Changes

*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

*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)

'''Arrested larval development'''(synonyms: inhibited development, hypobiosis, diapause)

*Long lifespan of several months (c.f. adult worms; a few weeks only)

*Long lifespan of several months (c.f. adult worms; a few weeks only)

*Larvae become arrested at an early stage in their development e.g. ''Ostertagia'' as EL4 (i.e. early fourth stage), equine cyathostomes as L3

*Larvae become arrested at an early stage in their development e.g. ''Ostertagia'' as EL4 (i.e. early fourth stage), equine cyathostomes as L3

*Termination of arrested development is spontaneous (i.e. a genetic alarm clock). Previously arrested larvae then resume their development and grow to adult worms

*Termination of arrested development is spontaneous (i.e. a genetic alarm clock). Previously arrested larvae then resume their development and grow to adult worms

=== Host Immunity ===

=== 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.

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''':

'''Worm population dynamics - Continuous 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.

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.

'''Factors Adversely Affecting Host Immunity'''

 

*''Nutrition''

**Gross deficiency or mineral/trace element deficiency e.g. cobalt

 

*''Reproductive status''

**"Periparturient relaxation in immunity" (PPRI) seen in breeding ewes and sows

 

**This is due to impaired cell-mediated immune response associated with  

 

#An increase in blood prolactin levels

#A shift of IgA from gut mucosa to mammary gland around parturition

 

*''Drug treatment''

**e.g. Repeated anthelmintic and corticosteroid treatment

 

*''Concurrent infection''

 

**Pathogenic effects of ''Nematodirus'' infection are exacerbated by concurrent coccidia infection in lambs

*''Previous experience of a parasite''

 

**A hypersensitivity reaction to ''Haemonchus'' occurs in some ewes

 

 

 

 

 

 

 

 

'''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 ==

== Pathogenesis ==

=== Introduction ===

=== Introduction ===

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

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).

*'''Species''' of worm and '''stage''' of life-cycle present (affects feeding, site and host reaction)

*'''Numbers''' of worms present (or invading).

*'''Numbers''' of worms present (or invading)

*'''Host immunity''' (affects worm population and pathogenicity).

*'''Host immunity''' (affects both 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).

*'''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 ===

=== Mechanisms ===

The nematodes responsible for PGE impair productivity by adversely affecting:

The nematodes responsible for PGE impair productivity by adversely affecting

 

*''Appetite''

a) ''Appetite'':

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

 

*''Digestion''

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

**'''Digestibility'''; this decreases with abomasal infection so there is a compensatory increase in intestinal digestion

 

**'''Gut microflora'''; abosomal infection causes a change in flora and increase in numbers

 

**'''Gut hormones'''; abosomal infection causes an increase in gastric pH increase in gastrin secretion  - cause of decrease in appetite?

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.

*'''Malabsorption of nutrients''': in intestinal infections due to villous atrophy - affects amino acids, fats and minerals.