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parasit 
9.22.97


Public Health Parasitology (nematodes)


today we're finishing up what we have to say about the nematodes. we'll 
discuss selected nematodes that have zoonotic potential.

It used to be 
that in the every day practice of veterinary medicine, vets would 
consider parasites in humans when newspapers published articles and 
parents got worried about it. As we will hear from Dr Wilson, it's now 
important to consider all potential zoonoses, from a liability 
standpoint, as petshops and breeders have all been sued when pet owners 
acquire parasitic infections from their pets. Potentially, if you deworm 
an animal and it isn't cured and someone picks up the parasite from it, 
you could be held liable (how incredibly lame). 

Dr Schad heard today 
that there was a meeting in Chester Co of people with Lymes dz, and some 
of them volunteered to test the Lyme vaccine - signed all the documents 
and release forms and stuff - and now they are suing the vaccine 
manufacturer because they had side effects from the vaccine! Now, drug 
companies will not be willing to test vaccines if they are held liable 
for htings like this. We just won't get any new vaccines.

LARVA MIGRANS: 
cutaneous (CLM) or visceral (VLM).

ancylostoma braziliense with southern 
US and south america and elswhere distribution is main etiological agent 
of CLM. you shouldn't think that only animals in the deep south will have 
a.braziliense. remember, HW extended its range from the south to the 
whole US probably in part through movement of dogs from south to north. 
people go on vacation and stuff and take their dogs with them, bringing 
parasites.  see hookworm lecture for life cycle detail, or item 3 on pg 
one of today's handout.

epidemiology: largely in southeastern US. 
infective larvae are susceptible to dessication, remember, so these do 
best in  moist, shaded areas. people at risk are people exposed to 
contaminated soil in moist areas. people in building trades eg plumbers, 
electricians, carpenters, marines in paris island - are high risk. people 
with prolonged intimate contact with the soil. people going in crawl 
spaces under houses. 

pathogenesis: please appreciate that these 
hookworm larvae do not establish intestinal infections in abnormal hosts. 
act as if person is a paratenic host instead. they wanter in the skin for 
as long as three months, some may encyst and become dormant. CLM is 
characterized mostly by moving larvae. One sees raised erythematous 
serpiginous unulating trails on the skin. the badly affected parts are 
usually plantar surfaces of the feet. but any place that makes prolonged 
contact with the soil can be a site of invasion. 

slide: a large breast 
with a very long trail from medial to the nipple out up into the axillary 
region. because this woman was pregnant and seen in a new england medical 
center where this dz is rare, there was a lot of concern about how to 
treat her

slide: same woman's buttocks covered with confluent lesions. I 
guess she was sunbathing and lying on the ground nude or in a bikini. 
yikes. this infection is very uncomfortable and itchy. she was finally 
successfully treated. 

prevention: as veterinarians, there is the basic 
concept that you treat animals not only to help them and cure them of 
ailments, but to prevent spread of infections to other animals of same or 
different species, including us. so you want to decrease the number of 
eggs going in to the environment - so it is desireable to restrict free 
ranging dogs. it's important to reduce numbers of stray cats and dogs. 
spay programs are useful. picking up after your pets is important. if you 
deal with clients who have small kids and if they consult you, sandboxes 
ARE favored places for feral cats to defecate. it's best to use 
sterilized sand to fill sandboxes.

TOXOCARIASIS

wandering ascaris 
larvae in humans causes VLM and OLM (ocular larva migrans)
etiology: 
toxocara canis, mainly, which is a really big worm. toxocara cati is also 
a possible, less important, etiological agent. the problem is that if you 
distinguish between them in biopsy tissue, you probably can't do a good 
job of it. you can't speciate them that way. so we don't really know how 
many infections are attributable to t. cati but we think relatively few.


