Borrelia afzelii

Classification

Higher order taxa:

Kingdom: Bacteria, Phylum: Spirochaetes, Class: Spriochaetes, Order: Spirochaetales, Family: Spirochaetaceae, Genus: Borrelia

Species

Borrelia burgdorferi, Borrelia lonestari, Borrelia recurrentis

Description and Significance

Borrelia afzelli is considered a new species of the Genus Borrelia and considered homologous to Borrelia burgdorferi with regard to phenotypic, genetic, and immunological characteristics. Diseases linked to this species of Borrelia are Lyme disease and Acrodermatitis chronica atrophicans (ACA) found, almost prevanlently, in Europe. Better understanding of the structure and function of this pathogen will create better methods of treatment to people with the diseases it causes.

Genome Structure

The genome sequencing of this particular strain is still underway as it is still a very new strain. However, all previous species of Borrelia have had linear chromosomes, ranging in sizes from 900-920kb pairs having circular and linear plasmids. Also, it is thought that the strain B. afzelii has recently derived from B. burgdorferi due to its lack of genetic variance. The genome of the bacterium Borrelia burgdorferi has a linear chromosome of 910,725 base pairs and at least 17 linear and circular plasmids with a combined size of more than 533,000 base pairs.

Cell Structure and Metabolism

Borrelia spirochetes are 5 to 25 µm long and 0.2 to 0.5 µm wide. The phenotype of the species afzelli include being, a motile, nonsporulating, spirally-shaped, aerobic, pathogen. Also, it is a gram negative bacterium and is generally transmitted through ticks. The bacterium has very specific nutritional needs and lives by regulating the lipoproteins within the host.

Ecology

Borrelia resides in the digestive tract of the tick or flea. The tick or flea usually inherits the bacteria by the usually infected, white-footed mouse. Once the tick has inherited the bacteria it is the host and can now be the transmitter of the disease LB. Since the tick lives by sucking the blood of its victim, the bacteria is transmitted through saliva by a bite of its victim.

Pathology

The most prevalent arthropod-borne infection in temperate climate zones around the world caused by Borrelia spirochetes is Human Lyme borreliosis (LB). LB is attained mainly by the transmition of Borrelia in the saliva of the bite of a tick or flea. In order for the bite to be infectious, the tick first must contain the bacteria within the lumen of its stomach. Being spirally-shaped, allows it to penetrate deep into its hosts avoiding recognition of an immune response. B. afzelii itself causes a distinct skin infection known as acrodermatitis chronica atrophicans (ACA). ACA is seen in the late stage of LB and can be diagnosed as, progressive, fibrosing skin process due to continuing infection of B. afzelii. It is followed by an inflammatory stage with bluish red discoloration and cutaneous swelling, often seen with recurring events even a year after its first notice. The early stages of LB can be noticed by a bulls-eye like marking on the surface of the skin, most notibly on the extremities.

References

Can it be Lyme Disease?---HealthandAge

eMedicine - Acrodermatitis Chronica Atrophicans: Article by Bozena Chodynicka, MD.

Genomic Sequence of a Lyme Disease spirochaete, Borrelia burgdorferi.

Jason Farlow, Danielle Postic, Kimothy L. Smith, Zack Jay, Guy Baranton, and Paul Keim Department of Biological Sciences, Northern Arizona University, Flagstaff, Arizona 86011-5640, Institut Pasteur, Paris, France Received 12 February 2002/ Returned for modification 31 March 2002/ Accepted 2 September 2002

Journal of Clinical Microbiology, December 2002, p. 4612-4618, Vol. 40, No. 12

ScienceDirect - FEMS Microbiology Letters: Homogeneity of Borrelia japonica and heterogeneity of Borrelia afzelii and ‘Borrelia tanukii' isolated in Japan, determined from ospC gene sequences.

The Lyme Disease Guide: Tick Life Cycle

Toshiyuki Masuzawa*, Tetsuro Komikado, Kazuhide Kaneda, Takako Fukui, Katsuji Sawaki and Yasutake Yanagihara Department of Microbiology, School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Shizuoka, Shizuoka 422, Japan Received 15 April 1997; revised 21 May 1997; accepted 28 May 1997. Available online 7 November 1997.