what are the two options for intermediate host function in an indirect nematode life cycle?1) definitive host ingests the intermediate host; i.e. snail is prey to deer (passive transmission) 2) intermediate host serves as vector; i.e. dog is prey to mosquito (active transmission)definitive nematode hostdomestic animals infected with adult stages of parasitic nematodes - sexual reproduction of parasite occurs hereintermediate nematode host- vertebrate/invertebrates - provide niche for development of larvae - provide advantages for transmissionparatenic nematode hosttransport - vertebrates/invertebrates - no development of larval stages - predator/prey relationship with definitive hosthypobiosisarrested development - inhibition of larval development, often due to environmental conditions - survival mechanism - resumed development when environmental conditions improve --> disease - refractory to some drugswhy are hypobiosis states refractory to some drugs?because the parasite is not in a high enough metabolic state to be affected by the drugshypobiosis: Ostertagia ostertagi life cycleacute onset of disease in spring --> larvae arrest in L4 in fall --> emerge the following spring - periparturient rise or "spring rise" in egg countsOrder Strongylidabursate nematodes - GI parasites - strongyle-type egg - egg passed in feces - L1-L3 in environment - male with copulatory bursasuperfamilies of Strongylida- Ancylostomatoidea - Strongyloidea - Trichostrongyloidea - MetastrongyloideaAncylostomatoideasuperfamily in the Strongylida order - "hookworms" - bent head, oral cutting plates or teeth - buccal capsule - plug feeders (eat tissues) - hematophagicprimary pathogenic mechanism in hookworm diseaseingestion of blood by adult worms in the small intestineBunostomum phlebotomum lifecycleruminant hookworm - infective larvae enter via mouth or skin - either tracheal migration or direct migration to GI tract - adult nematodes in small intestine; eggs are laid in SIwhat process happens to ruminant hookworms (Bunostomum phlebotomum) when they enter the skinexsheathment - L2 skin was retained as a form-fitting sheath around L3; protects larvae in the external environment - L3 casts off the sheath soon after entering hostpatency periodwhen there is evidence of parasitism; can actually give a diagnosis (i.e. eggs in the stool)prepatent period (PPP)before you can tell there is an infection, but there is one - often involves requisite developmental changescyclical seasonality is typical of _____ and ______ hookworm transmissionpercutaneous; oralstrongyle-type egg- diagnostic stage of hookworms and other members of the order Strongylida - oval-shaped - thin, transparent shell - contains developing embryo or larva, depending on time in the external environmentAncylostoma caninumcanine hookwormwhat special type of transmission does Ancylostoma caninum have?transmammaryhow would Ancylostoma caninum present clinically in humans?Cutaneous Larva Migrans - only able to migrate under the skinarrested L3 in skeletal muscle or gut wall is a good diagnostic example ofhypobiosislactogenic (transmammary) migrationonly occurs in Ancylostoma caninum - transmission of parasites to suckling pups - no tracheal migration; goes straight to intestineslife cycle of Ancylostoma caninum (without lactogenic migration or hypobiosis)skin penetration by L3 --> systemic blood circulation --> tracheal migration --> intestinedoes patency occur faster or slower with the transmammary route of Ancylostoma caninumfasterwhat is a factor that has been experimentally shown to increase Ancylostoma caninum excretion in milk?hormones - study with estradiol and progesteronewhat is the only hookworm species that has transmammary or prenatal infections in dogs and cats?Ancylostoma caninumwhat are some reasons why Ancylostoma caninum is such a potent pathogen?- transmammary/prenatal infections that skip the tracheal route - L4 stage of larvae can feed on blood --> leads ot much higher daily blood loss valueshookworm disease in dogs: intensity of exposure- arrested L3 burdens in dams (in stomach lining or muscle; hypobiosis) - heavily contaminated environmentwhy does host susceptibility to hookworm infection/disease decline with advancing age?- physiological resistance (larger hosts, have more blood to spare) - acquired immunitywhat is a practical demonstration of hypobiosis in effect, seen in Ancylostoma caninum infection?repopulation of the gut by arrested larvae in tissues (population comes back after certain period of time post-treatment)Strongyloideasuperfamily of the Strongylida order - large-bodied worms - bursate - buccal capsules - direct life cycles (some facultative exceptions) - migration in many species - strongyle-type eggs (except Syngamus) - predilection site = large intestine (except Syngamus and Stephanurus)What is the only Strongyloidea that doesn't have Strongyle-type eggs? What type does it have?Syngamus; bioperculated eggsWhat are the only Strongyloidea that don't have the large intestine as their predilection site?Stephanurus and SyngamusSyngamidaefamily under the superfamily Strongyloidea - contains genus Syngamus and StephanurusSyngamus tracheagapeworm; tracheal worm of fowl and game birds - huge females made of mostly ovarian tissuewhat are the only parasites that exist in the trachea of domestic birds?Syngamus trachea; adult worms in the tracheaLife cycle of Syngamus tracheaadult worms in trachea, reproduce there --> bioperculate eggs coughed up, swallowed, passed in feces --> L3 develops inside egg --> infection by ingestion of L3 in egg, hatched L3 or L3 in paratenic hosts --> L3 penetrate intestine and migrate to lungs --> PPP then permanently in copulaclinical signs of Syngamus tracheahemorrhagic tracheitis with mucus production (from immune response) - "gaping", shaking, gasping - young birds; coughing, severe pneumonia, deathHow can you diagnose Syngamus trachea?Bioperculate egg in the feces - opening on each end of eggStephanurus dentatusStrongyloidea of the Syngamidae family kidney worm in swinewhere will you find adult Stephanurus dentatus?found in peri-renal fat and walls of kidney of swineLife cycle of Stephanurus dentatusinfection --> immediate molt to L4 & migration to the liver via blood --> final molt in liver parenchyma --> migrate through peritoneum to the kidney --> adults complete development in kidney cysts --> eggs passed in urineroutes of infection of Stephanurus dentatus- ingestion of L3's - ingestion of infected earthworms (facultative intermediate hosts) - skin penetration by L3'swhat is the most common infectious stage of nematodes?L3at which two parasitic stages can pathogenesis occur with Stephanurus dentatus?L4 and adult stageL4 stage pathogenesis of Stephanurus dentatus(final molt at liver parenchyma) --> severe cirrhosis --> liver failure, deathadult stage pathogenesis of Stephanurus dentatus- inflammation and thickening of the kidney and ureter - green pus around kidneymain clinical sign of Stephanurus dentatus infectionfailure to gain weightStephanurus dentatus infection diagnosis*strongyle-type eggs in urine of adult reservoirs* necropsy (liver cirrhosis) meat inspectioncan Stephanurus dentatus be treated?yesGenus Oesophagostomumin the family Chabertiidaethe definitive hosts of most oesophagostomum species are _____, _____, ______, except for Oesophagostomum dentatum which affects _____cattle, sheep, goats; pigswhat is the primary clinical sign of oesophagostomum infection?enteritisoesophagostomum have what capsular feature?radial alaeLife cycles of oesophagostomum spp.adults live in colon --> "strongyle-type" eggs released in feces --> free-living larval dev. is quick to L3 --> infection by ingestion of ensheathed L3's --> exsheath in small intestine --> penetrate the mucosa of small and large intestine --> (possible hypobiosis) --> L4's energy, pass to colonin what stage can oesophagostomum spp. survive winters in the environment?L3'spathogenesis of oesophagostomum spp.L3 in nodules on GI tract with greenish pus --> intestinal