In general, our knowledge of tickbornediseases in cats is substantially less thanour knowledge of the comparable diseasein dogs or human patients. One exceptionto this generality is cytauxzoonosis, aprotozoal disease of cats caused byCytauxzoon felis. The organism issupposedly transmitted from bobcats,the primary reservoir host, to domesticcats via a tick vector (the ixodid tickDermacentor variabilis). Because of therapidly fatal nature of C. felis–inducedillness, the domestic cat has usually beenconsidered an accidental dead-end hostfor this infectious agent. Typical clinicalmanifestations include depression,lethargy, anorexia, fever, and jaundice.Cats often die less than a week from theinitial onset of clinical signs. Some cats,however, survive C. felis infections andafter recovery may remain asymptomaticcarriers for months to years. Initiallyreported in Missouri and surrounding

IN THIS ISSUE:Tickborne Diseases of Cats ........ 1Tickborne Diseases of Dogs....... 4Ask the Vet ................................ 7

disease transmission. Most tick-transmittedpathogens require a 24- to 48-hourperiod of attachment to the host beforesuccessful transmission of an infectiousorganism is possible. Fastidious groomingmay result in the early removal of mostticks from cats and, thereby, theprevention of disease transmission.Alternatively, serologic testing in catshas led to confusing and somewhatdiscordant data. Therefore, as describedbelow, polymerase chain reaction (PCR)testing should be used more frequently inthe future to clarify the role of tickborneorganisms as a cause of disease in cats.

A U G U S T 2 0 0 5 V O L U M E 3 , N U M B E R 3

A NEWSLETTER OF PRACTICAL MEDICINE FOR VETERINARY PROFESSIONALSA NEWSLETTER OF PRACTICAL MEDICINE FOR VETERINARY PROFESSIONALS

states, cytauxzoonosis is now reportedthroughout the southeastern, southcentral, and mid-Atlantic states. Assuch, cytauxzoonosis is an importantemerging tickborne disease of cats withan expanding geographic distribution.In C. felis–endemic regions, acaracidesshould be recommended routinely for catsin an effort to prevent this highly fatalinfection.

Recent molecular evidence indicatesthat cats can also be infected withAnaplasma phagocytophilum and anEhrlichia canis–like organism. Theinfrequent diagnosis of anaplasmosisand ehrlichiosis in cats may be relatedto a number of factors, including ageneral underrecognition of tickbornediseases in cats, potentially decreasedpathogenicity of tickborne organisms incats as compared with dogs or people,and the rapid removal of ticks from catsresulting in decreased opportunity for

Tickborne Diseasesof Cats

Edward B. Breitschwerdt, DVMProfessor of Medicine and Infectious DiseasesCollege of Veterinary MedicineNorth Carolina State University

2 HARTZ® COMPANION ANIMALSM • AUGUST 2005 • VOL. 3, NO. 3

Consulting EditorsAlbert Ahn, DVMVice President of CorporateCommunications and VeterinaryOperationsThe Hartz Mountain Corporation

Bruce TrumanSenior DirectorAnimal Health and NutritionThe Hartz Mountain Corporation

Associate EditorsJill A. Richardson, DVMDirector—Consumer RelationsThe Hartz Mountain Corporation

David LevyAssistant ManagerAnimal Health and NutritionThe Hartz Mountain Corporation

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A U G U S T 2 0 0 5 V O L U M E 3 , N U M B E R3

