VMED 5235

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VMED 5235 VETERINARY PARASITOLOGY PARASITES OF
SUCKLING PIGS
Many opportunistic organisms are present in the
warm environment of the new born pig that can
effect its future performance. Three parasites
are acquired very early by the newborn the
small intestinal threadworm, Strongyloides
ransomi, the coccidial protozoan, Isospora suis,
and the mange mite, Sarcoptes scabiei.
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Strongyloides ransomi, intestinal threadworm
(rhabditoid). The pig is the only host. Adult
females can be found deep in the mucosa of the
small intestine, more commonly in the duodenal
portion. Of worldwide occurrence, the intestinal
threadworm is more common in the warmer climatic
areas. Only females are present in the parasitic
generation. Adults are 2.1-4.2 mm (0.15 in) in
length. The filariform esophagus occupies 1/3 of
total body length.
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LIFE CYCLE OF THE INTESTINAL THREADWORM STRONGYLOI
DES RANSOMI
Prenatal infection may occur from larvae in sows
circulatory system with patency as early as 2-3
days after birth Transcolostral infection may
occur with patency 4 days after birth from larvae
sequestered in mammary fat with patency in 4 days
Embryonated eggs pass out in feces Eggs develop
to infective 3rd stage, direct cycle
or to Females and males,
indirect cycle Eggs from female develop to
infective 3rd stage
When infective larvae penetrate the skin or are
ingested, they enter circulatory system, heart,
lung, tracheal migration to small intestine in 3
days and begin egg production 3 days later, 6-10
days postinfection
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Littermate Hampshire Pigs
Control
Infected
182 lbs
82 lbs
Pathogenesis, signs and symptoms Death
generally occurs before pigs are 10-14 days old
if infection levels are high, but stunting and
unthriftiness are the usual sequelae of
Strongyloides ransomi infection. Diarrhea
followed by progressive dehydradion are the usual
signs. Pulmonary signs are possible during peak
lung migration. The economic loss because of
poor weight gains and reduced feed conversion
efficiency make it costly disease of young pigs.
Parasitized pigs require 3-18 more feed per
unit of gain than non parasitized pigs.
Infections run their course within 6-10 weeks
with peak egg production at about 2 weeks. A
good immunity develops and Strongyloides is
seldom encountered in slaughter pigs.
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5A
Diagnosis Finding thin-shelled, larvated eggs
in feces measuring 50 x 30 um, or finding adults
in the small intestine at necropsy with a history
of diarrhea and unthriftiness. Clinical
strongyloidiasis can be confused with
colibacillosis or coccidiosis most commonly.
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5B
The survivors of an outbreak of strongyloidiasis
several months after the pig crop was reduced by
75
A difference of 34 lbs less for infected pigs vs
control littermate
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Treatment Thiabendazole in a paste-syringe
formulation is effective for suckling pigs.
Levamisole is also effective in older pigs.
Ivermectin is effective against intestinal adults
and against somatic larvae in sows, preventing
transcolostral passage when sows are treated
10-14 days prior to farrowing. Doramectin is
also effective against adults and probably is
also effective against somatic larvae.
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Prevention and Control Strongyloides infective
larvae are relatively fragile, short lived, and
very susceptible to desiccation since they are
not sheathed. An environment where fecal
contamination is heavy and moist and protection
is afforded for larvae by debris, bedding and
shade, is ideal for Strongyloides transmission.
Strongyloides commonly becomes endemic on poorly
managed farms. Mortality of newborn pigs can
approach 75 under such conditions. Even in well
managed operations, it should be remembered that
Strongyloides can be introduced through breeder
sows by transmammary or prenatal transmission of
larvae originally picked up elsewhere.
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Porcine Coccidiosis
Isospora suis, pig coccidia Eight Eimeria spp,
and one Isospora sp. Are recognized from pigs in
the USA. Only the one Isospora, I. suis is
pathogenic to pigs. Porcine coccidiosis is
primarily a disease of suckling pigs of 5 to 15
days of age. The disease is being diagnosed with
increasing frequency in the midwest as well as
the southeastern hog belt. It has become a major
problem in swine operations with continuous
farrowing and in confinement rearing. Outbreaks
have been reported to be more numerous in August
through October.
