Trichostrongyloidea - cattle Flashcards
Common general characteristics of Trichostrongyloidea?
Most important group of nematode pathogens in grazing ruminants. Small, “hair-like”. Direct Life Cycle. ensheathed L3 is the infective stage. Mainly GI nematodes. Generally not migratory. PPP ~21 days.
What nematodes of Trichostrongyloidea from the bovine GIT would be found in the abomasum?
Trichostrongylus, Ostertagia, Haemonchus.
What nematodes of Trichostrongyloidea from the bovine GIT would be found in the Small Intestine?
Trichostrongylus, Cooperia, Nematodirus.
Ostertagia ostertagi
Cattle. Most common cause of parasitic gastritis in cattle. Direct lifecycle. In abomasum of ruminants. Eggs released from adults in abomasum and hatch in feces. Ensheathed L3 is ingested (L3 migrate from feces to grass), is exsheathed in the rumen and penetrates the lumen of the abomasal gland and develops to L4. (Possibility of entering a hypobiotic EL4 phase). Development from L4 to Immature adult and emerge into abomasum. 21 day PPP.
Ostertagia ostertagi pathogenesis
Extensive pathologic and biochemical changes in the abomasum with severe clinical signs. Most severe when emerging from abomasal gland (about 18 days unless it enters EL4). Thickened hyperplastic gastric mucosa. Increase in pH of abomasal fluid due to loss of functional gastric glands (parietal cells which produce HCl).
Over-wintered L3’s - survive on pasture and are ingested the next April/May
Where do ostertagia ostertagi develop in the cattle GIT?
Lumen of the Abomasal glands (parietal cells) in the mucosal layer.
What effects do the growing O. ostertagi have on the environment of the GIT.
Thickened hyperplastic gastric mucosa. Abomasal folds often edematous and hyperemic, and sometimes necrosis and sloughing of the mucosal surface occurs. Regional lymph nodes enlarged and reactive. Really heavy infections result in increased pH of abomasal fluid from around 2.0 to 7.0 (loss of functional gastric glands and replacement with undifferentiated cells). This leads to: - failure to activate pepsinogen to pepsin, with failure to denature proteins. - loss of bacteriostatic effect Enhanced permeability of abomasal epithelium to macromolecules like plasma proteins and pepsinogen (increased size of intercellular junctions). This results in leakage of plasma proteins into gut lumen/hypoalbuminemia/hypoproteinemia, and loss of pepsinogen into plasma.
What does the abomasum resemble with heavy O. ostertagi infections?
Moroccan leather. due to Ostertagiosis nodules.
There are two clinical forms of O. ostertagi in cattle. Why is this and when do they occur?
Type 1: Grazing calves, occurs July-October, due to larvae acquired from pasture, mortality low.
Type 2: Yearlings, occurs March-May, due to maturation of EL4’s from pasture during previous autumn, mortality high.
How do you dx Ostertagiosis? Is it on an individual basis or by herd?
Clinical picture and grazing history, diagnosis is by herd. Some diagnostic aids: fecal egg counts, serum pepsinogen, post-mortem
Can cattle develop immunity to Ostertagia?
Poop
Can cattle develop immunity to Ostertagia?
Yes, but it is slow and takes at least one grazing season. The second season, calves and adults are usually immune. Immune animals still carry burdens
Describe the difference between the terminology, first and second generation of O. ostertagi parasites. Which one(s) cause disease?
This is dealing with Type 1 Ostertagiosis. Ingestion of over-wintered L3’s leads to infection and this first generation parasite produces eggs that contaminate pasture. Ingestion of the large numbers of eggs on pasture sets up second the generation of parasites. The second generation is usually the only generation sufficient enough to produce clinical signs/disease.
What influences the inhibition of L3 O. ostertagi as L4’s (EL4)?
Temperature - exposure of free-living stages to lower temperature increases probability of inhibition as L4’s in abomasal glands. This sets up the possiblity of Type 2 Ostertagiosis for the next year.
The probability that the free-living L3’s will be exposed to lower temperatures increases if the cattle are rotated to contaminated pasture late in the season, or during dry summers which delays emergence of larva from fecal pats.
How do you treat Ostertagiosis?
Type 1 disease: use most currently available anthelminthics; move to clean pasture.
Type 2 disease: modern benzimidazoles; macrocyclic lactones.
