Pig Nematodes Flashcards
GI Nematodes of Pig
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**
Pig husbandry and parasites
Increasing parasite problems as we move from intenstive systems with slatted floors and no bedding to organic systems.
Pig nematodes and prevalence based on husbandry
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
Hyostrongylus rubidus- red stomach worm
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
Hyostrongylus rubidus- pathology
pathology is similar to ostertagia
nodule formation on surface of stomach
puncture wounds from gastric gland eruption– coffee granule appearance
Hyostrongylus rubidus- clinical signs and diagnosis
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.
Ascaris suum
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
Ascaris suum- direct life cycle
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.
Adult ascaris suum
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
Maturation of eggs in environment
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
Ascaris lumbricoides- human roundworm
extremely important parasite of humans in the developing world
Relationship btwn A. suum and A. lumbricoides
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
Clinical signs of A. suum
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
Ascaris suum in the PM room
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.
Diagnosis of A. suum
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
Ascaris suum- epidemiology
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.
Trichinella
important mostly because it’s a zoonosis
will infect any mammal but mostly carnivores and omnivores and pig is a major host
Trichinella spiralis life cycle
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.
Trichinella spiralis- modes of infection
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.
Trichinella- sylvatic cycle
[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
Trichinella domestic cycle
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.
Diagnosis of trichinella in pigs
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
Clinical signs of trichinella in man
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
Control measures of trichinella
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)
Trichuris suis whipworm- life cycle
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
Trichuris suis epidemiology
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
Clinical signs of trichuris suis
Seen in growers/finishers
reduced groth rate
loose feces to overt scouring
mucus in feces
occasionally fresh blood in feces in severe cases
Diagnosis of trichuris suis
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
Treatment of clinical outbreak of trichuris suis
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)
Trichuris trichuria (human whipworm)
excess of one billion people infected globally, still occurs in southern states of US
Oesophagostomum species
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
Life cycle of oesophagostomum species
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
Prevalence and epidemiology of oesophagostomum
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
Periparturient rise and Oesophagostomum
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.
Oesophagostomum pathology
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
Oesophagostomum- clinical signs
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.
Oesophagostomum egg
similar to hystrongylus- only diagnostic of oesophagostomum in INDOOR pigs
Anthelmintic resistance in pig nematodes
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.
