HIV (AIDS) Flashcards
What type of virus is HIV?
HIV is a retrovirus that infects CD4+ T cells and macrophages, leading to progressive immunodeficiency. HIV genomics is a positive-sense RNA with a diploid genome. There are two types of HIV, HIV-1 and HIV-2, with HIV-1 being the most prevalent worldwide. The HIV virion consists of a conical capsid made of p24 subunits (capsid protein) and a protective shell of p17 subunits (matrix protein). The virion envelope includes gp41 and gp120 glycoproteins.
What proteins are on the HIV envelope?
- GP41 facilitates viral entry
- GP120 is for docking
What proteins are inside the HIV core?
- P24 (capsid)
- P17 (matrix protein)
What enzymes does HIV have upon infection of a host cell?
- Reverse transcriptase
- Integrase
- Protease
How does HIV enter the cell?
- Binds CCR5 on macrophages (early infection).
- Binds CXCR4 on T-cells (late infection).
- GP120 is for docking
- GP41 facilitates viral entry
What is the definition of AIDS?
AIDS is defined as either:
1. CD4 count < 200 cells/mm³
2. The presence of an AIDS-defining condition
What are the major transmission routes of HIV?
- Sexual contact
- Blood exposure (needle sharing)
- vertical transmission (mother-to-child); 30% chance without antiretroviral therapies but less than 2% with appropriate medication
Which type of sexual exposure has the highest risk of HIV transmission?
Receptive anal intercourse (~1% per exposure).
- vaginal sex only has a .04 to .08 % chance (4 to 8 out of 10,000 exposures)
- needle stick injuries have a .2 to .6 % chance (20 to 60 out of 10,000 exposures)
What are the major risk factors for acquiring HIV?
- High viral load
- Presence of an STI
- Lack of circumcision
What is the clinical presentation of acute HIV?
2-4 weeks after exposure: fever, lymphadenopathy, sore throat, maculopapular rash, GI symptoms, painful mucocutaneous ulcers.
What are the most common symptoms of acute HIV infection?
- Fever is the most common manifestation (observed in ~80% of symptomatic cases), as the acute period is described as a “flu-like” or “mononucleosis-like” illness.
- Skin rash is the second most common symptom, with ~ 40–50% of patients developing a characteristic morbilliform rash on the trunk, which may extend to the face, limbs, palms, and soles during acute HIV. It is usually a non-pruritic red, maculopapular rash (flat or slightly raised small red spots).
- Many individuals experience myalgias (muscle aches) and arthralgias (joint pains) during acute HIV infection.
- Swollen lymph nodes are common, particularly in the neck (cervical nodes), but any lymph node region (axillary, groin, etc.) can be involved. The lymph nodes are usually mildly to moderately enlarged and tender.
- A sore throat often accompanies the fever (pharyngitis), however, unlike strep throat or EBV mononucleosis, the pharyngitis in acute HIV typically lacks pus or tonsillar exudates, but the throat pain can be significant.
- A persistent headache is another common complaint (about half of cases). In some patients this is mild, but in others it can be intense and may suggest aseptic meningitis if accompanied by neck stiffness.
- Diarrhea has been reported in nearly half of acute HIV cases, as well as nausea and sometimes vomiting. These GI symptoms, while not present in everyone, are significant because they are less typical in other causes of “flu-like” illness.
- Night sweats (waking up with sheets drenched from sweating) is a classic symptom in acute HIV and patients often find this unusual compared to ordinary colds or flu.
Are there some patients who do not have symptoms after exposure to HIV, especially in the acute period?
Not everyone will have symptoms – the presentation varies from person to person. Some may only have a high fever and fatigue, while others experience a broad range of symptoms. A small fraction of newly infected people (perhaps 10–20%) may notice no symptoms at all or only very mild ones and thus not realize they have acute HIV.
What test is used to diagnose acute HIV?
HIV RNA (viral load) is elevated, but HIV antibody (seroconversion) may not be detectable in the early period. For early detection during the serologic window, nucleic acid testing (NAT) is employed to detect HIV RNA and to determine the viral load.
How long can chronic HIV remain asymptomatic?
8-10 years, but some patients have persistent lymphadenopathy. Symptomatic pre-AIDS occurs only in some patients but not everyone. Prior to AIDS level disease patients may develop increase frequency of constitutional symptoms and opportunistic dermatologic or fungal infections.
When should routine HIV screening be performed?
- Once for all adults aged 13-75
- Annually for high-risk patients (MSM, IV drug users, sex workers, high-risk partners).
When do you screen pregnant women for HIV?
During the first prenatal visit and in the third trimester if high risk.
What is the preferred HIV screening test after the acute phase?
4th generation HIV antigen/antibody immunoassay (detects HIV p24 antigen and HIV antibodies).
What is the confirmatory test for HIV?
HIV-1/HIV-2 differentiation Immunoassay (preferred over Western blot).
In what instances should a patient be screened for HIV?
- STIs (syphilis, gonorrhea, chlamydia, HSV, trichomonas)
- High risk behaviors (unprotected sex, MSM, sex work, sharing needles, IV drug use)
- Unexplained oral candidiasis
- Oral hairy leukoplakia
- Pneumocystis jirovecii (PCP)
- Cryptococcal meningitis
- CMV retinitis
- Disseminated TB
What are the AIDS-defining conditions?
- Candidiasis (esophageal)
- Pneumocystis pneumonia (PCP)
- Kaposi sarcoma
- Disseminated histoplasmosis/coccidioidomycosis
- Toxoplasmosis
- Invasive cervical cancer
- MAC
- CMV retinitis
- Cryptococcal meningitis
- HIV encephalopathy
- Progressive multifocal leukoencephalopathy (PML)
What is the treatment for all HIV patients, regardless of CD4 count?
2 NRTIs + 1 Integrase inhibitor (INSTI).
What are the first-line antiretroviral therapy (ART) regimens?
Emtricitabine + Tenofovir + Dolutegravir OR
Emtricitabine + Tenofovir + Bictegravir OR
Abacavir + Lamivudine + Dolutegravir
What pre-exposure prophylaxis (PrEP) is used for high-risk HIV-negative individuals?
Emtricitabine + Tenofovir (Descovy or Truvada) daily.
What are the indications for giving post-exposure prophylaxis (PEP) for HIV?