A NEWSLETTER OF PRACTICAL MEDICINE FOR VETERINARY PROFESSIONALSAlthough various Ehrlichia, Anaplasma,

and Neorickettsia spp have been reportedto cause disease in cows, sheep, dogs,horses, and humans, the role of anyspecific species as a pathogen in catsremains less clearly defined. The firstevidence for naturally occurring felineehrlichiosis was provided by Charpentierand Groulade in France. Felineehrlichiosis was subsequently reported in1989 by Buoro and colleagues when theydescribed intracytoplasmic inclusions inmonocytes and lymphocytes derived fromthree cats in Kenya. By both light andelectron microscopy, the inclusions weremorphologically similar to Ehrlichia spmorulae, as observed on blood smearsobtained from other animals. Subsequently,morulae were described in stained bloodsmears obtained from cats in the UnitedStates, France, Brazil, and Sweden. Todate, no Anaplasma or Ehrlichia spp havebeen cultured from the blood of a cat;however, Bjoersdorff and colleaguesamplified and sequenced 16S rDNA(from an EDTA blood sample obtainedfrom a 14-month-old shorthaired catfrom Sweden) that was 100% similar tocanine and equine A. phagocytophilumstrains from the same region.Experimentally, inoculation of cats withA. phagocytophilum resulted inasymptomatic infection or mild feverand depression, and the developmentof neutrophilic and eosinophilicmorulae. Recently, several laboratories,including the North Carolina StateUniversity Vector Borne DiseasesDiagnostic Laboratory, have amplifiedA. phagocytophilum DNA from the bloodof acutely ill cats with fever, lethargy,inappetence and thrombocytopenia.These feline cases have been identified ingeographic regions that are endemic forcanine, equine, or human anaplasmosis.

Our research group has also describedE. canis–like infection in young cats fromthe southeastern United States, easternCanada, and France. Based on PCRamplification and DNA sequencing, theEhrlichia DNA amplified from the bloodof these cats was 100% similar to the

comparable E. canis DNA sequencesobtained from canine E. canis isolates.Because no isolates were made fromthese cats, a more complete geneticcharacterization was not possible;therefore, we are currently describingthese feline infections as E. canis–like.Antibodies could not be detected inthese cats by immunofluorescent assayusing E. canis antigens. Serum from allthree cats from Canada and the UnitedStates contained antinuclear antibodies.The predominant disease manifestationsincluded polyarthritis accompaniedby fever in one cat, bone marrowhypoplasia or dysplasia accompaniedby pancytopenia in one cat, and anemiaand thrombocytopenia in one cat. Indogs, neutrophilic polyarthritis hasbeen most frequently associated withE. ewingii infection. Neutrophilicpolyarthritis in the one cat was confirmedby cytologic analysis of joint fluid at1 and 3 years of age, suggesting thepossibility of chronic E. canis–likeinfection. Previous serologic studieshave reported an association betweenthrombocytopenia, hyperglobulinemia,and polyarthritis in cats that had E. canisantibodies.Other nonspecific clinicalabnormalities, including lethargy,anorexia, conjunctivitis, swelling in theventral neck region, and mild interstitiallung disease, were reported in these catsand can be observed in association withcanine ehrlichiosis.

There is increasing evidence that ticks,as well as fleas, can transmit Bartonellaspp. The extent to which various tickspecies are vector competent to transmitvarious Bartonella spp to cats, dogs, orhumans is unknown. There are numerousrecent reviews of bartonellosis thatprovide veterinarians with an excellentbackground for these emerging zoonoticinfectious organisms. Two reviews arecited in the suggested readings. Similar toEhrlichia spp, Bartonella spp can causelong-lasting intravascular infections incats and dogs. As with other vectorborneorganisms, blood serves as a food sourcefor fleas and ticks and as a means of

perpetuating future generations oftickborne organisms.

To further define the spectrum offeline tickborne infections and until suchtime as serologic testing is thoroughlyvalidated in experimentally or naturallyinfected cats, PCR testing will benecessary. In addition, until E. canis andother tickborne pathogens have beenisolated from cats and several isolates areavailable from disparate geographicregions for detailed comparative geneticstudy, the molecular evidence supportingE. canis infection in cats must be

HARTZ® COMPANION ANIMALSM • AUGUST 2005 • VOL. 3, NO. 3 3

interpreted with caution. Because tickexposure has not been clearly establishedin cats with E. canis–like infection, it ispossible that an Ehrlichia genotype, withcomplete or partial 16S rDNA homologywith E. canis, is capable of infecting catsand may have evolved with a differentmode of transmission as compared withtick transmission of E. canis to dogs.

