Opportunistic Infections Flashcards

1
Q

What is the most profound effect of HAART?

A
  • reducing OI related mortality in HIV infected people
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2
Q

What are OIs directly related to?

A
  • related to the overall immune function of CD4 T cells
  • HAART reduced OIs and improved survival, independent of antimicrobial prophylaxis (does not replace the need for antimicrobial prophylaxis in severe immune suppression
  • although hospitalizations and deaths have decreased dramatically due to ART, OIs remain a leading cause of morbidity and mortality in HIV infected persons
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3
Q

What are some of the AIDs indicator conditions?

A
  • cervical cancer, encephalopathy, lymphoma, wasting syndrome due to HIV
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4
Q

What are some of the bacterial OIs associated with HIV?

A
  • mycobacterium avid complex (MAC) infection- lungs

- recurrent bacterial infections can also occur such as repeated episodes of bacterial pneumonia or salmonella sepsis

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5
Q

What are some of the fungal OIs associated with HIV?

A
  • pneumoncystis carnii pneumonia, lungs
  • candidia- in the mouth, esophagus, trachea, bronchi, lungs or gut
  • histoplasmosis
  • coccidiomycosis
  • aspergillosis
  • cryptococcosis- outside the lungs particularly cryptococcal meningitis
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6
Q

What are some of the protozoal OIs associated with HIV?

A
  • toxoplasmosis of the brain

- cryptosporidium

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7
Q

What are some of the viral OIs associated with HIV?

A
  • CMV disease outside of the liver, spleen or lymph nodes and CMV retinitis
  • HSV systemic- encephalitis
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8
Q

What CD4 found is considered the danger zone?

A
  • under 200 (opportunistic infections can affect the body with a count over 200 though be conscious of this)
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9
Q

What is immune reconstitution inflammatory syndrome (IRIS)?

A
  • characterized by a fever, worsening clinical signs of the OI or symptoms of new OI
  • occur in the first few weeks after starting ART
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10
Q

What may IRIS occur with?

A
  • mycobacterial infections
  • pneumocystis carnii pneumonia
  • toxoplasmosis
  • hep B and hep C
  • tuberculosis
  • CMV infection
  • varicella zoster infection
  • cryptococcal infection
  • progressive multifocal leukoencephalopathy
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11
Q

When do OIs usually occur in respect to initiating an ART?

A
  1. shortly after initiation (within 12 weeks) of ART
    - subclinical infection unmasked by early immune reconstitution (not failure of ART)
    - start treatment for the OI- continue ART
  2. OI occurs over 12 weeks after initiation of ART in patients with CD4 cound >200 cells/mm3 and suppressed HIV RNA
    - - may be difficult to determine IRIS or new OI due to incomplete immunity
    - - start treatment for OI; continue ART; consider modifying ART if CD4 response to ART is suboptimal
  3. OI in patient with immunologic and virology failure on ART- clinical failure of ART
    - - start treatment for OI; modify ART for better virologic control
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12
Q

What is mucocutaneous candidiasis as an OI?

A
  • usually caused by candida albicans- other species are seen in advances immunosuppression
  • oropharyngeal and esophageal candidiasis are common here
    — most common in those with a CD4 count < 200
    (vulvovaginal candidiasis can also be an issue here)
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13
Q

what are the characteristics of oropharyngeal candidiasis?

A
  • pseudomembranous- painless, creamy white plaques on buccal, oropharyngeal mucosa and/or tongue; can be scraped off easily
  • erythematous - patches on anterior or posterior palate or tongue
  • angular cheilosis
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14
Q

What are the characteristics of esophageal candidiasis?

A
  • retrosternal burning or discomfort, odynophagia, fever

- endoscopy- whitish plaques +/- mucosal ulceration

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15
Q

What are the characteristics of vulvovaginal candidiasis?

A
  • creamy discharge, mucosal burning and itching
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16
Q

What is the treatment for mucocutaneous candidiasis?

A

treat for 7-14 days

  • oral fluconazole is the treatment of choice
  • effective and in some studies is superior to topical therapy
  • more convenient and generally better tolerated compared to topical
  • topical (nystatin suscpension, clotrimazole troches)
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17
Q

Should we be recommending primary prophylaxis for all those with mucocutaneous candidiasis??

A

NO

  • very low attributable mortality
  • acute therapy is highly effective
  • can lead to disease caused by drug resistant species
  • drug interactions
  • expensive
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18
Q

What is the cause of PC pneumonia?

A
  • caused by pneumocystitis jiroveci
  • ubiquitous in the environment - initial infection usually in early childhood - 2/3 of healthy children have antibodies by age 2-4 years old
  • PCP may result from reactivation or new exposure
  • in immunocompromised patients, possible airborne spread
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19
Q

What is the most common and life threatening OI?

A

-PCP pneumonia

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20
Q

Who is at most risk of being affected by PCP penumonia?

A
  • patients that are aware of their HIV infection or are not receiving ongoing HIV care or amoung those with advanced immunosuppression (CD4 counts <200 cells/mm3)
  • incidence of PCP has declined substantially with widespread use of prophylaxis and ART
21
Q

What are the signs that are associated with PCP?

A
  • progressive exertional dyspnea, fever, nonproductive cough, chest discomfort
  • hypoxemia: characteristic, may be mild or severe
  • subacute onset, worsens over days-weeks (fulminant pneumonia is uncommon)
  • chest exam may be normal, or diffuse dry rales, tachypnea, tachycardia (esp with exertion)
  • CXR- bilateral infiltrates
  • definitive diagnosis- organisms in sputum
22
Q

What is the duration of treatment for PCP?

A
  • 21 days
23
Q

What is the treatment of choice for PCP?

