Allelic Diversity in the Serum Amyloid A2 Gene and Amyloid A Amyloidosis in a Breeding Colony of Zebra Finches (Taeniopygia guttata).

A high incidence of amyloid A (AA) amyloidosis was observed in the research breeding colony of zebra finches at our institution. Some birds with hepatic AA amyloidosis were asymptomatic for comorbid conditions frequently associated with the development of AA amyloidosis, whereas other birds with comorbid conditions failed to develop AA amyloidosis, suggesting a potential genetic component to the disease. Sequencing the SAA2 gene from 20 birds yielded 18 distinct sequences that coded for 5 isoforms of the protein. Most of the amino acid substitutions are unlikely to affect the protein's structure or function, but 2 changes-R52L and V84M-were predicted to be disruptive. In particular, R52 is highly conserved across vertebrates, with only arginine or lysine found at this position in reported sequences to date. The atypical R52L substitution occurred in 2 otherwise healthy birds with hepatic AA amyloidosis, supporting the idea that this change is pathogenic.

Amyloidosis in a Captive Zebra Finch (Taeniopygia guttata) Research Colony.

Five birds in a captive zebra finch research colony were diagnosed with systemic amyloidosis within a 7-mo period by means of postmortem Congo red staining and green birefringence under polarized light. The liver was the most frequently and usually the most seriously affected organ, followed by the spleen and then the kidney. All 5 birds had been clinically affected with various inflammatory, infectious, and neoplastic conditions associated with amyloid A (AA) amyloidosis in humans and animals. Immunohistochemistry using antisera against duck AA protein revealed that tissues from 2 of the 5 birds were positive for the presence of AA protein and systemic inflammation-associated amyloidosis. Although the development of AA amyloidosis has been associated with chronic inflammation, trauma, and various infectious and neoplastic diseases as well as possible genetic predispositions and stresses linked to overcrowding, the root causes for individual cases of AA amyloidosis are incompletely understood. As far as we know, this report is the first description of AA amyloidosis in captive, research zebra finches.

A therapeutic dose of ketoprofen causes acute gastrointestinal bleeding, erosions, and ulcers in rats.

Perioperative treatment of several rats in our facility with ketoprofen (5 mg/kg SC) resulted in blood loss, peritonitis, and death within a day to a little more than a week after surgery that was not related to the gastrointestinal tract. Published reports have established the 5-mg/kg dose as safe and effective for rats. Because ketoprofen is a nonselective nonsteroidal antiinflammatory drug that can damage the gastrointestinal tract, the putative diagnosis for these morbidities and mortalities was gastrointestinal toxicity caused by ketoprofen (5 mg/kg). We conducted a prospective study evaluating the effect of this therapeutic dose of ketoprofen on the rat gastrointestinal tract within 24 h. Ketoprofen (5 mg/kg SC) was administered to one group of rats that then received gas anesthesia for 30 min and to another group without subsequent anesthesia. A third group was injected with saline followed by 30 min of gas anesthesia. Our primary hypothesis was that noteworthy gastrointestinal bleeding and lesions would occur in both groups treated with ketoprofen but not in rats that received saline and anesthesia. Our results showed marked gastrointestinal bleeding, erosions, and small intestinal ulcers in the ketoprofen-treated rats and minimal damages in the saline-treated group. The combination of ketoprofen and anesthesia resulted in worse clinical signs than did ketoprofen alone. We conclude that a single 5-mg/kg dose of ketoprofen causes acute mucosal damage to the rat small intestine.

Bilateral traumatic temporomandibular joint luxation in a rat.

Bilateral temporomandibular joint (TMJ) luxation was diagnosed postmortem in a female, 6-mo-old CD rat (Rattus norvegicus) after probable head entrapment and subsequent disentanglement from a protective jacket. Clinical antemortem signs included inability to close her mouth, prehend food and drink water, anxiety, and linear skin erosions extending down the right and left commissures of the mouth. Radiography revealed rostral displacement of the mandible with concomitant malocclusion. The combination of clinical signs, acute nature of the presentation, and torn appearance of the protective jacket were strongly indicative of a traumatic etiology. To our knowledge, this is the first reported case of TMJ luxation in a rat.