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Research in Veterinary Science xxx (2006) xxx–xxx

A health evaluation in a colony of captive collared peccaries(Tayassu tajacu) in the eastern Amazon

Pedro Mayor a,*, Yvonnick Le Pendu b, Diva Anelie Guimaraes c,Jurupytan Viana da Silva c, Hilma Lucia Tavares c, Montse Tello a, Washington Pereira d,

Manel Lopez-Bejar a, Ferran Jori e

a Department of Animal Health and Anatomy, Faculty of Veterinary, Campus Universitario, Autonomous University of Barcelona,

08913 Bellaterra, Barcelona, Spainb Universidade Estadual de Santa Cruz, Departamento de Ciencias Biologicas Km. 16, Rodovia Ilheus/Itabuna, Salobrinho, Ilheus, BA 45662-000, Brazil

c Laboratorio de Reproducao Animal, Centro de Ciencias Biologicas, Universidade Federal do Para, Rua Augusto Correa no 1,

Campus Universitario do Guama, Belem, PA 66-075-900, Brazild Laboratorio de Patologia Animal, Instituto de Saude e Producao Animal, Universidade Federal Rural da Amazonia, Department of Pathology,

Faculty of Veterinary, Av. Presidente Tancredo Neves no 2501, Bairro Terra Firme, Caixa Postal 917, Belem, PA 66077-530, Brazile CIRAD EMVT. TA 30/E, Epidemiology Unit, Campus International de Baillarguet, Montpellier 34398, Cedex 5, France

Accepted 7 December 2005

Abstract

This study pretends to determine baseline data on the health and mortality of a colony of captive collared peccaries in the EasternAmazon (Belem, State of Para, Brazil) during a 65-months survey. Thirty-nine out of 166 animals (23.5%) died and were examined post-mortem. Monthly mortality averaged 1.2%. The highest mortality rate was observed in newborns (74.4%). Abandonment by the motherand aggression were responsible for 24.1% and 13.8% of the total newborn deaths, respectively. Most frequent causes of non-neonataldeath were food poisoning (50.0%) due to an episode of accidental bitter cassava leaves ingestion and traumatism due to aggressionsbetween animals (10.0%). Results from serology for different infectious diseases showed that 4.9% (2/41) collared peccaries had antibod-ies against Brucella spp. and 9.8% (4/41) animals had antibodies to two different Leptospira spp. serovars, butembo and autumnalis. Thisis the first survey of morbidity and mortality in captive collared peccaries in the Amazon region.� 2006 Published by Elsevier Ltd.

Keywords: Mortality; Pathology; Health; Collared peccary; Tayassu tajacu; Wildlife production

1. Introduction

The collared peccary (Tayassu tajacu) is a widespreadmammal in the American continent and represents animportant source of meat, appearing as the most huntedspecies in the Amazon region (Bodmer et al., 1997). Forthat reason, it has been considered an interesting species

0034-5288/$ - see front matter � 2006 Published by Elsevier Ltd.

doi:10.1016/j.rvsc.2005.12.003

* Corresponding author. Tel.: +34 3 581 2482; fax: +34 3 581 2006.E-mail addresses: pedrogines.mayor@uab.es, mayorpedro@hotmail.

com (P. Mayor).

to be included in captive breeding programs (Bodmeret al., 1997; Sowls, 1997). Few information has been pub-lished so far on the potential and requirements for breedingthis species in captivity. Nevertheless, this situation ischanging and more information is being produced on thebiology and management of this species in captivity(Nogueira Filho and Nogueira, 2004; Mayor et al., 2005).Reliable knowledge on the pathology of the collared pec-cary is scarce and most of the existing studies were con-ducted in free-ranging populations from semi-arid regionsin Texas and Arizona (Samuel and Low, 1970; Sowls,1997; Noon et al., 2003). Baseline data on health aspects

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of captive collared peccary are necessary for the promisingdevelopment of the commercial production of the species inthe Amazon basin and other areas in Latin America. Nev-ertheless, the causes of morbidity and mortality in collaredpeccary and the role of this species as a potential source ofpathogens for other wild and domestic animals or men islargely unknown.

