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parasit
11/10/97
johnstone
internal parasites of horses

he 
gave out a bunch of handouts for today through wednesday and dr 
guerrero's slides which (not surprisingly) are not yet on the web.


internal parasites of horses
the horse population in US is about 15-20 
million. horses are mainly raised on pasture so parasites are important 
to deal with and control. 
table in handout: internal parasites of 
horses, common names, real names, location.

in descending order of 
importants:
small strongyles
large strongyles
ascarids
strongyloides
bots

pinworms
stomach worms
tapes
eyeworms and filarids
lungworms

clinical 
effects range from none to unthriftiness to diarrhea to colic to death

seriousness largely depends upon three factors: 
number of parasites 
present - the heavier the worm burden, the more signs
age of infected 
horse - younger are more susceptible - naive hosts, not immune
pathogenic 
potential of infecting species: not all parasites can cause same degree 
of pathology. small strongyles are more pathologic per worm than are some 
others. 

"parasites have no boundaries" - affect all ages.
horses tend 
to be susceptible at all ages, but pathogenic effects tend to be worse in 
young horses.

first parasite the foal meets: 
strongyloides larvae in 
colostrum. foals are born parasite free but this is the first one they 
meet. strongyloides westeri. initially infected via mares milk at 4-45 
days postpartum. PPP 5-7 days, so at 2 wks of age, foal may be passing a 
lot of s.westeri eggs from a patent infxn with parthenogenetic females. 
so there's a constant source of reinfection - percutaneous, oral, and 
transmammary. (L3) these three routes guarantee that almost all foals 
will be infected. can see 20000 eggs/grm in feces by 5 wks of age.


despite the fact that many nursing foals are wormy, they grow well, 
compensating by drinking more milk. also infxns are self limiting- 
immunity develops by 4-6 mos of age. animals that are not treated will 
clear the infxn by about 11-12 wks of age. if you use a drug effective 
against strongyloides eg fenbendazole (note that you don't need broad 
spectrum drug at this early age, but later on you do - early on, they're 
only infected with strongyloides) - and you treat a foal at 2, 4,6,8, etc 
weeks, it curtails the infxn, but delays the immune response. so it 
appears that acquisition of immunity is related to duration of infection. 
so a better approach might be to tx at 4 wks, and again at 8 wks. this 
provides enough stimulus for foal to develop quite good immunity, and 
infection won't bounce back after second tx, like it will if you dose q 
2-4 wks. 

broad spectrum of activity not necessarily important early in 
life. You don't need ivermectin, can use fenbendazole or any of the other 
benzamidazoles early in life.

parascaris equorum is the second parasite 
they meet. common infection in foals, yearlings, and less in two year 
olds. aquired resistance is strong, so rare in older horses. signs: 
coughing with mucoid nasal d/c commonly occurs in infected foals due to 
lung migration of larvae. light infections of adults in small intestine 
are usually asymptomatic. also due to migration through liver no clinical 
signs but white spots on liver. can also see severe pneumonia from lung 
migration of severe. adult worms can cause impaction, rupture, 
peritonitis, death but this is rare, requires heavy worm burden. 
would 
see it more if not treating with anthelmintics. egg is large, typical 
ascarid egg with thick sticky shell. round. sticky external coat means it 
sticks to everything in foal's environment. the usual clinical picture of 
adult ascarid infection is rough haircoat, unthrifty, potbelly. patent 
infections are often first seen at about 2-3 mos of age. PPP of p.equorum 
is 10-16 wks. so they have to be at least 10 wks old to have a patent 
infxn.

only three drugs against parascaris are effective against larval 
stages. ivermectin (IVM) is best - gets L3, L4, adult. fenbendazole (FBZ) 
is partly 
effective against L4 and fully against adult. Strongid C is 
effective against L3 but not L4 and also adults. most benzamidazoles are 
only effective against the adults in small intestines, not L3 or L4. 


