An excellent resource that details all aspects of health issues for dogs, and one that every conscientious dog owner should have is:
Carlson, Delbert G., DVM, and James M. Giffin, MD. Dog Owners's Home Veterinary Handbook (Revised and Expanded). Howell Book House, Macmillan Publishing Company, 866 Third Avenue, New York, NY 10022 USA (1992, 2nd ed). ISBN: 0-87605-537-4 (hardcover).
This comprehensive book is a complete guide to health care of dogs. It lets you know when you can treat the dog, or when you need to take it to the vet post-haste. It lists symptoms so that you may inform your vet of relevant information about its condition. The arrangement of the material facilitates rapid reference. Illustration of key procedures (pilling, taking pulse/temperature, etc). Lists poisonous substances, including houseplants. A must have home veterinarian handbook.Other books/articles that you may find of use include:
This is written by the Subcommittee on Dog Nutrition, Committee on Animal Nutrition, Board on Agriculture, National Research Council. It reads pretty well for something put out by a committee. Lots of references. Lots of tables of nutrient contents of various foodstuffs. Don't expect any discussions of what dog food is best! For the most part, consumers are left to figure this out for themselves.
There are also many sources of online information about general veterinary matters. The best place to start is Ken Boschert's NETVET site, at http://netvet.wustl.edu/.
Some help is available on VETMED, a moderated mailing list in which people ask about adn discuss veterinary problems -- not everyone subscribed is a veterinarian, of course, but quite often people here can point you to where you should look. Email to firstname.lastname@example.org with SUBSCRIBE VETMED yourfirstname yourlastname in the body of the message. Be sure to substitute your own first and lastnames in the subscribe command.
You can also do research and article searchs at most University libraries: ask the librarian about the following services: Agricola, BIOSIS Previews, CAB Abstracts (produced by Commonwealth Agricultural Bureaux), Focus on Veterinary Science & Medicine (produced by the Institute for Scientific Information). MEDLINE indexes about 60-70 veterinary journals and is a place to start, but is not as comprehensive as the above services. If the library does not have them separately, they are also available on the Dialog service, which most University libraries subscribe to.
Symptoms include depression, weakness, vomiting, diarrhea, dehydration, weight loss and shivering. A veterinarian may find decreased mental ability, a slow heart rate, poor pulse quality, and low body temperature. Blood tests may reveal increased kidney indices and electrolyte imbalances of low sodium and chlorine and high potassium. A simple test called ACTH stimulation confirms the disease.
Treatment traditionally involves replacing mineralocorticoids with fludrocortisone acetate (Florenef Acetate); glucocorticoids may also be replaced depending on the dog's condition. Dogs tend to be resistant to the desired effects of Florenef, thus high doses are required and side effects include increased thirst, urination, and urinary incontinence in some cases. An experimental drug that may soon be approved for use in animals is desoxycorticosterone pivalete (DOCP, available through Ciba Animal Health) injected subcutaneously. Preliminary studies are encouraging, and details may be found in JAAHA March/April 1995.
Normally, anal sacs are emptied when the dog defecates. Some dogs with overactive anal glands may require occasional help. Your vet can demonstrate the procedure.
A common indication of trouble with anal sacs is "scooting" (dragging the rear on the ground).
Impaction: occurs when the anal sacs fail to empty properly. This is more common in smaller breeds. Squeezing the sacs yourself as needed will control the problem.
Infection: complicates impaction. There is blood or pus in the secretions, and the dog may scoot (drag its rear on the ground). It may be painful. Check with your vet for an antibiotic you can apply after you empty the sacs.
Abscess: Signs of anal infection, with a swelling at the site of the gland. It goes from initially red to a deep purple. You will have to have it lanced and cleaned by the vet.
Dogs whose anal sacs become repeatedly infected and/or abscessed will need to have the glands removed. Surgery is uncomplicated, although the dog will have poor bowel control for the next few days after surgery. Try putting a pair of small boy's underpants, with the dog's tail through the third opening, on the dog to contain accidents.
Blood transfusions are the topic of much controversy. One school of thought is that the animal is likely to hemolyse the transfusion, so blood should be tranfused only in lifethreatening situations. The other school argues that transfusions have never been proven to be dangerous in this disease (and goes on to assume that they are therefore safe).
