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Infectious Disease > Week 6: HIV testing and treatment > Flashcards

Week 6: HIV testing and treatment Flashcards

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2
Q

Question: What is differential diagnosis and what tests to be performed?

A
  • HIV
  • allergic dermatitis
  • secondary syphilis
  • coxsackie
  • scarlet fever (throat swab rapid antigen test or culture
    *
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3
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Great start at Prevention & Treatment of HIV

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4
Q

HIV screening guidelines

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5
Q

Case

A
  • so not strep
  • has secondary syphilis
  • could have HIV depending on generation of test
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6
Q

Clinical course of HIV and CD4 count and viral load

A
  • viral load goes from nothing to very high around 10 million copies and very contagious but too soon to have antibody test
  • viral load could be high but Ab test could be negative
  • sero-conversion is Ab negative to Ab positive
  • CD4 cells are located everywhere in the body (test the blood)
  • HIV only infects via CD4 receptor and only activated CD4 cells
  • HIV is enveloped so when it replicates it takes a piece of the cell membrane with it
  • so CD4 goes down then back up as they are recruited and then slow decline around 100 cells per year
  • Immune system is constantly stimulated because HIV viral replication is very prone to mutation which keeps changing
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7
Q

HIV testing

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8
Q

Forms of HIV testing

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  • HIV Ab Elisa screen
  • Western blot
  • HIV Ab Elisa followed by automatic WB confirmation
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9
Q

Rapid HIV Testing

A

HIV Ab Elisa screen

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10
Q

HIV Confirmatory testing

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Western blot

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11
Q

3rd generation HIV screening

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  • HIV Ab Elisa followed by automatic WB confirmation
  • Antigens bind HIV antibodies from patient sample
  • Allows detection in early seroconversion
  • 6-8 week window period
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12
Q

Features of HIV Ab Elisa screen

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  • High sensitivity
  • false-positive possible
  • 6-8 week window period
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13
Q

Features of Western blot HIV testing

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  • High specificity
  • Confirmatory testing
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14
Q

Features of 4th generation HIV testing

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  • Antigens bind HIV Abs from patient sample & monoclonal Abs detect p24 antigen
  • Allows detection prior to seroconversion
  • Detect between 12-26 days from exposure
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15
Q

What is Acute Retroviral Syndrome?

A

Symptomatic acute HIV infection that occurs 2-4 weeks after infection which presents like nonspecific flu-like illness for 3-14 days

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16
Q

Diagnosis of Acute Retroviral Syndrome

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3rd or 4th generation HIV screening test negative or indeterminate with HIV RNA high

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17
Q

Are you contagious in Acute Retroviral Syndrome?

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Highly infectious at this time

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18
Q

Presentation of Acute Retroviral Syndrome

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Symptomatic acute HIV infection presenting as non-specific flu-like illness for 3-14 days 2-4 weeks post HIV infection

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19
Q

HIV screening algorithm

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20
Q

Continued case presentation

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21
Q

Potentially infectious agents of HIV

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  • Blood
  • Breast milk
  • Tissue
  • Semen
  • Vaginal secretions
  • Anal secretions
  • Visibly bloody fluids
  • Other bodily fluids
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22
Q

NOT infectious agents of HIV

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  • Urine
  • Saliva
  • Sweat
  • Tears
  • Nasal secretions
  • Sputum
  • Vomitus
  • Stool
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23
Q

Forms of higher risk HIV transmission risk

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  • Receptive anal sex 0.3% - 3%
  • Needle sharing 0.67%
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24
Q

