6.11 ‐ Strongylids II – Trichostrongyles and Strongyles – Flashcards
Trichostrongyles; General Features; development, threat, type of life cycle, survival strategies
- larvae develop in eggs to L3’s and hatch on pasture
- major parasitic threat to food production animals, especially on pasture
- direct life cycles (monoxenous)
- some use hypobiosis to remain in host when pasture environment is hostile to larvae
Trichostrongyles; life cycle
egg
-In environment > L1 > L2 > L3
-ingested by cattle
-abomasum/small intestine > L3 > L4 > adults
PPP = 2-3 weeks
Ostertagia spp.; general morphology, types
Medium‐sized or brown stomach worm
* Slender brown worm – up to 10 mm
* Ostertagia ostertagi – cattle
* Ostertagia circumcincta – sheep, goats
Ostertagia spp.; General Morphology ‐ Eggs
- thin‐shelled, morulated eggs (to 85 μm)
- Typical GIN egg
Ostertagia spp.; life cycle
- larvae develop in eggs and hatch on pasture
- L3’s are the infective forms – ingested
- L3’s enter gastric pits, develop and return to lumen
- mucosal migration
- hypobiosis is a major factor in the epidemiology and pathogenesis of disease – depends on environmental conditions on pasture (Larvae and eggs can survive on pasture over winter)
Ostertagia spp.; pathogenesis
- largely associated with developing L3’s in the gastric pits and their emergence
- developing larvae (arrow) cause direct damage to the gastric glands as well as induce inflammatory response and hyperplasia
- increased mucus, leakage through weakened tight junctions and loss of function of parietal cells ( decreased HCl)
Functionally,
* pH rises to near neutral
‐ no pepsinogen to pepsin conversion
‐ bacterial changes (dysbiosis) in abomasum
* leakage through altered mucosa (both directions)
‐ proteins, water, electrolytes to lumen
‐ pepsinogen to blood
* altered protein metabolism and inappetance give rise to emaciation
Ostertagia spp.; Lesions and Clinical Signs
- altered mucosa with single or coalesced nodules in the abomasum
- three distinct clinical presentations
‐ Type I
‐ Type II
‐ pre‐Type II
Type I ostertagiosis: where large burdens of O. ostertagi cause significant damage to gastric glands within the first grazing season. Type II ostertagiosis: where large encystsed/hypobiosed burdens of O. ostertagi emerge from gastric glands causing significant pathology.
Type 2 ostertagiasis occurs in cattle 2–4 years old and older adults, is the result of the emergence and development of hypobiotic larvae, and in addition to signs seen with type 1, hypoproteinemia with development of submandibular edema, fever, and anemia is a clinical sign.
Haemonchus spp.; morphology, important species and host
Large or Barberpole stomach worm
- slender–up to 30mm
- Haemonchus contortus – sheep*
Haemonchus spp.; general morphology, eggs
- thin‐shelled, morulated eggs (to 85 μm)
- typical GIN egg
Haemonchus spp.; life cycle
- larvae develop in eggs and hatch on pasture
- L3’s are the infective forms – ingested
- L3’s have only brief mucosal migration …but…
- hypobiosis is a major factor in the epidemiology and pathogenesis of disease – depends on environmental conditions on pasture
(FEW larvae or eggs survive on pasture over winter)
Haemonchus spp.; Pathogenesis, Lesions
- largely associated with developing L4’s and adults through blood‐feeding on the mucosa of the abomasum
- bood‐feeding causes anemia and hypoproteinemia as well as focal areas of haemorrhage in the abomasum
Haemonchus spp.; Clinical Signs
- in acute cases, profound anemia and hypoproteinemia
‐ pale carcass, watery blood
‐ edema
‐ often with little change in fat stores if many worms - in chronic cases, continuing blood loss gives:
‐ anemia and related edema (“bottle‐jaw)
‐ muscle weakness and fat depletion
‐ dark, hard feces
Nematodirus spp.; adult morphology etc.
- very slender – up to 25 mm
- multiple worms often found coiled together
Nematodirus spp.; General Morphology ‐ Eggs
- thin‐shelled, morulated eggs (up to 250 μm)
- other than size, typical GIN egg
Nematodirus spp.; life cycle
- larvae develop in eggs to L3’s and hatch on pasture (some after freezing stimulus)
- larvae develop deep between villi of small intestine and adults in lumen
- no hypobiosis
- larvae and eggs can survive on pasture over winter
Nematodirus spp.; Pathogenesis, Lesions, Clinical Signs
- adults can cause villus atrophy
- diarrhea, anorexia and resultant weight loss
Cooperia and Trichostrongylus species; what type of parasure, what hosts?
trichostrongyles
-infect a variety of ruminants
- with the exception of T. axei, these nematodes are largely host‐specific (e.g. cattle or horses or sheep/goats)
trichostrongyles of swine
- Hyostrongylus rubidus – red stomach worm
- similar to Ostertagia but less common now because of confinement rearing
Strongyles; general features; types, hosts, site of infection
- can be divided morphologically, taxonomically or functionally
- we will discuss migratory versus non‐migratory strongyles
(i.e. Strongylus spp. vs cyathostomes) - all parasites of equids with adults in the cecum and colon
Strongyles; General Morphology ‐ Eggs
- Typical GIN egg (that was in the notes but should be strongyle egg for horse, not GIN????)
