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9.23.97
parasit
dr hunter

THE PHYLA ACANTHOCEPHELA AND 
PLATYHELMINTHES


TAXONOMY:

acanthocephela		platyhelminthes
							|
				
trematodes and cestodes

acanthocephala == thorny headed worms. the 
proboscis contains thornlike structures used for attachement. separate 
sexes: males and females have the thorns which protrude out during 
attachment. the male has "cement glands" and a copulatory bursa. female 
has a uterine bell and eggs. you can see large hooks on the proboscis, 
these are curved chitinous structures. they are an important part of the 
pathogenesis.  they come in a variety of shapes and sizes. small hooks, 
large hooks, red hooks, blue hooks (ha ha). they look like cacti and can 
be diagnostic.

the one we need to know is MACRACANTHORYNCHUS 
HIRUDINACEOUS: uses an intermediate host. adults live in small intestine 
of the pig. adult worms attach there and cause pathology. the eggs are 
released in feces. egg + acanthor is ingested by dung-beetle or water 
beetle, and forms the acanthella stage which migrates into another part 
of hte insect and forms a cystocath and encysts in there. if a pig eats 
the beetle, the cystocanth will excyst and grow to adult worm.

diagnosis 
is by eggs in feces - thick brown shell, contains acanthor (infective 
stage for insect host). also ID of adult - no gut, no circulatory system. 
they obtain nutrition by absorbing across integument. have highly folded 
surface area. in terms of diagnosis the spiny proboscis is also very 
characteristic. sometimes is confused with a tapeworm or with ascaris 
suum. if you put the worm into water, it will puff up and look like a 
nematode so people confuse it with ascaris suum. when you put it into 
water, the spiny proboscis sticks out and you shoudl notice it. 

slide: 
eggs - oval, thick brown shell - multishelled. many layers of shell. 
acanthor is within egg. 

separate sexes: males smaller than females. 
during infection it takes 2-3 mos for patency (PPP 2-3 mos). once females 
are patent they stay so for 7-10 mos, males for a year. female can make 
75 million eggs per lifetime. after copulation males use cement glands to 
cement sperm into female and to keep out other sperm. males can also use 
the cement on other males to prevent them from being able to fertilize 
other females. 

pathogenesis: often asymptomatic. verey little 
detectable clinical dz. can see ulcers and granulomas at site of 
attachment, with necrosis and peritonitis which can kill the pig. disease 
(diarrhea and wt loss) is normally a function of worm burden. this is 
true of almost all worms. 

slide: small intestine of pig showing the 
small males and the larger females. worms are dorsoventrally flattened 
until immersed in water. 
slide: h&e stain. proboscis of worm is digging 
into the intestine, and is surrounded by necrosis and inflammatory 
response, which will cause peritonitis if untreated. basically we have 
mechanical disruption of the gut. and we can see the folds in the worm.


CONTROL is dependent on a couple things. one, removal of intermediate 
host. probably the best way is via sanitation - remove the feces and 
there won't be beetle grubs feeding. tx with levamisole and ivermectin 
kills adults. usually sanitation and treatment together will manage this.


other acanthocephalans to know about are 

moniliformis dubius: 
rat/cockroach life cycle. used to study insect immunity.

polymorphus 
minutus: small bright orange worm seen in duck, amphipod gammarus pulex 
is intermediate host. 

prosthenorcis spp: monkey/cockroach lifecycle. 
two forms of dz: acute or chronic. acute - death within a day or so 
associated with penetration of gut and acute peritonitis, or chronic 
associated with buildup of worms ovrer time causing diarrhea and 
emaciation.

slide: intestine of harbor seal- looks lik a caplet and a 
tablet of soething lying on top of it. unusual body structure.

slide: 
eggs - can see the multishelled structure and the thing inside the egg.

slide: necrotizing enteritis in a robin with a heavy worm load. these 
worms are normally asymptomatic, again, but can result in severe disease 
in some circumstances.

