Ruminant Lungworms Flashcards
Lungworms of large animals
two superfamilies: trichostrongyloidea and metastrongyloidea
Trichostrongyloidea
direct life cycle
dictyocaulus species- unusual in that it lives in the lungs (i.e. other trichostrongylids live in GI tract)
Cause parasitic bronchitis (husk)- mostly in dairy cattle
HIGHLY pathogenic
Metastrongyloidea
indirect life cycle with IMHs
Metastrongylus species in pigs (earthworm IMH)
Muellerius capillaris in sheep/goats (mollusc IMH)
Protostrongylus rufescens in sheep/goats (snail intermediate host)
NON pathogenic
Trichostrongyloidea lungworms
**Ditcyocaulus viviparus- cattle
dictyocaulus arnfieldi- horse and donkeys
Dictyocaulus filaria- sheep and goats
Dictyocaulus eckerti- deer and other cervids–nb: deer can be carriers of dictyocaulus viviparus
Life cycle of Dictyocaulus viviparus
Direct life cycle
Adult worms in mainstem of bronchi/trachea (live for 1-2 months or so)–> produce eggs which hatch in lungs–> L1 migrate up trachea and get swallowed–> L1 in feces (different from GI nematodes because they hatch internally)–> L2–>L3–>L3 is infective; gets ingested and penetrates intestinal mucosa–>moults to L4 in mesenteric lymph nodes–>lymphovascular route to lungs–>enter into alveoli–> young adults in bronchioles and small bronchi
nb: pilobolus fungus aids in dispersal of L3s- can get this fungus on fecal pats–> larvae move up to fungus–> get explosion of spores which carry/spreads larvae
Appearance of dictyocaulus viviparus (various life stages)
L1 larvae: 400-450 microns in length, 25 microns in width
L1 larvae present in feces, NOT eggs
Adults: up to 8cm in length and slender- threadlike, creamy appearance
Immunity to d. viviparus
Strong immunity follow infection, but immune response itself can cause pathology–> Ig and eosinophils produced–> happening in lungs, therefore lung damage
Cf. GI nematodes: takes 1-2 years for a strong IR
Immunity is boosted by natural challenge– immunity lasts for ~6 months and wanes if unchallenged.
NB: there is a vaccine for dictyocaulus
Clinical signs of parasitic bronchitis
Mildly affected animals (~100 worms): intermittent cough- with an increase in coughing after exercise
Moderately affected animals: coughing at rest, tachypnoe (>60), hyperpnea (crackles in posterior lung lobe)
Severly affected animals (1000 worms approx): harsh cough, tachypnea (>80), dysnpea, mouth breathing (air hunger)
Pyrexia due to secondary bacterial infection, emphysema
Pathogenesis of Parasitic bronchitis
penetration phase: d1-7: larvae migrating to lungs (no pathology)
prepatent phase: days 8-25: larvae migrating up through lungs- start to see clinical signs
Patent phase: days 26-60: mature adults in airways–> cause response in lung tissue
Postpatent phase: days 61-90: adults expelled from airways (recovery)
Prepatent phase: days 8-25
L4 and young adults migrating up respiratory tree
Acute inflammatory response (monocytes and eosinphils)
Mucus/cellular plugs produced by lung tissue–> collapse of alveoli
First clinical signs seen
Heavy infection: calves can die from day 15 onwards
Patent phase: days 26-60
Clinical signs worsen
lesions due to presence of worms in bronchi: Profuse inflammatory exudate; hyperplasia of bronchial epithelium; overinflation of alveoli ; interstitial emphysema and oedema; eosinophilia
lesions due to aspirated eggs/larve: granulomatous response to aspirated eggs.
Post-patent phase: days 61-90
expulsion of worms due to IR
Most animals: gradual recovery and strong acquired immunity
Some animals (up to 25%): clinical signs increase–> often fatal
due to either “alveolar epithelialisation” or bacterial infection (acute interstitial pneumonia)
Reinfection syndrome
heavy challenge in immune (previously infected or vaccinated)
IR kills larvae in lungs
Mild syndrome: coughing and slight tachypnea
Diagnosis: clinical signs, history and response to tx
Not a patent infection- no L1s, not normally fatal.
