IM4.1-20 | Fever and Febrile Syndromes — Graded Quiz

Correct. The smear findings — enlarged RBC, Schuffner's dots, ameboid ring forms, single parasite per cell — confirm Plasmodium vivax. For uncomplicated vivax malaria in pregnancy, chloroquine remains the drug of choice (NVBDCP India). ACT (artemether-lumefantrine) is used for falciparum; in the second trimester it is acceptable as an alternative but chloroquine is still first-line for vivax. Primaquine (for radical cure of hepatic hypnozoites) is ABSOLUTELY CONTRAINDICATED in pregnancy due to haemolytic risk to the G6PD-deficient foetus. Primaquine should be deferred to the post-partum period.

Schuffner's dots and ameboid rings with enlarged RBCs confirm P. vivax. In pregnancy, chloroquine (600 mg base stat, then 300 mg at 6, 24, 48 hours) is the drug of first choice for vivax. Primaquine for radical cure is absolutely contraindicated in pregnancy. ACT is reserved for falciparum or chloroquine-resistant vivax.

Correct. Disseminated Mycobacterium avium complex (MAC) is the most likely diagnosis. MAC is an opportunistic infection that occurs almost exclusively when CD4 falls below 50 cells/µL. It presents with prolonged fever, weight loss, hepatosplenomegaly, elevated alkaline phosphatase, and anaemia. Bone marrow biopsy showing intracellular (within macrophages) non-caseating granulomas with AFB is the characteristic pattern of disseminated MAC. Miliary TB can also cause this picture but typically produces caseating granulomas and occurs at higher CD4 counts; MAC is more specifically associated with CD4 <50. Treatment is clarithromycin + ethambutol ± rifabutin.

Disseminated MAC is the classic cause of HIV-associated FUO at CD4 <50/µL. Non-caseating granulomas with intracellular AFB on bone marrow biopsy is its distinctive pattern (versus caseating granulomas in TB). Treatment differs: MAC needs clarithromycin + ethambutol, not NTEP anti-TB regimens.

Correct. This patient has dengue with warning signs during the critical phase: abdominal pain/tenderness, ascites, haematocrit rise >20% above baseline (40% to 54% = 35% rise), and thrombocytopenia. WHO 2009 dengue guidelines do NOT recommend prophylactic platelet transfusion unless there is active significant bleeding — transfusion thresholds are generally <10,000-20,000 with bleeding or clinical deterioration. The cornerstone of management is careful IV fluid therapy with isotonic crystalloids (normal saline or Ringer's lactate), guided by haematocrit trends and haemodynamic parameters. Aspirin is contraindicated (antiplatelet effect and Reye's syndrome risk). Steroids have no proven benefit.

In dengue critical phase with warning signs, WHO 2009 guidelines mandate careful IV fluid therapy (isotonic crystalloids) guided by haematocrit, not empiric platelet transfusion. Platelet transfusion is only indicated for active significant bleeding. Aspirin is contraindicated due to antiplatelet effects. Steroids are not evidence-based for dengue vascular leak.

Correct. In an immunosuppressed patient on methotrexate, the Mantoux test and IGRA may be falsely negative due to impaired cell-mediated immunity — a negative result does not exclude active TB. CBNAAT (GeneXpert MTB/RIF) directly detects MTB DNA and rifampicin resistance gene mutations in sputum with sensitivity of ~88% and specificity of ~99% for smear-positive disease, and reasonable sensitivity even in smear-negative cases. Two negative CBNAAT results provide the best molecular evidence against active pulmonary TB. ADA has diagnostic utility in pleural/pericardial TB but not pulmonary. IGRA is for latent TB detection, not active TB exclusion.

In an immunosuppressed patient, both Mantoux and IGRA may be falsely negative due to T-cell anergy — they cannot reliably exclude active TB. CBNAAT (GeneXpert) on sputum is the best available test to rule out active pulmonary TB, with high specificity (~99%). Two negative CBNAAT results significantly reduce the probability of active pulmonary TB and should guide clinical decision-making.

Correct. This is septic shock from catheter-associated urinary tract infection. The Surviving Sepsis Campaign Hour-1 Bundle mandates ALL of the following within the first hour: (1) measure lactate, (2) obtain blood cultures before antibiotics, (3) administer broad-spectrum antibiotics, (4) 30 mL/kg IV crystalloid for hypotension or lactate ≥4 mmol/L, and (5) vasopressors (noradrenaline) to maintain MAP ≥65 if unresponsive to fluids. No single intervention takes priority in isolation — the bundle is concurrent. CT abdomen can follow once the patient is stabilised, not during the acute resuscitation phase.

In septic shock, the Surviving Sepsis Campaign Hour-1 Bundle requires simultaneous resuscitation: blood cultures, IV broad-spectrum antibiotics, IV crystalloid 30 mL/kg, lactate measurement, and vasopressors if MAP remains <65 mmHg despite fluid. No single step in isolation is the correct answer — the concurrent bundle is the evidence-based approach.

Correct. This clinical picture — FUO, elevated alkaline phosphatase suggesting hepatic infiltration, anaemia, residence in Bihar (hyperendemic belt for visceral leishmaniasis or kala-azar) — should immediately prioritise exclusion of visceral leishmaniasis (Leishmania donovani) and disseminated TB. rK39 antigen test is the rapid, highly specific first-line test for kala-azar (sensitivity ~94%, specificity ~97% in Bihar); bone marrow aspiration is confirmatory (Leishman-Donovan bodies on smear) and simultaneously allows biopsy for AFB culture and histology to exclude disseminated TB and haematological malignancy. In India's FUO series, kala-azar and extrapulmonary/disseminated TB are two of the three most common diagnoses that must be excluded in every classic FUO case.

