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120 Cards in this Set
- Front
- Back
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What is the common name for Strongylidea?
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bursate worms
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what is the disting feature of males of Order Strongylidea?
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copulatory bursa (cuticle expansion lobes supported by muscular rays) to grasp female at vulvar site to facilitate spicule insertion & movement of sperm (but less developed in Metastrongyloidea)
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describe the buccal area of Trichostrongyloidea?
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small or absent
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describe the buccal area of Strongyloidea?
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large with well-developed buccal capsule; leaf crown at opening & teeth at base where it opens to the esophagus
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describe the buccal area of Ancylostomoidea?
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large, bent dorsally, buccal capsul has pointed teeth or cutting plates at anterior opening
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describe the buccal area of Metastrongyloidea?
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usually lacks buccal cavity
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where are most Trichostrongyloidea found?
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in the abomasum or small intestine of ruminants
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where are most Strongyloidea found?
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large intestine of horses
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where are most Ancylostomoidea found?
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small intestine of a variety of mammals
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where are most Metastrongyloidea found?
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lungs, some in vascular or nervous system of mammals
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How are Strongylidea found in feces?
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morulated 'strongyle-type' eggs in feces (except Metastrongyloidea = L1 in feces)
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What is the general life cycle of Strongylidea?
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morulated eggs in feces à free-living L1-L3 à L3 (infective, non-feeding) à ingested
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what do Strongylidea require environmentally?
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moulting requires moisture, O2, & temp >50F
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how does Trichostrongyloidea infect hosts?
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generally only ingestion of pasture herbiage
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how does Ancylostomoidea infect hosts?
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generally skin penetration
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how does Metastrongyloidea infect hosts?
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ingestion of infected intermediate host or paratenic host
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What are the four superfamilies of Strongylidea?
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Trichostrongyloidea, Strongyloidea, Ancylostomatoidea, Metastrongyloidea
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what is the common name for Trichostrongyloidea?
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trichostrongyles
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what generas of Trichostrongyloidea infect the abomasum and duodenum of grazing ruminants?
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Cooperia, Haemonchus, Ostertagia, trichostrongylus (mnemonic C-HOT)
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what Trichostrongyloidea most severly affects sheep and goats?
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Haemonchus contortus
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what Trichostrongyloidea most severly affects cattle?
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Ostertagia ostertagi
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How long are Trichostrongyles?
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adults are <7mm
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what is the prepatenet period of Trichostrongyles?
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~3w
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what species are in the Trichosrongyloidea?
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Haemonchus contortus, Haemonchus placei, Ostertagia ostertagi, Teladorsagia (Ostertagia) circumcincta, Trichostrongylus axei, Trichostrongylus colubriformis, Cooperia punctata/pectinata, Cooperia oncophora, Cooperia curticei, Cictyocaulus viviparous, Dityocaulus filarial, Dictyocaulus arnfiedi
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where does Trichostrongylus axei infect?
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stomach or abomasum of ruminants and horses
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where does Trichostrongylus colubriformis infect?
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small intesting of ruminants
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what is the morphology of Trichostrongylus axei and Trichostrongylus colubriformis?
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adults < 7mm long, little or no buccal cavity, very few eggs
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describe the pathogenesis of Trichostrongylus axei and Trichostrongylus colubriformis infect?
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rarely causes disease alone, usually in association with Ostertagia, Haemonchus, or Cooperia
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what are the clinical signs of Trichostrongylus axei and Trichostrongylus colubriformis?
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watery diarrhea which requires 100,000 worms caused by plaque of eroded epithelium in stomach or duodenum
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What affect does Trichostrongylus axei have on horses?
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more pathogenic; advise not to co-graze horses with sheep or goats
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what is the prepatent time for Trichostrongylus axei and Trichostrongylus colubriformis?
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3 wks
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where does Ostertagia ostertagi infect?
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Ruminant abomasum, important in cattle (to lesser degree in llamas), worse in calves < 1yr
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where does Teladorsagia circumcincta infect?
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abomasum of sheep, goat, llama
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What is the common name for Ostertagia ostertagi and Teladorsagi circumcincta?
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brown stomach worm
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what is the morphology of Ostertagia ostertagi and Teladorsagia circumcincta?
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adults are 7-14mm long, brown in collor, broad shallow buccal cavity, female has vulvar flap and produces less than 100 eggs/day/worm
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what is the life cycle & transmission of Ostertagia ostertagi and Teladorsagia circumcincta?
