A System for the Infectious Diseases Examination

📋 Key Information Summary

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A structured infectious diseases (ID) examination begins with a targeted history: fever pattern (continuous, intermittent, relapsing, hectic), travel history (including transit stops), animal and arthropod exposure, sexual history, injecting drug use, immunisation status, and close-contact illness.
Fever of Unknown Origin (FUO) is defined as fever ≥ 38.3°C on multiple occasions lasting ≥ 3 weeks with no diagnosis after 1 week of inpatient investigation (or 3 outpatient visits); the three major categories are infection, malignancy, and autoimmune/inflammatory disease.
Classic FUO fever patterns — Pel-Ebstein (Hodgkin lymphoma), quotidian (tropical infections), double quotidian (visceral leishmaniasis, gonococcal endocarditis), and relapsing (Brucella, malaria) — should guide differential diagnosis.
HIV/AIDS examination requires systematic assessment: general inspection (wasting, cachexia), oral cavity (candidiasis, hairy leukoplakia, Kaposi sarcoma, aphthous ulcers), skin (seborrhoeic dermatitis, molluscum contagiosum, herpes zoster, Kaposi sarcoma), lymph nodes, parotid glands, and fundoscopy (CMV retinitis).
Persistent generalised lymphadenopathy (PGL) in HIV is defined as ≥ 2 non-continguously involved extra-inguinal sites for ≥ 3 months in the absence of other causes.
Parotid enlargement in HIV is typically bilateral, diffuse, and painless, associated with CD8 lymphocytic infiltration and Sjögren-like syndrome (diffuse infiltrative lymphocytosis syndrome, DILS).
CMV retinitis on fundoscopy shows characteristic "cottage cheese and ketchup" (haemorrhagic) or "brush fire" (granular, peripheral) lesions; urgent ophthalmology referral is essential.
A systematic ID examination proceeds head-to-toe: skin and mucous membranes, respiratory, cardiovascular (new murmurs in endocarditis), abdominal (hepatosplenomegaly), musculoskeletal (septic joints), and neurological (meningism, focal deficits).
Australian-specific considerations include high rates of CA-MRSA in remote Aboriginal and Torres Strait Islander communities, scrub typhus and melioidosis in northern Australia, Q fever in livestock workers, and mosquito-borne arboviruses (Ross River, Barmah Forest, Murray Valley encephalitis).
Risk factor assessment must include injecting drug use (endocarditis, hepatitis B/C, skin/soft-tissue infections), sexual history (STIs, HIV, hepatitis B), occupational exposure (Q fever, brucellosis, leptospirosis), and immunosuppressive therapy or comorbidities.
Always consider tropical infections in returned travellers within 12 months of travel: malaria within 3 months, dengue within 2 weeks, typhoid within 4 weeks, and rickettsial diseases within 3 weeks of exposure.
Aboriginal and Torres Strait Islander Australians experience 2–3 times the burden of infectious diseases; rheumatic heart disease, trachoma, scabies, invasive Group A streptococcal disease, and chronic suppurative otitis media remain disproportionately prevalent.

Introduction & Australian Epidemiology

Infectious diseases remain a major cause of morbidity, mortality, and healthcare utilisation in Australia. The approach to examining a patient with suspected infection demands a structured, systems-based assessment that integrates a detailed history with focused physical examination. Unlike many other medical disciplines, the infectious diseases examination is uniquely shaped by the host (immune status, comorbidities, age), the pathogen (bacteria, viruses, fungi, parasites), the environment (geographical exposure, occupational risk, community prevalence), and time (acute versus chronic infection).

Australia's unique epidemiological landscape includes geographically distinct infectious disease profiles: tropical infections in the Top End and Far North Queensland (melioidosis, scrub typhus, dengue, Ross River virus), zoonotic infections in rural and regional areas (Q fever, brucellosis, leptospirosis, Australian bat lyssavirus), and urban sexually transmitted and blood-borne infections (HIV, hepatitis B and C, syphilis, gonorrhoea). The burden of infectious disease is disproportionately borne by Aboriginal and Torres Strait Islander Australians, people experiencing homelessness, refugees and asylum seekers, men who have sex with men (MSM), people who inject drugs (PWID), and immunocompromised individuals.

This article presents a systematic framework for the infectious diseases examination, encompassing the clinical history, fever assessment, HIV/AIDS-specific examination, and a structured head-to-toe examination with integrated risk factor assessment. The approach is designed for Australian clinicians working across primary care, emergency medicine, and hospital settings.

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Key epidemiological data (Australia, 2023): Approximately 29,000 people are living with HIV in Australia (estimated prevalence 0.1%). Notification rates for syphilis (infectious) have increased >500% since 2010. Invasive Group A Streptococcal (iGAS) disease notifications have risen sharply since 2022. Melioidosis (Burkholderia pseudomallei) is endemic across tropical northern Australia with seasonal peaks during the monsoon.

Infectious Diseases History

The ID history is the cornerstone of the infectious diseases examination. It must be thorough, systematic, and hypothesis-generating. A well-taken history narrows the differential and guides targeted examination and investigation.

Fever History

Establish the presence, pattern, and characteristics of fever:

Onset: Acute (<7 days), subacute (1–4 weeks), or chronic (>4 weeks).
Pattern: Continuous (sustained, minimal diurnal variation — typhoid), intermittent (fever spikes with normal intervals — pyogenic abscess), remittent (fever with incomplete resolution — most bacterial infections), relapsing (afebrile periods between episodes — malaria, Brucella, Borrelia), hectic (wide swings with drenching sweats — deep-seated abscess, endocarditis).
Height: High spiking fevers (>39.5°C) suggest bacteraemia, malaria, or drug fever; low-grade fevers may indicate endocarditis, TB, or lymphoma.
Rigors: Shaking chills suggest bacteraemia (especially Gram-negative), malaria, or pyelonephritis. True rigors are distinct from chills and are highly suggestive of blood-stream infection.
Drenching sweats: Night sweats suggest TB, lymphoma, brucellosis, or HIV-related opportunistic infection.
Response to antipyretics: Paracetamol responsiveness is non-diagnostic, but failure to defervesce after adequate antipyretic therapy may indicate serious bacterial infection or non-infectious fever.

