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Nematodes - Roundworms
they're like an inflated tube (they have…
Nematodes - Roundworms
- they're like an inflated tube (they have hydrostatic pressure, which maintains their shape)
- separate sexes (sexual reproduction)
- muscles underlie their cuticle
- have a GIT (unlike cestodes)
- egg -> L1 -> L2 -> L3 -> L4 -> L5 -> adult
- L3s are the infective form for all except lungworms (L1s infective) and they can pause in this state (outer cuticle gets reinforced to protect them) until the environment is favourable
- MANY different routes of infection: fecal-oral, penetration of skin (some hookworms), transplacental (toxocara), transmammary (dog hookworms), predator-prey (trichonella), vector borne (heartworm)
- 1) Tracheal migration +/- somatic and 2) mucosal migration
Order: Rhabditida (rhabditids, threadworms)
- infect vertebrates only during part of their life cycle or accidentally
- very small microscopic worms
Strongyloides = threadworms
- S. stercoralis - dogs, cats, people, primates (L1 hatch in feces and can be found using baermann technique)
- S. papillosus - ruminants (L1 in egg in feces)
- S. westeri - equine (L1 in egg in feces)
- S. ransomi - swine (L1 in egg in feces)
- Things they all have in common: infect small intestine deep between villi, thread like adults (very small)
- life cycle "free living" outside the host. Males are non parasitic, females produce fertile eggs mitotically that mature to L1s and released in feces of infected host. Can get infected by oral route (mucosal migration), skin penetration (tracheal or somatic migration), or transmammary transfer of L3s
- S. stercoralis is especially bad for immunocompromised because L1s develop very quickly into adults. Infection generally cleared from healthy animals by 6 months of age
pathogenesis - usually non pathogenic in small animals, can cause blood enteritis, larvae in feces so required baermann for sensitivity
- treat with ivermectin (except be careful with collies due to idiosyncratic drug response)
Strongyloides westeri - Horses
- L1 in egg in feces -> egg will float on fecal float
- pathogenesis large numbers in small intestine can cause inflammation, edema and enteritis
- affects young animals only
- no transplacental transmission but there can be transmammary through milk
- eggs are thin shelled and NOT morulated. fully larvated in fresh feces. vs strongyles which are thin shelled and morulated
strongyloides ransomi - swine
pathogenesis - usually a neonatal problem. Causes malabsorption and leaky vessels from enteritis -> diarrhea and dehydration
- will see larvated eggs on fecal float
Order: Strongylida (strongylids, strongyles, trichostrongyles, hookworms, lungworms)
- Feed directly on the host rather than "sharing" nutrients
- most have a single host (except for lungworms)
- smaller than ascarids
- trichostrongyles and lungworms are slender
- hookworms and strongyles are stout bodied
- thin shelled eggs -> don't last long in environment
- called diff things depending on host - in ruminant or swine = gastrointestinal nematode. in human or primate = hookworm egg. in horse = strongyle egg
- most are primarily oral transmission (some penetrate skin) and eggs are found in feces
Ancylostoma caninum
- Think of capital A = prominent sharp teeth to clamp -> vicious blood sucking worm
- adult worms -> buccal cavity has 3 large pairs of teeth to clamp, may appear dark red if filled with blood and they are stout (tiny) but each worm can cause a lot of damage, their copulatory bursa (genitals) are on the posterior end
- common hookworm of dog small intestine
- more common in south and temperate regions
- eggs are thin shelled and morulated (lots of little blastospheres present -> they will develop quickly
- Direct Life cycle (no IH) = morulated eggs are passed into environment in feces of infected animal -> L1s develop to L3s -> L3s penetrate the skin of dogs (or humans) and undergo tracheal migration in young dogs or somatic migration in older dogs. If L3s enter via oral route, then this causes patent infections through a mucosal migration. Pups can be infected through transmammary route (somatic) and that will be a quicker PPP
- PPP = 2.5 weeks for transmammary and 3-4 weeks for other routes
- Clinical signs/pathogenesis - blood feeding worms cause anemia and protein loss (hypoproteinemia) -> decreased oncotic pressure -> edema in the abdomen. Also causes enteritis. Acute infections (50-100 worms) can cause death before clinical signs are present. Less acute infections can result in anemia, melena and emaciation
- treat with antihelmintics
Ancylostoma tubaeforme - cat version of hookworm
- eggs same as ancylostoma caninum (thin shelled and morulated)
- adults are smaller than caninum
- Life cycle the exact same as caninum. Morulated eggs passed in feces -> L1 develop to L3s -> L3s penetrate skin of cat or human -> tracheal migration in young cats/somatic migration in older cats (will hide out in tissues)
- pathogenesis likely the same as caninum
- treatment: same as roundworms in cats
Uncinaria stenocephala - the northern hookworm - "U" = untoothed and largely Unpathogenic. hookworm that has cutting plates instead of 3 pairs of teeth!