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L3 ingested from pasture > enter gastric glands, develop to L4 > emerge to gastric lumen or arrest in glands
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what is the pathogenesis of Ostertagia ostertagi and Teladorsagia circumcincta?
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L4/adults in gastric glands = de-differentiation of chief/parietal cells = loss of acid production, increase abomasal pH. Emerging adults = inflammation, Mucosal cells form hyperplastic lesion at infected gland opening = Moroccan leather, Leaky mucosa = loss of protein/fluid into lumen > protein catabolism, loss of nitrogen in urine = protein deficiency, hypoproteinemia, CS: anorexia, diarrhea, wt loss, poor growth (protein deficiency + anorexia), edema
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what is the prepatent time for Ostertagia ostertagi and Teladorsagia circumcincta?
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3 wks
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what is the transmission of Ostertagia ostertagi and Teladorsagia circumcincta limited by?
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host specific, does not cross-infect
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what are the clinical signs of Ostertagia ostertagi and Teladorsagia circumcincta infection?
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anorexia, diarrhea, decreased weight gain or weight loss, evidence of protein deficiency in matrix osteoporosis of bone (resulting in poor growth) and hypoproteinemia
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how is Ostertagia ostertagi and Teladorsagia circumcincta diagnosed?
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fecal egg counts, response to treatment (low egg count if many arrested L4); pepsinogen levels in serum (glands reverse causing pepsinogen leaks into serum)
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when does Ostertagia ostertagi and Teladorsagia circumcincta affect cattle?
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4-8w after turnout; cattle develop effective age-resistance = fewer patent animals
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what resistance does Ostertagia ostertagi and Teladorsagia circumcincta have?
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no anthelmentic resistance
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where does Haemonchus contortus infect?
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abomasum of ruminant; important in sheep/goats
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where does Haemonchus placei infect?
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abomasum of cattle; less pathogenic
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what is the morphology of Haemonchus contortus and Haemonchus placei?
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10-30mm, males = asymmetrical dorsal lobe of copulatory bursa, female ovaries twist around red (blood filled) intestine giving barber pole appearance
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what is the common name of Haemonchus contortus and Haemonchus placei?
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barber pole worm
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what is the life cycle & transmission of Haemonchus contortus and Haemonchus placei?
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Ingestion of L3 from pasture > L4 > L5 and adults feed on blood in abomasum/duodenum > morulated eggs > develop to L3 (5-7d)
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what is the pathogenesis of Haemonchus contortus and Haemonchus placei?
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Prepatent L5 and adult worms in lumen of abomasum = BLOOD-FEEDERS > anemia, hypoproteinemia; can occur within 1w of ingestion (large # of larvae)
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what are the clinical signs of Haemonchus contortus and Haemonchus placei?
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black or tarry feces (NOT diarrhea), pale MM, low PCV, rapid shallow breathing, high HR, edema of lips, intramandibular (bottle jaw), limbs
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what is the prepatent period of Haemonchus contortus and Haemonchus placei?
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3 wks
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what is the transmission of Haemonchus contortus and Haemonchus placei limited by?
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host specific, does not cross-infect
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when does Haemonchus contortus and Haemonchus placei affect livestock?
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Commonly a problem in LATE grazing season. Adults do not develop strong resistance.
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where does Cooperia punctata/pectinata infect?
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abomasum of ruminants and stomach of horses
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where does Cooperia oncophora infect?
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proximal small intestine of cattle
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where does Cooperia curticei infect?
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proximal smal intestine of sheep
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what is the morphology of Cooperia punctata/pectinata, Cooperia oncophora, and Cooperia curticei?
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5-10mm, anterior cuticle inflated with transverse striations
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what is the pathogenesis of Cooperia punctata/pectinata?
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adults deep in mucosa of proximal small intestine > enteritis, catarrhal inflammation, important in mixed infections with Ostertagia or Haemonchus
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what are the clinical signs of Cooperia punctata/pectinanta?
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anorexia, diarrhea, usually not sole source of disease
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what is the pathogenesis of Cooperia oncophora?
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rarely pathogenic
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what is the prepatent period of Cooperia punctata/pectinata, Cooperia oncophora, and Cooperia curticei?
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3 wks
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what resistance does Cooperia punctata/pectinata, Cooperia oncophora, and Cooperia curticei?
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some ivermectin resistance
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how is Cooperia punctata/pectinata, Cooperia oncophora, and Cooperia curticei diagnosed?
