Borrelia burgdorferi and Lyme Disease Detection
Overview
Borrelia burgdorferi is a bacterial eubacterial phylum spirochaete and a tick borne parasite.[1] It is one of the known causative agents for Lyme Disease. Borrelia burgdorferi was named after Willy Burgdorfer who first isolated the bacteria in 1982. The spirochete is a flat wave shape that is commonly 0.3 micrometers in width and ranges from 5 to 20 micrometers in length. It has both an outer and inner membrane with a thin layer of peptidoglycan separating the membranes. Seven to eleven bundled periplasmic flagella reside within the membranes and allow the bacterium to move through a highly viscosity medium, which increases its virulence factor. The flagellar filaments wrap around the cell and rotate in order to help the flagellar motor propel the bacteria in a signature corkscrew motion. The doubling time of the bacteria ranges from 24 to 48 hours. Borrelia burgdorferi is different from common pathogenic bacteria because it lacks the common virulence factors like toxins, a specialized secretion system, and lipopolysaccharides. The bacteria lacks common biosynthetic abilities and heavily relies on its host for nutrients and other factors for its survival.
By Roya Best
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Genetics
The genome of Borrelia burgdorferi is a linear chromosome with many smaller plasmids that are both linear and circular. The linear chromosome is about 950 kb and the linear and circular plasmids range from 9 to 62 kb, which all encode 853 genes. The genome of Borrelia burgdorferi was the third ever genome sequenced. Linear chromosomes are not common in bacteria, however, in Borrelia burgdorferi it seems to provide an advantage that has continued to allow the linear chromosome to persist. The Borrelia burgdorferi genetic sequence shows that the flagella are hidden between the two membranes compared to other organisms that have it externally radiating outward. The flagella are strategically positioned in order to provide Borrelia burgdorferi an advantage in hiding from the host immune system, as this is critical in its survival.
Borrelia burgdorferi lacks the classic genes to synthesize amino acids, fatty acids, enzyme cofactors, and nucleotides. It takes advantage of its host and obtains these important materials. The inability to synthesize these things is likely lost in coevolution with ticks and other hosts. Additionally, Borrelia burgdorferi lacks the genes to use the citric acid cycle, oxidative phosphorylation, and cellular biosynthesis. Borrelia burgdorferi however has the genes for and derives its energy from glycolysis and fermentation of sugars.
Borrelia burgdorferi interacts with platelets, endothelial cells, chondrocytes, and extracellular matrix when infecting a host. These interactions inhibit the proper function of various mechanisms in these infected areas. This leads to the symptoms of Lyme Disease.
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Lyme Disease History and Overview
Lyme Disease is an enzootic vector-borne disease that is transmitted by Ixodes tick. Lyme Disease was first discovered by Doctor Alan Steere in 1977 when he noticed that people were being infected with an unknown pathogen in the same geographic location during the same time of the year presenting with the same symptoms. The first confirmed case was in Lyme, Connecticut, thus providing the name of the Disease. In 1981 it was finally discovered that Borrelia genus bacteria were the causative agents of Lyme Disease.
There are a few Borrelia species that can cause Lyme Disease, however, Borrelia burgdorferi is the most common in the US. Lyme Disease is the leading vector-borne disease in the US. There are an estimated 476,000 cases each year of Lyme Disease in the US according to numbers from 2010 to 2018. However, this is most likely an underestimate because Lyme Disease is difficult to diagnose. Lyme Disease is endemic to the US, Europe, and Asia. Most cases are reported during the Spring and Summer months due to the life cycle of the reservoir, the Ixodes ticks. Common animals that can become infected with Borrelia burgdorferi are white-footed mice, chipmunks, dogs, white-tailed deer, squirrels, horses, opossums, and raccoons.
Research surrounding Lyme Disease is sparse due to the lack of federal funding. The annual NIH investment in research is much lower than in other infectious diseases. Thirty million dollars a year is allocated to Lyme Disease research which affects over 470,000 individuals annually. However, 36 million dollars is allocated to West Nile Virus which only affects about 3,000 individuals and 202 million dollars is allocated to Malaria which only affects under 2,000 individuals. The lack of funding surrounding Lyme Disease is highly controversial and why individuals with the disease commonly suffer due to improper diagnosis and must tolerate its symptoms.
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Transmission
Ticks become infected with Borrelia burgdorferi when they have a blood meal from an infected reservoir, such as a white-footed mouse or chipmunk. When an infected tick bites an animal or human, Borrelia burgdorferi will migrate from the tick’s midgut to the salivary glands and then into the bloodstream of the new host. The spirochete then travels from the bloodstream to various tissues within the new host. The location in which Borrelia burgdorferi lands is where the most symptoms will be experienced. While no virulence factors are found within Borrelia burgdorferi, symptoms will occur as a result of the inflammatory response and damage the bacteria causes when it replicates.
