 |
|
|
|
||||||
|
|||||||||
 |
|||||||||
|
|
 |
|
|
|||||||||||||||||||||
Introduction The Schistosomes are blood trematodes belonging to the Phylum Platyhelmintha. They differ from other trematodes in that they have separate sexes. The schistosomes remain in copula throughout their life span, the male surrounding the female with his gynephoric canal. They require definitive and intermediate hosts to complete their life cycle. The schistosomes differ from other trematodes in that infection is acquired by penetration of cercaria through the skin. There are 3 species of Schistosomes responsible for human disease i.e.. S. mansoni and S. japonicum are responsible for intestinal shistosomiasis and S. haematobium for urinary tract schistosomiasis. S. mekongi and S. intercalatum are less common. It is the eggs and not the adult worms which are responsible for the pathology associated infections Life Cycle
Schistosoma mansoni S. mansoni occurs in West and Central Africa, Egypt, Malagasy, the Arabian Peninsula, Brazil, Surinam, Venezuela and the West Indies. The intermediate host is Biomphalaria, an aquatic snail. Morphology The ova of S.mansoni are 114-175um long by 45-68 um wide. They are light yellowish brown, elongate and possess a lateral spine. The shell is acid fast when stained with modified Ziehl-Neelsen. The eggs are often viable when passes in fresh unpreserved stool and the miracidia show flickering of an excretory flame cell. A non viable egg is dark coloured and shows no internal structural detail or flame cell movement. Eggs can become calcified after treatment and are usually smaller, appear black and often distorted with a less distinct spine. Clinical Disease
The clinical disease is related to the stage of infection, previous host exposure, worm burden and host response.
Cecarial dermatitis (swimmers itch) follows skin penetration and results in a maculopapular rash which may last 36 hours or more.
After mating, the mature flukes migrate to the venules draining the large intestine. There, eggs are laid and they
penetrate the intestinal wall. They are excreted in the faeces often accompanied by blood and mucus.
It is the eggs and not the adult worms which are responsible for the pathology associated with S. mansoni infections.
The adult flukes acquire host antigen which protects them from the host's immune response.
The host's reaction to the eggs which are lodged in the intestinal mucosa, leads to the formation of granulomata and
ulceration of the intesinal wall. Some of the eggs reach the liver via the portal vein. The granulomatous response to these
eggs can result in enlargement of the liver with fibrosis, ultimately leading to portal hypertension and ascites. The spleen
may also become enlarged. Other complications may arise as a result of deposition of the eggs in other organs e.g. lungs.
Katayama fever is associated with heavy primary infection and egg production. Clinical features include high fever,
hepatosplenomegaly, lymphadenopathy eosinophilia and dysentery. This syndrome occurs a few weeks after primary infection. Laboratory Diagnosis Microscopy
Laboratory confirmation of S. mansoni infection can be made by finding the eggs in the faeces. When eggs cannot be found in the faeces a rectal biopsy can be examined. An ovum of
Schistosoma mansoni Serology Serological tests are of value in the diagnosis of schistosomiasis when eggs cannot be found. An enzyme linked
immunosorbent assay (ELISA) using soluble egg antigen, is employed at HTD. A summary of less common intestinal Schistosoma species
An ovum of Schistosoma japonicum Schistosoma haematobium Schistosoma haematobium causes urinary schistosomiasis and occurs in Africa and the Middle East; Pathogenesis The clinical disease is related to the stage of infection, previous host exposure, worm burden and host response.
Cercarial dermatitis (Swimmer's Itch) following skin penetration, results in a maculo-papular rash and can last 36 hours or more. The mature flukes of S. haematobium
migrate to the veins surrounding the bladder. After mating, the eggs are laid in the venules of the bladder and many penetrate through the mucosa, enter the lumen of the bladder and are
excreted in the urine accompanied by blood. Thus haematuria and proteinuria are characteristic, though not invariable features of urinary schistosomiasis. As with all Schistosoma
species, it is the eggs and not the adult worms which are responsible for the pathology associated with S. haematobium. In chronic disease, eggs become trapped in the bladder wall resulting in the
formation of granulomata. Following prolonged infection, the ureters may become obstructed and the bladder becomes
thickened resulting in abnormal bladder function, urinary infection and kidney damage. Chronic urinary schistosomiasis is associated with squamous cell bladder cancer. Laboratory diagnosis
The definitive diagnosis of urinary schistosomiasis is made by finding the characteristic ova of S. haematobium
in urine. They are relatively large, measuring 110 - 170 in length and 40 - 70 in width. They have an elongated ellipsoid shape with a prominent terminal spine.
Terminal urine should be collected as the terminal drops contain a large proportion of the eggs. The urine can either be centrifuged and the deposit examined microscopically for ova or it can be
A bladder biopsy is seldom necessary to make the diagnosis. A rectal snip may show the presence of ova as they sometimes pass into the rectal mucosa.
Serological tests can be of value when eggs cannot be found in clinical samples. An enzyme linked immuno-sorbent
assay using soluble egg antigen to detect antischistosome antibody is currently used at the Hospital for Tropical Diseases. An ovum of Schistosoma haematobium
a miracidium and egg of Schistosoma haematobium on a polycarbonate filter. |
|
|
|
| [UKNEQAS Parasitology] [Nematodes] [Cestodes] [Trematodes] [Unusual Helminths] |