I. suis
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ISOSPORA SUIS
Morphology and Life Cycle The usporulated oocyst
of Isopora suis is 17-25 x 16-21 um and contains
a hazy body between the sporont and the cell
wall. The sporulated oocyst contains two
sporocysts. The endo- genous stages are found
throughout the small intestine with most stages
being present in the jejunum and ileum.
Development stages differ in appearance from
those of Eimeria spp. There are probably two
asexual generations. Endogenous stages can be
found throughout the small intestine. Peak in
asexual development stages is 3 days after
Hazy Body
Unsporulated Isospora suis oocyst
infection, and mature sexual stages are present 5
days after infection. The prepatent period is 5
days and patency lasts for 5 to 8 days
Sporulated Isospora suis oocyst
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10A
Asexual stages
Sexual stages
Pathogenesis and Clinical Signs Clinical
disease occurs in pigs of 5 to 15 days of age but
is more frequent in those 7-10 days of age. Pigs
develop a yellow, fluid diarrhea, become
unthrifty and sometimes die. A fibrinonecrotic
or diphtheric membrane may be present in the
small intestine. The lesion is one of villous
atrophy or blunting. Asexual and sexual stages
are present in the epithelial cells. Oocysts can
be demonstrated in only about 50 of pigs
affected. Diagnosis can be made by demonstration
of the typical oocyst along with the clinical
signs. Poor response of diarrhea to broad
spectrum antibiotics or E. coli bacteria
vaccination of sows would tend to incriminate
coccidiosis. Histologic examination is the best
definitive diagnosis.
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10B
Isospora suis oocyst in fecal flotation
Fibrinonecrotic membrane in small intestine from
Isospora suis infection
Sporulated I. suis oocyst
Porcine coccidiosis
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Porcine Coccidiosis, Treatment and Control
There is no approved treatment for porcine
coccidiosis. Although amprolium in sow ration
for 3 weeks before and after farrowing has been
helpful in checking problems with neonatal
diarrhea, it is not approved for swine in the
USA. Sows are considered to be indirectly the
source of oocysts although it is un- common to
find sows passing oocysts on farms reporting
outbreaks of coccidiosis. In a national survey
of 77 sow fecal samples from farms with outbreaks
of coccidiosis, none were positive, however, 1 of
172 sow fecal samples from farms without a
history of neonatal coccidiosis was positive. I.
suis oocysts sporulate in as little as 12 hours
at 37 C, a temperature that reduces or inhibits
sporulation of Eimeria spp. Oocysts. Newborn
pigs usually are maintained in an environment
with a temperature of 32 to 35 C that is
favorable for sporulation of I. suis. Oocysts
have been shown to remain infective for 2 years.
Scrupulous attention to sanitation in the
farrowing quarters (and treatment when available
of sows) is of primary importance in the control
and prevention of coccidiosis in pigs. Sanitation
and thorough steam cleaning are the most
important strategies.
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SARCOPTIC MANGE
The sarcoptic mange mite of pigs is structurally
similar to those of other animals and man, but is
probably at least biological race because it is
not easily transferred to a different species of
host. Females, nymphs and larvae are in tunnels
in the upper 2/3 of the epidermis, males are on
the surface, more commonly in areas with few
hairs and tender skin such
as ears, face, neck, shoulders, inner surfaces of
hind legs, and tail. Distribution is worldwide,
more common in winter and where animals have
close contact with each other. Adults are
rounded with short legs, of which two end in
long, stalked pretarsi with suckers, and two end
in long whip-like setae. Spine-like projections
are present on the dorsal surface. Females are
about 380 um long and 270 um wide. Males are
smaller. Females, newly mated on the surface,
burrow into the epidermis forming tunnels 0.5 3.0
cm long in which they lay eggs. Larvae hatching
from eggs go through a nymphal stage and then
become adults. Female activity continues for 2
to 3 day intervals for about 2 months. The life
cycle requires 10 to 14 days to complete.
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Pathogenesis, Signs and Symptoms Pigs are known
to harbor sarcoptic mites all their lives with
little or no clinical effect. Lesions are due
more to the reaction of immunological sensi-
tization than simple irritation from burrowing
mites. Sensitized pigs experience pruritis and
inflammation. Early lesions consists of crusty,
scaly red papules or vesicles. Older lesions
become hyperkeratinized, dry, thickened,
appearing as stiff skin folds. Pruritis and
resulting trauma may result in coagulated crusts
oozing serum and blood. Lesions may be seen as
early as 2 weeks of age, but normally pigs are
weanlings before sensitization is sufficient for
development of lesions. Weak and malnourished
pigs which are immunologically less competent are
more severely affected than healthy litter mates.
