Schistosomiasis is a disease caused by parasitic worms of the Schistosoma type. It may infect
the urinary tract or intestines. Symptoms may include abdominal pain, diarrhea, bloody
stool, or blood in the urine. In those who have been infected a long time, liver damage,
kidney failure, infertility, or bladder cancer may occur. In children it may cause poor growth
and learning difficulty. The disease is spread by contact with water
that contains the parasites. These parasites are released from freshwater snails that have
been infected. The disease is especially common among children in developing countries as
they are more likely to play in infected water. Other high risk groups include farmers, fishermen,
and people using infected water for their daily chores. Diagnosis is by finding the
eggs of the parasite in a person's urine or stool. It can also be confirmed by finding
antibodies against the disease in the blood. Methods to prevent the disease include improving
access to clean water and reducing the number of snails. In areas where the disease is common
entire groups may be treated all at once and yearly with the medication praziquantel. This
is done to decrease the number of people infected and therefore decrease the spread of the disease.
Praziquantel is also the treatment recommended by the World Health Organization for those
who are known to be infected. Schistosomiasis affects almost 210 million
people worldwide, and an estimated 12,000 to 200,000 people die from it a year. The
disease is most commonly found in Africa, Asia and South America. Around 700 million
people, in more than 70 countries, live in areas where the disease is common. Schistosomiasis
is second only to malaria, as a parasitic disease with the greatest economic impact.
Classification Species of Schistosoma that can infect humans:
Schistosoma mansoni and Schistosoma intercalatum cause intestinal schistosomiasis
Schistosoma haematobium causes urinary schistosomiasis Schistosoma japonicum and Schistosoma mekongi
cause Asian intestinal schistosomiasis Avian schistosomiasis species cause swimmer's
itch and clam digger itch Species of Schistosoma that can infect other
animals: S. bovis — normally infects cattle, sheep
and goats in Africa, parts of Southern Europe and the Middle EastS. mattheei — normally
infects cattle, sheep and goats in Central and Southern AfricaS. margrebowiei — normally
infects antelope, buffalo and waterbuck in Southern and Central AfricaS. curassoni — normally
infects domestic ruminants in West AfricaS. rodhaini — normally infects rodents and
carnivores in parts of Central Africa Signs and symptoms
Above all, schistosomiasis is a chronic disease. Many infections are subclinically symptomatic,
with mild anemia and malnutrition being common in endemic areas. Acute schistosomiasis may
occur weeks after the initial infection, especially by S. mansoni and S. japonicum. Manifestations
include: Abdominal pain
Cough Diarrhea
Eosinophilia — extremely high eosinophil granulocyte count.
Fever Fatigue
Hepatosplenomegaly — the enlargement of both the liver and the spleen.
Hepatic schistosomiasis is the second most common cause of esophageal varices worldwide.
Genital sores — lesions that increase vulnerability to HIV infection. Lesions caused by schistosomiasis
may continue to be a problem after control of the schistosomiasis infection itself. Early
treatment, especially of children, which is relatively inexpensive, prevents formation
of the sores. Skin symptoms: At the start of infection,
mild itching and a papular dermatitis of the feet and other parts after swimming in polluted
streams containing cercariae. Occasionally central nervous system lesions
occur: cerebral granulomatous disease may be caused by ectopic S. japonicum eggs in
the brain, and granulomatous lesions around ectopic eggs in the spinal cord from S. mansoni
and S. haematobium infections may result in a transverse myelitis with flaccid paraplegia.
Continuing infection may cause granulomatous reactions and fibrosis in the affected organs,
which may result in manifestations that include: Colonic polyposis with bloody diarrhea;
Portal hypertension with hematemesis and splenomegaly; Cystitis and ureteritis with hematuria, which
can progress to bladder cancer; Pulmonary hypertension;
Glomerulonephritis; and central nervous system lesions.
Bladder cancer diagnosis and mortality are generally elevated in affected areas.
Pathophysiology Life cycle
Schistosomes have a typical trematode vertebrate-invertebrate lifecycle, with humans being the definitive
host. Snails
The life cycles of all five human schistosomes are broadly similar: parasite eggs are released
into the environment from infected individuals, hatching on contact with fresh water to release
the free-swimming miracidium. Miracidia infect freshwater snails by penetrating the snail's
foot. After infection, close to the site of penetration, the miracidium transforms into
a primary sporocyst. Germ cells within the primary sporocyst will then begin dividing
to produce secondary sporocysts, which migrate to the snail's hepatopancreas. Once at the
hepatopancreas, germ cells within the secondary sporocyst begin to divide again, this time
producing thousands of new parasites, known as cercariae, which are the larvae capable
of infecting mammals. Cercariae emerge daily from the snail host
in a circadian rhythm, dependent on ambient temperature and light. Young cercariae are
highly mobile, alternating between vigorous upward movement and sinking to maintain their
position in the water. Cercarial activity is particularly stimulated by water turbulence,
by shadows and by chemicals found on human skin.