ulcers form upon emergency of L4 --> severe enteritis - anemia, protein loss, weight loss - diarrhea - chronic ulcerative colitis - debilitating for wool and mutton productionoesophagostomum spp. diagnosisdifficult because in young animals, diarrhea may happen in the PPP with no eggs in feces, just due to nodules - nodules at necropsy disseminated in all ruminants, concentrated in cecum and colon in pigscan oesophagostomum spp. be treated?YesFamily Strongylidaein the superfamily Strongyloidea contains two sub-familiestwo subfamilies of StrongylidaeStrongylinae ("Large Strongyles") Cyathostominae ("Small Strongyles")Genus: Strongylusin the subfamily Strongylinae ("Large Strongyles") *MOST DESTRUCTIVE PARASITES OF HORSES*what species are in the genus of parasites most destructive to horses?Strongylus vulgaris Strongylus equinus Strongylus edentatusWho is the definitive host and where is the predilection site for all Strongylus spp.?Horses and donkeys Cecum and colonparts of the life cycle of genus Strongylus that are common to all equine strongyles- Adults live in cecum eggs passed in feces (L1) - development of L3 takes 2 weeks (in soil) - L3 penetrate intestinal mucosa *potentail migration* - nodules form in the mucosa of cecum and colon that burst to release adults into gutwhat migration pattern is unique to Strongylus vulgaris?after L3 penetrate intestinal mucosa: - L4 migrate to endothelium in *cranial mesenteric artery* - molt to L5 (young adults) in 2-3 months - return to intestine via arterial luminalife cycle of Strongylus equinusIngestion of L3's --> exsheath in mucosa --> Molt to L4's --> migrate to liver, stay for 6-7 wks --> migrate to pancreas --> molt to L5's --> return to large intestinespecial migratory places: Strongylus vulgaris = ________; Strongylus equinus = _______, _________; Strongylus edentatus = _________, _________cranial mesenteric artery; liver --> pancreas; liver --> flanks --> peritoneumLifecycle of Strongylus edentatusingestion of L3's --> exsheath in SI --> migrate to liver via portal vein --> molt to L4's in liver --> migrate to flanks --> molt to L5's in peritoneum --> return to LI --> nodular formation --> rupture of noduleswhat is the common mode of pathogenesis amongst large Strongyles?adults cause intestinal ulcers, bleeding, and scarring due to feeding on the mucosapathogenesis specific to Strongylus vulgaris- larvae cause inflammation in arterial walls as they develop from L4 --> L5 - rarely aneurysms and thinning of walls - fever, inappetence, colic (possibly fatal)diagnosis of Strongylus spp. infections- clinical signs - *strongyle-type eggs in feces of definitive hosts in patent infections* - necropsy; specific lesions related to migratory pathways & easily identifiable adults in the large intestineCyathostominaesubfamily of the family Strongylidae "Small Strongyles"what would be more pathogenic; an infection of 1 large strongyle or 1 small strongyle and why?1 large strongyle; small strongyles are too small, need many to cause pathogenesis (which can happen)life cycle of Cyathostomes: pre parasiticidentical to large strongyles - direct, free living larvae - during mid-summer L3's develop in 2 weekslife cycle of Cyathostomes: parasiticNO MIGRATION; L3 to L4 development inside mucosa of large intestine - may be arrested development in winter in temperate climatesLarval Cyathostomosis pathogenesisNEED LOTS - hemorrhagic enteritis - L4's in feces - peripheral edema - sudden onset diarrhea when larvae emerge into lumen - spring occurrence - unresponsive to some antihelminticsCyathostomosis diagnosisdiarrhea in spring recurrence of diarrhea after treatment fecal counts might be low because signs caused by emerging larvaecan Cyathostomosis be treated?yestrichostrongyloideathread-like roundworms superfamily, in the order Strongylida - not plug feeders like the others - mostly feed on bacteria, microbiomeGenuses of interest in the family trichostrongylidaeHOT! Haemonchus Ostertagia Trichostrongylustrichostrongyloidea genuses of interestHaemonchus, Ostertagia, Trichostrongylus, DictyocaulusGeneral Trichostrongyle Life Cycle*contamination* - eggs come into the environment through feces *development* - develop from egg to L3 (free living, motile larvae) in the environment *infection* - enter the host at L3 stage *maturation* - occurs in the abomasum/small intestine - L3 --> L4 --> adultsat what points in the life cycle of Trichostrongyles can you try to break the cycle with treatment?contamination development infection maturationmajor features of the Trichostrongyles- small, hair-like - BURSATE; large copulatory bursa - small buccal capsule (unlike hookworms, which have a large one for biting) - strongyle-type eggs (except Nematodirus)what are the typical predilection sites of Trichostrongyles?- Abomasum, stomach, small intestinewhat are the typical definitive hosts of Trichostrongyles?Ruminants, equine, swinewhat is special about the Trichostrongyles head?not much - lots of other worms have specialized heads for pathogenesis - their pathogenesis comes from eating bacteriaTrichostrongyles have a _______ biotic potential, laying _____ of eggshigh; lots_____ egg: ______ adult -->one: one; no amplification in the host, like with bacteria and viruseshow does age of the host affect Trichostrongyle infection?older hosts are harder to infect; more developed immunityCan Trichostrongyles overwinter?yesCan Trichostrongyles go through hypobiosis?yesWhat are Trichostrongyles' strategies for reproductive success?1) High biotic potential 2) Motile intermediates; allows dispersal 3) overwintering larvae 4) Arrested development; allows parasite to respond to changes in the environment 5) Periparturient rise 6) Drug resistanceHow does reproduction of the worm affect drug resistance?since they reproduce sexually, genetic recombination can occur, leading to drug resistance as a reproductive strategyPeriparturient Risereproductive strategy of Trichostrongyles - increase in number of nematode eggs produced by ewes in the period after parturition - exposes naive newborns to parasites - eggs sense that host is pregnant --> choose to hatch soon afterWhat can be wrong with the host to reduce parasite success?No host Wrong host species Immune host Dead host! sheds no eggsWhat factors reduce parasite success?- Host troubles - Antihelminthic drugs - competitors; other or same species - external environment - too cold, too dryWhy can Haemonchus have such a higher biotic potential than Trichostrongylus?Haemonchus feeds on blood; very rich diet, can make lots of eggsNematodirus spring flush of L3 from eggsmass hatching of L3 in the spring; lots of eggs in the environment for when lambs are feeding --> fecal egg count of the lambs declines going into summer as lambs build up immunitySurvival of many nematodes is associated with their ability to undergo _____hypobiosis (arrested development)Initiating factors in arrested development- seasonal influences on infective larvae on pasture - host immune responses to parasitic phase of life cycle - competition - presence of adult wormsconsequences of arrested development- survival of nematodes in hostile conditions - synchronous development of large numbers of larvae (usually a trickle) - metabolic depression --> less susceptible to anthelminticsWhat Trichostrongyle is an exception to the simple life cycle rule?Dictyocaulus viviparusWhat is most special about the Dictyocaulus viviparus life cycle?NO EGGS in the feces - live young are excreted from the host to environmentWhat is a key external agent in the Dictyocaulus viviparus life cycle?Pilobulus fungi - fungus grows in cow pat, where the larvae have been developing from L1-L3 - larvae crawl up the fungi - when the spores of the fungus burst, the larvae are dispersed with themDoes Dictyocaulus viviparus have tracheal migration?yesDictyocaulus viviparus is alungwormclinical signs of Dictyocaulus viviparus- coughing - no eggs in fecalDiagnosis of Dictyocaulus viviparus- clinical signs (mostly) - seasonal occurrence (might happen