A hospital-level cost-effectiveness analysis model for toxigenic Clostridium difficile detection algorithms.

BACKGROUND: Despite thorough analyses of the analytical performance of Clostridium difficile tests and test algorithms, the financial impact at hospital level has not been well described. Such a model should take institution-specific variables into account, such as incidence, request behaviour and infection control policies. AIM: To calculate the total hospital costs of different test algorithms, accounting for days on which infected patients with toxigenic strains were not isolated and therefore posed an infectious risk for new/secondary nosocomial infections. METHODS: A mathematical algorithm was developed to gather the above parameters using data from seven Flemish hospital laboratories (Bilulu Microbiology Study Group) (number of tests, local prevalence and hospital hygiene measures). Measures of sensitivity and specificity for the evaluated tests were taken from the literature. List prices and costs of assays were provided by the manufacturer or the institutions. The calculated cost included reagent costs, personnel costs and the financial burden following due and undue isolations and antibiotic therapies. Five different test algorithms were compared. FINDINGS AND CONCLUSION: A dynamic calculation model was constructed to evaluate the cost:benefit ratio of each algorithm for a set of institution- and time-dependent inputted variables (prevalence, cost fluctuations and test performances), making it possible to choose the most advantageous algorithm for its setting. A two-step test algorithm with concomitant glutamate dehydrogenase and toxin testing, followed by a rapid molecular assay was found to be the most cost-effective algorithm. This enabled resolution of almost all cases on the day of arrival, minimizing the number of unnecessary or missing isolations.

Establishing quality control ranges for temocillin following CLSI-M23-A3 guideline.

OBJECTIVES: This study aimed to establish acceptable quality control ranges for temocillin disk diffusion tests and Etest(®) minimal inhibitory concentrations. METHODS: According to Clinical and Laboratory Standards Institute (CLSI) guideline, a Tier 2 quality control study was performed and involves seven laboratories. Each of them tested 10 replicates of two quality control strains (Escherichia coli ATCC 25922 and E. coli ATCC 35218) on three different media lots and, for disk diffusion, two disk lots. RESULTS: Proposed zone diameter quality control ranges were 12-25 mm for E. coli ATCC 25922 and 19-28 mm for E. coli ATCC 35218. Proposed Etest quality control ranges were 3-24 mg/l for E. coli ATCC 25922 and 2-6 mg/l E. coli ATCC 35218. CONCLUSION: Based on our results, we would advise the use of E. coli ATCC 35218 as QC strain for temocillin susceptibility testing and Etest because ranges obtained are narrower than with E. coli ATCC 25922 and do not overlap temocillin breakpoint.

Unexpected urinary Schistosoma infection in a Belgian travel group returning from Malawi.

Urinary schistosomiasis, caused by Schistosoma haematobium, is a prevalent parasitic infection in certain areas of Africa and the Middle East. Humans can be infected by cercariae when they are in contact with contaminated freshwater. The adult worms reside in the veins of the vesical and pelvis plexuses. The urinary bladder, the seminal vesicles and the lower ends of the ureters are the most commonly affected organs. In this case report, we describe an unrecognised case of urinary schistosomiasis in a woman who was part of a Belgian travel group; two other patients out of eight were also infected. In Belgium, the number of reported cases of S. haematobium infection is limited. The aim of this report is to emphasize this parasitic infection should be suspected in patients who travel to endemic areas.

Mannan-binding lectin (MBL) gene polymorphisms in ulcerative colitis and Crohn's disease.

The inflammatory bowel diseases (IBD), Crohn's disease (CD), and ulcerative colitis (UC), are complex multifactorial traits involving both environmental and genetic factors. Mannan-binding lectin (MBL) plays an important role in non-specific immunity and complement activation. Point mutations in codons 52, 54 and 57 of exon 1 of the MBL gene are associated with decreased MBL plasma concentrations and increased susceptibility to various infectious diseases. If these MBL mutations could lead to susceptibility to putative IBD-etiological microbial agents, or could temper the complement-mediated mucosal damage in IBD, MBL could function as the link between certain microbial, immunological and genetic factors in IBD. In this study, we investigated the presence of the codon 52, 54 and 57 mutations of the MBL gene in 431 unrelated IBD patients, 112 affected and 141 unaffected first-degree relatives, and 308 healthy control individuals. In the group of sporadic IBD patients (n = 340), the frequency of the investigated MBL variants was significantly lower in UC patients when compared with CD patients (P = 0.01) and with controls (P = 0.02). These results suggest that MBL mutations which decrease the formation of functional MBL could protect against the clinical development of sporadic UC, but not of CD. This could be explained by the differential T-helper response in both diseases.