parasit exam 1

Strongylus vulgaris:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• True Strongyle (equine large strongyle)

• strongyle type egg

• large globoid buccal cavity w/ corona radiata + 2 teeth

• large copulatory bursa

2) L1-L3 in environ. → HORSE ingest free-living infective L3

3) ex-sheath → L3 penetrate GI mucosa + intima of arterioles → cr. mesenteric a. → gut wall nodules → L5 emerge into LI lumen

4) LI lumen

5) eggs shed in feces

6) fecal culture + Baermann

7) 6 mo

8) no, susceptible to all 3

9) larvae migrating in aa. → a. + gut wall lesions → verminous arteritis, aneurysms, thrombosis, infarcts, altered peristalsis → verminous colic, non-specific signs (lethargy, diarrhea/constipation, wt loss, poor-doer signs, fever if acute, etc)

Strongylus equinus:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• true strongyle (equine large strongyle)

• strongyle type egg

• large globoid buccal cavity w/ corona radiata + 3 teeth

• large copulatory bursa

2) L1-L3 in environ. → HORSE ingest free-living infective L3

3) ex-sheath → L3 penetrate gut mucosa → nodules in cecum → emerge as L4 → peritoneal cavity → liver → peritoneal cavity → L5 emerge into LI lumen

4) LI lumen

5) eggs shed in feces

6) fecal culture + Baermann

7) 6-11 mo

8) no, susceptible to all 3

9) larvae migrating in liver + peritoneum → liver + peritoneum + CECUM lesions → non-specific signs (lethargy, diarrhea/constipation, wt loss, poor doer signs, etc)

Strongylus edentatus:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• true strongyle (equine large strongyle)

• strongyle type egg

• large globoid buccal cavity w/ corona radiata + 0 teeth

• large copulatory bursa

2) L1-L3 in environ. → HORSE ingest free-living infective L3

3) ex-sheath → L3 penetrate gut mucosa → hepatic portal v. → nodules in liver → molt into L4 → travel via hepatic ligaments into retroperitoneal space → peritoneum → L5 emerge into LI lumen

4) LI lumen

5) eggs shed in feces

6) fecal culture + Baermann

7) 9 mo

8) no, susceptible to all 3

9) larvae migrating in liver + peritoneum → LIVER + peritoneum + gut wall lesions → non-specific signs (lethargy, diarrhea/constipation, wt loss, poor doer signs, etc)

Small strongyles:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• true strongyle (equine small strongyle/cyathostomes)

• strongyle type eggs

• short shallow buccal capsule

• copulatory bursa

2) L1-L3 in environ. → HORSE ingest free-living infective L3

3) ex-sheath → mucosal migration → emerge into LI lumen, hypobiosis possible as L3 submucosal cysts

4) LI lumen

5) eggs shed in feces

6) fecal culture + Baermann

7) 6-8 wks

8) resist most nicotinic agonists + benzimidazoles, susceptible to some MLs

9) plug-feeding adults → non-specific often subclinical signs (lethargy, diarrhea/constipation, wt loss, poor doer signs, etc), larval cyathostomiasis theoretically possible → potentially fatal

Oesophagostomum radiatum:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• true strongyle (cattle LI nodular worm)

• strongyle type egg

• copulatory bursa

2) L1-L3 in environ. → CATTLE ingest free-living infective L3

3) ex-sheath → L3 mucosal encystment in LI → emerge into LI lumen become adults, hypobiosis possible

4) LI lumen

5) eggs shed in feces

6) fecal culture + Baermann

7) 6-7 wks

8) no, susceptible to all 3

9)

• primary infxn relatively harmless → non-specific signs (lethargy, diarrhea/constipation, wt loss, poor doer signs, etc)

• re-infxn can be problematic → host immune system form NODULES around larvae in mucosa upon re-infxn → nodules caseate + calcify → nodules affect peristalsis + aborption → non-specific signs (lethargy, diarrhea, wt loss, poor doer signs, etc)

