Nematodes ID Flashcards
Dorsal nerve
Cuticle
Ovary
Pseudocoelom
Intestine
Excretory Canal
Uterus
Muscle
Hypodermis
Ventral Nerve
3 parts of the esophagus: Corpus, Isthmus, Bulb
What functions as hydrostatic skeleton?
Pseudocoelomic fluid and muscles. S shaped locomotion
Rectal commissure
Ventrolateral connective
Nerve rings- oesophageal and rectal
What is the line?
What is the purple circle?
Excretory Canal
Testis
Lips
Cutting plates
Leaf crown
First arrow and second arrow
Dorsal gutter
Teeth
Intestine
Rhabditiform (oesophagus)
Top: Spicula, Intestine, Testis
Bottom: Copulatory bursa, Cloaca, Ejaculatory duct, Vas deference
Left: Spicula, Anus, Lateral lobe, Bursal rays
Bottom: Dorsal lobe
Right: Copulatory bursa
Spicule
Gubernaculum
Telamon
Vulva flap
Top: Ovary, Intestine
Bottom: Eggs in the uterus, vulva, vagina
a. Intestine
b. Uterus
c. Ovary
d. Muscle cell
e. Ventral nerve cord
What are characteristic features of Nematodirus sp.?
Cephalic inflation, long thin spicules, very large eggs, spine on the tip of female tail
Nematodirus spathiger- sheep, cattle- SI
* Coiled around villus- villous atrophy, erosion of epithelium, diarrhoea
* LC: Direct. L1-L3 in egg. Need drying or cold to hatch. L3 burrows in mucosal glands, or coil around villi and moult to L4. Adult in lumen. PPP = 21 days
* HYPOBIOSIS COMMON
Nematodirus spathiger- sheep, cattle- SI
* Coiled around villus- villous atrophy, erosion of epithelium, diarrhoea
* LC: Direct. L1-L3 in egg. Need drying or cold to hatch. L3 burrows in mucosal glands, or coil around villi and moult to L4. Adult in lumen. PPP = 21 days
* HYPOBIOSIS COMMON
Nematodirus sp- sheep, cattle- SI
* Coiled around villus- villous atrophy, erosion of epithelium, diarrhoea
* LC: Direct. L1-L3 in egg. Need drying or cold to hatch. L3 burrows in mucosal glands, or coil around villi and moult to L4. Adult in lumen. PPP = 21 days
* HYPOBIOSIS COMMON
What are the other species like this that impact the animal that this impacts?
Nematodirus filicollis- sheep, small intestine
Other: N. spathiger and N. abnormalis
Nematodirus spathiger- sheep, small intestine
N. battus- sheep, cattle. Not in AUS but most pathogenic
What species of Nematodirus is found in cattle?
Nematodirus helvetianus
Cooperia- “wire worm”
Cattle, sheep. Small Intestine.
~9 mm, small cephalic vesicle, tranverse cuticular striations in the oesophageal region, longitudinal cuticular ridges on body. Spicules have a wing like expansion. No gubernaculum.
LC: Direct. L3 in mucosal glands. L4 has head in gland, body in lumen. Adult in lumen braced against villi. PPP= 15 days.
HYPOBIOSIS
Effects on host: villous atrophy, erosion of epithelium
Epi: Ingest larvae during wet season (summer or winter)
Cooperia- “wire worm”
Cattle, sheep. Small Intestine.
~9 mm, small cephalic vesicle, tranverse cuticular striations in the oesophageal region, longitudinal cuticular ridges on body. Spicules have a wing like expansion. No gubernaculum.
LC: Direct. L3 in mucosal glands. L4 has head in gland, body in lumen. Adult in lumen braced against villi. PPP= 15 days.
HYPOBIOSIS
Effects on host: villous atrophy, erosion of epithelium
Epi: Ingest larvae during wet season (summer or winter)
Cooperia punctata- cattle (“cattle bankrupt worm”)- sub tropical- small intestine.
What is the other worm that has the same host in a sub-tropical area?
Cooperia pectinata- cattle- small intestine
(C. punctata)
What is the other worm that has the same host in a temperate environment?
Cooperia oncophora- cattle, temperate
(C.surnabada)
What Cooperia use sheep as hosts?
C. curticei- vary in pathogenicity
Haemonchus
Features: 2-3 cm long, red, tooth in buccal capsule, prominent cervical papillae, “barber’s pole” in female, female with large vulval flap, asymmetrical dorsal ray, spicules with barbs
* LC: Direct. L3 burrows in abomasal glands moult to L4. re-emerge to lumen. PPP= 21 days.
* Effects on host: L4 and adult feed on blood. Ingest 0.05 ml/worm/day. Microcytic, hypochromic anaemia. Hypoproteinaemia- “bottle jaw.” DOES NOT CAUSE DIARRHOEA. Reduced exercise tolerance. Heavy infections- sudden death.
** Voracious blood sucker **
* Epi: high biotic potential- 5-10,000 eggs/day. Eggs will not hatch below 10C. Larvae not resistant to desication.
* Summer rainfall areas (increase in spring, maximum in Feb then decline. Overwinter as hypobiotic larvae) & winter rainfall areas (summers too hot and dry. Develop in spring (lambs) and autumn (lambing ewes)).
* Immunity- self cure when threshold reached. Resulting immunity is labile. Vaccine against gut wall proteins.
Haemonchus
Features: 2-3 cm long, red, tooth in buccal capsule, prominent cervical papillae, “barber’s pole” in female, female with large vulval flap, asymmetrical dorsal ray, spicules with barbs
* LC: Direct. L3 burrows in abomasal glands moult to L4. re-emerge to lumen. PPP= 21 days.
* Effects on host: L4 and adult feed on blood. Ingest 0.05 ml/worm/day. Microcytic, hypochromic anaemia. Hypoproteinaemia- “bottle jaw.” DOES NOT CAUSE DIARRHOEA. Reduced exercise tolerance. Heavy infections- sudden death.
** Voracious blood sucker **
* Epi: high biotic potential- 5-10,000 eggs/day. Eggs will not hatch below 10C. Larvae not resistant to desication.
* Summer rainfall areas (increase in spring, maximum in Feb then decline. Overwinter as hypobiotic larvae) & winter rainfall areas (summers too hot and dry. Develop in spring (lambs) and autumn (lambing ewes)).
* Immunity- self cure when threshold reached. Resulting immunity is labile. Vaccine against gut wall proteins.
Haemonchus
Features: 2-3 cm long, red, tooth in buccal capsule, prominent cervical papillae, “barber’s pole” in female, female with large vulval flap, asymmetrical dorsal ray, spicules with barbs
* LC: Direct. L3 burrows in abomasal glands moult to L4. re-emerge to lumen. PPP= 21 days.
* Effects on host: L4 and adult feed on blood. Ingest 0.05 ml/worm/day. Microcytic, hypochromic anaemia. Hypoproteinaemia- “bottle jaw.” DOES NOT CAUSE DIARRHOEA. Reduced exercise tolerance. Heavy infections- sudden death.
** Voracious blood sucker **
* Epi: high biotic potential- 5-10,000 eggs/day. Eggs will not hatch below 10C. Larvae not resistant to desication.
* Summer rainfall areas (increase in spring, maximum in Feb then decline. Overwinter as hypobiotic larvae) & winter rainfall areas (summers too hot and dry. Develop in spring (lambs) and autumn (lambing ewes)).
* Immunity- self cure when threshold reached. Resulting immunity is labile. Vaccine against gut wall proteins.
Haemonchus
Features: 2-3 cm long, red, tooth in buccal capsule, prominent cervical papillae, “barber’s pole” in female, female with large vulval flap, asymmetrical dorsal ray, spicules with barbs
* LC: Direct. L3 burrows in abomasal glands moult to L4. re-emerge to lumen. PPP= 21 days.
