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ID Review > Respiratory Infections > Flashcards

Respiratory Infections Flashcards

1
Q

Treatment for GAS pharyngitis? [2]

A

10 day course of penicillin or amoxicillin

Clinda [alt]

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2
Q

Presentation of lemierre’s syndrome?

A
  1. Pharyngitis
  2. Fever, lethargy, lateral neck tenderness/edema
  3. Septic emboli [bilateral nodular lung infiltrates + arthritis]
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3
Q

Treatment of lemierre’s?

A
  1. Augmentin/Unasyn

+/- anticoagulation

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4
Q

Diagnosis of lemierre’s?

A

CT with IV contrast showing a filling defect in the internal jugular vein

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5
Q

Presentation of diptheria?

A

Sore throat, low grade fever, and an adherent grayish pseudomembrane of the tonsils and pharynx.

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6
Q

Treatment of diptheria? [2]

A

Antitoxin

Abx

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7
Q

Complications of diptheria? [3]

A
  1. myocarditis [25%]
  2. delayed peripheral nerve conduction. [5%]
  3. Airway obstruction from pseudomembrane
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8
Q

Presentation of scarlet fever?

A
  1. sudden onset of fever, chills, malaise, sore throat
  2. exanthem appears 12–48 hours later that begins on the trunk and spreads peripherally
  3. Erythroderma (texture is of a sandpaper quality and erythema blanches with pressure
  4. strawberry tongue
  5. Pastia’s line formation with petchia in creases
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9
Q

Treatment of scarlet fever

A
  1. Penicillin for 10 days

2. Clinda for 10 days [alt]

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10
Q

What is Arcanobacterium Haemolyticum [micro]

A

A nonmotile beta-hemolytic, gram-positive bacillus

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11
Q

Who gets Arcanobacterium Haemolyticum infections?

A

10-30 year olds.

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12
Q

Presentation of Arcanobacterium Haemolyticum

A
  1. Pharyngitis
  2. 25-50% get a rash that is urticarial, macular, or maculopapular occur on the trunk and extremities while sparing the palms, soles, and face
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13
Q

Treatment of Arcanobacterium Haemolyticum

A
  1. Erythromycin [resistant to penicillin]

?Azithromycin

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14
Q

Seroprevalence of EBV in adults?

A

95%!

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15
Q

Who gets EBV?

A

Teens and young adults.

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16
Q

EBV complications?

A
  1. splenic rupture
  2. encephalitis
  3. autoimmune hemolytic anemia
  4. mild liver enzyme elevations.
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17
Q

Difference between EBV and CMV

A
  1. CMV is more mild with less sore throat and lymphadenopathy.
  2. Hepatitis is nearly ALWAYS present with CMV
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18
Q

Difference between EBV and acute retroviral syndrome

A

Mucocutaneous ulcerations and a rash are features more common with acute HIV syndrome versus infectious mononucleosis.
–> Screen all patients with suspected mono but negative testing for HIV.

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19
Q

HHV-6 infection in adults.

A

Rare
Occasionally, a mononucleosis-like syndrome with prolonged lymphadenopathy has been described during seroconversion of HHV-6 in adults

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20
Q

Etiology of chronic epiglotitis? [5]

A 
TB
Histo
Coccidio
Sarcoid
Viral
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21
Q

Diagnosis of chronic epiglotitis?

A

direct laryngoscopy and biopsy.

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22
Q

Who gets acute fungal sinusitis?

A

Immunocompromised

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23
Q

Causes of acute fungal sinusitis? [4]

A
  1. Aspergillus
  2. Mucorales
  3. Fusarium
  4. Occasionally dematiaceous molds
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24
Q

Definition of chronic sinusitis?

A

signs and symptoms that persist for at least 12 weeks.

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25
Q

Etiology of chronic sinusitis? [3]

A

gram-negative bacilli
MRSA
anaerobes.

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26
Q

What is Allergic fungal sinusitis?

A
  • Intense allergic response to chronic fungal colonization. - Typically among immunocompetent patients
  • Due to noninvasive growth of fungi in areas of compromised mucus drainage
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27
Q

Treatment of allergic fungal sinusitis?

