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30 Cards in this Set
- Front
- Back
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How do parasite problems increase in housing systems? |
Highly intensive = least amount of parasite problems - slatted floors, no bedding Indoor "extensive systems" - solid floors. Straw bedding Outdoor Systems Organic System = most parasite problems |
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Small intestine Nematodes: |
Ascaris Suum Trichinella Spiralis (also zoonotic) |
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Large Intestine nematodes: |
Oesophagostomum spp Trichuris suis |
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Life of ascaris suum: |
- Typical ascarid - Large, 40cm - Direct life cycle - PPP = 6-8 weeks - L3 inside egg is infective - Migratory Egg (L1 develops in egg) L2 - inside egg L3 - inside egg (infective stage) - earthworm can be paratenic host (won't develop in it) L3 hatches after ingestion (is inside the host) L3 travels to liver via portal circulation L3 in liver Travel in blood to lungs Travel up bronchial tree and swallowed Moult to L4 in SI Adults in small intestine Eggs Shed in feces |
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Clinical Signs of Ascaris suum |
Over clinical signs not usually seen - burdens with adult worms typically 1-5 individuals per host Reduced productivity (up to 10%) - food conversion efficiency - reduced weight gain - increased fattening time Occasionally impaction and/or obstructive jaundice - overdispersed population structure Occasionally transient pneumonia in young pigs due to migrating larvae Milk spot liver |
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What is milk spot liver? |
Cloudy white spots up to 1cm Fibrous repair of inflammatory reaction to migrating L2/L3 Common Liver condemnations - economically important! |
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Diagnosis of Ascaris suum |
Clinical signs and history (poor production) Faecal egg counts *50-70 micrometers (µm) in length * 40-60µm wide - can be very high (1000's epg) - can also detect in feces collected from pens Incidence of liver condemnations - in Europe, a serologic test measuring antibodies to parasite Hb to assess infection levels recently made available |
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Ascaris suum Epidemiology |
Can complete life cycle indoors (unlike trichostrongylids of ruminants) - infective stage is inside egg Each female worm -> 200,000 eggs per day - eggs extremely resistant (up to 5 years or more) Eggs need to develop in environment to become infective - unlarvated egg in fresh faeces (not yet infective) -> develops in environment (min of 4 weeks, depending on temp) -> larvated egg (infective) *optimal temp range 22-26 C *no development below 15C - leads to seasonal pattern (e.g. greatest incidence of "milk spot" in summer Highest burden in young growinng pigs - acquired immunity in adults Difficult/impossible to eradicate from indoor systems - improved hygiene reduces intensity of infection and increases age at whih piges are infected *slatted floors vs. straw *anthelmintic drugs routinely used for control - can overwinter (outdoor systems) |
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Ascaris infections in humans |
Developing world: Ascaris lumbricoides - very high morbidity, high mortality Developed world: Ascaris lumbricoides not present Ascaris suum occasional zoonotic infection - contamination of vegetables with pig excrement Can infect humans if eggs consumed |
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Trichinella overview |
Important worldwide due to zoonosis - economic cost of meat inspection and regulation - re-emerging in some countries (China, Eastern Europe) - wildlife reservoir; sporadic disease from eating undercooked wild game Small intestine nematode Trichinella spiralis most common species worldwide, and largest zoonotic risk - undercooked pork most important source of human infection Other trichinella species important in wildlife reservoirs |
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Trichinella spiralis Life Cycle |
L1 ingested in infected muscle tissue L1 infects SI mucosal epithelium L2 -> L3 -> L4 -> adult - occurs within small intestine in 2 days. - patency reached in 5 days post-infection In same host, adult -> newborn larvae (L1) - penetrate intestinal mucosa of same host Travel via lymph and blood - enter either mesenteric lymphatics of bloodstream (usually newborn larvae enter general circulation to distribute throughout body) L1 migrate to muscles Form encyst in muscle - cause skeletal muscle cells to re-differentiate into nurse cells |
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Trichinella nurse cells |
cells loses differentiation and becomes nurse cell, forms capsule, get angiogenesis and sinusoids. Orchestrated by products released by parasites within muscle cell Hidden from immune system Eventually becomes calcified (gritty tissues) |
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Trichinella clinical signs in man |
Infections usually light and asymptomatic Following heavy infections: - intestinal infection can cause transient enteritis (L1 to adult) 1-2 weeks later L1s in muscle cause - acute myositis - pyrexia - myocarditis - periorbital and facial edema - photophobia - ascites - eosinophilia Can be fatal Diagnosis: - muscle biopsy - ELISA - epidemiological information |
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Domestic cycle of Trichinella |
Pigs + rats - Trichinella spiralis Pig ----> human via undercooked pork Pig ----> Pig - Infected pig feed - Tail biting - Rats Pigs generally asymptomatic Generally in extensive management systems *low incidence of infection also present in horses |
