6 HIV Syphilis and Others Flashcards by Hannah Frank | Brainscape

Q

Why is HIV considered a retrovirus?

A

It uses reverse transcriptase for reverse transcription (turning its RNA into DNA) —> integrates its genetic material into host cell DNA —> new virus produced

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Q

What is the difference between HIV-1 and HIV-2?

A

HIV-1 is the virus primarily responsible for AIDS, and the one you will see in the US

HIV-2 is isolated in W. Africa, similar in genetic sequence but less aggressive

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Q

What are HIV’s targets in our body?

A

T cells - particularly CD4 T cells (Helper T cells)

Also infects B lymphocytes and macrophages (other types of WBCs) but it’s the T cells we care about

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Q

What are lymphocytes?

A

WBCs that defend against Protozoa, fungi, certain intracellular bacteria, and viruses

Include B cells and T cells

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Q

What do B cells do?

A

Make antibodies to attack antigens

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Q

What do T cells do?

A

T4 cells (CD4) are the helper T cells - enhance immune response, tell B cells to make antibodies

T8 cells (CD8) are the killer T cells - destroy foreign agents

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Q

HIV replication occurs in ….

A

Activated CD4 cells

HIV particle fuses to CD4 component of T cell
HIV incorporates into host T cell (use of reverse transcriptase)
New copies of HIV are released

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Q

Routes of transmission for HIV

A

Sexual transmission (exchange of infected body fluids)

Injected drug use

Occupational injury (ie needlestick)

Blood products (risk now 1:1,000,000)

HIV-infected mom to infant (risk 15-40% if mother untreated)

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Q

HIV is NOT spread by…

A

Casual contact

Requires infectious body fluid PLUS port of entry

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Q

Comparative risk of HIV transmission:

Insertive vaginal intercourse

A

1/10,000

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Q

Comparative risk of HIV transmission:

Receptive vaginal intercourse

A

1/1,000

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Q

Comparative risk of HIV transmission:

Receptive anal intercourse

A

1/50

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Q

Comparative risk of HIV transmission:

Shared drug needle

A

1/150

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Q

Comparative risk of HIV transmission:

Occupational needlestick

A

1/300

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Q

Primary (acute) HIV infection occurs ______ after exposure

A

2-6 weeks

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Q

How do 50-90% of patients with acute HIV infection present?

A

With a mono-like or flu-like illness

Lasts ~2 weeks and resolves spontaneously

Super easy to miss if you aren’t thinking about it

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Q

A patient with primary acute HIV will have a ______ HIV Ab test

A

Negative

Viral load is extremely high but body hasn’t made any antibodies yet

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Q

When is an HIV+ patient most infectious?

A

During acute primary infection 😬

If you don’t Dx them right, they are highly likely to transmit to partner(s)

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Q

Clinical SSx of primary HIV infection

A

Fever
Adenopathy
Sore throat
Rash***
Mucocutaneous ulcers***
Myalgia
Arthralgia
H/A
N/V/D

Looks a lot like the flu or mono, right?!

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Q

Lab findings for primary HIV infection

A

Elevated transaminases (LFTs)
Slight Leukopenia
Slight anemia
Thrombocytopenia

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Q

What is clinical latency for HIV?

A

Begins as the immune system responds to infection (acute illness resolves)

Patient seroconverts - now their Ab test will be positive

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Q

HIV infected patients will usually seroconvert within…

A

3 months

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Q

What happens to a patient’s HIV viral load when they are in clinical latency?

A

Decreases to a “set point” then slowly rises over time

HIV remains active in lymph nodes

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Q

What happens to a patient’s CD4 count during clinical latency?

A

CD4 T cell count slowly declines

Patient does pretty well though until CD4 <200

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Q

How long does clinical latency last in HIV?

A

Patients can remain asymptomatic (or minor LAD) for an average of 10 years

Approx 5% are long term nonprogressors

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Q

What happens as an HIV+ patient’s immune system deteriorates?