- infects both dogs and cats
- morphologically the same as ancylostoma but has cutting plates instead of teeth in the buccal region
- Eggs = morulated (just like ancylostoma) but they are LARGER than ancylostoma
- Life cycle (direct..one host) Morulated eggs passed in environment -> L1s develop to L3s -> L3s are hardy and freeze tolerant "northern hookworm" -> L3s are ingested rather than enter through skin -> no extra intestinal migration... once they are ingested, they develop into adults in the small intestine
- PPP = 2.5 weeks
- Pathogenesis/clinical signs - much less pathogenic. compared to ancylostoma but can cause anemia and hypoproteinemia -> edema. Mild enteritis.
- treatment: antihelmintics
Lungworms
- aka "metastrongylid nematodes"
- larvae hatch in fresh feces of cattle on pasture
Muellerius capillaris - Lungworm
- Metastrongylid nematode = true lung worm
- DH = sheep, goats
- IH = snails and slugs
- Life cycle = indirect that involves ingestion of IH followed by migration to predilection site of the alveoli and terminal bronchioles of the sheep/goats
- L1s are shed in feces (NO EGG STAGE) and this is the diagnostic stage -> you look for L1s in feces to confirm infection
- Pathogenesis - alveolar rupture, focal interstitial pneumonia and some granuloma formation
- Lesions/clinical signs - raised regions in the lung grossly, calcification of parts of the lung lobes
- treatment - no registered compounds... can try ivermectin
Filaroides and Oslerus spp
- Oslerus osleri = tracheal or bronchial infections
- Filaroides hirthi - terminal bronchioles or alveoli
- infects domestic or wild canids (dogs, wolves, coyotes etc)
- Morphology - eggs are thin walled and fully larvated eggs are laid by female = quickly hatch in bronchi. You can see the worm inside the egg. Adult worms are small and slender
- Life cycle - direct. L1s shed in environment -> ingested by canid -> tracheal migration gives adults in trachea/bronchi (O. osleri species) or in bronchioles/alveoli (F. hirthi species)
- PPP 10 weeks O. osleri and 5 weeks F. hirthi
- pathogenesis - hirthi usually asymptomatic and osleri can cause nodules -> released eggs/larvae can give rise to tracheitis/bronchitis with a wheezing cough. Heavy infections -> dyspnea
- diagnosis - finding larvae in sputum (coughed up saliva/mucous from respiratory tract) using Baermann technique and nodules can be seen with bronchoscopy
- Baermann technique is using the funnel, clamp, water and sample with gauze -> requires FRESH fecal
Aelurostrongylus spp - true lungworm of cats
- required IH -> goes up the food chain until it reaches cats
- infects small bronchioles and alveoli (similar to Filaroides hirthi)
Morphology - small, slender adults and larvae have a small bent tail with a dorsal spine
- Life Cycle larvae passed in feces and infect snail/slug (IH) -> frogs/rodents/lizards/birds act as paratenic hosts -> paratenic host gets ingested by cat and larvae migrate from stomach to lungs -> adults will settle in the bronchioles and alveoli
