dx: Lumbar puncture usually shows cerebrospinal fluid (CSF) findings of elevated white blood cell count (50-1000/µL) with lymphocytic predominance, normal glucose (>45 mg/dL), and normal to slightly elevated protein concentration <200 mg/dL (generally 100 mg/dL). Most patients have an increased red blood cell count as well. Diagnosis is usually confirmed by detecting viral DNA by polymerase chain reaction (PCR) in the CSF.

MRI: Usually involves (hemorrhage of) the medial temporal and inferior frontal lobes.

Tx: HSV meningitis is often self-limiting and does not require antiviral treatment. HSV encephalitis does require antiviral treatment. Empiric treatment with intravenous acyclovir should be started while awaiting PCR results as encephalitis is often associated with significant morbidity and mortality.

148
Q

Mycobacterial, HIV, mumps virus, tick-associated bacterial and spirochetal

A

Hx: immunosuppression or exposure history

HIV-associated aseptic meningitis generally follows a mononucleosis-like syndrome. Most commonly seen in acute HIV infection.

Viral load should be obtained to exclude acute HIV. Always a consideration in young adults and patients with high-risk behaviors.

149
Q

Cryptococcal meningoencephalitis

A

Hx: Cryptococcal meningitis is usually a subacute meningitis, and patients commonly present after weeks of symptoms. It is most commonly seen in immunocompromised patients (eg, those with HIV).

Symptoms are due to increased intracranial pressures (headache) from capsular swelling; almost all patients have markedly elevated opening pressure on spinal tap.

Tx: Intravenous amphotericin (plus flucytosine) is used for induction therapy

150
Q

🥶 🗿 Rubella (German measles)

A

Clinical presentation

  • Congenital:
    • Sensorineural hearing loss
    • Cataracts
    • Patent ductus arteriosus
  • Children:
    • Fever
    • Cephalocaudal spread of maculopapular rash
  • Adolescents/Adults:
    • Same as children + arthralgias/arthritis

Diagnosis

  • Serology

Prevention

  • Live attenuated rubella vaccine

A mild, vaccine-preventable viral illness. Symptoms develop 2-3 weeks after inhalation of infected respiratory droplets. Patients may be asymptomatic or have initial symptoms of low-grade fever and lymphadenopathy, particularly suboccipital, posterior 👂🏽 auricular, and posterior cervical. A fine, pink, maculopapular exanthem begins on the face, spreads quickly in a cephalocaudal pattern to the rest of the body, and lasts <3 days. Some patients also have petechiae or erythematous papules, known as Forchheimer spots, on the soft palate. Treatment is supportive.

Although postnatal infection is mild, prenatal infection can result in spontaneous abortion, fetal demise, or congenital rubella syndrome. Immunization with the measles, mumps, and rubella vaccine at ages 1 and 4 is the best method of prevention.

151
Q

Scarlet fever

A

A streptococcal infection that can cause fever, palatal petechiae, and a “sandpaper” texture rash. The rash usually begins and is most prominent within skinfolds (eg, axillae, groin) and then spreads to the trunk and extremities. In addition, the diagnosis is rare for patients under age 3.

152
Q

🦠 HPV

A

Human papillomavirus (HPV) is the most common sexually transmitted infection and has been linked to multiple diseases, including condylomata acuminata as well as vulvar, vaginal, anal, oropharyngeal, and cervical cancer. Persistent HPV infection (particularly with types 16 and 18) results in cellular dysplasia as the incorporation of viral DNA creates increased pro-oncogenic protein expression and inhibits normal cellular regulation. The HPV vaccination induces an antibody response that decreases the risk of future HPV infection and subsequent related diseases.

Disease associations

  • Cervical cancer
  • Vulvar & vaginal cancers
  • Anal cancer
  • Penile cancer
  • Oropharyngeal cancer
  • Genital warts

Vaccine indications

  • All girls & women* age 11-26
  • Boys & men age 9-21 (9-26 for men
  • who have sex with men; individuals with HIV)

The quadrivalent HPV vaccination has been shown to be highly immunogenic, safe, and well-tolerated in females aged 9 to 26. To be most effective, the vaccine should be given before a female becomes sexually active. It can be administered when a patient has an abnormal Pap test or when a woman is breast-feeding. It can also be given when a patient is immunocompromised because of a disease or medication. It is not recommended for use during pregnancy. The vaccine was recently approved for use in males aged 9 to 26 to reduce the likelihood of genital warts. As in women, it is most effective if administered before exposure to HPV through sexual contact.

