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Memórias do Instituto Oswaldo Cruz
Fundação Oswaldo Cruz, Fiocruz
ISSN: 1678-8060 EISSN: 1678-8060
Vol. 90, Num. 2, 1995, pp. 277-280
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Memorias Instituto Oswaldo Cruz, Vol.
90(2):277-280
mar./apr. 1995
Acute Human Schistosomiasis Mansoni
Ana Rabello
Centro de Pesquisas Rene Rachou - FIOCRUZ, Av. Augusto de Lima
1715, 30190 002 Belo Horizonte, MG, Brasil
Code Number: OC95054
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The acute schistosomiasis is the toxemic disease that
follow the Schistosoma cercariae active penetration
trough screen in the immunologicaly naive vertebrate host.The
clinical picture starts two to eight weeks after the first
contact with the contaminated water. Susceptible patients
present a syndrome comprising fever, diarrhea, toxemia and
hepatosplenomegaly. Diagnosis is based on epidemiological and
clinical features, presence of Schistosoma eggs in the
feces, enlargement of abdominal lymph nodes by ultrasonography
and by detection of high antibodies levels against the antigen
keyhole limpet haemocyanin. Different rates of cure have been
observed with specific medication and for the most severe
clinical presentations the use of steroids reduces the
systemic and allergic manifestations.
Key words: schistosomiasis - schistosomiasis mansoni - acute
phase
The initial phase of the Schistosoma infection
incorporates a large group of signs and symptoms which follows
the Schistosoma sp. cercariae active penetration
through skin. It comprises the pre-postural period and the
variable acute form which in the most severe presentation
corresponds to the Katayama fever of S. japonicum
infection. The acute form is a self-limiting clinical
picture resultant mainly from the underlying immune systemic
response occurring in the immunologicaly naive vertebrate
host.
The assumption that the basis of the toxemic illness of the
initial period of the Schistosoma infection is mainly
caused by a immune reaction against parasite toxins has
been accorded since the first reports of this condition in
monkeys (Fairly 1920) and humans (Dias Rivera et al. 1956,
Ferreira et al.1966). Although the acute form can be rarely
observed in re-infection (Katz & Bittencourt 1965) there is an
agreement on the fact that the susceptible organism prone to
develop a severe toxemic disease is the prime infected patient
(Dias Rivera et al.1956, Neves 1965, Ferreira et al. 1966,
Hiatt et al. 1979) and that the disease is predominantly self-
limiting, mostly benign, and invariably proceeds to
chronification (Dias Rivera et al. 1956, Neves 1965, Ferreira
et al. 1966).
Epidemiology
The incidence of the acute form of schistosomiasis mansoni is
certainly underestimated. This illness has been mainly
described as a disease of travelers. Many scientific
publications concerning this acute disease refer to groups of
tourists, fishermen or sailors originally from an non-endemic
country who have visited a tropical zone (Lunde & Ottsen 1980,
Evengard et al. 1990). However, as schistosomiasis is a
focally distributed disease (Pessoa & Amorim 1957, Kloetzel
1989), the acute form is also diagnosed in inhabitants from
endemic countries who do not live in endemic areas.
Nevertheless, acute disease is seldom recognized in infected
patients from endemic areas.
Clinical aspects
Different intensities of clinical manifestation are observed;
some patients evolve with a relatively severe picture while
others develop mild symptoms. The development of non-apparent
clinical form characterized by blood eosinophilia and a
positive immediate cutaneous reaction in the initial phase has
been described by Rocha et al. (1993).
Two to eight weeks after a first contact with natural water
infested by Schistosoma cercariae, susceptible infected
patients present a syndrome comprising a period of 2 to 30
days of fever (100%), diarrhea (94.4%), toxemia and weakness
(62%), weight loss (50%), abdominal pain (55.5%), cough
(66.7%), myalgia and arthralgia (61.1%), edema (50%),
urticaria (44.4%), nausea and vomiting (28.8%) and
hepatosplenomegaly the patients sought physician and/or
hospital (Rabello et al. 1995). The clinical findings
associated with the acute disease may be confounded with a
number of infections such as visceral leishmaniasis, typhoid
fever, malaria, miliary tuberculosis, viral hepatitis,
mononucleosis and bacterial infections (Neves 1986, Chapman et
al.1988).