Travel History

A detailed travel history is essential, including transit stops and layovers:

Destinations and dates: Map travel itinerary with precise dates, including rural and urban locations.
Incubation periods (from return to Australia):
- <2 weeks: dengue, malaria (falciparum), typhoid, rickettsial infections, viral haemorrhagic fevers.
- 2–6 weeks: malaria (vivax, ovale), typhoid, acute schistosomiasis, hepatitis A/E, amoebic liver abscess.
- 6 weeks–12 months: malaria (relapse vivax/ovale), visceral leishmaniasis, Strongyloides hyperinfection, TB.
Exposure details: Freshwater swimming (leptospirosis, schistosomiasis), bushwalking (tick bites — rickettsiosis), altitude (dengue mosquito habitats), animal markets.
Prophylaxis: Chemoprophylaxis compliance (malaria), pre-travel vaccinations (yellow fever, typhoid, hepatitis A/B), malaria prophylaxis regimen and duration.

Contact History

Close contacts with similar illness (respiratory viruses, meningococcal disease, food-borne outbreaks).
Known contacts with TB (duration and setting of exposure, ventilation, index case sputum smear status).
Household or sexual contacts with hepatitis B, HIV, or STIs.
Childcare or institutional contacts (gastroenteritis, respiratory infections, varicella, pertussis).
Healthcare worker contacts or recent hospital admission (nosocomial infection, MRO colonisation).

Animal Exposure

Livestock (cattle, sheep, goats): Q fever (Coxiella burnetii), brucellosis, leptospirosis, anthrax.
Cats: Cat-scratch disease (Bartonella henselae), Pasteurella multocida, Sporotrichosis, toxoplasmosis.
Dogs: Capnocytophaga canimorsus, Pasteurella, leptospirosis, echinococcosis.
Bats: Australian bat lyssavirus (ABLV), Hendra virus (via horses).
Native fauna (possums, bandicoots): Buruli ulcer (Mycobacterium ulcerans) — endemic in parts of Victoria and Far North Queensland.
Arthropods: Tick bites (rickettsiosis, Flinders Island spotted fever, Q fever), mosquito exposure (arboviruses), flea bites (murine typhus).
Rodent exposure: Leptospirosis, hantavirus, lymphocytic choriomeningitis virus.

Immunisation History

Verify completeness of National Immunisation Program Schedule (NIP) — especially childhood vaccines, influenza, pneumococcal (PCV13, PPSV23), COVID-19, shingles (zoster), hepatitis B.
Asplenia-specific vaccines: meningococcal ACWY, meningococcal B, pneumococcal, Haemophilus influenzae type b.
Occupational vaccines: hepatitis B (healthcare workers, plumbers), Q fever (abattoir workers, veterinarians, farmers), influenza, varicella (if non-immune).
Travel vaccines: yellow fever, typhoid, hepatitis A, Japanese encephalitis, rabies (pre-exposure for high-risk travel).
Immunocompromised patients: live vaccines contraindicated (MMR, varicella, yellow fever, BCG, oral polio).

Risk Behaviours

Sexual history (using the "5 Ps" framework): Partners (number, gender), Practices (oral, anal, vaginal; condom use), Protection (barrier methods, PrEP), Past STIs, Pregnancy prevention and plans.
Injecting drug use: Drug type, needle/syringe sharing, frequency, injecting sites, needle exchange engagement.
Alcohol and substance use: Chronic alcohol use predisposes to aspiration pneumonia, spontaneous bacterial peritonitis, and TB.
Occupational exposure: Healthcare workers (needle-stick injuries, TB, COVID-19), abattoir workers (Q fever, brucellosis), farmers (leptospirosis, Q fever), miners (histoplasmosis), plumbers/sewer workers (leptospirosis).
Recreational exposure: Camping (tick exposure), freshwater swimming (leptospirosis), diving (otitis externa), gardening (sporotrichosis, tetanus, Buruli ulcer).

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Mnemonic for ID History — "FAT TIGER": Fever pattern, Animal exposure, Travel history, Treatment (prior antibiotics, antivirals), Immunisation, Gender/sexual history, Exposures (occupational, recreational, environmental), Risk behaviours (IDU, alcohol, homelessness).

Fever Assessment & Fever of Unknown Origin

Physiology of Fever

Fever results from an upward shift in the hypothalamic thermoregulatory set-point mediated by pyrogens (exogenous — bacterial endotoxin, viral proteins; endogenous — IL-1, IL-6, TNF-α, prostaglandin E2). This is distinct from hyperthermia (heat stroke, neuroleptic malignant syndrome), where the set-point is normal but heat-dissipation mechanisms are overwhelmed or impaired.

Patterns of Fever

Pattern	Description	Classic Causes
Continuous (sustained)	Fever persists with minimal diurnal variation (<1°C fluctuation)	Typhoid (first week), pneumococcal pneumonia, typhus
Remittent	Fever fluctuates but does not return to normal	Most bacterial infections, infective endocarditis, TB
Intermittent (spiking)	Fever returns to baseline between episodes	Pyogenic abscesses, lymphoma, malaria
Relapsing	Distinct febrile episodes separated by afebrile periods	Malaria (vivax/ovale — 48 hr), Brucella, Borrelia recurrentis (relapsing fever), rat-bite fever
Pel-Ebstein	1–2 weeks of fever alternating with 1–2 weeks of apyrexia	Hodgkin lymphoma (rare but classic)
Double quotidian	Two fever spikes per day	Visceral leishmaniasis, gonococcal endocarditis, adult-onset Still's disease

Fever of Unknown Origin (FUO)

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Classic FUO Definition (Petersdorf & Beeson, modified): Fever ≥ 38.3°C on multiple occasions, duration ≥ 3 weeks, with no diagnosis established after 1 week of inpatient investigation (or 3 appropriately chosen outpatient visits including basic laboratory and imaging studies).

In modern practice, FUO is further categorised:

Category 1

Classic FUO

As defined above. The three major categories account for >90% of cases: infection (~25–35%), malignancy (~20–30%), and autoimmune/inflammatory disease (~20–30%).

Setting: Specialist ID/General Medicine

Category 2

Nosocomial FUO

Fever developing in hospitalised patient ≥ 24 hours after admission, not present or incubating at time of admission. Consider C. difficile, catheter-related BSI, line infections, drug fever, PE, VAP.

