Step Up - Infectious Diseases Flashcards
1
Q
Nosocomial pneumonia - Definition:
A
Occurs after the first 72h of hospitalization.
2
Q
Classic CAP presents with:
A
- Sudden chill.
- Fever.
- Pleuritic pain.
- Productive cough.
3
Q
Atypical pneumonia - Presents with:
A
Often begins with a sore throat and headache followed by a non productive cough and dyspnea.
4
Q
2 recommended methods of prevention:
A
- Influenza vaccine - Give yearly to people at incr. risk for complications and to health care workers.
- Pneumococcal vaccine - For patients >65yr and for younger people at high risk (eg those with heart disease, sickle cell disease, pulmonary disease, diabetes, alcoholic cirrhosis, asplenic individuals).
5
Q
Typical CAP - Common agents:
A
- S.pneumoniae (60%).
- H.influenza (15%).
- Aerobic gram(-) rods (6-10%) - Klebsiella (and other Enterobacteriaceae).
- S.aureus (2-10%).
6
Q
Typical CAP - Clinical features - Symptoms:
A
- Acute onset of fever and shaking chills.
- Cough productive of thick, purulent sputum.
- Pleuritic chest pain (suggest pleural effusion).
- Dyspnea.
7
Q
Typical CAP - Signs:
A
- Tachycardia, tachypnea.
- Late inspiratory crackles.
- Bronchial breath sounds
- Incr. tactile vocal fremitus.
- Dullness on percussion.
- Pleural friction rub (associated with a pleural effusion).
8
Q
Most cases of CAP result from?
A
Aspiration of oropharyngeal secretions because the majority of organisms that cause CAP are NORMAL INHABITANTS of the pharynx.
9
Q
CXR - Typical CAP:
A
- Lobar consolidation.
2. Multilobar consolidation indicates very serious illness.
10
Q
General approach to diagnosis of CAP - 1st step:
A
Differentiate lower respiratory tract infection from the other causes of cough and from upper respiratory tract infection.
11
Q
General approach to diagnosis of CAP - 2nd step - Once lower tract infection is suspected:
A
Next task is to differentiate between pneumonia and acute bronchitis - Clinical features NOT reliable - CXR the only reasonable method of differentiating between pneumonia and acute bronchitis.
12
Q
Studies have shown that if VITAL SIGNS are entirely normal, the probability of pneumonia in outpatients is less than?
A
1%.
13
Q
Atypical CAP - Common agents:
A
- Mycoplasma pneumoniae (MC).
- Chlamydia pneumoniae.
- Chlamydia psittaci.
- Coxiella burnetti (Q fever).
- Legionella spp.
- Viruses - Influenza (A, B), adenoviruses, parainfuenza virus, RSV.
14
Q
Atypical CAP - Clinical features - Symptoms:
A
- Insidious onset - headache, sore throat, fatigue, myalgia.
- Dry cough (no sputum production).
- Fevers (chills are uncommon).
15
Q
Atypical CAP - Clinical features - Signs:
A
- Pulse-Temperature dissociation - normal pulse in the setting of high fever is suggestive of atypical CAP.
- Wheezing, rhonchi, crackles.
16
Q
Atypical CAP - CXR:
A
- Diffuse reticulonodular infiltrates.
2. Absent or minimal consolidation.
17
Q
Sputum culture CAP:
A
The value of routine sputum collection for Gram stain and culture is controversial. The Infectious Disease Society of America has recently advocated performing sputum Gram stain and culture in ALL patients hospitalized with CAP.
18
Q
The following steps are appropriate in patients admitted to the hospital with suspected pneumonia:
A
- CXR (PA and lateral).
- Lab tests - CBC and differential, BUN, Cr, glucose, electrolytes.
- SaO2.
- Two pretreatment blood cultures.
- Gram stain and culture of sputum.
- Antibiotic therapy.
19
Q
Diagnosis of pneumonia - CXR:
A
- PA and lateral CXR REQUIRED to confirm the diagnosis.
- Considered sensitive - If CXR findings are NOT suggestive of pneumonia, do not treat the patients with antibiotics.
- After treatment, changes evident on CXR usually lag behind the clinical response (up to 6wks).
- Changes include interstitial infiltrates, lobar consolidation, and/or cavitation.
- False-negative chest radiographs occur with neutropenia, dehydration, infection with PCP, and early disease <24h.
20
Q
Do radiographic changes and clinical findings help in identifying the causative organism in CAP?
A
No, they do not help.
21
Q
Pneumoniae pearls:
A
- Alcoholics –> Klebsiella.
- Immigrants –> TB.
- Nursing home residents –> Nosocomial pathogen and predilection for the upper lobes (eg Pseudomonas).
- HIV(+) –> PCP + TB - still more likely to have a TYPICAL infectious agent.
- Legionella –> Organ transplant recipients, renal failure, chronic lung disease, smokers.
22
Q
Diagnosis of pneumonia - Sputum Gram stain:
A
Try to obtain in all patients:
- Commonly contaminated with oral secretions.
- A good specimen has a sensitivity of 60% and specificity of 85% for identifying gram(+) cocci in chains (S.pneumoniae).
23
Q
Diagnosis of pneumonia - Sputum culture:
A
Try to obtain in all patients REQUIRING hospitalization - Specificity is improved if the predominant organism growing on the culture media correlates with the Gram stain.
24
Q
Diagnosis of pneumonia - Special stains of the sputum in selected cases:
A
- Acid-fast stain (Mycobacterium spp.) if TB is suspected.
2. Silver stain (fungi, Pneumocystis carinii) for HIV/immunocompromised.
25
Diagnosis of pneumonia - Urinary antigen assay for Legionella in selected patients:
1. Test is VERY SENSITIVE.
| 2. Antigen persists in the urine for WEEKS (even after treatment has been started).
26
Diagnosis of pneumonia - Blood cultures:
Positive in 5%-15% of cases.
27
Test for microbial diagnosis for outpatients?
NOT required - Empiric treatment is often successful if CAP is suspected.
28
Treatment of CAP - Decision to hospitalize:
The decision to hospitalize or treat as an outpatient is probably the MOST IMPORTANT decision to be made and is based on severity of disease.
29
Uncomplicated CAP in patients WITHOUT significant comorbidities - Treat with:
Azithromycin or Clarithromycin (if comorbidities, give a fluoroquinolone).
30
Treatment of pneumonia - In people younger than 60yrs:
MC organisms are: S.pneumoniae, Mycoplasma, Legionella, Chlamydia.
- -> Macrolides (azithromycin, clarithromycin) or doxycyclin cover ALL of these organisms and are the first-line treatment.
- -> Alternative: Fluoroquinolones.
31
Treatment of pneumonia - In older adults and patients with comorbidities (more likely to have typical CAP) OR those treated with antibiotics in the last 3 months, treat with:
First-line agent --> Fluoroquinolone (levofloxacin, moxifloxacin).
32
Treatment of pneumonia - For outpatient, treatment is continued for?
5 days. DO NOT stop treatment until patient has been afebrile for 48h.
33
Treatment of pneumonia - Hospitalized patients:
A fluoroquinolone alone or a 3rd-gen cephalosporin + macrolide (ceftriaxone + azithromycin) is appropriate.
34
Treatment of hospital-acquired pneumonia:
Treatment is tailored toward gram(-) rods (any of the following are appropriate):
1. Cephalosporins with pseudomonal coverage: ceftazidime, cefepime.
2. Carbapenems: imipenem.
3. Piperacillin/tazobactam
- -> Macrolides are NOT used - as they are in CAP.
35
Complications of pneumonia:
1. Pleural effusion ("parapneumonic effusions").
2. Pleural empyema occurs in 1%-2% of all cases of CAP (up to 7% of hospitalized patients with CAP).
3. Acute respiratory failure may occur if the pneumonia is severe.
36
Complications of pneumonia - Pleural effusion:
1. Can be seen in >50% of patients with CAP on routine CXR. Empyema is infrequent in these patients.
2. Most of these effusions have an uncomplicated course and resolve with treatment of the pneumonia with antibiotics.
3. Thoracentesis should be performed if the effusion is significant (>1cm on lateral decubitus film) --> Send fluid for Gram stain, culture, pH, cell count, determination of glucose, protein, and LDH.
37
Ventilator associated pneumonias - Risk:
1. Normal mucociliary clearance of the respiratory tract is impaired (cannot cough).
2. Also, positive pressure impairs the ability to clear colonization.
38
Ventilator associated pneumonia - Findings:
1. New infiltrate on chest X-ray, purulent secretions from endotracheal tube.
2. Fever.
3. Rising WBC count.
39
Ventilator associated pneumonia - Treatment:
Combination of the following 3 different drugs:
1. Cephalosporin (ceftazidime or cefepime) OR penicillin (piperacillin/tazobactam) OR carbapenem (imipenem).
2. Aminoglycoside OR fluoroquinolone.
3. Vancomycin OR linezolid.
40
Lung abscess Pearls:
1. Areas most likely to be infected by aspirated material - POSTERIOR segments of the UPPER lobes and SUPERIOR segments of the LOWER lobes.
2. Aspirated material is more likely to affect the RIGHT lobe due to angle of the right main stem bronchus from the trachea.
