exam 2 Flashcards

Question

Neospora caninum life cycle

Answer 1

-the most important cause of bovine abortion in Canadian cattle -indirect -canid DH has meronogy and gametogony in intestines. -shed unsporulated oocysts which sporulate in environment. -cattle eat sporulated oocysts. merogony in IH. -causes tissue cycts and abortion. DH eats. -both DH, IH can have transplacental transmission

Answer 2

Early pregnancy: fetal death and resorption Mid pregnancy: * Abortion (typical) * Infected, neurological calf * Underweight, unable to stand, flexed or hyper-extended limbs, lack of coordination, decreased reflexes and sensory perception Late pregnancy: * Infected, but clinically normal – may infect their own offspring * Uninfected calf (rare) Infected cows may have problems with subsequent pregnancies

Answer 3

Endemic abortion (endogenous) – recrudescence of chronic infection Epidemic abortion (exogenous) – acute infection following ingestion of sporulated oocysts – abortion storms

Answer 4

diagnosis: clinincal and epidemiology. ELISA. tissues from abortuses control: prevent DH from eating abortuses, raw meat, dead cattle. do not breed seropositive cattle.

Answer 5

Relevant in sheep and goats Abortion storms in naïve animals Outcome depends on time of infection: * Early: fetal death and resorption * Mid: abortion or stillborn * Late: weak or normal lambs Tissue cysts common in sheep, goats, pigs Less common in cattle, horses and poultry

Answer 6

-indirect or direct -DH cats -IH get tachyziotes tissue cysts containing bradyziotes. -shed in cat feces -sporulate in environment -enter IH become cysts (humans, cattle, cats) can have prenatal infection and abortion. -DH eats tissue cycts with bradyziotes.

Answer 7

ndirect methods * Serology, IgG (chronic) and IgM (acute) Direct methods * Gross pathology: macroscopic necrosis in cotyledons * Histology, PCR

Answer 8

* Regional variation in seroprevalence in sheep (20-100%) * Prevent access of cats to sheep feed * Vaccines have been developed * To prevent zoonotic transmission: * After handling aborted or stillborn fetuses, thorough hand washing * Cook lamb and mutton to 70ºC or freeze at -20ºC for at least 3 days

Answer 9

-cattle lungworm -direct lifecycle -L3 ingested, transmucosal migration to lungs. shed as adults, L1-L3 translation in WET environment 5 days. -PPP 3-4 weeks

Answer 10

-Rare, but important cause of pneumonia in pastured cattle * Can be subclinical * Coughing, dyspnea, sawhorse stance * Morbidity and mortality can be high – Vaccine (irradiated L3) used in Europe, given to calves before first turn-out – Anthelmintics (especially ML): given at midpoint of first grazing season -baermann on fresh samples!! no eggs, L1

Answer 11

-small lungworms of sheep/ goats * Adult parasites live in lung parenchyma and/or small airways * Indirect life cycle with gastropod IHs L1 shed, then snail IH, L3 ingested by sheep. * Notable lung lesions but rarely clinical

Answer 12

-dermal nematode in cattle -skin lesions alopecia, scaling -in western CAD - Diagnosis: clinical symptoms, microfilaria in skin biopsy * Treatment: – ML kill the microfilaria and resolve skin lesions within 2-3 weeks – Adults resist treatment and survive for years

Answer 13

-PPP 6-8 weeks -L1 in dermis, fly eats translation in IH hornly L1-L3 then fly bites DH -L3 devleop to adults in hair follicle -development in IH 3 weeks

Answer 14

-L1 microfilarie in blood of cattle -L1-L3 in IH hornfly or mosquito which takes blood meal. -develop 12-16 days -go back to DH as L3 -adults live in peritoneal cavity. -little to no clinical significance

Answer 15

-cestodes -more pathogenic in sheep (lambs diarrhea, and weight loss) -eggs shed feces -free living mite with cytercercoids IH. develop in IH 1-4 months. -oral ingestion of mite. -adults in DH.

Answer 16

-eggs in feces ingested by sheep -sheep develop tissue cyst cystercerci -eaten by canines which shed eggs. Dx: * No clinical signs associated with adult stages in dogs or cysticerci in sheep Control: * No treatment for sheep * Treat dogs with praziquantel AT LEAST twice per year * Prevent dogs from eating infected sheep carcasses

Answer 17

* Most common in beef-eating countries other than Canada – Eastern Europe, Russia, eastern Africa and Latin America * Rare cause of carcass condemnation in feedlot cattle in Canada * Predator-prey indirect life cycles: – Human definitive hosts (DH) – Cattle intermediate hosts (IH) * Eggs immediately infective and resistant (18 mos)

Answer 18

-adults in humans, shed gravid segments and eggs -eaten by cattle -Cysticerci in cardiac and skeletal muscle of cattle. 12 week incubation period. -human eats infected meat with cystercerci.

Answer 19

Definitive hosts – Treatment of carrier people with cestocides – Goal: halt environmental contamination with immediately infective eggs – Prevent access to IH (raw or undercooked meat in endemic regions) – Cook meat to the safe internal temperature (160◦F|71◦C) * Intermediate hosts (cattle) – No treatment available or suitable – Meat inspection – Prevent livestock access to human feces -CFIA

Answer 20

Reportable disease under Health of Animals Act: meat inspectors, vets, and labs must immediately report even suspicion of disease to CFIA district vet -quarentine premises and source farms -license remaining animals to slaughter have enhanced inspection froze for 10 days. -lift quarentine after certain number of animals are negative.

