Nematodes Part 2 Flashcards
what nematode parasites are common in ruminants
Trichostrongyles
HOTC = Haemonchus, Ostertagia, Trichostrongylus, Cooperia
Describe morphological characteristics of HOTC parasites
Family Trichostrongyloidea
- small
- bursate
- males have copulatory bursa with spiracles
Trichostrongyle habitat
abomasum and small intestines of ruminants
Trichostrongyle distribution
generally throughout N. America but some more common in certain regions
Name two examples of Trichostrongyles - scientific name and common name
Ostertagia ostertagi = brown stomach worm, bankrupt worm
Haemonchus contortus = Barberpole Worm
describe how the eggs of the two examples of trichostrongyles differ
Haemonchus contortus = more roung
Ostertagia ostertagi = more egg shaped
Note that there is overlap
EGGS NON LARVATED
What is the food source of both Trichostrongyle examples
blood - both are blood feeders although Haemonchus is known to be more of an avid blood feeder
In the Trichostrongyloid life cycle what is the infective stage?
L3
Describe the Trichostrongyloid life cycle
-What is the prepatent period?
- Eggs shed in feces
- L1-L3 in feces - feed on fecal bacteria
- L3 ingested while DH (ruminant) grazing – exsheath in rumen
- enter wall of abomasum or SI – develop into L4
- develop to lumen-dwelling adult in muscosa of predilection site
NO MIGRATION OCCURS
Prepatent period = 3 weeks
Define hypobiosis and the process
*Clinically speaking, why is this significant
larval inhibition, arrest development/go dormant during unfavorable conditions
occurs as L4 in abomasum
* less susceptible to anthelminthics at this stage
What is PGE
Parasitic Gastroenteritis caused by a complex of mainly Trichostrongyloid nematodes
Clinical signs of PGE in cattle (8)
rough coat
weight loss
diarrhea
anemia – more common in sheep and goats
submandibular edema = bottle jaw
high fecal count
adult worms at necropsy – lesions specific to certain species (ie Ostertagia ostertagi moroccan leather)
What animals are more susceptible to acquiring PGE?
weanlings
adults = good immunity but if experiencing stress/ starvation this immunity can go down
What males prevention of PGE difficult?
- management of dz is labor intensive
- high egg numbers and survival of L3 = total eradication is unlikely
- resistance to preventative dewormers
What is the Brown Stomach Worm
Ostertagia ostertagi - Family Trichostrongyloidea - Phylum Nematoda
Discuss the pathogenesis of the Brown Stomach Worm
as developing, larvae destroys gastric glands - cell tight jxn rupture
damages HCL-producing parietal cells = pH becomes neutral = can no longer digest proteins = bacterial overgrowth
adult = some blood sucking –> anemia
Type 1 Ostertagiasis
who is affected/infected, effect of infection
young cattle - suckling, dairy heifers, stocker
damage during exodus of gastric glands = moroccan leather = pebbled appearance of abomasal mucosa
Type 1 Ostertagiasis pathology
large # larvae in pasture, daily ingestion
Type 1 Ostertagiasis Dx
Prognosis
- high egg counts in FF
- incremental to rapid onset of clinical signs
diarrhea, weightloss, bottle jaw, anemia, rough coat, death
Prognosis - good w/ tx, move to safe pasture
What is Pre-type II Ostertagiasis
ingestion of L3 that go into hypobiosis once in gastric gland – can last 3-4 months, no clinical dz seen
What is Type II Ostertagiasis
-Clinical signs
stimulated hypobiotic larvae acquired 3-6m prior
larvae resume developement - emerge from gastric glands
-gradual destruction of abomasum
-seen more in yearlings, calf replacement heifers and older stock
-signs of PGE
-high egg count
What is the Barberpole Worm?
Haemonchus contortus
Family Trichostrongyloidea
Phylum Nematoda
Barberpole Worm
- hosts
- habit and severity of effects
major cause of PGE in goats/sheep
pathogenic bloodsucker, most impt parasite in small ruminants except in cold climates
What are the signs of PGE in small ruminants?
weight loss rough hair/wool breaks anemia diarrhea - general PGE hypoproteinemia
Why is H. contortus such a problem? (5)
- year round transmission in Fl
- sheep and goat acquire little to no immunity
- deadly blood sucker
- very fecund
- resistant to most antihelmintics
Why are sheep and goats so susceptible to worms?
