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Treatment of gastritis in cheetahs (Acinonyx jubatus).

Three cheetahs (Acinonyx jubatus) had a clinical history of chronic spiral bacteria-associated gastritis and three cheetahs had no clinical history of gastritis. Gastric biopsies were obtained from all six cheetahs prior to treatment for gastritis and 3 wk and 1 yr posttreatment. The cheetahs were treated with tetracycline hydrochloride 500 mg p.o. q.i.d., metronidazole 250 mg p.o. q.i.d., and bismuth subsalicylate 300 mg p.o. q.i.d. Each drug was administered concurrently for 7 days. Following this treatment, each cheetah was maintained on 300 mg bismuth subsalicylate p.o. s.i.d. for 1 yr. The three cheetahs with a history of gastritis were culture positive for Helicobacter acinonyx and remained positive during the entire study. The three cheetahs with no clinical history of gastritis were culture negative for H. acinonyx, but gastric biopsies revealed Gastrospirillum-like bacteria (tentatively named Helicobacter heilmannii) pretreatment. Gastric biopsies were negative for H. heilmannii on subsequent examinations. Although the treatment did not eradicate H. acinonyx, it did provide symptomatic relief from the vomiting, anorexia, and weight loss associated with clinical gastritis. The use of endoscopically guided gastric mucosal biopsies for urease testing and histopathologic examination of Warthin-Starry-stained sections is a sensitive and specific method of diagnosing spiral bacteria-associated gastritis. Treatment of spiral bacteria-associated gastritis in cheetahs should include the rational use of antibiotics (tetracycline or amoxicillin and metronidazole), bismuth compounds, and omeprazole and evaluation of husbandry methods to reduce stress.

Acinonyx↗

Systemic candidiasis in a cheetah (Acinonyx jubatus).

Systemic candidiasis, with involvement of the spleen, liver, kidneys, and lymph nodes, was diagnosed in a geriatric captive cheetah (Acinonyx jubatus). The animal had a long clinical history of intermittent chronic gastritis associated with Helicobacter acinonyx and chronic renal failure, both of which were repeatedly treated with broad-spectrum antimicrobial therapy. Following euthanasia, a postmortem examination showed numerous microabscesses and granulomas composed of degenerate eosinophils and containing asteroids or Splendore-Hoeppli material throughout the body. Yeast, pseudohyphae, and infrequently branching septate hyphae, demonstrated with special stains, were identified as a Candida sp. by fluorescent antibody testing. Low genetic variation in cheetahs may increase their susceptibility to infectious agents. Additional factors contributing to the overgrowth and dissemination of Candida sp. in this case may have included changes in the bacterial flora of the alimentary tract as a result of repeated antimicrobial therapy and alterations in the topography of the alimentary mucosa caused by chronic gastritis.

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Chronic gastritis in tigers associated with Helicobacter acinonyx.

Helicobacter pylori-like organisms (HPLOs) were isolated from the gastric mucosa of two Sumatran tigers and identified by polymerase chain reaction analysis as Helicobacter acinonyx. At histological examination, both tigers revealed a chronic gastritis associated with HPLOs as demonstrated by immunolabelling and electron microscopy. This is the first isolation of H. acinonyx from tigers, in which, as previously reported in cheetahs, it may be a cause of gastritis.

Animals↗

Enhancing zona penetration by spermatozoa from a teratospermic species, the cheetah (Acinonyx jubatus).

Cheetahs (Acinonyx jubatus) produce poor quality ejaculates that can limit the efficiency of standard assisted reproduction including artificial insemination (AI) and in vitro fertilization (IVF). The purpose of this study was to: (1) further study sperm-oocyte interaction in this teratospermic species by examining the ability of malformed sperm to interact with various oocyte barriers; and (2) assess the potential of zona piercing for assisting IVF in a teratospermic felid. Zonae of salt-stored (SS), domestic cat oocytes were mechanically pierced (ZnPd) three times each. Semen was collected by electroejaculation from six male cheetahs and ejaculates were processed for IVF. Sperm aliquots from each ejaculate were assessed for a sperm motility index (SMI) over time. Zona-intact (ZnIn-SS) oocytes (n = 78) and ZnPd-SS oocytes (n = 74) were coincubated with spermatozoa in vitro for 6 h. The proportion of morphologically abnormal spermatozoa per ejaculate was high for all males (range 81.5% to 95.9%). SMI values at 0 and 6 h were variable, ranging from 50 to 75 and 0 to 40, respectively. Spermatozoa from all ejaculates bound to and penetrated the outer zona pellucida of ZnIn-SS and ZnPd-SS oocytes similarly (P > 0.05). The proportion of oocytes containing spermatozoa within the inner zona layer and the average number of spermatozoa per oocyte in this region were greater (P < 0.05) for the ZnPd-SS than ZnIn-SS oocytes (39.2% and 1.0 versus 12.8% and 0.2, respectively). Although zona piercing enhanced sperm penetration, there was no increase (P > 0.05) in pleiomorphic spermatozoa penetrating the inner zona pellucida or PVS.(ABSTRACT TRUNCATED AT 250 WORDS)