Sarcoptes infestations cause unthriftiness and
death in severe cases.
Early papular lesion
Old lesion in ear
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Diagnosis, Control Diagnosis is based on finding
adult mites, eggs, or immature stages in skin
scrapings. Scrapings from the edges of active
lesions made with a blunt scalpel or 3 bone
curette are placed in mineral oil. Skin debris
can be cleared with a drop of 10 KOH. The
presence of Sarcoptes justifies treatment to
prevent the carrier state. Many insecticides
available as sprays or dust, application of which
must include complete body coverage, ear canals
and under surface of body. The most effective
one is reported to be amitraz. Treatment should
be repeated at least once in 7-10 days. Because
transmission is usually from sows to suckling
pigs, sows can be treated before farrowing with
ivermectin twice, 7-10 days apart, or once with
doramectin
Chronic sarcoptic mange
Adult mite Egg
to prevent transmission to pigs of both Sarcoptes
and Strongyloides. Building should be cleaned,
disinfected and/or sprayed. Clean herds can be
kept clean by treating new animals before adding
to herd.
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Growing Pigs Four nematode parasites of growing
pigs are of importance in the swine population of
Louisiana, especially in the southern part of the
state. Ascaris suum, Oesophagostomum spp.,
Trichuris suis, and Metastrongylus spp.
1.33 lbs from one market hog
Ascaris suum, the large roundworm of swine
(ascarid). The pig is the only natural host,
although they have been reported from sheep,
cattle, rodents, etc. Adults live unattached in
the lumen of the small intestine. A.
lumbricoides of man and A. suum were thought to
be the same parasite. The one found in the pig
was called A. lumbricoides (var. suum). They are
now recognized as a different species.
Ascaris suum
A. suum is a common parasite of pigs worldwide.
From 50 to 75 of pigs are infected. It is more
common in growing pigs than mature pigs.
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Large, stout-bodied nematodes, pinkish-yellow
with 3 prominent lips surrounding the mouth.
Females are 18-37 cm (7-17 in), males 15-24 cm
(6-10 in). The life cycle is direct. A
hepato-tracheal migration route occurs. Females
lays eggs in 1-cell stage that pass out in the
feces. A single female can produce an estimated
250,000 to 2 million eggs daily. Eggs have thick
shells with a mammillated proteinaceous layer on
the exterior and measure 50-80 x66-68 um.
Three lips surround the mouth
Male tail with spicule extruded
Ascaris impacted intestine
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Ascaris suum eggs passed in feces develop to the
1st stage larvae (L1) in 17-22 days at
temperatures of 18-22 C, the L2 appears at 24-27
days and the L3 beginning on day 34. Eggs become
infective for mice in about 6 weeks. Then they
may remain infective for 7 years of longer in
protected areas of lots and pastures. When
ingested, the infective eggs hatch in the
digestive tract and the liberated larvae
penetrate the wall of the large intestine. A few
may pass via the lacteals to lymph glands and
other locations.
Ascaris eggs in fecal flotation
Most larvae are in the liver by day 2-4 after egg
ingested and in the lungs by days 4-7. Larvae are
in the intestine and molted to L4 by days 10-13.
At this time, some larvae are spontaneously
eliminated from the small intestine into the
cecum and colon. The molt from L4 to L5, young
adults is on days 21-30. At this time, larvae
are again eliminated. The prepatent period is
40-53 days. Large numbers of adults live in pigs
for only about 6 months, at which time they
begin to be expelled, but some pigs continue to
harbor a few worms for more than a year.
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Pig liver with milk spots
Ascarids blocking bile duct of pig liver
Pathogenesis, signs and symptoms
The larvae migrate through the liver and cause
hemorrhagic foci which microscopically show mild
eosinophilic infiltration an a few small lymph
nodules in portal areas. On repeated exposure to
larvae, there is an increase in connective
tissue, infiltrating eosinophils, and dilated
lymphatics which grossly appear as whitish spots
or milk spots. Such lesions disappear in 25 to
40 days. Migrating larvae cause a verminous
pneumonia which may cause death if large numbers
of larvae are involved. Clinical signs are that
of pneumonia, pigs have an asthmatic cough
thumps, and may breathe with difficulty.
