Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/18

Click to flip

18 Cards in this Set

  • Front
  • Back
Secondary Nematode Pathogens/Contributors
Haemonchus sp
Trichostrongylus spp
Bunostonum spp
Oesophagostomum sp
Chabertia sp
Trichuris sp
Secondary Nematode Pathogens/Contributors of Sheep
Nematodirus spp
Cooperia spp
Strongyloides sp
Bunostonum sp
Oesophagostomum sp
Chabertia sp
Trichuris sp
Names, Appearance, Life Cycle and Pathogenicity of Large Strongyles of Horses
Strongylus equinus, S. edentatus, S. vulgaris, Triodontophorus spp.
Gross appearance
Stout worms, 1.5-5cm long
Large buccal cavity
Bursa visible
Leaf crowns, teeth, dorsal gutter
Life cycle: L3 from grass  ingested  penetrate intestinal mucosa then:
S. Vulgaris migrates through mesentaeric artery PPP 6-7 months
S. edantatus through liver hepatic portal circulation and peritoneum. PPP 11-12 months
S. equinus swims to liver through peritoneal cavity then back to intestine PPP 9 months
Triodontophorus molts from L3  L4 in wall of intestine
Pathogenicity
Plug feeders: ulcers, bleeding, anemia
Life Cycle and Pathogenicity of Small Strongyles of Horses
Cyathostomes
Small worms < 1.5cm long
Life cycle
Ingest L3  larvae invade mucosa of LI
 Larvae may develop to L4 without interruption
Or  can arrest at EL3 stage
L4 emerge into gut lumen and mature to adult worms
PPP 8-12 weeks
Pathogenicity
Plug feeders (superficial mucosa)
Cyathostomosis
L3 local inflammatory response
Type 1: Larval emergence through summer. Tens or hundreds of thousands
Type 2: emergence of previously arrested larva
Serious disease, wt loss, severe diarrhea
Secondary Pathogens
Trichostrongylus axei
Cattle, sheep, pigs, horses
Pathogenicity is similar to Ostertagia but does not enter gastric glands  nodular lesions
Habronema/Draschia spp
Spiruroids occurring in stomach
Draschia found in torpics
Mild gastritis
Indirect lifecycle – Musca spp
Onchocerca spp
Filarial nematode, Indirect LC, cullicoides (midge) is intermediate host
Thelazia sp
Same as cattle, conjunctivitis, Indirect LC  flies (Musca)
Life Cycle of Trichinella spiralis
Life cycle:
L1 liberated from cysts by host digestive enzymes  invade intestinal mucosa  females lay prelarvae 5 days later  enter lymphatics  enter bloodstream  transported to muscles  develop into encysted L1 2-3 weeks later in striated muscle
Zoonosis of Trichinella spiralis
Humans can become infected by eating undercooked pork (or another infected mammal)
Outbreaks are becoming less frequent in US and Europe, may still be a problem in less developed countries
5 larvae ingested per gram of body weight is fatal
Periorbital edema, myalgia, fever, gastroenteritis, pruruitis, dermatological lesions, eosinophillia (in 20%)
Control:
Treatment of mammals rarely performed
Sub/non clinical
Meat inspection (most important method)
Detected via biopsy, enzymatic digestion methods, ELISA
Infected carcasses are destroyed
Roast meat evenly to at least 77°C internal temp
Freezing -15°C for 20 days
Macracanthorhynchus sp
Beetle intermediate host
Spiruroids: Ascarops stongylina and Physocephalus sexalatus
Stomach worms of pigs
Not very pathogenic (secondary pathogens)
Toxocara canis
Most prevalent nematode of dogs.
Almost ALL!! Puppies harbor this worm
Can cause serious disease in large numbers
Can invade human tissues
Impairment of vision, media attention
Typical ascarid: fleshy adult worm, up to 18cm long and lives in small intestine of dog, fox, and other canidae.
Egg is characteristic dark egg with a pitted surface
Significance/clinical signs
Pot-belly, diarrhea, vomiting, wt loss: young puppies
Can cause intestinal obstruction
Possible zoonosis
Zoonosis of Toxocara canis
3 disease syndromes in humans
Visceral larval migrans (VLM)
Eosinophilia, hepatomegaly, fever, asthma
Ocular larval migrans (OLM)
Unilateral partial impairment of vision
More common
Covert toxocarosis (-iasis)
Non specific clinical signs associated with high Ab titre
In most cases, Toxocara infections are not serious, and many people, especially adults infected by a small number of larvae (immature worms), may not notice any symptoms. The most severe cases are rare, but are more likely to occur in young children, who often play in dirt, or eat dirt (pica) contaminated by dog or cat stool.
Toxocara canis Lifecycle in Puppies
Larvae migrate via hepatotracheal route  small intestine  become adult  eggs passed in feces
PPP is about 4-5 weeks
Nematodes of Dogs
Toxocara canis- ascarid- small intestine
Toxascaris leonina- ascarid- small intestine
Uncinaria stenocephala- hookworm- small intestine
Ancyclostoma caninum- hookworm- small intestine
Trichuris vulpis- whipworm- cecum
Filaroides (Oslerus) osleri- lungs
Angiostrongylus vasorum- heart
Dirofilaria immitis- heart
Nematodes of Cats
Toxocara cati- ascarid- small intestine
Toxascaris leonina- ascarid- small intestine
Aelurostrongylus abstrusus- lungs
Lifecycle and Epidemiology of Toxocara canis in Other Warm-blooded Adults
Many animals can be paratenic (similar to intermediate) host
Larvae migrate  liver  via heart to lungs  stay in blood stream and back to heart  somatic tissues (liver, kidney, musculature)  granulomatous reactions  “waiting phase”
Will be protected from antiparasitics and remain inactive until:
Eaten: ie non-canid
Or pregnancy: female canids
Treated male canids are not very signficant
Epidemiology of Toxocara canis in Dogs
Infection of dogs is by ingestion of the L2, which can occur in four ways
Ingestion of embryonated egg
Prenatal infection
Transmammary infection
Ingestion of paratenic host
Infection of a paratenic host can occur by:
Ingestion of embryonated egg
Ingestion of larvae in the tissues of another paratenic host
Each female T. canis  250,000 egg/day
Eggs are not infected until L2
Eggs can survive 4-5 years, accumulated in environment
Ie: breeding kennels, city parks, etc
Lifecycle and Epidemiology of Toxocara canis in Other Warm-blooded Adults
Many animals can be paratenic (similar to intermediate) host
Larvae migrate  liver  via heart to lungs  stay in blood stream and back to heart  somatic tissues (liver, kidney, musculature)  granulomatous reactions  “waiting phase”
Will be protected from antiparasitics and remain inactive until:
Eaten: ie non-canid
Or pregnancy: female canids
Treated male canids are not very signficant
Epidemiology of Toxocara canis in Dogs
Infection of dogs is by ingestion of the L2, which can occur in four ways
Ingestion of embryonated egg
Prenatal infection
Transmammary infection
Ingestion of paratenic host
Infection of a paratenic host can occur by:
Ingestion of embryonated egg
Ingestion of larvae in the tissues of another paratenic host
Each female T. canis  250,000 egg/day
Eggs are not infected until L2
Eggs can survive 4-5 years, accumulated in environment
Ie: breeding kennels, city parks, etc