Practical pathology of aging mice

Pettan-Brewer, Christina; Treuting, Piper M.

Barbering, alopecia, dermatitis, and scarring are commonly seen in mice (Fig. 2) . Dermatitis may have a variety of causes including infectious agents, such as fur mites, or fighting with secondary bacterial infections. These will often respond to treatments such as removal of aggressive mice, topic and oral antibiotic, or corticosteroids (26) . In contrast, idiopathic ulcerative dermatitis in the B6 mouse does not respond to treatment. Affected B6 mice are usually pruritic leading to self-mutilation, disease progression and, often, euthanasia for humane reasons. The B6 chronic ulcerative dermatitis has been attributed to many causes (27, 28) most recently primary follicular dystrophy (29) . The clinical disease is variable, waxes and wanes, appears to have sex, and season predilections. As seen with other strain-specific diseases, the use of F1 hybrids has a decreased incidence of B6 dermatitis (1, 30); however, skin lesions remain a significant background factor in aging colonies (29) . Collectively, skin lesions in aging mouse colonies have variable presentations ranging from the very mild alopecia to severe ulcerative disease requiring euthanasia. Mild changes, such as ill-kept fur (Fig. 2B ) are often one of the first clinical signs noted in diseased mice. It is nonspecific and a result of decreased grooming. Alopecia in mice may present on the head ( Fig. 2A) or in a patches (Fig. 2C) . Barbering by cage mates may result in areas of hair loss; however, distinctive patterns (Fig. 3A) and the presence of one unaffected (dominant) mouse in the cage will help to rule out dermatitis. Histologically, dermatitis is also variable in presentation and severity, depending on etiology and chronicity. Mild lesions (Fig. 2E) with few scattered inflammatory cells may be noted in regions of clinical alopecia. Severe lesions may occur and are often a combination of ulceration, necrosis, and associated chronic-active inflammation. Healing is by dermal fibrosis and marked epithelial hyperplasia (Fig. 2F) . Like rectal prolapses, open skin lesions serve as a nidus for bacterial infection with skin commensals (Staphylococcal species) and result in smoldering inflammation that may affect physiological parameters such as inflammatory cytokines, leukograms, lymphadenopathy, and reactive amyloidosis (31) .