Parasit Exam Three

Transplacental Transmission

Adult stage in Toxacara canis. In mid-gestation of pregnancy, some arrested larvae in the adult dog become active. First Stage. ______________________ Transmission: -Larvae migrate to the placenta -Migrate to fetal liver (>d 43) -Following birth, larvae use tracheal route to SI -Patent by 21 days of age

Transmammary (Lactogenic Transmission)

Adult stage in Toxacara canis. In mid-gestation of pregnancy, some arrested larvae in the adult dog become active. Second Stage. _______________________ Transmission: -Some of the activated larvae migrate to the mammary glands -Late pregnancy and early lactation -Larvae ingested during suckling (develop directly in the gut) -Not as important as to pup infection as TP transmission

Gut (SI)

Adult stage in Toxacara canis. In mid-gestation of pregnancy, some arrested larvae in the adult dog become active. Third Stage. Some larvae migrate to the _____________ of the dam.

Refugia

Allowing susceptible worms to exist.

Baermann Technique

An apparatus to demonstrate larvae in feces. Used in the diagnosis of lungworms such as Dictyocaulus spp.

Tight Junctions

An area of fusion of the lipoprotein layers of the plasma membranes of adjacent abomasal epithelium cells. Maintains the integrity of the abomasum.

No. Sometimes you will deworm the animal, the symptoms go away, but they will become reinfected by the hypobiotic larvae becoming activated. (As in Ancylostoma caninum).

Are arrested larvae in muscle and gut walls killed by routine deworming?

Synonyms for Parelaphostrongylus tenuis

Pneumostrongylus tenuis Odocoileostrongylus tenuis Elaphostrongylus odocoilei Neurofilaria cornellensis

Strongyles

Primary ruminant genera of ____________________: 1. Trichostrongylus 2. Cooperia 3. Nematodirus

Premunition

Resistance to an infection which occurs when an acute infection has become chronic and lasts as long as the parasites remain in the body. Failure of larvae, whether acquired from the environment or from an arrested state, to take because of the presence of adults. Occurs in Ostertagia spp., possible treatment with subclinical infections in the future.

*H*aemonchus *O*stertagia *T*richostrongylus

The *complex* that generally causes parasitic gastroenteritis in the family of Trichostrongyles.

Nematodirus spp.

Thread-necked worm. CAN differentiage egg from other strongyles because it is *very large*. Female lays *very few* eggs. Life Cycle: Direct, except... 1. Larval stages develop within the egg and do NOT hatch until L3. 2. Eggs/L3 can survive on pasture for extended periods of time (survive freezing, but susceptible to dessication). 3. After ingestion, the L3 exsheaths in the abomasum. 4. Migrates between the villi in the *SI*. 5. Emerge as adults 15-26 days (PPP). 6. May undergo hypobiosis.

Strongyloides fuelleborni

Threadworm of primates. The primary threadworm of primates.

Trichostrongylus colubriformis

Tichostrongyle of sheep.

Trichostrongylus vitrinus

Trichostrongyle of cattle.

Trichostrongylus capricola

Trichostrongyle of sheep and goats.

Somatic

____________________ migration is an effective means of infecting the *fetus and pup*.

Protostrongylus spp.

Fine hairlike worm found in *bronchioles and lung parenchyma*. Most have a *dorsal spine* on tail of larva. DH: sheep, goats, lagomorphs IH: snails and slugs

Periparturient Rise

In Haemonchus spp. Occurs in lambing ewes. High egg shedding begins two weeks prior until 8 weeks post-lambing. Hypobiosis usually ends with lambing. Immunological relaxation. Results in egg shedding increase that coincides with period when *young susceptible lambs* are on pasture.

Uterus

In Haemonchus spp., the barber pole effect is from the ___________ wrapping around the gut.

Decreased, Increased

In Phase II of ostertagiasis, you would expect to find ______________ blood protein levels and _________________ blood pepsinogen levels due to the destruction of tight junctions.

Skin penetration and lactogenic transmission

In Strongyloides ransomi, infection is primarily by these two routes.

1. Strict sanitation 2. Good pasture management 3. Compost manure 4. Good nutrition

List good management practices that would help decrease the incidence of parasites without overloading on deworming medication, which ultimately leads to increased resistance.

Protostrongylus stilesi Protostrongylus rushi

Lungworm of bighorn sheep.

Hookworms

Medium-sized worms. Anterior end bent dorsally (hooked). Well developed buccal capsule with teeth or cutting plates. Located in the *small intestine* of most vertebrates. Voracious blood suckers.

Uncinaria stenocephala

Northern hookworm of carnivores. In northern US and Canada. Eggs and larvae survive freezing. Slight pathogenesis, clinical disease rarely observed. DH: dogs, foxes, wolves, rarely cats Life cycle (similar to A. caninum, but develop at lower temps). Transmission: -Oral route is most common -Cutaneous transmission not as successful -*NO transplacental or transmammary transmission*

Pointed, Large Intestine

Pinworms are unique in that the females have long, _________________ tails. They inhabit the ____________ ____________.

Enterobius vermicularis

Human pinworm. Physicians often suggest to parents that the best control is to *get rid of the dog or cat*. NO! Human pinworm is transmitted among humans ONLY. DH: humans (*children*), primates Life Cycle: Similar to Oxyuris equi.

Cutaneous Larva Migrans (CLM)

"Plumber's Itch". Similar to visceral larva migrans (VLM) except larvae penetrate and remain in the *cutaneous tissue*. Characterized by inflamed, pruritic, serpentine tracts in the skin. Caused by L3s of Ancylostoma braziliense.

Characteristics of All Strongyles

-Tend to be larger and stouter worms in the order -Adults in *large intestine* of herbivores -Well-developed buccal capsule -Females are oviparous -Males have well developed bursa and rays -Life cycle is direct -Infective form is L3 -Infection is by ingestion of L3

Routes of Infection for Toxascaris leolina

1. Direct - ingestion 2. Predation on paratenic host *NO transplacental or lactogenic transmission.*

Routes of Infection in Toxocara cati

1. Direct - tracheal migration 2. Lactogenic - transmammary 3. Predation on paratenic host 4. Ingestion of worms in vomit or feces *NO TRANSPLACENTAL TRANSMISSION*.

80

20% of a herd/flock harbors _______% of the parasites.

Vulgaris

A foal that is 24 weeks old (~6 months) will most likely have Strongylus _________________ eggs in its fecal exam.

Edentatus

A foal that is 44 weeks old (almost 1 year) will most likely have Strongylus _________________ eggs in its fecal exam.

Parascaris equorum

A foal that is twelve weeks old will most likely have _________________ _________________ eggs in its fecal exam.

Westerni

A foal that is two weeks old will most likely have Strongyloides _________________ eggs in its fecal exam.

Acute Hookworm Disease

A certain severity of Ancylostoma caninum infection. -Massive infection -Pale mm's -Tarry stool -Eggs in feces, but clinical signs may precede -Normocytic, normochromic anemia -Treat IMMEDIATELY!

