kennel cough (Bordetella) vaccination not needed

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Are pesticides and kennel cough vaccinations really needed?

kennel cough (Bordetella) vaccination not needed

Postby guest » Tue Sep 09, 2003 2:46 pm

Reviewer Lynelle Johnson, DVM, PhD, DACVIM
Publication Citation


Title: Prevalence of Bordetella bronchiseptica in cats attended by a veterinary practice in the Manawatu region
Author: Molyneux JM, Guilford WG, Hunter JEB, Gwozdz M, Fenwick SG, Jones BR
Journal: New Zealand Vet J
Volume: 48
Number:
Pages: 82-84
Date: 2000


Purpose of Study


Background
Bordetella has recently been recognized as a primary respiratory tract pathogen in cats, and several studies have suggested a high level of exposure to the organism as indicated by serum titers. High seroprevalence has been reported in the presence and absence of upper respiratory tract disease. Fatal infection has occurred in young kittens.

Hypothesis
The importance of Bordetella bronchiseptica in cats with upper respiratory disease can be determined by comparing isolation rates in cats with and without upper respiratory disease.

Findings of Study


Study Design
This was a prospective study examining healthy cats and cats with upper respiratory disease at Massey University in New Zealand. Cats housed singly (n =3 4) and cats from multiple-cat dwellings or cat colonies (n = 66) were included in the study. Samples for Bordetella culture were obtained from the nostril and oropharynx from each cat and placed in Amies transport media. Swabs were cultured on blood agar plates, MacConkey’s agar, and Bordetella-selective agar for 48 hours.

Study Results
Cats ranged in age from less than 12 months to > 12 years. Overall, Bordetella was isolated from seven of 100 cats, five from the oropharynx and two from the nasal cavity. Two of these seven cats had signs of upper respiratory tract disease. Of cats in single-cat households, two of 34 had signs of respiratory disease but neither had Bordetella isolated. One cat without respiratory disease had Bordetella isolated from the oropharynx.

Of cats (n = 26) in multi-cat households, four had signs of upper respiratory tract disease but none had Bordetella isolated. In cats (n = 40) from cat colonies, half had signs of upper respiratory tract disease and Bordetella was isolated from the nasal cavity in one cat and oropharynx in one cat. In cats without upper respiratory disease, Bordetella was isolated from the nasal cavity in one cat and from the oropharynx in three cats.

Commentary


Design Evaluation
This prospective study included appropriate populations to compare isolation rates for Bordetella among cats from typical households (single or multiple cat) and cats from a cattery. Both healthy cats and diseased cats were examined.

Results Evaluation
Most of the cats with respiratory disease were in a cattery, and yet Bordetella was isolated infrequently. The study results suggest that Bordetella is infrequently a cause of upper respiratory tract disease even in situations in which multiple cats are potentially exposed to infectious organisms.

The isolation rate for Bordetella was higher in multi-cat households (9%) than in single-cat households (3%), and this is in agreement with other studies. Bordetella was isolated from the oropharynx in five cats and the nasal cavity in two cats, although this did not seem to correlate with disease state.

Clinical Application
Bordetella was isolated infrequently in this region, even in situations in which infectious diseases are expected to have high prevalence. In this study, Bordetella was isolated only from adult cats; kittens were not at increased risk for Bordetella isolation.

Questions Raised
It would be interesting to obtain larger numbers of diseased cats from household environments to provide a better estimate of the prevalence of Bordetella in the natural population. Other causes for upper respiratory infection were not investigated or excluded in this study. The role of viral potentiation of Bordetella infection has not been investigated, but that question is beyond the scope of this study.

Summary
Bordetella was infrequently associated with upper respiratory tract disease in this population of cats from New Zealand.

ISI Abstract


Authors
Guilford, WG ; Hunter, JEB; Gwozdz, M; Fenwick, SG; Jones, BR

Article Title
Prevalence of Bordetella bronchiseptica in cats attended by a veterinary practice in the Manawatu region.