The most common way of getting schistosomiasis in developing countries is by wading or swimming
in lakes, ponds and other bodies of water that are infested with the snails that are
the natural reservoirs of the Schistosoma pathogen.
Humans Penetration of the human skin occurs after
the cercaria have attached to and explored the skin. The parasite secretes enzymes that
break down the skin's protein to enable penetration of the cercarial head through the skin. As
the cercaria penetrates the skin it transforms into a migrating schistosomulum stage.
The newly transformed schistosomulum may remain in the skin for two days before locating a
post-capillary venule; from here the schistosomulum travels to the lungs where it undergoes further
developmental changes necessary for subsequent migration to the liver. Eight to ten days
after penetration of the skin, the parasite migrates to the liver sinusoids. S. japonicum
migrates more quickly than S. mansoni, and usually reaches the liver within eight days
of penetration. Juvenile S. mansoni and S. japonicum worms develop an oral sucker after arriving
at the liver, and it is during this period that the parasite begins to feed on red blood
cells. The nearly-mature worms pair, with the longer female worm residing in the gynaecophoric
channel of the shorter male. Adult worms are about 10 mm long. Worm pairs of S. mansoni
and S. japonicum relocate to the mesenteric or rectal veins. S. haematobium schistosomula
ultimately migrate from the liver to the perivesical venous plexus of the bladder, ureters, and
kidneys through the hemorrhoidal plexus. Parasites reach maturity in six to eight weeks,
at which time they begin to produce eggs. Adult S. mansoni pairs residing in the mesenteric
vessels may produce up to 300 eggs per day during their reproductive lives. S. japonicum
may produce up to 3,000 eggs per day. Many of the eggs pass through the walls of the
blood vessels, and through the intestinal wall, to be passed out of the body in feces.
S. haematobium eggs pass through the ureteral or bladder wall and into the urine. Only mature
eggs are capable of crossing into the digestive tract, possibly through the release of proteolytic
enzymes, but also as a function of host immune response, which fosters local tissue ulceration.
Up to half the eggs released by the worm pairs become trapped in the mesenteric veins, or
will be washed back into the liver, where they will become lodged. Worm pairs can live
in the body for an average of four and a half years, but may persist up to twenty years.
Trapped eggs mature normally, secreting antigens that elicit a vigorous immune response. The
eggs themselves do not damage the body. Rather it is the cellular infiltration resultant
from the immune response that causes the pathology classically associated with schistosomiasis.
Diagnosis
Contemporary diagnosis involves detection of parasitic antigens by ELISA; all that is
required from the patient is a blood sample. This screening method is highly effective.
Microscopic identification of eggs in stool or, less commonly, the urine is another way
of arriving at a positive diagnosis. For the measurement of eggs in the feces of presenting
patients the scientific unit used is eggs per gram. Stool examination should be performed
when infection with S. mansoni or S. japonicum is suspected, and urine examination should
be performed if S. haematobium is suspected. Eggs can be present in the stool in infections
with all Schistosoma species. The examination can be performed on a simple smear. Since
eggs may be passed intermittently or in small amounts, their detection will be enhanced
by repeated examinations and/or concentration procedures. In addition, for field surveys
and investigational purposes, the egg output can be quantified by using the Kato technique
or the Ritchie technique. Eggs can be found in the urine in infections
with S. japonicum and with S. intercalatum Detection will be enhanced by centrifugation
and examination of the sediment. Quantification is possible by using filtration through a
nucleopore membrane of a standard volume of urine followed by egg counts on the membrane.
Investigation of S. haematobium should also include a pelvic x-ray as bladder wall calcification
is highly characteristic of chronic infection. Recently a field evaluation of a novel handheld
microscope was undertaken in Uganda for the diagnosis of intestinal schistosomiasis by
a team led by Russell Stothard from the Natural History Museum of London, working with the
Schistosomiasis Control Initiative, London. Tissue biopsy may demonstrate eggs when stool
or urine examinations are negative. The eggs of S. haematobium are ellipsoidal
with a terminal spine, S. mansoni eggs are also ellipsoidal but with a lateral spine,
S. japonicum eggs are spheroidal with a small knob.
Antibody detection can be useful in both clinical management and for epidemiologic surveys.
Prevention A few countries have eradicated the disease,
and many more are working toward it. The World Health Organization is promoting these efforts.
In some cases, urbanization, pollution, and/or consequent destruction of snail habitat has
reduced exposure, with a subsequent decrease in new infections.
Snails Prevention is best accomplished by eliminating
the water-dwelling snails that are the natural reservoir of the disease. Acrolein, copper
sulfate, and niclosamide can be used for this purpose. Recent studies have suggested that
snail populations can be controlled by the introduction of, or augmentation of existing,
crayfish populations. For many years from the 1950s onwards, vast
dams and irrigation schemes were constructed, causing a massive rise in water-borne infections
from schistosomiasis. The detailed specifications laid out in various UN documents since the
1950s could have minimized this problem. Irrigation schemes can be designed to make it hard for
the snails to colonize the water, and to reduce the contact with the local population.
