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Schistosomiasis
Schistosomiasis, AKA Bilharzia
Parasitic disease caused by several species of
flatworm
Affects many in developing countries (it’s estimated
that 207M have the disease and that of those, 120M
are symptomatic)
Can contract it by wading or swimming in lakes,
ponds and other bodies of water infested with the
parasite’s snail host.
Distribution Map
A Brief History...
First described by German pathologist:
Theodore Maximilian Bilharz
Bilharz performed autopsies on Egyptian
patients who had died from the disease:
found male & female parasite eggs in the liver
portal system, bladder.
Later seen in Japan, called Katayama fever
Life Cycle (Basic)
Life Cycle
(Eggs  larvae  into snail)
1. Parasite eggs released into freshwater
(from human urine, feces)
2. Eggs hatch  ciliated miracidia, free
swimming
3. Miracidia find & infect snail host
(different species prefer diff’t snail sp.)
4. Each miracidia transforms into many
fork-tailed, free swimming forms called
cercariae within 4-6 weeks of entering snail.
5. Cercariae leave snail and move into water at a rate
of 1500/day for up to 18 days.
Miracidia larva
with cilia
6. Cercariae find a human host,
penetrate skin, and differentiate into
larval forms called schistosomulae.
7. Migrate through the host’s skin,
gain access to the lymphatic system.
8. Travel to the lungs (stay 3-8 days
and ~70% are eliminated)
9. Migrate to liver portal system, mature into male &
female adults
Cercariae with forked tail
Life Cycle
(Into human  lymphatics  lungs  liver)
10. In liver, m & f pair up  female inserts
herself into the gynecophoral canal of male
 they are now ‘paired’.
11. Migrate to favoured sites:
S. mansoni – mesenteric venules of
large bowel & rectum
S. japonicum – mesenteric veins of the
small intestine
S. haematobium – perivesical venous plexus
surrounding the bladder
Life Cycle
(maturation  movement to target organs  egg production)
Paired male & female
12. Females release eggs.
Egg characteristics
- Covered in microbarbs  cling to vascular
endothelium
- Pores, which allow the release of
1) Antigens
2) Enzymes (aid in passage of eggs
through host tissues)
12. Eggs enter lumen of excretory organs
50%  passed out of body
50%  trapped in tissues, carried away by
blood circulation, lymph.
Life Cycle
(Egg release)
Cercariae penetrate skin  rash
- called schistosome or swimmer’s itch.
Eggs laid in target organs release antigens  cause
Katayama fever
- fever
- urticaria
- malaise
- diarrhea
Acute Infection
(Early)
Symptoms of chronic infection caused by eggs that travel
to various parts of body
Eggs remain trapped in host tissues  secrete Ags 
granulomatous inflammatory immune response
 Granulomas: macrophages surrounded by lymphocytes (CD4, CD8
Tcells), which aggregate at site of infection.
Fibroblast cells:
 During late stage of chronic infection, they replace the granulomas.
Their prolif. is stim. by factors produced by the schistosome egg, &
by cytokines from macrophages & CD4 Tcells.
Fibroblasts mediate collagen deposition in the granuloma,
leading to fibrosis (=fibrous connective tissues
development
Chronic Infection
(Late)
Granuloma
Genitourinary complications
 Eggs lodge themselves in wall of bladder & can develop into polyps
 Polyps can erode, ulcerate & cause hematuria (blood cells in urine)
 Eggs lodge in ureters and urethra, cause lumps and lesions 
kidney failure
 Eggs lodge into ovaries, the uterus, cervix, fallopian tubes  lumps
 complications incl. infertility
(For the men: eggs can also lodge into the testes and the prostate )
CNS complications
 S. haematobium and S. mansoni can migrate to the spine
 S. japonicum found in the brain and causes encephalopathy (general
brain dysfunction)
Chronic Infection
(When eggs meet the meet the genitourinary areas & CNS)
 The commonest presentation is terminal haematuria [sometimes
uniform or microscopic]
 Haematuria initially painless.
 Burning micturation and hypogastric pain
 Ureteric colic [due to the passage of coagulated blood from a
source of bleeding situated high up in the ureter]
 Pain and burning sensation in the epigastrium- due to involvement
of the submucosa of the stomach
 High urinary blood and protein levels are related to intensity of
infection and lower urinary tract pathology
 Pyelonephritis, glomerulonephritis nephrotic syndrome
 Long standing urinary schistosomiasis lead to reduced bladder
capacity
 Ureters liable to stenosis especially around their orifices causing
partial obstruction to urine flow
 Secondary bacterial infection may occur
 Hydroureter, hydronephrosis, pyelonephrosis, bladder / ureter
calcification
Carcinoma of bladder [squamous cell
type]
Diagnosis
Microscopic Detection
Take stool or urine sample
to detect eggs
S. haematobium eggs are
oval and have a spike at
the tip
S. japonicum eggs small
and almost spherical with
tiny spine
S. mansoni eggs have a
spike on the side (spine)
S. mansoni S. japonicum
S. haematobium
Diagnosis
Antibody tests
An earlier and more sensitive form of detection
Some complications
 Cross-reactivity with other helminthic infections (other
flatworm parasites)
 Can’t tell the difference between current and old infections
as antibodies stay long after infection is over.