A
  • Topical and systemic steroids
  • Surgery
  • Antifungals unproven
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28
Q

Treatment of viral sinusitis? [3]

A

nasal saline irrigation
inhaled corticosteroids
antipyretics

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29
Q

Treatment of bacterial sinusitis?

A
  1. Augmentin

2. Doxy [alt]

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30
Q

What prompts treatment of acute sinusitis with an abx?

A
  1. Symptoms lasting ≥10 days.
  2. Severe symptoms ≥3–4 days.
  3. Double sickening phenomenon (worsening symptoms after a period of improvement).
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31
Q

Intracranial complications of sinusitis? [5]

A 
Subdural empyema
Epidural abscess
Brain abscess
Meningitis
Venous sinus thrombosis
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32
Q

Extracranial complications of sinusitis? [3]

A

Orbital cellulitis
Orbital abscess
Subperiosteal abscess

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33
Q

When is abx recommended for acute COPD exacerbation? [2]

A
  1. Presentation with three cardinal symptoms: increased dyspnea, sputum volume, and sputum purulence.
  2. Presentation with two of the above cardinal symptoms if increased purulence is one of the symptoms.
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34
Q

What is the gram stain of pertussis?

A

gram-negative coccobacillus

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35
Q

Incubation period for pertussis?

A

1–3 weeks but typically is 7–10 days.

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36
Q

Who should get PEP for pertussis and with what?

A

Individuals with close contact to a person with pertussis (face-to-face contact within 3 feet of an infected individual).
–> Azithro

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37
Q

Sequelase of otitis media? [3]

A

Hearing loss.
Cholesteatoma.
Chronic perforation of tympanic membrane.

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38
Q

When should staph aureus be considered a pathogen for otitis media?

A

persistent otorrhea after insertion of tympanostomy tubes.

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39
Q

Finding of otitis media associated with mycoplasma pneumonia?

A

hemorrhagic bullous myringitis

–> Uncommon

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40
Q

Treatment of otitis media? [2]

A

Amoxicillin

Surgery if recurrent (myringotomy, adenoidectomy, and placement of tympanostomy tubes).

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41
Q

What is antigenic shift? Drift?

A

Drift refers to minor modifications (point mutations) within HA, NA, or both leading to localized outbreaks.

Shift refers to more radical changes in the antigenicity of HA, NA, or both (segment reassortment) leading to widespread disease or pandemics.

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42
Q

Most predictive findings of influenza in a local epidemic? [2]

A
  1. Fever

2. Cough

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43
Q

Who should be treated empirically for influenza [6]

A

patients who present after the onset of fever and cough during influenza season who are at high risk for complications…

  1. Young
  2. Old [>65]
  3. Pregnant + 2-4 weeks post partum
  4. Asthmatics
  5. DM, heart disease
  6. Hospitalized
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44
Q

Who gets the flu shot?

A

All older than 6 months, yearly.

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45
Q

Who gets chemoprophylaxsis for influenza? [4]

A
  1. Who present within 48 hours of exposure to an infected person.
    AND
    Who are at high risk of developing complications from influenza and have not been vaccinated.
    OR
    Who have been vaccinated within the past 2 weeks.
  2. Who are severely immunosuppressed with exposure in prior 48 hours.
  3. Outbreaks in nursing homes
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46
Q

Treatment of RSV [2]

A

Ribavirin [PO, transplant only] +/- IVIG

Palivizumab [not used in adults]

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47
Q

Complication of parainfluenza virus in hematopoietic stem cell transplant (HSCT) recipients?

A

risk factor for airflow decline and a cause of long-term pulmonary complications

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48
Q

Treatment of parainfluenza virus?

A

Supportive.

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49
Q

Who gets disseminated adenovirus infections? [2]

A

recipients of stem cell and solid organ transplants.

Those treated with Campath (alemtuzumab)

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50
Q

What is adenovirus a/w in HSCT? [2]

A

T-cell depleted graft recipients.

Acute graft versus host disease.

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51
Q

Treatment of adenovirus if disseminated?