Secondary bacterial pneumonia may occur. Larval
migration enhances the pathogenicity of swine
influenza as well as viral pig pneumonia
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The adult worms compete with the host for
nutrients, interfere with absorption of
nutrients, may occlude the small intestine and/or
block the bile duct resulting in icterus. Exact
dollar figures for economic losses are difficult
to obtain. Estimates go as high as 75 million
yearly in USA. Losses are from death, decrease
in weight gain, condem- nation of livers and
inefficient weight gain. Pigs infected with
ascarids require 6 more feed per unit of gain
than pigs not infected.
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Diagnosis, Prevention and Control Diagnosis is
by finding liver or lung lesions or adults at
necropsy and/or eggs in fecal flotation. Hepatic
lesions caused by A. suum need to be
differentiated from those caused by Stephanurus
dentatus. Management and sanitation can be used
effectively to control swine ascarids. The
McLean County System developed by USDA and
farmers in the 1920s still holds with some
modifications and additions

1. Clean farrowing quarters scrupulously,
scrubbing with hot lye solution to remove as much
feces and dirt as possible. Follow with high
pressure steam and a hot clear water rinse.


2. Wash sows with soap and water, scrub if
necessary to remove adhering eggs. 3. Use
clean pastures that have not been grazed for
years by pigs.
4. Haul sows and pigs to pasture, do no
drive on contaminated lanes, etc.
5. Take care not to track worm eggs into
building on dirty shoes. Pigs raised indoors
have a lower prevalence of ascarids, but fewer
worms per pig.

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Oesophagostomum spp., the nodular worms of swine
(strongyloid) The pig is the only host. Adults
are in the lumen of the large intestine. Two
species of Oesophagostomum are common worldwide
O. dentatum, the common nodular worm and O.
quadrispinulatum, the long-tailed nodular worm.
Two other species have been reported from the
southern states O. brevicaudum, the
short-tailed nodular worm, and O. georgianum.
Oesophagostomum dentatum en face
Robust worms, females 8-13 mm (1/2 in.) in
length, males 8 mm (1/3 in.). Short buccal
capsule, cuticle at anterior end inflated
forming the cephalic vesicle. Leaf crown
present. Eggs in early cleavage pass in feces,
hatch, and develop on the ground. Pigs become
infected by ingestion of infective larvae (L3)
while feeding on contaminated ground or
vegetation. larvae pass into the large
intestine, enter the mucosa where they remain for
days to weeks and molt to L4 then return to the
lumen. The prepatent period varies from 16 to 60
days depending on the species and strain of
Oesophagostomum.
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Oesophagostomiasis
PATHOGENESIS , SIGNS AND SYMPTOMS
The economic loss to the swine industry in the
U.S.has been estimated at more than 25,000,000.
The nodules formed in response to the larval
invasion of the mucosa of the large intestine
interfere with absorption of nutrients and
intestinal motility. The submucosal nodules
produced by quadrispinulatum are much larger (5
mm) than those produced by O. dentatum because of
a more intense inflammatory reaction. Without
secondary bacterial infections, the lesions heal
in 5-7 weeks. Heavy infections cause enteritis,
weakness, anemia, emaciation, constipation,
diarrhea, unthriftiness, and occasionally death.
Pigs heavily infected with Oesophagostomum spp.
required 3 more feed per unit of gain than pigs
not infected. Little or no immunity appears to
develop to nodular worms, resulting in older
swine being more heavily infected.
Oesophagostomiasis is believed to be a
contributing cause to the "thin sow" syndrome in
Great Britain.
Oesophagostomum mouth closed
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DIAGNOSIS Finding the nodules and/or adult
worms. Eggs of Oesophagostomum are almost
indistinguishable from those of Hyostrongylus,
but the eggs can be cultured and the infective
larvae differentiated. Eggs of O. dentatum are
60-80 x 35-45 Fm and have 4-16 cells when laid.
The eggs of O. quadrispinulatum are 60-70 x 30-40
Fm and those of O. brevicaudum are 52-67 x 30-45
Fm.
Nodules on mucosa of large intestine caused by
Oesophagostomum larvae
Infective 3rd stage larvae of Oesophagostomum
dentatum
Oesophagostomum dentatum egg in a fecal flotation
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Trichuris suis - the whipworm of swine
(trichuroid) The pig is the only natural
host, but man has been experimentally infected.
