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Multisystems > Path- HIV and Opportunistic Infections > Flashcards

Path- HIV and Opportunistic Infections Flashcards

1
Q

What family and genus does HIV belong to?
What is the structure of the genome?
It is enveloped or not?
What 3 cells does HIV virus have tropism for?

A

Family: retroviridae
Genus: Lentivirus

It is ssRNA + sense [2 copies per virus]
It is enveloped

Tropism for:

  1. CD4 T cells
  2. macrophages
  3. dendritic cells
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2
Q

What are the 3 major genes on the HIV genome?

A
  1. gag region [group antigen]
    - encodes p17 [matrix antigen], p24 [capsid antigen]
  2. pol region [polymerase]
    - p10 protease
    - p66/61 reverse transcriptase
    - p32 integrase
  3. env gene
    - gp120 surface antigen [binds CD4]
    - gp41 transmembrane antigen
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3
Q

Where does the HIV virus envelope come from?

A

It is a lipid envelope that is acquired from the host cell membrane

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4
Q

What are the 5 major groups of people infected by HIV?

What % of total HIV cases belong to each group?

A
  1. homosexual/bisexual men = 50%
  2. heterosexual contacts of high risk groups [IVDU] = 30%
  3. IVDU = 20%
  4. hemophiliacs <1%
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5
Q

What are the 3 major routes of transmission of HIV?

A
  1. Sexual [75%]
    - globally = hetero
    - US = homo/bi
  2. parenteral inoculation
    - IVDU
    - blood/blood component transfusion
  3. infected mother to newborn
    - intrapartum and peripartum
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6
Q

How long after infection does it take to develop acute retroviral syndrome?
How long does it take to resolve?
What is occurring during this phase to the immune system?
How does it present?
What marker will be high [and measurable] in serum?
What controls acute retroviral syndrome?

A

It occurs 3-6 weeks after infection and resolves in 2-4 weeks.

Occurring during the phase:

  1. widespread lymphoid seeding
  2. high virus production
  3. reduction in CD4+ T cells
Presentation:
[mononucleosis-like syndrome]
1. rash
2. cervical LAD
3. fever/vomiting/diarrhea

p24 capsid antigen will be high in serum.

ARS is controlled by CD8 cytotoxic T lymphocytes [which actually kill CD4 cells ;/]

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7
Q

Describe the chronic phase of HIV.
What does “latency” describe for chronic HIV?
What 2 infections are likely to occur with chronic HIV?

A

It lasts several years and has clinical latency [aymptomatic–> persistent LAD] but NOT microbiological latency.

Virus continues to replicate in lymphoid tissue.
CD4 cells gradually decline

  1. candida [thrush]
  2. zoster
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8
Q

What is the function of enzyme immunoassay [EIA] for HIV?

What determines sensitivity?

A

It is a screening test for antibodies/antigens

Sensitivity is determined by generation

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9
Q

What happens with each subsequent generation of HIV?

A

The window period [time from infection to positive test] is shortened with each generation.

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10
Q

What is detected on enzyme immunoassay for the first generation?
What is used as an antigen?
When will the person become positive?
What is the sensitivity/specificity?

A

EIA first generation detects:

IgG antibodies to HIV-1 using viral lysate as the antigen.
The person is positive 6-8 weeks after infection.
LOW sensitivity, LOW specificity

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11
Q

What is detected on enzyme immunoassay for the second generation?
What is used as antigen?
When does it detect infection?
What is the sensitivity/specificity?

A

IgG antibodies to HIV-1 using recombinant proteins/peptides as the antigen.

The person is positive about a week before generation 1 [5-7weeks]

It is more SPECIFIC than generation 1

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12
Q

What is detected on enzyme immunoassay for third generation?
What is used as antigen?
When does it detect infection?
What is the sensitivity/specificity?

A

IgG and IgM antibodies for HIV1 and HIV2.

Recombinant proteins/peptides aer used as the antigen.

Detects infection 3 weeks after infection.

More SENSITIVE than prior generations

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13
Q

What is detected on enzyme immunoassay for 4th generation?

When does it detect infection?

A

detects p24 antigen and HIV1/2 IgG and IgM

It detects infection in 2 weeks

*it does not differentiate p24 from IgG/IgM results

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14
Q

How long do rapid screening tests take to get results?
What are they detecting?
How does sensitivity compare to EIAs?

A

They get results in less than 30 minutes but detecting IgG/IgM in oral fluid, blood, plasma or serum.

It is less sensitive than EIAs but most dectect HIV1 and 2

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15
Q

What 3 serology confirmatory tests are used to confirm + EIAs or rapid tests?
Which are first generation? Second?
Which is used at Parkland?

