A 73-year-old Japanese man was referred to Hiroshima Prefectural Hospital with a 6-day history of fever. Nine days prior to admission, he had received a tick bite on his right knee while picking bamboo shoots. Three days after the bite, he developed a fever with shaking chills. Minocycline was prescribed at a local clinic, but his symptoms did not resolve. On admission, his consciousness was unclear. Petechiae were observed on his right lower limb (Picture 1). The tick bite site had formed an obscure eschar (Picture 2). His platelet count was 110×10/μL. The patient was suspected of having severe fever with thrombocytopenia syndrome (SFTS), and was treated with supportive measures. SFTS viral nucleic acid was detected through a polymerase chain reaction in his serum sample. The petechiae disappeared on the 12th day of admission (Picture 3), but the eschar remained at that time (Picture 4). The patient thereafter suc-

Severe Fever with Thrombocytopenia Syndrome.

Although severe fever with thrombocytopenia syndrome (SFTS) was first reported from Japan in 2013, the precise clinical features and the risk factors for SFTS have not been fully investigated in Japan. Ninety-six cases of severe fever with thrombocytopenia syndrome (SFTS) were notified through the national surveillance system between April 2013 and September 2014 in Japan. All cases were from western Japan, and 82 cases (85%) had an onset between April and August. A retrospective observational study of the notified SFTS cases was conducted to identify the clinical features and laboratory findings during the same period. Of 96 notified cases, 49 (51%) were included in this study. Most case-patients were of advanced age (median age 78 years) and were retired or unemployed, or farmers. These case-patients had a history of outdoor activity within 2 weeks before the onset of illness. The median serum C-reactive protein concentration was slightly elevated at admission. Fungal infections such as invasive aspergilosis were found in 10% of these case-patients. Hemophagocytosis was observed in 15 of the 18 case-patients (83%) whose bone marrow samples were available. Fifteen cases were fatal, giving a case-fatality proportion of 31%. The proportion of neurological abnormalities and serum concentrations of lactate dehydrogenase and aspartate aminotransferase were significantly higher in the fatal cases than in the nonfatal cases during hospitalization. Appearance of neurological abnormality may be useful for predicting the prognosis in SFTS patients.

/pdf/epidemiological-and-clinical-features-of-severe-fever-with-1qr3a73j5m.pdf

Epidemiological and Clinical Features of Severe Fever with Thrombocytopenia Syndrome in Japan, 2013-2014.

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease caused by a novel bunyavirus (SFTS virus, SFTSV). At present there is still no specific antiviral treatment for SFTSV; To understand which cells support SFTSV life cycle and whether SFTSV infection activates host innate immunity, four different cell lines (Vero, Hela, Huh7.5.1, and Huh7.0) were infected with SFTSV. Intracellular/extracellular viral RNA and expression of IFNα, and IFNs were detected by real-time RT- PCR following infection. To confirm the role of non-structural protein (NSs) of SFTSV in exogenous IFNα-induced Jak/STAT signaling, p-STAT1 (Western Blot), ISRE activity (Luciferase assay) and ISG expression (real-time PCR) were examined following IFNα stimulation in the presence or absence of over-expression of NSs in Hela cells. Our study showed that all the four cell lines supported SFTSV life cycle and SFTSV activated host innate immunity to produce type I IFNs in Hela cells but not in Huh7.0, Huh7.5.1 or Vero cells. NSs inhibited exogenous IFNα-induced Jak/STAT signaling as shown by decreased p-STAT1 level, suppressed ISRE activity and down-regulated ISG expression. Suppression of the exogenous Type I IFN-induced Jak/STAT signaling by NSs might be one of the mechanisms of SFTSV to evade host immune surveillance.

/pdf/severe-fever-with-thrombocytopenia-syndrome-virus-inhibits-2eo5egt2wr.pdf

Severe fever with thrombocytopenia syndrome virus inhibits exogenous Type I IFN signaling pathway through its NSs invitro.

Severe fever with thrombocytopenia syndrome virus (SFTSV) is a newly emergent tick-borne bunyavirus first discovered in 2009 in China. SFTSV is a growing public health problem that may become more prominent owing to multiple competent tick-vectors and the expansion of human populations in areas where the vectors are found. Although tick-vectors of SFTSV are found in a wide geographic area, SFTS cases have only been reported from China, South Korea, Vietnam, and Japan. Patients with SFTS often present with high fever, leukopenia, and thrombocytopenia, and in some cases, symptoms can progress to severe outcomes, including hemorrhagic disease. Reported SFTSV case fatality rates range from ~5 to >30% depending on the region surveyed, with more severe disease reported in older individuals. Currently, treatment options for this viral infection remain mostly supportive as there are no licensed vaccines available and research is in the discovery stage. Animal models for SFTSV appear to recapitulate many facets of human disease, although none of the models mirror all clinical manifestations. There are insufficient data available on basic immunologic responses, the immune correlate(s) of protection, and the determinants of severe disease by SFTSV and related viruses. Many aspects of SFTSV virology and epidemiology are not fully understood, including a detailed understanding of the annual numbers of cases and the vertebrate host of the virus, so additional research on this disease is essential towards the development of vaccines and therapeutics.

