Title

Subtitle

Dr. Jean Dodds on over-vaccinating........

 
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Abstract
January 15, 2015, Vol. 246, No. 2, Pages 205-211
doi: 10.2460/javma.246.2.205

 

Comparison of anamnestic responses to rabies vaccination in dogs and cats with current and out-of-date vaccination status

Michael C. MooreDVM, MPHRolan D. DavisMSQing KangPhDChristopher I. VahlPhDRyan M. WallaceDVM, MPHCathleen A. HanlonVMD, PhD;Derek A. MosierVMD, PhD
Veterinary Diagnostic Laboratory, College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506. (Moore, Davis, Hanlon); Statistical Intelligence Group LLC, 117 Firethorn Ln, Manhattan, KS 66503. (Kang); Department of Statistics, College of Arts and Sciences, Kansas State University, Manhattan, KS 66506. (Vahl); CDC, 1600 Clifton Rd, Atlanta, GA 30333. (Wallace, Hanlon); Department of Diagnostic Medicine and Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506. (Mosier)

This manuscript represents a portion of a thesis submitted by Dr. Moore to the Kansas State University Graduate School as partial fulfillment of the requirements for a Master of Public Health degree.

Presented to the Compendium of Animal Rabies Prevention and Control Committee of the National Association of State Public Health Veterinarians, Nashville, Tenn, June 2014.

The authors thank Drs. Sue Nelson, John Teeter, and Don Dinges for assistance in procuring samples.

Objective—To compare anamnestic antibody responses of dogs and cats with current versus out-of-date vaccination status.

Design—Cross-sectional study.

Animals—74 dogs and 33 cats.

Procedures—Serum samples were obtained from dogs and cats that had been exposed to rabies and brought to a veterinarian for proactive serologic monitoring or that had been brought to a veterinarian for booster rabies vaccination. Blood samples were collected on the day of initial evaluation (day 0) and then again 5 to 15 days later. On day 0, a rabies vaccine was administered according to label recommendations. Paired serum samples were analyzed for antirabies antibodies by means of a rapid fluorescent focus inhibition test.

Results—All animals had an antirabies antibody titer ≥ 0.5 IU/mL 5 to 15 days after booster vaccination. Dogs with an out-of-date vaccination status had a higher median increase in titer, higher median fold increase in titer, and higher median titer following booster vaccination, compared with dogs with current vaccination status. Most (26/33) cats, regardless of rabies vaccination status, had a titer ≥ 12 IU/mL 5 to 15 days after booster vaccination.

Conclusions and Clinical Relevance—Results indicated that dogs with out-of-date vaccination status were not inferior in their antibody response following booster rabies vaccination, compared with dogs with current vaccination status. Findings supported immediate booster vaccination followed by observation for 45 days of dogs and cats with an out-of-date vaccination status that are exposed to rabies, as is the current practice for dogs and cats with current vaccination status.


CITING ARTICLES
. (2016) Compendium of Animal Rabies Prevention and Control, 2016. Journal of the American Veterinary Medical Association248:5, 505-517. 
Online publication date: 17-Feb-2016.
Citation | Full Text | PDF (259 KB) | PDF Plus (306 KB) 
(2015) Letters to the Editor. Journal of the American Veterinary Medical Association 246:6, 594-596. 
Online publication date: 26-Feb-2015.

Citation | Full Text | PDF (487 KB) | PDF Plus (494 KB)  

 

 

 Re-Printed with permission from Dr. Jean Dodds

 Canine Vaccination Guidelines:  https://www.aaha.org/public_documents/professional/guidelines/caninevaccineguidelines.pdf

2011 AAHA Canine Vaccination Guidelines Members of the American Animal Hospital Association (AAHA) Canine Vaccination Task Force: Link V. Welborn, DVM, DABVP (Chairperson), John G. DeVries, DVM, DABVP, Richard Ford, DVM, MS, DACVIM, (Hon)ACVPM, Robert T. Franklin, DVM, DACVIM, Kate F. Hurley, DVM, MPVM, Kent D. McClure, DVM, JD, Michael A. Paul, DVM, Ronald D. Schultz, PhD, DACVM"

 

 

Chapter 8. Alternatives to Current Adjuvants:
a Veterinary Perspective

W. Jean Dodds, DVM

Hemopet, 11561 Salinaz Avenue, Garden Grove, CA 92843

www.hemopet.org; E-mail: [email protected]

Abstract

Veterinary practitioners are seeing more patients exhibiting signs of immunologic dysfunction and disease, many of which occur within 30-45 days of a vaccination. Vaccines and their adjuvants are implicated as the potential triggering agents in those animals that are genetically predisposed to adverse vaccine reactions, termed vaccinosis.  The number of adjuvants used in veterinary vaccines should be re-examined, as they exceed those used in human medicine. Discovery and implementation of new types of vehicles designed to enhance the immune response to vaccines should be encouraged. A multifaceted approach is required, including alternative strategies for containing infectious disease and reducing the environmental impact of conventional vaccines.  The periodicity between adult booster vaccinations should be increased to three years and monitoring of serum antibody levels (as an indirect assessment of protection against the clinically important infectious agents) should be fostered.

Key Words

Animals; Vaccines; Adjuvants; Vaccinosis; Alternative strategies.

Introduction

Countless animals have been vaccinated routinely and repeatedly without obvious untoward effects. In that regard, however, the veterinarian must determine what constitutes "acceptable" harm (Dodds, 1997, 1999; Smith, 1995).

In humans, causality questions about the adverse events associated with childhood vaccines are categorized by:  Can It (Potential Causality)? Did It (Retrodictive Causality) ? and Will It (Predictive Causality ) ? (Stratton, Howe, Johnston, 1994).  An updated report from this National Academy of Sciences Committee (201l) found convincing evidence for a causal relationship between some vaccines and adverse events for:  mumps-measles-rubella (MMR), varicella zoster (herpes virus), influenza, hepatitis B, meningococcal, and tetanus-containing vaccines. But, their rather surprising conclusion was that “few health problems are caused by or clearly associated with vaccines” ! 

Immunologic adjuvants act to accelerate, prolong, or enhance antigen-specific immune responses when used together with specific vaccine antigens (Altman & Dixon, 1989). Vaccine adjuvants are incorporated into vaccines to enhance their immunogenicity, but this increases the risk of autoimmune and inflammatory adverse events following the vaccination (Cerpa-Cruz, 2013).  For those killed vaccines available for human and veterinary use, potent adjuvants produce a more sustained humoral immune response and compete favorably with the longer protection typically afforded by MLV products. But, these adjuvants may also induce adverse effects (Cerpa-Cruz et al, 2013; Cruz-Tapias et al, 2013; Dodds, 1997; Israeli et al, 2009; Kuroda et al, 2004; Leventhal et al, 2012; Luján et al, 2013; Perricone et al , 2013; Shaw & Tomljenovic , 2013, 2014; Stejskal, 2013; Tomljenovic &  Shaw, 2012).

