Adverse Reaction To Vaccination

[schwarzbear]

Hi List,

My litter of 7 pups were vaccinated with Canvac 3 on the 19th December at 7-1/2 weeks of age. A week after the vaccination 3 of the pups developed a rash in their ears. Took to the vet and he said a reaction to the vaccine. I released 4 pups who had no problems with the full disclosure to all owners.

Well then the nightmare commenced for these 3 affected pups. The short story I lost the 2 girls and still waging the war with the little boy who is now 15 weeks old.

I was not aware when I asked for a "dead" vaccine that in actual fact the distemper portion of the vaccine which is a combo of 3 vaccines is "live". It seems the 3 pups had an adverse reaction to the distemper part.

Of course I have talked to many people and my question to my vet was if I breed again (who knows at this point in time) would I be able to give separate vaccinations with a week or more in between to not blast an immature immune system with the 3 combo. He said individual vaccines of the 3 where not available in Australia. I do know the parvo one is because the pup I am struggling with is waiting to have a dead parvo injection.

Would appreciate any input from other breeders. These are Rottweiler pups.

Thanks

[leopuppy04]

I have no advice but that's awful

[weiz4eva]

Im so sorry for your loss.

Weimaraners can also have reactions to vacs.

Most breeders will only give C3 a vac at 6wks then another at 10wks or 12wks then nothing for 12mths.they dont need We suggest ONLY c3 for all our dogs/puppies anything more than a c3 isnt needed.

[schwarzbear]

Im so sorry for your loss.

Weimaraners can also have reactions to vacs.

Most breeders will only give C3 a vac at 6wks then another at 10wks or 12wks then nothing for 12mths.they dont need We suggest ONLY c3 for all our dogs/puppies anything more than a c3 isnt needed.

Thank you for your replies much appreciated. The vaccine I used is C3. Did you know that the distemper portion is "live". I did not I thought all 3 were dead.

What I am asking is if anyone knows if you can get in Australia the single vaccines. I know you cab get the parvo one but don't know about the other 2.

[Alyosha]

So sorry to hear about your pups.

This is a list of all vaccines approved in Australia that cover Distemper:

http://services.apvma.gov.au/PubcrisWebClient/search.do;jsessionid=d42TPvdC1smTbNHKRGTX8CrSgJSqLJylx2XBp7r215hKjySvGdvM!1534907726

They all seem to be combinations. If you go into each entry some will say what components are killed or attenuated. If not, you can click on label details and you should find the info there.

In a different section on the same website you or your vet can report the adverse reaction: http://www.apvma.gov.au/use_safely/adverse/veterinary.php

Could it be worth avoiding the Distemper component for these pups or related ones? And just giving Parvac (killed parvovirus only vaccine)?

[Alyosha]

All the ones in Australia seem to be live distemper.

Just an extra thought...

Another option you may have, if you find a product elsewhere in the world that might suit what you need, your vet can apply through the same department - APVMA - for special permission to import it. This permission can be given when a vet specifically needs a medicine which is not available in Australia.

[Kustali]

I'm so sorry, there seems to be alot of puppies affected by the vaccines from all breeds, so scary.

An alternative is Homeopathy, i'll pm you a link

[Jumabaar]

I'm so sorry, there seems to be alot of puppies affected by the vaccines from all breeds, so scary.

An alternative is Homeopathy, i'll pm you a link

As far as I know there is no alternative, I have used homeopathic drops in conjunction with vaccines to give pups a boost. Even my holistic vet believes that dogs do need vaccinations- she just thoroughly believes they only need one shot at 12 weeks, a titre to check it has worked and thats it.

Sorry for your loss. Loosing them at that age is soul destroying.

Can I ask (purely for learning sake) how it was worked out that it was a reaction to the attenuated distemper and not the adjuvants that are used in killed vaccines?

Edited January 27, 2012 by Jumabaar

[hilaryo]

OMG what a nightmare for you schwarzbear

So sorry for the loss of your puppies and continuing struggle with the remaining affected puppy!

May I ask how the reation progressed from the rash on the ears?