- never evolved ability to acquire strong immunity to worms – originally from dry/deserts or cold mountains \
- browse by preference avoiding grass
What is Periparturient Rise?
massive outpouring of worm eggs by ewes and does while lactating
PRL suppresses immunity to worms
condition begins near parturition
ceases w/in few days of weaning
What are the 3 sources of Periparturient Rise?
- Hypobiotic larvae resume development, ewe/doe has reduced immunity at this point
- ingestion of larvae overwintered on pasture –mature in large numbers
- increased egg output from an existing adult population
What is the final outcome of Periparturient Rise?
- worm burdens maintained rather than expelled
- worms free to produce many eggs
- massive past L3 contamination develops
Name management principles
good nutrition
don’t overstock or overgraze
segregate classes of animals whenever possible
use mixed species/alternate grazing wherever possible – horses/cattle
Name the member of Family Strongyloidea learned
scientific and common name
Ancylostoma Caninum - 3 teeth
Hookworm of dogs
A. tubaeformae = cats - 3 teeth
A. braziliense = dogs and cats - 2 teeth
What kind of eggs do hookworms have?
non-embryonated/larvated eggs
What is the infective stage of hookworms?
Ancylostoma Caninum
L3 stage
Habitat for adult hookworm?
small intestine
Life cycle of Ancylostoma Caninum
- hookworm adult attached to small intestine of DH
- non-larvated eggs leave DH via feces
- eggs embryonate in environment - moist
- L1 develops in egg in 24 hrs and hatched
- L1 molts to L2 then matures to L3 but remains ensheathed (doesnt molt) NOW INFECTIVE
- infects DH
Name the 5 possible ways Ancylostoma Caninum can infect the DH
as ensheathed L3
- oral ingestion
- skin penetration
- prenatal/transplacental
- lactogenic infection
- ingestion of paratenic host
What is characteristic about oral ingestion of Ancyclostoma Caninum L3 larvae?
rarely occurs in nature
no larval migration, adult matures in small intestine
prepatent period = 15-18 days
What is characteristic about skin penetration of Ancyclostoma Caninum infective L3 larvae in dogs <3m old?
extensive migration = blood vessels/lympathic vessels –> heart –> lungs –> alveoli –> migrate to bronchioles/bronchi –> swallowed –> mature in small intestine
What is characteristic about skin penetration of Ancyclostoma Caninum infective L3 larvae in dogs >3m old?
extensive migration but follow more somatic route from blood vessels/lymphatic vessels
- **become hypobiotic – encyst in muscle = pool of infection
- mammary gland population at onset of lactation
- repopulate adult worms in SI if eliminated
What is characteristic about prenatal/transplacental infection of Ancyclostoma caninum infective L3 larvae?
rare
L3 enters blood stream, pass to placenta to fetus
source = hypobiotic larva in mom, infection occurs during pregnancy
What is characteristic about lactogenic infection of Ancyclostoma caninum infective L3 larvae?
L3s recovered from milk up to 20d after whelping
source = hypobiotic larvae migrate to mammary glands
adult mature in SI, no migration occurs in puppies
What is characteristic about paratenic host ingestion infection of Ancyclostoma caninum infective L3 larvae?
ingest rodent host w/ hypobiotic L3s
adults now mature in SI of DH no migration occurs
What is the pathogenicity of Ancyclostoma caninum
- anemia - site of attachment continues to bleed
- severity depends on age of host, # worms, overall health
- adults can have acquired immunity
- puppies most susceptible b/c no aquired immunity and low iron reserves
What are the clinical signs of an Ancyclostoma caninum infection?
- bloody diarrhea, mucus, black/tarry
- decreased appetite
- weakness
- poor growth/hair coat
- pale mucus membranes
- hemorrhagic pneumonitis -migrating larvae
- most eczema - skin penetration
Name the condition and specifics of the zoonotic hookworm discussed in class
Ancyclostoma braziliense causes Cutaneous Larval Migrans (CLM)
- L3 skin penetration marked by elevated, red and winding pruritic lesions
- rarely enter SI and mature to adults
- also called sand worms, plumbers itch, creeping eruption
What is the scientific name and family of the large equine pinworm discussed?