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requires fecal culture to obtain L3 or postmorten mucosal scrapings
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where does Nematodirus species infect?
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proximal small intestine of cattle and sheep
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what is the source of infection of Trichostrongyle in ruminants?
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entirely based on pasture grazing
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what determines the number of Trichostrongyle eggs on a pasture?
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adult worm population in grazing hosts
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what conditions are required for Trichostrongyle eggs to hatch and L1 to become L3?
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warmth, air, moisture
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what is the best time of the year for development and transmission of Trichostrongyles?
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summer and early fall in cool climates and winter and early spring in semi-tropical climates having hot/dry summers
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How is a large adult population of Trichostrongyles generated?
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ingestion of large numbers of larvae
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what is Type I Ostertagiasis?
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L4 do not arrest, they emerge and become egg laying adults in 3 weeks. Usually in calves in the Fall (cool temperate regions) or Spring (hot, semi-arid regions)
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what, other than ingestion of larvae, is another source of adult Trichostrongyles?
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arrested L4 stage larvae in gastric glands of the abomasum
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what is Type II Ostertagiasis?
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when L4 becomes activated to develop to adults (early spring in the North, early fall in the South)
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what occurs when an adult population of Trichostrongyles is removed?
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allows L4 to become a new adult population
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What should one know about anthelmintic treatment in Trichostrongyles?
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if it is active against L4
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What else stimulates arrested L4 Trichostrongyles to become adults?
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onset of lactation
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when is periparturient Haemonchosis important in ewes?
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all ages
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when is periparturient Ostertagiasis important in cows?
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usually at first calving only
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how can Trichostrongyles be controled?
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tactical or strategic treatment
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how are Trichostrongyles treated tacticaly?
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when susceptible animals are on heavily contaminated pastures must treat repeatedly due to reinfection or treat and move
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how are Trichostrongyles treated strategically?
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soon after uninfected animals are put on pasture they are treated to prevent adult worms from generating eggs to contaminate pasture (treat calves with repeating or long lasting adulticide in spring when put on pasture in cool temperater regions, and treat re-stocking calves with adult and L4 killing drugs in late fall) and (treat calves, long-yearlings in early fall (wet season) with adulticidal drugs; treat calves in late spring/early summer at start of the dry season with adult and L4 killing drugs in subtropical regions) and (to get optimal milk production, first lactation cows are treated just before calving) and (to prevent disease and minimize pasture contamination ewes and goats are treated before parturition)
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what determines host role in pasture contamination?
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host susceptibility; variation in susceptibility to infection 15-20% of herd and carry most of the adult worm burden and produce ~80% of eggs (can be refugia worm population to prevent drug resistance), age, premunition or concomitant immunity
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where does Dictyocaulus viviparous infect?
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bronchi of cattle
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where does Dictyocaulus filarial infect?
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bronchi of sheep/goats
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where does Dictyocaulus arnfiedi?
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bronchi of horses
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what is the morphology of Dictyocaulus viviparous, Dictyocaulus filarial, and Dictyocaulus arnfiedi?
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30-80mm, thin, small buccal cavity, male copulatory bursa is smaller than others, stout spicules, femles lay eggs with L1 that hatch while in host
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what is the lifecycle and transmission of Dictyocaulus viviparous, Dictyocaulus filarial, and Dictyocaulus arnfiedi?
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Infective L3 ingested from pasture > penetrate gut > lymph ducts and mesenteric lnn to thoracic duct > venous blood > lungs > L4 moults to L5 > adults lay eggs in lungs. Adults in primary/secondary bronchi, NO intermediate host; L3 live free on pasture; larvae susceptivle to dessication
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what is the pathogenesis of Dictyocaulus viviparous, Dictyocaulus filarial, and Dictyocaulus arnfiedi?
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"Worms + inflammatory exudates (osinophil and leukocyte) fills bronchi = blocks air flow
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how is Dictyocaulus viviparous, Dictyocaulus filarial, and Dictyocaulus arnfiedi diagnosed?
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L1 in fecal float or Baermann; dark brown food granules in larvae
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what is the treatment for Dictyocaulus viviparous?
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vaccination with atetenuated L3 in Europe, broad spectrum anthelmentics; avoid low, wet pastures
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what is a preventative measure for horses against Dictyocaulus arnfiedi?
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Donkeys have patent infection while horses have more pathological infection so don't graze donkeys with horses
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what determines the # of trichostrongyle eggs shed on pasture?
