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Vaccinations and How They Disrupt the Immune System
Patricia Jordan DVM, VND 

By Dr.Jeannie on Jun 14, 2010 in Dog Health - Immune System, Dog News The Latest Poop

There is historical evidence that the Chinese were the first to attempt the theory of vaccination during the Song Dynasty (960-1279).1 This procedure was called virolation and was first used with small pox crusts as snuff to blow up the nostrils of people they hoped to affect. Virolation by the Chinese predates the small pox work of Edward Jenner, Farmer Jesty and Lady Montague by five centuries.2 The Chinese discontinued the attempts at vaccination as they discovered the process did not help and actually made conditions worse for the patient. How intelligent this deduction was back in that period of time. The Chinese from the medical perspective saw the vaccine as a pathogen and invoked the Divergent Meridians to take the pathogen and translocate it to the interior of the body. In order to do this, to make the pathogen latent, the body had to expend its resources, Yuan Qi and Yin-Jing which is dense and heavy and kept the pathogen dormant (which the body does in the joints/bones/marrow).
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The problems in babies and in animals of all ages that are receiving a continuous yearly load of pathogen impact via vaccines, is that the Yuan Qi and Jing should not be disturbed at these young stages of development and thereafter so frequently in life. The additional problems of a poor diet , the use of excessive drugs like antibiotics and resultant Qi depletion is an overall lack of capability to maintain dormancy of the pathogens.
When overwhelmed with vaccinations in addition, these mechanisms leave the individual vulnerable. With so many resources being allocated to deal with the vaccines, what is left of the Vital Force to handle the vicissitudes of daily living? Poor nutrition and environmental toxins and chemicals along with the synthetic use of drugs all tax and handicap the body, so that the bodies are coming into immune compromise and depletion much too quickly.
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The vaccines themselves stimulate adverse reactions causing disease, disability, organ failure, cancer, autoimmune disease and sometimes death. The number of dog vaccines has grown from 4 administered only once or twice in a lifetime to 20 and often aggressively administered twice a year! The intent of this commentary is to introduce to the reader to just a few pathways of immunopathology resulting from vaccine administration. When dealing with a patient exhibiting any clinical signs, remember to obtain vaccine administration history and remember that the ancient Chinese were indeed able to link the correlation of vaccination to the disharmonies of health that followed.
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In lectures I have attended by veterinary vaccine researchers such as Drs. Ron Schultz, Richard Ford, Jean Dodd and Dennis Macy, the pathways to pathology from vaccination have been clearly associated. The only vaccine that Dr. Ron Schultz is still advocating is the 3 way vaccine for the three lethal viruses, distemper, adenovirus and parvovirus (and the rabies until we get the laws changed).3 For the cat, the only lethal virus he advocates vaccination for is the feline distemper. Dr. Schultz lays out the pathology that follows cats vaccinated with herpes virus or calicivirus vaccines if administered by injection. He also advises that these vaccines against the lethal viruses are only necessary once in a lifetime to a mature mammalian immune system in order to result in genetic imprinting, incorporation of the viral proteins into the genome to affect pathogen sensitization of the patient’s immune cells. Additional administration just increases the adverse events and vaccine induced disease. Lymphoma is now understood to result from chronic B cell stimulation, chronic stimulation by antigen, vaccines result in antigenic stimulation, adjuvant ensures the chronic stimulation.4
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The rabies virus vaccine is full of its own problems with autoimmune disease production and adverse events such as ascending paralysis and encephalitis which have occurred since Pasteur first started grinding up infected spinal cords and injecting them into subjects.5 There is evidence from as far back as 1954, published, and 1945, unpublished, that only one rabies vaccine injected into the mature body of a mammalian immune system is capable of sensitizing the patient for life against the rabies virus.6 Other work followed in the 1970’s. Research to confirm this is currently being performed by Dr. Schultz and his group as the vaccine manufacturers are not releasing their data that establishes this fact.7 There was a study done in France on cats and dogs vaccinated against rabies that showed that animals were still resisting a rabies viral challenge 5 years after vaccination.8 As well there are human cases where the rabies vaccine amnestic response has been effective for 14 years.9
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Humans have pathogen recognition of small pox for 92 years after vaccination. Once thought to be 50 years in duration and even less when they first started the procedure of vaccine administration, it is now well understood that most viral vaccines give pathogen recognition for the entire life of the patient.10 My clinical experience is that this amnestic can also be passed vertically from one generation to the next, why not, it is genetic incorporation we are talking about. Dr. Ron Schultz and Dr. Jean Dodd are on record that only one or two rabies vaccines will be sufficient for the life of the animal and are both working with the Rabies Challenge Fund to establish the scientific criteria necessary to change the laws regarding rabies vaccination in this country.
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In 1972 the American Veterinary Medical Association first recommended vaccinating yearly, despite the decades of successful use of vaccines administered only in the first year of life. Representatives from the drug manufacturers and several regulatory representatives were the ones whom advised the AVMA to institute a change to yearly vaccine recommendations, not active small animal practitioners and not immunologists.11 The AVMA enacted this radical change despite the clear acknowledgement that yearly vaccines were not necessary and that the current practice of only administering pediatric vaccines had been enough to successfully control infectious disease. What has resulted from this unscientific and non evidence based procedure of vaccination administration? Dr. Ron Schultz now sees autoimmune diseases in animals that previously did not exhibit this. Our farmed fishes that we now vaccinate due to the stress and disease that follow intensive farming practices are now being diagnosed with autoimmune diseases.12 The AVMA appointed Feline Vaccine Associated Sarcoma Task Force has a decade of research showing the vaccine induced cancers and not just in the feline species, not just at the injection site and not just sarcomas. The unparalleled rise of chronic degenerative diseases, cancer, allergies, asthma, autoimmune diseases, disability and deaths is illustrated in the following graphs using the increased rate of vaccination on humans 13
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Following is an incomplete list of adverse events and diseases that follow vaccination. After 25 years of being in the veterinary field, this list presented in 2007 at Warwick, Rhode Island is the first time in my veterinary career that any veterinary medical researcher has presented this information to veterinary professionals. (Schultz) Common Reactions included; lethargy, hair loss, hair color change at injection site (cutaneous vasculitis), fever, soreness, stiffness, refusal to eat, conjunctivitis, sneezing, and oral ulcers. Moderate reactions included; immunosuppression, behavioral changes, vitiligo, weight loss (cachexia), reduced milk production, lameness, granulomas/abscesses, hives, facial edema, atopy, respiratory disease and allergic uveitis (blue eye). Severe reactions triggered by vaccines included; vaccine injection site sarcomas, anaphylaxis, arthritis, polyarthritis, hypertrophy osteodystrophy, autoimmune hemolytic anemia, immune mediated thrombocytopenia, hemolytic disease of the newborn (neonatal isoerythrolysis), thyroiditis and glomerulonephritis. Disease or enhanced disease which with the vaccine was designed to prevent included; myocarditis, post vaccinal encephalitis or polyneuritis, seizures, abortion, congenital anomalies, embryonic/fetal death and infertility. Dr. Ron Schultz is one record with the statement that anytime you inject you could potentially kill the patient and to assume vaccination is safe is a serious misrepresentation of the facts.14 The AVMA is now on record with this caution not to assume the safety of vaccinations.
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From these post vaccinal reactions, it can be understood that vaccination is not an “innocuous” procedure and that the risk versus the benefit of vaccination must be reviewed. For more information on vaccine induced disease, review the United State’s Federal Registry of adverse vaccine events in humans and the reported adverse events that follow vaccination reported through VAERS. The factual link of vaccination to damage is the reason the National Childhood Vaccine Injury Compensation Act was made into law. Adverse events from vaccinations are grossly unreported in both human and veterinary medicine and the lack of a central independent site for registering vaccine adverse events leaves the veterinary medical professional at a serious advantage and unable to collect even an informed consent or full disclosure statement prior to the procedure. 15 The AVMA is on record with the statement that the canine immune system is not different from the mammalian immune system and thus the reporting of vaccine induced diseases in human medicine and research is relevant to what we see in practice. Oncology Diplomate Dr. Dennis Macy is a supporter of the Veterinary Vaccine Injury Compensation Act that would address vaccine injury from veterinary vaccines even though the only lawfully mandated vaccine for animals is the rabies vaccine. Since the suggestion that a single vaccination against only the lethal viruses was necessary by leading veterinary infectious disease experts, the author has studied what science did know about vaccine induced immunopathology and found the reasons to support a position of not causing disease in my patients through the additional vaccinations protocols still much too prevalent today.
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The following is a brief overview of some of the pathophysiology produced by vaccination reported in the scientific literature: the different ingredients in the vaccines, aluminum and mercury are linked to immune dysregulation as are the viruses, the mutators and carcinogens in the vaccines. The big moment of epiphany for the author was the reaction that the antigen in vaccines does much to dysregulate the immune system by the very interaction with immune cells leading to autoantibody production, autoimmune disease, loss of tolerance, immune mediated pathology, all four forms (type I-IV) of immune system reactions, oxidative damage, chronic inflammation, cancer, to even speeding up the aging process (Selye’s Disease)