 Can’t tell you anything about overall worm burden so we
can’t tell how serious the infection is
Diagnosis
Antigen tests:
 Detect antigens in blood with
immunoelectrophoresis
Molecular detection:
 20-25% of schistosomiasis
genome has been sequenced 
can use 2 probes to detect S.
mansoni DNA in human blood
 Genome sequencing has the
potential to yield DNA vaccines
Prevention
For travelers it’s easy- don’t swim in stagnant water
(running water is better, still not safe).
Harder in endemic areas  people are dependent on
nearby freshwater.
Focused on education, eliminating snail nesting grounds
Molluscicides can be used to eliminate snails.
Proper irrigation systems and engineering are key
There are ways to build irrigation and canalization systems
that don’t allow snails to inhabit the surrounding area
 However, many irrigation/canalization projects since the 50s have
ignored UN instructions, may have contributed to spread of the
parasite
Treatment
Swimmer’s itch and Katayama Fever are usually treated
symptomatically.
Chemotherapy is treatment of choice - Praziquantel is most widely
used drug.
Praziquantel
Extremely well tolerated, few side effects
Broad-spectrum antihelminthic drug
(antihelminthic= drugs that expel parasitic worms)
Cures schistosomiasis in 80–90% of patients, 90%
reduction in egg excretion in those not cured
Causes worm muscles contract – cannot hold onto
human tissues
Resistance has been reported in Egypt and Senegal
Treatment
Others:
Metrifonate  against S. haematobium
Niridazole  against S. japonicum
Oxamniquine  against S. mansoni
WHO recently approved use of combo of 3 drugs at
once (rule is always no more than 2) to cure a few
related diseases (incl. Schistosomiasis) in hopes that
eradication will be faster.
Genitourinary Schistosomiasis

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Genitourinary Schistosomiasis

  • 2. Schistosomiasis, AKA Bilharzia Parasitic disease caused by several species of flatworm Affects many in developing countries (it’s estimated that 207M have the disease and that of those, 120M are symptomatic) Can contract it by wading or swimming in lakes, ponds and other bodies of water infested with the parasite’s snail host.
  • 4. A Brief History... First described by German pathologist: Theodore Maximilian Bilharz Bilharz performed autopsies on Egyptian patients who had died from the disease: found male & female parasite eggs in the liver portal system, bladder. Later seen in Japan, called Katayama fever
  • 6. Life Cycle (Eggs  larvae  into snail) 1. Parasite eggs released into freshwater (from human urine, feces) 2. Eggs hatch  ciliated miracidia, free swimming 3. Miracidia find & infect snail host (different species prefer diff’t snail sp.) 4. Each miracidia transforms into many fork-tailed, free swimming forms called cercariae within 4-6 weeks of entering snail. 5. Cercariae leave snail and move into water at a rate of 1500/day for up to 18 days. Miracidia larva with cilia
  • 7. 6. Cercariae find a human host, penetrate skin, and differentiate into larval forms called schistosomulae. 7. Migrate through the host’s skin, gain access to the lymphatic system. 8. Travel to the lungs (stay 3-8 days and ~70% are eliminated) 9. Migrate to liver portal system, mature into male & female adults Cercariae with forked tail Life Cycle (Into human  lymphatics  lungs  liver)
  • 8. 10. In liver, m & f pair up  female inserts herself into the gynecophoral canal of male  they are now ‘paired’. 11. Migrate to favoured sites: S. mansoni – mesenteric venules of large bowel & rectum S. japonicum – mesenteric veins of the small intestine S. haematobium – perivesical venous plexus surrounding the bladder Life Cycle (maturation  movement to target organs  egg production) Paired male & female
  • 9. 12. Females release eggs. Egg characteristics - Covered in microbarbs  cling to vascular endothelium - Pores, which allow the release of 1) Antigens 2) Enzymes (aid in passage of eggs through host tissues) 12. Eggs enter lumen of excretory organs 50%  passed out of body 50%  trapped in tissues, carried away by blood circulation, lymph. Life Cycle (Egg release)
  • 10. Cercariae penetrate skin  rash - called schistosome or swimmer’s itch. Eggs laid in target organs release antigens  cause Katayama fever - fever - urticaria - malaise - diarrhea Acute Infection (Early)