2. Material and methods

2.1. Study site

The animals belong to an experimental breeding farmlocated in EMBRAPA-Amazonia Oriental research center,located in the Eastern Amazon region (Belem, State ofPara, Brazil; 01�24 0 S; 48�20 0 W). The climate is typicallyequatorial with an average annual temperature of 26 �C,and an average relative humidity of 78%. Between 2000and 2004, annual rainfall oscillated between 2370 mmand 3273 mm.

2.2. Animals

The experimental breeding stock was founded with 12animals captured in the wild and introduced at the end of1998 (n = 4) and at the beginning of 1999 (n = 8). Twentyanimals from a commercial breeding farm were also intro-duced in July 2000 in a separate large paddock. In March2004, the experimental farm comprised 127 individuals.During the experimental period, from November 1998 toMarch 2004, the total number of different animals presentin the farm was 166 individuals and stock grew regularlyfrom July of 2000 (n = 45) to March of 2004 (n = 127).

2.3. Management

Collared peccaries were enclosed in two kinds of pad-dock: 12 small paddocks with an area comprised between21 and 36 m2, and a single large floor paddock. In March2004, animal density in small paddocks was 0.24 collaredpeccaries/m2, ranging from 3 to 14 animals, which resultedin an average occupied space of 4.1 m2 per animal (range:2.6–7.2 m2). The single 450 m2 floor paddock hosted 18collared peccaries, in a surface of 25 m2 per animal. Ani-mals were maintained outdoors. Reproductive groupshad an initial proportion of 1:2–3 (male:females). Whenpossible, only one male was present per reproductivegroup. No reproductive or weaning program for pigletswas implemented during the study period. Consequently,piglets were always in direct contact with their relatives.The females were fed with 400 g of commercial pig pelletswith a calorific supply of 2500 kcal and a protein level of14% per kg of food, supplemented by local fruits. Waterwas always available.

During first year of study, coprological analyses wereconducted in the all introduced animals from the experi-mental farm. Since Strongyloides sp and Ascaris suis were

identified, a preventive dose of Ivermectin 1% (Ivomec�)at a dosage of 0.3 ml per 10 kg animal was administratedvia intramuscular every 6 months.

2.4. Monitoring of reproduction performances

Captive population was monitored from November1998 to March 2004. Reproductive parameters of femaleswere monitored regularly during that period as an addi-tional indicator of herd health. Recorded data were yearlydistribution of births, age of first parturition, prolificacy(number of piglets per birth), number of natural weanedpiglets per parturition, inter-birth interval (time comprisedbetween two consecutive births), number of births perfemale and year, and production of piglets per femaleand year.

2.5. Monitoring of mortality

Death occurrences were monitored during 65 monthsbetween November 1998 and March 2004. Every animalfound dead during the study period was collected and itsage, sex, weight, date of death and clinical history wererecorded. Animals were classified as newborns, juveniles,sub-adults and adults according to age (Lochmiller et al.,1987; NAHMS, 2000; Dubost et al., 2003). Since naturalweaning was conducted in the experimental farm, animalswith less than four weeks of age were considered newborns.Animals between four weeks and six months of age wereconsidered juveniles. Sub-adults were those animalsbetween six months and one year old, and we consideredadults those animals from one year old onwards.

Mortality was calculated on the basis of true mortalityrate and risk of mortality, according to Martin et al.(1987). Population at risk was the total number of animalsalive during a determined period. True mortality rate wascalculated as the ratio of the sum of deaths related to thepopulation at risk on a monthly and annual basis. Mortal-ity after the arrival of animals at the farm was calculated asa risk rate by dividing the number of deaths by the numberof animals that entered.

2.6. Monitoring of pathology

Pathological events were monitored through post-mor-tem examinations. Carcases of collared peccaries wereexamined within a few hours after death detection. The car-cases were examined in accordance to a standard protocol(Jori et al., 2001).

On the base of clinical history and macroscopic findings,the suspected causes of death were determined. Cases witha non-determined diagnosis were classified as ‘unknown’.

2.7. Disease survey

In December 2001 and in November 2003, blood sam-ples were collected from the cephalic or saphenous veins

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in 41 (77.4% of the total population) and 35 collared pec-caries (32.4% of the total population), respectively. Theserum was removed and frozen at �20 �C until analyses.All sampled collared peccaries appeared to be in good bodycondition and without any detectable clinical abnormali-ties. Haemolytic samples were discharged and not includedin the study.