We've got puppies being vaccinated this week with the C3.

[schwarzbear]

OMG what a nightmare for you schwarzbear

So sorry for the loss of your puppies and continuing struggle with the remaining affected puppy!

May I ask how the reation progressed from the rash on the ears?

We've got puppies being vaccinated this week with the C3.

[schwarzbear]

Hi Hilaryo,

To anybody who is going to vaccinate I would contact a homeopathic vet or person and get an immune booster. The 4 pups that were released I got my homeopathic lady to make up an immune booster which I sent to them. What it is Human Transfer factor capsules and Thuja drops. They were put on these a week before their second vaccination and they continued for 2 weeks after the vaccination. If I breed again this is what I will do with all of my pups.

To answer your question why I know it was the distemper portion is because my vet said so as did Camden University. Symptoms they are horrific. I truely believe that both girls died of distemper. For my pups it started with a rash in the ears then the pups became lethargic, progressed to neurological problems, diarrhea, pneumonia. I was either at the vet or the University nearly every day for weeks with these pups trying to save them. At Christmas because the Uni shut down and I was sick of all the chemicals I went the holistic way with my homeopathic lady and graduated to All Vets Natural for the homeopathic nosodes. By this time I only had Koopa (the boy).

A lot of people would say why did I not put them down. These were beautiful pups with temperaments to die for the best I have ever bred. I decided I needed to try and save them. They were not sick all the time it would come in waves and they were such sweet pups. The girls one I was going to keep she was stunning and the other girl was going to my grandchildren.

[Steve]

The only real threat you have in Australia for young puppies is Parvo and you can buy a killed parvo vax and give that yourself. Then at 16 weeks go a live C3. There hasn't been any distemper in 29 years but generally most agree we should still give em a shot.Its probably an acceptable risk if you don't.Kennel cough is pretty useless in my opinion and I don't ever vaccinate for it.

If your puppies and not any others vaccinated with that batch or not all of your puppies reacted this way and are having a reaction you have to assume its an immune system issue in your pups and that needs to be noted and considered when anyone is deciding on a mating in future .It's info you need to share for other breeders to be aware of in the hope that they can breed puppies less likely in the future to have a bad reaction. Keep in the back of your mind that even though these puppies reacted this way which is something you could see that there may be things going on with the other's immune system which has shown its self yet so you need to keep good notes on this litter for years.

So if you are keeping a pup from that litter for breeding you need to ensure you choose one which has had no reaction what ever to the vaccine for a start. This is advice given to us from Jean Dodds when she was in Australia.

There are also some other things you may be able to learn from what has happened to try to head off anything similar again but you will need to take a long look at the bitch and her mother, her immunity, vaccination status, whether she was having heart worm meds, what worm meds etc ,diet of the puppies, your worming protocol and which drugs were used ,what other things they may have been exposed to, you need to look at the history of immune system issues in both parents,their parents and their siblings and relatives and a bunch of other things to try to spot anything that starts to tell a story if you want to take it to that length.

Some years ago I took a litter to the vet ,all were checked, temps taken etc before the Vax went in .As I was leaving one was gagging and I said to the vet "that puppy is being sick" Her response was a smile and "probably sick of being in the crate" By the time I got home 2 were dead - 40 min drive in air conditioned back seat. the other 6 were fine - never missed a beat. Anaphylaxis.

[schwarzbear]

The only real threat you have in Australia for young puppies is Parvo and you can buy a killed parvo vax and give that yourself. Then at 16 weeks go a live C3. There hasn't been any distemper in 29 years but generally most agree we should still give em a shot.Its probably an acceptable risk if you don't.Kennel cough is pretty useless in my opinion and I don't ever vaccinate for it.

If your puppies and not any others vaccinated with that batch or not all of your puppies reacted this way and are having a reaction you have to assume its an immune system issue in your pups and that needs to be noted and considered when anyone is deciding on a mating in future .It's info you need to share for other breeders to be aware of in the hope that they can breed puppies less likely in the future to have a bad reaction. Keep in the back of your mind that even though these puppies reacted this way which is something you could see that there may be things going on with the other's immune system which has shown its self yet so you need to keep good notes on this litter for years.