fenbendazole inhibits patency of infection, and can be useful against 
light infections. with heavily infected foals, there is a danger treating 
with rapidly acting compounds, like piperazine, which is still used to tx 
ascarids in dogs and is still approved for use in horses but isn't used 
much in horses anymore - if you kill lots of these worms you may see a 
"toxemia like syndrome" resulting from an allergic response to the many 
dead and dying worms in the small intestine. so it is better to use a 
subtherapeutic dose, or less active compound, to kill some of the worms, 
then repeat the dose in 10-14 days.

gasterophilus - the bot fly. so, now 
it is summer. the bot fly is attacking the foal in the pasture. "bot" 
refers to the larval stages of these flies. very common in horses of all 
ages. the adult fly attaches her eggs to the side of the hair shaft of 
the host. the complete life cycle takes about 12 mos. adult bot flies 
actively deposit eggs between may and october, on the forelimbs and heads 
of horses. horses lick themselves, stimulating eggs to hatch. larvae 
migrate through oral mucosa to stomach. overwinter in stomach. pass out, 
pupate on ground, hatch in 1-2 mos. 

horse tongue - lesions causd by 
larvae which are migrating through mucosa. may also see periodontal 
ulcers caused by the larvae. 

bot larvae in stomach - really disgsting. 
take up a lot of space, it looks like. 
in light infxns, they are fairly 
innocuous, but you run the danger of some of the larvae actually 
perforating the stomach, causing peritonitis that can be fatal. he has a 
slide showing little holes in the stomach near the larvae - tiny hole, 
but enough to allow fluid to leak out of stomach. so while most botfly 
infections are innocuous, they shouldn't be ignored, or this can happen. 
because of the potential for this, control of botfly larvae must be 
incorporated into every equine parasite control program. many things have 
been used to treat these suckers. trichlorfon and dichlorvos, 
organophosphates developed in the 60s, were used for a while. the usual 
recommendation was to treat horses every 30-60 days during the 
season,then to tx again 3-4 wks post last killing frost (last frost kills 
any eggs left on horse and any adult flies that are around, so if you 
treat after the last one, you have no risk of reinfection til next 
season). the problem with these drugs was that it was dangerous to use 
them in pregnant mares. now, we use IVM or moxidectin (aka "quest"), each 
of which is effective. IVM is most effective, b/c it gets all the larval 
instars - migratory and in stomach - also very safe. so the 
organophosphates are not used as much, are still on approved list but not 
often used. some vets still use their leftover stock and stuff, but 
probably eventually will be totally superceded by IVM and moxidectin.


later in year, foal is infected with anoplocephala magna/perfoliata 
clustered around ileocecal valve. seen in cecum and at ileocecal valve. 
characteristic egg - D shaped egg. these are the horse 
tapeworms.frequency of infection varies a lot farm to farm, but w/in any 
locality localized heavy infxns may be seen, and then we may see acute 
obstructive colic from it. they aren't frequent, but a number of reports 
in literature do describe serious clinical conditions from teh tapeworms. 
A. perfoliata has been associated with intussusceptions, cecal 
impactions, and peritonitis secondary to gut perforation. 

slide: a case 
of cecal perforation which had been walled off. this horse did recover, 
after abscess was surgically managed.

generally little effort has been 
put into making drugs against anoplocephala b/c they are considered 
unimportant. no drugs are labelled for use against these beasts. so, we 
use small animal meds - droncit, praziquantel, very expensive.

mebendazole and fenbendazole have also been used.
pyrantel pamoate, 
however, is the only one really effective against equine tapeworms - but 
it isn't labelled for this use. it has a wide saftey margin, has been 
used a lot in horses over 10-15 yrs. if you want to tx tapeworms, you 
have to give 2x the dose that treats strongyles, however. 

stomach 
worms:
habronema muscae
draschia megastoma
trichostrongylus axei

widespread and common, but not that pathogenic. remember that the first 
two, the spirurids, require an intermediate host (housefly or stable 
fly). more importantly, they are responsible for summer sores. these 
arise from deposition of larvae in skin abrasions, producing these yucky 
lesions. they tend to heal spontaneously during the winter but are 
painful and ugly while they last. also they are very itchy and 
distressing to the horse. the adults of draschia produce tumorlike 
lesions in the stomach. occasionally, they have ruptured leading to 
peritonitis - but not often. 
trichostrongylus axei often occurs where 
donkeys/horses graze with cattle/sheep. it's the same spp infecting 
horses/donkeys/cattle/sheep/goats. so if horses and cattle graze 
together, they maximize the contamination of the pasture. where 
contamination is heavy yuo may see acute hemorrhagic gastritis in the 
horse. 

