Micro: PCP, Toxo, MAC in AIDS Flashcards

1
Q

What is a normal CD4 count?

A

450-1400

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2
Q

What are the 3 major clinical syndromes in pts w AIDS?

A

pulmonary - dyspnea and infiltrates (PCP most common)
neurologic - focal findings and mass lesion (toxo)
fever of unknown origin (FUO) - disseminated infections (MAC)

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3
Q

CXR has diffuse intersitial infiltrates what should you expect?
CXR has lobar infiltrate what should you suspect?

A

PCP (ground glass infiltrates)

s. pneumoniae

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4
Q

What is the phylogenetic status of PCP?

A

was believed to be parasite

it is actually a fungus

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5
Q

What is the microbiology of PCP?

A

2 prominent antigen groups, includes MSG complex

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6
Q

What is the life cycle/pathogenesis of PCP?

A

developmental stages: small pleomorphic trophozoite and cyst form (up to 8 intracystic bodies)
probably sexual phase
asexual replication by trophic form and sexual by cyst
MSG facilitates adherence to ECM, surfactant and mannose
MSG undergoes antigenic variation

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7
Q

What is the pathology of inf w PCP?

A

heavy airless lungs, thickened alveolar septa, foamy eosinophilic alveolar exudate w parasites
organism doesn’t invade lung tissue

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8
Q

How is PCP diagnosed?

A

CXR, PC in bronchopulmonary secretions by sputum or bronchoalveolar lavage
transbronchial or open lung biopsy may be necessary
LM: Giemsa stains nuclei of trophozoites, silver stains cyst walls, DFA, clusters of crushed ping pong balls
elevated LDH (up to 500)
+ beta-D-glucan
oxygen desaturation when exercising
PaO235 indicate severe dz and need for steroid treatment

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9
Q

What is the treatment for PCP?

A

high dose TMP-SMX (also used for prophylaxis if cd4 <200, once HAART raises this, can stop prophylaxis)
as organisms die can deteriorate due to dead contents filling alveolar spaces - combo w prednisone

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10
Q

What is the transmission of P. jiroveci?

A

person to person is rare

thought to be inhaled

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11
Q

What are lung symptoms that do NOT indicate PCP and necessitate search for a different dx?

A
lymphadenopathy
pleural EFFUSIONS (PCP can have pneumothorax)
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12
Q

What are signs of a poor prognosis for PCP?

A

pts who AREN’T immunocompromised

pts who present w pneumothorax

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13
Q

What is the microbiology and basic life cycle of t. gondii?

A

obligate intracellular parasite
oocyst, trophozoite/tachyzoite, and bradyzoite forms
oocyst released into environment, develops four sporozoites which are ingested to cause infection
sexual and asexual phases (asexual in body responsible for dz = tachyzoites and bradyzoites)

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14
Q

What is the reservoir of infection for t. gondii?

A

cats - only definitive hosts for sexual stages

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15
Q

What are the different modes through which humans can become infected w t. gondii?

A
eating undercooked meat w cysts
ingestion of oocyst from fecally contaminated hands or food
organ transplant or blood transfusion
transplacental
accidental inoculation of tachyzoites
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16
Q

What does t. gondii do in the body?

A

gets into phagosome and prevents fusion w lysosome, differentiates into tachyzoite and divides rapidly
form cysts in skeletal muscle, myocardium, brain

17
Q

What are the features of persistent infection w t. gondii?

A

dormant stage = bradyzoite

persistent inf w bradyzoites in immunocompetent, upon immunocompromise, cysts can reactive & cause symptoms

18
Q

What are the clinical manifestations of toxo?

A

usually asymptomatic in immunocompetent
encephalitis in HIV+
congenital can be severe

19
Q

How is toxo diagnosed?

A

serology - positive IgM in immunocompetent
AIDS - IgG+ on SERUM (IgM not helpful), ring enhancing lesion, PCR of CSF (negative doesn’t rule out)
usually improve w/i 10-14 days of rx, otherwise biopsy
tachyzoites on histology

20
Q

What is the treatment of toxo?

A

not necessary in immunocompetent, not pregnant
for HIV/AIDS - sulfadiazine w pyrimethamine and leucovorin, continue until lesions and CD4 improve
CD4 less than 100 need TMP-SMX prophylaxis if IgG+

21
Q

What is the microbiology of MAC?

A

slow growing, non-pigmented in culture

isolated from birds, fresh and salt water

22
Q

What is the pathophysiology of MAC?

A

inhaled into respiratory tract, ingested into GI
translocates across mucosal epithelium, infects macrophages in LP and spreads lymphatically to local nodes
spreads hematogenously in immunocompromised

23
Q

What are the clinical presentations of MAC?

A

immunocompetent: pulm dz
infects those w CF
in HIV: disseminated dz presents as nonfocal fever syndrome

24
Q

What are the three different kinds of pulm dzs that occur in immunocompetent individuals w MAC?

A

elderly smokers (men) w pre-existing lung dz (COPD) - chronic cavitary pneumonia that resembles tb
elderly non-smoking females - mild lingular or RML infiltrates, productive cough and weight loss
single pulmonary nodule

25
Q

What are the features of disseminated dz of MAC?

A

fever, night sweats, weight loss
lymphadenopathy, pancytopenia
abnormal liver fxn tests, watery diarrhea, RUQ pain

26
Q

How is MAC diagnosed?

A

culture for AFB

DNA probe can differentiate from tb

27
Q

What is the treatment for MAC?

A
either azithromycin (preferred) or clarithromycin +
ethambutol and rifamyin (rifabutin has less interxns w HAART than rifampin) +
HAART
28
Q

What is the prophylaxis for MAC?

A

azithromycin

not needed w CD4 above 100