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infection include the following: 1) hyperplastic lesions occur principally in descending colon (involves cecum and colon with pathogenic Helicobacter) 2) there is minimal inflammatory cell infiltrate of mucosa unless mucosalrosions occur (usually mild to moderate mixed inflammatory cell infiltrate with pathogenic Helicobacter), and 3) mortality is common in young mice, and colonic lesions in mice of all ages (nonfatal large bowel disease most often in aged mice infected with pathogenic Helicobacter).  Isolation and biotyping of C. rodentium are essential since nonpathogenic but related Citrobacter sp. can be found in mouse intestine.

 F. Treatment:  The disease is contagious but self-limiting.  Treatment with neomycin sulfate, tetracycline hydrochloride in drinking water reduces losses but does not completely eliminate the infection.  12.5 % sulfadimethoxine in the drinking water may also prove beneficial in managing mortality.  Good sanitation is probably the most important control method.  Rectal prolapses usually occur after Citrobacter rodentium has been eliminated from the gut.  The rectal prolapse may be reduced by using a moistened cotton micro swab.

 G. Control:  Use strict sanitation and microisolator cage barriers to prevent cage to cage transmission by fecal contamination. Depopulation and restocking with uninfected mice, and Cesarian rederivation have been successful methods for eliminating the infection.

II. Chronic Respiratory Disease

 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.  Although the incidence of infection with either organism is rare, the significance when present is very high, often leading to fulminating respiratory disease.  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 among 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 kDatingskincare I Sex En Index Php Option Com Content Task Blogcategory Id 15 Itemid 52 Dating Skin Care DORAa Dating Skin Contacts qDatingskincare I Sex En Index Php Option Com Content Task Blogcategory Id 15 Itemid 52 Dating Skin Care DORAw i Dating Dating Dates Boob