lungworm Flashcards
What are key factors in the epidemiology of Dictoycaulus viviparus?
- Female worms in cow’s lungs produce eggs containing fully developed larvae
- Eggs hatch in bronchi, and are transported up the windpipe, swallowed & excreted in faeces
- Infective larvae can remain viable in soil as well as on pasture over winter
- When ingest, infective larvae migrate to lungs provoking a strong, but short-lived immune response
- Adult lungworm live in the trachea causing parasitic bronchitis (husk)
- Deposition of newly hatched eggs/larvae may lead to parasitic pneumonia
What are important trends in the epidemiology of Dictyocaulus Viviparus?
- Prefers wetter climate (west coast)
- Sensitive to dehydration (2-3 weeks)
- Unpredictable epidemiology
- Failure to develop immunity in dairy cows (reduced vaccine use/increased reliance of antithelmics)
What are key factors in the epidemiology/life cycle of angiostrongylus vasorum (canine lungworm)?
- Live in pulmonary artery & occasionally right ventricle of dogs
- Foxes act as a reservoir of infection in the UK
- Intermediate host required for maturation of L1 larvae that have been excreted in the faeces of the definitive host
- Canines become infected by ingestion of L3 larvae, by eating the IH
- Following ingestion, L3 crosses intestine wall, enters abdominal lymph nodes & develops to L5
- L5 migrate toward the right side of the heart, through hepatic portal vein, caudal vena cava & liver
- Eggs intermittently released, transported through pulmonary vasculature to capillaries where they hatch
- The L1 larvae cross the capillary/alveolar walls to enter the alveoli, are subsequently coughed up, swallowed & excreted.
What is the life cycle of dicotycaulus viviparus?
- Already hatched L1 passed out in faeces contaminating pasture
- Under the right climate conditions, the larvae will develop to infectivity (l1 to L3) in as little as 1 week
- L3 survival stage on pasture
- Ingestion of infective L3 by cow
Inside the host :
- L3 penetrate the intestinal wall and migrate via the lymphatic and vascular system to the lungs in about 7 days
- Here they mature into adults
- Females lay eggs that hatch in the bronchi, and larvae and transported up the windpipe and swallowed to repeat the cycle
Why do we see such a variation in the immune response to Angiostronglyus vasorum compared to D. viviparus although both are lungworms?
- Adult antigens cause Type III hypersensitivity (immune complex deposition in many tissues), Complement activation & Immune infiltration in lungs & many tissues
- Egg deposition causes pulmonary inflammation/granuloma and pulmonary arteriolar vasoconstriction
How does the variation in immune response reflect in the clinical signs of angiostrongylus vasorum in dogs compared to d. viviparus in cattle?
Pulmonary artery obstruction, endarteritis and thrombosis occur, as well as parenchymal damage to various organs due to larvae migration. Fibrosis and induration of lungs and occlusion of the pulmonary arteries can cause pulmonary hypertension and right-sided cardiac failure, resulting in hydrothorax hydropericardium, liver congestion and ascites.
Disseminated intravascular coagulation can occur. Immune-mediated thrombocytopenia, and/or factor deficiency are less commonly described following infection, all of which result in a predisposition to, or spontaneously occurring haemorrhage. Embolic larvae to other organs, especially kidney and brain results in granulomatous haemorrhagic or infarcted foci.
How do eosinophils respond to lungworm infection?
Release cytokines or chemokines associated with induction of eosinophil-mediated tissue inflammation.
What factors induce migration of eosinophils into lung tissue?
Various infections, drugs, parasites, autoimmune processes, malignancies, and obstructive lung diseases have been associated with increased eosinophils in the lungs.
What do eosinophils do in lung tissue?
These eosinophils release harmful chemicals and proteins that can damage the tissues in the lungs.