This has been cited as a classic case of the relevance paradox because guidelines on how
to design these schemes to minimise the spread of the disease had been published years before,
but the designers were unaware of them. Treatment
Schistosomiasis is readily treated using a single oral dose of the drug praziquantel
annually. As with other major parasitic diseases, there is ongoing and extensive research into
developing a schistosomiasis vaccine that will prevent the parasite from completing
its life cycle in humans. In 2009, Eurogentec Biologics developed a vaccine against bilharziosis
in partnership with INSERM and researchers from the Pasteur Institute.
The World Health Organization has developed guidelines for community treatment of schistosomiasis
based on the impact the disease has on children in endemic villages:
When a village reports more than 50 percent of children have blood in their urine, everyone
in the village receives treatment. When 20 to 50 percent of children have bloody
urine, only school-age children are treated. When fewer than 20 percent of children have
symptoms, mass treatment is not implemented. The Bill & Melinda Gates Foundation has recently
funded an operational research program — the Schistosomiasis Consortium for Operational
Research and Evaluation to answer strategic questions about how to move forward with schistosomiasis
control and elimination. The focus of SCORE is on development of tools and evaluation
of strategies for use in mass drug administration campaigns.
Antimony has been used in the past to treat the disease. In low doses, this toxic metalloid
bonds to sulfur atoms in enzymes used by the parasite and kills it without harming the
host. This treatment is not referred to in present-day peer review scholarship; praziquantel
is universally used. Outside of the U.S., there is a drug available exclusively for
treating Schistosoma mansoni and one exclusively for treating S. hematobium. While metrifonate
has been discontinued for use by the British National Health Service, a Cochrane review
found it equally effective in treating urinary schistosomiasis as the leading drug, praziquantel.
Mirazid, an Egyptian drug made from myrrh, was under investigation for oral treatment
of the disease up until 2005. The efficacy of praziquantel was proven to be about eight
times than that of Mirazid and therefore Mirazid was not recommended as a suitable agent to
control schistosomiasis. Another agent, mefloquine, which has previously
been used to treat malaria, was recognised in 2008-2009 to be effective against schistosoma.
Mefloquine may be used in combination with praziquantel or artemisinins. Its mechanism
of action is not known but it causes extensive and severe morphological, histopathological,
and ultrastructural damage to adult and juvenile schistosomes, particularly, the worm tegument,
musculature, gut, and vitelline glands of female worms.
Epidemiology
The disease is found in tropical countries in Africa, the Caribbean, eastern South America,
Southeast Asia and in the Middle East. In these areas as of 2010 it affects approximately
238 million people 85% of whom live in Africa. An estimated 600 million people worldwide
are at risk from the disease. Worldwide an estimated 12,000 to 200,000 people
die related to schistosomiasis yearly. Schistosoma mansoni is found in parts of South
America and the Caribbean, Africa, and the Middle East; S. haematobium in Africa and
the Middle East; and S. japonicum in the Far East. S. mekongi and S. intercalatum are found
locally in Southeast Asia and central West Africa, respectively.
Among human parasitic diseases, schistosomiasis ranks second behind malaria in terms of socio-economic
and public health importance in tropical and subtropical areas. The disease is endemic
in 74-76 developing countries. They live in rural agricultural and peri-urban areas.
20 million have severe consequences from the disease. In many areas, schistosomiasis
infects a large proportion of children under 14 years of age.
History Schistosomiasis is known as bilharzia or bilharziosis
in many countries, after German physician Theodor Bilharz, who first described the cause
of urinary schistosomiasis in 1851. The first doctor who described the entire
disease cycle was Brazilian parasitologist Pirajá da Silva in 1908. The first known
case of infection was discovered in 2014, it belongs to a child who lived 6,200 years
ago. It was a common cause of death for Ancient
Egyptians in the Greco-Roman Period. Society and culture
Schistosomiasis is endemic in Egypt, exacerbated by the country's dam and irrigation projects
along the Nile. From the late 1950s through the early 1980s, infected villagers were treated
with repeated injections of tartar emetic. Epidemiological evidence suggests that this
campaign unintentionally contributed to the spread of hepatitis C via unclean needles.
Egypt has the world's highest hepatitis C infection rate, and the infection rates in
various regions of the country closely track the timing and intensity of the anti-schistosomiasis
campaign. See also
Genital schistosomiasis Trematode lifecycle stages
Tropical disease Male menstruation, a misunderstood symptom
caused by schistosomiasis References
Further reading André Ricardo Ribas Freitas and Rodrigo Nogueira
Angerami. Spinal Cord Schistosomiasis, Parasitic Diseases - Schistosomiasis, Prof. Rashika
El Ridi, ISBN 978-953-51-0942-6, InTech, DOI: 10.5772/53771. Available: http:www.intechopen.compdf/41921
External links Schistosomiasis at DMOZ
UNHCO site on Schistosomiasis River of Hope - documentary about the rise
of schistosomiasis along the Senegal river