255 Canine And Feline Heartworm Disease Flashcards
What is the lifecycle of D. Immitis?
Mosquito ingests microfilariae
-> [mosquito phase]L1->L2->L3 (10-14days) -> Larva acquire new host -> [tissue phase] L3 (3-4d)-> L4 (~2months cat/~45-65 days dog)-> [Bloodstream phase]-> developing adult (4-6 months cat/4-5months dog) -? Mature adult produce microfilariae (7-8m cat/6-7months dog)
- In dogs adults live 5-7 years & microfilariae 1-2 years
- in cats adults lie 2-4 years and microfilariae rarely circulate
What is the epidemiology of heartworm disease?
- Pivtal for heart worm transmission is a climate of adequate temperature and humidity to support a viable mosquito population, and sustain sufficient eat to allow maturation of ingested microfilariae into infective third stage (L3) larvae in the intermediate hoes.
- mosquito species maturation of larvae ceases at temperatures below 14degrees Celsius.
- decreases in winter months but presence of micro environments suggests the risk of transmission never reaches zero.
What is the pathophysiology of heart worm disease in cats?
Stage 1 = immature worms enter pulmonary arteries and cause acute parenchyma inflammatory reactions (subclinical). This is followed by a period when worms mature to adults and the host immune response is suppressed.
Stage 2 = worms start to die which results in marked inflammatory response. If infected cat survives it enters…
Stage 3 = permanent lung damage that includes type II alveolar cell hyperplasia and chronic respiratory disease.
- the pulmonary arterial response to adult heart worms is more severe in cats. A severe myointimal and eosinophilic response produces pulmonary vascular narrowing and tortoises, thrombosis, and hypertension.
- Eosinophilic infiltrates in lung parenchyma and pulmonary arteries leads to pulmonary oedema, pneumonia is, and type II cellular proliferation. Eventually diminished pulmonary function leads to hypoxemia, dyspnea, and potentially death.
- anaphylaxis can occur and lead to sudden death.
- Wolbachia pimientos is a gram -ve, intracelluar, endosymbiosis bacterium colonising a number of helminths, including D. Immitis. Wolbachia resides in D. Immitis and released in large numbers during melting, during microfilaria production, and upon death. Wolbachia-associated molecules (WAMs) involved in the hosts inflammatory response to D. Immitis. Heart worms free of Wolbachia spp. Do not produce inflammatory response that is as intense when they die.
What is the pathophysiology of heartworm disease in dogs?
Pulmonary hypertension/pneumonitis: primarily pulmonary vascular pathogen living in pulmonary artery. Direct contact with artery results in damage; including inflamed endothelium, villous myointimal proliferation, medial thickening and pulmonary thrombosis that results in dilation and tortuousity of pulmonary arteries. Pulmonary parenchymal disease occurs as inflammatory response and is characterised by eosinophilic and neutrophilic infiltrates, and chronically lead to irreversible lung fibrosis.
Wolbachia pipientis is gram -ve, intracellular, endosymbiosis bacterium colonising a number of helminths, including D. Immitis. They are relesed during molting, microfilaria production, and upon death of adult parasite. Wolbachia associated molecules (WAMs) are involved in inflammatory response and contribute to interstitial inflammation. Endothelial and medial thickening with obstruction to blood blow lead to diminished pulmonary vascular compliance, increased resistance and subsequent hypertension.
Right heart changes eccentric, or mixed eccentric and concentric hypertrophy is common in dogs with severe HWD. Hypertrophy does not correlate to severity of pulmonary hypertension. When worms die they are carrier to distal pulmonary arteries where they lodge and contribute to pulmonary changes and hypertension. Myocardial failure might be responsible for development of right dilated ventricle. Right sided congestive heart failure may develop in cases with no mild pulmonary hypertension.
Hepatic/renal disease: worms may reside in caudal vena cava which leads to hepatic and renal failure. Immune-complex glomerular disease is a common complication of HWD. Antigen-Antibody complexes produced that precipitate in glomeruli causing glomerulonephritis and subsequent proteinuria. Proteinuria enhances thrombus formation via decreases levels of plasma antithrombin III
Caval syndrome may arise when hemodynamic event cause transient or sustained decrease in pulmonary artery blood flow allows worms to fall into right ventricle. It is characterised by severe acute tricuspid regurgitation with poor cardiac output, intramuscular hemolysis, secondary hemoglobinuria, shock, and hypotension. Caval syndrome is rapidly fatal. Congestive failure ma or may not precede caval syndrome.
