1179450
case-report20232023
HICXXX10.1177/23247096231179450Journal of Investigative Medicine High Impact Case ReportsSwarath et al
Case Report
Leptospirosis-Induced Myocarditis and
Arrhythmias
Journal of Investigative Medicine High
Impact Case Reports
Volume 11: 1–5
© 2023 American Federation for
Medical Research
https://doi.org/10.1177/23247096231179450
DOI: 10.1177/23247096231179450
journals.sagepub.com/home/hic
Steven Swarath, MBBS1, Nicole Maharaj, MBBS1,
Rajeev Seecheran, MBBS, MHA2, Valmiki Seecheran, MBBS, MSc1,
Jessica Kawall, MBBS1, Stanley Giddings, MBBS3,
and Naveen Anand Seecheran, MBBS (MD), MSc, FACP, FRCP(E),
FACC, FESC, FSCAI3
Abstract
Cardiac manifestations in leptospirosis usually involve atrial arrhythmias, conduction abnormalities, and nonspecific ST-T
changes, while left ventricular dysfunction is rare. We present the case of a 45-year-old male without a pre-existing
cardiovascular history who developed atrial fibrillation and atrial and ventricular tachycardia, in addition to new-onset
cardiomyopathy in the setting of fulminant leptospirosis infection.
Keywords
leptospirosis, myocarditis, ventricular tachycardia, atrial tachycardia, atrial fibrillation, arrhythmia, heart failure
Introduction
Leptospirosis is a zoonotic disease caused by spirochetes of
the genus Leptospira.1 Severe disease causes multisystem
dysfunction, which includes cardiac involvement. Atrial
fibrillation (AF), first-degree atrioventricular block, and
nonspecific ST-T changes likely reflecting myocarditis are
seen in patients with systemic infection. However, these
patients rarely have significant left ventricular dysfunction
(LVD).2
We present the case of a 45-year-old male without a preexisting cardiovascular history who developed AF and atrial
(AT) and ventricular tachycardia (VT), in addition to newonset cardiomyopathy in the setting of fulminant leptospirosis infection.
Case Report
A 45-year-old South Asian male farmer with no significant
medical history presented to the emergency department with
chest pain and generalized myalgias. He was exposed to
“flood waters” a week before admission. He also reported
fever and “flu-like” symptoms, which seemingly resolved 2
days before seeking medical care. He was a lifelong nonsmoker and denied using alcohol or any illicit substances.
There was no pertinent travel or pet history.
His vital signs on admission were blood pressure of 86/58
mm Hg, heart rate of 102 beats per minute, pulse-oximetry
94% on room air, random blood glucose 184 mg/dL, and
temperature of 36.4 °C. On physical examination, he was
noted to be severely icteric. He had an S3 with no murmurs.
Air entry was decreased, and there were occasional scattered
crackles bilaterally. His abdomen was mildly distended,
however, nontender. He was alert and oriented without any
neurological deficits, and there was no anasarca with mild
pitting edema to the tibial tuberosity bilaterally. His chest
radiography revealed borderline cardiomegaly with mild
interstitial edema, and initial admission 12-lead electro­
cardiogram indicated sinus rhythm at 94 beats per minute
with no acute dynamic changes. The patient was immediately resuscitated with intravenous crystalloid infusion, and
his electrolytes were repleted judiciously. His coronavirus
rapid antigen test returned a negative result.
1
North Central Regional Health Authority, Mt. Hope, Trinidad and
Tobago
2
Kansas University Medical Center, Wichita, USA
3
University of the West Indies, St. Augustine, Trinidad and Tobago
Received March 31, 2023. Revised May 4, 2023. Accepted May 14, 2023.
Corresponding Author:
Naveen Anand Seecheran, MBBS (MD), MSc, FACP, FRCP(E), FACC,
FESC, FSCAI, Department of Clinical Medical Sciences, Faculty of Medical
Sciences, University of the West Indies, 2nd Floor, Building #67,
Eric Williams Medical Sciences Complex, Mt. Hope, St. Augustine,
Trinidad and Tobago.
Email: nseecheran@gmail.com
Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons AttributionNonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction
and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages
(https://us.sagepub.com/en-us/nam/open-access-at-sage).
2
Journal of Investigative Medicine High Impact Case Reports
Table 1. The Patient’s Admission Laboratory Data.