There are two types of AHA: primary, where the system destroys its own red blood cells for no apparent reason, and secondary, where the red cell membrane is changed (perhaps by a virus or parasite) and is then destroyed as abnormal. Prognosis for secondary AHA is much better and depends on how well the underlying cause can be treated. The prognosis for primary AHA is much worse, with only 50% of the animals living beyond 12 months.
If your dog has this problem check with your vet. There is an operation that can correct the problem of elongated palates. In any case, dogs should not be constantly panting and breathing noisily, so a vet check is in order.
In general, breathing anomalies should be investigated: noisiness, wheezing, excessive panting, excessive coughing.
Coloring (natural or artificial) in food can also directly color the stool so you can't be sure of anything without a chemical analysis. A sudden diet change/addition can also affect stool color.
Get a sample to the vet.
*Brucellosis may be passed to humans.* It can cause suppressed immune systems and sterility in humans. However, brucellosis in this form cannot be passed back to animals or other humans, as this disease is not adapted to humans.
Diagnosis can be quickly made, although animals tested less than three weeks after exposure will show negative. False positives are possible; followup diagnosis with more reliable methods should follow any initial positives.
Treatment for brucellosis is not generally very successful and often very expensive. Extensive antibiotic therapy, evaluation and additional testing will add up quickly, with no guarantee of success. No vaccine is available.
Any animal with brucellosis should not be bred, and should be eliminated from the kennel or other breeding stock before infecting the entire colony. Animals entering the breeding area, male and female, should be tested for brucellosis PRIOR TO breeding.
Parvovirus comes in several forms:
(summarized from Carlson & Giffin)
In the US, there is a current upswing in Parvo infections. Make sure your dog is up-to-date on its vaccinations. Don't let a too-young puppy roam where possibly infected dogs have been (for example, in the park). Contact with feces or un-vaccinated dogs is the primary source of transmission. Some breeds seem to be especially sensitive to parvo, such as Rottweilers.
Steps were taken to locate these recessive genes. By breeding an unknown dog to a known CHD, the pups were then rebred to CHD dogs and percentages were calculated. Most Malamutes today have been CHD rated. The percentage is the actual likelihood of CHD showing up in a breeding. Malamute breeders tend to agree that 6.25% (one great-great-great grandparent is a carrier) is the upper limit of acceptablity in a CHD rating.
Puppies are CHD rated now by taking the CHD factors of both parents and averaging them together. Example:
Dog 1.75% Bitch 2.01% --------------- (1.75 + 2.01)/2 = puppies 1.88%Needless to say, an non-CHD certified Mal or a Mal that is certified above a 6.25% should not be bred, in order to contain the disease. Non-CHD certified dogs can be CHD certified, but it is a very expensive procedure.
CHD may be diagnosed with various tests that include blood tests and x-rays.
The Complete Alaskan Malamute by Riddle and Seely covers this disease fairly well.
Coccidiosis is caused by protazoal parasites of either Eimeria spp. or Isospora spp. Crowding, poor sanitation, or stress may facilitate its spread.
Symptoms depend on the species of protozoa, the infective dose, and the amount of damage caused. They can range from mild diarrhea to severe, bloody diarrhea with subsequent dehydration and anemia. Following infection, the affected animal may become a carrier. Coccidiosis is a cause of diarrhea in puppies. It may result in death in puppies.
Treatment consists of supportive therapy once disease develops. Drug therapy is ineffective - all of the available agents are coccidiostatic agents; they can prevent infection, but will not treat an established infection. Good sanitation is essential in preventing coccidiosis. Most disinfectants are ineffective against coccidian oocytes, but boiling water and 2% formaldehyde are effective if they reach the oocyte. Scrupulous cleanliness is the best preventive, although it is no guarantee against Coccidiosis.
Because coccidia is an environmental contaminant that produces an opportunistic infection, stress of any kind, such as vaccination, may be all that it needs to manifest. Adult dogs are carriers, and the coccidia oocysts are pretty resilient to most common disinfectants. Coccidiosis may be a major problem in an unclean environment, but may crop up a well run operation as well. An adult carrier will serve as a potential source of infection to puppies. The fact that a kennel has problems with coccidia is not itself a scathing indictment of the kennel - it's just a fact of life that has to be dealt with.
