Opportunistic Infections Flashcards

1
Q

What OIs are likely between 350-250 CD4 cell counts?

A

Bacterial skin infections
Varicella Zoster
Kaposi’s sarcoma

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2
Q

What OIs are likely between 250-150 CD4 cell counts?

A

Oral Candiasis (~249)
Pneumocystis carinii pneumonia
Non-Hodgkin’s lymphoma

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3
Q

What OIs are likely between 150-50 CD4 counts?

A

Cryptococcal meningitis

Herpes simplex virus infections

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4
Q

What OIs are likely between 50-0 CD4 counts

A

CMV infections

Mycobacterium-avium complex

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5
Q

What is Carini pneumonia?

A

Organism with protozoal and fungal properties,
Classified as a fungus.
Part of normal colonization in the lungs.
Only immunocompromised are at risk for a disease.

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6
Q

What are the s/sx of Carini pneumonia?

A
Usually slow onset (days to weeks).
Fever
Fatigue
Dyspnea
Tachypnea
Non-productive cough
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7
Q

What is the most common form of PCP?

A

Pneumonia

Oral thrush is a common co-infection

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8
Q

How do you diagnose PCP?

A

CXR
ABG
Sputum culture

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9
Q

What is the first line treatment for moderate-severe PCP?

A

Bactrim 15-20mg/kg/d IV in 3-4 doses x 21 days

Switch to PO after clinical improvement

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10
Q

What is the first line treatment for mild-moderate PCP?

A

Bactrim 15-20mg/kg/d PO in 3 divided doses or Bactrim DS 2 tabs TID x 21 days

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11
Q

When are adjuvant steroids prescribed in PCP?

A

Pts with severe PCP and PaO2 < 70.

Must be started within 72 hours of treatment

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12
Q

What is the steroid regimen for PCP?

A

Started within 72 hours of treatment.
Mortality rates and rates of respiratory failure are reduced.
If patient is unable to take PO, use IV methylprednisolone (75% of PO prednisone dose)

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13
Q

What is the prednisone dose in PCP?

A

40mg BID days 1-5, then 40mg QD days 6-10, then 20mg QD days 11-21

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14
Q

In what patients do we have primary prophylaxis of PCP?

A
CD4 < 200, or
CD < 14%, or
A hx of oropharyngeal candidiasis, or
A hx of AIDS-defining illness, or
CD4 > 200 but < 250 if CD4 cell count monitoring (e.q. q3months) is not possible
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15
Q

What is first line primary prophylaxis therapy for PCP?

A

Bactrim DS 1 tab QD
OR
Bactrim SS 1 tab QD

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16
Q

When do we d/c primary prophylaxis therapy for PCP?

A

Patients who have responded to HAART with an increase in CD4 count to >/= 200 for >/= 3 months

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17
Q

What is the difference between primary and secondary prophylaxis therapy for PCP?

A

None, same regimen and reasons to d/c

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18
Q

What is toxoplasmic encephalitis?

A

Toxoplasma gondii.
Intracellular parasite (protozoa).
Passed to humans from raw or undercooked meat and by contact with feces from infected cats.

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19
Q

What are the s/sx of toxoplasmic encephalitis?

A
CNS infection
Typically assocaited with fever
Seizures
Focal neurological deficits
Other sx associated with encephalitis
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20
Q

How do you diagnose toxoplasmic encephalitis?

A

Serological testing for Toxoplasma IgG
Neuroradiological scans (CT or MRIs)
Brain biopsy

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21
Q

What does IgG show?

A

Past infxn

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22
Q

What does IgM show?

A

Current infxn

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23
Q

When do we take a brain biopsy for toxoplasmic encephalitis?

A

Usually reserved for patients refractory to empiric therapy

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24
Q

What is the 1st line therapy for toxoplasmic encephalitis?

A

Sulfadiazine + pyrimethamine + leucovorin for >/= 6 weeks

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25
Q

What do we use if pyrimethamine is not available or delayed?