- PPP 5-6 weeks
- Pathogenesis/lesions/clinical signs - adults and released eggs/larvae gives rise to focal pneumonia with granulomas, heavy infections cause cause chronic cough and dyspnea. Larvae can be diagnosed by examining sputum or with bauermann technique using fecal
- treat with fenbendazole
Crenosoma spp - true lungworm of dogs, wolves, foxes and raccoons
- requires a mollusc IH
- infects small bronchioles and alveoli
- Morphology small slender adults and the anterior cuticle has crenations (folds)
- females deposit L1 larvae or thin shelled eggs containing L1 larvae in feces -> can detect using baermann technique
- Life cycle L1 larvae passed in feces -> infects snail/slug as IH -> DH gets infected by eating the snail/slug containing L3 larva at this point -> larvae migrate from stomach to lungs -> adults settle in bronchioles and alveoli
- pathogenesis/clinical signs adults and released eggs/larvae give rise to focal lesions -> rhinotracheitis, bronchitis, nasal discharge
- larvae diagnosed by examining sputum or baermann technique with fecal
- treat with fenbendazole
Trichostrongyles
- eggs = thin shelled and morulated
- larvae develop in eggs to L3s and then hatch on pasture
- major parasitic threat to food production animals
- direct life cycles (monoxenous)
- some use hypobiosis (developmental arrest) to remain in host when pasture environment is too harsh to survive
- NO VERTICAL TRANSMISSION -> can only get infected by ingesting L3s from pasture
- Life cycle thin shelled, morulated egg passed in feces into pasture -> egg hatches and L1 develops to L3 -> animal eats L3 larvae from pasture -> develops into L4 and L5 in abomasum/small intestine
- PPP 2-3 weeks
Ostertagia spp. - brown stomach worm
- medium sized, slender brown worm
- ostertagia ostertagi affects cows
- ostertagia circumcincta affects sheep/goats
- eggs are thin shelled and morulated
- Life cycle thin shelled morulated eggs released into environment -> larvae hatch at L1 and mature to L3 -> L3s ingested by ruminant -> mucosal migration (develop in gastric pits and return to abomasum lumen) as adult and when environment is favourable for survival
- hypobiosis is a major factor for pathogenesis of disease if environment isn't right, they will arrest development until it's favourable
- pathogenesis/clinical signs - developing larvae cause damage to gastric pits -> inflammatory response and hyperplasia. Can see increase mucous and leakage through weakened tight junctions and loss of function of parietal cells (decreased HCL)
Loss off parietel cells = pH rises, bacterial changes (dysbiosis) in abomasum -> proteins, water, electrolytes in lumen and pepsinogen goes into blood -> altered protein metabolism and inappetence causes emaciation
- Lesions and clinical signs - altered mucosa with single or coalesced nodules in the abomasum.