To facilitate the generation ofnew information related to tickborneinfections in cats, veterinarians willhave to become more knowledgeableabout molecular versus serologic testingmodalities. I will briefly review someconsiderations when requesting molecular-based diagnostic testing on a cat withsuspected tickborne infection.

MOLECULAR DIAGNOSTICSAND PCR TESTING:DO’S AND DON’TS

PCR is a highly sensitive diagnostictechnique that can be used to detect smallquantities of bacterial, viral, or protozoalDNA or RNA in a patient’s blood, fluid,or tissue specimens. PCR does notamplify or detect antibodies or antigens,only DNA or RNA. Therefore, thetargeted organism must be in the samplefor its DNA or RNA to be detected.

When to Use PCR Testing■ Before administration of an antibiotic

or antiprotozoal drug to confirmactive infection (i.e., presence ofDNA equals presence of the organism):Antibody tests confirm exposure tothe organism and may or may not bereflective of active infection. When indoubt, store an EDTA-anticoagulatedblood sample in the refrigeratorbefore administering treatments. It isbetter to have a pretreatment sampleand not need it than to need thesample and not have it. Formalin

should be avoided because it denaturesDNA with prolonged exposure.

■ After completion of treatment toconfirm therapeutic elimination ofthe infection (i.e., failure to detectDNA supports treatment success):Conceptually, veterinarians can thinkof PCR testing as using the samelogic and approach as when culturingurine. It is best to perform PCRbefore antibiotic administration orafter treatment has been stopped. Iftreatment has not eliminated theinfection, waiting 2 to 3 weeks aftertreatment should allow the number oforganisms to increase in the blood ortissue sample to a level that can bedetected by PCR.

■ When the species of an infectiousagent is important for determinationof the appropriate type of drug to usefor treatment: For example, differentdrugs would be used to treat Babesiacanis and Babesia gibsoni infections indogs. Species-specific PCR allowsdifferentiation of the infecting species.

PCR: Points to Ponder■ Although this is a very sensitive test,

a negative PCR result will neverdefinitively eliminate the possibilityof an infectious agent.

■ Repeated negative PCR results fromthe same patient would stronglysupport therapeutic elimination of theinfectious agent.

■ In most instances, the use ofglucocorticoids will increase thenumber of infectious particles inthe blood. Therefore, corticosteroidadministration, particularly atimmunosuppressive doses, canenhance PCR detection of aninfectious agent.

■ If the PCR test is properly designedand performed, a false-positive resultshould not occur. PCR contaminationcan result in a false-positive result.However, good molecular diagnosticlaboratories run several controls to helpavoid or detect PCR contamination.Newer PCR approaches such asreal-time PCR greatly decrease thepossibility of PCR contamination ascompared to older, conventional PCRassays.

■ PCR assays performed by differentlaboratories can vary substantially inthe quality of the assay and testresults. Always know your laboratory.

SUGGESTED READINGBjoersdorff A, Svendenius L, Owens JH, Massung RF:

Feline granulocytic ehrlichiosis—A report of a newclinical entity and characterisation of the infectiousagent. J Small Anim Pract 40:20–24, 1999.

Bondy PJ, Cohn LA, Kerl ME: Feline cytauxzoonosis.Compend Contin Educ Pract Vet 27:69–75, 2005.

Bouloy RP, Lappin MR, Holland CH, et al: Clinicalehrlichiosis in a cat. JAVMA 204:1475–1478, 1994.

Breitschwerdt EB, Abrams-Ogg ACG, Lappin M, et al:Molecular evidence supporting Ehrlichia canis-likeinfection in cats. J Vet Intern Med 16:642–649, 2002.

Breitschwerdt EB, Kordick DL: Bartonella infection inanimals: Carriership, reservoir potential,pathogenicity, and zoonotic potential for humaninfection. Clin Microbiol Rev 13:428–438, 2000.