Forms of lower risk HIV transmission risk

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  • oral sex 0.06%
  • Insertive sex 0.03 - 0.14%
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25
CD4 count of HIV clinical Assessment
* Used to stage disease * Stage 1: asymptomatic CD4\>500 * Stage 2: CD4 200-500 * Stage 3: CD4 \<200, \<14%, or opportunistic disease or malignancy
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HIV Viral load of HIV clinical Assessment
* Used to monitor ARV therapy * Well controlled: viral load undetectable * Suboptimally or uncontrolled viral load detectable
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Stage 1 HIV
* asymptomatic * CD4\>500
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Stage 2 HIV
CD4 200-500
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Stage 3 HIV
* CD4\<200, \<14% * opportunistic disease or malignancy
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Well controled HIV
viral load is undetectable
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Suboptimally or uncontrolled HIV
* Viral load is detectable
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How is HIV viral load determined
HIV RNA Quantitative PCR
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Describe the natural history of HIV infection
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What stage are most new diagnosis of HIV?
* 38% of new HIV diagnosis in the U.S. already have advanced disease
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Why is it important to diagnose HIV early?
People who know they have HIV can begin treatment
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HIV treatment
* HAART/ART * results in viral suppression and markedly reduced transmission
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What is the best treatment for HIV?
Prevention but also treating those with HIV reduces risk of transmission with HAART/ART treatment
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When to start HIV treatment
ASAP in all HIV-infected adults as long as the patient is ready (A1 recommendation)
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HIV Treatment must start conditions
* opportunistic infections * Tuberculosis * HIV-AN, Co-infection with HBV or HCV * Pregnant women
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ARV agents mechanism of action
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ARV Mechanism of action cont.
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NRTI Antiretroviral Medications NRTI means?
nucleoside reverse transcriptase inhibitors
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NNRTI Antiretroviral Medications NNRTI means?
non-nucleoside reverse transcriptase inhibitors
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PI Antiretroviral Medications PI means?
Protease Inhibitor
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Types of antiretroviral medications 6 listed
* NRTIs * NNRTIs * PIs * Integrase Inhibitors * Entry inhibitors * Phamokinetic boosters
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Current NRTI Antiretroviral Medications
* Abacavir * didanosine * Emtricitabine * Lamivudine * Stavudine * Tenofovir AF or DF * Zidovudine
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Current NNRTI Antiretroviral Medications 5 listed
* Doravirine * Efavirenz * Etravirine * Nevirapine * Rilpivirine
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Current PI Antiretroviral Medications
\*Include booster\* * Atazanavir * Darunavir * Fosamprenavir * Indinavir * Lopinavir * Nelfinavir * Saquinavir * Tipranavir
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Current Integrase Inhibitors Antiretroviral Medications 4 listed
* Bictegravir * Dolutegravir * Elvitegravir (with cobicistat) * Raltegravir
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Current Entry Inhibitiors Antiretroviral Medications 3 listed
* Enfuvirtide * Ibalizumab * Maraviroc
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Current Pharmacokinetic Boosters Antiretroviral Medications 2 listed
* Ritonavir * Cobicistat
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HAART guidelines: Initial Regiment
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Describe prevention of HIV Resistance
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Explain steps of HIV infection & replication 10 listed
**FBIRITAABM** 1. **F**ree virus 2. **Binding and fusion:** to a CD4 molecule and one of two coreceptors (either CCR5 or CXCR4) Receptor molecules are common on the cell surface. Then the virus fuses with the cell 3. **Infection:** Virus penetrates cell and contents are emptied into cell 4. **Reverse Transcription:** Single strans of viral RNA are converted into double-stranded DNA by the reverse transcriptase enzyme 5. **Integration:** Viral DNA is combined with the cell's own DNA by the integrase enzyme 6. **Transcription:** When the infected cell divides the viral DNA is "read" and long chains of proteins are made 7. **Assembly:** Sets of viral protein chains come together 8. **Budding:** Immature virus pushes out of the cell taking some of the cell membrane with it. The protease enzume starts processing the proteins in the newly forming virus 9. Immature virus breaks free of the infected cell 10. **Maturation:** The protease enzyme finishes cutting HIV protein chains into infividual proteins that combine to make a new working virus
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How drug resistance arises in HIV Treatment
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Causes of HIV Resistance to Antiretrovirals (ARVs)
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ARVs AKA
Antiretrovirals
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CD4 coreceptors for HIV
CCR5 and CXCR4
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HIV Fusion Inhibitors
* Enfuvitide * Maraviroc
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Maraviroc MOA
CCR5 inhibitor to prevent binding and fusion of HIV
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Enfuvitide MOA
prevent HIV fusion with CD4 cells
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Contents of HIV virus capsid
* Single-stranded RNA * Three enzymes * Reverse Transcriptase * Integrase * Protease
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Drugs that target retroviral (HIV) reverse transcriptase
* NRTIs * NNRTIs
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Antiretroviral medications molecular targets 5 listed