So if you are keeping a pup from that litter for breeding you need to ensure you choose one which has had no reaction what ever to the vaccine for a start. This is advice given to us from Jean Dodds when she was in Australia.

There are also some other things you may be able to learn from what has happened to try to head off anything similar again but you will need to take a long look at the bitch and her mother, her immunity, vaccination status, whether she was having heart worm meds, what worm meds etc ,diet of the puppies, your worming protocol and which drugs were used ,what other things they may have been exposed to, you need to look at the history of immune system issues in both parents,their parents and their siblings and relatives and a bunch of other things to try to spot anything that starts to tell a story if you want to take it to that length.

Some years ago I took a litter to the vet ,all were checked, temps taken etc before the Vax went in .As I was leaving one was gagging and I said to the vet "that puppy is being sick" Her response was a smile and "probably sick of being in the crate" By the time I got home 2 were dead - 40 min drive in air conditioned back seat. the other 6 were fine - never missed a beat. Anaphylaxis.

[schwarzbear]

Thank you everybody that has replied. Also I made a mistake in the date they were vaccinated in November.

Have had no problems on my bitch line and as far as I know the father's is clear. Fortunately all the pups are in lovely pet homes so will never be bred with. If the boy makes it he will remain with me. It has been a real learning curve although rather painful.

[Steve]

You know what - over the years the times I've probably learned the most is when things go belly up . Its taught me to question everything and never to take the word of my vet or the drug companies which produce the product.

You cant underestimate the knowledge wisdom and understanding that comes from experience and listening to other's experiences. No amount of study or looking at isolated studies where variables arent taken into account can ever equal that.

Im so very sorry for what you have had to go through and how your puppies had to suffer - but Im sure at the end of the day it will make you a better breeder.

[asal]

From my own experience I dont entirely believe its the puppies parents at fault.

none of this happend until the vaccine companies came up with a "better" vaccine. forget the year but its over 10 years ago now. I bred my first pups in 1979 and up until about 1983 or there abouts never lost a pup after vaccination. same family of dogs in some cases same parents.

then the new u beaut more "effective" vaccine was released. that day I took 10 pups for their vaccinations. next morning all but 4 were dead. another two had their immune systems shut down over the next 2 weeks and they too died.

that was three litters of pups the parents of two of the litters had previous litters vaccinated with the "old" vaccines with no reactions whatever.

by the second lot of puppies to be vaccinated and equal death rate i realised this was the new reality to vaccination.

and yes when I phone the company was told, "its only the small breeds dying" change to a bigger breed.

and no they had no intention of researching a safer version.

so?

are our dogs really now carrying a "new" weakness gene. or like the murry grey cattle and collie dogs the victums of a new drug that was not tested for safety sufficiently. eg ivermectin.

this culling of the innocents because a new improved product is killing a percentage of who they are supposed to be vaccinating would never be tolerated if the babies were human surely?

at the time i raised the question on a forum and to my astonishment the replies came thick and fast. even adult dogs were dying after their booster shots. and its taken how long for it to be disclosed that the yearly shots are severe overvaccination but (maybe more likely didnt believe or want to), it was a guaranteed income.

only in the very recent past has it been acknowledged that once they have had their initila shots yearlies are not needed.

well thats for the survivors that is.

many vets flatly refuse to give a reduce dose. i have found the only way to have the puppies survive in reduce the dose so i will not use a vet who will not consider a half dose.

for goodness sake they give the same dose to a great dane weighing ten and more times that of a toy breed puppy. and yes it does work and no i havent lost any to disease

despite protests that the vaccine is not guaranteed to work at less than the recommended dose.

well given the choice that the full dose none of the dead puppies will ever catch any disease they are right on the ball there.

