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Leptospirosis in farmed deer in New Zealand: AreviewMA Ayanegui-Alcerreca a , PR Wilson a , CG Mackintosh b , JM Collins-Emerson a , C Heuera , AC Midwinter a & F Castillo-Alcala aa Institute of Veterinary, Animal and Biomedical Sciences , Massey University , PrivateBag 11222, Palmerston North, New Zealandb AgResearch Invermay , PO Box 50034, Mosgiel, New ZealandPublished online: 18 Feb 2011.

To cite this article: MA Ayanegui-Alcerreca , PR Wilson , CG Mackintosh , JM Collins-Emerson , C Heuer , AC Midwinter& F Castillo-Alcala (2007) Leptospirosis in farmed deer in New Zealand: A review, New Zealand Veterinary Journal, 55:3,102-108, DOI: 10.1080/00480169.2007.36750

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Review Article

Leptospirosis in farmed deer in New Zealand: A review

MA Ayanegui-Alcerreca*, PR Wilson*§, CG Mackintosh†, JM Collins-Emerson*, C Heuer*, AC Midwinter* and F Castillo-Alcala*

AbstractCurrent knowledge of leptospirosis in farmed deer in New Zea-land is reviewed. Over the past 25 years, leptospirosis has been reported to occur in individual cases as well as in herd outbreaks in farmed deer and in human cases linked to farmed deer. Sero-logical studies and evidence from bacterial culture suggest infec-tion is widespread. Mixing of young stock from several sources appears to be a signifi cant risk factor for outbreaks. The culture of Leptospira interrogans serovars Hardjobovis, Pomona and Copenhageni has been reported. Infection with serovar Hard-jobovis had the highest prevalence, either individually or mixed with serovar Pomona. Infection with serovar Copenhageni ap-pears uncommon and its pathogenicity in deer is unproven. Titres to serovars Australis, Ballum, Balcanica and Tarassovi have been reported. Deer appear to be maintenance hosts for serovar Hardjobovis, incidental or accidental hosts and prob-ably a maintenance population for serovar Pomona, since some infections persist for several months, and accidental hosts for serovar Copenhageni.

Serovar Pomona appears to produce clinical and probably sub-clinical disease, whereas serovar Hardjobovis appears to cause only subclinical disease, although the relative risk of disease causation has not been determined. Clinical disease is usually manifested by haemolysis, jaundice, renal lesions, haemoglobin-uria and often by sudden death. Renal lesions are commonly observed at slaughter and many are associated with leptospiral infections. Occupationally, slaughterhouse workers appear to be at greatest risk of contracting the disease from deer. Vaccination produces serological responses, but its effectiveness in protect-ing against disease, and prevention or reduction of shedding in urine, has not yet been confi rmed in deer. More robust knowl-edge of the epidemiology of leptospiral infections in deer, and the effectiveness of vaccines and vaccination regimes, is needed to assist the deer industry to develop a strategy to manage this disease.

KEY WORDS: Deer, farmed deer, New Zealand, leptospirosis, Leptospira, Pomona, Hardjobovis, Copenhageni, zoonosis, re-view

IntroductionLeptospirosis is a bacterial disease with worldwide distribution, caused by pathogenic spirochaetes belonging to the genus Lepto-spira (Sonrier et al 2000). It is a signifi cant disease of animals and humans. Leptospira spp are classifi ed into 17 genomospecies (23

serogroups), and seven are pathogenic and endemic to feral and domestic mammals (Faine et al 1999). All mammals can serve as maintenance hosts for one or more of the >250 known serovars of Leptospira (Plank and Dean 2000). There is an increasing ap-preciation of this disease and its zoonotic potential internationally (Faine et al 1999, Pp 7–9).

Serological evidence of a low prevalence in feral deer had been published prior to establishment of the deer farming industry (Daniel 1966, 1967), although two investigations later failed to detect serological evidence of infection in wild deer (Anonymous 1977, non-peer-reviewed; Hathaway et al 1981). The fi rst pub-lished report describing leptospiral disease in farmed red deer (Cervus elaphus) and wapiti (Cervus elaphus nelsoni) in New Zea-land was in 1980 (Anonymous 1980, non-peer-reviewed). Sub-sequently, there have been many outbreaks and individual cases of leptospirosis on deer farms, and infection is now recognised as being widespread (Ayanegui-Alcerreca et al 2004, non-peer-re-viewed; Ayanegui-Alcerreca 2006). Human cases associated with deer have been reported from deer slaughter premises (DSPs) (Bell 2005; Brown 2005; both non-peer-reviewed). Thus, leptospirosis is now a well-recognised clinical disease in farmed deer in New Zealand but there is limited knowledge of its prevalence, epide-miology, rate of incidence of clinical disease, subclinical effects, prevention and human health signifi cance (Wilson et al 1998). This paper reviews the literature on leptospirosis in farmed deer in New Zealand.

