antibodies is weak. Parasite DNA is detectable by dot-blot hybridisation using a radio-
labelled probe consisting of 340 bases from repetitive sequences of the parasite genome.
Parasite antibodies are detectable by the ELISA technique using a mixture of three
monoclonal antibodies against a 89 kDa secreted component of the adult worm.n 7.5.4SCHISTOSOMASPP
The life-cycle and basic biology of the schistosomes is described in section 4.8.1. The dis-
ease caused by these parasites is known as bilharzia, named after the person who first
described this disease. The adult stages of S. mansonican be easily maintained in labora-
tory mice and primates and the larval stages in the snail Biomphalaria glabrata.
An important aspect of the understanding of how this parasite is able to avoid the host’s
response has come about via the surgical transplanting of adult worms from mice to
monkeys. If the worms were transferred from a mouse to a monkey they survived, but
if the monkey was sensitised/immunised against mouse proteins the parasites did not sur-
vive. This implied that the parasite had somehow or other acquired host antigens/pro-
teins onto its tegument. Hence the monkey’s immune system recognised the worms
as mouse tissue. The monkey had been immunised to be anti-mouse and hence rejected
the worms.
From the above series of experiments it was deduced that during a primary infection
it takes the host about 7+days for the mouse to develop an adaptive immune response
involving the production of anti-worm antibodies and sensitised immune cells. During
this period the parasite has sufficient time to absorb host proteins onto its tegument
which provide the parasite with a molecular disguise. Thus it is not recognised as foreign
by the adaptive immune system. The parasites from the primary infection survive but the
host is now primed/sensitised and should there be a secondary infection the host is now
able to mount a more rapid attack on the parasite and is apparently able to destroy most
of the secondary invaders.
This system from the parasite’s point of view prevents the host from becoming over-
crowded and as a result both the host and the parasite are able to survive. The host
is partially protected or immunised by having a live parasite, a condition known as
non-sterile immunity. The type of immune response centres round the production of
antibodies against adult worm antigens.
However the surviving parasites mature and eventually produce eggs which pass out
of the host via the faeces. Some of these eggs migrate to the liver where they stimulate
a cell-mediated immune response leading to the formation of a granuloma (see sec-
tion 7.5). If soluble extracts of the egg (soluble egg antigen) is introduced into the hepatic
tissue, a cell-mediated response is invoked as well as the formation of granulomas. This
indicates that egg antigen and adult worm antigen are different, each provoking a different
type of immune response.
Egg granulomas cause a certain amount of damage and malfunctioning of certain
aspects of the liver, for instance interference in bile production and the destruction of
hepatic tissue which is replaced with collagen and fibrin to form scar tissue. The patho-
logy of the type just described is a result of the host’s immune response and is often
referred to as immunopathology.n 7.5.5SCHISTOSOMA MANSONI, S. JAPONICUMAND
S. INTERCALATUM
The adults of these three species of Schistosomaare found in the portal and mesenteric
blood vessels. Once the cercariae have made contact with the skin they begin to penet-PARASITOLOGY
Praziquantel at a dose of
40 mg/kg body weight
is highly effective
against most pathogenic
trematodes. Treatment
also appears to reverse
parasite gall bladder
abnormalities as
observed by
ultrasonagraphy.
The disease bilharzia
(schistosomiasis) is
caused by the trematode
parasite Schistosoma
spp. Urinary
schistosomiasis
is caused by S.
haematobiumand bowel
schistosomiasis by S.
mansoni, S. japonicum
and S. intercalatum.