SFTS Virus: Signs, Risks, and Prevention Measures

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease caused by the SFTS virus, a member of the Bunyaviridae family. First identified in China, it has since been reported in other parts of Asia, raising concerns due to its high fatality rate and potential for human-to-human transmission. The disease primarily affects individuals exposed to tick populations, making awareness and preventive measures crucial.

Early recognition and intervention are essential. Understanding how the virus spreads, the risks involved, and available protective strategies can help reduce infections and improve outcomes.

Transmission and Vectors

The SFTS virus is primarily transmitted through the bite of infected ticks, with Haemaphysalis longicornis identified as the dominant vector. This species, commonly found in East Asia, thrives in humid environments such as grasslands, forests, and agricultural fields, increasing the risk of human exposure in rural communities. The virus persists within the tick across multiple life stages, from larvae to adults, ensuring continuous transmission.

Beyond tick bites, evidence suggests the virus can spread through contact with infected animals, particularly livestock such as goats, cattle, and dogs. Farmers and veterinarians face higher risks when handling contaminated blood or bodily fluids. A study in Emerging Infectious Diseases found significantly higher seroprevalence rates of SFTS virus antibodies among individuals with frequent animal exposure, reinforcing livestock’s role in viral transmission.

Human-to-human transmission, though less common, has been documented in healthcare settings through direct contact with infected blood or secretions. Case reports from China and South Korea describe instances where family members and medical personnel contracted the virus while caring for patients. A study in The Lancet Infectious Diseases highlighted that nosocomial outbreaks, while rare, tend to occur in clusters linked to inadequate protective equipment or breaches in biosafety protocols.

Clinical Presentation

Symptoms typically develop within 7 to 14 days following a tick bite, beginning with fever, fatigue, and gastrointestinal disturbances. High fever, often exceeding 38.5°C (101.3°F), is an early and consistent sign. Patients frequently experience malaise, myalgia, dizziness, nausea, vomiting, diarrhea, and abdominal pain, often leading to dehydration and electrolyte imbalances.

As the disease progresses, thrombocytopenia and leukopenia become more pronounced. Platelet counts can drop significantly, increasing the risk of spontaneous bleeding. Leukopenia weakens the immune response, predisposing patients to secondary infections. A study in The Journal of Infectious Diseases found that over 85% of SFTS patients exhibited thrombocytopenia, with severity correlating with outcomes. Elevated liver enzymes and lactate dehydrogenase (LDH) indicate hepatic involvement and widespread cellular damage.

Neurological symptoms, including confusion, disorientation, seizures, and coma, emerge in severe cases. MRI findings in critically ill patients have revealed diffuse cerebral edema and white matter lesions. Research in Clinical Infectious Diseases reported that nearly 30% of hospitalized SFTS patients exhibited neurological impairment, with a higher prevalence among older individuals. These symptoms often indicate a poorer prognosis, emphasizing the need for close monitoring.

Possible Complications

As SFTS advances, complications arise due to vascular damage and multi-organ dysfunction. Hemorrhagic manifestations, including epistaxis, gastrointestinal bleeding, and subconjunctival hemorrhages, become more frequent as thrombocytopenia worsens. Disseminated intravascular coagulation (DIC) can develop, leading to both excessive bleeding and microvascular thrombosis. Autopsy findings from fatal cases have revealed fibrin thrombi in multiple organs, underscoring the severity of coagulation dysfunction.

Acute kidney injury (AKI) is a significant concern, particularly in patients with prolonged hypotension or systemic inflammation. Direct viral invasion of renal tissue, coupled with ischemic injury, contributes to declining kidney function. Elevated serum creatinine and blood urea nitrogen (BUN) levels indicate renal impairment, with some patients requiring temporary renal replacement therapy. A study in BMC Infectious Diseases noted that individuals with pre-existing renal conditions face a heightened risk of AKI following SFTS infection.

