Haemoglobin and met-haemoglobin as endogenous toxins

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AN INTRODUCTION TO CANINE BABESIOSIS

Canine babesiosis is a tick-borne disease caused by haemoprotozoan parasites of the genus Babesia128, named after Dr Victor Babes, who in 1887 established the aetiology of the cattle disease in Romania. The first report of canine babesiosis was in South Africa in 1885 by Hutcheon . The parasites were only recognised by Purvis and Koch, in 1896 and 1897, respectively, and Spreull successfully transmitted the disease in 189925 ,195. Babesiosis primarily affects erythrocytes but can involve multiple organs and can range from a relatively mild to a fatal peracute disease ,202. Although haemolytic anaemia is the hallmark of infection, numerous variations and complications can occur125.

CAUSATIVE AGENT

The parasites Babesia canis and B. gibsoni (phylum Apicomplexa) are responsible for canine babesiosis throughout the world. Babesia canis was previously described as a group of three biologically different subspecies, namely B. c. canis, B. c. vogeJi, and B, c. rossf16, which has been confirmed with PCR using restriction fragment length polymorphism analysis ,55. Using a phylogenetiC approach the three subspecies of B. canis belong to the clade of Babesia species sensu stricto where B. c. canis clusters with B. c. ross; whereas B. c. vogeJi may form a monophyletic group with B. divergens and B. odocoilepa, The proposed name for this group is the Babesids . Recently a B. canis was identified from a cat, which on PCR sequences of the internal transcribed and 5.8S rRNA regions of the ribosomal operon used for sub-speciation of B. canis was markedly different from the three recognized subspecies of B. canis12. This novel feline genotype of B. canis has been proposed to be a new subspecies, named B. canis subspp. presentil’12.
The small babesias in dogs are generally considered to be Babesia gibsonf6 ,202 and using peR, this group has been further subdivided into 2 subspecies: the North American and Asian subspecies230 . However, in one dog naturally infected with a small Babesia, it was shown that it was distantly related to B. gibsoni, but more closely related to B. microN, B. rodhaini, and Theileria equp9. It is therefore likely that the small Babesia fauna occurring in dogs is more diverse than has been assumed so far.
Babesia c. canis is found in Europe, B. c. vogeli in northern Africa, North America and South Africa131 and B. c. rossi in southern Africa 131,202,216. The pear-shaped trophozoite of B. canis measures 4-5 IJm long and is usually found in pairs within the erythrocyte, but up to eight or more may be present26 ,202. In comparison, B. gibsoni is much smaller; is round to oval in shape; measures 3 IJm long; and is found in Asia, Australia, North America and northern and eastern Africa26,96,150,202.
Schizogony occurs in the gut epithelial cells of the adult tick and results in the formation of large merozoites. The merozoites then undergo successive cycles of schizogony within various cell types, including oocytes. In the salivary glands, schizogony results in the formation of small, infective sporozoites. After the tick has attached to a canine host and feeds, sporozoites in the tick’s saliva enter canine erythrocytes with the aid of a specialized apical complex. Once inside the erythrocyte, the merozoite transforms into a trophozoite, from which additional merozoites develop by a process of merogony. These merozoites leave the cell to enter other erythrocytes. Trans-ovarial transmission can occur30 , and it is believed that ticks can remain infective for several generations195

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EPIDEMIOLOGY

Babesiosis is solely a tick-borne disease, with B. c. canis being transmitted by Dermacentor reticulatus, B. c. vogeli and B. gibson; by Rhipicephalus sanguineus, and B. c. rossi by Haemaphysalis leachf6 ,202,216. In experimental studies, Hyalomma marginatum and Dermacentor andersoni have been shown to transmit B. canis216.Babesia canis can infect dogs of all ages, although in a survey from the Onderstepoort Veterinary Academic Hospital (OVAH), 77% of infected dogs were younger than 3 years of age220. Other canids (e.g., wild dogs, jackals, and wolves) are also susceptible26. A seasonal variation in the number of cases has been reported at the OVAH186, with a higher incidence in the summer months (September to April in South Africa) and peaking in November. This seasonal variation has also been described in North America, with most cases of babesiosis occurring between March and October113 The source of infection is either carrier ticks or ticks feeding on dogs that are sick or are incubating the disease and then feeding on a susceptible dog26. Other possible sources of infection are carrier dogs and blood transfusions26.113.202.
According to reports, seroprevalence of B. canis in greyhounds from the southeastern United States is higher than that of the general pet population203. In California, up to 13% of dogs in animal shelters are seropositive to B. canis and 3% positive to B. gibsonf26. These dogs ould act as reservoirs for the disease203.

PATHOGENESIS

The inCUbation period following tick exposure is 10-21 days26. Dogs experimentally inoculated with B. canis-infected blood showed transient parasitaemia on Day 1 after inoculation. Organisms then disappeared from peripheral blood for about 10 days. A second more intensive parasitaemia developed after 2 weeks and peaked around Day 20 after inoculation26.

Declaration
Abstract
Index
Acknowledgements
Chapter 1 Overview of canine babesiosis  Research focus of this thesis
Chapter 2 Renal changes
Chapter 3 Haemoglobin and met-haemoglobin as endogenous toxins
Chapter 4 Cardiac changes
Chapter 5 Cardiac pathology
Chapter 6 Serum protein response
Chapter 7 Conclusions
References
Appendix
Scientific publications connected with this thesis

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