Evermann JF, Roelke ME, Briggs MB. 1986. Feline coronavirus infections of cheetahs. Feline Practice 16, 21-28.

Clinical and diagnostic features of the 1982-83 epizootic of Feline Infectious Peritonitis (FIP) and the effects on the cheetah population of Wildlife Safari in Oregon are presented in tabular format. Test producers and results are discussed, and photographs of affected cheetahs are included. The results of serologic testing of the survivors of the epizootic, as well as testing of new additions to the colony, were presented in a companion article.

Evermann_et_al_1986_Feline_coronavirus_infections_of_cheetahs.pdf

Evermann JF, McKeirnan AJ, Ott RL. 1991. Perspectives on the Epizoology of Feline Enteric Coronavirus and the Pathogenesis of Feline Infectious Peritonitis. Veterinary Microbiology 28, 215-244.

This review presents some current thoughts regarding teh epizootiology of the feline coronaviruses; feline infectious peritonitis virus (FIPV) and feline coronavirus (FEVC), with primary emphasis on the pathogenesis of these viruses in nature. Although the mechanism(s) whereby FIPV causes disease are still incompletely understood, there have been significant contributions to the literature over the past decade which provide a framework upon which plausible explanations can be postulated. Two concepts are presented which attempt to clarify the pathogenesis of FIPV and at the same time may serve as an impetus for further research. The first involves the hypothesis, originally promulgated by Pedersen in 19891, that FIPV is derived from FECV during virus replication in the gastrointestinal tract. The second involves a unique mechanism of the mucosal immune system referred to as oral tolerance, which under normal conditions promotes the production of secretory immunity and suppresses the production of systematic immunity. In the case of FIPV infection, we propose that oral tolerance is important in the control of the virus at the gastrointestinal tract level. Once oral tolerance is disrupted, FIPV is capable of systemic spread resulting in immune-mediated vasculitis and death. Thus, it may be that clinical forms of FIP are due to a combination of two events, the first being the generation of FIPV from FECV, and the second being the capacity of FIPV to circumvent oral tolerance.

Evermann_et_al_1991_Perspectives_on_the_Epizootiology_of_FEV_and_the_Pathogenesis_of_FIP.pdf

Evermann JF, Laurenson MK, McKeirnan AJ, Caro TM. 1993. Infectious Disease Surveillance in Captive and Free-Living Cheetahs: An Integral Part of the Species Survival Plan. Zoo Biology 12, 125-133.

During the formulative stages of developing the Species Survival Plan (SSP) for the cheetah, the impact of infectious disease upon its survival in captivity was of prime consideration, together with genetics, nutrition, physiology, and behaviour. This paper summarizes the results of an infectious disease surveillance program, initially designed to monitor the infectious agent associated with clinically normal and clinically ill cheetahs in captivity, but subsequently supplemented with data from free-living cheetahs. The focus was on two viral infections, feline infectious peritonitis (FIP) and feline rhinotracheitis virus. Results indicated that between 1989 and 1991, there was a n increase in the seroprevalence (number antibody-positive animals) of cheetahs to feline coronavirus from 41% to 64% in captivity. During this same time period, there were only two documented cases of FIP in cheetahs in the United States. The results suggest that feline coronavirus (feline enteric coronavirus-feline infectious peritonitis group) or a closely related coronavirus of cheetah is becoming endemic in the captive cheetah population. Further serologic results from 39 free-living cheetahs demonstrated that there was a high seroprevalence (61%) to feline coronavirus, although serum antibody titers were considerably lower than those encountered in captive cheetahs. The observation of a high percentage of free-living cheetahs, which were seropositive to feline herpesvirus (44%), was unexpected, since it has been generally regarded that this infection is primarily associated with cheetahs in captivity.

Evermann_et_al_1993_Cheetah_infectious_disease_surveillance.pdf

Good KM, Houser A, Arntzen L, Turnbull PCB. 2007. Naturally acquired Anthrax antibodies in a cheetah (Acinonyx jubatus) in Botswana. J. Wildl. Dis. 44, 721-723.

An outbreak of anthrax in the Jwana Game Reserve in Jwaneng, Botswana, was first observed when three cheetahs (Acinonyx jubatus) died of the disease in November 2004. In the aftermath of this event, banked serum samples collected from 23 wild-caught cheetahs were examined, by the inhibition enzyme-linked immunoassay (ELISA), for antibodies to the protective antigen (PA) of Bacillus anthracis. Of the 23 cheetahs, 16 regularly accessed the reserve. Antibodies to PA were detected in one cheetah collected in May 2004, indicating the disease was occurring well before it was first noticed. This appears to be the first demonstration of naturally acquired anthrax antibodies in cheetahs. The finding of one antibody-positive animal amongst at least 16 potentially exposed individuals is consistent with existing reports that it is uncommon for cheetahs to develop natural immunity to anthrax.

Good_et_al_2007_Anthrax_antibodies_in_a_cheetah_in_Botswana.pdf

Gosselin SJ, Tarr MJ, Balistreri WF, Kramer LW, Setchell KDR, Johnston OJ, Dresser BL. 1986. Dietary considerations in the pathogenesis of hepatic vascular lesions in captive cheetah. In Journal of the American Association of Zoo Veterinarians. Abstract.

The livers of more than 100 cheetah from zoos throughout North America were evaluated by light microscopy, histochemistry and electron microscopy. While estrogens can explain some hepatic function abnormalities, they did not appear to be the major cause of this hepatic vascular lesion.

Gosselin_et_al_1986_Pathogenesis_of_hepatic_vascular_lesions_in_cheetah.pdf

Gosselin SJ, Loudy DL, Tarr MJ, Balistreri WF, Setchell KDR, Johnston OJ, Kramer LW, Dresser BL. 1988. Veno-occlusive disease of the liver in captive cheetah. Vet Pathol 25, 48-57.

Liver tissues from 126 captive cheetah were evaluated by light microscopy and histochemistry; eight animals were evaluated by electron microscopy. The main hepatic lesion. a vascular lesion resembling veno-occlusive disease (VOD) of the liver and characterized by subendothelial fibrosis and proliferation of smooth muscle-like cells in the central veins, was seen in 60% of the sexually mature cheetah. Although this hepatic vascular lesion was seen in cheetah as young as 1 year of age, the most severe lesions; usually associated with liver failure, were found in cheetah between the ages of 6 and 11. There was no sex predisposition, and in approximately 40% of the VOD cases; liver disease was not suspected clinically or at necropsy. VOD was found in other felidae, especially in the snow leopard. High levels of vitamin A  in livers, as well as in diets of the cheetah could be a contributing factor in the development of VOD in some groups of cheetah.

Gosselin_et_al_1988_VOD_in_captive_cheetah.pdf

Gosselin SJ, Setchell KDR, Harrington GW, Welsh MB, Pylypiw H, Kozeniauskas R, Dollard D, Tarr MJ, Dresser BL. 1989. Nutritional considerations in the pathogenesis of hepatic veno-occlusive disease in captive cheetahs. Zoo Biology 8, 339-347.