Answer 21

-liver fluke The most important trematode of livestock – Rare in western Canada * Grey-brown leaf shaped fluke primarily in bile ducts * Can infect many species – cattle, sheep, goats, deer, horses, pigs * Infection occurs only where there is suitable aquatic snail habitat * Zoonotic

Answer 22

-eggs shed from cattle or sheep -eggs-> miracidium-> IN snail where they undergo asexual repro. -in snail go from sporocytys to redia. -cecaraie after snail and metacercaria on vegatation ingested by DH. -10-12 week PPP

Answer 23

* Often asymptomatic * Acute/subacute fasciolosis (in sheep) * Migrating juvenile flukes in liver tissue (prepatent) * Anemia, hypoalbuminaemia, sudden death * Submandibular edema (bottle jaw), ascites, eggs present * Chronic fasciolosis (in cattle) * Adult flukes in bile ducts * Generally sub-clinical * Reduced growth and fertility, progressive loss of condition * Post-mortem: chronic cholangitis, calcified bile ducts * In all livestock, migrating flukes can trigger Clostridial disease

Answer 24

-too dense to float -Coproantigen, antibodies in bulk tank milk Bloodwork: +/- anemia

Answer 25

-liver fluke DH caribo, eggs shed -eggs-> micarcidium which penetrates snail foot IH. undergoes asexual repro. to redia. -6-8 weeks develop outside host -after snail metacercaria on vegitation ingested by sheep, cattle (Dead end hosts) or cervideds (DH) -can be fatal for sheep

Answer 26

-liver fluke * Relatively common in cervids in western Canada: – Deer, elk, caribou are normal definitive hosts (shed eggs) * Livestock and other ungulates are dead end hosts -Chronic or asymptomatic in cattle – Flukes walled off in liver parenchyma – no eggs shed, no clinical signs, unless flukes activate clostridial spores in liver (bacillary hemoglobinuria, aka redwater disease)

Answer 27

* Rarely necessary in western Canada in cattle * In problem herds (herd level diagnosis), prevention: * Avoid known contaminated pastures * Avoid liquid manure as fertilizer from infected herds near water.

Answer 28

Control of F. hepatica in problem herds involves: * Treatment of all exposed ruminants on farm * Closantel (Flukiver) or triclabendazole in fall (resistance observed to latter in Europe) to kill juvenile flukes - SHEEP * Albendazole in early winter to kill adult flukes – DAIRY * Vaccination for Clostridial diseases (at least every 6 months)

Answer 29

-zombie ant fluke * Small fluke which lives in bile ducts * Incidental finding in cattle, sheep, deer, rabbits, gophers, people * Introduced into B.C. and Cypress Hills in Canada * TERRESTRIAL cycle – ant as second IH

Answer 30

-eggs shed from DH cattle -ingested by snail and miracirdium released first snail IH -caercarie in snail slime eaten by ant, develop 2 months. second IH with metacecarie which is ingested by DH cattle. -TERRESTRIAL, not aquatic, life cycle -PPP 8 weeks

Answer 31

-causes parasitic gasteroenteritis (PGE) -sub clinical disease causes major production losses (decreased feed intake, loss of protein) -diagnosis relies on quantitative fecal egg counts -Anthelmintic resistance is currently one of the MAIN CHALLENGES for parasite control

Answer 32

-most important nematodes in grazing ruminants – Direct life cycle, infective L3, PPP ~21d, eggs look very similar – Commonly occur as mixed infection -control with broad spectrum anthelmintics

Answer 33

-Ostertagia ostertagi* -Haemonchus placei

Answer 34

Cooperia spp.* Nematodirus spp

Answer 35

-worms mature in dig tract and lay eggs. -eggs shed in feces -L1-L3 in environment -L3 ingested and immature worms go into mucosa.

Answer 36

-abomasum * Most important parasitic nematode species in cattle in Canada and Northern US * L4 may enter arrested development (hypobiosis) to survive harsh weather conditions -morocco leather abomasum apperance. thick mucosa, red. -causes ostertagiosis

Answer 37

-no acid production from parietal cells. -pepsinogen cannot be activated to pepsin so no protein digestion, hypoprotenemia, malabsorptive diarrhea, bacterial overgrowth, increase abomasal pH.

Answer 38

-TYPE 1 summer (july to october): crazing calves, gradual onset, larvae on pasture, large number of adult worms so high FEC, bright green diarrhea watery, weight loss, anorexia. -TYPE 2 winter (march to may): larvae in dorment stage, yealrings can be off pasture, sudden onset. inhibited larvae emerge at once so low FEC. * Hypoalbuminemia, submandibular edema * Low morbidity, high mortality -diarrhea

Answer 39

-bovine abomasum -barber pole warm, BLOOD SUCKER -L4 may enter hypobiosis, not common in CAD more south -white on worm

Answer 40

* Hyperacute - Sudden death due to haemorrhagic anemia * Acute - Anemia, bottle-jaw, ascites, dark feces, anorexia * Chronic - Weight loss, weakness, anorexia * FEC can be low (PPP), or very high (Thousands of EPG -NOT DIARRHEA sucks blood. -hard to treat many resistance. -diagnose with L3, PCR.

Answer 41

Common and sometimes dominant GIN in cattle * Adults ~1cm long * Contributes to PGE as part of mixed infection * C. oncophora: mild pathogen, temperate areas, very common in Canada. C. punctana more in north USA. -parasitic stage develop on surface of SI mucosa -inappetance

Answer 42

-Development to L3 inside the egg * Eggs overwinter on pasture, hatch with temperature rises in spring * Shedding rare in animals > 6 months of age (immunity) * Pasture contamination predominantly from calves * Acute diarrhea in young calves in pasture

Answer 43

-bovine SI * Hookworm (Ancylostomatidae): Blood feeders * Ingestion of L3 or SKIN PENETRATION by L3 * Rare in Canada

Answer 44

* Only adult females are parasitic * Warm and wet regions of the World * Not seen in Western Canada * Unlike most GIN, transmit well off pasture * Larvated eggs, relatively small * Ingestion of L3 or SKIN PENETRATION -bovine SI

Answer 45

heterogenic cycle: where they survive in environment homogenic cycle: where they survive in host.

