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PARASITOS Y ENFERMEDADES PARASITARIAS
DE LOS ANIMALES DOMESTICOS


Dictyocaulus viviparus

Pathogenesis

Severe pathological changes can occur before patency due to larvae and immature adults migrating through the alveoli, bronchioles and bronchi and inducing an inflammatory response. Bronchiolar passages become clogged with inflammatory cells, including eosinophils, macrophages and neutrophils and if severe enough may result in collapse of alveoli distal to these cellular infiltrates because air cannot pass through these plugs. Air present in the alveoli is absorbed into the blood and the alveoli collapse because new air cannot pass the eosinophilic plug.  The severity of these lesions is directly related to the degree of infection such that heavy infections may lead to interstitial emphysema and pulmonary edema that is often fatal.

Patent disease is associated with adult worms in the bronchi and manifests as a bronchitis with a mucus exudate followed by pneumonia due to aspiration of eggs and L1's into the alveoli where they are surrounded by inflammatory cells, including macrophages and giant cells, and ingested. The bronchial epithelium is infiltrated by inflammatory cells and becomes hyperplastic.   Heavy infections may progress to emphysema and edema.

In lightly infected animals, recovery will occur following expulsion of the adult worm population. In moderate to heavy infections, the bronchial lesions may take several weeks or months to recover. However, during this recovery phase a small number of animals may succumb to a postpatent parasitic bronchitis or a secondary bacterial pneumonia.

The etiology of the syndrome, postpatent parasitic bronchitis, is unknown but is due to a proliferation of alveolar epithelial cells converting the thin, permeable alveolar epithelium into a thickened layer of cells that is much less permeable to the passage of oxygen and carbon dioxide, thereby compromising gaseous exchange at the alveolar surfaces. Interstitial emphysema and pulmonary edema are common complications of this syndrome and when this stage is reached, death is almost certain.

Pulmonary edema results from the onset of cardiac failure in animals with dyspnea. Alveoli fill with transuded fluid and the alveolar walls become lined with  protein "hyaline membranes" as water in the transuded fluid evaporates or is reaborbed. These membranes further compromise gas exchange at the alveolar epithelial surfaces and lead to a significant deterioration in clinical condition.

Images showing the development of parasitic bronchitis in cattle due to Dictyocaulus viviparus Dictyocaulus viviparus
(Images courtesy of Professor Max Murray, Glasgow University Veterinary School)

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1. Larva migrating up a bronchus.

2. Eosinophilic plug in a small bronchiole and collapse of surrounding alveoli.

3. Adults in a bronchus with exudation and intense cellular infiltration surrounding the bronchus.

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4. Adult worms in the   diaphragmatic bronchi.

5. Distribution of lung worm lesions in the diaphragmatic lobes. 6. Parasitic pneumonia with giant cells and macrophages engulfing aspirated eggs and newly hatched larvae

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7. High power - parasitic pneumonia with giant cells and macrophages engulfing aspirated eggs and newly hatched larvae 8. Post patent parasitic bronchitis
- diffuse epithelialization (swelling and proliferation of type II pneumocytes). Many macrophages are present in the lumen of these epithelialized alveoli
9. Reinfection lesion - dead worm surrounded by an eosinophilic necrotic area and proliferating lymphoid tissue.

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10. Gross picture of emphysema 11. Microscopic picture of emphysema 12. Pulmonary edema

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13. Hyaline membranes lining
the alveolar surfaces


    

 

Parásitos y enfermedades parasitarias de los animales domésticos
Dr. Colin Johnstone (autor principal)
Derechos de copia © Universidad de Pennsylvania