41
Lung abscess - Typical case:
The typical case is aspiration of a large volume of oropharyngeal contents or food, with resulting pneumonia and necrosis when adequate treatment is NOT administered.
42
By definition, a lung abscess is formed by?
One or more cavities, each >2cm in diameter.
43
Lung abscesses can be complications of the following:
1. Aspiration of organisms.
2. Acute necrotizing pneumonia.
3. Hematogenous spread of infection from distant site.
4. Direct inoculation with contiguous spread.
44
Lung abscess - Causative organisms:
Bacteria that colonize the oropharynx:
1. Oral anaerobes: Prevotella, Peptostreptococcus, Fusobacterium, Bacteroids spp.
2. Other: S.aureus, S.pneumoniae, and aerobic gram(-) bacilli.
45
Lung abscesses - Epidemiology/risk factors:
1. Main risk factor is predisposition to aspiration.
2. Poor dental hygiene.
3. Edentulous patients are less likely to aspirate oropharyngeal secretions.
46
Lung abscesses - Clinical features:
1. Majority --> Indolent course. Some present more acutely.
2. Cough - Foul-smelling sputum is consistent with ANAEROBIC infection - Sometimes blood-tinged.
3. Fever, chills.
4. Constitutional symptoms: Fatigue, malaise, weight loss.
47
Lung abscess - Diagnosis - CXR:
Reveals thick-walled cavitation with air-fluid levels.
| --> Look for abscess in dependent, poorly ventilated lobes.
48
Lung abscess - Diagnosis - CT:
May be necessary to differentiate between abscess and empyema.
49
Lung abscess - Diagnosis - Culture:
Consider obtaining cultures via bronchoscopy or transtracheal aspiration rather than simple expectoration to avoid contamination with oral flora.
50
Lung abscess - Treatment:
1. Hospitalization is often required if lung abscess is found. Postural drainage should be performed.
2. Antimicrobial therapy.
51
Lung abscess - Antimicrobial therapy:
1. Antibiotic regimens include coverage for the following:
a. Gram(+) cocci - ampicillin or amoxicillin/clavulanic acid, ampicillin/sulbactam, or vancomycin for S.aureus.
b. Anaerobes - Clindamycin or metronidazole.
c. If Gram(-) are suspected - Add fluoroquinolone or ceftazidime.
2. CONTINUE antibiotics until the cavity is gone or until CXR findings have improved considerably.
52
Lung abscess - Antimicrobial therapy - How long may it take?
This may take months!
53
TB - Transmission:
1. Occurs via inhalation of aerosolized droplets containing active organism.
2. Only those with active TB are contagious (eg by coughing, sneezing).
3. People with primary TB are NOT contagious.
54
Percentage of people with primary TB that will develop active disease in their lifetime?
Only 5-10%.
55
TB - Risk factors:
1. HIV(+)
2. Recent immigrants (within past 5yrs).
3. Prisoners
4. Health care workers
5. Close contacts of someone with TB.
6. Alcoholics
7. Diabetics
8. Glucocorticoid use
9. Hematologic malignancy
10. Injection drug users.
56
Primary TB - Clinical features:
1. Asymptomatic.
2. Pleural effusion may develop.
3. If the immune response is incomplete, the pulmonary and constitutional symptoms of TB may develop. This is known as progressive primary TB.
57
Primary TB - Radiographic findings:
1. Ghon's complex - calcified primary focus with an associated lymph node.
2. Ranke's complex - when Ghon's complex undergoes fibrosis and calcification.
58
Extrapulmonary TB - Sites:
1. Lymph nodes.
2. Pleura.
3. GUT.
4. Spine
5. Intestine.
6. Meninges.
59
Diagnosis of TB is challenging in HIV patients because:
1. PPD skin test result is negative.
2. Patients have "atypical" CXR findings.
3. Sputum smears are more likely to be negative.
4. Granuloma formation may NOT be present in the late stages.
60
Diagnosis of TB - CXR:
1. Classic --> Upper lobe infiltrates with cavitations.
2. Other possible findings:
a. Pleural effusion.
b. Ghon's complex and Ranke's complex - evidence of healed primary TB.
c. Atypical findings common in immunocompromised patients.
61
Diagnosis of TB - Sputum studies:
1. DEFINITIVE diagnosis is made by sputum culture - growth of M.tuberculosis.
2. Obtain 3 morning sputum specimens - culture takes 4-8wks.
3. PCR can detect more rapidly.
4. Diagnosis sometimes made by finding AFB on microscopic exam, but this is NOT definitive because other mycobacteria may colonize airways.
62
If PPD test is positive, what should be done?
A CXR to rule out active disease. Once active disease is EXCLUDED, 9 months of INH treatment is initiated (!).
63
A patient with a positive PPD test has how much lifetime risk of TB?
A 10% lifetime risk of TB --> This risk is reduced to 1% after 9months of INH treatment.
64
If patient has been BCG vaccinated, and we find positive PPD, do we give INH?
Yes, for 9 months, REGARDLESS of the BCG vaccination.
65
TB Treatment - Patients with active TB must be ISOLATED until sputum is negative for AFB. First-line therapy:
```
4-drug regimen:
1. INH
2. Rifampin
3. Pyrazinamide
4. Ethambutol or streptomycin
FOR 2 MONTHS!
```
66
TB Treatment - After the initial 2 month phase?
A phase of 4 MONTHS is recommended using INH and rifampin.
67
Prophylactic treatment for latent (primary) TB:
Consists of 9 months of INH after active TB has been excluded (negative CXR, sputum, or both).
68
ALL TB medications can cause?
Hepatotoxicity. Discontinue treatment only if liver transaminases rise to 3-5times the upper limit or normal.
69
Influenza - Transmission:
Orthomyxovirus --> Transmitted via respiratory droplets, typically occurring in winter months.
70
Influenza - Clinical findings:
Rapid onset of:
1. Fever
2. Chills
3. Malaise
4. Headache
5. Non productive cough
6. Sore throat
7. Nausea may also be present
71
Meningitis - Pathophysiology:
1. Infectious agents --> Frequently colonize the nasopharynx and respiratory tract.
2. These pathogens enter the CNS.
72
Meningitis - How do pathogens enter the CNS?
1. Invasion of the bloodstream, which leads to hematogenous seeding of the CNS.
2. Retrograde transport along cranial (eg olfatory) or peripheral nerves.
3. Contiguous spread from sinusitis, otitis media, surgery, or trauma.
73
Acute meningitis:
Onset within hrs to days.
74
Chronic meningitis:
Onset within weeks to months - commonly caused by mycobacteria, fungi, Lyme, or parasites.
75
Acute bacterial meningitis - Complications:
1. Seizures
2. Coma
3. Brain abscess
4. Subdural empyema
5. DIC
6. Respiratory arrest
76
Acute bacterial meningitis - Complications - Permanent sequelae:
1. Deafness
2. Brain damage
3. Hydrocephalus
77
Aseptic meningitis - Etiology:
1. Enteroviruses
2. HSV
3. Also by certain bacteria, parasites, fungi
78
Acute bacterial meningitis is a...?
MEDICAL EMERGENCY! Frequently fatal, even with appropriate treatment.
79
Acute bacterial meningitis - clinical features:
Characteristic triad:
1. Fever
2. Nuchal rigidity
3. Change in mental status
80
Meningitis - Symptoms:
1. Headache (may be more severe when lying down).
2. Fevers.
3. Nausea and vomiting.
4. Stiff, painful neck.
5. Malaise.
6. Photophobia.
7. Alteration in mental status (confusion, lethargy, even coma).
81
Meningitis - Signs:
1. Nuchal rigidity (may be ABSENT).
2. Rashes - Maculopapular with petechiae --> PURPURA is classic for N.meningitidis/ Vesicular lesions in varicella or HSV.
3. Incr. ICP and its manifestations - papilledema, seizures.
4. Cranial nerve palsies.
5. Kernig (only in 50%) and Brudzinki (only in 50%).
82
Diagnosis of meningitis - LP or CT first?
CT of the head, first --> If there are focal neurologic signs or if there is evidence of a space-occupying lesion with elevations in ICP.
83
Meningitis - Prophylaxis:
1. Rifampin
2. Ceftriaxone
for all close contacts of patients with meningococcus, give 1 dose of IM ceftriaxone.
84
Meningitis Treatment - Infants:
Cefotaxime + ampicillin + vanco (aminoglycoside if <4weeks).
85
Meningitis Treatment - 3mo to 50yrs:
Ceftriaxone or cefotaxime + Vancomycin.
86
Meningitis Treatment - >50yrs:
Ceftriaxone or cefotaxime + vancomycin + ampicillin.
87
Meningitis Treatment - Impaired cellular immunity (eg HIV):
Ceftazidime + Ampicillin + Vancomycin.
88
Encephalitis is often seen together with...?
Meningitis
89
Encephalitis - Viral causes:
1. HSV-1
2. Arbovirus - Eastern equine encephalitis, West Nile virus.
3. Enterovirus - polio.
4. Less common causes - Measles, mumps, EBV, CMV, VZV, rabies, prion diseases such as Creutzfeldt-Jakob.
90
Encephalitis - NON viral infectious causes:
1. Toxoplasmosis.
| 2. Cerebral aspergillosis
91
Encephalitis - Non infectious causes:
1. Metabolic encephalopathies.
| 2. T-cell lymphoma.
