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