Both vaccines protect against high-risk HPV subtypes (HPV-16 and HPV-18), and the quadrivalent additionally protects against subtypes that cause genital warts (HPV-6 and HPV-11). Either vaccine is recommended for use in women. Both vaccines are administered in three doses: time zero and then 1 to 2 months later, with the third dose being given 6 months after the initial dose. Pregnant women should not receive the vaccine because there is a lack of safety data in this population.

The ACIP also recommends that boys and men age 11 to 21 years receive the quadrivalent vaccine, although the vaccine may be given to boys as young as 9 years of age.

HPV 6 & 11​: Anogenital warts (condylomata acuminata)[benign]

Caused by human papillomavirus (HPV), a common sexually transmitted infection. Condyloma acuminata occur due to persistent infection with low-risk HPV strains 6 and 11, and patients with chronic tobacco use or immunosuppression (eg, HIV) have an elevated risk.

  • Sexual abuse in 👶🏽 children
  • Autoinoculation from other sites
  • Prenatal or perinatal

Clinical features

  • Multiple pink or skin-colored lesions
  • Lesions ranging from smooth, flattened papules to exophytic/cauliflower-like growths
  • Pink/flesh-colored, verrucous papules & plaques
  • Asymptomatic (most common)
  • Pruritic, friable lesions

Anogenital warts typically appear as clusters of soft, pink or skin-colored (fleshy) lesions in the internal or external vaginal, vulvar, and anal regions in women. Most lesions are exophytic, dry-appearing, and verrucous (ie, cauliflower-like), although some may appear sessile and flat. Genital warts are typically asymptomatic and nontender, although pruritic, friable lesions (eg, those that bleed with manipulation) may occur.

Laryngeal papillomas are caused by human papillomavirus (HPV) subtypes 6 and 11,

HPV can be transmitted via nonsexual contact such as vertical transmission during delivery, autoinfection from other areas of the body, or heteroinoculation from a caregiver (eg, diaper changes). However, because of the association with transmission via direct genital contact, an assessment for sexual abuse is required in all children, particularly those age ≥4.

Diagnosis is primarily clinical, based on the characteristic appearance of the lesions. Small anogenital warts are treated with topical agents that either chemically injure the lesion (eg, trichloroacetic acid, podophyllin resin) or stimulate an immune response to it (eg, imiquimod).

Treatment

  • Chemical: Podophyllin resin, 🔱trichloroacetic acid
  • Immunologic: Imiquimod
  • Surgical: Cryotherapy, laser therapy, excision (large bleeding lesions)

Anogenital warts in children are often self-resolving; therefore, asymptomatic patients typically require only observation. For those with symptomatic or unresolved disease, management options include topical treatments (eg, podophyllotoxin) and surgical removal. Although podophyllum is not recommended for extensive disease because of toxicity (peripheral neuropathy). Medical treatment with podophyllum, imiquimod, trichloroacetic acid, and 5-fluorouricil requires weeks or months of therapy to be effective.

HPV, in particular types 16, 18, and 31, have been linked to 🎒 cervical neoplasia 🦀.

153
Q

Giardiasis

A

Risk factors

  • Exposure to contaminated food or water
  • Fecal incontinence & crowding (eg, daycare, nursing homes)

Presentation

  • Acute
    • Loose, foul-smelling, fatty stools
    • Abdominal cramps
    • Flatulence
    • Weight loss
  • Chronic
    • Malabsorption (eg, lactose intolerance)
    • Profound weight loss
    • Vitamin deficiencies

Treatment

  • Metronidazole

Giardia is endemic in low-resource settings and is a frequent cause of travel-associated diarrhea. In high-resource settings, the most common risk factor for Giardia is exposure to oocysts shed by infected mammals (eg, beavers) into rivers and lakes.

During the acute phase, giardiasis causes histologic changes in the small intestine (eg, disruption of the microvilli on enterocytes). This results in malabsorption and subsequent loose, oily stools; weight loss; and flatulence. Treatment with metronidazole is highly effective.

Cx: Patients who are not treated are at high risk for chronic malabsorption. Lactose intolerance (due to brush border disruption) and fatty acid malabsorption (which causes the oily, malodorous stools) are the most common sequelae. Chronic malabsorption can lead to profound weight loss and vitamin deficiencies.

