We monitor the health of the Serengeti and Crater lions by routinely collecting blood samples whenever we handle the animals, and serious disease outbreaks have also led to several intensive veterinary investigations. The lion studies have provided important insights into the natural cycling of viral outbreaks, the ecological interactions that exacerbate disease outcomes, and the extent to which lions can withstand infections that are fatal in other species.

Whereas every lion is infected with feline herpesvirus (FHV) in the first few months of life, feline calicivirus, feline parvovirus, coronavirus and canine distemper virus (CDV) all strike the Serengeti and Crater populations in discrete outbreaks every 4 to 13 years. Outbreaks of these four viruses are associated with minimum threshold densities of susceptible hosts: survivors gain immunity against further subsequent infection by the same disease, so the population shows herd immunity until large numbers of young susceptibles are recruited into the population. This effect is also seen by the fact that the four viruses barely spread from one susceptible to another when most of the population is immune, but almost every susceptible lion becomes infected when most of the population is susceptible. Although calicivirus, parvovirus and coronavirus may cause mild illness, they do not increase cub mortality or reduce female fertility.

In contrast, canine distemper virus (CDV) has caused several fatal epidemics in canids within the Serengeti-Mara ecosystem, affecting silver-backed jackals (Canis mesomelas) and bat-eared foxes (Otocyon megalotis) in 1978 and African wild dogs (Lycaon pictus) in 1991. A CDV epidemic in the Serengeti lion population in 1994 resulted in fatal neurological disease characterized by grand mal seizures and myoclonus (involuntary twitching of the forelimbs and face). Over a third of the Serengeti lions died within 6 months, and most of the victims had encephalitis and pneumonia. Genetic analysis showed that the outbreak originated in domestic dogs and spread to lions, leopards, hyenas and bat-eared foxes.

Seroprevalence data revealed that the Serengeti lions had also been exposed to CDV in 1976 and 1981 but without any overt signs of disease. We originally speculated that the 1994 strain may have been unusually virulent, but subsequent outbreaks eventually led to a different conclusion. A second high-mortality CDV epidemic struck the nearby Ngorongoro Crater lion population in 2001, and further serological analyses indicated that at least five “silent” CDV epidemics swept through these populations between 1976 and 2006 without clinical signs or measurable mortality. Clinical and pathology findings suggested that hemoparasitism was a major contributing factor during the two fatal epidemics, and measurements of the magnitude of hemoparasite infection between 1984 and 2006 years demonstrated unusually high levels of Babesia during the 1994 and 2001 epidemics. In addition, only CDV-infected prides that were co-infected with high levels of Babesia suffered severe mortality; mortality rates were minimal in prides that were only infected with CDV or only suffered from high levels of Babesia. The common event preceding the two high mortality CDV outbreaks was extreme drought conditions with widespread herbivore die-offs, most notably of Cape buffalo (Syncerus caffer). As a consequence of heavy tick infestations of starving buffalo, the lions were infected by unusually high numbers of Babesia, infections that were magnified by the immunosuppressive effects of coincident CDV, leading to unprecedented mortality. Such mass mortality events may become increasingly common if climate extremes disrupt historic stable relationships between co-existing pathogens and their susceptible hosts and synchronize the temporal and spatial convergence of multiple infectious agents.

The 1994 CDV outbreak was first detected in the center of the Serengeti National Park, then spread south to the Ngorongoro Conservation Area, next moved to the Western Corridor near Lake Victoria and finally crossed the Kenyan border to the Maasai Mara Reserve about 8 months later. Could the epidemic have traveled so far and so fast solely by lion-to-lion transmission? Or did the virus repeatedly transfer from one host species to another? We first developed a simple stochastic susceptible–infected–recovered (SIR) model of disease transmission involving one to three sympatric species. The model successfully mimicked the erratic and discontinuous spatial pattern of lion deaths observed in the Serengeti lions under a reasonable range of parameter values, but only when one to two other carnivore species repeatedly transmitted the virus to the lion population. We subsequently built a highly realistic contact network model based on detailed behavioral and movement data from the long-term lion study. The results again suggested that the 1994 epidemic must have been fuelled by multiple spillovers from other carnivore species such as jackals and hyenas.

Lentiviruses closely related to feline immunodeficiency virus (FIV) are found worldwide in at least 25 nondomestic felid species. Serological surveys in free-ranging lions reveal an incidence as high as 90%. A phylogenetic analysis of gene sequences reveals six distinct FIV phylogenetic clades: FIV-A is found throughout the continent whereas FIV-B, C & F are restricted to East Africa and FIV-D & E are restricted to southern Africa. Three clades (FIV-A, B & C) occur in the Serengeti and Ngorongoro Crater and are as divergent from each other as lentiviruses from different feline species, i.e., puma and domestic cat. The FIV-Ple clades are more closely related to each other than to other feline lentiviruses, suggesting that the ancestors of FIV-Ple evolved in geographically isolated lion populations that converged recently in East Africa.

