Leptospirosis is a zoonosis with a widespread distribution
Leptospirosis can present with a wide array of clinical symptoms. Renal failure,
liver involvement, thrombocytopenia, myocarditis, neurological involvement, DIC
etc are the notable systemic complications.
We present the case reports of three patients who were referred with fever, chest
pain and ECG changes to a tertiary care centre.
55 year old presented with the complaints of
- fever of two days duration
- vomiting of a days duration
- myalgia of a days duration
Clinical examination was unremarkable other than for a Pulse rate of 100/min on
presentation with a supine blood pressure of 90/70. Auscultation of the chest showed
This patient a bus driver by profession had undertaken a pilgrimage to a hilltop
shrine which required him to walk 4 km uphill barefooted .He had undertaken the
pilgrimage 4 days prior to the day of admission.
His past history was non contributory. He does not consume alcoholic drinks. He
gave a history of 20 years of cigarette smoking.
He gave no family history of vascular events.
His ECG taken on presentation showed sinus tachycardia with ST elevation in the
anterior chest leads. The ST elevation pattern shows a concavity upwards which is
atypical for myocardial infarction. As also there is a sagging ST depression in
the inferior leads with low voltages in the frontal leads
A bedside Echocardiogram was done in view of his atypical symptoms, ECG changes
to rule out a myocardial infarction. Echo revealed normal LV and RV dimensions without
any RWMA which would suggest an AMI. There was no evidence of myocarditis or of
any pericardial pathology. ECG 2 ( 2 HOURS LATER )
Laboratory investigations –
Day 1 of admission-
Hb gm% 14, TLC 11850/cmm, Polymorphs 47%, Lymphocytes 16%, Eosinophils 1%, Band
forms 36%. ESR 15 mm/hr, platelet count 157,000/cmm CPK-MB 16 U/L ( 0-25 U/L )
Random Blood sugar 162 mg%
Blood Urea 44 mg/dl, serum creatinine 15 mg/dl, serum Na 134 meq/L, serum K 4.3
Urine examination- albumin nil, sugar yellow, microscopy 1-3 pus cells HPF
Day 2- Platelet count 136,000/cmm.
FBS 102 mg/dl
AST 21 ( 5-35 U ), ALT 24 ( 5-40 )
CPK-MB 20 U/L
CPK 900 U/L
Day 3 –
Hb 13.1 gm%, TLC 6400/cmm, P51%, L 37%, E 7%, M 1%, Band forms 3%, Meta 1% Platelets
LEPTOSPIRA Ig M antibody titre positive at 43.28
Control values ( Positive > 11, equivocal 9-11, negative < 9 )
Course in hospital- The patient was afebrile from Day 2 of admission His symptoms
of vomiting and chest pain subsided from the second day of admission He was started
on Injection Crystalline penicillin 20 lakh units given intravenous every 6 hourly.
The same was continued for 6 days.
The patient was discharged on the seventh day after admission with the advice to
continue Oral Doxycycline for 5 days.
He was re-evaluated 2 weeks after discharge. When he reported that he was back at
work without any undue symptoms.
58 year old was referred from a local hospital with the complaint of a retrosternal
chest discomfort with radiation down the left upper limb.
He had been admitted in the secondary care centre with the complaints of fever and
myalgia of two day duration associated with nausea, vomiting and diarrhea. The myalgia
was most prominent in the muscles of the back. On day two of admission in that hospital
he complained of giddiness.
Examination at the time of presentation revealed bilateral rhonchi over the lung
fields < 1/3 of the lung fields. The liver was palpable but not tender.
He denied ever being a smoker. He was not a known diabetic or hypertensive. He denied
any exert ional symptoms prior to admission. His family history was not significant
for vascular disease.
A bed side ECHO was done, which did not show any RWMA. There was no signs suggestive
of pericarditis or myocarditis.
In spite of the very significant ST elevation a decision as to not thrombolyse the
patient was taken, in view of the history of fever, and absence of a RWMA in spite
of the ECG changes. The pain too was atypical in it being not more than a mild chest
heaviness. As also the patient was fairly comfortable during the ECHO interrogation.
Repeat ECG ( 2 hours later )
In view of the atypicality of presentation and the regression of ECG changes a decision
of not to thrombolyse was stuck to. The patient was started on intravenous Penicillin.