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the adult worm population in grazing hosts
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what determines if we treat a trichostrongyle parasite infestation?
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parasite fencundity
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when do we treat animals for Ostertagia?
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200+ epg
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when do we treat animals for Haemonchus?
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1000+ epg
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where do trichostrongyle eggs and larvae develop?
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moisture, warmth, >50F, O2
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what do trichostrongyle eggs and larvae require for development?
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fecal pat incubator - moisture, warmth, >50F, O3
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what is the best time of the year for trichostrongyle development/transmission on pasture in cool climates?
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summer/early fall
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what is the best time of the year for trichostrongyle development/transmission on pasture in warm climates?
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winter/sprin
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what is the best time of the year for testing for dewormer resistance in trichostrongyles?
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END of grazing season whn you expect worm burden to be highest
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what is type I Ostertagiasis in trichostrongyles?
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L4 do not arrest; emerge and become egg-laying adults in 3w; usualy occurs in fall (cool temperate regions) or spring (hot, semi-arid regions)
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what is type II Ostertagiasis in trichostrongyles?
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L4 arrested in abomasal mucosa, particularly tend to arrest if L3 ingested at END of grazing season (fall in temperate or spring in tropical regions), reactivate at beginning of grazing season (early spring in temperate or fall in tropical) but also stimulated to reactivate by lactation or by removal of an existing population with dewormers (called premonition)
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in what species does periparturient haemonchosis occur?
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sheep In ewes
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briefly, what is periparturient haemonchus?
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type II ostertagiasis
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what occurs in periparturient haemonchosis?
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in ewes the emergence of L4 is stimulated by parturition. Adults develop and produce eggs to contaminate pastures for lambs to ingest L3. ewes debilitated by large adult worm burden
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how do we test for trichostrongyle resistance?
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sample at the time of dosing with drug and again at a period that does not allow patency (7-10d later does not allow patency of newly ingested eggs or L4s coming out of arrest) looking for a drop in egg count
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what can cause host resistance to trichostrongyles?
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individual variation, age in cattle (not sheep), and preminution or concomitant immunity
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when are cattle resistant to trichostrongyle?
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> 2yrs
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when are sheep resistant to trichostrongyle?
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never; deworm ewes at lambing, adults that are on heavily contaminated pastures, lambs on all pastures
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what is preinution or concomitant immunity to trichostrongyles?
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existing worm populations inhibit new infections and L4 activation
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how can we tacticaly treat cattle for trichostrongyles?
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when susceptible animals are on heavily contaminated pastures, show clinical signs must treat repeatedly or or treat and move
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how can we strategicly treat cattle for trichostrongyles?
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to prevent build-up of infective larvae on a pasture from egg-producing adult worms (L3 ingested or L4 arrested) treat soon after uninfected animals are put out to pasture to prevent pasture contamination with L3s
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when would we perform strategic treatment to prevent strongyles in cattle in cool temperate regions (including NC)?
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(1) treat newborn and overwinter calves in spring 3-6w after turnout, and repeat in 3w to minimize pasture contamination by removing L3s from pasture (2) treat older calves with adult worms and Lf-killing anthelmentic in late fall if they will be grazed the following spring to remove arrested L4
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when would we perform strategic treatment to prevent strongyles in cattle in subtropical south?
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(1) treat calves and long-yearlings (SSGs) in early fall (start of grazing season, wet season) with adulticide (2) treat calves at end of grazing season in late spring/early summer at start of dry season with adult/L4 killing drugs
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when would we perform strategic tretment of 1st calf heifers?
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at start of lactaion for optimal milk production
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how can we control trichostrongyles in sheep and goats?
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to prevent disease and minimize pasture contamination, treat ewes and goats before parturition (FAMACHA)
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how is the FAMACHA used in trichostrongyle control of sheeps and goats?
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selective deworming based on clinical signs of anemia; slow drug resistance
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what anthelmentics can be used on trichostrongyles?
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macrocyclic lactones (macrolides), benzimaidazoles (albendazole, fenbendazole), & levamisole
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what do macrocyclic lactones do in trichostrongyle control?
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kill adult and L4 forms of trichostronglyles, but not L4 of strongyles in horses
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what do benzimidazoles do in trichostrongyle control?
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kill adult and L4 forms of trichostronglyles, but not L4 of strongyles in horses
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what do levamisole do in trichostrongyle control?
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adulticide, does not kill L4 larvae; must repeat treatment since adults will emerge from L4 arrested
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