In December 2001, serological and immunological testsfor infectious diseases included brucellosis, leptospirosisand tuberculosis at the Laboratorio de Reproducao Ani-mal-CCBof theUniversidade Federal do Para. InDecember2003, serology for infectious diseases included pseudorabies,swine influenza virus, porcine circovirus type 2, porcine par-vovirus, porcine respiratory and reproductive syndrome,salmonellosis and swine erysipelas at the Veterinary Labora-tory of Infectious Diseases of the Department of AnimalHealth andAnatomy of the AutonomousUniversity of Bar-celona (Spain). Serologic survey of foot-and-mouth diseasewas performed at the Official Laboratory of the AgricultureMinistry in the State of Para (Brazil) in December 2003.

The slow agglutination test (SAT) and the rapid agglu-tination test (RAT), the complement fixation test (CFT)described by Alton et al. (1975), the salt-2-mercaptoethanoltube agglutination test (SMTA) and the ELISA test (Bru-cella-Ab I-ELISA�; Svanovir, Uppsala, Sweden) were usedaccording to the kit instructions to detect antibodiesagainst Brucella spp. (Lord and Lord, 1991).

The microscopic agglutination test (MAT) was per-formed for 22 leptospiral serovars, including autumnalis,butembo, castellonis, bataviae, canicola, whitcombi, cynopteri,grippotyphosa, hebdomadis, copenhageni, icterohaemorrha-

giae, javanica, panama, pomona, pyrogenes, hardjo, wolffi,shermane, tarassovi, andamana, patoce and sensot. Positivesera were considered to the end point of 50% agglutination,and microagglutination titters of P1:100 were consideredevidence of previous exposure.

0

20

40

60

80

100

120

140

Population risk

Popu

latio

n ri

sk (

n)

1-11

-98

1-2-

99

1-5-

991-

8-99

1-11

-99

1-2-

001-

5-00

1-8-

00

1-11

-00

1-2-

01

1-5-

01

Fig. 1. Monthly mortality rates and total population at risk in a colony of capti1998 and March 2004.

For the tuberculosis survey, all collared peccaries wereinjected intradermical with 1 ml M. bovis PPD providedby the Instituto de Tecnologia do Parana (Tecpar, Curit-iba, Brazil) in the eyelid using a 21-gauge needle, asdescribed by Monaghan et al. (1994).

An enzyme linked immunosorbent assay (ELISA) wasused to determine the antibody activity against swineinfluenza virus (Civtest� Suis Influenza; Hipra, Girona,Spain), porcine parvovirus (Ingezim� PPV; Ingenasa,Madrid, Spain), porcine respiratory and reproductive syn-drome (Herdchek� PRRS 2XR; Idexx, Westbrook,Maine, USA), pseudorabies (Herdchek� Anti-ADV GPI;Idexx, Westbrook, Maine, USA), salmonella (SalmonellaCovalent Mix ELISA�; Svanovir, Uppsala, Sweden) andswine erysipelas (Ingezim� Mal Rojo; Ingenasa, Madrid,Spain). All tests were performed according to the kitinstructions.

The complement fixation test (CFT) and the ELISAdescribed by Sakaki et al. (1978) and Ferris and Dawson(1988), respectively, were used to determine the antibodyactivity against foot-and-mouth disease.

An immunoperoxidase monolayer assay technique(IPMA) to detect antibodies to porcine circovirus type 2was performed as described by Balasch et al. (1999).

3. Results

3.1. Reproduction performances

Between September 1999 and March 2004, the experi-mental farm passed from 12 to 127 collared peccaries(Fig. 1). During this period, 136 piglets were born and106 individuals were naturally weaned. Parturitionsoccurred all year-around. A list of the reproductive perfor-mances of the herd can be found in Table 1.

