Pathogenesis
Etiology
- Dirofilaria immitis, large nematode parasite usually located in pulmonary arteries
.
Predisposing factors
General
- Infection common where parasite is endemic and if patients are not receiving chemoprophylactics.
- Travel to endemic areas (eg for vacation) without chemoprophylaxis.
Pathophysiology
- Clinical disease depends on:
- Number of worms present.
- Reactivity of the dog to the filarial and wolbachial antigens.
- Size of dog.
- Activity of dog.
- Number of dead worms present.
Artheriopathy
- After migration into the pulmonary vasculature, filariae causes mechanical damage to walls of pulmonary arteries.
- Vascular immune reaction is stimulated by either verminous antigens or wolbachial antigens.
- Endothelial cells are separated and appear inflamed. WBCs accumulate and intima thickens.
- Endothelium grows villous-like structures made of smooth muscle and intima
.
- Heartworms cause lining of heart and pulmonary arteries to become rough and disrupt blood flow.
Pulmonary hypertension Pulmonary Arterial Hypertension (PHT)
- Increase of peripheral resistance of pulmonary arteries occurs due to intimal and medial proliferative pathology.
- Usually mild or moderate in most cases. Cases with right-sided CHF often have severe pulmonary hypertension.
- Can also be caused by:
- Vasoconstriction which can be due to inflammatory reaction, attempts to compensate local hypoxia, reduction of modulation of smooth muscle tone caused by parasite metabolites.
- Anatomical obstruction of vessels by reduction of arterial lumen due to villous proliferations, emboli caused by live or dead parasites or even microfilariae, secondary thrombi due to endothelial damage and parasite tissue.
Cardiac lesions
- Pulmonary hypertension initially induces dilation of right ventricle with a compensatory hypertrophy of the myocardium.
- Right-sided congestive heart failure in severe cases.
- Presence of parasite inside heart can trigger mechanical valvular damage resulting in tricuspid regurgitation.
Caval syndrome Caval Syndrome
- Caused by massive infections of worms obstructing right ventricle or vena cava, causing intravascular hemolysis, right-sided congestive heart failure and death.
- Tricuspid valve insufficiency due to mechanical interference by worms.
Lesions in the pulmonary parenchyma
- Increased vascular permeability expands inflammatory reaction to alveolar or interstitial perivascular tissue.
- Vascular and perivascular inflammatory reaction is amplified during adulticide treatment.
- Epithelial cells type I affected with a consequent fibrosis and reduction of exchange of gases and capillary fragility.
Shock
- Experimental inoculation of extracts of adult parasites induce a grave shock apparently with immunological basis.
- Also induced with death of large numbers of microfilariae (usually >10,000/ml).
Lesions caused by microfilariae
- Can induce immune mediated pulmonary pathology.
Lesions in other organs
- Antigen-antibody complexes often cause protein-losing nephropathy (reversible).
Timecourse
- Disease has insidious onset - from months to years after infection.
- Adult worms can survive for 5-7 years.
- Microfiliariae can survive several months - 2 years.
Epidemiology
- Transmitted by many spp of mosquitoes but mainly members of the family,Culicidae.
- Microfilariae found in host blood.
- Microfilariae ingested in blood-meal by mosquito, rapidly transform to L1, then moult to L2 and L3.
- Adults, microfilariae, L3s
, L4s and young adults are found in dogs.
Diagnosis
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Treatment
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Prevention
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Outcomes
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