Abstract
Aims: To determine the prevalence by isolation of Bordetella bronchiseptica infection in healthy cats and in cats showing signs of upper respiratory tract (URT) disease attended by a veterinary practice in the Manawatu region. Methods: The nasal cavity and oropharynx of 100 cats of mixed sex and age were swabbed and the swabs cultured fur B. bronchiseptica. The population of cats surveyed was that attended by the Massey University Veterinary Teaching Hospital, and included healthy cats, cats with clinical signs of URT disease, cats with a recent history of URT disease, cats from single cat households, cats from multiple-cat households, and cats from a colony. Results: Bordetella bronchiseptica was recovered from 7 cats (5 from pharyngeal samples and 2 from nasal samples). Five of the 7 cats appeared to be healthy at the time of sampling, whilst 2 showed clinical signs of URT disease. Six of the 7 culture-positive cats were from a cat colony. The prevalence of B. bronchiseptica in healthy cats sampled was 7% and in cats with URT disease was 8%. Conclusion: This study confirms that B. bronchiseptica infection is present, but the prevalence of infection is low, in both healthy cats and in cats with URT disease attended by the Massey University Veterinary Teaching Hospital. It is unlikely that B. bronchiseptica infection is a frequent cause of feline URT disease of cats in this region.
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Hypothyroidism and kennel cough vaccine

Postby guest » Mon Mar 08, 2004 4:07 pm

Relationships Between Infections And Vaccinations And The Development Of Immune Mediated Thyroid Dysfunction
ACVIM 2002
Dr Peter A Graham, BVMS, PhD, CertVR, MRCVS
East Lansing, MI

Introduction

Hypothyroidism continues to be the most common endocrine disorder of the dog and remains a priority disease among dog breeders and exhibitors.

Hypothyroidism is manifested systemically by its association with an overall decreased metabolic rate. Clinical signs reflect lower metabolic rate and decreased tissue turnover and include obesity, predisposition to infection, alopecia or delayed hair growth cycle, skin changes, anemia, altered lipid metabolism, and possibly reduced reproductive efficiency.

In the dog, at least 95% of hypothyroidism is primary in nature, that is, the functional failure is located in the thyroid glands (not pituitary or hypothalamus). This primary hypothyroidism has been associated with two forms of disease processes; 1) lymphocytic thyroiditis (chronic atrophic autoimmune thyroiditis, autoimmune thyroid disease (AITD)) and 2) idiopathic (non-inflammatory) thyroid follicular atrophy. Some evidence even links these, and suggests that idiopathic non-inflammatory atrophic thyroid disease may be a late consequence of lymphocytic thyroiditis in some cases. Lymphocytic thyroiditis can progress through stages identifiable by laboratory tests, including subclinical thyroiditis, subclinical or partial hypothyroidism, hypothyroidism with circulating thyroid antibodies, and possibly hypothyroidism with no circulating thyroid antibodies 1.

Lymphocytic thyroiditis is characterized by focal and/or diffuse lymphoplasmacytic infiltration with macrophages. During this process, antibodies directed against thyroid antigens are released into the circulation. The most notable of these is thyroglobulin autoantibody (TgAA), and in humans, thyroperoxidase (TPO) antibody.

The recent availability of a commercial canine thyroglobulin antibody (TgAA) assay now allows us to use serologic evidence of thyroiditis to perform studies on its prevalence, epidemiology and progression 1.

In addition to the progressive forms of AITD, there are transient/subacute forms of thyroiditis in humans associated with clinical signs including lethargy, malaise, and painful neck. Whether these forms of thyroid disease exist in the dog is difficult for us to determine because of the expected subtle and non-specific nature of their clinical presentation 2.

Our studies at Michigan State University 1,3using thyroglobulin antibody as a marker for canine AITD have demonstrated:

Strong breed dispositions

A high prevalence in "healthy" populations

Slow, or in some cases no, progression from subclinical pathology to loss of functional reserve and thyroid failure

Possible transient forms-in some animals TgAA wanes with no negative thyroid functional sequelae

The slow progression rate of this disease hampers investigations into cause and effect relationships. Temporal associations with individual causal events are almost impossible when clinical disease may not occur for several years.

Associations Between AITD and Infections

To date, most available information associating AITD with infection is based on findings in experimental animals and in human clinical studies.

