13.1.1 Trichomonas gallinae
Trichomonad 19 microns - protozoa
Mouth, pharynx, esophagus, crop, proventri- culus.
Chickens, turkeys, pigeons, doves, eagles, falcon, and hawks.
Extremely common in the domestic pigeon in which it may cause serous disease. Also fairly common in the turkey and the chicken and may be responsible for disease in the morning dove.
A disease primarily of young birds 80-90% or more of adult pigeons are infected but show no evidence of disease. Infected squabs may die in 10 days.
Lesions - appear as small yellowish circumscribed areas in the mouth (esp. soft palate) - 3-14 days after infection.
These increase in size and extend to the esophagus crop, and the pro-ventriculus. The liver may also be involved with the extension to the heart and pancreas.
Not found beyond proventriculus. Inflammation and ulceration of the oropharyngeal mucosa associated with palisading of the parasites in mucosa - penetrating the underlying tissues to reach the liver abscesses in the liver considered to be the cause of death.
In the turkey and the chicken, lesions are more common in the crop, the esophagus and the pharynx. (uncommon in mouth) lesions in morning dove are similar to those in pigeons.
- a. Initial depression
- b. Ruffle feather
- c. Weak-emaciation
- d. Accumulation of greenish fluid and cheesy material in mouth and crop - (may exude from mouth)
- e. Pendulous crop - poultry
- f. Necrotic lesions
Organisms are numerous in the mouth and the crop. Immunity - Symptomless carriers immune to reinfection. Some species are more susceptible. Tumbler pigeon more susceptible according to Miessner and Hanson in 1936.
Transmission by adults to squabs occur in a few minutes after hatching through pigeon milk from crop. Transmission occurs in chickens and turkeys through contaminated drinking water from infected birds.
Made on the presence of lesions and organism in the mouth - crop.
Revent infection from wild pigeons by shielding drinking facilities.
Chicken-turkey, grouse, partridge, pheasant, and quail.
Cuticle of anterior end of worms form a characteristic swelling. The double plugged egg measures 6-65 x 25-28 microns.Earthworms - intermediate host. Needs to pass through worm to hatch. Infective stage in 14-21 days. Adults tunnel in mucosa - tunnels are packed with eggs.
Lesions - pathogenesis - small numbers of worms produce no lesions but large numbers cause marked inflammation varing from a simple catarrh to croupous inflammation with diphtheritic pseudomembranes.
Nematode some investigators show very little morphological difference between this species and C.
Annulata except the anterior bulbous swelling just behind the head of the latter.
Turkeys,ducks and wild birds. Life Cycle-direct
Ovoviviparous - Larvated eggs 58 x 35 microns
Lesion: Similar to those of Capillaria.
similar to other species - beetles and possible roaches (Blatella) serve as intemediate host.
Infection is by ingestion. There is no migration outside the stomach. The glandular mucosa of the gladular portion of the stomach is usually parasitized. The adult stage is usually seen 25 days after ingestion of 3rd stage larvae.
Heavy infections cause gastrointestinal disturbances which may lead to emaciation. The nematodes are usually in the lumena of the gastric glands. The catarrhal gastritis that results may lead to a chronic hypertrophic gastritis. The typical mucosal surface is characterized by irregular circumscribed wart-like thickenings with a finely verrucose surface.
Rotational grazing between equidae and ruminants is an effective means of controlling the most pathogenic nematode parasites in both host groups. Cross-infection with T.axei is one possible undesirable consequence of that management practice.
Other aspects of epidemiology follow tose previously discussed relative to ruminants.
Recovery of a strongyle-type egg in the fecEs indicates the possibility. Fecal culture with recovery and identification of infective third stage larvae permits positive antemortem diagnosis. " Diagnostic drenching", using a foumulation of thiabendazole, is a more practical alternative. Clinical improvement may be expected if T. axei is the primary etiological agent.
Scraping of the mucosa or washing of the stomach ebable postmortem diagnosis which further requires good light, contrasting background (usually white) and some magnification.