• nodules rupture (rare) → ulcerative colitis, peritonitis, death

Oesophagostomum columbianum:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• true strongyle (cattle LI nodular worm)

• strongyle type egg

• copulatory bursa

2) L1-L3 in environ. → CATTLE ingest free-living infective L3

3) ex-sheath → L3 mucosal encyst in nodules in LI → emerge into LI lumen become adults, hypobiosis possible

4) LI lumen

5) eggs shed in feces

6) fecal culture + Baermann

7) 6-7 wks

8) no, susceptible to all 3

9)

• primary infxn relatively harmless → non-specific signs (lethargy, diarrhea/constipation, wt loss, poor doer signs, etc)

• re-infxn can be problematic → host immune system form NODULES around larvae in mucosa upon re-infxn → nodules caseate + calcify → nodules affect peristalsis + aborption → non-specific signs (lethargy, diarrhea, wt loss, poor doer signs, etc)

• nodules rupture (rare) → ulcerative colitis, peritonitis, death

Chabertia ovina:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• true strongyle (sm rmt LI nodular worm)

• strongyle type egg

• large bell-shaped buccal capsule + 0 teeth

2) L1-L3 in environ. → SM RMT + sometimes cattle ingest free-living infective L3

3) ex-sheath → L3 mucosal encyst in nodules in LI → emerge into LI lumen become adults, hypobiosis possible

4) LI lumen

5) eggs shed in feces

6) fecal culture + Baermann

7) 6 wks

8) no, susceptible to all 3

9) usually non-specific poor doer signs but large #s of plug feeding adults can cause mucosal ulcerations

Oesophagostomum venulosum:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• true strongyle (sm rmt LI nodular worm)

• strongyle type egg

• copulatory bursa

2) L1-L3 in environ. → SM RMT ingest free-living infective L3

3) ex-sheath → L3 mucosal encystment in LI → emerge into LI lumen become adults, hypobiosis possible

4) LI lumen

5) eggs shed in feces

6) fecal culture + Baermann

7) 6-7 wks

8) no, susceptible to all 3

9)

• primary infxn relatively harmless → non-specific signs (lethargy, diarrhea/constipation, wt loss, poor doer signs, etc)

• re-infxn can be problematic → host immune system form NODULES around larvae in mucosa upon re-infxn → nodules caseate + calcify → nodules affect peristalsis + aborption → non-specific signs (lethargy, diarrhea, wt loss, poor doer signs, etc)

• nodules rupture (rare) → ulcerative colitis, peritonitis, death

Oesophagostomum dentatum:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• true strongyle (pig LI nodular worm)

• strongyle type egg

• copulatory bursa

2) L1-L3 in environ. → PIGS ingest free-living infective L3

3) ex-sheath → L3 mucosal encystment in LI → emerge into LI lumen become adults, hypobiosis possible

4) LI lumen

5) eggs shed in feces

6) fecal culture + Baermann

7) 6-7 wks

8) no, susceptible to all 3

9)

• primary infxn relatively harmless → non-specific signs (lethargy, diarrhea/constipation, wt loss, poor doer signs, etc)

• re-infxn can be problematic → host immune system form NODULES around larvae in mucosa upon re-infxn → nodules caseate + calcify → nodules affect peristalsis + aborption → non-specific signs (lethargy, diarrhea, wt loss, poor doer signs, etc)

• nodules rupture (rare) → ulcerative colitis, peritonitis, death

Stephanurus dentatus:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• true strongyle (swine kidney worm)

• strongyle type egg

• square buccal capsule

• bursa barely visible

• stout looking worm

2) L1-L3 in environ. → pig either:

• ingests free-living infective L3

• L3 penetrates host skin

• ingests L3 in paratenic host

3) ex-sheath → blood → liver → retroperitoneally to kidney wall + ureters

4) kidney + ureters

5) eggs shed in URINE

6) URINE culture + Baermann

7) 9-16 mo

8) no, susceptible to all 3

9)

• larvae migrating in liver ± skin if skin penetration infxn → LIVER lesions + skin lesions → non-specific signs (lethargy, diarrhea/constipation, wt loss, poor doer signs, etc) + sometimes death

