Ruminant Lungworms

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http://veterinarydiseases.blogspot.com/

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Dictyocaulus removed from the airways of a calf. Worms are large with females 6-8 cm and males 4-5 cm. L1 are passed in feces that have characteristic glycogen granules. Diagnosis is by Baermann sedimentation or sugar flotation.

Site and ID:

Dictyocaulus viviparous in large airways of a calf. Sheep and goats have D. filariae

Optimum Development•Direct life cycle. Prepatent period 25 days.

•Occurs sporadically in high rainfall, wet pasture conditions of winter and spring in the south, summer in the north

•L1-L3 stages are fragile (no sheath), non-feeding and very susceptible to heat and drought

•Lungworms oversummer in hosts (adults, +/- hypobioticL5) and overwinter as larvae on pasture or adults in hosts

•Major Problems Occur: In animals with no immunity, young age and large L3 exposure in winter-spring on crowded, wet pastures contaminated by older carrier cattle. Strong immunity develops in 1st exposure year.

Yearling calf with “anoxic syndrome” in the prepatent

(7-25 day) period. Due to migration phase of larvae in lungs after massive pasture exposure to lungworm L3

Dyspnea, anoxia and fever with open mouth breathing, grunting, frothing, tongue out

Pathogenesis of Dictyocaulus•Penetration: Clinical signs do not occur 1-7 days after infection. Larvae cause minor eosinophilic, granulomatous inflammation in lymph node and lung during early migration

•Prepatent: ‘Anoxic syndrome’ occurs in the third week, during the prepatent period after heavy exposure. Larvae cause bronchial pneumonia with eosinophilic exudate that blocks small airways, leading to atelectasis, edema, emphysema and secondary bacterial infection with some fatalities. Synergy with Pasteurella and a role in the bovine respiratory disease complex have been attributed to lungworms

•Patent: Patency occurs at 25-55 days. Adult worms cause frothy, mucopurulant exudate with cough, anorhexia, reduced weight gain.Granulomatous consolidation, especially the diaphragmatic and cardiac lobes, occurs with proliferation of the bronchial epithelium, increased macrophages, giant cells and eosinophils

•Recovery: Occurs at 55-70 days. Worms ‘self-cure’ due to immune response and clinical signs decrease. Some become ‘respiratory cripples’or die 7-8 weeks after infection due to alveolar epithelization.

Grossly visible pulmonary emphysema and atelectasis associated with bovine lungworms

Pulmonary emphysema, bovine lungworms

Emphysema occurs with ‘one way valve’ partial obstruction of airways, atelectasis is associated with complete airway obstruction.

Patent phase lesions:Lung lobe showing severe interstitial edema and inflammation. Lesions and worms are concentrated in the diaphragmatic and cardiac lobes. Note the frothy, mucopurulentexudate with adult lungworms in the airways.

Eosinophilic granulomatous inflammation characterizes

the response to lungworms

Histopathological Lesions

In some animals inflammation

eventually progresses to

alveolar epithelialization and death at 7-8 weeks

Carriers are important. Immune older animals shedding low numbers of larvae are a source of pasture contamination for young, non-immune stock. Lungworm losses occur sporadically in the US. In cool, wet climates in Europe lungworms can cause major problems (eg ‘husk’ in Scotland), where an irradiated L3 larvae vaccine was developed.

Sheep and goats (D. filariae) have a similar pattern of disease as cattle, but are more prone to chronic respiratory bacterial infections. Initial cough, nasal discharge are often concurrent with heavy GI nematode infections.

Muellerius - alveolar level “blister lesions” of this sheep and goat protostrongylid lungworm is transmitted by land snail intermediate hosts. Prepatent period is 5-7 weeks

Small, nodular eosinophilic, granulomatouslesions occur at the terminal bronchiolar and alveolar level. Muellerius is very common in goats.

Notched tail of Muellerius L1 from a goat. Dictyocaulus L1 have a ‘straight’tail and prominent glycogen granules

Protostrongylus is a related lungworm that resides more toward the terminal bronchioles, with larger infarct-like lesions on the serosal surface. Not considered to be clinically important.