Lyme disease in livestock

Lyme disease in livestock

Lyme disease in livestock

Previous authors: E HODZIC AND S W BARTHOLD

Current authors:
D M IMAI - Assistant, Clinical Health Sciences Professor, Comparative Pathology Laboratory, University of California, California, 95616, USA 
E HODZIC - Director of Core Facility, DVM, MSci, PhD, Davis School of Veterinary Medicine, University of California, One Shields Avenue, California, 95616, USA

Introduction

Lyme disease, or Lyme borreliosis, was first described in 1977 as a distinctive entity in a cluster of children from Lyme, Connecticut, USA. These children had symptoms resembling juvenile rheumatoid arthritis, a disease that does not cluster and is rare in children.107 Based upon similarities with recognized human clinical syndromes in Europe that were of unknown aetiology, but associated with the bite of Ixodes ricinus ticks, the causative agent was isolated from North American Ixodes scapularis ticks in 1981,20 and subsequently named Borrelia burgdorferi.53 Once the connection was made between vector, agent, and the human disease, Lyme disease has been diagnosed throughout the world, but its significance is greatest in North America and Europe.47, 89, 98, 100 Borrelia. burgdorferi has become an important public health problem and the most prevalent tick-borne disease in the United States.1, 64 It emerges across much of the northern hemisphere, causing considerable morbidity and in some cases mortality in humans, domestic animals, and occasionally wildlife.

The wide geographic distribution and the broad host range of both the vector and the bacterium provide ample opportunity for livestock species to be infected with B. burgdorferi. Most of what is known about Lyme disease, however, is based upon clinical studies in humans, and experimental studies in laboratory rodents. The amount of well-documented information on Lyme disease in livestock is limited.

Aetiology

Borrelia burgdorferi is a Gram-negative spiral or corkscrew shaped diderm bacterium, measuring 10 to 30 µm in length and 0,2 to 0,3 µm in diameter, with a lipoprotein-rich outer cell membrane and periplasmic flagella.53, 88, 114 For culture in vitro, this micro-aerophilic slow-growing organism requires a complex liquid medium, and an optimal temperature of 33 to 35 °C. 3

The genome of B. burgdorferi is small (~1.5 Mb) but complex, composed of 1 large, highly conserved linear chromosome and many small, highly variable linear and circular plasmids.24

Based on 16S ribosomal DNA gene sequences, the genus Borrelia belongs to the order Spirochaetales, family Spirochetaceae, but genomically unique and not closely related to any other bacteria, including the other spirochaetes. Other related genera include Spirochaeta, Cristispira, Treponema and Brachyspira (formerly Serpulina). It was first believed that B. burgdorferi was the only bacterium that could cause Lyme disease, but differences in morphology among isolates from diverse geographic locations suggested that additional spirochaetes may be involved in the aetiology.41

A major effort has been undertaken to analyse the phenotypic and genotypic diversity of B. burgdorferi isolates from around the world, using polymerase chain reaction (PCR) techniques that target 16S and 23S ribosomal DNA, flagellin, OspA, bdr genes, and intergenic spacers, as well as complete genome sequencing. It is now apparent that B. burgdorferi is genetically diverse, and is represented by more than 20 different genospecies grouped within the B. burgdorferi sensu lato (s.l.) complex. Borrelia. burgdorferi sensu stricto (s.s.) is present in the USA and Europe (but not in Eurasia and Asia); B. afzelii, B. garinii, B. valaisiana, B. spielmanii, and B. lusitaniae are present in Eurasia; B. japonica, B. turdae, and B. tanukii in Japan; and B. bissettii and B. andersoni in the USA.34, 51, 80, 89 The causative genospecies of Lyme disease in humans and livestock are B. burgdorferi s.s., B. afzelii, and B. garinii.  B. valaisiana has also been proposed as a causative agent of the human disease.59, 62, 116

Borrelia burgdorferi s.l. belongs to a guild of pathogens, including Ehrlichia and Babesia spp. and tick-borne encephalitis viruses, that are maintained within the same vector reservoir niches.112 Thus, co-infection with one or more of these agents can occur and may be responsible for ‘paraLyme disease’ syndromes. Since these other agents have a wide host range, they also infect livestock.

Epidemiology

Borrelia burgdorferi s.l. is geographically distributed in temperate regions of the northern hemispheres. These areas have the environmental conditions and reservoir hosts conducive to ixodid ticks. The range of B. burgdorferi s.l. was previously limited to northern Africa at its most southern extreme.2 Nevertheless, migratory birds, particularly seabirds, likely contributed to the expansion of its geographic distribution, with documentation of B. burgdorferi s.l. DNA in ixodid ticks or seropositivity in livestock, as far south as the Falkland Islands, Crozet Islands, and off-shore islands of New Zealand,76 and now, in Chile, Brazil, and Uruguay.4

Borrela burgdorferi and its vector ticks tend to be nonselective in their host range, and B. burgdorferi has been isolated from a wide variety of birds and mammals.2 Most hosts harbour subclinical infections. For example, in hyperendemic areas such as New York and Connecticut states in the USA, a high...

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