Parasitic Gastroenteritis

Introduction

Parasitic gastroenteritis (PGE) is a disease complex associated with a number of nematode species (mostly strongyles), either singly or in combination. It is characterised by:

• diarrhoea
• less than optimum productivity (sub-clinical disease)
• seasonal appearance
• hypoalbuminaemia.

PGE is of considerable economic importance in grazing livestock. It is a potential welfare problem, particularly on organic farms. Losses are associated with the cost of:

• replacement stock
• disruption of breeding programme
• impaired productivity, e.g. weight-gain, wool clip, milk yield, etc.
• treating clinically affected stock, e.g. drugs, labour, veterinary bills
• prophylaxis (prevention), e.g. drugs, labour, pasture management.

Aetiology

Strongyle nematodes are the main cause of PGE in grazing animals and, in particular, those found in two superfamilies, i.e. Trichostrongyloidea and Strongyloidea. Non-bursate nematodes are rarely responsible for PGE, although Strongyloides species (a member of the family Rhabditoidea and NOT a strongyle) may sometimes contribute to the disease.

Normally, only a few of the many roundworm species that are found in the alimentary tract of grazing stock are important as causes of PGE, e.g. in first season calves in northern Europe, Ostertagia species (an abomasal nematode) is the primary pathogen with Cooperia and Nematodirus species (intestinal nematodes) acting as contributory factors; other worms are rarely of clinical significance.

Epidemiology

Introduction

The epidemiology and pathogenesis of many strongyle infections of grazing animals are very similar. Infection by ingestion of an infective larva (L3), development to L4 and adult stages is generally restricted to gastric or intestinal mucosa (although a few species migrate around the body), adult worms eventually emerge to lie on the mucosal surface. The prepatent period is normally 2weeks, though may be 6+months for certain species or if development is "arrested".

Risk of disease depends on the balance between:

• rate of infection if the host; and
• host immunity.

Rate of Infection

The rate of infection of the host by infective L3 depends upon:

• host appetite (under normal circumstances this is fairly constant, increasing with host liveweight); and
• numbers of infective larvae (L3) on pasture (there are marked fluctuations in the number of L3 on pasture grazed by livestock during the year which help to explain the seasonal occurence of PGE).

Development from L1 → L2 → L3 is temperature dependent. Also, the L3 cannot feed as it is ensheathed (i.e. enclosed in the shed L2 cuticle). Its life-span therefore depends on how quickly its food stores are used up, and this too is temperature dependent as it is more active in warm weather.

a) Infective larvae (L3) overwinter on pasture:

• if infected stock grazed pasture previous year
• longer lifespan in colder weather

b) Larval numbers decline in the spring:

• heavy mortality of overwintered L3 (food reserves soon depleted as temperatures rise)
• diluted by spring grass growth

Host infected at turnout, patent infections develop and pasture contaminated:

• stock ingest remaining overwintered L3
• strongyle eggs passed out with faeces onto pasture

c) Development from egg to L3:

• strongyle eggs passed in host faeces for most of the grazing season
• development of egg to L3 depends on dung-pat microclimate and requires:
  • high relative humidity (nearly 100%) - dungpat acts as a "buffer" against drought; and
  • warmth (optimum temperature 25°C) - dungpat cannot buffer against changes in macroclimate temperature.
• development is therefore influenced largely by macroclimate and temperature. Net result = concertina effect.

d) Translation of infective larvae:

• movement of larvae from dungpat onto grass in order to infect final host
• L3 must cross a zone of repugnance around the dungpat (up to 45cm) - normally left ungrazed
• L3 cross zone by swimming in a film of moisture. Also, beetle and earthworm activity, rain splash, soil migration, etc.

e) Autoinfection peak in infective larvae:

• due to larvae reaching L3 stage simultaneously ("concertina" effect) and translation of L3 onto pasture
• factors affecting either egg - L3 development or translation will influence the timing of the peak, e.g. cold spring, dry summer
• decline in L3 after autoinfection peak due to a combination of (a) shorter lifespan in warmer weather; and (b) autumn flush of grass growth

f) Overwintering of larvae:

In temperate climates, some species can overwinter on the grass, while others cannot. In either case, nematodes may survive inside the host for long periods of time, not as normally developing adult worms (that would be expelled within a few weeks), but as larval worms that have become temporarily arrested in their development and may remain inside the host 'asleep' for many months.

