Nodular hyperplasia of lymphoglandular complexes in dogs: A potential diagnostic pitfall for rectal masses.

Lymphoglandular complexes are components of the gut-associated lymphoid tissue that are characterized by submucosal lymphoid aggregates invested by projections of mucosal epithelium. Reports of pathology involving these structures are rare in both human and veterinary literature. Here, the authors report 2 cases of rectal masses excised from dogs following a period of tenesmus and hematochezia. In both animals, the masses were composed of lymphoid tissue closely encompassing tubuloacinar structures. Immunohistochemistry and polymerase chain reaction antigen receptor rearrangement testing demonstrated that the lymphoid population was polyclonal, comprising T and B cells arranged in loosely follicular aggregates centered on the epithelial foci. In light of these findings, a diagnosis of lymphoglandular complex nodular hyperplasia was reported. To the authors' knowledge, this is the first report of this condition in dogs.

Th17 cytokines are critical for respiratory syncytial virus-associated airway hyperreponsiveness through regulation by complement C3a and tachykinins.

Respiratory syncytial virus (RSV) infection is associated with serious lung disease in infants and immunocompromised individuals and is linked to development of asthma. In mice, acute RSV infection causes airway hyperresponsiveness (AHR), inflammation, and mucus hypersecretion. Infected cells induce complement activation, producing the anaphylatoxin C3a. In this paper, we show RSV-infected wild-type mice produce Th17 cytokines, a response not previously associated with viral infections. Mice deficient in the C3aR fail to develop AHR following acute RSV infection, and production of Th17 cytokines was significantly attenuated. Tachykinin production also has been implicated in RSV pathophysiology, and tachykinin receptor-null mice were similarly protected from developing AHR. These animals were also deficient in production of Th17 cytokines. Tachykinin release was absent in mice deficient in C3aR, whereas C3a levels were unchanged in tachykinin receptor-null animals. Thus, our data reveal a crucial sequence following acute RSV infection where initial C3a production causes tachykinin release, followed by activation of the IL-17A pathway. Deficiency of either receptor affords protection from AHR, identifying two potential therapeutic targets.

Hepatic encephalopathy in two goat kids with common paternity.

Two juvenile, intact, female mixed-breed goats from a common sire were presented for periodic neurologic deficits, seizures, and a generalized loss of body condition that occurred over a 4-6-week period. On physical examination, both goats were thin, obtunded, blind, and ataxic. Laboratory diagnostics revealed increased serum bile acids (95 micromol/l; reference interval: 0-50 micromol/l) in one of the goats. Both goats exhibited progressive physical and mental deterioration, and were eventually euthanized. Upon necropsy, no significant macroscopic lesions were noted. Microscopic examination, however, demonstrated hepatocellular atrophy and anomalies in the hepatic microvasculature, including duplication of hepatic arteries, small-to-indistinct portal veins, and oval cell hyperplasia. In addition, spongiform change was microscopically identified throughout the parenchyma of the brain, most notably within the white matter and along the junction of gray and white matter. The diagnosis of congenital portal vein hypoperfusion (suggestive of a portosystemic shunt) with resultant hepatic encephalopathy was proposed in each case based on the characteristic microscopic lesions in conjunction with the signalment and history of the goats. The observation that the affected kids were sired by the same buck suggests a hereditary basis for the condition in these animals as well.