Setting: Inpatient consultation

Category 3

Neutropenic FUO

Fever in patient with ANC < 0.5 × 10⁹/L not explained by clinically or microbiologically documented infection. High risk of Gram-negative bacteraemia, invasive fungal infection.

Setting: Emergency — empirical broad-spectrum antibiotics

A fourth category — HIV-associated FUO — is defined as fever ≥ 38.3°C lasting ≥ 3 weeks (inpatient) or ≥ 4 weeks (outpatient) in a patient with confirmed HIV infection. Causes include disseminated Mycobacterium avium complex (MAC), Pneumocystis jirovecii, CMV, lymphoma, cryptococcosis, histoplasmosis, and drug fever.

Causes of FUO in Australia

Category	Common Causes in Australia	Key Diagnostic Clues
Infection (~30%)	TB (pulmonary and extrapulmonary), infective endocarditis, intra-abdominal abscess, osteomyelitis, HIV-related opportunistic infection, brucellosis, Q fever, melioidosis, amoebic liver abscess, CMV/EBV	Rigors, new murmur, hepatosplenomegaly, travel/occupational history, immunosuppression
Malignancy (~25%)	Lymphoma (Hodgkin and non-Hodgkin), leukaemia, renal cell carcinoma, hepatocellular carcinoma, atrial myxoma	Night sweats, weight loss, lymphadenopathy, hepatosplenomegaly, elevated LDH
Autoimmune/Inflammatory (~25%)	Adult-onset Still's disease, systemic lupus erythematosus, vasculitis (GCA, PAN), inflammatory bowel disease, sarcoidosis, drug fever	Rash, arthritis, temporal artery tenderness, young female patient, elevated ESR/CRP with negative cultures
Other/Miscellaneous (~10%)	Drug fever, venous thromboembolism, factitious fever, thyroiditis, tissue infarction, granulomatous hepatitis	Temporal relationship to medication, eosinophilia, normal WBC

Fever Assessment — Physical Examination Focus Points

Vital Signs & General Inspection

Temperature (tympanic, oral, or rectal — rectal most reliable in neutropenic patients), heart rate (relative bradycardia in typhoid, Legionella, brucellosis, myxoma), blood pressure (sepsis-related hypotension), respiratory rate, SpO₂. Assess general appearance — toxic, comfortable, cachectic.

Skin & Mucous Membranes

Rash (maculopapular — viral, drug, rickettsial; petechial/purpuric — meningococcal, DIC; erythema nodosum — TB, sarcoid, strep; eschar — rickettsiosis, scrub typhus), jaundice, injection sites (IDU), perianal lesions.

Lymph Nodes

Systematic palpation — cervical (anterior, posterior, submandibular, supraclavicular), axillary, epitrochlear, inguinal, femoral. Note size, consistency (rubbery = lymphoma, matted = TB), tenderness, mobility, laterality.

Cardiovascular

New or changing murmurs (infective endocarditis — mitral regurgitation most common), splinter haemorrhages, Janeway lesions, Osler nodes, Roth spots. Peripheral stigmata of IE often absent in right-sided (PWID-associated) endocarditis.

Abdominal

Hepatomegaly (liver abscess, hepatitis, malignancy), splenomegaly (EBV, malaria, endocarditis, lymphoma, leishmaniasis), renal angle tenderness (pyelonephritis), right iliac fossa tenderness (typhoid ileal perforation, amoebic caecitis).

Musculoskeletal & Neurological

Joint swelling (septic arthritis, reactive arthritis, endocarditis), bony tenderness (osteomyelitis, vertebral discitis), meningism, focal neurological signs, peripheral neuropathy (HIV, leprosy).

Investigations for FUO

Essential FBC, CRP, ESR, LFTs, LDH, ferritin, blood cultures × 2 sets (from separate sites) Urinalysis and midstream urine; chest X-ray; HIV serology (if not known negative)

Available CT chest/abdomen/pelvis with IV contrast FDG-PET/CT — high sensitivity for occult infection, vasculitis, and malignancy; increasingly first-line in FUO workup

Available Echocardiography (transthoracic, then transoesophageal if high suspicion) TEO is superior for prosthetic valve endocarditis, abscess, and small vegetations

Specialist Temporal artery biopsy, liver biopsy, bone marrow biopsy, tissue biopsy of identified lesions QuantiFERON-TB Gold / T-SPOT.TB for latent and active TB assessment

HIV/AIDS Examination

The HIV/AIDS examination is a focused, systems-based assessment designed to identify clinical manifestations of HIV infection, estimate immunological status from clinical signs, detect opportunistic infections and malignancies, and assess treatment-related complications. It complements laboratory markers (CD4 count, HIV viral load) and is essential for staging and monitoring.

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Clinical pearls — CD4 correlates: Oral candidiasis typically appears at CD4 < 200 cells/μL. Oesophageal candidiasis at CD4 < 100. CMV retinitis and MAC at CD4 < 50. Pneumocystis jirovecii pneumonia (PJP) at CD4 < 200. Kaposi sarcoma can occur at any CD4 count but is more common < 500. However, in the era of antiretroviral therapy (ART), many patients present with higher CD4 counts, and immune reconstitution inflammatory syndrome (IRIS) can unmask subclinical disease.

General Inspection

Nutritional status: Wasting syndrome (unintentional weight loss >10% baseline + chronic diarrhoea or fever >30 days in the absence of other cause). Assess BMI, temporal and thenar muscle wasting, mid-arm circumference.
Cachexia: Suggests advanced immunosuppression, disseminated malignancy (lymphoma, KS), or chronic opportunistic infection (MAC, cryptosporidiosis).
Fever: Continuous or intermittent — consider all opportunistic causes plus drug fever (abacavir hypersensitivity, nevirapine, dapsone).
Facial appearance: Lipoatrophy (sunken cheeks, temporal wasting — associated with stavudine, didanosine, zidovudine), facial wasting (loss of buccal fat).

