parasit lecture exam 1

4 types of symbiosis w/ example of each?

• phoresis = 1 organism (phoront) is carried by another w/o physiologic dependency

  • ex) bacteria carried on legs of housefly

• mutualism = 2 organisms living tgt that physiologically depend on each other

  • ex) ruminant + rumen microflora

• commensalism = 1 organism benefits from associating w/ the host but host is not harmed/benefitted

  • ex) clownfish + anemone

• parasitism = parasite physiologically depends on host for metabolic needs + habitat at the expense of host

  • ex) canine heartworm in dogs

Obligate vs facultative parasites?

• obligate = must live parasitic lifestyle or die

• facultative = opportunist that can survive w/o host

endoparasite vs ectoparasite

• endoparasite = parasite lives in internal organs of animals

• ectoparasite = parasite lives on the exterior of animals

infection vs infestation

• endoparasites INFECT = entry + development/multiplication of an infectious agent w/i the body of an animal

• ectoparasites INFEST = lodging, development, or repro of parasites on the surface of the body

accidental vs aberrant parasites?

• accidental parasite = wrong host + usually right location

  • usually develops in correct manner similar to that in its natural host

• aberrant parasite = right host + wrong location → can’t complete normal life cycle

  • usually happens in accidental parasites who get lost

pseudoparasite vs spurious parasite?

• pseudoparasite = non-parasite that resembles parasite

  • ex) pollen grain, fungal spores, free-living nematodes

• spurious parasite = parasite passing thru GI tract of non-host species that get mistaken as parasites of the non-host

  • ex) Eimeria oocysts that normally infect rmts found in dog feces → didn’t actually infect dog eggs just passing thru

What are the 3 types of hosts?

• definitive = where parasite reaches maturity + (if applicable) repro sexually

• intermediate = where parasite goes thru its larval/developmental stages

  • repro + metamorphosis may occur

  • essential to completion of life cycle

• paratenic = host that transports parasite where it remains viable but does NOT grow/develop

  • not essential to completion of life cycle

Direct vs indirect life cycles?

• direct life cycle:

  • only requires definitive host

  • parasite infects definitive host via environment

• indirect life cycle:

  • requires definitive host AND 1+ intermediate host(s)

  • environmental stage optional in some species

incubation period vs pre-patent period vs patent period

• incubation period = time b/t infxn + first clinical signs appear

  • usually shorter than pre-patent

• pre-patent period = time b/t infxn + parasite first becomes detectable

  • usually once eggs shed

• patent period =

presumptive vs definitive diagnosis of parasitism?

• presumptive = infxn presumed based on factors other than actual detection of parasite

  • ex) puppy is anemic, presume infected w/ parasites bc we know hookworms cause anemia in puppies before detectable

• definitive = parasite presence in host shown directly or indirectly

  • ex) fecal float indirectly shows parasite presence

How do you obtain a definitive ante-mortem diagnosis of parasitism?

• demonstrate presence of parasite in host tissues in LIVE animal

• ex) see worm moving under skin

What are the 2 clinical levels of parasitism?

• sub-clinical parasitism = parasites reduce host productivity w/o overt clinical signs

• clinical parasitism = parasites cause overt clinical signs

When do you use the suffix -iasis vs -osis?

• -iasis = parasite infxn w/o overt clinical disease

  • only req. detection of some stage of the parasite

• -iosis = parasite infxn w/ overt clinical disease as a result

  • req. detection of parasite, presence of clinical signs, and interpretation of these findings

What is premunition? What is required for premunition to exist?

• a state of resistance to re-infection after an acute infection becomes chronic

• persists only as long as infecting organisms remain in the body

• ex) sheep w/ chronic low-lvl of worms won’t get more worms bc all seats on bus taken

What are the 3 different goals for treatment of parasites?

