Cardio2.5- Heartworms

  1. What is the infective stage of D. immitus?
    L3 within the mosquito
  2. Describe the life cycle of D. immitus.
    mosquito picks up microfilaria from dog--> larvae develop into infective L3 within the mosquito--> mosquito takes another blood meal and deposits L3 into the skin--> larvae molt from L3 toL4 and L4 to L5 within subQ tissues--> L5 migrate to the vascular system--> migrate to the pulmonary vasculature, where they mature into adults (5 months)--> adult worms reproduce and release microfilaria into the blood--> repeat
  3. What stages of D. immitus are treatable/ preventable?
    L3/L4 subQ stage, adults in pulmonary vessels, microfilaria
  4. Which stages of D. immitus are NOT treatable, responsible for the lapse in time between infection and + antigen test/ treatment?
    migrating L5, young adults; takes 5 months for migration and  maturation from L5 to adult, which produce Ag and are susceptible to adulticides
  5. What is Wolbachia?
    intracellular, symbiotic gram negative rickettsial species that enhance the development of filarial parasites
  6. How do you tell a male from a female adult D. immitus grossly?
    the males have a screwed up head
  7. How species get heartworms?
    canines, cats, ferrets, muskrats, sea lions, and coatimundi
  8. What disease does heartworms cause in humans?
    coin lesions in lungs, subcutaneous, or ocular lesions
  9. What are the main differences b/w feline and canine HWD? (9)
    • innate resistance of the cat
    • higher level of aberrant migration in the cat
    • adult worm bigger relative to the cat than the dog
    • lighter worm burden in cats
    • microfilaremia very brief in cats
    • cats have a marked pulmonary reaction to parasites
    • difficult to definitively diagnose in cats
    • lack of safe adulticide therapy for cats
    • higher preventative doses in cats
  10. What is a possible reason that cats are more innately resistant to heartworms than dogs?
    the worms undergo abberant migration and cannot develop properly
  11. Why do worms sometimes cause sudden death in cats?
    when an adult worm dies (even just 1), it creates a pulmonary embolism and a SEVERE parenchymal reaction
  12. Why is US considered more useful for diagnosis of HW in cats than dogs?
    because the worms are so large relative to the size of the heart and lungs, so you have a higher chance of actually finding the worms
  13. What are common locations for aberrant HW migration in cats? (3)
    eyes, brain (ventricles), systemic arterial system
  14. When does pulmonary injury occur due to heartworms, and what are the clinical implications of this?
    while the L5 are maturing; this is before we can detect the infection, so we can't stop it from happening
  15. What are the consequences of pulmonary damage due to HW infection? (4)
    endothelial swelling, WBC and platelet activation--> arteritis, thrombi
  16. What are the 2 fundamental ways that HWs harm the host?
    damage to pulmonary arteries, injury to lung parenchyma
  17. HW cause ___________, which increases the resistance in the pulmonary arteries, causing ____________.
    villous arteritis; pulmonary hypertension
  18. Thrombosis around adult parasites can clinically be detected by __________.
    increased D-dimers
  19. Radiographic changes associated with HWD tend to be worse in ___________.
    the caudal lung lobes
  20. How does HWD cause cor pulmonale?
    villous arteritis and thrombosis--> increased pressure and pulmonary hypertension--> pulmonary arteries dilate from increased pressure--> pulmonary arteries become stiffer--> pressure increases further--> RV mixed hypertrophy b/c it must overcome higher pressure (RV not designed to work at high pressures)--> right heart failure
  21. What is the "horseshoe sign"?
    dilated caudal right and left lobar pulmonary arteries- seen with PHT and HWD
  22. How is pulmonary hypertension in HWD different from that in pulmonary stenosis?
    with HWD, there is no pressure gradient b/w the main pulmonary artery and the RV; in pulmonic stenosis, there pressure is much higher in the RV than in the pulmonary circulation
  23. How does lung injury occur in HWD? (6)
    pulmonary infarction from thrombosis, hypersensitivity pneumonitis (from parasites sequestered in lungs), inflammatory pulmonary edema, HARD in cats, lung fibrosis, hemosiderosis (from RBC injury or hemorrhage)
  24. Why is the pulmonary edema from HWD considered "inflammatory" pulmonary edema?
    you don't get pulmonary edema from R-CHF, therefore, if you get pulmonary edema with HWD, it must be from inflammation and increased vascular permeability (HWD does NOT cause L-CHF)