Oral Cavity Examination

Examine the oral cavity systematically — lips, buccal mucosa, hard and soft palate, tongue (dorsum, lateral borders, ventral surface), floor of mouth, gingivae, and oropharynx:

Finding	Description	Significance
Oral candidiasis (thrush)	White, curd-like plaques on buccal mucosa, palate, or tongue that can be scraped off leaving erythematous or bleeding base. Erythematous (atrophic) form — red, smooth patches on palate or dorsum of tongue.	CD4 < 200; marker of immunosuppression. If oesophageal symptoms present → oesophageal candidiasis (AIDS-defining, CD4 < 100).
Hairy leukoplakia	White, corrugated, vertically-oriented, non-scrapable plaques on lateral borders of tongue. EBV-associated epithelial hyperplasia.	Can occur at any CD4 count. Indicates HIV infection but does not correlate directly with degree of immunosuppression. Usually bilateral.
Kaposi sarcoma (oral)	Purple, violaceous, macular or nodular lesions on palate (most common oral site), gingivae, or tongue. Caused by HHV-8.	AIDS-defining. Can occur at any CD4 but more common with advanced disease. Check skin and lymph nodes concurrently.
Aphthous ulcers	Large (>1 cm), deep, painful ulcers on non-keratinised mucosa (buccal, soft palate, floor of mouth). Giant aphthous ulcers in HIV can be debilitating.	HIV-associated aphthous ulcers may require thalidomide or systemic corticosteroids. Distinguish from HSV and CMV ulcers (biopsy if persistent).
Gingivitis / Periodontitis	Linear gingival erythema (LGE), necrotising ulcerative gingivitis (NUG), necrotising ulcerative periodontitis (NUP).	Aggressive periodontal disease is an early marker of HIV. NUP is associated with severe immunosuppression.
Parotid enlargement	Bilateral, diffuse, non-tender parotid gland swelling. May be associated with cystic lymphoepithelial lesions (CLEL).	DILS (diffuse infiltrative lymphocytosis syndrome) — CD8+ lymphocytic infiltration. Usually good prognosis; associated with higher CD4 count. Unilateral enlargement warrants investigation for lymphoma.

Lymphadenopathy in HIV

Lymphadenopathy is extremely common in HIV and must be characterised systematically:

Persistent generalised lymphadenopathy (PGL): ≥ 2 extra-inguinal sites persisting ≥ 3 months in the absence of other detectable cause. PGL is common in early HIV infection and may be a reactive phenomenon.
Size: Nodes >1.5 cm (cervical/inguinal) or >1 cm (axillary) warrant attention. Nodes >4 cm or rapidly growing demand urgent investigation.
Differential diagnoses of lymphadenopathy in HIV:
- Reactive (HIV itself, concurrent infections — EBV, CMV)
- Infectious — TB (cervical, caseating), MAC, Bartonella (bacillary angiomatosis), fungal (histoplasmosis, cryptococcosis), toxoplasmosis
- Malignancy — non-Hodgkin lymphoma (most common HIV-associated lymphoma), Hodgkin lymphoma, Kaposi sarcoma, Castleman disease (HHV-8 associated)
Examine all node groups: Pre- and post-auricular, submandibular, submental, anterior cervical, posterior cervical, supraclavicular (Virchow node), infraclavicular, axillary, epitrochlear, para-aortic (palpable on deep abdominal palpation), inguinal, femoral, popliteal.

Skin Lesions in HIV

The skin is a window to immunological status in HIV. Examine the entire skin surface, including the scalp, behind the ears, intertriginous areas, perianal region, and soles of feet:

Condition	Appearance	CD4 Correlation
Seborrhoeic dermatitis	Erythematous, scaly plaques on scalp, nasolabial folds, eyebrows, and chest. More extensive and refractory than in HIV-negative individuals.	Can occur at any CD4; often early manifestation.
Herpes zoster	Dermatomal vesicular eruption. Multidermatomal or disseminated disease suggests severe immunosuppression.	Single dermatome — any CD4. Multidermatomal or recurrent — CD4 < 200.
Molluscum contagiosum	Flesh-coloured, umbilicated papules on face (especially periorbital), neck, trunk. Large (>1 cm) or numerous lesions in HIV.	CD4 < 200. CD4 < 100 — very numerous, refractory to treatment.
Kaposi sarcoma (cutaneous)	Purple/violaceous macules, patches, or nodules. Classic sites: palate, trunk, extremities, face. May have surrounding oedema. HHV-8 associated.	Any CD4 (immune reconstitution may improve lesions on ART).
Pruritic papular eruption (PPE)	Chronic, intensely pruritic, folliculocentric papules on extensor surfaces, trunk, and face. Eosinophilic folliculitis.	CD4 < 200 (usually). May improve with ART.
Bacillary angiomatosis	Violaceous to erythematous vascular papules resembling pyogenic granuloma. Bartonella henselae/quintana.	CD4 < 200. Must distinguish from Kaposi sarcoma (requires biopsy).
Scabies (crusted/Norwegian)	Thick, hyperkeratotic, crusted plaques — hands, feet, scalp, trunk. Highly infectious. Minimal pruritus despite extensive infestation.	Severe immunosuppression (CD4 < 200). High relapse risk — requires oral ivermectin + topical permethrin.

Parotid Enlargement

Bilateral parotid enlargement in HIV deserves specific discussion. It is part of the spectrum of DILS (diffuse infiltrative lymphocytosis syndrome), characterised by CD8+ T-lymphocytic infiltration of salivary and lacrimal glands. Features include:

Bilateral, diffuse, firm, non-tender parotid swelling (may be massive).
May be associated with sicca symptoms (dry eyes, dry mouth) mimicking Sjögren syndrome.
Cystic lymphoepithelial lesions (CLEL) — benign cystic structures within the parotid gland, bilateral, pathognomonic of HIV.
Associated with higher CD4 counts and relatively good prognosis (compared to other AIDS manifestations).
Differential diagnosis: Lymphoma (usually unilateral, rapidly progressive), parotitis (bacterial or viral — mumps, CMV), Sjögren syndrome, sarcoidosis.
Investigation: Ultrasound (cystic vs solid components), CT/MRI if concern for malignancy, FNA biopsy if unilateral or rapidly growing.

Fundoscopy in HIV

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CMV retinitis is an ophthalmological emergency. Patients with CD4 < 50 cells/μL presenting with new visual symptoms (floaters, visual field defects, blurred vision) must be assessed urgently. CMV retinitis can progress to retinal detachment and irreversible blindness within days.

