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parasit
11.4.97

dr schad

gastrointestinal helminthiases of 
dogs/cats.

as we know, so far we've talked about the worms in groups as 
they relate to each other biologically. now, we see the parasites in 
practice as mixed infections happening in particular hosts, so we'll do 
this now.

helminths of canine intestines:
these are presented in order 
of appearance, eg first ones happen to youngest host, and so forth.


ancylostomiasis - hookworm anemia
caused by ancylostoma caninum which 
lives in small intestine and is a bloodsucking nematode. a.caninum 
undergoes transmammary transmission and can appear in 2 week old pups. 
it's a voracious bloodsucker. they suck blood wastefully, puff it out at 
intervals. create bleeding ulcers. the emphasis is on hookworm anemia and 
bloodloss, but these also cause malabsorption, blunting of villi, 
diarrhea - but not as much as some other worms eg uncinaria.
the 
distribution of this parasite is nationwide, but tends to occur on an 
east-west gradient, being most common and prevalent in the east, less so 
in the west as rainfall decreases, and going south as summer gets longer 
and winters shorter it becomes more of a problem. infective stage is the 
L3, ensheathed in environment. L3 is eaten and grows L4->adult in SI - 
or, hypobiotic L3 in muscle can reactivate and grow that way, or can be 
transmammary transmitted to puppy. L3 in environment is resistant to 
chemicals. L3 in transport host may or may not be important. L3 
ensheathed is susceptible to dessication and cold. greatest prevalence is 
during summer, lowest during winter. in late winter/early spring before 
larvae appear in environment, the prevalence is already increasing. and 
it starts falling in August while there are still abundant larvae. why? 
b/c those larvae enter hypobiotic state.  and in early spring, arrested 
larvae are waking up.

anemia will develop in more mature animals in 
about 14-18 days. bloodloss peaks at time eggs first appear in feces. 
puppy infected by lactogenic route in this slide is very weak, can't 
stand on his own, and is very anemic with white mms.

"kennel anemia" is 
the situation we see in very young animals as above
also possible in old 
animals which haven't seen worm before or exposed to large infection. 
this is acute hemorrhagic anemia. animals on good diet will crank up 
hematopoietic machinery and reverse this anemia over time.
chronic anemia  
- seen in older animals which fail to maintain an adequate resistance. 
long standing less severe anemia, iron deficiency type anemia, 
hypochromic, microcytic anemia with small, pale RBCs

prophylaxis - you 
need to control the L3 not the egg. with ascarids you have to deal with 
an egg. but not here. they are susceptible to dessication. so you can 
treat soil with sodium borate, which isn't compatible with keeping a 
lawn. you can keep kennels/pens clean and dry. larvae are resistant to 
chemicals so you have to treat thoroughly if you use borate. 

chemoprophylaxis: milbemycin, ivermectin plus pyrantel - not actually. 
not so much prevention of infection, but prevention of adult worm, 
because this actually allows them to grow, but then gets rid of them 
every month before dz can develop. preparturient tx of bitch - will 
discuss w/toxocara. there is no vaccine currently available. 

dx: 
strongyle type egg in feces (fresh), can't tell from uncinaria 
stenocephala in pure infections. in 24 hr stools will see larvae, need to 
tell from filaroides or strongyloides. postmortem dx - pale organs, 
emaciation, intestinal hemorrhage, adult worms, attachment points.

tx: 
there's a chart in handout in back that's more up to date than the part 
in this section. ideally, check the stool again before 2 weeks (before 
new infxn could be patent). supportive tx: iron supplementation, high 
protein diet, and in young puppies blood transfusions.many puppies still 
die with transfusions.

resistant cases may involve arrested larvae. we 
regularly hear about animals that are hard to cure of these infections, 
animals that come back repeatedly being found to be infected often with 
no apparent exposure. a paper trained dog that never goes outside, or an 
animal treated in winter and found negative is positive again later in 
winter...probably due to hypobiosis. 

experiment: started with twelve 
dogs, six treated at a time when all the worms developing would have done 
so, at about 19 days. the dogs were treated with an anthelmintic that 
removes only adults. the treated dogs were worm free through 50 days. all 
the time, were kept in controlled environment with no potential exposure 
to infection. after fifty days, these dogs gradually became reinfected. 
this must have been due to reawakening of hypobiotic larvae. 

canine 
toxocariasis - caused by toxacara. this is not toxascariasis! toxocara is 
more pathogenic than toxascaris. and recall that baylisascaris is also 
seen in dog. we're not going to discuss it anymore, because other than 
its occurence we don't knwo anything about it. 

