History

A 2-year-old male fancy rat from a private rattery had lost weight and was found dead shortly thereafter in December 2009. The rat had had a lump in the region of the right ear base for an unknown duration, and purulent discharge was often noted draining from the mass into the right ear canal when palpated. At this facility, rats were kept in wire cages (5 to 8 rats/cage). No sick animals from this colony had previously been evaluated, although facial abscesses had been observed in some of the rats.

Clinical and Gross Findings

The rat weighed 0.285 kg (0.63 lb) at necropsy, and subcutaneous and visceral adipose tissues were minimal. Both tympanic bullae were irregularly rounded with expanded nodular bony projections, and they contained caseous tan exudate (Figure 1). The right tympanic bulla was also mottled black and brown. The caudal lobe of the left lung was largely replaced by multiple, coalescing abscesses containing tan-white caseous material; other lung lobes were wet and congested. Additional gross lesions included diffuse testicular atrophy, malocclusion of the incisors, and bilateral focal plantar pododermatitis (so-called sore hock).

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Photographs of the ventral aspect of the skull (A) and thoracic cavity (B) of a 2-year-old fancy rat that underwent weight loss and died. The rat had had a lump in the region of the right ear base from which purulent exudate could be expressed. In panel A, notice that the tympanic bullae (arrows) are bilaterally enlarged, irregular, and nodular. The right bulla is mottled dark brown to black, and both bullae contain tan-brown caseous exudate. In panel B, gross findings are indicative of bronchopneumonia with abscess formation in the left caudal lung lobe.

Citation: Journal of the American Veterinary Medical Association 240, 2; 10.2460/javma.240.2.155

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Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page →

Histopathologic and Microbiological Findings

Routine tissue samples were collected for histologic examination, those of most interest being samples of the lung lobes, tympanic bullae, cerebrum, testes, and kidneys. Samples of the tympanic bullae and lung tissue were submitted for microbiological culture.

Histologic examination of the left caudal lung lobe revealed ectasia, and the bronchi were filled with and obliterated by degenerate neutrophils, macrophages, fibrin, amorphous eosinophilic necrotic material, and karyorrhectic cellular debris. Ninety percent of the adjacent pulmonary parenchyma in this lung lobe was similarly effaced. Moderate, diffuse congestion and edema were present in the other lung lobes. The lumen of the trachea contained accumulations of degenerate and viable neutrophils, necrotic cellular debris, and fibrin.

The left tympanic bulla was effaced by multinodular proliferations of immature, woven trabecular bone (Figure 2). Abundant amounts of fibrous connective tissue and small blood vessels filled the space between these trabeculae. Bilaterally, the tympanic bullae also contained granulation tissue, macrophages, erythrocytes, and neutrophils (ie, evidence of osteomyelitis). The lumen of each bulla was diffusely obstructed by accumulations of degenerate and viable neutrophils, foamy macrophages, karyorrhectic cellular debris, edema, fibrin, and erythrocytes (evidence of otitis media). Moderate numbers of plasma cells and lymphocytes had infiltrated the adjacent soft tissue stroma.

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Photomicrograph of a transverse section of a portion of the left tympanic bulla of the rat in Figure 1. The lumen of the bulla (L) is filled with an exudate (E) composed mainly of neutrophils and caseous necrotic debris, granulating fibrous connective tissue, and erythrocytes. Notice that the bulla (B) is multinodular owing to proliferation of immature woven trabecular bone and that there is extension of the inflammatory changes into the bone (asterisk). H&E stain; bar = 1 mm.

Citation: Journal of the American Veterinary Medical Association 240, 2; 10.2460/javma.240.2.155

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The cerebrum contained a 1-mm-diameter necrotic region surrounded by an intense rim of degenerate and viable neutrophils, plasma cells, and foamy macrophages. The blood vessels in the adjacent neuropil had mild lymphoplasmacytic cuffing. Additional microscopic findings included marked diffuse testicular atrophy with spermatocyte degeneration and chronic, moderate membranous glomerulonephropathy.

A pure isolate of Mycoplasma pulmonis was cultured from samples of lung tissue. Culture of the tympanic bullae yielded M pulmonis as well as Escherichia coli and Actinomyces spp.

Morphologic Diagnosis

Severe, locally extensive necrosuppurative bronchopneumonia, bronchiolectasis, and abscess formation in the lungs; bilateral, severe, chronic suppurative otitis and osteomyelitis with reactive bone proliferation; and focal, moderate necrosuppurative encephalitis.

Comments

The gross and microscopic lesions in the rat of this report were characteristic of M pulmonis infection. Other differential diagnoses were infection with Corynebacterium kutscherii or chronic infection with cilia-associated respiratory bacillus; however, for this rat, infection with M pulmonis was confirmed on the basis of microbial culture results. Mycoplasma pulmonis is an important pathogen in both commercial and privately owned colonies of rats and mice. In laboratory and commercial settings in North America before the 1990s, Mycoplasma infections in rats were common with prevalence ranging from 8% to 78% in rat colonies.¹ Since that time, improved laboratory techniques as well as increased surveillance and monitoring of rat colonies have decreased the prevalence to 0% to 1%, as recently reported.² However, monitoring of privately owned ratteries rarely occurs and Mycoplasma infection remains a problem in nonlaboratory settings.

Mycoplasma pulmonis is the primary pathogen in the multifactorial respiratory tract condition in rats that is referred to as murine respiratory mycoplasmosis or chronic respiratory disease. Other agents that may be involved in chronic respiratory disease include cilia-associated respiratory bacillus, Sendai virus, sialodacryoadenitis virus, rat respiratory virus, or pneumonia virus of mice. Chronic infection with M pulmonis can lead to development of abscesses in the lungs and infection (via the auditory tube) of the middle ear. Treatment is possible with enrofloxacin (10 mg/kg [4.5 mg/lb], PO, q 12 h for 7 days) combined with doxycycline (5 mg/kg [2.3 mg/lb], PO, q 12 h for 7 days)³; however, this treatment will not affect any viral agents involved. Prevention is most important for this disease. Owners should separate sick rats from unaffected rats, avoid crowding at all times, clean cages regularly, feed an appropriate and complete diet, and provide fresh water at all times. For rats with chronic respiratory tract disease, it is important to clean bedding frequently because high levels of contamination with ammonia can exacerbate the clinical signs and cause progression of the disease.⁴ It is difficult to eliminate M pulmonis infection from a colony because of its persistent nature and common involvement in multifactorial disease. It is often necessary to depopulate commercial colonies completely. However, for pet rats, that may not be necessary; for pet rats, antimicrobial treatment and good husbandry may alleviate the clinical signs of the disease.

The microscopic changes in the kidneys of the rat of this report were consistent with chronic progressive glomerulonephropathy in rats, also called old rat nephropathy. This is a common renal disease in aged rats, particularly males, for which the exact pathogenesis is unknown. High-protein diets have been considered to be an important contributing factor to the development of this disease.⁴ Testicular atrophy also is a common degenerative change in aged rats. Sore hock generally develops secondary to trauma from wire cage housing. In the rat of this report, the lesions in the kidneys, testes, and hind limbs were unrelated to the Mycoplasma infection.