Perform fundoscopy with dilated pupils (tropicamide 1%) in all patients with CD4 < 100 cells/μL, and in any HIV patient with visual symptoms regardless of CD4 count:

Finding	Appearance	Significance
CMV retinitis — "Cottage cheese and ketchup"	Full-thickness retinal necrosis with yellow-white granular opacities (cottage cheese) and intraretinal haemorrhages (ketchup). Posterior pole involvement. Perivascular cuffing.	AIDS-defining. CD4 < 50. Requires systemic antiviral (IV ganciclovir or oral valganciclovir) ± intravitreal injection. Urgent ophthalmology referral.
CMV retinitis — "Brush fire"	Granular, peripheral retinal opacification without haemorrhage. Indolent, slowly progressive. Often asymptomatic initially.	Same urgency. Peripheral lesions may be missed without dilated fundoscopy.
HIV retinopathy	Cotton-wool spots (retinal nerve fibre layer infarcts), dot-blot haemorrhages, microaneurysms.	Most common ocular finding in HIV. Non-specific; reflects microvasculopathy. Usually asymptomatic. No specific treatment.
Toxoplasma chorioretinitis	White, fluffy, focal retinal lesion with overlying vitritis ("headlight in the fog"). Often adjacent to old pigmented scar.	CD4 < 100. Treat with pyrimethamine + sulfadiazine + folinic acid (leucovorin). Urgent ophthalmology referral.
Varicella zoster virus (VZV) retinitis (ARN)	Acute Retinal Necrosis: peripheral, multifocal, well-demarcated areas of retinal necrosis. Rapidly progressive. Vitritis, vasculitis.	Can occur at higher CD4 counts than CMV. IV aciclovir + intravitreal foscarnet. High risk of retinal detachment.

Additional HIV Examination Domains

Respiratory: Tachypnoea, crackles (PJP — subacute dyspnoea, dry cough, bilateral ground-glass appearance on CXR), focal consolidation (bacterial pneumonia, TB). Perform TB screening in all HIV patients (chest X-ray, symptom screen, interferon-gamma release assay).
Cardiovascular: HIV-associated cardiomyopathy (dilated cardiomyopathy), pericardial effusion (TB, KS), new murmurs (endocarditis — especially if PWID).
Abdominal: Hepatomegaly (hepatitis B/C co-infection, MAC, lymphoma), splenomegaly (MAC, lymphoma), ascites (peritoneal TB, KS).
Neurological: Focal deficits (toxoplasmosis, CNS lymphoma, PML — JC virus), meningism (cryptococcal meningitis), peripheral neuropathy (HIV-associated distal sensory polyneuropathy, antiretroviral drug toxicity — dideoxynucleosides), cognitive decline (HIV-associated neurocognitive disorder — HAND).
Anorectal examination: Perianal herpes simplex (chronic, ulcerating), perianal warts (HPV — high risk of anal dysplasia/carcinoma in MSM), Kaposi sarcoma, perianal abscess/fistula.

Systematic Infectious Diseases Examination & Risk Factor Assessment

The systematic ID examination extends beyond the HIV-specific assessment to encompass a comprehensive, head-to-toe approach applicable to any patient with suspected infection. This examination integrates findings from the targeted history with a structured physical assessment to localise infection, identify organ involvement, and stratify severity.

Step-by-Step Systematic Examination

General Appearance & Vital Signs

Assess for acute illness severity: sepsis screening (qSOFA — altered mentation, SBP ≤ 100 mmHg, RR ≥ 22/min). Temperature, heart rate (relative bradycardia clues — typhoid, Legionella, brucellosis), blood pressure, respiratory rate, oxygen saturation. Nutritional status, hydration, posture, comfort level. Presence of rigors or diaphoresis.

Head, Eyes, Ears, Nose & Throat (HEENT)

Eyes: Conjunctivitis (adenovirus, chlamydia), jaundice (hepatitis, leptospirosis, malaria), subconjunctival haemorrhage (dengue), keratitis (HSV, VZV). Ears: Acute and chronic suppurative otitis media (disproportionately common in Aboriginal children), mastoiditis. Nose/Sinuses: Acute bacterial sinusitis, mucormycosis (immunocompromised — DM). Throat: Pharyngitis (Group A Streptococcus, EBV, gonococcal), tonsillar exudates, peritonsillar abscess.

Neck

Cervical lymphadenopathy (unilateral — bacterial infection, malignancy; bilateral — viral, TB, lymphoma), thyroid tenderness (subacute thyroiditis), meningism (stiff neck, positive Kernig's and Brudzinski's signs), jugular venous distension (right-sided IE, pericardial effusion), Ludwig's angina (floor-of-mouth swelling — dental abscess).

Respiratory Examination

Inspection (accessory muscle use, tracheal deviation), percussion (stony dull = effusion, dull = consolidation), auscultation (crackles, bronchial breathing, pleural rub, absent breath sounds). Pleural effusion (parapneumonic, TB, empyema). Consolidation patterns (lobar — pneumococcal; atypical — Mycoplasma, Legionella). Cavitating lesions (TB, Staphylococcus aureus, anaerobic abscess).

Cardiovascular Examination

Infective endocarditis (IE): New or changing regurgitant murmur (mitral regurgitation most common in native valve left-sided IE; tricuspid regurgitation in PWID right-sided IE). Peripheral stigmata — Janeway lesions (painless erythematous macules on palms/soles), Osler nodes (painful nodules on fingertips), splinter haemorrhages (proximal nail bed — also trauma), Roth spots (retinal haemorrhages with pale centres). Sepsis: Warm peripheries (vasodilatory shock), bounding pulse. Pericarditis: Pericardial rub, friction rub.

Abdominal Examination

Liver: Hepatomegaly (hepatitis, liver abscess, malignancy). Tender hepatomegaly with right upper quadrant pain — amoebic or pyogenic liver abscess. Spleen: Splenomegaly (EBV, malaria, endocarditis, lymphoma, kala-azar). Ascites: Shifting dullness (peritoneal TB, SBP in liver disease, peritoneal carcinomatosis). Renal angle tenderness: Pyelonephritis. Psoas abscess: Pain on hip flexion (iliopsoas sign) — TB of lumbar spine, retroperitoneal abscess.

Musculoskeletal

Septic arthritis: Hot, swollen, tender joint with restricted range of motion (knee most common, then hip, shoulder, wrist). Osteomyelitis: Bony tenderness, overlying erythema, sinus tracts (chronic). Vertebral discitis: Spinal tenderness, limited flexion, neurological deficit if epidural abscess. Reactive arthritis: Asymmetric oligoarthritis, enthesitis (post-gonococcal, post-enteric, Chlamydia). Crepitus (surgical emphysema): Gas-gangrene (Clostridium perfringens), necrotising fasciitis.

