Exam 3 Flashcards
Ascaris suum Basics
- Pig ascarid
- small intestine
- Eggs can live in soil for years
- Young pigs are most susceptible and contribute most to environmental contamination
Ascaris suum Life Cycle
- Larvated egg ingested orally ->
- L3 hatches in intestine->
- migrates to liver ->
- lung ->
- trachea ->
- coughed up and swallowed ->
- Small intestine (L4, adult) ->
- Egg in feces
- Prepatent period is 8 weeks
- No in utero or transmammary transmission
Ascaris suum Pathologic Effects
Adult worms o In intestine o Malnutrition o Occlude lumen o Obstruct bile/pancreatic duct o Can cause perforation o Decrease weight gain & production
Migrating larva
o Liver fibrosis – milk spot (Not clinically relevant)
o Inflammation & secondary infections of lungs
Ascaris suum Public Health & Diagnosis
Public Health
• Zoonotic
• Undergoes same lifecycle in humans
Diagnosis
• History
• Fecal float for “fluffy” egg
• Necropsy – milk spot liver, pneumonia, adults in intestine
Ascaris suum Prevention/Control & Treatment
Prevention/Control
• Drugs alone not successful
• Prevent accumulation of eggs
• Treat sows 2 weeks before and on the day of transport to farrowing crates
• Clean sows with soap and warm water before farrowing
• Treat piglets again at weaning
Treatment • Piperazine • Pyrantel (approved to kill larvae) • Heavy Infections o ½ dose dewormer o full dose few days later
Basics of Stongyloides ransomi
- small intestine threadworm of pigs
- Parasitic and free-living life cycles
- Up to 50% mortality in infected baby pigs
- Can strike first weeks of life
Stongyloides ransomi Life Cycle
- Adult female in the small intestine ->
- larvated egg (L1) shed in environment & hatches ->
- L2, L3 enter host via ingestion or skin penetration ->
- can go to mammary gland (important transmission)
OR
- L3 from free-living cycle can infect host
- Pre-patant period – 5 days oral, 12 days skin
Stongyloides ransomi Pathology/Clinical Signs
• Usually asymptomatic
Acute disease
o Very young pigs- first few weeks of life
o Acute enteritis with bloody diarrhea
o Rapid emaciation and growth stunting
Chronic
o older pigs
o Tend to store up larvae in mammary glands rather than develop adults
Larvae tissue migration
o Lung symptoms
Skin penetration
o inflammation, sensitization, mange-like
Stongyloides ransomi Diagnosis
Antemortem
o Fecal float for larvated egg
o 50 mm, FRESH sample
Postmortem
o Small intestine scraping,
o adult worms, 1-2 mm
Stongyloides ransomi Treatment & Control
Prevent transmammary transmission
o Treat sows 1wk before parturition w/ Ivermectin
Treat 1wk old piglets
o Ivermectin
Reduce moist areas
Rotate out older sows
Physocephalus & Ascarops
- thick, white pig stomach worms
- 1-2 cm long- easy to see on necropsy
- Distinctive eggs in fecal floats
- Elongate (40 um long), thick-walled, larvated egg
- Use beetles as intermediate hosts
- Clinically insignificant and not typically treated
Hyostrongylus rubidis Basics
- Thin, red pig stomach worm
- Strongyle, <1 cm long
- Clinically significant
- Pasture operations in midwest and S
Hyostrongylus rubidis Life Cycle
- Adult in stomach ->
- strongyle egg ->
- motls from L1, L2, L3 on ground ->
- pig ingests L3 ->
- embeds in stomach mucosa ->
- L4 ->
- adult emerges in lumen of stomach
Hyostrongylus rubidis Pathology, Diagnosis, Treatment
Pathology
• Adult pigs at pasture
• Inappetance
• Gastritis, ulcers, melena, anemia
Diagnosis
• 65-75 micrometer strongyle eggs
• postmortem exam
Treatment
• Fenbendazole, ivermectin
Oesophagostomum Basics
- Nodular worm
- Strongyle
- Pig large intestine as adult
- L4 can insist in intestinal mucosa
- Pasture & poor management operations
- Affects feeder pigs
Oesophagostomum Life Cycle
- Adult in large intestine ->
- strongyle egg pooped onto ground ->
- molts L1, L2, L3 ->
- pig ingests L3 ->
- L4 encysts in intestinal wall ->
- adult in lumen of large intestine
Oesophagostomum Clinical Signs & Pathology
- Clinical disease is usually due to L4 encysted in intestinal wall
- Nodule formation
- Granuloma formation in large intestine
- Nodules with inflammation -> chronic diarrhea
- May not detect eggs in feces during clinical disease
- Encysted larvae don’t produce eggs!
