In 2002, the largest epidemic of West Nile virus(WNV) meningoencephalitis in humans ever record-

ed occurred.1 There were 4,155 laboratory-confirmedcases in humans (case fatality rate, 6.8%).2 TheCenters for Disease Control and Prevention (CDC)also reported WNV infection in numerous avian andmammalian species, including 16,739 birds reportedfrom 41 states and the District of Columbia, and

14,571 mammals, including 1 cat, 7 dogs, and 24 ani-mals of other species; the remainder of the infectedanimals were horses reported from 41 states.2

Little information has been published with regardto WNV infection in domestic pet mammals such asdogs and cats. After the 1999 epidemic in New YorkCity, 5% of domestic dogs tested had antibodies againstWNV.3 Additionally, a human serosurvey carried out inQueens, NY, during the same time revealed that 3%(weighted) of the humans surveyed were seropositiveagainst WNV.4 When the results were compared, theseroprevalence in dogs from the same area in Queenswhere the human serosurvey was completed was 11%;this was > 4 times that in humans, suggesting thatdomestic animals may be useful sentinel indicators forWNV and the potential risk of human exposure.

The purposes of the study reported here were toestimate WNV infection rates, assess environmentalvariables that correlated with seropositivity in dogs andcats, and assess whether pets should be considered aspossible sentinels for WNV and therefore of potentialhuman exposure. The survey was performed during anepidemic of WNV infection in the vicinity of Slidell, StTammany Parish, La, during summer and fall of 2002.

Materials and MethodsStudy design—This study used a cross-sectional conve-

nience sample of domestic dogs and cats from St TammanyParish and the city of Slidell, the largest city in the parish, todetermine the prevalence of WNV antibodies and identifyand evaluate potential environmental variables and other fac-tors that correlated with seropositivity during a WNV epi-demic in humans.

Study site—During 2002, without adjusting for thenumber of residents per state, Louisiana had the fourth high-est number of laboratory-confirmed WNV cases in humansin the United States and St Tammany Parish had the thirdhighest rate of WNV-induced human encephalitis in thestate.5,6 When adjusted for the number of residents per state,Louisiana ranked first in the United States for reportedhuman cases, with 6.7 WNV infections/100,000 residents.7

St Tammany Parish and the Slidell community were cho-sen as the study sites because of the number of human casesof meningoencephalitis caused by WNV. Of 12 cases reportedto the CDC by mid July 2002, 11 were from Louisiana, 4 ofwhich were from St Tammany Parish. Overall, St TammanyParish had 39 human cases from June 10 to August 29, 2002.5

St Tammany Parish has a human population of 191,268,with 69,253 households, and Slidell has a population of25,695, with 9,480 households.8 Slidell city limits includenumerous natural water sources such as sections of LakePontchartrain to the south, Pearl River to the east, andnumerous bayous and marshes throughout the city.

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Serologic survey of cats and dogs during an epidemic of West Nile virus

infection in humans

James C. Kile, DVM, MPH, DACVPM; Nicholas A. Panella, MSc; Nicholas Komar, ScD; Catherine C. Chow, MD, MPH; Adam MacNeil, MPH; Brent Robbins, DVM;

Michel L. Bunning, DVM, MPH

Objective—To estimate West Nile virus (WNV) infectionrates, assess environmental variables that correlatedwith seropositivity in dogs and cats, and assess whetherpets should be considered as possible sentinels forWNV and therefore of potential human exposure.Design—Cross-sectional serosurvey.Animals—442 dogs and 138 cats.Procedure—Serum samples were screened forseropositivity against WNV by use of the plaquereduction neutralization test.Results—116 (26%) dogs and 13 (9%) cats yielded pos-itive results. The odds of seropositivity against WNV foroutdoor-only family dogs were almost 19 times as greatas those for indoor-only family dogs and almost twice asgreat for stray dogs as for family dogs. Family dogs notreceiving heartworm medication were 2.5 times as like-ly to yield positive results for antibodies against WNV asfamily dogs receiving heartworm medication.Conclusions and Clinical Relevance—Seropositivitywas greater for outdoor family dogs than for indoorfamily dogs. Further investigation of the potential useof stray dogs as sentinel indicators for WNV infectionand the potential risk of human exposure is warrant-ed. (J Am Vet Med Assoc 2005;226:1349–1353).