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1. Lymphocyte suppression from canine polyvalent vaccines in dogs and in chickens with the avian pneumovirus vaccine. 16
2. Post vaccinal lesions of the nervous system and the role of the autoimmune process of pathogenesis. 17
3. Immune mediated glomerulonephritis, amyloidosis, uveitis, polyarthritis, non-regenerative anemia, renal organ failure and hepatic organ failure, auto-inflammatory syndrome, immune mediated inflammatory neuropathies, autoimmune encephalomyelitis, Gullian Barre Syndrome (post infectious auto-immune disease) Common Immune Deficiency, ischemic dermatopathologies (cutaneous vasculitis), post injection site granuloma, necrotizing panniculitis, vaccine induced type 2 diabetes, metabolic syndrome, heart disease, pericarditis, myocarditis, dilated cardiomyelopathy, acute coronary events, vaccine induced enhancement of viral infection, aberrant viral pathogenesis, IgE class switching and behavioral changes of increased anxiety, increased aggression and increased compulsive obsessive disorder.18
4. Molecular mimicry (example of how measles in MWR vaccine is able to cause SSPE subacute sclerosing panencephalitis which is autism), distemper and molecular mimicry leading to myelin sheath autoimmune inflammation, neuropathy, cognitive dysfunction, chronic inflammatory demyelinating polyneuropathies, and thimerasol in vaccines altering the function of the dendritic cells in antigen presentation 19
5. Particularities of the vasculature which promotes organ specificity of autoimmune disease. 20
6. Histamine dysregulation up or down as a result of vaccinations. 21
7. Inflammatory arthritis and intractable chronic arthritis. 22
8. Immune mediated thyroiditis 23
9. Thymic depletion 24
10. Autoimmunity, loss of tolerance 25
11. Vascular induction of mini-strokes, blood stasis 26
12. T cell suppression allowing co-infections with bacteria, viruses, fungus, yeast and parasites (intestinal and dermatophyte)27
13. Immunodeficiency (this imparts the necessity to NOT vaccinate in any situation the cats that are Felv or FIV positive and the necessity of knowing the immune status before any stressful immunosuppressive actions taken against them (e.g. anesthesia, spay, neuter). Vaccinating immunosupressed individuals increases adverse events and expression of the very infections they are being vaccinated against. This holds true for the patients undergoing chemotherapy and other immune suppressing medications e.g. cyclosporine (Atopica) prescribed for over reactive immune systems up regulated from damage associated with earlier vaccine administration.28
14. Cytokine cascade promotion and onset of inflammatory cascade 29
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The above list is not comprehensive as that would be beyond the scope of this commentary due to space limitations, it is however the outline of a second book on vaccine damage by this author. There is voluminous evidence for the association of cancer with vaccines and the International Agency for Research on Cancer and the World Health Organization have clearly established the information that adjuvant in vaccines are Grade 3 out of 4 carcinogens, with Grade 4 being the most likely to induce cancer.30 Dr. Rich Ford has stated that the adjuvant aluminum in the vaccines is one culprit in mutating our genome and specifically the P53 oncogene thereby ruining the individual’s ability to stop tumor genesis.31 The smoking gun proof of this is the presence of the blue grey aluminum foreign body retrieved from biopsy specimens of vaccinated individuals. The vaccines are causing cancer formation not just in cats but also dogs and ferrets and not just at the injection site of a vaccine. The fact that these very same vaccine ingredients are the same carcinogens in the childhood vaccines mandated by our government in the national childhood vaccine program is of serious concern. The rise in childhood brain cancer is the most highly associated vaccine administered cancer in children and this is of certain consequence to the current vaccines and vaccination protocols32
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It is understood now, that vaccination is not the same as immunization, that production of antibody is not the same as immunity and to the vaccinologists out there Dr. Ron Schultz states “this is an indefensible practice”.33 Since 1978 veterinary vaccine research authorities have been advising against yearly vaccinations.34 Vaccination has never been linked to any science or evidence based medicine but only to precedence and since 1978 to the generation of income.35 The problem with the veterinarians over-vaccinating is now causing public health problems. Emory University’s Rollins’ School of Public Health has a published a paper on how human illness is associated with use of veterinary vaccines.36 Others, like Dr. Traavik, Biosafety Officer for the country of Norway, are alerting us to the dangers of the recombinant vaccine technology, the use of chimera viruses that are transferring disease to man.37 Dr. Michael Fox has been concerned about the impact of the unregulated and uncontrolled use of these genetically engineered viruses in vaccines and the future this plaque is bringing upon mankind.38
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My research into the number of rabies vaccines recently recalled and the hundreds of thousands of human rabies vaccines recalled in the past for “failure to inactivate the rabies virus” are very disconcerting as is the recall of rabies vaccines due to unauthorized inclusion of human DNA in the vaccines. Vaccines do not enjoy any science of benefit and were never shown historically to even affect the level of infectious diseases. John Hopkins Bloomberg School of Public Health includes this information on their website. How far do we have to continue to keep ourselves immunized against the fact that the very act of vaccination is what is causing disease in this westernized world?
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Vaccination is an obstacle to cure; vaccination is the induction into a cycle of disease and disease management that is in every way a violation of the AVMA 1969 Veterinary Oath, in every way including public health and animal welfare.
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The use of TCVM will not be able to successfully restore health to our patients if vaccinations are allowed to continue to corrupt the patient’s immune system. Blood stasis, Qi depletion, Liver Yin Deficiency and Blood Deficiency will always be the root of disease while vaccinations remain the non-evidence based medical procedure that is the hallmark of conventional medicine. The body’s Qi will try to imprison these toxins and poisons in the joints bone and marrow, but the body with continual bombardment will be quickly depleted. Our patients deserve to have us conform to our duties spoken in the Veterinary Oath and our obligation to stay current with the advancements of scientific research. In my opinion, vaccination is not science based, nor evidence based medicine, but rather the risky business fulfilled by corporations able to control the licensing and the distribution, administration and promotion even the mandate by law of this poisoning of the blood. The Chinese were correct in the age of the Song Dynasty, the Dynasty associated with both Emperor’s Song and the people’s technological advancements. The ancient Chinese were able to abandon a practice that proved ineffective and proved an impediment to restoring health. This is an example where old medicine is new again and once again a gift to the world from the people of China.
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REFERENCES:
1. Temple R. The Genius of China: 3,000 Years of Science, Discovery, and Invention. New York: Simon and Schuster, Inc. 1986: 135.
2. Behbehani AM. The small pox story: life and death of an old disease. Microbiological Reviews Dec 1983; Vol 47 No.4: 455-509.
3. Schultz R. Everything you need to know about vaccines. Seminar Danbury, CT, June 15, 2007 Sponsored by Cavaliers of the Northeast.
4. Zangani MM et al. Lymphomas can develop from B cells chronically helped by idiotype specific T cells. Journal of Experimental Medicine 2007; 204 (5): 1181-1191.
5. Morden M. MD, Rabies Past Present in Scientific Review. Mokelumne, California: Health Research Publisher 1947: also Rabies Radio address WWRL, Jan 25, 1947
Ahasar HA, et al. Neuroparalytic complications after anti-rabies vaccine (inactivated nervous tissue vaccine). Trop Doct 1995 Apr; 25 (2):94.
Bernard KW, et al. Neuroparalytic illness and human diploid cell rabies vaccine. JAMA 1982 Dec 17; 248 (23):3136-8.
Bahri F et al. Neurological complications in adults following rabies vaccine prepared from animal brains. Presse Med 1996 Mar 23; 25 (10): 491-3. In French
McBean E, The Poisoned Needle: Suppressed Facts About Vaccination. ISBN-0-7873-059404
1957 reprinted April 1, 2009. ISBN-101442131292
6. Crick J. The vaccination of man and other animals against rabies. Postgraduate Medical Journal 1973 August; 49: 551-564.
Johnson HN. Experimental studies on the duration of immunity in dogs vaccinated against rabies. Bulletin of the World Health Organization 1954; 46: 32.
7. Fiala J. AVMA vaccine report surprises skeptics. DVM News 2003 Jan 1 Advanstar Communications http://veterinarynews.dvm360.com/dvm/article/articleDetail.jsp?id=43254
Schultz R, Everything you wanted to know about vaccinations. Seminar Danbury, CT June 15th, 2007 Sponsored by the Cavaliers of the Northeast
8. Aubert MF. The practical significance of rabies antibodies in cats and dogs. Scientific Review
1992; 11 (3): 735-760.In French
9. Malerczyk C et al., Duration of immunity an amnestic response with purified chick embryo cell rabies vaccine. J Travel Med 2007; 14:63-64.
10. Crotty S et al., Cutting Edge; Long term B cell immunity in humans after small pox vaccination. Immunol 2003 Nov 15; 171 (10):4969-73
Amanna J, Carlson NE et al., Duration of Humoral immunity to common viral and vaccine antigens. NEJM 2007; 357; 1903-15.
11. AVMA Council on Biological and Therapeutic Agents. Synopsis of Vaccination Procedures for Dogs. JAVMA 1973; 162 (3); 228-230.
12. Koppang EO, Bjerkas I., et al., Vaccination-induced systemic autoimmunity in farmed Atlantic salmon. J Immunol. 2008 Oct. 1; 181 (7): 4807-14.
13. http://genesgreenbook.com/content/proof-vaccines-didn’t-save-us has slideshow of graphs from public health sources. April 16, 2008
Schultz R., Tizzard I., Salk J., Siegel G., Swango L., Rude T., Safety, Efficacy the heart of vaccine use , experts discuss pros, cons in vaccine roundtable discussion. DVM Magazine 1988; 119: 16.
14. Schultz R. What Every Veterinarian needs to know About Canine and Feline Vaccines and Vaccination Programs with an Emphasis on Recombinant Vaccines, Warwick, RI April 16, 2008 sponsored by Merial