now the life cycle of t.canis has been discussed, we have the diagrams in 
the old handout. just remember - in all these cases of larva migrans, the 
human is substituting for the paratenic host. also, heavy transmission to 
very young children often involves a litter of puppies and a dam. even 
though the dam may not carry adult worm infections, when she is lactating 
and cleaning up the whelping box and ingesting the feces of the 
prenatally infected or transmammary infected pups she can get reinfected 
by swallowing the larvae passed by the pup. 

this infection 
traditionally has been thought of as a problem for something like 
80-90-100% of puppies. it's been thought that with the many alternate 
life cycles, no puppy could avoid infection. recently, as many as 80% of 
puppies are known to be infected in the south. in well cared for animals, 
you might find a much lower prevalence, however. puppies will kick out 
these infections in about 8 weeks time.

the female worm is a large worm, 
and these worms occur in large numbers. heavily infected puppies can 
really severely contaminate an area. these worms put out like 200,000 
eggs/female/day, so in a small place you get accumulations of millions of 
eggs. 

areas where many dogs are walked can be heavily contaminated. 
some surveys show that ten percent of all samples from public parks 
contain t. canis eggs. some confined areas like urban squares contain 
millions of eggs.

human aspect: as indicated in handout, severe VLM is 
limited to the very young child. well, largely limited. this is because 
very often in our culture, little kids are associated with young puppies. 
if you watch tv commercials, you often see a small child cuddling a small 
puppy. it's nice to look at and all, but it's not a good public health 
thing. it's dangerous because the puppy can be infected and because kids 
practice pica (eating weird crap) and may eat dirt, soil, feces, 
whatever. milder VLM is seen in adults and kids over 8 yrs old. 

wrt 
pathogenesis: just remember as we see in handout: eggs must be 
embryonated to be infected. if someone ingests dog feces - parents panic. 
they take kids to an MD. MDs do not know a lot about parasitology around 
here and then THEY panic. they call the vet. the question is, was this 
kid in danger of being infected. The question is: is the stool fresh? 
Well, the MD thinks you're being a smartass - but you're not. you need to 
find out whether or not the eggs were embryonated. if the stool has had 
time to sit around and have the eggs develop, there's a problem. if the 
stool was freshly passed, there is no risk of toxocara infection. in the 
case of acute infections, recently acquired - worms are usually still 
wandering. they leave tracks as you see in the handout, areas of 
hemorrhage, necrosis, inflammation, etc. in chronic infections, larvae 
become encapsulated in granulomatous lesions. even in a host that is 
responding strongly and making a good immune response, some larvae will 
continue to migrate and survive nicely. how do they do it? well, the 
worms have an epicuticle - thin exterior surface that can be shed. 
presumably they escape damage by shedding the epicuticle.

signs 
dependent on intensity of infection. if you have one or two larvae in the 
lung, it's not a huge deal. but if you have one larva in the eye, that 
can be a VERY big deal. so site of infection is important. immunity 
develops with exposure but reinfection is additive. inflammation is most 
important for the disease. 

intensity of infxn
site of larvae
frequency 
of reinfection
intensity of rxn

differential diagnosis of VLM from 
t.canis:
wheezy child
failure to thrive/puniness
anemia, eosinophilia

seizures
abdominal pain, often considerable with organomegaly

hepatomegaly, splenomegaly
generalized lymphadenophathy

the whiny, 
complaining, wheezy small child. 

slide: brain with larva coiled up in 
granuloma. 
clinical and autopsy findings of a two and a half year old 
infant with toxocara sp infection of brain and granulomatous lesions in 
liver. cause of death was "non accidental injury". relationship between 
toxocara infection and behavioral disorders is discussed. the parents 
beat this child to death because of his constant whining and crying - 
which was due to the VLM! another child in the house wasn't abused and 
wasn't infected.
This sad story tells many of us who have animals and 
always have that one really should be careful about where they defecate 
and about keeping them wormed.

OLM: in older kids or adults, lightly 
infected, worms have greater ability to wander and may eventually reach 
the eye. these are infections with few worms. at one time, when 
granulomas were found in the eye that looked like toxocara, it was 
assumed to be retinoblastoma and eye was removed. now, we don't assume 
that anymore. 