The need for differential antemortem diagnosis is reduced by the advent of broadspectrum anthelimintics. Thiabendazole, for instance, is effective against adult and larval stages of all equine species that are characterized by a strongyle eggs.
- Thiabendazole, drug
- Trichlorofon has fair activity
- Dichlorvos has no larval claim
- Phenothiazine is poor.
* (Not found in USA). The above measurements are for the third instars.
Adult the common bot fly is a large fly resembling a bee in appearance and buzzing with the one pair of conspicuosly spotted wings. The throat bot and nose bot flies are smaller, darker, with clear plain wings. See family Oestridae.
Horse bots are highly specialized parasites that attack horses, mules asses and perhaps zebras. Bots do not molest cattle, sheep, or other farm animals, even though they may be grazing in the same pasture with horses. If the horses are removed from such a pasture, the bot flies will die without laying their eggs on the other animals. Occasionally a young horse bot is found in the skin of a human being, who is evidently an accidental unfavorable host. Under these conditions the bots act very differetly from the way they do in horses: they burrow rapidly about in the skin and have never been known to grow to any considerable size or to reach the stomach or intestines, where they normally attach themselves in horses. In the human skin the minute larvae cause severe itches, leaving a raised, reddened, circuitous streak, suggesting in minature the work of a meadow mole in a field. How the larvae get into human skin is not known and cases are rare.
The common horse bot fly and the throat bot fly occur throughout the United States wherever horses are found, but they are much more numeous in some localities than in others. Throat bot flies are extremely abundant in the drier parts of the country and at the higher altitudes--that is, above 3000 feet. The presence of large number of horses in which they develop favors and abundance of horse bots. The nose bot appears to have become established in the Unites States, about 1998. It was first observed in the Western part of the Dakotas and in eastern Montana and since that time has spread over much of the region from Illinois to Eastern Washington and Oregon, and from Southern Canada to central Kansas.
The eggs of the common bot fly are ready to hatch 7 days after being laid on the horse legs, but hatching does not take place until they are rubbed by the warm lips of the horse. The bots may lie quietly in the eggs as long as 3 months awaiting this stimulus. When the horse bites the spots where the eggs are attached, the moisture warms them, and the bots push off the egg cap and adhere to the animals moist lips. They soon penetrate the mucous covering of the lips and tongue. They burrow there for about a month before going to the stomach. During this time they molt, or cast their skins, and increase considerably in size.
The eggs of the nose botfly hatch in 2 to 4 days, and the minute spiny larvae penetrate theskin of the horses lips and work toward the mucocus lining, where they continue to burrow for more than a month before passing to the stomach.
The eggs of the throat botfly hatch in about 6 days, and the young bots immediately crawl into the horses mouth. The first stage larvae soon establish themselves in pockets between the molar teeth, where they grow and molt to the second stage. After 3 to 4 weeks in the mouth they pass to the stomach and intestine, where they attached themselves in the pyloric or exit, end of the stomach and in the duodenum just below the stomach.
Horse owners soon become aware of the presence of horse bots because of annoyance the flies cause the animals. This is particularly true of the nose botfly, which lays its eggs around the lips of the hroses. The animal attacked reacts violently; it may run away and sometimes serious damage results. These flies prevent horses on pasture from grazing. The animals usually stand in groups, preferable on the highest spot available, with the nose of one resting on the back of another. Horses are often seen walking or trotting across a pasture with heads constantly nodding to avoid the attacks of nose flies.
Contrary to the belief of many persons, these flies do nto sting or otherwise hurt an animal. They just frighten them.
The newly hatch nose bots burrow into the lips and travel around in the mucous lining of the horses mouth; the young common bots burrowing habbit causes considerable irritation and perhaps at times interferes with feeding. In route to the stomach, the bots sometimes attach themselves in the pharynx have been known to cause swelling of the throat sufficient to prevent the passage of food. The tissue reaction is usually slight, however.
