Leptospirosis is a zoonosis of worldwide distribution caused by infection with L. interrogans, a pathogenic spirochete. The organism infects a variety of animals, especially rodents and animals associated with farming. Humans represent only incidental infection usually through work-related contact through skin or mucous membranes, typically after exposure to water or soil contaminated with urine from an infected animal or via drinking of or bathing in contaminated water. The main occupational groups at risk are farm workers, field agricultural workers, plumbers, sewer workers, sanitation workers and military troops.
Leptospira are spiral-shaped, thin, motile organisms with flagella. The most common serovars are icterohaemorrhagiae, which are usually found in rats (Rattus norvegicus). Urinary shedding of organisms from infected animals is the most significant source of Leptospira spp. because the spirochetes can persist for long periods of time in the renal tubules.
The natural course of leptospirosis comprises of two distinct clinical phases: septicemic and immune. Humans typically become ill seven to 12 days after exposure to leptospires. The first stage is called the septicemic phase (leptospiremic phase) because the bacteria may be isolated from blood cultures and cerebrospinal fluid (CSF). This phase is characterized by a nonspecific flulike illness with sudden onset of high fever, headache, myalgias (classically involving the paraspinal, calf and abdominal muscles)  and conjunctival suffusion. Conjunctival suffusion (reddening of the eye surface) is a characteristic physical finding in leptospirosis, and its presence in a patient with a nonspecific febrile illness should raise suspicion for diagnosis.
The second stage is called the immune phase (leptospiruric phase) when circulating antibodies can be detected and the bacteria can be isolated from the urine. This stage occurs as a result of the body's immunologic response by producing immunoglobulin M antibodies and can last longer than one month. During this stage, specific organ damage can be observed. Aseptic meningitis is one of the most important clinical syndromes that can occur in 80% of patients during the immune phase. Renal symptoms, such as uremia, azotemia, pyuria and hematuria, may occur. Pulmonary manifestations, although usually benign, can be potentially life threatening and range from chest pain, cough and dyspnea to pulmonary hemorrhage or acute respiratory distress syndrome. An increase in liver enzymes (up to five times normal) with a disproportionately high total bilirubin has been described as a prognostic indicator in leptospirosis . Varying degrees of jaundice, pancreatitis, hepatomegaly and myocarditis can also occur.
Weil's disease is the most severe form of leptospirosis. Patients can present with high fever (>40°C), significant jaundice, renal failure, hepatic necrosis, pulmonary involvement, cardiovascular collapse, neurologic changes and hemorrhagic diathesis, with a variable clinical course. Weil's disease can occur at the end of the first stage and peaks during the second stage but can occur at any time during acute leptospirosis as a single, progressive illness.
Acute renal failure is one of the most common complications of severe leptospirosis. Renal leptospirosis is usually described as a combination of acute tubular damage and interstitial nephritis.
A particularly serious type of lung involvement called severe pulmonary hemorrhagic syndrome is considered to be a major cause of death in patients with Weil's disease in developing countries, with profuse lung hemorrhage dominating the clinical picture .
Hepatic dysfunction is usually mild and reversible. Liver dysfunction in severe leptospirosis can be seen as conjugated serum bilirubin levels may increase to above 80 mg/dL, accompanied by modest elevations in transaminases, which rarely exceed 200 U/L .
Variable degrees of thrombocytopenia have been reported with leptospirosis. The pathogenesis of thrombocytopenia and hemorrhagic diathesis in leptospirosis is not well understood.
Overall, Weil's syndrome has a mortality rate of 5% to 10%. Important causes of death include renal failure, cardiopulmonary failure and widespread hemorrhage .
The diagnosis of leptospirosis requires a high degree of clinical suspicion because the disease's numerous manifestations can mimic other tropical infections or other nonspecific febrile illnesses, as well as noninfectious diseases such as small vessel vasculitides, systemic lupus erythematosus or even malignancies. The initial diagnosis of leptospirosis remains a clinical one, a presumed analysis in the appropriate epidemiologic and clinical context. Routine laboratory testing is nondiagnostic but may show elevated erythrocyte sedimentation rate, peripheral leukocytosis, variable degrees of cytopenias, mildly increased aminotransferases and increased serum bilirubin and ALP.
Isolation of the organism by culture of clinical specimens (blood, CSF, urine) during the first seven to 10 days of the illness is considered the gold standard of diagnosis. However, this method is difficult, requires longer than 16 weeks because initial growth may be slow and has a low sensitivity and specificity. The majority of leptospirosis cases are diagnosed by serologic testing of which MAT is most common
The vast majority of infections with leptospira are self-limiting, and it remains controversial if antimicrobials produce benefit in cases of mild leptospirosis without end-organ damage. The current choices of treatment for mild leptospirosis include oral doxycycline and amoxicillin. Parenteral high-dose penicillin G has long been considered the treatment of choice of fulminant leptospirosis. Recent trials have demonstrated that the broad-spectrum third generation cephalosporins cefotaxime and ceftriaxone are also acceptable agents for patients with severe leptospirosis [6, 7].
The use of steroids in patients with leptospirosis has not been well established. In the current case, the improvement of the patient's renal dysfunction, thrombocytopenia and hemoptysis may be attributed to the introduction of steroids. Several case reports have described the beneficial effects of glucocorticoids in severe leptospirosis with pulmonary hemorrhage , thrombocytopenia  and renal failure [10, 11].
Public health measures to prevent and reduce leptospirosis include identification of contaminated water sources, rodent control, prohibition of swimming in waters where risk of infection is high and informing persons of the risk involved in recreational water activities.
In the case of our patient, the diagnosis of leptospirosis was not initially considered because potential risk factors were not identified at the outset. The majority of cases of leptospirosis occur in the tropics, with infrequent incidences in temperate regions. Adding another atypical facet to the patient's presentation, in the United States, the majority of cases occur in the Southern and Pacific coastal states, with Hawaii having the most reported cases. Also, our patient presented in the wintertime. Most cases of leptospirosis occurring in temperate areas occur in the late summer to early fall . According to the NYC Board of Health, between 2008 and summer 2009, there were only three cases of leptospirosis in NYC (including our patient).