HIV and AIDS — DCE Clinical Case

Long Case — Advanced HIV presenting with Pneumocystis pneumonia and chronic hepatitis B

Patient scenario

Mr Michael Tane is a 42-year-old man who presents to the emergency department with a three-week history of progressive exertional dyspnoea, dry cough and low-grade fever. [1]

History of presenting complaint: [1]

• Three weeks ago: onset of exertional dyspnoea, initially on climbing one flight of stairs, progressing to dyspnoea on walking on the flat.
• Two weeks ago: dry non-productive cough, worse at night, associated with fever (up to 38.5 degrees Celsius), night sweats and fatigue.
• One week ago: oral thrush noticed by his GP, who prescribed oral nystatin. The GP also organised an HIV test, which returned positive.
• No haemoptysis, chest pain, weight loss beyond 3 kg, headache, visual changes, or neurological symptoms. [1]

Past medical history: Chronic hepatitis B (diagnosed 5 years ago, not on treatment). No prior hospitalisations. No prior HIV testing before this presentation. [1]

Medications: Nystatin oral suspension (started one week ago). No regular medications. No over-the-counter, herbal or recreational drugs reported (later confirmed on further history). [1]

Family history: Father with type 2 diabetes and ischaemic heart disease. Mother alive and well. No family history of HIV or hepatitis. [1]

Social history: Born in Vietnam, migrated to Australia at age 15. Works as a chef. Divorced 2 years ago, currently in a new relationship with a female partner (HIV status unknown). Social alcohol consumption (4 to 6 standard drinks per week). Smokes 10 cigarettes per day (15 pack-years). No injecting drug use. Sexually active with female partners; inconsistent condom use. Has two children aged 8 and 12. [1]

Examination findings: [1]

• Afebrile at triage (37.4 degrees Celsius), heart rate 108, blood pressure 118/72, respiratory rate 24, oxygen saturation 91 per cent on room air at rest, dropping to 85 per cent on walking 50 metres.
• Thin, cachectic appearance. Oral cavity shows thick white adherent plaques on the tongue and buccal mucosa consistent with oral candidiasis.
• Respiratory: bilateral fine inspiratory crackles throughout both lung fields, more pronounced at the bases. No wheeze, no consolidation, no pleural effusion signs.
• Cardiovascular: tachycardia, no murmurs, no signs of heart failure.
• Abdomen: soft, non-tender. Liver edge palpable 2 cm below the costal margin (chronic hepatitis B). No splenomegaly. No ascites.
• Small bilateral cervical and axillary lymphadenopathy (1 to 1.5 cm, rubbery, mobile, non-tender).
• Skin: no rash, no Kaposi sarcoma lesions.
• Neurological: alert and oriented, no focal deficits. [1]

Investigations: [1]

Candidate's opening statement (model answer — SASPOP format)

"Mr Michael Tane is a 42-year-old chef, born in Vietnam, presenting as a late presenter with newly diagnosed HIV-1 infection at CD4 80 cells per microlitre and viral load 340,000 copies per millilitre, complicated by moderate-to-severe Pneumocystis jirovecii pneumonia (PaO2 58 mmHg on room air, exertional desaturation, bilateral ground-glass infiltrates and elevated LDH), oral candidiasis, and chronic hepatitis B co-infection with high HBV DNA. [1]

He is hypoxaemic (PaO2 below 70 mmHg), which mandates adjunctive corticosteroids alongside high-dose co-trimoxazole for the PCP. His main problems are: (1) moderate-to-severe Pneumocystis pneumonia requiring admission, oxygen, co-trimoxazole and corticosteroids; (2) advanced HIV at CD4 80 — requiring ART initiation within 2 weeks of admission once the PCP is stabilising; (3) chronic hepatitis B co-infection with high HBV DNA, which means his ART must include dual anti-HBV agents (tenofovir plus lamivudine or emtricitabine); (4) opportunistic infection prophylaxis — co-trimoxazole for PCP and toxoplasmosis at CD4 80; (5) the risk of IRIS and CMV retinitis at his current CD4; (6) the psychosocial impact of a new HIV diagnosis on a recently divorced man with a new partner and two children; and (7) public health obligations including partner notification.* [1]

