Although the name Chikungunya was only coined in 1954 together with the first identification of the virus, epidemics of what was almost certainly the disease have been described since 1789. Considerable confusion has arisen in the past between Chikungunya and Dengue due to their somewhat similar clinical picture. Human Chikungunya infection is characterised by major epidemics interspersed with long periods of either none or only sporadic cases. Major epidemics can be as long as 20 years apart. The initial epidemic starts within populations of baboons and monkeys, the virus being transmitted by the Aedes furcifer-taylori mosquito. Humans are next infected. These early human infections result from encounters with infected Aedes furcifer- taylori mosquitoes usually near the sleeping areas of baboons, which are the natural hosts of the mosquito. The infected human contact developes a viremia which may be transmitted to any house mosquito usually Aedes aegypti. As the Aedes aegypti mosquito may feed from a number of hosts large epidemics soon follow. The typical acute attack is a viral type disease but with severe joint pains. In a retrospective study 88% recovered fully, but 3,7% still had occasional stiffness and mild discomfort 3-5 years later, 2,8% had continual stiffness and 5,6% persistent joint pains. Chikungunya has been claimed to cause a haemorrhagic fever but the bleeding tendency is very mild and seriously ill cases with shock were probably due to a combined infection with dengue. Epidemiological studies have shown that nearly twice the number of rheumatic complaints occurred in respondents with anti-Chikungunya antibodies than in those without. Nevertheless the prevalence of rheumatoid arthritis in these studies was very low, indicating that it is unlikely that Chikungunya infection could go on to cause a rheumatoid-like disease. Only two cases of destructive joint disease could be found that had developed from an almost certain Chikungunya infection. Despite the lack of destructive arthropathies noted in the epidemiological studies the morbidity from Chikungunya was significant. Nearly twice the number of rheumatic complaints were reported in respondents with anti-Chikungunya antibodies as in the general population. The arthritis appeared to consist more of arthralgias and stiffness rather than an inflammatory arthritis. The etiology of osteoarthritis is unknown but some workers have claimed that short lived inflammatory disease including infections may in some way damage joint cartilage and predispose to the later development of osteoarthritis. In this study there was significantly more osteoarthritis in respondents that were Chikungunya positive than those that were negative in the 30 to 40 age groups. In older groups this difference was lost. The reason for some patients recovering fully and rapidly and others developing a chronic arthritis following Chikungunya arthritis is unknown. Genetic factors may well play a roll. Tissue typing of patients with chronic joint symptoms has shown a significantly increased frequency of the DR7 antigen, and a negative correlation with the DR2 antigen. To date the therapy of the chronic arthritic symptoms of Chikungunya has proved difficult. An open pilot trial of chloroquine was undertaken which showed that it is probably effective in treating these chronic symptoms. Primate studies have shown that the baboon develops antibodies against Chikungunya but does not develop clinical symptoms. Arthroscopic studies of the knees of baboons infected with Chikungunya showed no arthritic changes. The baboon would appear to be an unsuitable model for further Chikungunya studies, but a model of chronic arthritis has been developed in the rabbit.
|Subject||Medical sciences: Diseases|
|Subject 2||Medical sciences: Diseases|
|Degree Type||Doctoral degree|