A

Cidofovir

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52
Q

Who with CAP should be sputum without blood cultures? [3]

A

Failed outpatient antibiotic therapy
Patients with structural or obstructive lung disease
Patients who have a positive Legionella urine antigen test

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53
Q

Patients who should get blood AND sputum cultures [8]

A
  1. Admission to the ICU
  2. Cavitary infiltrates
  3. Leukopenia
  4. Alcohol abuse
  5. Advanced liver disease
  6. Asplenia
  7. Positive pneumococcal urine antigen test
  8. Pleural effusion
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54
Q

What serotype does the legionella urine antigen detect?

A

1

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55
Q

In what organisms is acute and convalescent serologic testing used for diagnosis? [3]

A

Chlamydophila pneumoniae
Legionella species
Mycoplasma pneumoniae

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56
Q

Likely etiology of a mild, outpatient treated pneumonia? [5]

A 
Mycoplasma pneumoniae
Moraxella catarrhalis
Haemophilus influenzae
Chlamydophila pneumoniae
Respiratory viruses
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57
Q

Likely etiology of moderate, inpatient but non-ICU treated pnemonia? [7]

A

Streptococcus pneumoniae
Legionella spp.
Mycoplasma pneumoniae
Chlamydophila pneumoniae
Haemophilus influenzae
Aspiration (e.g., gram-negative enteric pathogens, oral anaerobes)
Respiratory viruses (e.g., influenza, RSV, parainfluenza, adenovirus)

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58
Q

Likely etiology of ICU treated pneumonia? [5]

A 
Streptococcus pneumoniae
Staphylococcus aureus
Legionella spp.
Gram-negative bacilli
Haemophilus influenza
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59
Q

Treatment of pneumonia as outpatient [3]

A
  1. Azithro
  2. Doxy
  3. Resp fluoroquinolone OR beta-lactam + azithro if risk factors OR abx use in last 3 months.
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60
Q

Treatment of inpatient non-ICU pneumonia?

A
  1. Resp fluoquinolone alone

2. Ceftriaxone + azithro

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61
Q

Who gets mycoplasma pneumonia?

A
  1. Young people <40 in the summer or fall
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62
Q

Presentation of mycoplasma pneumonia?

A

URI with constitutional symptoms that then progresses to a lower respiratory tract infection. Sore throat is often the initial finding. 1/3 have ear findings

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63
Q

Describe the radiologic findings in mycoplasma

A

Can be more extensive than the physical exam would indicate. Lower lobe unilateral or bilateral patchy infiltrates in one or more segments in bronchial or peribronchial distribution have been described.

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64
Q

Extrapulmonary sites of chlamydia pneumonia? [5]

A 
otitis media 
sinusitis
pericarditis 
myocarditis
endocarditis
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65
Q

Presentation of legionella pneumonia?

A

Initially present with milder disease involving malaise, nonproductive cough, and myalgias, but this can rapidly progress to more severe pulmonary symptoms with high fevers, faget’s sign.

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66
Q

Extrapulmonary manifestations of legionella? [7]

A 
Mental status changes.
Diarrhea.
Rash.
Hyponatremia.
Hypophosphatemia.
Elevated liver enzyme levels.
Elevated creatinine levels.
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67
Q

What is nosocomial pneumonia?

A

presents 48 hours or more after admission.

68
Q

What is Healthcare-associated pneumonia (HCAP)?

A

Pneumonias in..

  1. Hospitalized in last 90 days
  2. NH or LTACs
  3. Those getting parenteral abx in last 30 days
  4. Chemo in last 30 days
  5. Wound care in last 30 days
69
Q

What is VAP?

A

pneumonia that develops 48 hours or more after endotracheal intubation.

70
Q

Risk factors for MDR in VAP? [5]

A
  1. Prior intravenous antibiotic use within 90 days
  2. Septic shock at time of VAP
  3. Acute respiratory distress syndrome preceding VAP
  4. 5 or more days of hospitalization prior to the occurrence of VAP
  5. Acute renal replacement therapy prior to VAP onset
71
Q

Treatment of HAP/VAP

A

Antipseudomonal
AntiMRSA
–> 7 days of abx

72
Q

When should 2 antipseudomonals be used?

A

If the patient is being managed in a unit where >10% of isolates are resistant to an agent being considered for monotherapy or the patient possesses risk factors for MDR pathogens

73
Q

Presentation of pulmonary nocardiosis?

A

subacute or chronic fashion and include dyspnea, nonproductive cough, hemoptysis, as well as fever.