The definitive test for assessing a dog's deafness is the BAER test, which can tell whether a dog is unilaterally (one ear) or bilaterally (both ears) deaf. In breeds where deafness is a problem, you should insist on a puppy that has been BAER-tested.o
There is a mailing list for owners of deaf dogs that can help you answer many of your questions (mail email@example.com for information). In addition, you should look at their informative web site, http://www.cybervision.com/~cairo/deaf.html.
DJD can be ruled out with radiographic analysis such as OFA or Wind Morgan provide.
Distemper is the leading cause of infectious disease death in dogs, most commonly in unvaccinated puppies 3-8 months of age. Among infected dogs: half show little in the way of illness; many show mild symptoms; and in a few the illness is severe or fatal. Malnourished and ill-kept dogs tend to show more acute forms of the disease. Secondary infections and complications with distemper are common. Prognosis depends on how quickly the dog is diagnosed and treated, and which form of the disease the dog has.
There are two stages. Symptoms in the first stage include fever, loss of appetite, listlessness, and a watery discharge from the eyes and nose. It may appear like a cold -- but dogs do not get colds the way people do; a "cold" is therefore much more serious in a dog than in a person. Within a few days the discharge will thicken: a primary indication of distemper. Dry cough, pus blisters on the stomach, diarrhea (and associated dehydration) may follow. At this point, the dog may recover, or proceed on to the second stage which involves the brain. Dogs with brain involvement do not usually survive.
As of this writing, early screening for these conditions in the breeding stock is strongly advised to eliminate dogs with this condition. In addition, littermates and close relatives of affected dogs should be reconsidered as good breeding stock, as they are likely to carry some of the genes for these conditions.
The paper focused on Labrador Retrievers; however it is quite likely that as with Hip Dysplasia, Elbow Dysplasia is heritable in a number of other breeds as well.
The lesions primarily affect cartilage and secondarily bone, and can occur in the elbow, shoulder, hock, and/or stifle, though the elbow is by far the most common. When the condition is associated with inflammatory joint changes it is known as OCD.
Pain is present on flexing the joint. X-rays may show fragmentation of the joint cartilage, or a loose piece of cartilage in the joint.
OCD in the elbow has been proven in the Labrador to be hereditary, but no such proof has been shown for other forms of OCD or heritability in other breeds. However, it would be prudent to assume that outside of traumatic origin, a polygenetic mode of inheritance is at work.
Surgery is indicated to remove the pieces of cartilage, smooth both the top of the joint and the cartilage to stimulate new growth without flaps or chips. Recovery and prognosis are generally very good; there are many cases of dogs who had this surgery and went on to compete in obedience and agility once completely recovered. However, no matter how sucessful the surgery, the dog should not be bred if a hereditary cause is suspected.
This is a serious condition because it usually results in arthritis and efforts need to be made to be sure that the dog has enough exercise to keep fit, but not so much or of the wrong kind that would make the arthritis more severe. The condition should be handled surgically by an experienced orthopedic specialist.
It is thought to be genetic, and OFA now certifies dogs based on X-rays in the belief that its incidence will be reduced this way.
Grade I--minimal bone change on the anconeal processBecause awareness of these conditions is relatively new, there haven't been nearly as many assessments for elbow dysplasia as for hip dysplasia.
Grade II--additional subchondral bone changes and/or osteophytes
Grade III--well developed degenerative joint disease
In their reports, OFA separates ratings into dogs and bitches. Here are some stats, for the breeds with more than 1000 evalustions:
Rottweiler, 1042 bitches, 38.1% dysplastic--890 dogs, 47.9% dysplasticIt isn't known why males are consistently higher in percent dysplastic. This pattern is true for all 16 breeds listed as having more than 75 evaluations registered.
GSD, 2940 bitches, 18.2% dysplastic--2156 dogs, 23.9% dysplastic
Labs, 1398 bitches, 10.4% dysplastic--801 dogs, 15.2% dysplastic
Besides OFA, GDC will also evaluate and rate elbows.
PRA affects the entire retina and is the canine equivalent of retinitis pigmentosa. This disease manifests itself differently in different breeds. The most common form of PRA in the collie is detectable at early age (6wks and over). The form of PRA in Irish Setters is also early-onset. In Labrador Retrievers, on the other hand, the age of onset is much later, typically four to six years of age, making it much harder to find and isolate carriers in this breed.
