7 results found
Sharma H, Turner CE, Siggins MK, et al., 2019, Toxic shock syndrome toxin-1 evaluation and antibiotic impact in a transgenic model of staphylococcal soft tissue infection, mSphere, Vol: 4, ISSN: 2379-5042
Nonmenstrual toxic shock syndrome (nmTSS), linked to TSST-1-producing CC30 Staphylococcus aureus, is the leading manifestation of toxic shock syndrome (TSS). Due to case rarity and a lack of tractable animal models, TSS pathogenesis is poorly understood. We developed an S. aureus abscess model in HLA class II transgenic mice to investigate pathogenesis and treatment. TSST-1 sensitivity was established using murine spleen cell proliferation assays and cytokine assays following TSST-1 injection in vivo. HLA-DQ8 mice were infected subcutaneously with a tst-positive CC30 methicillin-sensitive S. aureus clinical TSS-associated isolate. Mice received intraperitoneal flucloxacillin, clindamycin, flucloxacillin and clindamycin, or a control reagent. Abscess size, bacterial counts, TSST-1 expression, and TSST-1 bioactivity were measured in tissues. Antibiotic effects were compared with the effects of control reagent. Purified TSST-1 expanded HLA-DQ8 T-cell Vβ subsets 3 and 13 in vitro and instigated cytokine release in vivo, confirming TSST-1 sensitivity. TSST-1 was detected in abscesses (0 to 8.0 μg/ml) and draining lymph nodes (0 to 0.2 μg/ml) of infected mice. Interleukin 6 (IL-6), gamma interferon (IFN-γ), KC (CXCL1), and MCP-1 were consistent markers of inflammation during infection. Clindamycin-containing antibiotic regimens reduced abscess size and TSST-1 production. Infection led to detectable TSST-1 in soft tissues, and TSST-1 was detected in draining lymph nodes, events which may be pivotal to TSS pathogenesis. The reduction in TSST-1 production and lesion size after a single dose of clindamycin underscores a potential role for adjunctive clindamycin at the start of treatment of patients suspected of having TSS to alter disease progression.
Bharucha T, Sharma D, Sharma H, et al., 2017, Ochromobactrum intermedium: an emerging opportunistic pathogen—case of recurrent bacteraemia associated with infective endocarditis in a haemodialysis patient, New Microbes and New Infections, Vol: 15, Pages: 14-15, ISSN: 2052-2975
Sharma H, Sarker S-J, Lambourne JR, et al., 2016, The selective outpatient treatment of adults with imported falciparum malaria: a prospective cohort study, QJM, Vol: 109, Pages: 181-186, ISSN: 1460-2725
Sharma H, Smith D, Kearns A, et al., 2013, Expression of toxic shock syndrome toxin-1 by epidemic meticillin-resistant Staphylococcus aureus 16, Spring Meeting for Clinician Scientists in Training, Publisher: ELSEVIER SCIENCE INC, Pages: 98-98, ISSN: 0140-6736
Wheeler RD, Sharma H, Groves M, et al., 2007, A case study of mixed cryoglobulinaemia associated with peripheral neuropathy, Annals of Clinical Biochemistry: International Journal of Laboratory Medicine, Vol: 44, Pages: 566-569, ISSN: 0004-5632
<jats:p> The clinical diagnosis of mixed cryoglobulinaemia is difficult due to heterogeneity in presentation. Symptoms include the classical triad of purpura, arthralgia and weakness, with one or more other organs involved. We discuss a case of cryoglobulinaemia that presented with sensory motor neuropathy and with features of mononeuritis multiplex syndrome, but which lacked other classical features. Laboratory testing revealed a profile typical of mixed cryoglobulins: immunoglobulin M (IgM) paraprotein, low fourth carbon (C4) and positive rheumatoid factor. Subsequent investigations failed to reveal an underlying infectious or neoplastic cause. This case demonstrates the need to include cryoglobulinaemia in the differential diagnosis for peripheral neuropathy, and the critical importance of using the correct collection procedure to isolate cryoglobulins. </jats:p>
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