Heartworm Flashcards
Describe HW lifecycle
L1-3 develop in Mosquito
Takes 8-17 days, requires warm, humid conditions and presence of cosymbiont Wolbachia spp
L3 infect dog when Mosquitoe feeds, deposit on skin and enter through hole.
Mature to L4 and live in muscle/aberrant sites
2-3months final moult to juveniles that migrate to lungs/heart
Mature in pulmonary arteries
Takes 6-9month for newly infected dog to have micrfilaria (if both male and female worms present)
The microfilaria are then ingested by new vector to continue cycle
Pathogenesis of HWD and complications in dogs
Presence of worm in pulmonary artery causes villous and myointimal proliferation as well as vascular endothelial damage releasing vasoconstrictive substances and pro-thrombotic factors.
Result is thickening and tortuosity of the pulmonary arteries with end stage being pulmonary hypertension
The affected arteries are also resistant to recruitment during exercise
COMPLICATIONS:
Caval syndrome - v high burdens with worms in heart. Jugular dist, hepatorenal congestion
PTE - seen with worms dying (naturally or with Tx) and also hypercoagulable state. Risk greatly increases if not cage confined during adulticidal therapy
RS heart changes - eccentric hypertrophy, tricuspid regurg, RSCHF in severe disease
Type III hypersenstivity damage to glomerulus (ICGN)
Eosinophilic pneumonitis seen with L5 migration (before Ag positive) and eosinophilic granulomatosus is seen with adult worm death or overzealous immune response. Often recurs despite treatment with prednisolone.
Diagnostic tests for HW - limitations
Ag detection - Ag from female worm
low burdens, male only burden or Ag blocking by host immune system will result in false negative test (or reduce magnitude of positive).
False positives also reported - confirm with different test type or with mf detection prior to adulticidal treatment.
Takes >8mo to be positive after infection
Microfilarial detection (modified knotts test improves sensitivity) 10-20% amicrofilaraemic, also negative if on ML treatment
Rads - pulmonary vasculature tortuosity, variable infiltrative lung changes, right ventricle enlargement (variable depending on severity of HWD)
Echo - can determine severity of PHT, rarely see the worms unless heavy burden
Baselines - proteinuria in 345%, fragmentation injury of RBCs, macrocytic non-regenerative anaemia; eosinophilia.
Evidence of hypercoagulability: increased Ddimers, shortened PT/APTT, increased fibrinogen
Adulticidal Tx for Canine HW, rationale.
Factors that increase risk of complication:
1) activity
2) more severe pulmonary disease
3) presence of heavy worm burden (unable to measure this reliably)
Baseline: CBC and biochem and UA with thoracic rads for monitoring
day 0-1 start macrocyclic lactone treatment
Give 28d course of doxy
-> reduces MF and kills Wolbachia both of which contribute to inflammatory reaction on worm death, thus by treating this first we reduce that reaction. Also gives time for all juveniles to reach adult stages prior to definitive Tx
+/- GCS or antihistamine if concerned about allergic reaction from Mf death, though this is rarely reported with newer drugs
Melarsomine (arsenical parasiticide) is given by IM injection 1 month after finishing doxy (allows clearance of all Wolbachia related antigens) then again at 90 and 91 days (split dose protocol)
This 3 dose protocol recommended by AHWS due to increased safety and high effficacy reported (up to 98% clearance)
Dose increase expense and duration of restriction
Exercise restriction for 8 weeks after last dose (and throughout treatment)
if clinical signs of PTE develop O2 therapy with low dose pred +/- vasodilators may be beneficial. Can also give pred as a preventative
No indication of benefit for antithrombotic or anticoagulant therapy during treatment
Retest 9mo after last melarsomine - if persistent ag or mf then repeat adulticidal treatment after doxycycline course.
Failure occurs due to: juveniles not dying in initial treatment; resistance (rare); lack of preventative compliance
Diagnosis of feline HWI
very challenging as not all have + Ag and seroconversion of Ab may not indicate current disease
AG + always indicates adult HW present so such cats shoul dbe montiored for HARD
Ab serology has a sensitivity of 30-89% with up to 50% of HWI cats on necropsy exam found to be negative .
Most infections do not produce microfilaria
Radiographs - evidence of enlarged lobar and peripheral pulmonary arteries is seen in HWD and sometimes HARD, along with bronchointerstitial pulmonary pattern
left pulmonary artery width >1.6x caudal 9th rib is strongly suggestive of HWI
CT - multifocal regions of consolidation or lobar consolidation suggestive of infarction.
BAL - eosinopohilic inflammation
Echo - 40-100% sensitive for detection of infection (smaller hearts make them easier to see than in dogs)
Pathogenesis of feline HARD and HW disease
HARD - migrating juvenile worms cause an acute vascular and parenchymal inflammatory response.
This results in pulmonary endomesoarteritis and occlusive hypertrophy with increased expression of proinflammatory mediators.
Results in death of most juvenile worms in the majority of infected cats.
HWI occurs in small percentage and because of low # of worms this rarely causes RSCHF, PHT or caval syndrome. The worms are able to suppress the hosts inflammatory response also minimising remodelling. Many cats are subclinical for the infection until the worms die - in this instance 80% of cats will clear the infection without issue. But in some cats the degrading parasite causes severe pulmonary inflammation and thromboembolism that can result in fatal lung injury from infarction (like because of small size of feline pulmonary arterial tree). The dying worms can also trigger an anaphylactoid reaction possibly resulting in bronchoconstriction and pulmonary oedema like in ARDS.
Heartworm preventatives
Macrocyclic lactones: selamectin, ivermectin, moxidectin, milbemycin
