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Heartworm Disease, Dog 419

• Jugular venous distention (right heart failure) • Cardiac response ○ Patchy mixed interstitial-alveolar pattern
and pulsation with a right apical holosystolic ○ Right ventricular enlargement secondary with perivascular infiltrates demonstrated
VetBooks.ir • Palpable fluid wave (ballottement) if abdomi- tricuspid regurgitation and eventual ○ Right heart enlargement Diseases and Disorders
to moderate-severe PH and subsequent
most frequently in caudal lung lobes
murmur are indicative of tricuspid regurgita-
tion due to chronic PH.
myocardial failure
○ Enlarged caudal vena cava if CHF is
nal distention (ascites) is noted.
present or imminent
of severe HWIs
• Discolored urine (hemoglobinuria), murmur ○ Right-sided CHF (ascites) in up to 50% • Diagnostic workup may be abbreviated or
of tricuspid regurgitation, tachypnea/ • Systemic response even forgone if finances do not allow for
dyspnea, collapse, and right-sided CHF and/ ○ Renal: glomerulonephritis, proteinuria, young, clinically normal dogs, with attendant
or left-sided forward failure indicate caval infrequent hypoalbuminemia, and increases in risk. Workup may be even more
syndrome. decreased antithrombin (increases pul- detailed in instances of severe, complicated
monary thromboembolic risk) HWD.
Etiology and Pathophysiology
• Female mosquitoes serve as intermediate DIAGNOSIS Advanced or Confirmatory Testing
hosts after feeding on microfilaria-positive • Heartworm antigen tests (ELISA and immu-
dogs. Diagnostic Overview nochromatographic) are specific, sensitive,
• Microfilariae molt twice within the mosquito The diagnosis is made in one of two contexts: and some are semiquantitative.
into L3 larvae and can infect another dog an incidental finding of a positive antigen test ○ False-negative results with low female
in 2-2.5 weeks during the warm months of in an overtly healthy dog (more common) or worm burdens, immature infections, or
summer. overt clinical signs caused by infection-related rarely due to antigen-antibody complexes
• Patent infection (microfilaremia) occurs 6-7 secondary lesions. The antigen test is the con- making antigen unavailable
months after inoculation of a susceptible firmatory test of choice, and additional testing ■ Heat treatment of serum can improve
host by infective (L3) larvae. is indicated based on severity of physical signs sensitivity of ELISA test if false-negative
○ Occult (amicrofilaremic) infections exist and thoracic radiographic changes. suspected
during this prepatent period; other causes ○ False-positive results are rare but should
of occult infection include immune- Differential Diagnosis be considered when positive results occur
mediated microfilarial destruction, unisex • Microfilaremia: Acanthocheilonema (formerly in areas of low heartworm incidence.
infections, acute high-dose or chronic Dipetalonema) reconditum microfilariae are • Microfilaria: when used as a diagnostic test
macrolide prophylactic administration. shorter, narrower, and have a blunted head for HWI, filter and modified Knott’s tests
• Disease severity is determined in part by compared with D. immitis microfilariae. preferred over wet direct blood smear
the duration of infection, number of adult D. immitis is < 6 microns in diameter ○ Indicated to ascertain presence of
heartworms, the host’s response to live and (less than red blood cells [RBCs]), whereas microfilariae in dogs with HWI before
dead heartworms, and amount of exercise. A. reconditum is > 6 microns in diameter institution of therapy; wet mount direct
Some changes may be permanent. (approximately ≥ RBC diameter). smear is adequate in this instance.
• Wolbachia sp (an obligate intracellular, • Coughing: primary bronchointerstitial • Echocardiography (p. 1094) for moderate
gram-negative bacterium) has a symbiotic disease, collapsing trachea, infectious tra- to severe HWI to assess PH and caval
relationship with D. immitis and possibly cheobronchitis, pneumonia, left-sided CHF syndrome
participates in the heartworm inflammatory (p. 1209) ○ Dilated pulmonary arteries
response by releasing endotoxins and antigens • PH: PTE (due to other causes); chronic ○ Parallel linear hyperechoic densities in
associated with worm death. pulmonary disease; cyanotic right-to-left pulmonary arteries (and sometimes the
○ Wolbachia spp are necessary for D. immitis shunting cardiac disease such as patent right heart and venae cavae) with large
reproduction. ductus arteriosus and ventricular septal worm burdens
○ Microfilariae produced in absence of defect with primary or secondary PH; and ○ Right ventricular eccentric and concentric
Wolbachia sp do not become infective in primary PH hypertrophy with flattened intraventricular
the mosquito. • CHF (left sided [respiratory signs] or right septum in severe cases
• Response of the pulmonary arteries sided [ascites or pleural effusion]): primary ○ High-velocity tricuspid regurgitation (TR)
○ Damage from direct contact and other or secondary myocardial failure, chronic or pulmonic insufficiency on Doppler
mechanisms (e.g., immune mediated, congenital or acquired valvular disease echocardiography with PH (TR Vmax
waste product release) to vessel intima • Pulmonary neoplasia (primary or metastatic), > 3 m/s)
○ Villous proliferation of the intima and granulomatous or other infiltrative pulmo-
subintimal smooth muscle hypertrophy nary disease TREATMENT
○ PH: results from obstruction of blood
flow (PTE) and reduced vascular compli- Initial Database Treatment Overview
ance induced by endothelial and medial • CBC, serum biochemistry profile, urinalysis: • Eliminate worm burden and microfilariae
thickening and probably biological incom- eosinophilia and basophilia sometimes (if present).
petence (failure of damaged vessels to identified. Evidence of hemolysis and ○ Reduce risk of adverse events to adulticidal
respond to vasodilatory stimuli); results in hemoglobinuria if class 4 (caval syndrome). therapy.
dilated, often tortuous and truncated Pathologic proteinuria common due to • Address complications.
pulmonary arteries glomerulonephritis; may be reversible with • Prevent future infection.
• Response of the pulmonary parenchyma treatment
○ Deposition of heartworm antigen in the • Electrocardiography (p. 1096) may demon- Acute General Treatment
microvasculature causes parenchymal strate a right axis shift (prominent S waves Pulmonary thromboembolism:
immune/allergic reactions (periarterial in leads I, II, III, and V 3 , indicating right • Oxygen therapy (oxygen cage at 40% O 2
edema and inflammation). ventricular enlargement) and/or atrial or or nasal insufflation at 50-100 mL/kg/min)
○ Corticosteroid-responsive allergic pneu- ventricular arrhythmias in class 2 and 3 HWI. (p. 1146)
monitis in 14% of HWIs • Thoracic radiographs (may be normal) • Cage rest
○ Severe chronic HWI causes irreversible ○ Dilated and sometimes tortuous, truncated • Corticosteroids: prednisone 1 mg/kg PO q
pulmonary fibrosis with PH. pulmonary arteries 24h for 7-10 days

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