• total elimination = completely eradicate parasites

• control = minimize parasite load without complete eradication

• sporadic treatment/removal = like surgically removing a parasite one time

Nematodes:

• AKA

• anatomical appearance

• body wall composition

• body cavity composition

• AKA: roundworms

• anatomical appearance:

  • spindle-shaped w/ tapering at 1 or both ends

  • unsegmented body

  • separate sexes

  • essentially 1 outer tube composed of 2 inner tubes (repro tube + GI tube)

• body wall:

  • cuticle = tough collagenous outer skeleton

    • antigenic

  • hypodermis = layer under cuticle that secretes materials to build cuticle

  • muscle cells = fibers run along long side of worm to contract longitudinally → mvmt

• body cavity:

  • pseudocoelom = coelom-like but not lined w/ mesoderm

  • contains fluid that’s highly toxic/antigenic to host

  • repro tube + GI tube

Describe the male + female nematode repro tracts

• male

  • coiled testis → vas deferens → enlarged seminal vesicle → muscular ejaculatory duct → cloaca

  • ± accessory organs like spicules/bursa

• female

  • ovary → oviduct → uterus → muscular ovejector → vulva

  • vulva location varies w/i body

  • uterus type varies

3 types of nematode reproduction strategies for egg development

• oviparous = female lays egg w/ undeveloped embryo

• ovoviviparous = female lays egg containing L1

  • female lays embryonated eggs

• viviparous = female gives birth to larvae instead of laying eggs

Brewer’s 11 roundworm taxa

• true strongyles

  • direct life cycle

  • egg to L1-L3 in environment

• trichostrongyles

  • direct life cycle

  • egg to L1-L3 (mostly) in environment

• hookworms

  • direct life cycle

  • egg to L1-L3 in environment

• lung worms (direct life cycle)

• lung worms (indirect life cycle)

• meningeal worm

  • indirect life cycle

  • snail/slug intermediate host

• ascarids

  • direct life cycle (mostly)

  • eggs

  • no free-living L3s

• pinworms

  • direct life cycle

  • eggs

  • no free-living L3s

• spirurids

  • indirect life cycle

  • arthropod intermediate host

• rhabditids

  • direct life cycle

  • free-living L3 + free-living life cycle

• enoplids

  • direct life cycle

  • no free-living L3s

Brewer’s 6 strongyle taxa

• hookworms

• true strongyles

• trichostrongyles

• lung worms (direct life cycle)

• lung worms (indirect life cycle)

• meningeal worm

Characteristics of true strongyles

• bursate nematodes = have copulatory bursa

  • large bursa w/ spicules

• well-developed buccal cavity + capsule

• buccal capsule often has corona radiata

• teeth deep inside buccal cavity

• direct life cycle

• fecal-oral transmission

Large vs small strongyles

• large strongyles

  • well-developed globoid buccal capsule

  • larvae migrate weird → more pathogenic

• small strongyles AKA cyathostomes

  • shorter + shallower buccal capsule

  • larvae migrate in gut mucosa → relatively less pathogenic

  • typically occur in larger #s

3 large strongyle species

• Strongylus equinus

• Strongylus vulgaris

• Strongylus edentatus

How do equine strongyles feed?

• adult strongyles suck a plug of gut mucosa into buccal capsule → teeth lacerate mucosal plug + secrete digestive/anticoagulative enzymes → suck blood

• few worms feeding not usually pathogenic but many can dmg mucosal integrity

What is the general life cycle of strongyles in equines?

adults in LI lay eggs → eggs shed in feces → egg in environment → L1 develops in egg → hatches → L2 → L3 retains L2 cuticle as protective sheath + becomes infective but UNABLE to feed → host eats free-living L3 in environment → L3 sheds sheath w/i host + penetrates intestinal mucosa → L4 in ~1 wk → larval migration path → re-emerge as L5/adult in LI

Life cycle of S. vulgaris:

1) how does it enter the body?

2) is there migration in the host?

3) where do adults live?

4) how does it exit the body?

5) pre-patent period?

1) fecal-oral transmission, horse ingests free-living L3 in environment while grazing

2) L4 penetrates arterioles of GI tract → migrate twds larger arteries → reach cr. mesenteric a. in 2-3 wks → migrate w/i arteries for 2-4 months → return to intestine via destroying subserosal capillaries → encapsulate w/i nodules in gut wall → L5 → L5 molts, rupturing out of nodules into LI lumen → adult

3) LI (cecum + colon)

4) eggs shed in host feces

5) 6 mo

Pathology of S. vulgaris

• larval migration w/i arterial intima of cranial mesenteric a. + branches → lesions in arteries

  • arteritis, thrombosis, infarcts, aneurysms

• sequelae include altered intestinal motility + tone + predisposed to colic

• clinical signs are non-specific: fever, anorexia, lethargy, diarrhea/constipation, anemia, ab. pain

What is verminous arteritis in horses d/t?