  25. What is HARD in cats?
    Heartworm Associated Respiratory Disease: hyper-reactive response of bronchiolar smooth muscle, causing medial hypertrophy and severe inflammation
  26. Pulmonary vascular disease associated with HWD leads to __(2)__; pulmonary parenchymal disease leads to ___________.
    cor pulmonale and RV dysfunction/failure; respiratory signs
  27. What respiratory signs are often present with advanced HWD? (4)
    cough, respiratory distress, abnormal lung sounds- loud bronchial sounds or crackles
  28. What signs do cats with HWD often present with? (6)
    vomiting, coughing, dyspnea, chylothorax (prob from R-CHF), CNS disease, spontaneous pneumothorax
  29. What are 3 acute syndrome of heartworm disease (not the chronic presentation)?
    caval syndrome, acute pulmonary embolism, sudden death
  30. Signs related to RV dysfunction. (8)
    • [due to decreased CO] weakness, exercise intolerance, syncope
    • [when it become R-CHF] increased jugular venous pressure, hepatomegaly, ascites
  31. What abnormalities might be found on cardiac auscultation of an animal with HWD? (5)
    • tympanic second heart sound
    • S2 splitting into separate aortic and pulmonic components
    • jugular venous pulse
    • soft ejection murmur (flow into dilated PA)
    • tricuspid regurg (relating to PHT)
  32. Why is there sometimes splitting of S2 sound with HWD?
    separate aortic and pulmonary components because PHT causes the pulmonic valve to snap shut under high pressure
  33. Why might there be a soft ejection murmur with HWD?
    PHT and dilated main pulmonary artery--> ejection murmur
  34. __(3)__ are the most practical methods of assessing severity of HW infection and disease.
    History, clinical exam, and thoracic radiography
  35. What are thoracic radiographic signs of HWD? (6)
    • RV enlargement (if cor pulmonale)
    • bulging of main PA
    • enlarged pulmonary arteries
    • increased interstitial opacity
    • patchy alveolar infiltrates
    • coin lesions (small granulomas)
  36. What is echo useful for in HWD diagnostics? (2)
    • Dx of caval syndrome 
    • Dx of HWD in cats (can see worms more easily)
  37. Since bulging main PA is an unreliable finding in cats with HWD, look for __________.
    tortuous lobar pulmonary arteries
  38. What does "pruning" of pulmonary arteries mean?
    abrupt stoppage of blood flow (seen with contrast) due to thrombosis with worms
  39. What is the classic appearance of HW on echo?
    adult parasites: double echoic lines with a hypoechoic center (lumen of worm)
  40. CBC/Chem findings common with HWD. (4 CBC, 3 Chem)
    • eosinophilia, basophilia, monocytosis, +/- mild non-regenartive anemia
    • inc globulins, decreased albumin (renal loss), +/- incr liver enzymes (if congestion)
  41. How does HWD lead to glomerular disease?
    caval syndrome--> hemolysis--> pigment nephropathy--> glomerular disease--> protein-losing nephropathy
  42. What are the newest guidelines for laboratory diagnosis of HWD? (3)
    • Ag test prior to starting preventative (dog)
    • Ag test annually in dogs (to identify resistance to macrocyclic lactones)
    • (?????) positive HW antigen test
  43. ___________ is the test of choice to diagnose HW in dogs; it has an excellent ___________.