Veno-occlusive disease (VOD) of the liver has been diagnosed in a large number of captive cheetahs. Some ingredients or contaminants present in the diet were suspected as possible causes for this non-infectious disease with high incidence. Eight different diets fed to cheetahs kept in North American zoos were analyzed for vitamin A levels and the presence or absence of plant estrogens, nitrosamines, nitrites, and aflatoxins. Three of the eight diets were considered to contain toxic amounts of vitamin A. In humans and rats, hypervitaminosis A has been associated with hepatic vascular lesions, mainly perisinusoidal fibrosis, which progress eventually to occlusive lesions similar to VOD. Plant estrogens were detected in appreciable amounts only in one of the exotic carnivore diets. The role of plant estrogens in the pathogenesis of VOD in captive cheetahs is not clear at this time and needs further investigation. Based on the liver pathology and diet analyses, nitrosamines or their dietary precursor and aflatoxins can be excluded as possible causes of VOD in cheetahs kept in North American zoos.

Gosselin_et_al_1989_Diet_and_VOD_in_cheetahs.pdf

Grisham J, Killmar L. 1997. Species survival plan (SSP) surveillance of feline immunodeficiency virus (FIV) in cheetahs Acinonyx jubatus in North America. Int. Zoo Yb. 35, 71-73.

In 1995 the North American Species Survival Plan for Cheetah Acinonyx jubatus held a workshop on feline immunodeficiency virus (FIV) to discuss the information currently available on the disease and the possible effects on the captive population of cheetah. FIV was first documented in 1986 in domestic cats and since then it has been reported in 16 non-domestic species. This paper highlights the protocols and recommendations concerning FIV that have been made by the SSP.

Grisham_&_Killmar_1997_Cheetah_North_American_SSP_and_FIV.pdf

Heeney JL, Evermann JF, McKeirnan AJ, Marker-Kraus L, Roelke ME, Bush ME, Wildt DE, Meltzer DG, Lukas CJ, Manton VJ, Caro TM, O'Brien SJ. 1990. Prevalence and implications of feline coronavirus infections of captive and free-ranging cheetahs (Acinonyx jubatus). Journal of Virology 64:1964-72.

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 coronarvirus. 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 coronarvirus structural proteins. There was a poor correlation between indirect fluorescent antibody results and the presence of coronaviruslike particles in cheetah faeces, 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 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 term 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.

Heeney_et_al_1990_Feline_coronavirus_infections_of_cheetahs.pdf

A study on the impact of capture and captivity on the health of Namibian farmland cheetahs was carried out by MUNSON and MARKER-KRAUS (1997) and the Cheetah Conservation Fund. The study demonstrated that significant liver damage is incurred by cheetahs during the first week following capture, and that progressive renal damage may occur over time. The aim of this study was to find a way of reducing stress for several days in recently captured cheetahs without handling or depending on oral medication.

Huber_et_al_1999_Method_of_stress_reduction_in_cheetah_translocations.pdf

Hugh-Jones ME, de Vos V. 2002. Anthrax and wildlife. Rev sci tech Off int Epiz 21(2):359-83.

Although livestock anthrax is declining in many parts of the world, with an increasing number of countries probably truly free of the disease, anthrax remains enzootic in many national parks and even in some game ranching areas. These infected areas can present a persistent risk to surrounding livestock, which may otherwise be free of the disease, as well as a public health risk. The authors use as examples the national parks in southern Africa, the Wood Buffalo National Park in northern Alberta, Canada, and the deer ranching counties in south-west Texas, United States of America, to present the range of problems, epidemiology, and control procedures. While many advances have been achieved in the understanding of this disease, research is required into the genotypic grouping of anthrax isolates, improved field diagnostic techniques, and oral vaccines, as well as to provide a better understanding of spore survival in soil and the ecology of the disease under natural conditions. In cheetahs, anthrax remains a rare event.

Hugh-Jones_&_de_Vos_2002_Anthrax_in_wildlife.pdf

Jacobson RH. 1991. How well do serodiagnostic tests predict the infection or disease status of cats? JAVMA 199(10):1343-7.

Serodiagnostic test results do not always predict the status of an animal as might be expected. When few false-negative and few false- positive test results are reported for a test (high test sensitivity and specificity), the assumption is that the test is a very accurate predictor of infection/disease status. This assumption is correct if disease prevalence is high. However, when disease prevalence decreases to, for instance, 0.1% such as may be seen after several years of a vaccination campaign, a test having sensitivity of 99% and specificity of 99% becomes a poor predictor of infected animals. In this scenario, a positive test result will be wrong 91% of the time. A negative test result, however, virtually always will correctly identify non infection animals when prevalence of infection remains low.

Jacobson_1991_Reliability_of_serodiagnostic_tests_in_cats.pdf

Junge RE, Miller RE, Boever WJ, Scherba G, Sundberg J. 1991. Persistent cutaneous ulcers associated with feline herpesvirus type 1 infection in cheetah. Journal of the American Veterinary Medical Association 198(6):1057-8.

Feline herpesvirus type 1 (FHV-1) infection in domestic cats is most commonly manifested as an upper respiratory tract infection and is know as feline viral rhinotracheitis (FVR). Clinical signs include serous to mucopurulent ocular and nasal discharge, conjunctivitis, and corneal and oral ulceration. Ulcerative skin lesions attributable to FHV-1 in domestic cats have not been commonly reported. The possibility of genetic susceptibility to viral disease has been proposed for cheetahs on the basis of the low genetic diversity in the species. Morbidity and mortality in cheetahs with feline coronavirus infections is much higher than reported in domestic felids. A similar increased sensivity to FHV-1 may result in a higher incidence of cutaneous ulcers in cheetahs than in domestic cats.

Junge_et_al_1991_Cutaneous_ulcers_associated_with_feline_herpesvirus_infection_in_cheetah.pdf

Cheetahs (Acinonyx jubatus) are susceptible to severe, often lethal disease following infection with Feline Coronavirus (FCV). We have investigated the molecular genetics of FCV of cheetahs focusing on the 7a7b genes which are believed to be associated with virulence. The methods utilized include RNA extraction, reverse transcription and nested polymerase chain reaction (PCR). Virus detection by PCR was compared to serology for FCV which is currently used for screening for infection. In addition, samples were collected from one institution at multiple time points over one year in order to evaluate the epidemiology of FCV in a captive population. The results thusfar show 1) that the antigenicity of the capture antigen significantly impacts results, 2) seronegative animals may be shedding virus while seropositive animals may not, 3) evidence of persistent infection, increased shedding during periods of stress, and direct and indirect transmission in captive populations, and 4) mutations occur in the 7a7b genes that may impact virulence.

Kennedy_et_al_2000_Characterization_of_Feline_Coronavirus_of_cheetahs.pdf

Kennedy M, Kania S, Stylianides E, Bertschinger H, Keet D, van Vuuren M. 2003. Detection of Feline Coronavirus Infection in southern African nondomestic Felids. J Wildl Dis 39(3):529-35.

