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  IN THIS Article
 ::  Introduction
 ::  Case report
 ::  Discussion
 ::  Acknowledgments
 ::  References

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Year : 1990  |  Volume : 36  |  Issue : 4  |  Page : 222-4

Leptospirosis with atrial flutter (a case report).

Department of Medicine, Kasturba Medical College, Manipal, Karnataka.

Correspondence Address:
Department of Medicine, Kasturba Medical College, Manipal, Karnataka.

How to cite this article:
D'Souza C, Dwivedi S, Balasubramanian R. Leptospirosis with atrial flutter (a case report). J Postgrad Med 1990;36:222

How to cite this URL:
D'Souza C, Dwivedi S, Balasubramanian R. Leptospirosis with atrial flutter (a case report). J Postgrad Med [serial online] 1990 [cited 2022 Jan 28];36:222. Available from:

  ::   Introduction Top

Leptospirosis is thought to be the most widespread zoonosis in the world[2]. It has been known since 1931, that leptospiral (L) infections occur in different parts of India among both animals and humans. However, the clinical presentation of leptospirosis is varied and cardiac involvement is usually not common with L Canicola[9]. The diagnosis of leptospirosis is not often suspected even in patients with suggestive clinical features. Moreover, facilities for confirmation of diagnosis either by serology or by isolation of the organism are not readily available. Hence the prevalence of this disease must be many times more than the actual cases recorded in the literature would suggest. The following case report, to the best of our knowledge, is the first record of leptospirosis from western Karnataka and should serve to prompt further studies about its prevalence in this region.

  ::   Case report Top

A 65-year-old male agriculturist from Karkala, South Kanara District of Karnataka was admitted with a history of fever, myalgia, vomiting, jaundice, oliguria and generalized seizures. His illness had begun 9 days earlier with fever, cough and body ache. Fever persisted for about 5 days; subsided and then recurred again after a relatively asymptomatic period of 2 days. It was accompanied by severe muscle pain and muscle soreness, which made him practically immobile. In addition, he had upper abdominal discomfort and vomiting. Oliguria developed on the 7th day of illness. On the 10th day he had 3 episodes of generalized seizures. His past medical history was unremarkable except for a prostatectomy for benign prostatic hypertrophy six years earlier. He was a vegetarian, didn't consume alcohol and didn't smoke.
Physical examination realed a drowsy patient with deep jaundice, mild dehydration and a flapping tremor. He was afebrile, there was no neck stiffness and had no skin rashes. There was bilateral conjunctival congestion with subconjuctival haemorrhage in the left eye. Severe tenderness of all muscles, particularly those of thighs and calf was present. Pulse was 112/min, inregularly irregular, BP 130/80 rim Hg, temperature 990F. There were no signs of congestive cardiac failure nor were there any murmurs. Bilateral rhonchii were present. Liver was just palpable, smooth, soft and non-tender. Spleen was not felt. Neurologic examination was normal except for the drowsiness.
Haemoglobin was 12 gm/dl; WBC count was 16,700 mm with 88% neutrophils, 10% lymphocytes, 1% eosinophils and 1% monocytes. ESR was 140 mm/hr. Urine analysis showed mild proteinuria, 10-20 RBC and 2-3 WBC/HPF Tests for urine bile pigments were positive and bile salts were negative. LFT revealed total bilirubin 19.2 mg/dl with 11.6 mg/dl direct bilirubin, SGOT 122 units/L, SGPT 60 units/L, alkaline phosphatase 374 units/L, total protein 6.3 gm/dl with albumin 3.7 gm and globulin 2.6 gm/dl. CPK was 1020 units/L with CPK-MB 15 units/L. Serum electrolytes were: Na+ 116 meq/L, K+ 5.4 meq/L. chloride 80 meq/L and total CO2 was 13 meq/L Serum calcium was 8.4 mg/dl and phosphate 8.4 mg/dl. Blood urea was 359 mg/dl and creatinine 7.5 mg/dl. Prothrombin time was 26 sec with a control of 11 sec. Bleeding time, coagulation time, platele count were normal and fibrin degradation products were not seen. Ryles tube aspirate and stool gave a positive reaction for blood. Blood sugar, chest X-ray, ultrasound abdomen were all normal; HBsAg was negative.
ECG revealed atrial flutter with abnormal F waves (See [Figure:1]). The F-F cycle length was 0.15 seconds representing a flutter rate of 430 per minute. There was a basic 2:1 A V block reflected by the alternate conduction and block of the flutter impulses. A progressive increase in the F-R interval of the conducted impulses i.e. F-R interval was shortest (0.10 seconds) just following the dropped beat and longest (0.14 seconds) just preceding the next dropped beat, was also noted. In addition, groups of 3 or 5 ventricular complexes with R-R interval of 0.28 seconds were separated by one R-R interval of 0.4 seconds. Echocardiography did not reveal any evidence of myocardial or valvular lesion.
Patient's convalescent serum sample was tested for leptospira antibodies and was found positive by MAT against L. canicola. Attempted isolation of the organism by guinea-pig inoculation of patient's urine was negative.
Patient was treated with ampicillin and fluid, electrolyte and acid base deficits were corrected. He made a complete clinical and biochemical recovery without dialysis and remains well on follow- up visits. Pulse has become normal in rate and rhythm. ECG has reverted back to normal (See [Figure:1]).