FIV causes feline AIDS in domestic cats (Felis catus), but most nondomestic cat species do not show major symptoms of disease. Although FIV is too prevalent in the Serengeti and Ngorongoro lions to provide a control group to measure the precise health effects of FIV infection, lions infected at early ages do not suffer shorter life spans than lions infected at older ages. Every Serengeti and Ngorongoro lion is FIV-positive by 4 years of age, and there is no evidence that these animals show higher age-specific mortality than uninfected populations. These host-health patterns and the extent of FIV genome variation are consistent with host-virus coadaptation. However, free-ranging FIV-infected Serengeti lions do show declines in CD4+ cells, reductions in the CD4+/CD8+ ratio and in CD8+βhigh cells, and expansion of the CD8+βlow subset relative to uninfected captive lions. Depletion in CD5+ T-cells in seropositive lions is linked with a compensatory increase in total CD52 lymphocytes. FIV-infected cougars also show declines in total lymphocytes, CD5+ T-cells, and CD52 lymphocytes as well as a significant reduction in CD4+ T-cells. Like lions, seropositive cougars show significant declines in CD8+ βhigh cells, but cougars lack a compensatory expansion of CD8+βlow cells compared to controls.

These results parallel the CD4+ diminution in HIV and SIV infected humans and Asian monkeys and suggest there may be unrecognized immunological consequences of FIV infection in lions and cougars, though it is not clear whether these effects compromise host health. The lion data should also be interpreted with caution since the seropositive individuals were all free-ranging animals whereas all of the seronegative animals lived in captivity. Further analysis in 2009 by the O’Brien lab suggested that FIV infection is associated with pathology in African lions in Botswana and the Serengeti. However, their analysis of the Serengeti lions only involved FIV+ lions, and these were all sampled in the aftermath of the 1994 CDV outbreak, which inflicted widespread morbidity and mortality. Health outcomes of the Serengeti outbreak were not affected by FIV serostatus. In contrast, their 2009 analysis of FIV pathogenesis in the Botswana lions includes FIV+ and FIV- individuals from the same population. The Botswana lions are infected by a different clade of FIV than their Serengeti counterparts, and it is possible that the southern-African clade is more pathogenic than the three clades (FIV-A, B & C) found in East Africa. Indeed, recent work from the Willett lab in Glasgow suggests that the FIV-E clade is better able to target CD4 cells than the FIV-B clade.

Infection with the cestode Spirometra spp. was studied in the Serengeti and Crater lions. These populations live in different habitats (with moister soils in the Crater) and the Serengeti lions are outbred whereas the Crater lions are inbred. Based on fecal samples collected between March 1991 and November 1992, over 60% of lions were infected and the median intensity of infection was 975 eggs per g of feces; cubs less than 9 months of age were already heavily infected. Intensity of infection was higher in the Crater population than in the Serengeti population, but Spirometra levels were not related to allozyme heterozygosity in 28 individuals. Thus it wasn’t possible to ascribe differences in levels of parasite infection to genetic rather than to ecological factors.

Trypanosomes cause disease in humans and livestock throughout sub-Saharan Africa. Various species have shown evidence of clinical tolerance to trypanosomes, but there has never been any evidence of acquired immunity to natural infections until we discovered a distinct peak and decrease in age prevalence of Trypanosoma brucei infection in Serengeti lions. This pattern is consistent with an exposure-dependent increase in cross-immunity following infections with the more genetically diverse species, T. congolense. The causative agent of human sleeping sickness, T. brucei rhodesiense, disappears in lions by 6 years of age apparently in response to cross-immunity from other trypanosomes, including the non-pathogenic subspecies, T. brucei brucei. These findings suggest novel pathways for vaccinations against trypanosomiasis despite the notoriously complex antigenic surface proteins in these parasites.

Bovine tuberculosis, caused by Mycobacterium bovis, is a pathogen of growing concern in free-ranging wildlife in Africa, especially in the lions and buffalo of Kruger National Park in South Africa. M. bovis was isolated from 11.1% (2/18) migratory wildebeest (Connochaetes taurinus) and 11.1% (1/9) topi (Damaliscus lunatus) sampled during a meat cropping program in the Serengeti ecosystem in 2000 and from one wildebeest and one lesser kudu (Tragelaphus imberbis) killed by sport hunters adjacent to Tarangire National Park. A tuberculosis antibody enzyme immunoassay was used to screen serum samples from Serengeti and Crater lions sampled between 1984 and 2000, and ungulates collected throughout the protected area network between 1998 and 2001. Serological assays detected antibodies to M. bovis in 4% of Serengeti lions, 6% of Tarangire buffalo and 2% of Serengeti wildebeest. The study revealed that bovine tuberculosis has been present in Serengeti lions since at least 1984 and that the incidence of the disease remained virtually constant for the following 16 years. Although the number of cases was small, bTB-positive lions often showed obvious signs of disease as well as higher mortality.

Rabid lions have been reported in Kenya and South Africa, and rabies is a serious public health issue for villagers in the greater Serengeti ecosystem and a serious conservation threat to African wild dogs (Lycaon pictus) inside the Serengeti Park and Ngorongoro Conservation Area. However, rabies has never been detected in these lions.