Feline coronavirus (FCoV) infects members of the Felidae family with results ranging from seroconversion with no disease to fatal feline infectious peritonitis (FIP). Infection of nondomestic felids with FCoV is of concern, particularly in endangered populations such as cheetahs (Acinonyx jubatus). In this investigation, we tested 342 animals in the Republic of South Africa and Namibia, including 140 animals from wild populations, for evidence of FCoV infection by serology and/or reverse transcription/nested polymerase chain reaction (RT/nPCR) on feces from 1999 through 2001. Past or current infection was evaluated. Of these, 195 animals had evidence of infection and included 41 animals from wild populations. Serology (indirect immunofluorescence) did not always correlate with viral RNA detection, as seronegative animals were occasionally virus-positive, while many seropositive animals were not shedding virus. Serology indicated the infecting virus was most closely related to type I FCoV. Antibody levels in the majority of animals were low, even in those actively infected. Ten of 48 animals tested at more than one time point by RT/nPCR were shedding virus at multiple time points possibly indicating persistent animals tested had evidence of current or previous FCoV infection. Testing by serology and RT/nPCR is recommended for screening for FCoV infection.

Kennedy_et_al_2003_Detection_of_Feline_Coronavirus_infection_in_African_nondomestic_Felids.pdf

Within the EEP Cheetah population numerous cases of hind limb paralysis have occurred in cubs over the past years. The Salzburg Zoo sent an EEP Cheetah Ataxia Questionnaire consisting of 14 questions to the EEP Zoos in order to obtain a general view of the cheetah cub ataxia problem within the EEP Cheetah population. The following results were obtained.

Kotsch_et_al_2001_Evaluation_of_cheetah_cub_ataxia_within_the_EEP.pdf

The U.S., South African and Japanese captive cheetah population is threatened by three highly prevalent diseases, bacterial gastritis, glomerulosclerosis and veno-occlusive disease, causing premature death of potential breeders. Additionally very poor breeding success, inappropriate captive management and a paucity of genetic variability are major problems in captive cheetahs in general. Due to lacking data concerning cheetahs within the EEP, a medical survey was sent to 88 zoos and private institutions. One part concerning the individual medical status of those cheetahs is still being processed. The results of the survey containing questions concerning management conditions are presented.

Kotsch_et_al_2002_Integrated_approach_to_cheetah_health_assessment_within_EEP.pdf

Langley RJ, Hirsch VM, O'Brien SJ, Adger-Johnson D, Goeken RM, Olmsted RA. 1994. Nucleotide sequence analysis of puma lentivirus (PLV-14): Genomic organization and relationship to other lentiviruses. Virology 202: 853-64.

The complete nucleotide sequence of an isolate of puma lentivirus (PLV-14) was obtained by an inverse polymerase chain reaction (I-PCR) technique and confirmed by conventional PCR. Both methods were used to amplify overlapping regions of proviral DNA, for cloning and sequencing, from genomic DNA isolated from PLV-14 infected Florida puma (Felis concolor coryi) peripheral blood mononuclear cells (PBMC). The provirus has a total length of 9100 nucleotides and the genomic organization of presumed protein coding regions are similar to those seen in other members of the lentivirus family, i.e., three large open reading frames gag, pol, and env as well as smaller intergenic regions that apparently encode regulatory proteins vif and 3' rev by positional and sequence similarity to those seen in other lentiviruses. Two additional open reading frames were identified in the env region and their function (if any) is unknown. The length of the PLV-14 long terminal repeat (LTR) was found to be shorter than the LTRs of feline immunodeficiency virus (FIV). .

Langley_et_al_1994_Puma_lentivirus_sequence.pdf

Lezmi_et_al_2010_Abnormal_prion_in_renal_globuli_of_felines.pdf

Lloyd C and Stidworthy MF. 2009. Acute disseminated toxoplasmosis in a juvenile cheetah (Acinonyx jubatus). Journal of Zoo and Wildlife Medicine 38, 475-478.

Both the behavioural and the morphological analyses confirm the special role of the dewclaw in the cheetah: a strong hook to stop running animals by using the energy of the victim itself. However, this would hardly be an explanation for the rather large dewclaw in the puma. The present finding of the puma as an intermediate between the cheetah and other large felids for dewclaw size, supports the idea that, despite some later reversal to a more primitive, typically feline structure, the puma originated from felids like the fossil cheetah-like cat Miracinonyx inexpectatus of North America, which had longer, more cursorial limbs (though maintaining fully retractile claws) and, as far as one can judge from phalanx size, larger dewclaws than the extant puma.

Lloyd_&_Stidworthy_2009_Dissiminated_toxoplasmosis_in_cheetah.pdf

Marker L, Munson L, Basson PA, Quaokenbush S. 2003. Mulicentric T-cell lymphoma associated with feline leukemia virus infection in a captive Namibian cheetah (Acinonyx jubatus). J Wildl Dis 39(3):690-5.

This case report describes a multicentric lymphoma in a four year old female wildborn captive cheetah (Acinonyx jubatus) in Namibia after being housed in an enclosure adjacent to a feline leukemia virus (FeLV) infected cheetah that had previously been in contact with domestic cats. The year prior to the onset of clinical signs, the wild-born cheetah was FeLV antigen negative. The cheetah subsequently developed lymphoma, was found to be infected with FeLV, and then rapidly deteriorated and died. At necropsy, the liver, spleen, lymph nodes, and multiple other organs were extensively infiltrated with neoplastic T-lymphocytes. Feline leukemia virus DNA was identified in neoplastic lymphocytes from multiple organs by polymerase chain reaction and Southern blot analysis. Although the outcome of infection in this cheetah resembles that of FeLV infections in domestic cats, the transmission across an enclosure fence was unusual and may indicate a heightened susceptibility to infection in cheetahs. Caution should be exercised in holding and translocating cheetahs where contact could be made with FeLV-infected domestic, feral, or wild felids.

Marker_et_al_2003_T_cell_lymphoma_with_feline_leukemia_in_a_cheetah.pdf

Miller-Edge MA, Worley MB. 1991. In vitro mitogen responses and lymphocyte subpopulations in cheetahs. Veterinary Immunology and Immunopathology 28:337-49.

Lack of genetic variability and apparent susceptibility of cheetahs (Acinonyx jubatus) to coronavirus infection has lead to speculation that this species may have immune system deficits. To establish a foundation for evaluation of the immune function, cheetah peripheral blood mononuclear cells (PBM) were stimulated by a panel of six mitogens, and responses compared with those of domestic cat PBM. Individual responses in both species were variable, but evenly distributed throughout the range of stimulation for each mitogen. Proliferation by PBM from domestic cats occured within the same range as that of the cheetahs. However, a significantly lower response to peanut agglutinin (PNA) was observed with domestic cat PBM. Although responses varied between animals, certain individual cheetahs were consistent responders. The decreased values could not be explained by lack of IL-2 responsiveness since exogenous IL-2 significantly enhanced mitogen-stimulated proliferation in 11 of 12 cheetahs tested. The phenotypic distribution of domestic cat and cheetah lymphocyte subpopulations was similar as assessed by immunofluorescence staining for surface immunoglobulin (sIg) and cytotoxic T (Tc) cells (using a specific monoclonal antibody, FT2). Values for B cells (31.2% sIg+) and Tc (28.7% FT2 +) were slightly higher in domestic cats as compared with cheetah PBM (13.3% sIg+; 19.0% FT2+). Even though no species-specific deficits were detected, a significant negative correlation between PHA-stimulated proliferation and percent FT2+ (Tc) cheetah cells was observed. This indicates that proliferation can be used indirectly to assess relative numbers of functional T helper cells in cheetahs. Our studies suggest that these aspects of the cheetah's immune system are comparable with the domestic cat, and establish a basis for in vitro assays evaluating antigen-specific responses.