In the stomach and intestines, the bots remain attached for several months. At the points of attachment deep pits are formed in the lining membranes which may serve as places of entry for germs. These larvae have also been known to perforate the gut wall causing peritonitis. If the infection is very heavy, digestion may be seriously interfered with, and clusters of bots attached at the exit end of the stomach may impeded the passage of food. These conditions may give rise to olic, which responds to anit-bot treatment. The nose bot also has the habit of reattaching itself in the rectum as it passes out. It causes irritation and itching at this site. Cases have been reported where these larvae have migrated to the brain, as well as the ovary of the horses.
Much damage caused by bots in the mouth and digestive tract of horses is subclinical, i.e., not recognized by stock owners.
At postmortem they are commonly seen. Recover from feces after treatment. Many bots and poor nutrition----signs. Few bots and good nutrition---signs. In the fall we can usually assume horses in the U.S. are infected; hence, treat for bots is part of a routine parasite control program.
An effective method of destroying the eggs in the fall consists of applying water at a temperature of 1050 to 1100 F with a sponge or swab. Applying the warm water with vigorous rubbing causes a high percetage of the eggs to hatch and larvae quickly die. This is a critical aspect of control and prevention of reinfection after treatment. Ideally the eggs should be removed soon after, the first killing frost.
This treatment should be administered not earlier than 1/2 month after frost. A fast of 18 hours should preceed use of CS, and no purgative should be given with due caution by a competent veternarian. The volatile liquid produces a limited area of inflammation in the stomach of a horse or mule, but this is not known to have serious consequences and disappears in a week or two. When the capsule is administered by inexperienced persons, however, there is danger that it may break in the mouth. For this reason CS2 is nearly always given by stomach tube, and in combination with other drugs (to improve spectrum of activity).
One of the most practical developments in medication for the removal of bots from equine is the community or area campaign for eradication by medicinal treatment of horses and mules. In the Middle West, the South and elsewhere, these campaigns have been carried out with considerable success. As a rule, area or community treatment is supported and arranged for by the county agent of farm advisor. Under ideal conditions, all the horses in a given area are treated at the same time and at one place or in a limited number of places where the animals are assembled.
A program of this type enables the veterinarian to see, examine and treat many animals in an efficient manner. It can become a good opportunity for client education. A saddle club, 4-H Club or boarding stable may sponsor a "horse health" clinic with your cooperation and encouragement.
13.4.1 Vahlkampfia lobospinosa- amoeba - 24 micronsProtozoa in cattle rumen and reticulum.
13.4.2 Entamoeba bovis - amoeba - 20 micronsProtozoa cattle, rumen reticulum feces.
13.4.3 Monas communis - flagellate - 4 micronsProtozoa cattle, rumen reticulum feces.
13.4.4 Trichomonas ruminatium - flagellate - 9 micronsProtozoa in cattle, sheep goat
13.4.5 Callimastix frontalis - flagellate - 12 micronsProtozoa cattle
13.4.6 Trypanosoma theilari - Trypanosome - to 70 micrinisProtozoa in stomach of fetus
13.4.7 Genera: Dasytrichia, Diplodinium, Entodinium, Isotri.Protozoa in cattle rumen, reticulum are all ciliates (commensals) 40-270 microns.
13.4.8 Paramphistomum liorcis - " Rumen fluke" - to 11 mmTrenatide
13.4.9 Paraonphistomum cervi - "Rumen fluke" to 11 mmTrematode
13.4.10 Cotylophoron cotylophoran - "Rumen fluke"Trematode
The above flukes are found in the rumen, reticulum and small intestine of ruminants (cattle, sheep, goat, deer) they belong to family Paramphistomatidae which include conical flukes (cone-shape-quite uncharacteristic). They are fleshy with thick bodies and circular in transverse section. A sucker is located at the base and tip of the cone. They are pink in color and maggot-like in appearance. Their distribution is world wide, however, are of greater importance in tropical and subtropical area.
May be difficult since signs occur before eggs are passed. However, those animals that are severely affected also have marked persistent diarrhea and often young worms are passed out in the feces and can be recovered. Probably this condition is most apt to occur in the younger stock maintained on pasture suitable for intermediate host. Eggs are distinctly operculated and measure 135 x 70 microns. Segmentation is also distinct, however, eggs has to be distinguished from those of Fasciola hepatica (see latter).
