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Flashcards in Schistosomiasis Deck (33):

In what forms can schistosomiasis occur and what are the main species associated with these forms of the disease?

S. masoni - intestinal/hepatic form
S. haematobium - urinary form


Outline the LC of Schistosoma spp.

Egg hatches to a miracicduim that enters the snail host. It then goes through sporocyst and cercaria stage (4 weeks p.i. of snail) which enters the human skin. This then becomes a schistosomulae which migrates through portal blood to the liver or bladder. Adults form and then either are in the bladder or enter mesenteric venules as paired adults. Eggs are passed in faeces and urine and can then infect snails.


How does the female worm exist?

In the gynaecophoric canal of the male worm.


Are there any species that infect cattle? Which ones are zoonotic?

S. bovis

S. japonicum and S.mattei are zoonotic


What clinical signs are seen in cattle infection?

Diarrhoea, wasting and aneamia


What pathology might you see straight away with schistosoma infection?

Penetration of the skin by cercariae can cause dermal lesions.


What is "katayama fever" and describe the clinical signs?

The acute form of schistosomiasis. It occurs 3-8 weeks p.i and is associated with maturation of the worms into adults. You see sings associated with eosinophils : eosinophilia, fever, coughing and urticaria. It is rarely seen in locals.


What is the cause of chronic schistosomiasis?

It is associated with the eggs in tissues and granuloma formation. (lymphocytic granuloma --> fibrosis)


Describe the different pathologies that one might see in the different forms of the disease.

Intestinal passage of eggs can lead to haemmorrhage. Thickening of the mucosa and inflammation can also cause intestinal polyp formation and therefore obstruction of the bowels.

Hepatic - eggs can become trapped in the presinusoidal blood vessels leading to portal hypertension, hepatosplenomegaly and haematemesis (vomiting blood). Periportal fibrosis can also lead to the above.

Urinary - escaping eggs can lead to haematuria, proteinuria and bladder polyps.
embolised eggs in the bladder can cause cacification and predispose to bladder cancer.
emobolised eggs in ureters can cause hydronephrosis and hydroureter (due to obstruction) and pyelonephrosis (acute inflammation)


How can the disease be diagnosed?

By detecting eggs in urine or kato smears.
Antibody or antigen detection (ELISA)


What is the treatment?

Pranziquantal - kills adults


What are common sites of transmission?

Slow moving water: streams, irrigation canals, lakes, rice fields and fishponds.


What are some forms of control not associated with drug treatment?

Education, sanitation facilities, adapting mollusc habitats & molluscicides, Providing safe water supplies.


How can drug treatments be used in a control program?

Periodic treatment
Targeted treatment
Selective treatment


Why are the above methods likely to be ineffective? What would be an ideal solution?

Reinfection rates are very high, so vaccination and chemotherapy would be the best option.


What evidence is there for immunity to schistosome infections in humans?

Seems to be a decreasing prevalence with age (after a peak in prevalence and intensity in teenage years) which cant be fully explained by reduced water contact. It is also thought that resistance is conveyed by age specifically rather than by duration of exposure to the worm.


How can it be shown that age is a factor and not reduced water exposure.

Treat all age groups to remove infection. Then monitor them closely to establish reinfection rates and water contact.


What antibodies is resistance associated with?

Increased IgE and IL-5 but reduced IgG4 (which may block IgE binding).


What does this imply?

Schistosomulae are killed by degranulation products.


What gene is associated with familial resistance to infection and what is its significance?

Sm1 gene which is located near other TH2 genes that are involved in cytokine production. It is not clear what the exact role of this gene is, although it seems to be involved in TH2 responsiveness to infection.


IS there a genetic link to worse disease?

Yes - familial link to increased fibrosis and associated pathology. This implies a TH1 modulation may need to occur to prevent excessive pathology.


How can puberty contribute to resistance?

Sex hormones may directly affect worms
Physiological changes e.g. skin thickening
DHEA is correlated to schistosome specific IgE levels.


What other interesting types of immunity have been demonstrated in animal models of disease?

Concomitant immunity - adult worms may survive by being coated by albumin or have different AGs to the schistosomulae.
Anti-fecundity immunity


What types of vaccine could be developed?

Irradiated cercariae - storage, logistics and safety prevent this in humans
Anti pathology.


What vaccines are in development?

Defined antigen vaccine - one is in clin. trials but dead ags are ineffective and recombinant ags have had variable effects.

P28 - codes for glutathione-S-transferase. This seems to lead to reduced worm burden and reduced fecundity of the worms. It may be because they have less ability to detoxify haematin (unwell worm) or they become more prone to immune attack in general.


Why is a TH2 response needed in response to a schistosome infection?

TH2 kills damaging LC stages through IgE production. It can also help to modulate inflammation.


Why is granuloma formation important to the LC of the worm?

Granuloma enzymes allow the egg to escape tissue.


What are the variations in granuloma formation in mice that are athymic or have B-cell deficiency?

Thymus = no granuloma
B-cells = normal granuloma (no lymphocytes)

The granuloma is essential to prevent host death due to toxic egg products.


How is the immune response to eggs modulated by TH2 cells~?

Th2 produce IL-10 which suppresses TH1 inflammation and fibrosis and APCs. Also produced by tregs and the APC itself. TH2 produces IL-5 which stimulates Eosinophils and IL-4 which stimulated beta cells.


Why might TNFa induce egg production?

It stimulates fibrosis/granuloma formation which is needed for the eggs to escape.


When does a TH2 bias begin to occur?

When eggs begin to deposit in tissues.


Which cytokines are involved?

IL-4 and IL-13 (IL-13 --> fibrosis)


How is this response induced?

Glycosylated egg antigens (lewis x trissacharide) is taken up by DCs which normally induce a TH1 response. However, the subcellular compartment in which the trissacharide is processed is seperate to that which TH1 antigens are processed.