Secondary or Decompensated Hookworm Disease

A certain severity of Ancylostoma caninum infection. -Moderate numbers of worms -Microcytic hypochromic anemia -Pale mm's -Emaciation, dull, lethargic -Stool dark and tarry with eggs -Usually secondary to another condition -Institute supportive therapy and anthelmintics

Chronic or Compensated Hookworm Disease

A certain severity of Ancylostoma caninum infection. -Small numbers of worms -Dogs appear healthy -Eggs in feces

Peracute Hookworm Disease

A certain severity of Ancylostoma caninum infection. -TM transmission of large numbers of L3s (50-100 can be fatal). -Acute blood loss -2 weeks old -Pale mm, soft/liquid diarrhea, dark to blood in feces -Often with no eggs in feces -Blood transfusion, antibiotics, anthelmintics -Best to prevent by *treating the pre and post whelping bitch*

Visceral Larva Migrans (VLM)

A prolonged somatic migration of larval parasites in an abnormal host. Used to describe human infection with the dog ascarid, T. canis. Could also apply to infections with T. cati, T. virulorum, and Baylisascaris procyonis. Infection Route: Large #s of eggs contaminate environment. Children while eating abnormal things ("pica"), may ingest dirt contaminated with T. canis eggs. Larvae migrate abnormally to liver, lungs, brain, or eye. Signs: human - irritability, intermittent fever, anorexia, hepatosplenomegaly, eosinophilia, hyperglobulinemia. Dx: history of pica, clinical signs, find larvae on biopsy, ELISA on patient.

Chronic Larval Cyathostomiasis

A sign of small strongyle infection in horses. Due to accumulation of larva over time. Inflammation and thickening of cecal and colonic mucosa occurs --> *granulomatous colitis*. Signs: *protein-losing enteropathy*, hypoalbuminemia, extreme gerneralized edema, loss of condition, failure to grow. Treatment: regular anthelmintics.

Acute Larval Cyathostomiasis

A sign of small strongyle infection in horses. Hypobiotic larvae emerge, leading to mucosal injury/ulceration. Seasonal from late winter --> early spring. Signs: acute watery diarrhea, dehydration, fever, potential death. Dx: no eggs or only a few in feces.

Subulura brumpti

Avian pinworm. Found in the ceca of poultry. Dx: thin shelled egg in feces. Treatment: none known.

Haemonchus placei

Barber-pole worm of cattle. Found in *abomasum*.

Haemonchus contortus

Barber-pole worm of sheep. Found in *abomasum*. *Most important parasite of sheep*. Needs 5 cm of rain/month and 58-98 F. Survive the winter or summer by residual adult worms in stomach or by hypobiotic larvae in stomach. Signs: *ANEMIA* (bloodsucking L4s and adults), three classic haemonchosis syndromes.

Trichostrongylus spp.

Black Scours or Bankrupt Worm. Direct life cycle. Usually found in mixed infections. Typical strongyle-type egg.

Ostertagia ostertagi

Brown/Medium/Western Stomach Worm. Found in the *abomasum* of cattle. *Most important helminth parasite of cattle in the U.S. and worldwide.*

Different Cooperia spp.

C. pectinata - cattle C. punctate - cattle C. oncophora - cattle C. curticei - sheep, goat

After the fecal crust forms, larvae are protected. There is enough moisture for development. Larvae can be *transported away from the pat* by rain, birds, insects, cattle (mechanical dispersal).

Can Ostertagia spp. larvae live inside fecal pats once in the environment?

Ostertagia spp. survive well under snow pack (ground insulation), which makes them a source of infection in early grazing season.

Can Ostertagia spp. overwinter in northern pastures?

Patent Phase, days 25-55

Certain phase of Dictyocaulus viviparus. -Adult parasites in bronchi and trachea -Severity of signs reaches apex -Period of greatest mortality -Severe bronchitis, emphysema -Consolidation of lobules -Hyaline membrane formation -Cellular exudate, frothy mucosa

Post-Patent Phase, days 55-70

Certain phase of Dictyocaulus viviparus. -Adult worms expelled -Impaired pulmonary function may continue -Chronic bronchiectasis -Chronic pneumonia

Prepatent Phase, days 7-25

Certain phase of Dictyocaulus viviparus. -Larvae mature in lungs -Bronchioles blocked by eosinophilic exudate -Moderate clinical signs: coughing, labored breathing, dyspnea, tachypnea, harsh bronchial sounds -Death can occur with massive infections

Penetration Phase, days 1-7

Certain phase of Dictyocaulus viviparus. -Migration from intestine to lung -Minor clinical problems

Dictyocaulus viviparus

Common lungworm of cattle. Usually occurs in outbreaks in herds. Follows periods of wet cool weather (*October*). Greatest problem seen in *calves and yearlings* (first exposure most severe). DH: cattle, buffalo, camels, wild ruminants Pathogenesis: involves four phases --> penetration, prepatent, patent, post-patent. PPP: 70 days Signs: light infection --> slight clinical signs. Heavy infection --> *partial to complete airway obstruction*. Can have pneumonia, alveolar collapse, emphysema, bronchitis, rapid breathing, dyspnea, coughing. Dx: clinical signs, herd problem, larvae in feces (Baermann technique), necropsy.

Dictyocaulus filaria

Common lungworm of sheep. Similar to D. viviparus. Emphysema and pneumonia not as great. Disease milder than in cattle. Common in Midwestern sheep. DH: sheep, goats

Toxocara cati

Common roundworm of cats. DH: felids Paratenic Hosts: rodents Life Cycle: 1. Adults in SI. Mate, lay eggs. 2. Eggs passed in feces. 3. Develop to infective stage in egg in 3-4 weeks. 4. Infection by ingestion of infective egg (contamination of feed or grooming). 5. Hatch in SI (duodenum). 6. Tracheal Migration --> route taken by most infective larvae. 7. Somatic Migration --> few larvae return to the heart and migrate throughout the body. Enter muscle, become dormant, remain viable for at least one year. Some arrested larvae may resume development in late gestation. 8. Lactogenic Transmission --> reactivation of arrested larvae. Larvae go to mammary glands. Occurs when queen is *acutely infected during the last part of pregnancy*. Usually due to ingestion of rodents. *Transplacental transmission does NOT occur!* *Tracheal migration often occurs in older cats.* Epidemiology: adult females produce large numbers of eggs, eggs resistant to environment, source of human infection (i.e. sand v-ball courts). Signs: Kittens - coughing, vomiting, dull haircoat, intermittent diarrhea with worms. Adults - asymptomatic. Dx: history, clinical signs, worms in vomit or diarrhea, eggs on fecal. Treatment/Control: most anthelmintics efficacious. Treat kittens at 6, 8, 10 weeks. Treat nursing dams.

