The traditional treatment, my stolen show dog endured. Another LW endured the preventive and 2 years later was worm free. The walnut advice has me a bit confused. From the, I freely admit, scanned advice, I see a digestive worm elimination? I hope I am wrong here. A digestive worm has many eradicators, we have hook, round, tape and the like.
A heartworm is a worm that puts itself into the heart, and multiplies like crazy. It is not, never has been, nor ever will be, a worm that reacts to a digestive system treatment as other worms are treated. If an ingestion of walnut works its way to the bloodstream, that is a new ballgame, but I can't see that?
Does the walnut invade the circulatory system to eradicate? I am completely stumped. I live in the deep south where, as Dianne states, the mosquito is our state bird. HW is transmitted by mosquitos. Period.
Having endured and survived HW treatment vis-a-vis the killer routine (If your dog is not healthy enough to endure the treatment, the cure will kill), and living in mosquito country, and dealing with this issue, to find a walnut can cure a killer worm that we spend thousands yearly to prevent or cure, my interest is indeed piqued:
I have lived with this, and I have treated this, and my dog survived this. I have only lived with this for a couple of decades, and being in the deep south, where we kill for blindness, I may be totally out of the loop. SO!
I prefer MerckVeterinaryManual for all technical 'advice'. Here is the spawn of the HW:
Heartworhttp://www.merckvetmanual.com/mvm/index.jsp?cf ... =heartworm
m (HW) infection is caused by a filarial organism, Dirofilaria immitis . At least 70 species of mosquitos can serve as intermediate hosts; Aedes , Anopheles , and Culex are the most common genera acting as vectors.
Treatment is as follows from Merck:
Treatment in Dogs:
The extent of the preadulticide evaluation will vary depending on the clinical status of the patient and the likelihood of coexisting diseases that may affect the outcome of treatment. Clinical laboratory data should be collected selectively to complement information obtained from a thorough history, physical examination, antigen test, and usually thoracic radiography.
The most important variables influencing the probability of postadulticide thromboembolic complications and the outcome of treatment are the extent of concurrent pulmonary vascular disease and the severity of infection. Assessment of cardiopulmonary status is indispensable for evaluating a patient’s prognosis. Postadulticide pulmonary thromboembolic complications are most likely to occur in heavily infected dogs already exhibiting clinical and radiographic signs of severe pulmonary arterial vascular obstruction, especially if CHF is present.
The only available heartworm adulticide is melarsomine dihydrochloride, which is effective against mature (adult) and immature heartworms of both genders. For Class I and II patients, melarsomine is given at 2.5 mg/kg, deep IM in the epaxial (lumbar) musculature in the L3-L5 region using a 22 g needle (1 in. long for dogs <10>10 kg). Pressure is applied during delivery and for 1 min after the needle is withdrawn to prevent SC leakage. The procedure is repeated on the opposite side 24 hr later. Approximately one-third of dogs will exhibit local pain, swelling, soreness with movement, or sterile abscessation at the injection site. Local fibrosis is uncommon.
Dogs with high worm burdens are at risk of severe pulmonary thromboembolism from several days to 6 wk postadulticide. Dogs with Class III infection receive the alternate (split-dose) regimen of 1 injection, followed in 1 mo by 2 injections 24 hr apart. Administration of a single initial dose results in a graded (~50%) worm kill and reduced pulmonary complications. By initially killing few worms and completing the treatment in 2 stages, the cumulative impact of worm emboli on severely diseased pulmonary arteries and lungs can be reduced. This 3-injection protocol is becoming the treatment of choice of many veterinarians regardless of stage of disease, due to its increased safety and efficacy. Other treatment protocols recommend the administration of prophylactic doses of ivermectin for 1-6 mo prior to administration of melarsomine, if the clinical presentation does not demand immediate intervention. The rationale for this approach is to greatly reduce or eliminate circulating microfilariae and migrating D immitis larvae, stunt immature HW, and reduce female worm mass by destroying the reproductive system. This results in reduced antigenic mass, which in turns reduces the risk of pulmonary thromboembolism.
Following melarsomine injection, exercise must be severely restricted for 4-6 wk to minimize thromboembolic lung complications. A low cardiac output should be maintained in order to reduce thrombosis and endothelial damage and facilitate lung repair. Adverse effects of melarsomine are otherwise limited to local inflammation, brief low-grade fever, and salivation. Hepatic and renal toxicity are seldom seen.
