The Brown Dog Tick Biology Essay

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Ehrlichia canis is one cause of the disease- monocytic ehrlichiosis, a disease that affects dogs worldwide (Edward B. Breitschwerdt, 1997). The family (Ehrlichiae) are a group of gram-negative, obligative cocci that are intracellular and infect both humans and canines (Lauren Bockino, et al., 2003).

The brown dog tick, Rhipicephalus sanguineous, is the vector by which the bacteria pass from one individual to another. Infection occurs via the salivary secretions at the site where the tick bites the dog during feeding (Lauren Bockino, et al., 2003). The tick becomes infected with either the larvae or nymph form of the bacteria and then passes it on to another dog as either an adult or a nymph (Lauren Bockino, et al., 2003). If a tick feeds on a dog within the acute phase of infection, then the tick is potentially able to infect other dogs for 155 days following detachment (Ettinger SJ, 2000).

The entire lifecycle of Ehrlicia is not fully understood, however it is thought to occur in three intracellular forms (Lauren Bockino, et al., 2003). The first being a very small spherical bodies, 1-2 micrometres in diameter, which develop into morulae. Morulae are large membrane-bound bodies within the cytoplasm of the leukocyte (Lauren Bockino, et al., 2003). These morulae then dissociate to form small granules called elementary bodies (Lauren Bockino, et al., 2003).

Ehrlicia has an incubation time of between 8 and 10 days, afterwhich the acute phase of infection occurs and this lasts up to 4 weeks (Lauren Bockino, et al., 2003). During this time, the Ehrlichia multiplies within the leukocytes in the blood stream and the mononuclear phagocytes in the liver, spleen and lymph nodes (Lauren Bockino, et al., 2003). The infected cells circulate in the blood stream and adhere to the vascular endothelium causing vasculitis and subendothelial tissue infection (Lauren Bockino, et al., 2003). Thrombocytopenia is observed at this stage, because platelets are being destroyed, and variable leukocyte counts and aneamia may also develop during the acute phase (Ettinger SJ, 2000).

If the dog is immunocompetent then it will eliminate the parasite within 9 weeks but if the dog fails to do this, it will develop parasitemia (Lauren Bockino, et al., 2003). This stage is characterised by variable persistence thrombocytopenia, leukopenia and anaemia and dogs that have an inadequate immune response will become chronically infected (Ettinger SJ, 2000).

Treatment of Ehrlicia is a course of doxycyclin for at least a month, however, there should be a dramatic improvement within the first 48 hours of treatment (Lauren Bockino, et al., 2003). Previous infection does not induce permanent immunity against Ehrlicia and dogs can become re-infected with either the same or a different Ehrlicial species (Lauren Bockino, et al., 2003). Therefore, the major control method for this disease is tick control as it is the vector of the disease and in particular preventing the tick from engorging on the dog (Lord, 2001). The dogs can be treated with fipronil (in sprays and spot-ons), amitraz (often in flea and tick collars), permethrin (sprays and shampoos) and deltamethrin (shampoos) - all of which have proven effective in preventing tick bites when applied regularly (Lord, 2001). Regular grooming of the dog will also remove any ticks that may be attached (Lord, 2001). If an infestation breaks out, thorough treatment of the dog and kennels is critical and the removed ticks should be disposed of correctly (Lord, 2001). Treatment of an infested kennel should be done by a professional pest operator as ticks tend to live in small crevices and cracks which could be missed by an inexperienced individual (Lord, 2001).

Canine Distemper Virus

Canine distemper virus is a highly contagious, systemic, viral disease that occurs globally (Merck, 2006). The clinical symptoms are fever, leukopenia, G.I. and respiratory catarrh, as well as frequent pneumonic and neurological complications (Merck, 2006). The disease is also seen in other species like foxes, wolves, ferrets and even lion (Merck, 2006) (Roelke-Parker ME, 1996).

Canine distemper virus is caused by a paramyxovirus that is very similar to the measles and rinderpest viruses (Merck, 2006). The enveloped virus does not survive well outside of the host as it is highly sensitive to most disinfectants and lipid solvents (Merck, 2006). Droplet infection is the main route of infection and infected dogs can shed the virus for several months via aerosol droplet secretions (Merck, 2006). Initially the virus replicates in the lymphatic tissue of the respiratory tract, a cell-associated viremia then results in infection of all lymphatic tissue which is followed by infection of the respiratory, G.I. and urogenital epithelium, CNS and optic nerves (Merck, 2006). Disease occurs after the virus has replicated in these tissues (Merck, 2006). The spread of the virus to other tissues in the body depends on the level of specific humoral immunity within the host during the viremic period (Merck, 2006).

Treatment involves protecting against secondary bacterial invasion (using antibiotics), maintaining a fluid balance in the dog (using electrolyte solutions) and controlling nervous manifestations (using anticonvulsants) as well as antipyretics to reduce fever (Merck, 2006). However, despite this, some dogs do not recover especially those suffering from acute neurological manifestations and these dogs are usually euthanased (Merck, 2006).

