Cattle GI nematodes

Question 1

Nematode genera in bovine GI tract

Answer 1

Abomasum: ostertagia, trichostrongylus, hemonchus (all trichostrongyloidea)

Small intestine: cooperia, nematodirus, trichostrongylus (all trichostrongyloidea), bunostomum, toxocara

Large intestine: oesophagostomum, trichuris

Question 2

Abomasal GI nematodes

Answer 2

ostertagia, trichostrongylus, haemonchus

Question 3

Trichostrongyloidea

Answer 3

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

Question 4

Ostertagia

Answer 4

** Ostertagia ostertagi- major problem in UK and USA

Ostertagia leptospicularis

NB: O. lyrata is a morphological variant of O. osteragi

Question 5

Life cycle of ostertagia

Answer 5

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.

Question 6

Gastric gland structure/function and how ostertagia effects it

Answer 6

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.

Question 7

Pathogenesis of ostertagiosis (heavy infection >40,000 adults)

Answer 7

1. distension of parasitized gastric gland lumen–> rupture of intracellular junctions leading to leakage of plasma proteins in the lumen–> hypoproteinemia
2. 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.

Question 8

Pathology of ostertagiosis

Answer 8

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

Question 9

Type 1 form of ostertagiosis

Answer 9

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.

Question 10

Type 2 ostertagiosis

Answer 10

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.

Question 11

Diagnosis of ostertagiosis

Answer 11

Clinical picture and grazing history

diagnose herd, not individual

Use of diagnostic aids: fecal egg counts, serum pepsinogen, serum antibody, PM

Question 12

Fecal egg counts (McMaster method)

Answer 12

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

Question 13

Serum pepsinogen

Answer 13

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

Question 14

Serum and milk antibodies

Answer 14

ELISAs for parasite antibody used in research

Good measure of exposure to infection

not commerically available

Question 15

Post-mortem

Answer 15

true worm burdens and speciation; adult worms are small (~1cm)

Question 16

Immunity to Ostertagia

Answer 16

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)

Question 17

Epidemiology of ostertagiosis

Answer 17

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.

Question 18

Epidemiology of Type I Ostertagiosis

Answer 18

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.

Question 19

Etiology of type II disease

Answer 19

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.

Question 20

Ostertagiosis in beef herds (UK)

Answer 20

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.

Question 21

Atypical forms of bovine ostertagiosis

Answer 21

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

Question 22

Treatment of ostertagiosis

Answer 22

Type 1: most currently available anthelmintics–> move to clean pasture

Type 2: modern benzimidazoles, macrocylic lactones, pre-benzimidazoles (higher dose rate)

Question 23

Control of ostertagiosis

Answer 23

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.

Question 24

Trichostrongylus axei

Answer 24

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)

Question 25

Pathology of Trichostrongylus axei

Answer 25

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.

Question 26

Hemonchus

Answer 26

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

Question 27

Hemonchus- site, appearance, pathology

Answer 27

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.

Question 28

Bovine hemonchus

Answer 28

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.

Question 29

Small intestine nematodes

Answer 29

cooperia, nematodus, trichostrongylus: all trichostrongyloidea family

bunostomum and toxocara

Question 30

Cooperia species

Answer 30

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

Question 31

Cooperia oncophora

Answer 31

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

Question 32

Trichostrongylus colubriformis

Answer 32

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.

Question 33

Nematodirus species in cattle

Answer 33

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.

Question 34

Bunostum phlebotomum

Answer 34

superfamily: strongyloidea

Cattle hookworm- sucks blood

Site: SI

Adult is 1-3 cm with a hooked anterior end

Question 35

Bunostum phelbotomum

Answer 35

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)

Question 36

Bunostum clincial signs and treatment

Answer 36

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.

Question 37

Toxocara vitulorum

Answer 37

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.

Question 38

Large intestinal bovine nematodes

Answer 38

oesophagostomum radiatum

trichuris

Question 39

Oesophagostomum radiatum

Answer 39

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

Question 40

Trichuris globulosa

Answer 40

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.