Cattle GI nematodes Flashcards
Nematode genera in bovine GI tract
Abomasum: ostertagia, trichostrongylus, hemonchus (all trichostrongyloidea)
Small intestine: cooperia, nematodirus, trichostrongylus (all trichostrongyloidea), bunostomum, toxocara
Large intestine: oesophagostomum, trichuris
Abomasal GI nematodes
ostertagia, trichostrongylus, haemonchus
Trichostrongyloidea
most important group of nematode pathogens in grazing ruminants
direct life cycle
L3 is infective stage
Mainly GI nematodes (except dictyocaulus (lungworm))
PPP approx 21 days
Ostertagia
** Ostertagia ostertagi- major problem in UK and USA
Ostertagia leptospicularis
NB: O. lyrata is a morphological variant of O. osteragi
Life cycle of ostertagia
Adults in absomasum produce eggs–> hatch in feces–> L1->L2->L3 (sheathed in L2 cuticle) ingested–> penetrate abomasal gland–>L4–>immature adult–> emerge 18 days post-infection–> adults in abomasum
NB: L4 can arrest development–> EL4 (hypobiosis) in response to climatic signals
Males and females; egg-L3 is free-living; climate dependent growth
Sheath removed in abomasal gland; grow 8-10 fold, then rupture out of gland. Adults found in lumen of abomasum.
Pathology of this infection is the major eruption of L4 out of gland.
Gastric gland structure/function and how ostertagia effects it
Acidic environment of normal gastric gland converts pepsinogen to pepsin. In parasitized animals, no longer get a steady secretion of HCl. Parietal cells are replaced by undifferentiated epithelial cells resulting in a build-up of pepsinogen. Cel junctions are leaky and pepsinogen can go into the blood. Pepsinogen increases the pH of the gastric gland.
Pathogenesis of ostertagiosis (heavy infection >40,000 adults)
- distension of parasitized gastric gland lumen–> rupture of intracellular junctions leading to leakage of plasma proteins in the lumen–> hypoproteinemia
- distension of parasitzed gastric gland lumen–> destruction of parietal cells–> replacement with undiffereniated cells–> decreased HCl secretion and increase in abomasal pH to 7–> bacterial overgrowth and leakage of pepsinogen into blood–> elevated plasma pepsinogen
NB: malodorous breath d/t bacterial explosion.
Ostertagiosis nodules on surface of abomasum-look like moroccan leather.
Pathology of ostertagiosis
hyperplasia of abomasal mucosa
hyperemic/edematous-regional LN reactive
moroccan leather appearance of mucosa
Putrid smell of abomasal contents d/t bacterial overgrowth
large numbers of adult worms- 1cm in length, reddish in color
Type 1 form of ostertagiosis
Grazing calves (usually first season)- occurs July-October due to larvae acquired from pasture 2-3 weeks previously
Clinical signs: profuse watery diarrhea (typically bright green); weight loss, occasionally submandibular edema (d/t hypoalbuminemia); high morbidity, low mortality providing animals are treated, also, dehydration, dull coats, staining of hindquarters.
Type 2 ostertagiosis
Yearlings (often housed); occurs March-May due to maturation of inhibited larvae acquired from pasture during previous autumn
Clinical signs: intermittent diarrhea (not always present)
submandibular oedema is common (hypoalbuminemia); weight loss; +/- moderate anemia, anorexia, and increased thirst; morbidity is low, mortality is high.
Diagnosis of ostertagiosis
Clinical picture and grazing history
diagnose herd, not individual
Use of diagnostic aids: fecal egg counts, serum pepsinogen, serum antibody, PM
Fecal egg counts (McMaster method)
Eggs separated from fecal debris by flotation in saturated salt solution
Nematode eggs float above debris in top of wells.