15. Kessler D., A new approach to reporting medication and device adverse events and product problems. JAMA 1993 June 2; 269 (21): 2785. Also available online http://www.vaccinationnews.com/Adverse_Reactions/VAERS/credible_estimates.htm
World Small Animal Veterinary Association 2007 Vaccination guidelines http://www.wsava.org/SAC.htm
16. Phillips TR et al., Effects of vaccine on the canine immune system. Canadian Journal of Vet Research 1989; 53:154-160.
Kapczynski, D.R., Tumpey T., Immune Functions Following vaccination with an inactivated avian pneumovirus. Western Poultry Disease Conference Proceedings 2002
Havarinasab S., et al., Immunosuppressive and autoimmune effects of thimerasol in mice. Toxicol Appl Pharmacol 2005; Apr 15; 204 (2): 109-21
17. Negina IuP, Comparative study of auto-antibody formation following immunization with different types of vaccines. ZH Mikrobiol Epidemiol Immunobiol 1980 May; (5): 69-72. Romanov, UA et al, Role of auto-immune processes in the pathogenesis of post vaccinal lesions of the nervous system. ZH Mikrobiol Epidemiol Immunobiol 1977 Oct; 10: 80-93.
Cestnir A et al, The experts peaks; how does a viral infection trigger an autoimmune disease? Viral Immunology 1995; 8 (4):187-192.
Yamamoto K, Possible mechanisms of autoantibody production and the connection of viral infections and human autoimmune diseases. Tohoku J Exp Med. 1994; 173:75-82.
18. Classen BJ, Vaccine induced inflammation linked to endemic Type 2 diabetes and metabolic syndrome. The Open Endocrinology Journal 2008; 2:915.
Lappin M et al, Investigation of the induction of antibodies against Crandell-Rees feline kidney cells lysates and feline renal cells lysates after parental administration of vaccines against feline viral rhinotracheitis, calicivirus and panleukepenia in cats. AJVMR 2005; 66 (3): 506-11.
Vitale, Gross, Majro, Vaccine induced ischemic dermatopathy in the dog. Veterinary Dermatopathy 1999; 10 (2): 131-142.
Affolter VK, Cutaneous vasculitis and vasculopathology 2004 World Small Animal Veterinary Association Congress.
Lator N et al., Neuropathy and cognitive impairment following vaccination with Osp A protein of Borrelia burgdorferi. Peripheral Nerve Society, Inc 2004
Clinician’s Brief: Lyme Nephritis yet no organisms in the kidney 2008 September.
Hutton TA et al, Search for Borrelia burgdorferi in kidneys of dogs suspected of Lyme nephritis. J Vet Intern Med 2008; 22:860-864.
Mckisic M et al, Cutting edge; T cell mediated pathology in Murine Lyme Borreliosis. The J of Immunol 2000; 164: 6096-6099.
American Heart Association Meeting 2003 Studies describing heart disease following small pox vaccination. Nov 10 Orlando, Fl http://eurekalert.org/pub_releases/2003-11/aha-sdh102203.php Kuenzle S et al., Pathogens specifically and autoimmunity are distinct features of antigen-driven immune responses in Neuroborreliosis. Infection and Immunity 2007 Aug; 75(8):3842-3847. Frick OL, Brooks DL. Immunoglobulin E antibodies to pollens augmented in dogs by virus vaccines. Am J Vet Res 1981; 44: 440-445.
HogenEsch H, et al., Effect of vaccination on serum concentrations of total and antigen specific immunoglobulin E in dogs. Am J Vet Res 2002; 63: 611-616.
Tater KC et al., Effects of routine prophylactic vaccination or administration of aluminum adjuvant alone or allergen specific serum IgE and IgG responses in allergic dogs. Am J Vet Res 2005; 66 (9):15772-7.
19. Faseb J. Molecular mimicry and immune-mediated diseases. The Scripps Research Institute, 1998 Oct; 12 (13):1255-65.
Owens GP et al., Screening random peptide libraries with subacute sclerosing panencephalitis brain derived recombinant antibody identifies multiple epitopes the C-terminal region of the measles virus nucleocapsid protein. Journal of Virology Dec 2006; 80(24): 12121-12130.
20. Binstadt BA, et al. Particularities of the vasculature can promote the organ specificity of autoimmune attack. Nature Immunology 2006 Mar; 7(3): 284-292.
21. Falus A and Meretey K, Histamine: an early messenger in inflamatory and immune reactions. El Sevier Ltd. 1992 Dept of Molecular Biology and Immunology Natural Institute of Rheumatology and Physiotherapy Budapest, Hungary.
Jutel M, Blaser k, Akdes C, The role of histamine in regulation of immune response Crameri (Ed): Allergy and Asthma in Modern Society: A Scientific Approach Chem. Immunol Allergy Basel, Karger: 91:174-187.
Bordatella pertussis whooping cough Bordatella vaccines and histamine effects http://tjclarkinc.com/bacterial_disease/whooping_cough.htm
22. Otto A, Extended from remarks given by Karen Vanderhoof-Forschner to the FDA Vaccine Advisory Committee Meeting 11/28/01; Lyme vaccine linked to auto-immune arthritis. Pharmacy Today 2001 January
23. Dodd Jean, Adverse Vaccine Reactions, Hemopet/Hemolife 938 Stanford St. Santa Monica, CA 90403 online: http://itsfortheanimals.com/Thyroid-articles.htm
24. Brennar J, Orgard U et al., Thymic Depletion Syndrome associated with a combined attenuated distemper parvovirus vaccine in dogs. Israel Journal of Vet Med 1988; 44(2): 151.
Cain MJ, Philosophy of Love Your Pets Immune Related Problems. Dr. Marvin J Cain, 7474 Green Farms Dr. Cincinnati, OH 45224-1210.
25. MacKay IR and Mitchison, Review Article Advances in Immunology, Tolerance and Autoimmunity, 2001 Mar 1; 344, (9):655-644.
Chen RT, Pless R, DeStefano F, Epidemiology of autoimmune disease reaction induced by vaccination. J Autoimmunity 2001; 16:309-318.
HogenEsch H, Axona-Oliver J, Scott-Moncreiff C, Synder, and Glickman LT. Vaccine induced auto-immunity in the dog. Adv Vet Med, 1996; vol 41:733-747. http://www.vet.perdue.edu/epi/gdhstudy.htm http://vonhapsburg.homestead.com/haywoodstudyonlinevaccines.html
Balomenos D and Mertinez CA, Cell cycle regulation in immunity tolerance and autoimmunity. Immunology Today 2000 Nov; 21 (11):551.
26. Reik L Jr., Disseminated vasculomyelinopathy: an immune complex disease. Ann Neurology 1980; 7: 291-295.
27. Auwaerter PG et al., Changes with T cell receptor V beta subsets in infants following measles vaccination. Clin Immunol Pathol 1996 May; 79 (2):163-70.
Beckenhauer WH et al., Immunosuppression with combined vaccines. JAVMA Aug 15 1983; (4):389-390.
Blumberg DA, Leukocyte response to diphtheria-tetanus-pertussis and diphtheria-tetanus immunization. Pediatric Infect Dis J 1991 Mar; 10 (3): 247-248.
Daniliuk OS et al., Immunodepressive action Vaccinia virus. Buell Eksp Bio Med Jul 1982; 94 (7): 73-74.
Ehrland W. Susceptibility to infection after vaccination, Br. Med J. Mar 11, 1972; 1:683.
Eibl MM et al., Abnormal T-lymphocyte subpopulations in healthy subjects after tetanus booster immunization. NEJM 1984 Jan 19; 310 (3):198-9.
28. Erasmus MC, Vaccine induced enhancement of viral infection. Institute of Virology 2009 Jan 22; 27 (4): 505-12.
29. Schultz RD, What everyone needs to know about canine vaccines and vaccination programs 2007 National Parent Club Canine Health Conference http://www.spinoneous.org/forum/uploaded/Admin/vaccinations2007.pdf
30. Memoranda WHO 1972 Vol 47 No. 1 Virus associated immunopathology animal models and implications for human disease 1. Effects of viruses on the immune system, immune-complex disease and antibody mediated immunologic injury. Memoranda WHO 1972 Vol 47 No. 2 Virus associated immunopathology; animal models and implications for human disease 2. Cell mediated immunity autoimmune disease genetics and implications for clinical research. Proceedings of a NATO Advanced Study Institute on vaccine design: the role of cytokine networks, held June 24-July5, 1996 in Cape Sounion, Greece: New York, NY: Plenum Press 1997.
Anshu Agrawal, Poonam K et al., Thimerasol induces TH2 responses via influencing cytokine secretion by human dendritic cells. Journal of Leukocyte Biology, 2007 February; 81:474-482. http://www.jleukbio.org
31. IARC International Agency for Research on Cancer; Summaries and Evaluations Surgical Implants and Other Foreign Bodies 1999 Feb 23; 74:24305-310.
32. Kass PH, et al., Epidemiologic evidence for a causal relation between vaccination and fibrosarcoma tumorigenesis in cats. JAVMA, 1993; 203:396-405.
Munday JS et al., Histology and Immunohistochemistry of seven ferret vaccination site fibrosarcomas. Vet Pathology 2003; 40:288-293.
Vascellari M, Melchiotti E et al., Fibrosarcomas at presumed sites of injection in dogs, characteristics and comparison with non vaccination site fibrosarcomas and feline post vaccinal fibrosarcomas. J Vet Med A Physiol Pathol Clin Med 2003 Aug; 50 (6): 286-91.
Morrison WB, Starr RM et al., Vaccine associated feline sarcoma. JAVMA 2001; 218:697-702. Smith C, Are we vaccinating too much? JAVMA 1995; 207 (4):421-425.
Researchers probe vaccine associated feline sarcomas. JAVMA June 1, 2005 http://www.avma.org/onlnews/javma/sep04/040915k.asp
Couto CG, Macy DW. Review of treatment options for vaccine-associated feline sarcoma. JAVMA1998; 213:1426-1427.
Macy D, Vaccine-associated feline sarcomas. Journal of Feline Medicine and Surgery 1999 Mar; 1 (1):15-21.
Macy D, Is it time for a Veterinary Vaccine Injury Compensation Act? http://www.catshots.com
Ford R, DVM, MS, Diplomate ACVIM Vaccines and vaccination building the protocol-implementing the guidelines June 25,2007 Framingham, MA Sponsored by Merial.
Bode A and Dong Z, Post translational modification of p53 in tumorigenesis. Nature Reviews Cancer 2004 Oct 14; 4 (10): 793-805.
33. Questions and Answers about vaccine ingredients American Academy of Pediatric Physicians October 2008 http://www.vaccinateyourbaby.org/pdfs/vaccine_ingredients.pdf
Felex CA, Slaye I et al., p53 gene mutations in pediatric brain tumors Pediatric Blood and Cancer 2006 Jul; 25(6): 431-436.
34. Schultz RD, Everything you need to know about vaccines. June 15, 2007 Danbury, CT Sponsored by Cavaliers of the Northeast.
35. Schultz RD, Scott F, Veterinary Clinics of North America 1978, 8 (4):755-768.
36. Phillips TR, Schultz RD. Canine and feline vaccines in Kirks Current Veterinary Therapy XI (Small Animal Practice). Philadelphia, PA: WB Saunders: 205.
Horzinek M, Schultz RD, Frequently asked questions. Oct 19, 2009 National Parent Club Canine Conference http://www.spinoneous.org/forum/uploaded/Admin/vaccinations2007.pdf
Wolf A, Vaccines of the past and the future. (WSAVA) World Small Animal Veterinary Association Conference 2001 Vancouver, British Columbia.
37. Berkelman RL, Human illness associated with the use of veterinary vaccines. Emerging Infections CID 2003(1 August); 37:407-414.
38. Fox MD, Genetically engineered and modified live virus vaccines; Public health and animal welfare concerns http://twobitdog.com/DrFox/Livevirus-vaccines-animal
Terje Traavik, genetically engineered pox viruses in cell cultures recombined with natural viruses to create new viruses with unpredictable and potentially dangerous characteristics. Contact terjet@genok.org
Terje Traavik, Scientific Director Center for Biosafety of Norway, Professor of Gene Ecology, University of Tromso, Norway. Background document in risk assessment of genetically modified (GM) viruses for management of animal populations. Terje Traavik, Biosafety Officer of Norway University of Tromso, Norway prepared for the Norway Canada workshop on risk assessment for emerging applications of LMOs. June 4-6, 2007. Montreal, Canada. Research report for DN No 1999-6 An Orphan Science; Environmental risks of genetically engineered vaccines reported to Directorate for Nature Management http://www.naturforvaltning.no

