I. Chronic Respiratory Disease
II. Pasteurellosis
III. Pneumocystis carinii
IV. Respiratory Neoplasms
V. Sendai Virus
A. Etiology: Mycoplasma pulmonis is a microorganism lacking a cell wall. Cilia-associated respiratory (CAR) bacillus is a gram-negative filamentous rod that moves by gliding motility. Both organisms can induce a chronic pulmonary disease syndrome.
B. Transmission: Transmission by direct contact with infected secretions has been reported. The incidence of infection with either organism is rare in research mice. Rats may act as asymptomatic carriers for Mycoplasma pulmonis.
C. Clinical Signs: Infection with either agent begins without
clinical signs. Adverse environmental factors, such as high cage
ammonia levels, and/or the acquisition of primary viral or bacterial respiratory
pathogens, activate subclinical infections. Early signs of overt
disease include an oculonasal discharge and torticollis (see photo).
As the organisms travel down the respiratory tract, labored breathing,
anorexia, and hunched posture occur. Other clinical signs include
snuffling, chattering, anorexia with weight loss, rough hair coat, hunched
posture, and reduced fertility. 
D. Pathology: In the upper respiratory tract, a purulent
discharge may be found on the nasal mucosa and within the tympanic bullae.
This purulent exudate can be found in the trachea and bronchi causing yellow
parenchymous foci which may progress to form bullae (bronchiectasis) and
red to grey areas of consolidation.
E. Diagnosis: Histological examination of lungs reveals
a purulent bronchopneumonia with moderate hyperplasia of the normally rare
peribronchial lymphoid aggregates (A.). Mycoplasma pulmonis
does not stain with histochemical stains due to the absence of a cell wall.
Examination of silver-stained respiratory sections will help identify the
presence of CAR bacillus, which will stain with silver and are present
within the cilia of the airways (arrow in B.).
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The preferred sites to culture for Mycoplasma are the nasopharynx and middle ear. The media needed for primary mycoplasma recovery must contain swine or horse serum and yeast extract supplementation. ELISAs are commercially available for serological screening for Mycoplasma pulmonis and CAR bacillus infections in mouse and rat colonies. PCR assays on nasal or tracheal samples are also used for diagnosis of both agents. CAR bacillus can not be cultured on cell-free media, and is diagnosed through histopathologic and serologic examination. Diagnostic tests usually identify Mycoplasma pulmonis and/or CAR bacillus along with other respiratory pathogens such as Pasteurella pneumotropica and Sendai virus.
F. Treatment: Overt disease is just suppressed by antibiotic therapy. Oxytetracycline (0.1 mg/ml water), ampicillin (500 mg/L drinking water), sulfamerazine (500 mg/L drinking water or 1 mg/4 gm food), and enrofloxacin (165 mg/L drinking water) have all been reported to reduce mortality. CAR bacillus was eliminated from experimentally infected mice that received either sulfamerazine or ampicillin treatments for 4 weeks. The carrier state of Mycoplasma pulmonis, however, is not affected by an antibiotic regimen.
G. Control: Since uterine colonization may occur, Cesarian derivation may not eliminate Mycoplasma infection. However, culture of uterus at the time of Cesarian delivery and subsequent testing of young provides a method of salvaging valuable infected mouse strains. Rigid sanitary measures are essential even in the face of a disease outbreak. Rats are known carriers and should never be housed with mice.
A. Etiology: Pasteurella pneumotropica is a Gram-negative, short pleomorphic rod with bipolar staining properties.
B. Transmission: Transmission by aerosol, fecal-oral, and contact with infected secretions (including venereal transmission) has been reported. The bacteria can be consistently isolated from the nasopharynx of subclinically infected mice and is considered an opportunistic pathogen, proliferating in the presence of other respiratory microbial pathogens.
C. Clinical Signs: The majority of infected immunocompetent mice
exhibit no clinical signs. Epidemics of conjunctivitis and panophthalmitis
have occurred in weanling and young adult mice (see photo). An upper
respiratory infection can be manifest by an oculonasal discharge or torticollis
from otitis media, and in the face of respiratory mycoplasmal and viral
diseases, dyspnea may occur. Subcutaneous abscesses, mastitis, metritis
and accessory sex gland abscesses are additional lesions observed in immune
deficient mice. 
