HIV Opp. Infections

Question 1

What is Immune Reconstitution Inflammatory Syndomre?

Answer 1

Refers to an exaggerated immune response, precipitated by the immune system recovering after successful trx with ART. The recovered immune system becomes more active, and may start to recognize and react to infections that were present b/o starting trx but were previously not detected due to weakened immune system.

Question 2

What are the 3 Opportunistic Infectiosn that have Prophylaxis available for?

Answer 2

PCP, Toxo and MAC.

Question 3

Highest risk of at CD4 below what?

– PCP (CD4 <____ cells/mm3)
– Toxo (CD4 <____ cells/mm3)
– MAC (CD4 <____ cells/mm3)

Answer 3

– PCP (CD4 <200 cells/mm3)
– Toxo (CD4 <100 cells/mm3)
– MAC (CD4 <50 cells/mm3)

Question 4

> ___ : usual pathogens
___-_____ : Usual pathogens but more
often than usual (e.g. TB,
thrush, HZ)
< ____: PJP
< ___-____ : MAC, CMV, Toxo, CMV,
Cryptococcus

Answer 4

> 500 : usual pathogens
200-500 : Usual pathogens but more
often than usual (e.g. TB,
thrush, HZ)
< 200: PJP
< 50-100 : MAC, CMV, Toxo, CMV,
Cryptococcus

Question 5

What organism* causes Penumocystits Pneumonia (PCP/PJP)?

• mode of transmission?

Answer 5

Pneumocystis jirovecii (formerly P Carinii) [FUNGUS not bacteria]

• Fungus ubiquitous to the environment
• 2/3 of healthy children have antibodies by age 2-4 years
• mode transmission: inhalation of spores.
• Pre-ART, PJP occurred in 70-80% of patients with AIDS
• 90% of cases in patients with CD4 count <200 cells/mm3
• 20-40% mortality rate
• ART-era, incidence is <1 case per 100 person-years

Question 6

How does PJP generally present? slow or fast onset?

• what xray finding is characteristics of PJP?

Answer 6

Progressive dyspnea, fever, non-productive cough,
chest discomfort. VERY slow onset.

• Chest x-ray: diffuse, bilateral, symmetrical “ground
  glass” interstitial infiltrates, butterfly pattern
  **symmetrical ground glass infiltrates.

Question 7

What is required for a DEFINITIVE DX OF PJP?

Answer 7

Requires isolation of bugs in tissue via bronchoalveolar lavage fluid or sputum samples.

Question 8

What is the PREFERRED PJP TRX?

• ALTERNATIVES?

Answer 8

Trimethoprim-Sulfamethoxazole (TMP-SMX) x 21 days.

Alt:
Dapsone (risk of hemolytic anemia) + TMP or
Pramiquie + Clind or
Atovaquone (antiprotozoal/ antimalarial –>

Question 9

What is the monitoring plan following PJP trx in terms of efficacy and safety?

• what is the biggest AE to watch out for with TMP-SMX in hiv pts?

Answer 9

Efficacy:
* Improved signs and symptoms, caution IRIS

Safety (TMP-SMX):
* Adverse reactions to TMP-SMX higher in HIV compared to those w/o.
- Rash is v. common (30-55%); push through unless have signs of SJS or anaphylaxis.
- watch renal dosing

Question 10

When would you consider PRIMARY PROPHYLAXIS FOR PJP?

• what is the primary prophylaxis drug and dosing regimen?

Answer 10

In pts with CD4 <200 cells/mm.

Trimethoprim-sulfamethoxazole (TMP-SMX)
* SS 1 tab daily

Alternatives: dapsone, atovaquone, aerosolized pentamidine

Question 11

When would you start secondary prophylaxis for PJP?

-what is the secondary prophylaxis drug and dosing regimen?

• when would you d/c primary or secondary prophylaxis?

Answer 11

• Start immediately after successful completion of PCP
  treatment
• Same medications as primary prophylaxis
• Patient is on ART and experiences immune recovery, defined as CD4 > 200 cells/mm3
  for ≥ 3 months

Question 12

What causes Toxoplasmic Enecephalitis (toxo)?

• mode of transmission? person to person?
• should all pts be tested for IgG aby to toxoplasma soon after dx?

Answer 12

• TE caused by protozoan Toxoplasma gondii (toxo)
• undercooked meat, cat poop. no person to person tranmission.
• yep!

Question 12

What causes Toxoplasmic Enecephalitis (toxo)?

• mode of transmission?
• should all pts be tested for IgG aby to toxoplasma soon after dx?

Answer 12

• TE caused by protozoan Toxoplasma gondii (toxo)
• undercooked meat, cat poop. no person to person transmission.
• yep!