 

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Lungworm Can Kill Your Dog

The lungworm Angiostrongylus vasorum (also known as French Heartworm) is a parasite that infects dogs. The adult of this particular lungworm lives in the heart and major blood vessels supplying the lungs, where it can cause a host of problems. Left untreated, the infection can often be fatal.

The lungworm parasite is carried by slugs and snails. The problem arises when dogs purposefully or accidentally eat these common garden pests when rummaging through undergrowth, eating grass, drinking from puddles or outdoor water bowls, or pick them up from their toys.

There are two main problems caused by dogs becoming infected with lungworm:
* Infection with lungworm can cause serious health problems in dogs, and is often fatal if not diagnosed and treated.
* Dogs infected with lungworm spread the parasite into the environment, as the larvae of the parasite are expelled in the dog’s faeces. This increases the chances of other dogs becoming infected.  Continue Reading ...

 

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ALL ABOUT VACCINE ISSUES & VACCINATIONS

W. Jean Dodds, DVM (1) and Ronald D. Schultz, PhD (2) 

There is little doubt that application of modern vaccine technology has permitted us to protect companion animals effectively against serious infectious diseases. Today, we can question conventional vaccine regimens and adopt effective and safe alternatives primarily because the risk of disease has been significantly reduced by the widespread use of vaccination programs, which convey underlying population or herd immunity.

