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Clinical 2 (Sam) > Opportunistic Infections > Flashcards

Opportunistic Infections Flashcards

1
Q

HAART

A

highly active antiretroviral

therapy

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2
Q

IRIS

A

immune reconstitution syndrome

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3
Q

Define Opportunistic Infections

A

Defined as “infections that are more frequent or more severe because of immunosuppression in HIV-infected persons”

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4
Q

Prior to _____, OI’s were the principal cause of morbidity and mortality in the HIV infected population

A

HAART

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5
Q

What had the most profound illness on reducing OI-related mortality in HIV-infected persons?

A

HAART

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6
Q

What are the 3 major OI’s

A

PCP
MAC
CMV

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7
Q

However, many patients, for whatever reason do not take HAART optimally, leading to ?

A

treatment failure and HIV progression

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8
Q

OI’s are directly related to overall immune function (______)

A

CD4+ and T cells

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9
Q

HAART reduces OI’s and improves survival, independent of __________ ________

A

antimicrobial prophylaxis

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10
Q

HAART does not replace the need for antimicrobial prophylaxis in _____ ______ _______

A

severe immune suppression

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11
Q

Although hospitalizations and deaths have decreased dramatically due to ART, OI’s remain a leading cause of ?

A

morbidity and mortality in HIV-infected persons

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12
Q

What are some AIDS indicator conditions? (AIDS-defining illnesses)

A
  • Cervical cancer, invasive
  • Encephalopathy, HIV-related
  • Lymphoma, Burkitt
  • Lymphoma, immunoblastic
  • Lumphoma, primary or brain
  • Wasting syndrome due to HIV
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13
Q

List and describe some bacterial opportunistic infections

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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14
Q

List and describe some fungal opportunistic infections

A
  • Pneumocystis carny (PCP) pneumonia - lungs
  • Candid - in the mouth, esophagus, trachea, bronchi, lungs or gut
  • Histoplasmosis
  • Coccidiomycosis
  • Aspergillosis
  • Cryptococcosis - outside the lungs particularly cryptococcal meningitis
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15
Q

List and describe some protozoal opportunistic infections

A
  • Toxoplasmosis of the brain

- Cryptosporidium

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16
Q

List and describe some viral opportunistic infections

A
  • Cytomegalovirus (CMV) disease outside the liver, spleen or lymph nodes and CMV retinitis
  • Herpes simplex virus (HSV) - systemic, encephalitis
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17
Q

The lower your immune system is, the _____ the incidence of OI

A

higher

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18
Q

What is the presenting symptom of HIV and leads for testing for HIV?

A

opportunistic infections

*basically a person with normal immune function would not get these infections, so if you present with one, they will test for HIV

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19
Q

Describe the management of an acute OI

A

1) Start treatment for the OI (if treatment exists)
2) Start HAART
- During treatment of acute OI
- Timing of start of HAART dependent on the particular OI (ex.. TB and cryptococcus)

Rationale:

  • decrease mortality from OI with earlier HAART start vs morbidity/mortality from IRIS
  • medications to treat both, side effects/toxicity - difficult to differentiate
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20
Q

What is IRIS?

A

immune reconstitution inflammatory syndrome (IRIS)

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21
Q

Describe IRIS (immune reconstitution inflammatory syndrome)

A
  • Characterized by fever, worsening clinical signs of the OI or symptoms of new OI
  • Occur in the first weeks after starting ART
  • May occur with a number of conditions (slide 12)
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22
Q

Describe the management of acute OIs in the setting of ART

A

1) OI occurs 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 > 12 weeks after initiation of aRT in patients with CD4 count > 200 cells/mm3 and suppressed HIV RNA
- May be difficult to determine whether 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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23
Q

All are examples of ____ infections:

  • Mucocutaneous candidiasis
  • Pneumocystis carnii pneumonia (PCP)
  • Cryptococcosis
  • Histoplasmosis
  • Coccidiomycosis
  • Aspergillosis
A

fungal

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24
Q

Mucocutaneous candidiasis:

Usually caused by ______ _______, other species seen in advanced immunosuppresion

A

Candida albicans

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25
Q

Mucocutaneous candidiasis:

______ and ______ candidiasis are common

A

Oropharyngeal and esophageal

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26
Q

Mucocutaneous candidiasis:

Most common in patients which what CD4 count?

A

<200 (but can occur at higher CD4 counts)

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27
Q

Vulvovaginal candidiasis (yeast infections) occur in who?