  • 11. Symptoms of chronic infection caused by eggs that travel to various parts of body Eggs remain trapped in host tissues  secrete Ags  granulomatous inflammatory immune response  Granulomas: macrophages surrounded by lymphocytes (CD4, CD8 Tcells), which aggregate at site of infection. Fibroblast cells:  During late stage of chronic infection, they replace the granulomas. Their prolif. is stim. by factors produced by the schistosome egg, & by cytokines from macrophages & CD4 Tcells. Fibroblasts mediate collagen deposition in the granuloma, leading to fibrosis (=fibrous connective tissues development Chronic Infection (Late)
  • 13. Genitourinary complications  Eggs lodge themselves in wall of bladder & can develop into polyps  Polyps can erode, ulcerate & cause hematuria (blood cells in urine)  Eggs lodge in ureters and urethra, cause lumps and lesions  kidney failure  Eggs lodge into ovaries, the uterus, cervix, fallopian tubes  lumps  complications incl. infertility (For the men: eggs can also lodge into the testes and the prostate ) CNS complications  S. haematobium and S. mansoni can migrate to the spine  S. japonicum found in the brain and causes encephalopathy (general brain dysfunction) Chronic Infection (When eggs meet the meet the genitourinary areas & CNS)
  • 14.  The commonest presentation is terminal haematuria [sometimes uniform or microscopic]  Haematuria initially painless.  Burning micturation and hypogastric pain  Ureteric colic [due to the passage of coagulated blood from a source of bleeding situated high up in the ureter]  Pain and burning sensation in the epigastrium- due to involvement of the submucosa of the stomach  High urinary blood and protein levels are related to intensity of infection and lower urinary tract pathology
  • 15.  Pyelonephritis, glomerulonephritis nephrotic syndrome  Long standing urinary schistosomiasis lead to reduced bladder capacity  Ureters liable to stenosis especially around their orifices causing partial obstruction to urine flow  Secondary bacterial infection may occur  Hydroureter, hydronephrosis, pyelonephrosis, bladder / ureter calcification
  • 16. Carcinoma of bladder [squamous cell type]
  • 17. Diagnosis Microscopic Detection Take stool or urine sample to detect eggs S. haematobium eggs are oval and have a spike at the tip S. japonicum eggs small and almost spherical with tiny spine S. mansoni eggs have a spike on the side (spine) S. mansoni S. japonicum S. haematobium
  • 18. Diagnosis Antibody tests An earlier and more sensitive form of detection Some complications  Cross-reactivity with other helminthic infections (other flatworm parasites)  Can’t tell the difference between current and old infections as antibodies stay long after infection is over.  Can’t tell you anything about overall worm burden so we can’t tell how serious the infection is
  • 19. Diagnosis Antigen tests:  Detect antigens in blood with immunoelectrophoresis Molecular detection:  20-25% of schistosomiasis genome has been sequenced  can use 2 probes to detect S. mansoni DNA in human blood  Genome sequencing has the potential to yield DNA vaccines
  • 20. Prevention For travelers it’s easy- don’t swim in stagnant water (running water is better, still not safe). Harder in endemic areas  people are dependent on nearby freshwater. Focused on education, eliminating snail nesting grounds Molluscicides can be used to eliminate snails. Proper irrigation systems and engineering are key There are ways to build irrigation and canalization systems that don’t allow snails to inhabit the surrounding area  However, many irrigation/canalization projects since the 50s have ignored UN instructions, may have contributed to spread of the parasite
  • 21. Treatment Swimmer’s itch and Katayama Fever are usually treated symptomatically. Chemotherapy is treatment of choice - Praziquantel is most widely used drug.
  • 22. Praziquantel Extremely well tolerated, few side effects Broad-spectrum antihelminthic drug (antihelminthic= drugs that expel parasitic worms) Cures schistosomiasis in 80–90% of patients, 90% reduction in egg excretion in those not cured Causes worm muscles contract – cannot hold onto human tissues Resistance has been reported in Egypt and Senegal
  • 23. Treatment Others: Metrifonate  against S. haematobium Niridazole  against S. japonicum Oxamniquine  against S. mansoni WHO recently approved use of combo of 3 drugs at once (rule is always no more than 2) to cure a few related diseases (incl. Schistosomiasis) in hopes that eradication will be faster.

Notes de l'éditeur

  1. Circariae need to find a human host within a day, or they die. Circariae find a human host and lose their tail as they’re penetrating the skin.
  2. Japonicum can release up to 2000 eggs/day!!
  3. Uticaria: itchy, raised, swollen bumps
  4. Uticaria: itchy, raised, swollen bumps