Neurological

Meningitis: Neck stiffness, photophobia, Kernig's sign (pain on knee extension with hip flexed), Brudzinski's sign (involuntary hip flexion on passive neck flexion), altered mental status. Encephalitis: Altered consciousness, seizures, focal deficits (HSV-encephalitis — temporal lobe predilection), behavioural changes. Brain abscess: Focal neurological deficits, headache, seizures, papilloedema. Peripheral neuropathy: Stocking-glove sensory loss (HIV, diabetes, diphtheria), mononeuritis multiplex (vasculitis, HIV, HBV/HCV).

Skin & Soft Tissue

Systematic skin survey. Rashes: Maculopapular (viral exanthem, drug reaction, rickettsial), vesicular (VZV, HSV, enterovirus), petechial/purpuric (meningococcaemia, DIC, thrombocytopaenia), erythema migrans (Lyme disease — not endemic in Australia but seen in returned travellers). Cellulitis: Erythema, warmth, swelling, tenderness — borders often poorly demarcated (Streptococcus pyogenes vs Staphylococcus aureus). Necrotising fasciitis: Pain disproportionate to appearance, crepitus, rapidly spreading erythema, haemorrhagic bullae, systemic toxicity. Abscess: Fluctuant, erythematous, tender mass — incision and drainage primary treatment. Wounds: Bite wounds (human, animal), traumatic wounds (tetanus risk), burns.

Genital & Perianal Examination

Genital: Urethral discharge (gonococcal vs non-gonococcal), genital ulcers (HSV — shallow, painful, grouped; syphilis — chancre, painless, indurated; chancroid — painful, undermined edges), genital warts (HPV), inguinal lymphadenopathy (lymphogranuloma venereum, syphilis, HSV). Perianal: Perianal abscess, fistula-in-ano, perianal herpes, condylomata lata (secondary syphilis — flat-topped, moist, grey-white papules).

Risk Factor Assessment — Integrated Framework

Host Factors

Age extremes (neonates — GBS, E. coli, Listeria; elderly — Listeria, Gram-negative UTI, pneumonia)
Diabetes mellitus (mucormycosis, malignant otitis externa, emphysematous pyelonephritis, foot infections)
Asplenia (overwhelming post-splenectomy infection — encapsulated organisms: S. pneumoniae, N. meningitidis, H. influenzae)
Immunosuppression (HIV, transplant, chemotherapy, biologics — TB reactivation, fungal infections, CMV, EBV-associated lymphoproliferative disease)
Chronic liver disease (spontaneous bacterial peritonitis, Vibrio vulnificus bacteraemia)
Chronic kidney disease / dialysis (access site infections, hepatitis B/C)
Pregnancy (Listeria, Toxoplasma, CMV, parvovirus B19, hepatitis E)

Exposure Factors

Healthcare-associated (MRO colonisation — MRSA, VRE, ESBL, CRE; C. difficile; catheter-associated UTI; central line-associated BSI)
Community-acquired (respiratory viruses, CA-MRSA skin/soft tissue, gastroenteritis)
Geographical (northern Australia — melioidosis, scrub typhus, Ross River virus; Victoria/Queensland — Buruli ulcer; central Australia — trachoma, rheumatic fever)
Zoonotic (Q fever, leptospirosis, brucellosis, Hendra, Australian bat lyssavirus)
Vector-borne (mosquitoes — dengue, Ross River, Barmah Forest, Murray Valley encephalitis, Japanese encephalitis; ticks — rickettsiosis)
Water/food (Vibrio parahaemolyticus, hepatitis A/E, Cryptosporidium, Giardia, amoebiasis)

Quick Reference: Syndromes and Empirical Approaches

Sepsis / Septic shock

Piperacillin-tazobactam 4.5 g IV q6h ± vancomycin (if MRO risk)

Per source

30 mL/kg crystalloid bolus within first hour. Source control essential.

Community-acquired pneumonia

Amoxicillin 1 g PO TDS + doxycycline 100 mg PO BD (or moxifloxacin 400 mg PO daily if severe)

5–7 days (minimum 5 days, afebrile ≥ 48 hr)

Add azithromycin 500 mg IV for Legionella if severe or ICU admission.

Meningitis (community-acquired, adult)

Ceftriaxone 2 g IV q12h + dexamethasone 0.15 g/kg IV q6h × 4 days (start before or with first dose of antibiotic)

10–14 days (N. meningitidis 7 days; S. pneumoniae 10–14 days)

Add vancomycin if penicillin-resistant pneumococci suspected. Add ampicillin if Listeria risk (age > 50, immunocompromised, pregnancy).

Infective endocarditis (native valve, empirical)

Flucloxacillin 2 g IV q4h + gentamicin 1 mg/kg IV q8h (adjusted) ± benzylpenicillin 1.8 g IV q4h (for HACEK coverage if indicated)

4–6 weeks (depends on organism and complications)

If prosthetic valve or MRO risk: vancomycin + gentamicin + rifampicin. TEE mandatory if TTE negative and high clinical suspicion.

Urinary tract infection — complicated / pyelonephritis

Ceftriaxone 1 g IV daily or ciprofloxacin 500 mg PO BD (if local resistance patterns permit)

7–14 days (guided by organism and clinical response)

Imaging (US/CT) if no response at 48–72 hr, suspicion of obstruction, or emphysematous pyelonephritis.

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When to refer to infectious diseases specialist: Fever of unknown origin >1 week, suspected endocarditis, prosthetic device infection, suspected MRO, melioidosis, brucellosis, complicated TB (meningeal, miliary, drug-resistant), HIV with opportunistic infection, returned traveller with fever from malaria-endemic region (urgent blood film), and necrotising fasciitis.

Special Populations

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Pregnancy

TORCH infections: Toxoplasma, Others (syphilis, VZV, parvovirus B19, HIV), Rubella, CMV, HSV. Serological screening recommended.

Listeria monocytogenes: Risk increases in 3rd trimester. Causes bacteraemia, chorioamnionitis, neonatal meningitis. Avoid soft cheeses, unpasteurised dairy, cold deli meats.