Toxascaris leonina

Common roundworm of dogs, cats, wild canids and felids. Big issue in zoos. Contains a single cell with *space between ova and inside of shell* (compared to T. canis/cati). DH: dogs, cats, wild canids, felids Paratenic Hosts: rodents, rabbits, chickens Life Cycle: 1. Adults in SI. Mate, lay eggs. 2. Eggs passed in feces. 3. Develop to infective stage in egg in *only* one week. 4. Infection by ingestion of infective egg (either direct or by paratenic host). 5. Hatch in SI, duodenum. 6. Invade and remain in mucosa, molt (L4). 7. Returns to lumen, develops to adult. PPP: 8-10 weeks *Paratenic host has mucosal migration.* Epidemiology: cooler climates, eggs resistant, rapid development in infective larva (why it is a problem in kennels, zoos, etc.). Signs: long PPP allows animal to be more immuno-competent. Large numbers may cause intestinal irritation. Dx: clinical signs, identify eggs in feces (space between ova and shell). Treatment and Control: most compounds approved for use in dogs and cats will remove this.

Toxocara canis

Common roundworm of dogs. Can differentiate eggs from T. leolina, because there is little space between the cell and the shell (T. leolina has large space between). *Most important source of adult worms in adult dogs.* Zoonotic! DH: Canids (dogs, wolves, coyotes, foxes) Paratenic Hosts: rodents, pigs, birds Life Cycle (puppy): 1. Adult roundworms found in the SI. Mate, lay eggs. 2. Eggs passed in feces. Develop to infective larva in egg. 3. Ingestion of infected egg. 4. Egg hatches, releasing larva in stomach and duodenum. 5. Larvae invade bowel wall. 6. Tracheal migration (migrate to lung from liver --> heart --> penetrate alveoli --> up bronchial tree --> swallowed and develop to adults). Affects *PUPPIES* (<12 weeks of age). *Probability decreases dramatically as puppy gets older.* *If adult dog consumes egg, somatic migration occurs (larvae --> liver --> lung --> heart --> lie dormant in muscle for 1 year).* PPP: 21 days Other routes of transmission: cannibalistic dog eating infective dog muscle, ingestion of worms in vomit or feces. Epidemiology: many adult dogs infected, paratenic hosts are long-term reservoirs, eggs VERY resistant to environment (may survive for years). Signs: Fetal puppy - accumulate in liver, fetal death. Newborn puppy - pulmonary hemorrhage from migrating larvae (death at 2-3 days of age). Nursing puppy - large numbers of prenatal larvae and moderate numbers of lactogenic larvae, coughing, hyperpnea, nasal discharge, *potbellied*, vomiting, dull, lethargic. Juvenile and Mature Dogs - usually asymptomatic, aberrant migration --> neurological disorders or larvae in unusual places. Dx: worms in vomit or diarrhea, eggs on fecal exam. Treatment: most anthelmintics effective, including heartworm preventatives. *These are not effective in arrested larvae!* Control: reduce environmental contamination, reduce exposure, reduce contact with paratenic host, *treat the bitch during and after gestation to reduce infection in puppies*, treat puppies at 2, 4, 6, and 8 weeks of age.

Small Strongyles

Cyathostominae

Small Strongyles

Cyathostomum spp. Cylicostomes spp. Cylicodontophorus spp. Cylicostephanus spp. Gyalocephalus spp. Also known as the cyathostomes, cylicostomes, trichonemes, or small redworms.

Hypobiosis

Developmental arrest of larvae. Used by Ostertagia spp. Larval development resumes due to pregnancy, stress, relaxation of immunity, or seasonally-related factors.

Pilobolus (a fungus)

Dictyocaulus spp. are unique in that they may use __________________ to disperse on the ground. The sporangia (reproductive body) explodes dispersing the larvae.

Ancylostoma caninum

Dog hookworm. In *SI*. Has three pairs of teeth. DH: dogs, foxes, wolves, coyotes, cats Paratenic Hosts: mice, rats, monkeys, beetles, roaches Life Cycle (direct): 1. Adults in SI, mate. 2. Eggs passed in feces (up to 20,000/day!). 3. Eggs hatch, develop to infective L3. 4. Infection either by *ingestion or skin penetration*. -Oral infection (more common): ingested, exsheath, penetrate SI mucosa and wall. Some larvae return to lumen and develop into adults. Other larvae enter circulation. Tracheal migration --> mature to L4 in lungs and return to SI. Somatic migration --> L3 become hypobiotic in muscle. -Skin penetration: infective L3 penetrate skin. Migrate via lymphatics and circulation. Larvae either undergo tracheal or somatic migration. 5. Hypobiotic larvae may become activated. -Transmammary (lactogenic) transmission --> migrate to mammary tissue. -Tracheal route --> mature into adults in SI. -Transplacental transmission. 6. If paratenic host is ingested, larvae develop directly in intestine. PPP: 2-4 weeks depending on migration pattern Pathogenesis: can be *persistent infections* (refractory egg shielding). After removing intestinal worms with an anthelmintic, worms return to gut within a week. Larvae hypobiotic in muscle continually reactivate in small numbers and migrate to SI ("larva leak"), but do NOT mature if adult worms present. Hookworms are plug feeders that chew and lacerate tissue. Wounds continue to bleed after worms move. Blood loss up to 0.1 ml/worm/day (big deal in smaller breeds). Epidemiology: common in dogs of ALL ages, prolific egg layers, eggs killed by freezing, larvae survive well in moist soil. Signs: depends on the route of transmission. -Skin penetration: contact points, pruritus, hyperkeratinization. Can be peracute, acute, chronic, or secondary. Signs range from being asymptomatic --> fatal. Dx: history, clinical signs, *ONLY strongyle-type egg in dogs and cats!*. Can definitely diagnose. Treatment and Control: sanitation, routine fecals, deworm dogs (dam prior to and after whelping, puppies at 2/4/6/8 weeks.

Crenosoma vulpis

Fox lungworm. Adult has *cuticle with folds*. Found in *bronchi (trachea)*. DH: foxes, wolves, raccoons, dogs IH: snails and slugs Life Cycle: 1. Larvae and eggs produced. Eggs hatch shortly after production. 2. Larvae in sputum or feces. 3. L1s pass, develop into L3s in slug or snail, DH becomes infected by eating mollusk. PPP: 19 days Signs: rhinotracheitis, bronchitis, *nasal discharge*.

Halicephalobus gingivalis

Free-living nematode. *Facultative* parasite of horses and humans. Associated with a proliferative granuloma. Infection Route: 1. Larvae gain access via skin lesion or mucous membranes (oral, nasal, preputial). 2. Hematogenous spread into several organs and tissues, including brain, spinal cord, eye, sinuses, kidneys, heart. 3. Larval stage may be seen on skin, in wounds, granulomas. Signs: hyperemic turbinates, proliferative granulomas on organs. Treatment: anthelmintic treatment not effective.

Syngamus trachea

Gapeworm or "Y worm" of birds. Found in *trachea and copula*. Adults are bright red. *Young* most susceptible. Egg has *polar caps*. DH: chickens, turkeys, pheasants Life Cycle: 1. Adults mate, female lays eggs. 2. Larvae develops to L3 in egg. 3. Options for infection... -Egg with L3 is ingested -Ingestion of hatched L3 -Ingestion of earthworm or other transport host containing L3 4. Larvae penetrate gut wall. 5. Migrate to *lungs via circulation*. 6. Two molts occur in lungs. 7. Migrate up the bronchial tree, copulate, suck blood. PPP: 18-20 days Signs: heavy migration can result in pneumonia and death, hemorrhagic tracheitis with excess mucus production leading to airway occlusion, obstructive tracheitis. Most common clinical sign is *gasping or gaping*. Dx: characteristic egg in feces, Y worms in airway (necropsy). Treatment: good sanitation, ivermectin and fenbendazole.