Laboratory value
Complete blood count, comprehensive metabolic panel and cardiac biomarkers
White cell count
Hemoglobin
Platelets
Serum sodium
Serum potassium
Serum creatinine
Blood urea nitrogen
Serum calcium
Serum magnesium
Fasting blood sugar
Alanine aminotransferase
Aspartate aminotransferase
Alkaline phosphatase
Serum albumin
International normalized ratio
Prothrombin time
Activated partial thromboplastin time
Total bilirubin
Conjugated bilirubin
Troponin I
Creatine kinase
Infectious diseases panel
Erythrocyte sedimentation rate
C-reactive protein
Blood cultures
Urine culture
Human immunodeficiency virus enzyme-linked immunosorbent assay
QuantiFERON-TB GOLD (Cellestis Limited, Carnegie, Victoria, Australia)
Biofire Respiratory Panel (RP 2.1) (Biofire Diagnostics (Salt Lake City, UT, USA))
Respiratory pathogen panel (BioFire) tests
COVID-19 test (Centers for Disease Control and Prevention’s 2019-nCoV Real-Time
RT-PCR Diagnostic Panel, Atlanta, GA)
Leptospirosis immunoglobulin M (IgM) antibodies
Hepatitis B surface antigen
Hepatitis C IgM antibodies
Hepatitis C immunoglobulin G (IgG) antibodies
Dengue IgM antibodies
Dengue IgG antibodies
Malaria thick and thin smears
Urine Legionella antigen
Patient’s value
Normal range
19.6
13.4
67
132
4.4
4.3
81
9.2
0.9
84
73
34
154
3.2
1.2
14.6
34
15.5
11.1
1.2
293
4.5-11.0 × 109/L
14.0-17.5 g/dL
156-373 × 103/µL
135-145 mEq/L
3.5-5.1 mEq/L
0.5-1.2 mg/dL
4-24 mg/dL
9.6-11.2 mg/dL
1.7-2.2 mg/dL
60-120 mg/dL
20-60 IU/L
5-40 IU/L
40-129 IU/L
3.5-5.5 g/dL
1-1.4
11-14 seconds
26-31 seconds
0.1-1.3 mg/dL
0.1-0.8 mg/dL
0.00-0.08 ng/mL
29-190 IU/L
55
42
Negative
Negative
Nonreactive
Negative
Negative
0-22 mm/h
0.0-1.0 mg/dL
Positive or negative
Positive or negative
Nonreactive or reactive
Positive or negative
Positive or negative
Negative
Positive or negative
Positive
Negative
Negative
Negative
Negative
Negative
Negative
Negative
Positive or negative
Positive or negative
Positive or negative
Positive or negative
Positive or negative
Positive or negative
Positive or negative
Positive or negative
Bold term indicates the patient’s admission diagnostic data.
He was subsequently admitted to the medical intensive
care unit, where he was empirically initiated on renallydosed intravenous piperacillin-tazobactam and tigecycline
for suspected leptospirosis infection. He also received the
routine management bundle for severe sepsis, excluding corticosteroid therapy. The following day, the patient incurred
respiratory failure with severe hypoxemia and was commenced on high-flow noninvasive ventilation. A bedside
2-dimensional transthoracic echocardiogram revealed a
moderate global hypokinesis with an estimated ejection fraction of 30% to 35% and mild-moderate mitral regurgitation.
A noncontrast computed tomography scan of the chest, abdomen, and pelvis revealed basilar, bilateral air-space disease
suggestive of aspiration pneumonitis. Eventually, his serologies returned positive for leptospirosis infection (Table 1).
The patient endured a rocky clinical course. He alternated
rapidly between AT, AF with rapid ventricular response, and
VT, for which he was defibrillated and started on low-dose
amiodarone infusion at 0.5 mg/min with vigilant hepatic
function monitoring (Image 1). During his ensuing hospitalization, he remained clinically unstable and could not
undergo further diagnostic testing to clinch or ascertain his
Swarath et al
3
tentative diagnosis of nonischemic cardiomyopathy and
myocarditis. He deteriorated into a vicious spiral of septic
and cardiogenic shock for which he was admitted on multiple inotropic supports; however, he ultimately succumbed to
his illness due to multiorgan failure.
Discussion
Image 1. The patient’s 12-lead electrocardiograms were
interspersed during his hospital course. (A). The patient’s
electrocardiogram displays atrial tachycardia with variable
block and nonspecific ST-T changes. (B) The patient’s
electrocardiogram displays atrial fibrillation with rapid
ventricular response, rate-related intraventricular conduction
delay, and secondary ST-T changes. (C). The patient’s
electrocardiogram displays ventricular tachycardia with several
features, including atrioventricular disassociation, prolonged
QRS duration exceeding 160 milliseconds, and ventricular
concordance.
Leptospirosis is a biphasic illness, initially presenting with
an acute febrile episode that reflects early sepsis onset, typically 1 week in duration. Subsequently, there is an afebrile
interval period, followed by a recrudescence of fever marking the onset of delayed immunity with sequelae of severe
multiorgan dysfunction such as pulmonary hemorrhage, fulminant hepatic failure, acute kidney injury, and cardiac manifestations.3 The pathophysiology of the cardiac involvement
of leptospirosis is not well elucidated. However, a glycoprotein fraction of the leptospiral cell wall has been postulated
to inhibit the Na-K ATPase and implicated as a potential
arrhythmogenic mechanism.4 The commonly observed electrocardiographic changes include conduction defects, nonspecific ST-T changes, and atrial arrhythmias.5-8 In addition,
leptospirosis can be complicated by myocarditis and endocardial inflammation consistent with vasculitis.6 However,
LVD is not usually seen.9 Our patient displayed a febrile
illness with constitutional symptoms, one prior to the index
presentation. He likely presented in the delayed immune
phase of illness with evidence of multiorgan involvement of
the hepatic, renal, hematologic, and cardiovascular systems.