A

non-HIV infected women

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28
Q

Vulvovaginal candidiasis (yeast infections) may be more severe or recur more frequently in advanced ________

A

immunosuppresion

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29
Q

Mucocutaneous candidiasis:

Oropharyngeal = _____

A

thrush

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30
Q

Mucocutaneous candidiasis:

Describe pseudomembranous oropharyngeal (thrush)

A

-painless, creamy white plaques on buccal, oropharyngeal mucosa and/or tongue; can be scarped off eailsy

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31
Q

Mucocutaneous candidiasis:

Describe erythematous oropharyngeal (thrush)

A

patches on anterior and posterior palate or tongue

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32
Q

Mucocutaneous candidiasis:

What is another type of oropharyngeal (thrush)

A

angular cheilosis

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33
Q

Mucocutaneous candidiasis:

Describe esophageal

A
  • Retrosternal burning or discomfort, odynophagia, fever

- Endoscopy - whitish plaques +/- mucosal ulceration

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34
Q

Mucocutaneous candidiasis:

Describe vaginal

A

creamy discharge, mucosal burning and itching

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35
Q

What is the drug of choice for treatment for mucocutaneous candidiasis?

A

Oral fluconazole for 7-14 days

  • effective and in some studies superior to topical therapy
  • more convenient and generally better tolerated compared to topical
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36
Q

List some other options for the treatment of mucocutaneous candidiasis ?

A
  • Topical (Nystatin suspension, clotrimazole troches)
  • Itraconazole oral solution
  • Posaconazole oral solution
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37
Q

Mucocutaneous candidiasis:

Is routine primary prophylaxis recommended? Why/why not?

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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38
Q

What is primary prophylaxis?

A

prevention BEFORE development of disease

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39
Q

What is secondary prophylaxis?

A

prevention of RE-OCCURRENCE (after treatment of OI)

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40
Q

What is PCP Pneumonia caused by?

A

Pneumocystis jiroveci

also called PCP - pneumocystis carinii

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41
Q

PCP Pneumonia:

_______ in the environment

A

Ubiquitous (present, appearing and found everywhere)

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42
Q

PCP Pneumonia:

Who is the initial infection caused in?

A
  • Initial infection usually in early childhood

- 2/3 of healthy children have antibodies by age 2-4 years old

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43
Q

PCP Pneumonia:

May result from ?

A

reactivation or new exposure

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44
Q

PCP Pneumonia:

In immunosuppressed patients, possible ________ spread

A

airborne

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45
Q

What is the most common life threatening OI?

A

PCP Pneumonia

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46
Q

In advanced immunosuppression, treated PCP associated with ____% mortality

A

20-40

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47
Q

Who do the majority of PCP infections occur in?

A

The majority of PCP cases occur among patients who are unaware of their HIV infection or are not receiving ongoing HIV care or among those with advanced immunosuppression (CD4+ counts < 200)

48
Q

Incidence of PCP has declined substantially with widespread use of _______ and ___.

A

prophylaxis and ART

49
Q

Describe the clinical manifestation of PCP?

A
  • Progressive exertion dyspnea, fever, nonproductive cough, chest discomfort
  • Hypoxemia: characteristic, may be mild or severe
  • Subacute onset, worsens over days-weeks (fulminant pneumonia is uncommon)

Fulminant = sever/sudden onset

  • Chest exam may be normal, or diffuse dry rales, tachypnea, tachycardia (especially with exertion)
  • CXR - bilateral infiltrates
  • Definitive diagnosis requires demonstrating organism in sputum
50
Q

PCP:

Untreated = ___% mortality

A

100%

51
Q

Describe the treatment of PCP

A
  • Treatment started before definitive diagnosis
  • 21 day treatment
  • DOC = TMP/SMX
52
Q

What is the dose of TMP/SMX

A

15-20 mg/kg/day IV

53
Q

Adjust dose of TMP/SMX for ?

A

Renal insufficiency

54
Q

Adverse reactions with TMP/SMX

A

Adverse reactions (seen in 20-85% of patients with AIDS): rash, SJS, fever, leukopenia, thrombocytopenia, azotemia (nitrogen in blood), hepatitis, hyperkalemia

55
Q

PCP treatment:

Who gets corticosteroids?

A

For moderate-severe disease (hypoxia) within 72 hours improved mortality

56
Q

PCP treatment:

What corticosteroids and what dose?

A

Prednisone 40mg Bid days 1-5 then taper

57
Q

PCP treatment:

What are some alternative therapeutic regimens for moderate-severe disease?

A
  • Clindamycin-primaquine

- IV pentamidine

58
Q

PCP treatment:

What are some alternative therapeutic regimens for mild-moderate disease?