74
Q

Presentation on imaging of pulmonary nocardiosis? [4]

A
  1. ill-defined nodules (occasionally cavitary lesions)
  2. reticulonodular
  3. diffuse pulmonary infiltrates
  4. pleural effusions.
75
Q

What is seen on gram stain of pulmonary nocardiosis?

A

Gram-positive, beaded, fine right-angle branching filaments that are usually weakly acid-fast

76
Q

Risk factor for pulmonary actinomycosis?

A

aspiration of oropharyngeal contents.

Periodontal disease and poor dentition are risk factors

77
Q

Characteristic finding of pulmonary actinomycosis on imaging?

A

Direct extension of a cavity or mass through an interlobar fissure

78
Q

Complications of pulmonary actinomycosis? [4]

A 
Invasion of anatomic barriers leading to... 
1 empyema
2 mediastinitis
3 pericarditis 
4 vertebral osteomyelitis.
79
Q

Treatment of pulmonary actinomycosis

A

penicillin

80
Q

Where is melioidosis endemic?

A

Southeast Asia, Australia

81
Q

What causes melioidosis?

A

Burkholderia pseudomallei

–> found in soil, vegetation, and water throughout tropical regions.

82
Q

Microbiology of Burkholderia pseudomallei? [aerobe or anaerobe? Gram stain? What media does it grow on, oxidase?]

A

aerobic facultative intracellular gram-negative bacillus that grows readily on routine culture media
Oxidase positive
–> Characteristic bipolar staining with a “safety pin”
appearance

83
Q

Risk factors for melioidosis? [4]

A

DM
CKD/lung disease
EtOH use
Typhoons

84
Q

Presentation of melioidosis?

A

High fever, dyspnea, purulent sputum production, and hemoptysis. Bacteremia is common. [Fever and sepsis syndrome..pneumonia, sepsis, gram negative bacteremia and shock from right location]

85
Q

Imaging findings found in melioidosis

A

diffuse miliary nodules, which may expand and cavitate

86
Q

Treatment of melioidosis

A

Carbapenems
Ceftaz
Transition for PO bactrim for at least 3 months of therapy

87
Q

Microbiology of Rhodococcus equi [gram stain, culture color]

A

pleomorphic gram-positive coccobacillus
salmon-pink color when grown in culture
Weakly acid fast

88
Q

Lung manifestations of rhodococcus?

A

Nodules, cavitation, pleural effusion, and abscesses

89
Q

Advantage of NAAT for TB diagnosis?

A

Provide a rapid distinction between M. tuberculosis and nontuberculous mycobacterial species in the setting of a positive sputum smear sample.

90
Q

How should treatment response to pulmonary TB be measured?

A

Repeat sputum culture during the 1st and 2nd months of treatment

91
Q

When would you extend therapy for pulmonary TB? [3]

A

Positive sputum cultures at 2 months into treatment
Cavitary lesions on initial chest film.
Drug-resistant TB

92
Q

Most common NTM that cause pulmonary lung disease? [4]

A
  1. MAC
  2. fortuitum
  3. abscessus
  4. kansasii
93
Q

Risk factors for NTM pulmonary disease?

A
  1. COPD

2. bronchiectasis

94
Q

M. abscessus is a/w increased mortality in what patient population?

A

Cystic fibrosis

95
Q

M. fortuitum is more common in what patient population?

A

History of gastroesophageal reflux disease and vomiting.

96
Q

Diagnosis of NTM pulm infection?

A
  1. Multiple positive cultures as NTM can colonize
    AND
  2. Clinical criteria (e.g., pulmonary symptoms, nodular or cavitary infiltrates on chest radiograph, and/or multifocal bronchiectasis on chest imaging).
97
Q

Treatment of MAC pulmonary infection?

A
  1. macrolide, ethambutol, and a rifamycin
  2. Consider aminoglycosides in severe cavitary disease and with macrolide resistance
    3x weekly with nodular/bronchiectatic category
    Daily therapy if cavitary
    Therapy for 12 months
98
Q

Treatment of M. kansasii pulmonary infection

A
  1. rifampin, ethambutol, isoniazid

Daily for 18 months

99
Q

Principles of treatment of M. abscessus infections

A

Can be HIGHLY resistant and should be tested as such
Isolates can acquire mutational resistance to clarithromycin and amikacin because the isolates have only one copy of the gene

Macrolide plus one or more of the following:
aminoglycosides, linezolid, cefoxitin, and clofazimine

100
Q

Oral options for treatment of M. fortuitum pulmonary disease? [5]

A

macrolides, quinolones, doxycycline, minocycline, and sulfonamides
Treat with 2 drugs for 12 months.