Due to the endemic nature of leptospirosis in Trinidad and
the patient’s contextual history (farmer being exposed to
“flood waters”), there was a high degree of clinical suspicion,
hence the prompt diagnosis and management, confirmed by
serological testing.10
Despite the association of leptospirosis and VT being
exceedingly rare, our clinical acumen deduced that leptospirosis-induced myocarditis was the chief culprit. Acute
myocarditis is associated with increased major adverse
cardiovascular events, including short-term mortality.11
This diagnosis should be considered taking into account
the patient’s symptomatology, the presence of VT (and non­
sustained VT on telemetry), and new-onset cardiomyopathy
(CMP) diagnosed by transthoracic echocardiography.12,13
The Lake Louise criteria delineate diagnostic criteria for
myocarditis; however, the patient remained critically ill and
hemodynamically unstable throughout his hospitalization,
precluding such an examination from being performed.14
The patient’s lack of pre-existing cardiovascular history,
contributing comorbidities, and absence of calcium on chest
computed tomographic scan also lent credence to this tentative diagnosis; however, we do acknowledge this is not
definitive.12 Coronary angiography was also not performed
to exclude an ischemic etiology due to his multiorgan
dysfunction syndrome, specifically his acute kidney injury.
4
The mechanism of VT may be attributed to the myocardial
inflammatory process secondary to a pathogenic infection
that may continue even after myocardial recovery.15 The
substrate involves an intricate milieu of formation of microreentry circuits triggered by the pro­arrhythmic effects of
cytokines leading to electrical remodeling.16-18 Most cases
with myocardial involvement describe normal or mildly
reduced left ventricular function.7,8 Moderate to severely
reduced left ventricular function is rarely encountered and
reported.19,20
The patient also displayed a multitude of atrial arrhythmias, including sinus tachycardia, AT, and AF with rapid
ventricular response. Atrial arrhythmias in leptospirosis have
been well documented in the literature.21,22 These arrhythmias may result from a plethora of metabolic, electrolyte
derangements, intravascular volume imbalances, and neurohormonal and catecholaminergic stress.23,24 Proposed mechanisms of these arrhythmias involve sympathetic nervous
system–induced calcium entry into cardiac myocytes and
spontaneous calcium release from the sarcoplasmic reticulum.25 Our patient illustrated several of the aforementioned
electrolyte abnormalities, including hyponatremia, hyper­
kalemia, hypomagnesemia, and hypocalcemia, all of which
were aggressively corrected despite his critical illness physiology of severe sepsis and cardiorenal syndrome (Table 1).
Currently, there are no specific treatment guidelines for
leptospiral myocarditis other than treating the underlying
sepsis and supportive therapy.26 Cardiac involvement portends a worse prognosis, and postmortem studies reveal a
high prevalence of myocardial involvement.27,28 Our patient
also displayed the dreaded Weil’s syndrome (jaundice, renal
and hepatic failure), which is also associated with a high
fatality rate.29,30
Our patient had clinical and laboratory prognosticators
associated with a severe disease and a high fatality rate. He
was initiated on parenteral beta-lactam antibiotic therapy
while awaiting confirmation of the septic screen. Apart from
beta-lactam antibiotics, intravenous doxycycline may be
used to treat severe leptospirosis; however, this was not
available in our setting. Tigecycline, a tetracycline antibiotic
in the same class as doxycycline, has not been studied as an
in vitro agent for treating human leptospirosis; however, it
has been used as salvage therapy for multidrug-resistant bacteria. Recent evidence shows that tigecycline possesses both
in vivo bacteriostatic and bactericidal effects on Leptospira
strains.31 Despite it being associated with increased mortality
among intensive care unit patients, the multidisciplinary
team opted for a synergistic combination as the patient spiraled down further.32,33
Conclusion
We present the case of a 45-year-old male without a preexisting cardiovascular history who developed AF and AT
and VT, in addition to new-onset cardiomyopathy in the
Journal of Investigative Medicine High Impact Case Reports
setting of fulminant leptospirosis infection. The clinician
should be aware of potentially lethal arrhythmias and newonset cardiomyopathy in a patient with leptospirosis.
Authors’ Contribution
All authors contributed equally to the manuscript, and all authors
read and approved the final manuscript.
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with respect
to the research, authorship, and/or publication of this article.
Funding
The author(s) received no financial support for the research, authorship, and/or publication of this article.
Compliance With Ethics Guidelines and Standards
All procedures performed in studies involving human participants
were in accordance with the ethical standards of the institutional and
national research committee and with the 1964 Helsinki Declaration
and its later amendments or comparable ethical standards.
Informed Consent
Written informed consent was obtained from the patient(s) for their
anonymized information to be published in this article.
ORCID iD
Naveen Anand Seecheran
https://orcid.org/0000-0002-7779-0181
Data Sharing Statement
All available data can be obtained by contacting the corresponding
author.
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