Human Subacute Thyroiditis (DeQuervain's Thyroiditis)

Subacute thyroiditis is a disease entity in humans which is usually transient with no long-term functional implications and is believed to associated with an acute viral infection. Evidence for the viral origin of this condition includes: a typical viral prodrome and self-limited course, clustered association with viral outbreaks, and association with viral seasonality. Infections associated with subacute thyroiditis include: measles virus, influenza, adenovirus, Epstein-Bar, mumps, human foamy retrovirus. Additionally, there are often increased viral antibodies during subacute thyroiditis, even when there is no clinical evidence of viral disease. Despite the majority of cases resolving with no long-term thyroid effects, there is evidence to suggest that in some cases, such an episode of subacute thyroiditis could result in the initiation of a chronic autoimmune thyroid disease 4. Circulating thyroglobulin antibody and TPO antibodies are found in 40 to 60% of cases which usually fade

Our recent data suggests that transient serum TgAA occurs in dogs, however, the existence of canine DeQuervain's has not yet been confirmed. The nature of its likely clinical presentation may however make it difficult to identify.

Congenital Rubella Infection

Congenital rubella infection in humans is one disease for which there is good evidence of a link with increased risk of adult onset AITD 5. 20 to 30% of adolescents with a history of congenital rubella have antibodies to thyroid antigens (TGAA/TPO) compared with only 12% of controls. In these cases, there is no active Rubella at time of AITD diagnosis.

Experimental Animals

Several observations in experimental animals have also suggested a significant link between infection and the development of AITD. For example, AITD can be induced in mice by infection with Reovirus 1.

The classical chicken obese strain (OS) model of thyroiditis has been shown to have an endogenous retrovirus (ev22) inherited as autosomal dominant.

In rats, "sterilization" of intestinal flora leads to decreased risk of AITD and reinstitution of flora returns risk. The presence of gut flora is required to develop AITD in thymectomized and irradiated rats. Again in rats, immunization with purified Yersinia enterocolitica outer membrane protein can induce lymphocytic thyroiditis 6.

Chronic Autoimmune Thyroiditis (human)

In naturally occurring human thyroiditis, there have been studies demonstrating serologic evidence for recent bacterial or viral infection in Hashimoto's thyroiditis 7 and antibodies to non-HIV retrovirus have also been found 8. Other evidence linking infections and thyroiditis includes lymphocytic thyroiditis following group A Streptococcal vaccination 9 and binding of Yersinia-release-protein-antibodies to thyroid antigens in Western blots.

Canine Autoimmune Thyroid Disease

No studies have yet examined the possible association between infection and occurrence of canine AITD.

Association Between Vaccination and AITD

Concerns about "over-vaccination" and possible association between vaccination and AITD have been raised by some veterinarians 10,11. In addition, one controlled study identified a temporal relationship between recent vaccination and immune-mediated-hemolytic anemia (IMHA), another autoimmune condition 12. With the exception of the IMHA study, other reports have been anecdotal or limited to case studies.

A 22-week controlled study of vaccinated puppies did demonstrate antibodies associated with autoimmune diseases, including anti-fibronectin and anti-laminin, but not against the tested thyroid antigen, thyroglobulin 13.

The slowly progressive nature of AITD in dogs and the only recent availability of tests to identify early subclinical disease, makes it very difficult to perform cause and effect studies. The epidemiologic study requirement for control populations is also difficult to meet.

Recent work at Michigan State University has attempted to address questions concerning the impact of vaccination on the occurrence and progression of canine AITD using questionnaire-based surveys in combination with laboratory tests of thyroid disease and dysfunction. In one study, we compared over 200 dogs with normal thyroid function, but serum TgAA (consistent with subclinical thyroiditis) with a similar number of TgAA negative euthyroid animals. Crude associations were found between the presence of serum TgAA and owner-reported exposure to parvo- and coronavirus vaccinations. Within the rabies vaccination responses, there was an association with 3 yearly vaccinations. These crude associations do not necessarily provide support for cause/effect relationships and confounding factors still have to be investigated. However, these findings do open the door for future work. Breed and age are likely to continue to be major predisposing factors for this disease. Vaccination and other environmental factors are likely to be minor but important contributing factors in its development.

We have also investigated the possible impact of vaccination on progression to thyroid dysfunction in animals that were already TgAA positive. While there was no association with the overall reported frequency of vaccination, there was an association with exposure to Bordetella vaccine. A follow-up questionnaire revealed that the dogs in this study were almost exclusively vaccinated by the intra-nasal route.