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Elemental sulfur identified in urine of cheetah, Acinonyx jubatus.

The urine of the cheetah, Acinonyx jubatus, is almost odorless, and probably for this reason, it has not attracted much attention from scientists. Using gas chromatography-mass spectrometry, we identified 27 and 37 constituents in the headspace vapor of the urine of male and female cheetah, respectively. These constituents, composed of hydrocarbons, short-chain ethers, aldehydes, saturated and unsaturated cyclic and acyclic ketones, 2-acetylfuran, dimethyl disulfide, dimethyl sulfone, phenol, myristic acid (tetradecanoic acid), urea, and elemental sulfur, are all present in the headspace vapor in very small quantities; dimethyl disulfide is present in such a low concentration that it cannot be detected by the human nose. This is only the second example of elemental sulfur being secreted or excreted by an animal. It is hypothesized that the conversion of sulfur-containing compounds in the cheetah's diet to elemental sulfur and to practically odorless dimethyl sulfone enables this carnivore to operate as if "invisible" to the olfactory world of its predators as well as its prey, which would increase its chances of survival.

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Genetic evidence for host specificity in the adhesin-encoding genes hxaA of Helicobacter acinonyx, hnaA of H. nemestrinae and hpaA of H. pylori.

Gastric and non-gastric species of Helicobacter were examined for the presence of the adhesin-encoding gene, hpaA, from the human-associated gastric Helicobacter H. pylori (Hp), and for adhesin subunit protein HpaA. Amplification of a 375-bp internal DNA fragment of hpaA by PCR demonstrated the presence of the gene in Hp and in two closely related gastric Helicobacters, H. nemestrinae (Hn) and H. acinonyx (Hx), but not in the more distantly related H. felis (Hf) and H. mustelae (Hm). The non-gastric Helicobacters, H. canis (Hc), H. muridarum (Hr), H. fennelliae (He) and H. cinaedi (Hi), were all negative for hpaA. An immunoblot assay of water extracts with adhesin-specific antibody confirmed these results. The deduced amino acid (aa) sequences of Hp HpaA and Hn adhesin A (hereafter termed HnaA) are very similar, having identical receptor-binding motifs (rbm); also, the hemagglutination (HA) properties of Hn and Hp cells were indistinguishable. In contrast, the rbm of Hx adhesin A (hereafter termed HxaA), compared to that of Hp, contained a non-conservative aa substitution (Ile to Thr); also, there was variance in five consecutive aa from 10 to 14 residues upstream from the rbm. We conclude that these aa substitutions in HxaA are probably responsible for the difference in receptor recognition of this adhesin, as evidenced by the resistance of Hx HA to inhibition with N-acetylneuraminyl-alpha(2,3)-lactose. These results are consistent with the biological similarity between the natural host(s) of Hp and Hn; i.e., human and non-human primates, and the dissimilarity between these hosts and the feline host, the cheetah.

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Analysis of the mitochondrial genome of cheetahs (Acinonyx jubatus) with neurodegenerative disease.

The complete mitochondrial genome of Acinonyx jubatus was sequenced and mitochondrial DNA (mtDNA) regions were screened for polymorphisms as candidates for the cause of a neurodegenerative demyelinating disease affecting captive cheetahs. The mtDNA reference sequences were established on the basis of the complete sequences of two diseased and two nondiseased animals as well as partial sequences of 26 further individuals. The A. jubatus mitochondrial genome is 17,047-bp long and shows a high sequence similarity (91%) to the domestic cat. Based on single nucleotide polymorphisms (SNPs) in the control region (CR) and pedigree information, the 18 myelopathic and 12 non-myelopathic cheetahs included in this study were classified into haplotypes I, II and III. In view of the phenotypic comparability of the neurodegenerative disease observed in cheetahs and human mtDNA-associated diseases, specific coding regions including the tRNAs leucine UUR, lysine, serine UCN, and partial complex I and V sequences were screened. We identified a heteroplasmic and a homoplasmic SNP at codon 507 in the subunit 5 (MTND5) of complex I. The heteroplasmic haplotype I-specific valine to methionine substitution represents a nonconservative amino acid change and was found in 11 myelopathic and eight non-myelopathic cheetahs with levels ranging from 29% to 79%. The homoplasmic conservative amino acid substitution valine to alanine was identified in two myelopathic animals of haplotype II. In addition, a synonymous SNP in the codon 76 of the MTND4L gene was found in the single haplotype III animal. The amino acid exchanges in the MTND5 gene were not associated with the occurrence of neurodegenerative disease in captive cheetahs.

