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Early symptoms are then further divided into localized which usually include a characteristic circular rash, fever, malaise and flu like symptoms. The symptoms of early disseminated infection are mainly due to the spread of the bacteria in the blood stream in two to three days after the initial infection and include dizziness, migrating pain in the muscles, palpitations, neuroborreliosis and infections of the lymph nodes. The disease could also lead to many cardiac anomalies like atrioventricular block.
The disease if not treated properly or left untreated could lead to its persistent chronic form. The major parts of the body that are usually affected by this late, chronic form of the disease are eyes, brain and heart. Extreme cases of the disease may also lead to paraplegias. Pathogenesis The pathogenic organism is present in the saliva of the ticks and transferred to the blood stream while the ticks are feeding on the human blood. The tick’s saliva protects the organism and allows it to invade the dermis while avoiding the initial protective system of the human body.
After invasion, an inflammatory response develops against the organism which is usually is the cause of its characteristics initial lesions. Neutorphils however fail to invade the site of infection, enabling the bacteria to survive linger at the site of infection. . RESPONSE OF THE IMMUNE SYSTEM Innate Immunity Innate immune response is usually the body’s first and immediate response to any foreign antigen; in this case the bacteria (Borrelia). The cells usually involved in providing the innate immunity are called as the natural killer cells which include neutrophils, dendritic cells, monocytes and granulocytes.
However in Lyme’s disease neutrophils usually fail to invade the site of infection which allows the organism to survive for a longer duration. In the absence of neutorphills, the dendritic cells acquire a primary role of killing the pathogen. The dendritic cells engulf the bacteria by the process of phagocytosis. After the bacterium is phagocytosed, it is either killed by lysosomal enzymes or by the production of toxic substances e.g. Nitric Oxide, that degrade bacterial cell membrane leading to its death (Dietrich and Hartung 2001).
Dendritic cells having acquired this primary role of killing the cells perform many other functions too in the early manifestation of the infection. The dendritic cells cause the release of several mediators e.g. IL8, 12 and 1 as well as TNF alpha. All these mediators released by dendritic cells play an important role in the early defenses against the disease as well as development of the acquired immunity. Complement system Apart from the innate response that is directly involved in the killing of foreign pathogens, one important aspect of immunity against borrelia infection is the activation of the complement system.
The complement system is a complex of 20 proteins which are activated by the antigen antibody complexes. Functions of the complement system involves: activation of specific immune mechanisms e.g. release of certain chemical mediators, direct
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