Miller-Edge_&_Worley_1991_Immune_response_in_cheetahs.pdf

Miller-Edge MA, Worley MB. 1992. In vitro responses of cheetah mononuclear cells to feline herpesvirus-1 and Cryptococcus neoformans. Veterinary Immunology and Immunopathology 30:261-74.

In vitro T cell function by domestic cats and cheetahs to two common pathogens, feline herpesvirus-1 (FHV-1) and Cryptococcus neoformans, was assessed. Peripheral blood mononuclear cells (PBM) were stimulated with two strains of UV-inactivated FHV-1, whole heat-killed organisms or capsular antigen of Cryptococcus neoformans, and proliferative responses measured. As a group, cheetah PBM responded significantly poorer than domestic cat PBM when cultured with FHV-1. However, individual cheetah responses varied widely. Supplementation of cultures with exogenous interleukin 2 (IL-2) significantly increased the level of response of individual cheetahs to both strains of FHV-1. Cheetah sera contained slightly higher neutralizing antibody titers to FHV-1 than did domestic cat sera, suggesting that B cells function adequately in cheetahs. When stimulated with Cryptococcus neoformans, both species had similar incidences of positive proliferative responses. These data demonstrate that cheetahs exhibit heterogeneous responses to specific antigens, similar to domestic cats. However, a lower group response to FHV-1 in cheetahs suggests species differences occur. In addition, level of variability in major histocompatibility complex (MHC) class I-like genes, as determined by Southern blot hybridization, does not appear to correlate with a uniform response in vitro functional assays. Therefore, additional mechanisms influence the final outcome of the immune response.

Miller-Edge_&_Worley_1992_Responses_of_cheetah_mononuclear_cells_to_pathogens.pdf

Munson L. 1993. Diseases of captive cheetahs (Acinonyx jubatus): results of the Cheetah Council Pathology Survey, 1989-1992. Zoo Biology 12(1):105-24.

Knowledge of the diseases of cheetahs is essential to prevent and treat conditions that can modulate fertility and longevity. Toward this aim, a comprehensive pathology survey was conducted under a directive from the Cheetah Species Survival Plan. To date, 31 adult cheetahs and nine cubs from 16 zoological parks have been evaluated. Also, liver biopsies from 67 female cheetahs from 22 zoological parks were examined. Veno-occlusive disease (VOD) affected 82% of deceased cheetahs and 51% of live female cheetahs, and was the cause of death in nine cheetahs. Glomerulosclerosis and nephrosclerosis affected 84% and 39% of the population, respectively, and caused renal failure in eight cheetahs. The severity of VOD and glomerulosclerosis increased with age, and was not associated with infertility. Chronic gastritis was noted in 91% of the study population, and 95% of these cases also had spiral bacteria. Feline infectious peritonitis caused the death of two cheetahs. Male cheetahs had testicular degeneration, atrophy, and/or spermatogenic arrest, but these cheetahs also had severe systemic illness. Most females did not have reproductive tract lesions that would cause infertility, including those with parovarian cysts. Ovarian histology suggested that infertile cheetahs were not ovulating. Most cubs died from pneumonia or other systemic infections. The results of this study indicate that serious diseases are prevalent in the North American cheetahs, but these diseases do not appear to be the cause of infertility in the population. However, these diseases do limit the life span and well-being of cheetahs in captivity.

Munson_1993_Dieseases_of_captive_cheetah.pdf

Munson L, Marker L, Dubovi E, Spencer JA. 2004. Serosurvey of viral infections in free-ranging Namibian cheetahs (Acinonyx jubatus). J Wildl Dis 40(1):23-31.

Cheetahs (Acinonyx jubatus) in captivity have unusually high morbidity and mortality from infectious diseases, a trait that could be an outcome of population homogeneity or the immunomodulating effects of chronic stress. Free-ranging Namibian cheetahs share ancestry with captive cheetahs, but their susceptibility to infectious diseases has not been investigated. The largest remaining population of free-ranging cheetahs resides on Namibian farmlands, where they share habitat with domestic dogs and cats known to carry viruses that affect cheetah health. To assess the extent to which free-ranging cheetahs are exposed to feline and canine viruses, sera from 81 free-ranging cheetahs sampled between 1992 and 1998 were evaluated for antibodies against canine distemper virus (CDV), feline coronavirus (feline infectious peritonitis virus; FCoV/FIPV), feline herpesvirus 1 (FHV1), feline panleukopenia virus (FPV), feline immunodeficiency virus (FIV), and feline calicivirus (FCV) and for feline leukemia virus (FeLV) antigens. Antibodies against CDV, FCoV/FIPV, FHV1, FPV, and FCV were detected in 24, 29, 12, 48, and 65% of the free-ranging population, respectively, although no evidence of viral disease was present in any animal at the time of sample collection. Neither FIV antibodies nor FeLV antigens were present in any free-ranging cheetah tested. Temporal variation in FCoV/FIPV seroprevalence during the study period suggested that this virus is not endemic in the free-ranging population. Antibodies against CDV were detected in cheetahs of all ages sampled between 1995 and 1998, suggesting the occurrence of an epidemic in Namibia during the time when CDV swept through other parts of sub-Saharan Africa. This evidence in free-ranging Namibian cheetahs of exposure to viruses that cause severe disease in captive cheetahs should direct future guidelines for translocations, including quarantine of seropositive cheetahs and preventing contact between cheetahs and domestic pets.

Munson_et_al_2004_Viral_infections_in_Namibian_cheetahs.pdf

Four 3 mo old cheetah littermates were dewormed with levamisole hydrochloride according to the regular deworming regimen of the Peaugres Zoo . Levamisole was administered subcutaneously at a dosage of 5 mg/kg. Shortly after the injection, all four cubs showed severe respiratory distress and seizures, and died within twenty minutes despite attempts at resuscitation.

Oevermann_et_al_2004_Presumed_levamisole_intoxination_in_four_cheetah_cubs.pdf

Olmsted RA, Langley R, Roelke ME, Goeken RM, Adger-Johnson D, Goff JP, Albert JP, Packer C, Laurenson MK, Caro TM, Scheepers L, Wildt DE, Bush M, Martenson JS, O'Brien SJ. 1992. Worldwide prevalence of lentivirus infection in wild feline species: Epidemologic and phylogenetic aspects. Journal of Virology 66(10):6008-18.

The natural occurrence of lentiviruses closely related to feline immunodeficiency virus (FlV) in nondomestic felid species is shown here to be worldwide. Cross-reactive antibodies to FIV were common in several free-ranging populations of large cats, including East African lions and cheetahs of the Serengeti ecosystem and in puma (also called cougar or mountain lion) populations throughout North America. Infectious puma lentivirus (PLV) was isolated from several Florida panthers, a severely endangered relict puma subspecies inhabiting the Big Cypress Swamp and Everglades ecosystems in southern Florida. Phylogenetic analysis of PLV genomic sequences from disparate geographic isolates revealed appreciable divergence from domestic cat FIV sequences as well as between PLV sequences found in different North American locales. The level of sequence divergence between PL V and FIV was greater than the level of divergence between human and certain simian immunodeficiency viruses, suggesting that the transmission of FIV between feline species is infrequent and parallels in time the emergence of HIV from simian ancestors.

