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Multisystems > Micro- PCP, Toxo & MAC Infections in AIDS > Flashcards

Micro- PCP, Toxo & MAC Infections in AIDS Flashcards

1
Q

What is the most prominent clinical manifestation of pneumocystis jiroveci?
What increases the frequency of getting pneumonia?

A

pneumonia

increases in frequency as the CD4 count decreases below 200

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2
Q

What dies phylogenetic and biochemical data suggest that PCP is?
What are the 2 main developmental stages?

A

Fungus

  1. small pleomorphic trophozoite [1-4 micron]
  2. cyst form [5-8micron] with thick cell wall and 8 intracystic bodies
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3
Q

What are the 2 antigen groups on PCP?

A
  1. 95-140 kDa major surface glycoprotein [MSG] complex represents family of proteins encoded by multiple genes that are immunogenic
  2. 35-55kDa migratory band that is the most common antigen recognized by the host and is the marker of infection
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4
Q

When are most healthy people exposed to PCP?

What is the reservoir and method of acquisition?

A

Most healthy children are exposed by the age of 4.

The reservoir and method of acquisition are not known, but presumed to be inhalation.

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5
Q

Describe the 3 life cycle stages of PCP?

A
  1. trophozoite stage - organisms multiply by binary fission [asexual]
  2. pre-cystic stages
  3. cyst stage- contains 6-8 intracystic bodies [sexual reproduction]
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6
Q

What role does the MSG complex play in the host-parasite relationship?
How does it allow PCP to evade host immune response?

A

It facilitates adherence to host proteins like:

  1. ECM proteins
  2. surfactant proteins
  3. mannose receptor

It undergoes antigenic variation to evade host immune response.

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7
Q

Where does the pathology primarily occur for PCP infection?

A

In the lungs:

  1. cysts in the alveoli induce inflammatory response
  2. frothy exudate with clumps of parasites blocking O2 exchange [IN the alveolar spaces]
  3. thickened alveolar septa

*** do NOT invade lung tissue

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8
Q

What CD4 count would you see symptomatic pneumonia from PCP?
Describe the progression of the disease and symptoms.
What does CXR show?

A

CD4 <200

Acute/subacute progressive pneumonia over several weeks

  • SOB, tachypnea, cyanosis, fever
  • pneumothoraces in severe cases

CXR shows bilateral insterstitial infiltrates

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9
Q

How is lab Dx of PCP made?

A
  1. CXR - diffuse central [perihilar] alveolar or interstitial infiltrates
  2. Identification of P. jiroveci in bronchopulmonary secretions [sputum/lavage]
    - stains for nuclei of trophozoites [Giemsa]
    - stains for intracystic stage [Giemsa]
    - stains for cyst walls [silver stain]
  3. if all else fails, transbronchial or open lung biopsy
  4. Immunofluorescence/monoclonal antibody [DFA]
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10
Q

What is treatment for PCP?

A

Trimethoprim-Sulfamethoxazole

alternates:
primaquine with clindamycin
atovaquone
IV pentamide, trimethoprim, dapsone
trimetrexate plus folinic acid
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11
Q

What is control/prevention for PCP?

When should prophylaxis be started?

A

TMP-SMX

alternates:
dapsone
atovaquone
pentamide [aerolized]

Prophylaxis should be started at CD4 count 200

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12
Q

Describe the microbiology of T. gondii.

  1. What type of pathogen is it?
  2. Where is it found in the host?
A
  1. sprozoan protozoa

2. obligate intracellular

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13
Q

What are the 3 major forms of T. gondii organism?

What occurs in each stage?

A
  1. Oocyst [12micron cell]
    - excreted in feces of infected animals
    - develops into 4 sporozoites which are ingested to cause further infection
  2. Tachyzoite
    - asexual stage found in body and responsible for ACUTE infection
    - banana shaped
  3. Bradyzoite
    - asexual stage found in the body
    - cyst like and are metabolically slow growing
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14
Q

What are the only know definitive host for sexual stages of T. gondii?
How do they get infected?
What happens once T. gondii is in their system?
When they excrete oocysts, how long until the oocysts sporulate in the environment and become infectious?
How long do the cats shed oocysts?

A

Cats are the only definitive hosts for sexual stages of T. gondii.

The cat eats meat that has toxoplasma tissue cysts. Viable organisms are released and invade epithelial cells of the small intestine. Asexual stage–> Sexual stage where they form and excrete oocysts.

Oocysts are unsporulated when they are excreted and take 1-5 days to sporulate.
Cats shed oocysts for 1-2 weeks

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15
Q

What are the 5 ways humans can be infected with T. gondii?

Which is the most common source of human infection?

A
  1. ingestion of undercooked meat with toxoplasma cysts *most common source of human infection
  2. ingestion of oocyst from fecally contaminated hands/food
  3. organ transplant/blood transfusion
  4. transplacental transmission
  5. accidental inoculation of tachyzoites
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16
Q

What are the clinical sequelae of a human being infected by T. gondii?

A

Parasite forms tissue cysts in:

  1. skeletal muscle
  2. myocardium
  3. brain
17
Q

What does serologic prevalence data indicate is the most common of human infections throughout the world?