My immediate management is admission, supplemental oxygen to maintain saturation above 92 per cent, high-dose co-trimoxazole with adjunctive corticosteroids for the PCP, co-trimoxazole prophylaxis dose once the treatment course is structured, oral fluconazole for the oral candidiasis, baseline resistance testing and ART preparation, ophthalmology review for CMV screening, hepatitis B assessment, and a sensitive, structured discussion with the patient about the diagnosis, treatment plan and partner notification."* [1]

Integrated management plan

1. Moderate-to-severe Pneumocystis pneumonia (the immediate priority): [1]

• High-dose co-trimoxazole (trimethoprim-sulfamethoxazole at 15 to 20 mg/kg/day trimethoprim component, in 4 divided doses) for 21 days. For a 65 kg man, approximately 4 double-strength tablets (960 mg each) four times daily.
• Adjunctive corticosteroids are mandatory because PaO2 is below 70 mmHg on room air: prednisolone 40 mg twice daily for 5 days, then 40 mg daily for 5 days, then 20 mg daily to complete 21 days. Corticosteroids reduce mortality in moderate-to-severe PCP by attenuating the inflammatory response to dying organisms.
• Supplemental oxygen to maintain saturation above 92 per cent. Monitor gas exchange; escalate to ICU if type 1 respiratory failure progresses.
• Monitor for co-trimoxazole adverse effects: rash, fever, neutropenia, thrombocytopenia, transaminitis, hyperkalaemia.
• If co-trimoxazole is not tolerated or fails: second-line is primaquine plus clindamycin, or intravenous pentamidine. [1]

2. Advanced HIV — ART initiation: [1]

• Start ART within 2 weeks of admission (once PCP is stabilising), because early ART reduces progression to further opportunistic infections without significantly increasing PCP-IRIS risk.
• Regimen: tenofovir disoproxil fumarate (TDF) 300 mg plus emtricitabine 200 mg plus dolutegravir 50 mg daily. This is the WHO-preferred first-line worldwide. TDF plus FTC also treats the hepatitis B. No significant drug interactions with the PCP therapy or fluconazole.
• Check HLA-B 5701 if abacavir is being considered (not needed here, but standard practice before any abacavir-containing regimen).
• Baseline resistance test before starting ART to exclude transmitted resistance.
• Target: viral suppression below 50 copies per millilitre within 12 to 24 weeks, then sustained for life. Treatment interruption is harmful — the SMART trial showed higher mortality and cardiovascular/renal/hepatic events with CD4-guided interruption [8].
• The START trial established that ART benefits all patients regardless of CD4 count, with a 57 per cent reduction in serious AIDS and non-AIDS events with immediate versus deferred therapy [1].

3. Chronic hepatitis B co-infection: [1]

• TDF plus FTC in his ART regimen provides dual anti-HBV coverage. HBV DNA should suppress over months.
• Monitor HBV DNA, liver function tests and HBV serology every 3 to 6 months.
• Hepatocellular carcinoma surveillance — liver ultrasound and serum AFP every 6 months (he has chronic HBV with high DNA, placing him in the high-risk category).
• Vaccinate against hepatitis A if seronegative.
• Hepatology referral for ongoing HBV management if liver function tests do not normalise or HBV DNA does not suppress. [1]

4. Opportunistic infection prophylaxis: [1]

• Co-trimoxazole 960 mg daily (or 480 mg daily if tolerated) for PCP and toxoplasma prophylaxis (toxoplasma IgG is negative, but co-trimoxazole still covers PCP). Continue until CD4 is above 200 for at least 3 months on ART.
• CMV screening — urgent ophthalmology review for dilated fundoscopy at CD4 80 (approaching the CD4 50 threshold). CMV IgG is positive (indicating latent infection). If CMV retinitis is found, treat with valganciclovir.
• MAC prophylaxis — azithromycin 1200 mg once weekly when CD4 drops below 50 (may be needed transiently before ART-driven CD4 recovery lifts him above 50).
• Ensure all vaccinations are up to date: pneumococcal, influenza, hepatitis A and B, COVID-19. Vaccinate before ART takes full effect to maximise immunogenicity (though live vaccines are contraindicated at CD4 below 200). [1]

