---start parasit.9.8.97----

9/8/97
Dr Johnstone
lecture 5.

the worms 
crawl in...the worms crawl out.

The superfamily strongyloidea

remember 
there are four superfamilies of bursate nematodes in the strongylida.


the strongyloidea infect ruminants, swine, and horses. general features:

large bodied worms, easily recognized grossly. copulatory bursa present. 
most have well developed buccal capsule with teeth or cutting plates. the 
life cycle is direct except for stephanurus, the kidneyworm of swine, 
which may use intermediate hosts, and syngamus, the gapeworm of birds 
which may use a paratenic host (transport host). most females pass 
strongyle type eggs, except syngamus. parasitic phase of life cycle may 
be migratory. some of these migrations are extensive. predilection is for 
mucosal intestine, except for stephanurus (urinary tract) and syngamus 
(respiratory tract). 

three families in the superfamily strongyloidea:


* family syngamidae:

** contains genus stephanurus:
stephanurus 
dentatus: only species in this genus. is found in kidney and perirenal 
tissue of swine. Is large worm. cuticle is transparent and can see 
internal organs through it. strongyle type eggs are seen in urine of 
infected hosts.infection acquired by ingestion of L3 via ingestion and of 
L3 infected earthworms, or by skin penetration of L3, and maybe by 
prenatal infection
remember predilection site is the kidney so this life 
cycle calls for migration from gut to kidney
L3 migrate to mesenteric LNs 
and molt to L4. then they go to liver by portal system or systemic 
system. then they molt to immature adults, and wander for 3+ mos (causing 
pathologic effects). then they migrate across peritoneal cavity into 
kidney. they either penetrate kidney at hilus or become encased in 
perirenal cyst. prepatent period is long - up to 19 mos. dx: strongyle 
type eggs in urine, necropsy. remember the prepatent period is really 
long, so you have to wait for pig to be at least 6 mos old before infxn 
is patent - so this is usually dx'd at meat inspection - eg, will see 
liver cirrhosis.
most of parasitic phase occurs in liver and that is 
where we see most pathology.

** contains genus syngamus
syngamus 
trachea: find in fowl, game birds esp pheasants. predilection site: 
bifurcation of the trachea. one interesting thing about this worm is that 
the males and females live in a state of permanent copulation. this is 
the one thing you will remember forever from parasit, and if you get this 
wrong on the test you fail no matter what. females have a reddish cast 
and clear cuticle so can see massive ovary packed with eggs.

how do 
birds get infected? assume it is. bioperculate eggs are laid by adult 
worm. eggs are coughed up and swallowed and passed in feces of host. L3 
develops inside the egg. sometimes eggs hatch. sometimes transport hosts, 
eg earthworms, snails, slugs - are used, but still direct life cycle 
because you don't have to use transport host. worm uses those to improve 
chances of being eaten by host. host can acquire infxn by ingesting 
hatched freeliving L3, L3 containing eggs, or infected transport hosts. 
worms exsheath in duodenum, migrate to lungs, mature, move to trachea and 
live. prepatent period only 12-17 (or 18-20 days, depending on book...) 
days. in young birds, migration through lungs may cause pneumonia, 
bronchitis, death.

disease: tracehitis: gaping, gasping, coughing. much 
more severe in young birds. causes severe hemorrhagic tracheitis with 
some obstruction of airways and difficulty in breathing. dx on clinical 
signs, necropsy, and bioperculate egg in feces.

CHECK THE WEB SITE!! i'm 
feeling tired and slow and am concerned about getting everything he says.


the egg is fairly thin shelled, and has operculata at both ends.

family 
chabertiidae contains genera chabertia and oesophagostomum.

chabertia 
ovina is found in colon of sheep (sometimes goats, cattle). fairly 
widespread through world, uncommon around here. easy to ID. 1.5 - 2 cm 
long with prominent buccal capsule shaped like a bell. no teeth. 
pathogenic effects are caused mainly by use of buccal capsule. adult 
grabs plug of colonic mucosa and digests it, leaving an ulcer. bleeding 
and protein loss occur.