Although killed or inactivated products make up about 15% of the veterinary biologicals used, they have been associated with 85% of the post-vaccination reactions, mainly because of the acute adverse responses induced by the adjuvants used in companion animal, wildlife and livestock species (Dodds, 1997; Luján et al, 2013).  Several years ago, an "all-killed" combination vaccine for dogs was marketed, but some users encountered minor problems with discoloration of the adjuvant and local reactions at the injection site. The product was subsequently withdrawn.  No other source of killed combination vaccine is available for dogs, although such products are now offered for cats. Ringworm and chlamydia vaccines introduced for use in cats are advertised as having the safety advantage of a killed product (Dodds, 1997).   This debate about the relative merits and safety of killed versus MLV vaccines has been ongoing in the veterinary literature, and was hotly debated in a comparison of the risks, costs, and convenience of killed versus modified live human polio vaccines (Stratton, Howe, Johnston, 1994).

Discussion

The landmark review by Altman & Dixon (1989) addressed the vehicles used as immunomodifiers in vaccines. Today, these include: aluminum salts (Clements & Griffiths, 2002; Leventhal et al, 2012; Luján et al, 2013; Tomljenovic & Shaw, 2011a, b); water-in-oil emulsions (Altman & Dixon, 1989); biodegradable oil vehicles (Kuroda et al, 2000); oil-in-water emulsions (Altman & Dixon, 1989); biodegradable microcapsules, nano- and microparticles  (Akagi et al, 2012; Altman & Dixon, 1989); immunostimulating complexes (Gupta & Siber, 1995); organic oils like squalene (Altman & Dixon, 1989; Gupta & Siber, 1995); liposomes and lipid A (Richards, Alving, Wassef, 1996; Nordly et al, 2009); oral vaccines (Lavelle & O’Hagan, 2006); and virosomes (Spickler & Roth, 2003).   Subunit, recombinant and oral vaccines also have become available and popular, but need adjuvants to boost their immune response which tends to be relatively poor otherwise (Gupta & Siber, 1995; Lavelle & O’Hagan, 2006; Perrie et al, 2008; Vogel, 2000).

Since then, the literature and vaccine industry has exploded with new types of adjuvants and numerous studies describing the safety and efficacy of adjuvants in human and animal vaccines (Cerpa-Cruz et al, 2013; Cruz-Tapias et al, 2013; Davis, 2008; Heegaard et al, 2011; Israeli et al, 2009; Kuroda et al, 2004; Macy, 1997; Perricone et al, 2013; Shaw & Tomljenovic 2013, 2014; Spickler & Roth, 2003; Stejskal 2013; Tomljenovic & Shaw 2011 a, b. 2012; Vanloubbeeck, Hostetter, Jones , 2003; Vogel 1995, 2000; Wilson-Welder et al, 2009).

Biodegradable polymeric nanoparticles are newer vaccine vehicle adjuvants that have entrapped antigens such as proteins, peptides, or DNA. These help control the release of vaccine antigens and optimize the desired immune response by selectively targeting the antigen to the body’s antigen-presenting cells. The efficient delivery of vaccinal antigens to these antigen-presenting cells, especially in dendritic cells, and their activation are some of the most important current issues in the development of effective vaccines (Akagi, Baba, Akashi, 2012; Vanloubbeeck, Hostetter, Jones, 2003).  While current vaccine adjuvants can successfully generate humoral antibody-mediated protection, other diseases such as tuberculosis and malaria require a cell-mediated immune response for adequate protection (Wilson-Welder et al, 2009).

Adverse Events Associated with Adjuvants

Adjuvants have been used safely in human and veterinary medicine for decades, especially those containing aluminum salts and monophosphoryl lipid A in human and animal vaccines, and  squalene in animal vaccines (Aucouturier, Dupuis, Ganne, 2001; Macy, 1997; Nordly et al, 2009; Perrie et al, 2008; Richards, Alving, Wassef, 1996; Vogel, 1995, 2000: Wilson-Welder et al, 2009). Nevertheless, as cited above, adjuvants can also produce numerous adverse effects.

Experimental studies have shown that simultaneous administration of even two to three adjuvants can overcome genetic resistance to autoimmunity (Tomljenovic & Shaw, 2012).   Because vaccines are viewed an inherently safe and non-toxic, toxicity studies are often excluded from the regulatory safety assessment of vaccines.  Children are especially at risk as they are more vulnerable to toxicity than adults and are regularly exposed to more adjuvants with vaccines than are adults.  Adjuvants impact the central nervous system at all levels and can do so by changing gene expression (Shaw and Tomljenovic, 2014). Further, it is now known that the neuro-immune axis, heavily targeted by adjuvants, plays a key role in brain development and immune function (Shaw & Tomljenovic, 2013, 2014; Tomljenovic & Shaw, 2011a, b, 2012).  

The autoimmune (auto-inflammatory) syndrome induced by adjuvants (ASIA syndrome) was  first defined in 2011 (Perricone et al, 2013). Presently, it includes four conditions that share similar signs and symptoms and result from hyperactive immune responses: siliconosis, macrophagic myofasciitis syndrome, Gulf war syndrome and post-vaccination phenomena (Cruz-Tapias, 2013; Perricone et al, 2013; Stejskal, 2013).  The common denominator in these syndromes was the triggering effect of the adjuvants, in combination with other environmental factors and genetic predisposition (Dodds, 1997, 1999).  When combined, these factors cause the failure of self-tolerance, which equates to autoimmunity (Dodds, 1999).  

Proving the ASIA concept was accomplished by the use of experimental animal models including those for:  rheumatoid arthritis, systemic lupus erythematosus, autoimmune thyroid disease, anti-phospholipid syndrome, and myocarditis. The experimental animal models  are now widely used to understand the mechanisms, etiology and pathogenesis of these diseases; and results could help promote development of new diagnostic, predictive and therapeutic methods (Cruz-Tapias et al, 2013; Davis, 2008; Perricone et al, 2013; Stejskal, 2013).

Mercury is thought to be yet another trigger of ASIA syndrome (Stejskal, 2013), and the use of mercury and mercury compounds has been widespread in medicine, despite its known toxicity.  Mercury and other heavy metals mainly affect the body in two ways: via toxic and immunological reactions – which cause hypersensitivity or autoimmunity. Studies show that metals, such as mercury, can be a risk factor for the development of various autoimmune diseases, such as autoimmune thyroiditis, multiple sclerosis, and kidney disease, and nonspecific symptoms such as chronic fatigue and myalgia. Animal studies have shown that mercury and other metals, such as nickel, chromium, silver and gold, might either be non-toxic or induce severe diseases, such as skin disease or autoimmunity, but this depends upon the individual animal’s genotype.  Endocrine status and the presence of chronic infections are factors that might predispose to the risk of sensitization (Perricone et al, 2013; Stejskal, 2013).

