Genetic characterization of canine distemper virus in Serengeti carnivores.

The lion (Panthera leo) population in the Serengeti ecosystem was recently afflicted by a fatal epidemic involving neurological disease, encephalitis and pneumonia. The cause was identified as canine distemper virus (CDV). Several other species in the Serengeti were also affected. This report presents CDV H and P gene sequences isolated from Serengeti lions (Panthera leo), spotted hyenas (Crocuta crocuta), bat-eared fox (Otocyon megalotis) and domestic dog (Canis familiaris). Sequence analyses demonstrated that the four Serengeti species carry closely related CDV isolates which are genetically distinct from other CDV isolates from various species and locations. The results are consistent with the conclusions that: (1) a particularly virulent strain of CDV emerged among Serengeti carnivores within the last few years; (2) that strain has recognizable shared-derived (synapomorphic) genetic differences in both H and P genes when compared to CDV from other parts of the world; and (3) that the CDV strain has frequently crossed host species among Serengeti carnivores.

Trichinella nelsoni in carnivores from the Serengeti ecosystem, Tanzania.

A survey of trichinellosis among sylvatic carnivore mammals from the Serengeti ecosystem (Tanzania) demonstrated the presence of Trichinella nelsoni in 5 of 9 species examined. Muscle samples were collected from carcasses of 56 carnivores from 1993 to 1995 and frozen before transport and examination. Following artificial digestion of the samples, collected larvae were analyzed by the random amplified polymorphic DNA technique. Trichinella nelsoni was identified in 1 bat-eared fox (Otocyon megalotis), 1 cheetah (Acinonyx jubatus), 1 leopard (Panthera pardus), 3 lions (Panthera leo), and 3 spotted hyenas (Crocuta crocuta). The numbers of bat-eared foxes (6), cheetahs (5), and leopards (3) examined were too small to reveal the roles of these carnivore species in the ecology of T. nelsoni. The numbers of lions and spotted hyenas examined, with a prevalence of 12% and 23%, respectively, suggest that these species may be reservoirs of T. nelsoni in the area under study.

Atrial septal defects in Florida panthers.

Ostium secundum atrial septal defects (ASDs) were observed in six (3 M, 3 F) of 33 (20 M, 13 F) (18%) Florida panthers (Puma concolor coryi) necropsied by veterinary pathologists between 1985 and 1998. A seventh ASD was found in a female panther necropsied in the field and is included in the pathological description but not the prevalence of ASDs in Florida panthers. One panther (FP205) with severe ASD also had tricuspid valve dysplasia (TVD). Atrial septal defects and/or TVD are believed to have caused or contributed to the deaths of three (9%) Florida panthers in this study. Mean diameter +/- SD of ASDs was 9.0 +/- 4.7 mm (range 3 to 15 mm). Gross pathological changes attributed to ASDs/TVD in severely affected panthers (ASD > or = 10 mm) (n = 4) included mild right ventricular dilatation (n = 3) and hypertrophy (n = 2), mild to severe right atrial dilatation (n = 2), and acute pulmonary edema (n = 3). Panthers with mild ASDs (ASD < or = 5 mm) (n = 3) had no other detectable gross pathological changes associated with the ASDs. Histological examination of lungs of three panthers with severe ASDs revealed mild to moderate dilatation with fibrosis and smooth muscle atrophy of the tunica media of medium to large caliber arteries (n = 2), interstitial and/or pleural fibrosis (n = 2), perivascular fibrosis (n = 1), and acute to chronic edema (n = 3). Twenty-six necropsied panthers were examined one or more times while living; medical records were retrospectively evaluated. Antemortem radiographic, electrocardiographic, and echocardiographic examinations were performed on two panthers with severe ASDs (FP20 and FP205). Thoracic radiographic abnormalities in both included right heart enlargement, and in FP205 (severe ASD and TVD), mild pulmonary overperfusion. Electrocardiographic examination of FP205 revealed a right ventricular hypertrophy pattern, while FP205 had a normal electrocardiogram. Echocardiographic examination of FP20 revealed marked right atrial dilatation; a bubble contrast study indicated regurgitation across the tricuspid valve. Echocardiographic abnormalities in FP20 included right atrial and ventricular lilatation, atrial septal drop-out, and severe tricuspid regurgitation; non-selective angiography revealed significant left to right shunting across the ASD. All panthers with severe ASDs ausculted (n = 3) had systolic right or left-sided grade I-V/VI murmurs loudest at the heart base. All male panthers with ASDs (n = 3) (100%) and 9 of 17 (53%) male panthers without ASDs in this study were cryptorchid.

African buffalo maintain high genetic diversity in the major histocompatibility complex in spite of historically known population bottlenecks.

Historical population collapses caused by rinderpest epidemics are hypothesized to have resulted in notable genetic losses in populations of the African buffalo. Polymorphism in the major histocompatibity complex (MHC) DRB3 gene was probed by means of restriction analysis of the sequence encoding the peptide-binding region. Nucleotide substitution patterns agreed with a positive selection acting on this fitness-relevant locus. Buffalo populations from four National Parks, situated in eastern and southern Africa, each revealed a surprisingly high allelic diversity. Current high levels of heterozygosity may be reconciled with historical bottlenecks by assuming that local extinctions were followed by fast recolonization, in accordance with the high dispersive capabilities of buffalo. The specific amplification of DRB3 alleles also enabled the assignment of individual genotypes. For each population sample a deficiency in the expected number of heterozygous animals was found. As overdominant selection on the MHC is predicted to yield an excess of heterozygous individuals, this may not be a locus-specific effect. Several other explanations are discussed, of which increased homozygosity caused by nonrandom mating of buffalo in populations seems the most probable.

Phylogenetic evidence of canine distemper virus in Serengeti's lions.

Recently an epizootic, reported to be due to a morbillivirus infection, affected the lion population of the Tanzanian Serengeti National Park. A morbillivirus phosphoprotein (P) gene fragment was amplified by PCR from tissue samples of several affected lions. Sequencing of the amplificates and subsequent phylogenetic analyses revealed that a wild-type strain of canine distemper morbillivirus (CDV) was involved. Vaccination of the local domestic dog population with proven safe CDV vaccines is proposed.

A canine distemper virus epidemic in Serengeti lions (Panthera leo).

Canine distemper virus (CDV) is thought to have caused several fatal epidemics in canids within the Serengeti-Mara ecosystem of East Africa, affecting silver-backed jackals (Canis mesomelas) and bat-eared foxes (Otocyon megalotis) in 1978 (ref. 1), and African wild dogs (Lycaon pictus) in 1991 (refs 2, 3). The large, closely monitored Serengeti lion population was not affected in these epidemics. However, an epidemic caused by a morbillivirus closely related to CDV emerged abruptly in the lion population of the Serengeti National Park, Tanzania, in early 1994, resulting in fatal neurological disease characterized by grand mal seizures and myoclonus; the lions that died had encephalitis and pneumonia. Here we report the identification of CDV from these lions, and the close phylogenetic relationship between CDV isolates from lions and domestic dogs. By August 1994, 85% of the Serengeti lion population had anti-CDV antibodies, and the epidemic spread north to lions in the Maasai Mara National reserve, Kenya, and uncounted hyaenas, bat-eared foxes, and leopards were also affected.