Recent analysis of a group of 25 individuals simultaneously
exposed to S. mansoni cercariae showed that morbidity
(measured by the clinical-sonographic index) is more severe in
children than in adults independent of level of water contact
and also more severe in patients with high egg output
irrespective of age or level of water contact (Rabello et al.
1995).
Pathology
According to anatomic post mortem reports (Bogliolo
1958), acute clinical form corresponds to an acute generalized
miliar dissemination of granulomas and S. mansoni
eggs, predominantly in the liver, the subserous layer of
the small and large intestines, lungs, spleen and in the lymph
nodes of the mesentery, epiploon, retroperitoneum, as well as
in the lymph nodes of the hilus of the liver, pancreas, lung
and spleen. The granulomas are observed uniformly in the
initial phase of formation, with local histolysis and
granulocytic exudation. The liver is enlarged with a softened
consistency presenting necrotic-exudative granulomas and
degeneration of the hepatocytes. The spleen presents as the
"acute infectious tumor" (acute splenits).
The liver biopsy which displays the above mentioned
granulomata consists on the firm diagnostic of acute
schistosomiasis. Of course, this invasive procedure is seldom
indicated.
Chronification of disease happens due to immunomodulatory
mechanisms dependent on cell-mediated immunity (Boros et al.
1975) results in progressive reduction and organization of the
granulomas (Raso & Neves 1965).
Laboratorial diagnosis
Until recently, acute schistosomiasis diagnosis was only based
on epidemiological and clinical features, presence of S.
mansoni eggs in stools and eosinophilia. Many times this
situation consists on a challenge to physicians, since chronic
infected patients from an endemic area may present an adjacent
disease with a clinical picture similar to the acute
schistosomiasis.
Different patterns of specific humoral responses have been
described for acute and chronic schistosomiasis. Although IgG,
IgM and IgE responses against egg and worm antigens using
indirect immunofluorescence were shown to be equivalent in
acute, intestinal, hepatointestinal and hepatosplenic
patients (Kanamura et al. 1979), the higher levels of IgG,
IgM and IgE anti-cercariae adult worm antigens ratios in acute
patients disclosed serological differences antigen-stage
related between different clinical phases (Lunde & Ottesen
1980). Indeed, the presence of a circulating cercariae 41 KD
molecular weight glicoprotein antigen was detected in
experimentally infected mice as soon as three days after
infection while increased levels of IgM levels to this antigen
were detectable since one week post-infection (Hayunga et al.
1986).
High IgA responses to the gut associated antigens in acute
as compared to the chronic schistosomiasis using sections of
liver granulomata (Kanamura et al. 1979) and paraffin
sections of adult worm and by an indirect immunofluorescence
technique been previously shown (Kanamura et al. 1991). High
levels of IgA1 against adult worm and egg antigens have been
demonstrated in a small number of recently infected patients
by Evengard et al. (1990).
More recently, the high levels of IgG and IgM response
antikeyhole limpet hemocyanin (KLH) were shown to be a
diagnostic simple and useful tool for the acute and chronic
differentiation achieving high sensitivity and specificity for
S. hematobium (Mansour et al. 1989), S. mansoni
(Alves Brito et al. 1992) and S. japonicum (Yusheng
et al. 1994). It has been demonstrated the existence of a
shared carbohydrate epitope between the 38 KDa antigen which
is expressed at the miracidia and schistosomula surface and
the KLH (Dissous et al. 1986). Based on anti-SEA and anti-KLH
detection dipsticks dot-ELISA and dot-DIA (dot-dye
immunoassay) tests for the serological differentiation of
acute and chronic forms were successfuly described, presenting
efficacies of 90.2%, 89.0% respectively compared to an
efficacy of 92.7% of the ELISA test using the same antigens
(Rabello et al. 1993).
The diagnostic usefulness of the detection of circulating
IgA anti-SEA in ELISA for the serological differentiation
between acute and chronic clinical forms has been recently
stablished. Sensitivity and specificity proved to be as high
as 100% for the acute serological definition. Moreover, it has
been found that the specific immune response of anti-KLH
antibodies and anti-SEA IgA and IgM antibodies correlate with
morbidity allowing for age and levels of water contact
(Rabello et al. 1995).
