Leptospirosis Clinical Presentation
- Author: Sandra G Gompf, MD, FACP, FIDSA; Chief Editor: Burke A Cunha, MD more...
History
A good clinical history is often the key to accurate diagnosis in leptospirosis. Important features include a plausible exposure history and a clinical picture consistent with the disease.
Leptospirosis occurs worldwide wherever risk of contact with the urine, kidneys, or conception products of infected animals exists. Typically, rodents, dogs, cattle, and pigs are considered reservoirs for this organism; however, increasing diversity of travel and exotic-pet trade are expanding the list. The leptospires may live for years in the renal tubules of animals and are excreted in the urine into standing water or soil. This explains sources of both direct infection (eg, body fluids or organs of infected animals) and indirect infection (eg, inoculated soil or water). In 2004, cases were linked to flood water in urban endemic regions of Hawaii. In tropical settings, leptospirosis is becoming more prevalent among travelers and residents. For example, recreational activities in rivers (eg, white-water rafting) may be a significant risk factor for infection with leptospires.
Leptospires can live outside the body for several weeks. They enter the body through disrupted skin or mucosal barriers, such as abrasions or waterlogged skin. Other means of infection have been documented, including inhalation of aerosolized leptospires and direct infection across intact mucus membranes or conjunctivae. After an incubation period of 2-30 days (typically 5-14 d), clinical symptoms ensue. A plausible history of possible exposure must precede clinical symptoms in order to consider the diagnosis of leptospirosis.
Expert consensus is that leptospirosis occurs as two recognizable clinical syndromes. A third syndrome of asymptomatic infection is more controversial. Anicteric leptospirosis is a self-limited disease similar to a mild flulike illness. Icteric leptospirosis, also known as Weil disease, is a severe illness characterized by multiorgan involvement or even failure. Two distinct phases of illness are observed in the mild form—the septicemic (acute) phase and the immune (delayed) phase. In icteric leptospirosis, the 2 phases of illness are often continuous and indistinguishable. At disease onset, clinically predicting the severity of disease is not possible. Subsequent sequelae depend on the serovar involved and the health, nutritional status, and age of the patient, as well as the rapidity of definitive and supportive treatment.
An acute illness follows any infection with any serovar of leptospirosis. Most of the following symptoms develop in varying degrees: high temperature (38-40°C), rigors, sudden headache, nausea and vomiting, anorexia, diarrhea, cough, pharyngitis, nonpruritic skin rash, and muscle pain. Muscle pains are typically localized to the calf and lumbar areas. This phase of illness lasts 5-7 days and either regresses to a relatively asymptomatic period or progresses to a more severe illness. In anicteric leptospirosis, the acute illness is followed by 1-3 days without fever and then progresses to 4-30 days of the immune (delayed) phase of the illness.
Physical
The physical examination findings differ depending on the severity of disease and the time from onset of symptoms. Patients may appear mildly ill or toxic. Early in the disease, temperatures as high as 40°C and tachycardia are common. Hypotension, oliguria, and abnormal chest auscultation at presentation may portend severe illness. When fever is severe and prolonged, hypotension and shock due to volume depletion may also occur. The fever typically subsides within 7 days.
Early in the disease, the skin is warm and flushed. Additional skin findings include a transient petechial eruption that can involve the palate. Later in severe disease, jaundice and purpura can develop. The classic ocular finding of conjunctival suffusion occurs early irrespective of disease severity. Conjunctival suffusion is characterized by redness of the conjunctiva that resembles conjunctivitis but that does not involve inflammatory exudates.
Uveitis is a common feature following acute leptospirosis; however, patients who receive antibiotics during the acute phase of illness may develop only mild uveitis.[7]
Muscle tenderness can occur with the myositis of early infection. This can be particularly prominent in the paraspinal and calf muscles but can involve any muscle. Neurologic examination can reveal signs of meningitis, including neck stiffness and rigidity and photophobia. Early in the disease, the stiffness on neck examination can be confused as muscular in origin; however, this symptom may actually represent early meningismus.
Lung examination results may be normal in early or mild illness. In severe illness, signs of consolidation due to alveolar hemorrhage may be found. In patients with cardiac-related pulmonary edema, rales and wheezes can be heard.
The incidence of pulmonary involvement has increased over the past few years, affecting up to 70% patients. Alveolar hemorrhage that manifests as dyspnea and hemoptysis is the main pulmonary manifestation. This clinical manifestation may be severe and can occur in the absence of typical presentations of Weil disease.
Pulmonary involvement has emerged as a serious cause of mortality, becoming the main cause of leptospirosis-associated death in some countries.[8, 9]
Myocarditis may occur in severe disease. All of the physical findings of biventricular heart failure can be found, including elevated jugular venous pulsations; a new S3 gallop; and dysrhythmias, including atrial fibrillation, heart blocks of varying severity, and ventricular ectopy.
Abdominal examination may reveal liver enlargement and tenderness due to hepatitis. Acalculous cholecystitis, which may be suggested by a positive Murphy sign, is a finding of profound systemic illness. Pancreatitis has also been described in severe cases.[10]
Heme-positive stool and even gross blood can be found on rectal examination in patients with DIC and bleeding.
In severe disease, delirium may develop either as a consequence of shock or independent of it. Delirium may be an early finding in severe disease. Late in disease and into convalescence, prolonged mental symptoms may persist, including depression, anxiety, irritability, psychosis, and even dementia.
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