- clinical signs are dependent on how many L3s they ingest from the environment (so as L3s buildup on pasture over the summer, the loads can be heavier in late summer)
- 3 distinct clinical presentations Type 1, Type 2, Pre-type 2. Type 1 = first grazing season within summer months.. will see green diarrhea from chlorphyll Type 2 = affects cattle that grazed last year and is more severe. Occurs in the spring when larva reactivate after overwintering in gastric pits. These cows are eating stored feed and will have brown watery diarrhea Pre-type 2 = late summer and fall, the L3s they ingest will go hide out in the gastric pits to overwinter. No clinical signs during this time, they're just hiding out
Haemonchus spp. - large or barberpole stomach worm
- Haemonchus contortus affects sheep
- slender worm
- eggs are thin shelled and morulated
- think of them as extra large hookworms (they blood feed in the gastric environment but don't destroy the gastric pits)
- Life cycle - thin shelled morulated eggs passed through feces on pasture -> L1s develop into L3s -> L3s ingested by animals -> brief mucosal migration -> adults blood feed in abomasum
hypobiosis is a major factor of disease - these eggs don't survive well in the environment so they overwinter in mucosa
pathogenesis - pretty much just caused by developing L4s and adults because of blood feeding -> anemia and hypoproteinemia and focal areas of hemorrhage
clinical signs - acute cases = profound anemia and hypoproteinemia -> pale mucous membranes, watery blood, edema. Chronic cases = anemia and edema, muscle weakness and fat depletion, dark hard feces
Nematodirus spp
- the one and only genus you can identify by looking at their eggs (eggs are 3x bigger than any other) remember "irus" sounds like iris of the eye and their eggs look like eyeballs
- adults are slender and are often found with multiple worms coiled together
- eggs = thin shelled, morulated but 3x the size of any other nematode egg -> often looks like an eye
life cycle - larvae develop into L3s inside eggs on pasture and then hatch -> L3s ingested by animal -> larvae develop into adults in between the villi of small intestine and then re-enter lumen
no hypobiosis
- larvea and eggs can survive on pasture over winter
Pathogenesis/clinical signs - adult worms cause villi atrophy, diarrhea, anorexia and weight loss
- Long PPP
Strongyles
- this is the parasite you'll find horses
- found in the large intestine (cecum or colon)
- divided into migratory (strongyles) vs nonmigratory
- eggs are typical nematode eggs (thin shelled and morulated)
- how to differentiate adult strongyles -> look at the shape of the buccal cavity
- strongylus spp have deeper than wide buccal cavities
- cyathostomes have wider than deep buccal cavities
- Life cycle NO VERTICAL TRANSMISSION - larvae develop in eggs on pasture and hatch -> L3s are ingested and either undergo dramatic extra-intestinal migrations (strongylus spp) or mucosal migration (cyathostomes) -> adults feed in the cecum and colon
- some hypobiosis occurs depending on species
Strongylus vulgaris - migratory strongyles
- pathogenesis largely associated with developing L4s as they move extraintestinally in the cranial mesenteric artery (can develop there for up to 2 months before moving back to intestine)
- Larvae in the vasculature cause arteritis and thrombosis particularly at the ileocolic artery. Thrombosis bc the larvae are swimming against arterial blood flow
- clinical signs - large numbers can cause sequelae from arteritis (pyrexia, anorexia, colic and death). Chronic infections can cause colic
PPP = 6 months or more
Strongylus equinus and strongylus edentatus - migratory strongyles
- same life cycle as other strongyles
- both species undergo a long and turtuous life cycle in the horse
- not highly pathogenic during larval migrations but heavy burdens of adults can cause hemorrhage and inflammation in the colon when the adults re-enter the cecum and colon (they will feed on blood and mucosa)
- PPP for equinus = more than 8 months. PPP for edentatus is more than a year
Cyathostomes - non migratory strongyles
- the most important equine nematodes (up to 40 different species that affect horses)
- Life cycle larvae develop in eggs and hatch on pasture -> L3s are the infective forms that are ingested -> mucosal migration to develop into adult and then they will go back to intestinal lumen
- hypobiosis occurs within the mucosa in some species and those that overwinter and come out in spring can lead to acute larval cyathostomiosis
- wide PPP (5 weeks - more than 20 months) depending on the species
Pathogenesis/lesions/clinical signs - mainly associated with the mucosal migration in cecum and colon (nodules form around the cysts and can impede motility/cause inappetance) -> when larvae leave the cysts it can lead to inflammation, edema and ulceration. Clinically you will see weight loss, anorexia, diarrhea and colic