L4 migration of Strongylus vulgaris in intima of arteries

S. edentatus life cycle:

1) how does it enter the body?

2) is there migration in the host?

3) where do adults live?

4) how does it exit the body?

5) pre-patent period?

1) fecal-oral transmission, horse ingests free-living L3 in environment while grazing

2) L3 → penetrate gut mucosa → migrate into hepatic portal vein → encapsulate in nodules in liver → molt into L4 exit nodules → migrate in liver for 2 months → leave liver via hepatic ligaments → migrate around retroperitoneal space → migrate into peritoneum → migrate into cecum → emerge into cecal lumen as L5 → adults

3) LI

4) eggs in feces

5) 6-11 mo

Pathology of S. edentatus

• larval migration in liver + peritoneum + retroperitoneal space + gut mucosa → inflammation, adhesions, lesions, acute septic/chronic hemorrhagic peritonitis

• clinical signs are non-specific: fever, anorexia, lethargy, diarrhea/constipation, anemia, ab. pain

Life cycle of S. equinus:

1) how does it enter the body?

2) is there migration in the host?

3) where do adults live?

4) how does it exit the body?

5) pre-patent period?

1) fecal-oral transmission, horse ingests free-living L3 in environment while grazing

2) L3 → penetrate gut mucosa → molt into L4 in nodules in cecum → exit nodules migrate to liver via peritoneal cavity → migrate in liver ~2 mo → migrate into peritoneal cavity molt into L5 → emerge into gut lumen → adults

3) LI

4) eggs in feces

5) 9 mo

Pathology of S. equinus

• does not usually cause clinical signs by itself → signs usually d/t S. vulgaris co-infection

• clinical signs are non-specific: fever, anorexia, lethargy, diarrhea/constipation, anemia, ab. pain

At what age(s) will you find strongyle eggs in foal feces?

• <6 wks → eggs prob from mare feces → just passing thru GI tract

• 6 wks - 6 mo → likely eggs from small strongyles

• >6 mo → could be large + small strongyles eggs

What is the significance of hypobiosis?

Life cycle of small strongyles?

Pathology of small strongyles

Management strategies for equine strongyles?

What is selective therapy in strongyle mgmt? What is the goal? What 2 observations does it rely on? What is the 80/20 rule? When is it contraindicated?

• use screening tool to treat animals above threshold lvl

• goal: avoid clinical signs + avoid resistance

• 2 observations:

  • parasites are unevenly distributed (overdispersed)

  • strongyle egg shedding in adults is consistent over time

• 80/20 rule = 20% of horses carry 80% of the parasites (high egg shedders)

• contraindicated in young animals

Which test would you use to determine if your horse has parasites?

centrifugal fecal float

Which test would you use to identify which horses are high egg shedders?

McMaster method to find eggs per gram (EPG)

Which test would you use to determine if an antiparasitic drug is working for your farm? How do you do it?

• fecal egg count reduction test (FECRT) = (EPG (pre-tx) - EPG (14 day post-tx))/EPG (pre-tx) * 100

Where do adult strongyles live in equines?

large intestine (colon + cecum)

How do strongyles get inside horses?

• fecal-oral transmission

• horse ingests free-living L3 strongyle larvae

How do nematodes move food through their intestine?

muscular pharynx pumps food in → forces food thru wimpy intestine

Which of the big 3 drug classes are large strongyles susceptible to?

all of them (benzimidazoles, nicotinic agonists, MLs)

Which of the big 3 drug classes are small strongyles susceptible to?

• MLs

• very resistant to benzimidazoles + nicotinic agonists

What are the tx recommendations w/i first year of foal’s life + why?