The immunological effects of these metals, including mercury, are immunomodulation, allergy or autoimmunity. Metals may act either as immunosuppressants or as immune adjuvants in vaccines.  The type of allergy induced by metals is delayed-type hypersensitivity and manifests often as a contact dermatitis. Thimerosal (merthiolate), like nickel, is one of the most frequent allergens in children and adolescents, and in companion animals vaccinated for rabies (Cruz-Tapias, 2013; Dodds, 1997, 1999; Perricone et al, 2013; Stejskal, 2013).  Thus, mercury and other metals can be added to the list of environmental agents that exert both specific and non-specific effects contributing to ASIA syndrome (Stejskal, 2013).

Vaxjo is a newly published, web-based vaccine adjuvant database (Sayers,  Guerlain,  Zuoshuang, et al.  2012).  It curates, stores, and analyzes vaccine adjuvants and their usages in vaccine development. Basic vaccine information stored includes: adjuvant name, components, structure, appearance, storage, preparation, function, safety, and vaccines that use this adjuvant. Currently over 100 vaccine adjuvants have been annotated in Vaxjo. These adjuvants have been used in over 380 vaccines against over 81 pathogens, cancers, or allergies.

Use of Adjuvants in Veterinary Practice (Aucouturier, Dupuis, Ganne, 2001; Heegaard et al, 2011; Luján et al, 2013; Macy, 1997; Spickler & Roth, 2003; Vanloubbeeck, Hostetter, Jones, 2003).

As discussed above with respect to the safety of adjuvants, use of alternative methodologies to protect against the common infectious diseases of animals appears to be justified (Dodds, 1997, 1999; Spickler & Roth, 2003).   This is particularly relevant because, unlike human vaccines, veterinary vaccines often contain a large number of substances that act alone or together as immune stimulating adjuvants (Macy, 1997). Nevertheless, reducing the exposure risk of susceptible animals to known infectious agents is a basic epidemiologic principle that should be emphasized (Dodds, 1997, 1999).  Finally, the issues raised in this article are timely and germane to parallel concerns about childhood vaccination. In humans, this topic is equally important and controversial. The two-volume publication from an expert advisory panel of the National Academy of Sciences offers fascinating and troubling reading (Stratton, Howe, and Johnston, 1994).

Conclusion

Veterinary practitioners are confronting increasing numbers of patients exhibiting signs of immunologic dysfunction and disease. In an increasing number of cases, the onset occurs within 30-45 days of vaccination. The evidence implicates vaccines and their adjuvants as potential triggering agents combined with genetic predisposition of the vaccinated host.  The number of adjuvants used in veterinary vaccines should be re-examined. At the same time, discovery and implementation of new types of vehicles that enhance the immune response to vaccines should be encouraged. A multifaceted approach to furthering the recognition of this situation, along with alternative strategies for containing infectious disease and reducing the environmental impact of conventional vaccines, is clearly needed. As a beginning, the periodicity between adult booster vaccinations can be increased to three years and monitoring of serum antibody levels (as an indirect assessment of protection against the clinically important infectious agents) can be implemented.

 

References

Akagi T, Baba M, Akashi M. 2012.  Biodegradable nanoparticles as vaccine adjuvants and delivery systems: regulation of immune responses by nanoparticle-based vaccine. Adv Polymer Sci  247: 31-64.

Altman A, Dixon FJ. 1989. Immunomodifiers in vaccines. In Vaccine Biotechnology, eds. JL Bittle, FA Murphy, Adv Vet Sci and Comp Med  33: 301-43: Academic Press.

Aucouturier J, Dupuis L, Ganne V. 2001. Adjuvants designed for veterinary and human vaccines.  Vaccine 19 (17-19):2666-72.

Cerpa-Cruz S, Paredes-Casillas P, Landeros-Navarro E, et al.  2013. Adverse events following immunization with vaccines containing adjuvants.  Immunol Res  56(2-3):299-303.

Clements CJ, Griffiths E. 2002. The global impact of vaccines containing aluminum adjuvants. Vaccine 20 Suppl 3:S24-33.

Cruz-Tapias P, Agmon-Levin N, Israeli E et al. 2013. Autoimmune (autoinflammatory) syndrome induced by adjuvants (ASIA) – animal models as a proof of concept. Curr Med Chem 20:4030-36.

Davis HL. 2008. Novel vaccines and adjuvant systems: the utility of animal models for predicting immunogenicity in humans.  Hum Vaccin  4(3):246-50.

Dodds WJ. 1997. Vaccine-related issues. In Complementary and Alternative Veterinary Medicine, eds. AM Schoen, SG Wynn, Ch. 40, pp.701-12: Mosby.

Dodds WJ. 1999. More bumps on the vaccine road. Adv Vet Med 41:715-732.

Gupta RK, Siber GR. 1995. Adjuvants for human vaccines--current status, problems and future prospects.   Vaccine 13(14):1263-76.

Heegaard PM, Dedieu L, Johnson N, et al. 2011. Adjuvants and delivery systems in veterinary vaccinology: current state and future developments.  Arch Virol 156 (2):183-202.

Israeli E, Agmon-Levin N, Blank M, et al. 2009.  Adjuvants and autoimmunity. Lupus 18(13): 1217-25.

Kuroda Y, Nacionales DC, Akaogi J, et al.  2004. Autoimmunity induced by adjuvant hydrocarbon oil components of vaccine.  Biomed Pharmacother 58(5):325-37.

Lavelle EC, O'Hagan DT. 2006. Delivery systems and adjuvants for oral vaccines. Expert Opin Drug Deliv 3(6):747-62.

Leventhal JS, Berger EM, Brauer JA, et al. 2012. Hypersensitivity reactions to vaccine constituents: a case series and review of the literature.  Dermatitis 23(3):102-9.

Luján L, Pérez M, Salazar E, et al. 2013. Autoimmune/autoinflammatory syndrome induced by adjuvants (ASIA syndrome) in commercial sheep. Immunol Res 56: 317-24.

Macy DW. 1997.  Vaccine adjuvants.  Sem Vet Med Surg (Sm An) 12(3):206-11.

Nordly P, Madsen HB, Nielsen HM, et al. 2009. Status and future prospects of lipid-based particulate delivery systems as vaccine adjuvants and their combination with immunostimulators.

Expert Opin Drug Deliv  6(7):657-72.

Perricone C, Colafrancesco S, Mazor RD, et al. 2013. Autoimmune/inflammatory syndrome induced by adjuvants (ASIA) 2013: Unveiling the pathogenic, clinical and diagnostic aspects.

J Autoimmun 47:1-16.

Perrie Y, Mohammed AR, Kirby DJ, et al. 2008. Vaccine adjuvant systems: enhancing the efficacy of sub-unit protein antigens.  Int J Pharm  364(2):272-80.