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Vaccine-induced protection against anthrax in cheetah (Acinonyx jubatus) and black rhinoceros (Diceros bicornis).

Institution of a policy of vaccination in endangered species with a vaccine not previously administered to it cannot be undertaken lightly. This applies even more in the case of cheetah (Acinonyx jubatus) with their unusually monomorphic gene pool and the potential restrictions this places on their immune responses. However, the recently observed mortalities from anthrax in these animals in the Etosha National Park, Namibia, made it imperative to evaluate vaccination. Black rhinoceros (Diceros bicornis), another endangered species in the park, have been vaccinated for over three decades but the effectiveness of this has never been evaluated. Passive protection tests in A/J mice using sera from 12 cheetahs together with enzyme immunoassay indicated that cheetah are able to mount seemingly normal primary and secondary humoral immune responses to the Sterne 34F2 live spore livestock vaccine. Overall protection rates in mice injected with the sera rose and fell in concert with rises and declines in antibody titres, although fine analysis showed that the correlation between titre and protection was complex. Once a high level of protection (96% of mice 1 month after a second booster in the cheetahs) had been achieved, the duration of substantial protection appeared good (60% of the mice 5 months after the second booster). Protection conferred on mice by sera from three of four vaccinated rhino was almost complete, but, obscurely, none of the mice receiving serum from the fourth rhino were protected. Sera from three park lions with naturally acquired high antibody titres, included as controls, also conferred high levels of protection. For the purposes of wildlife management, the conclusions were that vaccination of cheetah with the standard animal anthrax vaccine causes no observable ill effect in the animals and does appear to confer protective immunity. At least one well-separated booster does appear to be desirable. Vaccination of rhino also appears to be justified from the limited data obtained.

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Prevalence of Bartonella infection in wild African lions (Panthera leo) and cheetahs (Acinonyx jubatus).

Bartonella species are emerging pathogens that have been isolated worldwide from humans and other mammals. Our objective was to estimate the prevalence of Bartonella infection in free-ranging African lions (Panthera leo) and cheetahs (Acinonyx jubatus). Blood and/or serum samples were collected from a convenience sample of 113 lions and 74 cheetahs captured in Africa between 1982 and 2002. Whole blood samples available from 58 of the lions and 17 of the cheetahs were cultured for evidence of Bartonella spp., and whole blood from 54 of the 58 lions and 73 of the 74 cheetahs tested for the presence of Bartonella DNA by TaqMan PCR. Serum samples from the 113 lions and 74 cheetahs were tested for the presence of antibodies against Bartonella henselae using an immunofluorescence assay. Three (5.2%) of the 58 lions and one (5.9%) of the 17 cheetahs were bacteremic. Two lions were infected with B. henselae, based on PCR/RFLP of the citrate synthase gene. The third lion and the cheetah were infected with previously unidentified Bartonella strains. Twenty-three percent of the 73 cheetahs and 3.7% of the 54 lions tested by TaqMan PCR were positive for Bartonella spp. B. henselae antibody prevalence was 17% (19/113) for the lions and 31% (23/74) for the cheetahs. The prevalence of seropositivity, bacteremia, and positive TaqMan PCR was not significantly different between sexes and age categories (juvenile versus adult) for both lions and cheetahs. Domestic cats are thus no longer the only known carriers of Bartonella spp. in Africa. Translocation of B. henselae seronegative and TaqMan PCR negative wild felids might be effective in limiting the spread of Bartonella infection.

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Sequence variation in the mitochondrial DNA control region of wild African cheetahs (Acinonyx jubatus).

