Question
Weil’s disease.
Answer
Weil’s disease is the severe, icteric (jaundiced) form of leptospirosis, caused by pathogenic strains of Leptospira interrogans, representing the most life-threatening presentation of the disease.
Pathogenesis: after entry through cuts/abrasions or intact mucosa during contact with water/soil contaminated by infected animal (rodent) urine, the organism disseminates haematogenously, its outer-membrane components directly damaging vascular endothelium and producing widespread vasculitis and capillary leak, underlying the disease’s characteristic multi-organ involvement.
Clinical features (the classical triad plus haemorrhage):
- Jaundice — often disproportionately severe relative to the degree of hepatocellular necrosis on biopsy (canalicular cholestasis predominates over frank hepatocyte death), a distinguishing feature from viral hepatitis.
- Acute kidney injury — interstitial nephritis and acute tubular necrosis, presenting with oliguria/renal failure.
- Haemorrhagic manifestations — due to vasculitis and thrombocytopenia, ranging from petechiae/purpura to significant pulmonary haemorrhage in the most severe cases.
- Additional features can include myocarditis, aseptic meningitis (in the later immune phase), and myalgia (from myositis).
Laboratory diagnosis: dark-field microscopy/culture (Fletcher’s/EMJH medium) or PCR in the early leptospiraemic phase; Microscopic Agglutination Test (MAT) — the serological gold standard — and IgM-ELISA from the second week; supportive findings include deranged LFTs (raised bilirubin, only mildly raised transaminases), raised renal parameters, thrombocytopenia, and raised CPK.
Treatment: IV penicillin or ceftriaxone for severe disease, with supportive management of renal failure (dialysis if needed) and haemorrhage; doxycycline chemoprophylaxis for high-risk exposure.
Prognosis: significant mortality if untreated or in severe multiorgan involvement, making prompt recognition and treatment essential.