BORRELIA BURGDORFERI: THE CAUSATIVE AGENT OF LYME DISEASE

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Borrelia burgdorferi is a Gram-negative, highly motile, and microaerophilic spiral-shaped or helical bacterium in the genus Borrelia and family Spirochaetaceae. B. burgdorferi is a spirochaete because of its helical or spiral shape. It is the causative agent of the tick-borne infection, known as Lyme disease in humans. The phrase “Lyme” is from a town known as Lyme in Connecticut, USAwhere the disease was first discovered in the 1970’s. Lyme disease is a zoonotic infection that occurs worldwide especially in the United States of America where it was first discovered. Bacteria species in the genus Borrelia causes both human and animal diseases generally known as borreliosis. B. burgdorferi is transmitted to humans through the bite of a tick (Ixodes scapularis), and the bacterium is reserved in wild rodents (e.g., deer), tick, sheep, horses, mice and other rodents. It is noteworthy that B. burgdorferi unlike other bacterial species (known to have a circular chromosome) has a linear chromosome. B. burgdorferi has a small genome, and its genetic make-up has been completely sequenced as well. Lyme disease is rare in regions where deer are limited or scarce because the insect vector of the bacterium i.e., ticks in the genus Ixodes requires deer for its survival and mating processes.

PATHOGENESIS OF BORRELIA BURGDORFERI INFECTION

Human infection with B. burgdorferi occurs following a blood meal by an infected arthropod, usually the deer tick (I. scapularis) which obtains the bacterium after taking a blood meal from animal reservoirs of the pathogen. Animal reservoirs of B. burgdorferi include wild rodents, mice and horses. B. burgdorferi is spread from the bite site (i.e., the skin) through blood to other organs of the body including the joints, heart and the central nervous system (CNS). Without early treatment, B. burgdorferi infection in humans progresses into three (stages) with characteristic clinical symptoms. The initial stage of Lyme disease (stage I) occurs in the first month of a tick bite, and it is usually characterized by the appearance of a lesion (erythema migrans) on the skin of the tick-bitten human host. Usually, the skin lesion (which may remain unnoticed for some time) appears following the exit of B. burgdorferi from the bite site. Stage I is accompanied by flu-like symptoms such as malaise, severe fatigue, headache, chills and fever. The skin lesion is red in colour, circular, painless and expanding, spreading or diffusing in nature. Erythema migrans (Figure 1) is a characteristic circular rash that appears on the skin of tick infected individuals.

There is no organ involvement in stage I Lyme disease but lymphatic vessels could as well be affected leading to a local lymphadenopathy. In stage II, the heart and CNS becomes involved as the pathogenic bacterium becomes systemic and spreads via the bloodstream. There are usually cardiac and neurological disorders, meningitis, palsy and arthritis or joint pains especially at the knee and elbow regions. Stage II Lyme disease usually occurs weeks or months later after stage I of the disease process, and it marks the dissemination stage of B. burgdorferi infection in humans. Stage III of Lyme disease usually occurs in about 75 % of untreated individuals, and it is characterized by a continued and persistent or chronic arthritis. It occurs months to years later after the stage I and stage II of the disease process. CNS involvement in stage III is rare but causes chronic encephalomyelitis and seizures when it ensues.      

Figure 1. Photograph showing erythema migrans (arrows) on the skin of a person with Lyme disease. The migrating nature of the inflammation on the skin of a person suffering from Lyme disease is the reason for the name “erythema migrans”. Erythema migrans is a characteristic circular rash that appears on the skin of tick infected individuals. CDC.

LABORATORY DIAGNOSIS OF BORRELIA BURGDORFERI INFECTION

B. burgdorferi is a slow-growing bacterium. Thus, the culture of the organism is not usually carried out. Blood and cerebrospinal fluid (CSF) are obtained from tick-infested individuals for serological analysis and other molecular detection techniques (e.g., PCR). ELISA, western blotting and enzyme immunoassay (EIA) techniques are also available for the laboratory diagnosis of B. burgdorferi infection in humans. However, most of these tests are not too specific or sensitive due to the presence of some cross-reacting antibodies against other spirochaete species in the normal flora of the host. Immunity against B. burgdorferi infection in humans is slow and antibody-mediated.

TREATMENT OF BORRELIA BURGDORFERI INFECTION

Lyme disease in humans is treated with doxycycline, amoxicillin and macrolides (e.g., azithromycin) in the first stage of the infection. Cephalosporin (e.g., ceftriaxone) is used in the second stage of the disease. CNS invasion by B. burgdorferi as well as cardiac system involvement is treated with intravenous ceftriaxone, a cephalosporin that crosses the blood-brain-barrier (BBB). A combination of cephalosporin and any of the above mentioned antibiotics are usually used in the third stage of Lyme disease.  

PREVENTION AND CONTROL OF BORRELIA BURGDORFERI INFECTION

Human encroachment into wooden areas, forest areas and other man’s deforestation and reforestation activities coupled with increase in the natural reservoirs of the bacterium (e.g., tick, mice and rodents) have led to an increase in tick-borne diseases as a result of human contact with infected ticks. Humans should avoid tick bites by wearing long clothes when in the woods or around forest areas. Insect repellants or insecticides should be used by households in wooden or forest areas as this has been proven to be effective in warding-off ticks and reducing their populations too. People who visit forests or similar areas should properly check their body for tick attachment and remove same immediately. Generally, avoidance of exposure to ticks is critical to preventing B. burgdorferi infection in human population since Lyme disease cannot be spread from one human to another.

Further reading

Brooks G.F., Butel J.S and Morse S.A (2004). Medical Microbiology, 23rd edition. McGraw Hill Publishers. USA.

Gilligan P.H, Shapiro D.S and Miller M.B (2014). Cases in Medical Microbiology and Infectious Diseases. Third edition. American Society of Microbiology Press, USA.

Madigan M.T., Martinko J.M., Dunlap P.V and Clark D.P (2009). Brock Biology of Microorganisms, 12th edition. Pearson Benjamin Cummings Inc, USA.

Mahon C. R, Lehman D.C and Manuselis G (2011). Textbook of Diagnostic Microbiology. Fourth edition. Saunders Publishers, USA.

Patrick R. Murray, Ellen Jo Baron, James H. Jorgensen, Marie Louise Landry, Michael A. Pfaller (2007). Manual of Clinical Microbiology, 9th ed.: American Society for Microbiology.

Wilson B. A, Salyers A.A, Whitt D.D and Winkler M.E (2011). Bacterial Pathogenesis: A molecular Approach. Third edition. American Society of Microbiology Press, USA.

Woods GL and Washington JA (1995). The Clinician and the Microbiology Laboratory. Mandell GL, Bennett JE, Dolin R (eds): Principles and Practice of Infectious Diseases. 4th ed. Churchill Livingstone, New York.

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