Five hundred and twenty-five bp of mitochondrial control region were sequenced and analysed for 20 Acinonyx jubatus and one Felis catus. These sequences were compared with published sequences from another domestic cat, 20 ocelots (Leopardus pardalus) and 11 margays (Leopardus weidii). The intraspecific population divergence in cheetahs was found to be less than in the other cats. However variation was present and distinct groups of cheetahs were discernible. The 80 bp RS2 repetitive sequence motif previously described in other felids was found in four copies in cheetah. The repeat units probably have the ability to form secondary structure and may have some function in the regulation of control region replication. The two central repeat units in cheetah show homogenization that may have arisen by convergent evolution.

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The use of reference strand-mediated conformational analysis for the study of cheetah (Acinonyx jubatus) feline leucocyte antigen class II DRB polymorphisms.

There is now considerable evidence to suggest the cheetah (Acinonyx jubatus) has limited genetic diversity. However, the extent of this and its significance to the fitness of the cheetah population, both in the wild and captivity, is the subject of some debate. This reflects the difficulty associated with establishing a direct link between low variability at biologically significant loci and deleterious aspects of phenotype in this, and other, species. Attempts to study one such region, the feline leucocyte antigen (FLA), are hampered by a general reliance on cloning and sequencing which is expensive, labour-intensive, subject to PCR artefact and always likely to underestimate true variability. In this study we have applied reference strand-mediated conformational analysis (RSCA) to determine the FLA-DRB phenotypes of 25 cheetahs. This technique was rapid, repeatable and less prone to polymerase chain reaction (PCR)-induced sequence artefacts associated with cloning. Individual cheetahs were shown to have up to three FLA-DRB genes. A total of five alleles were identified (DRB*ha14-17 and DRB*gd01) distributed among four genotypes. Fifteen cheetahs were DRB*ha14/ha15/ha16/ha17, three were DRB*ha15/ha16/ha17, six were DRB*ha14/ha16/ha17 and one was DRB*ha14/ha15/ha16/ha17/gd01. Sequence analysis of DRB*gd01 suggested it was a recombinant of DRB*ha16 and DRB*ha17. Generation of new alleles is difficult to document, and the clear demonstration of such an event is unusual. This study confirms further the limited genetic variability of the cheetah at a biologically significant region. RSCA will facilitate large-scale studies that will be needed to correlate genetic diversity at such loci with population fitness in the cheetah and other species.

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[Anatomic features of the carpal joint of the cheetah (Acinonyx jubatuw), compared with the domestic cat (Felis catus)].

The anatomy of the carpal joint of the cheetah (Acinonyx jubatus) was examined in seven specimens using dissection and corrosion casts as well as radiography, and compared to well-known data of the domestic cat (Felis catus). It was found that in the cheetah, as in the domestic cat, the intermedioradial, ulnar and accessory carpal bones, as well as the first, second, third and fourth carpal bones and the sesamoid bone of the abductor pollicis longus muscle, develop in a regular manner. The bones had a similar shape and the ligamentous apparatus was comparable, the most striking differences being the connection of all compartments of the joint cavity and the mediocarpal joint, working as a screw joint. The syndesmosis between the intermedioradial and ulnar carpal bones, instead of a synovial connection, is another adaptation for stabilization of the carpus of the cheetah during locomotion. The joint capsule is little spacious and in all three recesses can be differentiated. The first extends proximally palmar the ulnar carpal bone between the styloid process of the ulna and the accessory carpal bone, the second also extends proximally mediopalmar of the intermedioradial bone, and the largest third recess is located on the dorsal surface and extends proximally, laterally to the inserting tendon of the extensor carpi radialis muscle.

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Helicobacter acinonyx sp. nov., isolated from cheetahs with gastritis.

Four strains of a novel Helicobacter species were isolated from the stomachs of cheetahs (Acinonyx jubilatus) with gastritis. These isolates were phenotypically similar to Helicobacter pylori. The isolates were gram-negative, spiral bacteria which grew under microaerophilic conditions at 37 degrees C, but not at 25 or 42 degrees C, and produced urease, catalase, oxidase, alkaline phosphatase, and gamma-glutamyl transpeptidase. The isolates did not ferment glucose, mannitol, inositol, sorbitol, rhamnose, sucrose, melibiose, amygdalin, or arabinose; hydrolyze hippurate or indoxyl acetate; or reduce nitrate. They did not produce H2S from triple sugar iron agar, and they did not grow in the presence of 1.0% glycine or 1.5% NaCl. They were resistant to nalidixic acid and sensitive to cephalothin and metronidazole. Cells were typically 0.3 by 2.0 microns and possessed tufts of two to five sheathed, monopolar flagella. The G+C content of strain 90-119 was 30 mol%. Cluster analysis of densitometry scans of polyacrylamide protein gels revealed more than 70% similarity of the cheetah isolates to H. pylori, less than 60% similarity to Helicobacter felis, and less than 50% similarity to Helicobacter mustelae. Complete 16S rRNA sequences were determined for two of the cheetah isolates. Phylogenetic analysis was performed by comparing the cheetah sequences to those of 19 reference strains, including H. pylori, H. felis (two strains), H. mustelae, Helicobacter muridarum, "Flexispira rappini," Wolinella succinogenes, Campylobacter coli, Campylobacter concisus, Campylobacter curvus, Campylobacter fetus, Campylobacter hyointestinalis, Campylobacter jejuni, Campylobacter lari, Campylobacter rectus, Campylobacter sputorum subsp. bubulus, a Campylobacter sp. (pig isolate), [Bacteroides] gracilis, and [Bacteroides] ureolyticus.(ABSTRACT TRUNCATED AT 250 WORDS)