Olmsted_et_al_1992_Worldwide_prevalence_of_feline_lentivirus_infection.pdf

Osofsky,S.A.1994. Serologic evaluation of free-ranging lions, leopards and cheetahs for feline lentivirus and feline leukemia virus in Botswana. Annual Conference of the American Associationof Zoo Veterinarians and Association of Reptilian and Amphibian Veterinarians; 399 p.

None of the cats tested demonstrated evidence of feline leukemia infection. Significant evidence of lentivirus exposure, which was defined as a positive result on at least the cougar lentivirus western immunoblot, was found in cats of all three species: eight of 31 sampled lions, three of 18 leopard and one of four cheetahs demonstrated evidence of exposure to a feline lentivirus. In domestic cats FIV seropositivity is strongly correlated with FIV infection. Exposed cats were found in geographically diverse parts of the country.

Osofsky_et_al_1994_Serologic_Evaluation_for_Feline_Lentivirus_and_Feline_Leukemia_Virus.pdf

Osofsky SA, Hirsch KJ, Zuckerman EE, Hardy WDjr. 1996. Feline lentivirus and feline oncovirus status of free-ranging lions (Panthera leo), leopards (Panthera pardus), and cheetah (Acinonyx jubatus) in Botswana: a regional perspective. Journal of Zoo and Wildlife Medicine 27(4):453-67.

Osofsky_et_al_1996_Botswana_lion_leopard_cheetah_FIV_-_FEL_V.pdf

Osofsky SA, Hirsch KJ, Zuckerman EE, Hardy WD. 1997. Lentivirus Infection in Lions, Leopards and Cheetahs in Botswana. Cat News, 27:25-25.

In this study evidence of current lentivirus infection has been found in lions, leopards and cheetahs in geographically diverse parts of Botswana.

Osofsky_et_al_1997_Lentivirus_Infection_in_Botswana_Cats_CatNews_27.pdf

Pearke Wilkerson AJ, Teeling EC, Troyer JL, Kahila Bar-Gal G, Roelke M, Marker L, Pecon-Slattery J, O'Brien SJ. 2003. Coronavirus outbreak in cheetahs: Lessons for SARS. Current Biology 14(6):227-8.

In November 2002, a flu-like outbreak caused by a coronavirus now known as SARS-CoV occurred in Guangdong Province in China. In the space of 9 months the disease traveled to 29 countries, infected 8098 people and caused 774 deaths. A fatal epizootic of a related coronavirus in captive African cheetahs at Winston Safari Park in the early 1980s may offer comparative insight into the prospects for a coronavirus-based epidemic. The affected animals died of feline infectious peritonitis (FIP), caused by a felinecoronavirus (FCoV, also called FIPV). The presence of a cheetah coronavirus (Aju-CoV, for Acinonyx jubatuscoronavirus) was inferred based upon the presence of FIPV antibodies and the observation of coronavirus-like particles. Comparisons of SARS-CoV,FCoV and Aju-CoV reveal important epidemiological lessons.

Pearks_Wilkerson_et_al_2003_Coronavirus_outbreak_in_cheetahs.pdf

Peirce MA, Laurenson MK, Gascoyne SC. 1995. Hepatozoonosis in cheetahs and wild dogs in the Serengeti ecosystem. African Journal of Ecology 33:273-5.

Hepatozoan spp. are apicomplexan parasites occurring in a wide range of mammals, birds, reptiles and amphibians. Between 1987 and 1991 within the Serengeti ecosystem, 24 cheetahs were examined for the presence of blood parasites. Microscopical examination revealed the presence of Hepatozoan in the leucocytes from thirteen cheetahs (54.2%). The highest parasitaemias occurred in October-November and might possibly be associated with increased tick activity during the short rainy season and with the use of habitat with long grass.

Peirce_et_al_1995_Hepatozoonosis_in_cheetahs_in_the_Serengeti.pdf

Phillips JA, Worley MB, Morsbach D, Williams TM. 1991. Relationship among diet, growth and occurrence of focal palatine erosion in wild-caught captive cheetahs. Madoqua 18(2):79-83.

Forty-four wild-caught captive cheetahs of various ages were examined in Namibia for focal palatine erosion (FPE), a disorder characterized as penetration of the palatine mucosa by the lower first molar. Length of captivity varied from one month to more than four years. While captive these animals were fed a variety of diets ranging from meat scraps, to carcasses of rabbits and large domestic hoofstock. The occurrence of FPE was related to the type of diet fed, but only during the time period when the permanent teeth were erupting. Diet had no effect on producing RPE if individual cheetah were more than eight months old at the time of capture. There was no evidence that FPE occurred in wild cheetahs.

Phillips_et_al_1991_Focal_palatine_erosion_in_cheetah.pdf

Captive cheetahs (Acinonyx jubatus) worldwide suffer from a number of health problems rarely observed in free-ranging ones, and unusual in other species, especially felids. These include diseases of the central nervous system (CNS) as well as non-CNS diseases. Among the neurological diseases, the encephalo- myelopathy represents a serious threat to the European Endangered Species Plan (EEP) cheetah population, whereas the leucoencephalopathy affects only the Species Survival Plan (SSP) North-American population. Both are degenerative disorders of the CNS white matter, affecting the spinal cord or the cerebellum, respectively. Futhermore, several cases of feline spongiforme encephalopathy (FSE), a disease caused by a prion and considered to be related to the bovine spongiforme encephalopathy (BSE), have been diagnosed in captive cheetahs. Most of the FSE-affected cheetahs were born in the United Kingdom (UK) and probably were fed with infected bovine carcasses. Among the non-CNS diseases, lymphoplasmacytic gastritis associated with Helicobacter spp. is prevalent in captive cheetahs worldwide (Europe, North-America, South-Africa, Japan). Mild gastritis has also been diagnosed in free-ranging cheetahs. Another important disease in the captive cheetah population is glomerulosclerosis. Systemic AA amyloidosis affecting the kidneys, liver and other organs is also frequently diagnosed in all captive populations. There is a high correlation between amyloidosis and chronic gastritis and glomerulosclerosis. Oxalate nephrosis and pyelonephritis are other frequently diagnosed renal diseases. Veno-occlusive disease of the liver resulting in progressive liver failure is a frequent disease in the North-American population but not in the European and South-African populations. Myelolipoma are common lesions seen in the spleen, sometimes also in the liver, but are however clinically not relevant. Among the infectious diseases, the clinical feline herpes virus (FHV) infection is widespread in captive cheetahs and frequently causes conjunctivitis, rhinitis and chronic facial dermatitis. Feline infectious peritonitis (FIP-caused by feline coronavirus [FCoV]) has been reported in cheetahs, but colitis caused by feline enteric corona virus (FECV) may deserve increased attention. Among parasites, in captive populations, massive infestation with Ascarid sp. is a common problem despite regular deworming. Pneumonia by lungworms (Aelurostrongylus abstrusus) has been reported. The primary cause of these unusual diseases is mostly unidentified and the reason for their high prevalence in captive cheetahs is unknown, but the low level of these disorders in free-ranging cheetahs suggests extrinsic causes as predisposing factors (Munson, 2005).

