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Infectious Diseases Flashcards

1
Q

How is HIV acquired/transmitted?

A

1) Sexual intercourse
2) Exposure to infected blood
3) Perinatal transmission

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2
Q

How does acute HIV infection present?

A

60% asymptomatic

If symptomatic - Fever, lymphadenopathy, sore throat, rash, myalgias/arthralgias, diarrhoea and headache (“mononucleosis-like illness”)

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3
Q

Does the presence of symptomatic acute HIV infection correlate with progression to AIDS?

A

Yes - those with prolonged symptomatic illness correlated with more rapid progression to AIDS vs those who had mild symptoms or were asymptomatic

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4
Q

What does seroconversion to HIV refer to?

A

The development of detectable antibodies against HIV antigens - this depends in part on sensitivity of test used

e.g. HIV antigen/antibody screening test (targeting IgM and IgG antibody to HIV-1 and 2 + p24 antigen) - 18-45 days

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5
Q

What does the Western blot test target and what are its disadvantages?

A

Tests for IgG antibody to HIV-1 proteins

Does not reliably detect HIV-2 or subtype O HIV-virus
Takes several days to weeks to return

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6
Q

What happens about 6 months after infection with HIV?

A

Reach “viral set point” - plasma viraemia (HIV viral load) reaches a steady-state level due to cytotoxic CD8 cells preventing further decline in CD4 cells

Note small % (e.g. 7%, more common in women and those who are asymptomatic) may achieve spontaneous virological control without ART but most of these do not durably sustain HIV control and eventually become viraemic and experience disease progression

Note this viral set point level is closely associated with rate of disease progression in the absence of ART - those with higher set points (and lower early CD4 cell counts + symptomatic acute HIV infection) predicted faster disease progression

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7
Q

What is the average time from HIV acquisition to AIDS (ie CD4 cell count <200)?

A

8-10 years
Following acute infection, seroconversion and establishment of viral set point, there is a period of chronic HIV infection that is characterised by relative stability of the viral level and a progressive decline in CD4 cell count

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8
Q

What symptoms/signs do people with chronic HIV infection (CD4 count >200) typically have?

A

Most few/no symptoms

If symptoms often generalised/non-specific eg fatigue, sweats, weight loss

Can get generalised lymphadenopathy without alternative cause

Can have recurrent infections eg candida, oral hairy leukoplakia, seborrhoeic dermatitis, bacterial folliculitis, HSV/VZV, molluscum contagiosum infections, STIs, strep pneumoniae infection

  • occasionally can get AIDS-defining illnesses at CD4 count >200

Can have accelerated comorbid disease eg CVD, osteoporosis, cognitive dysfunction, certain malignancies

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9
Q

What is the major reservoir for HIV?

A

Lymphoid tissue eg lymph nodes

Viral burden in peripheral blood mononuclear cells is relatively low

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10
Q

Why does AIDS develop?

A

Due to continuous, high-level replication of HIV leading to virus and immune-mediated killing of CD4 lymphocytes

Generally the rate of CD4 cell decline correlates with the viral load (HIV RNA level)

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11
Q

What happens to humoral immunity in HIV?

A

Wanes over time

B cells exhibit increased expression of markers of activation and proliferation and undergo terminal differentiation leading to increased immunoglobulin secretion (although most of the antibodies produced are nonspecific)

this can be detected on routine biochemistry as increased total protein

this confers increased susceptibility to certain infections eg S pneumoniae

ie HIV causes immune dysregulation, not just immune deficiency

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12
Q

What is AIDS?

A

Acquired Immune Deficiency Syndrome (AIDS)

It is the outcome of chronic HIV infection and consequent depletion of CD4 cells

Defined as CD4 cell count <200cells/microL OR presence of any AIDS-defining condition regardless of CD4 count

(note patients who achieve immune reconstitution with ART eg increase in CD4 count >200 are no longer considered to have AIDS)

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13
Q

What are AIDS-defining conditions?

A

Opportunistic illnesses that occur more frequently or severely because of immunosuppression

Prior to ART they were the principal cause of morbidity and mortality in HIV

Examples:
Candidal infections of respiratory tract/oesophagus
Coccidiodyomycosis
Extrapulmonary cryptococcosis
Cryptosporidiosis (intestinal >1mth)
CMV disease (other than liver,spleen,nodes and onset >1mth)
CMV retinitis
HSV resp disease/oesophagitis
Extrapulmonary histoplasmosis
Kaposi sarcoma
Burkitt/immunoblastic/CNS Lymphoma
NTM infection - disseminated or extrapulmonary
PJP
Progressive multifocal leukoencephalopathy
Salmonella septicaemia
Toxoplasmosis of brain
Wasting syndrome

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14
Q

What are some of the common dermatologic findings in AIDS?