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Ultrasonography of the liver, spleen, and urinary tract of the cheetah (Acinonyx jubatus).

Diseases of the abdomen of the cheetah (Acinonyx jubatus) include those affecting the liver, spleen, and urinary tract. The most common diseases of captive-bred cheetah are gastritis, gastric ulceration, glomerulosclerosis, and hepatic veno-occlusive disease, and are the most frequent causes of mortality in these animals. The purpose of this study was to describe the ultrasonographic anatomy of the normal liver, spleen, kidney, and urinary bladder of the anesthetized captive-bred cheetah. Twenty-one cheetahs were examined. Eight of the 21 animals had subclinical evidence of either gastritis or chronic renal disease. The ultrasonographic appearances of the liver, gall bladder, common bile duct, and spleen were evaluated and various measurements made. Statistical analyses of the measurements were performed on all the healthy and subclinically ill animals taking sex, age, mass, and anesthetic protocol into account. There were no significant differences in any parameters between the healthy and subclinically ill animals (P > 0.25) and data were combined for statistical analyses. The mean mass was 41.1kg ( +/- 8.8) and the mean age was 5.0 years (+/- 2.2). The mean thickness of the liver medial to the gall bladder was 67.0 mm (+/- 14.8) and the liver was within the left costal arch in 75% of animals, extended caudal to the right costal arch in 50% of animals for an average of 30 mm, and extended caudal to the sternum in 63% of animals for an average of 32.5 mm. The maximum mean hepatic vein diameter at the entrance to the caudal vena cava was 8.6 +/- 2.8 mm; the mean diameters of the portal vein at the hilus and that of the caudal vena cava as it entered the liver were 7.5 +/- 1.6 and 9.9 +/- 4.1 mm, respectively. The mean diameter of the caudal vena cava was significantly affected by the type of anesthetic used (P < 0.10). The mass of the animals was significant in explaining the variance in maximum portal vein diameters (P < 0.10). The mean maximum velocity of the hepatic vein flow at the entrance to the caudal vena cava was 25.3 +/- 2.8 cm/s (n=4), the hilar portal vein was 11.7 +/- 3.3 cm/s (n=7), and the caudal vena cava was 33.8 +/- 19.8 cm/s (n=5). The mean maximum gall bladder length and width, and the mean common bile duct diameters were 44.6 mm (+/- 10.4), 23.3 mm (+/- 5.0), and 8.1 mm (+/- 2.4), respectively. Age was significant in explaining the variance in gall bladder lengths (P<0.10). Urinary tract ultrasonography was performed only in animals that had normal urea and creatinine levels (n=13). Renal cortico-medullary distinction was present in all kidneys and a cortico-medullary rim sign was seen in 21 of 26 kidneys. Mean kidney length, height, and width was 63.9 +/- 5.7, 38.1 +/- 5.2, and 42.1 +/- 5 mm, respectively. The average resistivity index was 0.58 (n=5). Mean urinary bladder length, height, and width were 57.0, 19.2, and 34.9 mm, respectively.

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Prevalence and implications of feline coronavirus infections of captive and free-ranging cheetahs (Acinonyx jubatus).