Answer 46

-bovine LI * Nodular bowel worm * Life cycle similar to trichostrongyles, except pre-adult larvae create nodules in large intestinal mucosa * Limited pathogenicity

Answer 47

-bovine LI Whipworm * Host-specificity, T. globulosa (cattle) * Direct life cycle, larvated eggs infectious, PPP4-6 weeks * Transmits well off pasture (thick wall) * Very mild pathogen * Commonly seen during fecal egg counts in Canadian cattle – incidental finding

Answer 48

Infection thru ingestion of infective stages from PASTURE – Build up of large amounts of L3 on pasture * Possible sources of springtime pasture contamination – Overwintered eggs or larvae (esp. Nematodirus) on pasture – Reactivation of hypobiotic larvae * Peak pasture contamination: 2nd half of grazing season * Outcome of infection largely depends on immune status -rise in june/july

Answer 49

-history -clinical signs -fecal egg counts FEC. Trichostrongylid eggs are usually undistinguishable Not usually a very sensitive measure of parasite burden in cattle -coproculture + morphology

Answer 50

-management: quarentine, good husbandry, pasture management -anthelmintics: long acting rumen boluses Macrocylic lactones (ivermectin) -strategic treatments: cows in spring to reduce pasture contamination then graze young animals later -targeted selective treatment

Answer 51

-young animals, pasture transmission * Clinical disease is more common and widespread (worse in goats) * Anthelmintic resistance a huge global problem -anemia, bottlejaw, diarrhea, reduced production.

Answer 52

* Haemonchus contortus: anaemia, death in some cases * Trichostrongylus colubriformis, Teladorsagia circumcincta: chronic diarrhea, production loss * Nematodirus battus: problem in lambs

Answer 53

eggs on feces, hatch, L1-L3 in egg develop, grass as L3 eaten by DH. goes to L4 in stomach to adults then shed eggs.

Answer 54

-ewes have peri parturient rise L4 reactive where they are about to lamb have a drop in immunity and the nematodes reproduce and multiply. the hypobiotic L3 reactivate. rise in eggs shed. increase in spring. -leads to increase in pasture eggs FEC end of spring and summer -lambs turned out in pasture in fall and have increase in lamb FEC

Answer 55

-trichostrongylus axei -Haemonchus contortus -Teladorsagia circumcincta (Ostertagia-like)

Answer 56

-Cooperia sp -Trichostrongylus sp -Nematodirus sp

Answer 57

-Parasitic Gastroenteritis Reduced weight gain and diarrhea -Haemonchosis Acute anaemia, edema, lethargy, and death. caused by Haemonchus contortus (“Barber’s Pole worm”)

Answer 58

-* Typical trichostrongylid life cycle * Most pathogenic species in sheep, Worldwide distribution, main species in Canadian sheep flocks -red and white looking worm * One female: up to 10,000 eggs/day 5000 worms: 250mL blood loss/day -can have low FEC due to PPP or very high.

Answer 59

clinical signs (esp. lambs < 6 mos): - Hyperacute - Sudden death due to haemorrhagic anemia - Acute - Anemia, bottle-jaw, ascites, dark feces, anorexia - Chronic - Weight loss, weakness, anorexia -L3 at coproculture, PCR, anemia color of mucus membrane chart.

Answer 60

-head with cuticular expansion -develop to L3 inside egg -eggs overwinter on pasture -hatching triggered by temp rise in spring. -illness and death in lambs in PPP

Answer 61

-Teladorsagia circumcincta, Trichostrongylus colubriformis, and LI nematodes. -Occur in mixed infections – PGE * Distinguishable features in L3s (coproculture) or adult

Answer 62

* Maximize overall health, good nutrition and pasture management * Breed resistant hosts * Chemical treatments: targeted staregic treatments -drug resistance huge problem

Answer 63

-Macrocyclic lactones eg.: Ivermectin, Moxidectin -Benzimidazoles* used off label -Salicylanilides: eg.: Closantel (targeted activity)

Answer 64

* A heritable reduction in efficacy of a drug against a particular species of a parasite * Ability of parasite population to tolerate dose of drug that would be lethal to most parasites in a sensitive population * When drug efficacy <95% * There are reports of H. contortus resistance to all classes of drugs

Answer 65

-Heritable trait, present when within a population more individuals are able to tolerate doses of a drug that, in a normal population of the same species, would be harmful.

Answer 66

-animal is treated, only some survive which are resistant, restsant eggs shed on pasture.

Answer 67

-susceptible subset of the population present on pasture, not exposed to the anthelmintic treatment, that will subsequently re-infect the flock -If the population on refugia is composed by susceptible worms, this will dilute the concentration of resistant worms delivered on pasture after treatment

Answer 68

* Proportion of the parasite population not exposed to drug treatment – Parasites in untreated hosts – Parasites in external environment (free-living stages) * The larger the in refugia population, the less the selection pressure – Resistant nematodes breeding with susceptible nematodes will dilute the proportion of resistant genes

Answer 69

* Underdosing (guessing weight instead of dosing by exact weight) * Length of time used (BZ -30 years, IVM >20) * Frequency of Treatment * Pasture management: open/closed flocks * Size of in-refugia population

Answer 70

-not in spring, leads to many resistance due to small refugia pop. -dont treat then move to clean pasture as it will infect new pasture with resistance. -recommend: treat and move to contaminated pasture or keep in same pasture with refugia pop. which will dilute the resistant strain.