Acquiring the disease depends on many factors, including, density, distribution, and prevalence of infected ticks in the individual's area. Cases of Lyme Disease are the most common in the Northeast and Northern Central states within the US. The most reported cases occur May through August due to the life cycle of ticks, tick feeding time, and increase in human activity outdoors. A tick must be attached to its new host for over 36 hours in order to transmit the disease. Adult ticks and nymph ticks can transmit the disease. However, it is much more likely to be infected by a nymph tick because of its small size and the likelihood of remaining attached for over 36 hours.
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Life Cycle
Tick life cycle- Ticks are the only known natural agents that can infect animals and humans with Borrelia burgdorferi. The tick genus Ixodes can become infected with and transmit Borrelia burgdorferi between hosts and reservoirs.
The life cycle of the Ixodes ticks heavily influences the transmission of Borrelia burgdorferi between various animals and humans. The tick has a life span of two years and undergoes different life stages. The egg phase of ticks has no influence on Lyme Disease and Borrelia burgdorferi can not be contracted during this stage. The larva stage is when ticks must take a blood meal to survive and grow, thus feeding on small animals, usually mice. This stage is critical to Lyme Disease as ticks can become infected with Borrelia burgdorferi. The combination of taking a blood meal and feeding upon white-footed mice is key because white-footed mice are known as one of the main reservoirs for which ticks become infected with Borrelia burgdorferi. The next stage of a tick’s life cycle is the nymph stage. At this stage, ticks can infect others with Borrelia burgdorferi. At the nymph stage, ticks also can infect small animals and humans. Nymphs are extremely small in size and can evade detection by humans, thus being attached long enough to infect humans with Borrelia burgdorferi. Ticks during the nymph stage feed in the spring and summer, when Lyme Disease cases are reported the highest. After the nymph stage, ticks molt into adults. Adult ticks can infect other animals and humans with Borrelia burgdorferi. However, it is not common for adult ticks to transmit Borrelia burgdorferi to humans because of their large size, which allows them to be easily seen and removed.
Lyme Disease life cycle- Lyme disease itself goes through a life cycle during the transmission of Borrelia burgdorferi between hosts and reservoirs. Larva or nymphs acquire Borrelia burgdorferi during their first blood meal from an infected host. Once infected, Borrelia burgdorferi persists in the tick’s midgut. When the infected nymph bites an uninfected animal the bite triggers the Borrelia burgdorferi to replicate, escape from the tick’s midgut, and exit through the salivary glands of the tick to another host. This life cycle of Borrelia burgdorferi and Lyme Disease thus completes the enzootic cycle.
Stages and Symptoms
There are three stages to Lyme Disease: early localized stage, early disseminated stage, and late disseminated stage. With each stage, new symptoms develop, and old ones may persist or disappear.
Stage 1- Early Localized Stage Early localized Lyme DIsease occurs three days to one month after the initial tick bite. The local area of the bite will be the area that experiences the most symptoms. About 70% of individuals will develop a “bull’s eye” rash. This rash is characteristic of Lyme Disease and commonly leads to diagnosis. It may get as large as 15 cm and last up to three weeks if untreated. Symptoms at this stage include flu-like symptoms, such as fever, eye redness, neck stiffness, and headaches. Antibiotics at this stage are the most effective and can prevent further growth of Borrelia burgdorferi and sometimes lead to being cured of the disease.
Stage 2- Early Dissemination Stage The early dissemination stage of Lyme Disease occurs weeks to months after initial infection if left untreated. At this point, Borrelia burgdorferi begins to spread throughout the bloodstream and begins to affect other parts of the body beyond the initial bite site. General symptoms include fever, chills, fatigue, and lymphadenopathy. The heart may begin to be affected and lead to arrhythmias or myocarditis. About 4-8% of individuals experience cardiac symptoms. The musculoskeletal system may also be affected and lead to arthritis development. Arthritis is common with about 60% of those with Lyme Disease developing the symptom. Additionally, the nervous system may begin to be affected and present with loss of memory or facial paralysis. Neurological symptoms affect about 15-20% of individuals who are not treated.
Stage 3- Late Dissemination Stage Late disseminated Lyme Disease occurs after one year of initial infection and is also considered chronic Lyme Disease. Symptoms at this stage are long-term and may include encephalitis, meningitis, and severe arthritis. Arthritis at this point in the disease is commonly harsh on individuals' knees. Other symptoms from previous stages most likely would persist throughout this stage.
Evasion and Detection
Treatment
Prevention
Vaccines
Conclusion
References
Authored for BIOL 238 Microbiology, taught by Joan Slonczewski, 2022, Kenyon College