Abdominal Ultrasonography - The usefulness of the
abdominal ultrasonography on the diagnosis of acute
schistosomiasis was recently described (Lambertucci et al.
1994, Rabello et al. 1994). The most typical sonographic
findings of acute clinical schistosomiasis mansoni are
hepatosplenomegaly and periportal and peripancreatic lym-
phadenomegaly. Peri-portal lymphnodes may be seen surrounding
the portal vein and the hepatic artery in the hepatic hilus.
Size of peri-portal lymph nodes varies from 10 x 5 to 36 x
12 mm. They are round or ovoid, sharply delimited, with thin
surrounding hypoechoic halus and internal medium intensity
echos. The liver presents homogeneously enlarged in all acute
patients. All chronic control patients presented a normal
liver echogenicity. The spleen is enlarged with a diffusely
increased echogenicity in all acute patients, presenting
preserved shape and contours. No lymph nodes can be seen in
the chronic and non-infected control groups. The sonographic
aspects of lymph nodes, liver and spleen are not specific and
can also be seen in other infectious diseases such as acute
hepatitis and other viral diseases with mesenteric adenitis.
The differential sonographic aspects of acute schistosomiasis
is detailed discussed elsewhere (Rabello et al. 1994).
Treatment
Hospitalization may be necessary for patients presenting the
more severe clinical manifestations. Intense toxemia, fever,
vomits and diarrheia frequently provoque dehydratation.
Clinical support and strict attention should be provided to
the acutely infected patient.
Reduced therapeutic efficacy of schistosomicides drugs
during acute disease has been inputed to their relatively
inactivity against immature worms. However, althoug the
majority of these drugs are relatively inative in mice three
to four weeks after infection, at the earliest stage of
patency (five to six weeks after infection) high cure rate is
achieved (Sabah et al. 1986). Thus when diagnosis of the
infection through detection of Schistosoma eggs in the
feces becomes possible the antischistosomal action of usual
drugs is similar to that observed in the chronic stage.
Patency was shown to happen between 45 and 48 days after
infection in baboons (Damian et al. 1992)
Different rates of cure from 45% in children (Lambertucci et
al. 1988) to 90% in adults (Katz et al. 1983) have been
observed with the use of oxamniquine for the acute
schistosomiasis. Praziquantel offerred 90% of cure rate in a
series of adult patients treated three months after infection
(Katz et al. 1983). In a recent opportunity, therapeutical
efficacy of 85.7 % of 14 patients in the acute patent phase
treated with oxamniquine (20 mg/kg of body weigh) was observed
(Rabello et al. 1995). One patient from this group had been
treated with praziquantel (60 mg/kg of body weigh) in
association with prednisone (1 mg/kg/day for five days
beggining two days before oxamniquine) 37 days after water
contact based on clinical-epidemiological features. He
presented symptoms and S. mansoni eggs in his stools 60
days after treatment. Retreatment with oxamniquine alone was
efficient at this occasion.
Severe adverse reactions have been observed in some
occasions when the patient with the acute phase was treated
with niridazole, hycanthone or praziquantel (Bogliolo 1958,
Harries & Cook 1987, Chapman et al. 1988). Some authors
suggest that clinical deterioration after treatment could be
due to the liberation of antigens from the dead worms and
consequent increased formation of immune complexes (Harries &
Cook 1987).
A number of case reports refer to an improvement of symptoms
with the use of steroids during this stage of the disease
(Gelfand et al. 1981, Farid et al. 1989) and some authors
recommend the administration of prednisone associated with
schistosomicides (Lambertucci et al. 1989). Contrary opinion
refers to that possible deleterious effect with the use of
dexamethasone has been observed (Raso & Neves 1965). Steroids
can reduce the size of liver granuloma during the acute
diasease in mice (Lambertucci et al. 1989). Although there is
no case-control study available in the literature it seems
that for the most severe clinical presentations the use of
steroids for a short period of time reduces the systemic and
allergic manifestations.
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Copyright 1995 Fundacao Oswaldo Cruz (Fiocruz)
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