101
Q

IV options for treatment of M. fortuitum? [3]

A

Amikacin, cefoxitin, and imipenem

102
Q

Why should macrolides be used with caution in M. fortuitum?

A

Inducible erythromycin methylase gene that confers resistance to macrolides

103
Q

What is lights criteria?

A

If one of the following is present, fluid is defined as an exudate:
Pleural fluid protein/serum protein ratio greater than 0.5.
Pleural fluid LDH/serum LDH ratio greater than 0.6.
Pleural fluid LDH greater than two-thirds the upper limits of the laboratory’s normal serum LDH.

104
Q

What are the 3 phases of a pleural infection?

A

Exudative stage
Fibropurulent stage
Organizing stage

105
Q

Describe the following studies in pleural fluid in the exudative stage? [pH, glucose, PMN count, LDH, culture results]

A 
Thin, free-flowing fluid with low numbers of neutrophils present.
pH >7.2.
Lactate dehydrogenase (LDH) <1000 IU/L.
Normal glucose higher than 60 mg/dL.
Negative cultures.
106
Q

Describe the changes that occur in the pleural fluid in the Fibropurulent stage

A

Increasing numbers of neutrophils and fibrin deposition.
pH and glucose begin to fall.
LDH level increases.

107
Q

What occurs in the organizing stage of a pleural effusion?

A

Fibroblast formation and scarring take place producing a pleural peel that entraps and encases the lung.

108
Q

Most common cause of pleural effusion today?

A

Streptococcus anginosus group (milleri)

MRSA and GRN are common in hospital acquired pleural effusions

109
Q

What is empyema necessitans?

A

A chronic empyema that may erode the chest wall and present with a spontaneous draining abscess.

110
Q

What organisms cause empyema necessitans? [2]

A

TB and actinomycosis

111
Q

How might Entamoeba histolytica cause a pleural effusion?

A

subdiaphragmatic rupture

112
Q

How does pleural fluid of E. histolytica look?

A

anchovy paste or chocolate appearance

113
Q

Common causes of lung abscess [4]

A 
aspiration of oral anaerobic flora
[alcoholism, seizures, stroke ,drug overdose]
foreign body
compressing lymph node
Poor dentition
114
Q

Four characteristics of lung abscesses for classification

A
  1. The causative organism(s)
  2. Presence of a foul odor to expectorated sputum (putrid abscess)
  3. Duration of symptoms prior to abscess (acute, subacute, chronic)
  4. Presence or absence of associated conditions (e.g., lung cancer, immunosuppression)
115
Q

Where are lung abscesses typically located?

A
  1. posterior segment of the right upper lobe
  2. posterior segment of the left upper lobe
  3. superior segments of the lower lobes.
116
Q

Presence of foul smelling sputum is suggestive of what?

A

polymicrobial anaerobic infection

117
Q

What bacteria lead to lung abscesses? [9]

A 
Oral anaerobes
Staphylococcus aureus
Klebsiella pneumoniae
Pseudomonas aeruginosa
Group A streptococcus
Streptococcus anginosus group
Nocardia
Rhodococcus equi
Actinomyces
118
Q

What fungi lead to lung abscesses [6]

A 
Histoplasma
Blastomyces
Coccidioides
Aspergillus
Cryptococcus
Mucorales
119
Q

What parasites can lead to lung abscesses? [3]

A

Paragonimus westermani
Entamoeba histolytica
Echinococcus

120
Q

Treatment of a lung abscess

A

6-8 weeks of abx
Serial CXR to assess response
Surgical mgmt if not responding

121
Q

Treatment of aspiration pneumonia?

A

Normally supportive care.

Unasyn if the patient fails to respond within 48 hours.

