6212NATSCI - Revision of Helminths and Transmission Routes

Give the list of Helminth transmission routes.

Faecal-oral.

Zoonotic faecal-oral.

Food-borne.

Zoonotic food-borne.

Water-borne.

Vector-borne.

Intermediate host.

Give an example of helminth that transmits via faecal-oral.

Gastrointestinal nematodes.

Give an example of helminth that transmits via zoonotic faecal-oral.

Toxocara and Echinococcus.

Give an example of helminth that transmits via food-borne.

Taenia, Trichinella and Fasciola.

Give an example of helminth that transmits via zoonotic food-borne.

Acanthocephalans, Diphyllobothrium, Clonorchis and Anisakis.

Give an example of helminth that transmits via water-borne.

Schistosomiasis

Give an example of helminth that transmits via vector-borne.

Brugia and Onchocerca.

Give an example of helminth that transmits via Intermediate host.

Acanthocephalans and all trematodes.

What are Cestodes?

Class of parasitic worms in the flatworm phylum.

They are obligate parasites, also known as tapeworms.

Give the cestodes morphology.

Have no gut or true head.

The scolex is the anterior attachment organ with suckers or hooks, followed by reproductive segments called proglottids.

What three main genera of Cestodes have clinical relevance?

Diphyllobothrium.

Taenia spp.

Echinococcus.

Give examples of a food-borne zoonotic tapeworm.

Diphyllobothrium.

Taenia spp.

Describe the transmission route of Diphyllobothrium.

Through consumption of raw or undercooked fish.

Describe the lifecycle of Diphyllobothrium.

The un-embryonated eggs are passed in the faeces of the definitive host.

Eggs embryonate in water.

Coracidia hatch from eggs and are ingested by crustaceans, the first intermediate host.

Procercoid larvae develop in the body cavity of crustaceans.

Procercoid larvae are released from the crustacean develops into plerocercoid larva.

Infected crustaceans ingested by small fish, the second intermediate host.

Predator fish (known as the paratenic host) eats small fish and the plerocercoid invades tissue.

Definitive host ingests plerocercoids in infected fish.

Adults develop in the small intestine.

Lifecycle repeats.

Describe the different hosts of Diphyllobothrium.

First Intermediate host – crustacean.

Second intermediate host – small fish.

Paratenic host – predatory fish.

Definitive host – mammal hosts such as humans and other carnivorous, fish-eating mammals, and occasionally birds.

Describe the pathology of Diphyllobothrium.

Causes a wide spectrum of disease and severity.

Can alter the structure of gastrointestinal tact by enhancing secretion and gut mobility.

The body can also mount an immune response towards the worm and eggs, but this can cause damage to the host also.

It can also cause vitamin B deficiency in humans.

These can lead to abdominal pain, mechanical obstruction, vomiting and diarrhoea in the host.

Describe the prevalence and intensity of Diphyllobothrium.

Diphyllobothriosis, caused by Diphyllobothrium infection, is considered the most important fish-borne zoonosis with up to 20 million individuals infected.

Describe the prevention and treatment of Diphyllobothrium.

Cook fish adequately.

Freeze fish adequately.

Salting, smoking or pickling fish does not kill parasite.

Medicines are available to treat infection.

Describe the diagnosis of Diphyllobothrium.

Stool samples will be examined for fish tapeworm eggs or segments.

Describe the lifecycle of Taenia spp.

The eggs or gravid proglottids in mammals’ faeces and passed into the environment.

Mammals, such as cattle and pigs, become infected by consumption of eggs or gravid-contaminated vegetation.

Oncospheres hatch, penetrate the intestinal wall and circulate to musculature.

Oncospheres develop into cysticerci in the muscle.

Humans infected by ingesting raw or undercooked infected meat.

Scolex attaches to the intestine and adults live in the small intestine.

Describe the transmission route of Taenia spp.

Consumption of raw or undercooked infected meat.

Describe the different hosts of Taenia spp.

Intermediate host – cow or pig.

Definitive host – humans.

