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parasit 
9.10.97
dr schad


ASCARIDOIDEA (small animal) 
(roundworms)

nematoda -class
ascaridida -order
ascaridoidea -superfamily

ascaridae -family

if you talk about ascaridoid nematodes as "rounds," 
lumping them together, you lose information, and in this litigious 
society, if you don't distinguish between species esp wrt zoonotic 
potential, you may be vulnerable to lawsuit. so don't lump them all 
together under the name "roundworms"

we've arrived at this group 
now...they're large nematodes which lack bursae

today we'll talk about 
the whole group of ascaridoidea, and talk about small animal species.


these are lumen dwellers. they occur in all vertebrates. they do not 
attach to the gut like hookworms, they don't burrow into mucosa. they 
aren't in close association with the mucosa as is hemonchus. they are 
LUMEN DWELLERS that maintain position by swimming, and the swimming 
abrades the intestinal mucosa and causes the disease/pathology in the 
host.

thick walled eggs, unlike the other eggs we've seen so far. the 
eggs are UNembryonated - they have not undergone enough cell division to 
see the larval form within the egg yet. in these worms, the eggs passed 
in the feces do not embryonate until they pass into environment. 
infection is by ingestion of embryonated egg containing infective L2 
larva. 

parasitic development involves tracheal migration (sole 
migration in large animals) and may also involve somatic migration (in 
small animal species). paratenic hosts are commonly used by speies 
occuring in carnivores.

adult worms are large, thick, with three large 
fleshy lips often with denticles. these worms can be 15 inches long and 1 
cm thick!. definitive hosts include diverse aquatic and terrestrial 
vertebrates.

slide: some worms of the genus ascaris. they look like 
white spaghetti with tapered ends. male has curled tail, female is larger

slide: pile of toxocara canis - looks like whole pile of spaghetti. adult 
females grow to about 8 inches long.

slide: head of worm showing the 
three lips and the esophageal opening. can see denticles along one of the 
lips. will abrade surface of mucosa as worm moves around. off to the side 
we see alae, thin serrated projections of the cuticle.

slide: egg. thick 
shell with a large round mass inside. shell isn't smooth - is kind of 
pitted and rough looking.
slide: infective eggs - embryonated.

so there 
are no freeliving larval stages in the ascaridoidea.

ASCARIDS OF SMALL 
ANIMALS

toxocara canis - dog
toxocara cati (mystax) - cat
toxascaris 
leonina - dog, cat. occurs with the other two. 

the worms are in these 
thick shelled eggs when in the environment, so they are more resistant to 
environmental factors than the other worms we've discussed. they have a 
wide geographic - in fact global - distribution.

in the handout we 
include baylisascaris procyonis and columnaris, seen in north american 
wildlife. these spp are involved in larva migrans in people. is mostly in 
the raccoon, but b.procyonis has been recently observed in dogs. 
frequency in dogs unknown. this is because most vet practices do not 
speciate ascaroid spp. but the larvae of this worm is highly neurotropic 
in the non-definitive host, migrating to spinal cord and brain and doing 
a lot of damage.

slide: some morphological characteristics of these 
worms. t.leonina has long thin, tapered alae, and t.catae has shorter, 
broader alae which end bluntly.
t.canis looks very very much like 
t.leonina at the alar portion, but has pitted eggs, whereas t.leonina 
eggs are smooth. also, in the male, t.canis has a constriction distal to 
the spicule, and t.leonina does not. 

if you don't already know you 
should learn that these worms will emerge from the body spontaneously, or 
during fever. they may come out of the anus, or may migrate up the gi 
tract and exit from the mouth.  you can impress the owners by recognizing 
the difference between the species when they bring you the worm. 

these 
worms can also get into the bile duct or pancreatic duct and do 
unexpected damage. 

scanning EM of eggs: you can see the pitted surface 
very clearly on the t.canis eggs

LIFE CYCLE OF TOXASCARIS LEONINA
this 
one is the simplest life cycle. it is a mixed life cycle, or indirect 
life cycle.

* embryonated egg is ingested
* hatches and releases L2 
which invades intestinal wall

-if inside intermediate host, say, a 
mouse:

* worms undergo somatic migration- larvae move in circulation to 
the liver, lungs, to the tissues so they are disseminated into tissues 
and encysted where they develop to L3 (that's why this is intermediate 
host - developement occurs.)
* predation of infected intermediate host by 
cat/dog

* L3 takes up life in lumen of cat/dog gut
* L3 grows into L4
* 
adult - PPP 7-10 wks, survives 5-10 mos

-if egg ingested by dog/cat:

* 
no migration
* intestinal tissue phase (L2-->L3)
* return to lumen
* 
growth into adult
* PPP 7-10 wks, survives 5-10 mos

SO t.leonina is 
NEVER clinically important in very young animals!!

and, there is no 
somatic or tracheal migration in the dog or cat. therefore there is no 
transmammary or transplacental infection.