92
Encephalitis - Risk factors:
1. AIDS - toxoplasmosis when CD4 is <200.
2. Other forms of immunosuppression.
3. Travel in underdeveloped countries.
4. Exposure to insect (eg mosquito) vector in endemic areas.
5. Exposure to certain wild animals (bats) in an endemic area for rabies.
93
Encephalitis - Overall mortality:
About 10%.
94
Encephalitis - Clinical features:
1. Patients often have a prodrome of headache, malaise, and myalgias.
2. Within hours to days, patients become more acutely ill.
3. Patients frequently have signs and symptoms of meningitis (headache, fever, photophobia, nuchal rigidity).
4. Altered sensorium, possibly including confusion, delirium, disorientation, and behavior abnormalities.
5. Focal neurologic findings - Hemiparesis, aphasia, cranial nerve lesions, seizures.
95
Encephalitis - Diagnosis:
1. Routine lab tests - to rule out viral causes. Include CXR, urine and blood cultures, urine tox screen, and serum chemistries.
2. Perform LP --> Examine CSF.
3. MRI of the brain --> IMAGING STUDY OF CHOICE.
4. EEG --> Helpful in diagnosing HSV-1.
5. Brain biopsy --> In an acutely ill patient with a focal, enhancing lesion on MRI without a clear diagnosis.
96
Encephalitis - Management of possible complications:
1. Seizures - require anticonvulsant therapy.
| 2. Cerebral edema - Treatment may include hyperventilation, osmotic diuresis, and steroids.
97
DDX in patients with fever + altered mental status:
1. Infection --> Sepsis, UTI/urosepsis, pneumonia, bacterial meningitis, intracranial abscess, subdural empyema.
2. Medication/drugs --> Neuroleptic malignant syndrome (haloperidol, phenothiazines).
3. Delirium tremens.
4. Metabolic --> Thyroid storm.
98
Hepatitis in immunosuppressed:
By CMV, EBV, HSV.
99
Hep B is associated with...?
PAN
100
Hep C is associated with...?
Cryoglobulinemia
101
Course of hep B - Acute infection subclinical in?
70%.
102
Course of hep B:
Resolution --> 90%.
Chronic hep --> 5-10%.
Chronic carrier --> <1%.
103
Course of CHRONIC hep B:
Cirrhosis --> In 25%, 10-30yrs after onset.
104
HCC from hep B infection:
1. Chronic hep (5-10%).
| 2. Chronic carrier (<5%).
105
Course of hep C - Acute infection subclinical in?
75%
106
Course of hep C:
Chronic hep --> 85-90%.
Resolution --> 10-15%.
Fulminant --> <1%.
107
Course of CHRONIC hep C:
Cirrhosis --> In 10-20% of all patients - 20-30yrs after onset.
108
Hep E is particularly prevalent in:
1. India
2. Pakistan
3. Southeast Asia
4. Parts of Africa.
109
If transaminases are markedly elevated (>500), think:
1. Acute viral hepatitis.
2. Shock liver.
3. Drug-induced hepatitis.
110
Risk of developing cirrhosis or HCC in chronic hep B:
25-40%.
111
Risk of developing cirrhosis or HCC in chronic HCV:
10-25%.
112
In acute hep or in drug-induced hep is ALT more elevated?
In acute hep.
113
In chronic HBV or in chronic HCV is ALT higher?
In chronic HBV, but it varies.
114
Hep and Hep B treatment:
Active (vaccine) and passive (Ig) immunization are available for BOTH.
115
Chronic hep B Treatment:
1. IFN-alpha.
| 2. Lamivudine (nucleoside analog).
116
Chronic HCV treatment:
1. IFN-alpha.
| 2. Ribavirin
117
Botulism - General:
1. Ingestion of PREFORMED TOXINS (!!!!).
2. Toxins can be inactivated by cooking food at high temperatures.
3. Wound contamination is another source for botulism.
118
Botulism - Severity of illness:
Varies widely, from mild, self-limiting symptoms, to rapidly fatal disease.
119
Botulism - Clinical features:
1. Abdominal cramps.
2. Nausea.
3. Vomiting.
4. Diarrhea.
120
Botulism - Hallmark:
Symmetric, DESCENDING flaccid paralysis.
| Starts with dry mouth, diplopia, and/or dysarthria. Paralysis of limb musculature occurs later.
121
Botulism - Diagnosis:
1. DEFINITIVE diagnosis is IDENTIFICATION of toxin in serum, stool, or gastric contents (bioassay).
2. Identifying C.botulinum alone in food is NOT a reliable diagnostic indicator.
122
Botulism - Treatment:
1. Admit patient and observe respiratory status closely. Gastric laavge is helpful only within several hrs after ingestion of suspected food.
2. If suspicion is high, administer antitoxin (toxoid) as soon as lab specimens are obtained (do NOT WAIT for the results).
3. For contaminated wounds - Wound cleansing and penicillin.
123
DDX of food-borne botulism:
1. Guillain-Barre syndrome - Characteristically ASCENDING paralysis, but ONE VARIETY (Fischer) can be DESCENDING.
2. Eaton-Lambert syndrome.
3. Myasthenia gravis - EMG studies differentiate.
4. Diphtheria.
5. Tick paralysis.
124
Intra-abdominal abscess - Etiology:
1. Spontaneous bacterial peritonitis.
2. Pelvic infection (eg tubo-ovarian abscess).
3. Pancreatitis
4. Perforation of the GI.
5. Osteomyelitis of the vertebral bodies with extension into the retroperitoneal cavity.
125
Intra-abdominal abscess - Diagnosis:
CT or US.
126
Intra-abdominal abscess - Treatment:
1. Typically involves DRAINAGE of the abscess.
| 2. Antibiotic regimen should include broad coverage against Gram(-) rods, enterococci, and anaerobes.
127
Non infectious causes of cystitis or cystitis-like symptoms:
1. Cytotoxic agents (eg cyclophosphamide).
2. Radiation to pelvis.
3. Dysfunctional voiding.
4. Interstitial cystitis.
128
Host-dependent factors - Incr. risk for recurrent or complicated UTIs:
1. DM - Incr. risk for recurrent UTIs.
2. Patients with spinal cord injury.
3. Immunocompromised.
4. Any structural/functional abnormality that impedes urinary flow (eg incomplete voiding, neurogenic bladder, BPH, vesicourethral reflux, calculi).
129
Male risk factors - UTIs:
1. Uncircumsized males are at higher risk due to bacterial colonization of the foreskin.
2. Anal intercourse.
3. Vaginal intercourse with a female colonized with uropathogens.
130
Lower UTIs - When to obtain cultures:
1. Age >65.
2. Diabetes.
3. Recurrent UTIs.
4. Presence of symptoms for 7days or more.
5. Use of a diaphragm.
131
Major clinical feature to remember about LOWER UTIs:
In LOWER UTIs, fever is characteristically ABSENT.
132
Asymptomatic bacteriuria - Diagnosis:
2 successive positive cultures (>10^5CFU/mL) must be present.
133
Asymptomatic bacteriuria - Treat when?
Only in pregnancy or before urologic surgery.
134
Lower UTIs - Diagnosis - Dipstick analysis:
1. Leukocyte esterase test (+) --> Pyuria.
| 2. Positive nitrite test for presence of bacteria (gram(-)) --> Sensitive for Enterobacteriaceae.
135
Urinalysis - Most important finding:
Presence of WBCs.
136
Urinalysis - Adequacy of collection:
1. Presence of epithelial (squamous) cells indicates vulvar or urethral contamination.
2. If contamination is suspected, perform a straight catheterization of the bladder.
137
Urinalysis - Criteria for UTI - Bacteriuria:
>1 organism per oil-immersion field.
| Bacteriuria without WBCs may reflect contamination and is NOT a reliable indicator of infection.
138
Urinalysis - Criteria for UTI - Pyuria:
It is the most valuable finding for diagnosis: Greater than or equal to 10 leukocytes/μL is ABNORMAL.
139
Urinalysis - Other findings:
Hematuria and mild proteinuria may be present. Hematuria in and of itself does NOT require extended therapy.
140
Lower UTIs - Diagnosis - Urine culture:
1. Confirms the diagnosis (high specificity).
2. Traditional criteria --> >10^5 CFU/mL --> misses up to 1/3 of UTIs.
3. Colony counts as low as 10^2 to 10^4 CFU/mL are adequate for diagnosis if clinical symptoms are present.
141
Lower UTIs - Diagnosis - Blood culture:
Only indicated if patient is ill and urosepsis is suspected.
142
Complicated UTI:
1. Any UTI that spreads beyond the bladder (eg pyelonephritis, prostatitis, urosepsis) --> Risk factors for upper UTI: pregnancy, diabetes, and vesicoureteral reflux.
2. Any UTI caused by structural abnormalities, metabolic disorder, or neurologic dysfunction.
143
Complications - UTI during pregnancy:
Incr. risk of preterm labor, low birth weight, and other complications, especially in advanced pregnancy.