A

Lymph nodes and tissue damaged - “burnt out”

Virus may mutate and become more pathogenic

Body fails to keep up replacement of CD4 cells

HIV RNA viral load increases while CD4 count decreases

This is the SYMPTOMATIC INFECTION phase

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Q

SSx of HIV

A

Fever
Night sweats
LAD
Fatigue/malaise
Arthralgias
Weight loss
Oral hairy leukoplakia****** (latent EBV)
Thrush
Prolonged diarrhea
Cervical dysplasia (latent HPV)
Skin disorders (molluscum, dermatophytes, seborrheic dermatitis)
Kaposi’s sarcoma******
Recurrent HZV
ITP

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Q

Definition of Progression to AIDS

A

CD4 T cell count <200 cell/mcL OR

HIV+ AND 1 of 27 AIDS defining conditions (regardless of CD4 count)

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Q

What are some examples of AIDS defining conditions

A

Pneumocystis jiroveci (PCP) pneumonia
Toxoplasmosis of the brain
Mycobacterium avium complex, disseminated
CMV in specific organs
Candidiasis of esophagus, trachea, bronchi/lungs
Kaposi’s sarcoma
Invasive cervical cancer

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Q

Opportunistic pneumonia common in AIDS patients

A

Pneumocystis jiroveci pneumonia (PCP)

Causative organism is an airborne fungus

Can be a reactivated dormant infection

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Q

Clinical presentation of PCP

A

Nonspecific resp symptoms: fever, cough, SOB

May result in severe hypoxemia

CXR shows diffuse or perihilar infiltrates8

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Q

How is PCP diagnosed?

A

Via exam of sputum sample

Lab: elevated LDH (serum lactate dehydrogenase) in 95%

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Q

First line treatment for PCP

A

Bactrim DS (trimethoprim-sulfamethoxazole) and supportive care

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Q

What is the most common intracranial lesion in HIV patients?

A

Encephalitis caused by toxoplasmosis

Usually a reactivated infection

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Q

What is the causative agent of toxoplasmosis?

A

Toxoplasma gondii

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Q

How is toxoplasmosis acquired?

A

Via ingestion - cat feces, contaminated raw food, or utensils

Immunocompetent patients rarely have symptoms

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Q

Clinical presentation of toxoplasmosis in HIV patients

A

HA
Focal neurological deficits
Seizures
AMS

Can also cause retinitis, pneumonitis

Q

How is Toxoplasmosis diagnosed?

A

Multiple contrast-enhancing lesions on brain CT or MRI

Seropositive for toxoplasmosis

Q

What is the clinical presentation of Mycobacterium avium complex?

A

May cause pulmonary infection in immunocompetent patients

Causes systemic disease in advanced HIV - night sweats, weight loss, abdominal pain, diarrhea, anemia

Causative agent: Mycobacterium avium or Mycobacterium intracellulare

Q

What is the mode of transmission for MAC?

A

Bacteria found in soil and dust —> inhaled or ingested —> systemic infection in HIV pt

Q

How is MAC diagnosed?

A

Sputum acid fast bacillus (AFB) stain positive

Positive sputum cultures

Positive blood cultures

Q

Most common retinal infection in AIDS patients

A

CMV retinitis

Caused by Cytomegalovirus, a herpes virus common in the general population

Q

How is CMV transmitted?

A

Blood
Sexually
Perinatally

It’s super duper common in the general pop

Q

Clinical presentation of CMV retinitis

A

Pt complains of visual disturbances

Characterized by perivascular hemorrhages, white fluffy exudates on fundoscopic exam

If left untreated, can lead to blindness

Q

What is the important thing to know about candidiasis in HIV patients?

A

The more invasive the candida, the lower the associated CD4 count

Esophageal candidiasis, thrush, and recurrent vaginal candidiasis should all be red flags

Q

What is Kaposi’s sarcoma?