As this disease is transmitted by droplet infection, infected dogs should be quaruntined for several months due to the time taken for the animal to shed the virus (Merck, 2006). Canine distemper virus is killed by routine disinfecting of the environment as it can persist in serum or tissue debris (Hirsch, et al., 1991). The virus can only survive for a few hours at room temperature, however at lower temperatures (i.e.- just above freezing) in shady areas, it can survive for several weeks (Hurley, 2010).

Prevention of canine distemper virus is in the form of immunisation of puppies with modified live virus (MLV) vaccines, however, the success of these vaccines depends on the lack of interference by the maternal antibodies (Merck, 2006). To overcome this, puppies are vaccinated 6 weeks after birth and then every 2-4 weeks until the age of 16 weeks (Merck, 2006). As I mentioned earlier, the measles virus and the canine distemper virus are closely related and so measles virus induces immunity against canine distemper virus in the presence of high levels of maternal distemper anitbodies (Merck, 2006). Both MLV measle vaccines and a combination MLV vaccines (i.e.- a combination of MLV measles vaccine and MLV canine distemper vaccine) are available (Merck, 2006). The first vaccine should be the MLV measles vaccine and this should be followed by at least two more doses of MLV distemper vaccines between the ages of 12 and 16 weeks (Merck, 2006). In immunosuppressed dogs, postvaccinal illness can follow MLV vaccines and in such dogs annual revaccination is advised (Merck, 2006). This is because studies suggest that breaks in neurologic distemper that can occur in stressed, diseased and immunosuppressed dogs however the frequency of revaccination also depends on the prevalence of the disease (Merck, 2006).

Visceral Leishmaniasis

Visceral Leishmaniasis is a chronic, severe protozoal disease in humans, dogs and some rodents (Merck, 2011). It is characterized by lesions on the skin and mucous membranes, weight loss, lymphadenopathy, anemia, lameness, renal failure and sometimes nose bleeds (Merck, 2011). Canine leishmaniasis is a zoonoses and dogs act as a resevoir of the parasite for humans (Merck, 2011). There are nine species of sandfly that are either proven or thought to be vectors for the disease, these are all close relatives of the subgenus Larroussius, and depending on the geographical area in question (e.g.- in China, the two species are P chinensis and P alexandri) (Merck, 2011).

The parasites are transmitted as flagellate forms (promastigotes) by the bite of various species of phlebotomine sandflies, these flies do not travel far and complete their life cycle within an area of 1 kilometre in diameter (Merck, 2011). The females take in blood during feeding and this is done crepuscularly (Merck, 2011). Once inside the body, the promastigotes are engulfed by macrophages and transform into amastigotes, which do not have flagella (Merck, 2011). These amastigotes divide, in the macrophage, and spread to various organs around the body especially the bone marrow, lymph nodes, skin, spleen, liver and kidneys (Merck, 2011). There are two different mechanisms responsible for the signs and symptoms of the disease- the production of granulomatous inflammatory reactions and the formation of circulating immune complexes that are deposited in the renal glomeruli, blood vessels and joints (Merck, 2011).

Treatment is in the form of two drugs, meglumine antimonate and allopurinol, which are administered in different doses during the treatment process (Merck, 2011). In endemic areas, Leishmaniasis is controlled by rapd treatment of infected dogs, control of stray dogs and control of the sandfly vectors (Merck, 2011). Prevention of the disease is in the form of protecting dogs from being bitten by sandflies using various chemicals either on dog collars or applied onto the skin itself (Palatnik-De-Sousa C B, 2004). Use of deltamethrin collar have proven to be 86% effective against the sandflies (Richard Reithinger, 2001). At present, there is no effective vaccine against leismaniasis and treatment is expensive and often results in relapse (Merck, 2011). The only successful mode of control of the disease was by elimination (culling) of all dogs in eastern China, however this is no longer acceptable there or anywhere else (Merck, 2011). Dogs can be asymptomatic which is problematic when trying to eradicate the disease by treatment, and for this reason, culling of stray and homeless is the most effective way of controlling the disease. Owners are advised to bring their dogs inside during dusk and dawn to prevent the sandfly from biting.


I have looked at three very different modes of control of infectious disease in dogs- general cleanliness, vaccination and culling. Another obvious mode of controlling would be worming in dogs however, due to word limit, I was unable to include an example of this. In the first example, Monocytic Ehrlichiosis, the control mechanism was basic cleanliness of the dog and tick treatment as the pathogenesis of the disease is via the Brown Dog Tick vector and elimination of a bite from this vector results in fewer cases. Canine distemper virus, on the other hand, has an effective vaccination that is administered to puppies. This vaccination is mandatory in most countries and so limits the prevalence of the disease. In the third example, Visceral leishmaniasis, the only effective control mechanism is culling of infected dogs which is not an ideal solution but there are no known vaccines and treatment does not really work. Although there are a few methods that are relatively successful in preventing the infection of dogs by the sandflys, for example deltamethrin (Richard Reithinger, 2001).

By using these three infectious diseases, I have shown that an understanding of the pathogenesis of the disease will lead to development of efficient control mechanisms.