The adults are found in the cecum and colon
attached to the mucosa by the anterior "whip"
end. Common in the U.S., a high incidence is
reported in Wisconsin, North Carolina, and
California. The body is composed of a long
slender anterior and a much thicker posterior
end. The esophagus consists of a column of
cells, the stichosome. Females are 38-53 mm (1½
- 2 in.) in length, the males 33-48 mm (1½ in.)
Eggs pass in feces, develop until they contain
infective larvae (L1) in about 30 days. When
ingested by a pig while feeding on contaminated
ground, eggs hatch, and larvae penetrate into the
wall of the cecum and colon. After a few days
they return to the lumen and develop into adults.
The prepatent period is 41-45 days
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.PATHOGENESIS, SIGNS AND SYMPTOMS Adults are
considered blood suckers and firmly attached to
the mucosa by the "whip" or cephalic end.
Secondary invasion by other organisms also
occurs. Large numbers of worms may cause
inflammation of the cecum and colon the cecum
may be filled with a bloody mucus. Clinical
signs of heavy infections include emaciation,
stunted growth, head-down posture with lower
abdomen tucked up, anemia, diarrhea and dark or
bloody stools in severe cases. The complex
pathogenesis may result by suppression of mucosal
immunity to resident bacteria induced by the
worms. Clinically, trichuriasis can be confused
with swine dysentery.
DIAGNOSIS Demonstration of eggs by fecal
flotation and adults at necropsy. The eggs
measure 50-56 x 21-25 Fm. Heavy infections
produce a copious bloody diarrhea before worms
are adult, and examination of mucosal scrapings
may be.
necessary to find the worms. Because of the
long, prepatent period and early onset of
clinical signs in heavy infections, fecal
examinations may not be sufficient for
diagnosis.
Cecal trichuriasis
Trichuris suis egg
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Metastrongylus spp., the lungworms of swine
(metastrongyloid) The pig is the only natural
host. Guinea pigs have been infected
experimentally. Adults occur in the small
bronchioles of the lungs. Two species of
Metastrongylus
Pair of trilobed lips of Metastrongylus spp.
are common in pigs throughout the world. These
two species, M. apri (elongatus) and M.
pudendotectus are found in mixed infections. The
third species, M. salmi, is rare but has been
reported from the USA. The lungworms are very
important parasites especially under pasture
conditions.
Adults are long and slender and have two lateral
three-lobed lips. Females are 28-48 mm (1-2 in.)
in length and the males are 14-19 mm (1/2 - 3/4
in.). The females have a prevulvular swelling at
the posterior end. The three species can be
differentiated by variations in these
traits. The life cycle of Metastrongylus spp. is
indirect and requires an earthworm as an
intermediate host. At least 17 species of
earthworms can serve as an intermediate host.
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The embryonated eggs deposited by females in the
bronchioles are coughed up, swallowed, and pass
out with the feces of the host pig. When
ingested by an earthworm, the egg hatches
releasing the L1 which penetrates the walls of
the esophagus, crop, intestine, hearts, and blood
vessels. The larvae molt twice and become
infective (L3) in about two weeks. A single
earthworm may accumulate 2000 or more
Metastrongylus larvae during a life span of up to
4 years. Earthworms also spontaneously shed
infective larvae that are capable of remaining
infective for swine for 2 months or more in moist
soil at 13C. In the pig, larvae penetrate the
gut wall and migrate to mesenteric lymph nodes
where they molt to L4. They migrate from the
lymph nodes by the lymphatics to the lungs,
break out of the alveoli, and molt to L5 stage.
The prepatent period is 3-4 weeks.
PATHOGENESIS, SIGNS AND SYMPTOMS Clinical
effects are usually mild and begin about 3 weeks
after infection. Coughing, unthriftiness, and
eosinophilia are most severe in young animals.
Within 2 weeks after infection, blood eosinophil
levels may reach 10-15 in association with focal
accumulations of eosinophils around the worms in
alveoli and bronchioles. As female worms begin
to produce eggs in large numbers, an alveolar
granulomatous process begins. In chronic
infections, catarrhal bronchitis leads to
conspicuous muscular hyperplasia and
peribronchial fibrosis.
