dc.description.abstract | Hydatidosis (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 |