LIFE CYCLE OF T.CATI

* 
embryonated egg ingested
* hatches and L2 invades stomach

IN MOUSE 
(paratenic host)
* somatic migration
* encystion in tissues as L2 (so not 
intermediate host)
* feline predation

BACK IN CAT:
* enters stomach or 
intestinal wall (L3)
* enters lumen as L3 or L4
* grows into adult

If 
originally eaten by CAT, with NO PARATENIC HOST:

* tracheal migration
* 
returns to stomach via liver, lung, bronchial tree (L2)
* then goes to 
"back in cat" part of cycle

alternative routes: transmammary 
transmission, which implies somatic migration. prenatal infection not 
known to occur. 

so these larvae reach intestines as L2 then encyst in 
wall of intestine, and we see nodules in wall of intestine. 

LIFE CYCLE 
OF T. CANIS

* embryonated egg ingested
* hatches in intestine (L2 
released)
* migrates to liver
* migrates to lung of host.

IN YOUNG PUPS 
(under 5 wks)

* vast majority continue with tracheal migration
* L3 
migrates to stomach
* L4 develops, goes to intestine, becomes adult

IN 
OLDER PUPS OR MATURE DOGS

* more of the larvae undergo somatic migration 
after reaching lung
* dissemination to and encystation in tissues (L2)
* 
transplacental migration in females
* pregnancy: invasion of fetal liver 
(L3) --birth-->lung of neonate (see above)

so in pregnancy, worms are 
stored in fetal liver. at parturition, the larvae migrate to the lung. 
this has obvious implications for pathogenesis. 

PPP about a month, if 
the infection goes directly from ingestion on in young pups. if there is 
prenatal infection, it takes only about 21 days for eggs to appear in the 
feces.

there can also be transmammary transmission. also, mouse can be 
used as paratenic host as t.cati does. 

so these are very successful 
species. not so long ago, some studies done by the CDC found that in some 
practices as many as 80% of dogs 2-6 mos old had toxocara infections. 
Fewer than 20% of dogs over 1 yr were infected. figures are lower in this 
area and in dogs which get regular care. dogs will lose these infections 
with time. will self cure in a matter of months.  EXCEPTION: the 
greyhound, which will harbor the worm and remain susceptible to infection 
without developing age resistance.

so, what we see here in this species, 
t.canis, is that the larvae are stored in liver of feti and that birth is 
a synchronizing event which lets a whole bunch of them into the lungs 
ofthe neonate at the same time. so this can cause pathology. so in the 
case of t.canis infxns of the dog, one does see pulmonary toxocariasis, a 
verminous pneumonia. this isn't seen with t.cati where there is no mass 
migration or t.leonina, where larvae never go near the lungs


distribution of t.canis larvae in 6 2 month old pup littermates. early in 
infection many larvae are in liver and some in lungs. they accumulate in 
skeletal muscle as time goes on, and at that point they are not very 
pathogenic. arrested larvae in the muscle are of minimal consequence 
clinically (more important epidemiologically). in these puppies, very few 
went to GI tract.

PATHOGENESIS AND DISEASE

we already discussed 
pulmonary dz as consequence of t.canis.

INTESTINAL ASCARIASIS -  

can 
see massive abdominal bloating of puppies. clinically, ascariasis is seen 
in young pups and kittens. there's wt loss, vomiting, dehydration, 
possible death. depends on wormload. infected animals might be anything 
from clinically healthy to near death. the worm movements are the basis 
for enteritis, so there's vomiting, diarrhea, which leads to matting of 
coat, unkempt looking animal, there may be anorexia, etc.wen many worms 
are present in the intestine, this is painful and animal may be noisy. 
older animals become resistant and lose their worms but the greyhounds 
remain susceptible for life. 

acute conditions: a large population of 
ascarids can occlude the gut and cause rupture, leading to peritonitis.


ascarids can migrate into bile duct and occlude it and cause bile stasis 
and jaundice. to drive home this point about migration...here's an 
anecdote from many many years ago. dr schad's professor told this story 
about HIS professor, Liepert, from london school of tropical medicine, 
who was a fellow of the royal society (like nat'l academy of science 
here). so, prof Lieper(T?) went to a chicken yard to pick up some chicken 
feces to do a coccidia study. he and a student were bent over scooping up 
chickenshit. As the professor bent over, an ascarid came out of his nose 
or mouth and fell to the floor. Apparently, he'd acquired an infection a 
while ago. So the student who was with him wanted to save the worm - but 
the chickens ate it. oh well.

diagnosis is by clinical signs and seeing 
ova in feces. 
remember toxascaris leonina has a smooth shell. 


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