Neurological complications, particularly encephalopathy, further complicate disease progression. Patients exhibiting altered mental status, seizures, or coma often have extensive neuroinflammation, as evidenced by elevated cerebrospinal fluid (CSF) protein levels and abnormal electroencephalographic (EEG) activity. MRI scans in severe cases reveal diffuse cortical atrophy and white matter hyperintensities, suggesting potential long-term neurological impairment. Some survivors experience persistent cognitive deficits, raising concerns about lasting neurological damage.

Diagnostic Procedures

Diagnosing SFTS requires clinical assessment, laboratory findings, and molecular testing. Given the nonspecific early symptoms, initial suspicion arises in patients presenting with high fever, gastrointestinal distress, and hematologic abnormalities in endemic regions. Routine blood tests often reveal pronounced thrombocytopenia, leukopenia, and elevated liver enzymes and LDH, signaling systemic involvement. These findings necessitate targeted diagnostic methods for confirmation.

Reverse transcription-polymerase chain reaction (RT-PCR) is the gold standard for detecting viral RNA in blood samples, offering high sensitivity in the early stages. Viral loads typically decline after two weeks, reducing detection accuracy. Serological assays, such as enzyme-linked immunosorbent assay (ELISA) and indirect immunofluorescence assay (IFA), detect SFTS virus-specific IgM and IgG antibodies. These tests are useful in later stages when viral RNA may no longer be detectable, though they require paired serum samples to confirm seroconversion.

Treatment Approaches

Managing SFTS remains challenging due to the absence of a specific antiviral therapy. Treatment focuses on supportive care, including fluid resuscitation to address dehydration and electrolyte imbalances. Blood transfusions may be necessary in severe thrombocytopenia cases to reduce bleeding risks. Continuous monitoring of renal and hepatic function helps guide interventions and prevent deterioration.

Research has explored antiviral agents such as ribavirin and favipiravir, which have shown inhibitory effects against bunyaviruses in vitro. A study in Clinical Microbiology and Infection suggested early favipiravir administration might improve survival rates, particularly in patients with high viral loads. However, clinical trials assessing its definitive benefit remain limited. Immunomodulatory approaches, including corticosteroids and intravenous immunoglobulin (IVIG), have been considered in severe cases with pronounced inflammation, though concerns about secondary infections and prolonged viral shedding necessitate cautious use.

Geographic Distribution

SFTS was first identified in China in 2009, where it remains endemic, particularly in provinces such as Henan, Shandong, and Hubei. Since then, cases have been reported in South Korea and Japan, with increasing numbers over the past decade. Surveillance data indicate most cases occur between April and October, coinciding with peak tick activity. In Japan, infections have been clustered in agricultural regions, primarily among elderly individuals engaged in outdoor work.

Beyond East Asia, concerns about the virus’s potential spread have grown. Recent studies detected viral RNA in Haemaphysalis longicornis ticks in Russia, suggesting a broader geographic range. The presence of this tick species in Australia and the United States raises questions about future outbreaks outside Asia. While no confirmed human cases have been reported in these regions, ongoing ecological studies aim to assess the risk of zoonotic transmission. Climate change and increasing global trade in livestock may further contribute to the spread of infected tick populations, necessitating enhanced surveillance efforts.

Preventive Measures

Reducing the risk of SFTS infection requires minimizing exposure to tick vectors and implementing protective measures in high-risk environments. Individuals in endemic areas should wear long-sleeved clothing and use insect repellents containing DEET or permethrin when outdoors. Regular tick checks after spending time in grassy or wooded areas can help detect and remove attached ticks before transmission occurs. Farmers and livestock handlers benefit from tick control programs for domesticated animals, reducing indirect exposure risks.

Healthcare workers treating SFTS patients must adhere to strict infection control protocols to prevent nosocomial transmission. Personal protective equipment (PPE), including gloves, masks, and face shields, is essential when handling blood or bodily fluids. The World Health Organization emphasizes proper disinfection procedures in hospital settings, particularly during outbreaks linked to human-to-human transmission. Public health campaigns that educate communities about tick avoidance and early symptom recognition play a critical role in reducing infection rates. While vaccine development remains in early stages, ongoing research into immune responses to SFTS virus may pave the way for future preventive options.