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parasitology

exam 3

QuestionAnswer
strongyles common name the royal roundworm
strongyles sp infect horses
where do stronglyes live the lg int of host.
what is the infective stage of stonglyes L3 larva
cyathostomines live where lg int. cecal, ventral/dorsal colon
cyathostomines pp 6-12wks. up to 2 yrs
what stage of cyathostomines causes disease L4. disruption of intestinal wall. weakened mucosal barrier
larval cyathostominosis rare. diseases associate with mass emergence of encysted larvae from wall of lg int
larval cyathostominosis symptoms diarrhea, cachexia, colic, anorexia, protein-losing enteropathy, ventral edema. mass emergence!
what is protein- losing enteropathy losing protein into gut
small stronglyles clinical importance disease occurs within PP making diagnosis difficult. acute and chronic. seen in horse <5yr. dewormed with/in last 2 wks.
with larval cyathostominosis why do diarrhea and colic occur b/c of disruption of large int mucosa. protein losing enteropathy
small stronglyles mortality rate 50%
how is small stonglyes diagnosed via necropsy
small stronglyles CBC results neutrophilia, anemia?, eosinophilia
small stronglyles Chemistry results hypoalbuminemia, hyperglobulinemia, elevated total protein b/c of globulin
small stronglyles ultrasound results thickened lg int mucosa
small stronglyes types cyathostomins
large stronglyes types strongylus vulgaris strongylus equinus strongylus edentatus
strongylus vulgaris pp 6mo
strongylus edentatus pp 11 mo
strongylus equinus pp 9 mo
strongylus vulgaris life cycle larvae migrate in walls/lumen of sm.arteries and cranial mesenteric artery. arrive in lg int, mature and reproduce
strongylus vulgaris symptoms local inflammation. reaction along vessels and walls of artereies. get uneven thickening of wall. Turbulence causes blood to clot. thombosis and organ to die
strongylus edentatus life cycle larvae migrate retroperitoneally and through liver. arrive in lg int, mature and reproduce
strongylus equinus life cycle larvae migrate through peritoneal cavity, pancreas and liver. arrive in lg int, mature and reproduce
strongylus vulgaris pathology mainly caused by migration. peritonitis. arteritis, thrombosis, embolism, ischemia, infarction. verminous aneurysms
strongylus edentatus and strongylus equinus pathology peritonitis, liver pathology
strongylus vulgaris clinical signs and importance younger horses. disease occurs in pp period b/c caused by immature stages. peritonitis, colic by interruption of blood supply
Trichostrongylus axei common names stomach hair worm, bankrupt worm, black scour worm
Trichostrongylus axei hosts cattle, sheep, goats, horses, swine, rabbits, people
parascaris spp. common name equine roundworm
parascaris spp pp 12 wks
parascaris spp clinical signs lethargy, rough hair, poor wt gain, diarrhea, colic, pot-belly, impaction, intussusception, intestinal rupture
parascaris spp peak worm burden occurs when 4-5 mo of age. smaller peak at 9 mo. most gain immunity at 12-18 mo
parascaris spp egg shedding b/w 3-6 mo. peak at 4-5 mo. second peek at 8-10 mo
oxyuris equi common name equine pinworm
oxyuris equi lives where posterior portion of lg int
oxyuris equi pp 5 mo
what is special about oxyuris equi eggs female deposits (cement) eggs in perianal folds
oxyuris equi clinical signs intense anal pruritus. rubbing hind end on stalls, fence posts. broken tail hair. behaviorial issues.
oxyuris equi diagnosis scotch tape test
strongyloides westeri common name intestinal threadworm
strongyloides westeri pp with lactogenic transmission 7 days
strongyloides westeri pp with env transmission 10-14 days
strongyloides westeri clinical signs enteritis, diarrhea-dehydration, poor growth, "frenzy" syndrome
Draschia and Habronema common name stomach worm
Draschia and Habronema life cycle obligate indirect
Draschia and Habronema intermediate host flies. deposit eggs in horse mouth, wounds, eyes
Draschia and Habronema pp 2 mo
Habronema clinical signs summer sore. larvae in cutaneous wounds, ocular problems. adults live in mucosa
Draschia clinical signs cause large nodules near the margo plicatus (stomach)
goals of treatment of healthy horses control parasite pop w/in herds. not complete eradication. maintain refugia
internal dose program most common. treatment of all horses at fixed intervals throughout the year. shorter then ERP. suppressive deworming to minimize contamination. driver of anthelminitic resistance
strategic dosing treatment of all horses at fixed times of year, no diagnostics. fewer treatments, less intensity. exploiting seasonal biology. reduce worm burdens by removal of accumulated adult parasites.