A

Vascular neoplasm

Classic Kaposi’s: found in elderly Eastern European and mediterranean males

AIDS-related Kaposi’s: most frequent in homosexual men - lesions generally multifocal and widespread, with associated LAD

May occur at any CD4 T cell count

Q

Who should get screened for HIV?

A

Everyone 13-64 with voluntary opt-out

Anyone in whom TB treatment is being initiated

At each presentation for an STD

Annually in patients at risk - more often for MSM

Pregnant women

Q

What things should trigger diagnostic HIV testing?

A

Opportunistic infections (ie fungal) and TB

Sx consistent with established HIV:
Weight loss, recurrent fever, night sweats, extreme tiredness, LAD, diarrhea > 1 week, sores of mouth/anus/genitals, PNA, unexplained neuro Sx

Sx consistent with acute HIV

Q

What tests do we use for HIV screening and diagnostic testing?

A

HIV antibody test - only detects HIV 4-12 weeks after infection, once patient seroconverts

Rapid HIV tests (saliva or blood) - a (+) requires confirmation

Combination HIV Ab and antigen testing

Q

What will happen if you suspect acute HIV and you only test for antibody?

A

You’ll miss it

Then they’ll go out and infect someone else and you’ll feel terrible

Q

Can minors get HIV tests in AZ without parents knowing?

A

They can access STD testing without parental consent but HIV is not explicitly included

Q

__________ is recommended for all with HIV, including those with acute/early infection

A

Antiretroviral therapy (ART)

Clinical trial data suggest that individuals treated during early infection experience immunologic and virologic benefits

Q

________ testing should be performed prior to initiation of ART

A

Genotypic drug resistance testing - it will help guide selection of ART

Q

What is the treatment goal in HIV?

A

Suppress plasma HIV-1 RNA levels to undetectable AND prevent transmission

Q

Where should you refer patients?

A

HIVAZ.ORG

Q

When should you be concerned about possible HIV exposure?

A

Unprotected sex with someone who tells you they have HIV (or you think may have HIV)

Condom broke or fell off during sex

Rape or sexual assault

Work-related exposure to HIV (ie needle stick)

Sharing needles to inject any type of drug

Q

If utilizing post exposure prophylaxis, it must be started within _____

A

72 hours of exposure

Q

What is PrEP?

A

Pre-Exposure Prophylaxis

Daily med (Truvada) that may be prescribed by HIV specialist or PCP to prevent contraction of HIV for those at risk

Q

Normal CD4 count is _________

A

500-1400

Q

You may see ____ and _____ at any CD4 count

A

Thrush

Kaposi’s sarcoma

Q

Once an HIV patient’s CD4 count is <400, you should…

A

Start Bactrim DS prophylaxis for PCP

Q

Once a patient’s CD4 is <100, you should

A

Ensure they are on Bactrim DS prophylaxis for toxoplasma gondii (if they aren’t on it already for PCP - WHICH THEY SHOULD BE)

Q

Once a patient’s CD4 is <50, you should…

A

Start Azithromycin prophylaxis for disseminated MAC

Q

What is the causative organism for Syphilis?

A

Treponema pallidum

Q

Syphilis is transmitted through…

A

Direct contact with infected lesion (usually genitals, anus, lips, mouth)

Bacteria enter the skin and in 10-90 days create a painless chancre

Q

What are the different stages of syphilis?

A

Primary
Secondary
Latent
Tertiary
Neurosyphilis
Ocular Syphilis

Q

Clinical presentation of Primary Syphilis

A

PAINLESS chancre appears at location syphilis entered the body

Persists for 4-6 weeks then resolves

Q

Clinical presentation of secondary syphilis

A

Many possible manifestations

Rash (very common)

Condyloma lata

Mucous patches

Pt may also have systemic Sx such as malaise, LAD

Generally persists 2-6 weeks then enters latency

Q

What is the 2˚ syphilis rash like?

