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Arrested larval development
(Hypobiosis)
• temporary cessation in development of a nematode at a
precise point in its parasitic development
• affects only a proportion
• nature of the stimulus
• environmental one received by the free living infective stages
(cold autumn/winter conditions & dry conditions
• acquired and age immunity
• degree of adaptation to these seasonal stimuli and
therefore the proportional of larvae which do become
arrested seems to he a heritable trait and is affected by
various factors including grazing systems and the degree
of adversity in the environment.
epidemiological importance
• ensures the survival of the nematode during
periods of adversity
• subsequent maturation of arrested larvae
increases the contamination of the
environment and can sometimes result in
clinical disease.
PERIPARTURIENT RISE (PPR) IN FAECAL
EGG COUNTS
• An increase in the numbers of nematode eggs in the
faeces of animals around parturition.
• Etiology: temporary relaxation in immunity
(prolactin)
• Source of the PPR:
• Maturation of larvae arrested
• An increased establishment of infections
• An increased fecundity
• Importance of the PPR:
– new susceptible hosts
– Increased contamination of the environment lead to
clinical disease
Trichostrongyloidea
• Small, often hair-like
• Bursate group
• Parasitize the alimentary tract except
Dictyocaulus
• Few cuticular appendages
• Buccal capsule is vestigial
• Well developed bursa and two spicules
• Direct life cycle
• Ensheathed L3 is infective stage
• Ostertagia, Haemonchus, Trichostrongylus,
Cooperia, Nematodirus
Ostertagia
• Parasitic gastritis
• Hosts: Ruminants
• Site: Abomasum
– Adult on surface of abomasum
– larval stages occur in the gastric glands
• Species:
– Ostertagia ostertagi cattle
– 0. circumcincta sheep and goats
– 0. trifurcata sheep and goats
• Identification
– slender reddish-brown
– l.0 cm long
• Species differentiation is based on the structure of the
spicules
• Direct life cycle
• Eggs in feces----L3 ----2 weeks
• L3 exsheathes in rumen---enter lumen of abomasal gland---- L4– L5– -- 18
days ----emerge from gland--- mature
• Entire life cycle take 3 weeks
• Early fourth larval stage
PATHOGENESIS
• Reduction in the functional gastric gland
– Failure to activate pepsinogen to pepsin
– Loss of bacteriostatic effect
• Enhanced permeability of the abomasal
epithelium
– Hypoalbuminaemia
•
CLINICAL SIGNS
• Profuse watery diarrhoea
• Hind quarters heavily soiled with faeces
• Dull coat
• Inappetence
• Weight loss (leakage of endogenous protein)
Treatment
• Benzimidazoles (albendazole, fenbendazole or
Oxfendazole
• Ivermectin
• Febantel, Netobimin
HAEMONCHUS
(Barber pole worm)
• Blood sucking abomasal parasite
• Host: cattle, sheep, goat
• Species:
– Haemonchus contortus
– H. placei
– H. similis
• Size: 2.0-3.0 cm
• Barber’s pole appearance: white ovaries winding
spirally around the blood-filled intestine
• Microscopic: there are cervical papillae and a
tiny lancet inside the buccal capsule
– Female has vulval flap
– Male has asymmetrical dorsal lobe
• larvae moult twice in close apposition to the
gastric glands
• Prepatent period is 2-3 weeks in sheep and
four weeks in cattle
Female - vulva flap
Cervical papillae
Buccal lancet
PATHOGENESIS
• Acute haemorrhagic anaemia
• Acute haemonchosis:
–Acute haemorrhagic anaemia
–Progressive and dramatic fall in the packed
red cell volume
–At necropsy 2000 and 20000 worms
–Abomasal contents are fluid and dark brown
• Chronic haemonchosis
• Loss of weight, weakness and inappetence
rather than marked anaemia
TRICHOSTRONGYLUS
• Host: Ruminants, horse, fowl, pigs
• Infection site: Small intestine, except T. axei
and T. tenuis
• Species
– T. axei ruminants (abomasum),
horse (stomach)
– T. colubriformis ruminants
– T. vitrinus sheep, goat
– T. capricola sheep, goat
– T. tenius small intestine and
caeca of game birds
• Identification: small, hair like
• Length…. 7.00mm
• No buccal capsule
• Distinct excretory notch in oesophageal region
• Spicules are thick and unbranched
• Life cycle: Direct
• Exsheathment of L3 of intestinal species occurs in
the abomasum
• Parasitic phase is non-migratory
• Prepatent period
– Ruminants 2-3 weeks
– Horse 25 days
– Birds 10 days
• L3 of the intestinal species penetrate between
the epithelial glands of the mucosa with
formation of tunnels beneath the epithelium,
but above the lamina propria
• Haemorrhage, oedema
• Loss of plasma proteins
• Enteritis
• Villi destroy
Clinical signs
• rapid weight loss and diarrhoea
• inappetence and poor growth rates
Cooperia
• Host: Ruminants
• Site: small intestine
• Species:
– C. oncophora
– C. punctata
– C. pectinata
– C. surnobada
– C. curticei
• Identification: size similar to Ostertagia
• Very large bursa
• Watch-spring like posture
• Main generic features---small cephalic and
the transverse cuticular striations in the
oesophageal region
• The spicules usually have a wing like