• 4 anthelmintic tx’s:

  • 2-3 mo → target Parascaris w/ nictonic agonist/benzimidazole

  • weaning/6 mo → FEC to det. whether targeting Parascaris vs strongyles → det. which drug to use

  • 9 mo → target strongyles w/ MLs

  • 12 mo → target strongyles w/ MLs

Which true strongyle(s) infect rmt?

• Oesophagostomum spp.

• Chabertia ovina

Oesophagostomum spp. life cycle:

1) how does it enter the body?

2) is there migration in the host?

3) where do adults live?

4) how does it exit the body?

5) pre-patent period?

1) fecal-oral transmission, rmt/pig ingests free-living L3 in environment while grazing

2) L1-L3 in environ.→ L3 penetrate colon mucosa → encyst (can undergo hypobiosis) → emerge into lumen as adults

3) mainly LI

4) eggs in feces

5) 6-7 wks

Pathology of Oesophagostomum spp.

• primary infxn relatively harmless but large # of larval emergence can cause clinical signs

• re-infxn can cause host immune-mediated response to form nodules/“mini-abscesses” around encysted larvae → nodules calcify + interfere w/ LI fxn → non-specific “poor-doer” subclinical signs

  • rarely nodules rupture → ulcerative colitis, peritonitis, adhesions, death

Chabertia ovina life cycle:

1) how does it enter the body?

2) is there migration in the host?

3) where do adults live?

4) how does it exit the body?

5) pre-patent period?

1) fecal-oral transmission, rmt ingests free-living L3 in environment while grazing

2) L1-L3 in environ.→ L3 penetrate gut mucosa → molt into L4 (can undergo hypobiosis) → emerge into LI lumen as adults

3) LI

4) eggs in feces

5) ~6 wks

Pathology of Chabertia ovina?

• mostly subclinical non-specific signs

• large #s of plug-feeding adults can cause mucosal ulcerations → non-specific clinical signs (diarrhea, wt loss, anemia, etc)

What true strongyle(s) infect swine?

Stephanurus dentatus

Stephanurus dentatus life cycle:

1) how does it enter the body?

2) is there migration in the host?

3) where do adults live?

4) how does it exit the body?

5) pre-patent period?

1) 3 mechanisms:

• ingestion of L3

• ingestion of L3 in earthworms serving as paratenic hosts

• skin penetration by L3 thru unbroken skin

2) L3 migrate via blood to liver (can undergo aberrant migration) → wander in liver for 2-9 mo → exit thru liver capsule → migrate retroperitoneally to kidney + ureters → encyst → mature into adults

3) kidney + ureters

4) eggs in urine

5) 9-16 mo

Stephanurus dentatus pathology?

• urinary issues maybe? no one knows bc no one checking pig kidney fxn at slaughter

• aberrant migration can cause clinical signs depending on where the larva wondered off to (skeletal m, lungs, CNS, pancreas, spleen, etc)

What are the abomasal worms + their main hosts? (HOTT)

• Haemonchus (sm rmt)

• Ostertagia (cattle)

• Telodorsagia (sm rmt)

• Trichostrongylus axei (rmt + horses)

Haemonchus contortus life cycle:

1) how does it enter the body?

2) is there migration in the host?

3) where do adults live?

4) how does it exit the body?

5) pre-patent period?

1) sm rmt ingest L3

2) L1-L3 in environment → L3 ingested → L3 ex-sheath in abomasum → penetrate b/t gastric epithelial cells → emerge as L4 → mature into adults

3) abomasum

4) eggs in feces

5) 15 days

Haemonchus contortus pathology?

• larval emergence from gastric mucsoa not problematic

• voracious blood sucking adults + late stage larvae are problematic → anemia

• peracute hemonchosis: massive infxn of highly susceptible animal → losing mass amts of blood → sudden death often w/o signs

• acute hemonchosis: lose blood from Haemonchus → lose blood proteins (albumin + globulins) → decreased oncotic pressure → dependent edema (bottle jaw)

• chronic hemonchosis: chronic insidious blood loss d/t chronic infxn w/ lower # of parasites → non-specific clinical signs w/o obvious enemia + edema

How is Haemonchus managed?

• Haemonchus very resistant

• use FAMACHA system → only treat animals w/ anthelmintics that score >= 4/3 depending on specific individual

What are the 3 ways parasites develop drug resistance?