From the CDC, Epidemic Intelligence Service, 1600 Clifton Rd SE,Atlanta, GA 30333 (Kile); CDC, the National Center for InfectiousDiseases, 1300 Rampart Rd, Fort Collins, CO 80521 (Panella,Komar, Chow, Bunning); the National Immunization Program,1600 Clifton Rd SE, Atlanta, GA 30333 (MacNeil); and the StTammany Parish Department of Animal Services, 25026 Hwy 36,Abita Springs, LA 70420 (Robbins). Dr. Kile’s present address isUSDA, Food Safety and Inspection Service, Landmark Center,Suite 300, 1299 Farnam St, Omaha, NE 68102. Dr. Chow’s presentaddress is Hawaii State Department of Health, 1132 Bishop St,Honolulu, HI 96813. Mr. MacNeil’s present address is HarvardSchool of Public Health, 677 Huntington Ave, Boston, MA 02115.Dr. Bunning’s present address is Air Mobility Command, USAF,203 W Losey St, Scott Air Force Base, IL 62225.

Dr. Kile was an Epidemic Intelligence Service Officer at the time ofthe study.

Address correspondence to Dr. Kile.

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Study population, sample collection, and question-naire—Dogs and cats were sampled when evaluated at vet-erinary facilities (enrolled as family pets) or animal controlshelters (enrolled as strays). Participation in the study wasoffered to all 29 veterinary facilities within the parish, withfinal enrollment of 15 facilities (52% participation), includ-ing 10 from Slidell and 5 from 4 other cities in the parish.There were 33 participating veterinarians.

Veterinarians were asked to offer to all clients whoresided in St Tammany Parish serologic testing for WNV ofall dogs or cats that the client brought to the veterinary facil-ities. Veterinarians obtained standard consent from pet own-ers, who then completed questionnaires requesting generalinformation about the animals, including species, the reasonthe pet was being seen (eg, checkup, sick visit, or surgery),and the number of years the pet had lived at the givenaddress. The questionnaires also gathered information aboutenvironmental variables, including geographic locations ofthe animals within the parish, potential exposure to mosqui-toes because of indoor versus outdoor movement, and pre-ventive insecticide usage by the owners on their pets.

Additionally, all 3 animal control facilities in the parishwere enrolled, including 2 in the parish and 1 in Slidell. Straydogs and cats were sampled after capture, while awaitingadoption or euthanasia in animal control facilities. Animalcontrol personnel provided a general address for the animal’slocation at capture. Although the length of time that an ani-mal was stray could not be determined, for the purposes ofthis study, it was assumed that all stray animals had outdoorrather than indoor exposure.

Serologic assay—Three to 5 mL of blood was collectedfrom each animal via a standard venipuncture technique andtransferred to a serum separator tube that was centrifuged.The resulting serum samples were held at –20oC until tested.

Serum samples were screened for seropositivity againstWNV by use of the plaque-reduction neutralization test,which is the most specific test for the arthropod-borne fla-viviruses.9 Briefly, sera were diluted 1:5 and mixed with anequal volume of reference virus (WNV/NY99-4132 strain)for a final dilution of 1:10. Samples were incubated at 37oCfor 1 hour. The virus-serum mixtures were added in dupli-cate 0.1-mL aliquots to drained wells of cell cultures grownon 6-well plates. Plates were incubated at 37oC for an hour,and the wells were subsequently overlaid with a nutrientagarose mixture. A second overlay containing a neutral reddye was added 48 hours later. Plates were examined on thefollowing day for plaques (areas of dead cells that appear ascolorless areas against a red background of viable cells).Samples with ≥ 80% reduction in plaque-forming units,when compared with the back titration, were considered fla-vivirus-positive and were further titrated to determine endpoint titers. Positive samples were also screened for neutral-izing antibodies against St Louis encephalitis virus. Samplesthat yielded positive results from the SLE screening were sub-sequently titrated to determine virus identification. A 4-foldor greater titer for WNV or SLE virus was considered diag-nostic for that virus.

Geospatial analysis—The latitude and longitude weredetermined for each dog and cat in the study at the homeaddress for family pets and capture address for strays by useof a geographic information system.10 Two human WNVstudiesa,b were conducted concurrently in the same area as thedog and cat WNV serosurvey described here. For affectedhumans, the geocoded locations for the seropositive humanfever and serosurvey studies were recorded. A geographicinformation system software programc was used to assessgeographic distribution and geographic relationshipsbetween dogs, cats, and affected humans.