Skrjabinema caprae

Goat pinworm.

Ancylostoma tubaeformae

Hookworm of cats. In *small intestine*. DH: felids Paratenic hosts: mice, rats, monkeys, beetles, roaches Transmission: -Ingestion of L3 -Skin penetration of L3 -*NO transmammary/lactogenic* (unlike A. canis) -*NO transplacental/prenatal* (unlike A. canis) -*Paratenic hosts*

Bunostomum phlebotomum

Hookworm of cattle. Voracious blood suckers. Most common in southern US. Most common in yarded cattle. May be significant blood loss in calves. Life Cycle (direct): 1. Infection through skin or ingestion of L3s. 2. Tracheal migration. Treatment and Control: dry pastures and paddocks, most anthelmintics.

Bunostomum trigonocephalum

Hookworm of cattle. Voracious blood suckers. Potentially a progressive anemia. Causes dark tarry stool, anorexia, bottle jaw. Life Cycle (direct): 1. Infection through skin or ingestion of L3s. 2. Tracheal migration. Treatment and Control: dry pastures and paddocks, most anthelmintics.

Ancylostoma braziliense

Hookworm of dogs and cats. Buccal cavity has two pairs of teeth. Less pathogenic than other hookworms. In SE US, latin America, and Africa. Transmission: -Ingestion of L3 -Skin penetration of L3 -*NO transmammary/lactogenic* (unlike A. canis) -*NO transplacental/prenatal* (unlike A. canis) -*Paratenic hosts* PPP: 3 weeks Pathogenesis: *cutaneous larva migrans (CLM)* in humans.

Oxyuris equi

Horse pinworm. Medium-sized worms (LARGE for pinworms!). Egg is flattened on one side. DH: horse Life Cycle: 1. Adults mate, female migrates out of anus and lay eggs in perianal region. 2. Eggs placed with sticky cement-like substance --> very irritating. 3. Egg develops to infective stage in 4-5 days. 4. Eggs fall or rubbed off in cement flakes, drop to ground or in feed, rubbed on surfaces. 5. Infective egg ingested. 6. Egg hatches and larva migrates to mucosal crypts of ventral colon and cecum. 7. Mature and return to gut lumen. 8. Adult females lay eggs in 4-5 months. Signs: eggs in perianal region cause intense pruritus, cause rubbing of tail head, restless and loss of condition, hair loss --> rat tailed appearance. Dx: clinical signs, history, find eggs in perianal region ("scotch tape" test), observe adults in freshly voided feces. Prevention and Control: remove egg masses via soap and warm water (use paper towels), sanitation in stalls and paddocks, treat infected animals with anthelmintics.

Strongylus equinus

In the *cecum*. DH: horse Life Cycle: 1. L3s penetrate cecal and colonic wall. 2. Encyst in subserosal nodules and molt to L4 within wall. 3. After two weeks, L4s migrate to the *right side of the liver via the peritoneal cavity*. 4. L4s wander in the liver for two months and migrate to *pancreas or abdominal cavity where molting occurs*. 5. Juvenile adults (L5s) penetrate the large intestinal wall and return to lumen to mate. 6. Attached to mucosa and imbibe blood. PPP: 9 months Signs: less is known, infrequent pathogen, can cause heavy infections. Dx: history, clinical signs, eggs in feces (cannot differentiate species), may culture to infective L3 for ID. Prevention and Control: good management, deworming program.

Strongylus vulgaris

In the *cecum, ventral colon*. DH: horse Life Cycle (direct): 1. Adults are blood feeders. Attach to the gut mucosa using buccal capsule (*mucosal plug*). 2. Egg passed in feces. 3. Embryo develops to L1. 4. L1 hatches and develops to infective L3 on the ground. 5. L3 is ensheathed and mobile (*negatively geotropic, positively phototropic*). 6. Infection is by ingestion of L3's. 7. L3 is ingested and cast off sheaths in SI. 8. Penetrate the cecal and ventral colonic wall and molt to L4 within submucosa. 9. L4 migrate within intima of small submucosal arteries. 10. Reach major intestinal arteries by d 8-14. 11. End up in the *cranial mesenteric artery* by d 11-21. 12. Migrate in the intima for 2-4 months. 13. L4 migrate back to cecal wall via small arterial circulation. 14. Occlude small arteries which become inflamed and destroyed. 15. Nodules form around the larvae where final molt takes place. 16. Juvenile adult (L5) ruptures from the nodule. 17. Sheath is removed and L5s enter gut wall and lumen, attach to the gut wall, mates and lays eggs. PPP: 6 months (crazy long!) Signs: *Acute syndrome*: in young foals with large # of worms. Due to migration in gut wall and mesenteric arteries. Causes colic, fever, anorexia, depression. *Verminous colic*: the big problem. Seen in horses of all ages. Migration of L4 and immature adults in cranial/anterior mesenteric artery. Disruption of arterial wall causes arteritis/aneurysm/thrombosis/embolism. Infarcts of cecum and colon. Causes recurrent colic. -Causes overall poor condition, emaciation, rough hair coat. Epidemiology: *temperature and moisture are dominant factors in larval development*. Adequate moisture required for L1 and L2 survival. In arid regions, harrowing feces can reduce larva populations. L3s can survive > 1 year on pasture. *Survival decreases with increasing temps* (greater larval activity, less food reserves). Ensheathed L3 are resistant to cold and dry conditions/dessication. Egg-shedding is seasonal. *Any pasture that has held a horse within a year can be assumed to have L3 infective larvae*. Dx: history, clinical signs, eggs in feces (cannot differentiate species), may culture to infective L3 for ID. Prevention and Control: good management, deworming program.

Strongylus edentatus

In the *colon*. DH: horse Life Cycle: 1. L3s penetrate the large intestinal wall. 2. Migrate to *liver via portal veins*. 3. Form hepatic parenchymal cysts where they molt in 2 weeks. 4. L4s wander in liver for 2 months and migrate to cecal wall via hepatic ligaments and parietal retroparitoneum. 5. L4s molt to *L5s in right flank*. 6. Juvenile adults (L5s) return to large intestine via mesentery, through cecal and colonic walls and form *nodules*. 7. Maturation and mating occur in lumen of intestine. PPP: 6-11 months Signs: *Larval Migration*: liver has disruption of hepatic architecture, abdominal cavity has peritonitis and adhesions, and the large bowel wall has adhesions. -Overall fever, depression, lethargy, anorexia, colic, diarrhea/constipation, hematologic disorders. Dx: history, clinical signs, eggs in feces (cannot differentiate species), may culture to infective L3 for ID. Prevention and Control: good management, deworming program.

HCl, pepsinogen

In the gastric gland, parietal cells produce _______________ and chief cells produce ___________________.