144
Complications - Recurrent infections:
1. Usually due to infection with new organism, but sometimes is a relapse due to unsuccessful treatment of the original organism.
2. Risk factors include impaired host defenses, pregnancy, vesicourethral reflux, and sexual intercourse in women.
3. Generally the consequences are not significant unless the patient is at risk for upper UTI.
145
The following groups are considered to have complicated UTI:
1. Men
2. Diabetics
3. Renal failure
4. Pregnancy
5. History of pyelonephritis in last year
6. UT obstruction, indwelling catheter, stent, nephrostomy tube.
7. Antibiotic resistant organism .
8. Immunocompromised patients (HIV, transplant patients).
146
UTIs treatment - For uncomplicated UTI:
Empiric treatment is appropriate - do NOT wait for culture results.
If complicated EXTEND TREATMENT TO 7DAYS.
147
UTI treatment - Pregnant women with UTI:
1. Treat with ampicillin, amoxicillin, or oral cephalosporins for 7-10days.
2. Avoid fluoroquinolones (can cause fetal arthropathy(!)).
148
UTI treatment - UTIs in men:
1. Treat as uncomplicated cystitis in women, but for 7 days.
| 2. Perform a urologic workup if there are complications or recurrences, or if initial treatment fails.
149
UTI treatment - Recurrent infections:
1. If a relapse occurs within 2 weeks of cessation of treatment, continue treatment for 2 more weeks and obtain a urine culture.
2. Otherwise treat as for uncomplicated cystitis. If the patient has more than two UTIs per year, give chemoprophylaxis.
150
Pyelonephritis - Complications (unusual):
1. Sepsis occurs in 10-25% of patients with pyelonephritis. May lead to shock(!).
2. Emphysematous pyelonephritis - caused by gas-producing bacteria in diabetic patients.
3. Chronic pyelonephritis and scarring of the kidneys - rare unless underlying renal disease exists.
151
Pyelonephritis - Diagnosis - Urinalysis:
1. Look for pyuria, bacteriuria, and leukocyte casts.
| 2. As in cystitis, hematuria and mild proteinuria may be present.
152
Pyelonephritis - Diagnosis - Blood/urine cultures:
Blood cultures --> Obtain in ill-appearing patients and ALL hospitalized patients.
Urine cultures --> Obtain in ALL patients with suspected pyelonephritis.
153
Pyelonephritis - Diagnosis - CBC:
Leukocytosis with left shift.
154
Pyelonephritis - Diagnosis - Renal function:
This is usually preserved. Impairment is usually reversible, especially with IV fluids.
155
Pyelonephritis - Diagnosis - Imaging studies:
Perform these if treatment fails or in any patient with complicated pyelonephritis. Consider renal US, CT, IVP, or retrograde ureterogram.
156
Treatment for uncomplicated pyelonephritis:
1. Use outpatient treatment if the patient can take ORAL antibiotics. Treat based on gram stain.
2. Repeat urine culture 2-4 days after cessation of therapy.
3. If symptoms fail to resolve within 48hr, adjust treatment based on urine culture.
4. Further failure to respond --> Urologic investigation.
157
For recurrent pyelonephritis:
1. If relapse is due to the same organism despite appropriate treatment, treat for 6 weeks.
2. If relapse is due to a new organism, treat with appropriate therapy for 2 weeks.
158
Prostatitis - Acute or chronic bacterial is more common?
Chronic bacterial is more common.
159
Acute bacterial prostatitis occurs more commonly in?
Younger men.
160
Prostatitis - Pathophysiology:
1. Ascending infection.
2. May occur after catheterization.
3. Other causes - direct/lymphatic spread from the rectum.
4. Hematogenous spread (rare).
161
Acute bacterial prostatitis - Causative organisms:
Gram(-) organisms predominate - E.coli, Klebsiella, Proteus, Pseudomonas, Enterobacter, Serratia spp.
162
Chronic bacterial prostatitis - Prevalence:
True prevalence is difficult to determine because many cases are asymptomatic and are diagnosed incidentally.
163
Chronic bacterial prostatitis - Target:
40-70yrs.
164
Chronic bacterial prostatitis - Causative organisms:
Similar to acute bacterial prostatitis - Can occur from chronic prostatitis.
165
Acute or chronic bacterial prostatitis is a more serious condition:
Acute.
166
Acute prostatitis - Clinical features:
1. Fevers, chills - Patients may appear toxic(!).
2. Irritative voiding symptoms - Dysuria, frequency, urgency.
3. Perineal pain, low back pain, urinary retention may be present as well.
167
Prostatic massage in patients with acute bacterial prostatitis may cause:
Bacteremia. SKIP RECTAL EXAM if the diagnosis is straightforward, given the risk of inducing bacteremia.
168
Chronic bacterial prostatitis - Clinical features:
1. Patients may be asymptomatic. Patients do no appear ill. Fever is uncommon.
2. Patients frequently have recurrent UTIs with irritative voiding and/or obstructive symptoms.
3. There is a dull, poorly localized pain in the lower back, perineal, scrotal, or suprapubic region.
169
Prostatitis - Diagnosis:
1. DRE - Acute: boggy, exquisitely tender prostate. Chronic: enlarged and usually non tender.
2. Urinalysis - Numerous WBCs (!) in ACUTE prostatitis.
3. Urine cultures - Almost always positive in acute prostatitis.
4. Chronic prostatitis - Presence of WBCs in expressed prostatic secretions suggests diagnosis. Urine cultures may be positive (chronic bacterial prostatitis) or negative (non bacterial prostatitis).
170
Acute prostatitis - Treatment:
1. If it is SEVERE and the patient appears TOXIC, hospitalize the patient and initiate IV antibiotics.
2. If is it MILD, treat on an outpatient basis with antibiotics - TMP/SMX or a fluoroquinolone and doxycycline. Treat for 4-6 weeks.
3. Patients usually responds to therapy.
171
Chronic prostatitis - Treatment:
1. Fluoroquinolone. Prolonged course is recommended but DOES NOT guarantee complete eradication.
2. It is very difficult to treat. Recurrences are common.
172
MC STD:
Genital warts - Associated with HPV.
173
80% of cases of Reiter's syndrome are associated with?
Chlamydial infection.
174
MC BACTERIAL STD:
Chlamydial infection - Many are co-infected with gonorrhea (up to 40% of women and 20% of men.
175
Chlamydial incubation period:
1-3wks.
176
Chlamydial infection is a risk factor for...?
Cervical cancer, especially when there is a history of multiple infection.
177
Chlamydia - Clinical features:
1. Many cases are asymptomatic (80% of women, 50% of men).
2. MEN who are symptomatic may have any of the following: dysuria, purulent urethral discharge, scrotal pain and swelling, and fever.
3. WOMEN who are symptomatic may have purulent urethral discharge, intermenstrual or post coital bleeding, and dysuria.
178
Complications of chlamydia:
1. MEN --> Epididymitis and proctitis.
2. WOMEN --> PID, salpingitis, tubo-ovarian abscess, ectopic pregnancy, Fitz-Hugh-Curtis syndrome.
- -> Leading cause of infertility in women due to tubal scarring.
179
Chlamydia - Diagnosis:
1. Culture, enzyme immunoassay, and molecular tests such as PCR. NOT serology(!).
2. PCR replaces culture as the screening test of choice due to higher sensitivity.
3. Sexually active adolescents (particularly females) should be screened for chlamydial infection even if they are asymptomatic.
180
Chlamydial - Treatment:
1. Azithromycin (oral 1 dose) or doxycyclin (oral for 7 days).
2. Treat all sexual partners.
181
Gonorrhea is usually symptomatic in...?
Men.
| THEREFORE --> Complications occur more often in women due to undetected disease.
182
What other sites besides the genitalia can gonorrhea infect?
1. Pharynx
2. Conjunctiva
3. Rectum
183
Gonorrhea transmission:
1. Sexually
| 2. Neonatally
184
Gonorrheal complications (more often seen in women):
1. PID - possible infertility, chronic pelvic pain.
2. Epididymitis, prostatitis (uncommon).
3. Salpingitis, tubo-ovarian abscess.
4. Fitz-Hugh-Curtis syndrome (perihepatitis) - RUQ pain; elevated LFTs.
5. Disseminated gonococcal infection.
185
Gonorrhea - Clinical features - Men:
1. Gonorrhea is asymptomatic in up to 10% of carriers. These can STILL transmit the disease.
2. Most men have symptoms involving the urethra - eg purulent discharge, dysuria, erythema, edema of urethral meatus, frequency of urination.
186
Gonorrhea - Clinical features - Women:
Most women are asymptomatic or have a few symptoms(!).
| May have symptoms of cervicits/urethritis - eg purulent discharge, dysuria, intermenstrual bleeding, and dyspareunia.
