This worm is from which class of nematodes?
True or false: Trichostrongylus axei has a small buccal cavity.
Distinguish between the nematodes in the following:
- Large strongyle
- Small strongyle
Which part of the body host adult Trichostrongyles?
Stomach & small intestine
- What type of life cycle do Trichostrongyles have?
- At what stage are they infectious?
- Sheathed L3
What are the 2 True Strongyles that infect the LARGE INTESTINE of RUMINANTS?
Which fecal test would you want to run to identify a particular parasite?
Which environmental extremes would kill a strongyloid L3?
What are the 4 "abomasal worms"?
- Trichostrongylus axei
Which adult nematode has a "barber pole" appearance?
What is the MOST important parasite of sheep, goats, and camelids?
What are some unique physical features of the Trichostrongylus female?
- "Barber pole" appearance (white = ovaries; red = intestinal tract)
- Cuticular vulva flap
What are some unique physical features of the male Trichostrongylus?
- Red when fresh
- LARGE bursa
The lancet of the buccal cavity can be found in which nematode?
What is the pre-patent period of Haemonchus contortus?
Haemonchus and Ostertagia differ in how they penetrate the gastric epithelial cells. How does Haemonchus act?
Penetrates BETWEEN the epithelial cells
Haemonchus females are PROLIFIC egg layers. About how many eggs does each female lay per day?
5,000 - 6,000 eggs
A massive infection with Haemonchus is called what?
With a preacute massive infection of Haemonchus, the animal typically dies within 7 days, but no eggs are observed within that time - why is this?
Pre-patent period of Haemonchus contortus = 15 days
In an animal with a preacute hemonchosis infection, what would be some findings on necropsy?
- Pale organs
- Dark, blood GI contents
- Hemorrhagic gastritis
You have a goat with the following symptoms:
Pale mucous membranes, melana, edema, weakness, and lethargy
What is your diagnosis?
Explain the pathway to developing edema during an acute hemonchosis.
Anemia (due to blood sucking parasites & melana) -> Loss of albumin (blood proteins) -> Decreased oncotic pressure within vessels -> Leakage of fluid (edema)
What might be the necropsy findings in an animal with an acute hemonchosis?
- Thin/watery blood
- Pale carcass
- Edematous abdomen
During which state of hemonchosis might you find the least number of worms involved in the infection?
Chronic hemonchosis (100 - 1000 eggs)
Which stage of hemonchosis is NOT associated with anemia OR edema?
Which strongyloids have paratenic hosts?
What are the goals of "selective therapy"?
- Minimize the number of eggs in the envrionment
- Use drugs in a way that might limit resistance
What 2 factors does selective therapy rely upon?
- An uneven distribution of eggs
- Consistent eggs sheddering over time
Treating in a way that maintains the susceptible individuals and susceptible genes within the population.
Ostertagia and Telodorsagia are both worms that infect the absomasum. Which animals do the two infect?
- Ostertagia = cattle
- Telodorsagia = sheep, camelids, and goats
Which type of trichostrongyle is represented by the following?
What color are adult Ostertagia worms?
Haemonchus and Ostertagia differ in their penetration methods within the GI tract. How do Ostertagia penetrate?
Ostertagia penetrates the gastric glands of the abomasum.
Which is more damaging to the gastric mucosa, Haemonchus or Ostertagia?
What is the pre-patent period of Ostertagia?
- Ostertagia larval migration damages which cells within gastric glands?
- What effect does this have on the production of pepsin?
- Zymogen, parietal, and mucous secreting cells
- Because parietal cells are damaged, HCl is not produced and pepsinogen is not broken down to pepsin. Without pepsin, proteins cannot be broken down and proper digestion cannot occur. This will lead to a malabsorptive diarrhea.
Ostertagia causes damage to parietal cells within the gastric glands of the stomach. What could be some consequences of this damage?
- Loss of HCl production = increased pH
- Proliferation of bacteria
- Profuse diarrhea
- Protein not utilized
What nematode might cause these nodular changes in the abomasum?
There are 3 phases to ostertagiosis - explain those phases; number of days post infection, larval stages involved, etc.
- Phase I: days 1 - 17 post infection --> L3 enter gastric glands & develop into L4
- Phase II: days 18 - 35 post infection --> L5 exits gastric glands & destroys cells of glands
- Phase III: 35 - 70 days post infection --> death of adults & repair of gastric mucosa
What are the overall effects of ostertagiosis on an animal?
- Reduced weaning weight
- Reduced milk production
- Reduced breeding efficiency
Trichostrongylus axei also migrate through the gastric mucosa within cattle. Describe this gastric migration.
L3s migrate between gastric glands; causing little damage to the glands
Trichostrongylus axei causes white, circular plaques to develop in the gastric mucosa of ruminants. What effect does it have on the GI tract of horses?
What are the clinical signs of a Trichostrongylus axei infection in a ruminant?
- Weight loss
- Dark, green, watery stools
What might be the lab findings in a blood sample for an animal with a Type I ostertagiosis?
- High levels of pepsinogen in the blood
- Mild anemia
Type II ostertagiosis occurs during the winter months, but what exactly is occuring during that period?
L4 hypobiotic larva are emerging from the gastric glands all at once -> This results in mass destruction of the gastric glands
Type I ostertagiosis occurs during the summer months, but what exactly is occuring within that period?
A large amount of L3 larva are acquired and infect the animal within a short period of time.