* Effects on host: L4 and adult feed on blood. Ingest 0.05 ml/worm/day. Microcytic, hypochromic anaemia. Hypoproteinaemia- “bottle jaw.” DOES NOT CAUSE DIARRHOEA. Reduced exercise tolerance. Heavy infections- sudden death.
** Voracious blood sucker **
* Epi: high biotic potential- 5-10,000 eggs/day. Eggs will not hatch below 10C. Larvae not resistant to desication.
* Summer rainfall areas (increase in spring, maximum in Feb then decline. Overwinter as hypobiotic larvae) & winter rainfall areas (summers too hot and dry. Develop in spring (lambs) and autumn (lambing ewes)).
* Immunity- self cure when threshold reached. Resulting immunity is labile. Vaccine against gut wall proteins.
Haemonchus
Features: 2-3 cm long, red, tooth in buccal capsule, prominent cervical papillae, “barber’s pole” in female, female with large vulval flap, asymmetrical dorsal ray, spicules with barbs
* LC: Direct. L3 burrows in abomasal glands moult to L4. re-emerge to lumen. PPP= 21 days.
* Effects on host: L4 and adult feed on blood. Ingest 0.05 ml/worm/day. Microcytic, hypochromic anaemia. Hypoproteinaemia- “bottle jaw.” DOES NOT CAUSE DIARRHOEA. Reduced exercise tolerance. Heavy infections- sudden death.
** Voracious blood sucker **
* Epi: high biotic potential- 5-10,000 eggs/day. Eggs will not hatch below 10C. Larvae not resistant to desication.
* Summer rainfall areas (increase in spring, maximum in Feb then decline. Overwinter as hypobiotic larvae) & winter rainfall areas (summers too hot and dry. Develop in spring (lambs) and autumn (lambing ewes)).
* Immunity- self cure when threshold reached. Resulting immunity is labile. Vaccine against gut wall proteins.
Ostertagia “brown stomach worm”
Size: ~ 9 mm. Location: Abomasum (nodules).
Features: cervical papillae, spicules terminate in 3 stubby hooked processes, small vulval flap.
LC (O. circumcincta in sheep): Direct. L1-L3 in faeces (~2 weeks). L3 ingested. Exsheaths in rumen. Migrates into the lumen of abomasal gland. Moults to L4. L4 returns to lumen. PPP= 21 days.
HYPOBIOSIS- common (6 months) (inhibited in spring, emerge in autumn).
Effects on host: (O. circumcincta) pH rises to 6, protein digestion stops, plasma pepsinogen rises, hypergastrinaemia, hypoproteinaemia, anorexia, diarrhoea. ANOREXIA.
Immunity: develops in older animals, worm burden expelled, remaining worms small & produce few eggs.
Ostertagia “brown stomach worm”
Size: ~ 9 mm. Location: Abomasum (nodules).
Features: cervical papillae, spicules terminate in 3 stubby hooked processes, small vulval flap.
LC (O. circumcincta in sheep): Direct. L1-L3 in faeces (~2 weeks). L3 ingested. Exsheaths in rumen. Migrates into the lumen of abomasal gland. Moults to L4. L4 returns to lumen. PPP= 21 days.
HYPOBIOSIS- common (6 months) (inhibited in spring, emerge in autumn).
Effects on host: (O. circumcincta) pH rises to 6, protein digestion stops, plasma pepsinogen rises, hypergastrinaemia, hypoproteinaemia, anorexia, diarrhoea. ANOREXIA.
Immunity: develops in older animals, worm burden expelled, remaining worms small & produce few eggs.
Ostertagia “brown stomach worm”
Size: ~ 9 mm. Location: Abomasum (nodules).
Features: cervical papillae, spicules terminate in 3 stubby hooked processes, small vulval flap.
LC (O. circumcincta in sheep): Direct. L1-L3 in faeces (~2 weeks). L3 ingested. Exsheaths in rumen. Migrates into the lumen of abomasal gland. Moults to L4. L4 returns to lumen. PPP= 21 days.
HYPOBIOSIS- common (6 months) (inhibited in spring, emerge in autumn).
Effects on host: (O. circumcincta) pH rises to 6, protein digestion stops, plasma pepsinogen rises, hypergastrinaemia, hypoproteinaemia, anorexia, diarrhoea. ANOREXIA.
Immunity: develops in older animals, worm burden expelled, remaining worms small & produce few eggs.
What are the other two that affect the same hosts?
Ostertagia circumcincta- sheep, goat.
(Ostertagia trifurcata, Teladorsagia davtiani)
ABOMASUM
What are the other species that affects the same hosts?
Ostertagia trifurcata- sheep, goat
(Ostertagia circumcincta, Teladorsagia davtiani)
ABOMASUM
Ostertagia ostertagi - cattle- abomasum
* the most important nematode in cattle in temperate areas of the world
* basic life cycle similar to Ostertagia in sheep
* causes nodules in abomasum
* severe infestation gives morocco leather appearance
Differences from sheep:
- Faecal mass as a reservoir for larvae
- Inhibited larvae can emerge synchronously
* cattle dung pat- “helminthological time bomb”
* water content and temperature within dung pat play crucial role in hatching of eggs and the development of larvae
* larvae can survive for extended periods in faecal pat
* emerge following rain
TYPE 1 ostertagiasis: young animals, no immunity, occurs in spring, dianose with egg counts, plasma pepsinogen
TYPE 2 ostertagiasis: larvae emerge synchronously, 2-4 year old animals, precipitated by “stress” (calving), erratic in occurrence (some years, few cattle affected), occurs in autumn, diagnose with plasma pepsinogen
* HYPOBIOSIS– Europe overwinter. No hypobiosis in sub tropical areas.
Ostertagia ostertagi - cattle- abomasum
* the most important nematode in cattle in temperate areas of the world
* basic life cycle similar to Ostertagia in sheep
* causes nodules in abomasum
* severe infestation gives morocco leather appearance
Differences from sheep:
- Faecal mass as a reservoir for larvae
- Inhibited larvae can emerge synchronously
* cattle dung pat- “helminthological time bomb”
* water content and temperature within dung pat play crucial role in hatching of eggs and the development of larvae
* larvae can survive for extended periods in faecal pat
* emerge following rain
TYPE 1 ostertagiasis: young animals, no immunity, occurs in spring, dianose with egg counts, plasma pepsinogen
TYPE 2 ostertagiasis: larvae emerge synchronously, 2-4 year old animals, precipitated by “stress” (calving), erratic in occurrence (some years, few cattle affected), occurs in autumn, diagnose with plasma pepsinogen
* HYPOBIOSIS– Europe overwinter. No hypobiosis in sub tropical areas.
Ostertagia ostertagi - cattle- abomasum
* the most important nematode in cattle in temperate areas of the world
* basic life cycle similar to Ostertagia in sheep
* causes nodules in abomasum
* severe infestation gives morocco leather appearance
Differences from sheep:
- Faecal mass as a reservoir for larvae
- Inhibited larvae can emerge synchronously
* cattle dung pat- “helminthological time bomb”
* water content and temperature within dung pat play crucial role in hatching of eggs and the development of larvae
* larvae can survive for extended periods in faecal pat
* emerge following rain
TYPE 1 ostertagiasis: young animals, no immunity, occurs in spring, dianose with egg counts, plasma pepsinogen
TYPE 2 ostertagiasis: larvae emerge synchronously, 2-4 year old animals, precipitated by “stress” (calving), erratic in occurrence (some years, few cattle affected), occurs in autumn, diagnose with plasma pepsinogen
* HYPOBIOSIS– Europe overwinter. No hypobiosis in sub tropical areas.