- needle stick or body fluid exposure in a known HIV patient (semen, blood, vaginal fluid, NOT urine, saliva, or sweat)
- exposure to non-intact skin or mucous membranes
- recent recent sexual exposure to known HIV carrier
- high risk sexual activity such as commonless sex
What is post-exposure prophylaxis (PEP) for HIV?
Emtricitabine + Tenofovir + Integrase inhibitor for 28 days, must start within 72 hours of exposure.
Which NRTI requires HLA-B*5701 testing before use?
Abacavir (risk of hypersensitivity reaction).
What are the major toxicities of NRTIs?
Mitochondrial toxicity (neuropathy, pancreatitis, lactic acidosis).
Which NRTIs cause lipoatrophy?
Zidovudine, Stavudine.
Which NRTI is associated with renal toxicity?
Tenofovir.
Is Didanosine commonly used in antiretroviral therapy?
Didanosine (ddI) is an older nucleoside reverse transcriptase inhibitor (NRTI) that was previously used in the treatment of HIV but is now rarely used due to its significant toxicity and the availability of safer, more effective alternatives.
Is Stavudine commonly used in antiretroviral therapy?
Stavudine (d4T) is an older nucleoside reverse transcriptase inhibitor (NRTI) that was previously used for HIV treatment but is now strongly discouraged due to its severe toxicity and the availability of safer alternatives.
What are the common NNRTIs used in antiretroviral therapy?
Nevirapine, Efavirenz, Rilpivirine, Etravirine, and Doravirine.
What are the major side effects of NNRTIs?
Efavirenz: CNS effects (vivid dreams, confusion, anxiety), Nevirapine: hepatotoxicity.
What are the common protease inhibitors used in antiretroviral therapy?
Ritonavir (RTV), Indinavir (IDV), Saquinavir (SQV), Atazanavir (ATV), Darunavir (DRV), and Lopinavir
What are the side effects of protease inhibitors?
All protease inhibitors carry a risk for developing hepatotoxicity as well as metabolic syndrome seen with hyperglycemia, insulin resistance, hyperlipidemia, lipodystrophy.
What is the mechanism of integrase inhibitors?
Prevent viral DNA integration into the host genome. Due to metabolic toxicity, drug interactions, and cardiovascular risks, integrase inhibitors (INSTIs) (e.g., dolutegravir, bictegravir) are now preferred in first-line HIV treatment. Protease inhibitors are mainly reserved for treatment-experienced patients or in cases requiring high genetic resistance barriers. The main integrase inhibitors are Dolutegravir (DTG), Bictegravir (BIC), Raltegravir (RAL), and Elvitegravir (EVG, with cobicistat).
What are the common adverse effects with the integrase inhibitors that are used in antiretroviral therapy?
- Dolutegravir is associated with weight gain, insomnia, neuropsychiatric effects, minor risk of NTDs (revised), and there also a know metformin interaction, requiring a dose adjustment.
- Bictegravir is associated with weight gain, mild Gl upset, low interaction risk.
- Raltegravir is associated with increased CK, myopathy, rhabdomyolysis, and moderate weight gain.
- Elvitegravir is associated with Gl issues, CYP3A4 drug interactions, minor neuropsychiatric symptoms
What drugs are used to boost ART concentrations?
Ritonavir, Cobicistat (CYP3A4 inhibitors).
Which antiretroviral therapy medication prevents CCR5 entry?
Maraviroc (MVC) is a CCR5 antagonist used in HIV treatment. Unlike other antiretroviral drugs that target viral enzymes, maraviroc blocks the CCR5 co-receptor on CD4+ T cells, preventing HIV from entering host cells. It is not a first-line drug and is primarily used in treatment-experienced patients with CCR5-tropic HIV-1.
Which antiretroviral therapy medication antagonizes gp41?
Enfuvirtide (T-20) is a fusion inhibitor used in HIV treatment. Unlike other antiretrovirals that target viral enzymes or receptors, enfuvirtide binds to the HIV gp41 protein, preventing the virus from fusing with the host CD4+ cell membrane and entering the cell. It is not a first-line drug and is reserved for treatment-experienced patients with multidrug-resistant HIV.
What is immune reconstitution inflammatory syndrome (IRIS)?
Paradoxical worsening of pre-existing infections after starting ART. This tends to occur 1-2 months after starting ART. Management involves treating the opportunistic infection, but continuing with ART.
How do you prevent the most severe implications associated with IRIS?
Delay ART initiation for 2 weeks if the infection is due to Cryptococcus or TB meningitis.
What is the management strategy for patients experiencing HIV wasting?
Optimize ART.
What is the common cause for HIV associated lipodystrophy syndrome?
This is a multifaceted syndrome that can involve pure fat atrophy or fat accumulation. Fat atrophy is the preferential loss of subcutaneous fat, versus fat or muscle seen in HIV wasting. Fat atrophy most commonly is associated with NRTIs such as stavudine or zidovudine. That accumulation is truncal fat that resembles Cushing’s syndrome, but is not associated with any specific drug regimen. Both atrophy and accumulation of fat can be associated with metabolic syndrome (insulin resistance, hyperglycemia, or hyperlipidemia).
What is the most common cause for peripheral neuropathy in AIDS patients?
The most common cause of peripheral neuropathy in AIDS patients is HIV-associated distal symmetric polyneuropathy (DSPN). It is primarily due to direct HIV-related neuronal damage but can also result from antiretroviral therapy (ART)-induced toxicity. DSPN often occurs in advanced HIV/AIDS (CD4 <200 cells/µL) due to direct HIV-induced damage to dorsal root ganglia and peripheral nerves. Patients experience symmetric numbness, burning pain, tingling in feet (may progress to hands) in a stocking-glove distribution. Patients may also exhibit absent/decreased ankle reflexes. No motor involvement as this is purely a sensory disease. The management involves ART initiation (may slow progression) and symptomatic relief with Gabapentin, pregabalin, amitriptyline. Didanosine (ddI), Stavudine (d4T), and Zalcitabine (ddC) (no longer used), are also implicated due to mitochondrial dysfunction.
What live vaccines are contraindicated in HIV?
MMR and Varicella if CD4 < 200.
What vaccines are recommended for patients who have HIV?
- Hepatitis A and B where Hep A is recommended if HAV IgG negative or at risk (e.g., MSM, IV drug use, chronic liver disease) and given as a 2-dose series; and Hep B is given as a 3-dose series (0, 1, and 6 months apart) if HBsAg, anti-HBc, and anti-HBs negative. High-dose formulation (double-dose) is preferred due to lower immunogenicity in HIV patients.