• aberrant migrations relatively common → lesions in wherever they wandered off to

Trichostrongylus axei:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• trichostrongyle (cow + horse stomach hair worm)

• strongyle type egg

• copulatory bursa w/ stout spicules

• small/absent buccal capsule

• smallest rmt stomach worms

2) L1-L3 in environ. → CATTLE or HORSE ingest free-living infective L3

3) ex-sheath → L3 mucosal migration b/t gastric glands → L5 emerge into abomasum lumen become adults

4) abomasum lumen

5) shed in feces

6) fecal culture + Baermann

7) 3 wks?

8) no, susceptible to all 3

9)

• larval emergence → erosion of gastric gland epithelium but worse in horse

• similar nodular abomasal lesions like Ostertagia in rmt

• hyperemic gastritis in horse

Haemonchus placei:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• trichostrongyle

• strongyle type egg

• large copulatory bursa

• females have barber pole appearance

• small/absent buccal capsule

• largest of stomach worms

2) L1-L3 in environ. → CATTLE + sometimes sm rmt ingest free-living infective L3

3) ex-sheath

4) abomasum

5) eggs shed in feces

6) fecal culture + Baermann

7) 25-28 d

8) resistance

9)

Haemonchus contortus:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• trichostrongyle

• strongyle type egg

• large copulatory bursa

• females have barber pole appearance

• small/absent buccal capsule

• largest of stomach worms

2) L1-L3 in environ. → SM RMT + sometimes cattle ingest free-living infective L3

3) ex-sheath

4) abomasum

5) eggs shed in feces

6) fecal culture + Baermann

7) 15 d

8) resistance

9)

Ostertagia ostertagi:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• trichostrongyle

2)

3) ex-sheath

4) abomasum

5)

6)

7) 3 wks

8) no, susceptible to all 3

9)

Cooperia oncophora:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• trichostrongyle

2)

3) ex-sheath

4) abomasum

5)

6)

7)

8) no, susceptible to all 3

9)

Nematodirus spp:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• trichostrongyle

• large strongyle-type eggs w/ large + few cells in morula

2)

3) ex-sheath

4) abomasum

5)

6)

7)

8) no, susceptible to all 3

9)

Telodorsagia circumcinta:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• trichostrongyle

2)

3) ex-sheath

4) abomasum

5)

6)

7)

8) no, susceptible to all 3

9)

Trichostrongylus colubriformis:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• trichostrongyle

2)

3) ex-sheath

4) abomasum

5)

6)

7)

8) no, susceptible to all 3

9)

Hyostrongylus rubidus:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• trichostrongyle

2)

3) ex-sheath

4) abomasum

5)

6)

7) 20-25 d

8) no, susceptible to all 3

9)

Ollulanus tricuspis:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• trichostrongyle

2)

3) ex-sheath

4) abomasum

5)

6)

7)

8) no, susceptible to all 3

9)

10)

Syngamus trachea:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• direct life cycle (bird) lungworm

• oviparous + direct life cycle

• atypical strongyle eggs shaped like hybrid of Trichuris + Nematodirus = few, large cells in morula w/ bipolar opercula

• adults live in mated pairs copulating all the time → Y-shaped

• adults are bright red when fresh bc blood-suckers

2) L1-L3 inside egg in environ → bird eats infective L3 in egg OR free-living L3 OR L3 inside paratenic host (inverts)

3) ex-sheath L3 → GI mucosa → hepatic portal v. → liver → vena cava → heart → lungs

4) tracheal lumen

5) eggs in trachea coughed up + swallowed → non-embryonated eggs passed in feces

6) 17-20 d

7)

• adults in trachea → obstructive tracheitis → spasmodic dyspnea (gaping)

• larval migration → unproblematic, poss. hemorrhage, edema, pneumonia

8)

• gaping → presumptive dx

• detect atypical strongyle eggs in fecal float

• detect adults in trachea surrounded by bloody mucus @ necropsy

9)