Arrested Larval Development (synonyms: inhibited development, hypobiosis, diapause):

• Long lifespan - several months (c.f. adult worms - a few weeks).
• Larvae become arrested at an early stage in their development, e.g. Ostertagia as EL4 (i.e. early fourth stage), equine cyathostomes as L3.
• Mechanism for ensuring the survival of the parasite when climatic conditions adverse. Note seasonal pattern of arrested development, e.g. Ostertagia only need to arrest over winter.
• Stimulus for arrested development varies, e.g. falling temperatures - Ostertagia; drought - Haemonchus.
• Termination of arrested development - spontaneous (i.e. a genetic alarm clock). Previously arrested larvae then resume their development and grow to adult worms.

Host Immunity

Acquired host immunity affects both the establishment of recently ingested infective larvae as well as the course of infection of developing worms. When considering the effects that host immunity has on a worm burden, remember that animals grazing at pasture are continuously exposed to infection and not just challenged by a single large infection.

Worm Population Dynamics - Continous Infection: It is important to remember that a worm burden inside an animal grazing at pasture does not remain static, but is continually changing, i.e. as older adult worms are lost, more infective larvae are recruited. A state of equilibrium is reached, i.e rate at which L3 establish = rate at which adult worms are lost. In an immune animal, the same equilibrium exists, except that fewer of the L3 ingested become established.

Effects of Host Immunity on Worm Burden:

a) Reduction in establishment of larvae:

e.g. fewer L3 establish in an immune adult cow than a parasite naive calf.

b) Expulsion of an existing worm burden ("self cure"):

Due to immediate-type hypersensitivity reaction to antigen from incoming L3? Non-specific factor in grass?

c) Arrested development:

Minor role only; arrested development mainly caused by climatic changes, e.g. temperature changes (Ostertagia), drought (Haemonchus).

d) Stunting worm growth:

e.g. worm length.

e) Reduction in biotic potential:

Host immunity often reduces egg production by female worms. This results in a stereotyped pattern of worm egg output, regardless of the level of infection.

Factors Adversely Affecting Host Immunity:

a) Nutrition:

Gross deficiency; mineral/trace element deficiency, e.g. cobalt.

b) Reproductive status:

"Periparturient relaxation in immunity" (PPRI) seen in breeding ewes and sows. Due to impaired cell-mediated immune response - associated with an increase in blood prolactin levels/shift of IgA from gut mucosa to mammary gland around parturition?

c) Drug treatment:

e.g. repeated anthelmintic and corticosteroid treatment.

d) Concurrent infection:

e.g. pathogenic effects of Nematodirus infection exacerbated by coccidia in lambs.

e) Previous experience of a parasite:

e.g. hypersensitivity reaction to Haemonchus in some ewes.

Pathogenesis

Introduction

The pathogenic effects of a worm burden on the host depend on:

• Species of worm and stage of life-cycle present (affects feeding, site and host reaction).
• Numbers of worms present (or invading).
• Host immunity (affects worm population and pathogenicity).
• Nutrition (may affect both host resilience, ability of an animal to withstand the effects of infection, and host resistance, ability of an animal to prevent establishment and/or development of infection).

Mechanisms

The nematodes responsible for PGE impair productivity by adversely affecting:

a) Appetite:

Very important; the reduction in appetite is the main cause of impaired liveweight gain.

b) Digestion:

• Digestibility: decrease in abosomal infections - compensatory increase in intestinal digestion.
• Gut microflora: change in flora and increase in numbers in abosomal infections.
• Gut hormones: increase in gastrin secretion (abosomal infections due to an increase in gastric pH) - cause of decrease in appetite?
• Malabsorption of nutrients: in intestinal infections due to villous atrophy - affects amino acids, fats and minerals.

c) Protein metabolism:

Normally there is a dynamic equilibrium between dietary protein in the gut, amino acids absorbed into the circulation, protein synthesis in the liver, protein storage in the muscle and protein catabolism (i.e. protein breakdown). In PGE, this equilibrium is upset:

• dietary protein intake decreases
• dietary protein breakdown decreases
• amino acid absorption decreases
• change in distribution of protein synthesis (reduced muscle; increased haemoglobin, albumin, immunoglobulins)
• protein leak due to an increase in mucosal permeability

d) Mineral metabolism:

Decreased calcium and phosphorus absorption (villous atrophy) leads to a decrease in bone mineralisation (osteoporosis).

e) Energy metabolism:

Decrease in appetite leads to mobilisation of adipose tissue.