5. IRIS risk: [1]

• Counsel Mr Tane about the risk of immune reconstitution inflammatory syndrome in the first 4 to 8 weeks of ART — paradoxical worsening of the PCP or unmasking of a subclinical infection.
• ART is continued through IRIS (it is an inflammatory response, not treatment failure).
• Severe IRIS (respiratory compromise) is managed with corticosteroids. [1]

6. Psychosocial support and shared decision-making: [1]

• Frame HIV as a chronic, manageable condition with near-normal life expectancy on ART.
• Address the stigma, confidentiality and partner notification obligations. Offer facilitated partner notification through the sexual health service.
• Offer the HIV peer support worker and a named clinical contact.
• Offer psychology referral for adjustment to the diagnosis.
• Address smoking cessation (smoking is the single biggest modifiable cardiovascular risk factor in HIV). [1]

7. Partner notification and public health: [1]

• Offer HIV testing to his current female partner. If HIV-negative and at ongoing risk, discuss PrEP (tenofovir plus emtricitabine daily).
• Offer HIV testing to former partners (through the sexual health service).
• This is a legal and ethical obligation in most Australian jurisdictions — facilitated, supportive and confidential. [1]

Communication and shared decision-making

I would sit with Mr Tane in a quiet, private room, with an interpreter available if needed (he migrated from Vietnam at 15 and his English appears functional, but cultural sensitivity and the gravity of the conversation warrant checking his preferred language for medical discussions). I would deliver the diagnosis with honesty and compassion: [1]

• "You have HIV. This is a serious diagnosis, but HIV is now a treatable chronic condition. With daily medication, people living with HIV have a near-normal life expectancy."
• "You also have a chest infection called Pneumocystis pneumonia, which is a complication of the HIV. We are treating it now with antibiotics and a course of steroid tablets."
• "Once the pneumonia is improving, we will start HIV treatment — a single tablet once a day. The goal is to make the virus undetectable in your blood, and once it is undetectable, you cannot pass HIV to your partner through sex. This is called U equals U — Undetectable equals Untransmittable [2][3]."
• "You also have chronic hepatitis B. The HIV treatment we are choosing also treats the hepatitis B, so we are addressing both with the same medication."
• "We need to talk about your partner. She should be tested for HIV. If she is negative, there is a preventive medication she can take called PrEP. This is something the sexual health team can help arrange confidentially."
• "I want to reassure you: your children are not at risk from casual contact. HIV is transmitted through blood and sexual contact, not through sharing meals, hugs, or everyday life."

I would document the shared decision, provide written information in English and Vietnamese if available, and arrange a named contact for between-appointment questions. [1]

Probing questions and model answers

Examiner: Why is he having adjunctive corticosteroids for the PCP? [1]

"Corticosteroids are indicated for moderate-to-severe PCP, defined as a PaO2 below 70 mmHg on room air or an elevated alveolar-arterial gradient. Mr Tane has a PaO2 of 58 mmHg and an A-a gradient of 55 mmHg, placing him firmly in this category. The rationale is that the lung injury in PCP is driven largely by the inflammatory response to dying organisms rather than by the organisms themselves. When high-dose co-trimoxazole kills large numbers of Pneumocystis organisms, the resulting inflammatory cascade can worsen oxygenation, paradoxically worsening the patient before they improve. Corticosteroids, started at the same time as or slightly before the co-trimoxazole, attenuate this inflammatory response and have been shown in multiple studies to reduce mortality, respiratory failure and the need for mechanical ventilation in moderate-to-severe PCP. The standard regimen is prednisolone 40 mg twice daily for 5 days, then 40 mg daily for 5 days, then 20 mg daily to complete 21 days." [1]

Examiner: How does the START trial inform your management? [1]

"The START trial is the definitive evidence for the Treat All policy [1]. It randomised 4,685 asymptomatic ART-naive adults with CD4 above 500 to immediate ART versus deferred ART (until CD4 fell below 350 or an AIDS-defining illness developed). The trial was stopped early because immediate ART reduced the primary composite endpoint of serious AIDS events, serious non-AIDS events, or death by 57 per cent (hazard ratio 0.43). The benefit was driven by reductions in tuberculosis, Kaposi sarcoma, lymphoma, non-AIDS cancers and cardiovascular events. This established that ART should be started in everyone living with HIV regardless of CD4 count. For Mr Tane, who is far below the START entry threshold (CD4 80 versus above 500), the case is even stronger — he has advanced disease with an active opportunistic infection, and ART is the definitive therapy for his underlying immune deficiency. I will start it within 2 weeks of admission."

