Arrested larval development or hypobiosis allows nematodes to survive adverse environmental conditions by temporarily ceasing development at a precise stage. This ensures the parasite's survival during periods of adversity. When conditions improve, arrested larvae resume development, increasing environmental contamination and potentially causing disease. The periparturient rise in faecal egg counts occurs around birthing and is caused by a temporary relaxation in immunity, leading to increased parasite establishment, reproduction, and contamination risk for new hosts. Nematodes like Haemonchus contortus are blood-sucking parasites of ruminants that cause anaemia and clinical disease. Dictyocaulus viviparus causes parasitic bronchitis in ruminants and horses through a direct life
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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
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
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.