Answer 71

-suspected when poor response to treatment. resistant strain makes up large # of parasite pop. – Resistance goes undetected in its early phases – First sign is shortening of the Egg Reappearance Period - FEC Reduction test (FECRT) is widely used to detect AHR and combined with morphology and PCR

Answer 72

-Ideally done individually for all animals in a herd -Horses: often done only on high shedders -Cattle/sheep: often run on pooled fecal samples (20 animals) -use quantitative, centrifugation Wisconsin technique (detection limit of 1 EPG). Other methods – MacMaster, MiniFlotac Test, treat, re-test in 14 days

Answer 73

% Efficacy = ((pre-treatment FEC – post treatment FEC) x 100)/ pre-treatment FEC. -Drug resistance when FECRT less than 95% -fecal sample before treatment and 2 weeks later.

Answer 74

* Quarantine and anthelmintic treatment of purchased livestock and test FEC prior to introducing to herd * Good nutrition and management: – Lower stocking densities – Avoid using the same pasture in spring used in previous fall -mix age groups/ species (but not sheep and goats they have same parasites)

Answer 75

* Make informed choices on drug use * Monitor resistance status (regular FECRT) * Minimize and strategize anthelmintic use. treat groups not whole flock. dose on individual animals or heaviest in flock. * Targeted selective treatment (TST)

Answer 76

– Goal is to leave large refugia (in untreated animals, on pasture) – Treat only those with high FEC, poor body condition, high FAMACHA scores (anemic)

Answer 77

Targeted selective treatment: FEC approaches Can use absolute FEC i.e. treat all animals with FEC above a threshold * Animals with high FEC tend to stay high * High shedders are major source of pasture contamination. -FEC depend on season, host species, climate, management; pathogenesis depends on parasite species present -Can also use proportions of shedders: Treat only the top 20-30% of shedders

Answer 78

-limit access to IH -limited survival of free-living stages in barn environment

Answer 79

-red stomach worm -parasite of outdoor pigs (pasture transmitted) -Trichostrongyle with typical life cycle -Rarely causes clinical problems Possibly: Ulceration, stomach perforation Hemorrhage, anemia (blood feeder) Decreased milk yield and fertility.

Answer 80

-Large roundworm of pigs -Distribution: worldwide very common -Does well indoors and outdoors -Parasite of grower pigs (2-5 months old right before market where there is the highest prevalence and highest intensity on worms Morphology - big, white worms-30 cm long

Answer 81

-Adults in SI: extremely fecund females (200,000 eggs per female per day) -Eggs pass in feces: Larval development occurs entirely within egg temperature dependent development to L3 inside egg which is infective for next host. -Extremely hardy eggs (7-10 years) (in shaded and damp conditions) hard to clean in facility once there.

Answer 82

-ppp 6-8 weeks -no transplacental or transmammary -host eats eggs, uses hepato-tracheal migration where they migrate to liver, lungs, coughed up in trachea and reswallowed takes 6-8 wks. then go to gut and are shed in feces. -eggs in environment develop from L1-L3 inside egg. -L3 infective

Answer 83

-often asymptomatic -LARVE: if symptoms due to migrating larvae causing 1st infection physical damage to liver but worse in following infection where there is an allergic reactions due to eosinophilics (MILK SPOTS) -commended livers -lungs can get emphysema (heaves or thumps) from migrating larvae. -ADULTS: subclinical effects decreasing performance.rarley obstruction and perf of gut wall occluding the bile duct -ZOONOTIC and other animals, humans ingest eggs.

Answer 84

diagnosis: eggs in feces or liver spots at meat inspection -control: Benzimidazoles, ML, immunity develops to ascarids as they age >6 months. -treat before farrowing -treat pasture in spring and fall -good management and hygiene.

Answer 85

-global distribution -eradicated in CANADA swine -direct life cycle: adult nematodes in SI of host, L1 in muscles of same host. -Foodborne transmission only (no fecal or environmental stage) * Larvae of wildlife species freeze resistant!!! problems in bear meat. make sure cook all the way.

Answer 86

-muscle tissue has trichinella larvae of pig in barn, dies and pigs and rats in barn eat muscle. larvae grow up in SI and reproduce. -the larvae stay in newly infected animal and get to their muscle and lie dormant as L1 until they are ingested by next host -people are infected when they eat undercooked meat from infected host. -in pigs freezing kills these larvae!! -humans eating black bear meat, walruses, polar bears all have this.

Answer 87

-in people: subclinical, diarrhea, larvae in muscle can cause myalgia, fever, perioribital oedema, myocarditis (fatal) use serology, muslce biopsy -animals: occasional been in dogs/cats. usually detected in meat of food animals. -detect antibodies -larvae are not shed in feces, stay in muscle

Answer 88

Tx: In animals: not warranted or practical In people: Anthelmintics (ASAP), corticosteroids control: dont let pigs eat meat scraps, eachother, or rodents. -cook meat before human consumption -freezing kills T. spiralis but not T. nativa. need to cook meat only way.

