Canine distemper (CD) is a highly contagious infectious disease of canine and feline species caused by canine distemper virus (CDV) [6]. Canine distemper is a worldwide occurring infectious disease, caused by a morbillivirus of the family paramyxoviridae [10]. Besides canine distemper virus (CDV), the genus morbillivirus comprises measle virus, rinderpest virus, dolphin morbillivirus, pest-despetits ruminants virus, porpoise morbillivirus and phosine distemper virus [33]. Canine distemper virus is an enveloped, single stranded, negative- sense RNA virus [32], which contains six structural proteins: two membrane glycoproteins, the fusion(F) and hemagglutinin(H), the envelope –associated matrix (M) protein, the phosphoprotein(P), the large polymerase(L) and the nucleocapsid (N) protein [4]. Additional accessory genes, the C and V proteins are found mostly as extra transcriptional units, with in the P gene. The lipid envelope, surrounding the virion contains the two surface glycoproteins F and H, which mediate viral entry and exit from the host cell. Furthermore, the helical neoclocapsid core, containing the N, P, and L protein, initiates intracellular replication and is located within the envelope. The viral M protein connects the surface glycoproteins and nucleocapsid during viral maturation [25].
Host range of canine distemper virus encompasses all species of the families canidae (dog, dingo, fox, jackal, wolf), procyonidae (raccon, coatimundi, panda), mustelidae (weasel, ferret, fishers, mink, badger, marten, otter), the large members of the family felidae (lions, leopards, cheetahs, tigers) and the collared peccary (tayassu tajacu). At least seven distinct lineages of canine distemper are recognized worldwide, based on the sequence analysis of the H genes: Asia–1, Asia–2, American–1, American–2, Arctic-like, European wild life, and Europe. Additional lineage probably will be identified in the future [29]. Genetic analysis of strains causing outbreak shows that CDV does not become more virulent and spread to new host species in a region, but the same strain circulates among susceptible animals of several host species in a given geographic area [18].
CD is highly infectious and frequently lethal disease in dogs and has a high mortality rate after rabies. The disease is transmitted through aerosol and the virus has high affinity for lymphocytes and macrophages. The duration and severity of the disease depends mainly on the ability of the infected animal to quickly mount an immune response to CDV. If the serum antibody titer high level within 8–9 days of infection, the virus disappear from the lymphatic and the other tissues and the infection remains subclinical or mild. However, if the immune response is weak or delayed, the virus disseminates to many tissues causing an acute or chronic disease with high mortality [17]. Immunologically naïve populations may experience high death rates. The mortality rates due to CDV infection vary among susceptible species [3] and could be as high as 100% in ferrets [40]. Domestic dogs mortality rates will largely depends on the immune status of the animal ranging up to 50% [11]. Outbreak in Africa wild dogs have led to mortality rate up to 95% [39].
Canine distemper virus is spread by the respiratory route with initial viral replication in respiratory epithelium and alveolar macrophages [21]. The initial infection is in epithelial cells and lymphoid tissue in the nasopharynx [20]. After multiplication in regional lymph nodes, the virus enters the blood stream, where it circulates with in infected B and T-cells. Primary viremia is synchronous with the first bout of fever and virus that is spread to lymphoid tissue throughout the body, circulating gut- associated lymphoid tissues, and fixed tissue macrophages such as kuffer cells in the liver. Virions formed in these sites are carried by blood mononuclear cells during second viremia that coincides with the second peak of fever. Epithelium cells do not posses CD150 (SLAM) and the receptor that facilitates virus entry in to epithelial cells is yet to be defined [29].
Canine distemper virus may be shed in virtually all body secretions and excretions depending on the stage of infection. Transmission most commonly occurs through inhalation of air borne virus or direct contact between susceptible and actively infected dogs [3]. Fomite or environmental transmission of canine distemper virus is also possible, but the virus does not remain infectious for more than hours to a few days depending on the ambient temperature and other conditions. Fomites and environmental contamination is therefore of less importance for disease transmission than for a hardier virus such as canine parvovirus. Because the virus does not persist long in the environment, mildly affected and recovering animals plays an important role in maintaining transmission cycles in shelters [30].