oesophagostomum - members of this genus called 
"nodular worms" because they cause nodules in intestines of hosts. four 
species of importance

radiatum (cattle)
dentatu (pigs)
comubianum 
(sheep/goats)
venulosum (sheep/goats)

these are the ones with the ornate 
cuticular inflations at head end. males have copulatory bursa. worm is 
about helf as long as a pin, 1-2 cm long. buccal capsule is present but 
shallow. females pass strongyle type eggs. 

preparasitic phase - 
typically strongyle type. free living larvae, infection by ingestion of 
ensheathed L3.
parasitic phase - exsheathing in small intestine. L3 
penetrates mucosa, molts to L4. L4s emerge, pass to colon. the 
penetration of mucosa causes pathology. prepatent period is 45 days. this 
is what happens in a first infection. molt from L3 to L4 happens within a 
nodule. larvae may remain arrested as L4 for up to a year. in heavy 
infections, serious problems are due to penetration of intestine and 
diarrhea. nodules may be very hemorrhagic. the nodule is a host response. 
L4 emerge and get into lumen. in older animal you will see white, fibrous 
looking nodules. in young animal w/acute infection you might see diarrhea 
but not eggs in feces, because diarrhea is caused by L4 erupting from 
nodules (not patent infxn yet). in older animal, colon loaded with 
fibrous white nodules. animal will have intermittent diarrhea, and a few 
adults passing strongyle type eggs into feces. these nodules reduce 
absorptive area of colon. pathogenesis almost entirely related to 
production of nodules.

family strongylidae has two subfamilies: 
strongylinae and cyathostominae. all are strongyles of horses. the 
subfamily strongylinae has two genera: strongylus and triodontophorus. we 
will ignore triodontophorus. there are three strongyle spp we will 
review: vulgaris, equinus, edentatus. the cyathostominae contains many 
genera, all having same basic life cycle. these are the small strongyles 
and we will discuss them as a group as the cyathostomes. back to large 
strongyles. all three spp found in cecum and large colon of horses and 
donkeys.

life cycle of strongylus spp - we will review s. vulgaris 
specifically, but all three spp have similar versions. all have strongyle 
type egg. infected egg shed, hatches, L1 molts to L2, molts to L3, is 
ingested, exsheaths in the host.
then, for s.vulgaris, after 
exsheathment, L3 penetrate intestinal mucosa, molt to L4, enter 
submucosal arteries, migrate to root of cranial mesenteric a. by 21 d 
post infxn. here they grow for 3-4 mos. they molt to L5 there, then turn 
and go back down arterial tree to the serosal surface of cecum or colon. 
then the host produces a rxn around them on the serosal surface, forming 
a nodule, which later ruptures on the mucosal side, allowing adult worm 
to get into cecum or colon. this prevents peritonitis - nodule forms, 
seals off behind worm, then ruptures only inside gut. prepatent period 
6-7 mos.

s.equinus: more complicated life cycle. less common worm. L3s 
exsheath in mucosa, molt to L4s in nodules. L4s migrate to liver directly 
(through peritoneal cavity) and stay there 6-8 weeks. then they migrate 
to pancreas, and molt to L5s about 16-17 wks post infection. we know they 
go back to lg intestine but don't know how. prepatent period 8-9 mos. 
strongyle type eggs.

s. edentatus; L3 ingested by host. exsheath in sm. 
intestine. migrates to liver via portal vein. molts to L4. migrates under 
abdominal peritoneum to flanks. molts to L5. returns to large int. and 
forms nodules. nodules rupture and adult worms get into lg intestine.
ppp 
11-12 mos.

note: the nodule is basically a foreign body reaction by the 
host to the parasite. one thing parasites do to evade host responses is 
to coat themselves with host antigen. this hides parasite from immune 
response - antigenic mimicry - sometimes will see blood cells sticking to 
worm, or something. this is how worm is able to migrate to Lg intestine, 
then it stops mimicking so it does provoke foreign body rxn. or something 
like that. remember - parasite doesn't want to kill the host. it might be 
antigenic enough to provoke foreign body response, but not antigenic 
enough to get itself killed.

the large strongyles - pathogenesis. 

because of their life cycles, they have a prepatent phase, a larval 
migration phase, and an adult phase. so pathogenic effects are grouped 
into prepatent disease due to migrating larvae, and patent disease due to 
adults. prepatent disease has worse effects.