Examiner: What is the significance of the PARTNER studies for this patient? [1]

"The PARTNER and PARTNER2 studies provide the definitive evidence for the U equals U message that I will deliver to Mr Tane and his partner [2][3]. PARTNER followed serodifferent couples (predominantly heterosexual, some MSM) where the HIV-positive partner was on suppressive ART (viral load below 200). Across approximately 58,000 condomless sex acts, there were zero phylogenetically linked transmissions. PARTNER2, focusing exclusively on gay male serodifferent couples (where the per-act transmission risk of anal sex is higher than vaginal sex), confirmed the same finding across approximately 77,000 condomless sex acts. Combined, across over 126,000 acts of condomless sex, there were zero linked transmissions. This means that once Mr Tane's viral load is undetectable, he cannot transmit HIV to his partner through sexual contact. This is profoundly important for his psychosocial wellbeing, his relationship, his adherence motivation, and public health. Combined with HPTN 052, which showed a 96 per cent reduction in transmission with early ART [1], this underpins the treatment-as-prevention strategy."

Examiner: What is the D:A:D study finding and why does it matter? [1]

"The D:A:D (Data Collection on Adverse Events of Anti-HIV Drugs) study was a large observational collaboration that tracked cardiovascular events in over 23,000 HIV-positive patients [7]. It found that cumulative use of certain nucleoside reverse transcriptase inhibitors — specifically abacavir and didanosine — was associated with an increased risk of myocardial infarction. The abacavir signal has been debated (some studies found it and others did not), but it influenced prescribing away from abacavir in patients with high cardiovascular risk. For Mr Tane, this matters because I am not using abacavir (his regimen is tenofovir-based), which avoids the concern entirely. More broadly, the D:A:D study underscored that people living with HIV have an approximately 1.5 to 2-fold increased cardiovascular risk compared with uninfected controls, driven by chronic inflammation, endothelial dysfunction and drug effects. I will address this proactively with smoking cessation (he smokes 10 per day), lipid monitoring, and a statin if indicated."

Examiner: How would you manage a confirmed viral load above 200 copies per millilitre after he starts ART? [1]

"A confirmed viral load above 200 copies per millilitre on ART is virological failure. My approach is systematic. First, I check adherence — non-adherence is by far the most common cause, and I would have a sensitive, non-judgemental conversation about barriers (his recent divorce, work as a chef with shift work, the new diagnosis). Second, I check for drug interactions that might reduce ART levels. Third, I send a resistance test (genotypic) on the current viral load to identify resistance mutations. Fourth, I never add a single new drug to a failing regimen — this drives multi-class resistance. Instead, I change the entire regimen based on the resistance profile, using at least two (preferably three) fully active drugs, guided by the resistance test and the treatment history. If he has INSTI resistance from dolutegravir failure, I might need to use a boosted protease inhibitor (darunavir/ritonavir or cobicistat) plus a new INSTI with activity (such as bictegravir if the mutation pattern permits) or a different class. The goal is to re-establish viral suppression as quickly as possible to prevent further resistance, disease progression and transmission." [1]

Short Case — Lymphadenopathy and oral findings examination in advanced HIV

Examination instruction

"Examine this patient's lymph nodes and oral cavity. He is a 45-year-old man with known HIV. Present your findings and discuss." [1]

Systematic examination routine

Step 1 — Inspect at the end of the bed:

• General appearance — cachexia, wasting (HIV wasting syndrome), distress.
• Skin — look for Kaposi sarcoma (violaceous plaques or nodules), seborrhoeic dermatitis, molluscum contagiosum, folliculitis, herpes zoster scars, dermatophyte infections. [1]

Step 2 — Examine the lymph nodes systematically:

