Canine Leptospirosis--Epidemiology Based on MAT Titers from Large Databases
ACVIM 2008
George E. Moore, DVM, MS, PhD, DACVPM, DACVIM
West Lafayette, IN, USA

Introduction

Leptospirosis has been identified as a re-emerging infectious diseases in human medicine, and veterinary literature also documents an increase in reported cases of canine leptospirosis by US veterinary teaching hospitals in the 1990s. Leptospirosis is caused by tightly coiled filamentous spirochetes of the genus Leptospira. Leptospira are aerobic organisms with a cytoplasmic membrane and cell wall, surrounded by an outer membrane that allows solute exchange between the periplasmic space and the environment. Both salt water and drying disrupt this envelope. These spirochetes prefer warm and neutral or slightly alkaline environments and can survive in fresh water or moist soils for months. Leptospira are unable to synthesize fatty acids and only reproduce within animal hosts. In spite of this, leptospirosis has been referred to as a "disease of the environment", as human cases are typically caused by environmental exposure to the organism. Most veterinary cases probably derive from environmental exposure too.

Sorting Through Serogroups, Serovars, Reservoirs, and Data Sources

The taxonomy of the organism is complex and evolving through a greater understanding of molecular genetics; currently 12 species are classified, with more than 250 different serovars. Pathogenic serovars of veterinary interest belong to the species L. interrogans or L. kirscheri. Historically, the serovars of greatest concern for canine patients, and for which bacterins were produced, were Canicola and Icterohaemorrhagiae--the reservoir hosts for which were the dog and rat, respectively. Other serovars, i.e., Pomona, Hardjo, and Grippotyphosa, were historically associated with large animal infections. In the last 30 years, as our canine patients were less frequently in contact with livestock or living in rural settings, our minimal concern for these latter serovars diminished further. Although cats can seroconvert following leptospiral infections1, clinical disease in cats appears to be rare.

From the mid-1970s to early 1990s, there were few published reports of canine leptospirosis in the US. This may have been due to reduced infections in reservoir hosts or due to the effectiveness of the bivalent (Canicola and Icterohaemorrhagiae) bacterin. Nevertheless of reason, no apparent resurgence of these 2 serovars appeared. Through the 1990s, case series reports of canine leptospirosis began to document canine infections caused by nonvaccinal serovars. Serovars Grippotyphosa, Pomona, and Autumnalis were reported to cause canine disease in various locations across the United States.2,3 These reports were generally based on cases seen at one, often a referral, hospital location.

A larger study was published in 2002 based upon a review of university veterinary teaching hospital cases of canine leptospirosis from 1970-98.4 Highest prevalence was found in university teaching hospitals in Ohio, New York, California, Iowa, Wisconsin, and Michigan. The sources of such data, albeit geographically and temporally dispersed, would have high reliability due to the rigors of diagnosis typically applied at university hospitals. This study addressed patient risk factors but did not include diagnosis by serovar. The largest study to date utilized a commercial diagnostic laboratory database to investigate microscopic agglutination test (MAT) results from 2002-2004.5 Approximately 25,000 test results were evaluated, but the clinical status of each animal was not known. The magnitude of titer response was documented for each submission, and prevalence was estimated based on percent of tests positive. The relative occurrence of different serovars was also evaluated, as well as trends over the 3-year period. Reporting of different serovars is important due to potentially different clinical presentations and the possibility of cross-reaction, even after vaccination.6,7

Some may be concerned that leptospirosis is over-diagnosed based on serology. Conversely, it is possible that leptospirosis is under-diagnosed. Published scientific reports document diagnosed cases but do not clarify whether appropriate testing is done in all suspect animals. Leptospirosis is responsive to ampicillin, which may be administered in many patients presenting with renal and/or hepatic disease. Prospective studies are needed to ensure that all these patients are tested for seroreactivity to leptospira, and convalescent samples (2-4 weeks after the onset of clinical signs) are often needed to demonstrate seroconversion. The prevalence of mild or subclinical infections is also unknown, but one study recently showed that in some locations exposure in dogs is common.8

Diagnosis, and thus studies based on diagnosis, is hindered by lack of a sensitive, specific, low-cost, rapid and widely available diagnostic test for leptospirosis. Most cases of leptospirosis are diagnosed by serology, and the reference method is the microscopic agglutination test (MAT). The MAT is difficult to standardize and requires live organisms for antigens. Despite these and other drawbacks, the MAT is still the diagnostic norm for most laboratories rather than culture!

Would PCR testing improve the validity of laboratory data? PCR has the potential to be used in diagnosing leptospirosis but its impact remains undetermined. PCR is not available at many laboratories; and controlled studies have not defined the correlation between PCR and MAT, using a true "gold standard" in a large number of cases. A limitation of PCR-based diagnosis is the inability of most PCR assays to identify the infecting serovar. While this is not significant for individual patient management, the serovar identify has important epidemiological and public health value.

References

1.  Andre-Fontaine G. Vet Microbiol 2006;117:19.

2.  Birnbaum N, et al. J Small Anim Pract 1998;39:231.

3.  Adin CA, et al. J Am Vet Med Assoc 2000;216:371.

4.  Ward MP, et al. J Am Vet Med Assoc 2002;220:53.

5.  Moore GE, et al. Emerg Infect Dis 2006;12:501.

6.  Goldstein RE, et al. J Vet Intern Med 2006;20:489.

7.  Barr SC, et al. Am J Vet Res 2005;66:1780.

8.  Stokes JE, et al. J Am Vet Med Assoc 2007;230:1657.

Speaker Information
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George Moore, DVM, MS, PhD, DACVPM, DACVIM
Purdue University
W. Lafayette, IN


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