continuous daily treatment for strongyles daily admin of pyrantel tartrate to all horses. no diagnostics. creates lot of resistance
selective treatment of stongyles adult horses only. treatment of only horses set above a FEC threshold. allows portion of drug susceptible parasites to survive. increase refugia. fewer treatments, less intensity, reduce likelihood of resistance
80/20 rule 20% of mature horses will shed 80% of the eggs. horses remain in the same category throughout their adult life.
horse pasture management reduce overcrowding. mowing/dragging. pasture hygiene. alternate species grazing. keep young and old separate so can treat properly.
should managers treat and move horse herd? no. move herd first, let acclimate, then treat
selective therapy combine selective/strategic deworming. increase refugia, slow down anthelmintic resistance formation.
integrative treatments anthelmintics are combined with grazing menagement. selective (strategic) treatment
contributors to resistance 1. too frequent deworming 2.underdosing 3.treating all animals, regardless of need 4. treating and moving to clean pasture
side resistance if resistance to one member of a group, resistant to all
cross resistance occurs when resistance to one group confers resistance to another group
refugia the portion of the parasite pop not subject to drug selection pressure.
broad spectrum equine anthelmintics effective against what 1. large strongyles 2.small steongyles 3.ascarids 4.pinworms
benzimidazoles affects tubulin and microtubule assembly. starves the worm
tetrahydrorpyimidines/imidithiazoles acetylcholine agonists. paralyze the worms
macrocyclic lactones gates glutamate chloride channels. starvation. paralyze and starve worms
fenbensazole BZD. Panacur/safegaurd. broad spectrum. documented resistance to cyathostomins.
oxibendazole anthelcide E.Q. broad sepctrum. documented drug resistance to cyathostomins
benzimidazole resistance resist worms have isomers of tubulin that are less affected by BZDs. amino acid substitutions in the gene encoding tubulin
pyrantel salts poorly absorbed across mucosal barrier. broad spectrum. kills L4s as they excyst. restance reported for Cyathostomins, parascaris
piperazine common for chickens. no longer labeled for horses. Limited for ascarids and small strongyles
ivermectin borad spectrum. moderate ERP for small strongyles
moxidectin broad spectrum. encysted EL3, LL3, L4. not labeled for use in foals <6mo
ivermectin ERP 2months. now approx 4-6wks
moxidectin ERP 3 months. now spprox 4-6 wks
benzimidazoles/pyantel <2wks. now resistance
minimum treatment obj for targeting migrating large strongyles annual to biannual treatment with a macrocyclic lactone, persistent extra-intestinal activity
minimum treatment obj for controlling small strongyle pop stingle/twice yearly treatment when pop is arrested in tissues. minimal treatment 'selective deworming' of wormy, high FEC animals to reduce pasture contamination. preserve genetic diversity and susceptibility of worms to effective drugs
high shedding level >500 EPG
medium shedding level 200-500 EPG
Low shedding level <200 EPG
Treatment for low egg shedders 1. deworm twice yearly with effective dewormer 2.deworm at least once a year for tapeworm
Treatment for medium/ high egg shedders 1. deworm a min of twice a year with an effective dewormer. may require one or two additional treatments during grazing/transmission season 2.deworm at least once a year for tapeworms
parascaris control 1. clean mare's udders/teats 2.dedicated pasture for foals 3.feed young animals from containers 4.keep foals from infection keeps thousands of eggs off pasture
parascaris treatment effective drug therapy at 2-3 mo and 5-6 mo (weaning). BZD, macrocyclic lactones
oxyuris equi treatment pytantel, BZD
Strongyloides westeri treatment usually does not require treatment. Macrocyclic lactones, BZD. supportive care
Trichostrongylid PP 21 days
diagnosis of Trichostrongylid high FEC shedders, treatment efficacy
Trichostrongyle in cattle ostertagia. disease associated with large numbers. young and nutritionally stressed animals at greatest risk.