PRA has been detected as early as six weeks in puppies, and these puppies are usually blind by six to eight months. An electroretinography can be used to detect the early signs of PRA. Animals to be tested in this manner are anesthetized while lenses are placed on the eyes to record the retina's reaction to light. (Like wearing contacts.) In other cases, ophthalmological examination by ACVO-certified vets can pick up cases of PRA and confirm them with electroretinography if desired.
All dogs affected with PRA eventually go blind. Carriers show no clinical symptoms. Symptoms are subtle, starting with night blindness, some eye dilation, to progressive blindness. It's quite common to not notice anything is wrong until the dog is nearly completely blind. Proactive testing is always recommended, especially for breeding stock.
Current research is beginning to isolate the genetic markers for this disease. At present, there is a genetic test to identify carrier and affected dogs in the Irish Setter breed. Work is underway for one for the Labrador Retriever. This disease is thought to be a simple autosomal recessive gene. Thus two recessive genes are needed for a dog to be affected. A single recessive gene masked by the healthy dominant means the dog is a carrier. Therefore, an affected dog's parents are carriers or also affected.
NOTE: In October 1945 the Kennel Club of England added PRA to the list of disqualifications from winning any award in the show ring.
Signs of glaucoma include reddened conjunctival tissue (red eye), weeping, light sensitivity, or even enlargement of the eye. As pressure increases, the pupil can become dilated and the cornea cloudy. Early diagnosis is critical to save the vision of the dog, and involves treating the underlying causes of the increased pressure if at all possible.
There are several options in treatment, which depend on the extent to which the eye has been damaged, and the amount of vision that has been lost. In addition, some dogs will respond better than others to medications:
Cataracts may be stable or progressive. In the former case, owners may never be aware that their dog has cataracts until or unless the dog is examined. In the latter case, the dog often adapts very well to the gradual loss in vision until a certain point is reached. General diagnosis can be done by ophthalmoscopic examination; if a more detailed examination is needed, a slit lamp examination must be performed.
Surgery is the only option for cataracts that seriously impair vision. Most surgery involves removal of the lens; however, implants can also be performed. Recovery and prognosis for these dogs are generally good.
If we bred NN x Nrd we would expect half of the puppies to be affected the others normal. If we bred Nrd x Nrd we would expect the following:
In mild cases of retinal dysplasia, sight is probably not affected much, if at all. In severe cases, skeletal abnormalities are present.
To avoid confusion, do not move your furniture around (except for any piece that the dog does keep bumping into. Be sure the dog knows when you are near so it is not startled. When you go out on walks, establish habitual trails. Your dog will adjust quickly.
CERF (Canine Eye Registration Foundation)
South Campus Courts C, Purdue University, West Lafayette, IN 47906
Vanderlip, Sharon Lynn, DVM. The Collie: A Veterinary Reference for the Professional Breeder.
Dr. Lionel Rubin, V.M.D., U of PA Vet Sch on Retinal Dysplasia.
Carrig, Sponenberg, Schmidt, Tvedten, JAVMA, Nov 1988.
Oliivero, DVM, Retriever Field Trial News, June 1993.
Rubin, Lionel F. Inherited Eye Diseases in Purebred Dogs, Williams & Wilkins, Baltimore, 1989.
CERF Publication "Ocular Disorders Proven or Suspected to be Hereditary in Dogs". The publication can be ordered directly from CERF by calling their office at (317) 494-8179.
Barnett, KC, et al: Hereditary retinal dysplasia in the Labrador Retriever in England and Sweden. J of Small An Prac, 10:755, 1970.
Carrig, CB, et al: Retinal dysplasia associated with skeletal abnormalities in Labrador Retrievers. JAVMA, 170:49, 1974.
Carrig, CB, et al: Inheritance of associated ocular and skeletal dysplasia in Labrador Retrievers. JAVMA, 193:1269, 1988.
Neslon, B, MacMillan, A.: Multifocal retinal dysplasia in the field trial Labrador Retriever. JAAHA, 19:388, 1983.
A condition more commonly seen in larger breeds. Gas in the stomach causes it to swell. In some cases, the stomach rotates on its axis, closing off both ends of it. Digestive processes continue unabated and the stomach swells up. The cause of bloat is unknown.
Some forms of bloat are fatal untreated; survival depends on understanding what is happening and getting the dog to the vet, the earlier the better.
History is important: in nearly all cases, there is a history of overeating, eating fermented foods, drinking excessively after eating, or taking vigorous exercise after a meal (within two or three hours).