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Gross lesions are usually inconspicuous,
consisting of greyish, nodular foci, 1-3 mm in
diameter and focal emphysema on the margins of
lung lobes, especially the caudal margin of the
diaphragmatic lobe where the parasites normally
localize in light infections. In young pigs
heavy infections, worms are found in the
bronchioles of all lobes. In addition to being
pathogens, lungworms are important as synergists
contributing to the pathogenicity of influenza or
enzootic pneumonia of pigs (Mycoplasma).
Concurrent lungworm infection with either one of
these diseases increases ten-fold the severity of
lesions and increases significantly the
potentiation of clinical signs. Shope (1940)
theorized that during swine influenza epizootics,
viruses may be incorporated in larvated lungworm
eggs and remain viable in a "masked" state (not
recoverable) for the life of the egg. Lungworms
developing from such eggs could transmit swine
influenza by the "unmaskingor activation of the
virus by stress. Intermittent or continuous
shedding of influenza virus by carrier swine has
been proposed, however, as the interepizootic
viral survival mechanism.
Metastrongylus greyish, nodular lesions in pig
lung
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DIAGNOSIS Diagnosis is by finding worms at
necropsy or eggs in feces. The
mammillated, larvated eggs measuring
45-57 by 38-41 Fm can be confused with
embryonated Ascaris eggs which measure 50-80 by
45-55 Fm. Antemortem diagnosis is complicated
because of intermittent egg shedding and the poor
flotation results with sugar and NaCl solutions.
A solution of magnesium sulfate (MgSO4, sp.gr.
1.20) gives good results. Higher sp. gr. is
undesirable because of the large amount of debris
floated up.
Metastronglylus
Ascaris
Metastrongylus and Ascaris eggs in fecal
flotation.
A good haven for earthworm intermediate hosts for
lungworms
Female tail
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Adult Swine I. Hyostrongylus rubidus, red
stomach worm (trichostrongyloid) Ascarops
strongylina, thick stomach worm (spiruroid)
Physocephalus sexalatus, thick
stomach worm (spiruroid) The pig is the only
definitive host of the three stomach worms,
although many animals can be paratenic hosts for
the larval stage of the two thick stomach worms,
A. strongylina and P. sexalatus. The latter two
thick stomach worms are located primarily in the
pyloric region of the stomach, and the red
stomach worm, Hyostrongylus rubidus, along the
lesser curvature in the fundic area. All three
of the stomach worms are associated primarily
with pastured swine. They have a worldwide
distribution, are more common in areas of warm
climate and in older animals. H. rubidus is less
than 10 mm (1/4 in.) in length. When first
removed from the host, they are red in color.
They have cervical papillae and the males have a
bursa. A typical trichostrongylid, the red
stomach worm resembles Ostertagia of ruminants.
Cervical papilla, lateral view
Anterior end
Hyostrongylus rubidus
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Both thick stomach worms, A. strongylina and P.
sexalatus are spiruroids and more robust than H.
rubidus. Ascarops has a cervical alae on one
side only (5)and the pharynx has sclerotized
rings in a multiple spiral arrangement (6).
Physocephalus has cervical alae on both sides and
the pharynx has sclerotized rings arranged in a
single
spiral. The pharynx of Physocephalus is much
longer than that of Ascarops. The posterior of
males of both thick stomach worms have caudal
alae, large papillae and 2 unequal spicules.
They are 10-20 mm long (1/2 in.).
Hyostrongylus, male bursa
Physocephalus, cervical alae, dorsal-ventral
view, single rings of pharynx
Ascarops, cervical ala, lateral view
Ascarops, multiple spiral rings of pharynx
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THE RED STOMACH WORM
H. rubidus has a direct life cycle and like most
trichostrongyloids, the eggs hatch and the larvae
develop on the ground to infective L3 in about
one week. After ingestion, infections become
patent in about 3 weeks. L3 enter the pits of
the gastric glands, remain for 2 weeks as they go
through 2 molts, and return to the lumen as L5
young adults. Larvae can remain in the mucosa for
several months in a histotrophic stage similar to
Ostertagia of cattle and sheep and cause
formation of small nodules.