0

2

4

6

8

10

12

14

16

% Monthly mortality

Mon

thly

mor

talit

y (%

)

1-8-

01

1-11

-01

1-2-

02

1-5-

021-

8-02

1-11

-02

1-2-

03

1-5-

031-

8-03

1-11

-03

1-2-

04

ve collared peccaries in the experimental farm of Belem between November

Table 1Reproductive parameters of the captive collared peccary in the experi-mental farm from Belem (State of Para, Brazil)

n Value

Prolificacy (piglets per parturition) 34 1.87 ± 0.42Natural weaned piglets per parturition 34 1.32 ± 0.71Age at first parturition (in days) 10 595.2 ± 239.9Inter-birth interval (in days) 43 179.2 ± 55.6Litters per female and yeara 37 1.32 ± 1.34Newborns per female and yearb 37 2.42 ± 2.64

a Only females more than 500 days old and periods in mixed groups areconsidered.b Only newborns born alive are considered.

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3.2. Mortality during the study

Between November 1998 and December 2003, 39 col-lared peccaries died. The cumulated mortality of the totalpopulation was 23.5% (39/166). Mortality rate in animalsfrom the single large floor paddock was higher than thatfrom small paddocks (Table 2).

From November 1998 to December 1999, coincidingwith the introduction of 12 founders, no obit was recorded.The highest annual mortality rates were observed in 2001with 19.7%, respectively. In 2000, 2002 and 2003, annualmortality rates were 13.7%, 10.1% and 13.5%, respectively.

Table 2Death number and mortality rates in captive collared peccaries in accordancebetween November 1998 and March 2004

Large floor paddock Small

Newbornsa Juvenile, subadultand adultsa

Newb

Population at risk 30 50 106Digestive disorder – (0%) 5 (10.0%) 3 (2.8%Abandonment 6 (20.0%) – (0%) 1 (0.9%Traumatism due to aggressions 2 (6.7%) – (0%) 2 (1.9%Accidental traumatism 1 (3.3%) – (0%) – (0%)Unknown 3 (10.0%) 2 (4.0%) 11 (10Total 12 (40.0%) 7 (14%) 17 (16

a Mortality rates with respect to the population at risk of the age category.b Percentages are proportion of different primary causes of death with respe

0

5

10

15

20

25

30

0 1 2 3 4 5 6

%

Days

Fig. 2. Evolution of newborn mortality (in percentages) during the first two w1998 and March 2004.

Fig. 1 shows true monthly mortality related to the totalpopulation at risk in the experimental farm betweenNovember 1998 and March 2004. True monthly mortalityaveraged 1.2 ± 2.6% during the whole period of monitor-ing. It averaged 1.37% in 2000; 2.49% in 2001; 2.46% in2002, and 1.13% in 2003. Significant differences wereobserved in mortality rates among age groups. Mortalityrates according to age class were, in decreasing order: new-borns (74.4%), juveniles and sub-adults (17.9%) and adults(7.7%).

From the total death incidence, female occurrence wasalso higher than male death incidence (58.1% vs. 41.9%,respectively). Female mortality related to the total offemales present in the farm was slightly higher than thatof males (30.5% vs. 25%, respectively).

3.3. Causes of mortality in newborns

Mortality rate in newborns was 74.4% (29/39) of thetotal deaths and cumulated mortality was 21.3% (29/136)of the total newborn population at risk. Neonatal mortalitywas higher in newborns from the single large floor paddockthan that from small paddocks (40.0% vs. 16.0%, respec-tively). As shown in Fig. 2, most newborn mortality tookplace during the first two days of life (48.3%; 14/29).

to age category and paddock structure in the experimental farm of Belem

paddocks Whole experimental farm

ornsa Juvenile, subadultand adultsa

Newbornsb Juvenile, subadultand adultsb

Totaldeaths

110 136 160) – (0%) – (0%) 5 (50.0%) 8) – (0%) 7 (24.1%) – (0%) 7) 1 (0.9%) 4 (13.8%) 1 (10.0%) 5

– (0%) 1 (3.4%) – (0%) 1.4%) 2 (1.8%) 14 (48.3%) 4 (40.0%) 18.0%) 3 (2.7%) 29 (100%) 10 (100%) 39

ct to the total deaths of each age category.

7 8 9 10 11 12 13 14 of life

eeks of life (n = 30) in the experimental farm of Belem between November

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Table 2 shows the results from the 29 newborn necropsies.Most identified causes of death were abandonment by themother (24.1%) and traumatism due to aggressions (13.8%).