• big 3 work

• raise birds indoors

• keep turkeys + chickens separate

Filaroides osleri:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• direct life cycle (dog) lung worm

• ovoviviparous + direct life cycle lungworm

• adult males have spicules + papillae instead of bursa

• L1 tail short + S-shaped (kinked)

• egg contains fully-developed L1

2) dog ingests egg w/ L1 → L1 hatches inside host, auto-infxn + hyper-infxn possible

3) ex-sheath L1 in GI → blood/lymph → heart → lungs

4) sub-mucosal nodules in trachea + bronchi (tracheal bifurcation) = pathognomonic for F. osleri

5) eggs in lungs coughed up + swallowed → infective egg w/ L1 in feces/saliva/vomit

6) idk

7) adults in nodules → obstructive dyspnea + resp. signs → verminous nodular bronchitis (mainly in puppies)

8) fresh feces/saliva + Baermann + ID L1

9)

• big 3 should work (extra-label)

• prednisone to reduce inflammation

• prevent dogs from ingesting excretions from wild canids, difficult to prevent transmission from mom to pups

Filaroides hirthi:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• direct life cycle (dog) lung worm

• ovoviviparous + direct life cycle lungworm

• adult males have spicules + papillae instead of bursa

• L1 tail short + S-shaped (kinked)

• egg contains fully-developed L1

2) dog ingests egg w/ L1 → L1 hatches inside host, auto-infxn + hyper-infxn possible

3) ex-sheath L1 in GI → blood/lymph → heart → lungs

4) bronchioles + alveoli

5) eggs in lungs coughed up + swallowed → infective egg w/ L1 in feces/saliva/vomit

6) 4-5 wks

7) eggs w/ L1 in bronchioles + alveoli → granulomatous pneumonia (canine verminous pneumonia) mainly in puppies but usually asymptomatic

8) fresh feces/saliva + Baermann + ID L1

9)

• big 3 should work (extra-label)

• prednisone to reduce inflammation

• prevent dogs from ingesting excretions from wild canids, difficult to prevent transmission from mom to pups

Filaroides milksi:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• direct life cycle (dog) lung worm

• ovoviviparous + direct life cycle lungworm

• adult males have spicules + papillae instead of bursa

• L1 tail short + S-shaped (kinked)

• egg contains fully-developed L1

2) dog ingests egg w/ L1 → L1 hatches inside host, auto-infxn + hyper-infxn possible

3) ex-sheath L1 in GI → blood/lymph → heart → lungs

4) bronchioles + alveoli

5) eggs in lungs coughed up + swallowed → infective egg w/ L1 in feces/saliva/vomit

6) 4-5 wks

7) eggs w/ L1 in bronchioles + alveoli → granulomatous pneumonia (canine verminous pneumonia) mainly in puppies but usually asymptomatic

8) fresh feces/saliva + Baermann + ID L1

9)

• big 3 should work (extra-label)

• prednisone to reduce inflammation

• prevent dogs from ingesting excretions from wild canids, difficult to prevent transmission from mom to pups

Dictyocaulus viviparous:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• direct life cycle (bovine) lung worm

• ovoviviparous + direct life cycle

• tiny bursa

• L1 brown food granules + tail w/ blunt transparent projection

• infxn most common Sept-Oct in MW

• can overwinter on pasture

2) L1-L3 in environment → L3 helped disperse via fecal pat + Pilobolus sporangia cumshot → L3 ingested by bovid

3) ex-sheath L3 in GI → blood/lymph → heart → lungs

4) bronchi + bronchioles

5) eggs hatch in lungs → L1 coughed up + swallowed → L1 in feces

6) 4-10 wks

7) adults in bronchi + bronchioles → emphysema, consolidation of lobules → dyspnea, husky cough, other resp. signs, bronchitis, wt loss, secondary infxn → death or adult lung worms expelled → incomplete recovery (chronic impaired pulmonary fxn) or full recovery providing good immunity

8)

• fresh feces + Baermann + ID L1

• ID worms in airways at necropsy

9)

