ahicks51

When the depo shots are so straightforward, and the results are so dramatic, perhaps it would be best to have your vet contact Dr. Stack directly? (The only reason I'd hesitate is that they're very busy over there in Yuma.) If not, perhaps you should find another vet that is willing to do the procedure. I'm sure the one you have is very good, but when someone with as much experience with greys as Dr. Stack feels sufficiently confident to post "the fix" on the Internet, she must have very good reasons for doing so.

Frontline Plus is a combination of fipronil and (s)-methoprene. Fipronil is possibly a carcinogen, and possibly an endocrine disruptor: http://www.pesticideinfo.org/Detail_Chemic...?Rec_Id=PC35768 Then again, so is virtually everything else listed on pesticideinfo.org. However, it is not listed as an IARC carcinogen; it's not on the US NTP as a carcinogen, not on California Prop 65, or TRI. It is a "possible" carcinogen as per the US EPA, Category C: "Category C: Possible human carcinogen. The data show limited evidence of carcinogenicity in the absence of human data." This means in one test or another, it showed up as a carcinogen. This could mean it proved negative in 4-5 studies, and showed up as positive in one. Similarly, it shows up on the Colborn list as an endocrine disruptor, while four others show it as negative. It is NOT listed as a reproductive/developmental toxin, or as a "Chemical of Special Concern." Fipronil kills by gumming up the GABA channels in bugs, which humans don't have. Much better than organophosphates. This is what provides Frontline with the "quick kill." The methoprene is the "slow kill." It is an insect growth regulator (IGR), which gums up th e life cycle: the pests can't moult, so they die. Humans and dogs don't moult, so this is a pretty darned selective killer. Methoprene is less toxic than table salt to dogs: http://pmep.cce.cornell.edu/profiles/extox...oprene-ext.html (LD50 for sodium chloride is about 3,000 mg/kg, whereas methoprene is somewhere between 5,000 and 10,000. Anything over 5,000 is very safe indeed.) There are no reported issues with chronic toxicity, reproductive or teratogenic hazards, is "not" mutagenic, and not a carcinogen. When one goes out and compares labels with other products, Frontline is much safer than other products out there. It's also much more expensive. As for it being a carcinogen- a big fat, "yeah, maybe." But so little of it is used, and when compared to the alternatives- what are you going to use? Herbs and spices and good wishes? Program is lufenuron, a product lacking data: http://www.pesticideinfo.org/Detail_Chemic...?Rec_Id=PC38491 Big question marks there for "lack of data" with respect to being a carcinogen, reproductive toxin, or an endocrine disruptor. And this isn't a topical- this is something that is fed. Advantage is imidacloprid, a chloronicotinyl insecticide. It is more toxic than active ingredients in Frontline and Program, but very little of it needs to be used to achieve the same effect. There are some issues with chronic poisoning, reproductive issues, and teratogenic effects (issues mainly concerning bone growth and decreased body weight at higher concentrations). It may be a weak mutagen. It is a Group E carcinogen, meaning there is proof it is NOT a carcinogen in humans. High dosages did lead to thyroid lesions in rats. http://extoxnet.orst.edu/pips/imidaclo.htm Pick your poison!

The last time we went to re-test Coco's thyroid (several months ago), MSU informed us they were not doing T4 by dialysis, which I understand to be the most accurate technique. Hopefully things have changed and they're back to testing in that manner, but you might call their lab services number (they're infallible) if there is any doubt. I went with Jean Dodds over at Hemopet instead. I'm not sure if they do it on site (unlikely) or send it out, and I don't know which lab they use if they do send it out. It may just be IDEXX, same as about half the vets use anyway.

And a little tip for those of you who have hounds that don't like to stay still during the ophthalmological exam at your vet: some hounds have this great (vagal?) response when cleaning their ears. Coco won't hold his head steady for more than a couple of seconds, and he's a big guy- but cleaning the ear while the vet examines his eyes, and he'll hold still long enough for her to do her job just fine.

See, the weird thing is that he WAS on Flagyl- but hasn't been for several days- and his appetite has continued to diminish. The adopter is going to get him into the vet (who used to do work for a greyhound rescue group, so he has a little experience with the breed), but I'm trying to get to the root of the problem. I'd originally thought it was behavioral, but now am all but convinced it's medical.

OK, thanks everyone. Now an extension of that question: of course, giardia gives dogs the uncontrollable trots, but can it cause problems with urination? I'm trying to track down a problem with a dog we fostered. The vet put him on Flagyl (metronidazole), and I'm still in the dark as to why. Now he's messing in the house (#1 and #2), and seriously off his feed. Both are very odd as he has been fantastic about housebreaking, and has always had an appetite like a tiger shark. He's about 3-4 years old, and very strong, otherwise healthy.

The Merck Veterinary Manual advises that metronidazole (Flagyl) is about 65% effective for curing giardia. Panacur may be slightly better, I understand (if it IS giardia, of course). Good luck!

Like Batmom says- did a fecal panel get done anywhere along the line? Even if so, they may have missed it because of it being in an early stage.