Answer 89

* Maintains Canada’s disease-free status – surveillance, regulation and testing. – Test 18,000 slaughtered swine annually – Every 3-5 years, test 16,000 sows – Testing done by CFAP in Saskatoon * Prohibits feeding of meat products to pigs * Test all horses slaughtered in CFIA- regulated abattoirs for export certification * Reportable Animal Disease

Answer 90

-warmer climates, south USA -morph and life cycle of strongloides -adult female in SI, homogonic ad heterogonic lifecycles -percutaneous and oral transmission of L3 -prenatal and TRANSMAMMARY most common gives to nursing piglets (enteritis, diarrhea, anemia) -not zoonotic -control: hygeine, treat sows 14 days before farrowing or piglets less than 14 days.

Answer 91

Distribution: worldwide (pigs have own species) -Pasture-transmitted -Typical trichostrongyle life cycle & eggs L4 encyst in nodules in large intestine -Subclinical and clinical effects Piglets: diarrhea, weight loss, anorexia Finishing pigs: reduced weight gain Sows: reduced litter sizes and milk production Control: anthelmintics (ML) as per Ascaris -resistance: to benzimidazoles, pyrantel, and levamisole

Answer 92

Distribution: worldwide Large intestine of pigs Does well indoors (grower barn) Morphology typical whipworm “lemon-shaped” egg (hardy!) Life cycle L1 develops inside egg, infective Simple mucosal migration

Answer 93

Often asymptomatic Subclinical and clinical effects Anorexia, poor weight gain Large bowel diarrhea (Mucous +/-blood) DDx: swine dysentery caused by Brachyspira Hypoalbuminemia/anemia Control: benzimidazoles (not ML); hygiene Zoonotic, but natural transmission rare and doesn’t usually fully develop in people

Answer 94

Distribution: worldwide Pasture transmitted Indirect life cycle with earthworm IH pig passes larvated eggs in feces earthworm eats eggs, translation L1-L3 pig eats L3 in earthworm Verminous bronchopneumonia in young outdoor pigs (like husk in cattle) Treat with benzimidazoles, ML if needed

Answer 95

-pig tapeworm pigs are IH -immediately infective eggs, hexican larvae picked up by pigs, larve migrate to cystercrcoid in muslce tissue of pig. -people are infected with adult form by eating undercooked pork as DH. -people can also be IH (NOT IN CAD CFIA reportable) -leads to Neurocysticercosis and epilepsy in humans from migrating larvae. -can get muscle cystrcrcoids and brain -people can get autoinfection from feces -common latin america, eurpose, africa, india, asia

Answer 96

-burrowing mite of pigs * Transmit year round in housed pigs * Problem in Europe, not so much here * Thick scabs and crusts, highly pruritic, major production losses * Dx: deep skin scraping * Control: 2 doses of parenteral ML, given two weeks apart to all pigs; decontamination of fomites * Causes transient infestation in people

Answer 97

-outbreaks in winter, pigs only sucking louse, very large -itchy bites lead to self excoriation and weight loss -diagnosis: large and dark color easily visible, -Control: Topical organophosphates or single dose of ML often suffices due to residual effects * Treat all animals on premise, contagious and very species specific

Answer 98

-Eimeria spp. – harmless, generally adult pigs -Cystoisospora suis – pathogenic in piglets < 2 wks old: yellow-gray, pasty diarrhea – often no blood loss of condition/ dehydration High morbidity, low mortality Control: if known problem, treat week old piglets with toltrazuril; hygiene

Answer 99

-Eimeria sporulated oocyst 4 sporocysts each containing 2 sporozoites (8 sporozoites -Isospora sporulated oocyst 2 sporocysts each containing 4 sporozoites (8 sporozoites)

Answer 100

-Pigs are a common intermediate host for Toxoplasma gondii – most often acquired horizontally * Consume sporulated oocysts in feed or water contaminated with cat feces * consume tissue cysts in undercooked meat or rodents * pigs are a common source of human infection

Answer 101

-crop and small intestine (different species) -direct (C. contorta) and indirect life cycles with earthworm IH (C. annulata) - infective stage is L1 in egg -football shaped with polar plugs egg

Answer 102

-roundworm -SI, direct lifecycle infective stage is L3 in egg -migrating larvae can cause hemmorrahic enteritis (diarrhea) in mucosa. -adult worms are found in lumen of intestine and cause obstruction -Viable or calcified parasites may be found in the albumin part of hen’s egg

Answer 103

-cecum worm -direct lifecycle (earthworm can be PH), L3 in egg infective. -not pathogenic in poultry but acts as a shelter for protozoa Histomonas meleagridis causative agent for black head or Entero hepatitis in turkeys. -characteristics swelling in mesopharynx in male worm

Answer 104

-gapeworm, causes gasps for air open mouth breathing, tracheal obstruction. -adults in trachea blood feed (anemia) -life cycle direct or paratenic host. infective stage is L3 egg. -male in female in permanent copulations form Y

Answer 105

* All in all out, cleaning and disinfection between batches * Biosecurity to keep eggs from being tracked in and wild birds and earthworms out * Mainly a problem in backyard flocks, free-range, organic, and deep litter systems * If necessary (high FEC, histomoniasis): benzimidazoles or levamisole in feed or water

Answer 106

-dwarf tapeworm of poultry -hooks on rostellum have suckers and spines -indirect life cycle with slug or snail with cysticercoids. -asymptomatic or enteritis -young birds

Answer 107

-oviduct fluke (trematode) -lifecycle has 2 IH (snails and dragon fly naids) -causes salphingitis with fatal peritonitis

Answer 108

-chemidocoptes -not zoonotic -treat ivrmectin repeated in 2 weeks C. mutans – Scaly Leg C. gallinae – De-pluming Itch C. pilae – “Beak Rot” CLASS : ARACHNIDA

Answer 109

Dermanyssus (anus posterior in anal plate) On birds at night, environment during the day Life cycle complete in a few days; blood-feeders Infests domestic and wild birds -Zoonotic