A

Eosinophilic folliculitis
Xerosis
Prurigo nodularis
Molluscum contagiosum
Psoriasis exacerbation
Scabies infection
Mucocutaneous candidiasis
Oral hairy leukplaia
Seborrhoeic dermatitis
Herpetic infections

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15
Q

What are the common haematological abnormalities seen in AIDS?

A

Anaemia, leukopenia, lymphopenia, thrombocytopenia

Polyclonal hypergammaglobulinaemia

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16
Q

What is the prognosis of someone with advanced HIV infection (CD4 count <50)

A

In the absence of effective ART - 12-18 mths

Much better with ART but the predicted CD4 count recovery is less than that for an individual who started ART earlier in infection PLUS first 6-12 months after starting ART patients with low CD4 counts more likely to get Immune Reconstitution Inflammatory Syndrome (IRIS)

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17
Q

What is the average rate of decline of CD4 cells (CD4 slope)?

A

About 50 cells/microL per year

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18
Q

What factors influence rate of HIV disease progression/rate of CD4 T cell loss?

A
  • HIV viral load
  • HIV genotype - HIV-1 leads to faster disease progression that HIV-2
  • HIV subtype (A-J) - subtype D more virulent than others
  • HIV infections assoc with CXCR4 coreceptor (cf CCR5 coreceptor)
  • CD8 T cells - low numbers of HIV-specific CD8+ T cells correlate with poor survival
  • HLA-B57 allele - presence = better control and hypersensitivity to abacavir
  • CCR5-delta 32 mutation homozygosity - highly resistant to HIV infection
  • Coinfection with TB, syphillis, fungal or helminth infection
  • Patient age - older = more rapid progression
  • alcohol use - heavy alcohol use = low CD4 counts
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19
Q

What coinfection may actually increase CD4 cell count in HIV infection?

A

Human T-lymphotropic viral type 1 or 2 (HTLV-1, HTLV-2)

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20
Q

Which patients with HIV should be offered antiretroviral therapy (ART)?

A

ALL - regardless of CD4 count or viral load

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21
Q

What does ART achieve in HIV treatment?

A

Results in sustained suppression of HIV RNA, improves CD4 count/cellular immunity, reduces HIV-immune activation (eg chronic inflammation) and decreases HIV transmission to others

ART dramatically changes the course of HIV leading to a near-normal lifespan (particularly when initiated earlier in course of infection/at higher baseline CD4 count)

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22
Q

How much do you expect ART to increase CD4 count?

A

50-150 cells/microL at one year then slower increments (eg 50-100) until steady state reached

Nadir of CD4 rise often depends on CD4 count at time of starting ART - lower, the less likely they will reach higher numbers

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23
Q

What benefit does administering IL-2 to patients with HIV have?

A

Increases CD4 count compared to ART alone but no discernible clinical benefit

24
Q

What is IRIS and who does it predominantly affect?

A

Immune Reconstitution Inflammatory Syndrome (IRIS) is manifest as worsening of a known opportunistic infection that had been improving with treatment (“paradoxical IRIS”) or new signs/unmasking of a previously occult opportunistic infection (“unmasking IRIS”) due to the inflammatory response created by a reconstituting immune system

It typically occurs in the first 6 months following initiation of ART and is more common in:
- individuals with low CD4 counts at time of ART initiation (low CD4 baseline)
- higher level of viraemia at baseline
- those with more significant degrees of immunologic improvement on ART

No difference between different ART regimens

25
Q

What factors may be responsible for elite HIV control (i.e. maintenance of very low/undetectable levels of HIV RNA in absence of ART)?

A
  • infection with a defective HIV varient
  • host genetic polymorphism
  • HLA-B57

unclear if stem cell transplants that alter CCR5 coreceptor (generally required for HIV entry into CD4 T cells) or stem cell transplant (to eradicate lymphoid HIV reservoir) can achieve long-term HIV cure

26
Q

When should you initiate ART for HIV infection?

A

On same day of diagnosis, regardless of CD4 count

27
Q

What is the treatment of choice for acute HIV?

A

(ultimately depends on drug resistance testing + maximising patients compliance) but currently recommended initial treatments for most people combine a 2 drug NRTI backbone with third drug from INSTI class e.g.

Dolutegravir-abacavir-lamivudine (if HLA-B*5701 negative) [Triumeq]
OR
Bictegravir-tenofovir AF -emtricitabine [Biktarvy]
OR
Elvitegravir-tenofovir AF-emtricitabine-cobicistat (PI to boose elvitegravir) [Genvoya]

28
Q

How long is ART continued?