  ::   Discussion Top

Leptospirosis is a term applied to disease caused by all leptospiras regardless of specific serotype. Several serotypes are known to exist in India. They include Icteroliacipiorrliagiae, Canicola, Autoinanalis, Grippotyplzosa, Tarassovi, Senzaranga, Pobmona, Hebdomadis, Andantans, Biflxa, Hyos, Sejroe, Medanesis, Alankarso, Batavia and Sexkoebing[5],[8].
Reports of leptospirosis in animals and man have been recorded from Andaman islands, Calcutta, Assam, Haryana, Bombay, Madras, Hyderabad and avangere[1],[3],[4],[5],[6],[7],[8],[10] reservoirs of infection in apparently healthy dogs, sheep, goats, horse, cattle, buffaloes, rats, other rodents and camels have been documented and organisms have been isolated from contaminated pond water [5]. Studies have shown that in certain parts of India upto 18% of patients with jaundice and upto 24% of cases of pyrexia of unknown origin (PUO) gave positive serologic evidence of leptospiral infection [8].
Cardiac arrythmias including paroxysmal atrial flutter, atrial fibrillation, ventricular tachycardia, and ventricular premature beats are known to occur with serotypes icterohaemorrhagiae, pomona and grippotyphosa but are uncommon with canicola infections [9]. In addition to several typical features of leptospirosis, our patient also presented with, interesting electrocardiographic evidence of atrial flutter with complex A-V conduction pattern in which 2:1 ventricular response changes spontaneously to 3:1 response and a gradual prolongation of the F-R interval. The repetitive grouping of ventricular complexes and the characteristic F-R prolongation indicate the operation of a Wenkebach phenomenon and concealed conduction. This complex A-V conduction pattern can be readily explained by the mechanism of multi-level A-V block. [11] As indicated in ladder diagram, there are probably two levels a of A-V block due to differential refractoriness within the A-V node. A proximal level with a 2:1 A-V block with halving of the effective atrial rate, i.e. the number of impulses penetrating deeper into the junction is reduced to half of the flutter rate. Three out of four, sometimes five out of six of these effective impulses traverse the junction and depolorize the ventricles, the last of each such group being blocked by a distal Wenkebach type of block (i.e. conduction ratio of 4:3 or 6:5). The QRS duration is 0.08 secs. The apparent slight prolongation of QRS duration in some of the ventricular complexes is due to the superimposed F waves, which distort the QRS complexes.
Features typical for leptospirosis in this patient in addition to the biphasic febrile illness and hepatorenal syndrome were severe muscle pain and muscle tenderness, conjunctival suffusion; jaundice with leukocytosis, elevated ESR, elevated CPK, abnormal urinary sediment, predominantly conjugated hyperbilirubinaemia with only minimally elevated SGOT and haemorrhagic tendency. If any of these features - See ‘F’ are present in a patient with jaundice with negative HBsAg, leptospirosis should be suspected[2] Diagnosis is confirmed by isolation of the organism by blood culture in the first week and urine culture after 14th day or by serology. Early diagnosis is important, since an timicrobial drugs to be effective must be administered within 4 days of the onset of illness.

  ::   Acknowledgments Top

The authors would like to thank Dr. R Raghavan, Professor, Dept. of Veterinary Microbiology, Veterinary College, University of Agricultural Sciences, Hebbal, Bangalore and Dr. P Dwivedi, Immunopathologist, Indian Veterinary Research Institute, Bereilly, UP for doing leptospirosis serology in our patient.

  ::   References Top

1. Bhatnagar RK, Sant MV, Jhala. HI. Prevalence of leptospirosis in Bombay. Studies in man and animals, Ind J Pathol & Bacteriol 1967; 10:324-327.  Back to cited text no. 1    
2.Christie AB. Leptospiral infections. In: "Infectious Diseases -Epidemiology and Clinical Practice," 3rd Edition. Churchill Livingstone, Edinburgh; 1980, pp 848-867.  Back to cited text no. 2    
3.Dalal PM. Leptospirosis in Bombay. Report of five cases. Ind J Med Sci 1960; 14:295-301.  Back to cited text no. 3    
4.Das Gupta BM. Leptospirosis in India. Ind Med Gaz 1938; 73:449-453.  Back to cited text no. 4    
5.Joseph KM, Kalra SL. Leptospirosis in India. Ind J Med Res 1966; 54:611-614.  Back to cited text no. 5    
6.Krishnamurthi MV, Madanagopalan N, Tajmul Hussain A. Leptospirosis in Madras. J Assoc Phys Ind 1965; 13:737-740.  Back to cited text no. 6    
7.Nagaraja Setty KL, Narayan A. Leptospirosis-our experience of 2 years. J Assoc Phys Ind 1985; 33:22.  Back to cited text no. 7    
8.Ratnam S, Sundararaj T, Tlyagarajan SP, Rao RS, Madanagopalan N, Subramanian S, et al. Serological evidence of leptospirosis in jaundice and pyrexia of unknown origin, Ind J Med Res 1983; 77:427-430.  Back to cited text no. 8    
9.Sanford. JP. Leptospirosis. In: "Harrison is Principles of Internal Medicine". 12th Edition. JD Wilson, E Braunwald, J Isselbacher, RG Petersdorf, JB Martin, AS Fauci, RK, editors. New York: McGraw Hill, Inc; 1991, pp 663-665.  Back to cited text no. 9    
10.Sajith Kumar R, Varghese PK, Paulose KP, Raveendran M. Uptospirosis (Weil's syndrome) in Central Kerala. A clinical and epidemiological analysis. J. Assoc Phys India 1988; 36:74.  Back to cited text no. 10    
11.Schamroth L. In: “The Disorders of Cardiac Rhythm”, 2nd Edition. Oxford: Black-well, Scientific Publications; 1980, pp 51-52.   Back to cited text no. 11    

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