187
Disseminated gonococcal infection - Clinical findings:
Occurs in 1%-2% of cases; more common in WOMEN:
1. Fever, arthralgias, tenosynovitis (of hands and feet).
2. Migratory polyarthritis/septic arthritis, endocarditis, or even meningitis.
3. Skin rash (usually on distal extremities).
188
Gonorrhea - Diagnosis:
1. Gram stain of urethral discharge showing organisms WITHIN leukocytes is highly SPECIFIC for gonorrhea.
2. Obtain cultures in ALL CASES - May treat empirically because culture results take 1-2 days to return.
3. Consider testing for syphilis and HIV(!).
4. Obtain BLOOD CULTURES if disease has disseminated.
189
Gonorrhea - Treatment:
1. Ceftriaxone (IM, 1dose) --> also effective against syphilis.
2. Other: Cefixime, ciprofloxacin, ofloxacin.
3. Also give azithromycin (one dose) or doxycycline (for 7 days) to cover COEXISTENT chlamydial infection.
4. If disseminated, hospitalize the patient and initiate ceftriaxone (IV or IM for 7 days).
190
Why is it important, but often difficult, to identify patients with primary HIV infection?
Because of the benefits of EARLY antiretroviral therapy - High index of suspicion is necessary.
191
HIV transmission:
1. Sexually
2. Parenterally
3. Via semen
4. Blood
5. Fluids
6. Breast milk
7. Vaginal fluid
192
Risk of HIV transmission - Needlestick injury:
1/300
193
Risk of HIV transmission - Vaginal (male to female):
1/1.000
194
Risk of HIV transmission - Vaginal (female to male):
1/3.000
195
Risk of HIV transmission - Anal receptive:
1/100
196
Risk of HIV transmission - Mother to child:
With medications --> 2/100.
| Without medications --> 1/3.
197
Caesarian delivery is indicated if viral load is over?
1.000 copies.
198
Caesarian section is NOT indicated in an HIV(+) mother when...?
CD4>500
| Viral load <1.000
199
4 phases of typical HIV course:
1. Primary infection.
2. Asymptomatic infection.
3. Symptomatic infection.
4. Full-blown AIDS.
200
Pre-AIDS phase (symptomatic HIV infection):
1. 1st evidence of immune system dysfunction.
2. Without treatment this phase lasts about 1-3yrs.
3. The following frequently appear:
a. Persistent generalized lymphadenopathy.
b. Localized fungal infections (eg on fingernails, toes, mouth).
c. Recalcitrant vaginal yeast and trichomonal infections in women.
d. Oral hairy leukoplakia on the tongue.
e. Skin manifestations that include seborrheic dermatitis, psoriasis exacerbations, molluscum, warts.
201
What is used to indicate when to initiate antiretroviral therapy and PCP prophylaxis?
CD4 count - Also useful in assessing response to therapy.
202
If untreated (no retroviral therapy), CD4 count decreases at an average rate of about...?
50 cells per YEAR.
203
HIV viral load - Importance:
Used to assess response to and adequacy of antiretroviral therapy. Provides complementary prognostic information to the CD4 count.
204
HIV - Diagnosis - PCR:
PCR RNA viral load test --> Patients with ACUTE HIV infection have very high levels of viremia - This test is repeated to assess effectiveness of therapy.
205
HIV - Diagnosis - p24 antigen assay:
Less costly but less sensitive alternative to viral loading testing.
206
HIV seroconversion occurs in...?
3-7WEEKS.
207
HIV - Diagnosis - ELISA:
Screening test for detecting antibody to HIV - Becomes positive 1-12 weeks after infection.
A negative ELISA essentially EXCLUDES HIV (99% sensitive) as long as the patient has not had a subsequent exposure before testing (before seroconversion).
208
Diagnosis of AIDS:
1. Depends principally on the identification of an indicator condition or on finding in an HIV-1 seropositive patient with a CD4 cell count lower than 200.
2. There are many indicator conditions (AIDS-defining illnesses).
209
Antiretroviral therapy in HIV:
The importance of strict (100%) adherence to the triple-drug regimen CANNOT BE OVEREMPHASIZED, because even minor deviations may result in drug resistance.
--> Do NOT initiate triple-drug therapy in a patient who is NOT willing or able to fully comply with the prescribed regimen.
210
Antiretroviral therapy - Indications:
1. Symptomatic patients regardless of CD4 count.
| 2. Asymptomatic patients with CD4 count <500.
211
HAART consists of:
2 NucleoSide reverse transcriptase inhibitors and either:
- A NON nucleoside reverse transcriptase inhibitor.
- A PI.
212
HAART in pregnant women?
Generally recommended to be continued in pregnancy.
213
Opportunistic infection prophylaxis - Tests:
1. CXR (bilateral interstitial infiltrates).
2. LDL level (always elevated).
3. ABG (hypoxia or incr. A-a gradient).
4. Sputum stain for pneumocystis (very specific but not sensitive).
5. Bronchoscopy with bronchoalveolar lavage (most accurate test).
214
Opportunistic infection prophylaxis - Preferred agent:
TMP-SMX.
215
HIV(+) - TB treatment:
1. Screen all patients with a yearly PPD test.
| 2. Prescribe INH + pyridoxine if the patient has positive PPD.
216
Opportunistic infection prophylaxis - Atypical mycobacteria?
1. Start prophylaxis when CD4<100.
| 2. Clarithro/Azithro.
217
Opportunistic infection prophylaxis - Toxoplasmosis:
1. Give this to patients with CD4<100.
| 2. TMP/SMX.
218
Opportunistic infection prophylaxis - Vaccination:
NO LIVE-VIRUS VACCINES.
1. Pneumococcal polysaccharide vaccine (Pneumovax) - Every 5-6 YEARS.
2. Influenza vaccine - Yearly.
3. Hep B vaccine (if not already antibody positive).
219
HSV - Pathophysiology:
1. After inoculation, the HSV replicates in the DERMIS and EPIDERMIS.
2. Then travels via sensory nerves up to the dorsal root ganglia.
3. It resides as a latent infection in the dorsal root ganglia.
4. Where it can be reactivated at any time and reach the skin through peripheral nerves.
220
HSV - Transmission:
1. Transmitted by contact with people who have active ulcerations or shedding of virus from mucous membranes.
2. HSV-1 is typically associated with transmission through NON sexual personal contact (eg kissing), and HSV-2 through kissing.
221
Contracting one form of herpes confers some degree of...?
CROSS-immunity, rendering primary infection with the other form of herpes less sever.
222
Infection with genital herpes is associated with an increased risk of contracting...?
HIV.
223
HSV-1 - Oral lesions:
Involve group of vesicles on patches of erythematous skin.
| --> Herpes labialis (cold sores) are MC on the lips (usually painful, heal in 2-6WEEKS).
224
HSV-1 is associated with what palsy?
Bell's palsy.
225
Recurrences of HSV - Associated with:
1. Stress
2. Fever
3. Sun exposure
4. Infection
- -> Tend to be shorter and less frequent over time.
226
HSV-2 - Primary infection:
More severe + prolonged symptoms, lasting up to 3 weeks.
227
HSV-2 presents with:
1. Painful genital vesicles or pustules.
2. Tender inguinal lymphadenopathy.
3. Vaginal and/or urethral discharge.
228
Disseminated HSV - Usually seen in?
Immunocompromised.
229
Disseminated HSV - May result in?
1. Encephalitis
2. Meningitis
3. Keratitis
4. Chorioretinitis
5. Pneumonitis
6. Esophagitis
230
Neonatal HSV - Features:
1. Congenital malformations.
2. Intrauterine growth retardation.
3. Chorioamnionitis.
4. Neonatal death.
231
HSV and ocular disease?
EITHER form of HSV can cause ocular disease.
232
Herpetic whitlow:
1. HSV infection of the finger caused by inoculation into open skin surface - Common in health care workers.
2. Painful vesicular lesions erupt in fingertip.
3. May cause fever + axillary lymphadenopathy.
4. Treat with acyclovir.
- -> DO NOT mistake for PARONYCHIA - Incision and drainage should NOT be done for herpetic whitlow.
233
HSV - Diagnosis:
1. Can be made clinically when characteristic lesions are recognized.
2. If there is uncertainty, perform:
a. Tzanck smear - quickest test.
b. Culture of HSV (gold standard).
c. ELISA.
234
Tzanck smear:
1. Perform by swabbing the base of the ulcer and staining with Wright's stain.
2. Shows multinucleated giant cells. Does NOT differentiate between HSV and VZV.
235
Culture of HSV:
1. Perform by swabbing the base of the ulcer.
| 2. Results are available within 2-3 days.
236
ELISA for HSV:
1. 80% sensitive.
| 2. Results available within MINUTES to HOURS.
237
Syphilis - Transmission:
Direct sexual contact with infectious lesions.
238
MC presentations for syphilis:
1. Genital lesions (chancre).
2. Inguinal lymphadenopathy.
3. Maculopapular rash of secondary syphilis.
239
Syphilis chancre appears when?
3-4 weeks after exposure.
240
Syphilis chancre heals when?
In 14weeks, even without therapy.
241
Secondary stage of syphilis - When?
May develop 4-8 weeks AFTER the chancre has healed.
242
Secondary syphilis - Most characteristic finding:
Maculopapular rash.
243
Latent syphilis - Definition:
Presence of positive serologic test results in the ABSENCE of clinical signs or symptoms.
1/3 develops tertiary syphilis.