Leptospiral serovars present in New Zealand

Classifi cation of leptospires has been described by Faine et al (1999, Pp 57–66). The serovars isolated from animals in New Zealand are from the L. borgpetersenii and L. interrogans genomo-species. Serovars isolated from animals other than deer in New Zealand include Hardjobovis from cattle and sheep (Bahaman et al 1980, 1984; Mackintosh et al 1980b; Marshall et al 1982); Bal-lum from rats, mice and hedgehogs (Brockie 1977; Marshall and Manktelow 2002); Tarassovi from pigs and dogs (Ryan and Mar-shall 1976; Mackintosh et al 1980a); Balcanica from possums and cattle (Hathaway et al 1978; Mackintosh et al 1980c); Pomona from pigs, cattle, sheep and dogs (Te Punga and Bishop 1953; Mackintosh et al 1980a; Vermunt et al 1994; Bolt and Marshall 1995); and Copenhageni from rats (Brockie 1977). In New Zea-land, serovars Australis and Canicola have been reported only from humans (Midwinter and Fairley 1999, non-peer-reviewed). Serological evidence of serovars Hardjobovis, Pomona Copenha-geni, Tarassovi, Ballum, Balcanica and Australis, and cultural evi-dence for serovars Hardjobovis, Pomona, and Copenhageni, have been reported from deer in New Zealand (Wilson et al 1998), and reports are summarised in Tables 1 and 2.

* Institute of Veterinary, Animal and Biomedical Sciences, Massey University, Private Bag 11222, Palmerston North, New Zealand.

† AgResearch Invermay, PO Box 50034, Mosgiel, New Zealand.§ Author for correspondence. Email: p.r.wilson@massey.ac.nz DSP Deer slaughter premise

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Occurrence of leptospirosisClinical and research reports of leptospirosis in deer in New Zea-land are presented in Table 1, while a summary of quarterly Ani-mal Health Laboratory reports is presented in Table 2. The fi rst report of disease diagnosed as leptospirosis in farmed deer was in 1980 (Anonymous 1980). It was subsequently proposed that severe leptospiral disease was uncommon (Griffi n 1987) but no evidence was presented for that assertion. This was despite evi-dence of renal and hepatic lesions, suspected abortions, redwater, and positive serology in diagnostic laboratory reports (Table 2), and deer from which Leptospira spp had been isolated (Fairley et al 1984; Flint et al 1986). In non-peer-reviewed reports, lepto-

spirosis was described as “the most important disease of weaned deer in the central and northern North Island” after yersiniosis (Anonymous 1990), and that “a few outbreaks... are seen each year” (Anonymous 1991). Other reports also suggest that infec-tion is widespread amongst farmed deer (Flint et al 1988; Wilson et al 1998; Ayanegui-Alcerreca et al 2004; Ayanegui-Alcerreca 2006), and clinical disease and mortalities are common (Table 2). Observation of widespread infection is supported by anecdotal information from veterinary practitioners, and the observation of a large proportion of kidneys at DSPs containing lesions resem-bling those caused by leptospirosis, sometimes containing lepto-spires in histological sections (Wilson et al 1998).

Serological surveys show variation in the prevalence of various serovars. Flint et al (1988) sampled two deer herds in the North

Table 1. Summary of clinical and research reports of leptospirosis in deer in New Zealand.

