For thousands of years, cultures across the globe have known the identity and characteristics of tuberculosis. Due to its notoriety, tuberculosis has many names; some of these names are references to the person who discovered the diseases, but most of which simply reference the idea of the disease consuming the sufferer from within.
Most cases of tuberculosis are caused by an infection from the mycobacterium Mycobacterium tuberculosis. It is also possible for a person to contract the disease by eating meat or drinking milk from cattle infected with Mycobacterium bovis however, modern pasteurization and meat preparation practices have been successful killing any M. bovis bacteria present in meat or milk from infected cattle. In third world, countries were pasteurization is not standard; M. bovis is a common cause of tuberculosis in humans. Human beings are the only species capable of hosting Mycobacterium tuberculosis. M. tuberculosis is a highly aerobic pathogen and requires a high oxygen demand. The most significant characteristic of mycobacterium such as M. tuberculosis is their highly lipid cell wall which is unlike that of most bacterium. This waxy cell wall benefits M. tuberculosis in a variety of ways. Mycobacterial cells are neither Gram-negative nor Gram-positive, one of the most common characteristics used by medical professionals in identifying infections organisms as well as offering treatment options. Without a gram permeability mycobacterium are resistant to most treatments that have been developed to combat bodily infections. This waxy shell also allows mycobacterium to survive in environments of extreme osmolality and acidity. M. tuberculosis is also capable of forming endospores when outside of the body. These endospores are inactive versions of the cell which are capable of surviving conditions harsher than those which could be survived by the normal cell. Endospores are usually immune to common disinfectants, and can survive without nutrients. M. tuberculosis can often survive outside of the body for a period of weeks and still remain capable of infection.
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The transmission of tuberculosis occurs when TB cells are released by persons with an active tuberculosis infection release them into the environment via coughing, sneezing, or talking. A person with an active pulmonary TB infection can produce tens of thousands of infectious TB cells in a single sneeze. Tuberculosis has an incredibly small effective infection dose; as few as 10 cells can successfully cause an infection. Once infected, one of two scenarios occurs. Active tuberculosis is a state where the immune system cannot prevent tuberculosis cells from multiplying. An infected individual may develop tuberculosis symptoms soon after infection; others who are infected may harbor the tuberculosis bacteria in their body for years, and will experience active tuberculosis when their immune system becomes weakened for whatever reason. 90% of those infected usually experience latent TB infection, and risk a 10 percent chance of developing an active TB infection sometime in the future.
Tuberculosis incidences are closely monitored by the World Health Organization. It is suspected that a third of the worldâ€™s population has been infected with M. tuberculosis, however many of these infections are latent. As with many communicable diseases, tuberculosis is especially prevalent in third world countries, for example infection incidence is 32 and 49 (per 1,000,000) in the United States and Europe respectively however the incidence is 948 in South Africa. This is due to a variety of causes, including a low presence of other mycobacteria, however it is mainly due to malnutrition and poor sanitation. An additional reason for the incidence of tuberculosis in regions such as South Africa is the presence of high HIV prevalence, as many as 73 percent of those becoming infected with tuberculosis already were infected with HIV. HIV/AIDS inhibit the immune system and result in a decreased ability of the body to fight a mycobacterial infection. Other factors which result in decreased capacity for immune response such as a history of drug abuse, or diabetes also increase risk of tuberculosis infection. Damage to the respiratory system due to particle damage or smoking can also cause an increased risk of mycobacterial infection due to a decrease in macrophage function.
Tuberculosis infection takes place when the infected droplets reach lungs of the host. Bacteria will often take hold in the bronchiole or the alveoli. Tuberculosis bacteria are often immediately identified by the macrophages responsible for removing bacteria from the lungs. Whether or not the microphage successfully destroys the tuberculosis bacteria is dependent on the particular fortitude of the particular strain of M. tuberculosis as well as the strength of the particular macrophage. If the microphage is not successful, the M. tuberculosis will begin to multiply while within the macrophage. Unlike other bacteria, M. tuberculosis multiplies slowly. Common bacteria will often multiply in about an hour, M. tuberculosis will often take aver 24 hours per multiplication. M. tuberculosis multiplication is also different from other bacteria in that it does not cause the release of endotoxins or exotoxins which would elicit an immune response. It is not until bacteria number from 10,000 to 100,000 that an immune response is triggered, this can take anywhere from 1-3 months.