• big 3 should work ± efficacy against larvae

• natural infxn prod. good immunity

• EU has vax

Dictyocaulus filaria:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• direct life cycle (sm rmt) lung worm

• ovoviviparous + direct life cycle

• tiny bursa

• L1 toilet plunger head + brown food granules + tail w/ blunt transparent projection

• infxn most common Sept-Oct in MW

• can overwinter on pasture

2) L1-L3 in environment → L3 helped disperse via fecal pat + Pilobolus sporangia cumshot → L3 ingested by sm rmt

3) ex-sheath L3 in GI → blood/lymph → heart → lungs

4) bronchi + bronchioles

5) eggs hatch in lungs → L1 coughed up + swallowed → L1 in feces

6) 4-6 wks in goats + 8 wks in sheep

7) adults in bronchi + bronchioles → emphysema, consolidation of lobules → dyspnea, husky cough, other resp. signs, bronchitis, wt loss, secondary infxn → death or adult lung worms expelled → incomplete recovery (chronic impaired pulmonary fxn) or full recovery

8)

• fresh feces + Baermann + ID L1

• ID worms in airways at necropsy

9)

• big 3 should work ± efficacy against larvae

• natural infxn prod. good immunity

• EU has vax

Dictyocaulus arnfieldi:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• direct life cycle (horse) lung worm

• ovoviviparous + direct life cycle

• tiny bursa

• L1 brown food granules + tail w/ blunt transparent projection

• infxn most common Sept-Oct in MW

• can overwinter on pasture

2) L1-L3 in environment → L3 helped disperse via fecal pat + Pilobolus sporangia cumshot → L3 ingested by donkey/horse

3) ex-sheath L3 in GI → blood/lymph → heart → lungs

4) bronchi + bronchioles

5) eggs coughed up + swallowed → eggs hatch in GI → L1 in feces

6) 4-5 wks but infxn often not patent

7) adults in bronchi → usually asymptomatic, more pathogenic in horses, adult lung worms expelled, poss. dry cough + secondary infxns

8)

• fresh feces + Baermann + ID L1

• ID worms in airways at necropsy

9) big 3 should work + keep horses/donkeys separate

Why do Dictyocaulus spp. larvae have brown food granules?

L1-L3 in environment don’t feed → rely on stored food granules in GI tract

Protostrongylus spp:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• indirect life cycle (sm rmt) lung worm

• ovoviviparous + indirect life cycle req. gastropod IH

• L1 long tapered tail

2) L1 infect IH → L1-L3 in IH → L3 in IH ingested by sm rmt definitive host

3) ex-sheath L3 in GI → blood/lymph → heart → lungs

4) bronchioles + alveoli

5) eggs hatch in lungs → L1 coughed up + swallowed → L1 in feces

6) 4 wks

7) adults in bronchioles + alveoli → inflammation + epithelial desquamation (sloughing) of bronchioles + alveoli → mostly sub-clinical poor doer signs, can have lobular pneumonia (conical + yellow-gray), fibrinous pleuritis

8) fresh feces + Baermann + ID L1 long tapered tail

9) big 3 should work (extra-label)

Muellerius spp:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• indirect life cycle lung worms (sm rmt hair lung worm)

• ovoviviparous + indirect life cycle req. gastropod IH

• adults tiny + white (can’t see grossly)

• males have spiral tail

• L1 tail w/ undulating tip + dorsal spine

2) L1 infect IH → L1-L3 in IH → L3 in IH ingested by sm rmt definitive host

3) ex-sheath L3 in GI → blood/lymph → heart → lungs

4) alveoli w/i granulomatous nodules

5) eggs hatch in lungs → L1 coughed up + swallowed → L1 in feces

6) 4-6 wks

7) adults + eggs + L1 in alveoli → sub-pleural gray-green granulomatous nodules (old nodules are calcified) → mostly asymptomatic, resp. signs, pneumonia, fibrinous pleuritis, secondary infxns

8)