so, toxocara canis, 
agent of canine toxocariasis. recall that the alae merge gradually into 
the body. the enteritis produced by the ascarids is made very largely by 
swimming motions of the worms. the worms do not hang on to the mucosa. 
they swim for their lives. they are big worms. they rub against the 
mucosa. the anterior end especially rubs. the alae are in fact ridges and 
are very abrasive. there's a lot of loss of enterocytes, and this is the 
basis of the enteristis seen in these infections. agent for this disease 
is toxocara canis, which has a widespread national and global 
distribution. patent infections arising from prenatal infections can 
appear in less than a month's time. eggs, not larvae, pass in feces, so 
very resistant to environmental conditions. infective stage varies:


remember that the dog becomes resistant early in life. in young animal, 
can be infected by eating embryonated egg +L2 - also infective to 
paratenic hosts, humans (VLM, OLM). in older dogs, the larvae mostly 
follow somatic route and hang out in muscles, later to be transmitted to 
fetus, having migrated to fetal liver, where they are stored until 
parturition, when they are reactivated and start to undergo 
pulmonary/tracheal migration, eventually reaching intestine. lactogenic 
infection can also occur. 
pups can expel L4 and immature adults which 
are eaten by female, reinfecting her.
pulmonary disease may be seen in 
puppies. this is not something seen with toxascaris leonina, where larvae 
never go to lungs. 
paratenic hosts containing L2s are infectious. 

verminous pneumonia occurs in neonates - prepatent disease
patent 
toxocariasis in older pups, at least 4 wks or more -> anorexia, poor 
growth, loss of condition, poor haircoat. pups may be potbellied, noisy, 
may vomit/diarrhea, painful - may have diarrhea, dehydration, death. 
occasionally a puppy has a huge bundle of worms.

what about diagnosis? 
prophylaxis?
prophylaxis - as in hookworms - interceptor, milbemycin. see 
handout for environmental info.

dx: finding egg in feces. they float 
nicely. spherical, unembryonated thick shelled eggs with pitted surface. 
distinguish from t.leonina, with smooth surface and ovum that doesn't 
fill whole egg. recall ascarids can wander into bile ducts, out of noses, 
mouths, anuses...remember, in dog, you can't speciate on alae - t.cati is 
the one with the arrowhead alae.

can you prevent the infection from 
being transmitted to puppies? a study was done, treating bitches with 
oxfendazole while pregnant. 20 day tx of 5 mg/kg BID reduced infection in  
puppies to near zero. one can also and with less time involved use 
doramectin (sp?) (a pfizer product) which isn't approved, for 5-8 days 
prepartum, 1 mg/kg.

moving on to strongyloidiasis- threadworm infection. 
no vertical transmission. a lactating animal can pass larvae to a pup but 
only if she happens to get infected while she is lactating. it isn't 
genuine lactogenic transmission involving hypobiosis. these aren't 
particularly pathogenic. worms are embedded in mucosa down in crypts. 
they are quite minute. no parasitic males. if you do a scraping of mucosa 
or if some mucosa is sloughed, you see only the large females. you may 
also see small larvae. in strongyloides stercoralis, eggs hatch in small 
intestine, so larvae pass through gut as well. not in other strongyloides 
spp. 
infective stage again is L3, not ensheathed. dense population 
arising from heterogonic life cycle is possible. see handout diagram. L3 
penetrates skin of host either directly via two molts L1->L2->L3 in 
environment, or via sexual reproduction in environment, acting as 
amplifier. so heavily infected young dogs can come in. also recall that 
the larvae born from parasitic females can develop inside the host, 
causing autoinfection, increasing the worm burden within the host. 


strongyloidiasis in about a third of dogs and a fair number of humans is 
a chronic infection. we don't know how long it lasts in dog - in humans, 
30-40 yrs! adult worms don't live that long. but dogs infected for a long 
time may have occult infxns. no larvae in feces, but barren females in 
intestines. those females can resume ovipositioning if you put them into 
a naive animal. it seems that these long lasting females that go through 
barren stage will when immunity wanes give rise to some autoinfective 
larvae which will then grow up and replace their mothers in the gut. so 
the worms aren't really 40 yrs old. 

adult worms in mucosa...eggs 
hatching in mucosa...emerging larvae cause enteritis. a dog with 
strongyloidiasis presents with diarrhea, perhaps some weight loss, 
dehydration. mucoid diarrhea. sometimes, a dog that is very emaciated and 
depressed comes in - due to hyperinfective disease with rampant 
autoinfection. commonly associated with pulmonary involvement and 
wheezing/coughing. perhaps associated with immunosuppression.

the 
heterogonic cycle outside the host can lead to large numbers, makes it 
hard to get rid of even under good conditions in kennels. a few surviving 
worms can multiply out of control.

parasite is transmissible to human, 
no great treatments for it. be careful. potentially dangerous to people.


for diagnosis, look for L1 in feces, with characteristic large genital 
rudiment and very pointy pinpoint sharp straight tail (in lungworms, tail 
is kinked).

tx: fenbendazole or ivermectin.

there are chronic carrier 
animals passing few eggs, irregularly. suppose that while working with a 
kennel you have a problem getting rid of strongyloides from the premises, 
and you want to verify dogs free of strongyloides. you take stool sample, 
mix with ground peat moss, about 2 cc stool with peat moss, put it aside 
a few days, then Baermanize it and look for larvae.