First intermediate host, aquatic snail: Planorbis, Bulinus, Fossaria (USA) Pseudosuccinea, Segnitilia,(Australia). Crecariae encyst on vegetation and develop to metacercariae. When these are ingested by the definitive host they are released in the duodenum and then migrate back up to rumen. Complete life cycle takes approximately 6 months.
The adults do not seem to be pathogenic. However, the immature stages can cause hemmorrhage and inflammation of the small intestine while migrating. The degree and extent of damage produced depend on the number of worms present.
Digestive disturbances are the major signs that have been associated with this fluke, but only when they are migrating. In heavily infected animals they may become dull, weak, and develop anemia. Persistent, fetid diarrhea may result from the enteritis. Death may occur from exhaustion resulting from the diarrhea.
Albendazole is effective agaisnt immature stages. Tetrachlorethylene and hexachlorethylene and hexachlorethane are effective against adults.
Same as for Fasciola
Nematode in rumen, reticulum, omasum, sheep, goat, cattle, deer. Coprophagous beetles-intermediate hosts.
Nematode in cattle, sheep, goat, bision.
6. 7 mm. - Nematode in cattle Bison
Slender - like Trichostrongylus. Difficult to see grossly except when cleared of debri. If abomasal mucosa is washed clear they are readily visible by their reddish brown color.
No apparent buceal cavity present and two small cervical papillae appear in both sexes.
Spicules have three fairly easily distinguishable branches of which the main one is the terminal/part of body of spicules. The gubernaculum is racqet or spindle-shaped. The females are more difficult to identify between the closely related generic groups. Grasspiculagia, Teladorsagia. It is a specialist task.
In Ostertagia females, there is often a vulva flap presence and a double ovijector without prominent cuticular features. The shape of flap in some ranges aid in differenciation of species.
Direct. L3 is present within a week after the eggs are passed under optimal conditions of temperature. Preparasitic larvae do now withstand prolonged freezing esp. in areas of long winters.
On ingestion, L3 migrate into mucosa where two mols occurs.
Young adults emerge onto surface of mucosa. Some 4th stage larvae emerge onto mucosal surface, 4th molt is usually completed in 10 days after infection. Some larvae may mature by the 23 day. Others may remain in mucosa up to 3 months without becoming mature. Prepatent period is between 15-17 days. Inhibition of larval development assumes great importance in this group of parasites. Longevity of parasite infection is 9 months.
Is an important widespread and continuous problem in temperature zone and can be acute but more often chronic or subacute infection.
Small circular raised areas about 1-2 mm. in diameter are of diagnostic importance. In the nodule the worms develop and the adults may be found, projecting from nodule into lumen or free on mucosa.
Ostertagia sp. infectionis cheifly of importance in cattle. Two forms of disease observed.
In calves associated with adult parasites consisting of an abomasites with edema and necrosis. Decreased albumen levels - significant reduction in weight gain followed by death.
The other consist of a severe clinical entiry in housed cattle. Chronic diarrhea and emaciation frequently ends in death. In some cases more than 200,000 parasites may be present with 60% being immatures. Abomasum mucosa greatly thickened, edematous with some superficial necrosis and acute inflammatory exudate. Serum protein as low as 4-5 gr./100.
The gross abomasal tissue from bovine and the kodachromes (slide in library set) show the distinct nodules characteristic of larval mucosal invasion by Ostertagia. Of course, it is the infective larvae which invade and after moulting to L4 emerge through the small dark opening seen in each nodule, stages henceforth, including the adult, being free in the lumen partially buried in the nodular opening.
The length of time larvae remain in the nodules is the basic for the seasonality of clinical illness. In the early autumn a typical Ostertagia infection takes place in that with cooler weather and consequent survival of infective larvae, large numbers may be ingested. Within six hours after entering th host, these larvae penetrate into the abvomasa glands an during the next three weeks grow and moult, a nodule forming all the awhile. By the end of this time, the larvae leave the abomasal glands emerging from the nodule to grow to adults and the nodules of mucosa recovery rapidly over the next month though blood sucking by adults produces other pinpoint lesions. This is what happens in the autumn where adult worms predominate and is Type I Ostertagiasis. It is an ordinary infective process in which treatment is possible and recovery may be rapid.