• fresh feces + Baermann + ID L1 long tapered tail

• sub-pleural gray-green granulomatous nodules at necropsy

9) big 3 should work (extra-label)

Metastrongylus spp:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• indirect life cycle lung worm (swine lung worm)

• ovoviviparous + indirect life cycle req. earthworm IH

• adults have 6 lips + long-lived

• small bursa

• colorless egg w/ thick lumpy shell containing L1

• eggs + larvae v hardy, resistant to environmental extremes

• worldwide distribution but uncommon in US

2) L1 infect EARTHWORM IH → L1-L3 in IH → L3 in IH ingested by pig

3) ex-sheath L3 in GI → blood/lymph → heart → lungs

4) bronchioles

5) eggs in lungs → coughed up + swallowed → EGG w/ L1 in feces

6) 3-4 wks

7)

• larvae in lungs + adults in bronchioles → petechial hemorrhage + bronchiolar obstruction → verminous pneumonia + emphysema, non-specific poor-doer signs w/ husky cough, secondary infxns

• not as pathogenic as rmt lung worms

8)

• fresh feces + fecal FLOAT + ID egg w/ L1 → false negatives occur

• adults grossly visible at necropsy

9) big 3 should work + good sanitation + keep pigs indoors to prevent exposure to earthworms and feces

Aelurostrongylus abstrusus:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• indirect life cycle lungworm (cat lungworm)

• ovoviviparous + indirect life cycle req. gastropod IH

• adults are lil guys

• L1 have kinked tail w/ dorsal spine

• rare in MW

2) L1 infect IH → L1-L3 in IH → L3 in IH ingested by definitive host (cat/raccoon) or paratenic host that is then ingested by definitive host

3) ex-sheath L3 in GI → blood/lymph → heart → lungs

4) sub-pleural nodules in lung parenchyma

5) eggs hatch in lungs → L1 coughed up + swallowed → L1 in feces

6) not given but Dr. Google says 6 wks

7) adults in gray-white nodules in lungs → resp. signs + feline verminous pneumonia

8)

• fresh feces + Baermann + ID L1

• tracheal wash + ID L1 in sputum

9)

• MLs + benzimidazoles should work (extra-label)

• might resolve w/o tx

Crenosoma vulpis:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• indirect life cycle lungworm (fox + dog bronchiole worm)

• oviparous + indirect life cycle req. gastropod IH

• adults are smol + have notched/scalloped body

• L1 don’t have kinked tail unlike Filaroides + Aleurostrongylus

2) L1 infect IH → L1-L3 in IH → L3 in IH ingested by definitive host (fox/dog) or paratenic host that is then ingested by definitive host

3) ex-sheath L3 in GI → blood/lymph → heart → lungs

4) bronchi + bronchioles

5) eggs hatch in lungs → L1 coughed up + swallowed → L1 in feces

6) 19 d

7) adults in lungs → resp. signs + diffuse bronchointerstitial pattern in lung xray

8)

• fresh feces + Baermann/zinc sulfate flotation + ID L1

• tracheal wash + ID L1 in sputum

9) big 3 should work (extra-label) ± prednisone to control resp. inflammation

Most lung worms infxns are detected by identifying L1 in fresh feces. Which cannot be detected this way?

• Syngamus trachea → fecal float + ID atypical strongyle egg

• Metastrongylus spp. → fecal float + ID egg w/ L1

tl;dr “French heartworm” and why do we care?

• Angiostrongylus vasorum

• Metastrongyle but not a lung worm

• ovoviviparous + indirect life cycle req. gastropod IH

• definitive host is dogs

• larvae infects IH → dog ingests IH w/ larvae → larvae undergo blood-lung migration

• adults live in pulmonary aa. + R heart → eggs hatch in lungs → new larvae undergo tracheal migration → larvae shed in feces → infect IH

• important bc formerly an EU problem but has now been reported in Canada

tl;dr rat blood worm and why do we care?