Describe the pathology of Taenia spp.

Overall, it generally has few or no symptoms and is not generally fatal.

Taenia saginata (from cows) is usually asymptomatic but heavy infection can cause weight loss, abdominal pain, diarrhoea, headaches and nausea and more.

Taenia solium (from pigs) can cause cysticercosis.

Explain what Cystercosis, caused by T. solium is.

It occurs from consuming vegetables or water contaminated by faeces, or someone infected with T. solium.

It causes eggs to enter the intestine where they develop into larvae and infect the bloodstream and invade host cells.

It causes headaches, dizziness, seizures, dementia, lesions in brain, blindness and tumour-like growths. Alongside these, it causes major neurological problems like hydrocephalus, paraplegy, meningitis and death.

Describe the prevalence and intensity of Taenia spp.

Together with cystercosis, infections affect 50 million people globally. Disease is most common in the majority world.

Describe the prevention and treatment of Taenia spp.

Prevention is by properly cooking meat.

Treatment is generally with praziquantel and occasionally niclosamide.

Describe the diagnosis of Taenia spp.

Via stool sample examinations.

Give an example of a zoonotic faecal-oral tapeworm

Echinococcus

Describe the transmission route of Echinococcus.

Humans can be infected by hand-to-mouth transmission after touching a dog due to faeces contamination of pet fur.

Describe the lifecycle of Echinococcus

An adult in the small intestine of the definitive host produces embryonated eggs which are excreted in faeces. This is where humans can be and intermediate hosts are infected.

The oncosphere hatches and penetrates the intestinal wall.

The hydatid cyst in forms in various organs like the liver and lungs in the intermediate host.

The protoscolex forms from a cyst.

The scolex attaches to the intestine.

The definitive host is infected by ingesting the cysts of the infected organs on intermediate host.

Describe how human infection of Echinococcus occurs.

The egg hatches in the  digestive system and produces planula larva.

It penetrates the intestinal wall and carried by the bloodstream to the liver, lung, brain or other organ.

It settles and forms a bladder-like structure called a hydatid cyst.

There is no intestinal, patent infection of humans – it only forms cysts.

Describe the different hosts of Echinococcus.

Intermediate hosts – sheep, goats, cattle, camels.

Definitive hosts – carnivorous predators, i.e., dogs, wolves, foxes and lions.

Dead-end hosts – humans (corpses are seldom eaten).

Describe the pathology of Echinococcus

Pathology is always severe where hydatid or alveolar cysts form in the brain or organs.

If the cysts rupture, they can create secondary cysts in other sites within the body.

Rupture of cysts can produce a host reaction manifesting as fever, urticaria, eosinophilia and potentially anaphylactic shock.

Untreated infections of E. multilocularis have a high fatality rate.

Describe the prevalence and intensity of Echinococcus.

E. granulosus is found worldwide, but is more prevalent in rural, grazing areas where dogs can ingest organs from infected animals.

E. multilocularis is common in the northern hemisphere.

Describe the prevention and treatment of Echinococcus.

Infections often remain asymptomatic for years until the cysts grow large enough to cause symptoms in the affected organs.

Hepatic and pulmonary signs/symptoms E. granulosus are the most common clinical manifestations.  

Some E. multilocularis  cysts can be misdiagnosed as cancer.

Describe the diagnosis of Echinococcus.

Cysts are detected with ultrasound, x-ray computed tomography or other imaging techniques.

Emergence of symptoms.

Explain Trematodes from a transmission route point of view.

Digenean trematodes are obligate parasite flatworms.

They have complex lifecycles that always involve an intermediate host mollusc.

Give an example of a food-borne trematode.

Liver flukes, i.e., Fasciola spp., Clonorchis and Opisthorchis.

Describe the transmission route of Fasciola spp.

Foodborne transmission from eating cysts on plants.

A parasite for sheep, cows and vegans.

Cercariae encyst on vegetation at the side of ponds and streams.  

Describe the lifecycle of Fasciola spp.

Embryonated eggs are passed in faeces.

