Two confirmed cases of severe fever with thrombocytopenia syndrome with pneumonia: implication for a family cluster in East China

Zhu, Yueyong; Wu, Huanyu; Gao, Jie; Zhou, Xueping; RenYi, Zhu; Zhang, Chunzhe; Bai, Hongling; Abdullah, Abu S.; Pān, Hào

doi:10.1186/s12879-017-2645-9

Cited by 29 publications

(23 citation statements)

References 25 publications

(27 reference statements)

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“…Within the first week post-symptom onset, thrombocytopenia, leukopenia, and other clinical indicators return to normal levels in mild SFTS patients while viral titers decline out to 14 days post initial symptoms onset. Following the first clinical stage, severe SFTS patients reach the MOD/MOF stage, which is characterized clinically by elevated AST/ALT, and high viral titer reaching 1 × 10 8 viral copies/mL and can experience secondary bacterial or fungal infections, hemorrhagic manifestations, central nervous system (CNS) disorders, disseminated intravascular coagulation, shock, and acute respiratory distress [39,42,51,54,55]. The clinical disease courses for SFTS and HRTV disease has been well-described by several groups, which is characterized by three phases: Stage I (fever stage), Stage II (multiorgan dysfunction (MOD)/multiorgan failure (MOF) stage), and Stage III (convalescent stage) ( Figure 2) [42,[51][52][53].…”

Section: Clinical Disease Coursementioning

confidence: 99%

Immune Modulation and Immune-Mediated Pathogenesis of Emerging Tickborne Banyangviruses

2019

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In the last decade, the emergence of several, novel tickborne viruses have caused significant disease in humans. Of interest are the tickborne banyangviruses: Severe fever with thrombocytopenia syndrome virus (SFTSV), Heartland virus (HRTV), and Guertu virus (GTV). SFTSV and HRTV infection in humans cause viral hemorrhagic fever-like disease leading to mortality rates ranging from 6–30% of the cases. The systemic inflammatory response syndrome (SIRS) associated with SFTSV infection is hypothesized to contribute significantly to pathology seen in patients. Despite the severe disease caused by HRTV and SFTSV, there are no approved therapeutics or vaccines. Investigation of the immune response during and following infection is critical to the generation of fully protective vaccines and/or supportive treatments, and overall understanding of viral immune evasion mechanisms may aid in the development of a new class of therapeutics.

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Section: Clinical Disease Coursementioning

confidence: 99%

Immune Modulation and Immune-Mediated Pathogenesis of Emerging Tickborne Banyangviruses

2019

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“…The case fatality rate of SFTS is very high, ranging from 12 to 30% in China and 22 to 30% in South Korea and Japan [1, 5, 6]. SFTS was first recognized as a family cluster of infection in central China and family clusters SFTS has been reported in China and South Korea even after discovery of SFTSV [2, 3, 7–16]. Since discovery of SFTSV in 2010, more than 2000 confirmed SFTS patients were reported annually in China [17].…”

Section: Introductionmentioning

confidence: 99%

Severe fever with thrombocytopenia syndrome can masquerade as hemorrhagic fever with renal syndrome

Qin

Han

et al. 2019

PLoS Negl Trop Dis

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Background Severe fever with thrombocytopenia syndrome (SFTS) is an emerging viral hemorrhagic fever with a high fatality rate and high frequency of person-to-person transmission and is caused by SFTSV, a tick-borne Phlebovirus . Because SFTS has similar clinical manifestations and epidemic characters (such as spatial and temporal distributions) with hemorrhagic fever with renal syndrome (HFRS) in China, we reason that SFTS patients might be misdiagnosed as HFRS. Methodology/principal findings Acute-phase sera of 128 clinically diagnosed HFRS patients were retrospectively analyzed for Hantavirus IgM antibodies with ELISA. Hantavirus -negative patients’ sera were further analyzed for SFTSV IgM antibodies with ELISA. ELISA showed that 73 of 128 (57.0%) of clinically diagnosed HFRS patients were IgM antibody positive to Hantaviruses. Among the 55 Hantavirus -IgM negative patients, four (7.3%) were IgM antibody positive to SFTSV. The results indicated that the four SFTS patients were misdiagnosed as HFRS. The misdiagnosed SFTS patients had clinical manifestations common to HFRS and were unable to be differentiated from HFRS clinically. Conclusions Our study showed that SFTS patients could be clinically misdiagnosed as HFRS. The misdiagnosis of SFTS as HFRS causes particular concern because it may increase the risk of death of SFTS patients and person-to-person transmission of SFTSV without proper care for and isolation of SFTS patients.

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“…Although SFTSV infection in humans is believed to be predominantly mediated through bites from virus-infected ticks, the first human-to-human transmission of SFTSV through contact or exposure to patient blood was reported in 2012 [10]. Since then, possible human-to-human transmissions of SFTS have been reported in families, co-residents of villages, and even in the hospital setting [11–14]. Further, some secondarily infected patients died with high viral loads and clinical symptoms, including high fever and low platelet counts [15].…”

mentioning

confidence: 99%

Shedding and Transmission Modes of Severe Fever With Thrombocytopenia Syndrome Phlebovirus in a Ferret Model

Jeong

Park

et al. 2019

Open Forum Infectious Diseases

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Background Although human-to-human transmission of severe fever with thrombocytopenia syndrome phlebovirus (SFTSV) via direct contact with body fluids has been reported, the role of specific body fluids from SFTSV-infected hosts has not been investigated in detail. Methods To demonstrate the virus transmission kinetics in SFTSV-infected hosts, we adapted the ferret infection model, and evaluated the virus shedding periods, virus titers, and transmission modes from various specimens of infected ferrets. Results Large amounts of infectious SFTSV are shed through nasal discharge, saliva and urine from SFTSV-infected ferrets. Virus could be detected from 2 dpi and persisted until 12 dpi in these specimens compared to the relatively short virus shedding period in sera. Further, transmission studies revealed that SFTSV can be transmitted to close direct- and indirect-contact naïve animals through various mediums, especially through contact with serum and urine. Further, ferrets contacted with human urine specimens from SFTSV-positive patients were successfully infected with SFTSV suggesting urine specimens could be a source of SFTSV infection in humans. Conclusion Our results demonstrate that the SFTSV can be shed in various body fluids for more than 12 days, and that these specimens can be a source for direct or indirect transmission to close contact personals.

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Two confirmed cases of severe fever with thrombocytopenia syndrome with pneumonia: implication for a family cluster in East China

Cited by 29 publications

References 25 publications

Immune Modulation and Immune-Mediated Pathogenesis of Emerging Tickborne Banyangviruses

Immune Modulation and Immune-Mediated Pathogenesis of Emerging Tickborne Banyangviruses

Severe fever with thrombocytopenia syndrome can masquerade as hemorrhagic fever with renal syndrome

Shedding and Transmission Modes of Severe Fever With Thrombocytopenia Syndrome Phlebovirus in a Ferret Model

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