Trichostrongyle in sheep, goats, camelids haemonchus contortus. can bleed animal to death. multi drug resistant and widespread
ostertagia common name brown stomach worm. highly pathogenic. tissue damage to abomasum
ostertagia live where abomasum.
ostertagia life cycle direct. arrested dev in gastric pits. seasonal emergence.
type 1 disease many worms acquired over short period of time. usually young animals
type 2 disease occurs months after initial infection. older animals. 2nd season on pasture
type 1 disease worms acquired in south b/w october and march. larva begin to arrest in tissues april-sept.
type 1 clinical disease larvae mature in gastric glands of stomach. damage occurs when larvae leave glands to become adult worms and reproduce.
type 1 ostertagiosis characterized by 1. profuse watery diarrhea (bright green) 2.bottle jaw 3.loss of appetite, failure to gain wt. loss of BCS 4. young animals, 1st season on pasture
type 2 disease worms acquired in south late spring. dormant during late summer-fall months
type 2 ostertagiosis characterized by older cattle. associated with stress. clinical signs similar to type 1 but more severe. high mortality. watery brown diarrhea. rumen pH approaches neutral
cooperia cattle. calves. loss in ADG
Nematodirus cattle. seasonal hatching concentrates infective worms. calves in late spring. parasite develops w/in egg and primed for hatch
overall purpose of treating young animal reduce adult worm burdens and disease potential at high pasture infectivity (seasonal bio)
overall purpose of treating high FEC shedders reduce pasture contamination
overall purpose of targeting inhibited larvae seasonally with effective drug therapy to reduce overall or selected portion of parasite population
what parasite causes bottle jaw anemia Haemonchus contortus
Haemonchus contortus common name Barber pole worm
where do Haemonchus contortus live in the abomasum
Haemonchus contortus lifecycle direct
Haemonchus contortus pp 21 days
clinical signs of Haemonchus contortus anemia PCV <15%. Pale mucus membranes. bottle jaw
Clinical name for bottle jaw hypoproteinemia submandibular edema
why are goats so susceptible to worms 1. never meant to live in subtropical climate 2. never had to evolve the ability to acquire strong immunity to parasite challenge.
sheep adaptations for mitigating parasite disease risk predominately grazing animals. acquired immunity to reg parasite numbers
goat adaptations for mitigating parasite disease risk preferential browsers. ability to detox ingested plants (Tannin). absence of acquired immunity
can fecal egg counts be used to predict worm burden of clinically affected animals No because the larva amount cause the disease
FAMACHA scoring qualitative scale for visually assessing anemia in sheep and goats. used for prescribing anthelmintic treatment to at risk animals
FAMACHA scores are highly correlated to what hematocrit and disease risk
Ascaris suum common name swine roundworm
Ascaris suum sp infect swine
Ascaris suum live where small intesting
Ascaris suum lifecycle direct. rodents may be paratenic host. tracheal migration. must dev in env before infective
Ascaris suum pp 8 weeks
how are Ascaris suum spread mechanically to offspring sticky abuminous coats. eggs stick on mom teats.
Ascaris suum clinical signs 1. stunted growth and poor feed efficiency in piglets 2.grower/finished on contaminated pasture 3.pneumonia/respiratory disease from tracheal migration 4.liver condemnation
why is the liver of pigs infected with Ascaris suum commonly condemned at slaughter granulmatous "milk-spots". $17/ cwt.
Ascaris suum treatment 1. FBZ removal of adults and immature stages. no withdraw time 2. pytantel, daily to prevent migration. 24hr withdraw time
Ascaris suum zoonotic significance human Ascaris morphologically indistinguishable from swine. some think they are the same species.
Trichuris suis common name swine whipworm
Trichuris suis sp infect swine
Trichuris suis live where caecum and lg int
Trichuris suis lifecycle direct. larvae dev beneath epithelium in sm int before moving to caecum and lg int.
