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Background To analyze and discuss the transmission route of a cluster of cases of severe fever with thrombocytopenia syndrome bunyavirus (SFTSV). Method We performed an epidemiological investigation and a genetic analysis of patients with severe fever with thrombocytopenia syndrome (SFTS) caused by SFTSV, their close contacts and the surrounding population. Results We found that all patients had contact with the blood of the first patient. The comparison of gene sequences in the three isolated SFTSV strains showed that the strains were closely related. Six close contacts and nine individuals in the surrounding population were positive for SFTSV IgM antibody. Conclusion We suspect that the cluster outbreak was transmitted via blood and that the natural reservoir host of SFTSV exists in the patients’ environment.

Background We report a mononucleosis-like illnesses case due to co-infection with severe fever with thrombocytopenia syndrome virus (SFTSV) and spotted fever group rickettsia (SFGR), which to the best of our knowledge, has never been reported . Case presentation A 64-year-old male with an 11-day history of fever, sore throat, malaise, nausea, and non-pruritic rash was admitted to our emergency department. Prior to admission, he was bitten by ticks. Laboratory tests revealed a white blood cell count of 24,460 cells/μL with 25% atypical lymphocytes and 20% mononucleosis, thrombocytopenia. Test results were positive for SFTSV RNA, SFTSV-specific IgM antibody, and SFGR-specific IgM antibody. He was diagnosed with mononucleosis-like illnesses due to co-infection with SFTSV and SFGR. After administration of doxycycline, he recovered completely. Conclusions The clinical presentation may be atypical in co-infection with SFTSV and SFGR. This finding highlighted the importance of considering SFGR infection, as well as a SFSTV and SFGR co-infection for the differential diagnosis of patients bitten by ticks in SFTSV-endemic areas.

A 53-year-old male was admitted to the emergency room with 5-day history of fever, bilateral parotid gland swelling, and right esticular pain for 2 days. He also complained of headaches, genralized arthralgias, myalgias, and severe lumbago. He lived in a ural area in Northeast China and had worked in the field 2 weeks rior to the onset of symptoms. He was previously in good health, nd there was no history to suggest a sexually transmitted infecion. He was treated with ibuprofen for 2 days before admission ithout remission of symptoms. The physical examination on admission revealed swelling of the arotid glands bilaterally (Fig. 1) and right scrotum. The vital signs ere as follows: temperature, 37.5 ◦C; heart rate, 80/min; respiatory rate, 20/min; and blood pressure, 120/60 mmHg. Petechiae ere noted in the throat, and the abdomen was soft. Lymhadenopathy was palpable in the neck. There was no conjunctival uffusion, facial suffusion, or cutaneous petechiae. The neurologic xamination was unremarkable. Initial laboratory studies (Table 1) revealed that the leukoyte count was 4890/ L, the hemoglobin level was 12.8 g/dL, the

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease recently discovered in northeastern and central China that is caused by a novel bunyavirus, severe fever with thrombocytopenia syndrome virus (SFTSV). Humans are primarily infected through tick bites. Four previous reports have discussed SFTS infection from person to person, all cases of which were symptomatic. In this report, we analysed the epidemiological and clinical data for a cluster of cases, including one case of secondary-asymptomatic infection, and review the literature regarding SFTSV transmission from person to person. We conclude that SFTSV caused the asymptomatic infections via person-to-person contact with infected blood.