-histo: larva coiled up in eosinophilic abcess. you can 
see a white mass behind the pupil in severely affected eyes. these are 
serious manifestations of toxocariasis, not very common.

prevention: 
it's long been said that if the veterinarian can see puppies early 
enough, they can be wormed on a two week schedule - at 2, 4, 6, 8 wks. 
then you don't have these problems. but people usually don't bring in 
their puppies. but you should request that they do. there are very safe 
wormers for toxocara - like pyrantel. the idea is if you do this q 2 wks, 
you remove the worms from the transplacental transmission before any eggs 
show up. ppp about 3 wks for transplacental. 4 wks ppp for transmammary. 
then you get the ones they got from the environment, and at 8 wks, just 
another final dose. after 8 wks, pups usually clear infection. and don't 
forget to worm the dam because she can get a reinfection while immune 
suppressed from lactation. think about client education. have handouts 
about these things available to try to forestall lawsuits. 

Dr Schad 
says he sometimes wonders about people who leave vet school 2 yrs after 
this lecture and they walk around and take their dogs for walks in the 
same places as th patients and stuff....

RACCOON ROUNDWORMS

Baylisascaris procyonis

this has very recently been found in dogs, we 
have no idea of prevalence. think about this. in most practices, if a dog 
comes in and passes an egg of this type, it's just "roundworms" and you 
don't know the species. And this worm is very dangerous, so we should be 
making this distinction!

life history is in handout. it's pretty typical 
ascaris history which involves an intermediate host where larva does 
develop in CNS of intermediate host. transmission strategy is to cause 
weird behavior in affected intermediate hosts, which are then preyed upon 
by raccoons. 

this larva is very neurotropic and larva is very big.
eggs 
are not really pitted like toxocara are, they're just kind of rough. 
toxascaris is smooth. 

OCCULT ANCYLOSTOMIASIS:

Dr Schad remarks he used 
to work with a.caninum without wearing gloves, b/c he didn't htink it 
could be pathogenic to people. well, he was wrong. in the past few years 
a lot of cases have been published involving this occult form of 
ancylostomiasis that occurs in people.

a.caninum penetrates skin, 
migrates to lung, coughed up, swallowed, reaches intestine. not many 
develop and the ones that do do not lay eggs - they are sterile. we never 
realized this worm was in people before because of this lack of eggs. in 
Australia, some people presented with an acute abdominal condition, and 
their intestines were intensely inflamed - severe eosinophilic enteritis. 
lengths of intestine were removed. in some of these guts, they found a 
couple of hookworms that turned out not to be the hookworm of humans, 
which has only two teeth on each side, whereas a.caninum has three. later 
they found attached worms via endoscopy. normally hookworms  don't lead 
to a strong host response. in a.caninum infection in humans there is a 
violent reaction and we don't really know why. if larvae migrate to the 
tissues, they are just quiescent and not a problem, so there may be some 
VLM going on but if so the larvae are encapsulated and we don't notice 
them. for some time there was doubt that these people were infected with 
a.caninum, but more recently it's becoming accepted and proven and 
whatever. we've seen it in Louisiana and in Australia and we expect a lot  
more attention to be paid to this. in the handout there is an editorial 
Dr. Schad wrote a couple of years ago. read it. 

TRICHINOSIS

already 
covered last time. in this handout there is a diagram that is more 
epidemiological as opposed to simply a life history.

so realize that we 
talked about trichinosis in swine before but most people in the US who 
get trichinosis today get it from eating BEAR MEAT (YUK!!). in PA, the 
state wanted to limit number of claims against the state by farmers, and 
so they let people shoot bears. some bear have as many as 900 larvae per 
gram, which is enough to make a pig uncomfortable. so some guy shoots the 
bear and has it ground up and distributed into sausages, and gives the 
sausages to all his friends and relatives, and they all get trichinosis. 
ugh. so you should consider this as well. 
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