Ostertagia ostertagi - cattle- abomasum
* the most important nematode in cattle in temperate areas of the world
* basic life cycle similar to Ostertagia in sheep
* causes nodules in abomasum
* severe infestation gives morocco leather appearance
Differences from sheep:
- Faecal mass as a reservoir for larvae
- Inhibited larvae can emerge synchronously
* cattle dung pat- “helminthological time bomb”
* water content and temperature within dung pat play crucial role in hatching of eggs and the development of larvae
* larvae can survive for extended periods in faecal pat
* emerge following rain
TYPE 1 ostertagiasis: young animals, no immunity, occurs in spring, dianose with egg counts, plasma pepsinogen
TYPE 2 ostertagiasis: larvae emerge synchronously, 2-4 year old animals, precipitated by “stress” (calving), erratic in occurrence (some years, few cattle affected), occurs in autumn, diagnose with plasma pepsinogen
* HYPOBIOSIS– Europe overwinter. No hypobiosis in sub tropical areas.
Ostertagia ostertagi - cattle- abomasum
* the most important nematode in cattle in temperate areas of the world
* basic life cycle similar to Ostertagia in sheep
* causes nodules in abomasum
* severe infestation gives morocco leather appearance
Differences from sheep:
- Faecal mass as a reservoir for larvae
- Inhibited larvae can emerge synchronously
* cattle dung pat- “helminthological time bomb”
* water content and temperature within dung pat play crucial role in hatching of eggs and the development of larvae
* larvae can survive for extended periods in faecal pat
* emerge following rain
TYPE 1 ostertagiasis: young animals, no immunity, occurs in spring, dianose with egg counts, plasma pepsinogen
TYPE 2 ostertagiasis: larvae emerge synchronously, 2-4 year old animals, precipitated by “stress” (calving), erratic in occurrence (some years, few cattle affected), occurs in autumn, diagnose with plasma pepsinogen
* HYPOBIOSIS– Europe overwinter. No hypobiosis in sub tropical areas.
Ostertagia ostertagi - cattle- abomasum
* the most important nematode in cattle in temperate areas of the world
* basic life cycle similar to Ostertagia in sheep
* causes nodules in abomasum
* severe infestation gives morocco leather appearance
Differences from sheep:
- Faecal mass as a reservoir for larvae
- Inhibited larvae can emerge synchronously
* cattle dung pat- “helminthological time bomb”
* water content and temperature within dung pat play crucial role in hatching of eggs and the development of larvae
* larvae can survive for extended periods in faecal pat
* emerge following rain
TYPE 1 ostertagiasis: young animals, no immunity, occurs in spring, dianose with egg counts, plasma pepsinogen
TYPE 2 ostertagiasis: larvae emerge synchronously, 2-4 year old animals, precipitated by “stress” (calving), erratic in occurrence (some years, few cattle affected), occurs in autumn, diagnose with plasma pepsinogen
* HYPOBIOSIS– Europe overwinter. No hypobiosis in sub tropical areas.
Ostertagia ostertagi
a) in Southern Australia
b) in Europe and North America
Trichostrongylus axei “stomach hairworm” - sheep, cattle, horse, pig, man
Host: primarily parasitic in cattle; can occur in sheep, horses, pigs, humans
Location: abomasum/ stomach (intraepithelial)
Features: size ~6mm, spicules- unequal, dissimilar
Pathogenesis: damages epithelium, protein lost into lumen, mucus produced, pH rises, 40,000 can kill lamb
Epidemiology: important in mixed grazing
Trichostrongylus axei “stomach hairworm” - sheep, cattle, horse, pig, man
Host: primarily parasitic in cattle; can occur in sheep, horses, pigs, humans
Location: abomasum/ stomach (intraepithelial)
Features: size ~6mm, spicules- unequal, dissimilar
Pathogenesis: damages epithelium, protein lost into lumen, mucus produced, pH rises, 40,000 can kill lamb
Epidemiology: important in mixed grazing
Haemonchus
Features: 2-3 cm long, red, tooth in buccal capsule, prominent cervical papillae, “barber’s pole” in female, female with large vulval flap, asymmetrical dorsal ray, spicules with barbs
* LC: Direct. L3 burrows in abomasal glands moult to L4. re-emerge to lumen. PPP= 21 days.
* Effects on host: L4 and adult feed on blood. Ingest 0.05 ml/worm/day. Microcytic, hypochromic anaemia. Hypoproteinaemia- “bottle jaw.” DOES NOT CAUSE DIARRHOEA. Reduced exercise tolerance. Heavy infections- sudden death.
** Voracious blood sucker **
* Epi: high biotic potential- 5-10,000 eggs/day. Eggs will not hatch below 10C. Larvae not resistant to desication.
* Summer rainfall areas (increase in spring, maximum in Feb then decline. Overwinter as hypobiotic larvae) & winter rainfall areas (summers too hot and dry. Develop in spring (lambs) and autumn (lambing ewes)).
* Immunity- self cure when threshold reached. Resulting immunity is labile. Vaccine against gut wall proteins.
Cooperia- “wire worm”
Cattle, sheep. Small Intestine.
~9 mm, small cephalic vesicle, tranverse cuticular striations in the oesophageal region, longitudinal cuticular ridges on body. Spicules have a wing like expansion. No gubernaculum.
LC: Direct. L3 in mucosal glands. L4 has head in gland, body in lumen. Adult in lumen braced against villi. PPP= 15 days.
HYPOBIOSIS
Effects on host: villous atrophy, erosion of epithelium
Epi: Ingest larvae during wet season (summer or winter)
Nematodirus spathiger- sheep, cattle- SI
* Coiled around villus- villous atrophy, erosion of epithelium, diarrhoea
* LC: Direct. L1-L3 in egg. Need drying or cold to hatch. L3 burrows in mucosal glands, or coil around villi and moult to L4. Adult in lumen. PPP = 21 days
Cooperia- “wire worm”
Cattle, sheep. Small Intestine.
~9 mm, small cephalic vesicle, tranverse cuticular striations in the oesophageal region, longitudinal cuticular ridges on body. Spicules have a wing like expansion. No gubernaculum.
LC: Direct. L3 in mucosal glands. L4 has head in gland, body in lumen. Adult in lumen braced against villi. PPP= 15 days.
HYPOBIOSIS
Effects on host: villous atrophy, erosion of epithelium
Epi: Ingest larvae during wet season (summer or winter)
Important genera?
Rhabditida
Features: rhabditiform esophagus, tiny nematodes, most species free living, most feed on bacteria
Important genera: Strongyoides, Rhabditis, Micronema “accidental” parasites
* LC: Parthenogenetic female. Eggs hatch quickly (6 hrs). Heterogonic & homogonic life cycles. Rhabditiform & strongyliform larvae. PPP= 5-12 days (short). Auto-infection can occur (S. stercoralis).
* Diagnosis- eggs- faecal flotation, larvae- Baermann technique, in vitro culture, Serodiagnosis- ELISA
* Treatment: Ivermectin, oxibendazole
Strongyloides ransomi
* Prenatal infection
* Trans-colostral infection
* Invasive- dermatitis
* Pulmonary- pneumonia
* Intestinal- parasitic female burrow in small intestine- diarrhoea, reduced growth rate
* Piglets vs. gilts
* Major disease problem
* larvae survive for 3 weeks
* must eliminate moist conditions in environment
* LC: Parthenogenetic female. Eggs hatch quickly (6 hrs). Heterogonic & homogonic life cycles. Rhabditiform & strongyliform larvae. PPP= 5-12 days (short). Auto-infection can occur (S. stercoralis).
* Diagnosis- eggs- faecal flotation, larvae- Baermann technique, in vitro culture, Serodiagnosis- ELISA
* Treatment: Ivermectin, oxibendazole
What strongyloides use ruminants as a host?
S. papillosus- small intestine
* LC: Parthenogenetic female. Eggs hatch quickly (6 hrs). Heterogonic & homogonic life cycles. Rhabditiform & strongyliform larvae. PPP= 5-12 days (short). Auto-infection can occur (S. stercoralis).