Answer 110

-surface mite Ornithonyssus (anus anterior in anal plate) On birds all the time Life cycle complete in a few days Blood-feeders Infests domestic and wild birds; zoonotic

Answer 111

-causes * Tick paralysis – young chicks. * Vector – Avian spirochaetosis ( Borellia anserina), Rickettsia- Aegyptinella pullorum. -treat by cleaning environment

Answer 112

* Dermanyssus, Argas: ENVIRONMENT * Acaricides: pyrethroids, carbamates, organophosphates, spinosad (no withdrawal) * RESISTANCE is becoming a problem * Heat > 45ºC for several days between batches * Mite traps (dx as well) * Diatomaceous earth (SiO2), sulfur dust * Ornithonyssus: Extralabel ivermectin, 2 tx a week apart

Answer 113

-only have chewing lice -entire lifecycle on chicken diagnose: visual inseption treat: offlabel insecticide powders, repeat in few weeks when nits hatch

Answer 114

-bed bugs -poultry breeder flocks and dugs, infestation in chicken houses feather loss & irritation, lesions on the breasts and legs, and possibly anemia in severe cases production may suffer: fewer egg numbers and increased feed intake -Nocturnal feeders. need to look for them at nightime -Zoonotic

Answer 115

-stick tight flea, angular head, rounder body, long back legs. -Ceratophyllus gallinae, nest flea of chickens. long horizontal body, round head

Answer 116

-* Hosts: Turkey, chicken, guinea fowl, quail, pheasant, partridge and goose. * Disease: Typhlitis/Typhlohepatitis, Avian trichomonosis of Lower digestive tract. ex liver and cecum -trophozoite

Answer 117

Host: Pigeons (most), turkey, chicken, hawk, mourning dove, golden eagle. * Disease : Yellow button, Avian trichomonosis of Upper digestive tract, Canker. ➢ Localised: Throat-crop form/ yellow button. ➢ Generalized: Can spread to inner organs like heart, liver, lung, and air sacs. Lethal form ➢ Virulent strain –Jones’ Barn strain -oral route, milk

Answer 118

-trophoziote has single flagellum -transmitted directly: cecal flagellate shed in fresh feces (cloacal, drinking) or -Transmitted indirectly: cecal flagellate inside the larvae of cecal nematode Heterakis gallinarum (+/ inside earthworm paratenic host

Answer 119

-Mucosoflagellate of caecum that spreads to liver -Signs of histomoniasis in turkeys include listlessness, reduced appetite, drooping wings, sulphur-yellow droppings, and occasionally cyanosis of comb and wattles (blackhead). -Post Mortem – “bulls-eye” lesions on liver, caseous cores in caecum, histology, culture, or PCR -separate chickens (carriers) from turkeys, clean environment.

Answer 120

-causes coccidiosis in chickens -many species of eminera. -cecal, rectal, intestine, ilium -some are pathogenic and some are cryptic in the duodenum or jejunum. *Can trigger overgrowth of Clostridium perfringens causing necrotic enteritis

Answer 121

* Unsporulated oocysts are excreted in feces, sporulate in the environment. * Infective stage- Sporulated oocysts. * 2nd generation merozoites are responsible for pathogenesis. -create many genorations of shistoziotes in gut epithelium with gametogony. - sporogony in feces in eggs.

Answer 122

Diagnosis * PM lesions * Oocyst morphology * Molecular diagnosis: ✓ PCR. ✓qPCR control: treat ionophores (monension), amprolium (used in outbreaks in water) -sulphonamides

Answer 123

* Hygiene and good husbandry * Chemoprophylaxis: anticoccidials in feed and water: ionophores, toltrazuril, decoquinate, sulfonamides - RESISTANCE * Vaccines in feed, water, sprays or gels; injected into eggs or layers * reccomended to sue Alternating chemotherapy and Vaccines – replacing drug ‘Resistant’ strains with ‘Susceptible’ strains * Other: probiotics, herbal compounds

Answer 124

-1st gen: live wild type parasites (spoorulated oocysts) elict natural immunity -2nd gen: live attenuated strains, precocious development (fewer cycles of merogony) -3 rd gen: subunit vaccine, DNA vaccine combining genes

Answer 125

C. meleagridis – intestines – usually non- pathogenic C. baileyi – intestine, respiratory tract – pathogenic C. galli – proventiculus - Pathogenic

Answer 126

-Choriptes spp. -surface mites, cattle, horses, sheep -Cause of Chorioptic mange (mud- fever) -diagnosis: history/ apperance, puritis of pastern, heel, tailhead. -diagnosis: superficial skin scraping -treatment: ML doing foot washes, treat whole herd and animals.

Answer 127

Diagnosis: * Direct observation/clinical appearance * Collect and store fresh, frozen orethanol * Identify to genus level * Test for tick-borne pathogens IF CLINICAL

Answer 128

* Manual removal(within12-24hrs) -ticks must be on 12-24 hours to transmit disease * Environmental modification (short grass, wood chips, etc.) * Topical Repellents: sprays,wipes,powders (carbaryl, pyrethroids, permethrin...) * Moxidectin, isoxazolines

Answer 129

-Damalinia (Werneckiella) equi: Chewing, Located on Dorso-lateral trunk- -Haematopinus asini: Sucking, Mane, tailhead, fetlocks § **Eggs at base of hair

Answer 130

-horses with lice -early spring and winter. -Those with thick coats, young foals, senior horses, pregnant mares, and those who are ill or weak are highest risk § Can live off host for up to 3 weeks (fomites) § Species specific, don’t carry other diseases

