Effects of Pelleting, Irradiation, and Autoclaving of Rodent Feed on MPV and MNV Infectivity.

Murine norovirus (MNV) and mouse parvovirus (MPV) are among the most common adventitial viruses seen in laboratory mice, and infections arise in barrier facilities despite rigorous biosecurity programs. Some authors have implicated nonsterilized feed as a source of MPV in rodent facilities, but none have conclusively documented viral particles in the feed. In this study, we hypothesized that both viruses can resist the pelleting process but not subsequent irradiation or autoclaving, thus revealing a potential source of outbreaks in rodent facilities. To test this hypothesis, we contaminated powdered feed with 10-fold concentrations of MNV and MPV and fed it to both Swiss Webster (SW) and C57BL/6NTac (B6) mice to determine a 'powdered ID50' according to seroconversion over a 28-d period. We repeated the experiment by using powdered feed that we contaminated with increasing viral doses (as no. of powdered ID50) and subsequently pelleted; from these results, we determined a 'pelleted ID50.' Finally we assessed the effect of irradiation and autoclaving on contaminated pellets by using the same experimental design. The powdered ID50 was relatively low and identical in both mouse strains (2.51 × 10² pfu) for MNV but higher in B6 (copy number, 3.20 × 106) than SW (3.98 × 104 copies) for MPV. As hypothesized, mice were infected by contaminated rodent feed despite the pelleting process. Indeed, pelleting resulted in a 1- to 2-log increase in ID50 in both strains for MNV and MPV. Irradiation and autoclaving of infected pellets effectively prevented seroconversion of mice exposed to all doses of MNV, whereas a single mouse seroconverted at the highest dose of MPV (1.35 × 107 copies). These data suggest that both MNV and MPV remain infectious after conditions reproducing the rodent chow pelleting process and that nonsterilized rodent chow might be a source of viral outbreaks.

Urinary MCP1 and Microalbumin increase prior to onset of Azotemia in mice with polycystic kidney disease.

Urinary biomarkers may offer a more sensitive and less invasive means to monitor kidney disease than traditional blood chemistry biomarkers such as creatinine. CD1(pcy/pcy) (pcy) mice have a slowly progressive disease phenotype that resembles human autosomal dominant polycystic kidney disease with renal cyst formation and inflammation. Previous reports suggest that dietary protein restriction may slow disease progression in mice and humans with polycystic kidney disease. Accordingly, we fed pcy mice either a standard chow (22.5% protein) or a protein-restricted (11.5% soy-based protein) diet from weaning until 34 wk of age. Every 6 wk we measured markers of kidney disease, including serum creatinine, BUN, and serum albumin as well as urinary monocyte chemoattractant protein 1 (MCP1), microalbumin, and specific gravity. Progression of kidney disease was equivalent for both diet groups despite dietary protein restriction. Urinary biomarkers proved useful for early detection of disease, in that urinary microalbumin was elevated as early as 22 wk of age and urinary MCP1 was increased by 28 wk of age, whereas increases in serum creatinine and BUN were detected later (at 34 wk of age) in both diet groups. Thus, urinary microalbumin and MCP1 analyses provided earlier, noninvasive indicators for detection of kidney disease and disease progression in pcy mice than did serum creatinine and BUN.