Oxyuris equi
Family: Oxyruoidea = pinworms
What is the habitat of the large equine pin worm?
large intestine
What is the morphology of the adult Oxyuris equi?
eggs?
adults = whitish, thick bodies, club shaped/double bulbed esophagus
eggs - asymmetrical, operculated, unembryonated
Life cycle of Oxyuris equi
- oviparous female deposits egg in perianal region
- eggs embryonate
- eggs fall into bedding, food, water
- eggs ingested and hatch in SI
- larval development in crypts of SI
- larvae enter lumen, move to large intestine and develop into adults
What is “Pruritis Ani” / “Seat Itch” ?
pathology of Oxyuris equi
- rubbing leads to hairloss and secondary bacterial infection
- skin thick, scaly, rat tailed appearance
How is Oxyuris equi dx?
eggs at perineum or feces
“scotch tape” test
Name the member of Ascaroidea discussed?
What is its DH
Phylum Nematoda
Toxacara canis
DH = dogs, in small intestine
What morphological characteristic helps ID species of Ascarids?
alae modifications
What is unique about the Toxicara Canis life cycle?
eggs with L2 is infective to new DH = larva is inside egg
Describe the Toxicara Canis life cycle
- adults in SI of DH
- non-embryonated eggs leave via feces
- eggs embryonate L1-L2 in environment
- egg with L2 larvae is infective to DH
- enters DH via several routes
Name the 4 possible routes Toxicara canis can enter the DH
- ingestion = direct transmission
- prenatal/transuterine trasmission
- colostral/lactogenic transmission
- ingestion of paratenic host
Discuss direct transmission of Toxocara canis to dogs <3 months
ingest L2 larvea infective stage
Tracheal migration = penetrate intestine, mesenteric lymph nodes, liver, heart, pulmonary arteries, lungs MOLTS TO L3 - then alveoli, bronchioles, trachea, coughed and swallowed to stomach
molts to L4/L5 in small intestine and mature to adult
prepatent period = 3-4 wks
Discuss direct transmission of Toxocara canis to dogs >3 months
ingest L2 larvea infective stage
somatic migration = hatch, penetrate intestine, enters system circulation
L2 larvae encysts becomes hypobiotic, maturation occurs
Discuss prenatal/transuterine trasmission of Toxocara canis
Hypobitoic L2 larvae migrate to fetus
L3 mold in fetal liver
L3 in lungs at birth, migrate to stomach
L4/L5 in stomach - mature to adult
Eggs found in puppy feces by 23-40 days old
Discuss colostral/lactogenic trasmission of Toxocara canis
Hypobiotic L2 larvae in mammary tissues passed via colostrum
L2 directly to stomach - SI
NO MIGRATION
Discuss the paratinic host form of Toxocara canis transmission
Ingestion of encysted L2 in rodents
L2 directly to SI
No migration
Discuss the pathogenicity of Toxocara canis
More problematic in younger puppies Signs with heavy infections = Pneumonia due to migrations Vomiting, diarrhea Pot-belled appearance Focal lesions in CNS - migrations to wrong location = neuro disorders
What zoonotic dz is associated with Toxocara canis – discuss pathogenicity
Visceral Larval Margins
- chronic granulomatous lesions due to larval migrations
- humans = paratenic host , more often children
What is the species name of the example worm from the family Trichoroidea
Trichinella spiralis
Phylum Nematoda
What are the hosts of the Trichina worm?
Trichinella spiralis
Adult parasite in = SI
Larval parasite = in striated muscles
Possible hosts = pigs, rats, bears, wild boar, humans, horse, other mammals
What type reproductive method does Trichinella Spiralis female have?
Larviparous = eggs in uterus, gives birth to live larva
Discuss the epidemiology of Trichinella spiralis
Sylvanic and urban cycles, human. Infection usually due to ingestion of undercooked meat
What is unique regarding the life cycle of Trichella spiralis?
Nurse cells – parasite encysts as L1 and uses host tissue to protect themselves
Therefor the host acts as the DH and the IH = parasite is born in and encysted in the same host until eaten again
Discuss the life cycle of Trichinella spiralis
- Female deposits larvae into intestinal wall
- Larvae enter lymphatics
- Migrations to thoracic duct, heart, lungs, heart
- Enter systemic circulation
- Larvae encyst (encapsulate) in striated muscle
- Larvae excuse in SI when ingested by different host
- Mature to adults in SI
What are the pathological phases of Trichinella spiralis?
Clinical signs rarely seen in swine
2 phases in other hosts =
- Intestinal infection with adults - occurs in intestines 1-2 after ingested
- Skeletal muscle invasion by L1 - 2 week, larvae invade many cell types but only encapsulate in skeletal muscle
How do you dx Trichinella spiralis?
Muscle biopsy
Serum samples -skin sensitive test, elisa
Slaughterhouse inspection
How do you control Trichinella spiralis
Prevention cannibalism
Cook meath thoroughly
Freezing - some can resist freezing however
Name the example of Filaroidea
What is the habitat of the adult worm?