- thin‐shelled, morulated eggs
Strongyles; General Morphology ‐ Adults
- shapes of the buccal cavity differs between types of strongyles in horses
‐ Strongylus spp. (deeper than wide buccal cavities)
‐ cyathostomes (wider than deep buccal cavities)
Strongyles; General Life Cycle
- Larvae develop in eggs and hatch on pasture
- L3’s are the infective forms – ingested
- EITHER: dramatic extra‐intestinal migrations (Strongylus spp. – migratory strongyles)
- OR: mucosal migration
(cyathostomes – non‐migratory strongyles) - adults feed in the cecum and colon
- some hypobiosis occurs in some species and some species can overwinter as larvae on pasture
Migratory Strongyles –Strongylus vulgaris; pathogenesis
- largely associated with developing L4 as they move extraintestinally in the cranial mesenteric artery
- may develop there for up to 2 months before returning to the intestine
- larvae induce an arteritis and thrombosis, particularly at the site of development in ileocolic artery and the arteries that branch from this site
- usually insufficient adults to cause intestinal lesions that are attributable to their feeding
Migratory Strongyles – Strongylus vulgaris; Clinical Signs
- large numbers can give acute disease resulting from arteritis – pyrexia, anorexia, colic and death
- chronic infections may give intermittent colic
- origin of the colic undetermined
‐ may involve impairment of the blood flow either through emboli or inflammatory restriction of blood flow
– may involve local nerve damage as well
Migratory Strongyles – Strongylus equinus and S. edentatus
-nature of mugration and pathogenicity
- both species undergo quite long and tortuous life cycles in their equid hosts
- not highly pathogenic during the larval migrations ‐ heavy burdens can produce hemorrhage and inflammation in the colon as larvae re‐enter the intestinal tract and as adults feed on blood and mucosa
Non‐Migratory Strongyles – “Cyathostomes”; importance, general comments
- collection of non‐migratory strongyles that may consist of 40+ species
(of which more than a dozen are frequently encountered – often together in a single host) - treated as a group clinically and therapeutically
- clinically, these parasites are probably the most important equine nematodes
Non‐Migratory Strongyles – “Cyathostomes”; General Life Cycle
- larvae develop in eggs and hatch on pasture
- L3’s are the infective forms – ingested
- mucosal migration known or suspected for all cyathostomes
- hypobiosis within the mucosa of the host occurs in at least in some species and some species can overwinter as larvae on pasture
- PPP varies from 5 weeks to >20 months
Non‐Migratory Strongyles – “Cyathostomes”; Pathogenesis/Lesions/Clinical Signs
- primarily associated with the larval mucosal migrations (mainly cecum and ventral colon)
- nodules form around many of the encysted larvae and may impede motility, cause inappetance > poor weight gain
- larvae leaving these nodules can cause inflammation, edema and ulceration
- clinically, anorexia, weight loss, diarrhea, colic
- # end of hypobiosis in spring may give rise to “acute larval cyathostomiosis”
- adults in large numbers may give a non‐specific clinical signs such as unthriftiness or digestive upsets with some colic (either intermittent or recurring)
- larval mucosal migration in spring more serious
- mid‐winter deworming can induce inflammation when hypobiotic larvae die in situ
Syngamus trachea – “Gapeworm”; hosts
- gallinaceous and other birds
Syngamus trachea – “Gapeworm”; adult morphology
- Males (2‐6mm) and female (5‐40mm)
- male and female are permanently attached in copula
- form a “Y‐shaped” structure attached to trachea
Syngamus trachea – “Gapeworm”; Egg morphology
- elongate, ellipsoidal and smooth
- operculum at each end of egg
- morulated eggs, 85‐90 by 50μm
Syngamus trachea – “Gapeworm”; life cycle
- larvae develop from morulated eggs, some hatch
- larvae in eggs, in soil or in paratenic hosts are infective when eaten
- larvae penetrate gut and move to lungs
- break into alveoli, migrate to trachea
- attach to mucosa, suck blood and mate into pairs
PPP - 10 days
Syngamus trachea – “Gapeworm”; Pathogenesis/Lesions/Clinical Signs
- worms in trachea cause birds to gape and gasp
- increased mucus production
- mild anemia and reduced production most important
- some mortality in heavy infections asphyxiation
Syngamus trachea – “Gapeworm”; gross signs on PM
- paired, blood‐filled worms attached to trachea
- raised, ulcerated lesions at sites of attachment