154
Q

Acute rhinosinusitis

A

Clinical features

  • Nasal congestion and/or purulent drainage
  • Facial pressure/pain
  • ± Fever, cough, headache, loss of smell, ear pain

Etiology

  • Viral
    • No fever or early resolution of fever
    • Mild symptoms (eg, well-appearing, mild facial pain)
    • Improvement & resolution by day 5-10
  • Bacterial
    • Fever ≥3 days OR
    • New/recurrent fever after initial improvement OR
    • Persistent symptoms ≥10 days

Treatment

  • Intranasal saline, saline irrigation, NSAIDs
  • Antibiotics if bacterial

Rhinosinusitis is a common infection of the upper respiratory tract characterized by inflammation of the nasal passages and paranasal sinuses. Presenting symptoms include nasal congestion and/or purulent discharge in addition to facial pressure/pain that is exacerbated by leaning forward. Pain with palpation or percussion of sinuses is common. Additional symptoms may include fever, cough, headache, ear pain, and loss of smell.

Viral rhinosinusitis can be differentiated from bacterial rhinosinusitis by the duration and severity of symptoms. History suggestive of a viral etiology includes mild symptoms (eg, no fever or early resolution of fever, mild pain) and improvement by day 5-10. In contrast, the clinical course of bacterial rhinosinusitis is one of the following: severe in onset (ie, high fever for ≥3 days), persistent (ie, symptoms lasting ≥10 days without improvement), or biphasic (ie, recurrent fever after initial improvement).

Management of viral rhinosinusitis is supportive care, including intranasal saline, saline irrigation, and nonsteroidal anti-inflammatory drugs.

155
Q

Coxsackie virus

A

Herpangina is caused by Coxsackie virus and typically affects young children in the late summer or early fall. Patients have gray vesicles that progress to fibrin-coated ulcers. The oral enanthem is located in the oropharynx on the posterior soft palate, anterior palatine pillars, tonsils, and uvula. Unlike hand-foot-and-mouth disease, another condition caused by Coxsackie virus, herpangina is not associated with a rash.

156
Q

Neonatal tetanus

A

Clinical features

  • Difficult feeding, trismus
  • Spasms & hypertonicity: Clenched hands, dorsiflexed feet, opisthotonus

Treatment

  • Supportive care
  • Antibiotics & tetanus immune globulin

Prevention

  • Immunization
  • Hygienic delivery & cord care

Clostridium tetani is ubiquitous in the soil, and neonatal tetanus can result when at-risk infants are exposed to C tetani through unhygienic delivery or cord care practices. C tetani produces a toxin (tetanospasmin) that prevents inhibitory neurotransmitter release at the junction of upper and lower motor neurons. Uninhibited lower motor neurons lead to spasms and hypertonicity.

Neonatal tetanus presents in the first few weeks of life. Signs of umbilical infection are generally present, but the diffuse hypertonicity (opisthotonus) is the hallmark of neonatal tetanus. Feeding difficulty is due to trismus (lockjaw) from spasm of the muscles of mastication. Patients are at risk for life-threatening stridor and respiratory failure as the diaphragm and upper airway muscles contract. Treatment includes supportive care (eg, nutrition and respiratory support), antibiotics (eg, penicillin), and passive immunization with tetanus immune globulin. Routine immunization of children and pregnant women against tetanus has virtually eliminated neonatal tetanus in the developed world, but sporadic cases continue to occur among unimmunized communities.

157
Q

Bacterial Lymphadenitis

A

Lymphadenitis is diagnosed when the lymph node becomes tender and erythematous in addition to being enlarged. Although there are multiple causes for lymphadenopathy in children, the differential diagnosis can be narrowed by determining if the lymphadenopathy is acute or subacute/chronic, and if it is unilateral or bilateral. Acute, unilateral lymphadenitis in children is usually caused by bacterial infection. Staphylococcus aureus is the most common pathogen isolated, followed by group A streptococcus. Patients with bacterial lymphadenitis are usually less than 5 years old and nontoxic appearing. The affected lymph node is tender, warm, erythematous, and usually 3 to 6 cm in size. In some cases, the infection can progress to induration and fluctuance.

