Schistosomiasis. Flashcards
Describe the disease schistosomiasis - history, prevalence and risk factors.
– Schistosoma blood flukes are the cause of the disease Schistosomiasis –> It’s the most important macro-parasitic disease of humans (caused by a trematode parasite)
- Also known as Bilharzia as it was discovered by Theodor Bilharz when he found worms in portal veins in liver, which were trematodes with two unique sexes.
- Bloody urine was a well recognised disease symptom in ancient north Africa and several references to the disease have been discovered in papyrus.
– Second to malaria in public health ranking of parasitic infections - >230 million infected worldwide.
– People are at risk due to agricultural, domestic and recreational activities which expose them to infested water, especially children. Disease of poor and war.
How are schistosomes different from other trematodes?
- they have no secondary intermediate hosts
- they mature in the blood system of their definitive hosts
- they have two distinct sexes
- they are actively infective.
What are the three key species of schistosomes and how do they cause their pathology?
– Haematobium is in west, south-east Africa and Nile region. Urinary parasite - bladder, no significant reservoir host. Causes the bloody urine.
– Japonicum is in some areas of East Asia. Intestinal parasite, many reservoir hosts – dogs, cats, rodents, pigs and goats. Ironically no longer in Japan.
– Mansoni is found in Nile delta region as well as west and south-east Africa and some regions in south America. Intestinal parasite, no significant reservoir hosts.
Describe the schistosome life cycle.
–> Two-host life cycle
- Adult worms live in veins that drain certain organs of the host –> this varies with species – S. haematobium will live in veins of bladder, S. mansoni prefers veins of the large intestine and S. japonicum will prefer veins of the small intestine.
- The adult female worm will deposit eggs which will pass out in the faeces.
- -The eggs are embryonated and will hatch when exposed to fresh water. They release miracidium which will swim.
- The miracidia have photoreceptors and are positively phototropic.
In the snail:-
- the miracidia will actively penetrate snail host where it sheds its epithelium and develops into sporocysts which will reproduce asexually several times.
- There’s no redial stage and cercariae will eventually emerge from the daughter sporocysts where they will be released into water.
In human:-
– There’s no secondary intermediate host so cercariae will stay in water until they encounter human skin which they will then attach to and penetrate (active transmission) – they are attracted to the secretions of the skin, e.g. arginine.
(the parasite is often found in rivers/lakes where humans wash.)
– the schistosomules (larvae) will then enter the blood circulation and travel to the liver where they will mature into adult worms. They will then migrate to gut (intestinal mesenteric veins) or bladder depending on species and begin producing eggs.
– eggs are then released via faeces or by urine.
What are the schistosome’s strategies for success?
- The cerariae are released at morning to ensure that there will be people washing in lakes.
- The cercariae are also positively geotropic, i.e. they will go and find the host by thermal and chemical cues.
- They then attach and penetrate the host and cause damage to regions they penetrate – obvious vesicles are formed on the skin.
Immuniobiology
- Normal development of schistosomes requires cues from the host immune system –> TNF stimulates egg production, Cd4 lymphocytes.
- Concomitant immunity –while the host cannot defend against first wave of infection, second/third infections are unlikely to be successful —> immunity will kill subsequent invading larvae. However the schistosome has developed various strategies to avoid antibody dependent cell mediated cytotoxicity (ADCC):
- –> Molecular mimicry – the surface proteins have evolved in parasite to resemble the host’s surface proteins.
- –> Molecular masking – they can also sequester the host’s glycoproteins/lipids onto their surface.
- Can also modulate the immune system –> attack host antibodies by fabulating enzymes and manipulate the cytokine system.
What are the clinical stages of schistosomiasis?
Acute schistosomiasis – occurs when the schistosome begins producing eggs about 4-10 weeks after initial infection. Also called Katayama fever.
- By this time the host has had considerable exposure to the parasite’s antigens but release of eggs causes a high number of antigen releasing causing formation of large immune complexes that must be cleared by cells of the RE system.
- Granulomas are formed around eggs consisting of eosinophils, neutrophils ad macrophages.
- There’s an increased leucocyte count – eosinophilia.
- Enlargement of liver and spleen.
- Often asymptomatic – but fever, nausea, headache, diarrhoea and blood can occur – symptoms are more common with S. japonicum.
Chronic intestinal schistosomiasis – the intestines are affected.
- Occurs a number of years after infection.
- Pathogenesis – granulamatous inflammation around eggs trapped in tissues with fibrosis. All areas of small and large intestine may be involved –> large intestine shows more severe lesions.
- Colonic polyps are sometimes formed – especially in Egypt (unknown why)
Chronic hepatosplenic schistosomiasis – also seen a few years after infection.
– Eggs are trapped in liver and granulomas are formed around these eggs, leading to fibrosis and swelling of the abdomen. Similar to above but in liver.
For S. haematobium –> the symptoms are more chronic in nature since the bladder is commonly affected.
- Eggs can be trapped in the bladder leading to their calcification (accumulation of calcium salts) and can this can cause blood in urine (haematuria).
- Bladder cancer is also associated with the infection.
What are the treatment options for schistosomiasis?
only drug is Praziquantel (an antihelmintic)
- it is used in all Bilharzia cases even asymptomatic as the adults are long-lived – to prevent further transmission. – However once the parasite starts forming granulomas, any damage caused is irreversible but the treatment is used to kill parasites and prevent any further damage.
- The drug acts to paralyse the worm’s muscles by causing an influx in calcium.
What are the methods for schistosomiasis control?
- Education – stay out of dirty waters, sanitation etc. hard to make the uneducated, poor masses change their customs and traditions. Such efforts don’t have much success. Education is inversely related to disease.
- Clean drinking water – to reduce infective water contact and contamination of water sources.
- Chemotherapy – periodic treatment of Praziquantel. Best to target children at schools.
- Vaccines – there is currently one candidate Sm-p80 (DNA vaccine consisting of a protein from S.mansoni) in clinical trials.
- Vector control – difficult to control the snail vectors as they are aquatic.
- - Physical methods
- -> Draining snail habitats, clearing of vegetation.
- - Chemical methods
- -> Use of chemical molluscidies – however it’s difficult to apply on water (difficult to determine amount needed) and can have negative effects on other animals. The effects were also short-lived on snails.
- - Biological methods
- -> Introducing potential predators or competitors – Marisa cornuatietis (another species of freshwater snail) successfully controlled a species of snail in Puerto Rico which competed with and preyed on the vector snails
- -> Snail eating fish have been cultured and released as well
- -> If done correctly this method can be environmentally friendly – if not it can damage to ecosystem and potentially introduce a new invasive species.
- -> Not 100% - only reduction so risk of infection will remain.