3.3.1. Altered maternal behaviour

The clinical history associated with abandonment wascharacterized by weakness. The necropsy revealed cachec-tic body condition without any specific lesion.

3.3.2. Traumatism due to aggressions

The newborn death due to aggressions from adults wascharacterized by evident incisive lesions.

3.3.3. Digestive processesAmong the digestive causes of death, a continuous epi-

sode of diarrheas resulted in the death of three newbornsin a period of 6 days, representing 10.3% of the total neo-natal deaths. No digestive process causing the death ofnewborns from the single large floor paddock was detected.The clinical history was characterized by the presence ofwatery diarrheas and apathy that derived in extreme weak-ness, and death of the animal. It was not possible to deter-mine the cause of this episode of diarrheas.

3.3.4. Accidental traumatism

One case of death was included in this category becausethe animal became trapped in different facilities of the pad-dock. Macroscopically, accidental traumatism was charac-terized by internal haemorrhages and fractures.

3.3.5. Unknown

Fourteen cases (48.3%) of neonatal death were includedin this category either because lesions were not found, or thecarcases were in an advanced state of decomposition orbecause only some parts of the carcass could be recovered.Three cases were classified as ‘Unknown’ because it was notpossible to confirm if the observed traumatisms were thecause of death or if the other individuals had bitten the car-cass. Other six cases were classified as ‘Unknown’ because itwas impossible to determine if they were stillborn or if theydied within the first hours after parturition.

Although not included in Table 1, the occurrence of anindividual stillborn was observed (0.7% from the total pop-ulation at risk).

3.4. Causes of mortality in juveniles, sub-adults and adults

The results of the necropsies are presented in Table 2.Mortality rate in this category was 25.5% (10/39) of thetotal deaths and cumulated mortality was 6.2% (10/160)of the total juvenile, sub-adult and adult population at risk.The only identified causes of death were food poisoningand traumatism.

3.4.1. Digestive disorders

Digestive disorders appeared as the most common causeof death (50.0%). The main cause was an accidental lonely

episode of food poisoning which affected five individuals.These animals consumed bitter cassava (Manihot esculenta)leaves without previous treatment. No dead animal pre-sented apparent lesions in the digestive tract or neurologi-cal clinical sign.

3.4.2. Traumatism

Traumatism was the other cause of death and affectedonly one individual. It occurred as a result of aggression,and was recognisable at necropsy by the presence of pierc-ing wounds and haematoma. Nevertheless, aggressionswere also observed in living animals and, in most cases,they did not result in wounds.

3.4.3. Unknown

Four cases (40.0%) of deaths were included in this cate-gory. In one case, it was impossible to determine if theobserved traumatisms were due to aggressions of otherindividuals or because the animal became trapped in differ-ent facilities in the paddock.

3.5. Serologic survey

Among the 41 sampled captive collared peccaries in2001, two (4.9%) had antibodies to Brucella spp., and four(9.8%) animals had antibodies to two different Leptospiraspp. serovars, butembo and autumnalis at titers of 1:200and 1:100, respectively. Nevertheless, none of these collaredpeccaries showed evidence of disease. The two animals sero-positive to Brucella spp. were culled for sanitary reasons.

None of the sampled captive collared peccaries showedantibodies against pseudorabies, porcine influenza virus,foot-and-mouth disease, porcine circovirus type 2, porcineparvovirus, porcine respiratory and reproductive syn-drome, salmonellosis, swine erysipelas or tuberculosis.

4. Discussion

The establishment of captive breeding systems for localwildlife begins to arouse a growing interest in the Amazonregion. The development of the captive wildlife industrymight represent an increased opportunity for disease trans-mission as a result of increased animal density and the con-centration and movement of animals from differentregions. However, little information exists on the patholo-gies that could affect the mortality of captive neotropicalwildlife species in their local environment. In the case ofcollared peccaries, most existing information consists ondata from farms in semi-arid areas in Texas (Samuel andLow, 1970; Sowls, 1997). It is possible that climatic andecosystem conditions determine the prevalence of particu-lar pathologies in this species. Therefore, we find necessaryto report the results of the main causes of mortality andhealth events observed in an experimental farm from theEastern Amazon region.