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Sylvatic cycle of Trichinella |
Wild animals - predominantly carnivores - trichinella spiralis and at least 14 other species *differentiated by molecular markers, PCR Modes of infection: - predation - scavenging/carrion feeding - cannibalism - (ingestion of fresh feces from infected animals) Sylvatic cycle well established in Canada *eating wild game is source of infection for humans |
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Capsulated Trichinella species |
T. spiralis T. nativa (cold tolerant) - Canada Trichinella T6 (cold tolerant) - Canada |
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Uncapsulated Trichinella species |
T. pseudospiralis - Canada |
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Sources of Trichinella infection for man |
T spiralis: eating undercooked pork Infection of pigs is mainly a risk for: - outdoor systems (contact rodents/wildlife reservoirs - Countries/situations where untreated animal products used in pig feed - Countries where poor public health systems in place Not major problem where intensive pig husbandry practice and good public health systems *horse meat also source in some countries Other Trichinella species: eating wild game |
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Prevention of Trichinella infection in humans |
Education - consumer education about risk of eating raw or undercooked pork/wild game Farming of pigs in manner to minimize infection - intensive husbandry systems - certified feedstuffs (prohibit of uncooked food waste to pigs) - rodent control Surveillance of susceptible animals (domestic and sylvatic) - use standardized artificial digestion method post-slaughter or after hunting |
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Treatment of meat to inactive Trichinella prior to consumption |
Cook to core temp of not less than 71C for at least 1 minute Freezing (up to 15 cm thickness): frozen solid at least -15C for at least 3 weeks - will kill T spiralis - wild game strains may be cold tolerant Irradiation Curing/smoking/drying not considered safe! |
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Surveillance of T spiralis in pigs |
Examine muscle from carcass for detection of larvae Predilection sites: - diaphragm - tongue - masseters Use Recognized Standard Approacch |
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Standard Pepsin-HCL digestion method |
Artificial digestion with Pepsin-HCl - 5g of muscle digested - reference method in most countries - sensitivity of ~1 larvae per gram (when 5g used) *can be combined with PCR to confirm species identitiy |
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Trichuris suis overview |
"whipworms" Large Intestine nematode - adults live in large intestine with anterior ends embedded in mucosa Adults = 4-6cm long Eggs 50-70µm long shell less thick than trichinella? - Mild/moderate infections asymptomatic - Clinical disease not common but can be problematic - more common in outdoor systems (organic) - transmission can occur indoors but restricted to "traditional systems" (e.g. solid floors/straw) - typically poor hygiene - eggs survive in environment for several years (very resistant, 2-11 years!) |
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Trichuris suis life cycle |
Eggs in feces (environment) L1 inside egg - (minimum of 1-2 months maturation before infective, can be up to 12 months) L1 inside the egg is the infective stage Ingestion (inside host) L1 released from egg and penetrates large intestinal mucosa L2 -> L3 -> L4 Adults emerge in colon/caecum PPP 6-12 weeks |
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Clinical signs of trichuris suis |
seen in growers/finishers - reduced growth rate - loose feces to overt scouring - mucus in feces - occasionally fresh blood in feces in severe cases (facilitates invasion of pathogenic spirochetes) |
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Diagnosis of trichuris suis |
Fecal egg count - occasional heavy infestations (can see 10,000 epg) - howeer PPP 6-10 weeks, eggs only seen in feces of older pigs 10 weeks or more Negative FEC does not rule out diagnosis |
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Oesophagostomum ("nodular worm") |
O. dentatum and O. quadrispinulatum - common in most countries - present in indoor systems in N america and western Europe Large intestine nematode Usually subclinical (production impact) Adult worm stout: 1-3cm long |
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Life cycle of Oesophagostomum spp. |
Eggs in feces L1 L2 L3 - ingested and enters SI or LI mucosa Once inside host: - may induce nodules L4 emerge - L4 can arrest development in nodules in reinfections Adults in large intestine PPP = 18-21 days |
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Oesophagostomum Epidemiology |
- poor acquired immunity: infections intensities increase with age Most common in organic herds and conventional indoor hrds Periparturient rise in fecal egg output occurs in sows - piglets born into highly infected environment |
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Oesophagostomum Clinical and Sub-clinical signs |
Sub-clinical: contribute to reduced productivity - infection intensities of up to 5000 adult worms are sub-clinical - reduced weight gain in growing pigs Clinical syndromes: - infection intensities of >10,000 worms can cause: Growing pigs - accute diarrhea (not common, tends to occur in very poor hygiene/husbandry situations) Sows - older breeding stock carry heaviest infections - can contribute to "thin sow syndrome" - fertility? - poor milk yields - leads to increased piglet mortality/disease |