that's all about tha acanthocephalids


PLATYHELMINTHES:

trematodes and cestodes
trematodes include monogenea 
and digenea (flukes)

subclass MONOGENEA:

genera gyrodactylus spp, 
dactylogyrus spp

direct life cycle, eggs hatch, infective phase gets 
into host, infects it. 
ectoparasites on skin and gills of aquatic 
animals. pathogenesis is a function of parasite burden.

slide: SEM of 
gyrodactylus. they have a holdfast organ called a ____ that holds on to 
the host. 
slide: fin of fish with some of these guys on it.
slide: high 
power veiw of attachment structure - haptor?- hooklike thing that digs 
into host. 
slide: vaguely pinkstaining thing. note blind ended 
bifurcated gut. these parasites do not have anuses. waste products go 
through tubule system to be excreted. two of main spines of the haptor or 
hafcor or whatever it is are seen.

subclass DIGENEA (flukes)

- 
hermaphrodites (most)
-dorsoventrally flattened
- oral and ventral 
suckers for attachments. oral ones usuallyfound on anterior end, ventral 
ones about halfway down ventral side
- complex life cycle with 
invertebrate intermediate host (snail) and pediogenesis, which is larval 
development and division within intermediate host. so one egg goes into 
intermediate host and divides and becomes thousands of infective larvae.


slide: anatomy of trematode. basically a bag of reproductive organs. 
vitelline glands make yolk and shell of eggs. seminal vesicles are 
present too. you can have cross fertilization or self fertilization. 


many distinct developmental stages - eggs, sometthing, something else, 
yikes. all life cycles very similar though. many flukes use hypobiosis of 
egg or metacercaria. this allows area to be contaminated for a long time 
and for wide distribution. the paedogenesis is also an important 
amplification step. these worms are complex and sensitive to temperature 
and skin. can use chemotaxis to find intermediate host. there is a 
complex nervous system and reproductive system. 

sexual reproduction 
occurs within definitive host (self or cross fert). eggs are produced and 
they contain the stage called the miracidium which penetrates the skin of 
a snail (finds it by chemotaxis), and then undergoes asexual reproductive 
cycle and pediogenesis within snail. after that, they grow into free 
living cercariae which bust out of the snail, thousands at a time, and 
glom onto a food item like fish, crayfish, or encyst on grass, or 
something. then they are eaten, end up in host, excyst, grow, become 
adults. only one species of flukes develops cercaria which directly 
penetrate the skin of definitive host.

eggs of flukes are distinctive 
because of the unipolar operculum. eggs in feces can be unembryonated 
covered by yolk cells, or can contain the miracidium. 

slide: eggs of 
different flukes. the operculum is there because mericidium can digest 
the edge of it, making it pop off, so it can come out. mericidium is 
ciliated so it can swim to host (snail). once it gets to host, it 
secretes proteolytic enzymes so it can digest edge of snail, and it loses 
the cilia. it becomes a sporocyst, and divides so you get multiple 
daughter sporocysts. eventually you give rise to stage calld ridia, whch 
divides and produces daughter ridia. these stages can migrate through 
snail into pancreas and liver, where they become ridia, and which contain 
the cercaria - eg, cercaria are INSIDE the ridia. 

slide: miricidium

slide: ridia, with cercaria coming out. note the ridia is really just a 
big sac that the cercaria can break out of. the cercaria then can break 
out of snail - kill snail if enough burst out at once. 

cercaria stage 
has a tail that's like a helicoptor spiral type thing

metacercaria - 
once cercaria finds next host or vegetation, it loses tail and forms this 
metabolically inactive, resistant stage. can sit on pasture several years 
this way. 