annually) - L1's in feces of infected hosts - necropsy (also mostly..)what type of histological plug might you see in a Dictyocaulus viviparus infection?eosinophilicDictyocaulus viviparus controlvaccination in europe, anthelmintics in USAclinical signs of acute disease of Haemonchus(mostly in young animals) - anemia - severe edema - dark feces - sudden death from hemorrhagic gastritis in the hyper acute formclinical signs of chronic disease of Haemonchus(mostly in older animals) - weight loss - lethargy - mild anemia - ± edemawill you see diarrhea in Haemonchus infection?NO - but there is presence of eggs in fecesbarber-pole wormHaemonchus________ is the most important intestinal parasite of sheep, goats, and other ruminantsHaemonchuswhat are the two main clinical signs of HaemonchosisAnemia and Hypoproteinemiawhat is the underlying pathogenesis of Haemonchus?blood-feeding tendencieswhat is specialized on the Haemonchus females' heads?lancet to pierce mucosa and feed on bloodat peak infection, Haemonchus can consume ____% of RBC/day of a lamb20control strategies for Haemonchus- NO EFFECTIVE VACCINES - strategic drenching programs - rotational grazing - breeding tolerant/resistant sheep (limited use)FAMACHA/RefugiaA way to directly target animals with largest parasite burdens - anemia guidedescribe the distribution pattern of worms within a populationover-distribution; a few animals have the most wormsis it more effective as treatment to treat the whole herd equally or to target only those with the highest worm burden?target those with the highest worm burden - maintains refugia; helps prevent drug resistance from occurringOstertagiosis: clinical signs in bovine- Diarrhea; profuse and watery - Anorexia but still eating; weight loss with animals "starving" to death even though still eating - dehydration - sub-mandibular edema (bottle jaw)________ is the most important endoparasite of cattle worldwideOstertagiaPredilection site for Ostertagia isAbomasumcan Ostertagia overwinter?yeswhat part of the abomasum tissue would Ostertagia be found in?Glandular tissue; not at the surface of the epitheliumWhat effect do Ostertagia have on the glands of the stomach?destroy the glands; form nodules that stretch the glands and burst, leading to proliferation and dedifferentiation of the cells --> increase in pH due to lack of HCl productionPathogenic mechanism of OstertagiosisGrowth of larvae in gastric glands --> erosion of glands replaced with undifferentiated cells --> increase in abomasal pH --> permeable mucosa --> *elevated plasma pepsinogen* and hypoalbuminemia --> osmotic diarrheaWhat serum value is most unique to Ostertagiosis?Elevated plasma pepsinogenWhy does elevated plasma pepsinogen occur in Ostertagiosis?low pH is required to cleave pepsinogen to pepsinOstertagiosis diagnosis- seasonal cycle - clinical signs - plasma pepsinogen - response to ivermectin treatmentOSTERTAGIOSIS- 2 clinical entitiessame disease, just different ages/times of the year Type I: young cattle Type II: older animals; arrested L4 resume development and leave gastric glandsPattern of epidemiology of Ostertagia in Northern USwinter --> type II come out in spring --> type I come out in summer, fall --> winterPattern of epidemiology of Ostertagia in Southern USType II come out during mild winter --> Type I come out during mild winter --> arrested during hot summerTrichostrongyle species of concernTrichostrongylus colubriformis Trichostrongylus axeiTrichostrongylus colubriformis pathogenesispredilection site: small intestine (ruminants) --> distortion and flattening of villi --> protein loss & protracted diarrheaTrichostrongylus axei pathogenesispredilection site: stomach (ruminants, swine, horses) - nodulesTrichostrongylus can cause clinical disease alone, but especially so if found in association with _____ and/or _____Ostertagia; HaemonchusHaemonchus, Ostertagia, Trichostrongylus are the genera that infect the _____ and _____ of grazing ruminantsabomasum; duodenumof the HOT nematodes, sheep and goats are most severely affected by _____ _____Haemonchus contortusof the HOT nematodes, cattle are most severely affected by _____ _____Ostertagia ostertagiAscarids"roundworms" - contain some of the largest nematodes of domestic animals - relatively host-specific - non-bursateAscarid mouthsurrounded by 3 lips (other nematodes have more) - 1 dorsal, 2 ventral - can be seen on a regular microscope; good diagnostic no buccal capsule; not plug feedersAscarid eggsround, thick-walled, brown contain a single cell when passed in fecespredilection site of Ascaridssmall intestineAscarids have a ________ life cycledirect - can have paratenic hostsinfective stage of AscaridsL2vertical transmission of Ascaridsplacental or via mammary glandsAscarid species of dogs and cats- Toxocara canis (dogs) - Toxocara cati (cats) - Toxocara leonina (dogs and cats) - Baylisascaris procyonis (raccoons, dogs)what do ascarids do to counter peristaltic action and how does this affect the host?coil themselves against the small intestine wall - blunts the villi - can also knot and obstructwhich dog and cat ascarids are zoonotic?all of themeven though the ascarids are large, they might be difficult to see on radiographs becausethey are the same density as the tissueswhich dog and cat ascarids use a direct lifecycle and which use a paratenic host?all of them can do bothinitial steps of ascarid migration, before migratory options:embryonate egg ingested by host --> L2 hatches and penetrates wall of SI --> goes to liver via portal circulation --> goes to heart and then lungswhat two paths can Ascarids take once they've gone from heart to lungs?Tracheal migration or somatic migrationTracheal migration of Ascaridsin lungs --> break out of capillaries into alveoli --> up the bronchial tree to the pharynx --> coughed up and swallowed --> mature to adults in SISomatic migration of Ascaridsin lungs --> migrate through lungs, back to heart, into systemic circulation --> distributed throughout body --> L2's encyst in tissues --> hypobiosisWhat is the only Ascarid that doesn't have tracheal or somatic migration, or prenatal or transmammary transmission?Toxascaris leoninaToxocara canis indirect life cycle: dog eats paratenic hostmouse eats eggs with L2 larvae --> L2 hatches & migrates to the liver then lungs --> somatic migration --> dog eats mouse --> L2 molts to L3 and then to L4 and adult in the intestine of the dogParatenic hosts of Toxocara canisrodents and birdsToxocara canis life cycle: egg ingested by older dog; transplacental migrationegg containing L2 ingested by dog --> L2s hatch & migrate to the liver then lungs; mature dog, somatic migration --> transplacental migration of larvae to fetal liver --> lungs of neonatal pup --> tracheal migration within the pupToxocara canis life cycle: transmammary transmissionEncysted hypo biotic larvae activate and migrate to the mammary glands --> L3s ingested by nursing pups --> L3s in the pharynx --> molt to L4s in the stomach --> molt to adults in the SIwhat is one method for reducing transmammary transmission to toxocara canis to pups?weaning them earlier - transmission cycle starts around 6 weeks post-whelpingToxocara canis life cycle in an immature pupIngested eggs hatch & migrate to liver then lungs --> tracheal migrationin general, Toxocara canis molts from L3 to L4 in the _______, and from L4 to adults in the ____ ______stomach, small intestineWhat does Toxocara canis worm do in the small intestine?coils up to maximize its surface area - allows it to stay in the intestine - damages intestinal lining (blunts villi, prevents absorption) - most common pathologyWhere else besides the GI tract can you see signs of Toxocara caniskidneys - can form granulomasthree infection routes of Toxocara cati1) Paratenic host 2) Egg ingestion 3) TransmammaryDoes Toxocara cati migrate outside the cat's GI tract if it is ingested through a paratenic host?NO - no tracheal migrationDoes Toxocara cati migrate outside the cat's GI tract if it is ingested just as an egg?YES - can