For many veterinary practitioners canine vaccination programs have been “practice management tools” rather than medical procedures. Thus, it is not surprising that attempts to change the vaccines and vaccination programs based on scientific information have created significant controversy. A “more is better” philosophy still prevails with regard to pet vaccines. 

Annual vaccination has been and remains the single most important reason why most pet owners bring their pets for an annual or more often “wellness visit.” Another reason for the reluctance to change current vaccination programs is 
many practitioners really don’t understand the principles of vaccinal immunity. Clearly, the accumulated evidence indicates that vaccination protocols should no longer be considered as a “one size fits all” program. 

Giving annual boosters when they are not necessary has the client paying for a service which is 
likely to be of little benefit to the pet’s existing level of protection against these infectious diseases. It also increases the risk of adverse reactions from the repeated exposure to foreign substances.

So, have veterinarians really embraced the national policies on vaccination guidelines from the American Animal Hospital Association, American Veterinary Medical Association and Academy of Feline Practitioners? Does the public trust veterinarians to be up-to-date on these issues or are they unsure? Do they believe veterinarians have a conflict of interest if they seek the income from annual booster vaccinations? 

Given current media attention to vaccination issues, the public is more aware and worried about vaccine safety.

Some veterinarians today still tell their clients there is no scientific evidence linking vaccinations with adverse effects and serious illness. This is ignorance, and confuses an impressionable client. On the other hand, vaccine zealots abound with hysteria and misinformation. None of these polarized views is helpful.

Further, veterinarians are still routinely vaccinating ill dogs and those with chronic diseases or prior adverse vaccine reactions.  This is especially problematic for rabies boosters, as many colleagues believe they have no legal alternative, even though the product label states it's intended for healthy animals. 

For more information, see Duration of Immunity Study for Rabies Vaccine - Rabies Challenge Fund

Alternatives to Current Vaccine Practices 

1) measuring serum antibody titers; 
2) avoidance of unnecessary vaccines or over vaccinating; 
3) caution in vaccinating sick or febrile individuals; and 
4) tailoring a specific minimal vaccination protocol for dogs of breeds or families known to be at increased risk for adverse reactions. 
5) considerations include starting the vaccination series later, such as at nine or ten weeks of age when the immune system is better able to handle antigenic challenge; 
6) alerting the caregiver to pay particular attention to the puppy’s behavior and overall health after the second or subsequent boosters; and 
7) avoiding revaccination of individuals already experiencing a significant adverse event. Littermates of affected puppies should be closely monitored after receiving additional vaccines in a puppy series, as they too are at higher risk. 


Some Frequently Asked Questions – Some questions are part of the Guidelines for Vaccination of Dogs and Cats compiled by the Vaccine Guidelines Group (VGG) of the World Small Animal Veterinary Association (WSAVA) 

Q. Do dogs competing in agility or other events need more vaccines for protection than other pet dogs?
A. No, although if the event location has an exposure risk for Leptospirosis or Lyme disease , annual vaccination for these diseases should be considered. 

Q. Is there risk of overvaccinating with vaccines not needed for a specific animal?
A. Yes. Vaccines contain material designed to challenge the immune system of the pet, and so can cause adverse reactions. They should not be given needlessly, and should be tailered to the pet’s individual needs. 

Q. Are the initial series of puppy core vaccines immunosuppressive?
A. Yes. This period of immunosuppression from MLV canine distemper and hepatitis vaccines coincides with the time of vaccine-induced viremia, from days 3 to 10 after vaccination.

Q. Can anesthetized patients be vaccinated?
A. This is not preferred, because a hypersensitivity reaction with vomiting and aspiration could occur and anesthetic agents can be immunomodulating.

Q. Is it safe to vaccinate pregnant pets? 
A. Absolutely not. 

Q. Should pets with immunosuppressive diseases such as cancer or autoimmune diseases, or adverse vaccine reactions/ hypersensitibvity receive booster vaccinations? 
A. No. Vaccination with MLV products should be avoided as the vaccine virus may cause disease; vaccination with killed products may aggravate the immune-mediated disease or be ineffective. For rabies boosters that are due, local authorities may accept titers instead or accept a letter from your veterinarian. 

Q. If an animal receives immunosuppressive therapy, how long afterwards can the pet safely be vaccinated?
A. Wait at least 2 weeks.

Q. Should vaccines be given more often than 2 weeks apart even if a different vaccine is being given? 
A. No. The safest and most effective interval is 3-4 weeks apart. 

Q. At what age should the last vaccine dose be given in the puppy series?
A. The last dose of vaccine should be given between 14-16 weeks regardless of the number of doses given prior to this age. Rabies vaccine should preferably be given separately as late as possible under the law (e.g. 16-24 weeks).

Q. Should the new canine influenza vaccine be given routinely? 
A. No. It is intended primarily for pounds and shelters and high density boarding facilities, as nose-to-nose contact and crowding promote viral transmission. 

Q. Can intranasal Bordetella vaccine be given parenterally (injected)?
A. No. The vaccine can cause a severe local reaction and may even kill the pet. 

Q. Will a killed parenteral Bordetella vaccine given intranasally produce immunity?
A. No. 

Q. Are homeopathic nosodes capable of immunizing pets?
A. No. There is no scientific documentation that nosodes protect against infectious diseases of pets. The one parvovirus nosode trial conducted years ago did not protect against challenge. 

Q. Should disinfectant be used at the vaccine injection site?
A. No. Disinfectants could inactivate a MLV product.

Q. Can vaccines cause autoimmune diseases?
A. Vaccines themselves do not cause these diseases, but they can trigger autoimmune responses followed by disease in genetically predisposed animals, as can any infection, drug, or chemical / toxic exposures etc.

Q. Can a single vaccine dose provide any benefit to the dog? Will it benefit the canine population?
A. Yes. One dose of a MLV canine core vaccine should provide long term immunity when given to animals at or after 16 weeks of age. Every puppy 16 weeks of age or older should receive at least one dose of the MLV core vaccines. We need to vaccinate more animals in the population with core vaccines to achieve herd immunity and thereby prevent epidemic outbreaks.

Q. If an animal receives only the first dose of a vaccine that needs two doses to immunize, will it have immunity? 
A. No. A single dose of a two-dose vaccine like Leptospirosis vaccine will not provide immunity. The first dose is for priming the immune system. The second for boosting the immunity has to be given within 6 weeks; otherwise the series has to start over again. After those two doses, revaccination with a single dose can be done at any time.

Q. Can maternally derived antibodies (MDA) also block immunity to killed vaccines and prevent active immunization with MLV vaccines?
A.Yes. MDA can block certain killed vaccines, especially those that require two doses to immunize. With MLV vaccines, two doses are often recommended, particularly in young animals, to be sure one is given beyond the neutralizing period of MDA. 

Q. How long after vaccination does an animal develop immunity that will prevent severe disease when the core vaccines are used?
A. This is dependent on the animal, the vaccine, and the disease.

· The fastest immunity is provided by canine distemper virus (CDV) vaccines -- MLV and recombinant canarypox virus vectored. The immune response starts within mins - hrs and provides protection within a day without interference from MDA.

· Immunity to canine parvovirus (CPV-2) develops after 3-5 days when an effective MLV vaccine is used. 

· Canine adenovirus-2/hepatitis (CAV-2) MLV given parenterally provides immunity against CAV-1 in 5 to 7 days. 


Q. Can dogs be “non-responders” and fail to develop an immune response to vaccines?
A Yes. This is a genetic characteristic seen particularly in some breeds or dog families. Boosting them regularly will not produce measurable antibody. Some of these animals may be protected against disease by their cell-mediated and secretory immunity. 

Q. Are there parvovirus and distemper virus field mutants that are not adequately protected by current MLV vaccines?
A. No. All the current CPV-2 and CDV vaccines provide protection from all known viral isolates, when tested experimentally as well as in the field. The current CPV-2 and CPV-2b vaccines provide both short and long term protection from challenge by the CPV-2c variant.

Q. Are serum antibody titres useful in determining vaccine immunity?
A. Yes. They are especially useful for CDV, CPV-2 and CAV-1 in the dog, FPV in the cat, and rabies virus in the cat and dog. Rabies titers, however, are often not acceptable to exempt individual animals from mandated rabies boosters in spite of medical justifcation. Serum antibody titers are of limited or no value for (many of) the other vaccines.