Richards RL, Alving CR, Wassef NM. 1996. Liposomal subunit vaccines: effects of lipid A and aluminum hydroxide on immunogenicity.   J Pharm Sci 85(12):1286-9.

Sayers S,  Guerlain U,  Zuoshuang X, et al.  2012.  Vaxjo: A Web-Based Vaccine Adjuvant Database and Its Application for Analysis of Vaccine Adjuvants and Their Uses in Vaccine Development.  J Biomed Biotechnol  2012: 831486.

Shaw CA, Tomljenovic L. 2013. Aluminum in the central nervous system (CNS): toxicity in humans and animals, vaccine adjuvants, and autoimmunity.  Immunol Res  56(2-3):304-16.

Shaw CA, Li D, Tomljenovic L. 2014. Are there negative CNS impacts of aluminum adjuvants used in vaccines and immunotherapy?  Immunotherapy 6(10):1055-71.

Smith CA.  1995. Are we vaccinating too much?  J Am Vet Med Assoc  207:421-425.Spickler AR, Roth JA. 2003.  Adjuvants in veterinary vaccines: modes of action and adverse effects.  J Vet Intern Med  17(3):273-81.

Stejskal V. 2013. Mercury-induced inflammation: yet another example of ASIA syndrome. Israel Med Assoc J 15:714-15.

Stratton KR, Howe CJ, Johnston RB, Jr, eds. 1994.  In Adverse Events Associated with Childhood Vaccines: Evidence Bearing on Causality: National Academy Press.  

Tomljenovic L, Shaw CA. 2011a.  Aluminum vaccine adjuvants: are they safe?   Curr Med Chem 18 (17):2630-37.

Tomljenovic L, Shaw CA. 2011b. Do aluminum vaccine adjuvants contribute to the rising prevalence of autism?  J Inorg Biochem 105(11):1489-99.

Tomljenovic L, Shaw CA.  2012. Mechanisms of aluminum adjuvant toxicity and autoimmunity in pediatric populations.  Lupus 21(2):223-30.

Vanloubbeeck Y, Hostetter J, Jones DE. 2003. The biology of dendritic cells and their potential use in veterinary medicine.  Anim Health Res Rev  4(2):131-42.

Vogel FR. 1995. Immunologic adjuvants for modern vaccine formulations. Ann N Y Acad Sci  754:153-60.

Vogel FR. 2000. Improving vaccine performance with adjuvants.  Clin Infect Dis 30 Suppl 3:S266-70.

Wilson-Welder JH, Torres MP, Kipper MJ, et al. 2009. Vaccine adjuvants: current challenges and future approaches.   J Pharm Sci 98(4):1278-316.  

 

 

Chapter 10: Adverse Events Associated with Vaccines in
Veterinary Practice

W. Jean Dodds, DVM

Hemopet, 11561 Salinaz Avenue, Garden Grove, CA 92843

www.hemopet.org; E-mail: [email protected]  

 

Abstract

A more pro-active approach is still needed to standardize and individualize the production and use of veterinary vaccines in order to ensure their safety and efficacy. Progress is hampered, however, by the ongoing controversy surrounding vaccines, failure to comply with current national vaccine policies and guidelines, resistance to change, and denial of adverse events within the general veterinary community as well as within society as a whole.  One solution resides with the need for more focused educational efforts both within academic veterinary medicine, clinical practice, and the companion animal and livestock owner communities.

Key Words

Veterinary; Vaccines; Denial of adverse events; Education needs; Policies

 

Introduction

There is no doubt that application of modern vaccine technology has permitted us to effectively protect companion animals (and people) against serious infectious diseases (Dodds, 1997, 1999; Sinha, Lopez and McDevitt, 1990; Wellborn et al, 2011).

In animals, viral disease and recent vaccination with single or combination modified live-virus (MLV) vaccines, especially those containing distemper virus, adenovirus 1 or 2, and parvovirus are increasingly recognized contributors, albeit relatively rare, to immune-mediated blood disease, bone marrow failure, and organ dysfunction (Dodds, 1997, 1999; Schultz, 1998; Wellborn et al, 2011). Potent adjuvanted killed vaccines like those given for rabies virus or ovine bluetongue virus also can trigger immediate and delayed (vaccinosis) adverse vaccine reactions (Dodds, 2001; Frana et al, 2008; Hogenensch et al, 1999; Luján et al, 2013).  Genetic predisposition to these disorders in humans has been linked to the leucocyte antigen D-related gene locus of the major histocompatibility complex, and is likely to have parallel associations in domestic animals (Cruz-Tapias et al, 2013; Sinha, Lopez and McDevitt, 1990).

 It must be recognized, however, that we have the luxury of asking such questions today only because the risk of disease has been effectively reduced by the widespread use of vaccination programs (Dodds, 1997, 1999; Schultz, 1998; Smith, 1995; Wellborn et al, 2011).

Discussion

Several factors are known to contribute to the risk of adverse vaccine reactions, namely (Cruz-Tapias et al, 2013; Dodds, 1983, 1997, 1999, 2001, 2012, 2015 a,b; Luján et al, 2013; Stejskal, 2013; Tizard, 1990): genetic predisposition (family history and breed type), influence of sex hormonal change (estrus), and type of vaccine and adjuvant used (rabies and thimerosol, bluetongue virus and aluminum salts).   The clinical signs associated with vaccine reactions typically include fever, stiffness, sore joints and abdominal tenderness, susceptibility to infections, neurological disorders and encephalitis, collapse with auto-agglutinated red blood cells and icterus (immune-mediated hemolytic anemia, IMHA), or generalized petechiae and ecchymotic hemorrhages (immune-mediated thrombocytopenia, IMTP).  Hepatic enzymes may be markedly elevated, and liver or kidney failure may occur by itself or accompany bone marrow suppression (Dodds, 1983, 1997, 1999, 2001, 2015a). 

An augmented immune response to vaccination is seen in dogs with pre-existing inhalant allergies (atopy) to pollens (Dodds, 1997).   Furthermore, the increasing current problems with allergic and immunological diseases have been linked to the introduction of MLV vaccines more than 20 years ago.  While other environmental factors no doubt have a contributing role, the introduction of these vaccine antigens and their environmental shedding may provide the final insult that exceeds the immunological tolerance threshold of some individuals in the pet population (Dodds, 1999).  The accumulated evidence indicates that vaccination protocols should no longer be considered as a “one size fits all” program (Dodds, 2013).

In cats, while adverse vaccine reactions may be less common, aggressive tumors (fibrosarcomas) can occasionally arise at the site of vaccination (Schultz, 1998; Scott & Geissinger, 1999).  A recent study from Italy reported finding similar tumors in dogs at the injection sites of vaccinations (Vascellari et al, 2003). These investigators stated that their “study identified distinct similarities between canine fibrosarcomas from presumed injection sites and feline post-vaccinal fibrosarcomas, suggesting the possibility of the development of post-injection sarcomas not only in cats, but also in dogs”. Other cancers such as leukemia have been vaccine-associated (Dodds, 1999, 2001, 2012).