undergo tracheal or somatic migrationDoes Toxocara cati migrate outside the kitten's GI tract if it is infected through the transmammary route?NOIs there any migration of Toxoscaris leonina in the definitive host?NO molting in the intestineToxocara canis clinical signs- Respiratory signs - Pot belly (edema) - Abdominal distress - sickly-sweet smell on puppy's breathAscarid eggs of dogs: ______ ______ has a dimpled appearance like a golf ballToxocara canisAscarid eggs of dogs: ______ ______ is very brown, with visible blobs of protein materialBaylisascris procyonisAscarid eggs of dogs: ______ ______ has a smoother surfaceToxoscaris leoninaAscarid eggs of dogs: ______ ______ and ______ _____ have cervical alae, while _____ _____ does notToxocara canis; Toxoscaris leonina; Baylisascris procyonisAscarid eggs of cats: ______ _____ has a more dimpled appearanceToxocara catiAscarid eggs of cats: which have cervical alae?BOTH toxocara cati and toxoscaris leoninaVisceral Larva MigransCondition in humans which roundworm larvae migrate through the body, causing damage to internal organs - somatic migration in dead-end hostsBaylisascaris procyonisraccoon roundworm (ascarid) - direct or paratenic host transmission - common in raccoons but can infect dogs - many paratenic hosts - can have neurotrophic larvae ZOONOTIC! can be life threateningAscarids of poultryAscarida galli, Heterakis gallinarumAscaridia galliPoultry roundworm - No migration in chicken tissues - direct life cycle; eggs laid in feces, develop in environmentHow are Ascaridia galli eggs differed from other ascarids?more oval and more clearHeterakis gallinarumPoultry roundworm; pheasants, turkey, chickens, other fowl - No migration in definitive host tissues - direct or paratenic host - vector of a protozoanThe predilection site of Ascaridia galli is the ____ _____ and of the Heterakis gallinarum is the _____small intestine; cecumwhat protozoan does Heterakis gallinarum transport?Histomonas meleagridisHistomonas meleagridisprotozoan parasite of the cecum and liver - lives in the Heterakis gallinarum vector - causes Blackhead disease - young turkeys more susceptible than chickens; mortality can reach 100%to prevent Blackhead disease, you should never raise _____ and _____ togetherturkeys; chickensAscaris suumSwine roundwormAscaris suum lifecycledirect or indirect (through earthworm)Ascaris suum lifecycle pre parasitic phase- eggs in environment; thick-shelled - eggs don't hatch - paratenic host of earthworm or dung beetle eat eggs, which hatch in their gut with infective larvae, which go into PH tissuesAscaris suum eggs: in fresh fecesovoid, have rough protein coatAscaris summ eggs: after 3-6 weekssame characteristics are fresh feces, but contain an infective larva (L2)Ascaris summ direct life cycle: parasitic phaseingestion of egg --> hatches in DH SI --> L2 penetrates gut wall --> enter liver via portal vein --> L3 enter lungs --> tracheal migration --> L3 to small intestine --> L3 to L4 to immature adults to egg-laying adultsAscaris suum indirect life cycle: parasitic phasesame as direct, but DH ingests PH instead of eggsAscaris suum pathogenesis in the livermilk spot lesions caused by migrating larvae - granulomas and fibrosis under liver capsuleAscaris suum pathogenesis in the lungspneumonia, cough caused by migrating L3sAscaris suum pathogenesis in the small intestine(in heavy infections) diarrhea, weight loss - intestinal obstruction and rupture is rare - blockage of bile duct is rareAscaris suum epidemiologyResistant, sticky eggs (rough surface) - females lay lots of eggs - flies may spread eggsHow do you diagnose Ascaris suum?- clinical signs - characteristic egg in feces - necropsyWhat are the ascarid species of horses and donkeys?Parascaris equorum Parascaris univalensParascaris equorum has only a _____ life cycledirectParascaris equorum eggsround, with dense, sticky protein coat (some lose coat in float)Parascaris equorum clinical signs in foals: migrating larvae in the liverNO clinical signs "white spots" on liverParascaris equorum clinical signs in foals: migrating larvae in the lungs, bronchipneumonia, nasal discharge, coughingParascaris equorum clinical signs in foals: adults in the small intestinerare: impaction, peritonitis, deathfactors affecting Parascaris equorum epidemiology- fecundity of females (lay lots of eggs) - long-lived eggs (thick shell, survive for years) - pre parasitic development (infective stage develops fast; seasonal transmission between yearlings and foals)What is easier to treat: Ascaris suum or Parascaris equorum?Ascaris suumTo prevent the spread of Parascaris equorum, ____ and ____ should be separatedyearlings; foalsOxyurida of concern in dogs and catsNONEOxyuridaPinworms - one (female) or both sexes will have a long tapering tailOxyurida predilection sitelarge intestineOxyurida life cycle is always _____directOxyuris equi life cycleAdults in the cecum and colon --> *eggs on the perianal skin* --> L4 feed on the mucosa of the colon --> adults feed on intestinal contentsOxyuris equi pathogenesis- mucosal feeding of L4s --> erosion, ulcers - Perianal irritation caused by eggs massesOxyuris equi clinical signs- pruritus (due to egg mass) - tail rubbing (due to pruritus) - loss of hair (due to rubbing)Oxyuris equi diagnosis- clinical signs - egg masses on perineum - diagnostic eggCan Oxyuris equi be treated?yespinworm eggslightly flattened on one side, have plug at one end - reach infectivity in 3-5 days after being laidTrichocephalid nematodes to knowTrichuris spp., Eucoleus (Capillaria) spp., Trichinella spp., Dioctophyma renaleTrichuris spp.whipworm - found only in mammalsTrichuris spp. adultswhip-shaped body - anterior end = find, hairlike, embedded in intestine wall - posterior end = stout, laying free in lumenTrichuris spp. egglemon shaped with bipolar plugs single cell when passed in fecesTrichuris spp. life cycleDIRECT infective stage = egg, containing L1 develops in environment, does not hatch unless swallowed by definitive host - eggs very resistant (common to see reinfection after treatment) - longer prepotent periodheavy trichuris vulpis infectiondogs - diarrhea intermittent with normal stool - feces often containing mucus, maybe blood flecks - weight loss, dehydration, anemiaheavy trichuris discolor infectionruminants - young animals: hemorrhages into lumen of cecum (isolated and rare)heavy trichuris suis infectionpigs - catarrhal enteritis in young animals - diarrhea, dehydration, anorexia, slow growth - bacterial infection with C. jejuniCapilaridsHair worms "Eucoleus (Capillaria)"Eucoleus (Capillaria) adultsvery fine and small (hair worms) - partially embedded in mucous membrane or buried in tissue - hard to see wormEucoleus (Capillaria) eggsasymmetrical with bipolar plugs single cell when in feces similar to Trichuris, but smallerEucoleus (Capillaria) life cycleprobably direct - infective stage = egg containing L1 - larvae hatch in SI, penetrate mucosa, migrate via bloodstream to lungsEucoleus (Capillaria) aerophilus: adult worm locationepithelium of bronchioles, bronchi, tracheaEucoleus (Capillaria) boehmi: adult worm locationmucosa of nasal sinusesEucoleus (Capillaria) of domestic speciesEucoleus (Capillaria) aerophilus, Eucoleus (Capillaria) boehmiWhere will you find Pearsonema (Capillaria) plica?in the urinary tract; causes urinary capillariosis - won't find eggs in host fecesEucoleus (Capillaria) aerophilusprimarily a parasite of foxes, respiratory tract - can be seen in other hostsEucoleus (Capillaria) aerophilus: clinical signsusually only in severe infections of young animals, otherwise subclinical - cough, nasal discharge, dyspnea, anorexia, debilitation - tracheitis, bronchitis, sometimes pneumoniaEucoleus (Capillaria) boehmifoxes and other canids; nasal infectionEucoleus (Capillaria) boehmi clinical signsusually only severe infections, otherwise subclinical - Chronic rhinitis: chronic serous nasal discharge and reverse sneezing - secondary infection --> purulent discharge - intracranial migration: RAREwhat