Answer 131

§ History and clinical appearance § Often asymptomatic (Carriers) § Hair loss, irritation, pruritus, dandruff (anemia) § Nits on base of hair, recovery and id. Of adult

Answer 132

* Topical pesticides: sprays, wipes, powders, shampoos (carbaryl, pyrethroids, permethrin...) * Systemic/oral ML may work on sucking lice * Treat repeatedly( also environment & fomites) * Highly contagious (treat all horses in herd)

Answer 133

-in horses, leave little white eggs -Horses ingest L1, go to GI tract to develop, pooped out at L2/L3. -larvae L3 to pupae in environment then adult flies lay eggs on horse and horse bites eggs and resets -are zoonotic to people can be in eyes

Answer 134

§ Gasterophilus intestinalis: eggs on forelimbs and shoulders, L3 in cardiac region of the stomach § Gasterophilus nasalis: eggs in inter- mandibular region, L3 in pylorus and proximal duodenum § Gasterophilus haemorrhoidalis: eggs on hair of mouth and lips, L3 in rectum

Answer 135

* History and clinical appearance: – usually asymptomatic – High intensities anorexia, colic, anaemia, cachexia * Eggs on tips of hair (vs base) * L3 on gastroscopy, passed in feces in spring, post-mortem * Adults are cause of dangerous behaviour in some horses while laying egg -treat ivermectin or moxidexin in fall after first frost

Answer 136

-blood feeding females lay eggs in OLD/ manure -identify: Arista, four longitudinal dark stripes on thorax, prominent forward projecting proboscis - IH for Habronema and Draschia -keep clean stalls, ect.

Answer 137

-blood feeding females -slash feeders with painful bites § Stout antennae, no arista, often banded/patterned eyes, mouthparts face down § MECHANICAL DISEASE TRANSMISSION: § Equine Infectious Anemia § Anthrax (CFIA)

Answer 138

-blood feeding fly * C. sonorensis (in Canada, near US border, Okanagan) * Tiny, short, stout legs, long segmented antennae, thorax humped, patterned wings * Adult females blood feed * Lay eggs in moisture/water * Vector of Onchocerca and viruses (Vesicular Stomatitis, African horse -lead to sweet itch sickness) * Hypersensitivity (Queensland or sweet itch)

Answer 139

Symptoms § Allergic reaction to saliva of midges (Culicoides spp.) § Papules on skin, particularly around mane and tail § Horses may rub à hair loss, scabs -prevention: bring horse inside, fly sheets, feed omega 3. topical steriod or systemic antihistamines.

Answer 140

* Aquatic larval cycle. adult females blood feed *Culex tarsalis, C. pipens: Vectors of West nile V, WEEV, EEV *Aedes spp .* Setaria equina (nematode) * Major public health significance globally (malaria, trypanosomes, viruses )

Answer 141

Management: -Stabling schedule and hygiene - Screens (fine mesh for Culicoides) - Site selection for grazing and manure piles - Eliminate arthropod breeding sites (water) Topical Repellents: sprays, wipes, powders, back rubbers (malathion, pyrethroids, permethrin...) - Do not work for tabanids - Pesticides, do not use off label - Wound care to prevent myiasis

Answer 142

-IH stable fly -go to horses bite -larve in tissues or in GI tract, adult in GI tract, pooped out as larvated egg -develop L1-L3 in fly IH. 1 week Cutaneous habronemiasis (“Summer sores”) Diagnosis: * Larvae in skin scraping or biopsy * Adults on gastric lavage/scoping * NOT fecal float Treatment: Ivermectin (ML)

Answer 143

-large roundworm of horses -usually foals less than 6 months -occasionally adult older horses -50% foals shedding -worldwide distribution -eggs very resistant and sticky * Quasi-vertical transmission (mechanical -often asymptomatic, if very large number could have impaction

Answer 144

-egg with L3 ingested get in and use hepato tracheal migration -may cause coughing (resp signs in foals) -adults go into GI shed in feces as eggs with morula -eggs L1-L3 in environment for 3 weeks. -ppp 10-12 weeks

Answer 145

-SI nematode * Primarily patent in foals <6 months of age * Warm humid climates – BC * Pastured and stabled animals with suboptimal environmental hygiene * Eggs not particularly resistant * Vertical transmission (transmammary) – Larvae shed in milk for up to 8 weeks -treat mares before milk or foals at 1 week

Answer 146

-equine threadworm -ppp 10-14 days -homogonic cycle (3 days) where they go back into the mare or heterogonic cycle (7-10 d) where the adult males and females are prodocucing outside the host. -semi tracheal route or tracheal -also somatic route and will have larve in tissues get into colostrum and cause trans mammary infection in foals.

Answer 147

-mostly eradicated due to anthelmic treatment, pasture transmitted -Strongylus vulgaris causes pathogenesis: L3 ingested larvae migrate from meseteric to arota and live there for weeks to months, then develop in LI as adults. they damage the aorta by eating on it and cause lesions. -eggs with morula shed, leads to L1-L3 a few days in environment. -ppp 6 months

Answer 148

-colic related to strongulus -not common but MOST IMOPORTANT STRONGLY -lesions on aorta and crainial mesenteric artery and by from larvae destroying them

Answer 149

- no teeth not clinical LI nematode -liver/ mesentery migration PPP 1 year -larvae can be seen in mesentery/ liver

Answer 150

-larvae migrate, liver/ pancrease migration go to LI -PPP 1 year -diagnosis fecal float but all strongyl look the same so have to do a larval coPCR or dna testing, -not seen really ever due to anthelmic treatment

Answer 151

-Most abundant and diverse equine nematodes At least 60 known species Pasture transmitted -large intestine nematode