A
  • TMP IV
  • adjust the dose for the renal insufficiency - AE: rash, SJS, fever, leukopenia, thrombocytopenia, azotemia, hepatitis, hyperkalemia
  • corticosteroids: for moderate to severe disease (hypoxia) (within 72 hours- improved mortality)
  • prednisone 40 mg BID days 1-5 days then taper
24
Q

What are the alternative therapeutic regimens for moderate-to-severe PCP disease?

A
  • clindamycin-primaquine

- IV pentamidine

25
Q

Should prophylaxis be initiated in PCP pneumonia?

A
  • initiate: primary prophylaxis in patients with CD4 count <200 cells/mm3 or history of oropharyngeal candidiasis - consider for those with CD4 count <14% or AIDs defining illness
  • primary/secondary prophylaxis for life, unless immune reconstitution on ART
26
Q

What is the preferred treatment for primary/secondary prophylaxis

A

TMP/SMX 1 DS tab daily or 1 SS tab daily

- alternatives: TMP/SMX 1 DS tab three times a week

27
Q

When should prophylaxis for PCP be d/c?

A
  • when there is an increase in CD4 count >200 cells/mm3 for over 3 months
  • restart maintence therapy if CD4 count decreases to <200 cells/mm3 or if PCP recurs at CD4 count >200 cells/mm3
28
Q

What is the epidemiology of toxoplasma gondii?

A
  • disease usuaully caused by reactivation of latent tissue cysts in raw or undercooked meat or ingestion of sporulated oocysts (from cat feces) in soil, water or food
  • primary infection may be associated with acute cerebral or disseminated disease
  • no transmission by person to person contact
  • primarily occurs in patients with CD4 count <50 cells/mm3
29
Q

What is the clinical presentation of toxoplasma gondii (CNS)?

A
  • fever, headache, seizures, focal neurological abnormalities, mental status changes. coma
  • dissemination to eye, lung or other organs can occur
30
Q

Disseminaiton may occur to where in the body after toxoplasma gondii?

A
  • eye, lung and other organ involvement
31
Q

What is the preferred regimen of toxoplasma gondii encephalitis?

A
  • pyrimethamine and sulfadiazine and leucovorin
32
Q

What is the alternative regimen of toxoplasma gondii?

A
  • pyrimethamine and clindamycin and leucovorin
33
Q

What is the DOT of toxoplasma gondii?

A

over 6 weeks, longer is extensive disease or incomplete response

34
Q

What is the adjunctive treatment of toxoplasma gondii? (TG)

A
    • adjunctive corticosteroids should only be administered if clinically indicated for treatment of cerebral swelling; monitor closely and d/c as soon as possible. Monitor for development of other OIs
  • anticonvulsants should be administered to those patients with TE who have a history of seizures, but should not be administered as prophylactics to all patents
35
Q

When is prophylaxis important for those with TG?

A
  • use in primary prophylaxis if the CD4 count < 100 cells/mm3 and positive IgG T. Gondii serology
    • TMPSMX- 1 ds tab daily (also covers PCP)
  • d/c primary prophylaxis in those with a CD4 count >200 cells/mm3 for over 3 months on ART
  • reintroduced if the CD4 count decreases to <100-200 cells/mm3
36
Q

What is used as secondary prophylaxis for TG?

A
  • pyrimethamine and sulfadiazine and leucovorin
  • alternatives: pyrimethamine and clindamycin
  • atovaquone (+/- pyramethamine and sulfadiazine)
37
Q

What is the treatment of mycobacterial infections in those with HIV?

A
  • concomitant but staggered start of HAART in patient not already on HAART due to AE from medication and risk of severe IRIS - start of HAART based on CD4 count
38
Q

What is MAC?

A

mycobacterium avid complex

- in nontuberculosis mycobacteria

39
Q

Where are MAC organisms found?

A
  • everywhere in the environment - water and soil
40
Q

What is the transmission of MAC?

A
  • inhalation, ingestion, or inoculation via the respiratory or GI tract
  • generally occurs in those with CD4 counts, <50 cells/mm3
41
Q

What is the clinical manifestation of MAC?

A
  • dissemination multi-organ infection
  • localized manifestations: pneumonisitis, pericarditis, osteomyelisitis, skin or soft tissue abscesses, genital ulcers, CNS infection
  • fever, night sweats, weight loss, fatigue, diarrhea, abdominal pain, anemia, neutropenia
42
Q

What is the major risk factor associated with MAC?

A
  • CD4 count <50 cells/mm3
43
Q

What constitutes a diagnosis of MAC?

A
  • culture of organism from blood, bone marrow, lymph node or other normally sterile tissue or fluid
44
Q

What is the initial treatment associated with dissmeninated MAC?

A
  • > 12 months
  • at least 2 effective drugs, to prevent resistance
  • clarithromycin and ethambutol po daily (+/- rifampin)
45
Q

What is the alternative treatment to treating disseminated MAC?

A
  • azithromycin po daily and ethambutol po (+/- rifampin)

- if not on ART then initiate ASAP after effective tx

46
Q

What is needed for prevention of disseminated MAC?

A
  • lifelong chronic maintenance therapy after completion of initial therapy unless immune reconstitution on ART
  • consider d/c of secondary prophylaxis if treated >12 months, no signs or symptoms of MAC, and sustained (>6 months) increase in CD4 count to >100 count/mm3 on ART
  • restart secondary prophylaxis if CD4 count decreases to <100 cells/mm3
47
Q

When is primary prophylaxis warranted for disseminated MAC?

A
  • CD4 count under 50 cells/mm3
48
Q

What is used for primary prophylaxis of disseminated MAC?

A
  • azithromycin 1200-1250 mg po once weekly
  • clarithromycin 500 mg po BID
  • d/c primary prophylaxis when CD4 count is over 100 cells/mm3