onchocerca: lesions in skin are very itchy, intensely itchy, 
associated with mmf in the skin - little bluish things on the slide. it's 
also possible that these lesions are hypersensitivity rxns to the bite of 
culicoides. eye lesions also possible. usual dx made on basis of thinning 
hair, scaly patch on neck, head, chest and ventral midline, and confirmed 
by skin biopsy. these were common up to 5-10 yrs ago. then we got IVM 
which has strong activity against trichostrongylus, habronema and 
draschia adults and L3, dictyocaulus adults and larvae, and onchocerca 
mmf. so as long as you give the IVM you're covering them all. 

parasite 
protection programs in horses primarily are designed to control the 
strongyle. you can't rely on one drug. if you ignore IVM or moxidectin 
you won't get the minor spp, which may then become more of a problem. so 
you make a program primarily designed to control strongyles which are 
most pathogenic, but you use drugs strategically to take care of the 
minor spp as well. 

dictyocaulus arnfeldi- lungworm of horse/donkey. 
donkey is natural host. infections are common in donkeys - up to 50%. but 
nonpathogenic in donkeys. usual problem is common grazing of horses and 
donkeys together. most infxn asymptomatic, but when there is persistent 
coughing of young horses, late in season, could be this. low prevalence 
in horses, coughing occurs. L1 in feces is diagnostic. spike tailed 
larvae (?)
IVM very effective against L4 and immature and mature adults. 
should give IVM at least once, preferably twice, during the year.

last 
of the relatively minor spp in growing and adult horses: oxyuris equi, 
the pinworm. found in LI. females are larger than males. gravid females 
migrate to host anus and oviposit there. eggs adhere to perianal skin, 
attach to blankets, stable walls, bedding, etc. so while this is very 
nonpathogenic, it is very common as well. eggs are ovoid. clinical signs: 
anal irritation, pruritis. horses will rub their butts on anything they 
can find. will see loss of hair, rubbed tails. "rat tail" appearance. 
just about all the modern anthelmintics have good activity against 
pinworms. pyrantel pamoate is an exception in that it isn't very 
effective against the L4 in the colonic mucosa. all the others are good 
against adults and L4s (also except fenbendazole. the other 
benzimidazoles are good though).

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Dr Johnstone remarks that 
the rat tailed horse idea USED to really correlate with oxyuris equi, but 
now oxyuris equi is much less common, but you still see horses with 
rubbed tails who do NOT have oxyuris equi.

the strongyloidea

the bread 
and butter parasites of equine veterinary medicine. the large strongyles 
and the small strongyles. it is around  these parasites that all parasite 
programs coalesce. they are found wherever horses graze, so all horses 
become infected fairly early in life, as soon as they start grazing on 
grass.

development of nematode infxns in growing foals: first parasite 
is strongyloides. they will pretty much clear that at about 20 wks. the 
second nematode parasite they meet is parascaris equorum. again, even in 
absence of tx they will develop good immunity and fairly adequately deal 
with it and will have very low level infection as they get older.  then 
as they start grazing, they start to meet strongyles. horses do not 
develop a good immune response to them. if you don't treat growing foals, 
these infections will build up over the first two years of the horse's 
life. after 2 yrs, there appears to be an innate age resistance - 
infection tends to be dampened - but still much higher than ascarid or 
strongyloides infections in horses of same age. and these strongyles can 
be very pathogenic. so this is a threatening time in horses' life - 12 
wks to 2 yrs.