Answer 152

-inhibited hide in mucosa and are resistant to some treatments then come out in spring and can cause colic. -mucosal migration -inhibited or hypobiotic L3/L4. ppp- 2-3 months -LI nematode

Answer 153

* Clinical signs: – Simultaneous emergence of mucosal larvae (rare in Canada) – Diarrhea, weight loss, protein losing enteropathy, edema – Mortality as high as 50% -CAN OCCUR WITHOUT ANY EGGS BEING SHED IN FECES

Answer 154

* Dx: – Subadult and adult worms in feces – Larval culture (+/- PCR) from eggs in feces – Thickened walls of large intestine on ultrasound * Tx: – Egg Reappearance Period (ERP) following treatment varies with product; due to mobilization of inhibited larvae. treat then want to see 95% reduction and stay dead for awhile – Moxidectin is only product effective against inhibited larvae

Answer 155

-Overuse of anthelmintics has led to widespread resistance among equine parasites, especially cyathostomes -fecal egg count wont give whole picture of how sick a horse may be

Answer 156

* Maintain and monitor drug efficacy: – Determine which horses contribute the most eggs. some will be high shedders. – Leave parasite refugia by using Targeted Selective Treatment (TST) – Monitor drug efficacy (by FEC reduction test) * Use strategic treatments to maximize effect and minimize shedding (based on knowledge of life cycle) * Use non-drug methods of control (pasture and manure management)

Answer 157

-test and treat all horses in fall. classify shedders -moxidectin to encysted larval stages of small strongyl and bots. -praziquantel if cestodes. -test and treat moderate/ high shedders in the spring (cyathostomes) and again in 2-3 months. -do FECRT every 3 years to ensure efficacy.

Answer 158

-treat up to 4 times a year * (Treat foals at 1-2 weeks if Strongyloides) * Treat foals at 2-3 months and 6 months (with benzimidazoles) to get Parascaris -treat with ivermectin for small strongyles. -do FECRT yearly to ensure efficacy.

Answer 159

-large strongyles are not resistant to anything -small stronglyes are starting resistance to macrocyclic lactones -parascaris is starting resistance to pyrantel.

Answer 160

-don't relocate dewormed horse to "clean" pasture. -reduce stocking density -dispose manure 2x week. -dont feed off the ground -dont spread fresh manure on fields that horses are grazing -mow and harrow pastures periodically -separate weanlings from yearlings, adults.

Answer 161

– Coughing foal with no bacterial or viral cause – Diarrhea in 2-3 week old foal – Diarrhea, weight loss, low protein/albumin, edema – Spasmodic colic of unknown origin – Pruritus ani (explore non parasitic causes!) (rubbing tails raw)

Answer 162

-Large intestinal nematodes -pinworm of horses, caecum, colon, rectum. -worldwide distribution Stabled horses, poor hygiene Eggs environmentally resistant NOT ZOONOTIC - cause Pruritus ani lay eggs on tail of horse cause ithcing.

Answer 163

-egg with L3 travel orally into mucosa where they grow into adults -you wont see eggs until 5 months after PPP 5 months -shed in feces. egg translates in environment from egg with L1-L3 in a few days -treatment: washing tail, ivermectin on tail off label.

Answer 164

-connective tissue nematode -arthropod transmission -present in canada with vectors (BC) -IH is midge which will bite horse with L1, larve grow to L3 in midge then bites another horse and transfers L3 to horse where it grows into adults. 3-4 weeks in IH

Answer 165

-Often no C/S -Cutaneous onchocerciasis: Face, neck, and ventral midline Alopecia Crusting Pruritus -Tx: ML will kill larvae but not adults -microfilaria can be found in skin biopsy.

Answer 166

-lung nematode -Rare in Canada -Dyspnoea and cough -Not usually patent in adult horses – primary reservoir is donkeys and horses < 3 yrs old -Pasture transmitted

Answer 167

-ingested as L3 larvae. goes through tracheal migration to lungs, adults in Gi shed feces, L1-L3 environment. -inhibited, or hypobiotic L3/L4 -PPP 12-14 weeks

Answer 168

-Ileum and Caecum Most common species -Worldwide distribution, rare in western Canada Pasture transmitted -IH mite with cystercrcoid (infective) for 2-4 months. then ingested by horse. adults in GI. shed in feces are eggs with hexicanth larvae. -ppp 1-2 month -clinical: ileal impaction and spasmodic colic

Answer 169

* Clinical signs: often none – Foals with other health issues * Risk factor for ileal impaction and spasmodic colic (A. perfoliata) * Dx: eggs in feces 24 hrs post- treatment, coproantigen & serology (NA in Canada) * Tx: Single annual treatment with praziquantel in late fall

Answer 170

* Caused by Neorickettsia risticii (Gram-negative bacterial endosymbionts of flukes) * Flukes (Acanthatrium oregonense) of bats (horses get in water) * Freshwater snail first IH * Flying aquatic insects as second IH (caddisflies mayflies, damselflies, dragonflies...) * Horses accidentally ingest N. risticii inside cercaria in water or metacercaria in aquatic/adult insect * Severe acute diarrhea, laminitis, abortion * Dx: PCR blood/feces; Tx: oxytetracycline

Answer 171

“Moroccan leather” abomasum; infects gastric glands 1. Rupture of intercellular junctions → leakage of plasma proteins → hypoproteinemia 2. Destruction of parietal cells → increased abomasal pH → reduced conversion of pepsinogen to pepsin → reduced protein digestion CS: malabsorptive diarrhea, anorexia, increased blood pepsinogen, bacterial overgrowth (putrid smell)

exam 2 Flashcards

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