(1) President, Hemopet, 938 Stanford Street, Santa Monica, CA 90403; 

(2) Chairman, Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI 53706.

* Excerpted from: AKC Health Foundation, St. Louis, MO, 2007; J Sm An Pract 48, 528–541, 2007; 5th IVVDC Conference , Madison, WI , 2009.

Additional Literature

● Day MJ, Horzinek MC, Schultz RD. Guidelines for the vaccination of dogs and cats. J Sm An Pract, 48, 528-541 2007

● Dodds WJ. Vaccination protocols for dogs predisposed to vaccine reactions. J Am An Hosp Assoc 38: 1-4, 2001.

● Dodds WJ. Vaccine issues revisited: what’s really happening ? Proc Am Hol Vet Med Assoc, Tulsa, OK, 2007, pp 132-140.

● Paul MA (chair) et al. Report of the AAHA Canine Vaccine Task Force : 2006 AAHA Canine Vaccine Guidelines. J Am An Hosp Assoc 42:80-109, Mar-April 2006, 28 pp. American Animal Hospital Association 

● Schultz R D Considerations in designing effective and safe vaccination programs for dogs. In: Carmichael LE (editor), Recent Advances in Canine Infectious Diseases. Intern Vet Inform Serv, 2000. http://www.ivis.org.

● Schultz RD. Duration of immunity for canine and feline vaccines: a review. Vet Microbiol 117:75-79, 2006. 

“CORE” CANINE VACCINES * 

· Distemper 
· Adenovirus (Hepatitis)** 
· Parvovirus 
· Rabies 
_______________________________________
* vaccines that every dog and cat should have
** immunity provided by a CAV-2 vaccine 

CANINE VACCINE ADVERSE EVENTS *

· retrospective cohort study; 1.25 million dogs vaccinated at 360 veterinary hospitals
· 38 adverse events per 10,000 dogs vaccinated
· inversely related to dog weight
· vaccines prescribed on a 1-dose-fits-all basis, rather than by body weight. 
· increased for dogs up to 2 yr of age, then declined
· greater for neutered versus sexually intact dogs 
· increased as number of vaccines given together increased
· increased after the 3rd or 4th vaccination
· genetic predisposition to adverse events documented
__________________________________________________ ___________
* from Moore et al, JAVMA 227:1102–1108, 2005


VACCINE CONCLUSIONS FOR CANINES *

Factors that increase risk of adverse events 3 days after vaccination:

· young adult age 
· small-breed size
· neutering
· multiple vaccines given per visit 


These risks should be communicated to clients

__________________________________________________ _____

 

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Canine Heartworm Disease

Dr. Angelo Alcazaren's veterinary medicine blog

Life Cycle

Diagram of life cycle of heartwormFigure 1.  Diagram of heartworm life cycle from Hill’s Atlas of Veterinary Clinical Anatomy

Canine heartworm is a 23 to 30 cm long worm that resides inside the heart of the dog.  The female produces baby heartworms called microfilariae which spread out through all the blood vessels of the dog.  When mosquitoes feed on infected dogs, they suck in blood and the baby heartworms.  They molt three times inside the mosquito producing L3

larvae.  The environmental temperature must be warm or else they don’t develop.  The mosquito carrying the L3 larvae bites another dog.  The larvae will enter the bite wound, penetrate tissues and molts a fourth time producing L4 larvae after 7 days.  The L4 larvae further migrates into the deeper tissues for 60 to 90 days until they finally molt into the young adult worm.  The young worm reaches the inside of the heart through blood circulation.  The young worms become mature and mate in the pulmonary arteries.  They then settle in the right chambers of the heart and pulmonary arteries where they can survive for up to 7 years.  Birth and release of baby heartworms into the circulation takes about six and a half months.

 

Figure 2.  From shakervet.com
Diagnostic Trends and Issues

Adult heartworms in right ventricleThe use of heartworm drugs like Heartgard®, Interceptor®, Sentinel®, Revolution™ and ProHeart® has dramatically decreased infection among the canine population.  However, these drugs have affected the reliability of antigen blood tests used in detecting adult worms in the circulatory system.  So to correctly evaluate the heartworm status of a dog, these antigen blood tests should be backed up with other diagnostic procedures like physical examination, medical history, direct blood examination, x-ray examination and echocardiogram.

 

Microfilaria as seen under the microscopeFigure 3.  Microfilaria as seen under the microscope surrounded by red blood cells from commons.wikimedia.org

Periodic blood testing for heartworms is a way of monitoring the effectiveness of the above mentioned drugs.  If an area has a lot of infected dogs then the recommendation is to perform yearly testing.  If the pet owner switches from one drug to another, the recommendation is to test at the time of changing and then retest after four to seven months to make sure that the drug is working.  If there is a lapse of more than 8 weeks in the administration of medication, then retesting must be done on a yearly basis to detect possible infection.

 

 

 

 

Figure 4.  Witness® heartworm antigen test showing both positive and negative results from www.westernmedicalsupply.com

witness heartworm antigen test

 

 

 

 

 

 

Heartworm treatment Issues

The newest drug used for treating heartworm infection is melarsomine dihydrochloride known in the market as Immiticide®.  Its effectiveness, safety and ease of administration have replaced thiacetarsamide, the original heartworm treatment available to veterinarians for many years.  This drug has a flexible dosing regimen based on how infected the dog is.  The standard dosing regimen consists of two doses of the drug given 24 hours apart.  This is ideal for dogs that don’t show any symptoms or those that are in the early stages of the disease.  The other regimen involves giving the dog a single shot of the drug and then is observed for a month for any allergic reaction or circulatory problem.  When the month goes by without any incident, the dog is given the standard two dose regimen.  This is the regimen being used for dogs in the late stage of heartworm infection or class 3 in veterinary medical terms and for dogs with high amount of worms in their bodies as confirmed by various diagnostic procedures.  This is a more cautionary protocol since the one month interval gives the dog a chance to recover from whatever reaction the dog would undergo from a sudden demise of a whole lot of worms in the circulation.  The two more injections would make sure that all other existing worms and their larvae would be taken care of.  The issue, however, for this protocol is the increased time of treatment and increased cost since the drug is very expensive.  There is also the issue of trying to use this drug on very old dogs suffering from the disease and those suffering from other terminal illnesses.  In these cases, veterinarians are forced to seek other treatment options.  One such option, being circulated around the internet, is the so called “slow kill” treatment.  Heartworm drugs like ivermectin and milbemycin oxime are administered to infected dogs at the usual monthly interval and dosage for one or more years.  Most of the worms would die slowly while the remaining ones become either sterile or structurally abnormal.  This option would be more affordable for most pet owners since the cost of heartworm drugs is much lower compared to Immiticide®.  In addition to the heartworm drugs, the dog is also given an antibiotic doxycycline to kill a bacteria-like organism within the worms called Wolbachia.  This bacterium has a symbiotic relationship with the worm and research has shown that it causes an allergic immune response when the worm dies.  Treating the dog with this drug would kill these bacteria lessening the allergic immune response.

immiticide injection

 

 

 

 

 

 

 

 

Figure 5.  Sketch showing administration of Immiticide® intramuscularly in the epaxial (lumbar) muscles in the third through fifth lumbar region from www.drugs.com

Another treatment option is surgical removal of heartworms.  The dog is placed under general anesthesia and a flexible alligator forcep is inserted into the main artery leading to the heart.  The adult worms are then grabbed and pulled out of the heart one by one.  This treatment option is usually the preferred option in cases where there are too many worms in the heart and blood vessels or when the dog has signs of heart damage due to the worms.

frcps

 

Figure 6.  A picture of a Fujimon alligator forcep used in pulling out the heartworms through the main artery leading to the heart from Dr. Colin Johnstone’s website Parasite and Parasitic Diseases of Domestic Animals.

frcpxr

Figure 7.  A left side X-ray view of the Fujimon alligator forcep inside the heart from Dr. Colin Johnstone’s website Parasite and Parasitic Diseases of Domestic Animals.

2worm

Figure 8.  Adult heartworms extracted from the heart using the Fujimon alligator forcep from Dr. Colin Johnstone’s website Parasite and Parasitic Diseases of Domestic Animals.