- HPV, this is recommended for all patients ≤45 years (3-dose series) as it protects against cervical, anal, and oropharyngeal cancers.
- Influenza, just like everyone else, this is given annually and has the same indications as a non-infected individual. The Inactivated influenza vaccine (IIV) or recombinant influenza vaccine (RIV) is given and the Live attenuated influenza vaccine (LAIV) is contraindicated.
- Meningitis ACWY, this is recommended for all HIV patients aged 11–55 in a 2-dose primary series with booster every 5 years.
- Pneumococcus, PCV15 or PCV20 (if never vaccinated). If PCV15 is given, follow with PPSV23 at least 1 year later.
- TDaP, one Tdap dose if never received in adulthood, followed by Td booster every 10 years.
Why is HPV recommended in patients with HIV?
The human papillomavirus (HPV) vaccine is strongly recommended for patients with HIV, as they are at increased risk for persistent HPV infection, cervical cancer, anal cancer, and oropharyngeal cancers.
How many occurrences of pneumonia (Recurrent Pneumonia) are required to meet the definition of an AIDS defining disease?
Bacterial respiratory infections become more frequent with CD4 <200. Having ≥2 episodes of pneumonia in one year in an HIV patient meets an AIDS definition. Common bacteria (like Streptococcus pneumoniae or Haemophilus influenzae) cause typical lobar pneumonia, but infections may be more severe and sometimes atypical organisms (including Pseudomonas in very low CD4 counts) appear. Prevention: HIV patients should receive pneumococcal vaccination (PCV15 or PCV20 (if never vaccinated). If PCV15 is given, follow with PPSV23 at least 1 year later). There is no specific antibiotic prophylaxis for bacterial pneumonia, but PCP prophylaxis with TMP-SMX also helps reduce some bacterial pneumonias. Treatment: as in HIV-negative patients (e.g. ceftriaxone + azithromycin for community pneumonia, tailored to microbiology). Recurrent pneumonia may prompt investigation for underlying structural lung disease or drug-resistant organisms.
What respiratory pathogen should be screened for in all patients with HIV?
TB, use either interferon or PPD.
TB can occur at any CD4 count, even in relatively immunocompetent patients, and is often one of the first serious infections as immunity wanes. When the CD4 count is relatively high, TB tends to manifest apically. When the CD4 count is low, TB develops within the pleura (leading to pleural effusions [high ADA, lymphocytic rich, and require histopathologic confirmation evidenced with granulomas], lobar lung, and has an increased risk of disseminating. The clinical presentation includes a chronic cough, pleurisy, fevers, night sweats, weight loss (pulmonary TB), or extrapulmonary disease (e.g. lymph nodes, disseminated TB). All HIV patients should be tested for latent TB (e.g. IGRA or PPD). The PPD only needs to be 5 mm or more to count as positive. If either of these are positive, isoniazid (INH) with pyridoxine (vit B6) for 9 months is recommended to prevent active TB. Treatment for active TB in HIV is with the standard multi-drug RIPE therapy (Rifampin (or rifabutin), Isoniazid, Pyrazinamide, Ethambutol) for at least 6 months (extended to 9–12 months for CNS or bone disease). Drug interactions with antiretrovirals and the need for direct-observed therapy should be considered. Antiretroviral medications are usually delayed for 1-2 weeks to prevent immune reconstitution inflammatory syndrome (IRIS). It is very important to note that a thoracentesis may be required for diagnosis in symptomatic patients suffering from an acute infection. A thoracentesis typically reveals a lymphocyte-predominant, exudative effusion. Although malignancy may present with similar findings, an elevated adenosine deaminase level strongly suggests TB. As tuberculous pleural effusions are caused by a hypersensitivity reaction to M tuberculosis or its antigens, pleural fluid smear is usually aseptic (unlike tuberculous empyemas) and pleural biopsy with histopathologic confirmation is often required.
Once CD4 falls into the 200–500 range (Stage 2 HIV), what infections are common with HIV patients?
Patients are at increased risk for tuberculosis, Candida infections, herpes zoster, and herpes simplex outbreaks. Prophylaxis for opportunistic infections in this range is still limited (PCP and others start below 200), but clinicians should ensure latent TB therapy if needed and vaccinations (e.g. varicella, pneumococcal) before CD4 drops further.
What is the treatment for Kaposi sarcoma in HIV?
Start ART. Patients may need chemotherapy for extensive disease.
Kaposi sarcoma is a vascular malignancy caused by HHV-8 that can emerge even at higher CD4 counts. KS can present when CD4 is fairly high (10% of cases occur with CD4 >500) but is much more common with advanced immunosuppression (75% of cases have CD4 <200). Clinical presentation: purplish, red-brown or violaceous plaques and nodules on skin or mucosa that are usually painless. Lesions usually do not blanch and can ulcerate or bleed, while able to occur anywhere (often on the face, oral cavity, or legs), they may ulcerate or swell. Lesions can affect the visceral musica, such as the GI tract or lungs, but this occurs in late-stage disease, causing bleeding or respiratory symptoms. Generally no prophylaxis is indicated as non are specific for KS (no vaccine or chemoprophylaxis); controlling HIV with ART is key, as immune reconstitution reduces KS risk. Treatment: Initiation of ART often leads to regression of KS lesions. For advanced or visceral KS, chemotherapy, such as paclitaxel, liposomal doxorubicin or interferon-α. Local therapies involve radiation or cryotherapy for skin lesions. Monitoring for immune reconstitution inflammatory syndrome (IRIS) (worsening of lesions temporarily after ART start) is recommended. Prognosis improves significantly with effective HIV treatment.
What is the most common opportunistic infection in patients with HIV?
The most common opportunistic infection in HIV patients is Pneumocystis jirovecii pneumonia (PJP, formerly PCP), especially when the CD4 count falls below 200 cells/µL. Additionally, this is a common infection in patients who are immunocompromised from chronic immunosuppressive medications (cyclophosphamide), chronic steroid use, stem cell transplant recipients, and organ donor recipients.
When should a patient with HIV start PCP prophylaxis (Pneumocystis jirovecii pneumonia)?
