Occurrence of Helicobacter species other than H. hepaticus in laboratory mice and rats in Sweden.

The aim of this study was to determine which Helicobacter species other than H. hepaticus colonize laboratory mice and rats in Sweden. We analyzed 63 intestinal samples from mice and 42 intestinal samples from rats by partial 16S rDNA sequence analysis. Previously these samples had been found positive for Helicobacter species but negative for H. hepaticus in a polymerase chain reaction screening assay at the National Veterinary Institute in Sweden. H. ganmani, H. typhlonius, H. rodentium, an uncharacterized Helicobacter species ('hamster B'), and a possibly novel species were detected in mice. The possibly novel species was most closely related to H. apodemus strain YMRC 000216 (98.3% sequence similarity). Two different Helicobacter species were detected in rats: H. ganmani and H. rodentium. H. ganmani colonization of rats has not previously been reported.

Development and use of a simple polymerase chain reaction assay to screen for Helicobacter spp. and H. hepaticus in intestinal and fecal samples from laboratory mice.

A simple and sensitive duplex polymerase chain reaction (PCR) assay was developed for use in detection of Helicobacter species and H. hepaticus in laboratory mice. Bacteria were extracted and concentrated from fecal pellets and intestinal segments by use of buoyant density centrifugation. To improve quality assurance, an internal control (mimic) for detection of false-negative reactions was included. In addition, cartridges (Capillette) pre-filled with PCR reagents, were used to minimize the hands-on time required, thus reducing the risk of contamination with previously amplified material. Laboratory mice from Swedish animal houses sent to the National Veterinary Institute for health monitoring were found to have high prevalence of H. hepaticus.

Fatal acute intestinal pseudoobstruction in mice.

Here we describe the epizootiology and pathology of spontaneous, fatal acute intestinal pseudoobstruction that occurred in a mouse colony of 1000 breeding pairs, mainly of the C57Bl/6 strain and free from known pathogenic agents. Most of the mice affected were dams in the second week of lactation. At necropsy, segments of the small intestines were distended with fluid contents. Widespread apoptosis of the villus epithelium of the small intestine and superficial epithelial cells of the large intestine, associated with strong expression of active caspase 3, was a distinctive feature. Necrotic enterocytes, mucosal erosions, and acute mucosal inflammation were prominent in some mice, and morphologic signs of toxemia were generally present. No light microscopic neuronal changes were apparent in the gut, and no etiologic agents were identified. These results indicate that sudden activation of apoptosis in the trophically stimulated gut epithelium during peak lactation was instrumental for the fatal outcome of the condition, but the primary cause of the motility dysfunction of the bowel was not established.

Diabetes and myocarditis in voles and lemmings at cyclic peak densities--induced by Ljungan virus?

Although it is well-documented from theoretical studies that pathogens have the capacity to generate cycles, the occurrence and role of pathogens and disease have been poorly empirically studied in cyclic voles and lemmings. In screening for the occurrence of disease in cyclic vole and lemming populations, we found that a high proportion of live-trapped Clethrionomys glareolus, C. rufocanus, Microtus agrestis and Lemmus lemmus at high collective peak density, shortly before the decline, suffered from diabetes or myocarditis in northern Scandinavia. A high frequency of animals had abnormal blood glucose (BG) levels at the time of trapping (5-33%). In contrast, C. rufocanus individuals tested at a much lower overall density, and at an earlier stage relative to the decline in the following cycle, showed normal BG concentrations. However, a high proportion (43%) of a sample of these individuals kept in captivity developed clinical diabetes within five weeks, as determined by BG levels and a glucose tolerance test performed at that later time. A new picornavirus isolated from the rodents, Ljungan virus (LV), was assumed to cause the diseases, as LV-induced diabetes and myocarditis, as well as encephalitis and fetal deaths, were observed in laboratory mice. We hypothesize that LV infection significantly affects morbidity and mortality rates in the wild, either directly or indirectly, by predisposing the rodents to predation, and is at least involved in causing the regular, rapid population declines of these cyclic voles and lemmings. Increased stress at peak densities is thought to be an important trigger for the development of disease, as the occurrence of disease in laboratory mice has been found to be triggered by introducing stress to LV-infected animals.