Hepatitis E: High maternal mortality in 3rd trimester (up to 20–25% in developing countries; rare in Australia).

Antibiotic considerations: Avoid tetracyclines (tooth discolouration), fluoroquinolones (cartilage toxicity), aminoglycosides (ototoxicity — use only if essential), trimethoprim (1st trimester — folate antagonist; 3rd trimester — neonatal kernicterus risk). Safe: penicillins, cephalosporins, azithromycin, nitrofurantoin (avoid at term).

GBS screening: All women at 35–37 weeks gestation. Intrapartum prophylaxis with IV benzylpenicillin if positive.

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Paediatrics

Neonates (0–28 days): GBS, E. coli (most common causes of early-onset sepsis), Listeria, HSV (disseminated or CNS disease — aciclovir IV). Always perform blood culture, LP, and initiate empirical ampicillin + gentamicin.

Infants and children: Higher heart rate and respiratory rate norms. Fever without source in <3 months — low threshold for investigation and empirical antibiotics. Febrile seizure ≠ meningitis but consider if prolonged or focal.

Aboriginal and Torres Strait Islander children: Disproportionately high rates of suppurative otitis media, bronchiectasis, rheumatic fever, skin infections (scabies, impetigo, Group A Strep), invasive bacterial infections.

Immunisation schedules: NIP schedule adherence; assess catch-up vaccines in migrant, refugee, and Aboriginal children.

Dose adjustments: Most antibiotics dosed per kg body weight. Renal function (eGFR) differs in neonates and young children — adjust accordingly.

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Elderly

Atypical presentations: Elderly patients may present without fever (hypothermia in severe sepsis), with delirium as the sole presenting feature of infection, or with functional decline.

Common infections: UTI (most common cause of bacteraemia in elderly), pneumonia (high mortality), C. difficile (risk with broad-spectrum antibiotics and PPI use), pressure injury infections, herpes zoster.

Antibiotic considerations: Reduced renal clearance (adjust doses based on CrCl), polypharmacy interactions (warfarin + fluconazole, metronidazole; QTc prolongation with macrolides + other QTc-prolonging agents). Avoid nitrofurantoin if eGFR < 30 mL/min.

Immunosenescence: Reduced vaccine efficacy. Annual influenza, pneumococcal (PCV13 + PPSV23), shingles (Shingrix® — adjuvanted recombinant, preferred), COVID-19 boosters.

Endocarditis: Increasing incidence in elderly (degenerative valve disease, prosthetic valves, healthcare-associated bacteraemia).

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Renal Impairment

Dose adjustments: Penicillins, cephalosporins, vancomycin, aminoglycosides, fluoroquinolones all require renal dose adjustment. Calculate CrCl using Cockcroft-Gault (adults) or Schwartz formula (children).

Vancomycin: Extended-interval dosing (AUC-guided, target AUC/MIC 400–600). Trough levels alone are no longer recommended (2020 ASHP/IDSA guidelines). Dose based on actual body weight.

Dialysis patients: High risk of access site infections, hepatitis B/C (screening recommended), MRSA colonisation. Peritonitis in peritoneal dialysis (S. aureus, S. epidermidis, Pseudomonas — empirical cefazolin + ceftazidime IP).

Nephrotoxic drugs: Aminoglycosides (monitor levels, consider once-daily dosing), amphotericin B (use liposomal formulation), tenofovir (use TAF instead of TDF if renal impairment).

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Hepatic Impairment

Drug metabolism: Hepatically cleared drugs (metronidazole, azole antifungals, macrolides, rifampicin, isoniazid, pyrazinamide) may accumulate. Dose reduction or avoidance may be required in Child-Pugh B/C cirrhosis.

Spontaneous bacterial peritonitis (SBP): Suspect in any cirrhotic patient with ascites and fever, abdominal pain, or encephalopathy. Diagnosis: ascitic fluid neutrophil count > 250/mm³. Empirical: ceftriaxone 2 g IV daily. Prophylaxis: norfloxacin 400 mg PO daily (or TMP-SMX) in high-risk patients.

Coagulopathy: Cirrhotic patients may have prolonged INR affecting interpretation. Low platelets. Adjust invasive procedures accordingly.

Hepatitis co-infection (HIV+HBV): Entecavir or tenofovir (TDF/TAF) for HBV treatment. Discontinuation of HBV-active ART in HIV can cause severe hepatitis flare. Avoid single HBV-active agent without HIV-active backbone.

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Immunocompromised

HIV/AIDS: See HIV/AIDS Examination section above. Risk stratify by CD4 count for opportunistic infections.

Transplant recipients: Timeline-based approach — 0–1 month (donor/recipient-derived infections, surgical site), 1–6 months (opportunistic — CMV, PJP, Aspergillus, Nocardia, Listeria), >6 months (community-acquired infections + late opportunistic if ongoing immunosuppression). Prophylaxis: TMP-SMX (PJP + Toxoplasma), valganciclovir (CMV if D+/R−), nystatin or fluconazole (oral candidiasis).

Biologic therapy (TNF-α inhibitors): Screen for latent TB (IGRA + CXR) before initiation. Risk of TB reactivation, invasive fungal infections (histoplasmosis, coccidioidomycosis), hepatitis B reactivation.

Chemotherapy-induced neutropenia: Febrile neutropenia is an oncological emergency. Empirical antipseudomonal β-lactam (piperacillin-tazobactam or meropenem). Add vancomycin if haemodynamically unstable, suspected line infection, or MRSA risk. Add antifungals (caspofungin or liposomal amphotericin B) if persistent fever >96 hr.

Asplenia: Overwhelming post-splenectomy infection (OPSI) risk — educate patients about fever, travel precautions, prophylactic antibiotics (penicillin V 500 mg PO BD or erythromycin if penicillin-allergic).

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health — Infectious Diseases Examination

Aboriginal and Torres Strait Islander Australians experience a substantially higher burden of infectious disease compared to non-Indigenous Australians. The gap is most pronounced in remote and very remote communities but is also significant in urban settings. Understanding the social and cultural determinants of health — including housing overcrowding, limited access to clean water, health literacy, intergenerational trauma, and institutional racism — is essential for effective clinical assessment and management.