I know a UTI frequently causes urinary continence problems. Can a urinary tract infection also cause issues with inability to control defecation- either medically or psychologically? (i.e., so long as I've wet the carpet, I may as well poo, too!)

Minerva once ate a 3-pound box of dog treats. She's also eaten entire loaves of bread while we were out. She also once broke into the kibble bag and gorged herself. (I know- we're horrible people.) The bread made her sleepy. The dog treats were extruded later in the hallway, same as how they went in but in less-solid form. You might see a mess later on, but as best as I know, bloat (gastric torsion) is not a function of overeating so much as it is the stomach "twisting" like a balloon in the gut.

Ooooh! Oooh! Get us a name, for future reference. Best wishes for Bodie and you!

Really stupid question here- but isn't bilirubin detected in an urinalysis, rather than a blood panel? If so, did you, er, submit a urine sample for testing? Might be a good idea to wait, re-test, and go from there. Merck Veterinary Manual also notes that pigmenturia can produce a false positive for bilirubin; if the urine was a red color, this should have been detected immediately, but I *think* pigmenturia means there is hemoglobin and/or myoglobin in the urine. As bilirubin is a breakdown product of hemoglobin- excreted in urine- this would explain the cross-reactivity in the test. Then, of course, you need to find out why there was hemoglobin or myoglobin in the urine.

Treatment for existing heartworm infections is extremely dangerous. Here's what the Merck Veterinary Manual has to say (emphasis mine): "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 kg or 1.5 in. for dogs >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 mm Hg. Both the standard melarsomine protocol and the alternate regimen kill all or most worms in ~75% of dogs. Antigen testing is performed 6 mo after the first 2 doses of the standard protocol or 4-6 mo after the third dose of the alternate protocol. A positive test result should be followed by retreatment (2 injections, 24 hr apart) if the antigen test is strongly positive, if the patient is still symptomatic, and if the patient is an athlete or a working dog. Mild infection, a weakly positive antigen test, absence of clinical signs, advanced age, and a sedentary dog are factors that may negate the need for a repeat melarsomine treatment. Maintaining dogs on ivermectin/pyrantel pamoate to slowly kill residual worms over the following 20 mo is an alternative in nonperforming dogs with a post-melarsomine weakly positive antigen test result. Ivermectin/pyrantel pamoate administered monthly for ~2 yr beginning at 5-7 mo post-L3 inoculation eradicates most adult worms. Further, during this time period, some older worms are also killed. However, the use of ivermectin/pyrantel pamoate is seldom a substitute for melarsomine treatment because the slow kill may allow pulmonary pathology to progress in the interim. In caval syndrome cases (class IV), surgical removal of worms from the right atrium and orifice of the tricuspid valve is necessary to save the life of the dog. This may be accomplished by using local anesthesia and either a rigid or flexible alligator forceps, or an intravascular retrieval snare, introduced preferentially via the right external jugular vein. With fluoroscopic guidance, if available, the instrument should continue to be passed until worms can no longer be retrieved. Immediately following a successful operation, the clinical signs should lessen or disappear. Fluid therapy may be necessary in critically ill, hypovolemic dogs to restore hemodynamic and renal function. Within a few weeks following recovery from surgery, adulticide chemotherapy is recommended to eliminate any remaining worms, particularly if many are still visible echocardiographically." The 4-6 weeks of restricting activity is important as bits and peices of the worms break free; if they lodge in the lungs, cardiac arteries, or brain, that can be the end of Fluffy. What the vet is recommending is presumably starting heartworm prophylaxis- presumably as ivermectin- to prevent, as you note, additional microfilariae from swimming around the system and taking up residence in the heart, as they do. If the titer is low, and the existing number of worms is small, this is presumably a "better-than-nothing" tack, and if you're *really* lucky, only one or two worms have taken up residence in the heart. The existing worms cannot reproduce effectively, and may even perish from the treatment (I *think*- I'm admittedly a little vague on that aspect of Dirofilariasis). See also: http://www.vetmed.auburn.edu/distance/cardio/aiello.htm http://publications.royalcanin.com/renvoie...session=2138011 It is estimated that 50% of people who DO use heartworm preventatives don't use them correctly- hence the annual re-testing before handing out new meds. If one were to start prophylaxis on an animal that was already infected, it would be critical to stick with it for the remainder of the animal's life.

Happened with Coco once. He also has "floaters" from cholesterol. Thought they were pannus; vet says they're cholesterol, which explains why they "move" now and again. She said it wasn't dietary, but I cut back on the beef heart a bit, and they seem less common now- no idea why. The corneal abrasion came about- I don't know how. It may have been from cavorting, or possibly he scratched his eye on a muzzle while rubbing his face. It took a few weeks to clear, but his corneas look good- aside from the occasional tiny cholesterol "floater"- and his vision is that of Minerva, who can spot cats from low earth orbit.

You should be nice to your ants. Cook for 'em. http://www.cdkitchen.com/recipes/recs/609/...Ants95380.shtml I mean, to kill 'em. And stuff.

