Brian A. Summers

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 population4,5 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.

Canine Distemper Epizootic in Lions, Tigers, and Leopards in North America:

Canine distemper virus (CDV) infection occurred in captive leopards (Panthera pardus), tigers (Panthera tigris), lions (Panthera leo), and a jaguar (Panthera onca) in 1991 and 1992. An epizootic affected all 4 types of cats at the Wildlife Waystation, San Fernando, California, with 17 mortalities. CDV-infected raccoons were thought to be the source of infection in these cats. Two black leopards died at the Naibi Zoo, Coal Valley, Illinois, and 2 tigers died at the Shambala Preserve, Acton, California. Initial clinical signs were anorexia with gastrointestinal and/or respiratory disease followed by seizures. Canine distemper virus was isolated from 3 leopards, 3 tigers, and 3 lions that died or were euthanized when moribund. Monoclonal antibody testing identified the virus isolates as CDV. Gross and histopathologic findings were similar to those found in canids with distemper with a few exceptions. There were fewer lesions in the brain, and there was a pronounced type 2 cell proliferation in the lung, with inclusion bodies and CDV antigen demonstrated by immunohistology. Neutralizing antibody to CDV was found in high titers in serum from most animals but was absent or was found only in low titers in some cats that succumbed after CDV infection. There was a marked difference in neutralizing antibody titers when tests were done with different strains of CDV.

Pathogenicity of morbilliviruses for terrestrial carnivores

Many different species of the order Carnivora are susceptible to canine distemper and the mortality rate varies greatly between species. Ailuridae, Canidae, Hyaenidae, Mustelidae, Procyonidae, Ursidae, Viverridae and now Felidae have been reported to be susceptible to canine distemper virus infection. Although distemper outbreaks in dogs, fur farms and in zoo carnivores have been greatly reduced in recent years due to vaccination, there are still regular outbreaks in free-living carnivores. Unexpected outbreaks of canine distemper have occurred in exotic felids in a California wildlife park and in the Serengeti in Tanzania as well as in javelinas (collared peccaries, Tayassu tajacu) in Arizona. Although safe and efficacious in dogs, modified live canine distemper virus vaccines may be dangerous for a variety of zoo and wildlife carnivores, especially red pandas (Ailurus fulgens) and black footed ferrets (Mustela nigripes).

Climate extremes promote fatal co-infections during canine distemper epidemics in African lions.

Extreme climatic conditions may alter historic host-pathogen relationships and synchronize the temporal and spatial convergence of multiple infectious agents, triggering epidemics with far greater mortality than those due to single pathogens. Here we present the first data to clearly illustrate how climate extremes can promote a complex interplay between epidemic and endemic pathogens that are normally tolerated in isolation, but with co-infection, result in catastrophic mortality. A 1994 canine distemper virus (CDV) epidemic in Serengeti lions (Panthera leo) coincided with the death of a third of the population, and a second high-mortality CDV epidemic struck the nearby Ngorongoro Crater lion population in 2001. The extent of adult mortalities was unusual for CDV and prompted an investigation into contributing factors. Serological analyses indicated that at least five “silent” CDV epidemics swept through the same two lion populations between 1976 and 2006 without clinical signs or measurable mortality, indicating that CDV was not necessarily fatal. Clinical and pathology findings suggested that hemoparsitism was a major contributing factor during fatal epidemics. Using quantitative real-time PCR, we measured the magnitude of hemoparasite infections in these populations over 22 years and demonstrated significantly higher levels of Babesia during the 1994 and 2001 epidemics. Babesia levels correlated with mortalities and extent of CDV exposure within prides. The common event preceding the two high mortality CDV outbreaks was extreme drought conditions with wide-spread herbivore die-offs, most notably of Cape buffalo (Syncerus caffer). As a consequence of high tick numbers after the resumption of rains and 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.

Canine distemper encephalomyelitis: Variation with virus strain

Disease induced by 3 virulent strains of Canine Distemper Virus (CDV) was compared in specific pathogen-free Beagle dogs. All strains produced an encephalomyelitis but variation was observed in the severity, clinical course and resulting neuropathology. Infection with Snyder Hill strain of CDV was consistently acute; dogs either succumbed 14 to 19 days post-inoculation (PI) or recovered. Lesions in the neuraxis were those of a polioencephalomyelitis. In contrast, CDV strain A75-17 produced subacute to chronic disease in which demyelination was the predominant finding. Some dogs succumbed, generally around 28 to 42 days PI. Total recovery was again recorded for some members of the group. Others developed persistent central nervous system (CNS) infection but remained clinically stable until electively killed with barbiturate, up to 62 days PI. CDV strain R252 also induced delayed, predominantly white matter disease with a mixed pattern of mortalities, persistent infections and recoveries, similar to A75-17. Neutralizing antibody responses correlated with the disease course. Dogs which died had low serum titres or lacked serum antibody. Recovering dogs had the earliest and highest titres. A few dogs with persistent CNS infection had antibody in the cerebrospinal fluid also. Current concepts of the pathogenesis of canine distemper encephalomyelitis (CDE) are discussed and a basis for the strain-dependent clinical and pathological expression of CDE is proposed. Viral strain appears to be an important factor in this common disease of the canine CNS.

