Journal of Postgraduate Medicine
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Year : 2002  |  Volume : 48  |  Issue : 2  |  Page : 117-8  

Clinical profile of leptospirosis in South gujarat.

AM Clerke, AC Leuva, C Joshi, SV Trivedi 
 Department of Medicine, Government Medical College, Surat - 395 001, Gujarat, India., India

Correspondence Address:
A M Clerke
Department of Medicine, Government Medical College, Surat - 395 001, Gujarat, India.
India

Abstract

BACKGROUND: South Gujarat has been witnessing increasing incidence of leptospirosis for the last few years. AIM: To study the clinical profile of leptospirosis in South Gujarat. SETTINGS AND DESIGN: Prospective study during July-September 2000 at the New Civil Hospital, Surat, Gujarat. PATIENTS AND METHODS: All the consecutive cases with clinical suspicion of leptospirosis were screened for lgM antileptospira antibody on the first and the fourteenth day. A four fold or greater increase in agglutinin antibody titre on paired samples was considered diagnostic. If the patient died before the fourteenth day then initial titre greater than 1:15 was considered diagnostic. RESULTS: Total number of patients referred to the hospital were fifty, of which thirty-eight [33 males, with age 14-50 (30 +/- 10.51)] were diagnosed as having leptospirosis. Most common organs involved were liver (27, 71.05%) and kidney (24, 63.15%). Cardio-vascular (12, 31.5%), pulmonary (10, 26.35%), neurological (2, 5.26%) and haematological (8, 21%) involvements were less common. Six patients died because of pulmonary involvement in the form of alveolar haemorrhage, while one died because of cardiac involvement. CONCLUSION: Liver and kidney were the most commonly involved organs in severe leptospirosis. Pulmonary involvement, though uncommon, led to high mortality.



How to cite this article:
Clerke A M, Leuva A C, Joshi C, Trivedi S V. Clinical profile of leptospirosis in South gujarat. J Postgrad Med 2002;48:117-8


How to cite this URL:
Clerke A M, Leuva A C, Joshi C, Trivedi S V. Clinical profile of leptospirosis in South gujarat. J Postgrad Med [serial online] 2002 [cited 2021 Oct 26 ];48:117-8
Available from: https://www.jpgmonline.com/text.asp?2002/48/2/117/132


Full Text

Leptospirosis is a zoonotic disease with very wide geographical distribution. It is an infectious disease caused by spirochetes known as leptospira, of which more than 20 serogroups and more than 200 serovars are known. Among the patients infected with leptospirosis, 40% seroconvert asymptoma-tically.[1] Out of remaining 60%, 90% suffer the milder anicteric form and 10% the severe icteric form. South Gujarat has been witnessing epidemics of leptospirosis in the monsoon season for the last five years. The present study was carried out to study the clinical profile of patients having severe leptospirosis in South Gujarat.


  ::   Patients and methodsTop


All the consecutive patients referred to New Civil Hospital, Surat with clinical suspicion of leptospirosis during July to September 2000 were studied. All patients presenting with fever with chills, headache, conjunctival suffusion, myalgia and muscle tenderness were screened for lgM antileptospira antibody by ELISA (Virion; Serion, Germany). Blood samples were drawn on the first and the fourteenth days of presentation. Any patient presenting with the above clinical features and fulfilling any one of the above two lab criteria was defined as a case of leptospirosis. Case definition of leptospirosis as proposed by the National Institute of Communicable Diseases (NICD), New Delhi was followed.2 If the patient died before the fourteenth day then an initial titre greater than 1:15 was considered diagnostic.

Patients in the study group were subjected to detailed clinical examination and investigations for specific organ involvement were carried out. Serovar specific tests like microscopic agglutination test were not performed, as facilities were not available at our institution. Autopsy studies were not performed, as relatives of deceased patients did not give consent for the same.


  ::   ResultsTop


Out of the fifty suspected cases thirty-eight were diagnosed as having leptospirosis as per the definition given by NICD. All these thirty eight patients fulfilled the diagnostic criteria for leptospirosis as per NICD definition. All the patients were paddy farm workers from Surat district. The clinical and demographic profile is included in table.