BACKGROUND: Severe fever with thrombocytopenia syndrome virus (SFTSV), which can cause hemorrhagic fever-like illness, is a newly discovered bunyavirus in China. The pathogenesis of SFTSV infection is poorly understood. However, it has been suggested that immune mechanisms, including cytokines and chemokines, play an important role in disease pathogenesis. In the present study, we investigated host cytokine and chemokine profiles in serum samples of patients with SFTSV infection from Northeast China and explored a possible correlation between cytokine levels and disease severity. METHODS AND PRINCIPAL FINDINGS: Acute phase serum samples from 40 patients, diagnosed with SFTSV infection were included. Patients were divided into two groups--severe or non-severe--based on disease severity. Levels of tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, interleukin-6, interferon (IFN)-γ, IFN- γ-induced protein (IP)-10 and RANTES were measured in the serum samples with commercial ELISAs. Statistical analysis showed that increases in TNF-α, IP-10 and IFN-γ were associated with disease severity. CONCLUSIONS: We suggest that a cytokine-mediated inflammatory response, characterized by cytokine and chemokine production imbalance, might be in part responsible for the disease progression of patients with SFTSV infection.

CBC Leucocytes (n/mm3) 1980 3970–9150 Hemoglobin (g/dL) 17.4 13.1–17.2 Platelets (n/mm3) 30,000 85,000–303,000 CD4 ( L−1) 167 410–1590 CD8 ( L−1) 173 190–1140 CD4/CD8 0.96 0.60–3.20 CRP (mg/L) 7.25 0–8 Biochemical tests Creatine kinase (U/L) >23,000 39–308 Creatine kinase MB fraction (ng/mL) 246 0–7.2 Myoglobin (ng/mL) >1000 0–116 Creatinine ( mol/L) 299 59–104 Blood urea nitrogen (mmol/L) 24.7 3.2–7.1 Na+ (mmol/L) 121.1 136–145 K+ (mmol/L) 8.76 3.5–5.2 Ca2+ (mmol/L) 1.67 2.17–2.57 Alanine aminotransferase (U/L) 179 5–40 Aspartate aminotransferase (U/L) 548 8–40 Lactate dehydrogenase (U/L) 1613 135–225 Troponin I (ng/mL) 0.03 0.00–0.40 Fasting plasma glucose (mmol/L) 26 3.9–6.10 Albumin (g/L) 28.7 40.0–50.0 eceived in revised form 23 June 2012 ccepted 29 June 2012

Background During the spring of 2009, a pandemic influenza A (H1N1) virus emerged and spread globally. We describe the clinical characteristics and factors associated with the death of patients who were hospitalized with 2009 H1N1 influenza pneumonia in Shenyang, China, from November to December 2009. Methods We carried out a retrospective chart review of 68 patients who were hospitalized with pneumonia and confirmed to have 2009 H1N1 virus infection by a real time RT-PCR assay of respiratory specimens. Results Of the 68 patients we studied, 30 (44%) were admitted to an intensive care unit and 10 (14.7%) died. The median age of patients was 41 years (range, 18-66), and only one patient was over 65 years of age. The male to female ratio was 2.78:1 (50:18). Of the 68 patients, 23 (34%) had at least one underlying medical condition, 9 (13%) had a cigarette index ≥400 and 22 (32%) were obese. All patients underwent chest radiography on admission and the findings were consistent with pneumonia in all cases. All patients were treated with oseltamivir and treatment was initiated at a median time of seven days after the onset of illness. The laboratory test results indicated lymphopenia, hypoproteinemia and elevated lactic dehydrogenase and C reactive protein levels. Of the 68 patients, 33 (52%) showed a reduction in CD4 T cell counts. Of the 58 patients who survived, 31 (53%) had lymphopenia and 27 recovered from this condition after five days. Of the 10 patients who died, nine (90%) had lymphopenia and only two patients recovered from this condition after five days. Obesity and recovery from lymphopenia after five days were factors associated with death, as determined by multivariate logistic-regression analysis (obesity, odds ratio = 23.06; lymphocytopenia reversion, odds ration = 28.69). Conclusions During the evaluation period in Shenyang, China, 2009 H1N1 influenza caused severe illness requiring hospitalization in 68 patients, 10 (14.7%) of which died. Many of these patients were considered healthy adults and few were elderly (65 years or older). Obesity and lymphopenia, which was not restored after five days of treatment, were factors associated with poor outcomes of 2009 H1N1 influenza infection.