A
  1. Western blot
    - 1st generation
  2. Immunofluorescent Antibody Assay [IFA]
    - 1st generation
    - used at Parkland
  3. HIV1/HIV2 Differentiation Immunoassay
    - 2nd generation test
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16
Q

What antibodies are detected with Western Blot confirmatory serology?
What are the 2 drawbacks of this technique?

A

Detects Ab to gp120,gp41, p24

Drawbacks:

  1. technically challenging to perform
  2. first generation test
    - only detects IgG so lag behind 3rd and 4th generation EIAs by 3 weeks
    - LEADS TO FALSE NEGs
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17
Q

What is the HIV confirmatory serology performed at Parkland?
How does it work?
What are the 2 main drawbacks?

A

Immunofluorescent Ab Assay:

  1. fix HIV infected lymphocyte to a slide
  2. patients Ab bind the HIV antigens
  3. Anti-human Ab binds the patients Ab

Drawbacks:

  1. interpretation is subjective
  2. only detects HIV1
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18
Q

What are quantitative viral loads NOT approved for in the US?
What are they mainly used for?

A

Viral load cannot be used to DIAGNOSE HIV

Viral load can be used for:

  1. prediction of disease progression in infected individuals
  2. monitoring response to therapy
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19
Q

What are qualitative RNA assays used for?

A
  1. diagnosis of HIV
  2. confirmation of positive EIA
  3. screening blood products
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20
Q

What are the 4 main limitations of molecular assays/amplification tests?

A
  1. skill to perform test
  2. expensive
  3. time consuming to perform
  4. separate blood draw because plasma is needed as opposed to serum for screening tests
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21
Q

What is the new testing algorithm for HIV?

A
  1. 4th generation EIA [p24, IgG/IgM]
  2. confirm + with rapid IgG immunoassay that differentiates HIV1 and HIV2

Confirmed reactivity = diagnosis of HIV
If NOT reactive:
1. test for HIV1 RNA [neg = check if HIV- or HIV2 acute]

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22
Q

What is the testing algorithm used at Parkland?

A
  1. 3rd generation EIAs
  2. Confirm with IFA
  3. if IFA is negative–> sent to reference lab for WB or HIV2 Ab

RARE cases submit plasma for amplified molecular assay

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23
Q

What opportunistic infections occur in HIV patients with and CD4 count:

  1. over 200
  2. under 200
  3. under 100
  4. under 50
A
  1. bacteria, TB
  2. PCP
  3. toxoplasma
  4. CMV, MAC
24
Q

Describe the histology seen with pneumocystis jirovecii pneumonia.
How is diagnosis made?

A

Histology:

  1. interstitial infiltrates
  2. foamy alveolar exudate

Diagnosis with BAL [bronchoalveolar lavage] stained with GMS silver stain OR immunofluorescenc

25
Q

You suspect an HIV patient with CD4 below 200 has pneumocystic pneumonia. After taking a BAL and staining it with GMS silver stain, what would you expect to see?

A

small round clusters of black that look like crushed ping-pong balls

26
Q

What are the 4 major clinical presentations of CMV in a patient with CD4 below 50?

A
  1. colitis- hemorrhagic with colonic ulcers
  2. pneumonitis
  3. adrenalitis
  4. retinitis
27
Q

What family of virus does CMV belong to?

What does this dictate about like cycle and progression of disease?

A

It is a herpesvirus so it will have:

  1. primary infection -subclinical or mononucleosis-like
  2. latency
  3. reactivation -uncommon in immunocompetent
28
Q

What are characteristic features of CMV on histology that allow for its diagnosis?

A
  1. owl eye nuclear inclusion

2. granular cytoplasmic inclusions [unique among DNA viruses]

29
Q

Diagnosis testing varies for CMV depending on the disease manifestation. What confirms:

  1. retinitis
  2. adrenalitis
  3. pneumonitis
  4. colitis
A
  1. clinical exam by opthalmologist
  2. PCR of blood because it represents systemic involvement
  3. biopsy
  4. biopsy
30
Q

What type of organisms is cryptosporidium?
What does it cause in immunocompromised HIV patients?
What is diagnosis?

A

It is a protozoal parasite
It causes fatal diarrhea and severe dehydration because it infects the small bowel epithelium.

Diagnosis:

  1. stool sample with acid fast or immunofluorescent stain for 4-6 micron oocysts
  2. small bowel biopsy where it is seen on the luminal surface
31
Q

What is the natural niche of MAC?

How does infection in an HIV person start and progress?

A

Naturally found in soil and water.

Infection begins with GI tract and disseminates from there.

32
Q

Describe the gross and histologic appearance of the small bowel mucousa in a MAC infection.

A

Gross:
tan, nodular appearance

Microscopic:
macrophages packed with acid fast bacilli filling the lamina propria

33
Q

Why are granulomas NOT seen in MAC infections?

