Cardiac Leptospirosis

8/10/2019 Cardiac Leptospirosis

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Cardiac LeptospirosisIralphuaborque md14thbatch hdsdocharlabarda


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Introduction

Leptospirosis is a disease caused by pathogenicspirochetes of the genus Lconsidered the most common zoonosis in the world and the distribution(sparing the polar and desert regions), occurring with the greatest freqtropics. Humans and a wide range of animals, including mammals, amphibiareptiles may be affected. However, humans are rarely chronic carriers and,

considered accidental hosts [1].

Transmission occurs by direct contact with the body fluid of an acutely infecby exposure to soil or fresh water contaminated withthe urine of an anichronic carrier.


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Disease in humans is characterized by an acute febrile illness followed by mildsequelae or an even more severe, and often fatal, multiorgan involvement [1studies regarding with leptospirosis infection are very limited in Turkey that it mpresented as seroepidemiologic studies in animals or brief human case reporlimited numbers of Weil disease cases were reported mostly from north, southMarmara regions of Turkey. The sensitivity regarding with diagnosing and repoleptospirosis cases were increased in the last decade [2].

The aim of this case presentation and review is to report a case with leptospirwhich has caused severe acute myocarditis with dilated cardiomyopathy anrecovery after ten days antibiotherapy.


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Case

Our case was a 21-year-old white male who was drafted to complete hiarmy was sent to our center for the evaluation of altered consciousness wpeaked fever, generalised musculosceletal tendernessdyspnea and edema.

On first physical examination; the patient has altered sensorium and beco

Fever was 38.5 C, arterial blood pressure was 120/80 mmHg and pulse was 12 His past medical history was nonspecific. He suffered from the symptoms c

upper respiratory tract infection 5 days before hospitalization and thprogressively increased.


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Two days before hospitalization, he also had a loose stool two times with urinincontinence at the night. Owing to the association of these symptoms withpatient was referred to our hospital for further evaluation. His laboratory resulblood cell count (WBC): 8800/mm3, platelet count :143000/mm3, total biliruurea 123 mg/dl, creatinine 3.06 mg/dl, aspartate aminotransferase (SGOT)17aminotransferase (SGPT) 135 U/L, creatinine phosphokinase (CPK) 5717

dehydrogenase (LDH) 1155 U/L, myoglobin 4000 ng/ml, CPK-MB 32.2 ng/ml (T

Because of the detection of nuchalrigidity, a lumbar puncture was performed

The cerebrospinal fluid (CSF) analysis revealed colorless, clear CSF samcells/mm3, 59 mg/dl protein, 54 mg/dl glucose, 122.9 mg/dl NaCl and 61 mg


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The patient was started on intravenous crystallized penicillin 2 MIU 12 timclarithromycin 1000 mg flacon b.i.d. amprically to cover streptococcal, meningonegative 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 3tachycardic, with loud S1 and normal S2 with audible S3 without any murmur.

12 leads surface electrocardiography (ECG) was obtained. ECG demonstratandslightly Q-Tc prolongation (516 msec) and therewere negative T waves in theno bruits and he has wet crackles at 1/3 basal level of both pulmonary. He hamusculoskeletal tenderness without any jaundice and cyanosis but with 1(+) prThe laboratory results were given in table 1 and 2.the patient had the signs ccongestive heart failure such as pretibial edema, pulmonary ralles and hypoteconsulted with the cardiology clinic forechocardiograhic examination.


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Our patient underwent a complete two dimensional transthoracic echocand Doppler study at the left lateral decubitus position from multiple window

All measurements were performed with Wingmed system V (GE, Horteechocardiograph with a 2.5 MHz transducer. Echocardiographic measurperformed according to recommendations of the American Society of Echo(3).

The echocardiographic examination revealed diminished left ventricular syand segmental left ventricular wall motion abnormalities, which were septal,anteroapical, lateral hypokinesis and inferior akinesis with grade 1 diastolicThe cardiac output was measured as 1.5 lt/min with a left ventricular ejecti38 %. Left ventricle was dilated (66 mm) and a 0.2 mm thick minimal pericadetected localized only to left ventricle lateral wall border.


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A wide variety of infections were assessed for the differential diagnosis, inclusepsis, streptococcal infection, meningococcal infection, legionellosis, infection, ricketsioses, brucellosis, salmonellosis and some viral infections sucBarr virus, cytomegalovirus and human immunodeficiency virus. We finaleptospirosis infection with multiorgan involvement including cardiovascula

nervous system with symptoms of fever, somnolence, prostration and myacreatinine phosphokinase levels, prominent neutrophilia with positive MAGIgM-ELISA*** tests for the blood and/ or CSF specimens also helped us cdiagnosis of anicteric leptospirosis infection (Table-2).


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After completing the parenteral medical treatment (Penicillin-G 24 Mclarithromycin 1 gr b.i.d, 10 days; ramipril 2.5 mg/day and furosemide 20 madded to his treatment. On day 3 after the treatment, the patient wasrecovered and the repeat echocardiographic examination reveechocardiographic findings with a left ventricular diastolic internal diameter an ejection fraction of 68 %. The patient was discharged without any compli

day of hospitalization with only the suggestion of a control examination pereturned to active duty one month later.

Our patient has been followed so far. There is no recrudescence and anyfindings relating to myocarditis, or other leptospirosis manifestations at 10ththe first attack.


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Discussion:

zoonoticMulti-organ

involvementmyoper


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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 w

anterolateral, anteroapical, lateral hypokinesis and inferior ak

grade 1 diastolic dysfunction.

The cardiac output was measured as 1.5 lt/min with a left ven

ejection fraction of 38 %.


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Our case vs literature

Common symptom

response to treatment

Renal involvement assoc. with HTN, HPO

Recovery

QTc -prolongation


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Laboratory is ESSENTIAL.

In general, diagnosis is based on initially upon clinical suspicion, confirmed lalaboratory.

Isolating the pathogenic organism from the blood, CSF or urine samples are

standard for the diagnosis of this disease.

The serological tests are very important confirming the diagnosis of leptospirobecause of the long incubation period of the pathogen [1-2,4].


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Treatment

Depends on severity and duration of symptom

time of presentation.

Penicillin most recommended

We used penicillin-G and clarithromycin -mixed in

the best way to avoid leptospirosis is to keep aw

animals and areas that may be contaminated

urine.


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Conclusion;

The presentation of an anicteric form of leptospirosis is ospecific and may be overlooked unless there is a higsuspicion. Our case indicates that myopericarditis, acfailure, acute hepatitis and meningitis may be assoc

leptospirosis. Although these complications may be fadiagnosis and treatment with penicillin-G are very imprevent the morbidity and mortality.

In addition, this infection should be considered for thpatients with acute myopericarditis.

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Cardiac Leptospirosis