s.vulgaris is most 
pathogenic of the strongyle spp, due to prolonged migration in mesenteric 
aa system. larvae disturb endothelial linings, causing thrombi to form. 
with repeated infections and chronic insult to the walls of these 
arteries you also get degeneration of elastic fibers and dilation of aa - 
aneurysms form. usually you find an accumulation of clots and L4, which 
break off and block off whole parts of the arterial tree. major cause of 
colic and death.

if you look at the adults, all have a similar 
pathogenesis - they all feed by chomping onto the mucosa and digesting 
it. it leaves a bleeding crater which ulcerates, then heals into a scar.


small strongyles: the cyathostominae. there are many species - 30 to 50 
of 'em. we're just going to call them the small strongyles. they have 
identical pathological effects and life cycles. size: 6-22 mm. they have 
small buccal capsules. pathogenic effects due to parasitic phase is very 
small compared to large strongyles. these are still highly pathogenic 
nematodes. while there is no migration, the preparasitic life cycle is 
identical to large strongyles.
L3 exsheath and then penetrate mucosa of 
lg intestine. they become L4, molt to L5. hypobiosis occurs at early L3 
stage, though -after they exsheath and get settled in the mucosa. they 
encyst as L3 and overwinter in the intestinal mucosa. in spring/summer, 
they molt to L4, emerge into gut lumen. prepatent period varies with 
species. so when thousands of these larvae emerge at the same time you 
have a dramatic effect. 

note: 98% of strongyle type eggs in horses are 
from small strongyles. 
the larvae have overwintered. then they develop 
in waves. new eggs are laid. we see a big rise in fecal egg count in 
spring/summer. the eruption of lg numbers of the arrested larvae across 
mucosa cause acute diarrhea and colic routinely in the spring. 
unfortunately, many of the anthelmintics we use are not effective against 
arrested L3. only fenbendazole (panacur) (7.5 mg/day x 5 days) will kill 
95% of arrested L3. it won't kill the adults, though. most adults have 
become resistant to these drugs. you have to mix drugs together, or give 
consecutive treatments, or something.
------

9.8.97
3 pm
dr schad


HOOKWORMS

we've been going on about the STRONGYLIDA, the bursate 
nematodes. we went over trichostrongyloidea and strongyloidea. here is a 
suggestion: as you study these worms, do not try to learn all the facts 
about each species - learn about the main category, then learn the 
exceptions.

handout: hookworms, hookworm infections, and hookworm 
diseases

STRONGYLIDA characteristics in general:
* GI Parasites (some 
exceptions eg kidneyworm,lungworm, gapeworm)
* strongyle type eggs 
(exceptions: gapeworm et al)
* egg exits in feces (most of them)
* L1 --> 
L3 in outside environment

generally speaking, worms in this group have 
three larval stages outside the host, and the ensheathed L3 is infective 
form. the sheath helps L3 to avoid environmental chemicals and stuff. 
it's hard to kill the larvae out in the environment.

STRONGYLOIDEA- 
group to which hookworms belong
* has above characteristics
* mouth 
capsule
* plug feeders - some of which suck blood

ANCYLOSTOMATIDAE 
(hookworms, jointed stoma worms)

* has characteristics of strongylida 
and strongyloidea
* head end bent (hence HOOKworm, some people say) to 
the dorsal side
* oral cutting plates/teeth
* bloodsuckers (some, not 
all)
* often skin penetrators
* then migrate to intestine via circulation


slide: puppy gut with worms attached. hemorrhage obvious.

some of the 
blood lost in hookworm disease wells up around the worm and isn't 
actually sucked into the worm. the worms are very voracious. they 
actually pump the blood through and blow it out their ani. ancylostoma 
caninum is very nasty.

* transmitted via soil - geohelminths - because 
infective larvae found in soil
* infective larvae are ensheathed L3


SUBDIVISIONS:

group having oral cutting plates: all ruminant pathogens 
fall into this category
 
* bunostomum phlebotomum in cattle
* bunostomum 
trigonocephalum in sheep and goat
* uncinaria stenocephala in dogs and 
cats - a very common parasite in the fox which occurs more in dogs in 
semirural/rural areas. often called "northern dog hookworm" found ranging 
from arctic north as far south as georgia. seen in sled dogs (sledge 
dogs?)

group with teeth: (a.= ancylostoma)

* a. caninum - common k9 
hookworm - most common. three teeth per side
* a. tubaeforme in cats - 
also 3 teeth/side, also widespread.

neither of above seen in arid parts 
of country eg Utah, Nevada.