244
Early and late tertiary syphilis:
Early --> If serology has been positive for Patient may relapse back to secondary syphilis.
Late --> If serology has been positive for >1yr --> Not contagious during this time, none of the symptoms are present.
245
Syphilis - Diagnosis - Definitive diagnostic test:
Dark-field microscopy - examines a sample of the chancre with visualization of spirochetes.
246
Diagnosis of syphilis - Steps:
1. Obtain VDLR + RPR.
| 2. IF POSITIVE --> Confirm with FTA-ABS.
247
Diagnosis of syphilis - Non treponemal tests:
RPR and VDRL (most commonly used) --> Ideal for screening.
248
Diagnosis of syphilis - Treponemal tests:
FTA-ABS, MHA-TP --> For confirmation.
249
Diagnosis of syphilis - ALL PATIENTS should ALSO be tested for?
HIV infection.
250
Treatment of syphilis:
```
Benzathine penicillin (IM, 1 dose).
If allergic --> Doxycycline, tetracycline for 2 WEEKS(!).
```
251
Treatment of late latent syphilis or tertiary syphilis?
Give penicillin in 3 doses IM once PER WEEK.
252
Treatment of syphilis - How to ensure adequate response?
Repeat non treponemal tests every 3 months. Titers should decrease 4-fold within 6 months.
--> If they do NOT, that may signal treatment failure or reinfection.
253
RPR and VDLR may be falsely positive in...?
SLE(!).
254
Chancroid - Caused by?
H.ducreyi - Gram(-) rod.
255
Chancroid - Transmission:
Sexually
256
Incubation period of H.ducreyi:
2-10days.
257
Diagnosis of chancroid:
It is made CLINICALLY:
1. Painful genital ulcer (s).
2. Tender lymphadenopathy.
3. Syphilis RULED OUT (negative dark-field exam + negative serology).
4. HSV RULED OUT based on clinical presentation or negative culture for HSV.
258
Chancroid - Treatment options:
1. Azithromycin (oral, 1 dose).
2. Ceftriaxone (IM, 1 dose).
3. Oral course of azithromycin, erythromycin, ciprofloxacin.
- -> With treatment --> Most ulcers resolve in 1 or 2 weeks.
259
Lymphogranuloma venereum - Features:
1. PainLESS ulcer at the site of inoculation that may go unnoticed.
2. FEW WEEKS later --> tender inguinal lymphadenopathy (usually unilateral) and constitutional symptoms develop.
260
Lymphogranuloma venereum - If untreated?
Proctocolitis may develop with perianal fissures and rectal stricture.
--> Obstruction of lymphatics may lead to elephantiasis of genitals.
261
Lymphogranuloma venereum - Diagnosis:
Serology - complement fixation, immunofluorescence.
| --> Treatment is doxycycline - oral for 21days.
262
3 forms of pediculosis:
1. Pediculosis capitis (head lice).
2. Pediculosis corpora (body lice).
3. Pediculosis pubis (pubic lice or "crabs").
263
Pediculosis pubis - What is it?
A common STD caused by Phthirus pubis (the pubic or crab louse).
264
Phthirus pubis - Transmission:
Sexually, via clothes, or towels.
265
Pediculosis pubis - Main features:
SEVERE PRURITUS in the genital region is characteristic. Other hairy areas of the body may be involved.
266
Pediculosis pubis - Diagnosis:
Made by examination of hair under microscope (or possibly with the naked eye) - identification of adult lice or nits.
267
Pediculosis pubis - Treatment:
Permethrin 1% shampoo (Elimite).
268
Cellulitis is?
An inflammatory condition of skin + subcutaneous tissue.
269
Cellulitis is caused by?
A wide variety of bacteria, MC being group A streptococci or S.aureus.
270
Cellulitis - If untreated?
Cellulitis may lead to potentially life-threatening bacteremia.
271
Cellulitis - Fever?
May or may NOT be present.
272
Cellulitis - recurrences in the same area?
Patients with cellulitis are predisposed to recurrences in the SAME AREA because of damage that occurs to the LOCAL LYMPHATIC vessels.
273
Cellulitis - Diagnosis:
1. Essentially clinical.
2. Obtain blood cultures if the patient has fever.
3. Obtain tissue cultures if there is a wound, ulcer, or site of infection.
4. Obtain imaging (plain film, MRI) if there is suspicion of deeper infection.
274
Cellulitis - Treatment:
1. Base treatment on suspected pathogens from the patients history. Most patients require PARENTERAL antibiotic therapy.
2. Treat with a staph penicillin (oxacillin, nafcillin) or a cephalosporin (cefazolin).
3. Continue IV antibiotics until signs of infection improve --> Follow up with oral antibiotics for 2 weeks.
275
Erysipelas is a...?
Cellulitis that is usually confined to the dermis and lymphatics.
276
Erysipelas - Cause:
Usually caused by group A strep.
277
Erysipelas - Predisposing factors:
1. Lymphatic obstruction (radical mastectomy).
2. Local trauma or abscess.
3. Fungal infections.
4. DM.
5. Alcoholism.
278
Erysipelas - Complications:
1. Sepsis.
2. Local spread to subcutaneous tissues.
3. Necrotizing fasciitis.
279
Erysipelas - Treatment:
For UNcomplicated cases is IM or oral penicillin or erythromycin - Otherwise treat as for cellulitis.
280
Erysipelas has a high rate of...?
Recurrences.
281
Common pathogens in cellulitis - Local trauma, breaks in skin:
Group A strep (pyogenes).
282
Common pathogens in cellulitis - Wounds, abscesses:
S.aureus.
283
Common pathogens in cellulitis - Immersion in water:
1. P.aeruginosa
2. Aeromonas hydrophila
3. Vibrio vulnificus
284
Common pathogens in cellulitis - Acute sinusitis:
H.influenza.
285
Necrotizing fasciitis is...?
A life-threatening infection of deep soft tissues that rapidly tracks along facial planes.
286
Necrotizing fasciitis - Causes:
S.pyogenes (Group A) and C.perfringens.
287
Necrotizing fasciitis - Risk factors:
1. Recent surgery.
2. Diabetes.
3. Trauma.
4. IVDA.
288
Necrotizing fasciitis - Clinical features:
1. Fever + Pain OUT OF PROPORTION of appearance of skin in early stages, so a high index of suspicion is important.
2. Extension of infection leads to thrombosis of microcirculation --> tissue necrosis, discoloration, crepitus, and cutaneous anesthesia.
289
Necrotizing fasciitis may rapidly progress to...?
Sepsis, TSS, and multi-organ failure.
290
Necrotizing fasciitis - Treatment:
1. Antibacterial treatment alone is NOT sufficient.
2. Rapid SURGICAL exploration and excision of devitalized tissue is an absolute necessity!!!.
3. Broad-spectrum parenteral antimicrobial therapy is warranted.
291
Differentiating DVT from cellulitis:
1. Like cellulitis, acute DVT ALSO presents with erythema, warmth, and tenderness in the affected extremity.
2. Inflammation in DVT is usually restricted to the posterior calf.
3. Because Homans' sign and the palpation of venous cords are NOT sensitive in detecting DVT, VENOUS DOPPLER must sometimes be performed to differentiate between cellulitis and acute DVT.
292
Lymphadenitis - Often caused by?
Local skin or soft tissue bacterial infection - often hemolytic streptococci and staph.
293
Lymphadenitis - Presentation:
1. Fever.
2. Tender lymphadenopathy of regional lymph nodes.
3. Red streaking of skin from the wound or area of cellulitis.
294
Lymphadenitis - Complications:
1. Thrombosis of adjacent veins.
2. Sepsis.
3. Even death if untreated.
295
Lymphadenitis - Diagnosis:
Helpful diagnostic studies include BLOOD and WOUND cultures.
296
The following types of wounds are most likely to result in tetanus:
1. Wounds contaminated with dirt, feces, or saliva.
2. Wounds with necrotic tissue.
3. Deep-puncture wounds.
297
Incubation period for tetanus ranges from about?
2 days to 2 weeks. (GRADUAL onset 1 to 7 days)
298
Tetanus - Clinical features - Classic and earliest symptom:
Classic and earliest symptom is hypertonicity and contractions of the masseter muscles, resulting in trismus, or "lockjaw
299
Tetanus - Clinical features - Progression:
Generalized muscle contractions including:
a. Risus sardonicus - grin due to contraction of facial muscles.
b. Opisthotonus - arched back due to contraction of back muscles.
+ Sympathetic hyperactivity.
300
Tetanus - Diagnosis:
1. Mainly clinical.
| 2. Obtain wound cultures, but they are NOT a reliable means of diagnosis.
301
Tetanus - Treatment:
1. Admit patient to the ICU and provide respiratory support if necessary. Give DIAZEPAM for tetany.
2. Neutralize unbound toxin with passive immunization - Give a single IM dose of tetanus Ig (TIG).
3. Provide active immunization with tetanus/diphtheria toxoid (Td).
4. Thoroughly clean and debride any wounds with tissue necrosis.
5. Give antibiotics (metronidazole or penicillin G), although efficacy is somewhat controversial.
302
Osteomyelitis - 2 main categories:
1. Hematogenous osteomyelitis (MC in children) - occurs secondary to sepsis.
2. Direct spread of bacteria from any of the following:
a. Adjacent infection (eg infected diabetic foot ulcer, decubitus ulcer).
b. Trauma (eg open fractures).
c. Vascular insufficiency (eg peripheral vascular disease).