Pneumocystis pneumonia is common in patients with AIDS and typically causes, and, interstitial infiltrates. and pleural effusion are rare. In addition,
CD4 < 200 → Give TMP-SMX. Pneumocystis pneumonia is an AIDS-defining illness that is often seen in patients who were previously unaware of HIV infection. The underlying pathogen is an atypical fungus called Pneumocystis jirovecii. Healthy patients rapidly clear these organisms if inhaled, but those with an impaired cell-mediated immunity, they are at risk for a noninvasive infection that fills the alveoli and leads to slowly worsening pulmonary symptoms, such as an indolent fever, dyspnea (shortness of breath), dry cough, hypoxia, and bilateral interstitial infiltrate. The presentation of a subacute onset of fever, dry cough, and dyspnea, is progressive over days to weeks. Weight loss is also usually present. P jirovecii cannot be cultured, therefore, definitive diagnosis requires identification of the organism. First, a chest x-ray will reveal an infection, showing bilateral lobar infiltrates that typically appear as ground glass opacities (pleural effusions are rare). Next, Pneumocystis pneumonia is initially evaluated with an induced sputum sample, while a bronchoalveolar lavage (BAL) is the second-line diagnostic test. When evaluating respiratory secretions (sputum or BAL) a methenamine silver stain used to identify the cell wall of the pathogen, which often appears as a crescent, a crushed ping-pong ball, or a circular ring around a clear center. The first-line treatment is with trimethoprim-sulfamethoxazole, and is usually curative. The alternative medications are atovaquone, or aerosolized pentamidine.
How is PCP (Pneumocystis jirovecii pneumonia) worked up and diagnosed?
- CXR
- Induced sputum (first-line) or BAL (second-line)
- Methenamine silver stain of the sample
What fungal marker is usually positive in PCP?
Beta-D-Glucan Assay (fungal marker, positive in most PJP cases).
When are steroids added for PCP (Pneumocystis jirovecii pneumonia) in a patient with HIV?
If PaO₂ < 70 mmHg on room air (or A–a gradient ≥35), add corticosteroids to reduce inflammation and improve outcomes.
What is the treatment for PCP (Pneumocystis jirovecii pneumonia) in a patient with HIV?
Treatment for PCP is similar to prophylactic treatment and involves high-dose TMP-SMX, which is first-line therapy for PCP (15–20 mg/kg TMP IV or PO in 3–4 divided doses daily for 21 days). For those with sulfa allergy, IV pentamidine or atovaquone (PO) or clindamycin + primaquine + trimethoprim + dapsone, or can be used. If PaO₂ < 70 mmHg on room air (or A–a gradient ≥35), add corticosteroids to reduce inflammation and improve outcomes. Patients often show improvement after 5–8 days of therapy; adjunctive oxygen and respiratory support are given as needed.
What two organisms cause Disseminated Endemic Mycoses in patients who have HIV?
With CD4 counts under ~200 (especially <150), patients in certain regions are vulnerable to Histoplasmosis and Coccidioidomycosis. In endemic areas, these can become disseminated AIDS-defining infections. Histoplasmosis tends to cause disease when CD4 <150. Histoplasma capsulatum is endemic to Ohio/Mississippi River valleys and presents with fever, weight loss, cough, and often hepatosplenomegaly, lymphadenopathy, and mucosal ulcers in mouth or nose. Coccidioidomycosis causes disease when CD4 <250 and is endemic in desert Southwest US, and presents as chronic fever, weight loss, cough or meningitis. Histoplasmosis is an opportunistic infection in patients with HIV and usually presents as a febrile, wasting illness marked by fever, fatigue, weight loss, vomiting, and dyspnea. Chest radiograph is typically normal or reveals diffuse interstitial infiltrate; focal infiltrate and pleural effusion are rare.
When should a patient with HIV start prophylaxis for coccidiomycosis?
When in the Southwest region of the United States (California or Arizona) and CD4 counts are below 250. Give fluconazole prophylactically. For acute treatment can be with either fluconazole or amphotericin B (depending on severity; fluconazole for meningitis). Chronic maintenance therapy continues until immune reconstitution (CD4 >150 for >6 months on ART).
When should you start Histoplasmosis prophylaxis?
CD4 < 150 in endemic areas → Give Itraconazole.
In highly endemic areas, some experts give itraconazole prophylaxis for Histoplasma if CD4 <150. Otherwise, no routine prophylaxis – early detection via antigen tests is used. Treatment for acute Histoplasmosis is with inductive treatment with amphotericin B, then prolonged oral itraconazole.
When should you start Toxoplasma prophylaxis?
CD4 < 100 and Toxoplasma IgG+ → Give TMP-SMX.
Alternative regimens (if TMP-SMX is not tolerated) include Dapsone + Pyrimethamine + Leucovorin (if G6PD normal) or
Atovaquone ± Pyrimethamine + Leucovorin.
Toxoplasmosis is the most common opportunistic CNS infection (Toxoplasma Gondii Encephalitis) in AIDS patients and occurs with CD4 <100. It results from reactivation of latent Toxoplasma cysts (typically in patients with prior exposure, i.e. IgG positive). Patients present with subacute neurologic deficits and brain imaging shows focal brain lesions. Patients develop headache, confusion, fever, focal weakness, cranial nerve palsies, or seizures over days to weeks. Imaging (CT/MRI) shows multiple ring-enhancing lesions, often in basal ganglia. Diagnosis is established with clinical signs along with MRI and Toxo-IgG. All HIV patients with CD4 <100 who are Toxoplasma IgG positive should be on TMP-SMX DS daily (this double covers PCP and toxo). Alternative prophylaxis is dapsone + pyrimethamine + leucovorin if unable to take TMP-SMX. Pyrimethamine + sulfadiazine + leucovorin for at least 6 weeks is often the first-line therapy. (Leucovorin is given to prevent pyrimethamine-induced folate deficiency.) Clinical improvement is expected in 1–2 weeks. Lack of improvement might suggest an alternative diagnosis (e.g. CNS lymphoma, which is the second most common CNS pathology in HIV patients, occurring with CD count less than 50). If sulfadiazine cannot be used, clindamycin + pyrimethamine can substitute. After acute treatment, chronic maintenance therapy with lower-dose pyrimethamine-sulfadiazine is continued until CD4 >200 on ART for >6 months.
What is the most common cause for dysphagia or odynophagia in HIV?
The most common cause of dysphagia (difficulty swallowing) or odynophagia (painful swallowing) in HIV patients is esophageal candidiasis (caused by Candida albicans), especially when the CD4 count is <100 cells/µL. Diagnosis requires either a definite clinical presentation or endoscopy. Other causes for dysphagia (difficulty swallowing) or odynophagia (painful swallowing) in HIV patients require an endoscopy with biopsy to determine the culprit (CMV or HSV). When no organism can be defined, the likely culprit is aphthous ulcers (HIV-associated esophagitis), which has a different treatment approach (Steroids).