Strongyloides stercoralis

Intestinal threadworm of dogs and primates. Thrives best where hygiene is poor. DH: dogs, cats, primates, humans Human disease: -Chronic: can last for decades -*Autoinfection*: infective filariform larvae hatch in gut and re-infect host. (Internal - penetrate bowel wall. External - pass and penetrate perianal skin.) -*Hyperinfection*: massive disseminated infection. -Immunosuppressed individuals have died due to hyperinfection. Canine disease: -Autoinfection more likely with immunosuppression. Signs: diarrhea in puppies, chronic soft stool in primates. Epidemiology: significant zoonotic potential. Parasite maintained in kennels by transmammary transmission and skin penetration. Dx: clinical signs, larvae in feces, distinguish from hookworm. Treatment and Control: practice strict hygiene (let kennel staff know if dx), treat infected animals with Ivermectin and Fenbendazole.

Strongyloides westeri

Intestinal threadworm of equines. In *young foals* 2 weeks - 6 months. DH: horse, mule, donkey, zebra Signs: foals - catarrhal enteritis, diarrhea (*day 9-13 "foal-heat" diarrhea*). Mares only have arrested larvae in mammary glands. Dx: clinical signs, larvated egg in foal feces. Treatment: Ivermectin, Oxibendazole.

Strongyloides papillosus

Intestinal threadworm of ruminants. Primarily seen in young animals. Dam doesn't harbor adults, only arrested larvae. DH: sheep, goats, cattle Sign: lambs and kids - *diarrhea*, dehydration, emaciation, weakness, anemia, CNS signs, death. Dx: clinical signs, larvated egg in feces. Treatment: ivermectin, moxidectin, doramectin, albendazole, fenbendazole, oxfendazole.

Strongyloides ransomi

Intestinal threadworm of swine. Located in mucosal surface in SI, larvae dispersed in somatic tissues. DH: pigs Life Cycle: 1. Parthenogenetic females in SI produce larvated eggs. 2. Larvated eggs pass in feces. 3. Free-living (heterogonic) cycle: larvae hatch and develop to free living males and females. Adults mate and produce eggs. Larvae hatch and develop to infective L3 on the ground. Occurs when weather is favorable. 4. Homogonic life cycle: skip free-living stage. Weather unfavorable to free-living forms. Larvae hatch and directly develop to infective L3 on the ground. 5. Larvae penetrate skin or oral mucosa and are ingested. 6. Enter circulation and migrate to lung. 7. Tracheal migration (break into alveoli --> up bronchial tree --> swallowed). 8. Develop to adult female in SI. 9. Can also undergo transmammary (lactogenic) transmission where the larvae pass in colostrum and milk. PPP: 1 week Signs: larval migration causes skin hypersensitivity, petechial hemorrhages in lung, and catarrhal enteritis. Piglets - *diarrhea*, dysentery, anorexia, emaciation, anemia. (75% death loss in piglets, stunts growth). Dx: clinical signs, typical Strongyloides-type egg in feces (larvated, somewhat parallel sides). Prevention and Control: dry pastures/pens, concrete, confinement. Treatment: Ivermectin, Levamisole

Stongyloides spp.

Intestinal threadworms. Tiny worms in the intestines of many vertebrates. Lactogenic transmission important in many species. Most prevalent in young and immunodeficient animals. Parasitic forms are parthenogenetic (development from unfertilized egg) females. Parasitic females bury in the mucosal crypts of the gut (SI). *Eggs hatch prior to exiting body*. Auto-infection with filariform types. Common life history characteristics: -Two life cycle variations: free living (heterogonic) and parasitic (homogonic) -Major modes of transmission: ingested, skin or mucosal penetration, transmammary/lactogenic

Toxocara virulorum

Large roundworm of cattle. Emerging parasite in *Florida*. DH: cattle (*weanling calves*), water buffalo NO paratenic hosts. Life Cycle - Direct: -Infection by ingestion of embryonated egg. Infects pregnant cows and calves. -Tracheal migration in calves. Mature worms only found in 3-10 weeks old calves. Eggs not observed after calves > 6 months. -Somatic migration in adults. Mature worms not found in adult cattle. -Lactogenic transmission is the *most important route for calf infections*. PPP: 3 weeks in calves Signs: Young calves - anorexia, abdominal pain, diarrhea or constipation, dehydration, etc. Impaction and intestinal obstruction can occur. Mature cattle - asymptomatic. High infectious doses related to GI and somatic signs. Dx: clinical signs, necropsy, eggs in feces. Treatment: none approved, Fenbendazole, good management.

Chabertia ovina

Large-mouthed bowel worm. In *large bowel* of sheep. Direct life cycle. PPP = 50 days. Can cause diarrhea, often with blood. VERY LARGE buccal capsule.

Haemonchus spp.

Largest stomach worm. Small buccal capsule with single lancet. Life Cycle (direct): 1. Eggs passed in feces. 2. L1 develops in 24-48 hours and hatch. 3. L1 and L2 feed on fecal MOs. 4. L2 molts to infective L3 keeping L2 sheath (resistant to environmental pressures). 5. L3 ingested by host. 6. Exsheath in rumen, goes to abomasum. 7. L3 burrows into mucosa between gastric epithelial cells. 8. Molts to L4 and subsequently to adult (depends if hypobiosis occurs). Epidemiology: infection by ingestion of L3s on forage. Hatching of eggs and development is driven by *weather* conditions. Eggs and L3 INTOLERANT of drying and freezing (will get through the winters and summers *in the host*). Has a *periparturient rise and spring rise*, where there are large increases in egg numbers being passed. Signs: *ANEMIA* (bloodsucking L4s and adults), three classic haemonchosis syndromes. Dx: history, clinical signs, fecal, *FAMACHA*, necropsy. Treatment and Control: pasture management, deworming.

Small Strongyles

Life Cycle: 1. L3s penetrate the mucosa of the *cecum and colon*. 2. Some form cysts and remain for long periods and others remain for short periods of time. 3. Eventually all molt. 4. L4s return to the lumen and mature into adults. PPP: different for all 29 spp. Signs: mostly due to emergence from cysts of the arrested L3s. Causes fever, diarrhea, depression. Also cause cyathostomiasis (acute and chronic) and natural cyathostome infection (plug feeders). Epidemiology: *temperature and moisture are dominant factors in larval development*. Adequate moisture required for L1 and L2 survival. In arid regions, harrowing feces can reduce larva populations. L3s can survive > 1 year on pasture. *Survival decreases with increasing temps* (greater larval activity, less food reserves). Ensheathed L3 are resistant to cold and dry conditions/dessication. Egg-shedding is seasonal. Dx: history, clinical signs, eggs in feces (cannot differentiate species), may culture to infective L3 for ID. Prevention and Control: good management, deworming program. Treatment: *resistance to anthelmintics is common!*. Rotate drug classes to change the selection pressure against the parasites.