Prevention

heartgard by shakervet.com

Figure 9.  Heartgard® packaging from shakervet.com

Heartgard® is known by its generic name as ivermectin.  It is a huge chewable tablet that is quite palatable and is effective against a wide range of external and internal parasites.  It is used as a monthly preventive medication against heartworm and can still provide adequate protection even if you fail to give it for two months straight.  It is safe for all breeds of dogs except for the Collie breeds and Collie crosses which are more sensitive to its toxic effect at very high doses.  So, accidental ingestion of an excess amount of this drug by said breeds usually ends up in death.

interceptor from petplace.com

Figure 10.  Interceptor® packaging from petplace.com

Sentinel_large from www.serenityanimalhospital.net

Figure 11.  Sentinel® packaging from www.serenityanimalhospital.net

Interceptor® and Sentinel® are known by their generic name as milbemycin oxime.  It is a tablet given once a month and is highly effective not only against heartworms but also against other intestinal worms like hookworms, roundworms and whipworms.  Like Heartgard®, it can still provide adequate protection even if you fail to give it for two months straight.

proheart from petproductsontheweb.com

Figure 12.  ProHeart® tablet packaging from petproductsontheweb.com

proheart6 from www.proheart6dvm.com

Figure 13.  ProHeart®6 packaging from www.proheart6dvm.com

ProHeart® and ProHeart®6 are known by their generic name as moxidectin.  It is available in two forms: tablet (ProHeart®) and liquid for injection (ProHeart®6).  The tablet is also given once a month and like Heartgard®, Interceptor® and Sentinel® it can still provide adequate protection even if you fail to give it for two months straight.  The injection provides 6 months protection against heartworms with one single shot.  It is injected under the skin and can still provide adequate protection even if you fail to give it for four months straight.

Revolution_large

Figure 14.  Revolution® packaging from 1800petmeds.com

Revolution™ is known by its generic name as selamectin.  It is a liquid drug that is applied once a month on the skin of the neck of the dog in between the shoulder blades where it slowly spreads out and eventually is absorbed into the bloodstream.  It is not only effective in preventing heartworm but can kill fleas and their eggs, sarcoptic mange mites, ticks and ear mites.  It is much safer to use in Collie breeds as compared to Heartgard® and can also provide adequate protection even if you fail to apply it for two months straight.

Preventive medication using these drugs should be started when the dog reaches 6 to 8 weeks of age and it is recommended that the dog must be tested first using the antigen blood test and then followed up by a microscopic examination of the blood for baby heartworms if the result of the antigen blood test is positive.  If medication is missed for more than two months then the medication should be given continuously for a year and an antigen blood test performed 6 months after to see if there is any infection.

 

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A Healthier Respect for Ovaries
Ovaries and Longevity

David J. Waters, DVM, PhD, Diplomate ACVS
Director, Center for Exceptional Longevity Studies
Gerald P. Murphy Cancer Foundation

A recent study by my research group appearing next month in Aging Cell reveals shortened longevity as a possible complication associated with ovary removal in dogs (1). This work represents the first investigation testing the strength of association between lifetime duration of ovary exposure and exceptional longevity in mammals. To accomplish this, we constructed lifetime medical histories for two cohorts of Rottweiler dogs living in 29 states and Canada: Exceptional Longevity Cohort = a group of exceptionally long-lived dogs that lived at least 13 years; and Usual Longevity Cohort = a comparison group of dogs that lived 8.0 to 10.8 years (average age at death for Rottweilers is 9.4 years). A female survival advantage in humans is well-documented; women are 4 times more likely than men to live to 100. We found that, like women, female Rottweilers were more likely than males to achieve exceptional longevity (Odds Ratio, 95% confidence interval = 2.0, 1.2 - 3.3; p = .006). However, removal of ovaries during the first 4 years of life erased the female survival advantage. In females, this strong positive association between ovaries and longevity persisted in multivariate analysis that considered other factors, such as height, adult body weight, and mother with exceptional longevity.

In summary, we found female Rottweilers who kept their ovaries for at least 6 years were 4.6 times more likely to reach exceptional longevity (i.e. live >30 % longer than average) than females with the shortest ovary exposure. Our results support the notion that how long females keep their ovaries determines how long they live.

In the pages that follow, I have attempted to frame these new findings in a way that will encourage veterinarians to venture beyond the peer-reviewed scientific text and data-filled tables of Aging Cell to consider the pragmatic, yet sometimes emotionally charged implications of this work. Call it a primer for the dynamic discussions that will undoubtedly take place, not only between practitioners and pet owners, but also within the veterinary profession. Call it a wake-up call for how little veterinarians have been schooled in the mechanistic nuts and bolts underlying the aging process. Call it an ovary story. 

Do ovaries really promote longevity? Observed associations between exposures and outcomes may not necessarily be causal, so we explored alternative, non-causal explanations for the association between ovaries and exceptional longevity in our study. But we found no evidence that factors which may influence a pet owner's decision on age at ovary removal — for example, earlier ovariectomy in dogs with substandard conformation or delayed ovariectomy to obtain more offspring in daughters of long-lived mothers — could adequately account for the strong association.

There is another aspect of our data pattern that gives us further confidence that ovaries really do matter when it comes to successful aging. A simple explanation for the observation that ovaries promote longevity would be that taking away ovaries increases the risk for a major lethal disease. In Rottweilers, cancer is the major killer. We found, however, that by conducting a subgroup analysis that excluded all dogs that died of cancer, the strong association between intact ovaries and exceptional longevity persisted. After excluding all cancer deaths, females that kept their ovaries the longest were 9 times more likely to reach exceptional longevity than females with shortest ovary exposure. Thus, we observed a robust ovarian association with longevity that was independent of cause of death, suggesting that a network of processes regulating the intrinsic rate of aging is under ovarian control. This work positions pet dogs, with their broad range of lifetime ovary exposure, to become biogerontology's new workhorse for identifying ovary-sensitive physiological processes that promote healthy longevity.

Interestingly, our findings in dogs surface just as data from women are calling into question whether those who undergo hysterectomy should have ovary removal or ovary sparing. In fact, our results mirror the findings from more than 29,000 women in the Nurses’ Health Study who underwent hysterectomy for benign uterine disease (2). In that study, the upside of ovariectomy — protection against ovarian, uterine, and breast cancer — was outweighed by increased mortality from other causes. As a result, longevity was cut short in women who lost their ovaries before the age of 50 compared with those who kept their ovaries for at least 50 years. Taken together, the emerging message for dogs and women seems to be that when it comes to longevity, it pays to keep your ovaries.

But before we all go out and buy T-shirts with some romantic imperative like “Save the Ovaries”, perhaps we should step back and consider the following question: Why haven’t previous dog studies called our attention to this potential downside of ovariectomy? Reviewing the literature, an answer quickly bubbles up. No previous studies in pet dogs have rigorously evaluated the association between ovaries and longevity. Two frequently cited reports (3,4) provide limited guidance because: (1) longevity data are presented as combined mean age at death for a relatively small number of individuals of more than 50 breeds of different body size and life expectancy; and (2) ovarian status is reported as “intact” or “spayed”, rather than as number of years of lifetime ovary exposure. Comparing female dogs binned into the categories of “intact” versus “spayed” introduces a methodological bias that might lead one to conclude that ovaries adversely influence longevity, i.e. ovary removal promotes longevity. Because the reasons for ovariectomy (e.g., uterine infection, mammary cancer) increase with increasing age, it is expected that a large percentage of the oldest-dogs are binned as “spayed” despite having many years of ovary exposure. For example, a dog who at age 12 undergoes ovariohysterectomy for pyometra would be binned as “spayed”, despite 12 years of ovary exposure. In our study, we employed a more stringent study design — restricting the study population to AKC registered, pure-bred dogs of one breed, carefully quantitating the lifetime duration of ovarian exposure — in order to lessen the likelihood of such bias. And we reasoned that studying veterinary teaching hospital-based populations of dogs with artifactually low life expectancies (for example, 3.5 years is median age at death for Rottweilers in the Veterinary Medical Data Base)(5) was an inappropriate vehicle to describe the influence that ovaries have on aging. So we cast a wider net and collected data from Rottweiler owners nationwide, focusing our attention on exceptional longevity, not average age at death, as our study endpoint.