If your dog is able to belch or vomit, it is more likely a gastric upset. If it cannot, rush it to the vet or emergency care *now* for emergency surgery.
If your dog is at risk for gastric bloat, you should discuss it with your vet before a possible episode. Your vet may recommend (and demonstrate) some things you can try to do as life-saving measures while getting it to the vet.
Measures thought to reduce the risk of gastric torsion ("bloat") [From the Bloat Panel, sponsored by the Morris Animal Foundations, published in the August 1992 Irish Setter Club of America's Memo To Members.]
Giardiasis is a malabsorptive syndrome. The parasites adhere to the lining of the small intestine where they interfere with absorption of nutrients. Light cases of Giardia often go undetected and many dogs "self cure" by expelling and developing an immunity to the parasite. In heavier infections, Giardia can interfere with absorption of certain types of nutrients, especially fats and certain vitamins. Fats are not absorbed and result in excess mucus in the stools which are very pungent and diarrhetic.
The parasites interfere with normal metabolism by forming a physical barrier between the lumen of the intestine and the absorptive cells. Excess mucus results from malabsorption of fats while excess water results in the diarrhea. The intestinal lining is not usually injured so stools should not contain blood. The parasites feed on partially digested food in the lumen of the intestine. They do not compete directly with the host for food. Their metabolism is primarily anaerobic, meaning that they do not utilize oxygen in their respiration. They lack cellular organelles concerned with aerobic respiration such as mitochondria.
The active stage within the host is the trophozoite (feeding body); this is the only pathological form. The transfer stage of the parasite is the termed the cyst. Giardia forms cysts by extruding cellular food particles and other vacuoles and secreting a resistant cyst membrane around the cell. This highly resistant cyst is then passed from the host in the feces. Trophozoites may be passed but quickly die. Cysts that are passed into water can survive for an extended time, up to 1-2 months under proper conditions. Survival times on land are somewhat less. A new host becomes infected by drinking fecally contaminated water or eating the feces of an infected animal. While food-borne transmission is rare, it has been documented for humans. Dogs may become infected by drinking out of streams, lakes or ponds containing Giardia cysts. Other sources of infection are wild animals that visit the kennel area and deposit infected feces in an area accessible to the dog. Scats of other dogs or wild animals are potential sources of infection for domestic dogs. Giardia is potentially transmissible to humans so caution is warranted.
Giardia can be difficult to detect even for professionals. It is too small to be seen by the unaided eye. A high quality microscope is needed for proper diagnosis; phase contrast microscopy is helpful. A definitive negative diagnosis should include stools collected on multiple days since cyst production tends to be cyclic with millions produced one day and few the following day. The cyst is the diagnostic stage of Giardia. Cysts tend to be approximately 9-15 micrometers in length and 4-5 um in width. Cysts are identified by size, the presence of four nuclei, axostyles and claw-hammer shaped median bodies.
The current drug of choice is metronidazole, known by the trade name FLAGYL. Although highly effective it is a known carcinogen and mutagen in mice. Quinacrine (ATABRINE) can also be used but is not as effective. Treatment is usually one tablet per day for 7-10 days, depending on the weight of the dog. Recovery is usually uneventful but a dog may become reinfected after treatment. Thus, it is important to try to isolate and eliminate the source of infection.
Symptoms may not appear until a full year has passed since infection. Because of this, the disease is often mistaken for another problem. The most persistant sign is a soft, deep cough. After exercise, the cough may be so severe that that the dog faints. Weight loss, discharge of bloody sputum, listlessness, and weakness are also common (from Carlson & Giffin).
The rest of the information on heartworms was adapted from a very informative post by Kristin Thommes who posted it March 5, 1994.
In the mosquito, the microfilariae (L1) will molt twice, to the L2 and then the L3 stage. At the L3 stage, the larvae migrate to the mosquito's mouthparts. Then when the mosquito bites a dog, the larvae are deposited ON the dog's skin and then crawl into the bite wound left by the feeding mosquito. If a mosquito with the L1 or L2 larval forms bites a dog, they will NOT be transmitting heartworms to the dog. Likewise, if the L1 forms are not removed from the dog's circulation by a biting mosquito, they will die off. The L1 stage does NOT "mature" into adult worms in the dog. So, the L3 larvae that crawl into a dog bitten by a mosquito will develop in the dog's subcutaneous tissues to L4 and finally L5 life stages. These then enter the venous system and enter the heart. They travel to the pulmonary arteries and become full-fledged adult worms, ready to reproduce.