What are the clinical signs of HW disease?
- most HWI are asymptomatic
- weight loss, diminished exercise intolerance, lethargy, poor condition, dyspnea, syncope, and abdominal distension (ascites).
PE: weight loss, split-second heart sound, right sided heart murmur of tricuspid insufficiency, and cardiac gallop.
Right heart failure: jugular venous distension ad pulsation. - <10% cardiac arrhythmias and conduction disturbances uncommon in chronic HWD.
- pulmonary parenchymal manifestations could produce cough, pulmonary crackles, granulomatosis, muffled lung sounds, dyspnea, and cyanosis.
What tests are an option to diagnose heart worm?
- Serologic testing: ELISA antigen testing to detect gravid adult female heart worms. Antigen testing can be negative with low worm burdens; infection with male worms; or infection with young female worms with immature reproductive tracts, heart worm prevention medication (kill microfilariae), immunologic destruction of microfilariae by cats. Antigen tests are available at referral laboratories or as point of care tests.
- Direct blood smear: not a regular method. A single drop is used to examine microfilariae under microscope. This requires 20-50 microfilariae per ml of blood.
- Difil test and Knott’s test: blood is centrifuged or filtered to concentrate microfilariae. This is useful to test for microfilariae
- Dipetalonema reconditum: transmitted by fleas may be picked up by microfilaria tests. DOes not require expensive treatment.
What is the difference between D. Recondition and D. Immitis?
D. Recondition: usually few in blood, progressive motion, has a caved body, blunt head, curved or ‘buttonhook’ tail.
D. Immitis : usually many, stationary, straight body and tail, tapered head
What are the radiographic and ultrasonographic findings of pets with HW disease?
- Rads: strongly indicative HWI if show problems in right side of heart, blunted tortuous pulmonary arteries and enlargement)
- US: measure thickening of right side of heart and show live worms wiggling.
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How is HW prevented?
- Prevention of HW with marocyclic lactose antibiotics. This includes avermectins, and milbemycins, and derived from soil microorganisms streptomyces.
- these agents terminate tissue stage larval development (L3and L4) during first 2 months after infection and have a large temporal window of efficacy, and administered orally or topically or injection every 6-12 m
- Ivermectin is widely effective and protects when lapses occur.
- Individuals with ABCB1 (1[MDR1] and P-glycoproteins 1 [PGP1] gene mutation) are sensitive at high extra-label dosages
- Adulticide feature enhanced with 3-day course of doxycycline.
- Milbemycin is effective against L3 and L4 larval stages stopping development in first 6 weeks. It’s given monthly at reach back effect of 2 months
How is HWI managed?
1) kill tissue base L3 and L4 larvae with monthly ML heartworm Product containing moxidectin. Other high dose MLS can cause anaphylactic reaction
2) Kill Wolbachia. They possess inflammatory proteins that are released when adult worms die or are killed, and these proteins increase chances of severe circulatory reactions in canine host. Doxycycline for at least a month as soon as diagnosis is made
3)
What is the AHS-recommended heartworm management protocol for day 0:
Day 0 (diagnosis):
- +ve Ag test verified with microfilaria test.
- Apply EPA-registered canine topical product labeled to repel and kill mosquitoes
- begin exercise restriction
If dog i symptomatic:
- stabilise with appropriate therapy and nursing care
- prednisone prescribed at 0.5 mg/kg BID first week, 0.5 mg/kg SID second week, 0.2 mg/kg EOD for 3rd and 4th weeks.
What is the AHS-recommended heartworm management protocol for day 1
- Administer appropriate HW preventative
- If MF detected, pre-treat with antihistamine and glucocorticoids (if not on prednisolone)
- observe for 8 hours to reduce signs of reaction
What is the AHS-recommended heartworm management protocol for day 1-28?
- Administer doxycycline 10mg/kg BID for 4 weeks
- reduce pathology associated with dead HW
- Disrupts HW transmission
What is the AHS-recommended heartworm management protocol for day 30?
- Administer appropriate HW preventive
- Apply EPA registered topical product to repel and kill mosquitos
What is the AHS-recommended heartworm management protocol for day 31-60?
- 1 month wait period following doxycycline before administering melarsomine is recommended to allow time for Wolbachia surface proteins and other metabolites to dissipate before killing adult worms. It also allows time for worms to wither as they become unthrifty after Wolbachia endosymbionts are eliminated
