---start---
parasit
johnstone
11/6/97

parasites of swine

note: slides 
are on the website under parasitic diseases of swine under "slides for 
lecture 42" so you can look at them along with the notes, noteservice, 
handout, etc. Dr Guerrero's slides haven't arrived yet but the handout 
will show up monday.

swine industry like other aggie enterprises has 
changed in past 20 yrs. modern swine production is intense and profit 
depends on efficiency. emphasis is on health and productivity, nto 
healing disease. primary indicators are number of pigs per sow per year, 
and rate of wt gain. swine industry is in three parts
breeding, 
feeding/growing, finishing. sometimes all three operations exist on one 
farm, sometimes they are separate. 
pigs nurse for about 3 wks and are 
weaned at about 12 lbs/3 wks. they are starter pigs from about 3-8 wks 
til about 50 lbs. they grow up to 12 wks/80 lbs then they are finishers.

swine farming is important in north america including PA (west pa)


parasites of pigs - two tables in handout - no, three tables. 
don't 
worry about gongylonema, dioctophyma, they are less important.

nursing 
pigs - first parasite they meet is strongyloides ransomi which is 
transmitted via colostrum. short PPP. after ingesting L3 will see adults 
in small intestine within 5-7 days. pathogenic form the parthenogenetic 
female adult. within a week, this female will be laying eggs which will 
pass in the feces of piglets into environment, develop rapidly into L3s, 
causing reinfection of the piglets. so you can have rapid buildup of L3 
in environment. s. ransomi is widely distributed, fairly common in pigs 
as far as infections are concerned but not as important clinically as 
this might suggest. there are a lot of infections but many will be 
subclinical. commonest in S and SE US. found in all ages of pigs but most 
common in suckling pigs. there is multiplication in the free living cycle 
and by parthenogenetic parasitic adult females. when hygeine breaks down, 
can become  a significant problem. likes dirty, wet environment. 


infected pigs are stunted, gain less weight, have diarrhea, can have 
significant effect on growth rate. pathogenic adult females cause acute 
diarrhea, poor wt gain,strong immunity 

strong immunity does develop so 
this is primarily seen in nursing pigs. although older pigs can be 
infected they rarely show clinical signs. it is important to include 
s.ransomi as part of your ddx of diarrhea in nursing pigs. consider this, 
transmissible gastroenteritis, clostridial enteritis,  coccidiosis.

eggs 
are partially embryonated, tadpole like embryo.

cocciosis in swine: 
isospora suis - important in nursing and weanling pigs. very important 
clinically and economically. 8 spp of eimiria in swine, but those are 
nonpathogenic. only isospora suis is clinically importnant. seen in pigs 
5-10 d old. characterized by diarrhea, characteristic yellow frothy 
rancid diarrhea, and mortality is below 20% in uncomplicated infections 
but increases with concurrent infections.  so if they do die, will be dx 
at necropsy. alternatively finding large numbers of oocysts in feces is 
diagnostic. clinical dz in piglets has seasonal incidence. peak in july, 
august, september all over US, related to temperature - 32-35 (C?) is 
ideal temperature for sporulation. most swine operations are not air 
conditioned. warm humid conditions are idea. 
remember - oocysts must 
sporulate first to be infective. ingestion of contaminated water and 
sporulated oocysts is the route of infection. abdominal discomfort, poor 
wt gain, etc. small intestine has sloughed, cheesy, necrotic epithelium. 

treatment is of questionable value. the 4-10 day old piglet isn't eating 
so you can't medicate feed. you can't medicate water. it's too expensive 
and difficult to treat them individually, also. some say giving a 
coccidiostat to sow rations will prevent source of infection, but it'snot 
clear that infection comes from sow. sanitation is the best control. 
steam cleaning farrowing crates, disinfecting them between farrowings. 
clinical disease occurs when there has been a breakdown of 
hygiene/sanitation. once piglets are weaned, sows are removed, pens 
should be cleaned and rested. 


whipworms: trichuris suis (pin on slide)

thin anterior end which inserts into mucosa of cecum/colon
whips are 
common in pigs but clinical dz isn't always seen with infections. 
commonest in growing feeder pigs, slows rate of wt gain. may cause bloody 
diarrhea. eggs are thick shelled and resistant to dessication.  seen in 
2-6 mos old pigs, has resistant infective stage. older pigs have strong 
effective immunity. larval stages develop in submucosa causing prepatent 
disease - typhlitis. so you may not see eggs during outbreak of clinical 
disease related to larval mucosal stage. there may then be secondary 
infections esp with treponema hyodysenteriae - swine dysentery. stools 
are frank blood or disgusting dark red tarry feces. if a pig gets to this 
stage, passing sloughed mucosa and blood, it's on the way out. the mucosa 
is all eroded, and heads of worms are in submucosa and it's all bloody. 
they aren't bloodsuckers, but they disrupt blood vessels with their 
burrowing.
eggs are bioperculate ovoid eggs. 

