Lyme disease is caused by the spread of bacterial infection involving the Borrelia burgdorferi sensu lato genus. Lyme disease pathology and symptoms of the condition correspond to the progressive involvement of multiple organs and systems in the body. Evidence of bacterial infection has been found in the skin, heart, peripheral and central nervous systems, and the joints. In some cases the presence of bacteria in organs such as the heart has only been found after autopsy and may have played a role in the cause of a patient’s death due to long-term damage going undetected. The symptoms of Lyme disease are largely due to the immune system’s response to the spirochaetes’ presence in a particular organ or tissue, in addition to disruption of the hypothalamic-pituitary adrenal axis, and alterations in cell proliferation and death in brain tissue.
Tick Saliva and Lyme Disease Transmission
Following a bite from an infected tick of the Ixodes genus the saliva of the tick is transmitted with accompanying spirochaetes into the skin during feeding. This saliva has components which disrupt the normal immune response to a bite and which afford protection to the infectious spirochaetes allowing them to establish themselves in the local area. These spirochaetes then multiply and begin to spread outwards in the skin resulting in the characteristic bull’s eye rash, erythema migrans. The redness of this rash is due to the immune system’s provocation to mount an inflammatory response to the invading organism. Unfortunately, even as this inflammation occurs the neutrophils which should accompany it fail to materialise. Neutrophils are the immune system components which would aid elimination of the bacteria from the skin; thus, the spirochaetes continue to survive and thrive.
The reason for this failure of the neutrophils to converge on the infected area is the use by the spirochaetes of the protein plasmin found in the tick saliva to effectively hide from the immune system. Despite B. burgdorferi s.l. antibody production the plasmin confounds the immune system’s efforts which is further obstructed by the spirochaetes ability to reduce the expression of surface proteins that would be targeted by such antibodies. This avoidance of detection involves alterations in the VIsE surface protein which effectively inactivates certain immune system components such as complement. Additionally, the bacteria may take up a position in the body’s extracellular matrix that makes it difficult to reach by the cells of the immune system.
Early Disseminated Lyme Disease Pathology
Over the days and weeks after a bite from an infected tick, the spirochaetes slowly enter the bloodstream from where they can gain access to almost every tissue in the body through the circulation. Infection can then spread quickly through the system and cause symptoms at places far away from the initial tick bite. The erythema migrans rash may now arise in other locations on the body as well as the original location as the spirochaetes cause other localised inflammation. Once again, the body’s normal response leading to the elimination of the spirochaetes through the action of neutrophils is inhibited by the pathogen’s use of the protease plasmin from the ticks’ saliva. The Borrelia bacteria are also adept at other tactics to avoid detection by the immune system.
These tactics employed by the Lyme disease bacteria have potential ramifications for the development of autoimmune complications. Exposure to the spirochaetes creates a chronic inflammatory response which may begin to damage ordinary bodily tissues due to molecular mimicry employed by the bacteria to avoid detection. In their imitation of normal body cells the bacteria can confuse the immune system into attacking ordinary body tissues which goes some way to explaining the chronic symptoms of Lyme disease experienced by some patients even after eradication of the infection by antibiotics. Where the immune system has produced antibodies against its own cells it will continue to attack these cells even in the absence of the Borrelia bacteria, leading to persistent symptoms including joint pain. Effectively, Lyme disease may induce an autoimmune condition similar to rheumatoid arthritis which persists even after the causative agent, the Borrelia bacteria, is removed.
A Multisystem Effect
Borrelia burgdorferi s.l. infection creates multiple symptoms due to it multisytem effects. In a large number of those infected, the symptoms only go as far as an acute flu-like illness which is effectively fought by the body and which leads to no other persistent effects from the tick bite. Stage II, early disseminated Lyme disease, involves the cardiovascular system and/or the central nervous system, leading to myocarditis, meningoencephalitis, and polyradiculitis. The levels of inflammation during this stage are much higher in these tissues than anywhere else in the early acute stage and can lead to significant tissue damage if the infection continues unchecked. Progression into Stage III Lyme disease involves more bodily systems, including the joints, and exerts more serious effects such as dementia and transverse myelitis.
Continue Reading –> Lyme Disease Pathology – Central Nervous System