Robert_&_Walzer_2009_Pathological_disorders_in_captive_cheetahs.pdf

Captive cheetahs have larger adrenal cortices (adrenal hyperplasia) and higher level of fecal corticoids than free-ranging cheetahs, suggesting that chronic stress may contribute to many health problems of captive cheetahs  (Terio, 2004). Among the neurological diseases, the cheetah ataxia, caused by a degenerative spinal cord disorder affecting young and adult cheetahs, represents a serious threat for a sustainable captive cheetah population in Europe. Furthermore several cases of FSE have been diagnosed in European cheetahs. Although the disease has been reported in several large cat species, the relatively high incidence in cheetahs suggests that they may be more susceptible than other zoo felids. In North America, a neurological disease of undetermined aetiology and known as leucoencephalopathy has been reported in numerous adult cheetahs.

Robert_et_al_2006_Neurological_diseases_in_cheetah.pdf

Leukoencephalopathy is a recently described disease of cheetahs characterized by white matter degeneration in specific areas of the brain. A 12-year-old male cheetah (Acinonyx jubatus) presented with progressive hind-limb ataxia and incoordination of 22-month duration. Magnetic resonance imaging was utilized as a diagnostic technique. The regions of interest were defined as brain and spinal cord. Images produced by magnetic resonance did not show changes in the intensity of the cerebral white matter consistent with a chronic degenerative process. The absence of clear lesions on the MRI implies a final diagnosis can not be made until the animals' signs worsen, and a follow up MRI shows unequivocal lesions, or until C.N.S. lesions can be detected postmortem by means of histopathology. The animal's chronic neurologic signs, apparent occasional blindness, and slow recovery from anesthesia, associated with severe neurologic signs during recovery, indicate it will remain a strong clinical suspect of leukoencephalopathy. Should the animal in this case be found positive, it would suggest that the disease may be suspected clinically before magnetic resonance imaging is a diagnostic option.

Schulz_et_al_2003_Diagnosing_leukoencephalopathy_in_a_cheetah.pdf

Setchell KDR, Gosselin SJ, Welsh MB, Johnston OJ, Balistreri WF, Kramer LW, Dresser BL, Tarr MJ. 1987. Dietary estrogens - A probable cause of infertility and liver disease in captive cheetahs. Gastroenterology 93:225-33.

The cheetah in the wild is "racing towards extinction" mostly due to habitat destruction. Its survival will probably depend on accelerated captive breeding. At this time, however, reproductive failure and liver disease threaten the future of the captive cheetah population. Histopathological evaluation of more than 100 cheetah livers identified venocclusive disease as the main hepatic lesion responsible for liver disease in this species. Analysis of the commercial feline diet by high-performance liquid chromatography and gas-liquid chromatography - mass spectrometry revealed large amounts of two phytoestrogens identified as daidzein and genistein. These compounds were found to be derived from a soybean product that was a component of the cheetah diet, and their concentrations both ranged from 18 to 35 microg/g diet. The adult cheetah consequently consumes 50 mg/day of these weak estrogens. When extracts of the diet were tested for estrogenicity using a bioassay, a dose-related increase in uterine weight was observed. In 4 cheetahs studied, withdrawal of this feline diet by substitution with a chicken diet resulted in an improvement in conventional liver function tests and a normalization in the appearance of hepatic mitochondria. We conclude that the relatively high concentrations of phytoestrogens from soybean protein present in the commercial diet fed to captive cheetahs in North American zoos may be one of the major factors in the decline of fertility and in the aetiology of liver disease in this species. The survival of the captive cheetah population could depend upon a simple change of diet by excluding exogenous oestrogen.

Setchell_et_al_1987_Infertility_and_liver_disease_in_cheetahs.pdf

Spencer J, Marker-Kraus L, Kraus D, Evermann J, O'Brien S.  Seroepidemiology of antibodies to viruses in free-ranging Namibian cheetahs. Report, 1 p.

In Namibia, most of the free-ranging cheetahs live on farmlands where they can present problems to the farmers. As a part of the disease surveillance programme all captured animals are tested for the presence of antibodies to feline viruses as well as having DNA RFLP pattern assayed. To date 134 animals have been tested for antibodies to feline herpes, calici, panleukopenia, leukaemia, immunodeficiency and corona viruses. The tests employed include commercially available ELISA kits, immunofluorescent antibodies assays (IFA) and western blotting.The animals have been shown to be positive for herpes, calici, panleukopenia, leukaemia and coronaviruses as well as toxoplasmosis. Two individuals tested positive for feline immunodeficiency virus antibodies by IFA but were negative on western blotting.

Spencer_et_al_-_Seroepidemiology_of_antibodies_to_viruses_of_Namibian_cheetahs.pdf

Spencer JA, Burroughs R. 1991. Antibody response of captive cheetahs to modified-live feline virus vaccine. J Wildl Dis 27(4):578-83.

The antibody response of cheetah (Acinonyx jubatus) to modified live virus vaccine against feline panleukopedia (FPLV), herpes (FHV) and calici (FCV) viruses was assessed by means of an enzyme-linked immunosorbent assay (ELISA). In the first year of study, 82 cheetahs were bled pre-vaccination. Of these, antibody levels to FPLV were found in 100% of the animals. Only 54% were found to have antibodies to FHV and 99% had antibodies to FCV. One month after booster vaccination with the same vaccine, increased antibodies to FPLV, FHV and FCV were seen in 19 (58%), 18 (55%) and 25 (76%) of these animals, respectively (n = 33). In the second year of study, 65 cheetahs were bled pre-vaccination. Fifty three of these animals were negative for antibodies to FPLV while 28 were positive to FHV and 64 were positive for FCV. These animals were then bled 1,2 and 6 mo post booster vaccination. The antibody levels to the various viruses showed different trends with time.

Spencer_&_Burroughs_1991_Antibody_response_of_captive_cheetahs_to_vaccine.pdf

Spencer JA, Burroughs R. 1992. Decline in maternal immunity and antibody response to vaccine in captive cheetah (Acinonyx jubatus) cubs. J Wildl Dis 28(1):102-4.

Blood was collected from captive cheetah cubs (Acinonyx jubatus) from the ages of 4 to 12 wk and monitored for the decline in maternally derived antibodies to feline panleukopenia, herpes and calici viruses. A steady decrease was seen in most of the cubs. Antibody responses to inactivated and/or modified live virus (MLV) vaccine also were measured. The strongest responses were seen post vaccination with MLV vaccine only.

Spencer_&_Burroughs_1992_Decline_of_immune_response_to_vaccine_in_cheetah.pdf

Spencer JA. 1993. Lymphocyte blast transformation response and restriction fragment length analysis in the cheetah. Onderstepoort Journal of Veterinary Research 60:211-7.

An extensive genetic and physiological analysis of the cheetah by O'Brien et al. (1983; 1985; 1987) indicated that the cheetah showed monomorphism at the major histocompatibility complex. This led O'Brien (1985) to propose that the cheetah suffered from an immunodeficiency and was highly susceptible to diseases. It was therefore decided to investigate cell-mediated and humoral immune responses and to apply the limited restriction fragment length analysis (using Pst 1 and Barn H1 enzymes) of the cheetah MHC 1 and MHC II genes. Antibody responses to antigens (feline viruses), as well as mitogen-induced lymphocyte blast transformation responses, were shown to be intact and comparable with that of the domestic cat, indicating a competent immune system in the cheetah. It was also suggested by the results that some polymorphism does exist in the MHC class II genes, but possibly not in the MHC class I genes.

