THE EFFECT OF LYME DISEASE ON THE IMMUNE SYSTEM
Editor's Note: This paper on Lyme Disease was written by AP Biology student Copeland M. ('15)
Introduction
According to the Centers for Disease Control and Prevention, more than 30,000 cases of Lyme disease in the US are reported to CDC every year. This disease affects a lot of people and in some cases the symptoms of the disease are very persistent. Even so, we still don’t know how to stop the infection in many patients. It’s important to learn more about the disease and particularly how the immune system reacts to it so we can learn how to help the immune system fight it off.
Background
Lyme disease is an infection transmitted to humans from an infected tick bite and caused by the bacterium Borrelia burgdorferi. Ticks become infected by feeding on animals that are infected. Its symptoms in humans include fever, headache, fatigue, and a characteristic bulls eye skin rash. Patients are diagnosed based on symptoms, the possibility of exposure to infected ticks, and lab tests. Antibiotics are used to treat Lyme disease, but early intervention is vital. The disease has a good prognosis for patients treated in the early stages of the disease. They usually recover quickly and fully, but people diagnosed later on are more likely to have persistent symptoms. Lyme disease can be prevented by avoiding tick-infested areas, using insect repellent and covering skin.
There are three stages starting with early localized Lyme disease as stage one. This is the first four weeks of infection and the symptoms shown during this stage include lack of energy, headache, fever, and chills. It is possible, though, for someone to not notice any symptoms during stage one. Stage two is early disseminated infection and is one to four months after infection. If Lyme disease isn’t treated during its early symptoms the disease might get worse. Symptoms during this stage symptoms include a circular rash at the site of the bite, pain in the arms and legs, fainting, and memory loss. The third stage is late persistent Lyme disease after months or years of the disease not being properly treated. Symptoms include arthritis, numbness in hands, and heart problems.
The disease appears to have a hereditary factor, as lupus seems to run in families and be more prevalent in certain ethnic groups. Certain genes have also been linked with lupus, although they are not the sole cause of the disease. This is backed up by the fact that within pairs of identical twins, often (in 75% of cases) only one has the disorder. Not everybody with lupus-associated genes develops it. This information strongly suggests that SLE is caused by a mix of genetic and environmental factors.
Immune response- Chronic Lyme disease
Chronic Lyme disease is when a patient has not been successfully treated with antibiotics and the symptoms of the disease are persistent. The symptoms move from the symptoms of stage one (fever, headache, rash) through stage three (autoimmune) as time goes on. This can lead to a Lyme-triggered autoimmune reaction. Proteins antigens in Borrelia burgdorferi’s cell wall are very similar to some standard protein antigens in our cell membrane and the infection manages to survive in the body even when treatment is taking place. When Borrelia burgdorferi enters the body the immune system responds by producing antibodies. Those antibodies are supposed to attack pathogens, but in certain cases, the antibodies will also attack the body because the protein antigens in Borrelia burgdorferi are so similar to self-antigens in the body. The body continues to try to attack the Lyme bacteria, but it ends up harming parts of the body like the skin and joints and can lead to a number of other problems including diabetes and other autoimmune diseases. The brain may also be under attack in an attempt to rid the body of Lyme disease. The brain is particularly bad at recognizing and removing infections and its response to the infection is to release a toxin that causes damage to nerves. Like in the rest of the body, the brain ends up just harming itself more and not being able to get rid of the infection.
Why the Immune System is Ineffective
Another reason Borrelia burgdorferi can be so hard to get rid of is because it can be hard to know when you’ve been infected. In addition to disguising itself in the body as a normal antigen, it’s able to hide from the immune system for weeks. Elements in a tick’s saliva cover the spirochete, a group of spiral-shaped bacteria, and protect it when it punctures the skin. The saliva hides bacterium from the immune system so when a patient gets tested their results may come back as negative because the immune system still hasn’t started fighting the infection. Also, its inner structure makes it so nonspecific defenses, such as mucus, don’t stop the bacterium. The inner structure is called a flagellum, which is a whip-like structure that allows a cell to move. That structure makes it possible for the bacterium to propel itself through the barriers it comes in contact with and the ones that would stop other pathogens from coming in. Once the bacterium is in the body it begins to change its shape by modifying the proteins in its outer cell wall, further hiding it from the immune system. The immune system searches for specific cell-wall proteins, but the bacterium no longer looks has these antigens and therefore can’t be found. Additionally, in the early stages of the infection the spreads into tissue such as skin, joints, heart, bladder and spleen and can stay there for up to two years.
Variations in the Immune System
Lyme disease is not a uniform disease; it reacts differently in different bodies. One immune system won’t necessarily act like another when it comes in contact with Borrelia burgdorferi. A research project led by students at Johns Hopkins and Stanford University worked to find out how variations in immune response to Lyme disease change the outcome of the infection. To do this, they measured the levels of immune system molecules, which orchestrate the interaction between the immune response and the infection. The immune system molecules are cytokines, chemokines, and acute phase makers. They discovered that patients who had a high number of immune system molecules during their first visit had more severe symptoms and higher rates of antibody production. People who had low rates of immune system molecules turned out to be people who failed to have a strong immune response. The study shows that levels of immune system molecules are linked to symptoms of the disease.