Eggs become embryonated in water.

Miracidia hatch from eggs and seek out snail intermediate hosts.

Miracidia penetrate the snail where sporocysts develop into rediae which develop into cercariae.

The free-swimming cercariae cyst finds aquatic vegetation.

Metacercaria on vegetation is ingested by the definitive host.

Immature flukes excyst in duodenum, penetrate the intestinal wall and migrate through the liver parenchyma to biliary ducts.

The adult flukes find the hepatic biliary ducts

Describe the different hosts of Fasciola spp.

Intermediate – snails

Definitive hosts – ruminants and humans.

Describe the pathology of Fasciola spp

Frequently causes disease in ruminants.

Human symptoms of fasciolosis can either be acute or chronic.

The acute phase, where the immature worms penetrate the gut, cause symptoms of fever, nausea, swollen liver, skin rashes and extreme abdominal pain.

Chronic phase, where the worms mature in the bile duct, can cause symptoms of intermittent pain, jaundice and anaemia.

In sheep and cattle, symptoms include persistent diarrhoea, chronic weight loss, anaemia, and reduced milk production. F. hepatica can cause sudden death in both sheep and cattle due to internal haemorrhaging and live damage.

Describe the prevalence and intensity of Fasciola spp.

Affects more than 70 countries worldwide.

200,000 cases and 700 deaths annually.

Equivalates to 1 million DAYLs.

F. hepatica is distributed worldwide and causes £23 million in economic of livestock species in the UK alone.

F. hepatica has one of the widest geographical spread of any parasitic and vector-borne disease, but is considered more geographically restricted to SWANA.

Describe the prevention and treatment of Fasciola spp.

Livestock are often treated with flukicides (chemicals that are toxic to flukes).

Ivermectin, which is widely used for helminthic parasites, has love effectivity for F. hepatica.

Strict control of growth and sale of edible water plants such as watercress.

Some farms are irrigated with polluted water and so vegetables from there should be thoroughly washed and cooked before being eaten.

Reduce the lymnaeid snail population or separating livestock from areas with the snails

Describe the diagnosis of Fasciola spp.

Can be made from finding yellow-brown eggs in the stool.

An enzyme-linked immunosorbent assay (ELISA) test is the diagnostic test of choice and can detect the antihepatica antibodies in serum and milk.

Describe the transmission route of Clonorchis.

Foodborne transmission of fish-eating mammals, including humans.

Describe the lifecycle of Clonorchis

Embryonated eggs are passed in faeces.

The eggs are ingested by a snail where the eggs develop into a cercariae.

Free-swimming cercariae encyst in the skin or flesh of a freshwater fish.

Metacercariae in the flesh or skin of freshwater fish are ingested by the definitive host.

Excyst in duodenum.

Adults move to the biliary duct of the definitive host.

Describe the different hosts of Clonorchis.

First intermediate host – freshwater snail, dependent on area found (i.e., Parafossarulus manchouricus in China, Japan, Korea and Russia, but also Assiminea lutea in China and Melanoides tuberculata in Vietnam).

Second intermediate host – freshwater fish, and sometimes shrimp.

Definitive host – humans (major), but also dogs, cats, rats, pigs etc.

Describe the pathology of Clonorchis

Chlonorchiasis appears as jaundice, indigestion, biliary inflammation, bile duct obstruction and sometimes liver cirrhosis, cholangiocarcinoma and hepatic carcinoma.

It is also a major causative agent of bile duct cancer and is a group one biological carcinogen.

Describe the prevalence and intensity of Clonorchis.

C. sinensis is the most prevalent in Aisa and third-most in the world.

85% of infections occur in China.

15 million people estimated to be infected.

200 million people at risk of infection.

Infection rates are generally higher in men, fishermen, farmers, businessmen and catering staff.

Infection more serious in adults aged 40-60 and the elderly.

More cases in low or middle-class countries, increasing the disease burden and creating economic problems.

Clonorchiasis causes 275,370 DALYs globally.

Clonorchiasis-related ailments in the Guangdong province of China were $200 million by 2010.

