Usefulness of the Bristol Stool Form Chart scoring system for the laboratory processing of faecal samples in suspected Clostridioides difficile cases.

Clostridioides difficile infection (CDI) remains a threat to hospitalized patients. All patients with diarrhoea [defined as Bristol Stool Form Chart (BSFC) types 5-7] not attributable to another cause should be tested for CDI. Samples should quarter fill and take the shape of the specimen container. Use of the BSFC definition of diarrhoea to determine which samples should be tested for CDI in the laboratory was assessed. In this study, two-thirds of glutamate-dehydrogenase-positive, toxin-positive samples were rated BSFC type <5. Therefore, the BSFC should not be used by laboratories to determine which samples are tested for CDI.

Extensive projections of myenteric serotonergic neurons suggest they comprise the central processing unit in the colon.

BACKGROUND: 5-Hydroxytryptamine (5-HT, serotonin) is an important regulator of colonic motility and secretion; yet the role of serotonergic neurons in the colon is controversial. METHODS: We used immunohistochemical techniques to examine their projections throughout the enteric nervous system and interstitial cells of Cajal (ICC) networks in the murine proximal to mid colon. KEY RESULTS: Serotonergic neurons, which were mainly calbindin positive, occurred only in myenteric ganglia (1 per 3 ganglia). They were larger than nNOS neurons but similar in size to Dogiel Type II (AH) neurons. 5-HT neurons, appeared to make numerous varicose contacts with each other, most nNOS neurons, Dogiel Type II/AH neurons and glial cells. 5-HT, calbindin and nNOS nerve fibers also formed a thin perimuscular nerve plexus that was associated with ganglia, which contained both nNOS positive and negative neurons, which lay directly upon the submucosal pacemaker ICC network. Neurons in perimuscular ganglia were surrounded by 5-HT varicosities. Submucous ganglia contained nNOS positive and negative neurons, and calbindin positive neurons, which also appeared richly supplied by serotonergic nerve varicosities. Serotonergic nerve fibers ran along submucosal arterioles, but not veins. Varicosities of serotonergic nerve fibers were closely associated with pacemaker ICC networks and with intramuscular ICC (ICC-IM). 5-HT2B receptors were found on a subpopulation of non-5-HT containing myenteric neurons and their varicosities, pacemaker ICC-MY and ICC-IM. CONCLUSIONS & INFERENCES: Myenteric serotonergic neurons, whose axons exhibit considerable divergence, regulate the entire enteric nervous system and are important in coordinating motility with secretion. They are not just interneurons, as regularly assumed, but possibly also motor neurons to ICC and blood vessels, and some may even be sensory neurons.

Strain variation in early innate cytokine induction by Plasmodium falciparum.

Previous work has shown that human donors vary in the magnitude and pattern of cytokines induced when peripheral blood mononuclear cells (PBMCs) are co-cultured with Plasmodium falciparum-infected erythrocytes. Whether P. falciparum strains vary in their ability to induce cytokines has not been studied in detail and is an important question, because variation in cytokine induction could affect parasite virulence and patterns of clinical disease. We investigated the early inflammatory cytokine response to four P. falciparum laboratory strains and five field isolates. Initial studies showed that parasite strain, parasitaemia and PBMC donor all had significant effects on the magnitude of pro-inflammatory cytokine responses (IFN-gamma, GM-CSF, IL-1 beta, TNF-alpha, IL-6, P < 0.005 in all cases). However, we noticed that the most highly inducing parasite strain consistently reached schizont rupture more rapidly than the other strains. When timing of schizont rupture was taken into account, parasite strains no longer differed in their cytokine induction (P = 0.383), although donor effects remained significant (P < 0.001). These data do not support the hypothesis that P. falciparum strains vary in induction of early innate cytokine responses from PBMCs, and instead are consistent with the suggestion that conserved parasite products such as haemozoin or GPI-anchors are the parasite-derived stimuli for cytokine induction.

Friedreich's ataxia cardiomyopathy: case based discussion and management issues.

Cardiac involvement is common in Friedreich's Ataxia and is a common cause of premature death. Evidence regarding treatment of congestive heart failure in patients with Friedreich's Ataxia is lacking. The case of a 31-year-old male with advanced Friedreich's Ataxia who presented with an acute diarrhoeal illness and features of acute heart failure is discussed. We then review the reported cardiac manifestations of Friedreich's Ataxia and discuss management options.

Public health use of surveillance for West Nile virus in horses: Saskatchewan, 2003-2005.

West Nile virus (WNV) infection in horses was first reported in Canada in 2001 and in the province of Saskatchewan in 2002. This paper outlines the surveillance results of WNV in Saskatchewan horses from 2003 to 2005 and describes the usefulness of its inclusion in an integrated surveillance program in Saskatchewan. The number of human and horse cases was highest in 2003, the epidemic year and then substantially lower in 2004 and 2005. Horses provided additive information about WNV activity in rural areas with low human population, however, this required willingness and active participation by veterinarians and horse owners. Vaccination impedes the future use of horses in WNV surveillance for public health or veterinary purposes; however, for zoonoses where no vaccination is available, domestic animals would be useful components for surveillance. Integration of surveillance data from human and animal health provide the benefit of a more complex epidemiological picture that can be used to improve public health.

Eustachian tube function assessed with tympanometry.

On 15 normal ears and 14 pathological ears of adults with intact tympanic membranes, Eustachian tube function was measured by using tympanometry in an effort to reproduce the results published by Holmquist. His method appeared to be a promising tool for clinical determination of Eustachian tube function. However, our results on normal ears were not significantly different from our results on pathological ears and were inconsistent with Holmquist's results. In contrast to Holmquist, 60% of our normal ears were unable to attain achieved negative middle ear pressures of -100 mm to -250 mm H2O. Our normal ears, as well as our pathological ears, required repeated swallows to normalize negative pressure. Tests in both our groups were not always repeatable even though recorded applied nasopharyngeal pressure was identical. Therefore, our findings do not substantiate this procedure as a useful, reliable clinical tool for measuring Eustachian tube function on ears with intact tympanic membranes.