A

Bactrim 5mg/kg IV BID x 6 weeks

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26
Q

When do we use primary prophylaxis for toxoplasmic encephalitis?

A

CD4 < 100 and toxoplasma IgG +

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27
Q

When do we d/c primary prophylaxis for toxoplasmic encephalitis?

A

After response to HAART and CD4 > 200 x >/= 3 months

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28
Q

What is used for secondary prophylaxis of toxoplasmic encephalitis?

A

Sulfadiazine + pyrethamine + leucovorin

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29
Q

When do we d/c secondary prophylaxis for toxoplasmic encephalitis?

A

After completion of initial therapy, and CD4 > 200 on HAART >/= 6 months

30
Q

What is Cryptococcus meningitis?

A

Cryptococcus neoformans.
Encapsulated yeast.
The most common life-threatening fungal infection in AIDs patients.
Organism is ubiquitous in the environment and found in soil.
Exposure to aged bird droppings may increase the risk of infection.

31
Q

What are the s/sx of Cryptococcus meningitis?

A
Progressive development of fever and/or HA, neck stiffness, photophobia, CNS changes.
Disseminated disease (skin, pulmonary) with cryptococcus is common.
32
Q

What is the 1st line treatment for Cryptococcus meningitis?

A

Liposomal ampho B + 5-FU x at least 2 weeks.
Followed by fluconazole 400mg qd x 8 more weeks.
Then chronic suppression with fluconazole 200mg QD for at least 1 yr

33
Q

What is the primary prophylaxis for Cryptococcus meningitis?

A

None recommended

34
Q

What is the secondary prophylaxis for Cryptococcus meningitis?

A

Chronic suppression.

Fluconazole 200mg QD

35
Q

When do we d/c secondary prophylaxis for Cryptococcus meningitis?

A

After completion of initial therapy, patients must be asymptomatic, and have a sustained increase in CD4 > 100 after HAART x at least 3 months after the 1st year

36
Q

What does MAC/MAI stand for?

A

Mycobacterium avium complex/infection

37
Q

What is MAC?

A

Comprised of mycobacterium avium and Mycobacterium intracellulare.
Ubiquitous in nature, commonly inhabiting soil and water.
Typically begins w/colonization of the intestinal or respiratory tracts after organism ingestion or inhalation, with subsequent development of localized infection and sometimes seeding of the blood.

38
Q

What are the most common s/sx of MAC?

A
Typically a multiorgan system disease in AIDs patients
Fever
Night sweats
Anorexia
Weight
39
Q

What are the common s/sx of MAC?

A
Diarrhea
Abdominal pain
Increased LFTs
Anemia
Neutropenia
Thrombocytopenia
40
Q

What are the less common s/sx of MAC?

A

Hepatomegaly
Splenomegaly
Lymphadenopathy

41
Q

What are the ways to diagnose MAC?

A

Culture is gold standard, but some pts with - blood cx for MAC will have positive liver, bone marrow or lymph node biopsies, which would confirm the diagnosis.
Organism takes 2-6 weeks to grow.
Clinical improvement on empiric therapy also helps confirm a presumptive diagnosis.

42
Q

What is the first line treatment for MAC?

A

Clarithromycin 500mg BID + ethamutol 15mg/kg/d
OR
When DDIs/intolerance precludes the use of clarithromycin, Azithromycin 500-600mg/d + EMB 15mg/kg/d

43
Q

When do you d/c first line therapy for MAC?

A

Completion of at least 12 months of treatment, remain asymptomatic and have CD4 count > 100 for > 6 months on HAART, and negative cultures

44
Q

Who should receive primary prophylaxis of MAC?

A

Pts with CD4 < 50

45
Q

What is the primary prophylaxis therapy for MAC?

A
Azithromycin 1200mg qweek 
OR
Clarithromycin 500mg BID 
OR
Azithromycin 600mg twice weekly
46
Q

When do you d/c primary prophylaxis of MAC?