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ok. 
moving on. other hookworm of the dog: uncinaria. you rarely hear about 
uncinariasis.  6% of dogs in NJ have this. it's in eastern and northern 
US and alaska. it's a tissue feeder, not a blood sucker. it's a sloppy 
feeder, doesn't suck per se. 

infective stage is ensheathed L3 in 
environment. you want to remember that you could see an animal with a lot 
of strongyle type eggs, which has to be hookworms in dogs, and no anemia. 
either dog was briefly infected with ancylostoma, or it has uncinaria 
stenocephala. some call this the northern dog hookworm. fox = reservoir, 
and as foxes get into suburbs (have even been spotted in the city here!) 
it is more common. life cycle is like ancylostoma, but it lacks any 
vertical transmission. no problem in neonates from uncinaria. usually in 
young but not too young dog that you have problem. all these parasites 
acquired larva by larva or egg by egg from environment require time to 
build up to disease causing worm burden. this causes a protein losing 
enteropathy but not anemia.

we see blunting of villi, fusion of villi, 
malabsorption, diarrhea, protein losing enteropathy. loss of appetite, 
loss of condition, dehydration of diarrhea is severe. 

wrt dx: strongyle 
type egg. if stools are older, speciate larvae. 

toxascariasis: 
toxascaris leonina
small intestine dweller
usually not as severe as 
toxocara canis.
distribution nationwide but less common than toxocara

occurs in older pups/young adults. can become reinfected, unlike toxocara 
canis which doesn't usually reinfect a non-naive host. anterior end of 
this worm has long tapering alae. the alae are responsible for 
pathogenisis - worms swim, abrade mucosa. if eggs are ingested by a dog, 
there is no tracheal migration - goes into mucosa, hatches, and in 2-2.5 
mos grows to adult (PPP 2-2.5 mos). or, worms can use intermediate host. 
so infective stage is embryonated egg + L2 or larvae arrested in tissues 
of intermediate host. wrt clinical findings, as we've emphasized, there 
is no prenatal or lactogenic infection. doesn't occur in young puppies. 
no neonatal dz. direct development in intestine so no pulmonary disease. 
no lung migration. ingestion of eggs from environment is asynchronous, 
occurs over time. PPP long. so when worms do reach disease causing level, 
you're dealing with an older host animal and more resistant host animal

prophylaxis - free ranging animals - if you can protect against predation 
on intermediate hosts, you can gain some measure of prevention, but 
that's hard to do. fences, etc. 

dx: ovoid, unembryonated thick shelled 
smooth surfaced egg. adult worms with lanceolate anterior end. tx: 
fenbendazole et al, see handout. adult hosts fully susceptible to 
reinfection so may need to retreat several times a year to get new 
infections.

trichuriasis:
whipworm infection
remember anterior ends of 
worms are buried in the mucosa, the tails are hanging into lumen. these 
worms live in cecum and colon. the anterior ends undermine enterocytes 
and work themeselves in there doing some puncturing of cells adn 
capillaries. they cause a colitis or a typhlitis this way. diarrhea will 
alternate with normal stools. distribution is nationwide. infectious 
stage = embryonated egg in environment. no vertical transmission.  it 
takes time for eggs to be ingested and for worm burden to build up. 
infection usually becomes apparent in older animals. young dogs, older 
pups. intestine with heavy infection shows engorged blood vessels, bowel 
is flaccid and enlarged with sloughing of mucosa. egg is characteristic, 
smooth, ovoid, bioperculate. capillaria eggs similar but less symmetrical 
and pitted.
prophylaxis: as toxocara canis
check handout for more info

recheck for reinfection 3-4 mos post tx.

