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Parasitology > Pig Nematodes > Flashcards

Pig Nematodes Flashcards

1
Q

GI Nematodes of Pig

A

Stomach: hyostrongylus rubidus and trichostrongylus axei– ostertagiosis like disease

Small intestine: ascaris suum*** and trichinella spiralis** (zoonosis- muscle worms, humans get from eating undercooked pork)

Large intestine: oesophagostomum** and trichuris suis**

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2
Q

Pig husbandry and parasites

A

Increasing parasite problems as we move from intenstive systems with slatted floors and no bedding to organic systems.

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3
Q

Pig nematodes and prevalence based on husbandry

A

Hyostrongylus: outdoor

ascaris: very persistent, therefore present in outdoor, indoor extensive and indoor intensive

Oesophagostomum: present in outdoor and indoor extensive- not super common in indoor intesnive but it does happen

Trichuris: present in outdoor and indoor extensive

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4
Q

Hyostrongylus rubidus- red stomach worm

A

adult worms 5-8mm, present in stomach

roughly analagous to pig ostertagiosis

causes chronic gastritis in pigs

outdoor pigs only and rare in UK

life cycle is typical trichostrongyloid- direct

PPP=3 weeks

L4 can undergo hypobiosis

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5
Q

Hyostrongylus rubidus- pathology

A

pathology is similar to ostertagia

nodule formation on surface of stomach

puncture wounds from gastric gland eruption– coffee granule appearance

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6
Q

Hyostrongylus rubidus- clinical signs and diagnosis

A

Clinical disease predominantly in lactating sows

Clinical signs- inappetance, anemia, loss of condition, redcued fertility

diagnosis: eggs in feces

disease of outdoor pigs-permanent pastures

effectively eradicated in indoor systems.

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7
Q

Ascaris suum

A

most important pig parasite

large roundworm/white spot

typical ascarid

large rigid, ropey worms (females up to 40cm)

Direct life cycle but can employ paratenic host

L3 inside egg is infective

Migratory: heptotracheal

SI of pig- larvated eggs infective

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8
Q

Ascaris suum- direct life cycle

A

Adults in SI–>egg–>L1 in egg–> L3 (inside egg) is infective

Hatches after ingestion–> L3 travels to liver via portal circulation–> L3 in liver, then travels in blood to lungs–> travel up bronchial tree and swallowed–> L4 in SI–> final moult in SI

PPP=7-9 weeks

Earthworm can be paratenic host- pigs eat earthworm with L3 larvated eggs.

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9
Q

Adult ascaris suum

A

burdens with worms typically 1-5 individuals per host

however over-dispersed population structure i.e. few animals with large burdens some with 40-60 large adults in SI

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10
Q

Maturation of eggs in environment

A

eggs are very resistant, shells sticky, pitted

Unlarvated egg (not infective)–> development in environment minimum of 4 weeks or longer depending on temp (temp <15 degress will halt)–> L3 within egg= infective

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11
Q

Ascaris lumbricoides- human roundworm

A

extremely important parasite of humans in the developing world

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12
Q

Relationship btwn A. suum and A. lumbricoides

A

very closely related but separate species. each parasite can establish infection in each host but cross infection is inefficient.

Therefore, in areas where human infection with A. lumbricoides is endemic, pigs are not an important reservoir of infection

In areas where A. lumbricoides is not endemic, get sporadic cases of human infection with A. suum

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13
Q

Clinical signs of A. suum

A

overt clinical signs rarely seen due to low parasite burden

reduced productivity (up to 10%): decreased food conversion efficiency, reduced weight gain, increased fattening time

occasionally get obstructive jaundice

occasionally transient pneumonia in young pigs due to migrating larvae- BUT other causes of pneumonia in pigs much more common

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14
Q

Ascaris suum in the PM room

A

Milk spot liver- cloudy white spots up to 1cm

milk spots caused by fibrous repair of inflammatory reaction to migrating L3

Liver condemnations– economically important.