158
Q

Orbital cellulitis

A

Risk factors

  • Local infection (eg, sinusitis, dental infection, skin infection)
  • Orbital trauma

Clinical signs

  • Painful eye movements
  • Ophthalmoplegia
  • Proptosis
  • Visual changes

Diagnosis

  • Clinical
  • CT scan if diagnosis is uncertain

Treatment

  • Intravenous antibiotics
  • Surgical drainage for abscess

The most common risk factor for orbital cellulitis is sinusitis, particularly of the ethmoid or maxillary sinuses. Patients may have purulent rhinorrhea, fever, and facial pain, such as the right cheek tenderness in this child. The proximity of the sinuses to the orbital space allows the contiguous spread of bacteria (eg, Streptococcus species, Staphylococcus aureus) during episodes of severe sinusitis. The subsequent intraorbital infection causes inflammation of the extraocular muscles (ophthalmoplegia, painful eye movements) and orbital fat (proptosis).

Patients with suspected orbital cellulitis should undergo CT scan of the orbits and sinuses to identify drainable fluid collections within the orbit (ie, orbital abscess). Intravenous antibiotic therapy is the mainstay of treatment, and purulent material in the sinuses or orbit should be drained if present.

159
Q

⛑ MENINGITIS

A

<1 month

  • Group B Streptococcus
  • Escherichia coli & other gram-negative bacteria
  • Listeria monocytogenes
  • Herpes simplex virus

≥1 month

  • Streptococcus pneumoniae
  • Neisseria meningitidis

N meningitidis is the second most common cause of bacterial meningitis in children age 1 month to 10 years (behind Streptococcus pneumoniae) and is the most common cause among adolescents. The risk of acquiring meningococcal disease is 10-fold higher in children age <2 years compared with older children.

Dx:

  • Protein concentration [normal <40 mg/dL]
  • Glucose concentration [normal 40 - 70 mg/dL]
  • Leukocyte (WBC) count [normal 0 - 5 cells/mm3]
160
Q

Bacterial meningitis

A

Hx: Fever, severe headache, stiff neck, photophobia, drowsiness or confusion, nausea, vomiting. Brudzinski sign

🥇 S. pneumoniae🏇🏽 the most common cause and may occur in patients with other foci of infection (eg, pneumonia, otitis media, mastoiditis, sinusitis, or endocarditis) or following head trauma with leakage of cerebrospinal fluid (CSF).

N. meningitidis is the second most common cause of bacterial meningitis in children age 1 month to 10 years (behind Streptococcus pneumoniae) and is the most common cause among adolescents. The risk of acquiring meningococcal disease is 10-fold higher in children age <2 years compared with older children. Meningococcal disease often presents with a petechial rash on the extremities that may become purpuric as the infection progresses. The disease progresses rapidly and carries very high morbidity and mortality rates even with appropriate treatment. Empiric therapy for suspected bacterial meningitis should include a third-generation cephalosporin (eg, ceftriaxone) and vancomycin. N meningitidis is generally susceptible to penicillin and third-generation cephalosporins.

Group B Streptococcus is the most common cause of meningitis in neonates (age <28 days) and infants age <3 months.

L. monocytogenes meningitis develops most frequently in neonates, older adults (>50 years of age), and those who are immunocompromised (diabetes mellitus, liver or kidney disease, collagen vascular disorders, disorders of iron overload, HIV infection, transplant recipients, and patients taking anti-tumor necrosis factor α agents such as infliximab and etanercept)

Dx: CSF findings that predict bacterial etiology with ≥99% certainty include:

Protein concentration >250 mg/dL [normal <40 mg/dL]

Glucose concentration <40 mg/dL [normal 40 - 70 mg/dL]

CSF-blood glucose ratio <0.23

Leukocyte (WBC) count >2000/µL [normal 0 - 5 cells/mm3]

Neutrophil count >1180/µL

A computed tomography (CT) scan of the head should be done before lumbar puncture in mass lesion suspected patients, as well as patients who are immunocompromised, have a history of CNS disease, present with new-onset seizures, or have a decreased level of consciousness, focal neurologic deficits, or papilledema.

Tx:VancomycinAND anIV third-generation cephalosporin(eitherceftriaxoneorcefotaxime) (ANDampicillin in adults age >50) are empiric treatments for bacterial meningitis.

161
Q

Non-polio Enteroviral infection

A

Echoviruses and coxsackieviruses.