This farm is a representative example of peccary produc-tion since reproductive performances are considerably

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good for a species in a recent process of domestication. Theaverage reproductive production of 2.4 piglets per femaleand year suggests that collared peccary raised in captivitypresents interesting reproductive parameters for the zoo-technical development of this species in the Amazonregion.

Cumulated mortality rate observed in our study was23.5%. Mortality rates in adult individuals were consider-ably higher than that observed in the domestic pig(NAHMS, 2000) and wild boar (Nixdorf and Barber,2001). As a favourite hunted species, one would expect thatcollared peccaries under production would appear as ani-mals more susceptible to stress, when found in proximityof men, one of its main predators. This is the case for otherprey species of wildlife kept in captivity during a domesti-cation process (Jori et al., 2001). However, no death casesdue to stress caused by humans were recorded during thefirst years of this farm establishment. In that sense, collaredpeccaries demonstrate a great adaptation capacity to theirnew environmental conditions.

Data show that true monthly mortality rates presented aslightly increase from September 2000 onwards. In this per-iod, taking into account one particular mortality peakcaused by accidental food poisoning, monthly mortalitycould be considered as homogenously distributed duringthe experimental period.

Neonates had the highest observed mortality rates (74%from total deaths and 21% from newborn population atrisk). In our study, neonatal death in the single large-floorpaddock was higher than that in the small paddocks andmost neonatal deaths took place during the first two daysof life. Most common identified causes of neonatal deathwere abandonment by the mother and traumatism.

The most important infectious outbreak was a continu-ous episode of diarrheas in newborns indirectly caused bymalfunction in the drainage system in some paddocks.During the rainy season, stagnant water provides an idealbackground for the development of pathogens. Neverthe-less, because of the lack of histologic examination it wasnot possible to determine the infectious character of thisprocess.

The most important pathological cause of death in juve-nile, subadult and adult individuals was food poisoning.This digestive disorder took place in only one episodeand affected five individuals in the single large floor pad-dock which consumed leaves of bitter cassava (Manihotesculenta), containing high amounts of cyanogene gluco-side (McMahon et al., 1995). This toxin can cause neuro-logical signs such as paralysis and in some cases canresult in the death of the animal (Ngudi et al., 2003). Thisepisode, considered accidental, was caused by a mishan-dling of the food and therefore has poor casuistic value.

In spite of being the second most important cause ofdeath, traumatisms due to aggressions between animalsonly affected one individual. Le Pendu et al. (2005)reported that in the captive collared peccary aggressiveinteractions represent only 13% of the total interactions.

Furthermore, Venturieri (2002) did not record significantdifferences in terms of frequency of agonistic behaviourrelated to the animal density. In that sense, findings inour study shows a very low prevalence in deaths causedby traumatism, compared to other prey species of wildlifebred in captivity for production purposes (Jori et al., 2001).

Taking into account the occurrence of the accidentalepisode of food poisoning, non-neonatal collared peccariespresented a very low mortality rate with only five individ-ual deaths during the 65 months of our survey, probablydue to the high rusticity degree of the species (Sowls,1997). This fact confirms that, contrary to other highlyselected domestic animals, high resistance to local patho-gens might be one of the advantages of breeding wildlifespecies such as the collared peccary in their own environ-ment (Sowls, 1997; Jori et al., 2001).

In the wild, previous serologic surveys demonstrated theprevalence of exposure of collared peccary to selectedpathogens (Loan and Storm, 1968; Crandell et al., 1986;Hoon et al., 2003). In the Amazon region, the status ofthe collared peccary in regard to infectious diseases ispoorly known. In the Brazilian Atlantic Forest, free-rang-ing collared peccary populations living in close contactwith human settlements and domestic animals presentedhigh antibody titers against leptospirosis and brucellosis(Nava and Cullen, 2003).