No. of Serovar (MAT) Gross/ Origin and serovars micro.

species of deer Agea Region n tested Serovar and titre Prevalence (%) Culture lesions Type of study Reference

Wild Red Mixed-age NI (Kaingaroa) 109 8 PM 0.9 ND ND Serological survey Daniel (1966)

Wild Red, Fallow, Mixed-age NI and SI 279 8 0 ND ND Serological survey Daniel (1967)Virginian, Sika

Farmed Red 3–4 Months NI (Rotorua) 12/70 5 PM 1:100–1:12,800 66.6 Yes Clinical report Fairley et al (1984)

PM + HJ 8.3 PM, HJ

HJ 1:100 8.3

Farmed Red Weaners SI (Southland) 16/>100 ND PM 1:24–1:768 62.5 PM, HJ Yes Clinical report Fairley (1984)b

Wild ND SI (Nelson) 24 ND PM 16.6 ND ND Serological survey Inglis (1984)

PM + ICc 16.6 ND

ICc 8.3 ND

Farmed Red Adult hinds NI (Manawatu) 6 2 HJ 1:24–1:384 33 ND ND Vaccine trial Wilson and Schollum (1984)

Farmed ND ND SI (Nelson) 6/26 ND HJ 23 HJ ND Serological survey Flint (1985)

Farmed ND Yearlings SI (Nelson) 120d ND HJ, CP 32 ND ND Serological survey Williams (1985)b

Farmed Red Fawns, weaners SI (Southland) 4e 7 ND 62 PM (5/6) Yes Clinical report Fairley et al (1986)

16f PM, HJ 12 HJ (1/6)

Farmed Red Adult hinds SI (Nelson) 27 5 HJ 1:32–1:128 21.4 HJ (8/27), CP (3/27) ND Serological surveyg Flint et al (1986)

Farmed Red, Mixed-age NI and SI 360 7 HJ 1:10–1:10,240 39 ND ND Serological survey Flint et al (1988)Fallow (5 farms)

PM 1:10–1:320 14 ND

CP 1:10–1:320 43 ND

AS 1:10–1:20 13 ND

BL 1:10–1:80 47 ND

BT 1:10–1:160 53 ND

TS 1:10–1:80 26 ND

Farmed Red, Mixed-age NI and SI 309 tested, ND HJ, PM, CP PM Yes Retrospective study Wilson and McGhie (1993)Wapiti X Red, Fallow 345 dead

Farmed Red, Mixed-age NI (lower) 675 4–7 HJ 1:24–1:1,536 73.6 PM (1/10) Yes Serological surveyg Wilson et al (1998)Wapiti X Red (53 farms) PM 1:24–1:1,536 41.5 HJ (3/10)

CP 1:24–1:1,536 11.3 Not typed

TS 15.1 (6/10)

Farmed Red Adult hinds NI and SI 417 3 HJ >1:100 9.8 ND ND Serum bank survey Reichel et al (1999)

PM >1:100 1.4 ND

CP >1:100 0.2 ND

Farmed Red Adult hinds, SI (Southland) 75 3 PM 1:24–1:3,072 26 ND Yes Clinical report Dean et al (2005) weaners HJ 1:24–1:48 1.3 ND

a Weaner = 3–12 monthsb Non-peer-reviewedc lcterohaemorrhagiae (lC); now known as Copenhageni (CP)d 10 propertiese Clinicalf In-contactg Plus cultureMAT = microscopic agglutination test; micro. = microscopic; NI = North Island; SI = South Island; ND = not done or not described; PM = Pomona; HJ = Hardjo(bovis); AS = Australis;

BL = Ballum; BT = Bratislava: TS = Tarassovi

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Island and three in the South Island, and reported overall preva-lences of serovars Australis (13%), Ballum (47%), Bratislava (53%), Copenhageni (43%), Hardjobovis (39%) Pomona (14%) and Tarassovi (26%). However, in that study all positive results above a titre of 1:10 were included, in contrast to other reports in which titres of 1:96 and 1:100 were used as the positive thresh-old; titres above 1:80 were observed only for serovar Copenhageni (n=1), Bratislava (n=1), Pomona (n=2) and Hardjobovis (n=38). In another study, Wilson et al (1998) sampled 601 red and red x wapiti stags, mainly 1 and 2 years of age, and 21 adult hinds from 53 farms (10 or 12 deer per farm) in the lower North Is-land. Using a positive titre threshold of 1:96, serovar Hardjobovis was present on 74%, Pomona on 42%, Copenhageni on 11% and Tarassovi on 15% of farms. It is likely that positive titres to Tarassovi resulted from cross-reactivity, although that serovar was also reported by Flint et al (1988). The within-slaughter-line prevalence ranged from 8 to 100% of 12 samples between farms for serovars Pomona and Hardjobovis, and from 8 to 92% for serovar Copenhageni. Reichel et al (1999, non-peer-reviewed) suggested that the prevalence of leptospirosis in the national herd may not be as high as suggested by Flint et al (1988) and Wilson et al (1998), based on a 9.8% and 1.4% seroprevalence of titres �1:100 to serovars Hardjobovis and Pomona, respectively, in a randomly selected sub-sample of 417 sera from 1,150 samples, comprising two samples from each of 575 farms. However, the sampling strategy used in that study reduced the chance of detect-ing infection at the herd level compared with those used by Flint et al (1988) and Wilson et al (1998). An analysis for serologi-cal prevalence from samples in a serum bank from 14 herds in the lower North Island sampled in 1992–1993 (n=730 samples)

