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The Babesiosis disease in dogs and the B. canis parasite 

Introduction

Babesia is a genus of intra- erythrocytic protozoan parasites which conducts a parasitosic symbiotic relationship with its host, causing the tick- born Babesiosis disease in domestic animals (Julius P. Kreier, 1981; Charles M. Hendrix et al., 2006), of which anaemia is the major outcome (G.M. Urquhart et al., 1996). The Babesia parasite is transferred to its host by bites from infected ticks, functioning as the parasite's vector.

This essay will focus on B. canis: species associated with the Babesiosis disease in canines. Investigations concerning vast global cattle deaths held by Bapis (1892) and Smith and Kilborne (1893), led to the discovery and definition of Babesiosis as an epizootic hemoglobinuria cattle disease; caused by a protozoan agent using ticks as its transition vector (John W. Davis et al., 1971). These findings constituted a land-mark in the field of parasitology: the first to demonstrate the possibility of a protozoan parasite being transmittable to its mammalian host by an arthropod vector. Subsequent reports of mammals infected with the parasites, in respect to the distribution of the tick vector, have been documented globally (Julius P. et al.,1981). B. canis is specifically found in Southern Europe, Africa, Asia, USA, central and South America (G.M. Urquhart et al.,1996) and  is listed as a high risk exotic disease in the DACTARI and in the Pet Travel Schemes. (DACTARI Scheme).    

B. canis; a protozoan parasite

Babesia is a hetroxenous protozoan parasite, member of the Babesiidae family, suborder Piroplasmorina of the phylum Apicomplexa. These single- cell eukaryote organisms, known for their harmful photogenic effects on domesticated animals, are found mainly in vertebrates' erythrocytes. As a result of erythtophagocytosis they can also be found in endothelial liver or lungs cells (E.J.L. Soulsby, 1982). Reproduction intricates in both sexual and asexual manners, taking place in the invertebrate host- commonly an Ixodidae tick. (G.M. Urquhart et al.,1996; DACTARI Scheme). The canis specie presents a large pyriform shape: 4-5 μm long and 2.5-3 μm wide, often with a vacuole containing cytoplasm (Julius P et al.,1981, G.M. Urquhart et al.,1996). Pairs of pyriform forms typically lie with their pointed ends adjacent (E.J.L. Soulsby,1982;Norman D. Levine, 1985). There are three subspecies within the canis specie: canis, rossi, and vogeli; each having a specific vector and degree of virulence (G.M. Urquhart et al.,1996;DACTARI Scheme). The vector- an Ixodidae tickAs a tick-born parasite, B. canis infects the dog using ixodiae ticks as intermediate hosts.

Ticks are ectoparasites of the Arachnida class, order Acarina, and are obligatory bloodsuckers of vertebrate's hosts; ticks have an important position due to their duel activities as disease vectors and pathogenic organisms. The Ixodidae family is characterised by a chitinous scutum on the dorsal surface; usually living outside they attach themselves to passing hosts. Transovarial transmission, in which the parasites pass to the next generation of ticks by infecting the female progeny ovaries (Dwight D et al.,1995), enables ticks to serve as vector for parasite diseases. The predominant strains of the B. canis are Rhipcephalus sanguineus and Dermacentor marginatus (Julius P et al.,1981), which will generally be found when given a suitable host, temperature and humidity. 

B. canis infection and life cycle 

The complex life cycle of the B. canis comprises three sequential stages, which are amalgamated with the ticks' life cycle. In the Schizogony asexual stage the infective Sporozoites, which migrate to the tick's salivary glands, are injected into the dog's intestinal erythrocytes; liver; spleen; lymph nodes; and muscles during the tick's feed. In the erythrocytes, asexual fission occurs, giving rise to Merozoites that will rupture on release and invade new erythrocytes, where they produce further generations. The final generation form Telomerozoites that will mature and reform to create male and female gametocytes. In the next ticks' feed infected erythrocytes are injected into the tick's gut where the majority of the Telomerozoites are destroyed; the survivors undergo sexual phase- Gamogony. Gametocytes fuse to a vacuole-containing zygote and formation of motile club-shaped vermicules takes place. Next, the vermicules release and migrate to various tissues of the tick, including the salivary glands where they multiply asexually and mature to become infectious sporozites; these invade the dog in the tick's next feed. The infectious parasite perpetuates itself throughout generations of ticks via transovarian transmission; multiple fissions of the parasite inside the prone- to -hatch larva results in infected hatching tick's larvae. The nymph experiencing its first feed, and infectious sporozites in the saliva gland invading the host erythrocytes, perpetuates the life cycle (G.M. Urquhart et al.,1996; E.J.L. Soulsby, 1982; Jay R. Georgi et al.,1992).           

Babesioisis

Babesioisis is characterised by variety and severity of symptoms, depending on factors such as the virulence of the parasite strain; intensity of infection; abundance of ticks; immunity and resistance of the dog; presence of other diseases; and stress. The corephysiological mechanism of the b. canis is the destruction of erythrocytes resulting in hemoglobin loss in the blood stream. With changes in the chronice and acute profiles, clinical and diagnostic signs will include hemolytic anemia; hemoglobinemia and hemoglobinuria; fever; increased respiratory rate; anorexia; diarrhea; yellow faeces;  vomiting; progressively reluctant locomotion and overall debility. Late diagnosis and untreated cases may lead to death, as a consequence of the reduced ability of the blood to carry oxygen. Diagnosis will often be provisional based on the typified fever and anemia signs combined with epizootiological factors rather than blood examination, since presence of the parasite is unlikely to show in infected blood ( E.J.L. Soulsby, 1982; John W. Davis et al., 1971; Jay R. Georgi et al.,1992).Babesiosis is best treated with chemotherapy, optimally given proximate to the diagnosis. Treatment in early stages of the disease can bring an arrest within 24 hours; in severe cases supportive treatment is the main option. Drugs commonly used are Trypan blue and Acaprin (E.J.L. Soulsby, 1982; John W. Davis et al., 1971; Julius P. Kreier, 1981) . Prevention and control of Babesiosis is primarily carried out through elimination of the vector via regular tick control programmes and application of chemical acaricides on the dog; additionally a new 6 month vaccine is now available in Europe (DACTARI Scheme). Emphasis must be on control measures for dogs newly introduced to endemic areas, however native dogs are generally passively immune due to maternal colostrum transmission of antibodies (E.J.L. Soulsby, 1982; John W. Davis et al.,1971; Julius P. Kreier, 1981).     

Summary

In the UK, Babesiosis is ascribed to as a scarce disease and for now doesn’t currently constitute a probable hazard to UK dogs. As such, the danger of mal diagnosis is fairly high, leading to unsuitable treatment and possible death. Therefore, reinforcement of the local veterinarians' education regarding risks and the probability of patient infection is of high importance, alongside with research into this exotic disease. This improvement in veterinarian awareness together with pet owner's cooperation, including appropriate pre- travel treatment, will help control and constrain incidents of Babesiosis keeping the B. canis a rare parasite; and avoiding the possibility of it transforming to an  invasive species in the U.K.