In our study, the negative seroprevalence to variousinfectious pathogens reflects no recent exposure to thoseagents. It is worth to highlight that levels of specificityand sensitivity of those tests in collared peccaries are notknown and therefore, those results should be taken withprecaution. Nevertheless, among the total sampled popula-tion, 2.5% (2/41) had antibodies against Brucella spp. and4.9% (4/41) had antibodies to two different Leptospira

spp. serovars, butembo and autumnalis. Brucella suis type1 is known to readily affect wild swine producing abortionand infertility (Fowler, 1996) and has been previouslyreported in free-ranging collared peccaries in Venezuela(Lord and Lord, 1991). In our study, low antibody titersobtained suggests that some of the individuals might havebeen in contact with Brucella spp., in the past, since anti-bodies against this pathogen can last for several years inthe collared peccary (Lord and Lord, 1991). Nevertheless,further analysis such as bacteriological isolation from sero-positive animals would be necessary to confirm the circula-tion of Brucella suis strains in our surveyed colony.

Leptospirosis is presumed to occur sporadically in manyspecies of wild mammals from the Amazon forest (Bhartiet al., 2003). In the collared peccary, previous reportsshowed a prevalence of 23% of antibody titers in free-rang-ing herds of Arizona (Corn et al., 1987) and a prevalence of95% in a captive colony inMexico (Acoltzi et al., 1990). Themajority of Leptospira infections within stable host parasiterelationships occur without clinical disease (Leighton andKuijken, 2001). In farm animals, transplacental infectioncan result in infertility, abortion, and infected neonates.Unfortunately, no microbiological isolation was attempted

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in our study and the link with high neonatal mortalityremains unknown. Nevertheless, as in the case of Brucella,confirmation of the circulation of those pathogens in thecolony, should be accompanied by simultaneous isolationand identification of the suspected bacteria. In the absenceof such identification, serological results are only a qualita-tive index of exposure to some form of Leptospira spp. andBrucella spp. bacteria. Epidemiological investigations suchas monitoring of neonatal mortality and serial serologicalsurveys could help to confirm possible correlations betweensymptoms and the circulation of infective agents within thecaptive population of collared peccaries. Both diseases areof global zoonotic concern. In the case of leptospirosis,L. interrogans serovar autumnalis is considered of clinicalimportance for humans, and the human seroprevalence ofleptospirosis in the Amazon basin is surprisingly high(Bharti et al., 2003). Therefore, collared peccary keepersand persons exposed to the same common source for lepto-spira should maximize hygiene precautions in order tominimize the probability of ingestion of the organism(Leighton and Kuijken, 2001).

5. Conclusions

Our study documents mortality in captive collared pec-cary on the basis of macroscopic examination and somelaboratory testing. Unfortunately, gross examination isoften insufficient to lead to a diagnosis of the cause ofdeath. Without complete histological examination, conclu-sions regarding the cause of death might be incomplete.However, it is useful to report those cases, since, to ourknowledge, this is the first reported health data of collaredpeccary in captivity in the Amazon region. Serologic sur-veys and post-mortem examinations can be useful to buildup baseline data for the health assessment and for the well-development of collared peccary captive breeding systemsin the tropics, but they should be completed when possiblewith complementary diagnostic procedures such as bacteri-ology or histopathology. Our survey indicates a low exis-tence of pathological agents as primary cause ofmortality and a high mortality rate in newborns in the cap-tive collared peccary. Analytical studies should be neces-sary in order to determine the possible risk factors forthe occurrence and maintenance of these diseases in thecollared peccary. These results suggest that most com-monly studied pathogens appeared in very low levels orwere inexistent in this colony. However, efforts should bemade to produce more data from a larger number of farmsand individuals in order to build up a more complete base-line database on the health of this species under productionand to monitor its possible role as a reservoir or vector ofdiseases of sanitary and economic concern.

Acknowledgements

We thank the experimental station EMBRAPA-CPA-TU in Belem for supplying the experimental animals.

Equally we thank the collaboration of the Federal Univer-sity of Para-U.F.P.A. for the data collection, and the Offi-cial Laboratory of the Agriculture Ministry in the State ofPara for the foot-and-mouth disease laboratorial analysis.We also thank the European Union (Research for theDevelopment, INCO-DEV; Fith Framework Programme;contract no: ICA4-CT-2001-10045) and the Spanish Minis-try of Science and Technology (MCYT; AGL2001-4961-AND) for supporting the project. We acknowledge Dr.Francois Roger for kindly reviewing the manuscript.

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