is the best way to diagnose trichuris sp. and capilarids?fecal float, double centrifugation EXCEPT Pearsonema plica; do urine flotationthe only canine parasite eggs that could be mistaken for whipworm eggs belong to the _______ parasitescapillaridTrichuris eggs are ______, have a _______-walled shell, and are usually _______ than the Eucoleus eggslarger; smooth; brownerWhat is the difference between the plugs on Trichuris and Capilarid eggsTrichuris eggs have ridges on the plugs; capillarid eggs lack ridgesE. aerophilus egg: _____ surface, _____ sides Trichuris sp. egg: ______ surface, ______ sidesrough; parallel smooth; curvedDifference between E. aerophilus and E. boehmi eggsE. aerophilus has a network of interconnecting ridges; E. boehmi is pitted, giving a stippled appearanceShould you worry about reinfection with Trichuris eggs?YES - eggs are very resistant and take months to mature; treatment should be repeated 3x at monthly intervalsdo E. boehmi and E. aerophilus have the same treatment?NO; slightly different, that's why correct diagnosis is crucialTrichinella sp. adults- very small - unlikely to be found on gross examination - found embedded in mucosa of small intestine - not frequent in vet med, more human medTrichinella sp. larvaewill coil in striated muscle! - easiest way to identify infectionTrichinella sp. life cycleZOONOTIC; indirect? - Does not have a free-living stage!! Both adult and larval stages occur in sequence in same hostInfective stage of TrichinellaL1 (encysted first-stage larvae) - ingested through raw or undercooked meatCan Trichinella sp. infect non-mammals?YES - 8 different species, with wide range of hostsmost concerning Trichinella sp.?T. spiralis - does very well in domestic swine and humans2 phases of Trichinella pathogenesisEnteral phase: GI - mostly asymptomatic, transient diarrhea/nausea Parenteral phase: - 2 weeks post-infection; myalgia, possibly fatalTrichinella sp. diagnosisDetection of larvae: - muscle biopsy - clinical signs (muscle pain after eating raw meat) - serology - necropsy - meat inspectionCan you get rid of Trichinella by freezing?NO - but can be eliminated by cooking (increase temperature)Dioctophyma renale adultsGiant kidney worm - largest nematode of domestic species - deep red-purple in color - size and predilection site are sufficient for IDDioctophyma renale eggsdetected in urine sedimentation - typically contain 2 cells - serrated outside like a tireDioctophyma renal life cycleINDIRECT - eggs ingested by IH (annelid) - DH ingests IH or paratenic host (fish or frog) - larvae penetrate intestine wall, enter the peritoneal cavity, and kidney - PPP; 6 months or moreDioctophyma renale pathogenesisLarge adults cause pressure necrosis --> destruction of renal parenchyma - most infection unilateral and involve only the right kidney - production of eggs in abdominal cavity may cause liver lesion, hemoperitoneum, peritonitisDioctophyma renale diagnosis- urine sediment - clinical signs: distended right kidney - rads and US (most common) - laparotomy (adult worm free in abdomen)treatment of Dioctophyma renalesurgical removal of adults and affected kidneyMetastrongylus sp. general characteristicsLUNGWORM; Metastrongyle - parasite of the bronchi and bronchioles of swine - large white parasite - BURSATE; well-developed bursa - worldwide distribution; pigs on pastureMetastrongylus sp. diagnosisFecal flotation (sugar solution) - *larvated eggs*Protostrongylus rufescens general characteristicsLUNGWORM - smaller bronchioles of sheep and goats - worldwide - BURSATE; well-developed - mostly asymptomaticMuellerius capillaris general characteristicsLUNGWORM - lungs of sheep and goats - worldwide - BURSATE; well-developed - mostly asymptomaticProtostrongylus rufescens & Muellerius capillaris life cycleINDIRECT direct host: sheep and goats - release larvae, not eggs indirect host: SNAILS infective stage: IH containing L3P. rufescens and M. capillaris diagnosisBAERMANN - detection of L1 in the fecesP. rufescens and M. capillaris: _______ has a kinked tail with an accessory spine, ______ has a plain tailMuelleris; ProtostongylusMuellerius capillaris treatmentmoxidectin in sheep Eprinomectin in goatsProtostrongylus sp. treatmentFenbendazoleParelaphostrongylus tenuis general characteristicsparasite of the meninges of white-tailed deer - usually asymptomatic - causes 100% fatal neurologic disease in abnormal hostsParelaphostrongylus tenuis life cycleINDIRECT DH = white-tailed deer IH = snails Infective state: IH containing L3 - L3 move through the digestive tract, travel along spinal nerves to get to the brain - L1 migrate to the lungs, are coughed up, swallowed, shed in fecesParelaphostrongylus tenuis diagnosisPRESUMPTIVE - rarely matures in abnormal host - based on clinical signs and epidemiology (animals with neurological disease; animals that share their pasture with white-tailed deers)Aelurostrongylus abstrusus general characteristicsParasite in the lungs of cats (& rarely dogs) - Bursate, but reduced - worldwide - mostly asymptomatic - moderate --> cough and anorexia - heavy infections may be fatalAelurostrongylus abstrusus life cycleINDIRECT DH = cats and dogs IH = snail PH = mice and possible birds infective stage = IH/PH containing L3Aelurostrongylus abstrusus diagnosisBAERMANN - detection of L1 in the feceswhat do Aelurostrongylus abstrusus L1 look like?severe kink (S-shaped curve) and a dorsal spineAngiostrongylus vasorum general characteristicsparasite of the pulmonary arteries and lungs of dogs, coyotes, and foxes "french heartworm" not present much in US infections include clotting disorders (subcutaneous or intracranial hemorrhage)Angiostrongylus vasorum life cycleINDIRECT DH = foxes and dogs IH = wide range of molluskan PH = frogs infective stage = IH/PH containing L3Angiostrongylus vasorum diagnosisBAERMANN - detection of L1 in the fecesAngiostrongylus vasorum L1 appearancevery similar to A. abstrusus - severe kink - cephalic button on the anterior endFilaroides osleri general characteristicscanine tracheal and bronchial nodular worm - hemorrhagic wart-like nodules in the trachea and bronchi of dogs and other canids - spasmodic cough induced by exercise or exposure to cold air; NOT tracheal palpation - infections develop slowlyFilaroides hirthiCanine lungworm - lung parenchyma of dogs and other canids - usually doesn't cause clinical signs - infection develops faster than F. osleriFilaroides spp. lifecycleDIRECT infective stage = L1 - L1 passed in feces (dead) or saliva and is immediately infective to another hostFilaroides spp. transmission- ingestion of regurgitated stomach contents, lung tissue, or feces - maternal groomingFilaroides spp. diagnosisNOT Baermann; Centrifugal Zinc Flotation - detection of L1 in fecesFilariodes spp. L1 appearancesevere kinked (S-shaped curve) and lack a dorsal spine - F. osleri indistinguishable from F. hirthiFilaroides spp. treatmentVERY difficult - no drug recommendationsCrenosoma vulpis general characteristicsparasite of bronchioles, bronchi, & trachea of dogs, foxes, wolves, raccoons, and other wild carnivors - rare in North America - produces a non-fatal coughThe adult cuticle of ______ ______ is thrown into crenated foldsCrenosoma vulpisCrenosoma vulpine life cycleINDIRECT DH = domestic and wild carnivores IH = snails Infective stage = IH containing L3Crenosoma vulpis diagnosisBAERMANN - detection of L1 in the fecesCrenosoma vulpis larval shapeC-shaped curve when killed no kink or dorsal spineStrongyloides spp. general characteristicsParasite of small intestine of domestic animals and humans - intestinal threadworm - ZOONOTICwhat is special about Strongyloides females?they are parthenogenic (males do not exist --> asexual reproduction)Strongyloides spp. clinical signsmay be subclinical heavy infections = enteritis (adults), respiratory signs (larvae migration) severe/fatal infections in immunocompromised or immunosuppressed hostsmost important Strongyloides sp. to rememberStrongyloides stercoralis ZOONOTICWhat special types of infection