Outbreaks of Acute Necrotic Enteritis and Haemolytic Crisis and Renal Disease Associated with Clostridium perfringens in Captive Toucans (Ramphastos spp).

Four toco toucans (Ramphastos toco), one channel-billed toucan (Ramphastos vitellinus) and one white-throated toucan (Ramphastos tucanus) died in two disease outbreaks in the same aviary in 2011 and 2016. Post-mortem examination revealed diffuse necrotic enteritis (NE) as the cause of death of five of these six birds. Clostridium perfringens was identified by culture and real-time multiplex PCR for C. perfringens α-, ß-, ε- and ι-toxin genes in ligated intestine of one toucan from each outbreak. At another aviary, two keel-billed toucans (Ramphastos sulfuratus) died peracutely from severe haemolytic crisis with haemoglobinaemic nephrosis and cholestasis and acute tubulointerstitial nephritis. Mild NE was present in these birds and C. perfringens was demonstrated in liver by bacterial culture and real-time multiplex PCR for C. perfringens α-, ß-, ε- and ι-toxin genes. To the authors' knowledge, this is the first description of outbreaks of NE associated with C. perfringens in captive toucans. Although haemolytic crisis has been reported in humans with C. perfringens type A septicaemia and hepatic abscesses, this presentation appears not to have been described in C. perfringens infections in toucans or other avian species. The factors causing C. perfringens proliferation and disease in the toucans were not identified. PCR for C. perfringens NetB toxin and enterotoxin genes performed retrospectively on one of the C. perfringens isolates from the second outbreak and on paraffin-embedded tissues from one dead toucan from the first outbreak was negative. With the current C. perfringens toxin typing scheme, C. perfringens type A was identified in the first two outbreaks.

TRAUMATIC (FOREIGN BODY) PERICARDITIS IN A TOCO TOUCAN (RAMPHASTOS TOCO).

An approximately 10-yr-old, captive-born female toco toucan ( Ramphastos toco ) was presented due to an acute onset of depression and apathy. On visual and physical examination, it showed an abnormal posture and dehydration, respectively. Serum biochemistry revealed hyperuricemia (39.4 mg/dl) and elevated glutamic oxaloacetic transaminase (GOT; 1,050 U/L). Radiographs demonstrated an enlargement of the cardiac silhouette. The bird died 7 days after presentation, despite treatment with enrofloxacin, allopurinol, a preparation of hepatorenal protectors, and complex B vitamins with dextrose. Necropsy revealed severe fibrinohemorrhagic pericarditis with a 15 mm long and 2.5 mm diameter, rigid foreign body in the pericardial exudate. Microscopically, this foreign body was of vegetal origin.

Bilateral Renal Tubular Neoplasm in a Channel-billed Toucan (Ramphastos vitellinus).

An adult male channel-billed toucan (Ramphastos vitellinus) was presented with a history of weakness, dyspnea, and severe dilatation of the coelomic cavity, which was caused by accumulation of serohemorrhagic fluid. Radiographs revealed increased radiodensity and thickness of the descending aorta and a pectoral mass, and blood test results revealed anemia, hypocalcemia, hypoproteinemia, and hyperuricemia. On ultrasound examination, a hyperechoic enlarged soft tissue mass was found in the caudodorsal region of the coelom. The bird did not respond to supportive care and died. Postmortem examination revealed severe, bilateral nephromegaly due to multifocal to coalescing renal tubular adenomas (adenomatosis), which was complicated with renal gout and soft tissue mineralization. Relevant concurrent diseases included hepatic hemochromatosis, subcutaneous cestodiasis with cellulitis, and systemic amyloidosis. There are few documented cases of neoplasms in ramphastid birds and to our knowledge, this is the first report of a renal neoplasm in a channel-billed toucan.

Localized toxoplasmosis in a ring-tailed lemur (Lemur catta) causing placentitis, stillbirths, and disseminated fetal infection.

Localized, myocardial toxoplasmosis contributed to the death of a female ring-tailed lemur (Lemur catta) 1 week after the delivery of 4 stillborn offspring with disseminated toxoplasmosis; the diagnosis was obtained by histopathology and immunohistochemistry in all 5 lemurs. Varying degrees of placentitis and placental edema with intralesional Toxoplasma gondii immunolabeling were observed in the 3 available placentas. The dam had severe myocarditis, and T. gondii antigen was only detected in the myocardial lesions. Disseminated toxoplasmosis with mild encephalitis was noted in all 4 fetuses, and 2 of the fetuses had mild acute multifocal hepatic necrosis. Fetal death was attributed to placental insufficiency with subsequent hypoxia and amniotic fluid aspiration.