Describe the prevention and treatment of Clonorchis.

Drugs used include triclabendazole and praziquantel for example.

Adequate cooking and hand washing is also likely to decrease the chances of infection

Describe the diagnosis of Clonorchis.

Infection is detected by identification of eggs in faeces or duodenal aspirate.

An enzyme-linked immunosorbent assay (ELISA) test is the diagnostic test of choice.

Real-time PCR and loop-mediated isothermal amplification detects DNA and are highly sensitive and specific.

CT, ultrasounds and MRI can also be used for primary biliary cirrhosis detection.

Describe the transmission route of Opisthorchis.

Food-borne trematode parasite caused be eating raw or undercooked fish.

Describe the lifecycle of Opisthorchis

Embryonated eggs are passed in the faeces.

Eggs are ingested by the snail and develop into cercariae.

Free-swimming cercariae encyst in the skill or flesh of freshwater fish.

Metacercariae in flesh or skin of freshwater fish are ingested by the human host.

Excyst in duodenum

Adults end in biliary duct.

Describe the different hosts of Opisthorchis.

First intermediate host – Bithynia siamensis snails.

Second intermediate host – Cyprinidae fish.

Definitive host – humans and other mammals like dogs, cats, rats and pigs.

Describe the pathology of Opisthorchis

O. viverrine can cause cancer in humans and is classified as a group 1 biological carcinogen. Causes cancer due to the host’s immune reactions and specific parasite secretion. The infection is not immediately life-threatening, but cancer develops after 30-40 years where death can occur within 3-6 months of diagnosis.

Can be harmless without clinical symptoms.

Mild symptoms include dyspepsia, abdominal pain, constipation or diarrhoea.

Severe infection can cause enlargement of the liver and malnutrition.

In rare cases, cholangitis, cholecystitis and cholangiocarcinoma can develop.

Heavy infections can cause problems in the liver, gall bladder and bile ducts.

Describe the prevalence and intensity of Opisthorchis.

O. viverrine is found in Thailand, Loas, Vietnam and Cambodia. Highest prevalence in humans in northern Thailand. Specifically in places where raw fish dishes are common cuisine.

It is a major public health problem in Southeast Asia.

Thailand has the most incidence of opisthorchiasis-associated chancer, cholangiocarcinoma in the world (9.6% of Thailand population). The highest incidence reached 45.7%.

School children are most infected.

Was a mass treatment programme in after 1984 leading to a sharp decline in prevalence after 1994.

Describe the prevention and treatment of Opisthorchis.

Avoidance of raw or undercooked freshwater fish from countries where the parasite occurs.

Lightly salted, smoked or pickled fish can also contain parasites.

Cooking or freezing adequately can prevent infection.

Praziquantel is the treatment of choice. Albendazole is an alternative option.

Describe the diagnosis of Opisthorchis.

Stool specimen samples can be examined for eggs.

Ultrasound, CT or MRI can detect bile ducts containing flukes.

Blood tests can detect liver flukes, but this is unavailable in the USA.

Give an example of a water-borne helminth.

Schistosomiasis, AKA blood flukes,`                     

Describe the transmission route of Schistosomiasis.

Caused by helminths spread by fresh water that’s contaminated with parasites released from infected freshwater sails.

Describe the lifecycle of Schistosomiasis.

Eggs are shed from the infected human in faeces (S. mansoni, S. japonicum and S. mekongi) or urine (S. haematobium).

Eggs hatch and release miracidia.

Miracidia penetrate the snail tissue.

Sporocysts develop in sails and their successive generations.

Free-swimming cercariae released from snail into water.

Cercariae penetrate skin.

Cercariae lose tails during penetration and become schistosomulae.

Circulate the blood.

Migrate to portal blood in the liver and mature into adults.

Paired adult worms migrate to the mesenteric venules of the bowel/rectum (S. mansoni, S. japonicum and S. mekongi) where the eggs circulate to the liver and shed in stool, or the venous plexus of the bladder (S. haematobium) where eggs are shed in the urine.