* Diagnosis- eggs- faecal flotation, larvae- Baermann technique, in vitro culture, Serodiagnosis- ELISA
* Treatment: Ivermectin, oxibendazole
What strongyloides use horses as a host?
Strongyloides westeri- small intestine (transcolostral infection)
* transcolostral infection important diarrhoea in foals 2 weeks old
* LC: Parthenogenetic female. Eggs hatch quickly (6 hrs). Heterogonic & homogonic life cycles. Rhabditiform & strongyliform larvae. PPP= 5-12 days (short). Auto-infection can occur (S. stercoralis).
* Diagnosis- eggs- faecal flotation, larvae- Baermann technique, in vitro culture, Serodiagnosis- ELISA
* Treatment: Ivermectin, oxibendazole
Strongyloides of dogs, cats, and man?
S. stercoralis, small intestine
* can remain dormant for 37 years auto-infection can occur secondary infection in AIDS cases
S. papillosus- calf. Small intestine.
Rhabditis strongyloides
Micronema gingivalis
Order? General features?
Four superfamilies?
General life cycle?
Strongylida
* buccal capsule- and male has copulatory bursa
Superfamilies:
* Trichostrongyloidea- “trichostrongyles” abomasum, small intestine
* Strongyloidea- “strongyles” large intestine
* Metastrongyloidea- “lungworms”- lungs
* Ancylostomatoidea- “hookworms” small intestine
LC: direct. (egg- L1- L2) in faeces–> (L3)–> L4- male/female in host
What are the important species and where from this superfamily? Features?
Trichostrongyloidea (superfamily)
Features: vestigial buccal capsule, copulatory bursa
Abomasum: Haemonchus, Ostertagia, Trichostongylus axei
Small Intestine: Trichostrongylus (black scour worm- sheep), Cooperia (wire worm- cattle), Nematodirus (thin-necked intestinal worm- sheep/cattle)
Air passages: Dictyocaulus
What are the trichostrongyles that affect sheep and goats?
All of the ones we learned
T. colubriformis- sheep, goats- duodenum
T. vitrinus- sheep, goats- duodenum
T. rugatus- sheep, goats- duodenum
T. axei- sheep, cattle, goats, pigs, horses- stomach, abomasum
T. axei
T. rugatus
T. vitrinus
T. colubriformis
Distribution:
* higher rainfall areas
* main sheep raising areas
* species differ in regions
T. colubriformis in summer rainfall areas; T. vitrinus in cooler, moist areas; T. rugatus in dry areas
* same principles apply elsewhere in world
Life cycle of trichostrongylus
Eggs laid in faeces
L1 hatches–> L1 & L2 develop in feaces–> L3 retains cuticle of L2 as sheath (protected but cannot feed)–> L3 migrates out of faeces onto grass–>L3 climbs up grass–> ingested by sheep–> exsheaths in rumen–> develops in small intestine
PPP= 21 days
Development where?
Effects on host?
* development occurs in duodenum
* moult to L4 occurs after 5 days
* moult to adult occurs at 10 days
* nematodes are intraepithelial
Efects on sheep:
Cause villous atrophy, protein loss, reduced absorption of Ca and PO4 (absorption occurs in duodenum, lower intestine cannot compensate, blood Ca conc. has to be maintained within narrow range, hypophosphataemia, reduced bone growth), anorexia (feed intake reduced, mechanism not known, major effect on growth rate), diarrhoea (parasite secrete analogues of parasympathetic transmitters; increase frequency & strength of peristaltic waves; together with poor absorption, leads to diarrhoea; assessment of dag score)
Trichostrongylus
* Villus atrophy
* Normal villi compared with those in an infected sheep
* mucosal glands enlarged inflammatory cells in lamina propria
* Abnormal epithelial cells breaks in epithelium
* Hypoproteinaemia: breaks in epithelium an increased permeability of capillaries lead to - leakage of plasma proteins into gut, hypoproteinaemia/ hypoalbuminaemia associated with up to 20% reduction in wool production and reduced growth rate
* globulin concentration in blood rises as host immune response
How does the host respond to infection of trichostrongyles?
* Immune response only if > 5 months of age
* threshold of 3000 worms
* expulsion of worms rarely 100%
* Immunity is against incoming larvae; mainly cellular, antibodies play minor role
*goblet cell hyperplasia- increased mucus
* mucus entangles worms
* mucus of immune sheep paralyses worms
* eosinophils, mast cells > in lamina propria
* discharge histamine, serotonin, cytokines
* lead to expulsion on nematodes
* eosinophls can kill larvae
* can have scouring in immune sheep
* > 60,000 nematodes can kill young sheep
* in winter rainfall zone= deaths MID-WINTER
Seasonal patterns of trichostrongyles
* Winter rainfall zones- summer too hot and dry, autumn moist, larvae develop, winter moist- grass short, spring flush dilutes larvae, rising temperatures shorten survival time.
* summer rainfall zones- winter too cold or dry, larvae develop in spring, maximum numbers in summer
* northern hemisphere (temperate)- winters too cold, development occurs in spring, reaches maximum in autumn
Strongyloidea- “strongyles”- large intestine (main location)- rarely kidney or trachea
Features: bursa in male, large buccal capsule, leaf crown
Hosts: horses, ruminants, pig, birds, elephants, macropodid marsupials
Life cycle: L1-(L3)- faeces–> (L3)- herbage–> L3 migrates- into int. gland–> L4 emerges- to lumen–> final moult in lumen
PPP= long
Moults- extra migration
Superfamily: Strongyloidea
Family: Strongylidae
Subfamilies: Strongylinae- globular buccal capsule, called “large strongyles”
Genera: important in equines- Strongylus, Triodontophorus, Oesophagodontus, Craterostomum
Superfamily: Strongyloidea
Family: Strongylidae
Subfamilies: Cyathostominae- cylindrical buccal capsule, called “small strongyles”
Genera: Cyathostomum
Strongyles of equines
Subfamily Strongylinae
Genus- Strongylus (red-worms, blood worms)
Species/ host:
S. vulgaris- horse
S. edentatus- horse
S. equinus- horse
S. asini- donkey, zebra (not in AUS)
Location: caecum and colon
Strongylus equinus- horse- caecum and colon
Strongylus vulgaris- caecum and colon
Strongylus edentatus- caecum and colon
Strongylus vulgaris- caecum and colon- size: 14-24 mm
Strongylus vulgaris- caecum and colon- size: 14-24 mm
Strongylus vulgaris- size: 14-24 mm- horse- caecum and colon.
Life cycle: direct. L1 and L2 develop in faeces, feed on bacteria. Development to L3 stops below 8C. L3 exsheaths in small/large intestine. Migrates into intestinal wall. Migrates in wall of arteries and ascends to root of cranial mesenteric arteries. Remains for several weeks. Returns to gut in blood stream. Enters lumen. PPP= 6 months
Effects on host: Migrating larvae- aberrant migrations, damages arterial wall, thrombus formation, lesion “verminous arteritis,” not an “aneurysm,” thrombi occlude arteries, intermittent colic to infarction…… adults: blood feeders, lesions continue to bleed, anaemia, eosinophilia, elevated white cell count
* Epi: common, cosmopolitan- prevalence was 85%, now 25% in Victoria…. larvae most abundant on pastures in spring- desiccated in summer, winter stops larval development. Peak egg laying occurs 10 months after infection- almost an annual cycle. Foals develop immunity.
Strongylus vulgaris- size: 14-24 mm- horse- caecum and colon.