Dirofilaria immitis
Right ventricle, pulmonary arteries of dogs, cats, ferrets, sea lions, seals and others
Describe the prelarval stage of Dirofilaria immitis?
What is the vector/IH of Dirofilaria immitis?
Found in circulating blood
Tapered anterior end, may be straight or hooked
Mosquitoes - many species can transmit the parasite
What is the significance of Acanthocheilonema reconditum?
On blood smear can be confused for microfilaria of Dirofilaria immitis.
Appearance is different in that it is more curved and has a blunt head in comparison with Dirofilaria immitis
What are the characteristics of an occult Dirofilaria immitis infection?
Hidden infections characterized by
-single sex infection, adults are either strictly
female or strictly male
-low numbers
Mff not detectable in peripheral blood at this stage
Best dx with antigen tests to find mature adults
What is the microfilarial periodicity of Dirofilaria immits?
Nocturnal periodicity - Mff present in blood during evening hours
And
Incomplete periodicity - Mff never disappear completely from peripheral blood during 24 hour period
What is the prevalence and frequency of Dirofilaria immits?
Determined by signalment and habits - more common in males, outdoor dogs, between 3-15 yrs, larger breeds
Describe the Diofilaria immitis lifecycle
- Mff released by female worm into circulation
- Mosquito takes up Mff from blood
- Mff molt to infective L3
- infective L3 enters DH after mosquito bite
- Larvae migrates to heart and lungs and undergo L3-L5 molts
- Adult worms mature in heart and produce Mff after mating
What is the pre-patent period of Dirofilaria immitis?
5.5-7 m
Discuss the IH of Dirofilaria immitis
Mosquito vectors = 23 species can transmit dz
Distribution of species vary, feeding habits vary, and breeding sites vary
Carry infective L3 to DH
When does a dog become antigen-positive?
Without prophylaxis earliest 5 months but most at 7 months after infection
With macrocyclic lactose doses missed -earliest 9 months after infection
What is possible to occur of a macrocyclic lectins prevention dose is missed?
Delayed HW maturation and patient conversion to antigen positive status
When does a dog become Mff positive
No prophylaxis = earliest 6.5 months after infection
Pets receiving macrocyclic lactose may never develop nuff or they may appear only transiently in small numbers but adults will still be present if doses are missed
What is the gold standard for HW antigen test
DiroChek HW Ag test
What are 6 reasons why a pet may be Antigen positive but Microflilaria test negative?
- Maturing infection, Mff not in circulation
- Use of prevention w/o removing adult worms
- Use of microfilaricide w/o remove of adult worms
- Unisex female infections, no male present
- Dog is true immune-mediated occult - rare but some dogs can destroy Mff
- . failure to use Mff concentration test
What are 4 reasons why a pet would be Ag test negative but Mff test positive
- Jeff are those of another species- usually in lower numbers
- Mff acquired transplacentally - few numbers and seen in young dogs
- Adult worms were removed for have died but Mff persist
- Contamination of test materials
For what reason would hw Ag test be variable and Mff negative or positive
Fluctuation Ag levels due to # of female worms, ages of worms, quality of samples
-older worms not as fecund
Discuss the Pathogenicity/Clinical signs of Dirofilaria immtis
Dz in adult - right ventricular and pulmonary artery obstruction
Vilous endarteritis = inflamed vessels Vascular resistance = increased cardiac workload due to inflammation Decreased cardiac output Exercise intolerance Coughing Hemoptysis =blood in sputum Vena cava syndrome
Some dogs can be asymptomatic
7 ways feline hw infection differs from canine infection
1 similarity
- Cats less susceptible
- Few worms can cause dz 1-2 in cats whereas caine dz depends on dog size and number of worms
- Worms short lived in cats, long lived in dogs
- Worms in cats dont usually produce Mff
- Lungs most often affected in cats, vs heart and lungs in dogs
- Diagnosis usually requires more steps that dogs
- No treatment, can only treat symptoms
1 there are preventative available
What is the tx for Hw dz that has the greatest efficacy, what is its limitation
Melarsomine dihydrichloride
Kills adult worms, no activity against worms <4 months
What is “Slow Kill”
Continuous monthly use of preventative in conjunction with antibiotics
Current macrocyclic lactones are not approved for this use
Requires client compliance
Takes a long time to work
SHOULD ONLY BE USED WHEN IMMITICIDE CANNOT BE
