II. Arthropods
III. Corynebacterium bovis (Hyperkertitis Associated Coryneform)
IV. Fight wounds
V. Mousepox (Ectromelia Virus)
VI. Self-Mutilation
VII. Staphylococcal Furunculosis
A. Barbering: A female mouse may develop a fur-chewing vice
and chew the hair off a cagemate or her litter. The hair over the
nasal and orbital regions or the dorsal cervical area is most often barbered.
The exposed skin is intact and normal in appearance. The only cure
for barbering, if the client considers it a problem, is to remove the mouse
that has not been barbered.
B. Alopecia: Alopecia often with accompanying epidermal thickening is one of the most common lesions seen in genetically engineered mice (GEM). The causes of alopecia are frequently unknown, and may be related with the genotype of the mouse.
A. Etiology: Myocoptes musculinus (A.), Myobia
musculi (B.), and Radfordia affinis (C.) are common fur mites.
Psorogates
simplex, the follicular mite, is rarely seen.
B. Transmission: Direct contact spreads the mite. Fur mites are usually host-specific. Prevalence of infestation is low in conventional colonies of mice.
C. Clinical Signs: Usually no clinical signs are observed. Black haired mice are thought to have an increased sensitivity to mites manifested by pruritus and alopecia progressing to excoriation, ulcerative dermatitis, and cicatricial disfigurement.
D. Diagnosis: On live mice, plucking hairs from the pelt
and examining under a dissecting microscope may reveal the eggs (laid on
the hair shaft) or the mites (A.). If the pelt from a recently killed
mouse is cooled to room temperature, the mites will crawl up to the tips
of the hairs, looking like white specks (B.). If an animal has been
dead for a while, the mites may have migrated to another host.
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E. Treatment: Adults and weanlings can be dusted with silica dusts, pyrethrin dusts. Ivermectin solutions, using the horse preparations, have been made in concentrations providing 8 mg in every liter of drinking water. Treated water in bottles should be provided once a week for 3 weeks to eliminate the mites. Alternatively, 0.1% solutions in spray bottles can be used to deliver ivermectin. Care must be exercised as some mouse strains, such as the CF-1, will experience decreased production or death when treated with ivermectin. Treatment should be tailored to break the mite life cycle and to accommodate the research protocol or animal use.
F. Control: Regular examinations and treatments may eventually rid the colony of mites.
III. Corynebacterium bovis (Hyperkertitis Associated Coryneform)
A. Etiology: Corynebacterium bovis has been identified as the cause of a bacterial skin disease of nude mice referred to as "scaley skin disease". The condition typically affects adult homozygous nude mice of both genders, and is manifested as a hyperkeratosis with yellow-white flakes adherent to thickened skin.
B. Transmission: The bacterium is carried on the skin and in the oral cavity of mice, and is transmitted by direct contact and by fomite transmission (handling, flake contact, etc.). C. bovis has been cultured from affected nude mice, and also from skin of asympomatic hirsute immunocompetent mice. The association of bacterium with disease may be related to lack of hair since the hairless immunocompetent SKH-1 mouse is also susceptible to bacterial hyperkeratosis
C. Pathology: Affected mice may lose weight and are often
removed from study because of reports of poor growth of transplanted tumors
or hinderence of immunologic studies. Mortality is low and the hyperkeratosis
is transient but may recur. Histologic examination of the skin reveals
acanthosis, orthokeratotic hyperkeratosis with a mononuclear cell dermal
infiltrate (A.). Short, Gram-positive rods arranged in clusters (arrow)
and palisades can be recognized in the stratum corneum on Gram-stained
skin sections (B.).
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D. Diagnosis: The bacterium can be cultured by inoculating blood agar with skin or buccal swabs and grows in punctiform colonies after 48 hrs of incubation in aerobic conditions. The bacterium can also be detected in skin and environmental samples by a C. bovis-specific PCR test.
E. Treatment and Control: Antibiotics such as ampicillin or penicillin VK delivered in drinking water controls the disease but does not eliminate carriage of the bacterium. Control measures include ordering mice from C. bovis-negative mouse colonies, housing mice in sterile microisolator cages, and use of oxidant-based disinfectants on forceps or gloves used for animal handling, and environmental surfaces (including biosafety hoods, animal restrainers, etc.).
Mice (particularly males) may fight and can inflict severe wounds upon
each other. These usually are located on the face, back, and genital
areas. If tail biting occurs, the tail may become gangrenous and
slough. The wounds may become infected and develop into abscesses.
Wounds may be treated by lancing and flushing with a tamed iodine or antibiotic
solution. Topical antibiotic ointments containing aminoglycosides
should be avoided since ingestion of aminoglycosides can be toxic to mice
(the mechanism of toxicity is respiratory paralysis from ganglion blockade).