122
Q

Who with flu may lack fever? [3]

A
  1. Elderly
  2. Immunocompromissed
  3. Those on steroids
123
Q 
Describe the following flu strains..
H1N1
H3N2
H5N1
H7N9
A

1918 spanish flu, re-emerged in 1977
Emerged in 1968, Hong Kong Flu
Emerged in Hong Kong in 2003 [Egypt and Vietnam clusters]
Avian flu from China, ongoing.

124
Q

H7N9 clinical characteristics

A
  1. Fowl to person spread in wet markets
  2. Some person to person spread
  3. 22% mortality rate
  4. Tamiflu resistance increasing
125
Q

H5N1 clinical characteristics

A
  1. Found in Vietnam, Egypt, Indonesia
  2. Rare human to human transmission
  3. Mortality rate 60%
  4. Multi-organ failure and diarrhea have
    been more common than in seasonal flu.
126
Q

Influenza clinical characteristics

A
  1. Incubation 1-4 days [2 average]
  2. Shedding occurs 1-2 days before symptom onset
  3. Shedding continues for 5-7 days after symptom onset in adults. Can be prolonged if immunocompromised.
127
Q

Most common cause of pneumonia following influenza

A
  1. Strep pneumo
  2. GAS
  3. Staph aureus
128
Q

Resp complications of influenza infection? [5]

A
  1. ARDS
  2. Hemorrhagic pneumonitis
  3. Bacterial infection
  4. Toxic Shock from bacterial infection [strep or staph with staph being most common]
  5. Invasive aspergillus infection [rare, Netherlands mostly]
129
Q

Non-resp complication of influenza [7]

A
  1. Seizures
  2. Encephalopathy/Necrotizing encephalitis
  3. GBS [10x more common with infection than vaccine]
  4. Myositis/Rhabdo
  5. Pericarditis
  6. Myocarditis
130
Q

Describe resistance pattern of flu B?

A
  1. Intrinsic resistance to adamantanes
    (rimantidine and amantidine)
  2. Increased resistance to tamiflu
131
Q

How does tamiflu resistance occur?

A

point mutation H275Y in H1N1 viruses

H274Y in N2

132
Q

What is Baloxavir

A

Cap-dependent polymerase inhibitor
• Non inferior to oseltamivir
• Superior for influenza B in patients with risk
factors
• Shorter duration of shedding
• Resistance mutations emerge on treatment [>10% after a single dose!]

133
Q

Presenting features of adenovirus [7]

A 
URI
pharyngitis
pneumonia,
conjunctivitis [this with pneumonia is a good clue!]
hemorrhagic cystitis [immunocompromised]
gastroenteritis,
hepatitis
134
Q

Presentation of adenovirus in transplant patients

A

URI progresses to LRI in about half
severe hepatitis, encephalitis
hemorrhagic cystitis [not a/w dissemination, own syndrome], tubulointerstitial nephritis

135
Q

Treatment of human metapneumovirus

A

NONE APPROVED

Supportive

136
Q

Complication parainfluenza can cause in transplant patients?

A

COP

137
Q

Where does hantavirus occur?

A

Arizona, Colorado, New Mexico, and Utah. Yosemite, California

138
Q

What animal is a/w hantavirus infection?

A

Rodent exposure most via aerosolized rodent urine.

Also present in throat swab and feces, mucous
membrane contact, and skin breaches and can spread - but less likely.

139
Q

How does Hantavirus pulmonary syndrome present?

A

5 stages…

  1. Incubation (4-30 days)
  2. Febrile phase with Fever, myalgia, malaise occasionally N/V/abd pain
  3. Cardiopulmonary phase
  4. Diuretic phase
  5. Convalescent phase
140
Q

Describe the cardiopulmonary phase of hantavirus pulmonary syndrome

A
  1. Acute onset of cough an dyspnea with rapid progression of shock and pulmonary edema (4-24h non-productive cough and SOB
  2. Hypovolemia due to progressive leakage of high
    protein fluid from blood to lung interstitium and
    alveoli, decreased cardiac function

–> COMPLETE WHITE OUT OF CXR due to both CHF and ARDS

141
Q

What lab clues to dx of hantavirus pulmonary syndrome [4]

A

Thrombocytopenia (98%),
Hemoconcentration
left shift with atypical lymphs
elevated PT, abnormal LFTs

142
Q

Who gets nocardia infection [9]

A

Solid organ transplant, hematopoietic transplant, chronic steroids, alcoholism, diabetes, chronic granulomatous disease, CF, anti-TNF therapy, AIDS (less common)

–> May occur YEARS after transplant.

