This document summarizes key details about several genera of parasitic worms that infect horses and other animals. It describes the life cycles, hosts, geographic distribution, morphology, pathogenesis and clinical signs, diagnosis, and treatment of Triodontophorous, Trichonema/Cyathostomes, Oesophagostomum, and Stephanurus dentatus. The main points provided are that Triodontophorous and Cyathostomes are strongyles that infect horses, Oesophagostomum causes nodule formation in ruminants, and Stephanurus dentatus is a kidney worm of pigs that causes liver damage during migration of larvae.

1. Strongyloidea

2. Triodontophorous
Members of this genus are non migratory large
strongyles frequently occur in the large
numbers in the colon and contributes to the
deleterious effect of mixed strongyle infection.
Species
T. serratus
T. tenuicollis
T. brevicauda
T. minor

3. Trichonema/Cyathostomes
• This genus contains more than 40
species, popularly known as trichonemes,
cyathostomes or small strongyles.
• These parasites are present in the large
intestine of horses.
• Their effects on the host range from poor
performance to clinical signs of severe
entritis.

4. Trichonema
Definitive Host Spectrum
• 13 genera and approximately 44 species
in the horse; 3 genera and 30 species in
elephants
Intermediate Hosts
• None
Geographic Distribution
• Worldwide

5. Morphology
• Adults - mouth directed forward ; short,
thick-walled, cylindrical buccal capsule.
• Body lengths vary per species but about 1/4
to 1/2 inch long; males bursate with
spicules equal.
• Eggs - similar to large strongyle

6. Life Cycle (Stages)
• Free living stages same as large strongyles
• L 3 infective; exsheath in stomach, small
intestine but do not migrate - only forms
nodules
• L 3 enter walls of cecum, colon; develop and
molt; return to gut lumen as early L 5
• Prepatent period - 4 to six weeks up to 3 to 4
months

7. Pathogenesis
Sites of Infection
– Cecum, right ventral colon
Pathogenesis/Clinical Signs
– Infection with a large number of "arrested"
cyathostomin larvae causes a clinical disease
– Affected horses with persistent diarrhea,
emaciation, hypoalbuminemia

8. Pathogenesis
– Granulomatous colitis; masses of cyathostomin
larvae embedded in mucosa = bright red L 4
– May be large numbers of L 4 , early L 5 in feces
with watery diarrhea

9. Diagnosis & Treatment
Diagnosis
• Eggs identify family - Cyathostome eggs may be the
majority found
• Larval culture necessary for species identification -
number of gut cells are a factor in identification
Treatment
• Benzimidazoles - BZ resistance shown by several spp;
Moxidectin (best to date) – approved for horses
Ivermectin or other avermectins
• Pyrantel salt - probably some resistance

10. Other Control Measures
• Clean bedding in stalls
• Not running young foals with older, more immune
horses
• Rotation onto "clean" pastures
• Strategic, regular treatment programs
• Alternate dewormer types annually (one type each year,
using the same type each time a dewormer is
administered in one year)
• Pasture contamination due to large number of parasites
and eggs produced makes management difficult - it is
practically impossible to remove all parasites from a
horse's gut

11. Oesophagostomum spp.
(NODULAR WORM)
Definitive Host Spectrum
• Cattle, sheep, goats, wild ruminants, pigs, primates
(host specificity/parasite species)
Intermediate Host
• None
Geographic Distribution
• Worldwide

12. Species
O. columbianum sheep and goat
O. venulosum sheep and goat
O. radiatum cattle and buffalo
O. dentatum pig
O. quadrispinulatum pig

13. Morphology
Gross
Stout white worm 1.0-2.0 cm long.
Microscopically
• The buccal capsule is small.
• In many species, it is surrounded by leaf crowns.
• Around the anterior oesophagus, there is a
cuticular cephalic vesicle. This terminates in a
cervical groove.