Question 13

How does toxo present?

Answer 13

• Focal encephalitis:
• Headache, confusion, motor weakness, fever
• Without treatment –> seizures, coma, death

Question 14

What is requried for Toxo dx?

Answer 14

*Toxoplasmosis Ig G antibodies PLUS
* CT or MRI

Question 15

What is requried for Toxo dx?

Answer 15

*Toxoplasmosis Ig G antibodies PLUS
* CT or MRI

Question 16

Toxo Prevention and Management:

• What is the indication for Primary prophylaxis of Toxo?
• what is the primary prophylaxis regimen?
• What is acute treatment? (3 drugs)
• how long do you treat for?
• when can you d/c acute treatment?
• What are the maintenance therapy/secondary prophylactic drugs/regimen (3 drugs)?
  – When do you start Maintenance therapy/secondary prophylaxis? When to d/c?

Answer 16

> > Primary Prophylaxis:
* Indiaction: Toxoplasma IgG positive + CD4 < 100 cells/uL

• Primary Prophylaxis Regimen:
  TMP-SMX 1 DS PO daily

> > Acute Treatment:
pyrimethamine 50-75 mg PO daily +
sulfadiazine 1000-1500 mg PO q6h +
leucovorin 10–25 mg PO daily
x 6 wks or longer if incomplete clinical and radiological response at 6 wks. –> followed by chronic Maintenance therapy.
{think: PSA don’t let ur kids eat sand]

D/c: when CD4 > 200 cells/uL x 3 mos (from ART)
OR CD4 100-200 cells/uL and HIV RNA undetectable x 3-
6mos

> > Maintenance Therapy/SEcondary Prophylaxis:
Pyrimethamine 25–50 mg PO daily +
sulfadiazine 1000-2000 mg PO BID +
leucovorin 10–25 mg PO daily

• When do you start Maintenance therapy/secondary prophylaxis? When to d/c?
• Start immediately after acute treatment
• Discontinue when CD4 > 200 cells/uL x 6 mos (from ART)
  AND
  remain asymptomatic

Question 17

What Causes Mycobacterium Avium
Complex Disease (MAC)

• how transmitted?
• how presents?
• how dx?
• is colonization in resp and gi tract indicative of MAC disease?
• why should MAC cultures be watched fro growth for 406 wks?

Answer 17

MAC disease is caused by Mycobacterium avium
complex (MAC)
* Slow growing bacteria
* Ubiquitous to the environment

• • Transmitted through inhalation or ingestion of
    MAC bacteria

> > Clinical presentation:
* Disseminated, multi-organ infection (localized may be seen)
* Fever, night sweats, weight loss, fatigue, diarrhea
* Localized manifestations (symptoms vary by site)

> > Diagnosis:
* Isolation of MAC in blood cultures (or other tissue including lymph nodes,
bone marrow etc.)
* Possible colonization in respiratory or GI tract that is not indicative of disease
* MAC is slow growing and cultures should be watched for growth for 4-6 weeks

Question 18

Is MAC prophylaxis RECOMMENDED for ppl already on ART?

Answer 18

NO!!!

Question 19

When should pts NOT on ART receive primary prophylaxis for MAC?

• What is preferred regimen of PP for MAC?
• alternative?
• when can you d/c primary prophylaxis for mac?

Answer 19

IF:
* MAC blood culture negative AND
* CD4 <50 cells/mm3

Preferred: Azithromycin 1200 mg once weekly or clarithromycin 500
mg bid (recall it’s an atypical) [think: macrolides for the BIG MAC]

Alternatives:
* Rifabutin.
Rifabutin is in a class of medications called antimycobacterials. It works by killing the bacteria that cause infection. Antibiotics such as rifabutin will not work for colds, flu, or other viral infections.

• as soon as they are started on ART.

Question 20

What is Maintenance therapy/secondary prophyalxis for MAC?

• when can you d/c secondary prophylaxis for MAC?
• Completed at least __ months of therapy
• No ___ of MAC disease
• CD4 >___ cells/mm3
  for >__ months

Answer 20

> > Treatment and maintenance therapy (secondary prophylaxis):
* Clarithromycin 500 mg bid + ethambutol 15 mg/kg PO daily or
* Azithromycin 500-600 mg daily + ethambutol 15 mg/kg PO daily
* Third or fourth agent: rifabutin, fluoroquinolone, aminoglycoside

> > Discontinuation of secondary prophylaxis:
* Completed at least 12 months of therapy
* No signs and symptoms of MAC disease
* CD4 >100 cells/mm3
for >6 months