In the winter form the disease - Type II Ostertagiasis - the larvae remain in the abomasal glands. The reason for this winter inhibition of larvae is not yer understood. This s the essential difference in the two type and consequently in autumn nature parasites predominate while in the winter immutures predominate. Between the seasons, when disease incidence is minimal the numbers of adult and immature parasites approach equality.
In both types of Ostertagiaisis the signs appear at about the time of emergence of the young parasites from the abomasal pH rises from its acidic normal 2.0 or 3.0 to over 7.0 at which leve lpepsin and pepsinogen activities stop. This ceasation of peptic digestion occurs fairly early and may persist for five weeks or so. When the pH risen above 7.0, tisue fluids begin to pass intercellularly into the abomasal lumen and diarrhea begins within 24 hours and remains as long as the pH is up. Bloods proteins are gradually lost under these conditions and a hypoporteninaemia develops tissue fluids become more stagnate and the Bottle jaw Syndrome as well as generalized edema may be observed.
When the mucosal glands again become functional (after perhaps as much as five weeks) and the pH returns to acidic normal the idarrhea ceases and conditions gradually correct themselves provided adult worms have been removed.
The signs in the autumn Tyoe I are generally by no means so severe as in the winter form. Autumn grazing calves when infected heavily will show a failure to gain weight or a frand loss of weight accompanied by a diarrhea green in color from chlorophyll which is not broken down at pH over 7.0. There is hardly time for edema to develop, and dehydration is more the rule, eyes being sunken and at coat looks sparing. There is not anemia and no pyrexia. Mortality is usually low.
A much higher mortality can be expected with Type II. Cattle in out temperature area from Georgia through Maryland are usually outwintered rather than housed, no small stress to animal. Additionally non-productive cattle stock are often overwintered on a bare subsistence dier and malnutrition has a significant additive effect in the pathogenesis of this disease in which the ability to utilize even plentiful food is impaired. Animals lose weight to the point of emciation with a profuse watery diarhea (brownish to almost clear if housed rather than on pasture). The greater blood protein loss (perhaps because of less protein intake during winter) eventually shows up as tissue edema in this type Ostertagiasis and anemia is evident. Fecal egg counts are of very little value here since the problem is well advanced before adult worms even begin to lay eggs. The best means of confirming a history-based diagnosis is necropsy and through examination of abomasal contents. Worms may not be evident at first but when the lumen contents are washed over #80 standard screen to rid of particular matter, the worms which are held back by the screen can be sen. As many as 30,000 may be expected in a severely parasitized adult animal in which case nodules on the mucosal surface may be so numerous that they become confluent and a diagnosis based on abomasal lesions alone may not be possible.
Nematode in abomasum of sheep, goat, cattle.
Nematode in abomasum of cattle, deer
Nematode in abomasum of cattle, sheep, goats -Southeastern.
The worms are easily seen - ovaries are twisted around intestine containing blood giving characteristic appearance. Asymmetrically - placed dorsal ray in male. Vulva flap present. In H. contortus it is lingui - form and ear-lobe-like in H. Place Vula in posterior 3 r of body. (Mecestocirrus - vulva at tip of tail).
L3. May hatch at 90 C -- larvae enter mucosa develop, and worms return to surface of mucosa in 4th stage.
H. contortus prepatent period 12-15 days. H. placei prepatent period 26-28 days.
Adult feed for 12 minutes at a time and move to new site. Hemorrhage continues for 6-7 minutes. All are blood suckers in warmer regions and is often the most important nemotodiosis of domestic ruminants. Severe anemia is common and free bloods or blood clots are observed in lumen abomasum on necropsy.
Nematode In abomasum of cattle, sheep, goat.