showed 60% prevalence for serovar Hardjobovis (Ayanegui-Alcer-reca 2006). That author also reported a nationwide survey of 110 farms, on which Hardjobovis alone was present on 61%, Pomona alone on 3.6%, and both serovars together on 16.4% of farms, giving an overall farm prevalence of 82%. No differences were found between regions.

Sex and age of deer, and possibly serological interpretation, may contribute to variation in prevalence estimates between studies. It is likely that leptospirosis is under-diagnosed or mis-diagnosed on deer farms because many diseases and mortalities are not sub-ject to veterinary investigation (Wilson 2004; Castillo-Alcala et al 2007).

Host-serovar relationships for deerThe defi nitions of host-serovar relationships applicable to lepto-spirosis have been discussed by Hathaway (1981), and are sum-marised in Table 3. It would appear from the lack of bacterial cul-ture evidence and low seroprevalences reported for serovars Bal-canica, Ballum, Tarassovi and Australis (Flint et al 1988; Wilson et al 1998) that deer are only accidental hosts to these serovars, if indeed titres represented infection rather than cross-reactivity.

Serovar Copenhageni has been cultured from the urine of deer from one property in Nelson (Flint et al 1986), and there is sero-logical evidence of causation of acute disease in weaners on a farm in Hawkes Bay (IH Walker1, pers. comm.). These limited reports, coupled with its low prevalence in serological surveys (Flint et al

Table 2. Data summarised from quarterly veterinary diagnostic laboratory reports in various issues of Surveillance (Ministry of Agriculture and Forestry and its predecessors, Wellington, New Zealand) describing cases of leptospirosis in deer since fi rst reported in 1980.

Year No. of Location/ Signs/ Histology Mortality(Issue) cases Age/sex source lesions Serologya rate

1980 (3) 1 Adult hind NR/farm Haemolysis, redwater PM (PM, HJ, BL, TS in Nephrosis 1/42 5/12 tested on same farm)

1989 (3) 6 NR NI (5), SI (1)/farm Redwater PM NR NR

1990 (2) Several NR NI and central NI/farm Jaundice, anaemia NR Nephrosis 10%

1990 (3) 1 Yearlings NR Focal renal scarring PM NR 55/1,000

1991 (1) 2 Yearlings NI/farm Sudden death PM 1:200–1:12,800 Chronic interstitial nephritis 55/3,000

Weaners NI/farm NR PM

1991 (4) 1 Weaners NR/farm Jaundice, redwater, sudden death PM >1:800 Nephrosis, hepatic degeneration 10/60

1993 (1) 1 Yearlings NI/s’house WSK (27/30) NR Chronic interstitial nephritis

1993 (2) 1 Yearlings S’house WSK HJ 1:25,600; PM 1:800 NR

1993 (3) Several Yearlings SI/s’house WSK HJ, PM Leptospires in tubules

Weaners Farm Jaundice, redwater NR NR 4/350

1996 (2) 1 Yearling hinds NR/farm Diagnosed pregnant, did not calve HJ 1:50–1:400 NR

1997 (3) 1 Fawns NR/ farm Watery blood, sudden death PM Nephrosis, + leptospires in tubules 5/1,174

1998 (1) 2 NR NR/s’house WSK Not done Leptospires in tubules

1999 (4) 1 NR NR/s’house NR NR Nephritis, + leptospires in tubules

2000 (2) 2 Weaners NR/farm Sudden death, redwater NR Nephrosis 7/500; NR

2000 (3) Several Weaners NI/farm Sudden death, redwater PM Leptospires in tubules 25/176; NR

2003 (4) 1 Yearling hinds SI/s’house Enlarged spleen, dark kidneys BL Intravascular haemolysis