Is prophylaxis given for Candida in patients with HIV?
Routine prophylaxis is NOT recommended due to fluconazole resistance and the non-life-threatening nature of most Candida infections. Consider prophylaxis only in recurrent or severe esophageal candidiasis with fluconazole 100–200 mg daily. The risk factors for Candidiasis in HIV include CD4 count <200 cells/µL (increased risk for thrush and esophageal candidiasis), Not on effective ART, Use of inhaled corticosteroids, Poor oral hygiene, dentures, smoking, and antibiotic use (disrupts normal flora). Oropharyngeal Candidiasis (Thrush), occurs when Candida albicans infects the oropharynx and becomes more frequent as CD4 drops under ~500. Presentation: painless, creamy-white plaque lesions on the tongue or buccal mucosa that easily scrape off, sometimes with an erythematous base. It may cause altered taste or mild discomfort. By the time CD4 nears ~200, Candida often causes esophageal candidiasis, which is associated with odynophagia, retrosternal pain, difficulty swallowing, and is an AIDS-defining illness. Since prophylaxis is not indicated, the goals of care are to treat infections and manage symptoms. For oral thrush, topical antifungals (nystatin suspension or clotrimazole troches) can be used in mild cases; more severe or recurrent thrush responds well to oral fluconazole for 7–14 days. Esophageal candidiasis requires systemic antifungals – fluconazole PO/IV for 14–21 days is first-line, or itraconazole solution as an alternative. Patients often feel rapid symptom relief after starting therapy.
Aside from MAC and CMV, what are the common etiologies of diarrheal symptoms in HIV patients?
- Cryptosporidiosis
- Microsporidiosis
- Isospora
These infections of the GI tract are common at CD4 <200 and can cause chronic, debilitating diarrhea. Cryptosporidium parvum (Protozoa) cause chronic cryptosporidiosis – profuse watery diarrhea, dehydration, abdominal cramps, nausea, and malabsorption, often lasting >1 month. Microsporidia (Enterocytozoon, Encephalitozoon species, etc.) are intracellular fungi (formerly classified as protozoa) that also cause chronic diarrhea and biliary tract disease in AIDS. Patients often have a low grade fever and weight loss due to the persistent diarrhea. No specific primary prophylaxis is available for these; preventive measures include avoiding contaminated water or food (boil water if CD4 is low, avoid swimming in untreated water, etc.). Diagnosis requires a stool O & P. Treatment for Cryptosporidiosis is with nitazoxanide (no reliably curative treatment in AIDS but may reduce symptoms). Isospora is treated with TMP-SMX (bactrim). And Microsporidiosis is treated with albendazole as it is effective for some species (Encephalitozoon intestinalis) and fumagillin for others. The cornerstone is aggressive ART to improve immune function (often the only way to clear infection). Supportive care with hydration and antimotility agents is essential. These infections can be chronic unless the CD4 count improves.
What is the cause for this seen in HIV patients?
Oral hairy leukoplakia is an EBV-mediated disorder of the tongue epithelium that leads to white, hyperkeratotic plaques usually distributed along the lateral border of the tongue. It has characteristic vertical white striations that appear “hairy.” This is often treated with acyclovir.
Why does this skin finding occur with patients who have HIV?
Herpes Zoster (Shingles): Reactivation of varicella-zoster virus occurs more frequently in HIV patients as immunity declines (often in this CD4 200–500 range). Presentation: a painful, blistering rash in a dermatomal distribution (does not cross midline). HIV-related zoster can be severe, with potential for multidermatomal rash or complications like ocular involvement (herpes zoster ophthalmicus, aka Ramsay Hunt syndrome when the facial nerve is also involved) or disseminated zoster. Prophylaxis: There is no routine medication prophylaxis for zoster in HIV, but varicella vaccine is recommended in non-immune patients with CD4 >200 to prevent primary VZV infection or severe zoster. Treatment: High-dose acyclovir (or valacyclovir) for 7–10 days, started promptly, can hasten lesion healing and reduce complications. Postherpetic neuralgia is managed with pain control (nortriptyline, gabapentin, lamotrigine, capsaicin, or lidocaine). If eye involvement is suspected, urgent ophthalmology evaluation is needed.
Herpes Simplex Virus (HSV): HIV patients with moderate immunosuppression may have more frequent and severe HSV-1 or HSV-2 outbreaks. Recurrent oral and genital herpes lesions are common, and chronic HSV ulcers >1 month or HSV bronchitis/pneumonitis/esophagitis are AIDS-defining if they occur. Presentation: painful ulcerative lesions – for oral/lip HSV or genital herpes – that may be larger or slower to heal than in immunocompetent hosts. Chronic perianal or oral ulcers can develop in advanced cases. Prophylaxis: Daily suppressive acyclovir (or valacyclovir) may be used in individuals with very frequent or severe recurrences, but is not routinely required. Treatment: episodic therapy with acyclovir, valacyclovir, or famciclovir is effective; IV acyclovir is indicated for severe or disseminated HSV (e.g. HSV encephalitis). ART can reduce HSV outbreaks over time by improving immune function.
An HIV patient with multiple raised, red vascular skin lesions that may resemble Kaposi’s sarcoma but tend to be friable (bleed easily) and can have a verrucous (wart-like) surface, is likely … ?
Bacillary Angiomatosis (BA), which is caused by Bartonella henselae or B. quintana bacteria. BA occurs almost exclusively in immunocompromised hosts (CD4 often <100, average ~50). Patients often present with one or multiple raised, red vascular skin lesions that may resemble Kaposi’s sarcoma but tend to be friable (bleed easily) and can have a verrucous (wart-like) surface. Lesions can be papules or nodules and are found on skin or organs (bacillary peliosis in the liver/spleen). Patients often have systemic symptoms (fever, weight loss, night sweats). This condition has no specific prophylaxis, however, avoidance of cat scratches/fleas might help prevent B. henselae infection as cats are reservoirs. Treatment is with Erythromycin as the treatment of choice for BA and is given for at least 8–12 weeks. Alternatively patients can be given doxycycline. Lesions typically start resolving after a couple of weeks of antibiotics. ART is also important to prevent relapse. If there is extensive hepatic involvement or peliosis, additional rifamycin antibiotics may be added.