Buoro IBJ, Atwell RB, Kiptoon J, et al: Feline anemiaassociated with Ehrlichia-like bodies in three domesticshorthaired cats. Vet Rec 125:434–436, 1989.

Charpentier F, Groulade P: Probable case of ehrlichiosisin a cat. Bull Acad Vet Fr 59:287–290, 1986.

Chomel B, Kasten RW, Sykes JE, et al: Clinical impactof persistent Bartonella bacteremia in humans andanimals. Ann N Y Acad Sci 990:1–12, 2003.

Kidd L, Breitschwerdt EB: Transmission times andprevention of tick-borne diseases in dogs. CompendContin Educ Pract Vet 25:742–750, 2003.

Lappin MR, Breitschwerdt EB, Jensen WA, et al:Molecular and serologic evidence of Anaplasmaphagocytophilum infection in cats in North America.JAVMA 225(6):893–896, 2004.

Luria BJ, Levy JK, Lappin MR, et al: Prevalence ofinfectious diseases in feral cats in northern Florida.J Feline Med Surg 6:287–296, 2004.

Meinkoth J, Kocan AA: Feline cytauxzoonosis. Vet ClinNorth Am Small Anim Pract 35:89–101, 2005.

Stubbs CJ, Holland CJ, Reif JS, et al: Feline ehrlichiosis:Literature review and serologic survey. CompendContin Educ Pract Vet 22:307–317, 2000.

Wagner JE: A fatal cytauxzoonosis-like disease in cats.JAVMA 168:585–588, 1976.

PCR testing should be usedmore frequently to clarify the role of tickborne

organisms as a cause of disease.

4 HARTZ® COMPANION ANIMALSM • AUGUST 2005 • VOL. 3, NO. 3

and tick-transmitted organisms needa “home” for the maintenance andperpetuation of future generations.Therefore, on a daily basis, veterinariansand pet owners are confronted with anevolutionary cycle that has been ongoingfor millions of years.

Without question, veterinarians playa central role in the diagnosis, treatment,and prevention of tick-transmittedinfectious diseases of companion animals.They also play an important role inadvising the public as to the zoonoticpotential of pathogens that are transmittedby ticks to cats, dogs, and humans.Based on scientific evidence that hasbeen generated during the past severaldecades, tick-transmitted pathogens caninduce clinical manifestations rangingfrom acute fatal illnesses (e.g., RockyMountain spotted fever, ehrlichiosis, andbabesiosis) to chronic debilitating diseasestates (e.g., ehrlichiosis, babesiosis,borreliosis, bartonellosis). The family dogis an exceptional environmental sentinelfor establishing the potential forinfection with tickborne organisms in agiven locality. Although controversial,exposure surveillance for a spectrum oftickborne organisms in dogs can be usedto educate clients and physicians as tothe potential for human infection.Clearly, minimizing or eliminating tickinfestations in companion animals isperhaps of greater importance to thepet-owning public today than during anyprevious time in history. In addition tofacilitating improvements in health carefor companion animals, veterinarians arecontributing in a substantial manner to

Tickborne Diseasesof Dogs

Despite substantial progress inour understanding of the diseasemanifestations caused by several tick-transmitted pathogens, numerouschallenges continue to confront theveterinary profession. This is particularlytrue in the context of canine tickborneinfections. Depending on their geographiclocation, local environmental exposureto brush and high grass (well confinedor allowed to roam), utility (hunting,search and rescue, herding, householdcompanion), and individual personalities,dogs will experience highly variabledegrees of tick infestation. For example, itis uncommon for a golden retriever orLabrador retriever to stay on the sidewalkand not run through high grass and lowbrush, the favorite habitats of most ticks.In addition, management practices,particularly for kennel dogs, will greatlyinfluence the frequency and severity oftick infestations. For these reasons, tickexposure and tickborne infections, althoughmore frequent in medium- to large-breeddogs or hunting and herding breeds, canbe found in all dog breeds and in mostparts of the world. Clearly, the routine useof acaracide products plays an importantrole in killing ticks before pathogens canbe effectively transmitted; however,veterinarians should not assume thatany available product or combinationof products will be 100% effective inpreventing transmission of tickbornepathogens. Tick transmission of aspectrum of microorganisms constitutesa highly complex process that on anevolutionary basis seems to favor the tickand the microorganism. Ticks need blood,