Future investigative directions should include experimental vaccine studies and larger, more detailed controlled questionnaire studies.

Mechanisms of Autoimmune Disease

A variety of mechanisms could be responsible for an association between infection or vaccination and the later development of autoimmune diseases. These include: i) virus induced changes in self antigen expression; ii) molecular mimicry; iii) super antigens; iv) anti-idiotype antibodies; v) immune complexes; vi) heat shock proteins and vii) MHC induction of non-immune cells.

Financial support provided by Companion Animal Fund and Animal Health Diagnostic Laboratory of the College of Veterinary Medicine, Michigan State University.

REFERENCES

1. Graham, P.A., Lymphocytic thyroiditis. Veterinary Clinics of North America, 2001. 31(5): p. 915-933.

2. Emerson, C.H. and A.P. Farwell, Sporadic silent thyroiditis, post-partum thyroiditis, and subacute thyroiditis, in Werner and Ingbar's The Thyroid. A fundamental and clinical text, L.E. Braverman and R.D. Utiger, Editors. 2000, Lippincott, Williams and Wilkins: Philadelphia.

3. Graham, P.A., et al., A 12-month prospective study of 234 thyroglobulin antibody positive dogs which had no laboratory evidence of thyroid dysfunction. Journal of Veterinary Internal Medicine, 2001. 15.

4. Volpe, R., Subacute (deQuervain's) thyroiditis. Clinics in Endocrinology and Metabolism, 1979. 8(1): p. 81-95.

5. Tomer, Y. and T.F. Davies, Infection, thyroid disease, and autoimmunity. Endocrine Reviews, 1993. 14: p. 107-120.

6. Penhale, W.J. and P.R. Young, The influence of microbial environment on susceptibility to experimental autoimmune thyroiditis. Clinical and Experimental Immunology, 1988. 72: p. 288-292.

7. Valtonen, V.V., et al., Serological evidence for the role of bacterial infections in the pathogenesis of thyroid diseases. Acta Medica Scandinavica, 1986. 219: p. 105-111.

8. Josephson, S.L., N.S. Swack, and M.T. Ramirez, Investigation of atypical Western blot reactivity involving core proteins of human immunodeficiency virus type 1. Journal of Clinical Microbiology, 1989. 27: p. 932-937.

9. Toonoka, N., et al., Lymphoid thyroiditis following immunization with group A streptococcal vaccine. American Journal of Pathology, 1978. 92: p. 681-687.

10. Smith, C.A., Are we vaccinating too much? Journal of the American Veterinary Medical Association, 1995. 207(4): p. 421-425.

11. Dodds, W.J., More bumps on the vaccine road. Advances in Veterinary Medicine, 1999. 41: p. 715-732.

12. Duval, D. and U. Giger, Vaccine-associated immune-mediated hemolytic anemia in the dog. Journal of Veterinary Internal Medicine, 1996. 10(5): p. 290-295.

13. HogenEsch, H., et al., Vaccine-induced autoimmunity in the dog. Advances in Veterinary Medicine, 1999. 41: p. 733-747.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)
Peter A. Graham, BVMS, PhD, CertVR, MRCVS
Michigan State University
AHDL, PO Box 30076
Lansing, MI 48909
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kennel cough clinical disease in spite of vaccination

Postby guest » Sat Sep 04, 2004 11:08 am

Like other bacteria, there are different strains of the same organism that are somewhat antigenically different. The relevant antigens on Bordetella are the fimbrial antigens that affect adhesion to the mucosa. What vaccines (both IN and parenteral) are designed in part to do is to develop antibodies against these fimbrial antigens to prevent the bacteria from adhering, colonizing the mucosa and causing disease. Researchers at K. State presented data at ACVIM in 2000 demonstrating that the fimbrial antigens on bacteria isolated from clinical cases are significantly different from those on the strain used in the vaccine. This is not surprising since bacteria in the "wild" are mutating all the time and the vaccine strains were put on "hold" years ago and have continued to be used today. This drift away from the antigenic types in the vaccines has allowed the bacteria to "escape" and cause clinical disease in spite of vaccination.
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Postby Guest » Thu May 12, 2005 12:28 pm

very interesting...ImageImageImageImageImageImageImageImageImageImageImageImageImageImageImageImageImageImageImageImageImageImageImageImageImage
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mysterious kennel cough