A

Toxoplasmosis

18
Q

Describe the pathogenesis of T. gondii in a human host.

A
  1. ingestion of tissue cysts containing bradyzoites OR oocysts containing sporozoites
  2. toxoplasma is released from the cyst and uses special structure on the anterior of the cell to invade host target cells [infection is receptor mediated]
  3. inside cell, phagosome forms around the toxoplasma but it inhibits fusion of lysosome.
  4. in the phagosome it differentiates into trophozoite and divides rapidly
  5. spreads from GI to skeletal muscle, cardiac, placenta, retina, CNS
  6. causes cell death and focal necrosis by invading adjacent tissue
  7. in immunocompetent host, it becomes bradyzoite [dormant stage] and persists as asymptomatic cysts
19
Q

What is the host immune response against toxoplasma infection?

A

Humoral and cell-mediated immunity

  1. antibodies
  2. IFNg
  3. stimulation of CD8+ T lymphocytes
20
Q

Patients with AIDS or other immune dificiencies are at a higher risk for developing symptoms from acute toxoplasmosis, however most cases are thought to be related to _________________.

A

Recrudescent [dormant stage bradyzoites reactivating] infections

21
Q

What is the most common syndrome in HIV+ patients infected with toxoplasma gondii?
At what CD4 count does it occur?

A

Toxoplasmic encephalitis:
-seizures, altered mental status, fever, headache

occurs at CD4 count below 100

22
Q

An AIDS patient has a CD4 count below 200 and pneumonia-like symptoms. What pathogen are you most concerned about?
An AIDS patient has CD4 below 100 and new onset seizures, headache, fever, altered mental status. What pathogen are you concerned about?

A

200, pneumonia-like = PCP

100, encephalitis-like = toxoplasmosis

23
Q

Describe the relationship between incidence and severity of congenital toxoplasmosis and the trimester during which the acute infection was acquired?

A

Rate of infection increases as fetal age increases
Severity of disease decreases as fetal age increases

First trimester = severe complications, especially CNS, chorioretinitis

24
Q

How is lab diagnosis of toxoplasmosis made in symptomatic immunocompetent hosts?

A
  1. clinical presentation of lymphadenopathy

2. serology [IgM = acute infection]

25
Q

How is the lab diagnosis of toxoplasmosis/encephalitis made in AIDS patients?

A

Combo of lab tests, radiological images and biopsy

  1. 95% will have IgG [because it is recrudescent]
    * IgM is NOT useful because encephalitis is not an acute disease
  2. CT/MRI showing mass lesion surrounded by inflammatory borders that enhance with IV contrast
  3. PCR of CSF [specific, but not sensitive]

If IgG is + and radiologic imaging supports toxoplasmic encephalitis, treat empirically [without definitive Dx]. If it does not improve in 10-14 days:

  1. Brain biopsy
26
Q

What will histopathology of a brain biopsy of someone with toxoplasmic encephalitis show?

A
  1. tachyzoites ** definitive Dx

2. inflammatory cells

27
Q

What is treatment for toxoplasmosis in:

  1. immunocompetent, not-pregnant
  2. pregnant
  3. AIDS
A
  1. Nothing
  2. evaluated for treatment to prevent congenital infection
  3. sulfadiazine [clindamycin if they have sulfa allergy] with pyrimethamine and leucovorin AND HAART
28
Q

What is prevention for toxoplasmosis infection?

A
  1. avoid inadequately cooked meat
  2. avoid cat feces
  3. keep CD4 >100 [if below 100 start on TMP-SMX]
29
Q

What type of organism is MAC?

Where are they ubiquitous?

A

Slow-growing non-tuberculous mycobacteria
- M avium, M intracellulare

They are ubiquitous to soil and water and people are exposed daily. No problems unless immune compromised.

30
Q

In immunocompetent individuals, what do MAC organisms predominantly cause?
What are the 3 major presentations?

A

Pulmonary disease
1. elderly male smokers with COPD–> chronic cavitary pneumonia that resembles TB on CXR and course

  1. elderly female non-smokers with prior bronchiectasis–> lingular or right middle lobe infiltrates
  2. single pulmonary nodules
31
Q

What is the most common presentation of MAC in HIV?

What CD4 count does it present?

A

Disseminated disease

  • fever [often over 104]
  • cachexia, night sweats, weight loss
  • generalized lymphadenopathy [bc it grows in RES]
  • pancytopenia [from bone marrow involvement]
  • cholestatic/abnormal liver tests
  • watery diarrhea

It presents at CD4 count of 50

32
Q

How is the diagnosis of MAC made?

A
  1. culture for acid fast bacilli [blood, lymph node, stool, marrow, aspirates, etc]
  2. DNA probe to target rRNA genes to differentiate MAC from TB
33
Q

What is treatment for MAC?

A

ATLEAST 3 MEDS

  1. azithromycon or clarithromycin
    - preferably azithro due to fewer drug interactions with HAART
  2. ethambutol
  3. rifabutin [less drug interactions than rifampin]

Plus HAART

34
Q

What is prophylactic treatment for PCP when CD4 <100?

A

PCP and Toxo use TMP-SMX as prophylactic meds

MAC uses azithromycin when CD4 is below 100

Multisystems (29 decks)

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