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15
Q

Diagnosis of A. suum

A

clinical signs and history

fecal egg counts: very prolific/fecund parasites. egg numbers in the 1000s

incidence of liver condemnations- can be up to 25% of livers from herd affected

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16
Q

Ascaris suum- epidemiology

A

Can complete life cycle indoors

Each female lays up to 200,000 eggs per day and the eggs are extremely resistant. Difficult/impossible to eradicate from indoor systems

Improved hygiene reduces intensity of infection and increases age at which pigs are infected

Can overwinter (outdoor systems)

Predominantly disease of young pigs- a degree of age resistnace occurs d/t strong acquired immunity

There is a seasonal pattern: eggs passed in feces require minimum of 4 weeks maturation to become infective with optimal temp 22-26C; no development below 15c

therefore greatest incidence of milk spot in the summer.

17
Q

Trichinella

A

important mostly because it’s a zoonosis

will infect any mammal but mostly carnivores and omnivores and pig is a major host

18
Q

Trichinella spiralis life cycle

A

All occurs in the same host

L1 ingested in infected muscle tissue–> L1 infects SI mucosal epithelium. L1 moults to L2, L3, L4 and Adult within SI of new host in 2 days.

Adult produces newborn larvae (L1) which penetrate SI mucosa. L1 travels via lymph and blood and migrates to the muscles. L1 then encysts in muscles.

Adults mate and die off pretty quickly

L1s remain in tissue for life of host.

19
Q

Trichinella spiralis- modes of infection

A

related to whipworms

Predation

Carrion (larvae long lived in corpse)

Cannibalism

Ingestion of fresh feces from infected animals–when adults producing L1s, can go into feces.

20
Q

Trichinella- sylvatic cycle

A

[aside: T.britovi very common in europe- sylvatic cycle only, no domestic cycle, not of public health concern]

cycle in wild animals, predominantly carnivores

Temperate areas: fox, roden, brown bear, badgers, wild pigs (not species specific at all)

arctic areas: polar bears, wolves, foxes

Tropical areas: lions, leopards, bush pigs, hyenas

Eating wild game is a source of infection for humans

21
Q

Trichinella domestic cycle

A

Pigs tansmit to each other via infected swill, rats (carry parasite, pigs eat rats) or main route of infection is tail biting.

Pigs are generally asymptomatic

low incidence of infection also present in horses

generally in extensive management systems

Man can acquire infection via undercooked pork; also smoked sausages big source of infection.

22
Q

Diagnosis of trichinella in pigs

A

examination of muscle for larvae

main test done in abbatoir: artificial digestion of muscle - pepsin-HCl: will leave very noticeable muscle cysts which are resistant to enzymatic degradation.

prediliction sites: diaphragm, IC muscles, tongue, masseters

Serology: ELISA

23
Q

Clinical signs of trichinella in man

A

infections usually light and asymptomatic

following heavy infections:

intestinal infection can cause transient enteritis (L1-adult)

1-2 weeks later, L1s in muscle cause: acute myositis, pyrexia, myocarditis, periorbital oedema, ascites, eosinophila

Can be fatal (1% of cases)

Diagnosis: muscle biopsy, ELISA

24
Q

Control measures of trichinella

A

Meat inspection: EU-mandatory screening of pork

Prohibition of uncooked food waste to pigs (boil swill for 30 min)

Control of rodent population in piggeries

Proper carcase disposal to prevent cannibalism in pigs

consumer education: cooking of pork, wild game (curing/smoking/flaming, BBQing not always effective)

25
Q

Trichuris suis whipworm- life cycle

A

found in LI

Adults emerge in colon/caecum–> eggs in feces (undifferentiated)–> L1 develops inside egg–> minimum of 1-2 months maturation before infective (can take up to 12 months)–>eggs ingested–>L1 release from egg and penetrates LI mucosa–> moult to L2, L3, L4 and then to adult

