Clostridium difficile infection in rural Ontario: a retrospective multisite population-based study.

INTRODUCTION: We conducted a retrospective, population-based study to assess the prevalence of Clostridium difficile infections and the associated risk factors among inpatients and outpatients in our region. METHODS: We used laboratory data over a 2-year period to identify inpatient and outpatient cases of C. difficile infection. Data were collected from 3 local catchment areas for rural hospital laboratories in Sioux Lookout, Mount Forest and the South Huron Hospital Association in Exeter. We gathered demographic data and infection-specific information, including recent antibiotic use and recent or current hospital admission or nursing home stay. RESULTS: During the study period, 34 cases of C. difficile infection occurred in 29 patients, with an estimated crude annual rate of 24.3/100,000 population. Of the cases, 47.1% were diagnosed in outpatients. Most patients (76.5%) had taken antibiotics within the previous 90 days, and antibiotic use and hospital admission accounted for 47.1% of cases. Clindamycin was more commonly associated with C. difficile infections at the northern site and ciprofloxacin at the southern sites. There were 2 deaths from comorbidities. CONCLUSION: The estimated annual incidence of C. difficile infection in our study is similar to urban-based estimates. Almost half of the cases involved outpatients, indicating a need to recognize this illness as a serious outpatient condition. Antibiotic stewardship is an ongoing consideration, as most patients were exposed to antibiotic use before infection.

INTRODUCTION: Nous avons effectué une étude rétrospective basée dans la population pour évaluer la prévalence des infections à Clostridium difficile et les facteurs associés chez les patients hospitalisés et non hospitalisés de notre région.. MÉTHODES: Nous avons utilisé les données de laboratoire sur une période de 2 ans pour recenser les cas d'infections à C. difficile chez les patients hospitalisés et non hospitalisés. Les données ont été recueillies à partir de 3 bassins de population locaux pour les laboratoires hospitaliers ruraux de Sioux Lookout, de Mount Forest et de la South Huron Hospital Association à Exeter. Nous avons colligé les données démographiques et les renseignements spécifiques aux infections, y compris l'utilisation récente de l'antibiothérapie et les hospitalisations ou séjours en foyers de soins infirmiers récents ou en cours. RÉSULTATS: Au cours de la période de l'étude, 34 infections à C. difficile ont été dénombrées chez 29 patients, pour un taux annuel brut estimé de 24,3/100 000 habitants. Parmi ces cas, 47,1 % n'étaient pas hospitalisés au moment du diagnostic. La plupart des patients (76,5 %) avaient pris des antibiotiques au cours des 90 jours précédents et l'antibiothérapie et l'hospitalisation caractérisaient 47,1 % des cas. La clindamycine a le plus souvent été associée aux infections à C. difficile dans le site le plus au Nord et la ciprofloxacine, dans les deux sites plus au Sud. On a déploré 2 décès par suite de comorbidités. CONCLUSION: L'incidence annuelle estimée de l'infection à C. difficile au cours de notre étude a été similaire aux estimations obtenues en milieu urbain. Près de la moitié des cas s'observaient chez des patients non hospitalisés, rappelant la nécessité de considérer cette infection comme un grave problème de santé chez les patients externes. La bonne gestion de l'utilisation des antibiotiques demeure un enjeu constant puisque la plupart des patients avaient été exposés à des antibiotiques avant leur infection.

Do genetic mutations and genotypes contribute to onychomycosis?

BACKGROUND: The variability in susceptibility to onychomycosis for individuals exposed to the same environmental risk factors raises the possibility that there may be individuals with a genetic predisposition to dermatophyte infection. OBJECTIVE: To determine whether there are genetic mutations or genotypes which contribute to onychomycosis. METHODS: The PubMed database was searched for examples of immune deficiencies resulting in dermatophyte infections. RESULTS: There are mutations in the innate immune receptors Dectin-1 and its adaptor protein CARD9 which result in familial mucocutaneous infections. There are also specific human leukocyte antigen genotypes that are more common in individuals and families with a high prevalence of onychomycosis. In addition, some patients have been reported with insufficient levels of CD4+CD25+ regulatory T cells. These deficits impair a full innate and adaptive immune response and may result in chronic or recurrent infections. CONCLUSIONS: There are documented mutations and genotypes that contribute to familial and individual susceptibility to onychomycosis.