• Examine all five groups bilaterally using the pads of the fingers: cervical (submental, submandibular, upper deep cervical, posterior triangle, occipital), supraclavicular, axillary, epitrochlear and inguinal.
• For each node, note: size, site, consistency (soft, rubbery, hard), tenderness, mobility (mobile versus fixed), matting, and overlying skin changes.
• Always examine the left supraclavicular node (Virchow) with the patient sitting forward — a hard node here suggests lymphoma or gastric malignancy. [1]

Step 3 — Examine the oral cavity:

• Inspect the lips (angular cheilitis), buccal mucosa, tongue (dorsal and lateral surfaces), hard and soft palate, gums and oropharynx.
• Look for: oral candidiasis (white adherent plaques, not scrapable), hairy leukoplakia (white corrugated plaques on lateral tongue, EBV-associated), Kaposi sarcoma (violaceous lesions on palate), aphthous ulcers, periodontal disease, gingivitis.
• Attempt to scrape any white plaque with a tongue depressor — candidiasis may partially scrape off, hairy leukoplakia will not. [1]

Step 4 — Screen for other stigmata of HIV:

• Chest — fine crackles (PCP), signs of effusion or consolidation (bacterial pneumonia, TB).
• Abdomen — hepatomegaly or splenomegaly (disseminated infection, lymphoma, MAC).
• Eyes — offer fundoscopy for CMV retinitis if CD4 is low.
• Neurological — cognitive assessment (HAND), focal deficits (toxoplasmosis, PML).
• Genital examination — sexually transmitted infections, cervical/anal dysplasia. [1]

Presentation template

"This patient has generalised lymphadenopathy with 1 to 2 cm, rubbery, mobile, non-tender nodes in the cervical, axillary and inguinal chains bilaterally, no supraclavicular lymphadenopathy. In the oral cavity there is oral candidiasis with thick white adherent plaques on the tongue and buccal mucosa, and white corrugated plaques on the lateral border of the tongue consistent with oral hairy leukoplakia. There is angular cheilitis. There are no visible Kaposi sarcoma lesions on the hard palate. These findings in a patient with known HIV are consistent with advanced immunodeficiency, likely CD4 below 200. [1]

I would like to confirm the CD4 count and viral load, ensure the patient is on ART (and start immediately if not), screen for opportunistic infections including a chest X-ray and induced sputum for PCP, ophthalmology review for CMV retinitis if CD4 is below 50, and arrange a lymph node biopsy if any node is rapidly enlarging, fixed, matted, supraclavicular, or associated with B-symptoms, to exclude lymphoma."* [1]

Discussion questions

Examiner: What is the differential diagnosis of generalised lymphadenopathy in a patient with HIV? [1]

"The differential includes: HIV-related persistent generalised lymphadenopathy (the most common cause — reactive hyperplasia from chronic antigen stimulation), tuberculosis (especially in TB-endemic regions, typically matted nodes), atypical mycobacterial infection (MAC at CD4 below 50), non-Hodgkin lymphoma (rapidly enlarging, B-symptoms), Hodgkin lymphoma, Kaposi sarcoma lymph node involvement, cryptococcosis, and multicentric Castleman disease (HHV-8-associated). The red flags for biopsy are a node above 2 cm, rapid growth, fixation, matting, supraclavicular location, or B-symptoms." [1]

Examiner: How do you distinguish oral candidiasis from hairy leukoplakia? [1]

"Oral candidiasis appears as white, creamy, adherent plaques on the tongue, buccal mucosa or palate that may be partially scraped off, leaving an erythematous base. It is caused by Candida species and typically occurs at CD4 below 200. It is treated with topical antifungals (nystatin, clotrimazole) for mild disease or oral fluconazole for moderate-to-severe disease. [1]

Oral hairy leukoplakia appears as white, corrugated, non-scrapable plaques, almost always on the lateral border of the tongue, and is caused by Epstein-Barr virus replication in the tongue epithelium. It cannot be scraped off. It is essentially pathognomonic for HIV or other significant immunodeficiency. It is usually asymptomatic and often resolves with ART and immune reconstitution, though aciclovir or valaciclovir can be used if symptomatic.* [1]

Both are clinical markers of advanced immunodeficiency. The key bedside discriminator is whether the plaque is scrapable (candidiasis) or not (hairy leukoplakia)."* [1]