Edited January 29, 2012 by asal

[asal]

cannot name names for obvious reasons but quite a few vets have admitted to me they now no longer give the full dose. one was shocked to see a puppy he had just vaccinated colapse and die while he was still holding it. Never wants to experience that again.

so is it faulty parents or fault in the makeup of the new vaccines???????????

incidently i have no idea why vets bother to have insurance or the drug companies. even when a known faulty batch kills for example 600 before its withdrawn the owners of the dead are never told, nor compensation ever a possibility.

i know because one batch of kitten vaccine was contaminated and killed an entire litter of at the time extremely rare lilac himilayan kittens. we only discovered they were killed by the vaccine when a friend working at the company saw the recall notice and the death figures reported in by the vets and over 600 notifications of the dead were received at the office of the vaccine company before the recall went out.

Edited January 29, 2012 by asal

[asal]

trouble is reporting stuff like that is more likely to get you accused of being paranoid and being a conspirity nutter.

if you are thinking that...google Ivemectin n murry grey cattle...n collie dogs

did some myself. very interesting the ones who react have a gene all right that doesnt cope.

so is it the fault of the animals or people they carry a gene the new u beut wonder drug affects or the manufacturers for not designing one that doesnt kick into that gene? chicken before the egg really.

one of the leaders in the field of designing worming drugs in the very early days it was mooted should we select for worm risistant animals? or drenches to protect all?

they went the drench way and after decades of trying to outwit the constantly evolving worms to resistance to every one of them in an astonishing amount of time, he wondered if he and his collegues had made the wrong choice.

his name is Hugh Gordon. or H Mc Al to many. http://en.wikipedia.org/wiki/Hugh_Gordon

there have been some significant worm resistant strains of sheep that were not continued with unfortunately. so the choice was and still is out there.

as well they discovered strains of nemanaphargic fungi (guessing at the spelling) that actively hunt and eat worm larve in the field.

this is them

http://notexactlyrocketscience.wordpress.com/2007/12/15/prehistoric-meat-eating-fungus-snared-microscopic-worms/

there are strains that exist that eat the larval stages of sheep and cattle worms and inoculated onto feed and fed to cattle and sheep, they kill and eat the worm larve passed in the manure. years later the paddocks when tested still had the fungai working, fasinating stuff.

wonder if there are ones that hunt dog worm larve as well?

Edited January 29, 2012 by asal

[OSoSwift]

if you are thinking that...google Ivemectin n murry grey cattle...n collie dogs

interestingly I have Murray Grey Cattle, have never heard of them being more sensitive to Ivermectin

I have also used it on my herd many times.

Will read some more.............

[asal]

here is part of one i found

"1. EXPLANATION

Doramectin is a member of the avermectin class of compounds, which includes abamectin and ivermectin. It is a semisynthetic avermectin that has close structural similarity to abamectin and ivermectin. It is used as an endoparasitic agent in non-lactating cattle.

Doramectin was previously evaluated by the Committee at its forty-fifth meeting (Annex 1, reference 119), when it established an ADI of 0–0.5 µg/kg bw on the basis of a NOEL of 0.1 mg/kg bw per day for mydriasis in a 3-month study in dogs treated by gavage and using a safety factor of 200. An additional safety factor of 2 was applied because doramectin was not tested in CF-1 mice, which is the test animal most sensitive to the neurotoxic effects of this family of drugs. In 1997, the Joint FAO/WHO Meeting on Pesticide Residues (JMPR) concluded that the sensitivity to avermectins of CF-1 mice was due to a genetic variation that causes reduced expression of P-glycoprotein in the blood–brain barrier (FAO/WHO, 1998). The JMPR further concluded that the results of studies with CF-1 mice were not appropriate for establishing ADIs for avermectins.

P-glycoprotein was expressed in the brain and jejunum of all species studied. P-glycoprotein is a cell membrane protein that acts to remove a wide variety of lipophilic compounds from cells, including avermectins. In the capillary endothelium of the central nervous system, it serves as a functional component of the blood–brain barrier. In intestinal epithelium, P-glycoprotein can limit intestinal absorption of a range of compounds.