Statistical analyses—Statistical analyses were per-formed by use of a statistical software program.d Crude per-centages of positive and negative status for neutralizing anti-bodies against WNV were calculated for each type of studyanimal, and the proportions that yielded positive results werefurther examined. Data were stratified for analysis by envi-ronment type, environment exposure, years at address, pur-pose of visit to veterinary facility, application of flea controlproducts, and heartworm medication status. Pearson χ2 orFisher exact tests were used to determine associations.Confounding of variables for observed effect was examinedby use of stratified analysis, and when appropriate, Mantel-Haenszel adjusted odds ratios (ORs) and 95% confidenceintervals (CIs) were calculated to adjust for confoundingvariables. For all analyses, a value of P < 0.05 was consideredsignificant.

ResultsAnimals—Final enrollment in the study included

442 (76%) dogs and 138 (24%) cats. Blood sampleswere collected from August 29 through October 28,2002. Of the 580 enrollees, 453 (78%) were family petsand 127 (22%) were strays. Three hundred (52% of allanimals) were dogs from Slidell, with 248 family and52 stray dogs, and 142 (25%) were dogs from else-where in St Tammany Parish, with 119 family and 23stray dogs. Eighty-three (14% of all animals) were catsfrom Slidell, with 57 family and 26 stray cats, and 55(10%) were cats from elsewhere in the parish, with 29family and 26 stray cats.

Serologic results—Of 580 animals tested, 116 of442 (26%) dogs and 13 of 138 (9%) cats were seropos-itive for neutralizing antibodies against WNV, indicat-ing a significantly (P < 0.001) higher seroprevalence indogs than in cats (OR, 3.42; 95% CI, 1.86 to 6.29).

Animals were stratified by environment type orfamily versus stray status, and this association of high-er seroprevalence of dogs, compared with cats,remained significant (P < 0.001) for both groups; fam-ily dogs had odds of seropositivity > 5 times those offamily cats (OR, 5.11; 95% CI, 2.01 to 13.01), and straydogs had odds of seropositivity > 3 times those of straycats (OR, 3.28; 95% CI, 1.35 to 7.95 [P = 0.01]). Afteradjusting for environment-type status (family vs stray),this overall association remained (OR, 4.21; 95% CI,2.21 to 8.01).

After adjusting for species, stray animals had oddsof seropositivity that were twice those of family ani-mals (OR, 2.04; 95% CI, 1.27 to 3.29). In individualstrata, stray dogs had odds of seropositivity almosttwice those of family dogs (OR, 1.89; 95% CI, 1.12 to3.20 [P = 0.02]), and stray cats had odds of seroposi-tivity almost 3 times those in family cats (OR, 2.95;95% CI, 0.91 to 9.55 [P = 0.08]).

Level of outdoor exposure was examined for fam-ily dogs and cats by use of indoor-only status as the ref-erence group (Table 1). Significant (P < 0.001) differ-ences were observed for outdoor-only family dogs,which were almost 19 times as likely to yield positiveresults for antibodies against WNV as indoor-only fam-ily dogs.

Family dogs not receiving heartworm medicationwere > 2 times as likely to yield positive results as familydogs receiving heartworm medication (P = 0.01). After

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stratifying by level of outdoor exposure (Table 2), thisassociation between heartworm medication and WNVseropositivity was significant (P = 0.002) only for familydogs taken outdoors for walks. However, results of theBreslow-Day test for homogeneity of ORs were not signif-icant, indicating no difference in ORs across these strataof outdoor exposures. After adjusting for outdoor expo-sure, the overall association remained significant, indicat-ing a consistent association between not receiving heart-worm medication in family dogs and WNV seropositivity.

There were no significant differences betweenWNV-positive and -negative seroprevalences withregard to family dogs and family cats and whether theirgiven address was in Slidell or in other parish areas, thenumber of years the pet lived at the address, the pur-pose of the visit to the veterinary facility, or the appli-cation of flea control products on the pet.

Geospatial results—Assessment of canine, feline,and human cases in Slidell indicated that there were noWNV-seropositive family dogs or cats in the samehousehold with a WNV seropositive human. However,there was 1 household with a human case and aseronegative dog.

DiscussionThe WNV seroprevalence in domestic dogs in all

of St Tammany Parish in 2002 (26%) was higher thanthat reported in New York City in 1999 (5%), and theseroprevalence in cats in the parish was 9%, althoughthe data from the 2 studies are not suitable for statisti-cal comparison. The higher seroprevalence of infectionin the animals that were resident for < 1 year, althoughnot significant, suggests that most infections occurredin 2002. Otherwise, an increased seroprevalence wouldhave been expected in the other animals.