Dictyocaulus arnfieldi

Lungworm of horses. Eggs are *larvated*. DH: donkeys (natural host), horses, ponies Life Cycle: 1. Adults mate and lay eggs in air passages. 2. L1s hatch immediately after eggs passed with feces. 3. Direct development to L3s on ground. 4. Infection by ingestion. 5. Penetrate gut and migrate via *lymphatics and circulatory system* to the lung. PPP: 40 days Epidemiology: horses and ponies are infected from donkeys. Signs: commonly asymptomatic even with many worms, may be prolonged cough in horses. Dx: clinical signs, fecal (eggs in *very* fresh feces), larvae on Baermann. Prevention and Control: keep horses and donkeys separate, routine deworming, isolate and treat all new donkeys. Treatment: fenbendazole, ivermectin, levamisole, mebendazole, oxibendazole.

Protostrongylus sylvilagi Protostongylus boughtoni

Lungworm of rabbits and hares.

Ostertagia spp.

Males have a well-developed bursa and spicules. Typical strongyle-type eggs. DH: ruminant herbivores (cattle, sheep, goats, etc.) Life Cycle: 1. Adults mate and eggs are passed in the feces. 2. L1 develops, hatches, develops directly on the ground (L1 --> L2 --> L3). 3. L3 move away from fecal pat mechanically and on their own. 4. L3s are ingested while grazing, exsheath while on their way to the abomasum. 5. L3s enter gastric glands. 6. Develop to L4 in 4-5 days (increasing 10x in size). 7. Become L5s 12-14 days later. 8. Leave the *gastric gland, destroying it*. 9. In lumen, adults mate and female lays eggs in 3 weeks. 10. Patent for 1-2 months. Other Notes on Life Cycle: -*Larvae can pause development in response to unfavorable weather. Late fall conditions in Northern US and late spring conditions in the south*. -*Hypobiosis*: developmental arrest of larvae. L3s enter gastric glands, molt to L4s and stop development to wait for a more favorable day to resume development (Northern US: late winter/early spring, Southern US: late summer/early fall). Epidemiology: *young* animals most susceptible, larvae can live inside fecal pats after crusts form, larvae can overwinter in northern pastures, larvae are susceptible to dessication/direct sunlight./high temps. Pathogenesis: -Phases of Diseases: 1. Phase I, days 1-17: gastric glands involved 2. Phase II, days 17-35: adults emerge from the gastric glands 3. Phase III, > 35 days: recovery phase, adult expansion Signs: strongyle-type eggs present, calves that are wasting away and dying within weeks, diarrhea, *bottle-jaw*, anemia, rough hair coat, reduced production performance. Types I, Pre-Type II, and II of ostertagiosis. Dx: history, clinical signs (weight loss, diarrhea, anorexia, bottle jaw), strongyle-type eggs on fecal, necropsy. Prevention and Control: *pasture management*, deworm in May and late October (choose dewormer that kills hypobiotic larvae and is long-lasting). Cattle can develop immunity over years.

Parelaphostronglus tenuis

Meningeal worm of deer. A NON-lungworm protostrongylid. Found in *cranial venous sinuses and subdural spaces*. DH: white-tailed deer mostly, also moose/elk/caribou/mule deer/red deer/sheep/goats/llamas IH: snails and slugs Life Cycle: 1. Adults on meninges, mate and female lays eggs. 2. Eggs and a few hatched larvae are carried to lungs. 3. Eggs hatch in lungs. 4. Larvae move into airspace and migrate up the bronchial tree, swallowed and pass in feces. 5. Larvae in foot of the snail --> L3s. 6. Deer ingests snail/slug, larvae released. 7. Penetrate intestinal wall, migrate via the peritoneal cavity to the vertebral canal. 8. Migrating larvae invade the *dorsal horns of gray matter of spinal cord*. 9. Grow and molt (~1 month). 10. Enter subdural space, mature, migrate to cranium. PPP: ~11-17 weeks or more Signs: most white-tailed deer are NOT affected, CNS signs and blindness are rare. Symptoms in aberrant hosts (moose = Mad Moose Disease, death in caribou/reindeer, highly pathogenic in llamas/sheep/goats). Dx: larvae in meninges on necropsy, larvae in feces, clinical signs. Prevention and Control: keep pastures clean (*remove rocks/trees*), use a molluscicide, treat infected animals. Treatment: doramectin, fenbendazole, ivermectin, moxidectin, etc.

Swine Lungworms

Metastrongylus apri Metastrongylus pudendotectus Metastrongylus salmi

Different Nematodirus spp.

N. helvetianus - cattle (assoc. with clinical disease, particularly in young susceptible animals) N. spathiger - sheep and goats N. filicollis - sheep and goats N. battus - sheep and goats (can cause synchronized seasonally severe and debilitating diarrhea in lamb flocks)

1. Ingestion of L3 2. Skin penetration of L3 3. Transmammary/lactogenic 4. Transplacental/prenatal (minor) 5. Paratenic hosts (mice, rats, monkeys, beetles, roaches)

Name three of the five routes of potential transmission of the hookworm Ancylostoma caninum.

Barber-pole Worm Wire Worms Eastern Stomach Worms

Name two common names of Haemonchus spp.

Dictyocoulus spp. Strongyloides spp.

Name two genera of nematodes where you can find larvae in the feces.

Brown Stomach Worm Medium Stomach Worm Western Stomach Worm

Name two of the three common names of Ostertagia ostertagi.

Necator americanus

New World Hookworm of humans.

Oesophagostomum spp.

Nodular worms. Leaf crown present. Parasites of the *large intestine*. Life Cycle (direct): 1. L3s are ingested. 2. Penetrate mucosa of small and large intestine and form *cysts*. 3. Larvae grow and molt and return to lumen, pass to colon where they mature to adults. PPP: 40 days Pathogenesis: excessive inflammatory response on subsequent exposures causes nodule formation. When the nodule *caseates or calcifies*, larva must leave or die. Nodules interfere with peristalsis, nutrient absorption, and water retention. Causes ulcerative colitis, adhesions, peritonitis. Signs: Young animals - first infection. No signs for moderate infection. Diarrhea, anorexia with heavy infection. Older animals - nodule formation. Anorexia, weight loss, diarrhea. Dx: no eggs when larvae are in mucosa, eggs for ID when adults are in lumen. Typical strongyle-type egg.

FAMACHA

Novel idea for the treatment and control of Haemonchus contortus in goats and sheep. Measures the level of *anemia* or *blood loss* (NOT fecal egg counts) and treatment decisions are based on these levels. Treating only the ones that are infected leaves worms still out there. No selective pressure for the worms, less likelihood of resistance. Based on the idea that few individuals harbor the most parasites.

Different Oesophagostomum spp.

O. columbianum - sheep & goats O. venulosum - sheep & goats O. radiatum - cattle

Ancylostoma duodenale

Old World Hookworm of humans.

Timing

Ostertagiosis type is based on _______________.

Increased (Most larvae are on the lower 1 inch of the grass blade).

Overgrazing on pasture leads to ____________________ transmission of parasitism.

Dictyocaulus spp.

