Clostridium perfringens infections initially attributed to norovirus, North Carolina, 2010.

We investigated an outbreak initially attributed to norovirus; however, Clostridium perfringens toxicoinfection was subsequently confirmed. C. perfringens is an underrecognized but frequently observed cause of food-borne disease outbreaks. This investigation illustrates the importance of considering epidemiologic and laboratory data together when evaluating potential etiologic agents that might require unique control measures.

Evaluation of the North Carolina Violent Death Reporting System, 2009.

BACKGROUND: Violence is a leading cause of death in North Carolina. The North Carolina Violent Death Reporting System (NC-VDRS) is part of the National Violent Death Reporting System (NVDRS), which monitors violent deaths and collects information about injuries and psychosocial contributors. Our objective was to describe and evaluate the quality, timeliness, and usefulness of the system. METHODS: We used the Centers for Disease Control and Prevention's guidelines for evaluating public health surveillance systems to assess the system. We performed subjective assessment of system attributes by reviewing system documents and interviewing stakeholders. We estimated NC-VDRS's reporting completeness using a capture-recapture method. RESULTS: Stakeholders considered data provided by NC-VDRS to be of high quality. Reporting to the national system has taken place before the specified 6-month and 18-month deadlines, but local stakeholder reports have been delayed up to 36 months. Stakeholders reported using NC-VDRS data for program planning and community education. The system is estimated to capture all NVDRS-defined cases, but law enforcement officers report only 61% of suicides. LIMITATIONS: The law enforcement agencies we interviewed may not be representative of all participating agencies in the state. Data sources used to assess completeness were not independent. CONCLUSION: NC-VDRS is useful and well-accepted. However, completeness of suicide reporting is limited, and reporting to local stakeholders has been delayed. Improving these limitations might improve the usefulness of the system for planning and appropriately targeting violence prevention interventions.

Cluster of oseltamivir-resistant 2009 pandemic influenza A (H1N1) virus infections on a hospital ward among immunocompromised patients--North Carolina, 2009.

BACKGROUND: Oseltamivir resistance among 2009 pandemic influenza A (H1N1) viruses (pH1N1) is rare. We investigated a cluster of oseltamivir-resistant pH1N1 infections in a hospital ward. METHODS: We reviewed patient records and infection control measures and interviewed health care personnel (HCP) and visitors. Oseltamivir-resistant pH1N1 infections were found with real-time reverse-transcription polymerase chain reaction and pyrosequencing for the H275Y neuraminidase (NA) mutation. We compared hemagglutinin (HA) sequences from clinical samples from the outbreak with those of other surveillance viruses. RESULTS: During the period 6-11 October 2009, 4 immunocompromised patients within a hematology-oncology ward exhibited symptoms of pH1N1 infection. The likely index patient became febrile 8 days after completing a course of oseltamivir; isolation was instituted 9 days after symptom onset. Three other case patients developed symptoms 1, 3, and 5 days after the index patient. Three case patients were located in adjacent rooms. HA and NA sequences from case patients were identical. Twelve HCP and 6 visitors reported influenza symptoms during the study period. No other pH1N1 isolates from the hospital or from throughout the state carried the H275Y mutation. CONCLUSIONS: Geographic proximity, temporal clustering, presence of H275Y mutation, and viral sequence homology confirmed nosocomial transmission of oseltamivir-resistant pH1N1. Diagnostic vigilance and prompt isolation may prevent nosocomial transmission of influenza.

Neonatal-onset multisystem inflammatory disease responsive to interleukin-1beta inhibition.

BACKGROUND: Neonatal-onset multisystem inflammatory disease is characterized by fever, urticarial rash, aseptic meningitis, deforming arthropathy, hearing loss, and mental retardation. Many patients have mutations in the cold-induced autoinflammatory syndrome 1 (CIAS1) gene, encoding cryopyrin, a protein that regulates inflammation. METHODS: We selected 18 patients with neonatal-onset multisystem inflammatory disease (12 with identifiable CIAS1 mutations) to receive anakinra, an interleukin-1-receptor antagonist (1 to 2 mg per kilogram of body weight per day subcutaneously). In 11 patients, anakinra was withdrawn at three months until a flare occurred. The primary end points included changes in scores in a daily diary of symptoms, serum levels of amyloid A and C-reactive protein, and the erythrocyte sedimentation rate from baseline to month 3 and from month 3 until a disease flare. RESULTS: All 18 patients had a rapid response to anakinra, with disappearance of rash. Diary scores improved (P<0.001) and serum amyloid A (from a median of 174 mg to 8 mg per liter), C-reactive protein (from a median of 5.29 mg to 0.34 mg per deciliter), and the erythrocyte sedimentation rate decreased at month 3 (all P<0.001), and remained low at month 6. Magnetic resonance imaging showed improvement in cochlear and leptomeningeal lesions as compared with baseline. Withdrawal of anakinra uniformly resulted in relapse within days; retreatment led to rapid improvement. There were no drug-related serious adverse events. CONCLUSIONS: Daily injections of anakinra markedly improved clinical and laboratory manifestations in patients with neonatal-onset multisystem inflammatory disease, with or without CIAS1 mutations. (ClinicalTrials.gov number, NCT00069329 [ClinicalTrials.gov].).

Insulin autoantibodies are associated with islet inflammation but not always related to diabetes progression in NOD congenic mice.

Susceptibility to diabetes in humans and nonobese diabetic (NOD) mice is believed to arise from the combined effect of multiple genetic loci, resulting in immune-mediated destruction of the insulin-secreting beta-cells. Insulin autoantibodies (IAAs) are often present in humans for years, and in NOD mice for weeks, before the onset of diabetes. We have evaluated the expression of IAAs in NOD mice and in diabetes-resistant NOD congenic strains to characterize the association of autoantibody expression with insulitis and diabetes. In NOD congenic strains with genes that contribute to protection from insulitis and diabetes (Idd3, Idd5, Idd10, and Idd18), the prevalence of IAAs is reduced relative to NOD mice. In contrast, NOD.B10 Idd9 mice have a high prevalence of IAAs and a high degree of insulitis, despite a nearly complete resistance to diabetes. These data indicate that IAA expression is a phenotype that is associated with insulitis and correlates with overall disease progression in some strains of congenic mice but not in others. It is likely that patients with type 1 diabetes will also show non-major histocompatibility complex genetically determined variation in expression of autoantibodies and progression to diabetes.

Candida glabrata spinal osteomyelitis.

Invasive disease caused by Candida spp. is being appreciated with increased frequency especially associated with widespread use of immunosuppressive drug therapy. We report a case of spinal osteomyelitis and epidural abscess caused by Candida glabrata occurring in a patient who had been diagnosed with candidemia 3 months before that patient was treated with fluconazole. The infection was successfully treated with amphotericin B, but the patient eventually required surgical intervention for spondylolisthesis with impingement on the cauda equina.