Parasitology - Nematodes 2

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Sub-clinical nematode disease causes major production loss in livestock

Parasitic Gastroenteritis (PGE)

- term for disease caused by parasitic nematodes in gastro-intestinal tract

- disease of grazing livestock (predominantly young stock)

- Adult animals generally have strong acquired immunity

- often caused by mix species of parasitic nematode

Trichostrongyloidea

most important group of nematode pathogens in grazing ruminants

direct life cycle

L3 is infective stage

Mainly GI nematodes

PPP approx. 21 days

Life cycle of Ostertagia ostertagi (cattle) *main nematode in UK

adults in abomasum

eggs

hatch in faeces

L1

L2

L3 (ingested)

penetrate abomasal gland

L4(EL4 hypobiosis) *arrested larval development - remain in tissues

imature adult

Development of hatching eggs is dependent on temperature and humidity (warmer and damper = faster development) Summer PPP = 3 weeks, Spring = 1-2 months

Once L3 is ingested, abomasum gland is penetrated and moult L4, then rupture back out the tissue causing the pathology

Pathogenesis of ostertagiosis (heavy infection)

Hypoproteinaemia - leakage of plasma proteins into lumen

Elevated plasma pepsinogen - leakage of pepsinogen into blood

Bacterial overgrowth - decreased HCL secretion, increase in abomasal pH (pH2 to 7)

Pathology:

hyperplasia of abomasal mucosa

bumpy appearance

putrid smell of abomasal contents - bacterial overgrowth

large numbers of adult worms

2 clinical forms of Ostertagiosis:

Type 1. Grazing calves (1st season), July-October, due to larvae acquired from pasture 2-3 weeks previously

Clinical signs:

- profuse watery diarrhoea

-weight loss

- morbidity is high

- mortality is low (provided animal is treated)

Type 2. Yearlings (often housed), occurs March-May, due to maturation of inhibited larvae acquired from pasture during previous autumn

Clinical signs:

-intermittent diarrhoea

-build up of fluid in the jaw (submandibular oedema

-weight loss

-anorexia and increased thirst

morbidity is low

mortality is high

(show few symptoms but very pathogenic)

Diagnosis:

- clinical picture and grazing history

- diagnosis on herd, not individual basis

- Faecal egg counts (FECs)

- serum pepsinogen

- Post mortem

*2 peaks of ostertagiosis outbreaks - 1st = spring time (type 2) 2nd = Summer (type 1) - much more common

Immunity to Ostertagia:

- slow to develop

- take at least one grazing season

- second season calves and adults generally immune

- immune animals still carry low burdens

*ability to arrest in the tissues as an EL4 - trigger is the experience that the larval stages have in the environment (exposed to cold then digested by calf, receive signal that Winter is approaching and no point developing so go into arrest until following Spring when they will survive and infect)

Ovine Ostertagiosis (brown stomach worm) *ewes are key for transmission to lambs

weight loss/failure to gain weight

intermittent diarrhoea

appetite loss

Haemonchus contortus in sheep (Barber pole worm)

important pathogen in tropics and sub-tropics

anthelmintic resistance

very pathogenic nematode (poor immunity) - blood feeding

largest parasite in abomasum

causes haemorrhagic anaemia *pierces surface of abomasum, creating puncture wounds and feeds off blood = causes severe blood loss

can be long lived = significant blood loss

- typical trichostrongylid life cycle

- best adapted to tropical climates

- development L1-L3 rapid under optimal conditions

Hyperacute Haemonchosis (up to 30,000 adults) = sudden death due to severe haemorrhagic gastritis

Acute Haemonchosis (2,00-20,000) = clinical signs seen approx. 2 weeks post infection

Chronic Haemonchosis (several hundred worms) weight loss, weakness and inappetance (would effect economic stability of sheep farming due to decreased production)