Additionally, vaccination of pet and research dogs with polyvalent vaccines containing rabies virus or rabies vaccine alone was shown to induce production of antithyroglobulin autoantibodies, a provocative and important finding with implications for the subsequent development of hypothyroidism (Scott-Moncrieff et al, 2002). 

Post-vaccinal polyneuropathy is a recognized entity associated occasionally with the use mostly of canine distemper and rabies vaccines, and the ovine bluetongue virus vaccines, but any vaccine could presumably be implicated (Dodds, 1999, 2015b; Frana et al, 2008; Luján et al, 2013).   This can result in various clinical signs including muscular atrophy, inhibition or interruption of neuronal control of tissue and organ function, muscular excitation, incoordination and weakness, as well as seizures (Dodds, 1999, 2015b; Luján et al, 2013).

Certain breeds or families of dogs appear to be more susceptible to adverse vaccine reactions, particularly post-vaccinal seizures, high fevers, and painful episodes of hypertrophic osteodystrophy (HOD) (Dodds, 1997, 1999, 2001).   Therefore, we should advise companion animal breeders and caregivers of the potential for genetically susceptible littermates and relatives to be at increased risk for similar adverse vaccine reactions (Dodds, 1997, 1999, 2001).  In popular (or rare) inbred and line bred animals, the breed in general can be at increased risk, because of the genetic predisposition that promotes an adverse response to viral or other infectious agent challenge (Dodds, 1983, 1999).  The recently weaned young puppy or kitten being placed in a new environment may be at particular risk.  Furthermore, while the frequency of vaccinations is recommended to be spaced 2-4 weeks apart, some veterinarians advocate giving vaccines once a week in perceived or legitimate high exposure risk situations. This practice makes little sense scientifically or medically, and clearly can be harmful. 

In these special situations, appropriate alternatives to current canine vaccine practices include (Dodds, 1997, 1999; Twark & Dodds, 2000): measuring serum antibody titers; avoiding of unnecessary vaccines or over vaccinating; deferring vaccinations of sick or febrile individuals; tailoring specific minimal vaccination protocol for dogs of breeds or families known to be at increased risk for adverse reactions; starting the vaccination series later, such as at 9-10 weeks of age when the immune system is more able to handle antigenic challenge; alerting the caregiver to pay particular attention to the puppy’s behavior and overall health after the second or subsequent boosters; and avoiding revaccination of individuals already experiencing a significant adverse event. Littermates and close relatives of affected puppies should be closely monitored after receiving additional vaccines in a puppy series, as they too are at higher risk.

When an adequate immune memory has already been established, there is little reason to introduce unnecessary antigen, adjuvant, and preservatives by administering booster vaccines.  By measuring serum antibody titers triennially or more often, if needed, one can assess whether a given animal’s humoral immune response has fallen below levels of adequate immune memory. In that event, an appropriate vaccine booster can be administered (Dodds, 2001, 2013, 2015a; Lappin et al, 2002; McGaw et al, 1998; Moore & Glickman, 2004. Mouzin et al, 2004 a,b; Schultz, et al, 2002; Tizard, 1998; Twark & Dodds, 2000).

Killed (inactivated) virus vaccines containing adjuvants, like those for rabies virus or ovine bluetongue virus, can trigger immediate and delayed adverse vaccine reactions (Dodds, 1997, 1999, 2013, 2015a; Frana et al, 2008; Luján et al, 2013; Stejskal, 2013; Wilcox & Yager, 1986).   While there may be immediate hypersensitivity reactions, other acute events tend to occur 24-72 hours or up to a week afterwards, and as long as 45 days later in the case of more delayed reactions.   Documented reactions in the above citations include: behavioral aggression and separation anxiety, destruction and shredding of clothing and bedding; obsessive behavior, barking , fearfulness, self-mutilation, tail chewing;  pica, with eating wood, stones, earth, and feces; seizures and epilepsy; fibrosarcomas at the injection site; and autoimmune diseases such as those affecting bone marrow and blood cells, joints, eyes, skin, kidney, liver, bowel, and central nervous system; muscular weakness or atrophy; and chronic digestive problems.

Based upon experience in the United States, rabies vaccines are the most common group of biological products identified in adverse event reports received by the United States Department of Agriculture (USDA) Center for Veterinary Biologics (CVB) (Frana et al, 2008).  Currently, 14 rabies vaccines are labeled for use in dogs, but only one of them does not contain thimerosol (mercury) as a preservative (Dodds, 2015a).  These vaccines must meet the standard requirements established in the USDA Title 9, Code of Federal Regulations. This requires that the vaccine provide a protected fraction of  ≥ 88% when comparing vaccinated animals versus control animals (Frana et al, 2008).  All rabies vaccines are evaluated for safety prior to licensure, but these studies may not detect all safety concerns for a number of reasons: insufficient number of animals for low frequency events, insufficient duration of observation, sensitivities of subpopulations (e.g., breed, reproductive status, and unintended species), or interactions with concomitantly administered products.

Despite the serious under-reporting of vaccinal adverse reactions, the Report cited above (Frana et al, 2008), states that between April 1, 2004 and March 31, 2007, nearly 10,000 adverse event reports (all animal species) were received by manufacturers of rabies vaccines.  Approximately 65% of the manufacturer's reports involved dogs.

The Frana et al, 2008 Report further states that "Rabies vaccines are the most common group of biological products identified in adverse event reports received by the CVB."   During the 3-year period covered in this report, the CVB received 246 adverse event reports for dogs in which a rabies vaccine was identified as one of the products administered.

One of the most disturbing aspects of these findings is the failure to consider the potential impact of the presence of mercury as a preservative in all but one licensed canine rabies vaccine.  As discussed previously (Dodds, 2015a), mercury and other heavy metals (aluminum, nickel, chromium, silver and gold) can cause hypersensitivity or autoimmunity in people and animals such as autoimmune thyroiditis, multiple sclerosis, neurological disorders, kidney disease, systemic lupus erythematosus, rheumatoid arthritis, myocarditis, and unspecific symptoms such as chronic fatigue and myalgia.  (Cruz-Tapias et al, 2013; Luján et al, 2013; Stejskal, 2013).  Animal studies also have shown that these heavy metal-induced disorders occur in individuals with a susceptible genotype (Cruz-Tapias et al, 2013).

Other Issues with Over-Vaccination

Other issues arise from over vaccination, as the increased cost in time and dollars spent needs to be considered, despite the well-intentioned solicitation of clients to encourage annual booster vaccinations so that pets also can receive a wellness examination.  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 (Dodds, 1999, 2013; Hustead et al, 1999; Luján et al, 2013; Smith, 1995).   

