Elimination of Pasteurella pneumotropica from a mouse barrier facility by using a modified enrofloxacin treatment regimen.

Multiple NOD. Cg-Prkdc(scid)Il2rg(tm1Wjl)Tg(HLA-A2.1)Enge/Sz (NSG/A2) transgenic mice maintained in a mouse barrier facility were submitted for necropsy to determine the cause of facial alopecia, tachypnea, dyspnea, and sudden death. Pneumonia and soft-tissue abscesses were observed, and Pasteurella pneumotropica biotype Jawetz was consistently isolated from the upper respiratory tract, lung, and abscesses. Epidemiologic investigation within the facility revealed presence of this pathogen in mice generated or rederived by the intramural Genetically Engineered Mouse Model (GEMM) Core but not in mice procured from several approved commercial vendors. Epidemiologic data suggested the infection originated from female or vasectomized male ND4 mice obtained from a commercial vendor and then comingled by the GEMM Core to induce pseudopregnancy in female mice for embryo implantation. Enrofloxacin delivered in drinking water (85 mg/kg body weight daily) for 14 d was sufficient to clear bacterial infection in normal, breeding, and immune-deficient mice without the need to change the antibiotic water source. This modified treatment regimen was administered to 2400 cages of mice to eradicate Pasteurella pneumotropica from the facility. Follow-up PCR testing for P. pneumotropica biotype Jawetz remained uniformly negative at 2, 6, 12, and 52 wk after treatment in multiple strains of mice that were originally infected. Together, these data indicate that enrofloxacin can eradicate P. pneumotropica from infected mice in a less labor-intensive approach that does not require breeding cessation and that is easily adaptable to the standard biweekly cage change schedule for individually ventilated cages.

An outbreak of Pasteurella pneumotropica in genetically modified mice: treatment and elimination.

A closed breeding colony comprising genetically engineered, wild-type, and stock mice presented with varying degrees of bilateral mucopurulent conjunctivitis and panophthalmitis. The one mouse with unilateral corneal ulceration, a knockout animal, was submitted for necropsy, and bacterial culture samples were obtained from the affected eye and uterus. In addition, ocular swabs from another 12 clinically affected animals, consisting of knockout, transgenic, wild-type, and stock mice, were submitted for bacterial culture analysis. All samples revealed pure cultures of Pasteurella pneumotropica. At the time of the outbreak, there were approximately 600 mice in the affected colony, with the majority of clinical cases (58 of 79) involving knockout mice and the remainder (21 of 79) in the other strains. Treatment consisted of enrofloxacin in the drinking water at 85 mg/kg daily for 14 days. Within 7 days of initiation of treatment, all existing clinical cases had resolved and no new clinical cases developed. Four weeks after completion of treatment, two groups of mice were submitted for multiple organ bacteriological analyses. One group of mice represented those animals which had complete resolution of clinical signs, and the second group of mice represented those individuals which had remained asymptomatic throughout the outbreak. All post treatment bacterial culture samples were negative for Pasteurella pneumotropica. By using the oral enrofloxacin suspension in the drinking water rather than the parenteral counterpart, concerns regarding the pharmacokinetics, specifically drug bioavailability via the oral route, problems with aqueous immiscibility and drug degradation within an aqueous medium were not potentially confounding variables. The clinical management, ease of administration, and efficacy of using an oral antibiotic formulation for the treatment and eradication of Pasteurella pneumotropica from a large mouse colony are presented in this paper.