Lab investigations –
On admission in the previous hospital –
Hb 14 gm%, TLC 11,600/cmm, P 89%, L11%, ESR 30 mm/hr, platelet count 2.5 lakhs/
Serum AST 26 U/L, ALT 16 U/L,
S Na+ 136 meq/L, S K+ 3.7 meq/L
Urine routine and microscopy- albumin trace, sugar nil, pus cells 2-4 /HPF
Day 1 of admission-
Random blood sugar 223 mg/dl
S creatinine 1.2 mg/dl
S Na+ 134 meq/L, S K+ 37 meq/L
Hb 98 gm%, TLC 7900/cmm, P 85%, L11%, Band forms 4%. ESR 79mm/hr, Platelet count
Urine routine and microscopy – albumin trace, sugar orange, pus cells 0-2 /HPF
Creatinine phosphokinase CPK 1013 U/L ( 20-200 U/L )
CPK-MB 69 U/L ( 0-25 U/L )
Chest X ray P –A view showed no cardiomegaly, increased broncho-vascular markings
Hb 9.9 gm%, PCV 30%, platelets 80,000/cmm, 80,000/cmm, 79,000/cmm
Urine RBC 0-1/ HPF
FBS 287 mg/dl, PPBS 241 mg/dl
AST 97 U/L, ALT 36 U/L
Lipid profile total CHO 114 mg/dl, HDL 25 mg/dl, LDL 62 mg/dl, VLDL 27 mg/dl, TG
CPK MB 40 U/L
Platelet count 85,000/cmm, 81,000/cmm,
FBS 284 mg/dl
platelet count 91,000/cmm FBS 115mg/dl
Platelet count 93,000/cmm
Platelet count 108,000/cmm
Dengue Ig M was negative
Leptospira Ig M positive at a titre of 33.7 u/ml
Platelet count 148,000/cmm
Day 9 –
FBS 78 mg/dl, S creatinine 0.75 mg/dl
Platelet count 160,000/cmm
Urine albumin nil
Hb 12.5 gm%, TLC 7200/cmm, P 43%, L 50%, E 2%, Band forms 4%, Metamyelocytes 1%,
platelet count 187,000/cmm
Course in hospital – The patient was started on Injection crystalline penicillin
at a dose of 20 lakhs, intravenous every 6 hourly.
He was afebrile from the third day after admission.
He did not receive any blood products in spite of the low Hb and platelet count
He was discharged on the tenth day after admission on oral Doxycline with the advise
to continue the same for 7 days
58 year old male admitted in medicine ward with the complaints of, fever and body
ache of three days duration. He also complained of nausea and vomiting with generalized
pruritus. He also gave the history of diminished urine output for the past three
On examination the pulse rate was 90/minute, BP was 130/80 mm Hg in the supine.
He had bilateral basal crepitations over the lung fields. He had conjunctival suffusion.
He also had a swelling of the left knee.
He is diabetic and hypertensive on irregular treatment for the same. He denied usage
of tobacco and used to consume alcoholic drinks on a regular basis.
He had been investigated in the lines of Coronary artery disease following an episode
of chest pain. An ECHO done six years prior to the present admission was reported
as normal. He did 10 mins and 17 secs on the TMT at 11.8 METS, which was reported
as negative for inducible ischaemia.
He developed hypotension on Day 2 of admission with ST elevation on the ECG monitor.
A 12 lead ECG taken also showed the same.
ECHO done did not reveal any RWMA. There was no evidence of pericarditis or myocarditis
The patient was already on intravenous penicillin with the clinical diagnosis of
Hb 13.4 gm%, Total leucocyte count 7460/cmm
Differential count – polymorphs 80%, lymphocytes 10%, eosinophils 2%, monocytes
4%, band forms 2%, metamyelocytes 2%
ESR 66 mm/hour. Platelet count 82,000/cmm- 78,000/cmm
Blood urea 116 mg/dl, serum AST 26 u/l, ALT 55 u/l. S creatinine 4.29 mg/dl
S urea 125 mg/dl, creatinine 4.79 mg/dl. S Na+ 128 meq/L, S K+ 3.9 meq/L
Synovial fluid WBC’s 5500/cmm, Poly 70%, Lymph 30%, total protein 3.9 g/dl, sugar
Hb 13 gm%, PCV 38%, platelet count 50,000/cmm-69,000/cmm
Fasting blood sugar 168 mg/dl, S urea 99 mg/dl, creatinine 4.36 mg/dl, S Na+ 135
meq/L, S K+ 4 meq/L
Serum CPK-MB 19 U/L ( 0-25 U/L )
Hb 121 gm%, PCV 36%, platelet count 115,000/cmm
FBS 197 mg/dl, S urea 140 mg/dl, creatinine 4.94 mg/dl, S.Na+ 128 meq/L, S.K+ 3.5
Lipid profile- Total cholesterol 123 mg/dl, HDL 15 mg/dl, LDL 32mg/dl, VLDL 76mg/dl,
Triglycerides 381 mg/dl
CPK 35 u/l ( 20-200 u/l ), CPK-MB 8 u/l
FBS 132 mg/dl, S urea 151 mg/dl, S creatinine 4.64 mg/dl, S. Na+ 127 meq/L, S.K+
Hb 12.7 gm%, PCV 38%, platelet count 151/cmm
DENGUE IgM antibody – negative.