Compliance or Resistance to Current Vaccine Guidelines

For almost two decades, the issues discussed above on over-vaccination and vaccine safety for companion and livestock animals have been raised by vaccinologists and veterinary clinicians. (Dodds, 1983, 1999; Luján et al, 2013; Smith, 1995; Schultz, 1998; Tizard, 1990).  But, how has this still controversial knowledge impacted the veterinary profession and animal owner today? Have veterinarians really embraced the national policies on vaccination guidelines?  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 media information regarding autism and measles vaccination, the public is more aware and worried about vaccine safety (Dodds, 2013).

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 (Dodds, 1999, 2013; Schultz, 1998; Tizard, 1990).

Veterinarians are still routinely vaccinating ill dogs and those with chronic diseases or prior adverse vaccine reactions (Dodds, 2013). 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 (Dodds, 1999, 2013, 2015b; Frana et al, 2008).

See www.rabieschallengefund.org

 

Treatment of Vaccinosis

The diagnosis of vaccinosis is an exclusionary one -- i.e. typically, nothing will be found upon other testing to explain the symptoms.  The animal is given the oral homeopathics, Thuja (for all vaccines other than rabies), and Lyssin to help detoxify the rabies molecular energy (“miasm”).  If there are no holistic veterinarians in the area, these homeopathics may be available from human alternative or homeopathic pharmacies.

Therapy typically uses steroids in tapering doses over 4-6 weeks to stop the inflammatory process and clinical symptoms.  Therapy  begins with an injection of dexamethasone phosphate first, and if the animal improves right away, is continued with prednisone  at 0.5 mg per pound twice daily for 5-7 days, then tapered gradually over the next month to every other day. The use of steroids will cause an increase in water intake and urination, but the animal should be able to handle the drug at these tapering doses for a few weeks.  If a holistic veterinarian wants to try an alternative therapy to steroids, with homeopathic remedies and nutraceuticals, this approach can also work.  They just try it for several days to see if it will work (Dodds, 1983, 1997, 2013).

These patients should not receive further vaccine boosters, except in the case of rabies vaccine, where exemption should be sought on a case-by-case basis but may not be granted in some specific locales.

Conclusion

Much still needs to be standardized and individualized, where appropriate, to ensure the safety and efficacy of veterinary vaccines (Dodds, 2013, 2015a; Wellborn et al, 2011). There remains controversy, failure to comply with current national vaccine policies and guidelines (Wellborn et al, 2011), resistance to change, and denial of adverse events within the general veterinary community as well as within society as a whole (Dodds, 2013, 2015a).

References

Cruz-Tapias P, Agmon-Levin N, Israeli E et al. 2013. Autoimmune (autoinflammatory) syndrome induced by adjuvants (ASIA) – animal models as a proof of concept. Curr Med Chem 20:4030-36.

Dodds WJ. 1983. Immune-mediated diseases of the blood. Adv Vet Sci Comp Med 27: 63-196.

Dodds WJ. 1997. Vaccine-related issues. In Complementary and Alternative Veterinary Medicine, eds. A M Schoen, SG Wynn, Ch. 40, pp.701-12, Mosby.

Dodds WJ. 1999. More bumps on the vaccine road. Adv Vet Med 41:715-32.

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

 Dodds WJ. 2012. Complementary and alternative veterinary medicine: the immune system. Clin Tech Sm An Pract 17(1):58-63.

Dodds WJ. 2013. Top 10 facts you aren’t told about vaccines, Parts 1 & 2. Proc AHVMA Annual Conf, Kansas City, MO; Aug 24-27, 2013.

Dodds WJ. 2015a. Guest Editor Overview, Autoimmunity. J Am Hol Vet Med Assoc 38:14-18, Winter issue.

Dodds WJ. 2015b.  Canine seizure disorders and the immune system. Case studies.  J Am Hol Vet Med Assoc 39: 29-31, Summer issue.

Frana TS, Clough NE, Gatewood DM, et al.  2008. Special Report.  Postmarketing surveillance of rabies vaccines for dogs to evaluate safety and efficacy. J Am Vet Med Assoc 232:1000-02.

Hogenesch H, Azcona-Olivera J, Scott-Moncreiff C, et al. 1999. Vaccine induced autoimmunity in the dog. Adv Vet Med 41:733-44.

Hustead  DR, Carpenter T, Sawyer DC, et al. 1999. Vaccination issues of concern to practitioners. J Am Vet Med Assoc  214: 1000-02.

Lappin MR, Andrews J, Simpson D, et al. 2002. Use of serologic tests to predict resistance to feline herpesvirus 1, feline calicivirus, and feline parvovirus infection in cats. J Am Vet Med Assoc 220: 38-42.

Luján L, Pérez M, Salazar E, et al. 2013. Autoimmune/autoinflammatory syndrome induced by adjuvants (ASIA syndrome) in commercial sheep. Immunol Res 56: 317-24.

McGaw DL, Thompson M, Tate D, et al. 1998. Serum distemper virus and parvovirus antibody titers among dogs brought to a veterinary hospital for revaccination. J Am Vet Med Assoc 213: 72-5.

Moore  GE, Glickman LT. 2004.  A perspective on vaccine guidelines and titer tests for dogs. J Am Vet Med Assoc 224: 200-03.

Moore GE, Guptill LF, Ward MP, et al. 2005. Adverse events diagnosed within three days of vaccine administration in dogs.  J Am Vet Med Assoc 227:1102–08.

Mouzin DE, Lorenzen MJ, Haworth JD, et al. 2004a. Duration of serologic response to five viral antigens in dogs. J Am Vet Med Assoc 224: 55-60.

Mouzin DE, Lorenzen M J, Haworth JD, et al. 2004b. Duration of serologic response to three viral antigens in cats. J Am Vet Med Assoc 224: 61-6.

Scott-Moncrieff JC, Azcona-Olivera J, Glickman NW, et al. 2002. Evaluation of antithyroglobulin antibodies after routine vaccination in pet and research dogs. J Am Vet Med Assoc 221:515-21.

Schultz RD.  1998. Current and future canine and feline vaccination programs.  Vet Med 93:233-54.

Schultz RD, Ford RB, Olsen J, et al.  2002. Titer testing and vaccination: a new look at traditional practices. Vet Med 97: 1-13, (insert).

Scott FW, Geissinger CM. 1999. Long-term immunity in cats vaccinated with an inactivated trivalent vaccine. Am J Vet Res 60: 652-58.

Sinha AA, Lopez MI, McDevitt HO. 1990. Autoimmune diseases: the failure of self-tolerance. Science 248:1380-87.

Smith CA.  1995. Are we vaccinating too much?  J Am Vet Med Assoc  207:421-25.

Stejskal V. 2013. Mercury-induced inflammation: yet another example of ASIA syndrome. Israel Med Assoc J 15:714-15.

Tizard I. 1990. Risks associated with use of live vaccines. J Am Vet Med Assoc 196:1851-58.

Tizard  I, Ni Y.  1998. Use of serologic testing to assess immune status of companion animals. J Am Vet Med Assoc 213: 54-60.