What are the risk factors for Bacillary Angiomatosis?
Advanced HIV/AIDS (CD4 count < 100), exposure to cats (B. henselae), exposure to lice (B. quintana), and homelessness.
What are the clinical features of Bacillary Angiomatosis?
A vascular proliferative disease caused by Bartonella henselae or Bartonella quintana, commonly seen in immunocompromised patients, particularly those with advanced HIV/AIDS (CD4 < 100). Red or purple papules, nodules, or plaques that may ulcerate and bleed. Can resemble Kaposi’s sarcoma. Systemic symptoms include fever, malaise, weight loss, and night sweats.
How does Bacillary Angiomatosis present in organs other than the skin?
It can involve the liver (peliosis hepatis), spleen, lymph nodes, and bones, leading to systemic symptoms such as hepatosplenomegaly and bone pain.
What is the primary pathogen of Bacillary Angiomatosis associated with cat exposure?
Bartonella henselae.
What is the primary pathogen of Bacillary Angiomatosis associated with lice exposure?
Bartonella quintana.
What is the key histopathological finding in Bacillary Angiomatosis?
Lobular proliferation of small blood vessels with neutrophilic inflammation and bacteria visible on Warthin-Starry silver stain.
How do you differentiate Bacillary Angiomatosis from Kaposi Sarcoma?
Bacillary Angiomatosis has neutrophilic inflammation, responds to antibiotics, and can have systemic symptoms like fever. Kaposi Sarcoma has lymphocytic inflammation, is associated with HHV-8, and does not respond to antibiotics.
What are the complications of untreated Bacillary Angiomatosis?
Hepatosplenic disease, bacteremia, endocarditis, bone lesions, and systemic dissemination leading to multi-organ involvement.
What is the preferred antibiotic for Bacillary Angiomatosis in HIV patients?
Doxycycline or erythromycin for at least 3-4 weeks, with longer duration in disseminated cases.
Which diagnostic stain is used to visualize Bartonella species in Bacillary Angiomatosis?
Clinical presentation, skin biopsy showing neutrophilic inflammation and vascular proliferation, and Warthin-Starry silver stain for Bartonella spp. Blood cultures may also be positive.
The key elements are:
1. Perform a biopsy.
2. Warthin-Starry silver stain is done for confirmation.
What is the treatment for Bacillary Angiomatosis?
Oral erythromycin or doxycycline for at least 3-4 weeks. Severe cases may require IV antibiotics.
What environmental yeast commonly causes meningitis in HIV patients, usually at CD4 <100?
Cryptococcus neoformans causes Cryptococcal Meningitis and is an environmental yeast that causes meningoencephalitis in HIV patients, usually when the CD4 <100. Cryptococcal disease can also present with pulmonary infection or disseminated disease, but CNS involvement is most feared.Patients tend to present with subacute meningitis, fever, severe headaches, and malaise. Neck stiffness (brudzinski and kernig) and photophobia are often mild or absent in AIDS patients. However, elevated intracranial pressure is common, evidenced with papilledema and cranial nerve palsies. This is a tricky opportunistic infection because imaging can often be negative (or only indicate swelling and increased intracranial pressure observed with decreased size of ventricles or loss of sulci) and routine primary prophylaxis for Crypto meningitis is not recommended in the US (due to low incidence with ART and risk of resistance). Because of this, some regions perform routine serum cryptococcal antigen screening (the preferred test is latex agglutination) in patients with CD4 <100 and preemptively treat if positive. Treatment involves a two-week induction with Amphotericin B + flucytosine, followed by at least 8 weeks of high-dose fluconazole. Afterward, lower-dose fluconazole (200 mg daily) is given as secondary prophylaxis until CD4 >100–200 on ART. Management includes frequent lumbar punctures or CSF shunting to relieve high pressure. Symptoms generally improve over 2–4 weeks. Without treatment, cryptococcal meningitis is uniformly fatal.
How do you diagnose Cryptococcus in HIV?
Latex agglutination in CSF > Cryptococcal antigen in CSF > India ink stain of CSF
What is the treatment for Cryptococcal meningitis in HIV?
Amphotericin B + Flucytosine, then Fluconazole for maintenance.
How does Progressive Multifocal Leukoencephalopathy (PML) present in HIV?
Progressive focal neurological deficits (JC virus).
Progressive Multifocal Leukoencephalopathy (PML) is caused by JC virus reactivation in the brain, PML occurs in advanced AIDS typically when the CD4 <100 (mean CD ~80 at presentation). This is a progressive demyelinating neurologic disease that causes focal deficits (hemiparesis, aphasia, ataxia, visual field cuts) that worsen over weeks, often without fever. MRI reveals multiple white matter lesions without edema or mass effect. Other MRI evidence includes cortical atrophy due to profound demyelination of oligodendrocytes. There is no specific therapy to prevent JC virus. Additionally, there is no effective direct anti-JC virus therapy. The main strategy is ART initiation to restore immunity. Some patients show improvement in PML with immune reconstitution (IRIS must be monitored). High-dose glucocorticoids are used if IRIS causes significant inflammation. Prognosis is guarded – PML has high mortality, though a subset stabilizes or improves on ART.
What does MRI show in Progressive Multifocal Leukoencephalopathy (PML)?
Non-enhancing, white matter lesions with no edema.
How is Progressive Multifocal Leukoencephalopathy (PML) diagnosed?
LP (CSF JC virus PCR)
Progressive Multifocal Leukoencephalopathy (PML) can occur in not only HIV patients, but also in those who … ?
- Take Natalizumab (for Crohn’s disease and MS)
- Take Rituximab
- Take Eculizumab
- Leukemia
- Lymphoma
- Immunosuppressants
What virus is primarily responsible for Primary CNS Lymphoma in patients with HIV?
Primary CNS Lymphoma is an AIDS-defining malignancy and is a Non-Hodgkin lymphoma usually secondary to EBV-related diffuse large B-cell. This is a common manifestation in HIV patients when CD4 counts <50. It is the second most common cause of focal brain lesions in AIDS (after toxoplasmosis). The presentation is similar to toxo but often has a more rapid decline with focal neurologic deficits (aphasia, hemiparesis, weakness) and patients often exhibit altered mental status, memory loss, confusion, and seizures. Imaging usually shows a solitary mass lesion, often periventricular, with significant edema. Diagnosis is confirmed by brain biopsy or detecting EBV DNA in CSF with a compatible lesion. This has no measure for prophylaxis other than effective ART. Treatment involves high-dose methotrexate-based chemotherapy (often with rituximab) and/or whole-brain radiation. Outcomes tend to be very poor in advanced AIDS. Immediate ART initiation is done to improve immune function, as this is often fatal within months. Some patients respond to chemo-ART and achieve remission if immune recovery occurs. For systemic NHL in AIDS, combination chemotherapy similar to HIV-negative patients is used, with careful attention to infections and myelosuppression.
