Cardiac Leptospirosis

Iralphuaborque md14thbatch hdsdocharlabarda

Introduction
Leptospirosis is a disease caused by pathogenicspirochetes of the genus Leptospira. It is
considered the most common zoonosis in the world and the distribution is worldwide
(sparing the polar and desert regions), occurring with the greatest frequency in the
tropics. Humans and a wide range of animals, including mammals, amphibians, birds and
reptiles may be affected. However, humans are rarely chronic carriers and, therefore, are
considered accidental hosts [1].
Transmission occurs by direct contact with the body fluid of an acutely infected animal or
by exposure to soil or fresh water contaminated withthe urine of an animal that is a
chronic carrier.
Disease in humans is characterized by an acute febrile illness followed by mild self-limiting
sequelae or an even more severe, and often fatal, multiorgan involvement [1, 2]. The
studies regarding with leptospirosis infection are very limited in Turkey that it mostly
presented as seroepidemiologic studies in animals or brief human case reports. These
limited numbers of Weil disease cases were reported mostly from north, south and
Marmara regions of Turkey. The sensitivity regarding with diagnosing and reporting the
leptospirosis cases were increased in the last decade [2].
The aim of this case presentation and review is to report a case with leptospirosis infection,
which has caused severe acute myocarditis with dilated cardiomyopathy and full
recovery after ten days antibiotherapy.
Case
Our case was a 21-year-old white male who was drafted to complete his duty for the
army was sent to our center for the evaluation of altered consciousness with agitation,
peaked fever, generalised musculosceletal tendernessdyspnea and edema.
On first physical examination; the patient has altered sensorium and become agitated.
Fever was 38.5 C, arterial blood pressure was 120/80 mmHg and pulse was 120 bpm.
His past medical history was nonspecific. He suffered from the symptoms consistent with
upper respiratory tract infection 5 days before hospitalization and the symptoms
progressively increased.
Two days before hospitalization, he also had a loose stool two times with urinary and fecal
incontinence at the night. Owing to the association of these symptoms with lethargy, the
patient was referred to our hospital for further evaluation. His laboratory results were; white
blood cell count (WBC): 8800/mm3, platelet count :143000/mm3, total bilirubin 0.6 mg/dl,
urea 123 mg/dl, creatinine 3.06 mg/dl, aspartate aminotransferase (SGOT)176 U/L, alanine
aminotransferase (SGPT) 135 U/L, creatinine phosphokinase (CPK) 5717 U/L, lactate
dehydrogenase (LDH) 1155 U/L, myoglobin 4000 ng/ml, CPK-MB 32.2 ng/ml (Table-1).
Because of the detection of nuchalrigidity, a lumbar puncture was performed.
The cerebrospinal fluid (CSF) analysis revealed colorless, clear CSF sample with 45
cells/mm3, 59 mg/dl protein, 54 mg/dl glucose, 122.9 mg/dl NaCl and 61 mg/dl LDH.
The patient was started on intravenous crystallized penicillin 2 MIU 12 times daily, and
clarithromycin 1000 mg flacon b.i.d. amprically to cover streptococcal, meningococcal, gram
negative and atypical infections.
One day later, his clinical status was getting worse.
On day 2, his blood pressure was 124-59 mmHg, pulse 96/min and fever was 37.7 C. He was
tachycardic, with loud S1 and normal S2 with audible S3 without any murmur.
12 leads surface electrocardiography (ECG) was obtained. ECG demonstrated sinus rhytm
andslightly Q-Tc prolongation (516 msec) and therewere negative T waves in the leads . He has
no bruits and he has wet crackles at 1/3 basal level of both pulmonary. He has generalized
musculoskeletal tenderness without any jaundice and cyanosis but with 1(+) pretibial edema.
The laboratory results were given in table 1 and 2.the patient had the signs consistent with
congestive heart failure such as pretibial edema, pulmonary ralles and hypotension. He was
consulted with the cardiology clinic forechocardiograhic examination.
Our patient underwent a complete two dimensional transthoracic echocardiographic
and Doppler study at the left lateral decubitus position from multiple windows.
All measurements were performed with Wingmed system V (GE, Horten, NORWAY)