THE THICK STOMACH WORMS
The life cycles of both thick stomach worms are
similar, both requiring intermediate hosts which
are dung beetles. Transport or paratenic hosts
are common in the life cycles of both Ascarops
and Physocephalus. Paratenic hosts are usually
an amphibian, bird, or small mammal. Once in the
definitive host, larvae bore into the stomach
mucosa and molt before emerging again into the
lumen.
Dung beetle Phaeneus vindex
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PATHOGENESIS, SIGNS AND SYMPTOMS Stomach worm
infections usually are not pathogenic, but if
enough parasites are present, hyperemia,
catarrhal gastritis, and submucosal edema may be
present. In severe cases, a yellow
pseudomembrane forms with underlining erosions
and deep ulcers. Clinically inapparent
infections with H. rubidus, which is a blood
sucker, leads to reduced weight gains and a
reduction in feed conversion of 7.
Diagnosis H. rubidus eggs are almost
indistinguishable from those of Oesophagostomum
in both size and morphology. They are typical
strongyle-type eggs in the morula stage with thin
shells. Hyostrongylus eggs measure 60-70 x 30-38
Fm. Eggs of the thick stomach worms are
thick-shelled and embryonated and need to be
differentiated from those of Gongylonema.
Ascarops ova measure 34-40 x 18-22 Fm, those of
Physocephalus, 31-39 x 12-17 Fm, those of
Gongylonema 57-59 x 30-34 Fm. TREATMENT
Dichlorvos is effective against all three stomach
worms. Fenbendazole, levamisole, thiabendazole,
ivermectin and doramectin are effective against
H. rubidus.
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35
Stephanurus dentatus, the swine kidneyworm
(strongyloid) The pig is the only natural host
though cattle have been experimentally infected
and a few field cases of cattle infections have
been recorded in Alabama. The adult parasite
occurs primarily in the walls of the ureters,
pelvis of the kidney, and perirenal fat.
Juvenile worms are found in the liver.
Kidneyworms are sometimes found in the pancreas,
lungs, other abdominal organs, lumbar muscles,
and in the spinal canal.
Stephanurus occurs throughout the world but is
common in tropical and subtropical areas. In the
U.S., it is common only in the southeastern
states. A survey in Georgia in 1976 reported
Stephanurus infections in 95.3 of market hogs
and a liver condemnation rate of 77.7. USDA
veterinarians inspecting meat in south Georgia
processing plants say they have never failed to
find the parasite in swine carcasses. In
Illinois, on the other hand, they are quite
uncommon.
Male female Stephanurus in swine ureteral cyst
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36
Stephanurus dentatus adults are stout-bodied and
have a mottled appearance. Males are about 2-3
cm (1 inch) in length and females are 3-4.5 cm
(1½ inches). They can be easily seen by the
unaided eye in a parasitized carcass because of
their size and their mottled appearance which is
due to the worm's internal organs showing through
the cuticle. These worms have an inconspicuous
leaf crown around the mouth. The male copulatory
bursa is quite small and square in shape. The
majority of adult worms are found in
cysts communicating with ureters. Eggs are
deposited in urine and thereby pass out of
the body. As many as 1 million eggs may be
passed daily by heavily infected hogs. They
hatch in 1 to 2 days on the ground and develop
into infective larvae in less than a
week. Experimentally, infective larvae can
survive in earthworms for as long as a month when
ingested by them. The earthworm can serve as a
paratenic host and swine can become infected by
ingestion of the earthworm which harbors
infective Stephanurus larvae.
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37
Infection is by either oral ingestion or skin
penetration. Larvae which are ingested penetrate
the intestinal wall and are found in mesenteric
lymph nodes for a few days where they molt to L4.
Larvae begin reaching the liver 10 days
postinfection. Once in the liver, the larvae
develop quickly and begin molting to L5 at 24 to
31 days postinfection. They then pass from the
liver the peritoneal cavity where they seem to
wander a great deal into almost any part of the
body. Some may even pass through the placenta
and cause prenatal infection, but the majority
eventually reach the perirenal region where they
perforate the walls of the ureters and become
adults. The entire life cycle requires at least
6 months before reaching patency and studies on
numbers of eggs voided in urine of sows show that
eggs are practically never found in large numbers
in samples from sows less than 2 or 3 years of
age and the greatest numbers of eggs are passed
by sows which are 6-7 years of age. A sow has
been shown to pass eggs for at least 3 years
following initial infection. Sooner or later the
worms die and
disintegrate. A whitish mass, consisting of pus,
is usually associated with the dead parasites.
