Borrelia burdorferi, first identified in 1981 or 1982 is the causative agent of Lyme disease. All agree it is a small spirochete. It is hard to culture (fastidious) and lives in a low oxygen environment (microaerophilic). This is why some have experimented with hyperbaric oxygen therapies which saturate the tissues with oxygen. I do not know if these treatments are effective. They are experimental and not covered by insurance. This is not an option in my state to the best of knowledge. Three pathogenic groups of the organism have been identified. The term B. burdorferi sensu lato, confusing terminology is used to include all the pathogenic(disease causing) strains. The word stricto is added at the end to signify those strains of the organism in North America. So the American Lyme germ is called Borrelia burdorferi sensu stricto. Other species found in Europe and Asia are called Borrelia garinii and Borrelia afzelii. The clinical manifestations of the various strains may vary somewhat. B. burdorferi is transmitted by tick bites. The ticks are called vectors. The primary vector is Ixodes scapularis, the deer tick. Other ticks have been shown to also transmit the infection including: I. rinicus, I. pacificus, I. persulcatous and the Lone Star tick. To the best of my knowledge Lyme is only transmitted by tick bites. The ticks are so small that they are usually not seen. The ticks have nymph, larval and adult stages. The first two stages are generally invisible to the naked eye. it is believed that tick bites are necessary because factors within the tick saliva are known to promote infection. It also believed that the duration of tick attachment is related to the transmission of the organism. There is debate about how long the tick needs to be attached. In general, I have found that is difficult to accurately estimate the duration of attachment. Certainly an engorged tick suggest that transmission is very likely. Most tick bites are never observed. Lyme has been found in other insects such as flies and mosquitoes. I have reported estimates which state that 20% of these insects and others are infected. There is no evidence to suggest that other insects have the ability to transmit Lyme, although this remains an open question. The term deer tick is misleading. The major host for Ixodes is considered the white footed mouse. Most small mammals including dogs carry the infection. The larger adult ticks are frequently seen on deer. But there is a clear consensus that the tiny nymph forms of the tick are responsible for the majority of infections. Some have suggested that the infection can be transmitted transplacentally to an embryo in an infected mother. So far there is no evidence to support this hypothesis. Others have suggested that it may be transmitted sexually. The cite evidence that Lyme DNA may be seen in vaginal secretions. I believe this is unlikely. The germ is rarely seen in body fluids of any kind. Dead spirochetes are excreted through the kidneys. I suspect the material seen in genital secretion does not represent viable organisms capable of causing infection. Of course this possibility cannot be ruled out. Lyme has been shown to have the ability to thwart the immune system. There is agreement that the germ attaches to extracellular matrix proteins. Its surface proteins allow it to attach to mammalian cells. Vascular inflammation is noted during early infection. It is known to have the ability to down regulate surface proteins to evade immune responses. Another surface protein called VIsE is know to undergo extensive changes during invasion. This protein is the basis for the new specific C6 peptide antibody test. I has the ability to become an intracellular L-form which also helps it "hide out" from immune responses. It can shift to the spore like cystic form to avoid immune responses as well. It is known to have a complex genetic structure. It has 132 active genes compared to 20 for the spirochete which causes syphilis. It is know to contain a large number of cytoplasmic plasmids, which are extra pieces of DNA and normally help facilitate genetic changes and the development of resistance to antibiotics.
In the IDSA model it is not resistant to antibiotics. Short courses of standard antibiotics will eliminate it. When symptoms persist after treatment which these physicians feel is adequate they tend to call it "post-Lyme" syndrome. The implication is that the infection has triggered an autoimmune response which persists in the absence of persistent infection of the organism.
In the ILADS model persistent symptoms are do to ongoing infection with the organism. They point to animal studies which document the persistence of the organism after treatment. They also point to numerous other studies which document the persistence of the organism in many tissues, ranging from ligaments to nerve tissue which have been performed over the last 20 years. Finally, they refer to clinical trials which document the benefits of prolonged antibiotic therapy.