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generally define gastric spirurid nematdes
Habronema muscae
Habronema microstoma
Draschia megastoma
generally describe gastric spirurid nematodes
all require a fly host such as house or stable flies
adult worms are small
L3 may penetrate wounds and tissues, producing lesions
because they utilize flies as intermediate hosts, infections tend to be seasonal “summer sores”
infections are rare in well managed facilities
what are the major forms of gastric spirurid infection
gastric
conjunctival
cutaneous “habronemiasis”
describe infection caused by Habronema spp
inhabits the mucus layer of the gastric mucosa
may cause catarrhal gastritis
adult infections are not considered important
describe infection caused by Draschia megastoma
fundic region
provokes formation of large, tumor like masses near the margo plicatus
masses contain worms
how is gastric habronemiasis diagnosed
small larvated eggs may be difficult to find by standard fecal flotation methods
eggs may be identified in gastric lavage fluids
characteristic lesions in the stomach with Draschia
how is cutaneous habronemiasis diagnosed
regional, farm, animal history
charcacteristic lesions in aberrant sites once tumor, fungal/bacterial granuloma, others
cytology for eosinophilia
biopsy
PCR
generally describe Trichostrongylus axei
adults inhabit glandular portion of the equine stomach
adult worms are small, measuring just 8mm
eggs are strongyle type and are not usually differentiated from equine strongyles (smaller, one end slightly pointed) though larvae may be cultured for identification
lacks host specificity among livestock, infection is only common where horses are pastured with ruminants
what are the important small intestinal nematodes
Strongyloides westeri
Parascaris equoruum
Parascaris univalens
generally describe infection and transmission of S. westeri
nursing foals and weanlings
parasitic and free living cycles
transmammary is most important (may be infected at 5 days of age)
skin penetration
ingestion
describe the pathogenesis of S. wsteri infection
larvae migrate via venous system through lungs to develop in small intestines, PPP= 6-10 days
immunity to adults develops within 6 months
eggs are nearly only seen in nursing and weanling foals
what are the clinical diseases associated with S. westeri
Catarrhal enteritis- “foal heat” diarrhea at 9-13 days post partum, corresponding to post-partum estrus
respiratory distress
dermatitis- frenzy syndrome- massive percutaneous penetration
no clinical signs in adult horses
how is S. westeri diagnosed
clinical signs
finding eggs in feces
generally describe equine roundworm
Parascaris equorum and P. univalens- common infection in foals
large, robust, small intestinal ascarids
major pathogen of foals and weanlings, horses >12-24m are largely resistent
adult worm burdens peak at 4-5 months of age
what are important life cycle features of equine roundworms
eggs become infective L3 within 14 days
eggs may live >10 years on pasture and are highly resistant
female worms may produce >200,000eggs/day
no vertical transmission from mare to foal
adult worms feed on intestinal contents and compete with host
PPP= 80-110 days
foals self cure at 6m
what are the clinical signs of equine tapeworms
foals may develop coughing, nasal discharge and airway mucus
other common signs include unthiftiness, rough hair coat, pot belly and stunted growth
heavy infections may cause colic, and even intestinal blockage and ruptre
infection is accompanied by a marked eosinophilia
what is the pathology of equine roundworm
liver
-small focal hemorrhagic tracts with eosinophils
-as lesions resolve, fibrotic foci remain
lungs
-petechial hemorrhage, eosinophil infiltration
-subpleural lymphocytic nodules up to 1cm in size
Small intestine
-potential intestinal impaction/rupture in foals following treatment with a paralytic
how is equine roundworm diagnosed
fecal floatation
finding worms in manure
surgery or necropsy
what are the large intestinal nematodes in horses
small strongyles
S. vulgaris
S. equinus
S. edentatus
Oxyuris equi
generally define small strongyles (Cyathostomes, Cyathostomins)
currently most important parasite pathogen of equids when present in large numbers
treated as a group and little is known about indivdual species
small to medium sized, males are bursate
all live in cecum and ventral colon
describe the life cycle of Cyathostome
L3 develop directly or enter hypobiosis, surviving up to 2.5 years before resuming development
PPP= 5-12 weeks depending on species
describe the epidemiology of Cyathostome
seasonal transmission
peak in gulf coast is late september to april
hypobiosis is seasonal and greatest during late winter and spring
hypobiotic L3 makes up majority of population in host
describe the pathology caused by Cyathostome
mildly thickened and edematous large intestinal mucosa with eosinophilic infiltration
describe the clinical disease caused by Cyathostomiasis
poor growth and development
colic that is non fatal with sudden onset in young horses <4 years
profuse diarrhea with no other obvious cause
seasonal
infection with large numbers of L3 may cause similar signs
low grade, increased frewuency of colic has been associated with increased burdens