LEPTOSPIRA IgM antibody POSITIVE at a titre of 36.37 units/ml
Hb 12.4 gm%, PCV 37%, platelet count 223,000/cmm
FBS 177 mg/dl, urea 132 mg/dl, creatinine 3.24 mg/dl, S.Na+ 143 meq/L, S K+ 4.1
Urine – albumin trace, pus cells 1-3/HPF, Hb nil, myoglobin negative.
FBS 172 mg%, S urea 115 mg/dl, S creatinine 2.36 mg/dl, S.Na+ 132 meq/L, S K+ 4.6
Hb 125 gm%, PCV 38%, Platelets 323,000/cmm, Total leucocyte count 7910/cmm, Polymorphs
49%, Lymphocytes 37%, eosinophils 8%, monocytes 5%,Metamyelocytes 1%
S UREA 87 mg/dl, S creatinine 1.77mg/dl, S Na+ 131 meq/L, S K+ 4.8 meq/L. PPBS 345
Urine albumin- trace.
FBS 243 mg/dl
PPBS 341 mg/dl
FBS 290 mg%, S urea 46 mg/dl, S creatinine 1.06 mg/dl. PPBS 333mg%
FBS 243 mg%
Course in hospital
The patient developed effusions in both knees. The left knee effusion was aspirated
and the biochemistry and cytology of it suggested a transudate.
The patient went into an oliguric renal failure. He was dialysed for the same on
Day 2 of admission. He developed hypotension with ST changes on the ECG during the
course of dialysis. He did not require a second dialysis. His urine output improved
subsequent to the dialysis.
He had a mild chest heaviness with ECG changes suggestive of an acute myocardial
infarction during the course of dialysis. An AWMI was suspected.
The ECHO done at the bedside did not reveal any regional wall motion abnormality
which would suggest an AMI. He was started on vasopressors with which the blood
pressure picked up. He was not started on anti-platelet agents, nitrates, anti coagulants
or on fibrinolytic therapy, given the low platelets, acute renal failure, need for
dialysis and the a typicality of ECG changes and absence of RWMA on the ECHO.
His CPK-MB values taken on day 1 of pain and repeated 24 hours after the onset of
pain were both within normal levels.
ECHO done prior to discharge also did not reveal any changes which would suggest
an AMI or myocarditis.
The patient was afebrile from Day 3 after admission.
He developed an irritant dermatitis on Day 5 of admission which required oral steroids,
H1 receptor blockers and steroid creams.
He was relieved of his chest symptoms a few hours after the onset of pain without
any further recurrence.
His urine output improved following dialysis and the serum creatinine had normalized
with a normal urine output by the time of discharge.
His platelet count improved over the days.
The ECG and platelet count normalized by the time of discharge.
Leptospirosis is known to present as a myocarditis which in patients of leptospirosis
carries a poor prognosis. Myocarditis is associated with hypokalemia, acute renal
failure, disseminated intravascular coagulation and hepatic dysfunction, all of
which carry a bad prognosis.
The three patients reported here had been referred as patients of acute myocardial
infarction, given the ECG changes suggestive of the same. The quality of pain in
all three patients was not typical for coronary ischemia/ infarction. All the three
patients presented here had no echocardiographic features to suggest an AMI. Surprisingly
the three patients did not have any features of myocarditis either. All three patients
had low platelets, leucocytosis with a left shift on the peripheral smear. None
of the three required treatment along cardiac lines.
All three of them were seen two weeks after discharge from hospital when they reported
as to not having had any further chest symptoms.
A coronary angiogram was not done in any of the three subjects on follow up. All
three patients refused the same on follow up stating financial constraints as a
ST / T changes are known to occur in leptospirosis secondary to either myocarditis
or electrolyte imbalance. In the three reported cases none of the patients had features
of myocarditis on ECHO, nor was there significant imbalance in the serum electrolytes.
The objective is to bring to attention significant ECG changes in patients with
leptospiraemia. The ECG changes mimicked an Acute myocardial infarction in all three.
The changes resolved spontaneously, without any need for treatment for coronary
ischaemia. There was no loss of R voltages ( which would imply cardiac tissue loss
) in leads which showed ST elevation in the subsequent ECG’s prior to discharge.
The echocardiographic interrogation of the heart at presentation and pre discharge
did not show any RWMA suggestive of an AMI. As also the cardiac enzyme markers were
not raised enough to qualify for an AMI. Importantly all three patients had a vague
dull ache in the anterior chest which was not typical of coronary ischaemia. The
ECG changes resolved spontaneously with improvement in the clinical condition. The
ST elevation on the ECG was also typical for coronary artery disease as the ST elevation
was diffuse, not pertaining to arterial territories transgressing arterial boundaries.
As also it was significant that there were no reciprocal changes in any of the ECG’s.
In areas where leptospirosis is endemic it is imperative to entertain this diagnosis
in patients with ST elevation on the surface ECG with a history of fever.