Parasites of the air passages. *Adults live in the bronchi and bronchioles*. Direct life cycle. Prefer moist, temperate climates. Life Cycle (direct): 1. Adults live within bronchi, mate and pass eggs. 2. Embryonated eggs coughed up, swallowed, and hatch in intestine. 3. L1 pass out with feces. 4. L1-L3 development in fecal pat. 5. L3 ingested, exsheath, penetrate intestinal wall. 6. Migrate into the lymph vessels to *mesenteric lymph nodes*, molt to L4. 7. Enter circulation, migrate to lungs. 8. Develop into adults in bronchioles in ~4 weeks. Epidemiology: Midwestern prevalence greatest in Sep-Oct, larvae develop and mature in fecal pats, larvae are sluggish and disperse mechanically, may use Piloblus (a fungus, *sporangia explode dispersing larvae*). Larvae may live up to one year at 40 F. Continuation of infection by *overwintering, larvae on pasture or worms in host*. Severe outbreaks follow buildup of infective larvae. Prevention and Control: pasture management, ensure animals on good nutritional plane, routine deworming, larval vaccine *in UK*. Treatment: doramectin, levamisole, fenbendazole, ivermectin, moxidectin.

Trichostrongyle Characteristics

Parasites that are small in size. Their buccal capsule is absent or small. Adults live in herbivore *stomach and intestine*. Females are oviparous. Males have a well-developed bursa. Direct life cycle. Infection is by ingestion of L3s.

Pepsin

Pepsinogen is activated by HCl to ________________, which is the functional hydrolytic enzyme of the abomasum.

Phase II, days 17-35

Phase of disease in ostertagiasis. Adults emerge from the gastric glands. Cycle: 1. Young adults (L5s) emerge causing stretching and erosion of gastric glands. 2. Widespread erosion occurs, *destroying many functional chief and parietal cells*. 3. Decreased pepsinogen and HCl secretion. 4. Bacteria proliferate. 5. No pepsinogen to pepsin. 6. Tight junctions break down. (Pepsinogen --> blood, blood proteins --> gut). Signs: abomasal mucosa hyperplastic, "Morocco leather" appearance (gray-white nodules), hyperemia, edema. Consequences: impaired digestion, loss of appetite, diarrhea, dehydration, weight loss or poor weight gains.

Phase I, days 1-17

Phase of disease in ostertagiasis. Gastric glands involved. Cycle: 1. L3s invade gastric glands. 2. L3s grow and molt to L4 stage. 3. *Larvae damage chief, parietal, and mucus secreting cells.* 4. Cells replaced with undifferentiated cell types. 5. Inflammatory response induced by growing larvae produce a constant erosion of the epithelial lining of the gastric glands. 6. Cells replaced by immature *non-secretory* epithelial cells. Signs: Abomasal pH remains at 2-2.5. No diarrhea, infected animals eat well and gain weight. Plasma pepsinogen levels rise only slightly.

Phase III, >35 days

Phase of disease in ostertagiasis. Recovery phase, adult expansion. Gradual loss of worms. Gradual return to normal function.

Baylisascaris procyonis

Raccoon roundworm. DH: raccoons, dogs Paratenic Hosts: over 100 animal spp! (Parasite can cause CNS signs via VLM in PH that is lethal). Life Cycle: 1. Adults in SI. Mate, lay eggs. 2. Eggs passed in feces. 3. Develop to infective stage in egg in 4 weeks. 4. Infection by ingestion of infective egg. 5. Hatch in SI. 6. Penetrate gut wall. 7. Tracheal migration. 8. Return to lumen, develop to adults. PPP: 10-12 weeks Significance: larvae continue to grow as they migrate, very neurotropic, very pathogenic, deaths of children in US (i.e. kids sucking on wood chips). Control: deworm captive raccoons, keep raccoons out of barns/sheds/attics, destroy middens (poop spot), use care in handling raccoons, hand washing, deworm dogs with any ascarid-type ova. Dx and Treatment: fecal exam, most anthelmintics efficacious.

Hyostrongylus rubidus

Red stomach worm. Infects *stomach*. DH: swine Life Cycle (direct): 1. Similar to Ostertagia spp. where the larvae go into the *gastric glands*. 2. Ingestion of L3s. 3. Larvae enter mucosa. (gastric gland pits). 4. L3s molt twice and return to lumen. Pathogenesis: adults suck blood. Numbers dependent. Causes catarrhal gastritis with ulcerations. Signs: lose condition, unthrifty, diarrhea, anemia, dark tarry stool (melena). Dx: clinical signs, strongyle type eggs. Prevention and Control: sanitation, confinement. Treatment: fenbendazole, ivermectin, doramectin.

Resistant Populations

Select populations of worms that are NOT affected by anthelmintics. Has led to a scientific re-evaluation of how we CONTROL worms.

Skrjabinema ovis

Sheep pinworm.

Teladorsagia circumcincta

Small brown stomach worm of sheep. Found in the *abomasum* of sheep and goats.

Rhabditis (Pelodera) strongyloides

Small free-living nematodes. Commonly found in decaying matter. Located in the skin and hair follicles. DH: dogs, horses, cattle, swine, rodents, humans Signs: seen in animals kept on damp hay or straw bedding. Lesions on contact surfaces causing loss of hair, erythema, pruritis, crusting, ulcerative dermatitis, deep pyoderma, popular dermatitis. Dx: presence of characteristic skin lesions, presence of rhabditiform larvae recovered from skin scrapings, larvae in blood agar develop to adults in 1-2 days. Treatment and Control: remove wet/damp bedding, clean lesion, no approved treatment (use avermectin).

Cooperia spp.

Small intestinal worm. *Most prevalent GI nematode of cattle in U.S.* Penetrate into mucosa of SI. May undergo hypobiosis. Often present in high numbers = high number of eggs. Direct life cycle. Signs: gross lesions in upper portion of SI (catarrhal enteritis, thickening of gut), chronic watery diarrhea, inappetence, loss of plasma proteins. Epidemiology: *emerging problem because of developing resistance*.

Trichostrongylus axei

Stomach Hair Worm. *Abomasum* of ruminants, *stomach* of horses, rabbits, hares. Usually secondary to Ostertagia infections in cattle. Direct development. L3s can overwinter on pasture. Infections occur in spring. L3s on pasture die off as weather becomes warmer, but passed eggs contaminate pasture for following year. Ingested larvae enter the mucosa of abomasum, cause epithelial damage. Produce a *catarrhal enteritis*. Signs: usually asymptomatic, high numbers = *watery diarrhea* (black scours, dingleberries). Problems with grazing horses and cattle.

Large Strongyles

Strongylinae

Egg, larvae

Strongyloides fuelleborni passes as an ______________, not as _________________ as in Strongyloides stercoralis. This is a way to differentiate between the two.