FASCIOLA HEPATICA is most important fluke. affects cattle and 
sheep. adults are found in bile ducts of liver. are hermaphrodites. . 
eggs passed in feces of host. when they first pass they do not contain 
maricidium. look nondescript. in right conditions, which are temperature 
dependent, the eggs embryonate and give rise to mericidium which takes 
about 10 days. then the miracidium pops off operculum comes out and looks 
for intermediate host via chemotaxis. it uses a specific species of 
snail. we don't need to know the names of the snail kinds. in other parts 
of the world different snails are used. within the snail it grows and 
gives rise to cercaria. miracidium --> sporocyst-->ridia__> 
cercaria-->out of snail-->metacercaria (encysted stage)-->eaten --> 
marita excyst -juvenile form -->migrates, goes to liver, feeds 
**pathological stage**--> 6-8 weeks --> enters bile ducts

slide: adult 
f.hepatica. large worm. note pointed head and broad shoulders. is endemic 
to pacific NW, northern CA, idaho, montana, and SE texas, LA, florida. 
also parts of NM. availability of water is important because of the 
snails. eg in nevada it occurs in the mountains only. distribution is 
limited because of the need for the specific intermediate host. the 
distribution of the fluke is limited by distribution of specific snail 
species. in pacific NW, ther eis a peak of dz in late fall. in LA, peak 
of dz in early spring. this is due to climate, environment, etc. 


environment defines dz. warm temps are required for development of 
miracidium to sporocyst to ridia. you need 9-10 days at a warm 
temperature to get to the miracidium stage (I think he said that...). 
temp can also affect development of snail. 

in NW USA winter is cold, 
transmission is during late summer, disease is seen in autumn. 
in 
southern US there is summer drought. transmission is during winter, and 
disease during spring. temperatures are almost alwyas high enough for 
miracidium to develop from eggs. so during winter the snails come out 
onto pasture and get infected. 10-12 weeks later disease is developing. 


also sometimes in areas where fasciola is found, sometimes herbage that 
is infected can be brought in and they can get infected despite absence 
of snails.

pathogenesis: 

acute: ingestion of large amounts of 
metacercaria
juveniles in liver produce migratory tracts as they feed 
that lead to development of thrombi and ischemic coagulative necrosis

clostridium novyi is an anarobe that multiplies within the necrotic 
lesions, releases toxins, and leads to development of necrosis and 
hemorrhage and can lead to death due to the toxins. again, the more 
juveniles in liver, more likely to develop dz. can be prevented by giving 
broad spectrum abx.

slide: sheep liver - bile duct thickened and adult 
worm being pulled out. after they migrate through liver they get into 
bile and pancreatic ducts, and they can cause duct hyperplasia. in sheep, 
they are constantly being infected and they do not get immunity. cattle 
get infected once and get immunity. 

acute dz: see destructive tracts. 
this liver looks like swiss cheese to me. in sheep, because this can 
happen every yera, this damage can build up. if enough fibrosis occurs, 
can lead to loss of liver function. in cattle, this only happens once but 
sheep can have repeated insults.

chronic dz: associated with presence of 
flukes in bile duct. found only in sheep. leads to hyperplasia, fibrosis, 
wasting dz, calcification, hypoproteinemia, anemia. with chronic dz you 
have a loss of condition in the sheep as opposed to death. productivity 
goes down. 

acute dz is primarily in calves put on pasture for the first 
time.

control and tx:

dx: based on operculate eggs found in feces 
,unembryonated.
tx: albendazole, clorsulon. molluscucides also used to 
clear snails from pasture. move animals to fluke free pasture to reduce 
contamination. fluke free pasture concept means minimal standing water, 
soil quality etc. some pastures just more fluky than others. 


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note: acanthor is infective stage for the intermediate 
host. It's a developmental stage, like L1 or L3, for example. 

we just 
discussed f.hepatica

fascioloides magna - primarily parasite of deer, 
sometimes infects cattle and sheep. is seen throughout USA. present in 
cysts that connect to bile duct. in sheep/goats, juveniles stay in liver 
and never mature. they just keep migrating in the liver. they don't 
mature or produce eggs. in cattle, they do the same thing. juveniles in 
cattle can encyst in bile ducts but adults do not make eggs. so in 
cattle, sheep, goats infections are never patent. so you can't really 
diagnose it except at postmortem. eggs can be detected in deer feces. 