A

CD4 > 100 for >/= 3 months

47
Q

What is CMV?

A

Envoloped double-stranded DNA virus that is a member of the Herpesvirus family.
It can become latent within infected cells.
Transmission occurs through infected body fluids.

48
Q

Where can CMV manifest?

A

Various different organ systems in immunocompromised hosts, but in AIDs pts - 2/3 of cases are CMV retinitis
May also manifest as sophagitis, colitis, or neurologic CMV

49
Q

What may happen if CMV retinitis is not treated?

A

Rapidly progress to retinal necrosis and permanent blindness

50
Q

WHat are the s/sx of CMV?

A

Visual changes
Flashes of light
Blurred vision
Blind sports (floaters)

51
Q

How do you diagnose CMV?

A

Clinical diagnosis

Culture and antigen detection are the most sensitive methods for detecting CMV in histological samples

52
Q

What is the 1st line therapy for CMV retinitis: for sight threatening lesions?

A

Intravitreal injections of ganciclovir or foscarnet for 14 doses over a period of 7-10 days
PLUS
Valganciclovir 900mg PO BID x 14-21 days, then once daily

53
Q

What is the 1st line therapy for CMV retinitis: for small peripheral lesions?

A

Valganciclovir PO 900mg BID x 14-21 days, then once daily

54
Q

What is the 1st line therapy for CMV esophagitis or colitis?

A

Ganciclovir IV x 21-42 days or until resolution of sx.
PO valganciclovir if PO absorption is adequate.
Maintenance therapy usually not necessary, but should be considered after relapses.

55
Q

What is the 1st line therapy for CMV neurological disease (PROMPT initiation of treatment)?

A

Combination of ganciclovir IV + foscarnet IV to stabilize disease and maximize response, continue until symptomatic improvement.
Maintenance therapy with PO valganciclovir + IV foscarnet should be continued lifelong unless there is evidence of immune recovery.

56
Q

What is secondary prophylaxis of CMV retinitis?

A

Suppression

Valganciclovir 900mg once daily

57
Q

When do you d/c CMV therapy?

A

CD4 > 100 for >/= 3-6 months on HAART

58
Q

When is primary prophylaxis of CMV considered?

A

Pts with CD4 < 50 and CMV IgG +

59
Q

What is primary prophylaxis therapy for CMV?

A

Oral ganciclovir or valganciclovir

60
Q

Why do we not use primary prophylaxis for CMV?

A

High cost
Toxicity
Development of resistance

61
Q

How is primary prophylaxis monitored?

A

Fundascopic examinations by an opthalmologist

62
Q

What are Bactrim’s ADR?

A
Rash
SJS
Photosensitivity
Fever
Leukopenia
Thrombocytopenia
GI
Hepatitis
High K
63
Q

What is sulfadiazine’s ADRs?

A
Rash 
Fever
Leukopenia
Hepatitis
N/V/D
Crystalluria
64
Q

What are pyrimethamine’s ADRs?

A

Bone marrow suppression (increasing leucovorin can help with bone marrow suppression)
Rash
Nausea

65
Q

What are amphotericin’s ADRs?

A

Renal
Infusion rxns
Fever, Chills, Rigors (give APAP, diphenhydramine, hydrocortisone, meperidine)
Decreased K and Mg
Lipid formulations less likely to cause these

66
Q

What are fluconazole’s ADRs?

A

GI

LFTs

67
Q

What are clarithromycin’s ADRs?

A

GI

Taste disturbances

68
Q

What are azithromycin’s ADRs?

A

GI

69
Q

what are EMB’s ADRs?

A

Oculotoxicity: optic neuritis and loss of red-green color perception; loss of cisual acuity
USE smaller doses of 15 mg/kg/d to avoid

70
Q

What are ganciclovir/valganciclovir’s ADRs?

A

Bone marrow suppression (esp neutropenia)
GI
LFTs

71
Q

What is 5-FC’s ADRs?

A

Bone marrow suppression
Renal
GI