Edward B. Breitschwerdt, DVMProfessor of Medicine and Infectious DiseasesCollege of Veterinary MedicineNorth Carolina State University

the comparative medical understandingof these seemingly elusive infectiousagents.

CASE EXAMPLETo highlight the clinical complexity

and the challenges to our currentunderstanding of tick-transmittedinfectious diseases, I would like to use thefollowing example from a consultationwith a practice owner in Iowa. Theveterinarian contacted me because one ofhis “associates” had evaluated a dog thatinitially presented with acute onset ofweakness and mild anemia (hematocrit27%). Following “symptomatic therapy,”the hematocrit normalized for severalweeks (rechecked at least four times);however, on a subsequent recheck,the hematocrit was 12%, immune-mediated hemolytic anemia (IMHA)was diagnosed, and the dog wasimmediately referred to the Universityof Iowa College of Veterinary Medicine.In conjunction with the medicalmanagement of IMHA, serum was sentto the North Carolina State UniversityVector Borne Diseases DiagnosticLaboratory (VBDDL) for a tickbornepathogen serology panel. Unfortunately,the dog died before test results wereavailable, which is not surprising. Severalrecent studies indicate that approximately50% of IMHA referrals to tertiary carecenters die because of their disease. Inour laboratory, immunofluorescent assaydetected Babesia canis antibodies (titer1:64), and additional review of the dog’shistory determined that the dog hadtraveled to Arkansas during the previous

HARTZ® COMPANION ANIMALSM • AUGUST 2005 • VOL. 3, NO. 3 5

COMPLICATING FACTORS INCLINICAL CONFIRMATION

I believe that the above exampleof vectorborne infection is repeatedon a daily basis in veterinary practicesthroughout the United States, onlywith different organisms, different dogs,different owners, and different attendingclinicians. The same evolutionaryadaptations that facilitate the persistenceof many tickborne infections in dogsalso complicate clinical confirmation ofdisease causation. This is particularly truewhen assessing diagnostic test results foran individual dog residing in a highlyendemic area for vectorborne infections.For example, our research group hasgenerated PCR evidence (i.e., findingorganism-specific DNA) for the presenceof six different tickborne pathogens in asingle EDTA blood sample, obtainedfrom a Walker hound with extensive tickexposure. Most dogs in this kennel also

had antibodies to nearly every tickborneorganism for which we tested. Therefore,clinicians need to recognize that themammalian body functions as a componentof numerous complex ecosystems, whichfacilitates the evolutionary perpetuationof vectorborne bacteria, protozoa, andviruses. In practical terms, this meansthat the detection of antibodies,antigens, DNA, RNA, or the cultureof microorganisms from a sick dog in ahighly endemic tick environment doesnot directly support a cause and effectrelationship between detection of themicroorganism and those diseasemanifestations found in an individualpatient.

It is also increasingly obviousthat disease expression is frequentlymultifactorial, particularly in thoseinstances in which vectorborne organismsuse blood or the vasculature as a reservoir.

year. Conclusions we can draw from thisexample are as follows:

1. A diagnosis of IMHA secondary tobabesiosis was made (perhaps), buttoo late to benefit the dog or theowner.

2. Serologic evidence of B. canis exposuredoes not confirm active Babesiainfection. Polymerase chain reaction(PCR) testing would have documentedactive infection by detecting B. canis–specific DNA sequences in the dog’sblood sample. EDTA-anticoagulatedblood was not submitted to theVBDDL at the same time the serumsample was submitted, so PCR testingwas not a possibility. Because Babesiaspp are intraerythrocytic organisms,DNA must be extracted from theerythrocytes for PCR amplification.