Spencer_1993_Lymphocyte_blast_transformation_responses_and_RFLP_analysis_in_cheetah.pdf

Spencer JA. 1998. Absence of canine distemper antibodies in selected southern Africa nondomestic felids. S Afr J Wildl Res 28(1):8-9.

Sixty eight animals from various parks and zoos in southern Africa were tested for the presence of antibodies to canine distemper virus (CDV). The areas surveyed include: the Johannesburg and Pretoria zoos, the De Wildt Cheetah Breeding and Research Centre, Botswana (Ghanzi region), Namibia (Gobabis region), the Kruger National Park, Midkwe Game Reserve, and Umfolozi Game Reserve. The species tested include cheetahs (Acinonyx jubatus) (n=23), lions (Panthera leo) (n=41) and leopards (Panthera pardus) (n=4). None of the 68 animals surveyed tested positive for CDV antibodies indicating a lack of exposure to this potentially fatal disease.

Spencer_1998_Absence_of_canine_distemper_antibodies_in_non-domestic_felids.pdf

In this article an ancient art is presented: miniature. This consisted in painting with great patient and precision extremely minuscule subjects, as in the "Taccuino". This book can be considered the first illustrated tome on zoology (here are presented the illustrations of different animals, between which cheetahs, a leopard and a camel).

Steinel_et_al_1999_Characterisation_of_feline_parvovirus_sequences_from_carnivores.pdf

Terio KA, Marker L, Munson L. 2004. Evidence for chronic stress in captive but not free-ranging cheethas (Acinonyx jubatus) based on adrenal morphology and function. J Wildl Dis 40(2):259-66.

The cheetah (Acinonyx jubatus) is highly endangered because of loss of habitat in the wild and failure to thrive in captivity. Cheetahs in zoos reproduce poorly and have high prevalences of unusual diseases that cause morbidity and mortality. These diseases are rarely observed in free-ranging cheetahs but have been documented in cheetahs that have been captured and held in captive settings either temporarily or permanently. Because captivity may be stressful for this species and stress is suspected as contributing to poor health and reproduction, this study aimed to measure chronic stress by comparing baseline concentrations of fecal corticoid metabolites and adrenal gland morphology between captive and free-ranging cheetahs. Additionally, concentrations of estradiol and testosterone metabolites were quantified to determine whether concentrations of gonadal steroids correlated with corticoid concentration and to assure that corticosteroids in the free-ranging samples were not altered by environmental conditions. Concentrations of fecal corticoids, estradiol, and testosterone were quantified by radioimmunoassay in 20 free-ranging and 20 captive cheetahs from samples collected between 1994 and 1999. Concentrations of baseline fecal corticoids were significantly higher (p=0.005) in captive cheetahs (196.08±36.20 ng/g dry feces) than free-ranging cheetahs (71.40±14.35 ng/g dry feces). Testosterone concentrations were lower in captive male cheetahs (9.09±2.84 ng/g dry feces) than in free-ranging cheetahs (34.52±12.11 ng/g dry feces), which suggests suppression by elevated corticoids in the captive males. Evidence for similar suppression of estradiol concentrations in females was not present. Adrenal corticomedullary ratios were determined on midsagittal sections of adrenal glands from 13 free-ranging and 13 captive cheetahs obtained between 1991 and 2002. The degree of vacuolation of cortical cells in the zona fasciulata was graded for each animal. Corticomedullary ratios were larger (p=0.05) in captive cheetahs; however, there was no difference (p=0.31) in the degree of corticocyte vacuolation between the two populations. These data provide both morphologic and functional evidence suggestive of chronic stress in captive cheetahs. Further research into the role of hypercortisolemia in the pathogenesis of the reproductive abnormalities and unusual diseases of captive cheetahs is needed.

Terio_et_al_2004_Chronic_stress_in_captive_cheetahs.pdf

Terio KA, Munson L, Marker L, Aldridge BM, Solnick JV. 2005. Comparison of Helicobacter spp. In Cheetahs (Acinonyx jubatus) with and without gastritis. Journal of Clinical Microbiology 43(1):229-34.

Chronic gastritis causes significant morbidity and mortality in captive cheetahs but is rare in wild cheetahs despite colonization by abundant spiral bacteria. This research aimed to identify the Helicobacter species that were associated with gastritis in captive cheetahs but are apparently commensal in wild cheetahs. Helicobacter species were characterized by PCR amplification and sequencing of the 16s rRNA, urease, and cagA genes and by transmission electron microscopy of frozen or formalin-fixed paraffin-embedded gastric samples from 33 cheetahs infected with Helicobacter organisms (10 wild without gastritis and 23 captive with gastritis). Samples were screened for mixed infections by denaturant gel gradient electrophoresis of the 16s rRNA gene and by transmission electron microscopy. There was no association between Helicobacter infection and the presence or severity of gastritis. Eight cheetahs had 16s rRNA sequences that were most similar (98 to 99%) to H. pylori. Twenty-five cheetahs had sequences that were most similar (97 to 99%) to "H. heilmannii" or H. felis. No cheetahs had mixed infections. The ultrastructural morphology of all bacteria was most consistent with "H. heilmannii," even when 16s rRNA sequences were H. pylori-like. The urease gene from H. pylori-like bacteria could not be amplified with primers for either "H. heilmannii" or H. pylori urease, suggesting that this bacteria is neither H. pylori nor "H. heilmannii." The cagA gene was not identified in any case. These findings question a direct role for Helicobacter infection in the pathogenesis of gastritis and support the premise that host factors account for the differences in disease between captive and wild cheetah populations.

Terio_et_al_2005_Helicobacter_in_cheetahs_with_and_without_gastritis.pdf

Thalwitzer_et_al_2010_Seroprevalence_to_viral_pathogens_in_cheetahs_from_Namibia.pdf

Truyen U, Parrish CR, Harder TC, Kaaden O-R. 1995. There is nothing permanent except change. The emergence of new virus diseases. Veterinary Microbiology 43:103-22.

The sudden appearance of apparently new viruses with pathogenic potential is of fundamental importance in medical microbiology and a constant threat to humans and animals. The emergence of a "new" pathogen is not an isolated event, as for instance the frequent appearance of new influenza virus strains demonstrates. Often the new virus strains co-circulate with the older strains in a susceptible population, but a replacement of the older strains has been also observed. In rare instances the new viruses can cause dramatic epidemies or pandemics, such as those observed with the human immunodeficiency virus, canine parvovirus, or most recently, with the agent of bovine spongiform encephalogathy in the United Kingdom. The mechanisms of the emergence are not always clearly understood, but an altered host range appears to be a common event. Whether a true change in host range occurs, or whether the virus adapted to the host and replicated more efficiently, is often unknown. This review tries to summarize the facts that are known about a wide variety of "new" viruses of mammals, such as the simian, human and feline lentiviruses, the feline coronaviruses, the feline parvoviruses, the carnivore morbilliviruses, the influenza A viruses, and the transmissible spongiform encephalopathies. A particular emphasis will be put on the genetic mechanisms that might have taken place and that might have been responsible for their sudden appearance.