2004 (3) 3 Weaners NR Diffusely jaundiced PM >1:1,600 NR 3

SI/farm Depression, redwater PM >1:800 Chronic interstitial nephritis 20/450

Sudden death NR Leptospires in tubules 16/110

2005 (1) 1 Yearlings SI/s’house WSK PM Chronic interstitial nephritis

a Highest titre is given where availableNR = not reported; NI = North Island; SI = South Island; PM = Pomona; HJ = Hardjo; BL = Ballum; TS = Tarassovi; s’house = slaughterhouse; WSK = white-spotted kidneys; weaner = 3–12 months

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1988; Wilson et al 1998; Reichel et al 1999; Ayanegui-Alcerreca 2006), suggest that deer are an accidental host to serovar Copen-hageni.

Serological and culture evidence indicate that deer are common hosts to serovar Pomona (Table 1). The only report of persistent shedding of leptospires in deer (Fairley et al 1984) showed this serovar was shed for at least 8 months in one animal, and at least 2.5–5 months in other deer in the same herd. Those authors stated, however, that: “As might have been expected, vaccination did not prevent leptospiuria in animals which were already in-fected”, inferring but not confi rming that the deer from which urine was collected had been vaccinated. The period of shedding may have been longer in non-vaccinated deer. Thus, the proposi-tion by Fairley et al (1984) that deer may not be maintenance hosts for serovar Pomona lacks defi nitive evidence. Those authors presented evidence of transmission of serovar Pomona from cattle to deer, whereas Dean et al (2005, non-peer-reviewed) demon-strated transmission by newly introduced young deer. Serological evidence of serovar Pomona infection in longitudinal studies (Ay-anegui-Alcerreca 2006) suggested that farmed deer could at least be a maintenance population, if not an individual reservoir host.

The substantial evidence of widespread infection with serovar Hardjobovis (Tables 1 and 2), coupled with evidence of persistent infection within herds over 21 months (Ayanegui-Alcerreca et al 2004), provides strong support for the hypothesis that farmed deer are maintenance (reservoir) hosts and a maintenance popula-tion for this serovar.

Relationship between serovar and disease

Relationships between host status and expression of disease are summarised in Table 4. Most cases of clinical leptospirosis in deer have been associated with serological and/or bacterial cul-ture evidence of infection with serovar Pomona (Tables 1 and 2). However, while it appears that serovar Hardjobovis is not com-monly associated with clinical disease, it is not possible to rule

out that this serovar can, on occasion, cause clinical disease. Wil-son and McGhie (1993, non-peer-reviewed) reported that serovar Pomona was associated, serologically, with 90% of diagnostic laboratory submissions of suspected leptospirosis in deer, while serovar Hardjobovis was associated with 10% of cases submitted. Results from only two bacterial cultures were reported from 70 submissions, although few were requested or attempted, and both yielded serovar Pomona.

It is diffi cult to draw conclusions about causation of disease based on laboratory reports of serology alone. Many apparently healthy deer have been seropositive to a number of serovars (Wilson et al 1998). A recent survey of veterinary practitioners indicated that a small number had observed clinical signs and outbreaks associated with serovar Hardjobovis (Ayanegui-Alcerreca 2006), although it is common, in a clinical context, for assumptions about causation to be drawn based on serological evidence alone. One outbreak of redwater and jaundice in a group of weaner deer was associated with serological evidence of serovar Copenhageni, in the absence of titres to serovars Pomona or Hardjobovis (IH Walker, pers. comm.). Of 18 laboratory submissions for investigation of sud-den death, 16 yielded positive titres for serovar Pomona, whereas only two yielded Hardjobovis titres (Howell 1991, non-peer-re-viewed; Wilson and McGhie 1993).

In contrast to clinical disease, the appearance of renal lesions resembling those caused by leptospirosis are frequently diagnosed at DSPs. Wilson et al (1998) reported a higher prevalence of gross renal lesions from herds with serological evidence of infection, with both serovars Pomona and Hardjobovis, than from seroneg-ative herds. They produced histological evidence that suggested that leptospiral infection was likely to be the main cause of the lesions. However, only 3/10 kidneys sampled randomly, that were culture-positive, had histological lesions, suggesting that infection may not produce gross or histological lesions in all cases.