how is cyathostomiasis diagnosed
clinical signs
strongyle-type eggs in quantitative fecal
L3 cultures to differentiate from large strongyles
larvae are swept into species
<200EPG= low contaminator
200-500= moderate
>500= high
what are the important large strongyles
infect equine large intestine
S. vulgaris (most pathogenic equine helminth, but not the most common!)
S. edentatus
S. equinus
how are large strongyles generally defined
adults are medium to large, with a large buccal capsule bearing a corona radiata ± teeth
blood feeders
long PPP >6m
-S. vulgaris= 6-99
-S. edentatus= 9-12
-S.equinus= 8-9
describe the life cycle of large strongyles
direct, just like small
consumed from the grass
describe the pathology caused by Strongylus vulgaris
L4 cannot escape through the internal lamina so they migrate ithin the walls of major arteries, causing aortic aneurysms, thrombosis of cranial mesenteric and other arteries
infarction of the gut vasculature → necrosis and colonic death
horses rapidly develop compensatory collateral circulation
describe the pathology and disease of Strongylus edentatus
larvae are not as pathogenic despite being 2x bigger than vulgaris
L3 enter cecal/colic all → migrate via the portal veins to the liver → nodule formation → molt to L4 → hepatic migration → peritoneal migration → cecum → adhesions, colic
describe the pathology of Strongylus equinus
L3 enter the cecal/colic wall → nodular formation → molt to L4 → transverse peritoneum to right half of liver (which contacts cecum) → hepatic migration → enter pancreas/abdominal cavity → molt to L5 → penetrate large intestinal wall → lumen
how are large strongyles diagnosed
strongyle type eggs in fecal floatation exam- need to culture
no pathognomotic clinical pathologic changes of S. vulgaris but may include
-neutrophilia that progresses to eosinophilia
-normocytic anemia
-increased serum total protein
-decreased serum albumin
-increased serum beta globulin
generally define Oxyuris equi (equine pinworm)
pinworm species found in the equine small colon
medium to large worms with pointed tails
no tissue migration, but migration of adult to cement eggs in the perianal region causes pruritus
cementing fluid containing embryonated eggs, dries and flakes off, contaminating the environment
describe the life cycle of Oxyuris equi
PPP= 5 months
eggs develop to L3 stage in 4-5 days
eggs are operculated, with one side flattened and the other convex, ofte larvated
how is Oxyuris equi diagnosed
rat tail appearance of tailhead
eggs will be seen on fecal floatation if present are rare
collect from perianal region with clear tape, scrape with tongue depressor/lube
generally define Setaria equina
Filarioid nematode that infects horses, mules, donkeys in US
mosquitoes are vector, PPP= 8-10m
adult worms are found INCIDENTALLY in abdominal cavity
what are the major equine tapeworms and their locations
Anoplocephala perforliata
-common, large and small intestines
A. magna
-small intestine ± stomach
Paranoplocephala mamillana
-small intestine
one tapeworm generation per year
describe the life cycle of equine tapeworms
tranmitted to horses by mites that are ingested accidentally
develop in horse 1.5-2months
develop in mite 2-4 months
define Anoplocephala perfoliata by location, size, eggs, scolex
ileum, ileocecal junction, cecum, upper colon
smaller, up t8 8cm
larger
lappets at base of scolex
define Anoplocephala magna by location, size, eggs, scolex
jejunum ± stomach
up to 80cm
smaller
without lappets
describe the pathology of equine tapeworms
lesions are associated with the accumulation of parasites at the ileocecal junction
pathology is uncommon but may include inflammation, ulceration, small intestinal rupture, ileal obstruction, intussusception
unthriftiness, anemia, colic
how do you do antemortem diagnosis of equine tapeworms
eggs only found in about 50% of infected horses on fecal
serum ELISA used in UK
what are the species of equine stomach bots
Gasterophilus intestinalis
Gasterophilus nasalis
Gasterophilus hemorrhoidalis
1st-3rd larval stages are obligate parasites
describe the life cycle of Gasterophilus spp
eggs are deposited one at a time on the hairs of the face, chest and forelegs
eggs hatch within 1 weeks and enter the oral tissues to embed for 1 month
molt to 2nd instars, then pass to stomach
molt to 3rd instars and attach to cardiac/pyloric portions or first part of SI
develop for 8-10 months, pass in feces and pupate for 3-5 weeks
seasonal cycle, gastric populations peak in fall, exit host in spring
life cycle takes 1 year
describe G. intestinalis by egg location, larva location, spines, and incidence
legs and chest
non-glandular stomach
2 rows-blunt
common
describe G. nasalis by egg location, larva location, spines, and incidence
neck
pyloris to duodenum
1 row
less common
describe G. hemorrhoidalis by egg location, larva location, spines, and incidence
nose-face
rectum
2 rows sharp
rare
describe Gasterophilus clinical disease of the mouth
1st instars occupy fissues on surface of tongue
2nd instars reside in gingival pockets at base of molar teeth and may cause parasitic periodontitis, lingual lesions (tunnels with air holes), chewing problems
tunneling action excavates all tissues, including nerves and capillaries
what clinical disease does Gasterophilus cause in the stomach
pit like ulcers/erosions in the stomach, surrounded by hypertrophic mucosa cause mild gastritis, though large numbers may be present without clinical signs
generally describe Eimeria leuckarti in horses
protozoa
common in foals but clinical disease is rare
small intestinal epithelium, PPP= 16-37 days
oocysts are large, dark brown, and rarely seen, unless sheathers fecal floatation media is used