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By the time the body has produced an immune response, tuberculin bacterium have taken root in the lower-upper and upper-lower lungs, this area is known as the hilum where they have infected both the macrophages as well as the cells of the lung. The hilum of the lungs contains the blood vessels as well as the primary lymphatic vessels of the lung. Groups of T-cells and macrophages will form granulomas around M. tuberculosis infected cells. These groupings of T-cells will release large amounts of cytokines causing damage to lung tissue. In patients whose immune system is successfully managing the infection, this damage will usually heal and become scar tissue, an infection which is overcoming the body will often cause lesions, as well as cavities in the lung filled with necrotic tissue. If cellular immunity fails to develop before tuberculin bacteria reach the lymphatics, the infection will likely spread to all areas of the body.
The complications caused by tuberculosis which has spread to other parts of the body are similar to those experienced by the lungs, where tissue becomes infected and is subsequently destroyed by the bodyâ€™s immune response. M. tuberculosis infection is possible in all organs of the body, the brain, kidneys and bones are common places for secondary infections to develop. Secondary infections of the heart and skeletal muscles are rare.
Tuberculosis carries with it many symptoms which are common to other, less severe infections, such as coughing and loss of appetite. Technically speaking the only way to truly diagnose tuberculosis is to find the M. tuberculosis in a specimen from the patient. Because most tuberculosis infections begin in the lungs, and patients will often experience a productive cough, sputum is most often the specimen of choice for tuberculosis tests. Due to the previously mentioned slow multiplication rate of mycobacterium, these tests can take as long as 4-5 weeks to produce a culture large enough for proper testing. Once the disease has cultured in the patient, fluorescence microscopy is used to identify the mycobacterium. While sputum cultures can indicate the presence of TB, they are not useful in identifying whether or the scale of the infection, nor if the TB is in an active state (although TB symptoms are often sufficient to identify TB as active). An anterior-posterior x-ray of the chest is often used to identify the state of tuberculosis activity based on the damage apparent on the image. Those with active TB will present x-rays showing cavities and legions filled with necrotic tissue, fluid present in pleural space, and enlargement of the lymph nodes. Those with inactive TB will present x-rays showing scar tissue from previous infection or otherwise healthy lungs. These methods of testing are useful for the diagnosis of patients who are severely ill however they are not necessarily practical for large scale testing.
Persons in high risk settings such as prisons, nursing homes, and hospitals need to be tested for existing M. tuberculosis infection. Those who have an infection in an inactive state risk developing an active infection, in turn subjecting those around them to the risk of infection. Today the tuberculosis skin test is the most common method of tuberculosis testing. This test uses a purified protein extract from tubercle bacterium to test for an existing immune response. In the most common form of the test .1mL of the solution is injected under the skin of the individual. After anywhere from 48 to 72 hours after the test, the diameter of the induration (raised, hardened inflammation) is measured. A larger induration indicates an existing immune response, and therefore suggests that the patient is infected with tuberculosis. Those who have previously been infected with tuberculosis which has now been treated will usually show no response, as their immunity has likely waned. This test is subject both to false positives and to false negatives. Persons with a compromised immune system due to HIV or immunosuppressant drugs will usually show no immune response to the tuberculin injection regardless of infection. It is also possible for persons with existing infections from mycobacteria which are not tuberculosis to react to the tuberculin, producing a false positive.
