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Host range & prevalence
Although CDV was initially described as an infectious disease of domestic dogs, it has increasingly become known as a worldwide multi-host pathogen, infecting a wide range of carnivores (Beineke et al., 2015). Its ability to infect multiple species has led to mass mortalities in a range of carnivore species from wild canids, to felids, hyaenids, procyonids, ailurids, ursids, mustelids and viverrids. Distemper outbreaks have also been reported in marine mammals, including Baikal and Caspian seals (Kennedy et al., 2000; Mamaev, 1995), with the viral strains likely originating from terrestrial carnivores (Forsyth et al., 1998). More recently CDV was reported in non-human primates (rhesus monkey (Macaca mulatta) and cynomolgus macaques (Macaca fascicularis)) with high mortality rates (Qiu, 2011; Sun et al., 2010). Infections in these primates have raised several concerns of a potential zoonotic risk of CDV in humans. There are, however, no known reports of CDV infecting humans. Speculations regarding the potential adaptation of CDV to infect humans are outside the scope of this review and readers are referred to a review by Cosby (2012).
Reports of CDV outbreaks in large felids such as lions (Panthera leo), leopards (Panthera pardus) and tigers (Panthera tigris), have challenged the belief that the Felidae group of animals is resistant to CDV infection (Appel et al., 1994; Guiserix et al., 2007; Harder et al., 1996; Roelke-Parker et al., 1996; Seimon et al., 2013). When experimentally exposed to a highly virulent strain of CDV (Appel et al., 1974) or inoculated with homogenized tissues from a dead leopard infected with CDV (Harder et al., 1996), domestic cats (Felis catus) were seropositive with no signs of clinical disease or viral shedding (Ikeda et al., 2001).
Recent studies on the seroprevalence of captive and free-ranging cheetah (Acinonyx jubatus) from Namibia to several viral pathogens have shown that cheetah are able to be infected by CDV (seropositive) but, similar to domestic cats, do not show clinical signs (Munson et al., 2004; Thalwitzer et al., 2010). The last decade has seen numerous CDV outbreaks in various wildlife species worldwide. Outbreaks were confirmed in critically endangered species such as the Ethiopian wolf (Canis simensis), and Amur tiger (Panthera tigris altaica) (Gordon et al., 2015; Seimon et al., 2013). Concern for the conservation efforts of the giant panda (Ailuropoda melanoleuca) in China has also been raised due to several recent reports of CDV induced mortality in captive populations (Feng et al., 2016; Hvistendahl, 2015). These outbreaks have highlighted the lack of knowledge on the extent of CDV susceptibility in wildlife species. This is even more evident for African wildlife with most studies originating from Tanzania, Kenya and Botswana. The CDV epidemic of 1994 that spread through the Serengeti National Park, Tanzania, is probably the best known of all, killing one-third of the lion (Panthera leo) population and causing deaths in several other species such as bat-eared fox (Otocyon megalotis), African wild dog (Lycaon pictus), silver-backed jackal (Canis mesomelas) and spotted hyena (Crocuta crocuta) (Roelke-Parker et al., 1996). More recently CDV outbreaks occurred in several reserves within South Africa. Canine distemper in a lion population on a privately owned nature reserve in the Waterberg in December 2015 resulted in 95% mortality. This outbreak also infected other carnivore species, resulting in the first reported case of CDV mortality in an endangered brown hyena (Hyaena brunnea). Four months later the devastating effect of CDV was also observed in African wild dog populations of Kruger National Park and Tswalu Kalahari Reserve, South Africa, with the total eradication of two packs (26 animals in total).
Transmission & stability
Canine distemper is highly contagious and is readily transmitted between susceptible hosts through contact or aerosolized oral, respiratory and ocular fluids and exudates containing the pathogen. During the acute phase of infection other body excretions and secretions (e.g. urine, faeces, skin) can also contain the virus (Greene & Appel, 1990; Williams, 2001). Viral shedding may follow infection for up to 90 days and occurs even if the animal was subclinically infected (Appel, 1987; Greene & Appel, 1990). Canine distemper virus is extremely sensitive to UV radiation, heat, desiccation, oxidising agents, detergents and lipid solvents (Kingsbury et al., 1978). At room temperature the virus is short lived, surviving between 20 minutes and 3 hours in tissues and exudates. Although the virus is able to survive for several days at temperatures below zero if protected by organic material (Greene & Appel, 1984), transmission of CDV is largely dependent on the close association between affected and susceptible animals. To sustain an epidemic of CD, dense populations of susceptible individuals and the continued presence of a biological reservoir are required (Alexander et al., 2010; Williams, 2001). Owing to their wide distribution, domestic dogs (Canis familiaris) are key reservoirs for a variety of diseases and are considered as the primary reservoir for CDV infection (Alexander et al., 2010; Berentsen et al., 2013; Cleaveland et al., 2000; Flacke et al., 2013; Laurenson et al., 1997). Domestic dogs, from communities surrounding protected wildlife areas are often unvaccinated and occur in high densities with a rapid population turnover. These and wildlife come into contact as both may wander several kilometers in and out of the protected areas (Butler et al., 2004) increasing the risk of disease transmission, especially if these areas are unfenced. This risk of disease transmission between domestic dogs and wildlife is further augmented by a general lack of vaccination programs, particularly in rural areas. Pathogen maintenance in the system is further increased through interspecies transmission of CDV in a wide variety of hosts (Alexander et al., 2010). Interactions among potential vectors of CDV, such as jackal, hyenas and lions at kills provide a potential mechanism for subsequent cross-species transmission (Cleaveland et al., 2000). The amount of effort necessary to either prevent an epidemic or to eliminate an infection from a population could be determined by calculating the basic
reproductive number (R0), an estimation of the number of secondary infections resulting from one infected individual (Dietz 1993, Dantzler et al., 2016). This estimate may vary considerably for different populations infected as R0 is influenced by several factors such as the duration of the infectious period, the probability of infection during contact and the number of susceptible individuals contacted per unit of time (Dietz 1993).
CHAPTER I: Advances in canine distemper virus (CDV) pathogenesis research: a wildlife perspective
1. General introduction
2. Viral properties
3. Epidemiology
4. Pathogenesis
5. Diagnosis
6. Treatment & control
7. Conclusion
CHAPTER II: Genome sequences of three vaccine strains and two wild-type canine distemper virus strains from a recent disease outbreak in South Africa
CHAPTER III: Molecular phylogenetic analysis of canine distemper virus in South African wildlife
1. Introduction
2. Materials & Methods
3. Results
4. Discussion
CHAPTER IV: The role of Toll-like receptor polymorphisms in susceptibility to canine distemper virus
1. Introduction
2. Materials & Methods
3. Results
4. Discussion
5. Conclusion
CHAPTER V: General conclusion
REFERENCES
