Journal of Dr. NTR University of Health Sciences

: 2018  |  Volume : 7  |  Issue : 3  |  Page : 233--235

A case report of Weil's disease

Venkata Krishna Pothukuchi, Shaik Ahmed, Katreddy Venkata Narasimha Reddy 
 Department of General Medicine, Guntur Medical College and Government General Hospital, Guntur, Andhra Pradesh, India

Correspondence Address:
Prof. Venkata Krishna Pothukuchi
57-9-15, New Postal Colony, Patamata, Vijayawada - 520 010, Andhra Pradesh


We are reporting a case of Weil's disease which is a severe form of leptospirosis manifesting with fever, jaundice, renal failure and hemorrhagic manifestations as it is a very important public health problem and to focus that it is also occurring in our area. The treating physicians may be alerted to consider the leptospirosis in the differential diagnosis of fevers so that early empirical treatment can be given to avoid the multi-organ dysfunction and mortality.

How to cite this article:
Pothukuchi VK, Ahmed S, Reddy KV. A case report of Weil's disease.J NTR Univ Health Sci 2018;7:233-235

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Pothukuchi VK, Ahmed S, Reddy KV. A case report of Weil's disease. J NTR Univ Health Sci [serial online] 2018 [cited 2023 Jan 28 ];7:233-235
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Leptospirosis is one of the most common zoonotic diseases, favored by a tropical climate and flooding during the monsoon, but occurring world-wide.[1] Large epidemics are reported after monsoons and periods of unusually heavy rainfall. In India, Kerala, Tamil Nadu and Andaman's are endemic for leptospirosis. However now with better facilities to detect the disease, the disease is being reported from almost all parts of India.[2]

The differential diagnosis of leptospirosis depends on the epidemiology of acute febrile illnesses in a particular area. A high index of suspicion is needed in endemic areas, and leptospirosis must be considered when a patient presents with acute onset of fever, headache and myalgia. However, in locations where dengue fever or malaria is also present, the differentiation may be very difficult because of similar clinical manifestations. Laboratory confirmation is crucial, especially when these diseases are occurring simultaneously during the rainy season.[2]

We are encountering sporadic cases of leptospirosis particularly during the rainy season in Coastal Andhra Pradesh and there are no individual case reports from this area, and that is the reason we are presenting this case report.

 Case Report

A 69-year-old male agricultural laborer was admitted with a history of fever since 2 weeks and decreased urine output since 1-week. There was a history of hematuria, black discoloration of stools; bleeding gums and mucosal bleed over lips. On examination, icterus, conjunctival hemorrhages [Figure 1] along with mucosal bleed over lips and pedal edema were present. Cardiovascular system, respiratory system and abdominal examination revealed no abnormality. Empirical treatment was started with ceftriaxone and arteether. Blood was sent for investigations, including smear for malarial parasite and leptospiral antibody test. Platelet count was 82000/mm 3. Bleeding time and clotting time were within the normal limits. Hemoglobin was 9.2 mg/dL. His serum bilirubin was 3.2 mg/dL (direct-0.8 mg/dL, indirect-2.4 mg/dL), aspartate transaminase (serum glutamic oxaloacetic transaminase [SGOT]) was 39 IU, alanine transaminase (serum glutamate pyruvate transaminase [SGPT]) was 40 IU and serum alkaline phosphatise (ALP) was 136 IU. Serum creatinine was 5.8 mg/dL and blood urea was 158 mg/dL. Blood smear for malarial parasite was negative. Strip test for malarial parasite was also negative. Viral screening tests were negative. Leptospiral strip test for IgM antibodies was positive.{Figure 1}

Benzyl penicillin and doxycycline were given in addition to ceftriaxone and patient was treated conservatively with intravenous fluids and furosemide. Biochemical parameters on subsequent examination showed that serum bilirubin was 3 mg/dL, SGOT was 18 IU, SGPT was 26 IU, ALP was 136 IU, serum creatinine was 4.8 mg/dL and blood urea was 99 mg/dL. There were no further bleeding manifestations. Jaundice and renal parameters gradually improved with conservative management without any need for dialysis as were the case similar to our other sporadic cases of leptospirosis admitted in this season. He was discharged in good clinical condition with the advice to continue doxycyline for further 5 days. On further follow-up, patient was recovered fully.