3. Arkansas is highly endemic for B.canis. Iowa is not endemic for B. canis.The dog most likely acquired theinfection from a brown dog tick(Rhipicephalus sanguineus) while inArkansas.

Other considerations include:

1. Because of research by Dr. AdamBirkenheuer at NCSU (and othersaround the country), babesiosis isbecoming recognized as an emergingcanine and human infectious diseasein the United States.

2. Babesiosis is a definitive cause ofIMHA in dogs.

3. Based on recent studies, bothvisualization of Babesia organisms onblood smears and serologic testing areinsensitive diagnostic tests as comparedwith PCR.

4. Dogs, owners, and other animals travelfarther and more frequently than atany other time in history. Recentexamples of infectious agents that“travel” include SARS, monkeypox,West Nile virus, and canineleishmaniasis.

5. It takes only one brown dog tick totransmit B. canis.

When multiple factors simultaneouslyinduce chronic changes in structural,biochemical, and physiologic processesover a protracted period of time, diseaseexpression can be highly variable,even among a specific dog population.Because the factors that influence diseaseexpression can differ significantly amongindividuals within a given population,clinicians should anticipate a broadspectrum of clinical, hematologic, orbiochemical abnormalities when focusingdiagnostic emphasis on a single factoror test result. For example, diversedisease manifestations, includingepistaxis, IMHA, immune-mediatedthrombocytopenia, glomerulonephritis,polyarthritis, and myelofibrosis, havebeen historically attributed to Ehrlichiacanis infection in dogs. For a variety ofreasons, it is increasingly clear thatcanine ehrlichiosis is a disease complexthat is influenced by the infecting

Ehrlichia sp, the host immune response,coinfection with other vectorborne ornonvectorborne pathogens, and perhapsnumerous other factors yet to beclarified. In addition to E. canis, otherspecies (Ehrlichia chaffeensis, Ehrlichiaruminatum, and Ehrlichia ewingii) cancause ehrlichiosis in dogs and people. Inconjunction with numerous highlyvariable host factors, the infectingEhrlichia sp can influence diseaseexpression. For instance, polyarthritis indogs is more frequently associated withE. ewingii infection than with E. canis orE. chaffeensis infection. It is also possiblethat genetic variation in organismvirulence can influence disease severity.For instance, dogs infected with E. canisin Greece are likely to develop severebone marrow suppression that isfrequently not therapeutically responsiveto doxycycline. Both of these

The same evolutionary adaptations that facilitatethe persistence of tickborne infections also

complicate clinical confirmation of disease causation.

observations are in direct contrast to theoverall experience with E. canis infectionsin the United States (i.e., pancytopeniais rare and most dogs, despite chronicillness, respond hematologically afterdoxycycline administration). In addition,recent data indicate that the commonevolutionary history of Anaplasma,Babesia, Bartonella, Borrelia, Ehrlichia,and Rickettsia spp has resulted incomplex polymicrobial interactions thatinfluence the pathophysiology of diseaseexpression in dogs and human patients.For clinicians and diagnostic laboratories,confirming active infection caused bya single tickborne pathogen can bechallenging, particularly when evaluatingchronic rather than acute illness.

Seroconversion, culture, and PCR canall be used to support causation in anacutely infected individual. However,the microbiologic confirmation ofpolymicrobial tickborne infections in achronically ill patient using these samediagnostic modalities can be extremelydifficult or in certain instancesimpossible to achieve.