• Angiostrongylus cantonensis

• Metastrongyle

• definitive host is rats

• important bc parasite has spread to US + causes encephalitis in humans

Parelaphostrongylus tenuis:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• meningeal worm

• oviparous + indirect life cycle req. gastropod IH

• strongyle type egg (don’t need to ID)

• long red-colored adults

• L1 tail has dorsal spine

• prevalent in east half of US (where WTD are)

2) L1 infect IH → L1-L3 in IH → natural definitive host WTD eat IH but important accidental host is camelids

3) L3 in GI → GI mucosa → peritoneal cavity → follow spinal n. to dorsal horn gray matter → develop into L4 → migrate up vertebral canal cranially in subdural space → cranium

4) remain in subdural space or invade cranial venous sinuses

5) eggs deposited in blood → heart → lungs → hatch → L1 coughed up + swallowed → L1 passed in feces

6) 90-135 d in WTD (long)

7)

• asymptomatic in WTD

• larval migration in accidental hosts (aka camelid) dmg spinal cord → CNS deficits → often incapacitated before parasite can complete life cycle d/t neurological disease

8)

• fresh feces + Baermann + ID L1 in WTD

• hx + signalment + CNS signs in camelid to presumptively dx

• find worms in CNS at necropsy

9) anthelmintics don’t work bc can’t penetrate CNS → can only do supportive care + physical therapy

Ancylostoma caninum:

1) Brewer’s taxa? Parity? Life cycle type? Identifying physical characteristics? Prevalence/distribution if relevant?

2) Who is the definitive host? How does it enter the body?

3) Is there migration in the host? Hypobiosis?

4) Where do adults live?

5) How does it exit the body?

6) Pre-patent period?

7) What lesions/pathologies does it cause + how?

8) How to definitively dx or presumptively dx?

9) Tx options + strategies?

1)

• dog hookworm

• oviparous + direct life cycle

• strongyle type eggs

• hooked front end

• 3 pairs of teeth at entrance of big buccal cavity

• adults usually firmly attached to SI mucosa

• big bursa

2) L1 to infective L3 in environment → penetrate skin (most common in adult dogs) or ingested/lactogenic transmission (puppies)

3) migration depends on route of infxn:

• Percutaneous → L3 ex-sheath enter blood/lymph → heart → lungs → tracheal OR somatic migration

  • Tracheal: L3 in alveoli → trachea → coughed up + swallowed → SI

  • Somatic: L3 in alveoli → blood → muscles → HYPOBIOSIS → leak continuously/activated in big wave → migration to SI or mammary glands in lactating dams

• Ingestion/Lactogenic transmission → L3 ex-sheath enter GI mucosa → mucosal OR somatic migration:

  • Mucosal: L3 in GI mucosa → SI

  • Somatic: L3 in GI mucosa → blood → muscles → HYPOBIOSIS → leak continuously/activated in big wave → migration to SI or mammary glands in lactating dams

4) SI lumen

5) eggs in feces

6) 2-3 wks

7)

• migrating larvae → skin rash + petechial lung hemorrhage → dermatitis, respiratory signs + pneumonia

• blood-sucking adults + late-stage larvae → multifocal hemorrhagic enteritis → ANEMIC puppy + melena d/t bleeding sites in SI, non-specific poor doer signs, varies from fatal to asymptomatic:

  • peracute neonatal ancylostomiasis = late-stage cause sick neonatal puppy BEFORE eggs in feces detectable

  • acute ancylostomiasis = older pup gets large #s of L3 in short period of time but eggs in feces detectable

  • chronic (compensated) ancylostomiasis = asymptomatic mature dog w/ low # worms

  • secondary (decompensated) ancylostomiasis = malnourished mature dog req. less worms to have worse dz

8)

• anemic puppy = hookworms

• strongyle type eggs in SA feces = prob hookworms

• grossly visible adults in SI at necropsy

9)

• big 3 work on adults but NOT on hypobiotic larvae, strains popping up w/ emerging resistance

• tx puppies + mom every 2 wks from 2-8 wks

All of the lung worms are infective at L3 EXCEPT for?

Filaroides infective at L1