can occur for Strongyloides spp. in humans?Autoinfection & HyperinfectionStrongyloides spp. autoinfection in humansinfection with contact with the infective stage in the environment - can be internal or externalInternal autoinfectionL3 reinvade host by penetrating the bowel wall - can happen with Strongyloides spp. in humansExternal autoinfectionL3 reinvade host by penetrating the perianal skin - can happen with Strongyloides spp. in humansStrongyloides spp. hyperinfection in humansexplosive development of massive disseminated infection - patients with depressed cell-mediated immunity - caused death of many peopleStrongyloides spp. life cycleDIRECT transmission: skin penetration (L3) very short PPP 2 types of life cycle2 types of Strongyloides spp. life cycleHomogonic HeterogonicStrongyloides spp. homogonic life cycleinside the host - NO free-living adult stages in the environment - L3 become parthenogenetic femalesStrongyloides spp. heterogonic life cycleoccurs in the environment - Adult stages (male and female), free-living in the environmentWhat determines if Strongyloides will undergo a heterogonic or homophonic life cycle?the environment into which the feces is depositedStrongyloides spp. diagnosisBaermann Test; detection of L1 in the feces Coproculture/fecal culturewhy might coproculture be a good way to diagnose Strongyloides stercoralis?L1 don't have a characteristic structure; let them grow to L3, which have a distinctively long esophagusTreatment of StrongyloidesivermectinSpirulids to knowDracula Physically Sucked Her Dead Torso Dracunculus spp. Physaloptera spp. Spirocera lupi Habronema spp. Draschia spp. Thelazia spp.Dracunculus sp. general characteristicsparasite of the subcutaneous tissues of carnivores and humans D. insignis = raccoons, other carnivores D. medinensis = primates, dogsDracunculus sp. life cycleINDIRECT infective stage = IH/PH containing L3 females for blister in the skin to deposit larvaetreatment/control of Dracunculus sp.remove the whole worm! safe water!Physaloptera sp. general chracteristicsParasite of the stomach of carnivoresPhysaloptera sp. adultspinkish tend to live with the anterior end embedded in stomach mucosa in dogs, may be in anterior duodenumPhysaloptera sp. eggsclear and elliptical smooth shell wall with larva coiled insidePhysaloptera sp. life cycleINDIRECT infective stage = IH containing L3 IH = coprophagous beetles, crickets PH = cold-blooded vertebratesPhysaloptera sp. clinical signsMinor clinical significance adults often viewed during endoscopyPhysaloptera sp. diagnosisGastroscopy Fecal sedimentation; NOT float, because the egg is heavySpirocerca lupi general characteristics"Esophageal worm" parasite of the wall of the stomach or esophagus of canidsSpirocerca lupi eggsvery small narrow, ellipsoidal, cylindrical smooth shell wall with fully developed larva coiled insideSpirocerca lupi life cycleINDIRECT infective stage = IH containing L3 IH = copraphagous beetles PH = rodents, chickens, birds, reptiles, etcSpirocerca lupi clinical signsoften subclinical cystic nodules common finding: esophageal neoplasia and secondary pulmonary osteoarthropathySpirocerca lupi diagnosisGastroscopy (fibrotic nodules) Fecal sedimentation; high density eggsHabronema sp. and Draschia sp. adultsparasites of the stomach of horses and donkeys - stay close to the margo plicatusHabronema sp. and Draschia sp. eggslarvated eggs in fecesHabronema sp. and Draschia sp. larvae common namesswamp cancer, bursatti, summer sores, esponjaHabronema sp. and Draschia sp. life cycleINDIRECT infective stage = IH containing L3 IH = fliesHabronema sp. and Draschia sp. clinical signscutaneous habronemiosis (persistent cutaneous granulomas) - develop in minor wounds and areas of skin subjected to continuous wettingHabronema sp. and Draschia sp. diagnosisgastroscopy; adult worms found in tumor-like masses in the stomach fecal sedimentation; high densityHabronema sp. and Draschia sp. treatment/control/preventionIvermectin & moxidectin for adults Ivermectin for summer sores (larvae)Thelazia sp. general characteristics"Eye worms" Parasite of the conjunctival and lachrymal sacs of domestic and wild animalsThelazia sp. adultssmall, thin, yellowish-white worms deep, cup-like buccal cavity, prominent cuticular striationsZoonotic Thelazia spp.Thelazia californiensis Thelazia callipaedaThelazia sp. life cycleINDIRECT - worms are viviparous - L1 passed by female into the lacrimal secretion is ingested by the fly IH as it feeds - IH/vectors = drosophilid flies - IH are parasite and host specificThelazia sp. clinical signs/pathogenesisanimals: mild ocular symptoms, unilateral infections, corneal opacity, conjunctivitis, blindness in severe cases humans: generally mildThelazia sp. diagnosisidentification of adult with in the conjunctival sac - morphological examination - molecular methodsThelazia sp. treatment/controlremove the worm! doramectin!Onchocerca sp.parasite of domestic and wild animals; location depends on species and hostwhy might an Onchocerca sp. infection go unnoticed, even though the adults are large?worms will be intricately woven into the deep connective tissues, not free in the eye (like Thelazia)What is characteristic about the Onchocerca sp. cuticle?characteristic ridgesOnchocerca sp. life cycleINDIRECT DH = humans and animals Vector = black flies and/or biting midgesmost important Onchocerca sp. to rememberOnchocerca lupi - predilection site = EYES - ZOONOTICOnchocerca sp. clinical signs and pathogenesisInitial stage = non-specific signs Chronic stage = Typical nodules - excessive lacrimation - photophobia - conjunctivitisWhat happens if an animal has Onchocerca sp. infection in the retrobulbar space?Asymptomatic infectionOnchocerca sp. diagnosisidentification of the adult worm - morphological examination - molecular methods Microfilaria are found in the dermis - do a skin snip biopsyOnchocerca treatment/controlSurgical removal of the parasitic nodule!Dirofilaria immitis general characteristics of adultscanine heartworm - one of the most deadly parasites of dogs - parasite of the pulmonary arteries and right ventricle - non-specific characteristics; males are spirally coiled at the posterior endDirofilaria immitis, microfilariae characteristicsUnsheathed first-stage larvae can be detected 5-6 months post-infectionD. immitis definitive hostDogs, wild canids, ferrets, others Cats are not as good a hostD. immitis life cycleINDIRECT DH = canids, etc IH = mosquitoesD. immitis stages: _____ in heart and pulmonary arteries of DH, ______ circulate in the blood, ______ will ingest m.f. during blood mealadults; microfilariae; mosquitoFactors contributing to further spread of D. immitis- environmental and climatic changes; natural and those created by humans - relocation of microfilaremic dogs - expansion of microfilaremic wild canidsD. immitis pathogenesis (dogs): Live worms- can have no clinical signs for 5-6 months during PPP - physical obstruction of vessels, heart chambers, and valves by adult worms - progressive endarteritis and obstructive fibrosis --> pulmonary hypertension, right side failureD. immitis: _____ worm numbers appear to nearly occlude ______ arteries, potentially leading to _____ ______ and _______ blood flowhigh; smaller; physical obstruction; decreasedD. immitis pathogenesis (dogs): dead worms- as worms die, they collapse into distal vasculature --> thrombosis, blood flow obstruction, strong inflammatory response - permanent damage to vascular bedD. immitis clinical signs (dogs)- exercise intolerance - arrhythmias - coughing - dyspnea - weight loss - ascites - jugular venous distension - congestive heart failureCaval syndromeheavy heartworm infestation - large numbers of adults in pulmonary arteries - worms in post cava and right atrium interfere with tricuspid valve function - life-threatening condition resulting in hemolytic anemiaD. immitis abnormal migration sites- eyes - CNS - peritoneal cavity - Skin - peripheral vasculature4 disease stages of canine heartwormmild (just one clinical sign or