Hx: Fever, severe headache, stiff neck, photophobia, drowsiness or confusion, nausea, vomiting. Most cases occur in the summer and early fall. Children are most often affected. Most frequently identified cause of aseptic meningitis.

Dx: PCR for enterovirus is available.

162
Q

Arboviral infection

A

St. Louis encephalitis virus, California encephalitis virus, West Nile virus, and eastern equine are most common.

Hx: Most often presents as encephalitis but can present as meningitis or meningoencephalitis. Seen in patients living in or traveling to areas of arboviral activity or epidemic. Most cases occur in warmer months and when contact with mosquito vectors is most likely.

163
Q

HSV infection

A

Herpes viruses (eg, herpes simplex, varicella, Epstein-Barr) most commonly cause encephalitis in immunocompetent adults. HSV-1 most often presents as temporal lobe encephalitis; HSV-2 causes aseptic meningitis. HSV meningitis is often associated with primary genital infection.

Hx: Patients typically present with fever, altered mental status, agitation, headaches, and seizures that can rapidly progress to complete Clinical signs of meningeal irritation (eg, photophobia, nuchal rigidity) are usually absent in patients with pure encephalitis. unresponsiveness or coma.

Px: can show neurologic abnormalities, including hemiparesis, cranial nerve palsies, and exaggerated deep-tendon reflexes.

Dx: Lumbar puncture usually shows cerebrospinal fluid (CSF) findings of elevated white blood cell count (50-1000/µL) with lymphocytic predominance, normal glucose (>45 mg/dL), and normal to slightly elevated protein concentration <200 mg/dL (generally 100 mg/dL). Most patients have an increased red blood cell count as well. Diagnosis is usually confirmed by detecting viral DNA by polymerase chain reaction (PCR) in the CSF.

MRI: Usually involves (hemorrhage of) the medial temporal and inferior frontal lobes.

Tx: HSV meningitis is often self-limiting and does not require antiviral treatment. HSV encephalitis does require antiviral treatment. Empiric treatment with intravenous acyclovir should be started while awaiting PCR results as encephalitis is often associated with significant morbidity and mortality.

164
Q

Cryptococcal meningoencephalitis

A

Hx: Cryptococcal meningitis is usually a subacute meningitis, and patients commonly present after weeks of symptoms. It is most commonly seen in immunocompromised patients (eg, those with HIV).

Symptoms are due to increased intracranial pressures (headache) from capsular swelling; almost all patients have markedly elevated opening pressure on spinal tap.

Tx: Intravenous amphotericin (plus flucytosine) is used for induction therapy

165
Q

Viral (aseptic) meningitis

A

Protein concentration [normal <150 mg/dL] elevated

Glucose concentration [normal 40 - 70 mg/dL] normal

Leukocyte (WBC) count [normal 10 - 500 cells/mm3]

166
Q

Neonatal varicella-zoster infection (VZV)

A

Clinical features

  • Fever
  • Vesicular eruption (chickenpox)
  • Systemic involvement (eg, pneumonia, hepatitis, meningoencephalitis)

Treatment

  • Acyclovir

Prevention

  • Isolate infant from varicella contact
  • Administer varicella-zoster immune globulin to infant if maternal infection developed 5 days before or 2 days after delivery

Varicella-zoster virus (VZV), or chickenpox is transmitted via aerosolized droplets and is extremely contagious. Therefore, postexposure prophylaxis (PEP) is recommended for exposed individuals who are not immune, including patients who have not received 2 doses of VZV vaccine OR who have not had confirmed varicella infection. A single dose of VZV vaccine does not provide sufficient protection to consider a patient immune. For immunocompetent individuals, PEP is limited to immunization with the live VZV vaccine.

However, for high-risk patients who cannot receive VZV vaccine, PEP is achieved by administering passive immunization with varicella-zoster immunoglobulin (VZIG). Patients eligible for VZIG include neonates, pregnant women, and immunocompromised patients. VZIG for neonatal PEP is effective if maternal infection developed 5 days before to 2 days after delivery.

167
Q

Meningiococcus

A

In an infant with meningococcemia, watch out for Waterhouse-Friderichsen syndrome, which is characterized by a sudden vasomotor collapse and skin rash (i.e., large purpuric lesions on the flanks) due to adrenal hemorrhage. Fulminant meningococcemia can occur after a meningococcus infection, and approximately 10-20% of infants present with vasomotor collapse, large petechiae and purpuric lesions. The condition carries an almost 100% mortality.