Truyen_et_al_1995_Emerge_of_new_virus_diseases.pdf

Turnbull P. 2005. Anthrax vaccination evaluation study in cheetah. Animal Keeper's Forum 32(7/8):329.

It has been recognized for decades that anthrax (that disease now so notorious for its biological warfare and bioterrorism associations) is a common natural seasonal disease among the herbivorous species of the Etosha National Park, occasionally affecting livestock and wildlife in other parts of Namibia. Of particular concern all along has been the additional threat is poses to the already endangered black rhino in Etosha, but it was only very recently realized that cheetah were dying in substantial numbers there from this disease.

Turnbull_2005_Anthrax_vaccination_evaluation_study_in_cheetah.pdf

Tyler JW, Cullor JS. 1989. Titers, tests, and truisms: rational interpretation of diagnostic serologic testing. JAVMA 194(11):1550-8.

The recent availability of serologic tests has changed the practice of veterinary medicine. These assays not only assist with the diagnosis and treatment of recognized syndromes, but they permit identification of new, poorly defined disease entities. Assays kits are available for FeLV, dirofilariasis, rheumatoid arthritis, enterotoxigenic colibacillosis, and failure of passive transfere. The purpose of this report is to discuss the theory behind diagnostic serologic testing, rebut selected misconceptions, and suggest strategies for interpreting the results of diagnostic serologic tests. Also, the authors have provided adaptations of standard statistical methods, sample calculations, general references, and a glossary of terms.

Tyler_&_Cullor_1989_Rational_interpretation_of_diagnostic_serologic_testing.pdf

The clinical signs shown by four cheetahs which were diagnosed as having spongiform encephalopathy are presented. Chronic, progressive ataxia initially involving the hindlimbs, but later the forelimbs also was consistently seen. Some of the animals also had postural difficulties, hypermetria and muscle tremors. All showed some degree of central nervous involvement, but the pattern of signs varied. The signs observed included a change in behaviour, hyperaesthesia to sounds, ptyalism, prominent nictitating membranes and blindness. No abnormalities were detected on clinical examination, routine haematological and biochemical investigations. Radiography and myelography were carried out on three animals. Two showed no abnormalities and one had fused thoracic vertebrae, but these did not impede passage of contrast medium in the spinal canal.

Vitaud_et_al_1998_Feline_spongiform_encephalopathy_in_cheetahs.pdf

This study offers a guideline for the partial antagonism of tiletamine-zolazepam (T-Z) anaesthesia in cheetahs and evaluates the possible differences between the two benzodiazepine antagonists flumazenil and sarmazenil in the species. Four cheetahs were anaesthetized 3 times at an interval of 14 days with an average i.m. dose of 4,2 mg/kg T-Z. In trials 2 and 3 Flumazenil at 31 ug/kg and Sarmazenil at 0,1 mg/kg respectively were applied i.m. 30 min after initial T-Z application. When comparing the duration and recovery from anaesthesia a highly significant difference could be established between T-Z- with and without antagonist. No significant difference could be determined between the two antagonists. The authors generally advocate caution when benzodiazepine antagonists with a novel species.

Walzer_&_Huber_1999_Comparison_of_two_benzodiazepine_antagonists_in_cheetah.pdf

Walzer C, Huber C. 2002. Partial antagonism of tiletamine-zolazepam anesthesia in Cheetah. J Wildl Dis 38(2):468-72.

This study evaluated partial antagonism of tiletamine-zolazepam (TZ) anesthesia in cheetahs (Acinonyx jubatus) and differences between two benzodiazepine antagonists, flumazenil and sarmazenil, in this species. Four cheetahs were anesthetized three times at an interval of 14 days with an average intramuscular dose of 4.2 mg/kg TZ. In trials 2 and 3 flumazenil at 0.031 mg/kg and sarmazenil at 0.1 mg/kg, respectively, were applied intramuscularly 30 min after initial TZ injection. There was a highly significant difference between the duration of TZ anesthesia with and without antagonist. Use of the antagonists significantly shortened duration and recovery and eliminated excitatory behavior during the recovery phase. No significant differences could be determined between the two antagonists. We recommend the use of sarmazenil and flumazenil to antagonize TZ anesthesia in cheetahs.

Walzer_&_Huber_2002_Partial_antagonism_of_Zoletil_anesthesia_in_cheetah.pdf

Environmental or behavioural enrichment have in recent years become household terms within the zoo community. This paper summarises the strategies developed and implemented for felids in the Salzburg Zoo. In all felid species it was possible to increase the daily activity budget and induce novel previously not observed behavioural patterns. Within the described strategies two are to be considered particularly successful: scatter feeding in all species and the provision of live fish as prey to the jaguars.

Walzer_1997_Enrichment_strategies_for_felids_at_Salzburg_zoo.pdf

This paper describes a nerval disease of cheetah cubs which is characterised by acute onset of hind limb ataxia-paresis. The clinical presentation, serological and pathological findings in three different clusters during the 1995 – 1997 period are examined. The authors suggest a possible viral etiology: ataxia progression was inhibited by the application of the anti herpes drug (Acyclovir) and prednisolon. A oronasal FHV-1 infection may trigger an immunologic process leading to ataxia with myelin destruction.

Walzer_et_al_1998_Acute_hind_limb_paresis_in_cheetah_cubs.pdf

Walzer C, Url A, Robert N, Kübber-Heiss A, Nowotny N, Schmidt P. 2003. Idiopathic acute onset myelopathy in cheetah (Acinonyx jubatus) cubs. Journal of Zoo and Wildlife Medicine 34(1):36-46.

Numerous cases of ataxia, hind limb paresis, and paralysis have occurred in cheetah (Acinonyx jubatus) cubs over the past 10 yr within the European Endangered Species Program population, including 12 in mainland Europe, two in the British Isles, one in Namibia, and one in Dubai. The condition is the most important medical factor limiting European cheetah population growth. Eight cubs at the Salzburg Zoo, Austria, were affected. They demonstrated upper motor neuron lesions when alive und bilateral, symmetrical myelin degeneration of the spinal cord on necropsy. Ballooning of myelin sheaths surrounded mostly preserved axons, and no spheroids, characteristics of acute axonal degeneration, were found. Myelin loss markedly exceed axonal degeneration. The syndrome's etiology is unclear, although viral, bacterial, parasitic, genetic, nutritional-metabolic, toxic, and physical causes have been considered.

Walzer_et_al_2003_Idiopathic_acute_onset_myelopathy_in_cheetah_cubs.pdf

Wildt DE, Grisham J. 1993. Basic research and the cheetah SSP program. Zoo Biology 12:3-4.

Throughout history, the cheetah has sustained the reputations for being difficult to propagate in captivity. In 1988, at its mid-years meeting in Kansas City, the SSP Committee mandated that all cheetahs in North America be designated as a research population and decided to implement and manage a systematic research program focusing upon basic reproduction, genetics, behaviour, nutrition, and disease.

Wildt_&_Grisham_1993_Cheetah_SSP_program.pdf