Leptospirosis is an acute and often severe infection that frequently affects the liver or other organs and is caused by the multiple serovars of Leptospira interrogans.[3] In 1885, Adolf Weil described the clinical hallmarks of this disease as an acute process characterized by splenomegaly, jaundice, and nephritis. With time, the designation Weil's disease came to signify severe leptospirosis characterized by diverse clinical findings, particularly fever, jaundice, acute renal injury, refractory shock, and hemorrhage (especially pulmonary hemorrhage).[4]

In general, clinical manifestation can be divided into two distinct clinical syndromes. 90% of patients present with mild anicteric febrile illness associated with influenza-like illness with headache and myalgia; 10% are severely ill with jaundice and other manifestations (Weil's disease). In icteric leptospirosis (Weil's syndrome), persistent high fever and jaundice are usually associated with hepatic dysfunction, renal insufficiency, hemorrhage and multi-organ failure (MOF). Hemorrhage can occur as petechiae, purpura, conjunctival hemorrhage and gastrointestinal hemorrhage. MOF is associated with a very high mortality. Myocarditis and hemorrhagic pulmonary infiltration are other complications, which may prove fatal.[2]

Leptospirosis should be suspected on the basis of an appropriate exposure history combined with any of the infection's protean manifestations. A high index of suspicion prompting elicitation of a detailed exposure history is critical and guides confirmatory testing. Weil's disease is suggested by elevated levels of blood urea nitrogen and serum creatinine in conjunction with mixed conjugated and unconjugated hyper bilirubinemia with aminotransferase elevation to <5 times the upper limit of normal.[4] When a patient is jaundiced, the bilirubin level is markedly raised but transaminase and alkaline phosphatase concentrations may not rise much beyond the upper limit of normal.[5] Jaundice is not associated with fulminant hepatic necrosis or hepatocellular damage, but rather with abnormal laboratory values.[4] Hematologic abnormalities are variable but common: Leukocytosis (typical in severe disease), leukopenia, hemolytic anemia, mild to moderate anemia, and thrombocytopenia.[4] The anemia frequently observed in Weil's syndrome has been ascribed on clinical impression to blood loss, renal failure, and/or an ill-defined hemolytic process. However, hemolytic anemia associated with leptospirosis in animals is well documented and is due to hemolysins with phospholipase activity.[6]

Higgin and Cousineau in their study quoted that jaundice in guinea pigs infected with Leptospira icterohaemorrhagiae appeared to be the result of hepatocellular damage associated with a markedly increased production of bilirubin from the extravascular erythrocytes degradation. Incidentally, the participation of the last process is plausible as most of the old worn out red blood cells in the circulatory system are phagocytosed in the spleen, the bone marrow and the liver. Hence, the reticuloendothelial cells of these organs produce most of the bilirubin that is formed in the body. A high content of bilirubin in the blood can be produced, at least theoretically, by the RE cells of the body phagocytizing red blood cells at such a rapid rate that the parenchymal cells of the liver cannot effectively excrete all the bilirubin brought to them. The bilirubin in the blood stream increases and jaundice occurs.[7]

It is unlikely that the early nonspecific illness of leptospirosis will be diagnosed unless there is a clear suggestion of the diagnosis in some occupational or recreational exposure, or if there is an outbreak. Clinical clues that may suggest the diagnosis of leptospirosis over other causes of acute fever are disproportionate myalgia, jaundice, conjunctival suffusion, pretibial rash and lymphocytic meningitis.[5]

The IgM ELISA is particularly useful in making an early diagnosis, since it is positive as early as 2 days into the illness, a time when the clinical manifestations may be nonspecific, and it is extremely sensitive and specific (93%).[3]

Penicillin (e.g., 1.5 million units every 6 h intravenously) or ceftriaxone (1 g daily intravenously) is the drug of choice in severe leptospirosis and is especially effective if started within the first 4 days of illness.[3]

In our patient blood urea nitrogen and serum creatinine levels were raised. Our patient had bleeding manifestations in the form of sub conjunctival hemorrhages and history of bleeding from gums along with anemia. However when the patient was admitted in our hospital there was no evidence of fresh bleeding, and vital signs were stable. The bleeding time and clotting time were within normal limits, so further coagulation profile was not done. However, the prothrombin and activated partial thromboplastin times are not necessarily elevated in severe leptospirosis.[4] Bilirubin was also raised without elevation of transaminases. Raise of unconjugated hyperbilirubinemia in our patient may be due to hemolysis [4],[6] or extravascular red blood cell destruction [7] in addition to minimal involvement of the liver that was rarely described in the literature.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


1Dockrell DH, Sundar S, Angus BJ, Hobson RP. Leptospirosis. In: Colledge NR, Walker BR, Ralston SH, editors. Davidson's Principles & Practice of Medicine. 21st ed. Edinburgh: Churchill Livingstone; 2010. p. 331-2.
2Dutta TK, Christopher M. Leptospiros — An Overview. J Assoc Physicians India 2005;53:545-51.
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6Trowbridge AA, Green JB 3rd, Bonnett JD, Shohet SB, Ponnappa BD, McCombs WB 3rd. Hemolytic anemia associated with leptospirosis. Morphologic and lipid studies. Am J Clin Pathol 1981;76:493-8.
7Higgin R, Cousineau G. The pathogenisis of leptospirosis II. Jaundice in experimental leptospirosis in guinea pigs. Can J Comp Med 1977;41:182-7.