* Fusion inhibitors * CCR5 inhibitor * Reverse transcriptase * Integrase inhibitors * Protease inhibitors
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Old guidelines of HAART
2 NRTIs + (II or boosted-PI or NNRTI)
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Most recent HAART guidelines
2 NRTIs + Integrase inhibitor
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How to prevent HIV Drug Resistance?
3 agents of at least 2 different classes
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If a person is taking adequate antiretroviral therapy, can they develop drug resistance?
No, if the virus is not replicating, no new mutations can occur!
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How does HIV resistance arise?
* Basically the drugs stop the virus from replicating but if something happens where drug resistance is formed than drug resistant virus will predominate
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Causes of HIV Resistance to ARVs
* Inadequate drug therapy * Poor adherence causing subtherapeutic drug levels * Poor absorption causing subtherapeutic drug levels * Drug-drug interactions * Infected with resistant virus during initial infection * Superinfection with resistant virus
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How to determine if a patient is infected with a drug resistant strain of HIV?
Genotype testing * Compares the genetic makeup of the patient's HIV versus the wild-type strain * Identifies known mutations which are associated with resistance to specific genes
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When to order HIV genotype?
* At acute infection/entry into care * Suboptimal suppression of viral load after starting HAART * Virologic failure during ART * USed to assist in selecting active drugs for a new regimen
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Case
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ARV drug-interactions
* HIV medications are metabolized by the cytochrome P450 mechanism in the liver * These antiretroviral medications have many potential drug-interactions with other medications that are also metabolized by this system * Inducers: can decrease levels of other drugs * Inhibitors: can increase levels of other drugs * Check for drug-drug interactions prior to starting any new medication or if someone has side-effects
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Drug interactions of "Boosters"
* Ritonavir or Cobicistat * Drug induced Cushing's * Intranasal, inhaled, intra-articular, IM steroid in patients on ritonavir or cobicistat * Beclomethasone appears safe * Statins, SSRIs, others
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Antiretrovirals that require acidic stomach
* Atazanavir * Rilpivirine
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Drug interactions of Integrase Inhibitors
* Avoid cations * DTG increases metformin
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Case
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Why screen ALL pregnant women for HIV?
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What is the effect of HAART on the risk of vertical HIV transmission
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Case
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Question
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Methods of reducing acquisition of HIV 11 listed
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Explain HIV virus distribution after infection
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PEP vs PrEP
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What is HIV PEP?
Post-exposure prophylaxis
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When is HIV PEP indicated?
* Given after high-risk exposure to reduce risk of HIV infection * Start within 72 hours of exposure
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HIV PEP dosing
28 day course of daily 3-drug regimen
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What is HIV PrEP?
Pre-exposure prophylaxis
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When is HIV PrEP indicated?
* Daily regimen given before exposure to reduce risk of HIV infection * Start at least 7 days prior to exposure
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HIV PrEP dosing
Daily 2-drug regimen
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HIV PEP drugs
Start 3 drug regimen \<= 72 hours from exposure 2 NRTIs (Tenofovir/emtricitabine) + II (Raltegravir)
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HIV PEP
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HIV PEP Side effects
* Mild nausea * Diarrhea * Headache
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HIV PrEP contrainidications 3 listed
* Active HIV * Renal dysfunction * Caution with HBV
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PrEP drugs
Currently only one FDA-approved formulation * Tenofovir disoproxil fumarate (TDF)/Emtricitabine (FTC) 1 tab qday * Approved for adolescents & adults \>= 35 kg (77 lbs)
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Question
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Case
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Case CXR
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What are the general clinical clues of HIV infection? 11 listed
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What are the lab clinical clues of HIV infection? 5 listed
* Leukopenia * Anemia * Thrombocytopenia * Polyclonal hypergammaglobulinemia * Endocrinopathies
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Common Bacterial Pulmonary syndromes associated with HIV
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Common mycobacterial pulmonary syndromes associated with HIV
* M. tuberculosis * M. avium complex
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Common viral pulmonary syndromes associated with HIV
* Influenza * RSV * CMV
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Common parasitic pulmonary syndromes associated with HIV
* Toxoplasmosis * Strongyloides
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Common Fungi pulmonary syndromes associated with HIV
* Pneumoncystis jirovecii * Cryptococcus * Histoplasmosis * Coccidiodomycosis * Blastomycosis * Aspergillus
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Common non-infectious pulmonary syndromes associated with HIV 6 listed
* Kaposi's Sarcoma * Non-Hodgkin's Lymphoma * Bronchogenic carcinoma * Lymphocutic interstitial pneumonitis (LIP) * Crack lung * Primary pulmonary hypertension