Can’t discriminate btwn different trichostrongyle eggs (except nematodirus)
Usually >1000 epg for type 1 ostertagiosis
There is NOT a linear relationship between fecal egg count and parasite burden- i.e. sometimes disease is cuased by pre-patent parasites e.g. type II ostertagiosis or nematodirus
LOW FEC DOESN’T RULE OUT A DIAGNOSIS OF PGE
Serum pepsinogen
indirectly assayed by measuring hydrolyzing activity of serum on albumin
actually measure amount of tyrosine
U tyr=micromoles of tyrosine released per liter of serum per minute
Normal value: 1 U tyr
Parasitized animals: 3-5 U tyr
specific for abomasal parasitism
Serum and milk antibodies
ELISAs for parasite antibody used in research
Good measure of exposure to infection
not commerically available
Post-mortem
true worm burdens and speciation; adult worms are small (~1cm)
Immunity to Ostertagia
slow to develop; takes at least one grazing season, but normally 2
Second season calves and adults generally immune
immune animals still carry burdens (greater proportion of burden are inhibited L4)
Epidemiology of ostertagiosis
Centers on the build-up of large numbers of infective L3 stages on pasture. More metabolically active in spring–> if no host, will die off in the summer.
Epidemiology of Type I Ostertagiosis
Development of egg to L3 is temp dependent. Development in June is slower than in july (concertina effect)
Over-wintered L3s (survived on pasture from previous grazing season)–> April/May: calves ingest over-wintered L3s and patent infection is established. 1st generation of parasites generally insufficient to cause clinical disease but produce eggs which contaminate the pasture. The concertina effect means that large numbers of 2nd generation reach L3 at the same time (July/August) and are ingested by calves.
2nd generation of parasites produce clinical signs 2-3 weeks after infection.
Etiology of type II disease
Exposure of free-living stages to low temperatures increases probability of inhibiton as L4s in abomasal glands
Larvae taken up in September/October and many will arrest in the tissues. Once temperatures increase, get reactivation of inhibited larvae.
Predisposing factors to type II disease:
ingestion of large numbers of L3s delayed to autumn caused by:
- grazing mgmt: moving animals to contaminated pasture late in the grazing season
- climate: dry summers delay emergence of larvae from fecal pats.
Ostertagiosis in beef herds (UK)
Dams are an additional source of pasture contamination, however egg output from adults is generally low
Ostertagiosis is uncommon in spring claving herds because calves aren’t weaned until autumn (over-wintered larvae are dead). Little contribution to pasture contamination during early grazing season.
Ostertagiosis is more common in autumn calving herds because calves are weaned in the spring and so epidemiology is similar to that of dairy calves.
Atypical forms of bovine ostertagiosis
Early season type 1: if calves put out early (March/early april) occasionally sufficient over-wintered L3s to cause disease 4-6 weeks after turnout
Ostertagiosis in adult cattle: unusual because of acquired immunity but occasionally cases can occur (unexposed stock moved to endemic area)
Occasional type 2 disease in cows debiliated by intercurrent disease
Treatment of ostertagiosis
Type 1: most currently available anthelmintics–> move to clean pasture
Type 2: modern benzimidazoles, macrocylic lactones, pre-benzimidazoles (higher dose rate)
Control of ostertagiosis
grazing management/prophylactic medication- avoid grazing heavily contaminated pasture and peak season “dose and move” allow limited exposure to larval infection “safe pasture”
Monitor: FEC/growth-reduce worming
Worm at housing: stock susceptible to type II disease.
Trichostrongylus axei
Site: abomasum (L3 ex-sheaths in abomasum)
Very small worm; less than 1cm and thin
Excretory notch in oesophageal region is a diagnostic feature
Infects a range of host species including cattle, sheep, goat, horse
L3 in sheath taken up from pasture; move into epithelial/gastric mucosa (NOT GLANDS)
Pathology of Trichostrongylus axei
Hemorrhage/edema/enteritis
large flattened, mucosal erosions/nodules- sub-epithelial tunnels (larvae migrate under)
Rarely a primary pathogen in the UK (imp. in subtropics)
In UK, often contributes to clinical signs of PGE as part of a mixed infection
L3 particularly resistant to cold and dessication–> in UK, over-winter occasionally on pasture in sufficient number to cause clinical problems in the spring.
Hemonchus
largest GI nematode
Not important in cattle in the UK
Hemonchus placei/contortus and Hemonchus similis
Mainly a tropical parasite, but present in temperate regions as wel (mainland Europe)
Several reports of BZ and IVM resistance
H. contortus important in sheep in the UK
L3s don’t over-winter–> can’t tolerate the cold in the UK
Hemonchus- site, appearance, pathology
Found in abomasum
blood feeding parasite–> causes anemia
Looks like a barber’s pole: white ovaries/blood filled intestine
lancet develops before final moults
feeds on mucosal vessels; adults move freely on mucosal surfaces (highly fecund)
Pierce surface- causes more blood loss than they actually take up
V. different from strongyles (hookworms) as they have no biting mouth parts.
Bovine hemonchus
in tropics: outbreaks during rainy season, end of long dry season (hypobiotic larvae- L4s can remain arrested and re-start just before rainy season)
Immunity in cattle >2 years
Immunity can be broken down during drought- poor nutrition/heavy challenge.