168
Q

Ludwig angina

A

Ludwig angina is a rapidly progressive cellulitis of the submandibular space. Most cases arise from dental infections in the mandibular molars that spread contiguously down the root into the submylohyoid (and then sublingual) space. The infection is usually polymicrobial with a mixture of oral aerobic (eg, viridans streptococci) and anaerobic bacteria.

Patients develop symptoms rapidly with systemic (fever, chills, malaise) and local compressive (eg, mouth pain, drooling, dysphagia, muffled voice, airway compromise) manifestations. Physical examination findings are often striking due to mass effect from edema. The submandibular area is usually tender and indurated, and the floor of the mouth is often elevated, displacing the tongue. Anaerobic, gas-producing bacteria may cause crepitus.

CT scan of the neck confirms the diagnosis and rules out an abscess. Most patients are treated with intravenous antibiotics (eg, ampicillin-sulbactam, clindamycin) and removal of the inciting tooth. Drainage and surgery are rarely required as the process is cellulitic and typically nonsuppurative. Impaired respiratory status requires prompt attention and early intervention with a mechanical airway.

169
Q

Tick-borne paralysis

A

Tick-borne paralysis is characterized by rapidly progressive ascending paralysis (which may be asymmetrical), absence of fever and sensory abnormalities, and normal CSF examination. Ticks must feed for 4-7 days and are typically found on patients after meticulous searching. Removal of the tick results in spontaneous improvement in most patients.

170
Q

Chagas disease

A

A chronic protozoal disease caused by Trypanosoma cruzi. The organism is common throughout Latin America, and should be considered in a symptomatic patient who has recently immigrated from that area. The two primary manifestations of Chagas disease are megacolon/megaesophagus and cardiac disease. Megacolon or megaesophagus (focal GI dilatation) occur secondary to destruction of the nerves controlling the GI smooth muscle. The pathophysiology of Chagas heart disease is not well understood, but probably represents a prolonged myocarditis secondary to the protozoal infection.

171
Q

🔥🍗Guillain-Barré syndrome

A

Pathophysiology

  • Immune-mediated demyelinating polyneuropathy
  • Preceding gastrointestinal (Campylobacter) OR respiratory infection

Clinical features

  • Paresthesia, neuropathic pain
  • Symmetric, ascending weakness
  • Decreased/absent deep-tendon reflexes
  • Autonomic dysfunction (eg, arrhythmia, ileus)
  • Respiratory compromise

Diagnosis

  • Clinical
  • Supportive findings
    • Cerebrospinal fluid: ↑ protein, normal leukocytes
    • Abnormal electromyography & nerve conduction

Management

  • Monitor autonomic & respiratory function
  • Intravenous immunoglobulin or plasmapheresis

Bacterial or viral infection induces autoantibodies to motor nerves with resulting demyelination and neuropathy

Dx: Weakness and paresthesias; ascending pattern; respiratory muscle fatigue; autonomic dysfunction; decreased DTRs

Nerve conduction studies show acute peripheral polyneuropathy;

Cerebral spinal fluid (CSF) analysis shows a high protein concentration with normal white blood cell (WBC) counts (albuminocytologic dissociation). The CSF protein level may be elevated due to increased permeability of the blood-nerve-barrier. CSF red blood cell (RBC) and glucose levels should be normal.

Tx:

Gold standard treatment includes intravenous immunoglobulin (IVIG) or plasmapheresis. Patients should be monitored closely due to risk of respiratory failure. Most patients take several months to recover.

Cx: Neuromuscular respiratory failure is a life-threatening complication found in up to 30% of patients. Once GBS is suspected in a hemodynamically stable patient, the next step in management is to assess pulmonary function with spirometry. Forced vital capacity (FVC) and negative inspiratory force monitor respiratory muscle strength, and serial pulmonary function testing should be performed given the potential for rapid progression of disease. A decline in FVC (≤20 mL/kg) indicates impending respiratory failure warranting endotracheal intubation. Additional indications for elective or emergency intubation include respiratory distress (eg, tachypnea, accessory muscle use), severe dysautonomia (eg, heart rate and blood pressure instability), or widened pulse pressure Tx: Mechanical ventilation is required in approximately 30% of patients who have GBS, as it can cause sudden hypercarbic respiratory failure.