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Case
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What is Pneumocystic jirovecii and where is it found?
Ubiquitous yeast in the environment
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Pneumocystic jirovecii infections caused by?
Disease from reactivation or new infection
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Who is most commonly infected with Pneumocystic jirovecii
Majority of cases of Pneumocystis pneumonia are in patients who are unaware of their HIV status or CD4 \<200
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A common co-infection of Pneumocystic jirovecii
Oral Candidiasis (thrush) is a common co-infection of Pneumocystic jirovecii
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Clinical presentation of Pneumocystic jirovecii
* Subacute, progressive dyspnea, non-productive cough, pleuritic chest pain * Hypoxemia, especially with activity (LDH\>500)
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Pneumocystic jirovecii CXR findings
Variable * Classic: diffuse, bilateral interstitial infiltrates * May be normal in early disease
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Chest CT of Pneumocystic jirovecii
Patchy-ground glass attenuation
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Treatment of Pneumocystic jirovecii
* TMP/SMX high dose x 21 days * Add prednisone if pO2 \< 70 mmHg or A-a gradient \> 35 mmHg
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PCP Prophylaxis When and What
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Case
120
Opportunistic infections with CNS involvment classes of disease
* Meningitis * Encephalitis * Neurosyphilis * CNS Lymphoma
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Opportunistic infections with CNS involvment: Meningitis 5 listed
* Cryptococcus * M. tuberculosis * Listeria monocytogenes * Typical bacterial * Typical viral
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Opportunistic infections with CNS involvment: Encephalitis
* Reactivation of latent infections * CMV, HSV, VZV * JV virus: PML (Progressive Multifocal Leukoencephalopathy) * Toxoplasma gondii
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Opportunistic infections with CNS involvment: Neurosyphilis
syphilis
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Opportunistic infections with CNS involvment: CNS lymphoma
CNS lymphoma
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How is Toxoplasma gondii encephalitis caused?
* Reactivation of latent tissue cysts * Primary infection is from undercooked meat or shed in cat feces
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Toxoplasma gondii encephalitis clinical presentation
* Focal encephalitis with headache, confusion, seizure or motor weakness & fever
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Toxoplasma gondii encephalitis CT/MRI
Single or multiple contrast-enhancing lesion with edema
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Toxoplasma gondii encephalitis Treatment
* Pyrimethamine + Sulfadiazine + Leukovorin for 6 weeks * Long-term secondary prophylaxis
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Toxoplasma gondii encephalitis reactivation prophylaxis When and What
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Case
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Case cont
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Classes of Causes of pancytopenia
* Bacterial * Mycobacterial * Viral * Malignancy * Fungal * Malnutrition * Drug/toxin
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Bacterial Causes of pancytopenia
Sepsis
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Mycobacterial Causes of pancytopenia
* M. Tuberculosis * M. avium complex
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Viral Causes of pancytopenia
* CMV * Parvovirus B-19
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Malignancy causes of pancytopenia
Lymphoma
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Fungal Causes of pancytopenia
* Cryptococcosis * Blastomycosis * Coccidiodomycosis * Histoplasmosis
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Drug/toxin Causes of pancytopenia
* Fapsone * Alcohol * Additive to cocaine
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Case cont cont.
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What is Mycobacterium avium Complex and where is it found?
AFB (Acid-Fast Bacteria) that is ubiquitous in the environment
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How is infection with Mycobacterium avium Complex transmitted?
* Inhalation * Ingestion
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Risk factors for Mycobacterium avium Complex infection
* CD4 \< 100; Most are \< 50 * HIV RNA \> 100,000 copies/mL
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Mycobacterium avium Complex Clinical presentations
Can present as Disseminated multi-organ infection or local infection
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Clinical presentation of disseminated multi-organ infection of Mycobacterium avium Complex
* Fever * Night sweats * Weight loss * diarrhea * Abdominal pain * Anemia * Elevated Alk Phos * Lymadenopathy * Hepatosplenmegaly
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Clinical presentation of local Mycobacterium avium Complex infection
* Pneumonia * Colitis
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Treatment of Mycobacterium avium Complex infection
Clarithromycin + Ethambutol + Rifabutin
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The challenges of Treating Mycobacterium avium Complex infections
* Drug-interactions with HAART * Medication toxicity
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MAC AKA
Mycobacterium avium Complex
149
Mycobacterium avium Complex prophylaxis What and When?
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Opportunistic infections at any CD4 level
PPD or IGRA reactive
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Opportunistic infections at CD4 \< 200 cells/uL
PJP Prophylaxis
152
Opportunistic infections at CD4 \< 100 cells/uL
Toxoplasma prophylaxis
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Opportunistic infections at CD4 \< 50 cells/uL
MAC Prophylaxis
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Case
155
Assesing need for prophylaxis

Infectious Disease (82 decks)

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