Small intestine nematodes
cooperia, nematodus, trichostrongylus: all trichostrongyloidea family
bunostomum and toxocara
Cooperia species
C. oncophora: temperate areas (UK) mild pathogen (larvae don’t migrate to tissues; all development in SI); contributes to PGE, very widespread
C. punctata and C. pectinata: sub tropical and tropical areas (more pathogenic)
Cooperia species in cattle: adults approx. 1cm long
Cooperia oncophora
Small intestinal nematode
common in temperate regions, including the UK
contributes to PGE as part of a mixed infection
sometimes predominant parasite (one of the least fecund species, population stability- no boom in numbers)
Parasitic stages develop on surface of SI mucosa
Mild pathogen: inappetance and decreased weight gain
Epidemiology v. simialr to O.ostergi
relatively resistant to anthelmintics
Trichostrongylus colubriformis
Small intestinal nematode
Adult worms less than 1cm
can also infect sheep and goats
life cycle and epidemiology same as trichostrongylus axei (of abomasum) –L3 in sheath taken up from pasture, exsheaths and moves into epithelia
Rarely a primary pathogen in the UK but contibutes to PGE
Very pathogenic when present in large numbers–> parasitic stages penetrate epithelium causing enteritis and tissue damage.
Nematodirus species in cattle
Nematodirus helevetianus- contributes to PGE as part of a mixed infection
Nematodirus battus and nematodirus spathiger: occur in cattle but much more important in sheep
Nematodirus egg is 2x the size of other trichostorngylid eggs
Also, nematodirus egg has large blastomeres within it.
Bunostum phlebotomum
superfamily: strongyloidea
Cattle hookworm- sucks blood
Site: SI
Adult is 1-3 cm with a hooked anterior end
Bunostum phelbotomum
Life cycle is typical hookworm:
Adult in SI–> eggs produced and passed in feces. L1-L3 sheathed in L2 cuticle. L3 can be ingested and go directly to SI, or percutaneous and migrate to lungs. L3–>L4 in bronchi trachea/coughed and swallowed to SI.
percutaenous (pulmonary migration)
oral route (no migration)
PPP=6 weeks (percutaneous)
Needs warm and wet conditions- don’t overwinter well
Small burdens in temperate regions
Mainly problem in tropics at end of dry season (hypobiotic larvae)
Bunostum clincial signs and treatment
Several hundred adult worms needed for clinical signs
>2000 can lead to death
Anemia; hypoalbuminemia; weight loss; sometimes diarrhea; pedal deramatitis–> foot stamping/itching due to penetration of infective larvae.
Treatment may need to incorporate improved indoor hygiene.
Toxocara vitulorum
largest intestinal parasite of cattle (30cm)
Worldwide distribution but not a problem in the UK
serious buggalo parasite in some areas
thick, albuminous, pitted shell that’s highly resistant.
non-infective egg- need to larvate to L3 to be infective
Similar life-cycle to T.cati;
L3 trans-mammary infection-ALD (no tissue migration)
Exposured to infection from birth but build-up immunity
Infection via larvated egg- no tissue migration in calf, but migration in older animals.
Large intestinal bovine nematodes
oesophagostomum radiatum
trichuris
Oesophagostomum radiatum
Site: LI
Apperance: long stout worms, 2cm
Not blood feeders; live in lumen of LI
Strongyloidea but NOT a hookworm
Not a major UK pathogen, more important in tropics and sub-tropics.
Nodules formed by O.radiatum on serosal surface of LI. Clinical signs associated with larval stages as larvae penetrate mucosa and LI and nodules are formed due to IR
Trichuris globulosa
Whipworm
Thin anteriod end, thick bulbous end protruding into lumen
light infections common- not a major pathogen
if clinical signs- individual cases rather than outbreak
egg has bipolar plugs
unembryonated egg is un-infective, L1 is infective stage.