asymptomatic), moderate, severe, cavalD. immitis pathogenesis (cats): dead worms- tend to harbor very few adult worms (usually just one) - usually asymptomatic - can develop HARD - GI and sometimes neuro signs - sudden death without warning (common)HARD in catsHeartworm-Associated Respiratory Disease - due to migration of young adult worms in the lungs - persistent tachypnea, intermittent coughing, increased respiratory effortheartworm is a ______ organ diseasemultipleseverity of heartworm disease is postulated to depend mainly on1) numbers of adult worms 2) duration of infection 3) individual host responseD. immitis diagnosis; dogs*history, lack of preventative, exercise intolerance* - antigen testing (ELISA); detect mature, adult female Ag - microfilariae testing - modified Knottsmodified Knott'sconcentrated blood test to find microfilariae of D. immitisimaging of heartworm: adult worms are very _____echogenicD. immitis diagnosis (cats)limited because cats often have single-worm infection - modified Knotts - antigen and Ab testwhat are the limitations of doing Ag or Ab testing for heartworm in cats?tests for female Ag or Ab; unisex infections of only males or immature infections may not be detectedD. immitis microfilariae identificationTapered headD. immitis dx interpretation: Ag +, microfilariae -"Occult" or Amicrofilaremic infection - early infection, not yet reproducing - adult females present, no males - low microfilaremia - after treatmentD. immitis dx interpretation: Ag -, microfilariae +Unexpectedly negative antigen tests - other microfilaremic species - mild infection - appearance of m.f. before antigenemia; RARE - *presence of Ag-Ab complexes: most common!*Immune-complex dissociation (ICD) for heartworm testingnot done routinely, but could be used if suspecting an Ag-Ab complex causing a false-negative - complex most common in cats - can happen after treatment or with mixed blood samplesPlatyhelminthesphylum of flatworms important ones: Cestodes and TrematodesTrematodes are divided intoDigenea MonogeneaMonogenea, general characteristicsgroup of flukes (trematodes) - most are ectoparasites of aquatic animals - Gyrodactylus spp., Dactylogyrus spp.Monogenea life cycleDirect - hermaphrodites - viviparousMonogenea feedingfeed on epidermis, blood, mucusMonogenea pathogenesisfunction of parasite burden - excessive mucus secretion - hemorrhage, tissue loss --> secondary infections - inflammation - can be lethal in heavy infectionsGyrodactylus spp.Trematode, monogenea - ectoparasite on skin and gills of aquatic animals - Haptor for attachmentGyrodactylus spp. treatmentshard to eradicate completely - copper sulfate baths - diluted formalin - hydrogen peroxide - praziquantelDigenea families to knowFasciolidae Paramphistomatidae Dicrocoelidae Troglotrematidae Diplostomatidae SchistosomatidaeDigenea general characteristics- nearly all are hermaphrodites - adults possess oral and ventral suckers - eggs found in feces, urine, sputum, mucusDigenia predilection sites- bile & pancreatic ducts of liver - small intestine - rumen - lungs - circulatory systemDigenea lifecycles, generalcomplex - alternating sexual (definitive host) and asexual (intermediate host) reproductionDigenea lifecycles, steps- eggs in feces, etc - enter freshwater, hatch, release miracidium - intermediate host = snail: asexual reproduction to cercaria - metacercaria can get encysted on vegetation, or go to second IH, or cercaria directly ingested - definitive host = mammal: adult worms reproduce sexually, lay eggsMiracidiumfree-swimming larvae, which hatch from eggs in fresh water in Digenea life cycle - eaten by snailsCercarialarvae of Digenea, which have been produced out of asexual reproduction in the intermediate host (snail)Metacercariaencysted stage of flukes3 ways for the DH to get infected by a digenean parasite1) eat metacercaria encysted on vegetation 2) eat infected secondary IH 3) direct penetration of skin by larval cercariawhich families of Digenea use the method of infection from eating metacercaria encysted on vegetation?Fasciolidae, ParamphistomatidaeFasciola hepaticaliver flukeFasciola hepatic adultlarge flattened "shoulders" leaf-likeF. hepatica eggsfound in feces - operculate - unembryonated - dx based on detection - can remain viable in feces for weeksF. hepatica life cycleindirect, typical Digenea life cycle ZOONOTICF. hepatica pathogenesis, acute diseasedue to ingestion of large numbers of metacercaria - direct damage caused by migration of juveniles - secondary Clostridium infectionWhat anaerobe can multiply within F. hepatica lesions and what does it cause?Clostridium novyi; "black disease" - can lead to death in severe casesF. hepatica pathogenesis, chronic diseaseassociated with presence of adults in bile duct - hyperplasia, fibrosis, calcification - hypoprotenemia, anemia, wasting diseasewhat effects do adult F. hepatica have in the liver?- bile duct hyperplasia - blood feeding --> anemiaF. hepatica distributionworldwide but discontinuouswhat affects the pattern of disease with F. hepatica?environmentF. hepatica treatment/controlmost drugs active against adults only kill the IH (snails) move to fluke-free pasturestwo important Fasciolidae species to knowFasciola hepatica Fascioloides magnaFascioloides magna, general characteristics- deer are the normal host - form cysts in liver that connect to the bile duct - in sheep & goats, juveniles don't mature and continue to migratewhat species are important in the Paramphistomatidae family?Paramphistomum cervi, P. microbothroidesParamphistomatidae spp. general informationRumen flukes - typical digenean life cycle - adults relatively harmless - worms migrate from small intestine into rumen - eggs confused with F. hepaticaP. microbothroides adultsdistinctive ventral sucker at posterior endwhat families of Trematodes infect the host via ingestion of a second intermediate host?TDD Troglotrematiae Diplostomatidae DicrocoeliidaeNanophyetus salmincolaTrematode in the Troglotrematidae family intestinal fluke - ID by eggs in stool - Metacercaria found in salmonids (second IH) - parasite is host to Neorickettsia helminthoecaParagonimus kellicottiTrematode in the Troglotrematidae family NA lung fluke - adults found in pairs in lungs - respiratory disease due to migration in lungswhat is special about the Paragonimus kellicotti egg?"collar" around the openingAlaria spp.Trematodes in the Diplostomatidae family intestinal fluke - complex life cycle; many definitive hosts - have special mesocercaria stage - vertical transmission via milk ducts to sucklings - can be pathogenicMesocercariaspecial larval stage found in intermediate, paratenic hosts - special to Alaria spp. - migrate to the lungs to form metacercariaDicrocoelium dendriticumTrematode in the Dicrocoeliidae family - small - lancet-shaped; no "shoulders"Platynosomum fastosumTrematode in the Dicrocoeliidae family - fluke of bile and pancreatic ducts of cats - metacercaria found in amphibians, lizards, geckos; "lizard poisoning" - terrestrial life cyclewhat family of Digenea infect the host via direct percutaneous infection by cercaria?Schistosomatidae (schistosomes, blood flukes)Schistosomatidae of veterinary importanceHeterobilharzia americana (dog) Schistosome bovis, S. nasale (cattle) S. indium (horses, cattle, goats) S. japonicum (cattle)Schistosomatidae parasites of humansS. mansoni, *S. japonicum*, S. haematobiumSchistosoma japonicum adultshugging! live togetherSchistosomatidae spp. general characteristics- cercaria are directly infective - live long - eggs remaining in host cause chronic disease (granulomas)Heterobilharzia americanadog schistosomes - DH = dogs, raccoons, bobcats, nutria, rabbit - predilection site = mesenteric veins - eggs evoke granuloma - usually asymptomatic, can cause dzmain pathogenesis of schistosomesgranuloma formationSwimmer's itchSchistosomiasis (avian, sometimes mammalian, schistosomes) - cercaria penetrate skin, but die - delayed-type hypersensitivity reactionwhich trematodes have a predilection site in the