Twark L, Dodds WJ.  2000. Clinical application of serum parvovirus and distemper virus antibody titers for determining revaccination strategies in healthy dogs. J Am Vet Med Assoc 217:1021-24.

Vascellari M, Melchiotti E, Bozza MA, et al. 2003. Fibrosarcomas at presumed sites of injection in dogs: characteristics and comparison with non-vaccination site fibrosarcomas and feline post-vaccinal firosarcomas.  J Vet Med 50 (6): 286-91.

Wellborn LV (chair), et al. 2011. Report of the AAHA Canine Vaccine Task Force: 2011 AAHA Canine Vaccine Guidelines. J Am Anim Hosp Assoc 47(5):1-42.   www.aahanet.org

Wilcock BP, Yager JA. 1986.  Focal cutaneous vasculitis and alopecia at sites of rabies vaccination in dogs.  J Am Vet Med Assoc 188:1174–77. 

Vaccines - Titers

There is growing concern, and controversy, with regards to

"are we over-vaccinating our companion animals???"

 

The following is an excellent 2013 article published in TODAY'S  VETERINARY PRACTICE, May/June 2013

 http://www.todaysveterinarypractice.com/article.asp?articleid=T1305C02#article

 

Peer Reviewed ...VITAL VACCINATION SERIES ... 

ANTIBODY TITERS versus VACCINATION 

 

TION SERIES
Antibody 
TiTers
PEER REVIEwEd

by:  Richard B. Ford, DVM, MS, Diplomate 

 

Richard B. Ford, DVM, MS, 
Diplomate ACVIM & ACVPM 
(Hon), is Emeritus Professor 
of Medicine at North Carolina 
State University’s College of 
Veterinary Medicine. He is a 
retired Brigadier General from 
the USAF Reserve, where he 
was assigned to the Office 
of the Surgeon General at the Pentagon. Dr. Ford 
is also a past president of the NAVC Conference 
and continues his role as a member of the scientific 
program committee. His clinical interests are in the 
field of companion animal infectious disease; he is 
a prolific author and serves on both the AAHA Canine Vaccination Task Force and AAFP Feline Vaccination Advisory Panel. Dr. Ford received his DVM 
from Ohio State University and completed a small 
animal internal medicine residency at Michigan 
State University. He held a previous faculty position 
Richard B. Ford, DVM, MS, 
Diplomate ACVIM & ACVPM 
(Hon), is Emeritus Professor 
of Medicine at North Carolina 
State University’s College of 
Veterinary Medicine. He is a 
retired Brigadier General from 
the USAF Reserve, where he 
was assigned to the Office 
of the Surgeon General at the Pentagon. Dr. Ford 
is also a past president of the NAVC Conference 
and continues his role as a member of the scientific 
program committee. His clinical interests are in the 
field of companion animal infectious disease; he is 
a prolific author and serves on both the AAHA Canine Vaccination Task Force and AAFP Feline Vaccination Advisory Panel. Dr. Ford received his DVM 
from Ohio State University and completed a small 
animal internal medicine residency at Michigan 

Richard B. Ford, DVM, MS, Diplomate ACVIM & ACVPM (Hon), is Emeritus Professor of Medicine at North Carolina State University’s College of Veterinary Medicine.

 

He is a retired Brigadier General from the USAF Reserve, where he was assigned to the Office of the Surgeon General at the Pentagon. Dr. Ford is also a past president of the NAVC Conference and continues his role as a member of the scientific program committee. His clinical interests are in the field of companion animal infectious disease; he is a prolific author and serves on both the AAHA Canine Vaccination Task Force and AAFP Feline Vaccination Advisory Panel. Dr. Ford received his DVM from Ohio State University and completed a small animal internal medicine residency at Michigan State University. He held a previous faculty position at Purdue Universityare in the field of companion animal infectious disease; he is a prolific author and serves on both the AAHA Canine Vaccination Task Force and AAFP Feline Vaccination Advisory Panel. Dr. Ford received his DVM from Ohio State University and completed a small animal internal medicine residency at Michigan State University. He held a previous faculty position at Purdue University. 

 

for more information with regards to vaccines research, please check out this link:

http://www.petwelfarealliance.org/vaccine-research.html 

 

  • What are the indications for performing titers?
  • When interpreting antibody titers, what test limitations apply?
  • How should test results be interpreted when making vaccination decisions for individual patients?

CORRELATION OF TITERS & IMMUNITY
Antibody titers measured in laboratories and by in-clinic and antibody test kits typically record results as positive or negative, and include a brief description of the result's significance. However, questions remain:

  • How well does a positive antibody titer (or test kit result) correlate with protective immunity in a patient? 
  • How well does a negative titer (or test kit result) correlate with susceptibility in a patient? 

When interpreting antibody titers, a few facts must be clear:

  1. The only true test of protective immunity involves exposure (challenge) to a virulent pathogen in which nonvaccinates (controls) are infected and manifest clinical illness while vaccinated animals remain healthy. Animal vaccines are licensed based on this premise.
  2. Interpreting antibody test results depends on understanding what results do and do not represent. In the clinical setting, antibody levels offer diverse and distinct clinical applications (see It's All About PIE, below). 
  3. Different classes of antibody, also called immunoglobulin (Ig), have specialized functions (identified and categorized as IgA, IgG, IgE, or IgM). In veterinary medicine, the antibody titers used to assess protective immunity typically represent the IgG class. 
  4. When using an in-clinic test kit to measure (qualitative or semiquantitative) antibody levels, results are reported as either positive (indicates protection) or negative (indicates susceptibility) and must be correlated with gold standard laboratory tests, such as virus neutralization (VN) or hemagglutination inhibition (HI), in order to accurately represent a defined threshold of antibody. Both in-clinic tests have been correlated through VN, HI, or challenge testing results. While the correlation studies were conducted independently through universities, the data is available through the respective companies that manufacture the in-clinic test kits.
  • What are the indications for performing titers?
  • When interpreting antibody titers, what test limitations apply?
  • How should test results be interpreted when making vaccination decisions for individual patients?

CORRELATION OF TITERS & IMMUNITY
Antibody titers measured in laboratories and by in-clinic and antibody test kits typically record results as positive or negative, and include a brief description of the result's significance. However, questions remain:

  • How well does a positive antibody titer (or test kit result) correlate with protective immunity in a patient? 
  • How well does a negative titer (or test kit result) correlate with susceptibility in a patient? 