The WNV seroprevalence in domestic dogs in allof St Tammany Parish was 15 times as great as theWNV seroprevalence in humans in the same area and10 times as great as that reported in humans in the1999 New York City study. Seroprevalence in cats in allof St Tammany Parish was 5.5 times as great as inhumans in the same area. Of the 2 human WNV stud-ies that were conducted concurrently in the same area,1 studya found that 5 of 55 (9%) febrile outpatients hadIgM antibodies against WNV. The second studyb foundthat 21 of 1,226 (2%) randomly selected Slidell resi-dents were seropositive against WNV. The high sero-prevalence in domestic animals relative to that in

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Table 1—Odds ratios (ORs) and 95% confidence intervals (CIs) for seropositivity against West Nilevirus (WNV) associated with environmental exposure and other factors in owned dogs and cats dur-ing a human epidemic in St Tammany Parish, La, 2002.

Dogs Cats

Seropositive SeropositiveVariable (% [proportion]) OR 95% CI (% [proportion]) OR 95% CI

Where pet staysIndoor only 11 (2/19) Ref Ref 5 (2/41) Ref RefOutdoor only 69 (48/70) 18.55 3.94–87.34 18 (2/11) 4.33 0.54–35.02Both in and out NA NA NA 3 (1/34) 0.59 0.05–6.81Pet door 20 (19/94) 2.15 0.46–10.14 NA NA NAWalks only 9 (17/180) 0.89 0.19–4.17 NA NA NA

Heartworm medicineYes 22 (73/328) Ref Ref 11 (2/18) Ref RefNo 42 (13/31) 2.52 1.18–5.39 5 (3/63) 0.40 0.06–2.60

Flea controlYes 24 (73/305) Ref Ref 5 (3/57) Ref RefNo 26 (14/55) 1.09 0.56–2.10 8 (2/25) 1.57 0.25–10.00

Ref = Referent category. NA = Not applicable.

Table 2—Crude (unadjusted), strata-specific, and environment exposure-adjusted associationsbetween exposure to heartworm medication and WNV seropositivity in owned dogs during a humanepidemic in St Tammany Parish, La, 2002.

Analysis type Received heartworm Seropositive ORand variable medication (% [proportion]) (95% CI)

Crude (unadjusted) No 42 (13/31) 2.52 (1.18–5.39)*Yes 22 (73/328)

Strata-specificIndoor only No 0 (0/2) NA

Yes 6 (1/16)Indoor except for walks No 31 (5/16) 5.64 (1.68–18.92)*

Yes 8 (12/161)Dog door No 29 (2/7) 1.58 (0.28–8.84)

Yes 20 (17/84)Outdoor only No 100 (6/6) NA

Yes 65 (41/63)Environment adjusted† 4.24 (1.66–10.85)*

*Significant (P � 0.05) association. †Breslow-Day test for homogeneity of ORs revealed no significant (P � 0.05) difference in ORs across strata; therefore, the adjusted (Mantel-Haenszel) OR is reported.

NA = Not available (2 X 2 tables contained cells with 0 observations, so an OR could not be calculated).

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humans may have been associated with different expo-sure variables, including feeding preferences of infect-ed mosquitoes and host-vector susceptibility and dis-tribution.

After adjustment for environment type and envi-ronmental exposure, dogs had higher WNV seropreva-lence than cats. This suggests that there were variablesrelated to being canine or feline that were associatedwith WNV infection, and those variables should be fur-ther studied. For instance, studies11,12 assessing mos-quitoes and heartworm infection (also a vector-bornedisease) in dogs and cats have revealed that heartwormdisease is detected at lower rates in cats than in dogs.Suggested reasons for this difference include cats nottolerating mosquito bites as well as dogs and differingfeeding behavior of vector populations with respect tothese animals. A higher prevalence of antibodiesagainst WNV in dogs than cats suggests that dogswould make a better sentinel species than cats.

The odds of seropositivity were approximately twiceas great for stray dogs as for family dogs, and althoughnot significant, stray cats had almost 3 times the WNVseroprevalence as family cats. Furthermore, outdoor-onlyfamily dogs and family dogs with a dog door had a high-er WNV seroprevalence than indoor-only family dogs.These findings indicate higher WNV seroprevalence foranimals with greater outdoor exposure.

