Equine stomach/SI/LI/cecum Flashcards
(27 cards)
Gasterophilus intestinalis
common bot, look like honey bees, do not feed, 1 cycle per year, oviposition sites dependent on species; pale yellow eggs on forelegs that horses have to lick to hatch. Leads to gingival myiasis. Gastric myiasis where bots attached to mucosa and leave pits at attachment. Bots usually don’t cause pathology in stomach. May cause hemorrhage if a lot. Causes annoyance.
Gasterophilus nasalis
Chin bot, yellow eggs laid under the chin. hatch spontaneously and burrow into mouth and invade gums between molars. Burrow into tissues of mouth and then larvae migrate to stomach, mature bots passed with feces. do not feed, 1 cycle per year, oviposition sites dependent on species. Leads to gingival myiasis. Gastric myiasis where bots attached to mucosa and leave pits at attachment. Bots usually don’t cause pathology in stomach. May cause hemorrhage if a lot. Causes annoyance.
Treatment of gasterophilus
Control flies which is difficult, wash areas of horse with warm water to hatch eggs, use macrocyclic lactone in fall (ivermectin)
Habronema
in stomach, H in pharynx. larvated eggs hatch in feces, larvae ingested by fly maggots, reach infective stage when flies pupate, when they emerge the larvae moves to proboscis, flies feed on secretions from hosts’ eyes and transmit the larvae. Free in stomach, may penetrate mucosa. Chronic gastritis and ulcers
Draschia
tumor like growths in stomach, head constricted from body. larvae penetrates submucosa, nodules form fibrous tumors in stomach. cavities have worms and necrotic material and interferes with stomach emptying
What are the two forms of Habronemiasis/draschiasis?
Gastric: larvae deposited near mouth, swallowed, mature and produce eggs. Cutaneous: larvae deposited on conjunctiva or in sores. can cause granular conjunctivitis.
clinical signs of summer habronemiasis?
cutaneous form, more common where horses can’t swish flies with tail, rapid granulation with serosanguinous drainage and hemorrhage, pruritic. wounds heal spontaneously when weather cools
diagnosis of habronemiasis?
gastric form hard to diagnose and usually post mortem. cutaneous form can see lesions and a biopsy shows many eosinophils
treatment and control of habronemiasis
control flies, gastric form of draschia hard to treat but use ivermectin. cutaneous form: macrolides should kill larvae, corticosteroids to reduce inflammation, DMSO, or surgery.
Strongyloides westeri
Threadworms, first patent infection seen in foals. Larvated eggs mature to filiform stage in environment. Skin penetration or L3 ingestion leads to tracheal migration. Imbed in SI mucosa. Mares can have larval stages in tissues that are activated by parturition to move into mammary tissue so transmammary transmission. large numbers cause mucosa erosion.
Clinical signs, diagnosis, treatment of threadworms
Most do not have clinical signs until 3-4 weeks of age. self-limiting, look for larvated eggs in feces of foals. use ivermectin-if 24 hour after foaling transmammary transmission reduced. Concerns about resistance to ivermectin in parascaris equorum leads to diminished drug use.
Parascaris
Large roundworm in the small intestine of foals. adults produce very large numbers of eggs that are passed into the feces and become infective in about 2 weeks. infective larvated eggs may survive in environment and after ingestion, undergo tracheal migration. PPP is 3 months and no transmammary transmission. infection mostly in foals. EGGS look like Balisascaris procyonis!
Parascaris pathogenesis
Minimal damage to liver, inflammaton of lung, interfere with nutrients so cause little weight gain. Large numbers may cause obstruction and intussusception and rupture of SI. Many may purge at 6 months but others remain infected.
Clinical signs and treatment of parascaris
respiratory signs, pyrexia, nasal discharge, dull hair coats. identify eggs in fecal float, kill worms slowly or impaction may occur. wash sticky eggs from udder of mare. using macrocyclic lactones or pyrantel causes obstruction. use benzimidazoles (fenben) instead. resistance to ivermectin and pyrantel. foals should receive four treatments of anthelmintics. 1st at 2-3 months of age with fenben, 2nd before weaning at 5-6 months, 3rd and 4th at 9 and 12 months to target strongyles and tapeworms.
Strongylus vulgaris
Used to be common cause of colic but now due to ivermectin it is rare. cecum and colon. ear shaped teeth at base of buccal capsule. Strongyle type eggs in feces, infective L3 are ingested, penetrate intestinal wall, L4 penetrate arterioles and migrate to the cranial mesenteric artery, move to cecum and colon and become adults. Eat mucosa and cause diarrhea. ONLY nematode with larval development in arterial system. PPP 6-7 months. 32 intestinal cells! causes most mortality.
Clinical signs and treatment for Strongylus vulgaris
thrombosis and thickening of arterial walls. colic, intolerance to exercise, jaundice, fever. Do fecal culture and Baermann. Macrocyclic lactones and regular deworming controls parasites well due to long PPP.
Other strongylus
Can cause liver damage, in cecum and colon as adults and cause diarrhea. can cause peritonitis and death. edentatus has 18-20. equinus has 16.
Cyathostomiasis
Trichonema, small strongyles, cyathostomins, cyathostomes. MOST important nematode of horses. Large intestine and cecum
life cycle of cyathostomins
some species are nonmigratory. have external and internal leaf crowns and teeth. Strongyle type eggs on pasture, L3 on grass is infective stage, don’t migrate extra-intestinally. can go to fourth stage or undergo hypobiosis and resume after dormancy. PPP is 6 weeks to 3 months.
Clinical signs, treatment of cyathostomins
adults usually cause no infection, larvae cause clinical disease that is inflammation of the mucosa of cecum and colon. excystment: L4 that emerge are huge, can cause hemorrhage, edema, congestion. Larval cyathostomiasis: disease caused by large emergence of larvae from intestinal mucosa and submucosa. similar to type 2 ostertagiasis. Leads to diarrhea with low egg counts, anemia, hypoproteinemia, poor weight gain. do fecal float and EPG, identify adults by necropsy. resistance becoming to macrocyclic lactones, moxidectin effective against mature encysted larvae. fenben good for inhibited larvae. deworm only when higher than 200 epg. do FECRT every few years.
Anoplocephala perfoliata
medium tapeworm in caudal SI, cecum, part of colon. pumpkin seed shaped with lappets.
Anoplocephala magna
large tapeworm, in SI and rarely in stomach and cecum. short segments, no lappets.
Life cycle of Anoplocephala
Egg with pyriform apparatus, cysticercoid develops in mites, mite is ingested and adult develops in SI or at ileocecal junction. PPP is 6-10 weeks. See inflamation and ulceration of mucosa, peritonitis. no signs with light infection.
Diagnosis and treatment of Anoplocephala
history, fecal float, most horses don’t pass eggs in feces, PCR. use prazi after tapeworm transmission.