A
  • Oral TMP/SMX
  • Dapsone and TMP
  • Primaquine plus clindamycin
  • Atovaquone suspension
59
Q

When do you start ART (antiretroviral therapy) after PCP treatment?

A

If not on ART then initiate, when possible, within 2 weeks of diagnosed PCP, if signs of clinical improvement

60
Q

PCP primary prophylaxis:

Who should we initiate this in?

A
  • patients with CD4 count < 200
  • patients with history of oropharyngeal candidiasis
  • consider for those with CD4 <14% or AIDS defining illness
61
Q

How long is PCP primary/secondary prophylaxis for?

A

For life (unless immune reconstitution on ART)

62
Q

What is the preferred treatment for PCP primary/secondary prophylaxis?

A

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

63
Q

What is the alternate treatment for PCP primary/secondary prophylaxis?

A

TMP/SMX 1 DS tab three times/week

64
Q

When should we discontinue PCP prophylaxis?

A

in patients on ART with sustained increase in CD4 count > 200 for > 3 months

65
Q

When should you restart maintenance therapy for PCP prophylaxis?

A

-If CD4 count decreases to < 200
or
-If PCP recurs at CD4 count > 200

66
Q

All are examples of ______ infections:

  • Toxoplasma gondii encephalitis (TE)
  • Cryptosporidiosis
  • Microsporidiosis
A

parasitic

67
Q

Toxoplasma gondii Encephalitis:

What is it caused by?

A

T gondii (a protozoa)

68
Q

Toxoplasma gondii Encephalitis:

What is disease usually caused by?

A

reactivation of latent tissue cysts

69
Q

Toxoplasma gondii Encephalitis:

Primary infection may be associated with ??

A

acute cerebral or disseminated disease

70
Q

Toxoplasma gondii Encephalitis:

What is the primary infection acquired from?

A

tissue cysts in raw or undercooked meat or ingestion of sporulated oocysts (from cat faces) in soil, water or food

71
Q

Toxoplasma gondii Encephalitis:

Is it transmitted from person-person?

A

No

72
Q

Toxoplasma gondii Encephalitis:

Rarely occurs in patients with CD4 > ____

A

200

73
Q

Toxoplasma gondii Encephalitis:

Primarily occurs in patients with CD4 < ____

A

50

74
Q

Toxoplasma gondii Encephalitis:

symptoms?

A

CNS:

-fever, headache, seizures (10%), focal neurological abnormalities (60-90%), mental status change, coma

75
Q

Toxoplasma gondii Encephalitis:

Dissemination may occur and cause ?

A
  • retinochoroiditis (eye)
  • pneumonia (lung)
  • other organ involvement
76
Q

Toxoplasma gondii Encephalitis:

What imaging is involved?

A

CR, MRI of brain: multiple contrast-enhancing lesions, often with edema

77
Q

Toxoplasma gondii Encephalitis:

Detection of organism using ____ _____

A

brain biopsy (invasive)

78
Q

Toxoplasma gondii Encephalitis:

Almost all HIV+ patients with TE toxoplasmosis are positive for what antibody

A

IgG

79
Q

Toxoplasma gondii Encephalitis:

Preferred treatment regimen?

A

Pyrimethamine + Sulfadiazine + Leucovorin

this is very expensive, why we don’t use it in NA

80
Q

Toxoplasma gondii Encephalitis:

Alternate treatment regimen?

A

Pyrimethamine + Clindamycin + Leucovorin

does not protect against PCP so will need additional PCP prophylaxis

81
Q

Toxoplasma gondii Encephalitis:

Potential treatment regimen?

A

TMP/SMX can be considered an option if there is a valid reason not to use the preferred regimen

82
Q

Toxoplasma gondii Encephalitis:

Duration of treatment?

A

> 6 weeks, longer if extensive disease or incomplete response

83
Q

Toxoplasma gondii Encephalitis:

When should adjunctive corticosteroids be administered and what do you need to monitor?

A

Only if clinically indicated for treatment of cerebral swelling; monitor closely and discontinue ASAP. Monitor for development of other OIs

84
Q

Toxoplasma gondii Encephalitis:

When should anticonvulsants be administered?

A

to patients who have a history of seizures, but should not be administered as prophylactics to all patients

85
Q

Toxoplasma gondii Encephalitis:

Monitor for?

A
  • Clinical improvement
  • Radiological improvement
  • Adverse effects
86
Q

Toxoplasma gondii Encephalitis:

Time of starting ART ?

A

No set recommendation but many will start within 2-3 weeks of toxoplasmosis diagnosis

87
Q

Toxoplasma gondii Encephalitis:

Who should get primary prophylaxis?