The Committee at its fiftieth meeting (Annex 1, reference 134) accepted the conclusions of the JMPR and considered that it was no longer necessary to apply an additional safety factor of 2 for avermectins and milbemycins that had not been tested in CF-1 mice. Doramectin was re-evaluated by the Committee at its present meeting in order to determine whether removal of the additional safety factor of 2 was appropriate. On the basis of the Committee’s decision taken at its fiftieth meeting, the present Committee concluded that use of an additional safety factor of 2 in establishing the ADI for doramectin was no longer necessary.

No new data were provided to the Committee. The literature was reviewed for published information on the toxicity of avermectins considered relevant to this evaluation. The Committee reviewed information on the mechanism of the toxicity of ivermectin in a subpopulation of collie dogs and observations of its toxicity in a subpopulation of Murray Grey cattle. The Committee also considered a published review of the relative sensitivities of mice, rats, rabbits, dogs and non-human primates to avermectins. The relative potencies of doramectin, ivermectin and abamectin were also considered. The Committee examined information about variants of the human gene that codes for P-glycoprotein and reviewed observations in humans.

2. BIOLOGICAL DATA

2.1 Toxicological studies

2.1.1 Genetic basis for sensitivity to the toxicity of avermectins

(a) Collie dogs

The genetic basis for the sensitivity of collies to avermectins was studied in 13 clinically normal collies, previously identified as being sensitive or insensitive to ivermectin. Seven animals were identified as sensitive after displaying typical clinical signs of neurotoxicity, including depression, ataxia, mydriasis, salivation or drooling, after receiving a single oral dose of 120 µg/kg bw. The objective of the study was to determine whether altered gene expression of P-glycoprotein or a polymorphism of the canine Mdr1 gene that codes for P-glycoprotein exists in avermectin-sensitive collies. The sensitivity of the CF-1 mouse strain to the neurotoxic effects of avermectin has been traced to a polymorphism of the murine Mdr 1 gene resulting in decreased expression of P-glycoprotein (Umbenhauer et al., 1997).

The level of Mdr1 expression was similar in sensitive and insensitive collies, as determined by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) analysis. Sequence analysis of canine Mdr1 by RT-PCR was conducted on RNA isolated from blood leukocytes obtained from the sensitive and insensitive collies and also from other breeds (one beagle, two golden retrievers and one Staffordshire terrier cross-bred dog). Sequence analysis of clones from three ivermectin-sensitive collies revealed an identical four-base pair deletion in the first 10% of the transcript. This deletion causes a frame-shift mutation resulting in the production of a truncated, non-functional protein. The same four-nucleotide deletion was detected in all samples from ivermectin-sensitive collies, which were also homozygous for the deletion. Insensitive collies had a heterozygous genotype, with one mutant allele and one wild-type allele. Blood samples from all the other breeds showed homozygosity for the wild-type. The investigators concluded that their study provided evidence that the sensitivity of collies to ivermectin results from a frame-shift deletion of four base pairs in the canine Mdr1 gene (Mealey et al., 2001).

(b) Observations in Murray Grey cattle

Murray Grey cattle on one farm in the central tablelands of New South Wales, Australia, were reported to be sensitive to the toxicity of avermectin B1. The first cases were noted in October 1985, in 50 Murray Grey heifers aged 18–26 months treated with avermectin B1 at an estimated dose of 175–200 µg/kg bw by injection. Three of the heifers died within 2 days of treatment.

Two weeks later, 144 Murray Grey cattle aged 4–18 months and weighing 200–450 kg were treated with avermectin B1 at an estimated dose of 120–200 µg/kg bw by injection. The numbers of males and females treated were not stated. Within 48 h of treatment, three steers weighing 400–450 kg developed severe neurological signs, and all three were slaughtered for necropsy. A fourth steer in this group showed mild neurological signs and was slaughtered 19 days after treatment.

A field trial was conducted on this farm with 208 Murray Grey cattle, comprising 90 steers that had been treated with avermectin B1 1–2 months earlier and a second group of 118 cattle that had not been treated previously. The animals were weighed and treated with the recommended therapeutic dose (200 mg/kg bw) or injected with the vehicle only. One steer in the group that had not been treated previously developed neurological signs 42 h after treatment and was slaughtered for necropsy.