expansion in the middle region and bear
ridges
• No gubernaculum
• Females usually have a small vulval flap
• Life cycle: direct
Pathogenesis
• Penetrate the epithelial surface of the small
intestine and cause a disruption
• Villous atrophy
• Reduction in the area available for absorption
• Diarrhoea
• Clinical Signs
• Loss of appetite,
• Poor weight gains
• Diarrhoea
• Suhmandibular oedema
Nematodirus
• Host: Ruminants
• Site: small intestine
• Nematodirus battus sheep, occasionally
calves
• N. filicollis sheep and goats
• N. spathigur sheep and goats
• Identification: Adults are slender
• Size: 2.0 cm long
• Intertwining of the thin, twisted worms
produces an appearance similar to that of
cotton wool
• A small hut distinct cephalic vesicle
• The spicules are long and slender with fused
tips
• Development to the L3 takes place within the
egg shell
Pathogenesis
• Disruption of the intestinal mucosa, particularly
in the ileum
• Severe damage to villi and erosion of the
mucosa leading lo villous atrophy
• Ability of the intestine to exchange fluids and
nutrients is grossly reduced
• Diarrhoea
• Enteritis
• Carcass has dehydrated appearance
Clinical signs
• Diarrhoea
• Thirsty
• Infected ewes continue to graze
• Inappetent and diarrhoeic lambs congregate
round drinking places
• Diagnosis
• Clinical signs (Fecal egg count is of low value)
• Treatment
• levamisole, milbemycin
Dictyocaulus
Parasitic bronchitis
• husk, hoose, verminous pneumonia or
dictyocaulosis
• Host: Ruminants, horse & donkeys
• Site: Trachea and bronchi, particularly of the
diaphragmatic lobes
• D. vivipurus cattle and deer
• D. filaria sheep and goats
• D. arnfieldi donkeys and horses
• Slender thread-like worms up to 8.0cm in length
• Life cycle
• Ovo-viviparous females
• L1 migrate up the trachea, are swallowed and pass out in
the faeces
• Larvae: Sluggish, and their intestinal cells are filled with
dark brown food granules
• L3 stage is reached within five days
• L3 penetrate the intestinal mucusa and pass to the
mesenteric lymph nodes where they moult.
• Then the L4, travel via the lymph and blood to the lungs.
and break out of the capillaries into the alveoli about one
week after infection.
• The final moult occurs in the bronchioles a few days later
and the young adults then move up the bronchi and
mature.
• The prepatent period is around 3-4 weeks.

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Larval arrest and immunity in nematode parasites

  • 1. Arrested larval development (Hypobiosis) • temporary cessation in development of a nematode at a precise point in its parasitic development • affects only a proportion • nature of the stimulus • environmental one received by the free living infective stages (cold autumn/winter conditions & dry conditions • acquired and age immunity • degree of adaptation to these seasonal stimuli and therefore the proportional of larvae which do become arrested seems to he a heritable trait and is affected by various factors including grazing systems and the degree of adversity in the environment.
  • 2. epidemiological importance • ensures the survival of the nematode during periods of adversity • subsequent maturation of arrested larvae increases the contamination of the environment and can sometimes result in clinical disease.
  • 3. PERIPARTURIENT RISE (PPR) IN FAECAL EGG COUNTS • An increase in the numbers of nematode eggs in the faeces of animals around parturition. • Etiology: temporary relaxation in immunity (prolactin) • Source of the PPR: • Maturation of larvae arrested • An increased establishment of infections • An increased fecundity • Importance of the PPR: – new susceptible hosts – Increased contamination of the environment lead to clinical disease
  • 4. Trichostrongyloidea • Small, often hair-like • Bursate group • Parasitize the alimentary tract except Dictyocaulus • Few cuticular appendages • Buccal capsule is vestigial • Well developed bursa and two spicules • Direct life cycle • Ensheathed L3 is infective stage • Ostertagia, Haemonchus, Trichostrongylus, Cooperia, Nematodirus
  • 5. Ostertagia • Parasitic gastritis • Hosts: Ruminants • Site: Abomasum – Adult on surface of abomasum – larval stages occur in the gastric glands • Species: – Ostertagia ostertagi cattle – 0. circumcincta sheep and goats – 0. trifurcata sheep and goats
  • 6. • Identification – slender reddish-brown – l.0 cm long • Species differentiation is based on the structure of the spicules • Direct life cycle • Eggs in feces----L3 ----2 weeks • L3 exsheathes in rumen---enter lumen of abomasal gland---- L4– L5– -- 18 days ----emerge from gland--- mature • Entire life cycle take 3 weeks • Early fourth larval stage
  • 7. PATHOGENESIS • Reduction in the functional gastric gland – Failure to activate pepsinogen to pepsin – Loss of bacteriostatic effect • Enhanced permeability of the abomasal epithelium – Hypoalbuminaemia •