Postby guest » Mon Jul 11, 2005 8:27 am

UNEXPLAINED DEATHS, CANINES - USA (MULTISTATE)
**********************************************
A ProMED-mail post
<http://www.promedmail.org>
ProMED-mail is a program of the
International Society for Infectious Diseases
<http://www.isid.org>

[1]
Date: 14 May 2005
From: A-Lan Banks <A-Lan.Banks@thomson.com>
Source: Newsweek, MSNBC News, 13 May 2005 [edited]
<http://msnbc.msn.com/id/7832310/>

A mysterious respiratory disease is sweeping greyhound tracks across the country, killing dozens of dogs and forcing owners to halt racing as researchers hunt for a vaccine to control the outbreak.

Dr Lisa Zerbel, a veterinarian in Massachusetts who is treating some of the sick dogs, said she thinks the illnesses are caused by a new strain of the influenza virus that is more virulent than the common one known as "kennel cough". But other experts say it is too soon to pinpoint the cause.

Wonderland Greyhound Park, in this blue-collar city north of Boston, has been the hardest hit. Since May 4, 16 of its dogs have died from the influenza-like illness, and the track has suspended racing indefinitely and quarantined its 1200 greyhounds.

Racetracks in Colorado, Iowa, and Rhode Island have also reported greyhound deaths over the past month, while other states are seeing a rash of nonfatal cases, according to Massachusetts officials. "The reason this is happening is because greyhounds travel from track to track, and they may be incubating the illness without someone knowing," Zerbel said. Necropsies on 2 of the greyhounds at Wonderland found the dogs died of pneumonia, a
complication that can be caused by infection by either bacteria or a virus.

"The most frustrating thing about it so far is it tends to be very silent early on," Zerbel said. "It's not until the late stages that they start to show signs indicating that they need treatment." By then, she said, a sick greyhound may be racing at a track in nother state.

Gary Guccione, secretary and treasurer of the National Greyhound
Association in Abilene, Kansas, said similar outbreaks have plagued
racetracks for the past 3 years. "A major outbreak like this used to happen once every 6 or 7 years," he said. "Now it seems to be coming on with more frequency and with greater strength. We're in desperate need of a good vaccine." There is already a vaccine for kennel cough, but the Massachusetts State Racing Commission does not require it, and it is unlikely it would be effective in this case, said Dr Alexandra Lightbown, the commission's chief veterinarian. In the meantime, all greyhounds at Wonderland are being treated with antibiotics as a preventive measure.

Virginia Tech's Dr Brad Fenwick, a specialist in greyhound medicine, is leading the search for a new vaccine. He hopes to conduct experiments on a vaccine this summer. Track owners around the country are funding his research.

He said he doubts the deaths at Wonderland and other tracks are from a new strain of influenza. But he said it is not clear yet whether the infections are caused by bacteria or by a virus. Bacterial pneumonia can result from a variety of illnesses, and in greyhounds it can progress from mild to life-threatening in a matter of hours.

At Dairyland Greyhound Park in Kenosha, Wisconsin, roughly 1/4 of the track's greyhounds have become ill in recent weeks, though none has died, said Scott Larrivee, a spokesman for state regulators. Dairyland suspended racing this week.

Several greyhounds have died at Bluffs Run racetrack in Council Bluffs, Iowa, according to Sally Prickett, a state veterinarian. She is awaiting lab results.

She said kennel cough usually hits younger dogs because their immune systems are weaker. But this disease is striking older dogs, and appears more serious, she said.

******
[2]
Date: 14 May 2005
From: ProMED-mail<promed@promedmail.org>
Source: Tucson Citizen and The Arizona Republic, 13 May 2005 [edited]
<http://www.tucsoncitizen.com/inde>

Ailing dogs cancel races; Tucson Greyhound anticipates resuming business on Tuesday.
--------------------------------------------------
Tucson Greyhound Park expects racing to return to normal next week after a disruption caused by a mysterious respiratory disease that has swept across the country. David Romo, director of racing, said the track is in the 2nd week of cancellations and said the disease has afflicted about 380 dogs -- about 80 per cent of its total. He said the track plans to resume racing on Tuesday but he couldn't say whether it would be able to stage a complete card.