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38
Ascaris milk spot lesions of swine liver.
Surface is smooth, color is normal. Lesions
resolve within 25 to 45 days if animal is not
reexposed.
Stephanurus lesions of swine liver. Surface is
irregular, color is purplish, Large lesions have
hemorrhagic centers and extent deeply into the
parenchyma.
Stephanurus egg in urine
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39
Life Cycle of Stephanurus dentatus
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40
PATHOGENESIS, SIGNS AND SYMPTOMS Aside from
general unthriftiness and arrested development
(which are symptoms common to parasitic
infections of all kinds) skin lesions may occur.
The urine sometimes contains pus and posterior
paralysis can be caused by a worm penetrating the
spinal column (but most cases of hindquarter
paralysis of swine are due to other causes).
The principal injury inflicted by kidneyworms
involves the liver and kidneys. The migrating
larvae cause an inflamed tract wherever they
migrate and often cause abscesses and adhesions.
Extensive grayish scars on the surface of a
healed liver look like the milk spots associated
with ascarid larval migrations. Such livers,
parasitize kidneys and other organs are condemned
for human consumption, as are the pork loins
which are frequently parasitized. When the
infection is excessive and is accompanied by pus,
large portions of a carcass, or sometimes an
entire carcass must be condemned. Condemnation
accounted for a 51 loss in value of livers,
kidneys, and loins to the swine industry in 1975
according to an estimate by the U.S. Department
of Agriculture. Other losses include,
condemnation of whole carcasses, lowered market
price, increased rate of infection with other
diseases, and increased death of pigs. Liver
condemnation losses were estimated at 14.9
million in 1984. Feed conversion efficiency of
infected pigs is reduced by 9.
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41
DIAGNOSIS The finding of worms 1 to 1½" long in
the perirenal site of a necropsied pig is itself
almost sufficient for diagnosis. Verification
can be made by observing the black and white
mottled appearance, orange-red anterior end, and
square male bursa. Finding the large (100 x 60
Fm) symmetrical strongyle-like eggs of
Stephanurus in the urine is diagnostic, but it is
not generally practical to do this and clinical
problems are usually associated with larval
migration and thus occur before
patency. TREATMENT Fenbendazole, ivermectin,
doramectin and levamisole are the only
anthelmintics on the market with label claims for
kidneyworm. Fenbendazole, ivermectin and
doramectin kill all stages. Levamisole kills
adult worms only.
Stephanurus egg in urine sample
Male female Stephanurus dentatus
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42
The fact that kidneyworm eggs are not usually
passed by infected swine until they are 2 years
old led workers at the Coastal Plain Experiment
Station in Georgia to breed only gilts for
maintaining the swine herd. Gilts are bred only
once and after having produced their first litter
are sent to market before mature kidneyworms can
develop in them. Additional contamination of the
premises is prevented by removal of gilts and
boars before they can pass many kidneyworm eggs.
Larvae from previous contamination can survive a
maximum of 6 months whether free of or in
earthworms.
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43A
Benefits By following the gilt-only management
system for 3 or 4 semi-annual farrowings,
Stephanurus can be eradicated from a contaminated
farm in 18 months or less. If reintroduction of
Stephanurus is prevented, former management
practices can be resumed. The elimination of
kidneyworms eradicates a costly problem. The
lower price paid for southern hogs compared to
those from the Midwest is based on the lower
carcass yield of southern hogs because of
condemnation of parts and necessary trimming of
high-value cuts such as loins. no special
equipment is needed. The small decrease in
number of pigs per gilt-litter is more than
compensated for by the higher sale price of
gilts, reduced maintenance expense, and the
reduction in chronic disease problems.
Chronic stephanuriasis
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43B
Gongylonema pulchrum, gullet worm of swine
Globocephalus urosubulatus, hookworm of swine
Gongylonema in situ
Globocephalus egg
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44
Macracanthorhybnchus hirudinaceus
June beetle
Anterior, probsoscis
Egg in fecal flotation
In situ, small intestine
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45
Trichinella spiralis, trichina worm (trichuroid)
Demodex phylloides, follicular mite
Heamatopinus suis, hog louse
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46
Balantidium coli cyst in large intestine mucosa
Lesions in large intestine resembling Hog Cholera
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47
HOGS ARE BEAUTIFUL