Why study exceptional longevity? Why not average longevity? We thought studying the most exceptionally long-lived individuals would tell us something about what it takes to age successfully. It’s the same rationale used by Thomas Perls and investigators of the New England Centenarian Study (6) and by other scientists who study long-lived humans in other parts of the world (7). The approach even garners support from the mathematical field. In a seminal book on the origins of creative genius, the mathematician Jacques Hadamard wrote: “In conformity with a rule which seems applicable to every science of observation, it is the exceptional phenomenon which is likely to explain the usual one.” (8) Hadamard was trying to understand how the brain gets creative so he studied people with extreme creativity. When it comes to studying aging, we’re solidly in the Hadamard camp. That is why in 2005 we established the Exceptional Longevity Data Base, launching the first systematic study of the oldest-old pet dogs (9). But folks in the opposing camp might justifiably fire back: “Don’t study extreme longevity. Extreme longevity is much more about luck than it is about genes, or environment, or ovaries.” 

So to address the possibility that the “strangeness” or outlier nature of dogs with exceptional longevity could be forging a misleading link between ovaries and longevity, we studied a separate cohort of Rottweiler dogs. This data set was comprised of 237 female Rottweilers living in North America that died at ages 1.2 to 12.9 years — none were exceptionally long-lived. Information on medical history, age at death, and cause of death was collected by questionnaire and telephone interviews with pet owners and local veterinary practitioners. In this population, we found females that kept their ovaries for at least 4.5 years had a statistically significant 37% reduction in mortality rate (1). This translated into a median survival of 10.4 years for females with more than 4.5 years of ovary exposure — 1.4 years longer than the median survival of only 9.0 years in females with shorter ovary exposure (p < 0.0001). Taken together, if you take out ovaries before 4 years of age you cut longevity short an average of 1.4 years and decrease the likelihood of reaching exceptional longevity by 3-fold.

Up to this point, my ovary story has centered around a summarizing of methodologies and results. The reader has been given opportunity to see the gist of our findings within the context of previous dog studies and late-breaking studies in women. Now, let us pivot our attention a bit away from the results to focus on the recipients of these results — DVMs and pet owners. 

We can start by tackling the question: Just how receptive will DVMs be to these new research findings? It’s hard for old dogs to learn new tricks. But one thing is sure — blossoming change is rooted in real communication. The anthropologist Gregory Bateson wrote: “The pre-instructed state of the recipient of every message is a necessary condition for all communication. A book can tell you nothing unless you know 9/10ths of it already.” (10). I call this “Bateson’s Rule of the 9/10ths”. If Bateson is right, then we will want to do something about the pre-instructed state of veterinarians. Because when it comes to the biology of aging, the state is virtually a blank slate. None of us received training in the biology of aging as part of our DVM curriculum — whether we graduated 30 years ago or last summer. Therefore, most DVMs are ill-prepared to receive messages examining the mechanistic underpinnings of the aging process. A Batesonian prescription for positive change would be to ratchet up the biology of aging IQ of practicing veterinarians. We agree. That is why we established the first gerontology training program for veterinarians in 2007 (11). We believe that by helping veterinarians “know” more about aging, they will be more able and more receptive to communicating the things that promote healthy longevity in their patients — things like preserving ovaries.

For certain, DVMs will be asked by pet owners to help them make their decision about age at spay in light of this new information. The question will be asked: Just how generalizable are these findings in Rottweilers to other segments of the pet dog population? It is impossible to say at this time. It will demand further study. Alas, 10 years from now, we might just find out that a longevity-promoting effect of ovaries in dogs is limited — limited to large breeds, urban but not rural dogs, or only those individuals with particular polymorphisms in insulin-like growth factor-1. These restrictions should not only be expected, they should be celebrated. It will mean that we have looked more deeply into how ovaries might influence healthy longevity. It will mean that our initial findings have been contextualized. And it is this contextualization of information that marks scientific progress — the kind of progress that guides sound clinical decision making. For it is context that determines meaning (12).

Our provocative findings in Aging Cell mean that it’s time to re-think the notion that taking away ovaries has no significant downside to a dog’s healthy longevity. Perhaps it would help us if we thought of lifetime ovary exposure as information — information that instructs the organism. Just how long and how healthy a female lives reflects what her cells, tissues, and organs thought they heard from the message received. Of course in biology, there is no single message but a symphony of messages, enabling each individual to successfully respond to environmental challenges. Our findings suggest that ovaries orchestrate that symphony. Taking away ovaries in early or mid-life makes for muddled information, less than perfect music. 

Information muddling can ensnarl decision-making. Our research takes an important first step toward disentangling the thinking about ovaries and longevity. We must never be paralyzed by the incompleteness of our knowledge. Our knowledge will always be incomplete — subject to revision, primed for further inquiry. This uncertainty, although invigorating for the investigator, is often painful for the practitioner who seeks simple, fact-driven algorithms to guide his action. Just as scientists will be called upon to forge ahead with their scientific inquiries, so too will practitioners be counted on to master the uncertainty. Together, we must navigate what the Danish philosopher-theologian Soren Kierkegaard called the gap “between the understanding and the willing.” That is, we must ask the right questions and make smart choices so that our action (the willing) is in synch with our knowledge (the understanding). Under just what circumstances will a particular individual benefit from specific lifestyle decisions? This is perhaps the most prescient, overarching question in the wellness and preventive medicine fields facing both human and veterinary health professionals today. How can we promote healthy longevity? Antioxidant supplementation or calorie restriction? Ovary removal or ovary sparing? 

Undoubtedly, there will be protagonists and antagonists in this ovary story. The protagonists will be open-minded to following a new script. They will embrace the idea of ovary sparing for critical periods of time to maximize longevity. They might even recognize the need for some sort of “ovarian mimetic” in spayed dogs to optimize healthy aging. The antagonists in this story — the defenders of the old script — will dismiss as trivial the notion that ovaries regulate the rate of aging and influence healthy longevity. Lines will be drawn and opinions will fly. But that's what healthy debate is — antagonists and protagonists keeping a high priority issue front and center, not allowing it to fade into the woodwork. It would seem that, in light of the new scientific findings, a contemporary dialogue should balance the potential benefits of elective ovary removal (13) with its possible detrimental effects on longevity. 

References

1. Waters DJ, Kengeri SS, Clever B, et al: "Exploring the mechanisms of sex differences in longevity: lifetime ovary exposure and exceptional longevity in dogs." Aging Cell October 26, 2009

2. Parker WH, Broder MS, Chang E et al: "Ovarian conservation at the time of hysterectomy and long-term health outcomes in the Nurses' Health Study." Obstet Gynecol 113: 1027-1037, 2009 

3. Bronson RT: "Variation in age at death of dogs of different sexes and breeds." Am J Vet Res 43: 2057-9, 1982

4. Michell AR: "Longevity of British breeds of dog and its relationships with sex, size, cardiovascular variables and disease." Vet Rec 145: 625-629, 1999

5. Patronek GJ, Waters DJ, Glickman LT et al: "Comparative longevity of pet dogs and humans: implications for gerontology research." J Gerontol A Biol Sci Med Sci 52: B171-8, 1997

6. Perls TT, Hutter Silver M, Lauerman JF: Living to 100: Lessons in Living to Your Maximum Potential at Any Age, New York, NY, Basic Books, 1999

7. Franceschi C, Motta L, Valensin S et al: "Do men and women follow different trajectories to reach extreme longevity?" Aging (Milano) 12: 77-84, 2000

8. Hadamard J: The Psychology of Invention in the Mathematical Field. New York, NY, Oxford Univ Press, 1945, p. 136

9. Waters DJ, Wildasin K: "Cancer clues from pet dogs." Sci Am 295: 94-101, 2006

10. Bateson G, Bateson MC: Angels Fear: Towards an Epistemology of the Sacred. New York, NY, Bantam, 1988, p 163

11. Gerontology Program for DVMs co-sponsored and organized by Gerald P. Murphy Cancer Foundation, Purdue University Center on Aging and the Life Course, P&G Pet Care; for more information go to www.gpmcf.org

12. Waters DJ, Chiang EC, Bostwick DG: "The art of casting nets: fishing for the prize of personalized cancer prevention." Nutr Cancer 60: 1-6, 2008

13. Kustritz MV: "Determining the optimal age for gonadectomy of dogs and cats." J Am Vet Med Assoc 231: 1665-75, 2007

© GPMCF 2009

 


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