A

Usually non-pruritic

Characteristically on palms and soles of feet

Not contagious

Q

What is condyloma lata?

A

Moist, heaped, wart-like papules

Occur in intertriginous areas (ie gluteal folds, perineum, perianal area)

Highly contagious

Q

What are the mucous patches associated with secondary syphilis?

A

Painless flat patches involving the oral cavity, pharynx, genitals - not painful (pt might not be aware of them)

Occur in 6-30% of cases

Highly infectious

Q

Clinical presentation of latent syphilis

A

Asymptomatic (duh)

No longer sexually transmittable

May persist for years

Q

Clinical presentation of tertiary syphilis

A

Most do not develop tertiary syphilis, but is does in ~15% of those who are UNTREATED

Can appear 10-30 years after initial infection

Can damage heart, blood vessels, brain, and nervous system

Q

What is neurosyphilis?

A

Can occur at any stage of the disease

Paralysis, difficulty with coordination, dementia

Q

What is ocular syphilis?

A

Changes in vision, blindness associated with syphilis

Can occur at any stage

Q

How is syphilis diagnosed?

A

Bacteria (from chancre) visible on microscopy (not commonly used)

Serology
• Rapid Plasma Reagan (RPR) or Venereal Disease Research Lab (VDRL) test - both are antibody tests
• Titer indicates disease activity (low 1:4, high 1:128)
• Low titer may be a false positive from another illness
• Confirm RPR with treponemal antibody test: FTA-ABS

Q

What additional diagnostic studies do you need if neurosyphilis or ocular syphilis are suspected?

A

LP with VDRL on spinal fluid to confirm

Refer to neurologist

Q

What is the standard treatment for syphilis?

A

Benzathine pen G 2.4mu IM x 1

Additional doses required if syphilis present for >1 year (3 doses at 1 week intervals)

Q

Syphilis treatment for PCN allergic patients

A

Oral Azithromycin or oral doxycycline

Exception: treat HIV patients and pregnant patients with PCN (REFER)

Q

What do you need to do after treating your syphilic patient?

A

Check RPR titer to confirm treatment success at 3, 6, 12, and 24 months
(4 fold decrease = adequate response)

Q

Why do we want to treat pregnant mothers for syphilis with pen G regardless of their allergy?

A

PREVENT CONGENITAL SYPHILIS

Q

What is congenital syphilis?

A

Untreated syphilis during pregnancy esp in early syphilis can lead to stillbirth, neonatal death, or infant disorders such as deafness, neuro impairment and bone deformities

Q

How do we prevent congenital syphilis?

A

Screen all pregnant women at 1st prenatal visit

If risk is high, screen and obtain sexual history again at 28 was and at delivery

If pregnant pt is PCN allergic, consider desensitization with oral PCN

Monitor serology closely to confirm successful treatment

Q

What is the causative organism for Lymphogranuloma venereum (LGV)?

A

Chlamydia trachomatis

Q

LGV is rare in the US but when diagnosed it usually occurs in …

A

MSM

Q

Clinical presentation fo Lymphogranuloma venereum

A

Causes systemic infection

Unilateral inguinal bubo

Self-limited genital ulcer or papule at site of inoculation

Anal discharge and rectal bleeding

Q

What do you do to diagnose LGV?

A

R/o syphilis

If LGV suspected, contact county health dept

May be able to do genital, rectal, or lymph node specimen swab for Chlamydia

Q

Treatment for Lymphogranuloma venereum

A

Erythromycin or Doxycycline

Q

Causative organism for chancroid

A

Haemophilus ducreyi

Q

Clinical presentation of chancroid

A

Painful TENDER genital ulcer

Lesion produces foul-smelling discharge (it’s contagious)

Inguinal amenities (buboes)

If suspected:
• R/o syphilis
• contact county health department - requires special culture

Q

Treatment for chancroid

A

Azithromycin, ceftriaxone, or ciprofloxacin