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dc.contributor.authorOmwandho, Charles A
dc.date.accessioned2013-05-12T08:45:29Z
dc.date.available2013-05-12T08:45:29Z
dc.date.issued1989
dc.identifier.citationMaster of Scienceen
dc.identifier.urihttp://erepository.uonbi.ac.ke:8080/xmlui/handle/123456789/22322
dc.description.abstractHydatidosis (hydatid disease) and echinococcosis refer to infections by the metacestode (larval) and strobilar (adult) stages of Echinococcus granulosus. The infection is a cyclozoonosis of major public health and economic importance in all the inhabited continents. Except in special cases, it is a dead end infection in man. In Kenya, hydatid disease has been reported in man, domestic and wild animals. A report by Eugster (1978) indicated that in Kajiado District alone 44.7% of cattle, 9% of sheep and 6.3% of goats had hydatid cysts. Human hydatidosis in Kenya is mainly found among the Suk in West Pokot, the Rendille, the Shangilla, the Maasai and the Turkana. Sporadic cases are known to occur' in other parts of Kenya among the Luo and Kikuyu (Okello and Kyobe 1981). Turkana District of Kenya is reported to have the highest incidence of human hydatidosis in the world and the number of patient.s seeking treatment in the DistricCls about 96 per 100,000 population annually (0' Leary 1~.76, French and Nelson 1983) . As this figure represents mainly self diagnosed cases, it underestimates the real incidence which is presumably much higher (Okello 1986). Although infection, prevalence and mortality rates due to hydatid disease may appear low in comparison with those for some other diseases, the morbidity associated with the disease is considerable and hydatid patients often requi re multiple surgical interventions. Extensive secondary hydatid disease often becomes )noperable and the involvement of bones usually requires amputation. Economic losses due to hydatidosis include the cost of hospitalization, the incapacity to do work especially after surgery and loss of life in some cases. Large amounts of livestock viscera are also condemned due to heavy infections with hydatid cysts. A large number of serological tests and their attendant problems in hydatid disease of man and animals have been described [Rickar-d 1979). These tests have suffered from lack of sensitivity, specificty or both (Yong and Heath, 1979). The serological diagnosis and sero-epidemiological studies of human hydatid disease have been based to a large extent on IIArc 511 antigen I first described by Capron et al (1967) and later "- characterized by Bout et al (1974). The sensitivity and specificity of these tests have been very poor and an , unacceptably high number of false negatives have been recorded (Okello and Chemtai 1981). Detection or .hydatid disease in livestock before slaughter is usually clinically impossible since the infected animals show no clinical signs, hence collection of epidemiological data for hydatid disease particularly to establish prevalence have mainly depended on collection of data in slaughter houses and in most cases, accurate and reliable records are not available. Both surgery and chemotherapy have been used in treatment of hydatid disease in Kenya. However, due to lack of adequate surgical facilities, late diagnosis and other complications such as the occurrence of multiple cysts in the abdomen and thorax, surgical treatment is possible in less than 50% of the cases in Turkana (Okello 1986). The recurrence rate is high among the surgically treated individuals (20% in Turkana) and many of the recurrent cases are inoperable (French 1984). Inoperable hydatidosis is thus a major problem and the need for medical treatment has long been realized: The benzimidazole carbamate group of drugs including flubendazole, mebendazole and albendazole have been used in experimental treatment of human hydatid disease. In view of the economic and public health importance of hydatidosis, there is need to investigate and fully understand the course of the disease in individuals undergoing various types of treatment such as surgery and chemotherapy. This study was undertaken to determine the effects ot albendazole therapy on serum protein levels and leucocyte counts in hydatid patients. Results indicated abnormal reduction +n serum protein concentrations on adrni s sion of patients but thi~..was found to recover over the treatment period with albendazole t"herapy. Electrophoretic studies using cellulose acetate membrane and SDS polyacrylamide gels showed a reduction in albumin and pre-albumin levels accompanied by elevated levels of IgG. In most cases (75%), albumin levels were as low as one third the amounts in normal subjects while pre-albumin was eliminated altogether from circulation at the height of infection. Determination of IgG levels using Ion Exchange Chromatography showed 2 -3 fold elevation on admission of patients but this later underwent a gradual decrease towards normal values with treatment. It was suggested that the reduction in serum protein concentrations may have resulted from impaired synthesis and release of albumin by the liver due to hydatid infection, loss of appetite observed in patients during early days post-admission, low dietary protein uptake by the patients and probably the loss of proteins in urine due to glomerulonephritis consequent to deposition of immune complexes in the kidneys of these patients. The loss of protein in urine due to glomerulonephritis was also suggested by Okello (1988). The elevation in circulating IgG in patients was thought to have resulted from its increased production aimed at combating the infection and to replace the IgG that is lost from circulation after penetrating the hydatid cyst membranes. The presence of hydatid cysts was. shown to suppress leucocyte proliferation in the patients. However, the use of albendazole led to a temporary decrease Ln,IYJl1phocyte, monocyte and neutrophil counts. This was followed by a proliferative burst .. ending with a gradual decline to normal levels in 8 out of 12 (66.6%) cases. In 2 out of 12 (16.7%) cases, there was an immediate elevation in absolute and differential leucocyte counts followed by a gradual decline while in another 2 cases, initial administration of albendazole was followed by a progressive decline in lymphocyte and neutrophil counts, accompanied by a consistent increase in monocyte and eosinophil counts throughout therapy. It is likely that the latter WPXP r-:>cn~ .- (xix) Iwhich the hydatid cysts were already undergoing regression at the beginning of therapy. Eosinophil counts were well above the normal range in 6 out of 12 (50%) cases and did not exhibit consistency in counts in response to albendazole administration. Total haemoglobin r packed cell volume and erythrocyte counts were normal in all the cases studied showing that hydatid disease is not associated with anaemia. The initial decline in leucocyte counts at the beginning of therapy is suspected to have resulted from the elimination of old leucocytes (probably defective) by albendazole. This hypothesis remains to be tested. From this study r it was concluded that chemotherapeutic use of albendazole restores serum protein concentration accompanied by polyclonal leucocyte proliferation in hydatid patients. The detailed mechanisms by which albendazole contains hydatid disease remains unclear and heeds to be investigated further.en
dc.language.isoenen
dc.publisherUniversity of Nairobien
dc.titleEffects of albendazole therapy on serum proteins and leucocyte counts in hydatid patientsen
dc.typeThesisen
local.publisherFaculty of Science. University of Nairobien


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