- do not deworm mid winter in case there are a ton of them overwintering -> would lead to an intense inflammatory response when they die hiding out in mucosa
Syngamus trachea - "Gapeworm"
- hosts are gallinaceous and other birds
- males and females are permanently attached in copula -> form a Y shaped structure attached to trachea
- eggs = ellipsoid, elongated and smooth. Operculum at each end of egg and they are morulated
- larvae hatch in soil -> ingested and penetrate gut -> move to lungs and migrate to trachea -> attach to mucosa, suck blood and mate into pairs (form Y shaped)
- PPP is 10 days
- pathogenesis worms in trachea cause birds to gasp for air, increased mucous production, mild anemia
Oesophagostomum - pimply gut worm
- found in the large intestine
- pathogenesis is caused by the larva entering the mucosa (inflammatory response) and then when the larva leave, the nodules they produced become ulcerated
Order: Oxyurida (pinworms, oxyurids)
- highly host specific
- affects large intestine -> usually not very pathogenic, but they are irritating
Oxyuris = horses
Enterobius = humans
Syphacia = rodents
general morphology
- thicker body and long tapering tail -> pin worms
- eggs are asymmetrical... looks like they've been dropped
general life cycle direct (one host)
- females will deliver eggs to perianal region (causes irritation) -> eggs mature to contain larvae -> fecal oral transmission route -> eggs hatch in intestine and mature in large intestine
Oxyuris equi - horse pinworm
- will find white eggs in the perineal region of the horse -> pruritis/irritation in the area
- worms are thick in anterior region and then thin out to become pointy and curved tail (pin shaped)
- eggs are asymmetrical (look like they've been dropped)
- adults found in the lumen of the cecum/colon
- infective form is L3 inside egg in the environment
Order: Ascaridida (ascarids)
- eggs VERY resistant in the environment and they mature to become L3 infective forms in the environment (can live a while in this state)
- fecal oral transmission most common route (animal will ingest egg containing L3 from environment and then larva will hatch inside GIT of animal)
- L3s penetrate small intestine and undergo migration (tracheal more likely or somatic)
- after migration, larvae reach small intestine again and rapidly mature to adults and produce eggs
- robust, heavy bodied roundworms
- infect small intestine of definitive hosts except for Heterakis gallinarum which lives in the cecum
- adults very host specific
- PPP varies but usually long due to migration
- paratenic hosts may be involved -> larvae will remain as L3 and hide out hoping to get ingested by right host
- don't typically cause clinical signs, sometimes diarrhea and often pot belly appearance -> massive numbers can lead to obstructions
- Edema (pot belly) appearance due to inflammatory response -> leaky vessels
- Ocular or visceral larval migrans can occur (both associated with tracheal migration)
Toxocara canis - roundworms
- transmission: fecal oral, vertical (transmammary or transplacental)
- large heavy bodied adults in small intestine
- thick shelled, sub-spherical pitted egg (outer surface) with a single cell when passed through feces
- many pups are born with this through transplacental infection
- direct life cycle (one host)
- egg passed in feces -> larva develop to L3s within pitted egg -> infective eggs ingested
- fate of L3 in host depends on age and immune status
- pups less than 3 months = tracheal migration with PPP 4-5 weeks
- pups 3-6 months primarily somatic migration (larvae will hide out in tissues)
- 6 months or older = only somatic migration (can't successfully do tracheal.. granulomas block them)
- most pups infected in utero by transplacental migration of larvae from bitch to fetus**
- if mom is infected with L3 larvae hiding out in somatic migratory state, pregnancy can mobilize the larvae and they will enter the liver and and lung of fetus and wait for birth of pup -> once born they will go right to the gut of the pups to form adults. PPP 3 weeks in this case
- some larvae may enter the pups once born through milk -> they will go right to alveoli and then to pups small intestine to complete life cycle
- mom can also get infected by ingesting larvae in feces of pups or eating paratenic hosts
- clinical signs: in light infections no sign, in heavy infections you'll see stunted growth, unthriftiness, dull skin and coat, cachexia, worms in vomit and feces
- Can cause eosinophilic gastroenteritis of lung problems if migrating larvae are abundant -> eosinophilia in dogs and in humans you'll see ocular migrating larvans or cutaneous larval migrans
- treat with fenbendazole (panacur), milebmycin (interceptor) or selamectin (revolution)