Geographic variation in the prevalenceof tick-transmitted pathogens also presentsan important challenge for veterinaryclinicians. It has become increasinglyobvious that ticks in different geographicregions or localities can transmitdifferent pathogens. For example, inthe northeastern United States, Ixodesscapularis can transmit Anaplasmaphagocytophilum, Borrelia burgdorferi,Babesia microti, and Bartonella vinsonii(arupensis). In the southeastern UnitedStates, dogs are more frequently exposedto Dermacentor variabilis, Amblyommaamericanum, and Rumex sanguineus,which could result in infection withAnaplasma platys, B. canis, Bartonellavinsonii (berkhoffii), E. canis, E. ewingii,

the potential for the transmission of thesepathogens. Also useful would be a meansof tracking companion animal infectiousdiseases maintained by an organizationsuch as the Centers for Disease Controland Prevention or the Infectious DiseasesSociety of America. Currently, nodatabase exists to address local, regional,or national concerns about these diseasesin companion animals.

SUGGESTED READINGAdelson ME, Rao RV, Tilton RC, et al: Prevalence

of Borrelia burgdorferi, Bartonella spp., Babesia microti,and Anaplasma phagocytophila in Ixodes scapularis tickscollected in northern New Jersey. J Clin Microbiol42:2799–2801, 2004.

Birkenheuer AJ, Breitschwerdt EB: Canine babesiosis.Stand Care Emerg Crit Care Med 6(2):1–4, 2004.

Birkenheuer AJ, Levy MG, Breitschwerdt EB:Development and evaluation of a seminested PCRfor detection and differentiation of Babesia gibsoni(Asian genotype) and B. canis DNA in canine bloodsamples. J Clin Microbiol 41:4172–4177, 2003.

Breitschwerdt EB, Atkins CE, Brown TT, et al:Bartonella vinsonii supsp. berkhoffi and relatedmembers of the alpha subdivision of the Proteobacteriain dogs with cardiac arrhythmias, endocarditis, ormyocarditis. J Clin Microbiol 37:3618–3626, 1999.

Breitschwerdt EB, Blann KR, Stebbins ME, et al:Clinicopathologic abnormalities and treatmentresponse in 24 dogs seroreactive to Bartonella vinsonii(berkhoffii) antigens. JAAHA 40:92–101, 2004.

Breitschwerdt EB, Hegarty BC, Hancock SI: Sequentialevaluation of dogs naturally infected with Ehrlichiacanis, Ehrlichia chaffeensis, Ehrlichia equi, Ehrlichiaewingii or Bartonella vinsonii. J Clin Microbiol36:2645–2651, 1998.

Daszak P, Cunningham AA, Hayatt AD: Emerginginfectious diseases of wildlife—Threats to biodiversityand human health. Science 287:443–449, 2000.

Goodman RA, Hawkins EC, Olby NJ, et al: Molecularidentification of Ehrlichia ewingii infection in dogs:15 cases (1997–2001). JAVMA 222:1102–1107, 2003.

Kidd L, Breitschwerdt EB: Transmission times andprevention of tick-borne diseases in dogs. CompendContin Educ Pract Vet 25:742–750, 2003.

Kordick SK, Breitschwerdt EB, Hegarty BC, et al:Coinfection with multiple tick-borne pathogens in aWalker Hound kennel in North Carolina. J ClinMicrobiol 37:2631–2638, 1999.

Lappin MR, Breitschwerdt EB, Jensen WA, et al:Molecular and serologic evidence of Anaplasmaphagocytophilum infection in cats in North America.JAVMA 225(6):893–896, 2004.

Mylonakis ME, Koutinas AF, Breitschwerdt EB, et al:Chronic canine ehrlichiosis (Ehrlichia canis): Aretrospective study of 19 natural cases. JAAHA40:174–184, 2004.

Tuttle AD, Birkenheuer AJ, Juopperi T, et al: Concurrentbartonellosis and babesiosis in a dog with persistentthrombocytopenia. JAVMA 233:1306–1310, 2003.

Weinkle TK, Center SA, Randolph JF, et al: Evaluationof prognostic factors, survival rates, and treatmentprotocols for immune-mediated hemolytic anemia indogs: 151 cases (1993–2000). JAVMA 226:1869–1880, 2005.