A

Indefinitely

Treatment interruption is associated with increased mortality/AIDS/non-AIDS related morbidity

29
Q

Can ART in acute HIV infection alter disease course?

A

Initial enthusiasm for “functional cure” has not been confirmed but early treatment does appear to reduce HIV RNA set point / increase CD4 count and reduce transmission risk - all favouring early treatment

30
Q

Who should be tested for HIV?

A
  • All patients with signs and symptoms of HIV
  • Patients with high-risk known or possible exposure to HIV (eg MSM, transgender, sex for money, IVDU)
  • patients seeking screening for STIs
  • patients considering PrEP
  • patients with TB (as HIV infection may led to faster disease progression and has important treatment considerations)
  • patients with HBV (overlapping risk factors + treatment considerations)
  • patients with HCV (overlapping risk factors, potential for accelerated liver disease, drug-to-drug interactions between treatments)
  • everyone at least once in their lifetime
  • pregnant women
31
Q

What is the preferred HIV testing algorithm?

A

1) Combination HIV antigen/antibody test
followed by
2) Confirmatory HIV antibody differentiation immunoassay (if 1 positive)

If both positive = HIV infection
If 1 positive, and 2 negative = indeterminate result/?false positive
-> In this case should test HIV RNA

HIV antigen/antibody detects HIV-1 and HIV-2 antibodies + HIV p24 antigen + group M and group O infections; 99% sens and spec; however not as sensitive as HIV RNA testing for acute infection

32
Q

If HIV antigen/antibody test is negative does that mean the patient does not have HIV?

A

Yes - in most cases

HOWEVER occasional false-negatives
- mostly if test performed in “window period” after acquisition but before antigen/antibodies can be detected; this window period may be up to 21 days (avg 8-10 days)
- false negatives rarely reported in very advanced HIV disease due to waning of antibody response

33
Q

What are the causes of false positive HIV testing? (ie positive antigen/antibody assay followed by negative differentiation assay and negative HIV RNA test)

A
  • Cross reaction alloantibodies from pregnancy
  • autoantibodies due to collagen-vascular disease, autoimmune disease, malignancy, chemotherapy
  • influenza vaccination
  • recent COVID-19 vaccination
34
Q

Why has Western Blot testing disappeared from most HIV testing regimens?

A

Because it takes up to 2 months to turn fully positive
AND
only reliably detects IgG to HIV-1 (not HIV-2)
AND
does not reliably detect subtype O virus

35
Q

What are some of the pre-HIV treatment considerations / screening tests that you should perform in a patient with newly diagnosed HIV?

A

1) Assess general health incl osteoporosis risk
2) Assess need for prophylaxis or treatment of opportunistic infections
- serum cryptococcal antigen if CD4<100
3) Check CD4 count and HIV RNA load
4) Check immune status and immunise appropriately
5) Screen for HBV and HCV
6) Assess for cardiovascular disease risk factors (as some antiretrovirals increase CVD risk) eg fasting lipids, HbA1c, renal function, baseline liver/FBC
7) test HIV for resistance mutations (HIV genotypic resistance)
8) assess for risk factors for non-adherence (eg depression, social issues) and treat as appropriate
9) counsel on importance of adherence to treatment
10) HLA-B*5701 allele testing - if considering treatment with abacavir

36
Q

What are the 6 classes of antiretroviral drugs currently licensed for use in Australia?

A

1) Nucleoside and nucleoside reverse transcriptase inhibitors (NRTIs)
2) Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
3) Protease inhibitors (PIs)
4) Integrase strand transfer inhibitors (INSTIs)
5) Entry inhibitors/fusion inhibitors
6) CCR5 inhibitors

37
Q

Have there been any reported cases of dolutegravir or bictegravir resistance in HIV treatment?

A

No

38
Q

How do Nucleoside and nucleotide reverse transcriptase inhibitors (NRTIs) work?

A

NRTIs (eg lamuvidine, emtricitabine, abacavir, zidovudine) work by inhibiting HIV RNA-dependent DNA polymerase (reverse transcriptase) by acting as structural analogues for thymidine or adenosine when DNA is reverse transcribed inside cells leading to premature DNA chain termination and inhibiting of viral replication

Because of this MOA, they also have the potential to inhibit human intracellular DNA polymerases including those necessary for mitochondria to replicate - thus mitochondrial dysfunction is the source of many of the potential toxicities of this class of drug

39
Q

Who is at risk of Abacavir hypersensitivity syndrome?

A

Patients with HLA-B*5701 allele (5-8% of Australian population)

40
Q

Why are Non-nucleoside reverse transcriptase inhibitors (NNRTIs) no longer used frequently in HIV treatment?

