G.I Nematodes of Cattle Flashcards
What is Parasitic Gastroenteritis?
What age group does it effect?
A generic term for disease caused by parasitic nematodes in gastro intestinal tract.
A disease of grazing livestock and usually affects young stock.
Adults animals generally have a strong acquired immunity.
PGE is most often caused by a combination of parasites.
What parasitic species are found in the cattle abomasum?
- Ostertagia
- Trichostrongylus
- Haemonchus
**ABOMASUM- OTH (OVER THE HILL) **
What is the superfamily associated with abomasal parasites?
Trichostrongyloidea
What parasitic species are found in the cattle small intestine and what is the superfamily they fall under?
- Cooperia
- Nematodirus
- Trichostrongylus
- Bunostomum
- Toxocara
- Cooperia, Nematodirus, Trichostrongylus: Superfamily Trichostrongyloidea (same as Abomasal superfamily)
- Bunostomum: Superfamily Strongyloidea (hookworm)
- Toxocara: Superfamily Ascaridoidea
What are the parasitic species found in the large intestine and what superfamily do they fall under?
- Oesophagostomum: Superfamily Strongyloidea
- Trichuris: Superfamily Trichuroidea
Superfamily Trichostrongyloidea:
Direct/ Indirect lifecyle?
Infective stage?
PPP?
Most important nematode parasites for grazing cattle
Direct life cycle
L3 infective stage
PPP: 21 days.
Remember that parasitic species in the same superfamily will SHARE characteristics. So when in doubt, think about other species in that family!!!
Of the abomasal parasites, name them in order from largest to smallest. Describe them in two words.
- Haemonchus- Largest
- Osteragia- Middle
- Trichostrongylus- smallest
All are hairlike and round.
Describe the life cycle events of Ostertagia ostertagi and its PPP.
- Adults are in the abomasum
- Produce eggs which are excreted in the feces
- Eggs hatch and moult from L1- sheathed L3 in the environment. (Optimal conditions are warm climates) In winter moulting time is increaed.
- Sheathed L3 is ingested and migrates to abomasum where it penetrates abomasal glands.
- Within the abomasal glands, L3 moults to L4.
- L4 can either become hypobiotic (EL4) and arrest in tissues due to a climactic signal OR L4 can moult to the juvenile adult. Takes roughly 7-10 days for L4 to develop post infection
- Juvenile adults erupts from abomasal gland approx. 18 days post infection and matures to adult in Abomasum.
- PPP=21 days.
What is the major pathogenesis of O. ostertagi?
The eruption of the juvenile adult from the abomasal glands 18 days post infection. especially if there are heavy worm burdens.
Describe how O. ostergi pathogenesis works.
In a normal gastric gland:
**Chief cells (zymogen cells) secrete pepsinogen
Parietal cells secrete HCl. **
Pepsinogen is convereted to pepsin (breaks down proteins into AA) in the presence of a low pH attributed to the HCl produced from Parietal cells.
Abnormal gastric gland:
- Distension of parasitized gastric gland lumen. This causes:
a. ) Rupture of intercellular junctions. cuasing leakage of plasma proteins into lumen resulting in a HYPOPROTEINEMIA.
b. ) Destruction of parietal cells and replacement with undifferentiated cells. This causes decreased levels of HCl production and therefore an increase in abomasal pH (pH2–> pH7). This increase in pH will cause BACTERIAL OVERGROWTH. The increase in pH will also cause failure to activate pepsinogen to pepsin causing a leakage of pepsinogen into blood resulting in **ELEVATED PLASMA PEPSINOGEN. **
O. ostergi Pathology:
What does this parasite cause to the abomasum i.e appearance, growth, etc..?
- Hyperplasia of abomasal mucosa
- Hyperemic/ edematous
- Morrocan leather appearance due to nodules on surface of abomasum.
- Putrid smell of abomasal contents due to bacterial overgrowth.
- Large #’s of adult worms
What are the two clinical forms of Ostertagiosis and describe them.
Occurs in what age cattle?
What time of year?
When are larvae acquired?
Type 1 (summer) Ostertagiosis:
– most common form
– occurs in pasteured , young grazing calves.
– occurs from July- October.
– Larvae acquired from pasture 2-3 weeks previously.
– Worms maturing without going into ALD, hypobiotic state.
**Type 2 (winter) Ostertagiosis: **
– occurs in housed yearlings.
– occurs from March- May
– due to maturation of inhibited larvae acquired from pasture during previous autumn.
– Occurs when larvae have remained in an arrested state instead of becoming metabolically active in fall. Now they become active and mature into adults.
What are clinical signs of Type 1 ostertagiosis?
- Profuse, watery diarrhea
- weight loss, dehydration & stained hindquarters d/t diarrhead d/t diarrhea
- Occasionally–> SM edema (bottle jaw)
- high morbidity (infection rate)
- low mortality
- dull coats
Clinical signs of type 2 ostertagiosis:
- **Intermittent diarrhea (not always present) (vs. Type 1 where diarrhea is always present) **
- SM edema is common
- weight loss
- +/- anemia
- Anorexia
- increased thirst.
- Low morbidity
- HIGH MORTALITY due to the eruption of heavy worm burdens from the abomasal glands.
How do we diagnose Osteragiosis?
Diagnose based on herds not individuals.
Diagnostic aids:
FEC
Serum pepsinogen
Serum antibody
PM inspection (nodules)
How can we use FEC as a diagnostic tool for O. ostertagi?
McMaster method?
What parasite egg is exceptional to the rest in the Trichostrongylus superfamily?
The McMaster Method: eggs are separated from feces by flotation in saturated salt solution. Nematode eggs float in liquid of specific gravity 1.1-1.2.
**Note: We cannot differentiate between different Trichostrongylus eggs. We must grow them to the infective L3 stage to be able to identify. **
The exception to this rule is the Nematodirus egg which is much larger than the rest, therefore identifiable.