303
Osteomyelitis - Causes:
MC is S.aureus and CN staph.
304
Osteomyelitis - Sites:
1. Long bones (tibia, femur, humerus).
2. Foot and ankle.
3. Vertebral bodies.
305
Osteomyelitis - Risk factors:
1. Open fractures.
2. DM --> Predisposition to infection and peripheral vascular disease.
3. Use of illicit IV drugs.
4. Sepsis.
306
Osteomyelitis - MC finding:
Pain over the involved area.
307
Osteomyelitis - Finding with chronic disease:
A draining sinus tract through the skin may form in chronic disease.
308
Common bugs in osteomyelitis - Catheter septicemia:
S.aureus
309
Common bugs in osteomyelitis - Prosthetic joint:
CN staph
310
Common bugs in osteomyelitis - Diabetic foot ulcer:
Polymicrobial organisms.
311
Common bugs in osteomyelitis - Nosocomial infections:
Pseudomonas spp.
312
Common bugs in osteomyelitis - IVDA, neutropenia:
Fungal spp., Pseudomonas spp.
313
Common bugs in osteomyelitis - SCA:
Salmonella spp.
314
Up to what percentage of patients with open fractures do patients eventually develop osteomyelitis?
Up to 10%.
| Use of orthopaedic hardware increases this risk (foreign body is the site of bacterial colonization).
315
Osteomyelitis of the vertebral bodies due to M.tuberculosis is called:
Pott's disease.
316
Osteomyelitis - Diagnosis - WBC:
May or may NOT be elevated - NOT useful for diagnosis.
317
Osteomyelitis - Diagnosis - Normal ESR, CPR:
Do NOT exclude diagnosis.
| --> Useful in monitoring response to therapy.
318
Osteomyelitis - Diagnosis - Most direct and accurate means of diagnosis?
Needle aspiration of infected bone or BONE BIOPSY (obtained in operating room).
319
Osteomyelitis - Diagnosis - Plain radiography?
Earliest radiographic changes (periosteal thickening or elevation) are NOT evident for at least 10 DAYS.
--> Lytic lesions only in advanced disease.
320
The most effective imaging study for osteomyelitis:
MRI - For diagnosis + Assessing the extent of disease process.
321
Osteomyelitis - Treatment:
Give IV antibiotics for EXTENDED periods (4-6wks). Initiate antibiotic therapy only after the microbial etiology is NARROWED based on data from cultures.
322
Chronic osteomyelitis refers to:
Bone necrosis and soft tissue compromise or to a relapse of previously treated osteomyelitis.
--> Very challenging to treat and almost impossible to completely eradicate.
323
Acute infectious arthritis - Pathogenesis - Microbes penetrate via:
1. Hematogenous spread - MC route.
2. Contiguous spread from another locus of infection (eg osteomyelitis, abscess, or cellulitis).
3. Traumatic injury to the joint.
4. Iatrogenic (eg from arthrocentesis, arthroscopy).
324
If a patient has a painless range of motion of involved joint, septic arthritis is very...?
Unlikely.
| Micromotions of joint cause SEVERE pain in septic arthritis.
325
Acute bacterial arthritis - Causative organisms:
1. S.aureus is MC overall in adults + children. Also various strep spp.
2. N.gonorrhoeae --> MCC in young, sexually active.
3. P.aeruginosa, Salmonella spp. --> SCA, Immunodef., IVDA.
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Risk factors for acute infectious arthritis:
1. Prior joint damage (eg RA).
2. Joint prosthesis.
3. DM.
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Acute infectious arthritis - Diagnosis - 1st step:
Perform a joint aspiration ("tap") and analysis of synovial fluid in all patients suspected of having a septic joint.
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Acute infectious arthritis - Diagnosis - Studies to order on aspirated synovial fluid:
1. WBC with differential - usually >50.000 WBC/mm^3 with >80% PMNs --> Most helpful test.
2. Gram stain of fluid --> 75% is gram(+), 30-50% is gram(-).
3. Culture - aerobic/anaerobic.
4. Crystal analysis (!) --> Acute gout arthritis may present as septic one.
5. PCR on synovial fluid --> If gonococcal arthritis is suspected and Gram + cultures are negative.
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Acute infectious arthritis - Diagnosis - Blood cultures:
Positive in >50% of all cases (frequently negative in gonoccocal arthritis).
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Acute infectious arthritis - Diagnosis - Other lab abnormalities:
1. Leukocytosis - in about half of patients with a septic joint.
2. Elevated ESR - Up to 90%.
3. Elevated CRP - For monitoring.
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Acute infectious arthritis - Diagnosis - Imaging studies:
1. Plain radiographs - Generally not useful.
| 2. CT or MRI - Helpful if the sacroiliac or facet joints are involved.
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Acute infectious arthritis - Treatment:
Prompt antibiotic treatment:
1. Do not delay in initiating antimicrobial therapy, when acute infectious arthritis is suspected.
2. If the Gram stain is negative, but AIA is still suspected, treat EMPIRICALLY, until culture and sensitivity results are available.
333
AIA - Treatment - Drainage:
Daily aspiration of affected joint as long as effusion persists is one treatment option.
HOWEVER --> Surgical drainage is better.
334
Complications of septic arthritis:
1. Destruction of joint and surrounding structures (eg ligaments, tendons) --> Stiffness, pain, loss of function.
2. Avascular necrosis - if hip is involved.
3. Sepsis.
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Gonococcal arthritis - Presentation:
1. Acute mono- or oligoarthritis, and often progresses within days in a migratory or additive pattern.
2. Knees, wrists, hands, ankles are the MOST commonly involved.
3. Tenosynovitis is often present in the hands/feet.
336
Gonococcal arthritis - Signs of disseminated infection:
1. Fever
2. Chills
3. Rash (macules, papules, and/or pustules)
- -> Admit to the hospital.
337
Septic arthritis - MC joint affected:
Knee.
| Also --> Hip, wrist, shoulder, ankle.
338
Septic arthritis in immunosuppressed or connective tissue diseases:
Polyarticular arthritis - and a WORSE prognosis.
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Malaria - General features - Caused by:
```
1 of 4 organisms:
1. P.falciparum
2. P.ovale
3. P.vivax
4. P.malariae
(+knowlessi).
```
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Malaria - Clinical features:
Symptoms may include:
1. Fever
2. Chills
3. Myalgias
4. Headache
5. Nausea
6. Vomiting
7. Diarrhea
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Malaria - Fever patterns:
P.falciparum --> Usually, constant.
P.ovale, P.vivax --> Usually, spikes every 48hrs.
P.malariae --> Usually spikes every 72hrs.
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Malaria - Onset of illness:
Usually occurs WEEKS to MONTHS after infection, but it is dependent on the specific cause.
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Malaria - Diagnosis:
1. Identify organism on peripheral blood smear.
| 2. Blood smear must have Giemsa stain.
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Which microorganism is by far the most serious and life-threatening?
P.falciparum.
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Malaria treatment - Chloroquine resistance - What to give?
1. Quinine sulfate and tetracycline.
| 2. Atovaquone-proguanil and mefloquine.
346
P.falciparum infection may require?
IV quinidine + doxycycline.
347
For hypnozoites in P.vivax and P.ovale infections - What to give?
Add a 2-week regimen of primaquine phosphate.
348
Malaria prophylaxis - What to give in chloroquine resistant areas?
Mefloquine is the agent of choice.
349
Rabies - A rare documented route of infection:
From a corneal transplant.
350
Rabies - Incubation period:
Typically ranges from 30-90days, but varies considerably.
351
Rabies - Symptoms in progressive order:
1. Pain at the site of bite.
2. Prodromal symptoms of sore throat, fatigue, headache, nausea, and/or vomiting.
3. Encephalitis - Confusion, combativeness, hyperactivity, fever, seizures may be present.
4. Hydrophobia - usually progresses to coma and death.
- -> Some patients may present with ASCENDING paralysis.
352
Rabies - Diagnosis:
1. Virus or viral antigen. Virus can be isolated in saliva as well.
2. 4-fold increase in serum antibody titers.
3. Identification of Negri bodies histologically.
4. PCR detection of virus RNA.
353
Rabies prophylaxis:
Rabies vaccine is available for at-risk individuals - Those with potential occupational exposure, such as veterinarians, wild-life officials, and lab workers.
354
Rabies - Treatment (post exposure management):
1. Clean the wound thoroughly with soap.
2. For wild animal bites (eg bat or raccoon), the animal should be captured if possible, destroyed, and sent to a lab for immunofluorescence of brain tissue.
3. If the patient was bitter by a healthy dog or cat in an endemic area, the animal should be captured and observed for 10days.
