Download SCHISTOSOMIASIS BILHARIZIASIS

SCHISTOSOMIASIS
BILHARIZIASIS
Is a human disease syndrome due to
infestation by Schistosoma
Most human schistosomiasis is caused by
1. Schistosoma haematobium discovered by
Theodor Bilharz in Cairo in 1861 (mainly
UTS).
2. Schistosoma mansoni (mainly GIT).
3. Schistosoma japonicum (mainly GIT).
EPIDEMIOLOGY
NILE RIVER
Schistosomiasis is a major source of morbidity
and mortality.
The endemic areas are limited to tropical and
subtropical zones, which exist around the
world.
The spread continues because of
a. water resource contamination in developing
countries
b. the migration of infected populations.
At least 200 million people in at least 74
countries have active schistosomal
infection. Of these, approximately 120
million people have symptoms, and 20
million are severely ill.
Disease prevalence tends to be worse in
areas with poor sanitation, increased
freshwater irrigation usage, and heavy
schistosomal infestation of human and/or
snail populations.
S mansoni and S haematobium infections
predominate in sub-Saharan Africa.
S mansoni is endemic in parts of South
America and the Caribbean.
S japonicum is common in China, Indonesia,
and the Philippines.
GLOBAL DISTRIBUTION
LIFE CYCLE
• The ovum is passed in the urine or faeces
of infected individuals and gains access to
fresh water where the ciliated miracidium
inside it is liberated; it enters its
intermediate host, a species of freshwater
snail, in which it multiplies .
• Large numbers of fork-tailed cercariae are
then liberated into the water, where they
may survive for 2-3 days.
• Cercariae can penetrate the skin or the
mucous membrane of the mouth of their
definitive host, humans. They transform
into schistosomulae and moult as they
pass through the lungs and are carried by
the blood stream to the liver and so to the
portal vein where they mature.
The male worm is up to 20 mm in length and
the more slender cylindrical female,
usually enfolded longitudinally by the
male, is rather longer .
Within 4-6 weeks of infection they migrate to
the venules draining the pelvic viscera,
where the females deposit ova.
LIFE CYCLE
PATHOLOGY
The pathological changes and symptoms
depend on species and stage of infection.
Most of the disease is due to the passage of
eggs through mucosa and to the
granulomatous reaction to eggs deposited
in tissues.
The eggs of S. haematobium pass mainly
through the wall of the bladder, but may
also involve rectum, seminal vesicles,
vagina, cervix and uterine tubes.
• S. mansoni and S. japonicum eggs pass
mainly through the wall of the lower bowel
or are carried to the liver.
• The most serious, although rare,
consequences of the ectopic deposition of
eggs are transverse myelitis and
paraplegia.
• Granulomas are composed of
macrophages, eosinophils, epithelioid and
giant cells around an ovum.
Later there is fibrosis and eggs calcify, often
in sufficient numbers to become radiologically
visible.
Eggs of S. haematobium, and of the other
two species after the development of portal
hypertension, may reach the lungs.
CLINICAL MANIFESTATION
1. URINARY TRACT
2. GIT AND LIVER
3. GENITAL TRACT
4. PULMONARY
HYPERTENTION
5. SPINAL CORD
Patients with acute schistosomiasis
(Katayama fever)
During the early stages of infection there may be
itching lasting 1-2 days at the site of cercarial
penetration.
After a symptom-free period of 3-5 weeks,
acute schistosomiasis (Katayama syndrome) may
present with allergic manifestations such as
urticaria, fever, muscle aches, abdominal pain,
headaches, cough and sweating.
On examination
Hepatomegaly, splenomegaly,lymphadenopathy
and pneumonia may be present. There is
eosinophilia and schistosomiasis serology may
be positive. These allergic phenomena may be
severe in infections with S. mansoni and S.
japonicum but are rare with S. haematobium.
The features subside after 1-2 weeks.
Chronic schistosomiasis
is due to egg deposition and occurs months
to years after infection. The symptoms and
signs depend upon the intensity of infection
and the species of infecting schistosome.
S. haematobium
Humans are the only natural hosts of S.
haematobium, which is highly endemic in
Egypt and East Africa, and occurs
throughout Africa and the Middle East .
Infection can be acquired after a brief
exposure such as swimming in freshwater
lakes in Africa.
• Painless terminal haematuria is usually the
first and most common symptom.
• Frequency of micturition follows, due to
bladder neck obstruction.
• Later the disease may be complicated by
frequent urinary tract infections, bladder or
ureteric stone formation, hydronephrosis,
renal functional abnormalities
• and ultimately renal failure with a
contracted calcified bladder.