What is HIV-associated dementia?
Cognitive decline in advanced HIV; treated with ART.
HIV Encephalopathy (AIDS Dementia) occurs with severe immunosuppression (CD4 <200) and can lead to HIV-associated neurocognitive disorder. The presentation is gradual cognitive decline, memory impairment, poor concentration, apathy, and motor abnormalities (gait instability, slow movements) in the absence of another cause. It is a diagnosis of exclusion after ruling out CNS opportunistic infections. There is no specific prophylaxis (this condition results from HIV itself), and effective ART is the best prevention. Treatment involves initiation or optimization of ART, as thus is the mainstay treatment and often stabilizes or improves cognitive function over weeks to months. Supportive care (safe environment, psychostimulants or antidepressants if indicated) and rehabilitation therapies can help manage symptoms. Improvement with ART underscores the importance of viral suppression to prevent HIV-related brain damage.
When should you start Mycobacterium Avium Complex (MAC) prophylaxis?
CD4 < 50 (if not on ART) → Give Azithromycin.
Disseminated Mycobacterium Avium Complex (MAC) infection is a late-stage AIDS condition seen at CD4 counts <50 cells/µL. MAC is an atypical mycobacteria found in soil and water that can spread throughout the body when immune defenses are very low. Patients tend to have a non-specific presentation of this systemic illness, and involves profuse watery diarrhea persistent fever, drenching night sweats, weight loss, abdominal pain, chronic diarrhea, diffuse lymphadenopathy. Cutaneous lesions are uncommon and are usually nodular and ulcerating. Often there is anemia and elevated alkaline phosphatase from liver involvement. MAC can affect any organ. The common physical exam findings include hepatosplenomegaly, lymphadenopathy, and sometimes lung nodules or bone lesions. The diagnosis for MAC involves either a blood culture or tissue biopsy. MAC is often prevented with prophylaxis when the CD4 <50 and patient is not yet on effective ART with azithromycin 1200mg weekly (or clarithromycin BID) to prevent MAC. This prophylaxis may be discontinued once patient is on ART and CD4 >100 for ≥3 months. Treatment for acute infections is with a macrolide, such as clarithromycin or azithromycin + ethambutol is (first-line). Often with a third drug like rifabutin is used as well. Therapy is prolonged (≥12 months) and can be stopped only after at least 12 months of treatment and CD4 >100 for 6+ months on ART (to prevent relapse). Patients often show clinical improvement after a few weeks of therapy; persistent bacteremia should clear with successful treatment.
What is the presentation of CMV retinitis in HIV?
Cytomegalovirus (CMV) retinitis occurs in HIV-infected patients when there is severe immunosuppression, specifically when the CD4 count falls below 50 cells/µL. It is an AIDS-defining illness and is caused by reactivation of latent CMV in patients with advanced HIV. Patients notice floaters, blurred vision, visual field defects, or painless vision loss. The fundoscopic exam shows retinal hemorrhages and yellow-white, fluffy lesions (“pizza-pie” appearance ‘cotton-wool spots’). If untreated, progressive retinal necrosis leads to retinal detachment and blindness. Fundoscopy classically shows fluffy yellow-white retinal lesions with hemorrhages (“pizza pie” or cottage cheese with ketchup appearance) in the areas of CMV infection. Routine primary prophylaxis for CMV (e.g. with valganciclovir) is not recommended due to drug toxicity. The best prevention is maintaining CD4 counts via ART. Patients with CD4 <50 should have regular dilated eye exams to catch early retinitis. Valganciclovir oral is often first-line for CMV retinitis in mild cases. For sight-threatening lesions (near the macula or optic nerve), induction therapy with IV ganciclovir or foscarnet and intravitreal antiviral injections is recommended. Oral valganciclovir is given for less severe cases or maintenance therapy. After 2–3 weeks of induction, maintenance therapy (secondary prophylaxis) with oral valganciclovir is continued until CD4 >100–150 on ART. Prompt treatment can preserve vision, but advanced retinitis may lead to permanent vision loss.
Other CMV manifestations include colitis (watery or bloody diarrhea), esophagitis, and encephalitis, but retinitis is most frequent. When spread of CMV occurs, leading to GI symptoms, patients may also have fever, weight loss, night sweats, malaise, abdominal pain, and diffuse lymphadenopathy. The diagnosis for disseminated infection causing diarrheal manifestations is with clinical symptoms, plus endoscopy with biopsy showing both microscopic and macroscopic features of CMV. Treatment is with ganciclovir or valganciclovir.
What histological finding is associated with CMV?
CMV is often associated with patients with advanced AIDS, increasing the risk for cytomegalovirus (CMV) pneumonia and diarrhea, and can cause fever, cough, dyspnea, and diffuse pulmonary infiltrates. CMV is commonly treated with ganciclovir. The presence of “owl’s eye” inclusion bodies on histopathology strongly supports a CMV infection.
What is the most common opportunistic eye infection in patients with AIDS?
Cytomegalovirus (CMV) retinitis, typically seen in patients with CD4 counts <50 cells/μL.
How is CMV retinitis diagnosed?
Slit lamp or fundoscopy: Retinal findings of necrosis, hemorrhage, and exudates.
CMV DNA PCR: Confirms systemic CMV infection in blood or aqueous humor.
What is the first-line treatment for CMV retinitis?
Oral valganciclovir for mild disease.
Intravitreal ganciclovir or foscarnet injections for sight-threatening lesions (near macula or optic nerve).
What is foscarnet, and when is it indicated for CMV retinitis?
Foscarnet is a pyrophosphate analog that inhibits viral DNA polymerase.
Indications:
CMV retinitis resistant to ganciclovir.
Patients intolerant to ganciclovir (e.g., severe neutropenia).
What are the side effects of foscarnet?
Nephrotoxicity: Monitor creatinine and electrolytes.
Electrolyte imbalances: Hypocalcemia, hypomagnesemia, and hypokalemia.
Seizures: Due to electrolyte disturbances.
