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parasitology
9.17.97
Dr. Lok
lecture 12

superfamily 
Spiruroidea and introduction to superfamily filaroidea
(handout)


so 
far, with the exception of one group, we've been talking about nematodes 
which mostly inhabit the GI tract, either lumen or mucosa - and most of 
these parasites have direct life cycles, only one host, and fecal/oral 
route of infection.

the exceptions to that would be the metastrongyles 
(lungworms) which use mollusck or anelid hosts as well.

today we're 
going to go into two superfamilies which are different. the spiruroidea 
and filaroidea.

notice three evolutionary trends these worms go through


1. use of arthropod intermediate hosts or vectors.
2. these particular 
groups also opt out of the GI tract as predilection site, and move into 
other tissue sites.
3. rise of vivparity - giving birth to live young 
instead of oviparity - laying eggs.

we'll also see worm progeny residing 
in peripheral tissues of host instead of host feces - an adaptation to 
use of bloodsucking arthropods as vectors.

the group we're starting with 
is the spiruroidea. three main genera:

spirucerca - dogs

habronema/draschia - horses
thelazai - interesting parasites.

getting 
right into it.

Spirucerca spp: adults are fairly large, reddish, often 
seen coiled up.
are found in large nodules in esophageal wall or anterior 
gastric mucosa. these nodules kind of communicate with gut lumen via a 
fistula - can see worm hind end protruding into lumen through fistula. 
females lay eggs into lumen this way. egg stage is diagnostic. seen in 
dogs and infrequently cats. only about half the size of a strongyle egg. 
thin shelled, parallel sided, containing vermiform embryo. might call 
this "larvated egg." when you see this in fecal float, it looks a bit 
like a paperclip (um, not on this slide it doesn't!). this parasite is 
found mostly in subtropics and tropics but has been found as far north as 
CT, USA!

spirocerca lupi: dog (or cat) passes eggs in feces. feces 
passed into environment and different invertebrates break it down. 
coprophagous beetles ingest the eggs of s.lupi, and eggs hatch and 
develop through L3 inside the beetle. this is an obligatory event in the 
life cycle of spirucerca spp. this is the obligatory use of an 
intermediate arthropod host. now you have the beetle harboring L3 
infective larvae. beetle will be eaten perhaps by dog or cat, resulting 
in infection of dog or cat, but usually insectivores eg rodents, 
chickens, reptiles, or whatever, will eat the beetle, adn then become 
paratenic hosts which are then eaten by definitive host. in paratenic 
host, L3 encysts within tissue. 

note the predatory prey relationship 
between definitive host and paratenic host.

what happens next? L3 
penetrate stomach wall of host and migrate by way of celiac artery into 
thoracic aorta, then they go back anteriorly and cross into the lumen of 
the esophagus somehow. this takes about 3 mos. back in esophagus or 
anterior stomach, that's where larvae invade the mucosa and form nodules, 
adn grow into adults which takes another 3 mos. so PPP is about 6 mos 
total for spirocerca.

spirocerca spp cause some pretty bizarre 
pathology. remember you can infer pathology from life cycle. one of the 
first things you see in these dogs is damage to intima of thoracic aorta. 
the lumen isn't silky white anymore. it has a lot of round, raised, pink 
to red lesions caused by migrating larvae.  frequently these result in 
aneurisms in the aorta. obviously if the adults are inhabiting golf ball 
sized cysts in esophageal lumen, this can cause dysphagia, obstructive 
disease - blockage of esophageal lumen occurs sometimes. note: can have 
many worms in one nodule.

so far things make sense - but, we also see 
stranger stuff. these cysts in the esophageal lumen and stomach can 
undergo a neoplastic like transformation. the parasite can cause 
formation of fibrosarcoma in intestine. this is rare - parasites are not 
usually responsible for malignant transformation! these tumors can then 
metastasize to the lung or wherever.  further evidence that the parasite 
is elaborating a soluble mutagen into host tissue is the changes we see 
in thoracic vertebrae - bony outgrowths, spondylosis - also see problems 
in leg bones aka long bones.

slide: large nodules on chest xray. one 
main diagnostic aid. also diagnose by seeing egg in feces

control: keep 
dog from eating paratenic hosts harboring L3. indoor dogs have reduced 
risk. can avoid feeding uncooked offal from free ranging chickens.


treatment - diethylcarbamazine or something else.

quick recap: 
spirocerca
first we see infection by ingestion of infected intermediate 
*or* paratenic host
bizarre migratory pattern through celiac 
artery/thoracic aorta, nodules in esophagus. can see metastatic 
fibrosarcomas. 

next parasite: quick mention of gongylonema- large 
worms, reddish. similra in terms of life history to spirocerca. uses 
coprophagous intermediate host (dung beetles). final host ingests 
intermediate hosts. this is a fairly benighn parasite. is found oftenest 
in cow. can be seen in any mammal. if you do lg animal pathology you'll 
see them frequently but they're usually incidental. don't cause clinical 
disease.

habronema/drachia - parasites in equine stomach. 
life cycle: 
adults in stomach, lay eggs which hatch into L1 in feces. eggs are 
embryonated when they are layed and they hatch nearly immediately. fly 
larvae ingest L1s. L1s grow to infective L3 at about the same time the 
fly larvae emerge from pupae. fly puts L3s near mouth, lips of horse, and 
on cutaneous lesions. host licks lips and swallows larvae which mature to 
adult stages. larvae left  on cutaneous lesions will stay there. the 
files deposit the L3s as they are feeding, btw.

so there's a subtle 
change in relationship between final host and intermediate host. ehre it 
is reverse. the intermediate host is predating the final host. the 
intermdiate host is now a VECTOR _ an intermediate host with directed 
action toward the final host.