Epidemiology of infection in deerLittle was known about the epidemiology of leptospiral infections in farmed deer, but this has been the subject of recent research

1 IH Walker, Hawkes Bay Veterinary Services, Waipukurau, New Zealand

Table 3. Epidemiological defi nitions of leptospiral host status (Hathaway 1981).

Host status Epidemiological defi nition

Maintenance or reservoir host An animal that is capable of acting as a natural source of infection for its own species

Incidental or accidental host An animal that gets infected with a serovar hosted by another animal species, but in which the serovar does not persist

Maintenance population Population of a species of animals that acts as a continuous reservoir of infection in a specifi c ecosystem

Alternative maintenance population In general, defi ned by the reservoir animal, but if not present other animal species can serve as a maintenance population

Table 4. Relationship between leptospiral host category and clinical and/or subclinical expression of disease (Heath and Johnson 1994).

Maintenance (reservoir) host Incidental (accidental) host

High susceptibility to infection, but low pathogenicity to the host Relatively low susceptibility, and high pathogenicity for the host

Endemic transmission within species (high titre prevalence) Sporadic transmission within the host species (low titre prevalence)

Tendency to cause more chronic than acute disease Tendency to cause acute and severe rather than chronic disease (high titre in(low titre in positive-culture animals, mild pathology) culture-positive animals, acute and dramatic pathology)

Long kidney phase (long-term shedders) Short kidney phase (short-term shedders)

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(Ayanegui-Alcerreca 2006). It appears that serovar Hardjobovis is endemic in the majority of herds (Flint et al 1988; Wilson et al 1998; Ayanegui-Alcerreca 2006). The majority of reports of clinical disease associated with leptospirosis in deer are from those in their fi rst year of life (Table 1). One instance of death of a 4-day-old calf with lesions typical of leptospirosis and the pres-ence of spirochaetes in renal tubules was reported by Fairley et al (1986). In a review of laboratory submissions for leptospirosis in deer from 1987 to 1992, Wilson and McGhie (1993) reported that 77% of reported mortalities occurred in deer <12 months of age. The majority of deaths occurred during autumn, correspond-ing to a period when animals are commonly moved from farm to farm and mixed with other animals. Fairley et al (1986) pro-vided evidence of infection of young deer with serovar Pomona transmitted from cattle recently introduced to the property, and Dean et al (2005) demonstrated introduction of infection with serovar Pomona to a property by newly introduced weaner deer. It is likely that infection with serovar Copenhageni was by associa-tion with rats (Flint et al 1986).

Data on samples from a serum bank of 10 weaners, yearlings and adult deer from 14 farms observed over a 2-year period suggested an age difference in the prevalence of serovar Hardjobovis, being 7–31% in weaners at 3–4 months of age, increasing to 50% at 15 months of age, and 71% in adults. This demonstrated that where infection was endemic it occurred primarily in the fi rst year of life (Ayanegui-Alcerreca 2006).

Clinical signs and gross pathologyWith the exception of two cases reported by Wilson and Mc-Ghie (1993) in which serovar Hardjobovis was implicated, and one case of sudden death with jaundice and redwater associated with serovar Copenhageni (IH Walker, pers. comm.), all clini-cal cases in deer confi rmed as leptospirosis have been associated with serovar Pomona. A recent survey of veterinary practitioners (Ayanegui-Alcerreca 2006) confi rmed that few cases were attrib-uted to serovar Hardjobovis. Dean et al (2005) provide the only report of confi rmed leptospirosis in live deer, describing lethargy and red urine observed on the fl oor of the deer yard when treat-ing the mob in the face of an outbreak, a phenomenon observed by others (PR Wilson, unpubl. obs.). Photosensitisation, corneal opacity and jaundice were reported by Bertram (1986, non-peer-reviewed) in a young red deer with a titre to Pomona of 1:200 and histological lesions suggestive of leptospirosis, but in the absence of leptospires. The principal presenting sign of leptospirosis in case reports (Fairley et al 1984, 1986; Dean et al 2005) and in submis-sions to veterinary diagnostic laboratories was sudden death with or without gross pathology (Wilson and McGhie 1993; 40% of investigations), and redwater (Table 2). Poor reproductive per-formance was investigated in 4% and abortion in 2% of labo-ratory submissions but leptospirosis could not be confi rmed as the cause. Other signs prompting investigation for leptospirosis included jaundice, low weight gain, anaemia and fading.