E. chaffeensis, Rickettsia rickettsii, andother less pathogenic spotted fever grouprickettsiae, such as Rickettsia montana andRickettsia rhipicephalus. These geographicdifferences can be problematic whendetermining the causative pathogen,particularly because many tick-transmittedinfections result in a prolonged subclinicalcourse. Therefore, a dog or cat might beinfected in an endemic area whereveterinarians are very familiar with thedisease manifestations but become illmonths to years later after moving to anarea where the disease is not endemic andveterinarians are far less familiar with thedisease manifestations. This emphasizesthe importance of obtaining a travelhistory for all sick animals when a vector-

transmitted infectious disease is adiagnostic consideration.

CONCLUSIONSTick-transmitted infectious diseases

will continue to challenge the creativityof the medical professions. Futureresearch efforts must substantiallyimprove our ability to detect the presenceof tick-transmitted pathogens in ourpatients. For several tick-transmitteddiseases, there is a serious need for bettertreatment modalities. The currentlyavailable treatments for diseases suchas babesiosis, bartonellosis, ehrlichiosis,and borreliosis may only induce a stateof remission, rather than eliciting atherapeutic cure. Because the diagnosisand treatment of these diseases willremain challenging for the clinician andexpensive for the client, developmentof a “tick vaccine” that would preventtransmission of all or most tickbornepathogens would seem to have greatmedical utility. In the interim, the use ofproducts that kill ticks before or shortlyafter attachment to the pet will minimize

6 HARTZ® COMPANION ANIMALSM • AUGUST 2005 • VOL. 3, NO. 3

Development of a “tick vaccine” that wouldprevent transmission of tickborne pathogenswould seem to have great medical utility.

Albert Ahn, DVM, is Vice President of Corporate Communicationsand Veterinary Operations at The Hartz Mountain Corporation.

ASK THE VET

HARTZ® COMPANION ANIMALSM • AUGUST 2005 • VOL. 3, NO. 3 7

Q

A

A client of mine mentioned that she sawsomething on the news regarding thediscontinuation of the Hartz AdvancedCare Flea and Tick drops for cats. Couldyou explain what is going on with thissituation?

Hartz has decided to voluntarily discontinue sales ofour Hartz® ADVANCED CARE® 4 in 1® Flea and TickDrops Plus+ for Cats and Hartz® ADVANCED CARE®

3 in 1® Flea and Tick Drops for Cats as of March 31,2006. In addition, Hartz has implemented labelchanges to these products this summer.

This move is being made following discussionswith the Environmental Protection Agency, whichregulates topical insecticides. Those discussions wereprompted by concerns over the number of adversereactions that have been reported by cat owners. Ifyou or your clients have any questions about thissituation, please contact the Hartz ConsumerRelations Department at 800-275-1414. Please beassured that Hartz will offer you any support neededto address customer concerns.

QA

WE WANT TO HEAR FROM YOU!• Have questions or comments? Call our Consumer Relations Department at 800-275-1414 and ask to speak to a Hartz staff

veterinarian or email us at feedback@hartz.com.

• To obtain a Hartz Veterinary Catalog of products, please call 800-999-3000 x5118 or email us at feedback@hartz.com.

Articles found in the Hartz Companion AnimalSM newsletter can be copied and distributed to your colleagues, staff, and clients.

Additional newsletters may also be obtained by contacting us at feedback@hartz.com or by phone at 800-275-1414.

What is the dose of grapes and raisinsthat can cause poisoning in dogs?

According to current information,1 the lowestdocumented toxic grape and raisin doses are 0.7oz/kg and 0.11 oz/kg, respectively. The mechanism ofaction and toxic principal are unknown at thistime but are currently being studied. Reportedhistopathologic lesions seen with raisin and/orgrape poisoning include proximal renal tubulardegeneration and necrosis.

REFERENCE1. Gwaltney-Brant S, Holding JK, Donaldson CW, et al: Renal failure

associated with ingestion of grapes or raisins in dogs [letter]. JAVMA218(10):1555–1556, 2001.

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