Trichuris suis pp 7-9 wks
Trichuris suis clinical significance stunted growth and poor feed efficiency in piglets. anemia, diarrhea, dehydration, dysorexia, wt loss. grower/finisher on contaminated pasture
what age piglets are most affected by Trichuris suis 8-14 wks
Trichuris suis attachment to lg int causes what inflamm response. colitis. mucosal necrosis and edema. focal hemorrhage
Trichuris suis zoonotic significance human Trichuris morphologically indistinguishable from swine. many think they are the same species. recent interest for use of "induced infections" in humans for treatment for autoimmune disorders
hygiene hypothesis microbes/parasites and humans co-evolved to keep immunity "in check"
Oesophagostomum dentatum common name swine nodular worm
Oesophagostomum dentatum species infect swine
Oesophagostomum dentatum lifecycle direct. must dev in env. larvae penetrate intestinal wall and dev. return to lumen as sub mature adult worms (L4). become adult and reproduce
Oesophagostomum dentatum live where lg int
Oesophagostomum dentatum pp 6-7wks
Oesophagostomum dentatum clinical significance stunted growth and poor feed efficiency in piglets, grower/finished on contaminated pasture. economic loss from condemned sausage casings
with Oesophagostomum dentatum why do piglets have stunted growth and poor feed efficiency nodule formation in gut and associated inflammation. enteritis. dysorexia. blood stained feces
stephanurus dentatus common name swine kidney worm
stephanurus dentatus species infect swine
stephanurus dentatus live where adult in ureters. eggs passed in urine.
stephanurus dentatus lifecycle direct (Facultative indirect). larvae penetrate stomach wall, enter hepatic blood supply. extensive/destructive systemic migration
how long does the systemic migration of stephanurus dentatus last 3-9mo. liver capsule. peritoneal cavity. peri renal tissues.
stephanurus dentatus pp 9-16mo
stephanurus dentatus clinical significance pathology associated with extensive systemic migration. liver cirrhosis. lack of growth in herd. condemnation of liver and kidney and pork loin (choice cuts) at slaughter.
strongyloides ransomi common name swine threadworm
strongyloides ransomi species infect swine
how are piglets commonly infected with strongyloides ransomi lactogenic route of hyobiotic larvae.
strongyloides ransomi pp in lactogenic route 7 days
Trichinella sp zoonotic significance traditionally associated with ingestion of pork from infected domestic swine
treatment and prevention of parasitism in swine 1. hygiene 2.animals segregated by age group 3.wide selection of anthelmintics
Ascaridia galli common name poultry round worm
Ascaridia galli sp infect poultry
Ascaridia galli lifecycle direct. dev in int. no tracheal/somatic migration
Ascaridia galli pathology comes from what penetration and inflammation in duodenal mucosa. emaciated. decreased egg production
poultry most suceptible to Ascaridia galli at what age young birds. acquired immunity >3mo
Heterakis gallinarum common name poultry cecal worm
Heterakis gallinarum sp infect poultry
Heterakis gallinarum lifecycle direct and facultative indirect. earthworm as paratenic host. must dev in env
Heterakis gallinarum pathology thickening of cecal mucosa
Heterakis gallinarum contrast with H.isolonche nodular typhlitis, casesous lesions, diarrhea, wasting and death
capillaria sp infect poultry
capillaria lifecycle direct and facultative indirect. earthworm as paratenic host, maybe IH
capillaria live where intestine, espohagus, crop
capillaria pathology emaciation, hemorrhagic diarrhea w/intestinal sp. hyperplasic of crop/esophagus. croupous inflammation, dysrexia, death
syngamus trachea common name gape worm
syngamus trachea sp infect poultry
syngamus trachea lifecycle direct and facultative indirect. earthworm paratenic host. tracheal migration.
syngamus trachea reproduce where larger bronchi and trachea
syngamus trachea migration through lung is associated with what ecchymoses, edema, lobar pneumonia.
syngamus trachea "gape" behavior open mouth, dyspnea, asphyxia from accumulated mucous in mouth
Spiruid nematodes sp infect poultry
Spiruid nematodes live where gizzard, proventriculus, esophagus
Spiruid nematodes lifecycle obligate indirect lifecycle. orthoptera/coleoptera as IH.
Spiruid nematodes pathology emaciation, hemorrhagic diarrhea w/intestinal sp.
treatment and prevention of parasitism in poultry production 1. confinement and off ground 2. avoid hypercontamination 3. segragate by age 4.wide selection of anthelmintics
Created by: ejohnson17