The only detailed descriptions of necropsy fi ndings typical of lep-tospirosis in deer are by Fairley et al (1984, 1986), and Dean et al (2005). Jaundice, enlarged kidneys that were sometimes pale with radial bands of tissue, swollen liver with rounded borders, red urine and anaemia have been described, but were not observed in all cases. Dean et al (2005) described the absence of gross lesions in two deer which died suddenly from leptospirosis. Of 33 labo-ratory reports reviewed by Wilson and McGhie (1993), jaundice was described in 73% of cases, and redwater in 33%, renal lesions in 33%, hepatic lesions in 6% and decreased fat reserves in 6%.

Gross renal lesions, ranging from small to large numbers of red and/or white spots, red and/or white mottling, and fi brotic scar-ring were frequently observed at slaughter in apparently clinically healthy animals (Wilson et al 1998). Some kidneys contained severe lesions, suggesting active pathology, and leptospires were isolated from some of those kidneys. A higher frequency of kid-neys with lesions was observed in deer from seropositive than se-ronegative lines. The extent of lesions in kidneys from some herds and individuals suggest reduction of growth rate may occur in young animals.

HistopathologyThe main histopathological lesions considered to be specifi c to leptospirosis were in the kidney (Table 2), and lesions in some other organs, particularly the liver (Wilson and McGhie 1993), were usually typical of acute septicaemic disease. Those authors described the frequency of lesions in 34 cases submitted to di-agnostic laboratories for histopathology, including haemoglobin-uric nephrosis (26%), nephrosis (18%), visible leptospires (41%), haemoglobin casts (15%), interstitial nephritis (24%), nephritis (6%), and other lesions (21%).

Fairley et al (1984, 1986) provided the most comprehensive his-topathological description of leptospirosis from clinical cases. Hepatic lesions included centrilobular necrosis, hepatocellular vacuolation and sometimes retention of bile, erythrophagocytosis and haemosiderin pigmentation. Renal lesions included cortical segmentation with radial bands of infl ammatory tissue, infi ltra-tion of mononuclear cells, interstitial infl ammation and oedema, nodules of lymphocytes, and fi brosis. Tubules were often dilated and contained casts and hyaline droplet degeneration. Glomeru-lar lesions including peri-glomerular fi brosis, and proliferation of Bowman’s capsule and glomerular atrophy, were seen in areas with interstitial pathology. Leptospires were often seen in tubules when stained with the Warthin-Starry (silver) stain.

Wilson et al (1998) described histopathological lesions related to various categories of gross lesions observed in kidneys at a DSP as summarised above. Lesions in kidneys with white spots consisted of extensive focal interstitial infi ltration of lymphocytes and plas-ma cells in the cortex, and accumulation of leucocytes in tubules, typical of leptospirosis in other species. Leptospires were observed in the tubules of kidneys from 3/10 culture-positive kidneys.

Treatment and vaccinationTreatment of clinical cases of leptospirosis in deer in New Zea-land has been reported by Howell (1991), and Dean et al (2005). Anecdotal reports from veterinarians suggest use of streptomycin or oxytetracycline, as recommended by Mackintosh (1993, non-peer-reviewed), is common. These antibiotics are commonly used for prophylactic treatment of in-contact deer when outbreaks are experienced or exposure is imminent, such as described by Dean et al (2005). Vaccination has been reported, either in the face of an outbreak (Fairley et al 1984; Dean et al 2005), often with con-current prophylactic antibiotic treatment, or where management of risk either to humans or animals is desired (Howell 1991).

In a small study of serological responses to vaccination, few re-sponses were reported in six deer to a sensitising dose, while all but one produced a serological response following a booster dose

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4 weeks later (Wilson and Schollum 1984). Initial responses were similar to those observed in cattle, but titres fell to undetectable levels after 3–5 months whereas titres reported in cattle gener-ally persisted for 12 months. Serological responses were signifi -cantly greater in deer that were seropositive before vaccination. Annual vaccination of hinds to provide passive immunity to their calves prior to weaning, followed by vaccination of the weaners in autumn, has been recommended in herds at risk (Mackintosh 1993).

