Leptospirosis

Leptospirosis is an acute systemic infection caused by various pathogenic Leptospira serovars, a natural focal disease with rodents and pigs as the two main reservoirs. Features are abrupt onset with early high fever, myalgia, weakness, conjunctival suffusion, calf tenderness, and superficial lymphadenopathy (septic/toxic phase); the middle phase may show pulmonary hemorrhage, diffuse lung bleeding, myocarditis, hemolytic anemia, jaundice, bleeding tendency, nephritis, meningitis, respiratory failure, or heart failure; most recover in the late phase, though some have post-febrile complications like uveitis and occlusive cerebral arteritis related to post-infectious allergy. Diffuse pulmonary hemorrhage, myocarditis, hemolytic anemia, and hepatic/renal failure are common causes of death.

Common Symptoms

Bleeding tendency; meningeal signs; hemoptysis; irritability; convulsions; fatigue; photophobia; remittent fever; oliguria

Causes and Pathogenesis

Leptospires enter through intact or broken skin and mucosa, rapidly spread via lymphatics and blood causing bacteremia, then invade organs, tissues, cells, even the subarachnoid space and anterior chamber; this penetration may relate to flexible spiral motility and hyaluronidase. Depending on serovar virulence and host response, different clinical forms result: virulent icterohaemorrhagiae, autumnalis, australis, and canicola serovars more often cause jaundice/hemorrhage; milder interrogans (influenza-typhoid), 7-day fever, especially pomona cause mild disease; but virulent serovars can cause mild anicteric forms and vice versa, depending on host immunity. Pathogenesis: Early infection-toxic microvascular dysfunction has mild morphological but marked functional changes; adhesion and toxins cause ultrastructural changes (mitochondrial swelling, lysosome increase). As disease progresses, organs (lung, liver, kidney, heart, striated muscle, nodes, CNS) develop functional and morphological damage. Tissue damage is generally mild and recovers without scarring. Neutrophils first increase with weak phagocytosis; monocyte-macrophages proliferate. Specific antibodies appear ~1 week after onset, peaking at ~1 month (agglutinin titers up to 1:10,000); IgM appears first; blood leptospires then disappear, but renal leptospires are unaffected and are shed in urine. Post-febrile complications relate to hypersensitivity.

Treatment

Drug therapy, supportive therapy

Preventive Measures

Integrated mass measures centered on environmental improvement and vaccination. 1. Eliminate/manage sources: (1) Rodent control (rodent carrier rates up to 48.7%) using chemical, mechanical, and ecological methods. (2) Manage water and feces; improve wells, latrines, animal pens; pen pigs; use composted manure; prevent urine/feces from entering water; vaccinate pigs with veterinary leptospiral vaccine in April-May. 2. Cut transmission: transform natural foci (ponds, bogs, cold water fields); drain rice paddy water 1 week before harvest; apply fertilizers/lime nitrogen; children should not fish/swim in endemic water; workers in mines, sewers, piggeries, slaughterhouses should wear rubber boots and gloves. 3. Chemoprophylaxis: oral doxycycline 0.2 g/week during endemic season for susceptibles. 4. Vaccination: phenol-inactivated multivalent (3- or 5-serovar) vaccine; subcutaneous injection 1 ml then 2 ml at 7-10 days, children half dose; immunity lasts ~1 year; complete 1 month before endemic season (late April/early May).

Department to Visit

It is recommended to visit the Infectious Diseases department; an appointment can be booked on this platform before the visit.

Warm reminder: The above information is for health science reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek medical attention at a regular hospital promptly.