Can seeds help mice with the daily grind?

Some laboratory mice gnaw food pellets without ingesting much of the gnawed material, resulting in the production of waste material called 'orts'. The fact that this food grinding behavior is not seen in all individuals of a particular strain suggests that it might be abnormal, and thus indicate a welfare concern. Furthermore, the increased rate of feed consumption and cage soiling is undesirable from a husbandry perspective. To try to determine possible motivations for the behavior, and identify potential treatments, outbred Crl:CD1(Icr) mice exhibiting food grinding were selected for one of three treatments placed in the feeder: no enrichment, a chewing device, or sunflower seeds. Both enrichment groups showed a significant decrease (P < 0.05) in ort production when compared with baseline measurements, but only mice provided with sunflower seeds maintained the decreased rate of food wastage after the treatment was withdrawn. A relationship between body weight and ort production was also found, in that cages with greater average body weights had lower levels of ort production. This suggests that a simple need to gnaw cannot alone explain food grinding, and that a nutritional motivation may also be involved.

Pneumocystis carinii causes a distinctive interstitial pneumonia in immunocompetent laboratory rats that had been attributed to "rat respiratory virus".

A prevalent and distinctive infectious interstitial pneumonia (IIP) of immunocompetent laboratory rats was suspected to be caused by a putative virus, termed rat respiratory virus, but this was never substantiated. To study this disease, 2 isolators were independently populated with rats from colonies with endemic disease, which was perpetuated by the regular addition of naive rats. After Pneumocystis was demonstrated by histopathology and polymerase chain reaction (PCR) in the lungs of rats from both isolators and an earlier bedding transmission study, the relationship between Pneumocystis and IIP was explored further by analyzing specimens from 3 contact transmission experiments, diagnostic submissions, and barrier room breeding colonies, including 1 with and 49 without IIP. Quantitative (q) PCR and immunofluorescence assay only detected Pneumocystis infection and serum antibodies in rats from experiments or colonies in which IIP was diagnosed by histopathology. In immunocompetent hosts, the Pneumocystis concentration in lungs corresponded to the severity and prevalence of IIP; seroconversion occurred when IIP developed and was followed by the concurrent clearance of Pneumocystis from lungs and resolution of disease. Experimentally infected immunodeficient RNU rats, by contrast, did not seroconvert to Pneumocystis or recover from infection. qPCR found Pneumocystis at significantly higher concentrations and much more often in lungs than in bronchial and nasal washes and failed to detect Pneumocystis in oral swabs. The sequences of a mitochondrial ribosomal large-subunit gene region for Pneumocystis from 11 distinct IIP sources were all identical to that of P. carinii. These data provide substantial evidence that P. carinii causes IIP in immunocompetent rats.