Equine Strongyles Flashcards
What are the 2 groups of equine strongyles?
Large strongyles - Strongylus vulgaris - Strongylus equinus - Strongylus edentatus Small strongyles (Cyathostominae)
How do you morphologically differentiate among the large strongyles?
- S. vulgaris: ear shaped teeth
- S. equinus: one large tooth, 2 smaller teeth
- S. edentatus: no teeth
Strongylus vulgaris - general characteristics
Host: horses, donkeys, mules, zebras
- oval buccal capsule
- ear shaped teeth at base
Strongylus vulgaris - life cycle
Females lay eggs, eggs hatch –> L1 emerges –> L2 –> L3 (ensheathed infective stage) –> L3 exsheath in SI, enter submucousa of cecum/colon and walls of submucosal arterioles –> L4: cecal and colic aortic artery, cranial mesenteric artery, small arteries of intestinal wall, enter tissue (nodules) –> adults in nodules –> nodules rupture –> adults enter lumen of cecum/colon
S. vulgaris pathology - migrating larvae
- arteritis
- thrombi
- emboli
- intestinal nodules
S. vulgaris pathology - adults
- intestinal nodules
- promote granulation, scarring
S. vulgaris pathology - larval damage
- intestinal nodules - minor
- arteritis - major
- verminous arteritis
S. vulgaris - arterial system
- inflamed/thickened walls
- thromboemboli
- posterior aorta: tracks/debris from migrating L4, damages smooth endothelial surfaces, aneurysms of cranial mesenteric artery
Strongylus vulgaris - clinical signs in adult equid
- anemia/bleeding ulcers
- confluence of attachment sites
- diarrhea
- unthriftiness, weight loss
- heavy infection with large strongyles: debilitation, weight loss, colic
Strongylus vulgaris - clinical signs in foals
Infected with 75-100 adult S. vulgaris = 30 ml of blood lost/day
Strongylus equinus - general characteristics
Hosts: horses, donkeys, mules, zebras
- one large tooth (dorsal, long arrow) and 2 smaller teeth (ventral, short arrows)
- dark red or black
Strongylus equinus - life cycle
Females lay eggs, eggs hatch –> L1 emerges -> L2 –> L3 (ensheathed infective stage) –> L3 exsheaths in SI, migrate to cecum/colon, encapsulate in subserosal nodules –> L4 enters peritoneal cavity, migrates to liver and back to SI thru abdominal cavity (pancreas), forms nodules in gut wall and ruptures into cecum/colon –> adults mature in cecum/colon
Strongylus equinus - pathology
Not as pathogenic as S. vulgaris
- mainly due to larvae
- hemorrhagic nodules in intestines
- nodules, fibrotic tracts in liver
- nodules in pancreas
Strongylus edentatus - general characteristics
Hosts: horse, donkey, mules, zebra
- no teeth!
- smooth buccal cavity
Strongylus edentatus - life cycle
Females lay eggs –> hatch with L1 emerging –> L2 –> L3 (ensheathed infective stage) –> L3 exsheaths in SI, migrate to cecum/colon, right ventral colon, thru gut wall, enter vessels, hepatic portal vv to liver, L3 wander in liver –> L4 exit liver thru hepatic ligaments, tissue under parietal peritoneum to right abdominal flank –> adults via mesentery, return to LI, enter cecum/colon by nodule formation, nodule rupture, mature in cecum/colon
Strongylus edentatus - pathology
Mainly due to larvae
- perivascular thickening
- subperitoneal cysts
- nodules and fibrous tissues
Large strongyles - general signs
- anemia
- poor weight
- fever
- depression
- lethargy
- colic
- soft feces
- rough hair coat
- death is possible
S. vulgaris - specific signs
- high fever
- inappetence
- colic
- gangrenous enteritis
- intestinal stasis, torsion or intussusception
- possible rupture, arteritis
- especially cranial mesenteric artery
Diagnosis of large strongyle infections
- fecal float: strongyle type eggs
- L3: strongylus spp.
- S. vulgaris: palpation of cranial mesenteric artery, arteriography, clinical signs
Epidemiology of large strongyles
Southern US - year round - max transmission in cooler seasons Britain/Canada - max transmission mid-summer to mid-fall
Is equine strongyle PPP in weeks or months?
Months!