Oesophagostomum Diagnosis & Treatment
Diagnosis
• Postmortem
• Presumptively based on history
Treatment
• Fenbendazole (resistance reported)
• Pyrantel
(resistance reported)
• Ivermectin
Trichuris suis Basics
- Whipworm- in cecum & large intestine
- Common in all ages > 6 weeks old
- Produces fewer eggs than Ascaris suum
- Eggs survive years in the environment
- Reinfection is common
Trichuris suis Life Cycle
- Adult in large intestine produces egg ->
- Pig ingests larvated egg ->
- adult in Large I & cecum
- PPP = 6 weeks
- affects growers and adults
Trichuris suis Pathology/Clinical SIgns
- Head embeds in mucosa and damages intestinal epithelium
- Most severe damage in pigs 10-16 wks old
- Anemia
- Bloody D
- Rectal prolapse
- Stunted growth
Trichuris suis Diagnosis & Treatment/Control
Diagnosis
• Fecal float- “fecal jewel” egg
• Adult- whip-like – attached to mucosa
Treatment/Control o Hygiene! eggs persist in environment o Routine treatments o Relocate operation due to envir contamination o Fenbendazole
Globocephalus, Gonglyonema, & Macracanthorrhynchus hirudinaceous
Globocephalus
• hookworms in small intestine of pig
• strongyle type egg
• rare
Gonglyonema
• Pig Esophageal worm
• Clinically insignificant
• Requires beetle intermediate host
Macracanthorrhynchus hirudinaceous
• Acanthocephalan- “spiny headed worm”
• Requires beetle intermediate host
Metastrongylus Basics
- Swine lungworm
- 8.5 cm long and thin
- Most common in MW & S
- Earthworm intermediate host is a reservoir for transmission
- Clinical signs occur relatively late
Metastrongylus Life Cycle
- Adult in lung ->
- egg coughed up and swallowed ->
- larvated egg in feces ->
- earthworm ingests larvated egg ->
- pig ingests earthworm
Metastrongylus Pathology & Clinical Signs
- Migrating larvae -> irritation, inflammation -> cough & secondary infections
- Chronic adult infection - lung consolidation, cough, secondary infections
- Modest clinical and economic significance
Metastrongylus Diagnosis & Treatment
Diagnosis
• Fecal float- larvated eggs, 55 x 40 um
• Adults are deep in airways
Treatment
• Fenbendazole
• Ivermectin
Stephanurus dentatus Basics
- Swine kidney worm
- Strongyle
- Usually in SE
- Likes warmth & humidity
Stephanurus dentatus Life Cycle
- Adult in perirenal area lays eggs in ureter ->
- ground via urine ->
- L3 into host via oral or skin penetration ->
- L4 migrates to liver & stays 4-9 months = liver damage ->
- Migrates thru retroperitoneal tissue
- Earthworms are paratenic hosts (reservoir) Facultative intermediate hosts- NOT required for development
- PPP = 9-16mo
Stephanurus dentatus Pathology
- Due to L4
- Hemorrhage, necrosis, fibrosis of liver
- Stunting
- Meat destruction due to migration
- Aberrant migration to spinal cord = necrosis & inflammation
Stephanurus dentatus Diagnosis
Problematic young pigs
o No adult worm in young pigs
o Past clinical history
Postmortem diagnosis
o Livers with necrosis and fibrosis and worms
o Adult worms around kidney
Adult swine
o Strongyle eggs in urine
Stephanurus dentatus Treatment & Control
Treatment
• Doramectin
• Fenbendazole
• Kills adults
Control
• Due to long PPP if you breed very young gilts you can eliminate worm in pop
Trichinella spiralis Basics
o Trichinellosis or Trichinosis
o Larvae (L1) in muscle, and adults in intestine of infected mammals
o Infects essentially all mammals
o 10,000 people infected every year & Serious disease and death in people
o Transmitted in undercooked meat
o Pork, (horse) in domestic cycle
o Wild pigs, bear, seal, walrus, cougar in sylvatic cycle
o Typically occurs as outbreaks
o Economic importance
Trichinella spiralis Life Cycle
- L1 ingested from pig muscle ->
- Excyst in small intestine ->
- Embed in mucosa ->
- Molts L2, L3, L4, adult in 5 days ->
- Produce more L1 ->
- L1 enters lymphatics then blood stream ->
- Enters tissue then muscle cell ->
- Muscle induces cyst form ->
- Chronic infection (months to years)
- Entire life cycle in one host
- No stages in feces
Trichinella spiralis Sources of Infection
- Backyard operations or poorly managed swine operations- dead pigs, cannibalism, tail biting, rodents
- Hunted wild animal meat products
- Unusual sources- horse meat
Trichinella spiralis Pathology in Humans
• Dose dependent
Intestinal Phase
• 1 week after infection may get clinical signs
• Nausea
• Vomiting
Migration Phase • 2-3 weeks PI; acute trichinellosis • Severe inflammation in skeletal muscle- diaphragm, tongue, periorbital • Heart (myocarditis), cause of death • Lungs, liver • CNS (encephalitis, meningitis)
Muscle Phase- Chronic
• Mild to severe inflammation, tissue dysfunction
Trichinella spiralis Diagnosis in Pigs
Muscle digestion in acid
• Pepsin and HCl
Microscopic inspection of muscle
• Tissue squash, histology
ELISA serology
• Antibodies develop after ~ 40 days
• Mostly used for surveys
Trichinella spiralis Diagnosis in Humans & Prevention
Diagnosis • Eosinophilia, muscle pain, periorbital edema, gastroenteritis, pruritis and skin eruption • Biopsy • ELISA serology • Outbreaks • History
Prevention
• Education on proper food prep
• Good rodent management on pig farms
• Cook your meat!
Taenia solium Basics
- Pork tapeworm of humans
- Humans get cysticercus & adult
- Pigs only get cysticercus (pork measles)
- Causes neurocysticercosis in humans
Taenia solium Life Cycle
- Adult in human SI ->
- egg in human feces ->
- pig ingests ->
- cysticercus in pig muscle ->
- human ingests ->
- develops into adult tapeworm
How do humans get cysticercus?
- Ingestion of eggs from human feces
* Potentially retroperistalsis