- treatment of heavy infections needs to be done slowly so it doesn't cause an obstruction -> use panacur (this starves the worms)
- if human ingests, they can get visceral or ocular larval migrans
Toxocara cati - common name = arrowhead worm
- Transmission can be fecal oral or vertical (transmammary most common
- Worm has the arrowhead and eggs look the same as toxocara canis. only way to tell them apart from toxocara canis is by knowing whether it came form a cat or a dog
- worms found in small intestine of cats
- transmammary infection through milk is most common route of infection
- infective eggs with L3s inside are found in the environment or passed to kittens through moms milk -> small intestine -> undergo tracheal migration in kittens and somatic migration in older cats
- older cats can get infected by eating paratenic hosts
- not as pathogenic as toxocara canis, can cause vomiting (even with moderate burdens) and unthriftiness/diarrhea with heavy numbers
- kill slowly with revolution
Toxocaris leonina
- Transmission = fecal oral only and mucosal migration only
- infects both cats and dogs but not as pathogenic as toxocara spp and worm burdens are usually not as heavy
- eggs are smooth on the outside with an undulating membrane on inner surface and they have a single cell or pair of cells inside the egg that do not fill the egg shell
- same life cycle as other toxocaras (infective L3 inside egg is ingested through oral route either from environment or paratenic host) -> eggs release L3 in small intestine -> mucosal migration! no tracheal (larva penetrate gastric pits and mucosa to further their development before returning to SI lumen as adult
- PPP ~2 months
- treatment is same as toxocara (revolution in cats) and revolution, panacur, interceptor for dogs
Parascaris equorum
- Transmission through fecal oral only and tracheal migration
- infects horses, ponies and donkeys (tends to affect younger animals)
- adult worms are heavy bodied and white (up to 50 cm long)
- eggs are sub spherical and have a thick protein coat thats sticky and will easily stick to blades of grass to be ingested
- direct life cycle with tracheal migration through liver and lung = NO vertical transmission because there is no somatic migration
- clinical signs = unthriftiness, anorexia, hypoalbuminemia and heavy burdens -> impaction colic
- diagnose by finding eggs in feces
- treat with fenbendazole (which will kill slowly and ensure no impaction)
- PPP 10-12 weeks
Ascaris suum
- infects swine and is zoonotic
- worms are heavy bodied .. look like giant beans and white
- eggs are sub-spherical with a thick protein coat
- life cycle is direct with tracheal migration through liver and lung (no vertical transmission) = have to get infected by ingesting eggs
- Can cause "milk spots" on liver, pulmonary hemorrhage and edema due to eosinophilic granulomas in the lung and mild enteritis
- diagnose by finding eggs in feces
- treat/control by all in all out farrowing facilities with good hygiene, deworming sows prior to farrowing and using in feed antihelmintics to decrease burden in young
- PPP 6-8 weeks
Ascaridia galli
- infects birds
- worms are heavy bodied
- eggs have smooth shell
- Mucosal migration -> infective L3 in egg is ingested -> small intestine and hatches -> larvae enters gastric mucosa to mature into L4 and then re-enters small intestine lumen to mature into adult
- can cause hemorrhagic diarrhea during larval mucosal migration, decreased production parameters
- diagnose by finding eggs in feces
- PPP 30-50 days
- seen more often in turkeys or egg laying operations because broiler birds don't even live long enough for one life cycle
Heterakis gallinarum - "cecal worm"
- found in chickens, turkeys and many other species
- SLENDER worms and found in the ceca
- eggs are thick and smooth shelled
- eggs embryonate into L3 after passing through feces and enter host or paratenic host -> larvae migrate to ceca and enter mucosa -> complete life cycle inside mucosa -> move back to ceca lumen -> undergo 3 molts -> adults
- PPP 24-30 days
-true intermediate host for Histomonas meleagridis
Baylisascaris procyonis - raccoon roundworms
- infects racoons (DH) and other species as IHs
- adults are large worms up to 20 cm
- eggs are thick and smooth shelled
- tracheal migration, no vertical transmission
zoonotic threat -> causes visceral larval migrans in humans (will affect organs)
if it ends up in racoon, then it does its normal thing and infects small intestine. if a paratenic host like any other animal OR A HUMAN ingests the infective egg -> visceral larval migrans! Will hide out in organs in the body and cause damage
Order: Spirurida (spirurids, filarids, Dracunculus)
- NOT luminal parasites in the small/large intestine
- mainly stomach worms, but some are in eyes or connective tissues
Drashia Megastoma and Habronema spp.
