Leptospirosis Clinical Presentation

Updated: Jul 08, 2021
  • Author: Sandra G Gompf, MD, FACP, FIDSA; Chief Editor: Michael Stuart Bronze, MD  more...
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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.

The exposure history may reveal direct contact with body fluids or organs of infected animals, or indirectly (eg, via contaminated soil or water). Direct exposure often occurs in occupational cases, while indirect exposure is more typical of cases contracted during travel or recreational activities rivers (eg, white-water rafting). Onset of clinical illness occurs abruptly, after an incubation period of 2-30 days (typically 5-14 d).

Expert consensus is that leptospirosis occurs as two recognizable clinical syndromes: anicteric and icteric (the existence of a third syndrome of asymptomatic infection is more controversial). Anicteric leptospirosis is a self-limited, 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.

An acute illness follows infection with any serovar of leptospirosis. Most of the following signs and symptoms may develop in varying degrees:

  • Headache

  • Fever (38-40°C)

  • Rigors

  • Muscle pain (typically localized to the calf and lumbar areas)

  • Nausea and vomiting

  • Anorexia

  • Diarrhea

  • Dry cough

  • Pharyngitis

  • Conjunctival suffusion

  • Nonpruritic skin rash

Despite reports of fever as a cardinal symptom, research by the Hawaii Department of Health found that the presence of fever varied. [25, 34] In serologically confirmed cases, 5% of patients gave no history of fever, and 55% were afebrile at the time of presentation. Myalgias and headache were universally reported at the time of presentation and were the chief complaint in 25% of patients.

The natural course of leptospirosis falls into 2 distinct phases. The acute phase of illness lasts 5-7 days and is followed by a 1-3 day period of improvement in which the temperature curve falls and the patient may become afebrile and relatively asymptomatic. Subsequently, leptospirosis either regresses to a relatively asymptomatic illness or progresses to a more severe illness.

Recurrence of fever indicates the onset of the second, immune stage. Nonspecific symptoms, such as fever and myalgia, may be less severe than in the first stage and last a few days to a few weeks. Many patients (77%) experience headache that is intense and poorly controlled by analgesics; this often heralds the onset of meningitis.

Aseptic meningitis is the most important clinical syndrome observed in the immune anicteric stage. Meningeal symptoms develop in 50% of patients. Cranial nerve palsies, peripheral facial palsy, [35] encephalitis, and changes in consciousness are less common. Mild delirium may also be seen. Meningitis usually lasts a few days but occasionally lasts 1-2 weeks. Death is extremely rare in anicteric cases.

Abdominal pain with diarrhea or constipation (30%), hepatosplenomegaly, nausea, vomiting, and anorexia are also seen. Acalculous cholecystitis may be seen rarely but is clinically significant. [36]

Uveitis (2-10%) can develop early or late in the disease and has been reported to occur as late as one year after initial illness. Iridocyclitis and chorioretinitis are other late complications that may persist for years. These symptoms first manifest 3 weeks to 1 month after exposure. Subconjunctival hemorrhage is the most common ocular complication of leptospirosis, occurring in as many as 92% of patients.

Renal manifestations include hematuria. Oliguric or anuric acute tubular necrosis may occur during the second week due to hypovolemia and decreased renal perfusion.

Weil syndrome, the severe form of leptospirosis, primarily manifests as profound jaundice, renal dysfunction, hepatic necrosis, pulmonary dysfunction, and hemorrhagic diathesis. Pulmonary manifestations include cough, dyspnea, chest pain, bloodstained sputum, hemoptysis, and respiratory failure.


Physical Examination

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 findings 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. [37]

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.

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. [38, 39, 40] 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.

Rash may present as a macular or maculopapular eruption with erythematous, urticarial, petechial, or desquamative lesions. Adenopathy may be noted.



The infection may progress to severe systemic inflammatory syndrome with hemorrhagic features. Findings of disseminated intravascular coagulation may occur with bleeding.

The onset of mental status alterations indicates progression to parenchymal involvement of the cerebral cortex with meningo-encephalitis, heralding a high mortality risk.

Severe and diffuse alveolar hemorrhage with massive hemoptysis can occur in the absence of typical Weil disease.

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.

Acalculous cholecystitis is a finding of profound systemic illness. Pancreatitis has also been described in severe cases. [38, 39, 40]

Uveitis, iridocyclitis, and chorioretinitis may occur late into illness and may persist for years.