definitive host: deer. adults found in large cysts connected to bile 
ducts. again they are hermaphrodites, can cross or self fertilize. eggs 
pass in feces as unembryonated eggs, they enter water, and in right 
conditions will embryonate and form maricidium - and it will digest 
operculum and come out of egg and look for a snail. within the snail, the 
ciliated maricidia which have penetrated snail lose the cilia and undergo 
pediogenesis --> mericidia to sporocyst to ridia to cercaria. the 
cercaria leave the snail and look for  appropriate vegetation in a water 
hole, and encysts into metacercaria stage. when eaten, excysts, becomes 
juvenile phase, and starts migrating. can lose way and end up in lungs 
causing damage. in sheep and goats juveniles stay migratory. in cattle 
can encyst but do not connect to bile ducts so never have patent 
infection. 

wide distribution across states. presence of it in deer 
population precludes sheep farming in many areas. the parasite is very 
destructive to sheep. esp in areas around great lakes where this is in a 
lot of deer. 

slide: sheep liver - much destruction. many tracts through 
liver. a single juvenile because it never matures can cause a lot of 
damage by repeatedly migrating through the liver.

slide: deer liver with 
huge cysts containing adult worms. they radiate from bile ducts. adults 
are within cysts. eggs pass out through bile ducts into the feces. 

slide: deer liver surface. can see large tracks of hemorrhage and 
necrosis where juveniles migrated through and were feeding in the liver. 
the white areas are fibrosis. so in the past this has also occured in 
this liver. many large areas become fibrotic over time if there are 
repeated infections. 

slide: deer liver with very large cyst within it. 
can see the adult within the cyst. 
slide: very large adult within a 
cyst. one way to tell it from f.hepatica is that f.magna is about 2-3 
times as large as hepatica. 

Dicrocelium dendriticum:

small lancet 
shaped flukes found in bile and pancreatic ducts of sheep, cattle, and 
pigs. two intermediate hosts (others just had one, snail). here, there is 
the land snail and the ant. the land snail is pretty independent of 
moisture. so this pathogen can be found in dry habitats as well as moist 
habitats. development in ant affects behavior. this fluke doesn't migrate 
through liver parenchyma.  "juvenile" is the immature adult that can't 
yet produce eggs. so with this fluke, there is no parenchymal migration, 
so pathology is bile duct fibrosis and cirrhosis. sheep do not get immune 
so this gets worse over time. 

although mainly found in sheep can also 
be found in man. eggs contain maricidium when they are passed. the 
maricidium + egg is eaten by snail. it doens't hatch and find snail. 
within snail, it undergoes pediogenesis. cercarian stages develop. so 
then they are secreted in slime balls by the snail, and ants come along 
and eat the slime balls. the cercaria invade the ant, migrate through it 
and form metacercaria. the metacercaria can form in ant brains, and they 
affect ant behavior. during nightime temperatures ant acts normal, but 
when it gets warm, the mandibles of the ant will clamp shut on the 
nearest piece of vegetation. so instead of going to its nest, it stays 
out with its ass hanging out, so to speak, clipped to a piece of herbage. 
if it isn't eaten, it lets go at night, and goes about its business. if 
it is eaten, life cycle continues within definitive host. 

slide: egg. 
looks like any other egg. is a lot smaller than fasciola eggs though. 
about 50% smaller. also has an operculum. 
slide: adults. much smaller 
than f.hepatica. about 4-5 mm. dorsoventrally flattened and lack pointy 
head/flattened shoulder morphology. more teardrop shaped. 

PLATYNOSUM 
FASTOSUM: fluke of bile and pancreatic ducts of cats. found in SE USA and 
west indies. metacercaria found on amphibians, lizards, and geckos, so 
definitive host most be carnivorous. 

slide: adult fluke within 
hyperplastic bile duct

PARAMPHISTOMATIDAE: patent infections in cattle 
sheep and goats. high infective dose causes development of dz as 
parasites migrate back from the small intestine through the abomasum and 
into the rumen. adults are relatively harmless. vetnral sucker present at 
posterior of worm. typical fluke life cycle with aquatic snail as 
intermediate host.
pathogenesis associated with the migration of the 
juveniles. 

slide: one of these flukes. can see blind gut, ventral 
sucker, oral cavity
slide: adults - kinda round and sluglike. can see the 
oral suckers and the ventral suckers. the appearance is diagnostic. they 
arne't really flat. in these worms, the ventral sucker is all the way at 
the posterior end. in  most of others, is about halfway down.