small strongyles are mucosal grazers/plug feeders/shallow 
buccal capsule. larvae are more pathogenic than adults. most of our 
current anthelmintics aren't that effective against the larvae of the 
small strongyles/cyathostomes. adults are of secondary clinical 
importance, though. larvae more problems. 
diarrhea, loss of condition in 
spring - emergence of L4 cyathostomes from gut wall. these L4 were 
aquired in previous season, overwintered in gut wall as arrested L3. so 
you see horses are infected year round, but the infections show large 
peaks in late spring/summer. these adults come from arrested L3s which 
emerge as L4 (around Feb/Mar) and mature into adults, which then produce 
large numbers of eggs which contaminate pasture, setting up infections 
for newly weaned, grazing foals. so pastures can become heavily 
contaminated with these eggs early in grazing season. when these larvae 
emerge in large numbers, can cause acute, life threatening, diarrhea. 
usually they call it "larval cyathostomiasis" - presents as sudden onset 
diarrhea, nonresponsive to tx, seasonal occurence, rapid wt loss, in 
heavy infections may see reddish L4s in feces, sometimes a mild recurrent 
colic and peripheral edema (from low serum albumen, suggesting leak 
through colonic mucosa). the seasonality suggests involvement of 
environmental inducing agent. 

two problems with tx of these affected 
horses- 
1. none of the currently available approved drugs are effective 
against arrested L3 in mucosa. 
2. removal of L4 and adults from lumen of 
colon apparently results in feedback effect on arrested L3, inducing them 
to resume development. so this exacerbates the problem. so, until 
recently, tx was limited to fluids, steroids, to releive intense 
inflammatory response and support animal during diarrhea.  BUT, sure 
enough, more recently, work has shown that if you give larvicidal doses 
of fenbendazole, you can kill the arrested L3 in mucosa as well as the 
other larval forms. unfortunately, due to drug resistance, it doesn't 
work well against adult small strongyles - many adults are resistant to 
the benzimidazoles. but it works well for the arrested L3 even in 
resistant strains! note that IVM andMOX get L4s and adults, but not 
arrested L3s. 
so - to tx the cyathostomes: 10 mg/kg daily x 5 days of 
fenbendazole in an offlabel usage. this may be approved within the next 
6-12 mos.

so. to summarize briefly. if you consider the small 
strongyles, look at the egg counts - there is not only a seasonal effect 
of adult worms,but since they lay eggs, we see a seasonality to strongyle 
egg counts. although horses are infected through the year, peak is late 
spring/summer. so we concentrate treatments to prevent this peak from 
occuring. so we treat in advance of the peak. 95% or more of strongyle 
egg counts, btw are due to small strongyles. only 4 or 5% are due to the 
large strongyles eg strongylus vulgaris. so in the larger scheme of 
things, small strongyles may have replaced s.vulgaris as our main 
concern, but on a worm to worm basis, s.vulgaris is way more pathogenic.


large strongyles
strongylus vulgaris
masses of them in colon of infected 
horse seen on a slide. 
if you use a drug against s.vulgaris, that drug 
will also work against other large strongyles, so we will just discuss 
this one which is most pathogenic, bc of migrations of larvae through 
mesenteric arteries, causing thrombi, arterial pathology, occluding blood 
supply to gut. changes can be caused by relatively few migrating worms. 
affected vessels are thickened, much larger than normal, sometimes can be 
palpated on rectal exam. but you don't see them a lot in well cared for 
horses anymore. on radiograph with injected dye, we see the anterior 
mesenteric artery is very dilated, thickened, inflamed.
note that adults 
are also pathogenic - deep buccal capsule, plug feeds on colonic mucosa, 
there is an ear shaped tooth visible behind the buccal capsule on this 
section. basically they grab a plug of mucosa,digest it, and leave a hole 
there. so.

parasites. another ad - for panacur aka fenbendazole. 

so.

talk about controlling these parasites, focusing mainly on strongyles.
to 
reiterate: in first 6 mos of horses' life, parasite control is directed 
against strongyloides and parascaris. after that, strongyle infxns become 
focal point for control program. b/c these animals on the chart are 12-24 
wks old, all the eggs in the feces are from small strongyles. ppp of 
large strongyles are 6-12 mos. this doesn't mean that s.vulgaris isn't 
there - it could be migrating through cranial mesenteric arterial tree, 
causing problems - remember, prepatent infxn in s.vulgaris is a problem! 
you have to treat those too.