Rheumatic Heart Disease (RHD)

Aboriginal and Torres Strait Islander Australians have among the highest rates of acute rheumatic fever (ARF) and RHD globally. ARF disproportionately affects children aged 5–14 years in remote NT, QLD, and WA. Secondary prophylaxis with benzathine penicillin G (BPG) 4-weekly is essential. Sore throat and skin sores (Group A Streptococcus) are the initiating infections. Auscultation for new murmurs (mitral regurgitation most common) is critical in any febrile child in endemic areas.

Scabies and Skin Infections

Scabies prevalence in remote communities is 5–10× higher than the general Australian population. Scabies drives secondary bacterial infection (Streptococcus pyogenes, Staphylococcus aureus impetigo), which in turn is a major risk factor for post-streptococcal glomerulonephritis and invasive GAS disease (necrotising fasciitis, bacteraemia). Mass drug administration (MDA) programs — ivermectin-based — have been piloted in NT communities. Examine skin thoroughly in every ID assessment.

Tuberculosis (TB)

TB notification rates in Aboriginal and Torres Strait Islander Australians are 5–10× higher than non-Indigenous Australians, with highest rates in the NT. Both pulmonary and extrapulmonary TB occur. Latent TB infection screening with IGRA is recommended for at-risk populations. Consider TB in any chronic respiratory illness, FUO, or lymphadenopathy in this population.

Trachoma

Australia is the only high-income country where trachoma (Chlamydia trachomatis serotypes A–C) remains endemic, exclusively in remote Aboriginal communities. WHO SAFE strategy: Surgery for trichiasis, Antibiotics (azithromycin), Facial cleanliness, Environmental improvement. Assess for trachoma in any child with chronic conjunctivitis in remote settings.

Chronic Suppurative Otitis Media (CSOM)

CSOM rates in Aboriginal children are among the highest in the world. Prevalence in some remote communities exceeds 40% in children under 5 years. CSOM causes conductive hearing loss, which has profound impacts on language development, education, and social outcomes. Otitis media with effusion (OME) progresses to AOM and CSOM without timely intervention. Examine ears with pneumatic otoscopy in every paediatric ID assessment.

Melioidosis

Burkholderia pseudomallei is endemic in tropical northern Australia (Top End, North Queensland). Aboriginal and Torres Strait Islander people are disproportionately affected due to higher rates of diabetes, hazardous alcohol use, chronic kidney disease, and outdoor occupational/recreational exposure. Peaks during the wet season (November–April). Pneumonia is the most common presentation; prostatic and neurological involvement occur. Consider in any febrile patient in northern Australia during the wet season with risk factors.

COVID-19 and Influenza

Aboriginal and Torres Strait Islander Australians experienced disproportionate morbidity and mortality during the COVID-19 pandemic, particularly in remote communities with limited healthcare access. Influenza vaccination rates, while improving, remain below target in some communities. Culturally safe communication and community-led health promotion are essential.

Cultural Safety & Communication

Effective ID examination requires culturally safe practice. Use Aboriginal Health Workers and Practitioners (AHW/Ps) as key members of the clinical team. Allow adequate time for consultations. Be aware of "sorry business" (mourning) and its impact on clinic attendance. Avoid shame-based communication. Consider gender-concordant examination where preferred. Interpreters may be required for patients whose primary language is not English (many remote communities speak English as a second, third, or fourth language).

⚠️

Clinical priority: In any febrile Aboriginal or Torres Strait Islander child from a high-RHD-burden area (NT, northern WA, northern QLD), always auscultate for a new cardiac murmur and consider ARF as a differential. ARF missed diagnosis leads to RHD progression and premature cardiac death.

📚 References

1. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework. Canberra: AIHW; 2023. Available from: aihw.gov.au
2. Australasian Society for Infectious Diseases (ASID). Antibiotic Guidelines for the Prevention and Treatment of Infection in the Community and Hospital Settings. Melbourne: ASID; 2022.
3. Royal Australian College of General Practitioners (RACGP). Guidelines for Preventive Activities in General Practice (Red Book). 9th ed. Melbourne: RACGP; 2018.
4. Menon A, Penn D, Ludwig KN. Fever of unknown origin: a systematic approach to diagnosis and management. Am Fam Physician. 2022;105(5):486–494.
5. Cunha BA. Fever of unknown origin: focused diagnostic approach based on clinical clues from the history, physical examination, and laboratory tests. Infect Dis Clin North Am. 2007;21(4):1137–1187.
6. Panel on Opportunistic Infections in Adults and Adolescents with HIV. Guidelines for the Prevention and Treatment of Opportunistic Infections in Adults and Adolescents with HIV. Washington, DC: Department of Health and Human Services; 2024. Available from: clinicalinfo.hiv.gov
7. Australasian Society for HIV, Viral Hepatitis and Sexual Health Medicine (ASHM). HIV Management Guidelines for Australia. Sydney: ASHM; 2023.
8. Currie BJ, Ward L, Cheng AC. The epidemiology and clinical spectrum of melioidosis: 540 cases from the 20 year Darwin prospective study. PLoS Negl Trop Dis. 2010;4(11):e900.
9. RHDAustralia (Rheumatic Heart Disease Australia). ARF/RHD Clinical Guidelines. Darwin: Menzies School of Health Research; 2020.
10. Communicable Diseases Network Australia (CDNA). National Surveillance Case Definitions. Canberra: Department of Health and Aged Care; 2023.
11. World Health Organization (WHO). WHO Alliance for the Global Elimination of Trachoma by 2020 (GET 2020). Geneva: WHO; 2023.
12. Tong SYC, Davis JS, Eichenberger E, Holland TL, Fowler VG. Staphylococcus aureus infections: epidemiology, pathophysiology, clinical manifestations, and management. Clin Microbiol Rev. 2015;28(3):603–661.
13. Baddour LM, Wilson WR, Bayer AS, et al. Infective endocarditis in adults: diagnosis, antimicrobial therapy, and management of complications. Circulation. 2015;132(15):1435–1486.
14. Australasian College for Emergency Medicine (ACEM). Guidelines on Fever in the Immunocompromised Patient. Melbourne: ACEM; 2021.
15. National Centre for Immunisation Research and Surveillance (NCIRS). The Australian Immunisation Handbook. 11th ed. Canberra: Department of Health and Aged Care; 2024. Available from: immunisationhandbook.health.gov.au