• change drug’s target site

• make enzyme that chops up drug

• make pump to pump out drug

What is refugia?

• susceptible population of parasites

• want to maintain refugia to avoid disease + avoid resistance

Ostertagia ostertagi life cycle:

1) how does it enter the body?

2) is there migration in the host?

3) where do adults live?

4) how does it exit the body?

5) pre-patent period?

1) cattle ingest L3 while grazing

2) L1-L3 in envrionment → L3 ingested → L3 ex-sheath → penetrate gastric glands of abomasum → L3 molt into L5 in gastric glands w/i 2 wks → L5 emerge from gastric glands into abomasum

3) kidney + ureters

4) eggs in urine

5) 9-16 mo

Ostertagia ostertagi pathology?

Trichostrongylus life cycle:

1) how does it enter the body?

2) is there migration in the host?

3) where do adults live?

4) how does it exit the body?

5) pre-patent period?

1) 3 mechanisms:

• ingestion of L3

• ingestion of L3 in earthworms serving as paratenic hosts

• skin penetration by L3 thru unbroken skin

2) L3 migrate via blood to liver (can undergo aberrant migration) → wander in liver for 2-9 mo → exit thru liver capsule → migrate retroperitoneally to kidney + ureters → encyst → mature into adults

3) kidney + ureters

4) eggs in urine

5) 9-16 mo

Trichostrongylus pathology?

Teladorsagia circumcinta life cycle:

1) how does it enter the body?

2) is there migration in the host?

3) where do adults live?

4) how does it exit the body?

5) pre-patent period?

1) 3 mechanisms:

• ingestion of L3

• ingestion of L3 in earthworms serving as paratenic hosts

• skin penetration by L3 thru unbroken skin

2) L3 migrate via blood to liver (can undergo aberrant migration) → wander in liver for 2-9 mo → exit thru liver capsule → migrate retroperitoneally to kidney + ureters → encyst → mature into adults

3) kidney + ureters

4) eggs in urine

5) 9-16 mo

Teladorsagia circumcinta pathology?

Cooperia life cycle:

1) how does it enter the body?

2) is there migration in the host?

3) where do adults live?

4) how does it exit the body?

5) pre-patent period?

1) 3 mechanisms:

• ingestion of L3

• ingestion of L3 in earthworms serving as paratenic hosts

• skin penetration by L3 thru unbroken skin

2) L3 migrate via blood to liver (can undergo aberrant migration) → wander in liver for 2-9 mo → exit thru liver capsule → migrate retroperitoneally to kidney + ureters → encyst → mature into adults

3) kidney + ureters

4) eggs in urine

5) 9-16 mo

Cooperia pathology?

Nematodirus life cycle:

1) how does it enter the body?

2) is there migration in the host?

3) where do adults live?

4) how does it exit the body?

5) pre-patent period?

1) 3 mechanisms:

• ingestion of L3

• ingestion of L3 in earthworms serving as paratenic hosts

• skin penetration by L3 thru unbroken skin

2) L3 migrate via blood to liver (can undergo aberrant migration) → wander in liver for 2-9 mo → exit thru liver capsule → migrate retroperitoneally to kidney + ureters → encyst → mature into adults

3) kidney + ureters

4) eggs in urine

5) 9-16 mo

Nematodirus pathology?

What species are trichostrongyle infections most significant?

rmt → most common + often pathogenic

What are the 6 most significant trichostrongyles that infect rmts?

• Haemonchus

• Ostertagia

• Trichostrongylus

• Teladorsagia

• Cooperia

• Nematodirus

What trichostrongyle(s) infect pigs?

Hyostrongylus

What trichostrongyle(s) infect cats?

Ollulanus

General etiology of ruminant parasitic gastrogenteritis (PGE)?

• infxn by mixed strongyle species (mostly trichostrongyles)

  • cattle → Ostertagia ostertagi

  • sm rmt → Haemonchus contortus

• larval emergence + adult feeding erode gastric mucosa + glands

Can Stephanurus dentatus eggs be identified from fecal culture + Baermann sedimentation?

• no

• Stephanurus dentatus eggs will only be in urine, not feces