"The dogs have been getting better; it just has to run its course," Romo told The Arizona Republic. "It's been horrible." The ailing dogs have also slowed business at Tucson Greyhound Park. "It hurts everyone involved," said general manager Marshall Kueker. The food and beverage people are not working. The mutual people are not working and kennel operators are not generating any revenue."

The disease has caused cancellations throughout the country and killed dozens of dogs as researchers hunt for a vaccine to control the outbreak. No Tucson greyhounds have died.

Dennis Young, assistant general manager at Phoenix Greyhound Park, said 4 days of racing had to be canceled in April. When racing resumed, only 12 races were run during mid-week programs, as opposed to the usual 15, because of the number of sick dogs.

On 18 Jan 2005, Tucson Greyhound Park quarantined all of its dogs because of an outbreak of kennel cough. But racing was not disrupted.

******
[3]
Date: 14 May 2005
From: ProMED-mail<promed@promedmail.org>
Source: Boston Herald [edited]
<http://news.bostonherald.com/localRegional/view.bg?articleid=82973&format=>

Race flu may kill your pet: CDC probes possible link to humans
--------------------------------------------------------------
The devastating and shadowy malady that is claiming the lives of greyhounds at Revere's Wonderland racetrack may have even deadlier ambitions: lovable Fido and perhaps even his master. The federal government's top scientists are exploring whether a deadly dog flu that has ripped through greyhound tracks across the country -- and is suspected in Massachusetts -- could leap to humans. The strain of canine influenza has already popped up in other dogs in animal shelters around the country. "Obviously, there is nothing to stop it from going from greyhounds to terriers or shepherds," said Ruben Donis, chief of the molecular genetics section of the influenza
branch of the federal Centers for Disease Control in Atlanta. "Humans, we can't say anything at this point," Donis said.

There is little the typical dog-owning family can do to protect its pet, experts said. Instead, the onus is on greyhound handlers to follow strict hygiene protocols so the virus that has devastated racers doesn't jump to the general dog population.

Revere's Wonderland dog track has been struck by the deadly contagion. 2 more greyhounds died there Wednesday, bringing the death toll to 18 in roughly a week. In Rhode Island, 13 dogs have died at Lincoln Park.

Meanwhile, veterinarians treating sick and dying greyhounds at Wonderland's gated, barracks-like kennel compound yesterday enforced a strict quarantine -- one aimed at not only dogs, but humans as well.

Dr Lisa Zerbel, a veterinarian at North Shore Animal Hospital who is treating Wonderland's 1200 greyhounds, rejected a request from a Herald reporter to enter the compound, located in an industrial section of Lynn. Zerbel said even casual human contact with the infected dogs could spread the killer illness beyond the hot zone. "Just down the street, we have a pet store, many animal hospitals," Zerbel said. "We want to assume it could be easily spread."

As vets battle the epidemic, state officials are now scrambling to nail down exactly what is killing the dogs -- and to prove whether it is linked to the flu-like killer that has affected an estimated 10 000 dogs nationwide. These include a few hundred domestic dogs as well.

And the federal CDC may help in that research, with plans to request a tissue sample from some of the dead Massachusetts dogs, Donis said. This summer, the CDC also plans to begin testing the blood of track workers in other states -- the 1st step in determining whether the canine flu may have already leaped to humans.

A sliver of good news: The mystery dog flu appears not to be the kind of killer that some scientists have seen in the so-called "avian influenza" -- a canine malady that has infected and killed people in Asia. Donis said the illness sweeping through greyhound populations appears to be milder. That said, flu, right after it jumps to a new species, can prove unpredictably
virulent. The 1918 influenza epidemic eventually lost its killer status, but not before millions died in the few years after its outbreak, Donis said.

[byline: Scott Van Voorhis]

ProMED-mail
<promed@promedmail.org>

[see also:
2004
---
Undiagnosed illness, canine - USA (FL)(02) 20040730.2081
Undiagnosed illness, canine - USA (FL) 20040701.1753]
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