* a. braziliense- in cats and dogs - more 
tropical species. in US ranges across gulf coast. not a bloodsucker. 
produces diarrhea and so forth. major importance in human parasitology - 
zoonotic. "creeping eruption" - larvae migrate in skin and leave itchy 
raised track.

HOOKWORMS OF RUMINANTS:

B.phlebotomum and 
B.trigonocephalum. do best in warm, wet areas eg gulf coast of texas, 
Louisiana, Florida. wet warm summers in NE US as well. is a parasite of 
some importance in dairy calves raised on manure packs or hutches esp if 
hutches aren't moved. another good environment is the feedlot.

life 
cycle of Bunostomum spp:
* eggs pass in feces, hatch in environment, 
-->L1-->L2-->ensheathed L3 -->eaten by cow or penetrates skin of cow, 
exsheathes migrates into circulation, carried to lung, breaks into 
alveoli, moves up into trachea, gets coughed up, gets swallowed. 
prepatent period is long at 4-8 wks. L4 is an avid bloodsucker
as well so 
you can have clinically significant prepatent disease - anemia may set in 
before eggs are found in feces. the freeliving larvae take 3-5 days to 
become infective in warm moist summer weather.

pathogenesis:

1. skin 
penetration phase
2. respiratory phase
3. intestinal phase

the migratory 
pathway often called "tracheal migration" - see p 6 handout on tracheal v 
somatic migration. 

one reason to learn about life cycle is to organize 
knowledge and try to figure out pathology. so these larvae migrate 
through lungs and may cause pathology there if enough larvae are moving 
at the same time. in intestine can have disease with lower levels of 
parasite than it takes to cause disease in the lung. the bloodsucking of 
L4 and adult can cause anemia, iron deficiency, edema, diarrhea, 
dehydration.
skin penetration phase - when conditions are favorable 
(warm, wet, numerous larvae) will see cattle stamping, licking legs - 
manure splashes on legs, and larvae migrate into skin - animals tend to 
be restless and unthrifty. the respiratory phase can cause a pneumonia if 
infection is heavy. intestinal phase - big thing is worms attaching to 
mucosa and plug feeding, and sucking out blood.

hookworm anemia is 
really a pure iron deficiency anemia. associated with this is edema, 
diarrhea, dehydration. in ruminant, edema often manifests as "bottlejaw"


diagnosis: strongyle type eggs in feces - except w/prepatent disease. 
necropsy.

HOOKWORMS OF DOGS AND CATS

Ancylostoma caninum:
three teeth 
on each side, really scary looking vampyric worm :)

life cycle of 
a.caninum:
many alternatives available :)

adult worms in small intestine 
feeding on mucosa, sucking blood, blunting villi, laying eggs: egg passed 
in feces...L1..L2...L3. infective ensheathed L3 penetrates skin or is 
ingested. remember L3 is susceptible to dessication. takes 5-10 days to 
become infective, btw, in summer. in winter, at this latitude, there is 
no freeliving larval development. but worms can overwinter in host in 
hypobiotic state. so, ensheathed L3 enters host via skin or mouth. if 
they come in through mouth, go directly into intestine, go into mucosa 
for a short distance, come back out into intestine. no tracheal 
migration. those entering through skin migrate to lungs as before, via 
circulation. then what happens is related to age of animal and 
resisstance, natural or acquired. in young animal, larvae will do the 
tracheal migration we discussed. in older animal, esp older females, 
worms do not leave circulation in lungs, but rather continue, reach 
musculature, and become arrested there. this is somatic migration. they 
become encysted in muscle tissue. wait, they aren't encysted. they are 
just coiled up. they are largely benign at this state. they're not 
causing disease here. now, these larvae, at parturition, will migrate to 
mammary tissue and be involved in transmammary transmission. so these 
activated worms can be passed in milk. from 1-3 weeks postpartum the # of 
larvae in the milk rapidly drops off. eg, huge spike at parturition, then 
by week 4 they're almost all gone. but if you dose mom with estradiol and 
progesterone, you can induce another spike. it's probably the hormones of 
parturition/lactation whch activate these larvae. note: larvae are not 
all gone despite the drop off in numbers which pass in the milk. the next 
pregnancy and lactation will produce more spikes despite isolation of 
bitch from reinfection. spikes will get smaller though, unless 
reinfection eventually occurs. if reinfection does occur, bitch will not 
be resistant to this kind of infection.