    Antigen test directed against adult female antigen; negative predictive value (neg. test very reliable)
  44. How can a dog be occult HW positive, but microfilaria negative (reasons why we prefer the antigen test)? (3)
    • single sex infection (hopefully its just F, we can still detect them with antigen test but they can't produce mf without males)
    • immune -mediated destruction of mf
    • chronic treatment with a preventative drug
  45. How is HWD usually diagnosed in cats?
    combined antibody test and antigen test; Ab test is specific for HW exposure, Ag test is specific for HW infection
  46. Why is it important to use a combination of Ab and Ag tests to diagnose HWI in cats?
    Ag tests detect Ag from F worms; you often get neg Ag tests in cats, even when they have HWI; Ab tests tell us if the cat has been exposed, but there may not be any worms in the cat (aberrant migration and failure to initiate an infection)
  47. Why can't transplacental infection with HW lead to a patent infection?
    microfilaria MUST go through a mosquito to develop to L3
  48. Contrast D. immitus from A. reconditum. (3)
    adult A. reconditum live in the SQ tissues, non-pathogenic, IH is flea
  49. What 2 tests are for the detection of microfilaria? (2)
    Knott's test or Millipore Filter test
  50. If you see microfilaria incidentally on a blood smear, how do you proceed?
    try to distinguish it from A. reconditum: D. immitus is wider and has a tapering head (as opposed to a blunt head); A. reconditum has button hook tail
  51. What are the different patient classifications for HWD? (4)
    • Asymptomatic 
    • Symptomatic for HWD: respiratory signs, cor pulmonale, R-CHF
    • Concurrent dz or aged patient
    • Acute Syndromes of HWD: acute PE, caval syndrome, death
  52. What are the methods of txt for HWD? (2)
    • immiticide (adulticide)- Melarsomine dihydrochloride
    • slow kill adults
  53. How can you handle txt of HWD when there is concurrent Wolbachia species?
    Wolbachia improve fertility of adult worms; prior killing of Wolbachia with Doxycycline for 4 weeks prior to adulticide therapy
  54. What is the preferred treatment procedure for an uncomplicated case of HWD?
    • 2 stage therapy:
    • 4 weeks of Doxy therapy
    • initial injection of Immiticide followed 1 month later with 2 injections 24 hours apart
  55. Describe the management of HWD (aside from the adulticide and actual killing of the worms).
    • strict cage rest for 2-4 weeks, observe for PE
    • treat PE with prednisolone
    • follow up with Ag test 4-6 months later
  56. What are the principles of txt of HWD in a complicated case with pulmonary signs? (2)
    treat for 7-14 days with prednisolone and doxycycline; then 2 stage treatment of adulticide therapy
  57. What are the principles of txt of HWD in a complicated case with R-CHF? (2)
    • Pimobendan (dog), furosemide, sildenafil, ACEi, spironolactone, STRICT cage rest, prednisone--> stabilize CHF for 2-4 wk prior to adulticide therapy
    • 2 stage adulticide therpay
  58. Why should you never give a beta blocker to  HWD dog?
    causes caval syndrome because the worms migrate backwards due to high pressure
  59. When do you start a preventative in a HW+ dog?
    immediately (Ivermectin, moxidectin)
  60. What issues are related to slow kill of adults in HWD therapy? (3)
    • takes too long- continued pulmonary damage
    • not cost effective (given twice monthly)
    • macrocyclic lactone resistance is emerging
  61. What macrocyclic lactones are used to prevent HWI? (5)
    ivermectin (oral), milbemycin oxime (oral), selamectin (topical), moxidectin (topical), moxidectin (injectable- every 6 months)
  62. What is caval syndrome?
    large worm burden with severe pulmonary hypertension--> worms move retrograde into tricuspid valve orifice, RA, and caudal vena cava--> low cardiac output and hepatic congestion
  63. What are the features of caval syndrome? (3)
    hemoglobinuria (due to RBC fragmentation and hemolysis), DIC, severe hepatocellular injury
  64. Describe the diagnosis and management of caval syndrome.
    TR murmur + echo; forceps/snare removal of worms
  65. If an animal on adulticide therapy gets a PE, how do you proceed? (4)
    corticosteroids, oxygen, rest, analgesics
  66. What is the best way to avoid macrocyclic lactone resistance in HWs?
    avoid selective pressure on microfilaria or adult worms by not using slow kill methods for txt
Card Set
Cardio2.5- Heartworms
vetmed cardio2.5