[whoo boy am I sleepy!]

larvae that are 
ingested by horse will be able to complete their growth to adultyhood in 
stomach of horse. L3 which didn't get put near there will not grow or 
anything. but they do cause a lot of pathology.  we call it "summer 
sores" or "swamp cancer" because it is worse in the summer when there are 
more flies around. often we see it on the face - "cutaneous 
habronemiasis". 

slide: cutaneous habronemiasis on face and legs of 
horse. they do a lot of damage to horse skin. also sometimes larvae are 
deposisted at eye area. sometimes you see ulcers near the medial canthus.


dx: noticing egg stages - very small larvatedeggs seen in feces. at PM 
see the nodules ont he stomach wall. tx o cutenaous lesiosn is by 
ivermectin therapy - some other things also work. steroids topically to 
lesion will usually help it resolve.

prevention and control: proper 
manure management to keep fly load down, stacking manure so heat kills 
larvae. good wound practicies - keep 'sm covred.

mild stomach pathology 
from adults. main clinical concern cutnaeous lesions due to L3 put onto 
the horse. 

mostly transmitted by fly depositing egg near horse mouth.


thelazia: 
slide: eye o dog containing t.californiensis. can see worm on 
cornea. this parasite is found in birds, mammals, etc. t. california is 
seen most often.

adult stages never found in GI tract. whole show 
involves eyes. eggs get into lacrimal fluid and hatch in lacrimal 
secretions.  L1-L3 growth occurs in the fly. later L3 will depsit eggs on 
eye. insect vector.

[note - seehandout. i am literally falling asleep]

this is not an important parasite. can see tearing and photophobia. dx is 
by recognition.

tx - ivermectin drench. some benzomitazoles. 

causes a 
little ocular pathology, that's all. is important biologically to 
complete evolutionary change into non-GI tract parasite which uses 
arthropod vector.

next - filarioidea:
best example of this is 
dirofilaria immitis - dog heartworm, which we will talk about tomrrow in 
detail. today we will talk about other filarid worms.

genera: difilaria, 
dipetalonema, onchocerca, setaria, stephanofilaria

note in the handout, 
the names of some genera in bold type. those are the ones we haev to 
remember. there are many species names we do not have to know, but the 
names of hte genera are very important.

filarids are long, slender 
nematodes, up to about 30 cm for a female adult.  we saw a lot of wild, 
jazzy looking nematodes within the ascaridoidea. these worms today are 
nondescript. no papillae, etc. life cycle involves obligatory blood 
feeding arthropid vector. we never find these parasites in GI tract of 
final host. other nematodes have oviparity. these give birth to live 
young! eggs hatch IN the uterus. motile embryos, called microfilaria, are 
born. in some species, microfilaria don't actually break the egg 
membrane, but just stretch it. microfilarai get into peripheral tissue of 
host, or blood. some go out into skin. there are many places these can go 
to be picked up by blood feeding arthropods.

filaria that cause dz in 
humans:

hundreds of millions of people worldwide affected. Lymphatic 
dwelling filaria are pan-tropic in distribution. includes wuchereria and 
brugia. L1-L3 occur in mosquito vector. microfilaria are found in 
peripheral circulation. this causes a spectral disease in 
humans/primates. lung dz, pulmonary eosinophilia, but mainly the best 
known thing is elephantiasis - huge lymphadenopathy, caused by adult 
stages of these worms in lymphatic duct of host.

skin dwelling filariae 
eg onchocerca volvulus. also limited to tropics, but only african and 
american.not seen in asia.vectors are black flies. microfilaria are found 
in skin where they are picked up by black flies. L1-L3 in the fly. causes 
ocular and skin dz in humans. adults are found in subq nodules. adult 
stages cause unsightly and uncomfortable nodules (which contian the adult 
worms, up to 20 cm in length, coiled up. the microfilarial stage is more 
important- migrates through skin and can cause dermal atrophy, pruritic 
papular dermatitis due to collagenase release and inflammatory response, 
eosinophilic infiltrate, etc. also see depigmentation of skin, and 
sometimes we'll see some lymphadenopathy in extremities similar to the 
elephantiasis but not as bad. if microfilaria invade eye - can get in 
cornea and cause punctate or progressive sclerosing keratitis and 
blindness, or can cause retinopathy and blindness. in some areas in 
Sudan/Savannah region of west africa, almost all adult males who work in 
fields are blinded by these parasites and are led around by little kids. 
there are treatments for this, the treatment of choice is ivermectin. 
(one of the few times where a veterinary drug was borrowed by MDs to 
treat a human medical problem...was just licensed as Mectazan for human 
use about 6-8 yrs ago and is now being distributed through areas where 
this parasite is endemic. 

re: elephantiasis: it can resolve when worms 
go away.

look at onchocercidae of animals section in notes - 
o.cervicalis is a parasite of horses with similar life cycle to human 
pathogen o.volvulus. it has a microfilarial stage in the skin as well. it 
has been incriminated as cause of skin dz in horses - nonseasonal 
pruritic skin dz in horses. it's not known if it causes ocular dz in 
horses. might cause periodic uveitis. diagnosis by skin biopsy.

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