Tuberculosis is believed to have existed as long as man; written mentions of the disease date back to Hippocrates. During this era and for some time after, tuberculosis was often treated as an inevitable hereditary disease which can in hindsight be recognized as being caused by latent infections due to proximity to family members with an active form of the disease. It was not until the late 1800â€™s that tuberculosis began to be fully understood, and for mycobacterium tuberculosis to be deemed the sole cause of the disease. By the turn of the 20th century sanatoriums were developed. Sanatoriums began as private resource facilities for renowned physicians whom had taken it upon themselves to search for a cure. Sanatoriums began to become places to isolate anyone with tuberculosis. Facilities for the wealthy were often much like hospitals; however facilities for the poor were more often prisons where one went to die. Advances have been made in medicine such that most cases of tuberculosis are entirely treatable so long as the patient has access to the proper medications. Because humans are the only known carriers of the disease, it is entirely possible to completely eliminate its incidence in the population. In countries such as the United States, a patient is more than likely to recover from a case of tuberculosis, however due to lack of healthcare in the third world, a person developing tuberculosis faces a significant risk of death. Effective treatment for tuberculosis is only limited to those who can afford it. Efforts are being made by the World Health Organization to implement a strategy to diagnose those harboring the disease and subsequently get them treatment; however there are significant funding gaps in obtaining the equipment necessary to accomplish either of these.
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Once a tuberculosis infection has been identified, treatment will usually begin. Tuberculosis treatment relies heavily on antibiotics to kill any mycobacteria in the body; this is difficult due to the aforementioned waxy cell wall of mycobacteria. One of the first anti-tuberculin medications was Isoniazid, which when activated by bacterial enzymes to prevent fatty acid synthase. This in turn prevents the synthesis of an important component of the waxy mycobacterial cell wall, mycolic acid. A reduction of mycolic acid levels often is not sufficient to eliminate a tuberculosis infection. Isoniazid treatments are only sufficient to halt the further multiplication of M. tuberculosis. Therefore Isoniazid is often administered alongside the antibiotic rifampicin, as well as two other drugs which work to prevent the synthesis of molecules necessary for mycobacterial cell walls. Patients with tuberculosis are always treated with a multitude of drugs, even if the drugs share a common effect; this is to prevent the development of drug resistant strains of tuberculosis.
Statistically speaking, if a strain of M. tuberculosis develops in a person being treated by a single drug develops a resistance to that drug; it is likely that the drug resistant strain will thrive and infect others. If a patient receiving multiple treatments develops a drug resistant strain, it is likely that the remaining two medications will be able to kill the bacteria and prevent the spread of a drug resistant strain. The cultured samples taken from the patient will always be tested to predict the most effective treatment regimen. However, if the treatment of a tuberculosis patient is not properly managed, it is possible that their infection may become resistant to all four of the medications which are typically used in standard treatment cycle. This produces multi drug-resistant tuberculosis. There are other medications, often ones which are less effective or more expensive which may be used. Treatment using these medications may often take longer, and also expose the patient to the risk of developing extensively drug-resistant tuberculosis. Persons infected with extensively drug-resistant tuberculosis harbor bacteria which are resistant to most bactericidal agents.
The development of drug resistant tuberculosis is one of the concerns regarding liberal use of antibiotics. Persons harboring an inactive form of M. tuberculosis who receive antibiotic treatment for an unrelated condition risk slowly exposing their M. tuberculosis strain to that particular antibiotic such that it will become resistant. Most western physicians have limited their use of antibiotics however countries such as China are still heavily criticized for using antibiotics in the treatment of conditions such as the common cold.
There has been no significant improvement to the treatment of tuberculosis in over 30 years. Efforts are being made to find a compound which will seek out tuberculosis bacterium in a dormant state rather than simply targeting the enzymes necessary for them to multiply. Fluoroquinolens are the most promising compounds thus far. In addition to actively targeting the inactive bacterium, it also has a longer half-life which reduces the ability of the bacterium to recover or develop a resistance. Additional medications are also being tested; however no treatment regimen has surpassed the standard first line treatment of isoniazid, rifampicin, pyrazinamide and ethambutol. These new medications may however be used as a second or third line treatment in the event of a developed resistance to other medications.