In dogs, canine distemper virus infection may result in subclinical infection or clinical disease. It is estimated that 75% of the infections occur as subclinical infections. The clinical disease has been characterized by systemic signs (dermatological, respiratory and gastrointestinal) with frequent nervous disfunction [18]. A transient fever usually occurs 3–6 days after infection and there may be a leucopenia (especially lymphopenia) at this time but these signs may go unnoticed. The fever subsides for several days before a second fever occurs, which lasts < 1 weeks. This may be accompanied by serous nasal discharge, mucoprulent ocular discharge, and anorexia. Hyperkeratosis of foot pads (hard pad disease) and epithelium of the nasal plane may be seen [1]. Canine distemper virus affects both white and gray matter in the central nervous system. Thus, various neurological signs may be observed including behavioral changes, seizures, cerebellar and vestibular signs, visual deficits, paresis, paralysis, limb weakness, tremors, and myoclonus ( is a gray matter sign characterized as a rhythmic jerking of single muscle or muscle groups) [2]. Seizure and myoclonus are typically gray matter signs, while visual deficits and different motor impairment are mainly signs of white matter dysfunction [18]. Signs of leptomeningitis, such as cervical rigidity and generalized hyperesthesia, may also occur [24].
In suspected cases of distemper, a complete blood count and thoracic radiographs used to access leukocyte responses and pneumonia respectively. In dogs presenting with neurologic disease suspected to be due to CDV, routine cerebrospinal fluid (CSF) analysis carried out to distinguish CDV infection from other diseases. The presence of CDV- specific antibody in CSF can confirm the diagnosis but requires special laboratory [36]. Routine diagnosis of canine distemper virus by immunoflourescence (IF) is applied to various specimens, including conjuctival, nasal, and vaginal smears, using polyclonal or monoclonal antibodies. This tests is not sensitive and can detect canine distemper virus antigens only within 3 weeks after infection, when the virus is still present in the epithelial cells [4]. Serological methods such as ELISA and seroneutralization (SN) assays, have a little diagnostic value because high titers of antibodies to canine distemper virus may be the result of previous vaccination or subclinical or clinical infection [23]. Definitive diagnosis of canine distemper by virus isolation on canine cells is fastidious and time consuming, taking several days to weeks, notably when applied to clinical specimen [14, 37]. During life, clinical diagnosis can be confirmed by finding typical cytoplasmic and intranuclear inclusion bodies in the smears of cells of the respiratory epithelium and peripheral blood. Unfortunately, these inclusion are not present in all cases, hence their absence does not preclude the diagnosis of distemper [21]. Distemper inclusions in canine erythrocytes are irregular to round to ring shaped and stain magenta with Romanowsky and Diff-Quik stains (the inclusions may stain with other rapid blood stains). Distemper inclusions are transient [5]. These inclusions appear as homogeneous, red to purplish, red or pale blue, pleomorphic but homogeneous cytoplasmic inclusions; they are found in neutrophils, monocytes, lymphocytes and erythrocytes. They probably occur in the early viremic stage and before clinical illness [38]. RT-PCR has been applied successfully to diagnosis of canine distemper [34, 37].
Control of canine distemper virus infection is based on adequate diagnosis, quarantine, sanitation, and vaccination with attenuated canine distemper virus vaccines. The virus is very fragile, and susceptible to standard disinfectants. Thorough disinfection of premises, however, can be very challenging. For treatment, hyper immune serum or immune globulin can be used prophylactically immediately after exposure. Antibiotic therapy generally has a beneficial effect by lessening the effect of secondary opportunistic bacterial infections [29]. Canine distemper virus is monotypic virus as defined by polyclonal antisera and a single exposure to the virus normally confers long- lasting immunity in dogs. In general, the introduction of live attenuated canine distemper virus vaccines in the 1950s and their extensive use drastically reduced the incidence of the canine distemper in dogs [15]. Therefore, previous underreporting of canine distemper in Ethiopia together with its strain makes this study mandatory. The principal objectives of the present study were to assess the occurrence of canine distemper relative to other contagious infectious and non infectious disease of dogs in Addis Ababa, and to isolate and characterize CDV from clinical cases of canine distemper.