355
Rabies Treatment - Post exposure management - For a known rabies exposure:
For a known rabies, both of the following should be performed:
1. Passive immunization - Administer human rabies Ig to patients, into the wound as well as in the gluteal region.
2. Active immunization - Antirabies vaccines in 3 IM doses into the deltoid or thigh over a 28-day period.
356
Candidiasis - Risk factors:
1. Antibiotic therapy.
2. DM.
3. Immunosuppressive therapy.
4. Immunocompromised hosts (incr. risk for BOTH mucocutaneous + systemic candidiasis).
357
Candidiasis - Typical presentation:
Mucocutaneous growth.
358
Candidiasis - MC affected areas:
1. Vagina - yeast infection.
2. Mouth, oropharynx - "thrush".
3. Cutaneous candidiasis.
4. GI tract (esophagus).
359
Candidiasis - Disseminated or invasive disease:
May occur in immunocompromised.
1. Sepsis/septic shock.
2. Meningitis.
3. Multiple abscesses.
360
Candidiasis - Diagnosis:
1. Mucocutaneous candidiasis is primarily clinical; KOH preparation demostrates yeast.
2. Invasive candidiasis is diagnosed by blood or tissue culture.
361
Candidiasis - Treatment:
1. Remove indwelling catheters or central lines.
2. Acceptable treatments for oropharyngeal candidiasis --> Clotrimazole, Nystatin, Oral ketoconazole, fluconazole.
3. Vaginal candidiasis - Miconazole or clotrimazole cream.
4. Cutaneous candidiasis - Oral nystatin powder, keeping skin dry.
362
Systemic candidiasis - Treatment:
1. Amphotericin B
2. Fluconazole.
3. New agents --> Voriconazole and caspofungin.
363
FUO - Definition:
1. Fever >38.3C.
2. Continuing "on several occasions" for at least 3 weeks.
3. No diagnosis over this time period despite 1 week of inpatient workup.
- -> 3 outpatient visits now substitute for 1 week in the hospital.
364
FUO - Etiology:
1. Infection - MCC.
2. Occult neoplasms - 2nd MCC (lymphomas, leukemias).
3. Collagen vascular diseases.
4. Other causes.
365
FUO - Infectious etiology:
1. TB and other mycobacterial infection.
2. Occult abscesses (eg hepatic, retroperitoneal).
3. UTI/complicated UTI.
4. Endocarditis.
5. Sinusitis.
6. HIV.
7. Inf. mono + other viruses.
8. Malaria and other parasitic infections.
366
Persistence of fever in the ICU, despite antimicrobial therapy, should raise the index of suspicion for:
1. Fungal infection.
2. Antimicrobial resistance.
3. Infections requiring surgical intervention (eg occult abscess, wound necrosis).
4. Drug fever.
367
FUO - Collagen vascular disease etiology:
1. SLE
2. Still's disease (!)
3. PAN
4. Temporal arteritis
5. Polymyalgia rheumatica
368
FUO - Other causes:
1. Granulomatous diseases (Sarco, Crohn).
2. Drug fevers.
3. Pulmonary embolism.
4. Hemolytic anemia.
5. Familial mediterranean fever (!).
6. Gout.
7. Subacute thyroiditis.
8. Factitious illnesses.
369
Approach to fever - Most sources define fever as:
Body temperature >37.5C measured by a modern ORAL thermometer.
--> Rectal thermometers are slightly higher than oral or axillary thermometer readings.
370
Approach to fever - Hyperthermia vs fever:
Hyperthermia --> An elevation in body temperature not caused by "raising the thermostat" (ie, no change in the hypothalamic set-point).
--> Usually, caused by the inability of the body to dissipate heat.
371
Approach to fever - Hyperthermia etiology:
1. Neuroleptic malignant syndrome.
2. Malignant hyperthermia
3. Heat stroke.
372
Approach to fever - Hyperthermia response to antipyretics:
Hyperthermia does NOT respond to antipyretics, but rather to external cooling measures (eg ice, fans) and mediacations specific to the cause (eg dantrolene for malignant hyperthermia).
373
Approach to fever - Fever occurs when?
There is an elevation in the hypothalamic set-point. It is a natural response to an inflammatory process.
--> Usually responds to antipyretics.
374
Approach to fever - Treat fever with antipyretics when:
1. Fever is really hyperthermia.
2. Fever is dangerously high: >41.
3. Patient is pregnant.
4. There is significant cardiopulmonary disease (incr. O2 demand may cause ischemia).
5. The patient wants asymptomatic reliefs (chills, myalgias).
375
Catheter-related sepsis - Etiology:
1. Central venous catheters are a common cause of ever and sepsis in the hospital, especially in the ICU.
2. MC organisms --> S.aureus and S.epi.
376
Catheter-related sepsis - Risk factors:
1. Emergent replacement of catheter.
2. Femoral lines.
3. Prolonged indwelling of the line.
377
Catheter-related sepsis - How many patients with catheter-related sepsis have clinical evidence of infection at the site of insertion (ie erythema, purulence)?
ONLY 50% --> High index of suspicion is required.
378
Catheter-related sepsis - If you suspect catheter-related, what should be done?
Promptly remove the catheter and send the tip for culture. This alone typically leads to resolution of fever and a decrease in leukocytosis.
--> Antibiotics are usually initiated. Narrow the spectrum once the organism is identified.
379
Catheter-related sepsis - Only central venous catheter or also arterial or peripheral venous catheters are involved?
ONLY CENTRAL.
380
Neutropenia - Definition:
1. By absolute neutrophilic count (ANC) Severely increased risk of infection.
381
Neutropenic fever - Etiology:
1. Bone marrow failure (eg due to toxins, drugs).
2. Bone marrow invasion.
3. Peripheral causes (hypersplenism, SLE, AIDS).
4. Isolated neutropenia (agranulocytosis) --> drug side effects.
382
Neutropenic fever - Important to keep in mind:
Because neutropenia severely compromises the patient's ability to mount an inflammatory response, fever may be the only manifestation of a raging infection.
383
MC infections seen in neutropenic patients:
1. Septicemia.
2. Cellulitis.
3. Pneumonia.
384
Obtain the following for any neutropenic patient with a fever:
1. CXR
2. Panculture (blood, urine, sputum, line tips, wound) (!!!).
3. CBC.
4. Complete metabolic panel.
385
Neutropenic fever management - If fever persists beyond 4-5days despite broad spectrum antibacterial therapy, then:
Give:
1. Antifungal drugs - IV ampho B.
2. Consider G-CSF.
386
IM from EBV or CMV is milder?
From CMV.
387
IM DDX in patients with fever, lymphadenopathy, and pharyngitis:
1. Acute HIV infection.
2. Strep infection.
3. CMV.
4. Toxoplasma.
388
In which patients presenting with IM-like symptoms, is it important to perform diagnostic tests for HIV, CMV, and toxoplasma?
In pregnant patients --> Can have adverse effects on the fetus.
389
One infection with EBV confers lifelong immunity?
YES - Usually it does.
390
IM - incubation period:
2-5 weeks.
391
IM - Signs:
1. Lymphadenopathy - >90% of patients - Tonsillar or cervical (especially POSTERIOR cervical) --> May be quite enlarged, painful, and tender.
2. Pharyngeal erythema and/or exudate - frequently present.
3. Splenomegaly - Present in half of patients.
4. Maculopapular rash.
5. Hepatomegaly - In 10% of cases.
6. Palatal petechiae and eyelid (periorbital) edema - may occur in a minority of cases.
392
IM - Common lab abnormalities:
1. Lymphocytosis.
| 2. Elevated aminotransferases.
393
CMV mononucleosis - MC seen in:
Sexually active adolescents/young adults. Milder than EBV-associated IM.
394
CMV mononucleosis - Features:
1. Fevers
2. Chills
3. Fatigue
4. Headaches
5. Splenomegaly
395
CMV mononucleosis - Cervical lymphadenopathy and pharyngitis?
It is usually, ABSENT.
396
CMV mononucleosis - Heterophile antibodies?
Negative.
397
IM - Diagnosis:
1. Serology.
2. Peripheral blood smear.
3. Throat culture.
398
IM - Serology:
A. Monospot test - detection of heterophile antibody.
- -> Positive within 4 weeks of infection with EBV mono and are undetectable by 6 MONTHS.
- -> NOT WITH CMV.
- -> Rapid heterophile tests are highly sensitive and specific, particularly in adolescents.
399
IM - Diagnosis - EBV-specific antibody testing:
Perform in cases in which diagnosis is not straightforward (usually done by indirect immunofluorescence microscopy or by ELISA).
400
IM - Peripheral blood smear:
Usually reveals lymphocytic leukocytosis with large, atypical lymphocytes.
401
IM diagnosis - Throat culture:
Perform if pharyngitis is present to RULE OUT a 2o infection with β-hemolytic strep.
402
IM - Complications:
1. Hepatitis.
2. Neurologic complications (rare): meningoencephalitis, Guillain-Barre syndrome, Bell's palsy.
3. Splenic rupture - rare.
4. Thrombocytopenia, hemolytic anemia.
5. Upper airway obstruction due to lymphadenopathy - rare.
403
IM - When to return to sports?
Concern is splenic rupture - Patients should wait 3 to 4 weeks from symptom onset before returning to sports as splenic rupture is very RARE after 4 weeks.
404
Community-acquired pneumonia - Definition:
Occurs in the community OR within the first 72h of hospitalization.