Most of the patients had multiorgan involvement; liver was the most common 27 (71.05%), which manifested as jaundice, pruritus, and tender hepatomegaly. Hepatic encephalopathy was very rare despite severe jaundice. There was conjugated hyperbilirubinaemia (serum bilirubin 11.3 ? 10.35 mg/dl), and only a mild rise in serum transaminases (AST 45 ? 9.26, ALT 42 ? 9.97) with marked rise in serum creatinine phosphokinase levels. Liver functions returned to normal without leaving any sequel. Kidney involvement manifested with oliguria and features of azotaemia (serum creatinine 3.16 ? 2.46 mg/dl and blood urea (113.48 ? 76.80). Ultrasonography of abdomen showed enlarged kidneys. Except for two patients who required haemodialysis, all the patients were managed conservatively. Renal functions returned to normal in due course. Pulmonary involvement was seen in 10 patients (26.31%) as gradual to sudden onset of breathlessness and haemoptysis. X-ray chest showed bilateral alveolar infiltrates and sputum showed haemosiderin-laden macrophages. Arterial blood gas analysis showed severe hypoxia and increased alveolar-arterial oxygen gradient. All patients with pulmonary involvement were given pulse steroid therapy and mechanical ventilatory support. Cardiovascular involvement manifested as hypotension and cardiac arrhythmias (sinus bradycardia and first-degree atrioventricular block). Haematological involvement manifested as thrombocytopaenia, prolonged bleeding time, upper gastrointestinal haemorrhage and petechial spots. Six patients died because of pulmonary involvement in the form of alveolar haemorrhage, while one died because of cardiac involvement.

Majority of the patients who were negative for leptospira antibodies, were suffering from alcoholic liver disease; two patients had viral hepatitis and two patients turned out to have renal failure due to reasons other than leptospirosis.


  ::   DiscussionTop


Leptospirosis is characterised by the renal and hepatic involvement; extensive pulmonary disease is not commonly discussed.[1],[3] In the present study, liver and kidney though the commonest organs involved, were not responsible for mortality. On the other hand, there was high incidence of pulmonary haemorrhage and the resultant high mortality. Respiratory manifestations have been reported sporadically in the literature.[4],[5],[6],[7],[8],[9] Mortality due to leptospirosis is two fold higher in cases with pulmonary involvement.[5] Dupont et al have implicated dyspnoea and alveolar infiltration as independent poor prognostic factors, associated with high mortality.[7] Alveolar haemorrhage has been reported even before the onset of renal or hepatic involvement.[8]

The pathogenesis of alveolar haemorrhage in leptospirosis is not well understood. The occurrence of alveolar haemorrhage in the absence of coagulopathy or thrombocyto-paenia in many cases is presumably due to capillary fragility which is characteristic of the disease.[9] The basic pathology in leptospirosis is vasculitis.[1]The commonest cause of alveolar haemorrhage, in patients without leptospirosis is vasculitis. Thus, it should be considered to be the most important factor for the pathogenesis of alveolar haemorrhage in leptospirosis too. The most important diagnostic test for immune mediated alveolar haemorrhage is antineutrophil cytoplasmic antibody (ANCA). Studies on the role of ANCA in leptospiral alveolar haemorrhage have not been carried out so far. In view of the high mortality associated with the condition, other treatment modalities like immunosuppression and plasmapheresis should be explored, as attempted by Borer et al.[11]

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1Speelman Peter. Leptospirosis. In: Braunwald, Fauci, Kasper, Hauser, editors. Harrison’s Principles of Internal Medicine. 15th edn. New York: McGraw Hil Publications; 2001. p.1055-57.
2National institute of communicable diseases. Case definitions of epidemic prone disesases. Delhi: NICD; 1998.
3Sitprija V. Leptospirosis. In: Weatherall, Ledingham, Warrel. editors. Oxford Textbook of Medicine. 3rd edn. Oxford: Oxford University Press; 1996. p. 689-91.
4Sehgal SC, Murhekar MV, Shagunan AP. Outbreak of leptospirosis with pulmonary leptospirosis in north Andaman. Indian J Med Res 995;102:9-12.
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7Dupont H, Dupont Perdrizet D, Perie JL, Zehner Hansen S, Jarrige B, Daijardin J B. Leptospirosis. Prognostic factors associated with Mortality. Clin Infect Dis 1997;25:720-4.
8Allen P, Raffery S, Phelan D. Masive pulmonary hemorrhage in leptospirosis. Intensive Care Medicine 1989;15:322-4.
9Courtin JP, Carre P, Poubean P. Diffuse alveolar hemorrhage and Myositis in icterohaemorrhagic leptosprirosis, rapid control by a single bolus corticosteroid. Rev Mal Respir 1994;11:601-3.
10Joseph Lynch and J .Leatherman . Alveolar Haemorrhage Syndrome In: Fishman editor. Fishman’s Pulmonary diseases and disorders. 3 rd edn. New York: McGraw Hill Publications; 1998. p. 1193-210.
11Borer A, Metz I, Gilad J, Riesenberg K, Weksler N, Weber G, et al. Massive pulmonary hemorrhage caused by leptospirosis successfully treated with nitric oxide inhalation and hemofiltration. J Infect 1999; 38:42-5.

 
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