The reason that the odds of seropositivity were 2.5times as great in family dogs not receiving heartwormmedication as those receiving heartworm medicationcould not be determined from the available informa-tion. Results suggest that environment-exposure vari-ables do not explain this association. After adjustingfor outdoor exposure, the overall association remainedsignificant, indicating a consistent association betweennot receiving heartworm medication in family dogsand WNV seropositivity. Whether heartworm medica-tion is protective against infection with WNV shouldbe assessed.

Results of this study substantiate the need for fur-ther investigation of the potential use of dogs as sen-tinel indicators for WNV and the potential risk ofhuman exposure. For arboviral diseases, a useful sen-tinel species for risk of human exposure would havesimilar vector-feeding patterns as humans, be highlysusceptible to mosquito-borne infection yet resistant todisease, survive infection, develop detectable antibod-ies but not develop sufficient viremia to infect mosqui-toes, and not infect other species.13,14 Domestic dogsfulfill these criteria.15,16

Studies17-20 using domestic pet mammals, such asdogs, as sentinels have evaluated environmental healthhazards to humans. The design and findings of suchstudies reflect the importance of the shared environ-ment of domestic pets and humans and of using variedanimal sentinel species in monitoring programs. Thestudies also report on animal disease cases as earlymarkers or sentinel indicators of disease risk tohumans, including using animals to monitor remedialactivities against the exposure variables.

During 2002, St Tammany Parish used sentinelchicken flocks to detect WNV activity via 30 flockswithin the parish and 2 to 3 flocks in Slidell.e Blood sam-

ples were collected from birds twice per month. Dataindicated that seroconversion in the sentinel chickenflocks was 9% from April to December, which was onlya third that in dogs of the same parish. Because the great-est prevalence of antibodies against WNV was detectedin stray dogs (48% in St Tammany Parish and 33% inSlidell), an option for public health departments wouldbe testing a random selection of captured stray dogsevery week at animal control facilities. This informationcould be used to provide a warning regarding WNVtransmission to mammals in the region. In addition, thisinformation could possibly be used to predict humancases within the area as well as for monitoring the effec-tiveness of mosquito control measures.

a. Chow CC, Kruger J, Asamoa K, et al. West Nile fever amongpatients with unexplained febrile illness during an epidemic ofWest Nile meningoencephalitis—Slidell, Louisiana, 2002, inProceedings. 52nd Annu Epidemic Intelligence Service Conf2003;71.

b. Vicari AS, Zielinski-Gutierrez E, Montgomery SP, et al.Household-based seroepidemiological survey of West Nilevirus infection—Slidell, Louisiana, 2002 (abstr), in Proceedings.52nd Annu Epidemic Intelligence Service Conf 2003;4.

c. ArcView, version 8.2, ESRI, Redlands, Calif.d. SAS, version 8.02, SAS Institute Inc, Cary, NC.e. Palmisano C, St Tammany Parish Mosquito Abatement

Control, Slidell, La: Personal communication, 2002.

References1. CDC. Provisional surveillance summary of the West Nile

virus epidemic—United States, January–November 2002. Morb MortalWkly Rep 2002;51:1129–1133.

2. CDC. Final West Nile virus update for 2002, reported April15, 2003. Available at: www.cdc.gov/ncidod/dvbid/westnile/surv&controlCaseCount02.htm. Accessed Jun 2, 2004.

3. Komar N, Panella NA, Boyce E. Exposure of domestic mam-mals to West Nile Virus during an outbreak of human encephalitis,New York City, 1999. Emerg Infect Dis 2001;7:736–738.

4. Mostashari F, Bunning ML, Kitsutani PT, et al. EpidemicWest Nile encephalitis, New York, 1999: results of a household-based seroepidemiological survey. Lancet 2001;358:261–264.

5. Office of Public Health, Department of Health andHospitals, State of Louisiana. West Nile virus encephalitis outbreak,2002. Available at: www.oph.dhh.state.la.us/infectiousdisease/west-nileprog/docs/WNtab103102.pdf. Accessed Feb 9, 2003.