liver and bile duct?FFDP Fasciola hepatica Fascioloides magna Dicrocoelium dendriticum Platynosomum fastosumwhich trematodes have a predilection site in the rumen?Paramphistomum spp.which trematodes have a predilection site in the intestine?Nanophyetus salmincola Alaria marcianaewhich trematodes have a predilection site in the lungs?Paragonimus kellicottiwhich trematodes have a predilection site in the circulation?Schistosomesthe liver fluke ______ ____ is a model for the type of life cycle with infection via ingested metacercaria encysted on vegetation, and is of major veterinary importanceFasciola hepaticaCestodestapeworms, under the phylum PlatyhelminthesCestodes, general life cycleegg in feces --> ingested by IH; Hexacanth larva hatches in gut, Metacestode develops --> 3 possibilities of transmission --> Adult in GI tract of vertebrate DHwhat are the 3 possibilities of cestode transmission after development of metacestode in the IH?1) ingested by definitive host directly 2) ingested by 2nd intermediate host, 2nd metacestode develops, ingested by DH 3) ingested by 2nd intermediate host, 2nd metacestode develops, ingested by paratenic host, ingested by DHCestodes, general characteristicsNo gut; absorb food through surface Hermaphrodite (both sex organs in each proglottid) Almost all require at least 2 hosts to complete life cycleproglottida segment of a tapewormAdult tapeworm characteristics- Chain (strobila) of independent units - one end anchored in wall of host intestine by scolex - bud off in segments (proglottids)strobilaChain of proglottidsscolexthe anterior end of a tapeworm, bearing suckers and hooks for attachment.Adult tapeworm: all stages of development are displayed in a _______ way, from the ______ to the distal end of the wormlinear; scolexAll segments of a tapeworm are served by ______ osmoregulatory and nervous systemscommonthe most mature proglottids on a tapeworm are _________ from the scolexfurthestoncospherefirst stage larva of tapeworms; infective for first (or only) intermediate host - consists of an embryo surrounded by two embryonic membraneshexacanthtapeworm embryo - contains 6 hookswhat are the two orders of cestodes important for veterinarians?Cyclophyllidea Pseudophyllideafamilies of vet importance in the order CyclopyllideaTHAD Taeniidae Hymenolopididae Anoplocephalidae Dilepididaegenera of vet importance in the order PseudophyllideaDiphyllobothrium SpirometraCyclophylliea general characteristicsfour radial muscular suckers on scolex - used for attachment and locomotion - most scolices has a rostellum longer than wide segments genital pore lateral - for fertilization - no opening for release of eggsWhat happens to the eggs in Cyclophyllidea?the are not released via an opening in the segment because there isn't one - eggs accumulate until segment is packed - gravid segments detach, pass out with feces or crawl out of host anus - ID of gravid segments can be diagnosticTaeniidae spp. general characteristicsCyclophyllidea family - T. sag, T. solium, T. serials, T. taeniaeformisspecial aspects of Tania solium, Tania saginata life cycleoncospheres develop into cysticerci in the muscle --> humans infected by ingesting raw or undercooked meat that is infectedcysticercosisCaused by larvae of pork tapeworm Taenia solium - clinical signs in dogs - creation of multiple cysts (can be neuro involved)Echinococcus granulosus, Echinococcus multilocularis general characteristics- small tapeworm of dogs (4-5 segments) - scolex with armed rostrum & 4 suckers - larval tapeworm of several hosts, including humansechinococcosis (hyatid disease)caused by the larval stage of custodies of the genus Echinococcus - dangerous for humans and caninesechinococcosis of E. granulosuscystic echinococcosis (cysts grow but don't infiltrate); most common formechinococcosis of E. multilocularisalveolar echinococcosisechinococcosis of E. vogelipolycystic echinococcosisechinococcosis of E. oligarthrusextremely rarehyatid cyst componentshyatid sand, brood capsule, daughter cyst, protoscoliceshyatid sandfluid from a hyatid cyst that contains protoscolicesimportant Anoplocephalidae speciesAnoplocephala perfoliata, Anoplocephala magna, Paranoplocephala mamillanaAnoplocephala perfoliataequine tapeworm (horses, donkeys) - adults can be pathogenic --> serious, persistent diarrhea - found in the cecum and ileum, clustered near the iliocecal valveAnaplocephala magna, Paranoplocephala mamillanahorse & donkey tapeworm - parasites of the small intestines - relatively non-pathogenicAnoplocephala spp. life cyclegrazers ingest mites infected with cysticercoids --> cysticercoids develop into adult tapeworms in intestine --> mature to gravid proglottids --> gravid proglottids detach, are passed in feces, disintegrate, release eggs --> eggs ingested by forage mites --> oncosphere develops into cysticercoid in mite body cavityDiplylidium caninumflea tapeworm, double-pored dog tapeworm - in family Dilepididae - mainly dogs and cats, sometimes humans - spread by fleas and biting lice - develops quickly in definitive host - proglottid has 2 lateral poresDipylidium caninum life cycleflea larvae eat tapeworm egg --> flea matures --> pet eats flea --> parasite larvae migrate to SI where they mature ---> proglottids containing eggs are shed in feceswhat two species have a life cycle similar to Dipylidium caninum?Amoebotaenia sphenoides (same except IH = earthworm, DH = fowl) Choantaenia infundibulum (IH = housefly, DH = fowl)Hymenolepis nanatapeworm that spreads by autoinfection - in the family HymenolepididaeDavaineidae tapeworms are found in what type of DH?birdsPseudophyllidea general characteristics- scolex has 2 shallow longitudinal grooves (bothria) - segments have uterine pore for release of eggs - require at least intermediate hostsbothriatwo shallow longitudinal grooves on the scolex of Pseudophyllidea - used for attachment and locomotion - Diphyllobothrium & Spirometra have no hooksDiphyllobothrium latum"fish tapeworm" found in dogs around the Great Lakes; seen quite often in seals and dolphins - 1st IH = Copepod - 2nd IH = fish - DH = mammalsSpirometra mansonoidesfound more often in cats than dogs humans can serve as 2nd IH --> human sparganosisAdult cestodes (tapeworms) reside in the ______ _____ of DH, with eggs and gravid segments found in or near _____ _____small intestine; host feceswhy are Acanthocephalans named as such?Acanth = thorn, Cephala = head; they have thorny headsAcanthocephalans, general characteristics- separate sexes - no gut - high reproductive output - cement glands in males (seal vagina after copulation; sexual competition)Macracanthoryhnchus hirudinaceus general characteristicsfound in SI of pigs, occasionally infects dogs and other mammals - IH = dung/May/water beetles - related parasite = Macracanthoryhnchus ingens (millipede IH, raccoons and dogs affected)Oncicola canis, Oncicola spp, general characteristicsrarely found in SI of dogs, cats, etc - IH = unknown (dung beetle?) - possible paratenic hoststypical Acanthocephalan life cycleeggs shed in feces --> eggs ingested by IH --> mature from acanthor to cystacanth --> DH ingests infected beetle IH --> cystacanth excysts in host small intestine --> adults in SIM. hirudinaceus eggs- generic Acanthocephalan egg - presence of acanthor (fully-developed larva in egg)M. hirudinaceus diagnosis- dependent on presence of eggs - ID of adults (presence of spiny proboscis, no gut or circulatory system) - do not confused with ascaris suum or cestodesattachment of M. hirudinaceus- no mouth or GI system - proboscis attaches via hooks to host - necrosis at local site - flattened villiM. hirudinaceus pathogenesis- can be asymptomatic - ulceration & granuloma formation at site of infection - acute or chronicM. hirudinaceus acute pathogenesisperitonitis - mechanical disruption of intestine wallM. hirudinaceus chronic pathogenesis- related to worm burden - competition for nutrients - diarrhea, wasting, failure to thrive

Parasitology Unit 1

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