ascaris suum - most common 
parasite in pigs. also has egg resistant to dessication that survives in 
environment a long time. commonest nematode in swine despite indoor 
raising of swine, b/c egg is so persistent and sticky. remember that 
parasitic phase is mandatory. after infection, eggs hatch, go to liver, 
then lungs, coughed up, swallowed, stomach, SI, mature, lay eggs. this 
pathway is directly related to pathogenesis. they cause disease mainly in 
pigs 2-5 mos. migratory phase through liver and lungs is big problem. 
clinical effects are poor wt gain, respiratory distress (prepatent) or 
impaction in heavy patent infections. because pigs are raised inside now 
and we have good drugs, the infection levels are lower than they used to 
be so it is unlikely to see the impaction. more common to manifest as 
poor weight gain - economic impact more than clinical problem. slide of 
that skinny dirty pig in the corner by the fence is due to ascaris suum. 
these days, this is more neglect and abuse than a problem with ascaris 
suum. more usual picture is pig who is depressed, has ears hanging down, 
normal stool, poor wt gain. can see milkspot lesions in liver due to 
migration of larvae. can see hemorrhage in lung and clinical effects like 
coughing, wheezing, etc. in light infections may see an occasional cough. 
egg is round, thickshelled, pitted. 

hyostrongylus rubris - stomachworm 
of pigs. used to be really common in swine, but has declining prevalence 
with rise of indoor farming. in third world countries, pigs are still 
raised outside, so you still see this stuff there. this worm is a blood 
sucker. it penetrates the gastric mucosa. it causes anemia, anorexia loss 
of condition

esophagostomum - nodule worm. found in colon as adults. 
larvae incite nodular host response. may remain hypobiotic in nodules for 
a long time. the more a pig is exposed,the more likely to be an 
immunological response to the larvae - will see lots of nodules with 
dead/dying larvae, and few adults in colon. but can still have disease 
due to large numbers of nodules in colon. 
common in adults and causes 
'thin sow syndrome' which has important manifestations in reducing litter 
size and weaning weights. also seen in feeder pigs causing poor growth 
rates and diarrhea. due to arrested development/larval inhibition, there 
can be periparturient rise from arrested larvae reawakening at 
parturition and maturing to adults. 

typical strongyle type eggs. 
remember that high egg counts do not correlate with number of worms! 
clinical syndrome may not be because of adults anyway. 

stephanurus 
dentatus, kidney worm. important nematode. commonest in SE and SCMidwest. 
feral swine have high prevalence and are reservoir. complex life cycles 
with several routes of infection makes it hard to control. long PPP 9-16 
mos. patent infxns found in sows over 2 yrs old. lesions are seen where 
migrating larvae and imm adults are found - liver and kidney. can be 
found in almost any body part. main site is liver and kidney. PPP gave 
rise to the gilts only breeding system - gilts were raised and had their 
first litters and were shipped out. this was not economical but was based 
up on logic of PPP. worms have transparent cuticle. hemorrhagic lesions 
in liver, fibrosis. more significant than ascaris suis. they migrate in 
liver a lot, not just passing through. typical strongyle type egg, found 
in urine of infected animals, not feces. 

metastrongylus apri - swine 
lungworm
midwest and southeast
feral swine affected
earthworm 
intermediate host required - low prevalence in confined pigs. 
causes 
coughing, pneumonia - secondary infections may occur.
bronchi and 
bronchioles contain thin, long, angelhair worms. hard to see against grey 
mucosa. usually not heavy infections. long thin worms which irritate 
bronchi. eggs is fairly characteristic, kind of round, with thick shell, 
and coiled larva(?)

controlling swine nematodes:
two aspects to control 
- primary aspect in outdoor pigs is use of anthelmintics, and in indoor 
pigs anthelmintics and hygiene. can't control parasites without hygeine. 

FDA approved parasiticides:
levamisole, piperazine, pyrantel, 
thiabendazole, ivermectin, doramectin, dichlorvos, fenbendazole. many 
older drugs no longer marketed, however, b/c ivermectin, doramectin are 
taking over the market. 

http://www.cvm.fda.gov/index/iHNADA.html

searchable FDA veterinary drug database

consider method of transmission, 
type of production system, and distribution of parasites in host 
population. refer to table listing methods of transmission. it's 
basically divided into direct, mixed, indirect, and other life cycles. 


swine raised outdoors - all these parasites will be seen
indoor 
production almost completely eliminates parasites requiring intermediate 
hosts. stephanurus dentatus isn't really transmitted indoors, probably 
because of long PPP and vulnerability of preparasitic larvae to dryness. 
ascaris however has a direct life cycle component, direct ingestion of 
egg, so will be transmitted indoors. so we'll see coccidia, strongyloides 
in suckling pigs, coccidia, ascaris suum, nad trichuris iin growing 
weaned pigs, and in adult pigs we'll see oesophogostomum, hyostrongylus, 
and stephanurus, and outdoor adult pigs will aslo have metastrongylus. so 
we see b/c there are two kinds of production systems lots of parasites in 
outdoor pigs, and lower levels of infection indoors, with several 
exceptions - strongyloides, coccidia, and ectoparasites like sarcoptic 
mange and lice. think back to approved parasiticides. the reason 
ivermectin is so popular is that it is broad spectrum, effective against 
most internal parasites and the two important ectoparasites. so parasite 
control of indoor animals is really controlled as a group, not as "endo" 
or "ecto" parasites. ivermectin is also popular because it is available 
as premixed feed additive. you have large numbers of stubborn animals 
which are large and can hurt you. so ivermectin is really the way to go. 
pigs raised indoors will crowd together, rub up alot, and mange and lice 
are prevalent, and ivomec will kill those parasites. so synopsis of 
lecture is "use ivermectin and your problems are solved."