tapeworms: in definitive hosts, 
generally nonpathogenic. only time problems are seen is when you have a 
huge population of worms when they can cause impaction or occlusion of 
gut. except for the infections invovling the echinococcus, where a lot of 
potential tapeworms are ingested at once, the inoculum is not large 
enough to produce such a big infection. all tapeworms use intermediate 
hosts, too. so you don't see them in young animals. only after animals 
start to hunt, except for say dipyllidium which rides on fleas. 
dipyllidium, although totally nonpathogenic, is most important of these 
in practice. the suckers are blind ending, the proboscis/rostellum has 
only tiny tiny hooks. so really it doesn't cause disease. it is important 
b/c owners do not like it. Georgi says it really isn't worth the effort 
to consider these parasites as being primarily involved when animals are 
scooting. flea control is needed to control this. new spot on 
insecticides are helpful. diagnosis - ovum within egg packets of 
segments.

remember that tapeworm eggs are infective when they are 
passed. if the species is zoonotic, you or your staff will be at risk. so 
be careful! remember the stage in the egg is a hexacanth larva with 6 
hooks. if you focus up and down you should be able to see those 6 hooks 
(except in pseudophyllidean)
you can also look just at the segments - 
dipyllidium segments are biconvex. mesocestoides is rectangular, longer 
than it is wide, club shaped or baseball bat shaped. taenia is 
trapezoidal - larger segments, with lateral genital pores.

taeniasis: 

t.pisiformis or t.hydatigena, small intestine.
the armed rostellum isn't 
really that bothersome, and the suckers are blind suckers. these are also 
pretty nonpathogenic. 
t.pisiformis cysticerci form in peritoneal cavity 
of rabbit
t.hydatigena cycsticerci form in liver peritoneal cavity of 
ruminants (not the same as echinococcus, though). do not confuse them 
with echinococcus granulosus or multilocularis which are more dangerous. 
prophylaxis: avoid predation, prevent scavenging or hunting. 
dx: younger 
segments are trapezoidal to square; older segments get distorted, have 
lots of eggs/branched uteri and lateral genital pore. 

taenia egg looks 
like echinococcus egg. round. very thick shell.

cats

cats handle 
parasites more easily than dogs for some reason

remember that in cat 
there are two kinds of ascarids - toxocara cati and toxascaris leonina


toxocariasis in the feline - transmammary transmission possible. refer to 
the dog section. infective stage is L2 in milk or in paratenic host or in 
egg in environment. there is no prenatal infection/storage of larvae in 
fetal livers.
older cats often show some interesting manifestations of 
toxocariasis.  susceptible throughout life. 

in kittens, toxocara cati 
rarely causes the very heavy infections we sometimes see in pups. see 
moderate intensity infections, with unthriftiness, potbellied appearance, 
diarrhea, and thickened intestines, probably from worms swimming as 
discussed. leukocytosis with eosinophilia up to 35%.

repeatedly infected 
cats have very markedly thickened intestines, easily palpated. the 
muscular layers are hugely thickened. 
verminous pneumonia is rare but 
pulmonary arterial hyperplasia is usual.
worms can also migrate and get 
into bile ducts or other wierd places.

prophylaxis - see t.canis
deworm 
queens before partiurition to reduce environmental contamination. destroy 
expelled worms
deworm kittens at 4-8 wks, then every 6-8 wks til 1 yr 
old. dispose of expelled worms which contain a lot of eggs. 
clean litter 
pans regularly (eggs not infective when passed, need to sit, so prompt 
feces removal is very effective). clorox will remove sticky coats on eggs 
so they do not stick to litter pan or whatever.
tx: many effective 
anthelmintics; few approved in cats. febantel is probably best.
dx: 
typical toxocara egg w/pitted surface

ancylostomiasis:
ancylostoma 
tubaeforme - small intestine
distribution: worldwide in warm humid areas

no vertical transmission known, but can apear in quite young kittens as a 
patent infection, b/c ppp only about 2 wks. not likely to be pathogenic 
until larger worm burden acquired, however, from environment. 
this worm 
has three teeth per side, as does a.caninum. can cause a lot of tissue 
damage but isn't that an efficient of a blood sucker, need a lot of worms 
to cause a clinical anemia. in rare, heavy infections may see signs as in 
a.caninum. usually isnb't present in enough numbers to cause clinical 
signs. 
dx: strongyle type egg in fresh feces, L1 in 24 hr feces - 
distinguish from aleurostrongylus which has a kinked tail.

toxascariasis 
- see dog section
dipylidium caninum 0- see dog section

taeniasis:

taenia taeniaformis: larvae has tapeworm shaped body
infective stage - 
strobilocercus in rodent livers (rats, mice)
most taenias are in more 
rural animals but cats can easily get this anywhere due to urban rodent  
populations.
normal taenid life cycle
need intermediate host as in all 
tapeworms.
rarely if ever pathogenic
prophylaxis: prevention of predation

dx: finding appropriate egg in feces or gravid segments
remember all 
taenid eggs are similar so be careful; echinococcus is moving east...
tx 
praziquantel etc


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