Life cycle: direct. L1 and L2 develop in faeces, feed on bacteria. Development to L3 stops below 8C. L3 exsheaths in small/large intestine. Migrates into intestinal wall. Migrates in wall of arteries and ascends to root of cranial mesenteric arteries. Remains for several weeks. Returns to gut in blood stream. Enters lumen. PPP= 6 months
Effects on host: Migrating larvae- aberrant migrations, damages arterial wall, thrombus formation, lesion “verminous arteritis,” not an “aneurysm,” thrombi occlude arteries, intermittent colic to infarction…… adults: blood feeders, lesions continue to bleed, anaemia, eosinophilia, elevated white cell count
* Epi: common, cosmopolitan- prevalence was 85%, now 25% in Victoria…. larvae most abundant on pastures in spring- desiccated in summer, winter stops larval development. Peak egg laying occurs 10 months after infection- almost an annual cycle. Foals develop immunity.
Strongylus vulgaris- size: 14-24 mm- horse- caecum and colon.
Life cycle: direct. L1 and L2 develop in faeces, feed on bacteria. Development to L3 stops below 8C. L3 exsheaths in small/large intestine. Migrates into intestinal wall. Migrates in wall of arteries and ascends to root of cranial mesenteric arteries. Remains for several weeks. Returns to gut in blood stream. Enters lumen. PPP= 6 months
Effects on host: Migrating larvae- aberrant migrations, damages arterial wall, thrombus formation, lesion “verminous arteritis,” not an “aneurysm,” thrombi occlude arteries, intermittent colic to infarction…… adults: blood feeders, lesions continue to bleed, anaemia, eosinophilia, elevated white cell count
* Epi: common, cosmopolitan- prevalence was 85%, now 25% in Victoria…. larvae most abundant on pastures in spring- desiccated in summer, winter stops larval development. Peak egg laying occurs 10 months after infection- almost an annual cycle. Foals develop immunity.
Strongylus vulgaris- size: 14-24 mm- horse- caecum and colon.
Life cycle: direct. L1 and L2 develop in faeces, feed on bacteria. Development to L3 stops below 8C. L3 exsheaths in small/large intestine. Migrates into intestinal wall. Migrates in wall of arteries and ascends to root of cranial mesenteric arteries. Remains for several weeks. Returns to gut in blood stream. Enters lumen. PPP= 6 months
Effects on host: Migrating larvae- aberrant migrations, damages arterial wall, thrombus formation, lesion “verminous arteritis,” not an “aneurysm,” thrombi occlude arteries, intermittent colic to infarction…… adults: blood feeders, lesions continue to bleed, anaemia, eosinophilia, elevated white cell count
* Epi: common, cosmopolitan- prevalence was 85%, now 25% in Victoria…. larvae most abundant on pastures in spring- desiccated in summer, winter stops larval development. Peak egg laying occurs 10 months after infection- almost an annual cycle. Foals develop immunity.
Strongyles of equines
Strongylus edentatus
Features: buccal capsule is wider anteriorly than posteriorly, no teeth in buccal capsule, very common species, larger than S. vulgaris (2.3-4.4 cm)
Life Cycle: L3 exsheaths in caecum. Burrows into gut wall. Enters portal veins. Migrates to liver. Spends 8 weeks in liver. Migrates to sub-peritoneal tissues. Returns to gut via mesentery. PPP= 10 months.
Effects on host: aberrant larvae found in many organs, migrating larvae cause lesions, adults cause anaemia
Strongyles of equines
Strongylus edentatus
Features: buccal capsule is wider anteriorly than posteriorly, no teeth in buccal capsule, very common species, larger than S. vulgaris (2.3-4.4 cm)
Life Cycle: L3 exsheaths in caecum. Burrows into gut wall. Enters portal veins. Migrates to liver. Spends 8 weeks in liver. Migrates to sub-peritoneal tissues. Returns to gut via mesentery. PPP= 10 months.
Effects on host: aberrant larvae found in many organs, migrating larvae cause lesions, adults cause anaemia
Strongyles of equines
Strongylus edentatus
Features: buccal capsule is wider anteriorly than posteriorly, no teeth in buccal capsule, very common species, larger than S. vulgaris (2.3-4.4 cm)
Life Cycle: L3 exsheaths in caecum. Burrows into gut wall. Enters portal veins. Migrates to liver. Spends 8 weeks in liver. Migrates to sub-peritoneal tissues. Returns to gut via mesentery. PPP= 10 months.
Effects on host: aberrant larvae found in many organs, migrating larvae cause lesions, adults cause anaemia
Strongyles of equines
Strongylus equinus
Features: 3 teeth in buccal capsule, deepest buccal capsule, tropical species
Life cycle: L3 exsheaths in caecum, L3 migrates into gut wall. Peritoneal cavity & liver. Spends 6-7 weeks in liver. Migrates via pancreas to gut. PPP= 8 months
Effects on host: anaemia.
Genus- Triodontophorus- 3 teeth, carried
Features: name means “bearing 3 teeth”
Life cycle: L3 exsheaths in caecum. L3 migrates into gland. moults to L4. L4 emerges into lumen. Final moult in lumen. PPP= 9 weeks.
Effects on host: graze on epithelial lining of gut, occur in groups, cause ulceration & blood loss.
Genus- Triodontophorus- 3 teeth, carried
Features: name means “bearing 3 teeth”
Life cycle: L3 exsheaths in caecum. L3 migrates into gland. moults to L4. L4 emerges into lumen. Final moult in lumen. PPP= 9 weeks.
Effects on host: graze on epithelial lining of gut, occur in groups, cause ulceration & blood loss.
Strongyles of equines
Subfamily- Cyathostominae (cyathostomes, small strongyles)
* 13 genera, 51 species worldwide, all have cylindrical buccal capsule, occur in large numbers (15,000)
Genus- Cyathostomum
Life cycle: L3 exsheath in caecum. Enters caecal glands. Moults to L4. L4 re-emerges to lumen. Final moult in lumen. PPP= 5 weeks (minimum)
HYPOBIOSIS important: seasonal pattern, following removal of adults, emergence may be synchronous
* Effect on host: adults feed on gut content, not pathogenic, very large number cause diarrhoea (1x10^6). Normally 115,000 larvae encysted. Visible from external surface. Massive emergence causes severe diarrhoea.
* Diagnosis- finds eggs in faeces, use McMaster chamber, >300 epg pathogenic, larval culture to identify genera
Strongyles of equines
Subfamily- Cyathostominae (cyathostomes, small strongyles)
* 13 genera, 51 species worldwide, all have cylindrical buccal capsule, occur in large numbers (15,000)
Genus- Cyathostomum
Life cycle: L3 exsheath in caecum. Enters caecal glands. Moults to L4. L4 re-emerges to lumen. Final moult in lumen. PPP= 5 weeks (minimum)
HYPOBIOSIS important: seasonal pattern, following removal of adults, emergence may be synchronous
* Effect on host: adults feed on gut content, not pathogenic, very large number cause diarrhoea (1x10^6). Normally 115,000 larvae encysted. Visible from external surface. Massive emergence causes severe diarrhoea.
* Diagnosis- finds eggs in faeces, use McMaster chamber, >300 epg pathogenic, larval culture to identify genera
Strongyles of equines
Subfamily- Cyathostominae (cyathostomes, small strongyles)
* 13 genera, 51 species worldwide, all have cylindrical buccal capsule, occur in large numbers (15,000)
Genus- Cyathostomum
Life cycle: L3 exsheath in caecum. Enters caecal glands. Moults to L4. L4 re-emerges to lumen. Final moult in lumen. PPP= 5 weeks (minimum)
HYPOBIOSIS important: seasonal pattern, following removal of adults, emergence may be synchronous
* Effect on host: adults feed on gut content, not pathogenic, very large number cause diarrhoea (1x10^6). Normally 115,000 larvae encysted. Visible from external surface. Massive emergence causes severe diarrhoea.
