Borreliosis (Lyme-like disease) is the fastest growing tick borne infection in the world.
What’s in a name?
Lyme disease is a controversial name and a very misunderstood disease. Technically the name Lyme disease refers to infection with Borrelia burgdorferi sensu stricto bacteria, common in the East Coast of USA. In Europe and in Russia it is called Lyme borreliosis and caused by the Borrelia burgdorferi sensu lato group of which the American Borrelia is a member. Relapsing fever Borrelia has a global distribution (including our neighbours Indonesia, Thailand, Japan and India and the West coast of USA).
In Australia we have Lyme-like illness the causative agent has not yet been isolated, similar to Brazil where they have named the Brazilian Lyme-like disease, Baggio- Yoshinari syndrome.
The causative agent has not been observed as a spirochete but only a round form. All illness caused by a Borrelia species should be called borreliosis, which is a complex infection which can have delayed onset and broad symptomology. Borrelia affects multiple body systems and is pleomorphic, that is it can change its form from spirochaete (spiral shaped) to round bodies and cysts. Untreated it can have high morbidity and mortality.
In Australia we have Lyme-like illness. The causative agent has not yet been isolated.
Borrelia can be transmitted by a tick bite and potentially by any blood sucking insect can transmit Borrelia. See Ticks in Australia. In humans Lyme borreliosis is caused by at least three different strains of the Borrelia bacteria. In the USA, the predominant strain is Borrelia burgdorferi sensu stricto, while in Europe it is B. garinii and B. afzelii. Other European strains include B. valarisiana, B. lusitanae and in Asia B. japonica. Relapsing fever borrelia include B. parkeri, B.hermsii, B.miyomotoi (Genospecies table). In addition there is another class of Borrelia that has hybrid characteristics of B. burgdorferi sensu lato and relapsing Borrelia named reptile-associated Borrelia. This class of Borrelia has not been associated with disease because it has not been identified in humans. Currently we don’t know which Borrelia causes Australian and Brazilian Lyme-like illness. Research into this area will deliver the answer. Donations to the Karl McManus Foundation will help to deliver the answers sooner.
Although Lyme disease has been named after the town Lyme in Connecticut, where this disease was first identified in 1975, borreliosis as an infectious disease was identified in Europe back in the early 1920’s. The diversity of borreliosis symptoms – skin problems, arthritis, neurological, cardiac, ophthalmological – were already characterised. Some European examples include Bannwarth’s syndrome for neurological symptoms, chronic lymphocytic meningitis, poly meningoradiculitis, erythema migrans rash (see above- presentation can range from 10-90%). The development of EM is dependent on the genospecies of Borrelia (Tjsse-Klasen et al 2013). Read more on signs and symptoms of borreliosis.
The many names that describe an infection with Borrelia whether related to the town in the USA where it was described or the many European descriptions of symptoms can lead to confusion. It would be correct and appropriate for the World Health Organisation (WHO) to decide on a global name for an infection with Borrelia.
Lyme is an old disease, not a new disease.
Diagnosis of borreliosis relies on clinical symptoms, a history of a tick bite, though not always known. Confirmation with testing is often not possible. Borrelia – the bacteria that causes Lyme disease –is the only known bacteria with 21 or more plasmids, 12 linear and 9 are circular*. These plasmids code for active genes, pseudogenes and phages (bacterial virus) which can be used for survival and assist with dissemination in the host. They can also assist in exchange of antibiotic resistant genes. This genetic variability decreases the reliability of diagnostic tests to confirm diagnosis. Read more about Testing.
*To compare, Staphylococcus aureus – the bacterium that causes antibiotic resistant golden staph infection – has only one plasmid. So imagine the plasmid capability of Borrelia bacteria.
Borrelia also has the unique ability to release blebs which are fragments of DNA enclosed in a membrane that is pinched off from the bacteria. They may contain plasmid DNA incorporated into the genome by horizontal transfer. The role of blebs is not clear but they may contribute to the inflammatory response in the body and to tissue damage (MacDonald & Kuehn, 2012; Charon et al, 2009)
Borrelia can live in a symbiotic fashion in biofilm with other micro-organisms (Sapi et al 2012). Pathogen colonies living in biofilms can be resistant to antibiotics.
Borrelia reproduces very slowly. Borrelia infections are treated with antibiotics. For more information seeCurrent Treatments. The common penicillin-based antibiotics (Beta-lactams) kill bacteria with a cell wall and when the bacteria are dividing. However, Borrelia has a slow reproduction time. Although we do not know the rate in host tissue (in vivo), in lab experiments (in vitro) it has been shown to divide once every 24-48 hours (Jutras et al, 2013). This is unlike Streptococcus throat bacteria which reproduce every 20 minutes. Streptococcus bacteria need to be treated for 480 life cycles which equals 7 days of antibiotic treatment.
So, 480 life cycles of Borrelia would be close to 480 days.
In theory to treat Borrelia infection for 480 life cycles you may need to take antibiotics for 2.5 years in order to get the infection under control. The aim of antibiotic treatment is to decrease the bacterial load so that the immune system can control the infection. Therefore earlier Lyme and other tick borne infections are treated faster the recovery.
The treatment of neuroborreliosis is even more complicated as penetration into the central nervous system (CNS) by many antibiotics is limited, so the treatment time for neuroborreliosis would be more than 3 years. This is not unlike mycobacterium tuberculosis (TB) infection in the CNS where treatment involves more than 3 years of antibiotics.
Another diversion tactic to overcome a hostile environment encountered in the host is for Borrelia to change from the spirochete shape to cell wall deficient L form (intracellular form) or to the cyst form. This ability is referred to as pleomorphism (or polymorphism) – the existence of an organism in two or more distinct forms during the life cycle.
The existence of the intracellular form of Borrelia may explain why blood tests for antibodies for Borrelia in chronic infectious states are negative as Borrelia blood levels are low and the immune system is evaded.
To confidently treat Lyme Borreliosis, three different classes of antibiotics need to target the three different cell forms. However Herxheimer reaction needs to be considered as accumulating toxins from bacterial lysis can cause tissue damage (Pound & May, 2005).
There are similarities between borreliosis and syphilis as they are both caused by spirochete bacterium. It is well established that syphilis can be transmitted sexually and in utero from mother to baby and via blood transfusion. Although there is scientific evidence that supports both relapsing fever Borrelia and Borrelia burgdorferi sensu lato can be transmitted in utero, CDC USA only lists this for relapsing fever Borrelia. Similarly there is scientific evidence that Borrelia burgdorferi sensu lato may be transmitted sexually but this is not supported by the CDC USA.
Borrelia has been found in blood that is stored for donation and individuals with/or being treated for borreliosis should not donate blood.
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Borreliosis is a public health issue
Furthermore, the onset of symptoms is probably dependent on the bacterial load, (number of tick bites, exposure) virulence of the strain and genospecies, slow replication of Borrelia, the number of co-infections delivered by exposure and the genetic makeup of the host. Because of these factors latency of the symptoms are not attributed to Borrelia infection or to the tick bite.