echocardiograph with a 2.5 MHz transducer. Echocardiographic measurements were
performed according to recommendations of the American Society of Echocardiography
(3).
The echocardiographic examination revealed diminished left ventricular systolic function
and segmental left ventricular wall motion abnormalities, which were septal, anterolateral,
anteroapical, lateral hypokinesis and inferior akinesis with grade 1 diastolic dysfunction.
The cardiac output was measured as 1.5 lt/min with a left ventricular ejection fraction of
38 %. Left ventricle was dilated (66 mm) and a 0.2 mm thick minimal pericardial fluid was
detected localized only to left ventricle lateral wall border.
A wide variety of infections were assessed for the differential diagnosis, including bacterial
sepsis, streptococcal infection, meningococcal infection, legionellosis, mycoplasma
infection, ricketsioses, brucellosis, salmonellosis and some viral infections such as Ebstein-
Barr virus, cytomegalovirus and human immunodeficiency virus. We finally diagnosed
leptospirosis infection with multiorgan involvement including cardiovascular and central
nervous system with symptoms of fever, somnolence, prostration and myalgia. Elevated
creatinine phosphokinase levels, prominent neutrophilia with positive MAG*. MAT**, and
IgM-ELISA*** tests for the blood and/ or CSF specimens also helped us confirming the
diagnosis of anicteric leptospirosis infection (Table-2).
After completing the parenteral medical treatment (Penicillin-G 24 MIU/day and
clarithromycin 1 gr b.i.d, 10 days; ramipril 2.5 mg/day and furosemide 20 mg/day were
added to his treatment. On day 3 after the treatment, the patient was dramatically
recovered and the repeat echocardiographic examination revealed normal
echocardiographic findings with a left ventricular diastolic internal diameter of 49 mm and
an ejection fraction of 68 %. The patient was discharged without any complication at 13th
day of hospitalization with only the suggestion of a control examination periodically. He
returned to active duty one month later.
Our patient has been followed so far. There is no recrudescence and any symptoms or
findings relating to myocarditis, or other leptospirosis manifestations at 10th month after
the first attack.
Discussion:
zoonotic
Multi-organ
involvement
myopericarditis
Cardiac involvement in leptospirosis
Common but underestimated
Our patient
Auscultation: Loud S1 and S3 without any murmur
ECG: slightly Q-Tc prolongation and significant negative T- waves
ECHO:
diminished left ventricular systolic function and
segmental left ventricular wall motion abnormalities, which were septal,
anterolateral, anteroapical, lateral hypokinesis and inferior akinesis with
grade 1 diastolic dysfunction.
The cardiac output was measured as 1.5 lt/min with a left ventricular
ejection fraction of 38 %.


Our case vs literature
Common symptom

response to treatment
Renal involvement assoc. with HTN, HPO
Recovery

QTc -prolongation


Laboratory is ESSENTIAL.
In general, diagnosis is based on initially upon clinical suspicion, confirmed later by the
laboratory.
Isolating the pathogenic organism from the blood, CSF or urine samples are the gold
standard for the diagnosis of this disease.
The serological tests are very important confirming the diagnosis of leptospirosis infection
because of the long incubation period of the pathogen [1-2,4].
Treatment
Depends on severity and duration of symptoms at the
time of presentation.
Penicillin most recommended
We used penicillin-G and clarithromycin -mixed infections
the best way to avoid leptospirosis is to keep away from
animals and areas that may be contaminated by their
urine.
Conclusion;
The presentation of an anicteric form of leptospirosis is often non-
specific and may be overlooked unless there is a high clinical
suspicion. Our case indicates that myopericarditis, acute renal
failure, acute hepatitis and meningitis may be associated with
leptospirosis. Although these complications may be fatal, early
diagnosis and treatment with penicillin-G are very important to
prevent the morbidity and mortality.
In addition, this infection should be considered for the feverish
patients with acute myopericarditis.