TROGLOTREMATIDAE:

nanophyetus salmincola: pacific NW range. typical 
lifecycle with snail intermediate. metacercaria found in salmonids. this 
fluke is a host to neorickettsia helminthoeca which causes salmon 
poisoning in dogs. the cercaria penetrate salmon and form metacercaria 
inside the fish. dogs eat the fish and get very ill, can die - from 
effects of rickettsia?

paragonimus kellicotti
typical fluke life cycle 
with snail intermediate
metacercaria found in crayfish
adults occur in 
pairs in cysts in the lungs and are hermaphrodites
can cause respiratory 
disease
praziquantel, fenbendazole and albendazole for treatment


definitive host can be a dog. eggs laid in feces. miracidia penetrate 
snail, cercaria are free swimming and find crayfish. crayfish eaten by 
dogs or people carry in metacercaria, juvenile migrates to lungs, adults 
reproduce, eggs coughed up, swallowed, and passed in feces. 

slide: egg. 
this egg has a liplike structure around the operculum making it easier to 
see. 

as of 1989 this parasite was seen in dogs and cats in most of the 
states east of mississippi uncommonly. is much more common west of 
mississippi because of sparseness of snail vectors. 

slide: cyst from 
lung of dog, containing two adults. 
slide: h&e stained histo prep of 
lung cyst with two adults
slide: xray showing lung cyst in cat. 


DIPLOSTOMADIAE:

alaria spp.
typical life cycle with snail intermediate

mesocercaria stage found in tadpoles and paratenic hosts. metacercaria 
found in lungs of definitive host (dog, cat) depending on how infection 
occurs. adults found in intestine of host. 

life cycle - adults found in 
say, cat, or mink. eggs pass. infect snail. cercaria are released from 
snail and infect frogs, and form mesocercaria. mouse eats frog and forms 
metacercaria. mouse eaten by mink or cat and life cycle continues into 
adult stage. 

there can be vertical transmission of this spp through 
milk. during lactation, mesocercaria will migrate to mammary glands as 
well as lungs during initial infection. adults are pretty harmless, but 
migration of mesocercaria can cause pulmonary damage and pneumonia.


SCHISTOSOMATIDAE:
typical life cycle, snail intermediate
no metacercaria, 
instead - cercaria infect definitive host directly. separate sexes, found 
paired in veins. eggs (with no operculum) are associated with 
granulomatous pathology. "swimmers itch" - bird schistosomes infect 
people swimming in lakes or whatever. but in people, they die in the 
skin. eggs normally found in feces or urine. 

this family has many spp. 
in man, s. mansoni, s. hematobium, and s.japonicum are the major 
pathogens that affect man. lots of people in africa and asia are 
infected. veterinary parasites:

s.bovis in cattle and sheep
s. indicum 
horses cattle goats and buffalo
s. nasale cattle- this one is found in 
nasal cavity
s. mathei sheep

heterobilharzia americana - found in dogs


male and female pair off for life. so i guess syngamus isn't the only one 
that does that. the female is smooth and is within a groove of the male. 
male can't develop without a female. 

eggs have spikes that can be used 
to distinguish between species. 

pathology associated with these eggs is 
normally because the deposition of them into veins and other tissues eg 
liver, lung, gut, where they can get caught and they are large and full 
of enzymes - they provoke granulomatous response. a large inflammatory 
response will occur. these worms can live for 30 yrs, so this can get 
quite serious. can see liver failure or chronic pneumonitis. 

cercaria 
have forked tail. they swim with tail at anterior end, like others. 


once cercaria find host they penetrate with proteolytic enzymes, and form 
the schistosomium stage. this undergoes a migratory sequence through 
different tissues, eventually giving rise to adults in the vein. the 
avian ones will die when they enter human skin, causing local 
granulomatous response. 






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