143
Q

What imaging should be ordered on those with pulmonary nocardia?

A

MRI of the brain as it commonly disseminates there with single or multiple abscesses

144
Q

Who gets skin manifestations of nocardia? [2]

A

Immunocompetent host in tropical region (N. brasiliensis)

Immunocompromised patient who gardens or walks barefoot

145
Q

Describe the skin manifestations of nocardia

A
  1. Sporotrichoid lesions

2. Mycetomas: chronic, progressive, lower limbs, draining sinuses (similar to Actinomycetes)

146
Q

Treatment of nocardia?

A

TMP/SMX is mainstay (skin = monotherapy)
Empiric Amikacin + imipenem/meropenem + TMP/SMX for transplant/disseminated disease

–> High rates of drug resistance.

147
Q

Who gets Rhodococcus infections?

A

T cell immunosuppressed - HIV+ & CD4<100; organ transplant. with proper exposure [farm, soil, horse manure].

148
Q

How is rhodococcus diagnosed?

A

Culture followed by 16S rRNA, MALDI-TOF

Blood cultures may be positive (>25%)

149
Q

What will tissue biopsy in rhodococcus show?

A

necrotizing granulomatous reaction; microabscess

150
Q

Treatment of rhodococcus infection?

A

vancomycin + imipenem/meropenem +
fluoroquinolone OR rifampin for 2-3 wks then oral FQ + azithro/clari or rifampin

Linezolid an alternative for vanco anchor

151
Q

What organisms give a safety pin appearance on gram stain? [5]

A 
Yersinia pestis
Vibrio parahemolyticus
Burkholderia mallei &amp; pseudomallei
Haemophilus ducreyi
Klebsiella granulomatis (granuloma inguinale)
152
Q

Complications of Melioidosis?

A

Metastatic abscesses: skin ulcers or abscesses more
common than bone, spleen, brain, prostate
Can become latent & reactivate like TB (rare)

153
Q

What causes glanders? Who gets this disease?

A

Burkholderia mallei & is rare in humans

Requires close contact w/ infected animals (horses, donkeys, mules)

154
Q

How do you handle glanders?

A

Looks EXACTLY like meliodosis. Dx and treat same way.

155
Q

What type of infection is an IUD a/w?

A

Pelvic actinomycosis

156
Q

Diagnosis of actinomycosis

A

Culture, histopathology (sulfur granules)

–> Easily made culture negative with small amounts of abx.

157
Q

Microbiology of actinomycosis?

A

Gram-positive, anaerobic, non–spore-forming bacteria
Often forms a tangled mass of branching filaments
Molar tooth colony appearance on plates

158
Q

Most common presentation of actinomycosis?

A

Oral-cervicofacial disease with lumpy jaw following dental procedure; erosive, destructive, draining sinus tracts.

159
Q

Treatment of cervicofacial actinomycosis

A

Penicillin for 6-12 months
Doxy [alt pen allergy]
Clinda [alt pen allergy]

160
Q

When should a sore throat be treated as strep in an adult?

A

ONLY with microbiologic diagnosis

–> Not ONLY if cantor score is high

161
Q

Ddx for strawberry tongue [3]

A
  1. Strep infection
  2. Staph toxic shock
  3. Kalasaki disease
162
Q

When should you SCREEN asymptomatic people for GAS? [2]

A

– Community outbreaks of invasive GAS or RF (eg, dorm)

– Family or personal h/o rheumatic fever

163
Q

Eradication regimen for GAS? [3]

A
  1. 10 days of amoxicillin-clavulanate
  2. clindamycin [alt]
  3. PCN plus rifampin (4 days) [alt]
164
Q

Diagnosis of Arcanobacterium Haemolyticum?

A
  • -> Failure to respond to strep treatment
  • -> Throat culture
  • -> Looks like strep with rash but throat culture and rapid strep are negative [strep excluded]
165
Q

What is herpangina?

A

Oral lesions present only with sore throat
Due to enteroviruses [coxsackie]
No hand or foot manifestations

ID Review (25 decks)

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