Diagnosis of parasitic bronchitis
Clinical signs, time of year
Grazing/vax/anthelmintic history
L1 larvae present in feces (50-1000 L1/g, baermann technique)– not present during pre-patent phase
Bronchoalveolar lavage, eosinophilia
ELISA: detects AB to adult and L3 antigens; reflects exposure to infection
Epidemiology of bovine lungworm
temperate regions with high rainfall
In UK, disease usually july-sept/oct
L3 can overwinter on pasture
carrier animals are important
small number of L3s cause infection
small numbers of worms sufficient to cause disease (100-1000)
Development L1-L3 rapid in optimal conditions (warm and wet, ~7 days)
Traditionally disease of 1st season grazing calves, now common in adults
Changing age distribution of parasitic bronchitis
recently, disease more common in adult cattle
- no previous history of lungworm or vax
- anthelmintic usage in 1st and 2nd years so no immunity
susceptible to heavy challenge
also, stocking densities have increased with an increase in intensive farming.
Prevention of bovine lungworm
vax with irradiated L3 vax (2 doses of 1000 irradiated L3s 4 weeks apart)
vax 1st season calves before turnout
oral vax: very effeceitve but not sterile immunity (therefore don’t mix with unvax animals)
immunity boosted by infection
Treatment of bovine lungworm
anthelmintic drugs (use early to reduce pathology)
mildly infected animals: treat and move to clean pasture
severely affected: house, hydrate, NSAIDS to damp down IR, abx if pyrexic
Anthelmintics may exacerbate clinical signs in severly affected animals d/t parasite death. Use levamazole with heavy infection because it just paralyzes the worms, rather than killing them and releasing antigen (like BZ)
Dictyocaulus arnfieldi
donkeys and horses
life cycle similar to D. viviparus except EGGS (not L1s) in feces
PPP=2-4 months
reaches patentcy in donkeys and foals/yearlings in horse
does NOT reach patentcy in adult horses.
Ubiquitous in donkeys–true definitive host (usually no clinical signs)
Diagnosis of D. arnfieldi
Donkey: eggs or L1s in feces; close exam (harsh lung sounds)
Horse: usually no eggs or L1s; clinical signs (chronic cough or tachypnea); grazing/anthelmintic histroy (i.e. co grazing with donkeys)
Response to anthelmintic tx
Tracheal wash- eosinophilia to confirm infection
Dictyocaulus filaria
Host: Sheep and Goats
Area: seen more in warmer climates but sporadic UK cases
PPP: 5 weeks
Causes sporadic disease- usually in lambs/yearlings in autumn
Milder clinical signs than d. viviparus: chronic cough/unthriftiness; nasal discharge; dysnpea in severe cases
Diagnosis: L1 in feces
Treat flock, move to clean pasture
Metastrongyloid lungworms
Pig: metastrongylus apri, M. salmi, M. pudendotectus
pig IMH: earthworm
Sheep/Goats: muellerius capillaris (IMH mollusc) and protostrongylus rufescens (snail IMH)
none are particularly pathogenic
Life cycle of Metastrongylus spp. in pigs
Ubiquitous
Adults in small bronchi and bronchioles–> eggs produced in feces–> L1 ingested by earthworm–> moult to L2, then L3 in IMH–> earthworms ingested by pigs–> L3 penetrate intestinal mucosa–> L4 in LN–>lymphovascular route to lungs, come out of capillaries into alveoli–> adults
PPP=4 weeks
nb: earthworms can remain infected for a very long time
Metastrongylus species, appearance, clinical signs and diagnosis
Slender white worms, adutls 6cm long
Clinical signs: mostly light and asymptomatic
Heavy infections: coughing, dyspnea, nasal discharge
Most prevalent in pigs 6-8 months old- infection depends on access to earthworms
Diagnosis: eggs in feces (MgSO4 flotation)
Muellerius capillaris
Sheep and goats, but goats more affected
Widespread and common
Brown “hair-like” worms found in alveoli
IMH= molluscs
NOT pathogenic
cause lead shot lesions in lungs
Diagnosis: L1 in feces (smaller than D. filaria, with a dorsal tail spine)
Protostrongylus rufescens
Sheep and goats
less common than muellerius
adults in bronchioles: red 4-6cm
NOT pathogenic
IMH= snails
Lung lesions larger than M. capillaris
heaviest infection in ADULT sheep and goats (as for M. capillaris)