Describe the different hosts of Schistosomiasis.

Reservoirs for S. japonicum – cattle, dogs, cats, rodents etc.

Intermediate hosts ^ - Oncomelania snails.

Reservoir for S. mekongi – dogs.

Intermediate hosts ^ - Neotricula aperta snails.

Reservoir for S. mansoni – frequently wild primates but is not considered a zoonosis as its primarily a human parasite.

Intermediate hosts ^ - Biomphalaria snails.

Describe the pathology of Schistosomiasis

Individual may develop cercarial dermatitis in the first 12 hours of infection due to irritation of the point of entrance.

Acute includes fever, myalgia, cough, bloody diarrhoea, chills or lymph node enlargement.

Symptoms may also include neurological effects like spinal cord inflammation, headaches, motor paralysis and visual and speech impairment.

Chronic infection can cause abdominal pain, diarrhoea, bloody stool and blood in the urine.

Those who have been infected for a long time may experience liver damage, kidney failure, infertility or bladder cancer.

In children, schistosomiasis may cause poor growth and learning difficulties.

Describe the prevalence and intensity of Schistosomiasis.

78 countries where schistosomiasis transmission is recorded.

51 countires require treatment for high prevalence.7

90% of infected people live in Africa.

1.8 million DALYs lost to schistosomiasis.

200,000 deaths estimated annually.

Describe the prevention and treatment of Schistosomiasis.

It is a neglected tropical disease.

Corticosteroids can be used to alleviate hypersensitivity reaction and reduce inflammation.

Praziquantel can be used to kill schistosomes and prevent chronic infections.

In some cases, urbanisation, pollution and consequent destruction of snail habitat have reduced exposure and decreased new infections.

Elimination of snail populations using molluscicides have been attempted to prevent schistosomiasis in the past but was expensive and ineffective.

Centres for disease control and prevention advices avoiding drinking or contact with contaminated water.

Describe the diagnosis of Schistosomiasis.

Finding parasite’s eggs in a person’s urine or stool.

Confirmed by finding antibodies against the disease in blood.

Imaging modalities like X-rays, ultrasounds or CT etc can be used to evaluate severity of infected organs.

Give examples of a soil-transmitted nematodes

Ascaris lumbricoides and Trichuris trichuira.

Describe the transmission route of Ascaris.

Faecal-oral/soil from drinking infected water or food.

Describe the lifecycle of Ascaris

Adults in the small intestine produce both unfertilised (will not undergo further development) and fertilised eggs that are released in faeces.

Embryonated egg with larvae are ingested by the host.

The hatched larvae enter circulation and migrate to the lungs.

Larvae are coughed up and swallowed, re-entering the gastrointestinal tract. Maturation proceeds in the small intestine.

Describe the different hosts of Ascaris.

Humans and swine are the major hosts for Ascaris.

Ascaris sp. Eggs may be found in dog faeces but does not indicate true infections.

Describe the pathology of Ascaris

Minor infections have no presented symptoms.

Bad infection symptoms will include bloody sputum, cough, fever, abdominal discomfort, intestinal ulcers and the passing of worms.

Can cause Loffler’s syndrome.

Can also be accompanied by pulmonary infiltration and eosinophilia.

There has been observations of decreases in fertility in infected women.

Describe the prevalence and intensity of Ascaris.

A. lumbricoides is primary distributed in tropical and subtropical regions in the world.

It is particularly common in areas with poor sanitation and hygiene practices.

0.8-1.3 billion individuals are infected with the worm, primarily in Africa and Asia. Of this, 120-220 million are symptomatic.

2700 deaths were directly attributable to infection of 2010.

Describe the prevention and treatment of Ascaris.

Prevention requires educated hygienic habits/culture and effective faecal treatment systems.

Infection may occur when food is handled without removing or killing the eggs on hands, clothes hair, raw vegetables/fruit or cooked food that is reinfected by handlers and containers.

Bleach does not readily kill eggs but it will remove their sticky film to allow rinsing of eggs.