172
Q

😼Cat bite

A

Cats have long, sharp teeth that can inoculate oral flora deep into skin, reaching soft-tissue structures (eg, nerves, tendon sheaths). Therefore, cat bites are much more likely to cause serious infection than dog or human bites

Tx: Antibiotic prophylaxis is recommended in addition to routine wound care (eg, copious irrigation). Oral flora of cats includes Pasteurella multocida (gram-negative coccobacilli) and oral anaerobes.

Amoxicillin/clavulanate is the agent of choice for prophylaxis; amoxicillin has activity against P multocida, and the addition of clavulanate provides coverage against oral anaerobes.

“Cat-scratch disease” (Bartonella henselae) is uncommon and does not require antibiotic prophylaxis in immunocompetent individuals.

173
Q

🕷 Spider Bites

A

Brown recluse spider bites commonly occur as patients are putting their clothes on, although they often go unrecognized initially; over the course of a few days, a deep skin ulcerdevelops at the site of bite with an erythematous halo and a necrotic center, which can progress to an eschar. With basic wound management, the lesion often heals without scarring. Debridement should be avoided in the early stages of necrosis but may facilitate healing once the lesion is stable and well-demarcated; severe cases may require skin grafting.

Black widow spider bites often lead to more pronounced local and systemic manifestations due to effects of the toxin. These include muscle pain (a prominent finding), abdominal rigidity (sometimes mimicking a surgical abdomen), and muscle cramps (seen in >60% of patients). Patients commonly develop nausea and vomiting within hours of the bite.

174
Q

dog bites

A

Most experts suggest a short course of antibiotics should be started for cat, human, or monkey bites. Only 4% of dog bites become infected (and therefore do not necessarily need antibiotic prophylaxis), compared with 35% of cat bites and 50% of monkey bites (which require antibiotics in most cases). Cat bites are usually deep punctures. Human bites almost invariably become infected.

175
Q

Brain abscess

A

Microbiology

  • Staphylococcus aureus
  • Viridans streptococci
  • Anaerobes

Pathogenesis

  • Direct spread (eg, otitis media, mastoiditis, sinusitis)
  • Hematogenous spread (eg, endocarditis)

Clinical findings

  • Headache, vomiting
  • Fever
  • Focal neurologic deficits, seizure
  • Ring-enhancing lesion on neuroimaging (CT, MRI)

Treatment

  • Aspiration/surgical drainage
  • Prolonged antibiotic therapy

A single brain abscess is usually the result of direct extension from an adjacent tissue infection (eg, otitis media, sinusitis, dental infection). The 2 most commonly isolated organisms are viridans streptococci and Staphylococcus aureus. Symptoms are often nonspecific, which may delay diagnosis. Patients frequently have headaches that are severe, unilateral, and resistant to analgesics. Fevers are an unreliable predictor, occurring in ~50% of patients. If diagnosis is delayed, focal neurologic deficits or seizures may emerge.

Brain imaging (CT scan, MRI) typically reveals cerebritis initially, but within 1-2 weeks the infection consolidates to a ring-enhancing lesion with central necrosis. Diagnosis requires CT-guided aspiration or surgical biopsy to obtain tissue for Gram stain and culture (bacterial, fungal, mycobacterial). Most patients are treated with empiric, intravenous antibiotics (eg, metronidazole, ceftriaxone, and vancomycin) and aspiration of the lesion.

176
Q

Cutaneous larva migrans (CLM)

A

Cutaneous larva migrans (CLM) is a creeping cutaneous eruption caused by dog (Ancylostoma caninum) or cat (A braziliense) hookworm larvae. Most infections are acquired from walking barefoot on contaminated sand (beaches) or soil. Humans are incidental hosts, and larvae are typically unable to penetrate the dermal basement membrane. As a result, cutaneous infection without deeper penetration is the norm.

Most infections occur in the lower extremities (~70%), and symptoms usually start with a pruritic, erythematous papule at the site of larvae penetration (which may go unnoticed). Within a few days, patients develop symptoms related to larvae migration: intensely pruritic, serpiginous, reddish-brown cutaneous tracks. Although most cases resolve spontaneously after a few weeks, antihelmintics (eg, ivermectin) are usually given to aid clearance.