  • 8. CLINICAL SIGNS • Profuse watery diarrhoea • Hind quarters heavily soiled with faeces • Dull coat • Inappetence • Weight loss (leakage of endogenous protein) Treatment • Benzimidazoles (albendazole, fenbendazole or Oxfendazole • Ivermectin • Febantel, Netobimin
  • 9. HAEMONCHUS (Barber pole worm) • Blood sucking abomasal parasite • Host: cattle, sheep, goat • Species: – Haemonchus contortus – H. placei – H. similis • Size: 2.0-3.0 cm • Barber’s pole appearance: white ovaries winding spirally around the blood-filled intestine
  • 10. • Microscopic: there are cervical papillae and a tiny lancet inside the buccal capsule – Female has vulval flap – Male has asymmetrical dorsal lobe • larvae moult twice in close apposition to the gastric glands • Prepatent period is 2-3 weeks in sheep and four weeks in cattle
  • 11. Female - vulva flap Cervical papillae Buccal lancet
  • 12. PATHOGENESIS • Acute haemorrhagic anaemia • Acute haemonchosis: –Acute haemorrhagic anaemia –Progressive and dramatic fall in the packed red cell volume –At necropsy 2000 and 20000 worms –Abomasal contents are fluid and dark brown • Chronic haemonchosis • Loss of weight, weakness and inappetence rather than marked anaemia
  • 13. TRICHOSTRONGYLUS • Host: Ruminants, horse, fowl, pigs • Infection site: Small intestine, except T. axei and T. tenuis • Species – T. axei ruminants (abomasum), horse (stomach) – T. colubriformis ruminants – T. vitrinus sheep, goat – T. capricola sheep, goat – T. tenius small intestine and caeca of game birds
  • 14. • Identification: small, hair like • Length…. 7.00mm • No buccal capsule • Distinct excretory notch in oesophageal region • Spicules are thick and unbranched • Life cycle: Direct • Exsheathment of L3 of intestinal species occurs in the abomasum • Parasitic phase is non-migratory • Prepatent period – Ruminants 2-3 weeks – Horse 25 days – Birds 10 days
  • 15. • L3 of the intestinal species penetrate between the epithelial glands of the mucosa with formation of tunnels beneath the epithelium, but above the lamina propria • Haemorrhage, oedema • Loss of plasma proteins • Enteritis • Villi destroy
  • 16. Clinical signs • rapid weight loss and diarrhoea • inappetence and poor growth rates
  • 17. Cooperia • Host: Ruminants • Site: small intestine • Species: – C. oncophora – C. punctata – C. pectinata – C. surnobada – C. curticei • Identification: size similar to Ostertagia • Very large bursa
  • 18. • Watch-spring like posture • Main generic features---small cephalic and the transverse cuticular striations in the oesophageal region • The spicules usually have a wing like expansion in the middle region and bear ridges • No gubernaculum • Females usually have a small vulval flap • Life cycle: direct
  • 19. Pathogenesis • Penetrate the epithelial surface of the small intestine and cause a disruption • Villous atrophy • Reduction in the area available for absorption • Diarrhoea • Clinical Signs • Loss of appetite, • Poor weight gains • Diarrhoea • Suhmandibular oedema
  • 20. Nematodirus • Host: Ruminants • Site: small intestine • Nematodirus battus sheep, occasionally calves • N. filicollis sheep and goats • N. spathigur sheep and goats
  • 21. • Identification: Adults are slender • Size: 2.0 cm long • Intertwining of the thin, twisted worms produces an appearance similar to that of cotton wool • A small hut distinct cephalic vesicle • The spicules are long and slender with fused tips • Development to the L3 takes place within the egg shell
  • 22. Pathogenesis • Disruption of the intestinal mucosa, particularly in the ileum • Severe damage to villi and erosion of the mucosa leading lo villous atrophy • Ability of the intestine to exchange fluids and nutrients is grossly reduced • Diarrhoea • Enteritis • Carcass has dehydrated appearance
  • 23. Clinical signs • Diarrhoea • Thirsty • Infected ewes continue to graze • Inappetent and diarrhoeic lambs congregate round drinking places • Diagnosis • Clinical signs (Fecal egg count is of low value) • Treatment • levamisole, milbemycin
  • 24. Dictyocaulus Parasitic bronchitis • husk, hoose, verminous pneumonia or dictyocaulosis • Host: Ruminants, horse & donkeys • Site: Trachea and bronchi, particularly of the diaphragmatic lobes • D. vivipurus cattle and deer • D. filaria sheep and goats • D. arnfieldi donkeys and horses
  • 25. • Slender thread-like worms up to 8.0cm in length • Life cycle • Ovo-viviparous females • L1 migrate up the trachea, are swallowed and pass out in the faeces • Larvae: Sluggish, and their intestinal cells are filled with dark brown food granules • L3 stage is reached within five days • L3 penetrate the intestinal mucusa and pass to the mesenteric lymph nodes where they moult. • Then the L4, travel via the lymph and blood to the lungs. and break out of the capillaries into the alveoli about one week after infection. • The final moult occurs in the bronchioles a few days later and the young adults then move up the bronchi and mature. • The prepatent period is around 3-4 weeks.