Vaccine
There is only one licensed vaccine against Lyme disease. The vaccine, named LYMERix, was developed by SmithKline Beecham and licensed in 1998. LYMERix is given in three doses and works by stimulating the antibodies that attack the Lyme bacteria in an infected tick in a human. It was found to be effective in preventing Lyme disease 78% of the time and 100% effective at preventing asymptomatic cases, which is when a person is infected but never shows symptoms.
By 2002 LYMERix was withdrawn from the market despite proving to be effective. There are no vaccines on the market today and no known plans of another attempts of creating one.
Treatment
Treatment differs between patients whose Lyme disease was diagnosed in its early stages than when diagnosed later. When caught early, the patient can use antibiotics for a few weeks and a topical medicine for the bulls eye rash. This is often found to be successful. If the disease is caught later on or if symptoms persist after taking antibiotics a different approach will be taken. They may be given a combination of antibiotics for a longer duration to help the symptoms. If Lyme disease symptoms are still a problem after treatment it might mean that the patient has post-Lyme syndrome, which is an autoimmune response. This means the patient won’t have a response from antibiotics.
According to the Centers for Disease Control and Prevention, more than 30,000 cases of Lyme disease in the US are reported to CDC every year. This disease affects a lot of people and in some cases the symptoms of the disease are very persistent. Even so, we still don’t know how to stop the infection in many patients. It’s important to learn more about the disease and particularly how the immune system reacts to it so we can learn how to help the immune system fight it off.
Background
Lyme disease is an infection transmitted to humans from an infected tick bite and caused by the bacterium Borrelia burgdorferi. Ticks become infected by feeding on animals that are infected. Its symptoms in humans include fever, headache, fatigue, and a characteristic bulls eye skin rash. Patients are diagnosed based on symptoms, the possibility of exposure to infected ticks, and lab tests. Antibiotics are used to treat Lyme disease, but early intervention is vital. The disease has a good prognosis for patients treated in the early stages of the disease. They usually recover quickly and fully, but people diagnosed later on are more likely to have persistent symptoms. Lyme disease can be prevented by avoiding tick-infested areas, using insect repellent and covering skin.
There are three stages starting with early localized Lyme disease as stage one. This is the first four weeks of infection and the symptoms shown during this stage include lack of energy, headache, fever, and chills. It is possible, though, for someone to not notice any symptoms during stage one. Stage two is early disseminated infection and is one to four months after infection. If Lyme disease isn’t treated during its early symptoms the disease might get worse. Symptoms during this stage symptoms include a circular rash at the site of the bite, pain in the arms and legs, fainting, and memory loss. The third stage is late persistent Lyme disease after months or years of the disease not being properly treated. Symptoms include arthritis, numbness in hands, and heart problems.
The disease appears to have a hereditary factor, as lupus seems to run in families and be more prevalent in certain ethnic groups. Certain genes have also been linked with lupus, although they are not the sole cause of the disease. This is backed up by the fact that within pairs of identical twins, often (in 75% of cases) only one has the disorder. Not everybody with lupus-associated genes develops it. This information strongly suggests that SLE is caused by a mix of genetic and environmental factors.
Immune response- Chronic Lyme disease
Chronic Lyme disease is when a patient has not been successfully treated with antibiotics and the symptoms of the disease are persistent. The symptoms move from the symptoms of stage one (fever, headache, rash) through stage three (autoimmune) as time goes on. This can lead to a Lyme-triggered autoimmune reaction. Proteins antigens in Borrelia burgdorferi’s cell wall are very similar to some standard protein antigens in our cell membrane and the infection manages to survive in the body even when treatment is taking place. When Borrelia burgdorferi enters the body the immune system responds by producing antibodies. Those antibodies are supposed to attack pathogens, but in certain cases, the antibodies will also attack the body because the protein antigens in Borrelia burgdorferi are so similar to self-antigens in the body. The body continues to try to attack the Lyme bacteria, but it ends up harming parts of the body like the skin and joints and can lead to a number of other problems including diabetes and other autoimmune diseases. The brain may also be under attack in an attempt to rid the body of Lyme disease. The brain is particularly bad at recognizing and removing infections and its response to the infection is to release a toxin that causes damage to nerves. Like in the rest of the body, the brain ends up just harming itself more and not being able to get rid of the infection.
Why the Immune System is Ineffective
Another reason Borrelia burgdorferi can be so hard to get rid of is because it can be hard to know when you’ve been infected. In addition to disguising itself in the body as a normal antigen, it’s able to hide from the immune system for weeks. Elements in a tick’s saliva cover the spirochete, a group of spiral-shaped bacteria, and protect it when it punctures the skin. The saliva hides bacterium from the immune system so when a patient gets tested their results may come back as negative because the immune system still hasn’t started fighting the infection. Also, its inner structure makes it so nonspecific defenses, such as mucus, don’t stop the bacterium. The inner structure is called a flagellum, which is a whip-like structure that allows a cell to move. That structure makes it possible for the bacterium to propel itself through the barriers it comes in contact with and the ones that would stop other pathogens from coming in. Once the bacterium is in the body it begins to change its shape by modifying the proteins in its outer cell wall, further hiding it from the immune system. The immune system searches for specific cell-wall proteins, but the bacterium no longer looks has these antigens and therefore can’t be found. Additionally, in the early stages of the infection the spreads into tissue such as skin, joints, heart, bladder and spleen and can stay there for up to two years.