What is ganciclovir, and how does it treat CMV retinitis?
Ganciclovir is a guanosine analog that inhibits viral DNA polymerase after being phosphorylated by CMV UL97 kinase.
It prevents viral replication and reduces retinal inflammation.
How does CMV develop resistance to ganciclovir?
UL97 gene mutation: Reduces ganciclovir phosphorylation, preventing its activation.
UL54 gene mutation: Alters viral DNA polymerase, reducing binding of ganciclovir.
What is the mechanism of action of valganciclovir?
Prodrug of ganciclovir with higher oral bioavailability.
Converts to ganciclovir in the body, where it inhibits viral DNA polymerase after activation by UL97 kinase.
What are the complications of untreated CMV retinitis?
Blindness: Due to progressive retinal necrosis.
Contralateral eye involvement: Without systemic treatment.
CNS involvement: CMV encephalitis or ventriculitis.
What is immune reconstitution inflammatory syndrome (IRIS), and how does it relate to CMV retinitis?
IRIS is a paradoxical worsening of symptoms due to the immune system recovering after starting antiretroviral therapy (ART). In CMV retinitis, IRIS can cause retinal detachment or severe inflammation.
How is CMV retinitis managed in patients with advanced HIV?
Treat CMV first: Valganciclovir or intravitreal therapy.
Initiate ART after 2 weeks to avoid IRIS.
Regular ophthalmologic follow-up to monitor for complications.
Why is regular screening important for CMV retinitis in AIDS patients?
Early detection prevents blindness.
Fundoscopic exams are recommended for HIV patients with CD4 counts <50 cells/μL.
What is the most common renal complication associated with HIV?
HIV-associated nephropathy (HIVAN), a collapsing form of focal segmental glomerulosclerosis (FSGS).
What are the clinical features of HIVAN?
Nephrotic syndrome (proteinuria >3.5g/day), progressive renal insufficiency, and normal to large echogenic kidneys on ultrasound.
What is the pathophysiology of HIVAN?
HIV directly infects renal epithelial cells, leading to podocyte injury, glomerular collapse, and tubulointerstitial inflammation.
How is HIVAN diagnosed?
Clinical suspicion with nephrotic-range proteinuria in an HIV patient; definitive diagnosis with renal biopsy showing collapsing FSGS.
What is the treatment for HIVAN?
Antiretroviral therapy (ART) is the mainstay of treatment; ACE inhibitors or ARBs can be used to reduce proteinuria.
Which HIV medications are associated with nephrotoxicity?
Tenofovir (especially TDF, causes proximal tubular damage), indinavir (causes nephrolithiasis), and atazanavir (causes crystalluria).
What is the difference between tenofovir disoproxil fumarate (TDF) and tenofovir alafenamide (TAF) in terms of nephrotoxicity?
TAF has lower renal toxicity compared to TDF due to its reduced systemic exposure.
What opportunistic infections in HIV patients can cause renal disease?
CMV nephropathy, BK virus nephropathy, and tuberculosis-associated renal disease.
Which HIV-related renal condition can mimic lupus nephritis?
HIVAN, as both can present with nephrotic syndrome and diffuse proliferative glomerulonephritis-like features.
Why is proteinuria screening important in HIV patients?
Proteinuria may be the first sign of HIVAN; routine urine analysis is recommended in all HIV patients.
When should dialysis be considered in an HIV patient?
If there is progressive renal failure despite ART, nephroprotective measures, and treatment of underlying causes.
What prophylactic measures should be taken in HIV patients to prevent nephropathy?
Early initiation of ART, avoiding nephrotoxic drugs, and controlling hypertension and diabetes.
What is the significance of acute kidney injury (AKI) in HIV patients?
HIV patients have a higher risk of AKI due to opportunistic infections, drug toxicity, and volume depletion.
How does HIV-related immune complex kidney disease differ from HIVAN?
Immune complex disease presents with mesangial proliferative glomerulonephritis and immune deposits, whereas HIVAN has collapsing FSGS.
Which patients are at highest risk for developing HIVAN?
African American patients with APOL1 gene variants have the highest risk of developing HIVAN.
What is the recommended HIV screening protocol for pregnant women?
All pregnant women should be screened for HIV at the first prenatal visit. High-risk women should be re-screened in the third trimester.
What is the recommended treatment for HIV-positive pregnant women?
All HIV-positive pregnant women should receive combination antiretroviral therapy (ART), regardless of CD4 count or viral load.
What is the goal of HIV treatment in pregnancy?
To achieve an undetectable viral load (<50 copies/mL) by delivery to reduce perinatal transmission risk.
What is the preferred ART regimen for HIV-positive pregnant women?
A regimen containing two NRTIs (e.g., tenofovir/emtricitabine or abacavir/lamivudine) plus an integrase inhibitor (dolutegravir) or a boosted protease inhibitor (atazanavir/ritonavir).
What is the risk of vertical transmission of HIV with and without ART?
Without ART, the transmission risk is ~25-30%. With ART and appropriate management, the risk decreases to <1%.
What is the preferred mode of delivery for an HIV-positive woman with a viral load <1000 copies/mL?
Vaginal delivery is safe if the viral load is <1000 copies/mL at 36 weeks.
What is the preferred mode of delivery for an HIV-positive woman with a viral load ≥1000 copies/mL?
A scheduled cesarean section at 38 weeks is recommended to reduce transmission risk.
What is intrapartum management for HIV-positive women in labor?
If the viral load is ≥1000 copies/mL, IV zidovudine (AZT) is given during labor.
If <1000 copies/mL, IV zidovudine is not needed.
How is neonatal HIV prophylaxis managed?
Low-risk neonates (maternal viral load <50 copies/mL) receive zidovudine (AZT) for 4 weeks.
High-risk neonates (maternal viral load ≥1000 copies/mL) receive combination therapy with zidovudine, lamivudine, and nevirapine for 6 weeks.
When should HIV testing be performed in neonates born to HIV-positive mothers?
HIV DNA PCR is performed at birth, 2-4 weeks, 2 months, and 4-6 months. Diagnosis is confirmed with two positive results.
Can HIV-positive mothers breastfeed?
No. In developed countries, breastfeeding is contraindicated due to transmission risk. In resource-limited settings, exclusive breastfeeding may be recommended if formula is unavailable.
What postpartum care is required for HIV-positive mothers?
Continue ART indefinitely and monitor viral load/CD4 counts. Ensure infant HIV prophylaxis and proper follow-up testing.
