Both wild and laboratory rats and, to a lesser degree, mice are the natural hosts of murine respiratory mycoplasmosis (MRM).  Hamsters, guinea pigs, and rabbits may carry the causative bacteria, Mycoplasma pulmonis, but do not develop lesions Mycoplasma pulmonis is transmitted horizontally by direct contact by aerosol and vertically by in utero transmission.  Venereal transmission may be possible.  Once inside the host, the bacteria damages host cells by causing dysfunction of the cilia of respiratory and genital tract epithelial cells.  In the respiratory tract, M. pulmonis preferentially colonizes the nasal passages and middle ears.  The bacteria competes for host cell nutrients and metabolites and may also produce toxic peroxides and nonspecific mitogens  Clinical signs are most commonly observed in older animals and MRM may be asymptomatic in young animals.  Signs include rales and dyspnea, snuffling and chattering, ocular and nasal discharge, rubbing of eyes, and head tilt.  In severe cases, weight loss and reduced fertility may occur.  The severity of disease is dependent upon the interaction of host, pathogen and environmental factors.  The hosts' age, strain, immune status, and presence of concurrent infections can exacerbate the disease.  Additionally, dietary deficiencies of vitamins A and E may add to the severity of disease.  More than 40 strains of M. pulmonis exist, which vary in virulence.  Temperature, humidity, and intracage ammonia levels are important environmental factors,.

  Diagnosis of MRM is dependent on cultural isolation of M. pulmonis.  The lower sensitivity and specificity of commercially available ELISA test kits make them less desirable.  Gross and histopathologic lesions are commonly present but are not diagnostic.  Gross lesions of the upper airways include suppurative rhinitis, otitis media, laryngitis, and tracheitis.  In the lung, suppurative bronchopneumonia, atelactasis, bronchiectasis and abscesses can occur.  When widespread, bronchiectasis and abscesses lead to the "cobblestone" lung appearance commonly seen in endstage disease.  Histopathologic lesions include suppurative exudates in airways.  Microscopic lesions have a neutrophilic response, accumulation of plasma cells and lymphocytes, and include epithelial hyperplasia and metaplasia.

  Murine respiratory mycoplasmosis must be differentiated from other bacterial pneumonias such as infection with Coryne-bacterium kutscheri, Streptococcus, cilia-associated respiratory (CAR) Bacillus infection, and mycotic pneumonia.  Concurrent infections with Sendai virus, pneumonia virus of mice, and other viruses are common.

  M. pulmonis infection is a serious complication of research with rats due to its effects on the immune, respiratory, and reproductive systems.  It is also a primary causes of early mortality in affected colonies.  However, the use of SPF rats has limited its prevalence.  Treatment with tetracycline or tylosin may suppress clinical signs in pet rats, but caesarian derivation and barrier maintenance, along with rigorous testing, is necessary in research facilities.

- by Sarah Kanagy, Class of 2005

- edited by Dr. Leon Thacker,   ADDL Director

References

1.  Brown MB, Peltier M, Hillier M, Crenshaw B, Reyes L: 2001.  Genital mycoplasmosis in rats; a model for intrauterine infection.  Am J Repro Immunol. 46 (3): 232-241.

2. Hodge LM, Simecka JW: 2002.  Role of upper and lower respiratory tract immunity in resistance to Mycoplasma respiratory disease. J Infec Dis 15: 186(2) 290-294.

3. Kohn DF and Clifford CB.  Biology and Disease of Rats.  Laboratory Animal Medicine, 2^nd ed.  Academic Press, New York. 121-165.

4. Laber-Laird K, Swindle MM, Flecknell P: 1996.  Handbook of Rodent and Rabbit Medicine.  Elsevier Science, Ltd., Tarrytown, NY. 13-14.

5. Percy DH and Barthold SWB: 2001.  Pathology of Laboratory Rodents and Rats.  Iowa State University Press, Ames, IA  126-130.