Eggs can be reduced by hot composting methods.

Completely killing them may require rubbing alcohol, iodine, specialised chemicals or cooking heat.

Infections can be treated using ascaricides like albendazole.

Piperazine is a flaccid paralysing agent that blocks the response of Ascaris muscle to acetylcholine which immobilises the worm and prevents migration. Worms can then be passed out in the faeces but intestine or biliary duct blockages can be caused.

In cases of severe infestation, worms may cause bowel obstruction requiring emergency surgery for removal.

Describe the diagnosis of Ascaris.

Faecal smears.

Larvae may be found in fluids aspirated from the lungs.

White blood cell counts may demonstrate peripheral eosinophilia.

X-rays may also be able to detect large blockages caused by the worms.

Give examples of vector-borne nematodes.

Brugia malayi and Onchocera volvulus.

Describe the transmission route of Brugia malayi.

Vector-borne via a biting fly.

Describe the lifecycle of Brugia malayi.

Mosquito takes a blood meal and L3 larvae enter the skin.

Adults mature in the lymphatics.

Adults produced sheathed microfilariae that enter peripheral circulation.

Mosquito takes a blood meal and ingests the microfilariae.

Microfilariae shed sheaths, penetrate the mosquito’s midgut and migrate to the thoracic muscles.

It matures into a L3 larvae.

It migrates to mosquito head and proboscis and is transferred into the host when the mosquito takes a blood meal.

Describe the different hosts of Brugia malayi.

The typical vector for Brugia spp. filariasis is mosquito species of the genera Mansonia and Aedes.

The final host is humans.

Southeast Asian cats are also hosts.

Describe the pathology of Brugia malayi.

Marked by infection and swelling of lymphatic system.

Caused by the presence of worms in the lymphatic vessel and resulting inflammatory response of the host.

Enlargement of the limbs (usually the legs) and caused by the repeated inflammation of the lymphatic vessels.

Secondary bacterial infection is common amongst patients with filariasis.

Describe the prevalence and intensity of Brugia malayi.

Infects 13 million people in south and southeast Asia and is responsible for nearly 10% of the world’s total cases of lymphatic filariasis.

Infection is endemic or potentially endemic in 16 countries, where it is most common in southern China and India.

Describe the prevention and treatment of Brugia malayi.

While there is no licensed vaccine to prevent lymphatic filariasis, recent research has produced vaccine candidates with good results in experimental animals.

Vector control has been effective in virtually eliminating lymphatic filariasis in some regions, but vector control combined with chemotherapy (where entire at-risk populations are treated annually with safe medicine combinations) produces the best results.

A goal of community-based efforts is to eliminate microfilariae from the blood of infected individuals in order to prevent transmission to the mosquito which is primarily accomplished through the use of drugs.

Secondary bacterial infection is often observed with lf and rigorous hygiene practices like washing with soap and water daily and disinfecting wounds can help heal infected surfaces.

Describe the diagnosis of Brugia malayi.

Tender or enlarged inguinal lymph nodes or swelling in extremities can alert medical professionals to infection.

Stained blood films can aid diagnosis – specifically that of the tail portion, presence of a sheath and size of the cephalic space.

PCR based assays are highly sensitive and can be used to monitor infections in both humans and mosquito vectors.

Describe the transmission route of Onchocera volvulus.

It is an arthropod-borne nematode via female biting blackflies of the genus Simulium.

Describe the lifecycle of Onchocera volvulus.

Blackfly takes a blood meal and the L3 larvae enter the bite wound.

Larvae migrate to the subcutaneous tissues.

Adults mature in subcutaneous nodule.

Adults produce unsheathed microfilariae that typically are found in the skin and lymphatics of connective tissues, but also occasionally in peripheral blood, urine and sputum.

Blackfly takes a blood meal and ingests the microfilariae.

Microfilariae penetrate the blackfly’s midgut and migrate to the thoracic muscles.

Microfilariae mature into L3 larvae.

L3 larvae migrate to the head and blackfly’s proboscis to be transferred when biting.