A

1) They aren’t active against HIV-2
2) high rates of genetic resistance to these agents
3) risk of hepatotoxicity
4) risk of neuropsychiatric adverse effects eg depression, suicidality

41
Q

What is the MOA of non-nucleoside reverse transcriptase inhibitors (NNRTIs)?

A

They bind directly to reverse transcriptase enzyme and block RNA-dependent and DNA-dependent polymerase activities disrupting enzyme activity and viral replication

Unlike NRTIs they do not inhibit human DNA polymerases

42
Q

How do HIV protease inhibitors work?

A

They inhibit HIV-1 and HIV-2 proteases and prevent cleavage of gag-pol polyprotein during maturation of the newly formed viral particle resulting in productive of immature, non-infectious virus

43
Q

What is unique about ritonavir (a HIV protease inhibitor)?

A

It is not used for its antiretroviral activity but rather as a pharmaco-enhancer by exploiting its activity as a CYP450 (3A4) inhibitor to boost levels of concomitantly administered protease inhibitors or the INSTI elvitegravir

44
Q

What are the main side effects of HIV protease inhibitors?

A

Metabolic eg hyperglycaemia, hyperlipidaemia

GI intolerance

Liver eg hepatotoxicity, transminase elevations, indirect hyperbilirubinaemia, cholelithiasis

Renal/GU - kidney stones, renal insufficiency

Cardiac - prolonged PR interval/1st deg AV block

Skin - rash throughout to SJS

45
Q

How do Integrase strand transfer inhibitors (INSTIs) work?

A

INSTIs (eg dolutegravir, raltegravir) prevent the integration of HIV DNA into the nucleus of the host cell

All available INSTIs are metabolised by glucuronidation via UGT1A1 to varying degrees influencing their potential for drug-to-drug interactions with medications metabolised by CYP450

46
Q

What are some examples of drug-to-drug interactions between HIV INSTIs and other medications?

A

Dolutegravir (and bictegravir to lesser degree) increase serum creatinine (not a true renal impairment, rather inhibits an enzyme OCT-2 in renal tubule cells that is important for excretion of creatinine and metformin) however no metformin dose adjustment is required

May have to increase dose of Dolutegravir if CYP450 inducers eg phenytoin, carbamazepine etc

47
Q

What are the main side effects of HIV integrase inhibitors eg dolutegravir?

A

Generally well tolerated

Headaches, fatigue, nausea, rash
Increased creatinine (not reflecting true renal impairment)

Hypersensitivity reactions can occur

48
Q

What do you use for HIV and HBV co-infection?

A

Regimen containing emtricitabine plus tenofovir e.g. Biktarvy or Genvoya

49
Q

Which HIV medications are not suitable for treatment of HIV in pregnancy?

A

Complex and requires specialist involvement re choice of ART plus doses (especially third trimester)

Dolutegravir - increased risk of neural tube defects

Darunavir - less effective

50
Q

Do you need to give ART during delivery to prevent mother-to-child transmission if mother is taking ART?

A

No, not if she has undetectable viral load near delivery

If HIV viral load >1000 or viral load unknown - then given intrapartum Zidovudine; if viral load detectable but <1000 case-by-case basis

51
Q

What parameters constitute high-severity PJP?

A

PaO2 <70mmHg on RA (on ABG) or SpO2 <94% on RA

If not meeting one of these parameters - treat as low-to-moderate severity PJP

52
Q

What is the treatment for low-to-moderate PJP?

A

PO Trimethoprim-Sulfamethoxazole 5/25mg/kg up to 480/2400mg Q8H for 21 days

53
Q

What antibiotic do you give patients with low-to-moderate severity PJP who have nonsevere hypersensitivity to Trimethoprim-sulfamethoxazole?

A

Clindamycin + Primaquine
OR
Trimethoprim + Dapsone
OR
Atovaquone

54
Q

What antibiotic do you give patients with low-to-moderate severity PJP who have SEVERE hypersensitivity to Trimethoprim-sulfamethoxazole?

A

Clindamycin + Primaquine
OR
Atovaquone

55
Q

How do you treat high-severity PJP?

A

Trimethoprim-Sulfamethoxazole IV Q6-8Hr

56
Q

What antibiotic do you give patients with high severity PJP who have hypersensitivity to Trimethoprim-sulfamethoxazole?

A

Clindamycin + Primaquine
OR
Pentamidine

PLUS
Prednisolone 40mg BD

57
Q

What is the duration of therapy for PJP in adults?

A

Acute treatment usually 21 days followed by maintenance therapy
- in HIV patients - continue until CD4 count >200 for 3 mths
- in patients without HIV - depends on immunosuppression/comorbidities

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