So if a dog is on Heartgard and is tested for heartworms using the Knott's test, chances are the dog will test negative even if there are adult worms present. There is a different, more expensive test for dogs who may have sterile worms. It uses a blood sample to test for antigens produced by the adult heartworms. If the dog has heartworm antigen, it has a greater than 99% chance of having heartworms. This test should be used on any dogs that are on Heartgard since they will not have microfilariae in their bloodstream. Likewise, if there are only low numbers of circulating microfilariae, the Antigen test will give a positive result where the direct Knotts (Filter) test may be negative. Just like the standard Knotts test, the Antigen test will be negative if the dog was infected less than 6 months ago.
It is therefore very important for those dogs on the monthly medication to be tested with the Antigen test rather than the Knotts!
No. If a dog was infected and had circulating microfilaria, and these microfilariae were transplanted into a healthy dog via a transfusion, the healthy dog would NOT get adult heartworms because the lifecycle could not be completed within the body of the dog. A mosquito is needed for development from the L1 to the L3 stage.Could a pregnant bitch with heartworms give them to her own puppies?
No, for the same reason as above, you need the mosquito for the intermediate stages between microfilarae and adult worms. While the placental barrier will keep the microfilarae out, even if this barrier broke down (which can happen), the pups will not be infested.How do those medications work anyway?
There are basically 2 types of medication available that will help to prevent adult heartworm formation in dogs that are negative. One type is the daily medication Diethlycarbamazine (DEC). It works by killing any larvae that have crawled into the dog from the mosquito within approximately the past 36 hours. DEC kills L3 larvae. Once they molt into L4's, DEC will not kill them and these larvae may develop into adult worms.
Most common ways that a dog will contract heartworms while on medication include not being given medication on a regular basis (e.g. completely missed dosages); traveling from a winter environment to a summer environment like Florida without giving the dog heartworm medication; not WEIGHING the dog while on the medication: the dog outgrows its dosage; and the dog vomiting or having severe diarrhea after being given its medication. What should you do if you forget your dog's medication? *IF* the dog is on daily medication, give the dog a monthly tablet within 45 days of the missed dose. Depending on what you feel comfortable with, you can then restart the dog on the daily medication, or continue giving the medication once a month. *IF* your dog is on monthly medication, give the medication anytime you remember, even if more than 45 days has passed. Giving heartgard to a dog with heartworms will not hurt the dog, and until 6 months has passed the dog will appear to be negative anyway. However, you should NEVER give daily medication to dogs who may have circulating microfilariae. The daily medication can cause an anaphylactic reaction if given to a dog with microfilariae present. Giving monthly medication will prevent the dog from acquiring a heavy worm load by being bitten by multiple infected mosquitoes. Just be certain to have the dog tested 6 months after the missed dose to be sure that the dog did not acquire heartworms.
As of 1997, there is a new treatment method for dogs with heartworm. I have been informed that Immiticide (Melarsomide) is an intramuscular injectable heartworm treatement that obsoletes Caparsolate. I do not know how this functions or how it differs in treatment considerations for the dog.Treatment for heartworms is difficult on the dog and prevention is easy. If your dog tests positive for heartworms and you decide to treat it, here is what will happen: Your vet will want to take a blood sample to begin with to check the dog's liver function. The treatment that kills the adult worms uses a drug called Caparsalate. This drug is given twice a day for 2 days while the dog is in the hospital. The dog must be kept quiet (caged) for 4 weeks after the adult worms have been killed. It takes 7 to 17 days from the time of treatment for the adult worms to die. Within this time, dead worms will fragment and travel to the dog's lungs. If dead worms are numerous, some of the blood vessels to the lungs will become blocked, and this is inevitable. However, if the dog is kept quiet and only allowed to move around enough to go outside, the blockage of pulmonary vessels may remain subclinical. If the dog is allowed to run around, the heart rate increases and many dead worm fragments will travel to the lungs at the same time. This is what you want to avoid. About 4 weeks after Caparsalate has been given, the dog will be given a high dose of ivermectin to kill the remaining microfilaria that are circulating. Although this is a high dose of ivermectin, it is below the lowest dose known to cause mild, self-limiting toxic side effects in Collies. Obviously, after being treated, dogs should be kept on heartworm preventative!