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parasitology
exam 3
| Question | Answer |
|---|---|
| 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
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