Describe the different hosts of Onchocera volvulus.

Vector – blackfly (g. Simulium).

Final host – human.

Describe the pathology of Onchocera volvulus.

Onchocerciasis which causes severe itching.

Long-term infection can cause keratitis, an inflammation of the cornea in the eye and ultimately leads to blindness.

Is also though to cause the nodding syndrome, affecting children 5 to 15 and is currently observed in South Sudan, Tanzania and Northern Uganda. However, the cause of the disease is unknown, but O. volvulus is found in the same areas.

Describe the prevalence and intensity of Onchocera volvulus.

187 million people are at risk of O. volvulus infection.

17-25 million people infected and 0.8 million showing some impairment of vision.

O. volvulus has not directly caused a single death but has cost 1.1 million disability adjusted life years.

Describe the prevention and treatment of Onchocera volvulus.

Due to the reliance of water to breed, artificial water systems, such as hydroelectric power plants, built in Africa provide ideal conditions all year for blackfly development and make controlling its spread difficult.

Mosquito nets and insecticides will aid in preventing transmission.

Most effective treatment involves using ivermectin, although resistance to this drug has reported to develop.

Describe the diagnosis of Onchocera volvulus.

Diagnosed by finding microfilariae in skin snips or adults in biopsy specimens of skin nodules.

Give an example of a food-borne nematode.

Trichinella spp.

Describe the transmission route of Trichinella spp.

Oral ingestion of cyst or larvae-contaminated tissue, but congenital and mammary transmission can occur in rats.  

Describe the lifecycle of Trichinella spp.

Intermediate host is infected by eating infected meat scraps or cannibalism.

Host ingests undercooked infected meat.

Larvae released into the small intestine.

Adults mature in small intestine.

Larvae deposited in mucosa.

Encysted larvae in striated muscle.

In the sylvatic cycle, it is spread via predation or scavenging.

Describe the different hosts of Trichinella spp.

Intermediate hosts – rats and pigs predominantly.

Final hosts – humans, bears, foxes etc.

Describe the pathology of Trichinella spp.

Light infections may be asymptomatic.

Intestinal invasion can be accompanied by gastrointestinal symptoms like diarrhoea, abdominal pain and vomiting.

Larval migration into muscle tissues can cause periorbital and facial edema, conjunctivitis, fever, myalgias, splinter haemorrhages, rashes and peripheral eosinophilia.

Occasional life-threatening manifestations include myocarditis, central nervous system involvement and pneumonitis.

Describe the prevalence and intensity of Trichinella spp.

In swine, prevalence varies from country to country and regionally.

In wild animals, Trichinella infection rates vary from region to region and seem to increase in colder climates.

Foxes, wolves and bears have the highest infection rates, but small mammals, such as skunks, raccoons and rats provide the highest risk to infecting the domestic pig.

Countries in Eastern Europe and Asia report hundreds or thousands of cases annually.

Describe the prevention and treatment of Trichinella spp.

Long-standing meat inspection programs in some European countries have drastically lowered prevalence rates amongst domestic swine.

Can be prevented by cooking pork meat properly or by freezing it. However, freezing is no an effective method for killing larvae.

In animal populations, pigs or wild animals would be prevented from eating uncooked meat, scraps or carcasses of any animals, including rats, which may be infected with trichinella.

In countries of the EU, as well as Switzerland, a trichinella test is required by law in regulation.

Smoking, curing and drying are not sufficiently effective measures for killing larvae.

Cold-resistant trichinella species, such as Trichinella nativa, can occur in the meat of other animal species.

Treatment is either by thiabendazole or mebendazole.

Describe the diagnosis of Trichinella spp.

Artificial digestion is used to detect the presence of encysted trichinella larvae in suspected muscle tissue. The meat sample is dissolved by a digestive solution, and the remains are examined for the presence of larvae.

Give examples of a zoonotic faecal-oral nematodes

Toxocara canis and Baylisascaris procyonis.

Describe the transmission route of Toxocara canis.

Zoonotic faecal-oral in dogs.