* Diagnosis- finds eggs in faeces, use McMaster chamber, >300 epg pathogenic, larval culture to identify genera
Strongyles of equines
Subfamily- Cyathostominae (cyathostomes, small strongyles)
* 13 genera, 51 species worldwide, all have cylindrical buccal capsule, occur in large numbers (15,000)
Genus- Cyathostomum
Life cycle: L3 exsheath in caecum. Enters caecal glands. Moults to L4. L4 re-emerges to lumen. Final moult in lumen. PPP= 5 weeks (minimum)
HYPOBIOSIS important: seasonal pattern, following removal of adults, emergence may be synchronous
* Effect on host: adults feed on gut content, not pathogenic, very large number cause diarrhoea (1x10^6). Normally 115,000 larvae encysted. Visible from external surface. Massive emergence causes severe diarrhoea.
* Diagnosis- finds eggs in faeces, use McMaster chamber, >300 epg pathogenic, larval culture to identify genera
Strongyles of equines
Subfamily- Cyathostominae (cyathostomes, small strongyles)
* 13 genera, 51 species worldwide, all have cylindrical buccal capsule, occur in large numbers (15,000)
Genus- Cyathostomum
Life cycle: L3 exsheath in caecum. Enters caecal glands. Moults to L4. L4 re-emerges to lumen. Final moult in lumen. PPP= 5 weeks (minimum)
HYPOBIOSIS important: seasonal pattern, following removal of adults, emergence may be synchronous
* Effect on host: adults feed on gut content, not pathogenic, very large number cause diarrhoea (1x10^6). Normally 115,000 larvae encysted. Visible from external surface. Massive emergence causes severe diarrhoea.
* Diagnosis- finds eggs in faeces, use McMaster chamber, >300 epg pathogenic, larval culture to identify genera
Strongyles of ruminants
Family- Chabertiidae
Subfamilies- Chabertiinae- globular buccal capsule, tissue feeders
Genera- Chabertia
Chabertia ovina
Hosts: sheep, goats, cattle
Location: colon (first coil)
Features: bell-shaped buccal capsule with no teeth, size 1.5-2.0 cm, tiny leaf crown
Life cycle: L3 exsheaths in small intestine. Enters mucosal glands. Moults to L4. L4 returns to lumen. Migrates to large intestine. Final moult in large intestine. PPP= 8 weeks.
Effect on host: feed on mucosa, cause haemorrhage, excess mucus production, diarrhoea, cosmopolitan parasite but more prevalent in temperate areas, strong immunity develops, usually only few worms present, 200 pathogenic, females lay 3000 eggs/day, eggs of “strongyle type”
Strongyles of ruminants
Family- Chabertiidae
Subfamilies- Chabertiinae- globular buccal capsule, tissue feeders
Genera- Chabertia
Chabertia ovina
Hosts: sheep, goats, cattle
Location: colon (first coil)
Features: bell-shaped buccal capsule with no teeth, size 1.5-2.0 cm, tiny leaf crown
Life cycle: L3 exsheaths in small intestine. Enters mucosal glands. Moults to L4. L4 returns to lumen. Migrates to large intestine. Final moult in large intestine. PPP= 8 weeks.
Effect on host: feed on mucosa, cause haemorrhage, excess mucus production, diarrhoea, cosmopolitan parasite but more prevalent in temperate areas, strong immunity develops, usually only few worms present, 200 pathogenic, females lay 3000 eggs/day, eggs of “strongyle type”
Strongyles of ruminants
Family- Chabertiidae
Subfamilies- Oesophagostominae- cylindrical buccal capsule, gut content feeders
Genera- Oesophagostomum (nodule worms)
Life cycle: L3 migrates into glands in small and/or large intestine. L4 emerges and migrates to large intestine. PPP= 5-6 weeks.
Oesophagostomum radiatum (the nodule worm of cattle)
Location: caecum/ colon
Features: cylindrical buccal capsule, small leaf crown, no external leaf crown, cervical collar in 2 parts
Life cycle: typical of genus
Effect on host: susceptible (young) host, no reaction. Resistant animals, intense reaction. Nodule filled with eosinophils, larva killed, caseous lesion calcifies. Nodules causes Hb & plasma proteins to leak into gut. Interfere with gut motility. Anorexia, reduced weight gains. Adults cause diarrhoea. Strong immunity by 12 months of age.
Oesophagostomum radiatum (the nodule worm of cattle)
Location: caecum/ colon
Features: cylindrical buccal capsule, small leaf crown, no external leaf crown, cervical collar in 2 parts
Life cycle: typical of genus
Effect on host: susceptible (young) host, no reaction. Resistant animals, intense reaction. Nodule filled with eosinophils, larva killed, caseous lesion calcifies. Nodules causes Hb & plasma proteins to leak into gut. Interfere with gut motility. Anorexia, reduced weight gains. Adults cause diarrhoea. Strong immunity by 12 months of age.
Strongyles of ruminants
Oesophagostomum columbianum (the nodule worm of sheep)
Location: colon
AND
Oesophagostomum venulosum
Location: caecum
* non-pathogenic, some scouring; very common in sheep. Prolific egg layers (3000/female/day). Typical strongylid eggs.
Strongyles of the pig
Oesophagostomum dentatum
Nodule worm of the pig
Other species: Oe. quadrispinulatum- significant pathogen in pigs
AND ONE MORE ON ANOTHER CARD
Stephanurus dentatus (the kidney worm of the pig)
Location: peri-renal fat in cysts attached to ureter
Distribution: limited to warm, moist areas in AUS, tropical & subtropical areas worldwide.
Life cycle: eggs passed in urine. L3 ingested or can penetrate skin. Migrate to liver via portal system (3 days) or aorta (8-40 days). Migrate in liver for 2-3 months. Migrate to perirenal area or anywhere in the body. PPP= 9 months.
Effect on host: fibrosis in liver, abscesses in carcass, organs condemned at slaughter, weight loss.
Diagnosis: eggs in urine. Elevated liver enzymes.
Stephanurus dentatus (the kidney worm of the pig)
Location: peri-renal fat in cysts attached to ureter
Distribution: limited to warm, moist areas in AUS, tropical & subtropical areas worldwide.
Life cycle: eggs passed in urine. L3 ingested or can penetrate skin. Migrate to liver via portal system (3 days) or aorta (8-40 days). Migrate in liver for 2-3 months. Migrate to perirenal area or anywhere in the body. PPP= 9 months.
Effect on host: fibrosis in liver, abscesses in carcass, organs condemned at slaughter, weight loss.
Diagnosis: eggs in urine. Elevated liver enzymes.
Syngamus trachea (the gape worm)
Hosts: poultry, many other species
Location: trachea
Features: cup-shaped buccal capsule, up to 10 teeth, pair appear Y shaped grossly.
Life cycle: eggs coughed up, swallowed. L1-L3 within egg**. Molluscs, oligochaetes paratenic hosts. L3 ingested. Migrate to trachea via liver then lungs. PPP= 2 weeks.
Effect on host: cause excess mucus production, block airways, respiratory distress- birds stand “gaping.” Blood feeders.
Diagnosis- eggs in feaces (ellipsoidal thin-shelled eggs with a thick operculum at both sides.
Syngamus trachea (the gape worm)
Hosts: poultry, many other species
Location: trachea
Features: cup-shaped buccal capsule, up to 10 teeth, pair appear Y shaped grossly.
Life cycle: eggs coughed up, swallowed. L1-L3 within egg**. Molluscs, oligochaetes paratenic hosts. L3 ingested. Migrate to trachea via liver then lungs. PPP= 2 weeks.
Effect on host: cause excess mucus production, block airways, respiratory distress- birds stand “gaping.” Blood feeders.
Diagnosis- eggs in feaces (ellipsoidal thin-shelled eggs with a thick operculum at both sides.
Trichostrongyles of ruminants
* Infections always mixed
* All animals are infected all the time
* Control rather than eradicate- eradication is impossible & would leave susceptible sheep and cattle
What is the economic impact of trichostrongyles in small ruminants?