Brain, spinal cord, liver, kidney, lung, heart, spleen, intestines, skeletal muscles, adrenals, lymph nodes and peripheral nerves from the four initial cases, the case found in the field trial and one normal treated animal were examined macroscopically and histologically. No pathological changes were found that would explain the severe neurological syndromes observed. The concentrations of avermectin B1 in plasma and/or serum, liver, brain and spinal cord from the five clinically affected animals and the normal animal were assayed by high-performance liquid chromatography with fluorescence detection. The average concentration of avermectin B1a was 56 µg/ml in brain tissue from affected animals and 4 µg/ml in brain tissue from the normal animal.

Two additional field trials were undertaken with Murray Grey cattle in other areas of New South Wales and in Victoria. A total of 83 cattle were treated with at least twice the normal therapeutic dose of avermectin B1. No adverse reactions occurred. The authors stated that no other incidents of toxic effects of avermectins have been reported in Murray Grey cattle. They also noted that the farm on which the adverse reactions were seen had maintained a virtually closed herd for approximately 15 years (Seaman et al., 1987).

2.1.2 Relative sensitivities of mice, rats, rabbits, dogs and non-human primates to the toxicity of avermectins

The relative sensitivities of the central nervous system in mice, rats, rabbits, dogs and non-human primates to avermectins have been reviewed (Lankas & Gordon, 1989). The studies conducted with ivermectin addressed acute toxicity in mice, rats, dogs and rhesus monkeys treated orally; short-term studies of toxicity in rats, dogs and rhesus monkeys; and studies of developmental and reproductive toxicity in mice, rats and rabbits. The studies with abamectin given by oral administration comprised long-term studies of toxicity and carcinogenicity in mice and rats, a 1-year study of toxicity in dogs and a study in rhesus monkeys given single doses.

The authors concluded that clear species differences exist in the sensitivity of the central nervous system to the toxicity of avermectin, rodents being the most sensitive. A dose of 0.2 mg/kg bw in mice and slightly higher doses in rats resulted in clinical signs of central nervous system toxicity, comprising tremors and ataxia, while these doses caused no adverse effects in rabbits, dogs or rhesus monkeys.

The authors described a study of acute toxicity in which groups of two male and two female rhesus monkeys were given abamectin or ivermectin at single oral doses of 0.2, 0.5, 1, 2, 8, 12 or 24 mg/kg bw. The time between administration of the next higher dose to the same group of monkeys was 2–3 weeks. The authors noted that the minimum single oral dose of ivermectin or abamectin that was toxic (2 mg/kg bw) was approximately 10-fold greater than the human clinical dose of ivermectin. Emesis was the only toxic effect observed in rhesus monkeys after an oral dose of ivermectin of 2 or 8 mg/kg bw; the clinical signs of toxicity observed after a dose of 24 mg/kg bw were emesis, mydriasis and sedation. The authors compared the effect at 8 mg/kg bw with effects seen in a child (age and sex not stated) after the apparently accidental ingestion of approximately 8 mg/kg bw. The toxic effects observed in the child were emesis, mydriasis and sedation. In view of the similarity of the toxic effects observed in rhesus monkeys and the child, the authors proposed that rhesus monkeys are an appropriate model for predicting the acute toxic effects of ivermectin in humans. The NOEL for acute effects after administration of abamectin or ivermectin to rhesus monkeys was 1 mg/kg bw.

The review of the developmental and reproductive toxicity of ivermectin included the results of studies conducted in mice, rats and rabbits. The reported NOELs for maternal toxicity in mice, rats and rabbits were 0.1, 5 and 3 mg/kg bw per day, respectively. The reported NOELs for developmental toxicity in mice and rabbits were 0.2 and 1.5 mg/kg bw per day, respectively. A NOEL of 0.2 mg/kg bw per day was reported for neonatal and developmental toxicity in a multigeneration study in rats (Lankas & Gordon, 1989)."

this is the link to the whole article

http://www.inchem.org/documents/jecfa/jecmono/v49je02.htm#2.1.1.2