Abstract
Systemic AA amyloidosis, also known as reactive or secondary amyloidosis, is a major problem in captive cheetahs but is not present in wild cheetahs. Some factors associated with the high rate of incidence in captive cheetahs include chronic lymphoplasmacytic gastritis, genetic homogeneity, and high-rearing density. The authors of this study postulated that horizontal transmission of amyloid fibrils in feces may play a role in accelerating AA amyloidosis in captivity. AA amyloid fibrils were isolated from feces of a cheetah with amyloidosis, and this fraction showed high levels of transmissibility when administered intravenously to mice that were primed for amyloidosis by injections of silver nitrate. Recipient mice showed severe amyloid deposition in the spleen 10 days after injection. As a comparison, mice injected with equal amounts of amyloid fibrils isolated from the liver of the same cheetah had milder manifestations of the disease, suggesting that fecal transmission may be more potent. Thus, the authors concluded that fecal-oral transmission may be one mechanism whereby AA amyloidosis maintains its stronghold on the captive cheetah population. The manner in which amyloid fibrils enter the feces is not known, but it may be derived from the amyloid present in the small intestines of affected cheetahs. It should be noted that oral transmission was not reported in this study.
Zhang B, Une Y, Fu X, et al. Fecal transmission of AA amyloidosis in the cheetah contributes to high incidence of disease. Proc Natl Acad Sci USA
Sudden death syndrome (SDS) is not uncommon in rapidly growing broiler chickens that die suddenly and unexpectedly with no discernable cause. The condition has been recognized for decades, but the pathogenesis has remained obscure. Recent evidence suggests that some broilers may be predisposed to cardiac arrhythmias, which result in fatality. Olkowski and colleagues hypothesized that the increased susceptibility of the myocardium to arrhythmia in some rapidly growing broilers is associated with specific pathologic alterations in the myocardium as a result of metabolic strain, and acute heart failure occurs in this setting during high levels of stress. Broilers subjected to stress developed severe ventricular arrhythmias, and some experienced sudden death. Extensive evaluation of cardiac tissues revealed spongy or vacuolated sarcoplasm, cytoplasmic eosinophilia, and nuclear pyknosis in myocytes that had lost striations in the mural left ventricular myocardium. Interstitial edema was sometimes observed. Purkinje cells of affected chickens demonstrated spongy or vacuolar change. Apoptosis of Purkinje cells was confirmed by Caspase-3 staining. The authors suggest that these changes in the Purkinje system may underlie the predisposition to sustainment of malignant arrhythmias that ultimately cause sudden death.
Olkowski AA, Wojnarowicz C, Nain S, Ling B, Alcorn JM, Laarveld B. A study on pathogenesis of sudden death syndrome in broiler chickens. Res Vet Sci
It is well known that autoimmune diseases occur much more frequently in women than men. Possible reasons for this observation include difference in sex hormones, heightened cellular and humoral responses in women compared with men, and direct or indirect effects of sex chromosomes. The authors of this study used a mouse model in which the testes-determining Sry gene was deleted from the Y chromosome, resulting in XX and XY− ovary-bearing mice. In addition, they replaced Sry as a transgene on an autosome, creating XXSry and XY− Sry testes-bearing mice. This genetic manipulation allowed XX and XY− comparison in a female hormonal background, as well as XXSry and XY− Sry in a male hormonal background. Mice underwent gonadectomies at 4 weeks of age. The XX sex chromosome complement conferred greater susceptibility to both experimental autoimmune encephalitis and pristine-induced lupus in SJL mice. XY− mice had higher levels of Th2 cytokines (IL-13, IL-4, and IL-10) than XX mice, while XX mice showed an increase in IL-13Rα2. The authors concluded that the female sex chromosome complement has a direct effect on promoting susceptibility to two distinct autoimmune diseases, which is unlikely to be mediated by indirect effects of differences in gonadal hormones.
Smith-Bouvier DL, Divekar AA, Sasidhar M, et al. A role for sex chromosome complement in the female bias in autoimmune disease. J Exp Med
Helicobacter species are associated with chronic inflammation and neoplastic transformation in humans and animals, including ferrets and mice. Specifically, H. pylori infection is implicated in the development of gastritis and gastric lymphoma in humans, and other Helicobacter species have been associated with gastric lymphoma in cats. The purpose of this retrospective study was to better characterize the strains of H. heilmannii (Hhe) that colonize the gastric mucosa of domestic cats and to explore the potential association between Hhe infection and gastric lymphoma in this population. Gastric tissues from 47 cats were examined and classified as gastritis (14/47), lymphoma (31/47), or normal (2/47). Twenty-nine samples were positive for argyrophilic organisms by Warthin-Starry stain, and 22 of these were determined to be Hhe strains 1–4. There was a strong association between Hhe positive status and diagnosis of lymphoma, particularly lymphoblastic lymphoma, in which 13/17 cases were positive for Hhe. These results highlight the need for prospective studies and provide preliminary evidence for clinical trials assessing the use of antibiotics in eradication of Helicobacter-associated feline gastric lymphoma.
Bridgeford EC, Marini RP, Feng Y, Parry NMA, Rickman B, Fox JG. Gastric Helicobacter species as a cause of feline gastric lymphoma: A viable hypothesis. Vet Immunol Immunopathol
Myxomatous mitral valve disease (MMVD) is a major cause of morbidity and mortality in dogs. The myxomatous degeneration of the valve leaflet is accompanied by destruction of the fibrosa layer, expansion of the spongiosa layer, and excessive accumulation of acidic mucopolysaccharides. MMVD is a progressive condition that can lead to coalescing nodules at the valve edge that interfere with coaptation during systole. The authors of this study set out to determine the regional distribution and phenotypic alterations of the stromal cell population in the valves of dogs with varying stages of MMVD. They studied mitral valve leaflets from 4 normal dogs and 27 dogs with MMVD. The distribution of vimentin-positive cells was altered in MMVD. Instead of being located throughout the valve as they were in normal dogs, specimens from dogs with MMVD showed decreased density of vimentin-positive cells with disease progression, and very few vimentin-positive cells in myxomatous regions. Cells positive for α-smooth muscle actin were absent in normal dogs but present at the ventricularis valve surface in dogs with late-stage disease. There was also a slight increase in mast cells in the distal zone of leaflets from affected dogs. Overall, the results provide temporal and spatial information on the stromal cell alterations in MMVD that may increase our understanding of the pathogenesis of this condition in dogs and humans.
Han RI, Black A, Culshaw GJ, French AT, Else RW, Corcoran BM. Distribution of myofibroblasts, smooth muscle-like cells, macrophages, and mast cells in mitral valve leaflets of dogs with myxomatous mitral valve disease. Am J Vet Res