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.
Serum Pepsinogen
- Specific for abomasal parasitism
- Useful in calves but less reliable in older animals where often get values of >1 with low burdens
- Indirectly assayed by mearuing hydrolyzing activity of serum on albumin.
- Results expressed in units of tyrosine
Post Mortem Test
This is the most important test becasue it shows the true worm burden and we can speciate them and distingusih them morphologically.
Immunity to Ostertagia
- Slow to develop
- takes at least one grazing season
- **second season calves and adults are generally immune. **
- Immune animals can still carry burdens ( a greater proportion of the burdens are inhibited L4)
Epidemiology of Ostertagiosis:
the epidemiology of ostertagiosis centres on the build up of infective L3 stages in the pasture.
When would it be the most safe to relase cattle back into pasture?
Would want to release cattle into pasture in the later summer (mid July) because by then pasture should be clean of infective L3’s due to the increasing temperature. If there is no susceptible host for them, they will die off in these temperatures.
Epidemiology of type 1 ostertagiosis:
- Over wintered L3’s (survive on pasture from previous grazing season)
- In April or May, Calves ingest over wintered L3’s and patent infection is established. (Remember: 1st generation parasites are generally insufficient to cause clinical disease)
- In May or July, 1st generation adult parasites produce 2nd generation eggs which contaminate the pasture.
Note: Concertina Effect: Large numbers of 2nd generation eggs reach L3 at the same time in pasture.
- In July or August, Large numbers of L3’s appear on pasture and are ingested by calves.
- This 2nd generation of parasites produces clinical signs in 2-3 weeks after infection. **PPP= 3 weeks. **
Classic type 2 disease predisposing factors?
- **Ingestion of large #’s of L3 delayed to autumn caused by: **
- Grazing management: moving animals to contanimated pasture late in the grazing season.
- Climate: Dry summers delay emerence of larvae from fecal pats.
Comment on Ostertagiosis in Beef herds
Ostertagiosis is uncommon in spring calving herds because they are usually weaned in autumn when the over wintered L3’s have already died off therefore they have little contribution to pasture contamination during early grazing season.
However, autumn calving herds are weaned during the spring therefore ostertagiosis is more common. This is because when they are weaned the pasture grazing calves will ingest over wintered L3’s just like dairy cattle and then type 1 ostertagiosis proceeds.
Treatment of Osteratgiosis:
Type 1?
Type 2?
Type I disease:
-Currently available anthelmintics and move to clean pasture.
Type 2 disease:
Modern benzimidazoles.
Macrocyclic lactone
Pro benzimidazoles
How can we control Ostertagiosis?
Grazing Management and Prophylaxis:
avoid grazing heavily contaminated pasture at peak season (dose & Move)
allow limited exposure larval infection ‘safe pasture’
FEC
worm at housing (stock susceptible to type 2 disease)
Trichostrongylus axei:
Site?
Size?
Diagnostic feature?
Hosts infects?
Climate/ Area?
- Abomasum
- less than 1 cm (smallest of the 3 abomasal parasites- Haemonchus is the largest)
- Excretory notch in the esophageal region.
- Cattlle, sheep, goat, horse
- **Rarely a PRIMARY PATHOGEN in the UK, usually contributes to PGE as a part of a mixed infection. **
- L3 particularly resistant to cold and desiccation.
Trichostrongylus axei pathology:
Hemorrhage
edema
enteritis
Haemonchus:
Largest GI nematode in the abomasum (o. osteragi is 2nd, trich axei is 3rd)
not important parasite in cattle in the UK.
Hemonchus contortus affects both cattle and sheep but is **much more important in sheep. **
Mainly Tropical parasite
present in temperate regions also.
Haemonchus:
Site?
Appareance?
Causes what? think about the name
Diagnostic features?
- Abomasum
- Barbers pole worm (red and white swirl) red is blood filled intestines and white is the eggs in the ovaries.
- Blood feeding parasite causing anemia.
- Size 2-3 cm.
- Lancet (develops before final moult)
- Adults move freely and feed on mucosal surfaces (highy fecund)
- Very pathogenic due to severe blood loss.
Cooperia:
- C. oncophora:
- temperate areas (UK)
- mild pathogen
- contributes to PGE (T. axei also) - C. punctata
- C. pectinata
These two are tsub tropical and tropical area and more pathogenic.
Cooperia oncophora
Found in what kind of areas?
What does it cause?
Epidemilogy?
Anthelmintics
Common in temperatre regions (UK)
Contributes to PGE
Not very fecund
Mild pathogen causing inappetance and reduced weight gains.
Epidemiology similar to O. ostertagi.
Dose limiting species: resistant to anthelmintics
Trichostrongylus Colubriformis:
Site?
Size?
Lifecycle & epidemiology?
Causes?
- Small Intestine
- < 1cm
- Can also infect sheep and goats.
- Lifecycle and epidemiology similar to T. axei
- Contributes to PGE
- In large #’s will cause enteritis.
Nematodirus Helvetianus
Nematodirus Battus
Nematodirus spathiger
N. helvetianus: Contributes to PGE as part of a mixed infection.
N. Battus & N. spathiger occur in cattle but much more important in sheep.
Bunostomum Phlebotomum
Superfamily?
Site?
Size?
Characteristics?
Strongyloidea
Small Intestine: Hookworm
1-3 cm.
Distinctive cutting plates
Bunstomum Phlebotomum:
Lifecycle?
PPP?
Conditions/ Climate?
Cause:
LIfecycle is typical hookworm:
- Percutaenously
- Orally ingested
PPP= 6 weeks
Wet/ Warm conditions: Temperate regions.
Cause:
- Anemia
- hypoalbuminemia
- Pedal dermatitis (hypersensitivty)- Penetration of infective larvae
Oesophagostomum radiatum:
Site?
Length?
Superfamily?
Causes?
Large Intestines
2cm
Strongyloidea but not a hookworm
Causes nodules on serosal surface of L.I.
Tichuris globulosa
Egg characteristics?
Adult characteristics?
‘Whipworm’
Egg: Bi polar plugged
Adult: threaded tail “misnomer”
Toxocara Vitulorum:
Small intestines
Largest intestinal parasite of Cattle.
Egg: Thick pitted shell: highly resistant.
Typical Ascarid
Toxocara Vitulorum:
Lifecycle?
Transmission?
Migration?
PPP?
L3 transmammary infection - most important. Can trnasmit infection up to 30 days.
ALD (no migratory phase in transmammary infection–straight to GI)
Exposed to infection from birth but build up immunity.
Infection via larvated egg
Note: No tissue migration in the calf.
Tissue migration in adult.
3-4 weeks.
What are the main species that contribute to Bovine parasitic Gastroenteritis?
- O. ostertagi
- C. oncophora