Control of trichostrongyles
Epidemiology of trichostrongyloidosis
- Moisture- needed for development of L3 in faeces and needed for larvae to migrate onto pasture. Effective rainfall- P/E > 0.3 (growing season correlates with larvae on pasture). Lateral movement limited (<0.5 m) & assisted by heavy rain and floods. Vertical movement- films of moisture. Can ascend up to 7 cm. Negatively geotropic, respond to light intesity, become anydrobiotic on grass, survival limited by lipid reserves.
- Temperature- mild AUS temps have little effect except Haemonchu > 10C. Low temp can slow egg hatching and development in some species. High temp shorten survival times on L3s on pasture. Interaction with humidity. Significant in tropical climates.
- Grazing factors- do not graze uniformly, avoid certain plants, avoid contaminated areas, distro of pellets & larvae in paddock not uniform. Type of veg affects larval survival: height, species. Stocking rate- initially higher stocking rates, lead to heavier contamination, very heavy stocking rates may reduce infections.
- Host factors- age, genetic susceptibility- skewed worm burdens and faecal egg counts, can select for resistant sheep, breed differences- merinos more susceptible than cross- breeds. “periparturient rise” or “spring rise” in faecal egg count. Relaxation of immunity. Increased prolactin 5 weeks before parturition and then decline until weaning. INcreased susceptibility to L3s. Re-emergence of inhibited larvae. Increased fecundity. Important interaction with time of lambing in AUS.
- Management factors- time of lambing, grazing management, nutritional status of animals, strategic use of anthelmintics,
Hypobiosis in trichostrongyles
* Temporary cessation in the development of a nematode at precise point in its parasitic development (L4)
* Factors supporting hypobiosis- unfavorable climtic conditons & immune status of animals
* Factors supporting the resumption of the development of inhibited larvae- hormonal changes & alternations in the components of immune system during the PRR & density dependence of parasite
Diagnosis of trichostrongyloidosis antemortem and postmortem
Dag score as well (0-5)
FECs: useful for diagnosis in sheep and cattle under the age of about 9 months, variability and degree of infection and (light, moderate, and heavy), give rough guide only > 500 epg pathogenic. Host immunity may suppress egg production. Concentration of eggs in faeces affected by digesta, diarrhoea, fasting, feed quality, size of host. Egg counts higher in young sheep, in Merinos. Can be carried out in the field. Difficult to ID eggs to genus need to carry out larval culture.
Fecundity of worms:
Haemonchus 5000-20,000 eggs/female/day
Trichostrongylus 10-200 eggs/female/day
Nematodirus 50 eggs/female/day
* Indicates presence of female worms only, neglects males and inhibited larvae
Faecal cultures
Diagnosis of Trichostrongyloidosis
Pasture larval counts
* Direct quantification from pasture: estimate number of larvae/kg of herbage, slow, does not detect low levels of contamination, non random distro of larvae in paddock makes sampling difficult, can be useful in comparing paddocks
* Introduction of worm-free “tracer” animals- mimic the grazing patterns of the resident flock, costly, time consuming, not all ingested larvae develop into adults
Total worm counts- direct assessment, can ID genera and species, can only do 1 or 2 counts, usually animals from tail of mob, pathogenicity affected by host age and nutritional status
Pathogenicity in sheep
Control of trichostrongyloidosis
* Paddock spelling- effective over summer, not effective after autumn break, harrowing in summer
* Crops- sowing to crops reduces contamination, use of stubbles
* Alternate grazing- alternating sheep and cattle reduces contamination (except T. axei), goats and sheep have some parasites, horses and kangaroos may be of use
* Anthelmintic drugs- timing of treatments: more effective in summer in southern AUS, winter treatments have limited effects
Two genera with pigs as the host in the stomach?
T. axei and Hyostrongylus rubidus (direct. L3 in gastric glands. PPP=21 days. Causes diarrhoea, weight loss, controlled on concrete floors)
Ollulanus tricuspis (stomach)- CAT
* minute nematode (1 mm)
* female has a tail with 3-4 short cusps
* viviparous (L3 develops within uterus)
* not very pathogenic
* Transmitted in vomit
Amidostomum anseris- “gizzard worm”- birds
* Ducks, geese, swans
* junction of gizzard and proventriculus
* Larvae penetrate gizzard lining
* highly pathogenic
AND
Trichostrongylus tenuis
* found in caecum
* wide host range
* nodules and mortalities in galliform birds
* controls wild grouse populations
3 common nematodes vs. age of the horse
Superfamily Ancylostomatoidea- hookworms
* Features: head bent dorsally, large buccal capsule, teeth or cutting plates, bursa in male, infect the host either orally or by skin penetration
* Location: small intestine
* Food: blood
* Hosts: dogs, cats, ruminants, pigs, humans
Life Cycle of Superfamily Ancylostomatoidea
Ancylostoma caninum- hookworm of dogs
Life cycle: females lay 15,000 eggs/day, skin penetration important, transmammary infection important
Effects on the host: use blood for food & respiration, females use 0.1 ml/day, black tarry faeces, microcytic, hypochromic anaemia, heavy infections (pups) cause death, strong immunity following exposure, can cause eosinophilic enteritis in man
Epi: common in warm climates, less common in southern AUS, sandy or loam areas ideal for larvae
Diagnosis: eggs in faeces, egg counts high (> 5000 epg), eggs small (<65 micrometers)
Ancylostoma caninum- hookworm of dogs
Life cycle: females lay 15,000 eggs/day, skin penetration important, transmammary infection important
Effects on the host: use blood for food & respiration, females use 0.1 ml/day, black tarry faeces, microcytic, hypochromic anaemia, heavy infections (pups) cause death, strong immunity following exposure, can cause eosinophilic enteritis in man
Epi: common in warm climates, less common in southern AUS, sandy or loam areas ideal for larvae
Diagnosis: eggs in faeces, egg counts high (> 5000 epg), eggs small (<65 micrometers)
Ancylostoma braziliense- hookworms of dogs
* common in tropical and sub-tropical regions
* less pathogenic- can cause hypoproteinaemia and diarrhoea
* primary cause of “cutaneous larva migrans” or “creeping eruption” in man
* tortuous erythematous inflammatory tracts within dermis associated with severe pruritis
Ancylostoma braziliense- hookworms of dogs
* common in tropical and sub-tropical regions
* less pathogenic- can cause hypoproteinaemia and diarrhoea
* primary cause of “cutaneous larva migrans” or “creeping eruption” in man
* tortuous erythematous inflammatory tracts within dermis associated with severe pruritis
Uncinaria stenocephala- hookworms of dogs
* common in cooler area
* L3 are ingested
* no extra-intestinal migration
* less pathogenic
* eggs > 65 micrometers
Uncinaria lucasi- hookworms of seals/ sea-lions
* serious pathogen in northern hemisphere seals
* transmammary transmission most important route of infection
* larvae penetrate skin
AND
Uncinaria hamiltoni- causes anaemia in AUS sea-lions
Ancylostoma tubaeforme- hookworm of cats
Ancylostoma braziliense- hookworm of cats
Uncinaria stenocephala- hookworms of cats
Hookworms of ruminants
Bunostomum phlebotomum- cattle- small intestine
Bunostomum trigonocephalum- sheep- small intestine
Features: found mainly in warm areas, skin penetration, transcolostral infection
PPP= 7 weeks
* cause anaemia, hypoproteinaemia, 1000 fatal burden
Infection with 25 nematodes is fatal in sheep, goats, and wild ruminants in Africa, South America, and Indonesia
Gaigeria pachyscelis
Hookworms of pigs
Globocephalus spp.
Distribution: occur in tropical areas of the world- not in AUS
Pathogenic effects: anaemia, weight loss, emaciation
Ancylostoma duodenale- hookworms of humans
Necator americanus- hookworms of humans
Superfamily Metastrongyloidea- lungworms
Features- small buccal capsule, reduced bursa, mainly found in respiratory system*** (or connected to it- vascular and nervous system)
Dictyocaulus filaria
* Features- long thin worm (10 cm), small buccal capsule, “spongy” spicules
* Life cycle: L1 in faeces. Characteristic cap on larva’s head. L1-L3 in faeces. L3 migrates onto herbage, ingested. Exsheaths in abomasum. Migrate to lungs via lymphatics. PPP= 21 days.