I used to think that feeding raw was all about the bones and chewing physically removing plaque. It *does* work, but I think the mechanism is different; if it were the physical action of bones and flesh abrading away tartar, then how would they know how to stop? Why don't the gums- which are softer- get torn up? Now I think it's due to the virtual absence of carbohydrates. While bagged food is rich in starch, sugars, and plant material, raw food has very little carbohydrate content. There is no nutritional requirement for carbohydrates in the canine. Anyway- it sure works. Although Minerva still needs brushing, they're vastly improved over when we used bagged food. It's remarkable.

A diagnosis of LSS is made much easier after reading what Dr. Stack has to say on the subject. I showed this to my vet; she'd never seen it before, I don't think. http://home.comcast.net/~greyhndz/lumbosacral.htm

Isoflurane, probably with propofol induction. Yes, it is safe. The thing you want to stay away from: barbituates. As these have generally been phased out, sighthounds are much safer off these days. A few old-timers somewhere might still use the "bad stuff," but isoflurane and related fluorinated anaesthetics offer many characteristics that make them vastly more appealing than those from previous generations. In the past five years or so, virtually all vets should have migrated from older, less safe compounds to newer, more reliable anaesthetics. ETA: And brush those teeth! Soft, children's size tooth brush with enzymatic paste for use on pets.

I agree that you should pursue the possibility of your pup having an autoimmune disorder. However, if you wish to follow the allergy route, I would suggest changing the HVAC filters to high efficiency filters such as a high-performance 3M Filtrete air filter. The higher end filters from 3M with the red labels have efficiency numbers around 700-1000, and the purple-blue label ones run numbers over 1200. In conjunction with a vacuum that has HEPA filtration (to keep dust from getting knocked back into the air), that will reduce the number of allergens. Have you determined if there is a food allergy at hand? If not, and you are not smitten with your food, you might try Nutro; Purina ONE isn't the best stuff out there, contrary to what Purina has to say. I am not particularly enamored with Nutro, but it's a good starting place. Unless you find he does particularly well on Purina, I would recommend trying something new. Similarly, if you're up to it, feeding raw food may have some benefits. I didn't used to be a raw feeding whacko, but I've turned into one.

How did you determine the types of allergies? Skin patch test? Blood test? Elimination (trial-and-error)?

I think that's the best route, right there; check with the vet, but capturing "first rain" in the morning before feeding and bringing the sample in for analysis might save a lot of heartbreak. Check with your vet, but I think fasting for 12-16 hours is a big must for accurate urinalysis. And if you have a specific gravity test done, it should be by refractometry, rather than dip stick.

If you want to kill all the grass, just cut it as short as you can (weed whacker), and spray with Roundup. Keep the dogs off of it for a week or so. Another solution is to cover with black or clear plastic, and anchor the edges. If done in summer, it'll work pretty fast. Move the plastic around until the whole yard has been killed. But, of course then the weeds will come up from seeds so a germination inhibitor like oryzalin (Surflan, practically non-toxic) will be required. Of you could just get a weed whacker and cut it with that. It takes a little longer, but it works well enough in irregular yards.

I'm a little surprised they want to admit him, as kennel cough is highly infectious. The incubation period is about 7-10 days; has your dog been in contact or close proximity to other, strange dogs in that period of time? If not, it may not be kennel cough. ETA: Sorry; when I picked up Tito, they said the incubation period was 7-10 days. A web-based resource (with references) says it's 3-4 days. Also notable: The cause of kennel cough is frequently canine adenovirus, or canine parainfluenza. Canine distemper can also do it, too. Many 5-in-1, 6-in-1, and 7-in-1 vaccines offer protection against one or more of these pathogens. If you've kept up with your vaccinations, although it is still possible they didn't "take," it might be less likely that kennel cough is the cause.

From the Merck Veterinary Manual (emphasis mine): "Evaluation of serum chemistries, including BUN, creatinine, calcium, phosphorus, and serum electrolytes, is useful in many urinary tract disorders and can provide a crude indication of glomerular filtration rate (GFR). Although elevations in BUN and creatinine are supportive of renal dysfunction, these tests are influenced by nonrenal factors as well. For example, dehydration can cause increases in BUN and serum creatinine not associated with renal failure. BUN can also be influenced by diet and GI bleeding and is considered inferior to creatinine for evaluating GFR. Serum creatinine levels can be falsely lowered in patients with severe muscle wasting and falsely elevated in patients with severe muscle damage. Although BUN and serum creatinine increase as GFR declines, this relationship is not linear. Large changes in GFR early in renal disease cause only small increases in BUN and serum creatinine, while small changes in GFR in advanced renal disease may be associated with large changes in BUN and serum creatinine." Wish I could be more help, as I really don't know about kidney issues other than what I've read here and there.

Dr. Feeman's treatise on the subject may be useful: http://www.animalmedicalcentreofmedina.com...y%20Failure.pdf Specifically: "Diagnosing kidney disease can be difficult because both BUN and creatinine levels can also be elevated with dehydration or urinary obstruction." Was the urine tested for density by refractometry? There should be a number (USG), and it may have been taken by dipstick test or refractrometry; the latter is the desired test as dipstick tests aren't terribly accurate. If it was high, he may have been very dehydrated.