Few studies of protection against either natural or artifi cial chal-lenge, or the effectiveness of various vaccination regimes, have been reported in deer despite there being three leptospiral vac-cines registered for use in this species in New Zealand. Fairley et al (1984) demonstrated that vaccination did not stop shedding of leptospires from animals already infected with serovar Pomona. Recent research (Ayanegui-Alcerreca 2006) has shown good im-munological responses to vaccination with Leptavoid 3 (Scher-ing-Plough Coopers Animal Health New Zealand, Upper Hutt, NZ), transfer of colostral antibody and lack of interference with serological responses by colostrum-derived antibody. That author also described 44% reduction in urine shedding, determined by dark-fi eld microscopy, and 55% reduction in kidney leptospiral culture in vaccinated deer grazing with non-vaccinated deer.

There may be differences in effi cacy between different vaccines. Despite the need for further validation of effi cacy in whole-herd vaccination programmes, these observations prompted Wilson et al (2005, non-peer-reviewed) to suggest that vaccination will likely play an important role in any industry strategy for manag-ing the risk of leptospirosis to animals and humans within the deer industry in New Zealand.

Effects of leptospirosis on productionAyanegui-Alcerreca (2006) reported weight gain of deer to ap-proximately 12 months of age in a herd infected with both Hard-jobovis and Pomona. The mean liveweight of animals with evi-dence of infection since weaning at 3 months was 3.7 kg lower than that for deer with no evidence of infection (p=0.037). On the same property, 94/97 (97%) pregnant hinds that had been vaccinated prior to the rut reared a calf to weaning, whereas 82/93 (88%) hinds not vaccinated reared calves to weaning (p=0.04). These data suggest that production losses due to leptospirosis may occur on some farms. This observation needs to be replicated, since only one herd was studied.

Human cases of leptospirosis associated with contact with deer

Leptospirosis is hyper-endemic in New Zealand and it is a fre-quent cause of disease in farmers and meat workers (Crump et al 2001); the zoonotic potential of leptospirosis from deer has been reviewed by Wilson and Davies (2003). Observations of shed-ding in urine in clinical cases and from in-contact deer (Fairley et al 1984, 1986), and from an infected herd without clinical dis-ease (Flint et al 1986), along with isolates from kidneys of appar-ently clinical normal deer at a DSP (Wilson et al 1998), suggest a risk to humans associated with both live and dead deer. There are unpublished reports of farmers, veterinarians and slaughter-house workers contracting leptospirosis. Bell (2005) described acute febrile disease and non-specifi c clinical signs in humans,

including fever, malaise, myalgia, meningitis and conjunctivitis, as well as anorexia, abdominal pain, nausea and vomiting caused by leptospirosis. Other clinical forms included ‘fl u’, jaundice, haemorrhage, and enlargement of the spleen and liver, and the most severe form was hepatic and renal failure or massive pulmo-nary haemorrhage (Weil Syndrome), which is sometimes fatal. Bell (2005) reported eight cases of disease in workers at DSPs in Southland in 2002–2003, and the rate of risk was 5/38 workers in the second year of study. Brown (2005) reported two severe cases requiring hospitalisation in workers from a DSP in Otago, and a cost of approximately $5,000/case to the DSP. To date, no fatalities have been reported.

ConclusionsConvincing serological, bacteriological and pathological evidence of infections of deer in New Zealand with Leptospira serovars Hardjobovis, Pomona, and Copenhageni has been reported. Most serological surveys suggest infection is widespread on deer farms in this country, but the rate of incidence of clinical disease is not able to be determined from existing data. It seems that in New Zealand, deer are a maintenance host for serovar Hardjobovis, and there is widespread infection but little, if any, disease. At the individual level, deer appear to be incidental or accidental hosts to serovar Pomona, which sometimes causes severe disease; at the population level, deer could act as an alternative maintenance population. Clinical leptospirosis, both as individual cases and outbreaks, has been frequently reported in laboratory reports rela-tive to other diseases in deer, and mainly associated with serovar Pomona. Clinical presentation and epidemiology appear similar to that in cattle in New Zealand. The role of deer in human cas-es of leptospirosis is becoming more apparent. More research is needed to defi ne vaccine effi cacy and control strategies for lepto-spirosis in farmed deer in New Zealand.

AcknowledgementsThis review was made possible by funding from DEEResearch Limited and Schering-Plough Coopers Animal Health New Zea-land, and scholarship funding from CONACyT, an agency spon-sored by the Government of México, for a PhD project conducted by MA Ayanegui-Alcerreca.

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Submitted 19 January 2006

Accepted for publication 17 January 2007

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