* Effects on host: block ariways, excess mucus production. Damage epithelium. Loss of mucociliary escalator. Interstitial pneumonia. Alveoli fill with fluid. Detachment of alveolar macrophages. Consolidation of lung lobules.
* Clinical signs: chronic cough, laboured breathing, secondary bacterial infection, eosinophilia, death
* Diagnosis- find larvae in faeces.
Dictyocaulus filaria
* Features- long thin worm (10 cm), small buccal capsule, “spongy” spicules
* Life cycle: L1 in faeces. Characteristic cap on larva’s head. L1-L3 in faeces. L3 migrates onto herbage, ingested. Exsheaths in abomasum. Migrate to lungs via lymphatics. PPP= 21 days.
* Effects on host: block ariways, excess mucus production. Damage epithelium. Loss of mucociliary escalator. Interstitial pneumonia. Alveoli fill with fluid. Detachment of alveolar macrophages. Consolidation of lung lobules.
* Clinical signs: chronic cough, laboured breathing, secondary bacterial infection, eosinophilia, death
* Diagnosis- find larvae in faeces.
Dictyocaulus filaria
* Features- long thin worm (10 cm), small buccal capsule, “spongy” spicules
* Life cycle: L1 in faeces. Characteristic cap on larva’s head. L1-L3 in faeces. L3 migrates onto herbage, ingested. Exsheaths in abomasum. Migrate to lungs via lymphatics. PPP= 21 days.
* Effects on host: block ariways, excess mucus production. Damage epithelium. Loss of mucociliary escalator. Interstitial pneumonia. Alveoli fill with fluid. Detachment of alveolar macrophages. Consolidation of lung lobules.
* Clinical signs: chronic cough, laboured breathing, secondary bacterial infection, eosinophilia, death
* Diagnosis- find larvae in faeces.
Dictyocaulus filaria
* Features- long thin worm (10 cm), small buccal capsule, “spongy” spicules
* Life cycle: L1 in faeces. Characteristic cap on larva’s head. L1-L3 in faeces. L3 migrates onto herbage, ingested. Exsheaths in abomasum. Migrate to lungs via lymphatics. PPP= 21 days.
* Effects on host: block ariways, excess mucus production. Damage epithelium. Loss of mucociliary escalator. Interstitial pneumonia. Alveoli fill with fluid. Detachment of alveolar macrophages. Consolidation of lung lobules.
* Clinical signs: chronic cough, laboured breathing, secondary bacterial infection, eosinophilia, death
* Diagnosis- find larvae in faeces.
Dictyocaulus filaria
* Features- long thin worm (10 cm), small buccal capsule, “spongy” spicules
* Life cycle: L1 in faeces. Characteristic cap on larva’s head. L1-L3 in faeces. L3 migrates onto herbage, ingested. Exsheaths in abomasum. Migrate to lungs via lymphatics. PPP= 21 days.
* Effects on host: block ariways, excess mucus production. Damage epithelium. Loss of mucociliary escalator. Interstitial pneumonia. Alveoli fill with fluid. Detachment of alveolar macrophages. Consolidation of lung lobules.
* Clinical signs: chronic cough, laboured breathing, secondary bacterial infection, eosinophilia, death
* Diagnosis- find larvae in faeces.
Lungworms of sheep
Protostrongylus rufescens
* Features: to 65 mm long, slender, red worm, in small bronchi and bronchioles
* Life cycle: L1 in faeces. Penetrates foot of snail (Cernuella). L1-L3 in snail. Sheep ingests snail. Migrates via lymphatics to lung.
* Effects on host: mild pneumonia, most infections subclinical
* P. stilesi- major pathogen in Rocky Mountain sheep- transcolostral transmission
Lungworms of sheep
Protostrongylus rufescens
* Features: to 65 mm long, slender, red worm, in small bronchi and bronchioles
* Life cycle: L1 in faeces. Penetrates foot of snail (Cernuella). L1-L3 in snail. Sheep ingests snail. Migrates via lymphatics to lung.
* Effects on host: mild pneumonia, most infections subclinical
* P. stilesi- major pathogen in Rocky Mountain sheep- transcolostral transmission
Lungworms of sheep
Protostrongylus rufescens
* Features: to 65 mm long, slender, red worm, in small bronchi and bronchioles
* Life cycle: L1 in faeces. Penetrates foot of snail (Cernuella). L1-L3 in snail. Sheep ingests snail. Migrates via lymphatics to lung.
* Effects on host: mild pneumonia, most infections subclinical
* P. stilesi- major pathogen in Rocky Mountain sheep- transcolostral transmission
Muellerius capillaris
* Feature- tiny coiled worms in alveoli
*Life cycle- L1 with kinked tail, snail and slug intermediate hosts
* Effects on the host: high prevalence, virtually non-pathogenic in sheep, can be highly pathogenic in goats
Muellerius capillaris
* Feature- tiny coiled worms in alveoli
*Life cycle- L1 with kinked tail, snail and slug intermediate hosts
* Effects on the host: high prevalence, virtually non-pathogenic in sheep, can be highly pathogenic in goats
Muellerius capillaris
* Feature- tiny coiled worms in alveoli
*Life cycle- L1 with kinked tail, snail and slug intermediate hosts
* Effects on the host: high prevalence, virtually non-pathogenic in sheep, can be highly pathogenic in goats
Dictyocaulus viviparus (“husk”)
Lungworm of cattle
* Major pathogen of cattle
* cough laboured breathing
* Hypersensitivity reaction
* Disease mainly in calves
* Develop strong immunity
* X-irradiated larvae provoke immunity
Lungworm of equines
Dictyocaulus arnfieldi
* In trachea of horses, donkeys, and otehr perissodactyls
* only mildly pathogenic
* direct life cycle
Diagnosis- Baermann technique, larva with point on tail
Parelaphostrongylus tenuis
Life cycle of Parelaphostrongylus tenuis
Parasites of red deer
Elaphostrongylus cervi
* Occur in connective tissues and meninges
* L1 enters blood and reaches lungs
* snail intermediate host
* no clinical signs in normal host
* neurological signs in other ruminants
Aelurostrongylus abstrusus
Features: tiny nematode in alveoli, very common parasite
* Life cycle: lays eggs, eggs hatch, L1 in faeces, L1-L3 in slug or snail, cat eats molluscs or, rodents, birds, reptiles- paratenic hosts, larvae enter bloodstream to reach lungs
PPP= 6 weeks
* Effects on host: generally subclinical, mild cough, weight loss, eosinophilia
* Diagnosis- Baermann for larvae, differentate from Strongyloides cati by shape of tail
Aelurostrongylus abstrusus
Features: tiny nematode in alveoli, very common parasite
* Life cycle: lays eggs, eggs hatch, L1 in faeces, L1-L3 in slug or snail, cat eats molluscs or, rodents, birds, reptiles- paratenic hosts, larvae enter bloodstream to reach lungs
PPP= 6 weeks
* Effects on host: generally subclinical, mild cough, weight loss, eosinophilia
* Diagnosis- Baermann for larvae, differentate from Strongyloides cati by shape of tail
Lungworms of pigs
Metastrongylus apri, M. salmi, M. pudendotectus
* Location: large worms found in bronchi
* Life cycle: eggs coughed up, swallowed, passed in faeces. Intermediate hosts: earthworms; pig ingests earthworm. Larvae migrate to lungs via lymphatics
* Effects on the host: respiratory airway disease; obstruct airways. Transmit swine influenza virus (in egg).
Name 3- who do they impact and where?
Lungworms of dogs
Lungworms of dogs