Stephanurus dentatus

Swine kidney worm. Adults in *kidney, ureters, perirenal tissue*, larvae in *liver*. DH: pigs Life Cycle: 1. Eggs pass in urine, develop to L3. 2.Options of infection... -L3 *ingested* and enter stomach wall, molt to L4, migrate to *liver*. -*Skin penetration* by L3. Molt to L4 in skin or muscle. Migrate to *liver*. -*Paratenic host* carrying L3. Earthworm ingests L3 and earthworm is ingested by pig. 3. ALL L4's end up in the liver! 4. Migrate for 3-9 months and cause a great deal of destruction. 5. Migrate to *kidney* (may be in perirenal fat, wall of ureter, etc.), and perforate the renal duct and create cysts. 6. Females are prolific. Live up to 3 years, producing up to 1 MILLION eggs/day! PPP: 9-16 months Pathogenesis: local irritation, skin penetration. Liver --> fibrosis, cirrhosis, abscesses, adhesions. Other sites and organs with aberrant migration (axial musculature --> loin chops condemned). Kidney, surprisingly, not markedly pathogenic. Dx: find strongyle-type egg *in urine*. Control: sanitation, gilt-only breeding (gilts slaughtered after one litter, can be unprofitable), anthelmintics. Treatment: doramectin, fenbendazole, levamisole, ivermectin.

Oesophagostomum dentatum Oesophagostomum brevicaudum

Swine nodular worms. Found in pigs and peccaries. Life Cycle (direct): 1. Ingestion of L3s. 2. Penetrate into the small and large intestinal mucosa, form nodules and L4s return to lumen. PPP: 20 days Pathogenicity: up to 5000 adults --> subclinical infection. >5000 leads to weight loss, reduced litter size, reduced weaning weights due to nodule formation. Dx: strongyle-type egg in feces. Treatment and Control: sanitation, most anthelmintics work.

Rodent Pinworms

Syphacia obvelata - mouse Syphacia muris - rat Aspicularis tetraptera - mouse Passalurus ambiguous - rabbit

Muellerius capillaris

The hair lungworm. Adults found in *subpleural pulmonary alveoli*. They are deeply embedded within the tissue or nodules. Adult has *cuticular spine*. DH: sheep, goats, chamois IH: various species of land snails Life Cycle: 1. Adults in alveoli and granulomatous nodules. 2. Female lays eggs that hatch in lungs. 3. L1 are coughed, swallowed, and pass with feces. 4. L1 enter snail and develop to infective L3 (via penetration of foot or ingestion). 5. Snail ingested and larvae released. 6. Larvae into wall of intestine --> lymphatics --> mesenteric lymph nodes --> blood and lymph --> heart --> lungs (alveoli). PPP: 6-10 weeks Signs: sheep --> subpleural granulomatous nodules, most sheep asymptomatic, heavily infected sheep develop cough/bronchopneumonia. Goats --> interstitial pneumonia, often severe. Dx: finding L1 in feces, necropsy. Epidemiology: infected by eating snails, larvae live in snail as long as snail lives, larvae resist freezing and some drying, L1 most active at low temps. Treatment: fenbendazole, levamisole.

Protostrongylus rufescens

The red lungworm. Found in the *bronchioles*. Second most pathogenic lungworm of sheep after Dictyocaulus. DH: sheep, goats, deer IH: snails and slugs Life Cycle: 1. Female lays eggs that hatch before being passed. 2. L1 consumed by IH, develop to L3. 3. IH consumed by DH. 4. Larvae migrate to lung. PPP: 5-6 weeks Signs: bronchitis --> focal pneumonia. Similar to Dictyocaulus spp. More worms = worse clinical signs.

Metastrongylus spp.

The swine lungworms. Part of the super family! Adults in *bronchi and bronchioles*. Has six lips. DH: pigs, wild boar, rarely sheep/cattle/humans (that means humans were eating earth worms?! Hi Dom) IH: earthworms Life Cycle: 1. Adults in bronchi, mate, lay eggs, coughed up, swallowed, and pass in feces. 2. Eggs must be ingested by an *earthworm*. 3. Develop to an infective L3 in earthworm. 4. Pig ingests infected earthworm. 5. L3 penetrates gut wall, migrates to the mesenteric lymph node and molts to L4. 6. Migrates via circulation to lung and into airspace. 7. Advance up the bronchial tree as they develop. PPP: ~3-4 weeks Epidemiology: eggs may survive for long periods in soil and for years in earthworm (*concentrating numbers*), can even survive for weeks after death of earthworm. Signs: hemorrhage where larvae enter lung, blockage of airway by adults --> verminous pneumonia and emphysema. Nodules form around dead worms (can be confused with TB). May be a vector of viral diseases like swine influenza, hog cholera. Typical husky cough, loss of condition, retarded growth. Dx: primarily the *husky cough*, eggs in feces (thick-shelled, mamillated, smaller than Ascaris), adults in bronchioles. Prevention and Control: keep pigs from earthworms, sanitation. Treatment: doramectin, fenbendazole, ivermectin, levamisole.

Ostertagia bisonis Ostertagia kazakhstanica

Two species of Ostertagia that affect pronghorn, bison, mule deer, and cattle. Found in the West-central region of North America.

Ostertagia mossi Ostertagia dickmansi

Two species of Ostertagia that affect white-tailed deer.

1. No transplacental transmission. 2. Tracheal migration occurs in OLDER cats (T. canis = puppies).

Two ways that T. cati migration differs from T. canis.

Acute Haemonchosis

Type of classic syndrome associated with Haemonchus spp. Morbidity high. Anemia present in ALL animals. Edema prominent. *Feces blackened* with high epg's. Animals weak, lethargic, wool loss. Ewes suffer agalactia. Utilize necropsy findings.

Hyperacute/Peracute Haemonchosis

Type of classic syndrome associated with Haemonchus spp. Rare. Occurs when susceptible animals have a massive exposure. *Extremely anemic.* Sudden mortality. Utilize necropsy findings.

Chronic Haemonchosis

Type of classic syndrome associated with Haemonchus spp. Widespread. Low number of worms over long period of time. Anemia and edema present. Clinical malnutrition. Insidious blood loss.

Pre-Type II Ostertagiosis

Type of ostertagiosis. Non-clinical entity. Period from acquisition of inhibition-prone larvae until unhibited larvae resume development. Northern US: fall to spring, Southern US: spring to fall.

Type I ("Summer") Ostertagiosis

Type of ostertagiosis. Occurs in late summer, early fall in the northern US, or in late winter/early spring in the southern US. Pastured young cattle. Rapid acquisition of larvae which invade mucosa, molt, and return to lumen (*NO hyperbiotic larvae*). Large number of worms in gut. High morbidity. Signs: profuse diarrhea, rapid weight loss, anorexia, submandibular edema (*bottle-jaw*). Dx: strongyle-type eggs in feces, increased plasma pepsinogen, hypoalbuminemia, mild anemia. Upon necropsy, find adult worms in abomasum, hyperplastic/edematous folds of abomasum, elevated abomasal pH with litmus paper.

Type II ("Winter") Ostertagiosis

Type of ostertagiosis. The clinical entity when large numbers of inhibited larvae resume development. Signs: profuse diarrhea, rapid weight loss, anorexia, submandibular edema (*bottle-jaw*).

Ocular Larva Migrans (OLM)

Unique sequela to infection by T. canis. Somatic larvae migrate into human eye (usually retina). Dx: ELISA for Toxocara Treatment: difficult, may not return to full function.

1. Strongyloidea (Equine strongyles, nodular worms) 2. Trichostrongyles (HOT Complex) 3. Hookworms 4. Metastrongyloidea (most lungworms)

What are the four superfamilies in the order Strongylida?