- ruminant strongyles is in weeks
Cyathostomes - general characteristics
Family: Strongylidae Subfamily: Cyathostominae - horses, donkeys, hinnies, mules, zebras - cylindrical buccal cavity - 2 leaf crowns
Cyathostomes - life cycles
Females lay eggs, eggs hatch –> L1 emerges –> L2 –> L3 (ensheathed infective stage) –> L3 exsheaths in SI, migrate to cecum/colon, encyst in crypts of Liberkuhn, ALD, mucosa or submucosa of cecum/colon –> L4 enter lumen of cecum/colon –> adults mature in cecum/colon
Hypobiosis in cyathostomes
Presumed signal received by pasture L3s - season of year (falling temps) - some emergence throughout the year Hypobiotic early L3s - stimulated to repopulate cecum/colon - become adults dependent of season - influenced by immune status/age of host
Larval cyathostomosis
Synchronous emergence of large numbers of arrested L4s in early spring
- hypobiotic larvae can be > 50% total larval population
- south: summer
- north: winter
- number of adults in gut might be influenced by treatment
- naive horses initial infection
- results in majority of worms developing without hypobiosis
- reinfection or frequent exposure (most worms arrest)
Hypobiosis may be used by the cyathostomes as a mechanism of ________
Controlling the numbers of adult worms in the gut
- treating horses with anthelmintic to eliminate adult cyathostomes from the gut will stimulate development of hypobiotic EL3s to repopulate cecum and colon with adult worms
What is the predominant contributor to fecal egg count and pasture contamination?
Cyathostomes
- FEC may not accurately reflect worm burden due to ALD
- FEC may not reflect number of adult nematodes (animals with high number of adults may have low FEC)
Small strongyle pathology
Larval cyathostomes in colon wall
- nodule formation
- hemorrhagic (black to dark red)
Small strongyle clinical signs with adults
- generalized disruption of mucosa
- superficial ulceration
- general debilitation
- intermittent soft feces
Small strongyle clinical signs with larvae
- disruption in normal gut motility
- hemorrhagic, catarrhal, or fibrinous enteritis
- colic: intussusception, cecal tympany
Small strongyles are severe in horses _______
Under 2 years
- inflammation
- penetration/emergence
- lymphocytes, plasma cells, eosinophils
- most pathological event is L4s emerging from tissue!!
Protein losing enteropathy
- hypoalbuminemia
- increased intestinal permeability
- thickened mucosa/poor absorption
Small strongyles are _____ than large strongyles
Less severe
- graze more on surface
- smaller buccal cavity
- only serious in large numbers
Small strongyle pathology due to all life stages
- intense inflammation possible in response to proteins released from cyst
- adults attach to large bowel mucosa
- may cause superficial ulceration
- leakage of extracellular fluids
Larval cyathostomiasis
Verminous enteritis
- acute onset
- severe diarrhea
- rapid weight loss
- pyrexia
- colic
- ventral edema
- L4 in diarrheic feces on gloves
Small strongyle infection - diagnosis
Strongyle type eggs
- cannot identify larvae, eggs to species
Treatment and control of large strongyles
Approved: Fenbendazole, Oxfendazole, Oxidbendazole, Pyrantel salts, Ivermectin, Moxidecin Pasture management - remove manure - alternate grazing with ruminants - avoid overcrowding and wet pastures
Larvae on pasture
Only 10% large strongyles, 90% cyathostomes
- need moisture, shade, relatively low temperature
- conditions favorable to movement lead to exhaustion and death (non feeding L3)
- do not live longer than 3 months
Maximal transmission of strongylid parasites
- cooler seasons (fall, winter, spring)
- high pasture numbers of L3s
Current goals of parasite management
- prevent clinical disease
- reduce level of infection below disease-threatening threshold
Approaches to parasite management
Targeted selective anthelminic treatment schemes
- only treat animals with high FECs
Selective anthelmintic therapy
Broadly used in ruminants, makes use of FEC
- has become important in horses, only horses that exceed a certain FEC are treated
- interval between FECs as long as possible/as short as necessary
- high and low shedders are identified
Value of SAT relies on stability of ______ over time
FEC
- consistency can be estimated measuring repeatability of eggs shedding
Recommendations
- targeted anthelminic treatment of high shedders
- results in reduction of pasture contamination
- reduces worm burden in whole pasture group
- lowers risk of developing drug resistance
Fecal egg count reduction test
- compare efficacy of anthelmintic
- detect resistance
- determine correct interval between anthelmintic treatments
- ensure low contamination on pasture
Delaying resistance
Use correct dosing
- use slow rotation of anthelmintics
- maintain refugia from treatment
- limit anthelmintic treatments
- resistance occurs (benzimidazole and pyrantel pamoate)
Pasture management
- collection of feces
- pasture harrowing, alternate grazing
- prevalence of resistance increasing
- cyathostomes need to be considered when designing a control program