Variations in the Immune System
Lyme disease is not a uniform disease; it reacts differently in different bodies. One immune system won’t necessarily act like another when it comes in contact with Borrelia burgdorferi. A research project led by students at Johns Hopkins and Stanford University worked to find out how variations in immune response to Lyme disease change the outcome of the infection. To do this, they measured the levels of immune system molecules, which orchestrate the interaction between the immune response and the infection. The immune system molecules are cytokines, chemokines, and acute phase makers. They discovered that patients who had a high number of immune system molecules during their first visit had more severe symptoms and higher rates of antibody production. People who had low rates of immune system molecules turned out to be people who failed to have a strong immune response. The study shows that levels of immune system molecules are linked to symptoms of the disease.
Vaccine
There is only one licensed vaccine against Lyme disease. The vaccine, named LYMERix, was developed by SmithKline Beecham and licensed in 1998. LYMERix is given in three doses and works by stimulating the antibodies that attack the Lyme bacteria in an infected tick in a human. It was found to be effective in preventing Lyme disease 78% of the time and 100% effective at preventing asymptomatic cases, which is when a person is infected but never shows symptoms.
By 2002 LYMERix was withdrawn from the market despite proving to be effective. There are no vaccines on the market today and no known plans of another attempts of creating one.
Treatment
Treatment differs between patients whose Lyme disease was diagnosed in its early stages than when diagnosed later. When caught early, the patient can use antibiotics for a few weeks and a topical medicine for the bulls eye rash. This is often found to be successful. If the disease is caught later on or if symptoms persist after taking antibiotics a different approach will be taken. They may be given a combination of antibiotics for a longer duration to help the symptoms. If Lyme disease symptoms are still a problem after treatment it might mean that the patient has post-Lyme syndrome, which is an autoimmune response. This means the patient won’t have a response from antibiotics.
Glossary
|
Antibiotics -- medicine that inhibits the growth of or destroys microorganisms
Antibodies -- blood protein produced in response to and counteracting a specific antigen. They combine chemically with substances that the body recognizes as alien, such as bacteria, viruses, and foreign substances in blood Autoimmune -- relating to disease caused by antibodies or lymphocytes produced against substances naturally present in the body Bacterium -- a member of a large group of unicellular microorganisms that have cell walls but lack organelles and an organized nucleus, including some that can cause disease |
Borrelia burgdorferi -- Bacterial species of the spirochete class
Spirochete -- a group of spiral-shaped bacteria, some of which are serious pathogens Flagellum -- a whip-like structure that allows a cell to move. Found in all three domains of life Nonspecific defense -- a barrier that helps prevent pathogens from entering the body Pathogen -- a bacterium, virus or other microorganism that can cause disease |
Works Cited
Lyme Disease. (2015, January 6). Retrieved March 3, 2015, from http://www.cdc.gov/lyme/
Why is Chronic Lyme Disease chronic? (n.d.). Retrieved March 3, 2015, from http://www.columbia-lyme.org/patients/ld_chronic.html
Lyme Disease Diagnoses. (n.d.). Retrieved March 3, 2015, from http://www.lymedisease.org/lyme101/lyme_disease/lyme_diagnosis.html
Lyme Borrelia May Induce Auto-Immune Disease. (2012, August 20). Retrieved March 3, 2015, from http://www.lymediseaseneogen.com/2012/08/20/lyme-borrelia-may-induce-auto-immune-disease/
How Does Lyme Disease Evade the Immune System? (2013, August 29). Retrieved March 3, 2015, from http://www.holtorfmed.com/lyme-disease-evade-immune-system/
Immune system research may help predict who gets long-term complications from Lyme Disease. (2014, April 16). Retrieved March 3, 2015, from http://www.sciencedaily.com/releases/2014/04/140416171951.htm
Why is Chronic Lyme Disease chronic? (n.d.). Retrieved March 3, 2015, from http://www.columbia-lyme.org/patients/ld_chronic.html
Lyme Disease Diagnoses. (n.d.). Retrieved March 3, 2015, from http://www.lymedisease.org/lyme101/lyme_disease/lyme_diagnosis.html
Lyme Borrelia May Induce Auto-Immune Disease. (2012, August 20). Retrieved March 3, 2015, from http://www.lymediseaseneogen.com/2012/08/20/lyme-borrelia-may-induce-auto-immune-disease/
How Does Lyme Disease Evade the Immune System? (2013, August 29). Retrieved March 3, 2015, from http://www.holtorfmed.com/lyme-disease-evade-immune-system/
Immune system research may help predict who gets long-term complications from Lyme Disease. (2014, April 16). Retrieved March 3, 2015, from http://www.sciencedaily.com/releases/2014/04/140416171951.htm