15. life cycle
– Eggs are passed in feces, develop, L 1 hatch
– L 1 develop to infective L 3 in the environment
in 6-7 days
– L 3 are ingested by DH
– Larvae exsheath and penetrate the wall of the
intestine (anywhere from pylorus to rectum)
and become enclosed in nodules - over time
these can become caseous and fibrotic
– Larvae (now L 4 ) leave the nodules and
begin maturation
– Prepatent period - 30 to 50 days

16. Pathogenesis
• Sites of Infection
– Large intestine adults
• Pylorus to rectum (in nodules) - larvae
Pathogenesis/Clinical Signs
• Cattle
• Resistance develops by 2 years, so disease is
seen only in young stock
• Nodules may be 1-5 mm in diameter, contain
caseous material and may become calcified
• Clinical signs - anorexia, emaciation, profuse dark
green diarrhea

18. Pathogenesis in sheep
• Nodules do not appear unless there has
been prior exposure and sensitization
• Nodules consist of the larva, leucocytes and
foreign body giant cells surrounded by
fibroblasts
• Nodules, when extensive, interfere with
digestion, absorption and bowel movement

19. Pathogenesis in sheep
• Suppurative nodules may rupture and cause
peritonitis.
• Adults are plug feeders and cause thickening
of the bowel wall and excess mucus
• Clinical signs - anorexia, weight loss,
emaciation and dark green mucoid,
sometimes bloody, diarrhea; perhaps death

20. Pathogenesis
Pigs
• Nodule formation causes enteritis, anorexia and
bloody feces
• In severe infections death is possible

21. Diagnosis & Treatment
Diagnosis
– Because most of the clinical effects are due to the nodules,
necropsy may be necessary for confirmation
– Eggs in feces cannot be distinguished from other strongylid-
type eggs and need to be cultured to the L 3 stage to confirm
Oesophagostomum
Treatment
– Benzimidazoles (e.g. fenbendazole); BZ-resistance reported
– Levamisole (ruminants)
– Morantel (cattle)
– Avermectins are particularly effective: Ivermectin,
doramectin
Other Control Measures
– Good management coupled with routine anthelmintic
treatment is the best control

22. Stephanurus dentatus
Kidney worm of pig
Definitive Host Spectrum
• Pigs, rarely and accidentally cattle, donkeys
Intermediate Host
• Earthworms may act as paratenic hosts
Geographic Distribution
• Worldwide, except northern Europe

23. Morphology
A large stout worm upto 4.5 cm long, with a
prominent buccal capsule and transparent
cuticle through which the internal organs
may be seen.
The colour is usually pinkish.
The size and site are diagnostic.

25. Life Cycle (Stages)
• Eggs are passed in urine
• Eggs hatch, larvae molt twice
• Infection of DH may occur 4 ways
• Ingestion of L 3
• Skin penetration by L 3
• Ingestion of earthworm containing L 3
• Transplacentally

26. Life Cycle (Stages)
• Ingested larvae arrive in the liver via the portal
circulation; percutaneous larvae arrive in the
liver via the lungs and the systemic circulation
• Migrate in liver 3 or more months - extensive
migration of L4 may cause great damage in the
form of abscesses and secondary bacterial
infections
• Larvae then penetrate through the liver capsule
and migrate to the perirenal tissues, ureters,
etc.
• Prepatent period - 6 to 16 months

27. Pathogenesis/Clinical Signs
Sites of Infection
Kidneys and perirenal tissues
Pathogenesis
Most pathology is caused by the larvae
• Skin penetration causes the formation of nodules and
enlargement of superficial lymph nodes
• Liver migration causes fibrosis, abscess formation,
cirrhosis, adhesions
• Economic loss from liver condemnation
Adults may cause thickening of the ureters and cystitis
Clinical signs - decreased weight gain, weight loss,
stiffness of the hind legs

28. Diagnosis & Treatment
Diagnosis
• Eggs in urine - highest concentration of eggs in
the last part of the first micturition in the morning
• Necropsy
Treatment
• Levamisole - kills adults only
• Ivermectin & fenbendazole - kill adults and
immature stages