Stomach - Equine, pig, man (other) very wide host range. T. longispicularis - abomasum and small intestine - 6.1 mm T. rugatus - small intestine - sheep, goat. T. colubriformis - small intestine - sheep, goats, others -6 mm T. vitrinus - small intestine - rarely abomasum - 65 mm - T. retortaeformis - small intestine - goat, rabbit, hare
T. falculatus - small intestine -goat, antelop
T. probolurus - small intestine - sheep, camels, man
T. capricola - rarely abomasum 6.8 mm
There are a few other species in domestic fowl. It is important for the veterinarian to know that T. axei is found in a large numbers of host, species and that it produces unusual lesions in horses, which make it important from the standpoint of stock and pasture location. This species has been reported in more than 40 species of animals. There is no evidence of immunity in horses.
Pathogenesis unique in equine. L3 penetrates mucosa - enter muscular - is - mucosa where it produces local hypermia, lymphatic and catarrhal inflammation, necrosis, erosion and proliferation. Pad or cushion-like thickenings observed in glandular stomach (fundus) - diameter 1 - several cmm - circumscribed hyperplastic area are seen which are whithsh at first - later become eroded in the center and the lesion appear as depressed reddish craters with lighter color walls - raised plaques - Diphtheric membrane necrotic. Many worms in walls mucus and mucosal crypts - revealed by scraping surface on necropsy.
Probably none over 10 mm - all are small pale reddish brown in color, anterior end simple - with no buccal cavity. Naked vulva (non flap), characteristic bursae and spicule. Worms are not too host specific. Therefore control is difficult.
Life Cycle - Typical of the family.
Pathogenesis - not too pathogenic. Apparently are blood suckers and produce considerable toxins: 2000-10,000 worms produce symptoms which vary. A disease primarily of lambs and yealdings rather than adults.
Few symptoms except weakness and inability to stand.
May last throughout summer and fall - anorexia, unthriftiness -weakness, constipation or diarrhea which may be black according to Australian reports which also cites a form of bone involvement which is associated with leg weakness, spontaneous fracturs have also been reports - femur and humerus involved - anemia rarely observed.
Under experimental work the nematodes depresses protein digestion, interfere with calcium and phophorous utilization and decreases phosphorus and calcium retntion in the blood.
Difficult - tentative on eggs - but not too characteristic. Identify adult worms or larvae on fecal culture.
Albendazole recently has been shown to be effective against all stages including the inhibited larvae in mucosa (hypobiosis).
- 1. Ciliates - gener same as in cattle - Protozoa
- 2. Trichostrongylus axei (See Bovine) for other species in stomach and intestine
- 3. O. circumcinta - "Medium Stomach Worm" - 12 mm. - Nematode abomasum of sheep, goat, antelope, deer, elk, muck, ox, reindeer.
- 4. O. trifurcata - stomach worm - 7 mm - nematode abomasum of sheep, and goat less commonly cattle.
- 5. O. occidentalis - Stomach worm 16 mm - males Nematodes abomasum in sheep, musk, ox.
- 6. Mashllagia marshalli - stomachworm 20 mm - Nematode
- Sheep, goat occasionally in intestine. Tropical and subtropical. Spicule branches long and slender with delicate transparent membrane attached to one but surrounds all three branches-females difficult to differentiate from Ostertagia unless gravid. Eggs are very large - 180 200 microns x 75 to 100 microns with dark segments etc.
First molt in egg, so it is the L2 which hatches (L1 larvae being protected). Infection is by ensheathed L3. The parasite has very long prepatent period of 3 months.
- 7. Haemonchus contortus - "twisted stomachworm - nematode (see Bovine).
Nematode in stomach - pharynx thickened with spiral rings
Nematode in stomach - pharynx with thick ringlike spirals - inflation of cutical anterionaly with cervical alae.
Nematode a trichostrongyle.
Swine stomach worms are of very common occurance but clinical illness appears to be the exception rather that the rule. When clinical signs do occur they are associated with poor growth, gastritis, anemia, and sporadic death losses.
