Characterization of the Gastric Immune Response in Cheetahs (Acinonyx jubatus) WithHelicobacter-Associated Gastritis

Abstract

Captive cheetahs have an unusually severe progressive gastritis that is not present in wild cheetahs infected with the same strains of Helicobacter. This gastritis, when severe, has florid lymphocyte and plasma cell infiltrates in the epithelium and lamina propria with gland destruction, parietal cell loss, and, in some cases, lymphoid follicles. The local gastric immune response was characterized by immunohistochemistry in 21 cheetahs with varying degrees of gastritis. The character of the response was similar among types of gastritis except that cheetahs with severe gastritis had increased numbers (up to 70%) of lamina proprial CD79aþCD21-B cells. CD3þCD4þ T cells were present in the lamina propria, and CD3þCD8aþ T cells were within the glandular epithelium. Lymphoid aggregates had follicular differentiation with a central core of CD79aþ/CD45Rþ B cells and with an outer zone of CD3þ T cells that expressed both CD4 and CD8 antigens. MHC II antigens were diffusely expressed throughout the glandular and superficial epithelium. No cheetah had evidence of autoantibodies against the gastric mucosa when gastric samples from 30 cheetahs with different degrees of gastritis were incubated with autologous and heterologous serum. These findings indicate that T-cell distribution in cheetahs is qualitatively similar to that in other species infected with Helicobacter but that large numbers of lamina propria activated B cells and plasma cells did distinguish cheetahs with severe gastritis. Further research is needed to determine whether alterations in the Th1:Th2 balance are the cause of this more plasmacytic response in some cheetahs.

Novel urease-negative Helicobacter sp. ‘H. enhydrae sp. nov.’ isolated from inflamed gastric tissue of southern sea otters

“…In captivity, cheetahs infected with this bacterium have severe gastritis and gastric ulcers; in the wild, though colonized with the same gastric helicobacter, stomachs histologically are, in large part, normal (Eaton et al 1993a,b). Authors have attributed the severe gastric disease noted in captive cheetahs to stress of captivity and other undefined variables that trigger gastritis and ulcers (Terio et al 2012). Authors have also argued that generations of inbreeding of the cheetah has created a genetic bottleneck, resulting in the lack of genetic diversity in this species, resulting in a population that, when subjected to captivity, expresses increased susceptibility to gastric H. acinonychis (O'Brien et al 1987, Munson et al 2005.…”

Integrating evolution in the management of captive zoo populations

“…Evidence for the role of inflammation in captive endangered species can be found in cheetahs, which are particularly susceptible to gastritis, perhaps due to the presence of the bacteria Helicobacter (Terio et al. ). Gastric inflammation may also be caused by autoimmune disease mediated by the presence of Helicobacter (D'Elios et al.…”

Comparative Serum Fatty Acid Profiles of Captive and Free-Ranging Cheetahs (Acinonyx jubatus) in Namibia

“…Despite obvious improvements in husbandry since cheetahs were first kept in captivity, they still suffer from a range of unusual diseases not typically seen in other large captive felids. These include glomerulosclerosis [1–4], renal amyloidosis [4], lympho-plasmacytic gastritis [2,5,6], veno-occlusive disease [2,7], splenic myelolipomas, cardiac fibrosis [2,4], adrenal cortical hyperplasia [1,2,4,8] with lymphocytic depletion of the spleen [2], pancreatic atrophy [2] as well as several ill-defined disorders of the neurological system [2,9]. Some of these chronic degenerative diseases eventually affect the majority of cheetahs in captivity and are considered to be the primary cause of morbidity and mortality in adult animals [2,10].…”