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SN9 SHORT NOTE 5M

Write a short note on leptospirosis.

General Medicine · Final Professional

Aetiology

Leptospirosis is a zoonosis caused by spirochaetes of the genus *Leptospira* (pathogenic species *L. interrogans*). It is one of the commonest zoonoses worldwide, and in India causes large monsoon-associated outbreaks, particularly in Kerala, Tamil Nadu, Gujarat, Maharashtra, Andaman and Nicobar Islands and Odisha.

Reservoir and transmission:

  • Rodents (especially rats) are the principal reservoir, excreting leptospires in urine for life without illness; also dogs, cattle, pigs and buffaloes.
  • Humans are infected through contact of abraded skin or mucous membranes with water, soil or mud contaminated by animal urine — hence outbreaks after flooding and heavy rainfall.
  • Occupational risk: paddy field workers, sewer and drainage workers, sanitary workers, veterinarians, abattoir workers, miners, fishermen and military personnel.
  • Recreational risk: swimming, rafting and wading in floodwater.

Incubation: 2–30 days (usually 7–12).

Pathogenesis

Leptospires penetrate mucosa or broken skin, disseminate haematogenously to all organs, and cause a generalised vasculitis with endothelial damage, which underlies the multi-organ manifestations. Damage to hepatocyte tight junctions causes cholestatic jaundice with only modest hepatocellular necrosis — explaining the characteristic pattern of very high bilirubin with only modestly raised transaminases, which is a valuable diagnostic clue.

Clinical Features — Two Phases

PhaseTimingFeatures
Leptospiraemic (septicaemic)Days 1–7Abrupt high fever with rigors, severe myalgia — classically of the calf and lumbar muscles, intense headache, conjunctival suffusion (redness without discharge or pain) — highly characteristic, nausea, vomiting, abdominal pain, rash
Immune (leptospiruric)After a brief defervescence, from day 7Antibody-mediated: aseptic meningitis, uveitis, rash, and — in severe cases — jaundice, renal failure and haemorrhage. Leptospires appear in the urine

Most infections (about 90%) are mild and anicteric, and self-limiting.

Severe Leptospirosis — Weil's Disease

The severe icteric form, with a triad of:

1. Jaundice — deep, with a characteristic orange-yellow ("orange cast") hue

2. Acute kidney injury — non-oliguric renal failure with hypokalaemia (a distinctive feature caused by impaired sodium reabsorption and potassium wasting)

3. Bleeding — from thrombocytopenia and vasculitis: epistaxis, gastrointestinal bleeding, and pulmonary haemorrhage

Other severe manifestations:

  • Severe pulmonary haemorrhage syndrome — a leading cause of death, with haemoptysis, hypoxia and ARDS; may occur with little or no jaundice, and can progress within hours.
  • Myocarditis with arrhythmia and heart failure; aseptic meningitis; rhabdomyolysis; uveitis (often weeks later).
CLINICAL PEARL

Fever with severe calf myalgia and conjunctival suffusion in a patient exposed to floodwater is leptospirosis until proved otherwise. Two further pointers strongly support it: jaundice with a high bilirubin but only mildly raised transaminases (very different from viral hepatitis, where transaminases are in the thousands), and acute kidney injury with HYPOkalaemia rather than the hyperkalaemia expected in renal failure. This triad of clues distinguishes it from dengue, malaria, hepatitis and scrub typhus, which share the clinical setting.

Investigations

  • Microscopic agglutination test (MAT) — the reference standard; requires paired sera with a fourfold rise, so it is retrospective and available only in reference laboratories.
  • IgM ELISA — the practical test; positive from the end of the first week; widely used, and repeat testing may be needed if taken very early.
  • PCR — detects leptospiral DNA in blood in the first week and in urine from the second week; the most useful early test.
  • Dark-field microscopy of blood or urine — insensitive and unreliable; rarely used.
  • Culture on Ellinghausen–McCullough–Johnson–Harris (EMJH) medium — slow (weeks) and low yield.
  • Supporting: CBC (neutrophilic leucocytosis — a useful contrast with the leucopenia of dengue, thrombocytopenia), markedly raised bilirubin with modest transaminase elevation, raised creatine kinase (from myositis), renal function with hypokalaemia, urinalysis (proteinuria, haematuria, granular casts), coagulation profile, and chest X-ray for pulmonary haemorrhage.

Management

  • Start antibiotics early — do NOT wait for serological confirmation, which is usually retrospective. Benefit is greatest when treatment begins within the first 4 days.
  • Mild disease: oral doxycycline, or amoxicillin/azithromycin (doxycycline is avoided in pregnancy and young children).
  • Severe disease: intravenous penicillin G or ceftriaxone.
  • Watch for the Jarisch–Herxheimer reaction — fever, rigors and hypotension shortly after the first antibiotic dose, from release of spirochaetal antigen; supportive management.
  • Supportive care determines survival in severe disease: careful fluid and electrolyte management with potassium replacement, renal replacement therapy (which has markedly improved outcomes and should be started early), mechanical ventilation and transfusion for pulmonary haemorrhage, and management of myocarditis. Corticosteroids for pulmonary haemorrhage remain of uncertain benefit.

Prevention

Rodent control, avoiding wading in floodwater, protective footwear and gloves for at-risk occupations, covering skin wounds, safe water supply, and health education before and during the monsoon. Chemoprophylaxis with weekly doxycycline is used for high-risk exposed groups and during outbreaks and floods in endemic districts of India — a measure of demonstrated effectiveness in this setting.

NEEDS VERIFICATION

Antibiotic doses and the doxycycline chemoprophylaxis regimen — confirm against current national guidance.

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