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Letter
Hantavirus Infection with
Marked Sinus Bradycardia, Taiwan
To the Editor: Hantaviruses are enveloped RNA viruses belonging
to the family Bunyaviridae (1,2), for which a
number of species have been identified, including the Hantaan, Seoul,
Puumala, Dobrava-Belgrade, and Sin Nombre viruses (1,2).
Each hantavirus is associated with a specific rodent reservoir (1,2).
Hantaan virus, found throughout northeastern Asia, causes a life-threatening
illness known as hemorrhagic fever with renal syndrome (HFRS). Main symptoms
and signs of HFRS are fever, myalgia, severe vascular leakage with ascites
and retroperitoneal edema and pain (abdominal, loin, or headache), shock,
acute renal failure, proteinuria and hematuria, thrombocytopenia, and
bleeding complications (3). Seoul virus, found
worldwide, and Puumala virus, found in Scandinavia and Eastern
Europe, cause mild forms of HFRS. Sin Nombre virus, found
in the United States, causes hantavirus pulmonary syndrome, which is characterized
by increased pulmonary capillary permeability and pulmonary edema and
can progress to severe respiratory distress syndrome and shock as a result
of low cardiac output (4,5).
Despite the fact that HFRS is frequently reported in People’s Republic
of China, no indigenous cases of HFRS have been reported in Taiwan. Previous
serologic studies found that the Seoul strain is endemic in the areas
of Taiwan and two isolated islands nearby, Kinmen and Matzu; in contrast,
in the People’s Republic of China, the Hantaan and Seoul strains concurrently
predominate (6,7).
Our patient, a 38-year-old man, had onset of sore throat, headache, cough,
myalgia, and intermittent fever (up to 38.3°C) on February 2, 2001. A
resident of Matzu for more than 30 years, he had traveled to the People’s
Republic of China 3 months before the symptoms began. Laboratory tests
at a local hospital showed thrombocytopenia (58,000/mL) and leukopenia
(3,800/mL). Because his symptoms persisted, he was transferred to the
National Taiwan University Hospital on February 7, 2001. Initial tests
there showed a temperature of 36.4°C, heart rate 74 beats/min, and respiratory
rate 18/min; there was no skin rash. The rest of the physical examination
was normal. He had a platelet count 73,000/µL; leukocytes 5,670/µL with
59.1% segments, 19.8% lymphocytes, and 18.2% monocytes; urea nitrogen
7.4 mg/dL; and creatinine 0.94 mg/dL. Urinalysis showed proteinuria (300
mg/dL). His chest radiography was normal. Abdominal ultrasound showed
a fatty liver.
After admission, the patient’s laboratory values gradually improved and
his proteinuria subsided. He had no fever. On February 10, 2001, he had
marked sinus bradycardia (as low as 33 beats/min) and became fatigued.
His blood pressure was 120–130/70–80 mmHg. No abnormal serum electrolytes,
urea nitrogen, creatinine, creatine kinase, and troponin-I were noted.
Echocardiogram showed normal atrium and ventricle size, good left ventricle
contractility, and small amount of pericardial effusion. His heart rate
gradually increased. He was discharged on February 15, 2001, without event.
A substantial increase of serum immunofluorescent immunoglobulin (Ig)
G titers (1:640 on February 6; 1:5120 on February 19, 2001) and positive
IgM titers of 1:80 against hantavirus antigen (Seoul type) confirmed that
this virus was responsible for the illness.
A few reports of hantavirus infection with cardiac involvement have been
published. A case report by Chun and Godfrey showed right atrium dilation
with diffuse atrial hemorrhage, interstitial edema, and vascular congestion
without surrounding myocardial fibers and conduction system involvement
in a 19-year-old soldier who died from epidemic (Korean) hemorrhagic fever,
sinus tachycardia, paroxysmal supraventricular tachycardia, and congestive
heart failure (8). Marked sinus bradycardia (as low as
34 beats/min) in a patient with a severe form of hemorrhagic fever with
renal syndrome (acute renal failure) has been reported (9).
However, this finding was not observed in patients with mild cases of
the disease.
The possibility that our patient acquired the infection during his travel
to the People’s Republic of China 3 months earlier is extremely low because
of the length of the incubation period (typical incubation period 4–28
days) (10) and the different hantavirus strains prevalent
in the People’s Republic of China (6). Although viral
genetic sequence data from the patient and rodents in Matzu were not available
in this study, our patient was infected with the Seoul strain, which is
highly seroprevalent in rodents in Matzu (6,7).
In summary, this case was probably the first indigenous case of hantavirus
infection in Taiwan. Its characteristics suggest that marked sinus bradycardia
should be included as a protean manifestation of hantavirus.
Yuan-Hong Liu,*† Jyh-Hsiung Huang,‡ Po-Ren Hsueh,* and Kwen-Tay Luh*
*National Taiwan University Hospital, Taipei, Taiwan; †En Chu Kong
Hospital, Taipai, Taiwan; and ‡Department of Health, Taipei, Taiwan
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