A

the patient is severely immunocompromised and cannot form a granuloma.
the best the body can do is make macrophages to ingest the acid fast bacilli

34
Q

How is diagnosis of MAC infection made?

A
  1. mycobacterial blood culture

2. biopsy of GI, lung, lymph node

35
Q

Before HAART, what % of HIV patients had CNS involvement at autopsy?
What % had clinically evident neurological disease?

A

90% had CNS involvement at death

40-60% had clinically evident neurological disease

36
Q

What 5 symptoms are associated with HIV encephalopathy?

A
  1. dementia
  2. ataxia
  3. motor abnormality
  4. bladder/bowel incontinence
  5. seizures
37
Q

What is the gross appearance of HIV encephalopathy?

A
  1. ventricular dilation
  2. sulci widening
  3. generalized atrophy
38
Q

What is the microscopic appearance of HIV encephalopathy?

A
  1. microglial nodules with macrophages
  2. multinucleated giant cells
  3. HIV antigens identified with immunostains
  4. necrosis/gliosis
39
Q

What is the most common CNS mycosis for a patient with HIV?

What is the clinical presentation?

A

Cryptococcus neoformanns –> meningitis [with some parenchymal involvement]

40
Q

What 2 tests are used to diagnose cryptococcus?

What is used as confirmation?

A

Crypto is a budding yeast with pseudohyphae and a polysaccharide capsule.

  1. India Ink on CSF- negative stain that highlights the capsule
  2. Latex agglutination test on CSF for the polysaccharide capsule
    - more sensitive than india ink
    - titered to follow response to therapy

Confirm with culture because some strains do no have significant capsular material

41
Q

How does cryptococcus parenchymal brain infection appear?

A

“soap bubbles” because the yeast forms clusters with capsular material

42
Q

What organism causes Progressive Multifocal Leukoencephalopathy [PML]?
What cells does it infect?
What is the result?

A

JC polyomavirus [papovaviridae DNA]

PML is caused by reactivation of latent infection that will infect oligodendroglial cells.

The result is multifocal demyelination –> global encephalopathy.

43
Q

How is Dx of PML made?

A
  1. imaging
  2. PCR
  3. biopsy
44
Q

What is seen grossly and microscopically in PML?

A

Grossly:
white matter takes on a granular appearance

Micro:

  1. gliosis
  2. single intranuclear inclusions in oligodendroglial cells
45
Q

You do an MRI and notice multifocal ring enhancing lesions at the cortex near the grey white junction. What is the likely organism?

A

Toxoplasma gondii [protozoa]

46
Q

How is T. gondii diagnosis made?

A
  1. empiric therapy
  2. biopsy
  3. serology
47
Q

What are the 2 ways T. gondii can appear on a biopsy?

A
  1. tear drop shaped tachyzoite [active]

2. cyst with internal bradyzoites [inactive]

48
Q

What CNS cells does CMV infect?

What does it cause?

A

Infects:

  1. neurons
  2. glial cells [ependymal]
  3. endothelial cells

causes:

  1. encephalitis
  2. ventriculitis/choroid plexitis
  3. radiculoneuritis
49
Q

How is the Dx of CMV in the CNS made?

A
  1. biospy
  2. PCR
  3. serology [negative is helpful]
50
Q

What are the 3 main malignancies associated with HIV?

A
  1. Kaposi sarcoma [HHV8]
  2. Non-Hodgkin lymphoma
  3. oral hairy leukoplakia
51
Q

Kaposi sarcoma is caused by what agent?

What does this same agent also cause?

A

HHV a gamma herpesvirus [lymphotropic] that also causes:

  1. primary effusion lymphoma
  2. body cavity based lymphoma
52
Q

Kaposi sarcoma is a _______ tumor. It is often [unifocal/multifocal].
What does the cell proliferation look like?
What are there markers for?

A

It is a vascular tumor that is often multifocal.
It has spindle cell proliferation with slit-like vascular spaces.

there are smooth muscle and endothelial cell markers

53
Q

Where are the tumors likely to be located for Kaposi sarcoma?

A
  1. mucous membrane
  2. GI
  3. skin
  4. lung
  5. nodes
54
Q

What virus is most often associated with the following non-hodgkin lymphomas:

  1. systemic [nodes/viscera] = 80%
  2. primary CNS =20%
  3. body cavity based = <1%
A
  1. EBV in 50% of cases
  2. EBV in all
  3. KSHV
55
Q

Describe what type of mitogen EBV is .

A

It is a POLYclonal B-cell mitogen that is followed by emergence of a monoclonal population

56
Q

What virus drives oral hairy leukoplakia?

What cells proliferate and where?

A

EBV driven squamous proliferation on lateral aspect of the tongue.

Multisystems (29 decks)

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