parasite control in equine vet med is based 
mainly on effective drug use. it is important for many reasons to not 
rely exclusively on drugs.management practices are also useful in 
limiting buildup of larvae on pasture. also, in the horse strongyles 
especially, we've seen emergency of drug resistance. the more you use 
drugs, the more likely drug resistance becomes. 

management factors of 
parasite control:
avoid overcrowding - in all grazing animals. the more 
horses there are, the more likely to increase pasture contamination.

remove feces from pasture - useful, but labor intensive. you can control 
strongyles almost exclusively just by daily removal of feces from 
pasture.
compost feces - high temp kills eggs/larvae
harrow pastures

alternate/mixed grazing on farms where horses are raised with cows/sheep. 
mixed grazing with cattle or sheep works b/c cross transmission is 
limited to trichostrongylus axei - so each species is a cleaner upper for 
the other host's pathogens. but in this way you can select for 
trichostrongylus which can then become a real problem in all of the 
animals. 

main features of control program:
include all the horses in 
the program - even though younger are more vulnerable, older horses carry 
infection and will constantly seed the pasture with eggs so they must be 
included in parasite control program. 
new horses should be quarantined 
and treated (preferably, do fecal egg count)
set up strategic program 
based on epidemiologic principles - seasonal effects of temperature and 
moisture on life cycles that produce infections that are concentrated in 
the grazing season. 

supplement basic strategy with additional 
treatments
rotate drugs slowly to prevent resistance
always follow dosage 
recommendations
do periodic fecal exams to check effectiveness of program 
and to detect emergence of drug resistance. there are already reports of 
resistance to ivermectin in cattle/sheep nematodes in australia. 

"every 
season is parasite season" according to this ad. that is true, with a 
caveat. while every season is parasite season, some seasons are better - 
late spring, summer, early fall is when most parasites are most 
prevalent.  

again - these infections peak in the summer. this must be 
taken into account in development of any control program, notwithstanding 
catchy ad slogans.
control of strongyles with pyrantel - it only gets 
adult small strongyles. you get rid of all the adults, reducing egg count 
to nothing,but then the arrested L3, plus L4 and L5 come and develop and 
a new patent infection occurs w/in 4-5 wks. this is why they were saying 
to treat every 4-8 wks with pyrantel. 
if you look at fenbendazole you 
see the egg counts drop but do not go to zero - because some of the 
adults are resistant. 
ivermectin, however - you treat with ivermectin 
and the egg counts drop and don't come up again for 10-12 wks. ivm has a 
residual effect, for one, and is also effective against L4 and L5, so 
fewer are left to emerge. all that's left is the arrested L3s. it takes 
longer for them to grow. so with this drug you only have to treat every 
12 wks.
moxidectin/quest - has a longer residual effect - 12-16 weeks. 


remember - basic strategy is to kill the beast by getting rid of the 
summer peak. optimal worm control: right tool, right time, right 
treatment. 

putting it all together 
the field of parasite control in 
horses has moved quickly in the past five years. we know much more about 
epidemiology of these infections than we did and have new drugs. 

July - 
tx for bots (ivm)
september - tx for tapes (pyrantel)
nov - tx for bots 


in april-sep tx q 4-8 wks (depending on drug) "routine control program" 
mainly against strongyles. eg Ivomec or pyrantel or whatever 

in Nov/Dec 
- tx for larvae - remember, IVM and MOX get the encysted stages and the 
adults and L4s in lumen,but not early L3 arrested larvae. Fenbendazole, 
however, is effective against the arrested L3. so give fenbendazole 5 day 
tx at some point during winter.

note that if your routine tx is 
pyrantel, you don't have to give separate dose for tapes, and if your 
routine tx is ivm, you don't have to give separate doses for bots, or 
whatever. then you can rotate the next year and use different drugs.


this doesn't account for ascarids and strongyloides. you would bring them 
into this program once they start grazing. during their first year, you 
have to use ivm or mox to get the migrating strongylus vulgaris.

daily 
wormers like strongid c - dr j doesn't like them - "biologically 
insulting" - causes rapid emergence of drug resistance. 
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