- stomach worms of horses
- cause problems when they set up in gastric mucosa
- L1s in fecal material and maggots of stable flies or horse flies eat them and become IH, so either L3s or IHs are ingested for horse to get infected
- L3s move directly to gastric pits and develop as adults
pathogenesis/clinical signs adult worms large tumour like nodules
pathogenesis/clinical signs larvae - larvae enter the skin of the animals from flies -> causes "summer sores" which are inflammatory lesions on the skin. Summer sores = inflammatory lesions -> weeping wounds which attract more flies -> flies enter wound and you get snowball effect
Filarids
- all require some blood sucking insect as IH
- generally infect connective tissues or body cavities
- long slender adults at predilection site
- tiny pre-L1s (microfilaria) in blood or skin
Acanthocheilonema reconditum
- DH = dogs
IH = FLEAS
- microfilaria much smaller compared to heartworm microfilaria
- adults found in connective tissue
Morphology - adults are slender. PreL1 microfilaria have parallel sided anterior end shaped like broomstick handle
Life cycle - indirect because it requires fleas. microfilaria found in blood of dogs. fleas blood feed on infected dog -> PreL1s develop to L3s inside fleas and then re-enter the dog by an unknown route
PPP = 2 months
non pathogenic, asymptomatic
Dirofilaria immitis - Heartworm
- most commonly seen in dogs but can infect other species
- adults usually located in right caudal lobar artery, other branches of pulmonary arteries and in heavy infections, they will back up into right ventricle
morphology - adults are slender and larvae (preL1 microfilaria) have a tapered anterior end
Life cycle - indirect (requires mosquitos). Female mosquito bites an infected dog and ingests microfilaria from their blood -> microfilaria develop from preL1 to L3s in mosquito -> mosquito bites another dog and deposits infective L3 larva into dogs subcutaneous tissue and they migrate into bloodstream -> move to pulmonary arteries (this is where adults mature) and overcrowding can push them to right ventricle -> male and
females reproduce microfilaria within 6-7 months
- if you kill adult worms, their microfilaria can still be present in blood for up to 2 years and be transmitted to mosquitos who bite the dog
- PPP= 6-7 months
pathogenesis - blood vessels in pulmonary circulation are damaged bc of worms = inflammation and endothelial thickening (arteritis), worms that die can cause thromboemboli in the lung. Both of these give rise to increased vascular resistance -> pulmonary hypertension -> right ventricular heart dilation & hypertrophy and congestive heart failure
Diagnosis
1) Antigen test (most sensitive) -> will detect proteins made by adults
2) Microfilaria tests = Knott's test or difil (will differentiate acanthocheilonema from dirofilaria immitis)
Antigen tests will detect proteins made by adult worms Limitations = no use in prepatent period (before there are adults), no sue with senile (old) worms, no use with single worm infections, no use with single sex infections
Testing
First time seeing dog/no history = do microfilaria test and antigen test
Second year (if on preventatives) just do antigen test
Order: Enoplida (trichurids [whipworms], dioctophyme, capillarids, trichinella)
- all have an elongated esophagus surrounded by specialized cells called stichocytes
- highly host specific
- trichuris - found in cecum, colon
- capillaria - found in epithelium of intestine, respiratory tract or urinary tract
- trichinella - intestine (larvae in muscle). Never leaves the host
Adults = slender and white
eggs oval with bipolar plugs
- larvae usually found in intestinal tract or muscle cells
- Life cycle larvae mature in eggs and infect the next DH or IH. Oral transmission is normal route.