1970 survey in Indian on month old feeder pigs from several Southern states - 19% Ascaops 1% Physocephalus and 0% Hyostrongylus rubidus. 1952 survey on market weight pigs from only Georgia -- 77% Ascarops, 52% Physocephalus and 45% Hyostrongylus. these surveys illustrate the prevalence of swine stomach worms and also theincidence seems to be declining, probably due to differences in management practices in recent year--notably confinement operations, and the use of temporary vs. permanent pastures of past. All three stomach worms occur mainly with pastured swine. Hyostrongeylus rubidus is exceptionally poor in resistance to cold and dryness compared to other trichostrongylids. In the 1970 survey 04% Hyostrongylus could have been due to the fact that they were winter pigs and pastured in colder months. The 1952 survey was done on summer pastured pigs.
All three of these worms burrow into the stomach mucosa and cause some irritation but do not result in clinical signs unless there are heavy infections or the animals are poorly nourished or under some stress. In mild cases, an excess of thick mucous covers the mucosa of the stomach, constitutng a catarrhal gastritis. In severe cases, a yellow pseudomembrane forms and deep ulcers may be present.
Clinical Signs and History: All these stomach worms are associated primarily with pastured swine and where clinical signs occur, they are referable to gastritis and anemia. Aside from affecting young pigs, there are reports of parasitic gastritis developing in sows under that stress of lactation. Sometimes these sows develop bleeding gastric ulcers which lead to melena and anemia.
A. Fecal egg exams: show small, thick shelled embryonated eggs of Ascarops and Physocephalus. Hyostrongylus eggs are almost indistinguishable from Oesophagostomum eggs, however, this leads to difficulty in diagnosis. B. Necropsy: Because worms and eggs can be present without disease a definitive diagnosis can be made only findings both the worms and pathogenic evidence of gastritis on necropsy. At necropsy, worms are found closely associated with the mucosa in thick mucous or under a diptheritic membrane. They should be identifed as to species.
Control measure are to avoid pastures or moist, damp places conductive to Hyostrongylus development anything leading to reduced ingestion of dung beetles or transports hosts will control Ascarops and Physocephalus. At the Tifton Experimental Station, they have found that plowing a strip around temporary pastures helps control stomach worms and other parasites because pigs tend to defecate in the barren strip rather than the pasture.
Nematode in stomach wall - see esophagus
Nematode stomach and dumdenum of dog, fox, cat, bobcat, lynx - Nematode
Nematode stomach of dog, fox, cat, bobcat, cyote, lynx.
The amove 3 nematodes are spiurids which require an intermediate host to complete life cycle. The physolopterid worms utilize orthoptera and beeltes as intermediate hosts and are stout. Their cuticle in both sexes is posteriorly extended to form a sheath which projects beyond the caudal end of the worm. In the fertilized female the vulva is covered with a ring of brown cement material. The eggs are larvated an measures 40 x 34 microns for P. rara and 49 -58 x 30 -34 for P. praleputialis.
Worms are found attached to gastric mucosa on which they feed or suck blood.
larvated eggs with a refractile nature. Adults when observed in stomach look like ascarids, though not attached.
Nematode (In canine only)
Nematode (In feline only)
Nematode (see intestine) - In heavy infections the above ascarids my migrate to any portion of G.I. Tract and may be frequently vomited.
Nematode stomach do, cat, mink, pole cat and wild carnivores.
A large head-buld characteizes this genus. It is armed with 11 transverse rows of spines while the anterior 2/3 of the body bear large flat cuticular spines. The eggs are oval with a thin cap at one pole: they hve a greenish shell ornamented with fine granulations in one cell morula stage - 69 x 37 microns.
Eggs hatch in water and the larvae are ingested by intermediate host - (cyclops) which are later ingested by fish - frogs or reptiles in which they become encysted - on ingestion by final host larvae migrated thru liver and other organs also mature in stomach.
Yellow mosaic lesion observed in liver - with burrows filled with necrotic material in the parenchyma. Thick wall cysts may be observed in stomach wall - peritonitis - very pathogenic in cat.