Case Report: Leptospirosis after a Typhoon Disaster Outside the Endemic Region, Japan

ABSTRACT.

Leptospirosis is a zoonotic disease that primarily affects people in tropical and subtropical areas worldwide. Owing to the temperate climate of Japan, leptospirosis is not endemic across the country. Domestic cases of leptospirosis have been mainly reported in Okinawa and the southwestern subtropical islands, but not in the other regions. Here, we describe a case of leptospirosis that developed and was diagnosed outside the domestically endemic region. Notably, disease onset occurred shortly after the patient experienced a flood after a typhoon disaster. With global warming, the international prevalence of leptospirosis may change. Physicians outside currently endemic areas must be aware of this tropical disease.

INTRODUCTION

Leptospirosis is a major zoonotic disease that affects people living in tropical and subtropical regions.^1,2 In Japan, domestic cases of leptospirosis are commonly reported in Okinawa and the southwest subtropical islands; those diagnosed in other regions are considered imported cases from abroad.^3,4 Thus, Japanese physicians rarely suspect this tropical disease when a patient has no history of traveling overseas. Sporadically, however, leptospirosis cases have been increasingly diagnosed outside the subtropical regions in Japan,^5–7 indicating that the disease-endemic area may be spreading due to the global warming and globalization.^8,9 Here, we present a case of leptospirosis that occurred outside the southwest subtropical islands after typhoon floods.

CASE REPORT

In September 2022, a ferocious typhoon hit the Chugoku region of Japan. Two weeks later, a 69-year-old Japanese man with hypertension and diabetes presented with fever that had persisted for 3 days. He lived in Hiroshima prefecture and denied traveling abroad or to the southwest subtropical islands of Japan. On his first visit, he was alert, and his vital signs were stable, except for elevated body temperature. Physical examination revealed conjunctival congestion but no myalgia, jaundice, hepatosplenomegaly, or superficial lymphadenopathy. Laboratory findings revealed elevated serum levels of C-reactive protein (CRP, 14.8 mg/dL) and creatinine (1.78 mg/dL), suggesting acute kidney injury. Data for leukocytes (7,600/µL) and liver function testing (aspartate aminotransferase [AST], 20 U/L; alanine aminotransferase [ALT], 16 U/L; total bilirubin, 0.6 mg/dL) were within normal ranges. Computed tomography revealed no remarkable findings in his chest or abdomen.

Under the provisional diagnosis of bacterial infection, he was hospitalized and received empirical treatment with intravenous ceftriaxone. A few hours after the initiation of antibiotic therapy, he developed a high fever, reaching 41 °C, accompanied by disturbed consciousness and urinary incontinence. Suspecting encephalitis or meningitis, we performed head computed tomography, head magnetic resonance imaging, and lumbar puncture, all of which yielded normal findings. With the use of antipyretic medications, his consciousness gradually improved. On the second day of hospitalization, his laboratory data deteriorated, with leukocytosis (10,600/µL) and elevated serum levels of CRP (27.32 mg/dL), ALT (28 U/L), AST (90 U/L), and creatinine (3.33 mg/dL). We escalated antibiotic therapy with a combination of meropenem and minocycline. Subsequently, the clinical symptoms and organ function of the patient improved, and the patient was discharged from the hospital on day 14.

During admission, our repeated interviews revealed that the area around the patient’s home had been flooded after the typhoon 2 weeks before disease onset. On the basis of this history, we suspected that this case was a waterborne infection. We submitted the patient’s paired serum samples to the National Institute of Infectious Diseases (Tokyo, Japan) for microscopic agglutination testing for leptospirosis, in which we observed more than a 4-fold elevation for Leptospira interrogans serovar Rachmati, leading to a definitive diagnosis of leptospirosis (Table 1).

Table 1.

Results of microscopic agglutination testing for Leptospira species

Species	Antibody titers
	Day 4	Day 14	Day 29
Leptospira borgpetersenii serovar Castellonis	< 50	< 50	< 50
Leptospira borgpetersenii serovar Javanica	< 50	< 50	< 50
Leptospira borgpetersenii serovar Poi	< 50	< 50	< 50
Leptospira interrogans serovar Australis	< 50	< 50	< 50
Leptospira interrogans serovar Autumnalis	< 50	< 50	< 50
Leptospira interrogans serovar Bataviae	< 50	< 50	< 50
Leptospira interrogans serovar Canicola	< 50	< 50	< 50
Leptospira interrogans serovar Copenhageni	< 50	< 50	< 50
Leptospira interrogans serovar Hebdomadis	< 50	< 50	< 50
Leptospira interrogans serovar Icterohaemorrhagiae	< 50	< 50	< 50
Leptospira interrogans serovar Kremastos	< 50	< 50	< 50
Leptospira interrogans serovar Pomona	< 50	< 50	< 50
Leptospira interrogans serovar Pyrogenes	< 50	< 50	< 50
Leptospira interrogans serovar Rachmati	< 12.5	100	100
Leptospira kirschneri serovar Grippotyphosa	< 50	< 50	< 50

DISCUSSION

Herein, we describe a case of leptospirosis, a zoonotic disease caused by the genus Leptospira. The clinical characteristics of the present case were typical of the disease, with acute-onset fever, conjunctival congestion, liver dysfunction, acute kidney injury, and the development of Jarish–Herxeimer reaction.¹⁰ Serological finding corroborated the diagnosis of this rare disease. This spirochete infection is a representative acute febrile disease in tropical regions. A recent eco-epidemiology study found that Leptospira species can be detected in environmental water and soil across the country; however, most of them are nonpathogenic to humans.^11,12 In the southwestern subtropical islands, a high diversity of environmental-derived Leptospira species, including human pathogenic species, is confirmed, suggesting the endemicity of the disease.³ In fact, outdoor activities with exposure to freshwater in such Japanese subtropical regions are recognized as risk factors for disease.¹³

The patient had no history of traveling to leptospirosis-endemic regions, which indicated that the infection occurred in the vicinity of his residence in Hiroshima prefecture. Spirochetes colonize the renal tubules of reservoir animals (mostly mice) and contaminate the soil and water environment through excretion from urine.¹⁴ Leptospirosis outbreaks secondary to floods have been reported in countries with high incidences of the disease.^15–17 Thus, we assumed that the spirochete infected the patient through flooding after the typhoon disaster.

The prevalence of tropical diseases, including leptospirosis, may have changed with climate change. Physicians outside of regions where the leptospirosis is endemic must keep this in mind when seeing patients.