• Pain in the iliac fossa or in the loin and
radiates to the groin.
• association of S. haematobium infection
with squamous cell carcinoma of the
bladder.
• Disease of the seminal vesicles may lead
to haemospermia. Females may develop
schistosomal papillomas of the vulva, and
schistosomal lesions of the cervix may be
mistaken for cancer. Intestinal symptoms
may follow involvement of the bowel wall.
• Ectopic worms cause skin or cord lesions.
• The severity of S. haematobium infection
varies greatly, and many with a light
infection are asymptomatic. However, as
adult worms can live for 20 years or more
and lesions may progress, these patients
should always be treated.
LIVER AND GIT
(Mainly S. Mansoni and Japanicum
– Bloody diarrhea
– Abdominal pain: RUQ pain, cramping
– Hematemesis (with portal hypertension)
– Ascites (with portal hypertension)
– Vulvar or perianal lesions
– On examination: Hepatosplenomegaly
– Abdominal tenderness
– Heme-positive stool and/or bloody diarrhea
– Ascites
Note: Hepatic failure and jaundice
are not features of hepatic
schistosomiasis
OTHER SITES AFFECTED BY
SCHISTOSOMIASIS
Pulmonary hypertension
– Dyspnea on exertion .
– Cough .
– Palpitations .
– Atypical chest pain .
– Pedal edema (with right heart failure)
Central nervous system (CNS)
– Seizures and/or mental status changes
(with cerebral involvement)
– Paralysis (with spinal cord involvement)
Skin
DIAGNOSIS
1. CLINICAL
2. HEMATOLOGICAL, BIOCHEMICAL
3. CONFIRMED BY
Detection of ova in urine deposit of terminal
stream (especially after exercise) or from
stool, biopsy or snip from rectum and
bladder wall. Ovum has terminal spine in
S. Hematobium and lateral spine in S.
mansoni
Serological tests ELISA for screening
4. Radiological and scope examination
SPECIFIC TREATMENT
Aim to stop egg-laying and reduce adult worm load
up to 90%
Three main drugs
• Praziquantel 40mg /kg for all types and as a
single dose is treatment of choice. Induce
parasitological cure in 80% of people and over
90% reduction in egg count in the remaining
individuals. Side effects like nausea and
abdominal pain are uncommon. Early therapy
reverse pathological changes like hepatomegaly
and bladder wall thickening and even large
granuloma.
Oxamniquine (old drug not used)15mg/kg/12hr
for 2 days in S.mansoni
Metrifonate (old drug not used) 7.5mg/kg every
2ws (1month)
Surgery in special circumstances and for some
complications like ureteric stricture, and small
fibrotic urinary bladder. Diathermy for rectal
papiloma removal. Neurosurgical procedures may
be needed for neurological complications if
chemotherapy is ineffective.
COMPLICATIONS OF
SCHISTOSOMIASIS
BILHARIZIASISIN GENERAL
1. Pulmonary hypertension
2. Cor pulmonale
3. Portal hypertension.
4. Obstructive uropathy.
5. Squamous cell carcinoma of the bladder.
6. Gastrointestinal bleeding
7. Carrier for salmonella
8. Neurological complications
Prognosis
• Almost all patients improve with treatment.
• Most patients with early disease or without
severe end-organ complications recover
completely.
• Surprisingly, patients with hepatic and
urinary disease, even with fibrosis, may
improve significantly over months or years
following treatment.
• Resolution of pulmonary disease is less
well documented.
Patients with heavier worm burdens are
less likely to improve and are more likely
to require re-treatment.
Treatment is indicated for patients with
end-stage complications of portal
hypertension and severe pulmonary
hypertension, but these patients are
much less likely to benefit.
Co-infection (with malaria, HIV, or hepatitis
worsens the prognosis.
PREVENTION
Travelers to endemic areas should avoid exposure
to freshwater that is likely to be contaminated.
No accepted prophylactic regimens have been
developed.
No vaccines are currently available, although
vaccine development is increasingly promising.
Early treatment after high-risk exposures should
minimize morbidity.
Prevention for groups residing in endemic
areas is more difficult than prevention for
travelers.
Improved sanitation to decrease
freshwater contamination with
sewage should decrease disease
prevalence.
Decrease occupational and recreational
contact with contaminated water may be
useful. These interventions are
particularly problematic with children.
Molluscicides to decrease the prevalence
of the snail hosts have some usefulness
but require frequent reapplication and
are used less frequently now than in the
past.
Mass treatment of targeted populations with
the newer less toxic antischistosomal
agents may have utility. It can be
combined with molluscicide treatment if
needed.
Vaccines hold the promise of significantly
reducing infection in endemic areas