Trichuris suis adults=4-6cm long

Infective stage= L1 inside the egg

Adults emerge: anterior ends embedded in mucosa of LI and caecum

PPP= 6-12 weeks

26
Q

Trichuris suis epidemiology

A

Common in UK, but present in low numbers

Mild/moderate infections are asymptomatic

Clinical disease not common but can be problematic

Transmission can occur indoors but restricted to traditional systems i.e. solid floors/ straw

Typically poor hygiene

More common in outdoor systems (organic)

eggs survive for several years in the environment- very resistant

27
Q

Clinical signs of trichuris suis

A

Seen in growers/finishers

reduced groth rate

loose feces to overt scouring

mucus in feces

occasionally fresh blood in feces in severe cases

28
Q

Diagnosis of trichuris suis

A

fecal egg count: lemon shaped with bipolar plugs

occasionally heavy infestations: can see 10,000s epg

however, PPP 6-10 weeks– eggs only seen in feces of pigs 10 weeks old or older

negative FEC doesn’t rule out diagnosis (i.e. in v. young pigs)

at PM see mild colitis, and embedded adults in LI

29
Q

Treatment of clinical outbreak of trichuris suis

A

can be difficult to eradicate due to egg persistence

in feed, TX with anthelmintics- BZ rather than IVM- may need to retreat (6 weeks later)

withdrawal periods of drugs e.g. flubendazole=7 days

washing and disinfection of environment

may need to depopulate housing (flame gun to clean)

30
Q

Trichuris trichuria (human whipworm)

A

excess of one billion people infected globally, still occurs in southern states of US

31
Q

Oesophagostomum species

A

Nodular worm

Oesophagostomum dentatum and quadrispinulatum

Common strongylid parasite in UK

usually sub-clinical but economically important

Adult worm= 1-2 cm

Cuticle, quite large strongylid parasites

32
Q

Life cycle of oesophagostomum species

A

Adults mature in LI–> eggs in feces–> L1, L2–>L3 ingested (infective stage) and enters SI or LI mucosa–> may induce nodules–> L4 emerge from mucosa–> L4 can also arrest development in nodules in reinfection–> adults mature in LI

IR to L3 movement into the tissues causes most of the pathology

33
Q

Prevalence and epidemiology of oesophagostomum

A

Highest prevalence in older pigs

Life cycle can be completed indoors- L3s can survive or develop in feces-contaminated concrete and skin and can be transmitted by flies

Infection intensity reduced by improved hygiene but prevalence remains high in indoor systems

Infection accumulates with age– higher burdens in sows than fatteners

Increasing acquired immunity–> increasing numbers remain arrested in nodules

34
Q

Periparturient rise and Oesophagostomum

A

periparturient rise in fecal output important in sows

occurs seconday half or pregnancy to weaning

piglets born into highly infected environment

can be prevented by one dose of anthelmintic 1 week before farrowing

Outdoor pigs: L3s overwinter poorly in temperate regions like UK, but L4 can arrest in nodules.

35
Q

Oesophagostomum pathology

A

Diffuse enteritis in colon and caecum

O. quadrispinulatum- most pathogenic species- forms distinct nodules

O. dentatum- forms indistinct nodules

Acute infections: hemorrhage of nodules and secondary infection, form small abscesses

Chronic infections: fibrous nodules

36
Q

Oesophagostomum- clinical signs

A

burdens up to 5,000 adult worms are probably clinically inapparent

reduced productivity

growing pigs: reduced weight gain

sows: poor milk yields (knock-on effect to piglets); contributes to thin sow syndrome; likely to affect fertility of sows; older breeding stock carry heaviest infections d/t larval arrest.

Diarreha in very heavy infections (10,000 adult worms)- very uncommon.

37
Q

Oesophagostomum egg

A

similar to hystrongylus- only diagnostic of oesophagostomum in INDOOR pigs

38
Q

Anthelmintic resistance in pig nematodes

A

reports confined to oesophagostomum to date

generally susceptible to 3 main classes of drugs

ineffective against larvae in nodules

much less problematic than in sheep

No UK reports of resistance.

Parasitology (12 decks)

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