A

CD4 count < 100 and positive IgG T. Gondii serology

88
Q

Toxoplasma gondii Encephalitis:

What is the primary prophylaxis treatment?

A

TMP/SMX - 1 DS tab daily (also covers PCP)

89
Q

Toxoplasma gondii Encephalitis:

Alternative prophylactic treatment?

A
  • TMP/SMX 1 DS tab three times/week
  • dapsone-pyrimethamine plus leucovorin (also covers PCP)
  • Atovaquone (with or without pyrimethamine/leucovorin also can be considered)
90
Q

Toxoplasma gondii Encephalitis:

Discontinue primary prophylaxis if?

A
  • If CD4 count > 200 for > 3 months on ART

- Reintroduced if the CD4+ count decreases to <100-200

91
Q

Toxoplasma gondii Encephalitis:

What is the preferred treatment for secondary prophylaxis?

A

Pyrimethamine + Sulfadiazine + Leucovorin

92
Q

Toxoplasma gondii Encephalitis:

What is the alternative treatment for secondary prophylaxis?

A

Atovaquone +/- Pyrimethamine or sulfadiazine

93
Q

Toxoplasma gondii Encephalitis:

When should you discontinue secondary prophylaxis?

A

If completed initial therapy for TE and remained asymptomatic with regard to signs and symptoms of TE and have a sustained increase in their CD4+ counts of > 200 after ART (> 6 months)

94
Q

Mycobacterium tuberculosis:

Co-infection as initial presentation or presents after starting _____ (IRIS)

A

HAART

95
Q

Mycobacterium tuberculosis:

What is the treatment?

A

concomitant but staggered start of HAART in patient not already of HAART due to adverse due to adverse effects from medications and risk of severe IRIS - start of HAART based on CD4 count

96
Q

Significant drug interactions between TB meds and ________

A

antiretrovirals

97
Q

Where are MAC organisms?

A

everywhere in the environment - water, soil

98
Q

How is MAC transmitted?

A

inhalation, ingestion or inoculation via the respiratory or GI tract

99
Q

Who does MAC generally occur in?

A

among persons with CD4+ counts < 50

100
Q

Without ART or chemoprophylaxis in AIDS patients incidence of disseminated MAC disease = ___%

A

20-40

101
Q

What is the major risk factor for disseminated MAC

A

CD4 count < 50

102
Q

Symptoms of MAC?

A
  • Usually a disseminated multi organ infection
  • Localized manifestations: lymphadenitis (cervical or mesenteric), pneumonitis, pericarditis, osteomyelitis, skin or soft tissue abscesses, genital ulcers, CNS infection
  • Fever, night sweats, weight loss, fatigue, diarrhea, abdominal pain, anemia, neutropenia
103
Q

How is MAC diagnosed?

A

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

104
Q

Disseminated MAC:

Strategy for treatment

A

initial treatment followed by chronic maintenance therapy

105
Q

Disseminated MAC:

What is the initial treatment?

A

> 12 months

-At least 2 effective drugs, to prevent resistance

106
Q

Disseminated MAC:

What is the preferred treatment?

A

Clarithromycin 500mg PO BID + Ethambutol 15 mg/kg PO daily (+/- Rifabutin)

107
Q

Disseminated MAC:

What is the alternative treatment ?

A

Azithromycin 500-600mg PO daily + Ethambutol PO (+/- Rifabutin)

108
Q

Disseminated MAC:

When do you start ART?

A

If not on ART then initiate ASAP after effective treatment

109
Q

Disseminated MAC:

How long is maintenance therapy after completion of initial therapy ?

A

Lifelong (unless immune reconstitution on ART)

110
Q

Disseminated MAC:

When should you consider discontinuation of secondary prophylaxis?

A

Consider discontinuation of secondary prophylaxis if treated > 12 months, no signs or symptoms of MAC, and sustained (>6 months) increase in CD4 count to > 100 cells on ART

111
Q

Disseminated MAC:

When should you restart secondary prophylaxis ?

A

if CD4 count decreases to < 100

112
Q

Disseminated MAC:

Indication ?

A

CD4 count < 50

113
Q

Disseminated MAC:

Drugs ?

A
  • Azithromycin 1200-1250 mg PO once weekly
  • Clarithromycin 500 mg po BID
  • Alternative: Rifabutin 300 mg PO daily
114
Q

Disseminated MAC:

Discontinue primary prophylaxis in patient on ART when ?

A

CD4 count > 100 for > 3 months

115
Q

GO OVER CASES

A

PROB WON’T BUT OKAY

Clinical 2 (Sam) (18 decks)

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