/pdf/baseline-mapping-of-severe-fever-with-thrombocytopenia-3c73frh726.pdf

Baseline mapping of severe fever with thrombocytopenia syndrome virology, epidemiology and vaccine research and development.

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging tick-borne disease. The primary symptoms associated with SFTS are fever, thrombocytopenia, leukopenia, nausea, and vomiting. Disease progression shows high mortality rate accompanied with multiple organ failure, bleeding tendency, and altered mentality. However, only supportive care has been the basis for the treatment of SFTS. We are reporting two patients who showed central nervous system manifestation, but cured them with ribavirin together with plasma exchange in an early state. The first case is a 60-year-old male, who was admitted to the hospital with a 7-day history of fever, chills, and thrombocytopenia. He was treated with empirical antibiotics; however, he experienced persistent high fever and an altered mentality has occurred. On hospital day 6, the SFTS virus (SFTSV) result from a real-time reverse transcription-polymerase chain reaction (RT-PCR) was confirmed positive. Therefore, ribavirin (30 mg/kg as initial loading dose, 15 mg/kg qid for 4 days and then 7.5 mg/kg qid as maintenance dose) was administered orally for 11 days and plasma exchange was performed for 5 days. The clinical outcome has improved. The second case is a 48-year-old male, who was admitted to the hospital with a 10-day history of fever, chills, myalgia, diarrhea, and thrombocytopenia. He was treated with empirical antibiotics. On hospital day 3, ribavirin (30 mg/kg as initial loading dose, 15 mg/kg qid as maintenance dose) was administered orally for 4 days and plasma exchange was performed for 4 days due to his high fever and altered mentality after a positive SFTSV result from a real-time RT-PCR. The patient had a successful recovery.

/pdf/two-treatment-cases-of-severe-fever-and-thrombocytopenia-1dt7d84mey.pdf

Two Treatment Cases of Severe Fever and Thrombocytopenia Syndrome with Oral Ribavirin and Plasma Exchange.

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious and hemorrhagic disease recently described in China and western Japan. A 71-year-old healthy Japanese woman noticed a tick biting her after harvesting in an orchard and removed it herself. She developed diarrhea, anorexia, and chills eight days later. Because these symptoms continued, she visited a primary care physician 6 days after the onset. Laboratory data revealed thrombocytopenia, leukocytopenia, and elevated liver enzymes. She was then referred to our hospital. Although not completely fulfilling the diagnostic criteria used in a retrospective study in Japan, SFTS was suspected, and we detected SFTS virus in the patient’s blood using RT-PCR. However, she recovered without intensive treatment and severe complications 13 days after the onset. In this report, we present a mild clinical course of SFTS virus infection in Japan in detail.

/pdf/mild-clinical-course-of-severe-fever-with-thrombocytopenia-3z6xo89kwa.pdf

Mild clinical course of severe Fever with thrombocytopenia syndrome virus infection in an elderly Japanese patient.

Phlegmonous gastritis (PG) is a rare, acute, severe infectious disease of the gastric wall that is often fatal due to Streptococcus spp. A 77-year-old man with diabetes and a gastric ulcer was urgently admitted due to prolonged nausea and vomiting. Computed tomography revealed widespread diffuse thickening of the gastric wall, and PG was suspected. The patient expired less than 9 hours after admission despite intensive treatments. Later, an analysis of the blood and gastric juice revealed group A streptococcus (GAS) and virulence factors associated with toxic shock syndrome (TSS). We herein diagnosed a patient with an extremely aggressive course of PG caused by GAS TSS.

Phlegmonous gastritis associated with group A streptococcal toxic shock syndrome.

Capnocytophaga canimorsus sepsis in a methotrexate-treated patient with rheumatoid arthritis

A 71-year-old man with myelodysplastic syndrome (MDS) receiving treatment with azacitidine developed extensive watery diarrhea for three consecutive days. As a result of high-grade dehydration, the patient was urgently admitted to the hospital and fluid replacement therapy was initiated. However, the patient's diarrhea did not improve. Vibrio cholerae non-O1/non-O139 was detected in a fecal culture. On the fourth day, the patient died due to circulatory collapse. An autopsy revealed extensive necrosis of the intestinal mucosa. Vibrio cholerae non-O1/non-O139-induced diarrheal disease often develops in patients with hepatic cirrhosis and has a serious clinical course. We herein report a fatal outcome of Vibrio cholerae O67 infection in an immunocompromised MDS patient.

Fatal diarrheal disease caused by Vibrio cholerae O67 in a patient with myelodysplastic syndrome.

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Mild clinical course of severe Fever with thrombocytopenia syndrome virus infection in an elderly Japanese patient.

Phlegmonous gastritis associated with group A streptococcal toxic shock syndrome.

Capnocytophaga canimorsus sepsis in a methotrexate-treated patient with rheumatoid arthritis

Fatal diarrheal disease caused by Vibrio cholerae O67 in a patient with myelodysplastic syndrome.