D. Pathology: Infected tissues are characterized by mucopurulent inflammation with mild necrosis.
E. Diagnosis: Cultures of the ocular, skin or glandular tissues usually reveal mixed infections of Pasteurella pneumotropica with other bacterial flora. Pasteurella pneumotropica is likely to be isolated in pure cultures from abscesses in immune deficient mice. An ELISA is commercially available to identify antibody in colonized mice.
F. Treatment: Enrofloxacin at 165 mg/liter of drinking water for 2 weeks has been effective in eliminating colonization.
G. Control: The primary concern for disease is in immune deficient mice. Mice should be obtained from colonies free from infection. Do not house infected with uninfected mice.
Pneumocystis carinii is an opportunistic pathogen of the
respiratory tract of mice, rats and probably all domestic mammals and man.
It is believed to be a fungus that is spread by the inhalation of infective
cysts. Mice that are immunosuppressed, either by treatment or by
virtue of a hereditary immunological defect, may develop a fatal
pneumonia. Affected mice display hunched posture, tachypnea, and
weight loss when the pneumonia has consumed a significant portion of the
lung. Affected lungs are diffusely red and fail to deflate when the
chest is opened (A.). Histologically, interstitial pneumonia is accompanied
by histiocytic alveolitis, with alveoli filled with eosinophilic foamy
material that may contain some degenerated macrophages or few neutrophils
(B.). PAS and Giemsa stains are needed to visualize the trophozoite
stages, and a silver stain is used to demonstrate the argyrophilic cysts
(C.). Sulfameraxine/trimethroprim antibiotics are used to treat or
prevent clinical disease in immunologically stressed mice (such as the
thymic deficient nude and severe combined immunodeficient mice).
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Benign respiratory tumors, primarily adenomas of the alveolar lining cells or of terminal bronchiolar epithelial cells, are common in certain strains (A strain) and older mice. Malignant neoplasms, such as squamous cell carcinoma, occur infrequently.
A. Etiology: Sendai virus is an RNA paramyxovirus of the parainfluenza type 1 group.
B. Transmission: Direct contact is the primary means of viral spread. The virus is not environmentally stable, but can be transmitted by fomites because of the quantities of virus excreted from infected mice. The incidence of infection is low.
C. Clinical Signs: Infected mice may exhibit labored breathing and decreased fecundity. In DBA/2 and immune deficient mice, the infection is almost always fatal. This virus is immunosuppressive and may predispose to secondary bacterial infections. Generally, no clinical signs are observed in mice in endemically infected colonies. In clinically apparent infections, signs are variable but may include chattering, mild respiratory distress to labored breathing, and decreased fecundity in adults, deaths (possibly whole litters) in neonates and sucklings, and poor growth in weanling and young adult mice.
D. Pathology: The lungs of affected mice may be mottled
with red and tan foci in the parenchyma (A.). Exudate in the major
airways may be seen. Histological examinations reveal characteristic interstitial
pneumonia with perivascular and peribronchiolar lymphoid infiltrates, hyperplasia
of alveolar macrophages, and foci of alveolar and bronchiolar epithelial
necrosis with a neutrophilic infiltrate (B.). Observation of squamous
metaplasia of the bronchial epithelium is associated with the reparative
stage of the infection.
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E. Diagnosis: Histologic lesions in susceptible mice and PCR can identify Sendai virus in acute infections. Commercially available ELISA and IFA can be used to identify antibody titers in recovering mice..
F. Treatment: In static colonies, the disease will run its course; no latent infection occurs. In breeding colonies, cessation of breeding for 60 days, elimination of all suckling mice during this time period, and purposeful mixing of weanlings and adults to insure maximum viral exposure of all susceptible mice will prevent infections of future litters.
G. Control: Prevention of exposure or deliberate exposure are the two main approaches to control Sendai virus infection.
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