When interpreting antibody titers, a few facts must be clear:

  1. The only true test of protective immunity involves exposure (challenge) to a virulent pathogen in which nonvaccinates (controls) are infected and manifest clinical illness while vaccinated animals remain healthy. Animal vaccines are licensed based on this premise.
  2. Interpreting antibody test results depends on understanding what results do and do not represent. In the clinical setting, antibody levels offer diverse and distinct clinical applications (see It's All About PIE, below). 
  3. Different classes of antibody, also called immunoglobulin (Ig), have specialized functions (identified and categorized as IgA, IgG, IgE, or IgM). In veterinary medicine, the antibody titers used to assess protective immunity typically represent the IgG class. 
  4. When using an in-clinic test kit to measure (qualitative or semiquantitative) antibody levels, results are reported as either positive (indicates protection) or negative (indicates susceptibility) and must be correlated with gold standard laboratory tests, such as virus neutralization (VN) or hemagglutination inhibition (HI), in order to accurately represent a defined threshold of antibody. Both in-clinic tests have been correlated through VN, HI, or challenge testing results. While the correlation studies were conducted independently through universities, the data is available through the respective companies that manufacture the in-clinic test kits.
  • What are the indications for performing titers?
  • When interpreting antibody titers, what test limitations apply?
  • How should test results be interpreted when making vaccination decisions for individual patients?

CORRELATION OF TITERS & IMMUNITY
Antibody titers measured in laboratories and by in-clinic and antibody test kits typically record results as positive or negative, and include a brief description of the result's significance. However, questions remain:

  • How well does a positive antibody titer (or test kit result) correlate with protective immunity in a patient? 
  • How well does a negative titer (or test kit result) correlate with susceptibility in a patient? 

When interpreting antibody titers, a few facts must be clear:

  1. The only true test of protective immunity involves exposure (challenge) to a virulent pathogen in which nonvaccinates (controls) are infected and manifest clinical illness while vaccinated animals remain healthy. Animal vaccines are licensed based on this premise.
  2. Interpreting antibody test results depends on understanding what results do and do not represent. In the clinical setting, antibody levels offer diverse and distinct clinical applications (see It's All About PIE, below). 
  3. Different classes of antibody, also called immunoglobulin (Ig), have specialized functions (identified and categorized as IgA, IgG, IgE, or IgM). In veterinary medicine, the antibody titers used to assess protective immunity typically represent the IgG class. 
  4. When using an in-clinic test kit to measure (qualitative or semiquantitative) antibody levels, results are reported as either positive (indicates protection) or negative (indicates susceptibility) and must be correlated with gold standard laboratory tests, such as virus neutralization (VN) or hemagglutination inhibition (HI), in order to accurately represent a defined threshold of antibody. Both in-clinic tests have been correlated through VN, HI, or challenge testing results. While the correlation studies were conducted independently through universities, the data is available through the respective companies that manufacture the in-clinic test kits.
  • What are the indications for performing titers?
  • When interpreting antibody titers, what test limitations apply?
  • How should test results be interpreted when making vaccination decisions for individual patients?

CORRELATION OF TITERS & IMMUNITY
Antibody titers measured in laboratories and by in-clinic and antibody test kits typically record results as positive or negative, and include a brief description of the result's significance. However, questions remain:

  • How well does a positive antibody titer (or test kit result) correlate with protective immunity in a patient? 
  • How well does a negative titer (or test kit result) correlate with susceptibility in a patient? 

When interpreting antibody titers, a few facts must be clear:

  1. The only true test of protective immunity involves exposure (challenge) to a virulent pathogen in which nonvaccinates (controls) are infected and manifest clinical illness while vaccinated animals remain healthy. Animal vaccines are licensed based on this premise.
  2. Interpreting antibody test results depends on understanding what results do and do not represent. In the clinical setting, antibody levels offer diverse and distinct clinical applications (see It's All About PIE, below). 
  3. Different classes of antibody, also called immunoglobulin (Ig), have specialized functions (identified and categorized as IgA, IgG, IgE, or IgM). In veterinary medicine, the antibody titers used to assess protective immunity typically represent the IgG class. 
  4. When using an in-clinic test kit to measure (qualitative or semiquantitative) antibody levels, results are reported as either positive (indicates protection) or negative (indicates susceptibility) and must be correlated with gold standard laboratory tests, such as virus neutralization (VN) or hemagglutination inhibition (HI), in order to accurately represent a defined threshold of antibody. Both in-clinic tests have been correlated through VN, HI, or challenge testing results. While the correlation studies were conducted independently through universities, the data is available through the respective companies that manufacture the in-clinic test kits.
  • What are the indications for performing titers?
  • When interpreting antibody titers, what test limitations apply?
  • How should test results be interpreted when making vaccination decisions for individual patients?

CORRELATION OF TITERS & IMMUNITY
Antibody titers measured in laboratories and by in-clinic and antibody test kits typically record results as positive or negative, and include a brief description of the result's significance. However, questions remain:

  • How well does a positive antibody titer (or test kit result) correlate with protective immunity in a patient? 
  • How well does a negative titer (or test kit result) correlate with susceptibility in a patient? 

When interpreting antibody titers, a few facts must be clear:

  1. The only true test of protective immunity involves exposure (challenge) to a virulent pathogen in which nonvaccinates (controls) are infected and manifest clinical illness while vaccinated animals remain healthy. Animal vaccines are licensed based on this premise.
  2. Interpreting antibody test results depends on understanding what results do and do not represent. In the clinical setting, antibody levels offer diverse and distinct clinical applications (see It's All About PIE, below). 
  3. Different classes of antibody, also called immunoglobulin (Ig), have specialized functions (identified and categorized as IgA, IgG, IgE, or IgM). In veterinary medicine, the antibody titers used to assess protective immunity typically represent the IgG class. 
  4. When using an in-clinic test kit to measure (qualitative or semiquantitative) antibody levels, results are reported as either positive (indicates protection) or negative (indicates susceptibility) and must be correlated with gold standard laboratory tests, such as virus neutralization (VN) or hemagglutination inhibition (HI), in order to accurately represent a defined threshold of antibody. Both in-clinic tests have been correlated through VN, HI, or challenge testing results. While the correlation studies were conducted independently through universities, the data is available through the respective companies that manufacture the in-clinic test kits.
  • What are the indications for performing titers?
  • When interpreting antibody titers, what test limitations apply?
  • How should test results be interpreted when making vaccination decisions for individual patients?

CORRELATION OF TITERS & IMMUNITY
Antibody titers measured in laboratories and by in-clinic and antibody test kits typically record results as positive or negative, and include a brief description of the result's significance. However, questions remain:

  • How well does a positive antibody titer (or test kit result) correlate with protective immunity in a patient? 
  • How well does a negative titer (or test kit result) correlate with susceptibility in a patient? 
  • What are the indications for performing titers?
  • When interpreting antibody titers, what test limitations apply?
  • How should test results be interpreted when making vaccination decisions for individual patients?

CORRELATION OF TITERS & IMMUNITY
Antibody titers measured in laboratories and by in-clinic and antibody test kits typically record results as positive or negative, and include a brief description of the result's significance. However, questions remain:

  • How well does a positive antibody titer (or test kit result) correlate with protective immunity in a patient? 
  • How well does a negative titer (or test kit result) correlate with susceptibility in a patient? 

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