In Bihar with FUO and elevated ALP suggesting hepatic involvement, visceral leishmaniasis and disseminated TB must be the primary targets. rK39 antigen is the rapid initial screen; bone marrow aspiration provides the simultaneous diagnostic yield for kala-azar (LD bodies), TB (AFB), and haematological malignancy. Empiric anti-TB therapy without confirmation is inappropriate — it risks missing kala-azar, which worsens dramatically on untreated steroids or with delayed diagnosis.

Correct. Heat cramps are the mildest heat-related illness: painful muscle cramps (typically calves, thighs, abdomen) in a person performing sustained muscular work in heat, caused by sodium depletion from sweating with replacement of fluid but not electrolytes. The patient is alert with normal blood pressure and temperature — excluding heat exhaustion (which has systemic signs: weakness, dizziness, nausea, headache, mild temperature elevation, possible hypotension) and heat stroke (hyperthermia >40°C, CNS dysfunction, hot dry skin). Treatment is oral salt solution (ORS) or IV normal saline — correcting the sodium deficit resolves the cramps. Heat cramps are NOT a fever syndrome; temperature is normal or mildly elevated.

The clinical picture (painful muscle cramps with profuse sweating, normal temperature and BP, normal cognition) following exertion with water-only replacement fits heat cramps — the mildest heat-related illness. Sodium depletion from sweat is the mechanism. Oral salt replacement (or IV saline if severe) is the treatment. This is distinct from heat exhaustion (systemic symptoms, mild hypotension) and heat stroke (CNS dysfunction, hyperthermia >40°C, anhydrosis).

Correct. This is classical Hodgkin lymphoma (Reed-Sternberg cells with mixed cellularity pattern). Malignant B symptoms (fever, night sweats, weight loss >10%) in lymphoma are caused by tumour-derived cytokines — particularly IL-1, IL-6, and TNF-alpha — which act as endogenous pyrogens. These cytokines stimulate hypothalamic COX-2, elevating PGE2 and raising the thermoregulatory set-point in exactly the same mechanism as infection-driven fever. This explains why antipyretics provide temporary relief. Exogenous pyrogens (LPS, microbial products) are the mechanism in infection, not malignancy. Hyperthermia (set-point-independent heat generation) is not the mechanism in lymphoma.

Fever in Hodgkin lymphoma is caused by endogenous pyrogens (IL-1, IL-6, TNF-alpha) released by the tumour and reactive cells, which act on the hypothalamic COX-2/PGE2 pathway to raise the set-point — the identical mechanism to infectious fever. Exogenous pyrogens are microbial products, not tumour-derived. This is why antipyretics provide symptom relief in B-symptom fever.

Correct. The governing principle of empiric therapy in FUO is a benefit-risk decision framework: empiric treatment is justified when two conditions are simultaneously met — (1) the clinical probability of a specific diagnosis is high enough to make treatment plausible, AND (2) the cost of withholding treatment (disease progression, irreversible organ damage, mortality risk) outweighs the risk of misidentification. The classic example is: empiric IV artesunate for severe malaria if smear is negative but clinical suspicion is very high. Empiric corticosteroids are specifically contraindicated before excluding TB and kala-azar (both worsen catastrophically). Broad-spectrum antibiotics do not cover TB, fungal, or autoimmune causes.

Empiric therapy is governed by two simultaneous conditions: high enough clinical probability of a specific diagnosis, AND the cost of delay (irreversible harm) exceeding the risk of treating without confirmation. It is not a default response to duration. Empiric corticosteroids are contraindicated before excluding TB and visceral leishmaniasis. This principle is the foundation of clinical decision-making in FUO management.

Correct. This patient has dengue without warning signs in the febrile phase. WHO 2009 guidelines allow safe outpatient management with adequate oral hydration (ORS, coconut water, fruit juice), paracetamol (not aspirin or NSAIDs), rest, and clear return precautions. The haematocrit rise from 43% to 48% is modest (<20% rise above baseline), and without warning signs (abdominal pain, persistent vomiting, bleeding, liver enlargement, rapid platelet drop, clinical fluid accumulation), he does not meet criteria for admission. Daily platelet and haematocrit monitoring is essential to detect critical phase progression. There is no dengue immunoglobulin; platelet transfusion is only for active significant bleeding.

Dengue without warning signs can be managed safely as an outpatient: oral hydration, paracetamol (not aspirin/NSAIDs), rest, and return precautions. Daily platelet and haematocrit checks are essential. ICU admission is for severe dengue; prophylactic platelet transfusion is not indicated without active bleeding. There is no approved dengue immunoglobulin.

Correct. Adult-onset Still's disease (AOSD) is the classic non-infectious, non-malignant cause of FUO with: (1) daily quotidian spiking fever, (2) evanescent salmon-coloured rash appearing with fever peaks, (3) arthralgia/arthritis, (4) markedly elevated ferritin (often >5,000–10,000 ng/mL), (5) neutrophilic leukocytosis, and (6) negative ANA/RF. Glycosylated ferritin fraction <20% (normal >50%) is a specific marker of AOSD and HLH. HLH would show pancytopenia, splenomegaly, elevated triglycerides, and haemophagocytosis on marrow biopsy — a more severe picture. SLE typically shows a malar (not evanescent) rash with positive ANA. Negative cultures exclude septicaemia.

The classic triad of AOSD: (1) daily spiking quotidian fever, (2) evanescent salmon rash appearing only during fever, (3) arthralgia/arthritis — combined with markedly elevated ferritin, neutrophilia, and negative cultures — establishes the diagnosis. Glycosylated ferritin fraction <20% (versus normal >50%) is a specific marker. HLH has a more severe phenotype with pancytopenia and haemophagocytosis. SLE causes a malar rash, not evanescent, with positive ANA.