Early events in canine distemper demyelinating encephalomyelitis

SummaryThe early neuropathological development of demyelinating Canine Distemper Encephalomyelitis (CDE) was studied in SPF dogs. Neural tissues were examined up to 30 days post infection (PI). Three phases of activity were observed. The primary event (first observed 8 days PI) was a nonsuppurative encephalomyelitis associated with the initiation of central nervous system (CNS) infection by virus-laden lymphocytes. At 24 days PI noninflammatory demyelination occurred in well defined, subependymal foci. Cell fusion and syncytia formation accompanied this early demyelination. The third phase, found at day 30 PI in one dog showing signs of recovery, was a second wave of nonsuppurative inflammation. The initial encephalomyelitis was widely disseminated throughout the CNS but subsequent demyelination appeared to be initiated from within the ventricular system. Myelin was phagocytosed by endogeneous CNS macrophages often infected with Canine Distemper Virus (CDV). The possible importance of viral induced cell fusion as well as immune factors in the mechanism of demyelination are discussed.

Status of Borrelia burgdorferi infection after antibiotic treatment and the effects of corticosteroids: an experimental study.

Sixteen specific-pathogen-free beagles were infected with Borrelia burgdorferi. Three groups of 4 dogs were treated with antibiotics for 30 consecutive days starting 120 days after tick exposure; 4 dogs were untreated controls. At day 420 after tick exposure and again before euthanasia, 2 dogs of each group were treated with prednisone for 14 days. All dogs contracted infection and 11 developed acute arthritis 50-120 days after exposure. After day 120, one of 12 antibiotic-treated dogs and 2 of 4 untreated dogs became lame. Antibiotic therapy reduced the frequency of Borrelia-positivity in subsequent skin biopsy samples. After prednisone treatment, both control dogs developed severe polyarthritis. At euthanasia, single tissues of the antibiotic-treated dogs and multiple tissues of all control dogs were Borrelia-positive by polymerase chain reaction. Viable spirochetes were not recovered from antibiotic-treated dogs. Two antibiotic-treated dogs showed histologic evidence of minimal lesions, whereas all control dogs had mild polyarthritis with periarteritis.

Factor VIII-related Antigen in Canine Endothelial Neoplasms: An Immunohistochemical Study

Canine vascular tumors (47 hemangiomas, 36 hemangiosarcomas) were investigated for the endothelial cell marker factor VIII-related antigen (F VIII RAg). The primary antibody was a commercial rabbit anti-human (r/h) F VIII RAg antiserum. All (100%) hemangiomas and 32 (89%) of 36 hemangiosarcomas stained for F VIII RAg. One hemangiosarcoma (3%) was negative, and three tumors (8%) were equivocal in staining. Rarely, the interpretation of stained immature endothelial cells was difficult. The r/h F VIII RAg antibody was a positive marker of normal, reactive, and neoplastic endothelial cells in the dog.

Necrotizing Meningoencephalitis of Maltese Dogs

The clinical and pathologic features of five young Maltese dogs with a necrotizing meningoencephalitis were studied and compared with published reports of the necrotizing meningoencephalitis of Pug dogs. The ages of the Maltese dogs ranged from 9 months to 4 years. Four dogs were male, and one was female. The dogs had a history of seizures with or without other neurologic signs for 3 days to 20 weeks prior to death. Cerebrospinal fluid examination in three dogs revealed a pleocytosis and elevated levels of protein. At necropsy, the cerebrum was asymmetrically swollen in four dogs, with a loss of distinction between the gray and white matter and mild to moderate asymmetrical dilation of the lateral ventricles. Histologically, there was extensive necrosis and nonsuppurative inflammation of the cerebral gray and white matter, overlying meninges, and adjacent thalamus and hippocampus. The 4-year-old dog had the longest duration of clinical signs and had little inflammation but extensive atrophy of affected areas, with astrocytosis. The clinical course and pathologic changes in these Maltese dogs are indistinguishable from those in reported cases of necrotizing meningoencephalitis of Pug dogs, indicating that this lesion is probably not unique to Pug dogs.

Canine distemper virus infection and encephalitis in javelinas (collared peccaries)

SummaryCanine distemper virus has been isolated in dog lymphocyte cultures from the brains of three javelinas that became moribund with signs of encephalitis. Canine distemper viral antigen was demonstrated predominantly in neurons and morbillivirus-like structures were seen by electron microscopy in brains of diseased animals. Serological studies suggest that CDV infection may be common in javelinas.