prenatal transmission - if you 
look at some old literature they thought this was a big deal. now they 
think only about 2% of larvae found in a new puppy got there prenatally. 
very little transmission across placenta. 

transport host/paratenic 
hosts: man is a dead end transport host - but mice can host hookworm 
larvae in their musculature for their whole lives. the arrested larvae in 
the tissues don't age. they just sit there. then if a dog ate the mouse 
it would be like eating the larvae directly and dog would develop 
disease.

you could substitute an insect for the mouse as well...

ppp 
depends a lot on age of animal. 14-21 days is often cited in literature. 
depends on resistance factors. ppp is foreshortened in mammary and 
prenatal infxn - can be as short as 11 days.

ok. a word about some of 
the other spp at this point. 

*** prenatal and transmammary transmission 
occur only with a. caninum. the other species only have oral or 
percutaneous transmission.

ok. hookworm diseases...
some spp are 
bloodsuckers, others are not. diseases differ.

a. caninum: a 
bloodsucker. before it becomes a bloodsucker, while entering the host, 
can cause a hookworm dermatitis if it is abundant. this doesn't happen a 
lot in the US but has been described often in europe, where interdigital 
spaces may show tracks, penetration points, etc, and dogs may be itchy, 
bite feet, etc.
respiratory phase may be seen in laboratory induced 
infections but are not seen clinically in nature. in human, respiratory 
phase is well described, proabably because people whine more :)
when we 
talk about this dz in dog, mostly we're talking about anemia. to see 
anemia there must be a bloodsucking species, which a.caninum is. remember 
that being parasitized doesn't mean having a disease - number of 
parasites is a factor, age/size of animal, etc.  so if there are enough 
worms to overcome host defenses and they suck a lot of blood you will see 
iron deficiency anemia.

hookworm anemia - break down into newborn, older 
animals, mature/resistant animals 

if you have heavy transmammary infxn, 
can see acute hemorrhage into intestine as the worms reach adulthood 
between 5-7 days from first blood meal, puppies go downhill fast. it's 
hard to save these puppies.

in more resistant or somewhat older animal, 
you have blood loss starting at about 6-7 days, and eggs appearing in 
feces at about 17 days. this animal will become anemic, may shed some 
eggs, but will eventually compensate for blood loss and survive if on 
adequate diet with iron and protein. these animals will be anemic for a 
period of time, and have diarrhea, but we don't see acute fatal anemia 
like in puppy.

in animal which has seen the parasite before it will 
shunt larvae off into somatic route. then you do not see the frank 
hookworm anemia. another factor is that beginning at about 8 mos in 
female or 11 mos in male, even w/o prior exposure, dogs begin to shunt 
more larvae into the somatic route. you can see hookworm anemia in older 
animal, but is less common.

a.braziliense and uncinaria stenocephala do 
not suck blood but cause malabsorption, enteritis, diarrhea (as do the 
bloodsuckers as well)

all the hookworms cause blunting of the villi, 
loss of absorptive surface, loss of tissue fluid and protein.

a word 
about a. tubaeforme - we don't understand the reason - here's another 
hookworm looking a lot like a. caninum - but it doesn't have transmammary 
transmission. it rarely causes a frank anemia in cats. someone estimated 
it takes 200 worms to cause anemia. that's a lot of worms. not 
impossible, but it's a lot of worms. so cats do have hookworm infxns and 
diarrhea, but would hav to have a really heavy load to cause an anemia.


wrt the diagnosis and treatments: pyrantel pamoate, mebendazole, 
fenbendazole
dx: strongyle type eggs in feces

see handout for rest of 
details.

----end----