Class III patients should be stabilized prior to melarsomine administration. Stabilizing treatment variably includes cage confinement, oxygen, corticosteroids, and heparin (75-100 U/kg, SC, tid) for 1 wk prior to the alternate melarsomine treatment protocol.
Patients with right-sided CHF should be treated with furosemide (1-2 mg/kg, bid), a low-dose angiotensin-converting enzyme (ACE) inhibitor such as enalapril (0.25 mg/kg, bid, possibly increased to 0.5 mg/kg, bid after 1 wk pending renal function test results), and a restricted sodium diet. Digoxin, digitoxin, and arteriolar dilators, such as hydralazine and amlodipine, should not be administered. Digoxin is not effective for cor pulmonale; arteriolar dilators, and occasionally even ACE inhibitors, are likely to cause systemic hypotension.
Postadulticide thromboembolic complications can occur 2-30 days following treatment, with signs most likely 14-21 days after treatment. Clinical signs are coughing, hemoptysis, dyspnea, tachypnea, lethargy, anorexia, and fever. Laboratory findings may include an inflammatory leukogram, thrombocytopenia, and prolonged activated clotting time or prothrombin time. A postinjection increase in serum CK may be noted. Local or disseminated intravascular coagulopathy may occur when platelet counts are <100,000/µL. Treatment for severe thromboembolism should include oxygen, cage confinement, a corticosteroid at an anti-inflammatory dosage (eg, prednisone at 1.0 mg/kg, PO, sid), and low-dose heparin (75-100 U/kg, SC, tid) for several days to 1 wk. Most dogs respond within 24 hr. Severe lung injury is likely if, after 24 hr of oxygen therapy, no improvement is noted and partial pressures of oxygen remain <70>40,000/µL), depending on the type of macrolide given. However, the microfilarial count is usually lower, and mild adverse reactions occur in ~10% of dogs. Most adverse reactions are limited to brief salivation and defecation, occurring within hours and lasting up to several hours. Dogs, especially small dogs (<10>40,000/µL) may develop tachycardia, tachypnea, pale mucous membranes, lethargy, retching, diarrhea, and even shock. Treatment includes IV balanced electrolyte solution and a soluble corticosteroid. Recovery is usually rapid when treatment is administered quickly. Microfilarial counts are not routinely performed, and thus severe reactions are seldom expected. Treatment specifically targeting circulating microfilariae may be started as early as 3-4 wk following adulticide administration. More commonly, microfilariae are eventually eliminated, even from non-adulticide-treated dogs, after several months of treatment with prophylactic doses of the macrocyclic lactones. No drugs are currently approved as microfilaricides by the FDA. However, licensed veterinarians are permitted extra-label use of certain drugs if a valid veterinarian-client-patient relationship exists. The use of monthly administered HW chemoprophylactics as microfilaricides is governed by this regulation. The macrocyclic lactones are the safest and most effective microfilaricidal drugs available. Livestock preparations of these drugs should not be used to achieve higher doses for the purpose of obtaining more rapid results. The macrolide of choice for killing microfilariae quickly is milbemycin (0.5 mg/kg, PO, 1 dose). Performance of a microfilariae test is recommended at the time the antigen test is performed (6 mo after the adulticide treatment).
Developing Larvae: Ivermectin/pyrantel pamoate, administered monthly for 1 yr to dogs with larvae that are no more than 4 mo post-L3 inoculation, prevents the development of infection. Continuous monthly administration of prophylactic doses of ivermectin, alone or in combination with pyrantel pamoate, is also highly effective against late precardiac larvae and young (<7 mo postinfection) quasi-adult HW. Comparable capability of the other macrocylic lactones has not been reported. This extended protection is important in dogs of unknown medical history that may have acquired HW infections because of lack of preventive drug administration or lack of compliance.
Now of course, with dogs with the merling gene, at least the aussie, collie and BC, they must NOT take ivermectin. MY lab mixes take it. A collie downward gene is cautioned NOT to use ivermectin. The studies are not specific, however, the caution is there.
Heartguard is, of course, ivermectin, as is the ivermectin found in your feed & seed HW products. Jury out, but cautioned against.
This is all that I know on the HW subject ,but to miscall is a death sentence. So I look forward to the studies carried out. As my h-cap friends know, I do love me some data.
Emphasis added. By me.
The bolding.
, and I'd think LWs would be more prone to it because of the homogeneity.