Sanitization of contaminated footwear from onychomycosis patients using ozone gas: a novel adjunct therapy for treating onychomycosis and tinea pedis?

BACKGROUND: Ozone gas possesses antimicrobial properties against bacteria, viruses, and yeasts. Previously, we demonstrated the efficacy of ozone in killing ATCC strains of the dermatophyte fungi Trichophyton rubrum and Trichophyton mentagrophytes. OBJECTIVE: To test the efficacy of ozone gas in sanitizing onychomycosis patient footwear contaminated with fungal material as a means of minimizing the risk of reinfection. METHODS: Swabs of footwear from onychomycosis patients were cultured prior to and after ozone exposure to test the ability of ozone to sanitize these items. RESULTS: We identified contamination of footwear from most onychomycosis patients, a potential source of reinfection in these individuals. Furthermore, ozone gas was effective in sanitizing contaminated footwear. CONCLUSION: Ozone gas is effective in sanitizing footwear and represents a novel adjunct therapy to be used in conjunction with antifungal medications and/or devices to better treat onychomycosis and tinea pedis patients in both the short and the long term.

Preventing and curing citrulline-induced autoimmune arthritis in a humanized mouse model using a Th2-polarizing iNKT cell agonist.

Invariant natural killer T (iNKT) cells are innate lymphocytes with unique reactivity to glycolipid antigens bound to non-polymorphic CD1d molecules. They are capable of rapidly releasing pro- and/or anti-inflammatory cytokines and constitute attractive targets for immunotherapy of a wide range of diseases including autoimmune disorders. In this study, we have explored the beneficial effects of OCH, a Th2-polarizing glycolipid agonist of iNKT cells, in a humanized mouse model of rheumatoid arthritis (RA) in which citrullinated human proteins are targeted by autoaggressive immune responses in mice expressing an RA susceptibility human leukocyte antigen (HLA) DR4 molecule. We found for the first time that treatment with OCH both prevents and cures citrulline-induced autoimmune arthritis as evidenced by resolved ankle swelling and reversed histopathological changes associated with arthritis. Also importantly, OCH treatment blocked the arthritogenic capacity of citrullinated antigen-experienced splenocytes without compromising their global responsiveness or altering the proportion of splenic naturally occurring CD4(+)CD25(+)FoxP3(+) regulatory T cells. Interestingly, administering the Th1-promoting iNKT cell glycolipid ligand α-C-galactosylceramide into HLA-DR4 transgenic mice increased the incidence of arthritis in these animals and exacerbated their clinical symptoms, strongly suggesting a role for Th1 responses in the pathogenesis of citrulline-induced arthritis. Therefore, our findings indicate a role for Th1-mediated immunopathology in citrulline-induced arthritis and provide the first evidence that iNKT cell manipulation by Th2-skewing glycolipids may be of therapeutic value in this clinically relevant model, a finding that is potentially translatable to human RA.

Severe necrotizing pancreatitis following combined hepatitis A and B vaccination.

Necrotizing pancreatitis is a severe form of pancreatitis and is associated with substantial morbidity and mortality. We report a case of necrotizing pancreatitis that developed following combined hepatitis A and B vaccination. No other causes of pancreatitis could be determined. Although confirming the diagnosis is challenging, 3 main factors suggest a possible link to the vaccine: the chronology of the events, the patient's human leukocyte antigen genotype and the incongruent immune response to the vaccine components. This report serves to alert physicians to the possible development of necrotizing pancreatitis after vaccination.