Trichuris spp. (whipworm)
- infects the cecum and colon of many mammals (including humans)
- each host has its own species of trichuris (host specific)
- eggs are football shaped (oval) with prominent plugs at each end and single cell fills yellow-brown egg shell
- adults are shaped like a whip (anterior 2/3 narrow and the remainder is much broader)
life cycle direct (one host) - infective eggs mature with an infective larva inside (eggs very environmentally resistant and frost resistant) -> animal eats L3 inside egg -> mucosal migration in small intestine before forming adults -> adults live in large intestine (anterior end engorged in mucosa) and they lay eggs there
- PPP = 2 months or more *Won't find in pups bc of long PPP
- clinical signs - malabsorption, protein loss, diarrhea, some worms may blood feed. clinical signs can occur during prepatent period
Eucoleus (Capillaria) spp.
- highly host specific and one host can be infected with multiple capillaria species
- all have prominent stichocytes around the esophagus
- some use intermediate hosts
- morphology of eggs - oval shaped with prominent plugs at each end but shell is irregular/wavy looking less smooth than trichuris spp**. Single cell fills yellow brown egg shell
- morphology of adults - slender and fine hair like appearance
life cycle many use earthworms as IHs, eggs will be in feces or urine depending on location of adults in host, C. hepatica lays eggs throughout the liver and this kills the liver perenchyma
- PPP 4-8 weeks
- pathogenesis/lesions/clinical signs - usually mild or asymptomatic, there are respiratory forms that can cause wheezing or coughs, if there are large burdens of worms in large intestine -> damage of epithelium -> enteritis -> diarrhea and emaciation
- capillaria species in birds = capillaria contorta, capillaria caudinflata and capillaria obsignata -> C. contorta causes wall of crop to be thickened due to numerous worms (clinical signs usually weakness and unthriftiness). C. caudinflata and C. obsignata causes edematous intestinal wall and reddish fluid, necrosis of mucosa in heavy infections
Dioctophyme renale = Giant Kidney Worm
- normally affects minks, but will also infect dogs
- uses invertebrate as IH and often fish become paratenic hosts
- usually infects the right kidney
morphology - females can be huge (up to 100cm long), males have copulatory bursa, adults are bright red colour, eggs have typical bipolar plugs with a pitted outer shell
- life cycle eggs passed through urine -> larva develop to infective form -> passed up food chain through invertebrate IH or fish as paratenic host -> eaten by dog or mink -> larvae leave intestinal tract and penetrate ONE KIDNEY ONLY (USUALLY RIGHT KIDNEY) otherwise host would die where they mature and destroy the kidney
- PPP = 3-5 months
Trichinella spiralis
- Females are long and slender and uterus contains developing larvae -> females live deeply embedded in GIT for short period and shed L1 larvae into intestine
- males have two cloacal flaps at their tail
- life cycle larvae shed by females become encysted in muscle tissue of animal -> any other human or animal that ingests the animal with cysts will get infected
- one female lays 1500 larvae
- pathogenesis/clinical signs migrating larvae that encyst in muscle can cause muscle pain, inflammation and eosinophilia. Larva feeding in the gut -> gastroenteritis and diarrhea
diagnosis biopsy of muscle tissue. Trichinella is not freeze tolerant -> so if you freeze pork meat, it will kill the parasites