6. CDC. Available at: www.cdc.gov/od/oc/media/wncount.htm.Accessed Feb 9, 2003.

7. Weathermax D. West Nile virus. CDC EIS Bull 2002;Fall:3–9.8. US Census Bureau. US census 2000. Available at: www.cen-

sus.gov/main/www/cen2000.html. Accessed Nov 22, 2002.9. Petersen LR, Marfin AA. West Nile Virus: a primer for the

clinician. Ann Intern Med 2002;137:173–179.10. Geocode.com. Available at: www.geocode.com. Accessed

Mar 24, 2003.11. Labarthe N, Serrao ML, Melo YF, et al. Mosquito frequency and

feeding habits in an enzootic canine dirofilariasis area in Niteroi, State ofRio de Janeiro, Brazil. Mem Inst Oswaldo Cruz 1998;93:145–154.

12. Miller M. Feline dirofilariasis. Clin Tech Small Anim Pract1998;13:99–108.

13. Langevin SA, Bunning M, Davis B, et al. Experimental infec-tion of chickens as candidate sentinels for West Nile virus. Emerg InfectDis 2001;7:726–729.

14. Apperson CS, Hassan HK, Harrison BA, et al. Host feedingpatterns of established and potential mosquito vectors of West Nilevirus in the eastern United States. Vector Borne Zoonotic Dis 2004;4:71–82.

15. Austgen LE, Bowen RA, Bunning ML, et al. Experimentalinfection of cats and dogs with West Nile virus. Emerg Infect Dis2004;10:82–86.

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16. Blackburn NK, Reyers F, Berry WL, et al. Susceptibility ofdogs to West Nile virus: a survey and pathogenicity trial. J Comp Pathol1989;100:59–66.

17. van der Schalie WH, Gardner HS Jr, Bantle JA, et al. Animalsas sentinels of human health hazards of environmental chemicals.Environ Health Perspect 1999;107:309–315.

18. Backer LC, Grindem CB, Corbett WT, et al. Pet dogs as sentinelsfor environmental contamination. Sci Total Environ 2001;274:161–169.

19. Bukowski JA, Wartenberg D, Goldschmidt M. Environmentalcauses for sinonasal cancers in pet dogs, and their usefulness as sen-tinels of indoor cancer risk. J Toxicol Environ Health A 1998;54:579–591.

20. Bukowski JA, Wartenberg D. An alternative approach forinvestigating the carcinogenicity of indoor air pollution: pets as sen-tinels of environmental cancer risk. Environ Health Perspect 1997;105:1312–1319.

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Selected abstract for JAVMA readers from the American Journal of Veterinary Research

Objective—To determine the hemodynamic effects of lidocaine (administered IV to achieve 6 plasmaconcentrations) in isoflurane-anesthetized cats.Animals—6 cats.Procedure—Cats were anesthetized with isoflurane in oxygen (end-tidal isoflurane concentration set at1.25 times the predetermined individual minimum alveolar concentration). Lidocaine was administered IV toeach cat to achieve target pseudo–steady-state plasma concentrations of 0, 3, 5, 7, 9, and 11 µg/mL, andisoflurane concentration was reduced to an equipotent concentration. At each plasma lidocaine concentra-tion, cardiovascular and blood gas variables; PCV; and plasma total protein, lactate, lidocaine, andmonoethylglycinexylidide concentrations were measured in cats before and during noxious stimulation.Derived variables were calculated.Results—In isoflurane-anesthetized cats, heart rate, cardiac index, stroke index, right ventricularstroke work index, plasma total protein concentration, mixed-venous PO2 and hemoglobin oxygen satu-ration, arterial and mixed-venous bicarbonate concentrations, and oxygen delivery were significantlylower during lidocaine administration, compared with values determined without lidocaine administra-tion. Mean arterial pressure, central venous pressure, pulmonary artery pressure, systemic and pul-monary vascular resistance indices, PCV, arterial and mixed-venous hemoglobin concentrations, plasmalactate concentration, arterial oxygen concentration, and oxygen extraction ratio were significantlyhigher during administration of lidocaine, compared with values determined without lidocaine adminis-tration. Noxious stimulation did not significantly affect most variables.Conclusions and Clinical Relevance—In isoflurane-anesthetized cats, although IV administration oflidocaine significantly decreased inhalant requirements, it appeared to be associated with greater cardio-vascular depression than an equipotent dose of isoflurane alone. Administration of lidocaine to reduceisoflurane requirements is not recommended in cats. (Am J Vet Res 2005;66:661–668)

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April 2005

Assessment of the hemodynamic effects of lidocaine administered IV in isoflurane-anesthetized cats

Bruno H. Pypendop and Jan E. Ilkiw

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