The extent and progression of exposure to feline infectious peritonitis (FIP) virus in the cheetah, Acinonyx jubatus, was monitored by a world-wide serological survey with indirect fluorescent antibody titers to coronavirus. The indirect fluorescent antibody assay was validated by Western blots, which showed that all indirect fluorescent antibody-positive cheetah sera detected both domestic cat and cheetah coronavirus structural proteins. There was a poor correlation between indirect fluorescent antibody results and the presence of coronaviruslike particles in cheetah feces, suggesting that electron microscopic detection of shed particles may not be an easily interpreted diagnostic parameter for FIP disease. Low, but verifiable (by Western blots [immunoblots]) antibody titers against coronavirus were detected in eight free-ranging cheetahs from east Africa as well as from captive cheetahs throughout the world. Of 20 North American cheetah facilities screened, 9 had cheetahs with measurable antibodies to feline coronavirus. Five facilities showed patterns of an ongoing epizootic. Retrospective FIP virus titers of an FIP outbreak in a cheetah-breeding facility in Oregon were monitored over a 5-year period and are interpreted here in terms of clinical disease progression. During that outbreak the morbidity was over 90% and the mortality was 60%, far greater than any previously reported epizootic of FIP in any cat species. Age of infection was a significant risk factor in this epizootic, with infants (less than 3 months old) displaying significantly higher risk for mortality than subadults or adults. Based upon these observations, empirical generalizations are drawn which address epidemiologic concerns for cheetahs in the context of this lethal infectious agent.

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Immunohistochemical screening for viral agents in cheetahs (Acinonyx jubatus) with myelopathy.

Numerous cases of acute-onset progressive ataxia, hindlimb paresis and paralysis of unknown aetiology occurred during 1993 to 2003 in cheetahs (Acinonyx jubatus) within the European Endangered Species Programme (eep). This study describes the immunohistochemical investigation of a possible viral aetiology of the "cheetah myelopathy". Antibodies to feline herpesvirus type 1, canine distemper virus, canine parvovirus and Borna disease virus were applied to formalin-fixed and paraffin-embedded brain and spinal cord sections from 25 affected cheetahs aged between three-and-a-half months and 13 years. Using the avidin-biotin complex technique, none of the antibodies gave positive immunosignals in either the brain or the spinal cord tissue.

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Epizootic gastritis associated with gastric spiral bacilli in cheetahs (Acinonyx jubatus).

An outbreak of vomiting in a group of captive cheetahs (Acinonyx jubatus) was investigated, and histologic examination revealed chronic gastritis characterized by infiltration of lymphocytes and numerous plasma cells and epithelial erosions. Lymphoid follicles, globule leukocytes, scattered neutrophils, and (in one animal) abscessed gastric glands were inconsistent findings. In addition, necropsy of three cheetahs revealed gastric mucosal hyperplasia. Two kinds of bacteria were identified in the stomachs of infected cheetahs. Numerous long, tightly coiled motile Gastrospirillum-like organisms were seen in gastric mucus and in Warthin-Starry-stained sections of mucosa. These bacteria could not be cultured but were transmitted to conventional mice in homogenates of gastric mucosa from infected cheetahs. Ultrastructural examination revealed helical filaments on some of these bacteria. In addition, a smaller Helicobacter sp. was isolated. This organism could be cultured in vitro under microaerophilic conditions. One or both of these bacterial species was probably responsible for the gastritis in these cheetahs.

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Systemic AA amyloidosis in captive cheetahs (Acinonyx jubatus).

Ongoing disease surveillance of necropsied captive cheetahs (Acinonyx jubatus) (n = 141) revealed a high prevalence of renal amyloidosis (n = 54 [38%]; age 1 to 16 years). The prevalence increased from 20% in pre- 1990 necropsies to 70% of cheetahs necropsied in 1995. In 74% of the cheetahs with amyloidosis, renal failure was determined to be the sole or partial cause of death. Papillary necrosis was seen only in affected cheetahs and involved 25% of these animals. Amyloid was present predominantly in the medullary interstitium, with minimal glomerular involvement. The amyloid deposits were immunohistochemically identified as AA type using antisera to both human and canine protein AA. A high percentage (52%) of animals with renal amyloid also had subsinusoidal hepatic AA amyloid deposits. Inflammatory diseases were identified in 100% of affected cheetahs. The most common inflammatory disease was chronic lymphoplasmacytic gastritis. The prevalence and severity of gastritis was higher in cheetahs with amyloidosis, and the prevalence of severe gastritis increased from 16% to 43%, coinciding with the increase in prevalence of amyloidosis. These findings suggest that cheetahs have a high prevalence of systemic amyloidosis in response to inflammation and that renal amyloidosis is an increasingly significant cause of morbidity and mortality in captive cheetah populations. Factors of potential importance in the apparent high prevalence of AA amyloidosis in cheetahs are currently being investigated in our laboratories.

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