Prevention is by separating the fighting animals.
V. Mousepox (Ectromelia Virus)
A. Etiology: Ectromelia virus, the agent of mousepox, is a DNA poxvirus of the vaccinia subgroup.
B. Transmission: Natural infections occur via the fecal-oral route, urine contamination or by direct contact. Skin abrasions are thought to provide the main route of entry. Inoculation of mice with poxvirus-infected tumor cells or serum products have also caused disease outbreaks. Severity of disease is dependent on the mouse strain. Incidence of disease is rare, with sporadic epizootics usually resulting from passage of infected cells or other biological material into naive mice.
C. Clinical Signs: Clinical signs are dependent on the genotype of the mouse strain, with strain A, C3H and BALB/c representing suceptible strains, and C57BL/6 considered a resistant strain. In acute disease, there is high morbidity and high mortality with affected animals exhibiting hunched posture, conjunctivitis and facial swelling. Subacute to chronically infected animals develop a cutaneous vesicular body rash which often progresses to swelling, necrosis and sloughing of the extremities. Deaths are sporadic.
D. Pathology: Lesions from animals dying from acute disease include visceral congestion, splenomegaly, white necrotic foci in the liver and spleen, and peritoneal exudate. In addition, focal pancreatic necrosis, erosive enteritis and vesicular pox lesions on the extremities can also be found. Although clinical and gross lesions are suggestive of the disease, histological demonstration of intracytoplasmic inclusion bodies (arrows) in epithelial cells surrounding vesicular skin ulcers, in small intestinal cells and in pancreatic cells is helpful to confirm the diagnosis.
E. Diagnosis: Ruleouts for these signs include Tyzzer's disease, MHV, salmonellosis, skin parasites, ringworm, bite wounds, and arthritis. Electron microscopy and PCR provide excellent forms of documentation of pox virions in infected cells. Serological tests using ELISA, HAI and IFA help screen mouse colonies for the presence of infection.
F. Treatment: None.
G. Control: If the animals are readily available commercially, exterminate the infected colony, sanitize the facility and repopulate with uninfected mice. Valuable mouse strains may be rederived if they can survive the acute infection. Identify the source of virus, and implement measures to prevent re-introduction.
A. Otitis Media: Otitis media has been reported to result
in enough irritation to cause the animals to scratch the base of the ears
with the hind feet. The scratching can lead to excoriation and ulceration
of the skin of the neck and subsequent inoculation of the wounds with environmental
bacteria contaminating the feet. The resultant dermatitis evokes
a more intense scratching reflex until a large ulcerative pustular dermatitis
results from the self-mutilating activity. Parenteral antibiotic
therapy appears to be of little help for the otitis media or the dermatitis.
Clipping of the toenails or applying an Elizabethan collar will allow resolution
of the dermatitis with or without medicinal therapy. Certainly, the
value of the animal will dictate the decision to treat or euthanize.
B. Ulcerative Dermatitis Syndrome: Black mice of a C57BL genotype are prone to develop a dermatitis with alopeica and epidermal ulcers. Mice will scratch the dorsal cervical region, shoulder and caudal axillary regions until ulcers form. The ulcerated areas often scar, causing restriction of forelimb movement. Ectoparasite infestation may exacerbate the syndrome, but the syndrome develops in mite-free mice. The disease appears to be multifactorial, and dietary factors may play a role in disease expression.
C. Chemical Irritants: Forceps disinfected with germicidal
solutions are often used to transfer the mice from dirty to clean microisolator
cages. The forceps are dipped in the germicidal solution and mice
are either grasped by the tail or by the loose skin over the neck.
Improperly diluted quaternary ammonium solutions can chemically burn the
skin of mice and induce an ulcerative dermatitis. Skin lesions must
be monitored and treated for secondary bacterial infections and self-mutilation.
VII. Staphylococcal Furunculosis
Staphylococcal species common to the flora of the skin and mucous
membranes of mice are Staphylococcus aureus and S. epidermidis.
Although S. aureus has not been recognized as a primary pathogen,
several reports point to its role in outbreaks of cutaneous infections
in athymic nude mice. Thymic deficient nude mice develop conjunctivitis
and facial abscesses from which S. aureus can be recovered in pure
culture (A.). Inoculation of the bacteria into the skin apparently
occurs from grooming or bite wounds, and although the skin usually remains
intact, the resultant abscesses progressively enlarge and occasionally
spread subcutaneously to form disfiguring lumps, primarily about the face
and head. Histologically, the abscess contains a core of bacteria
(arrow) surrounded by neutrophils, macrophages and fibrocytes (B.).
The condition does not respond well to antibiotic therapy. S.
aureus is considered a pathogen in nude mice and the presence
of these bacteria denotes a breakdown in the pathogen-free status of the
environment.
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