Friday, April 26, 2013


MYCOPLASMA Mycoplasma refers to a genus of bacteria that lack a cell wall.[1] Without a cell wall, they are unaffected by many common antibiotics such as penicillin or other beta-lactam antibiotics that target cell wall synthesis. They can be parasitic or saprotrophic. Several species are pathogenic in humans, including M. pneumoniae, which is an important cause of atypical pneumonia and other respiratory disorders, and M. genitalium, which is believed to be involved in pelvic inflammatory diseases. Mycoplasma is the smallest known cell and is about 0.1 µm in diameter. Origin of the name The name Mycoplasma, from the Greek mykes (fungus) and plasma (formed), was first used by Albert Bernhard Frank in 1889. He thought it was a fungus, due to fungus-like characteristics.[2] An older name for Mycoplasma was Pleuro pneumonia-Like Organisms (PPLO), referring to organisms similar to the causative agent of contagious bovine pleuropneumonia (CBPP).[3] It was later found that the fungus-like growth pattern of M. mycoides is unique to that species. [edit] Characteristics There are over 100 recognized species of the genus Mycoplasma, one of several genera within the bacterial class Mollicutes. Mollicutes are parasites or commensals of humans, other animals (including insects), and plants; the genus Mycoplasma is by definition restricted to vertebrate hosts. Cholesterol is required for the growth of species of the genus Mycoplasma as well as certain other genera of mollicutes. Their optimum growth temperature is often the temperature of their host if warmbodied (e. g. 37° C in humans) or ambient temperature if the host is unable to regulate its own internal temperature. Analysis of 16S ribosomal RNA sequences as well as gene content strongly suggest that the mollicutes, including the mycoplasmas, are closely related to either the Lactobacillus or the Clostridium branch of the phylogenetic tree (Firmicutes sensu stricto). [edit] Cell morphology The bacteria of the genus Mycoplasma (trivial name: mycoplasmas) and their close relatives are characterized by lack of a cell wall. Despite this, the cells often present a certain shape, with a characteristic small size, with typically about 10% of the volume of an Escherichia coli cell. These cell shapes presumably contribute to the ability of mycoplasmas to thrive in their respective environments. Most are pseudococcoidal, but there are notable exceptions. Species of the M. fastidiosum cluster are rod-shaped. Species of the M. pneumoniae cluster, including M. pneumoniae, possess a polar extension protruding from the pseudococcoidal cell body. This tip structure, designated an attachment organelle or terminal organelle, is essential for adherence to host cells and for movement along solid surfaces (gliding motility), and is implicated in normal cell division. M. pneumoniae cells are pleomorphic, with an attachment organelle of regular dimensions at one pole and a trailing filament of variable length and uncertain function at the other end, whereas other species in the cluster typically lack the trailing filament. Other species like M. mobile and M. pulmonis have similar structures with similar functions. Mycoplasmas are unusual among bacteria in that most require sterols for the stability of their cytoplasmic membrane. Sterols are acquired from the environment, usually as cholesterol from the animal host. Mycoplasmas generally possess a relatively small genome of 0.58-1.38 megabases, which results in drastically reduced biosynthetic capabilities and explains their dependence on a host. Additionally they use an alternate genetic code in which the codon UGA encodes the amino acid tryptophan instead of the usual stop codon. They have a low GC-content (23-40 mol %). [edit] First isolation In 1898 Nocard and Roux reported the cultivation of the causative agent of CBPP, which was at that time a grave and widespread disease in cattle herds.[4][5] The disease is caused by M. mycoides subsp. mycoides SC (small-colony type), and the work of Nocard and Roux represented the first isolation of a mycoplasma species. Cultivation was, and still is difficult because of the complex growth requirements. These researchers succeeded by inoculating a semi-permeable pouch of sterile medium with pulmonary fluid from an infected animal and depositing this pouch intraperitoneally into a live rabbit. After fifteen to twenty days, the fluid inside of the recovered pouch was opaque, indicating the growth of a microorganism. Opacity of the fluid was not seen in the control. This turbid broth could then be used to inoculate a second and third round and subsequently introduced into a healthy animal, causing disease. However, this did not work if the material was heated, indicating a biological agent at work. Uninoculated media in the pouch, after removal from the rabbit, could be used to grow the organism in vitro, demonstrating the possibility of cell-free cultivation and ruling out viral causes, although this was not fully appreciated at the time .[4] [edit] Small genome Recent advances in molecular biology and genomics have brought the genetically simple mycoplasmas, particularly M. pneumoniae and its close relative M. genitalium, to a larger audience. The second published complete bacterial genome sequence was that of M. genitalium, which has one of the smallest genomes of free-living organisms.[6] The M. pneumoniae genome sequence was published soon afterwards and was the first genome sequence determined by primer walking of a cosmid library instead of the whole-genome shotgun method.[7] Mycoplasma genomics and proteomics continue in efforts to understand the so-called minimal cell,[8] catalog the entire protein content of a cell,[9] and generally continue to take advantage of the small genome of these organisms to understand broad biological concepts. [edit] Taxonomy The medical and agricultural importance of members of the genus Mycoplasma and related genera has led to the extensive cataloging of many of these organisms by culture, serology, and small subunit rRNA gene and whole genome sequencing. A recent focus in the sub-discipline of molecular phylogenetics has both clarified and confused certain aspects of the organization of the class Mollicutes.[10] Originally the trivial name "mycoplasmas" has commonly denoted all members of the class Mollicutes. The name "Mollicutes" is derived from the Latin mollis (soft) and cutes (skin), and all of these bacteria do lack a cell wall and the genetic capability to synthesize peptidoglycan. Now Mycoplasma is a genus in Mollicutes. Despite the lack of a cell wall, many taxonomists have classified Mycoplasma and relatives in the phylum Firmicutes, consisting of low G+C Gram-positive bacteria such as Clostridium, Lactobacillus, and Streptococcus based on 16S rRNA gene analysis. The order Mycoplasmatales contains a single family, Mycoplasmataceae, comprising two genera: Mycoplasma and Ureaplasma. Historically, the description of a bacterium lacking a cell wall was sufficient to classify it to the genus Mycoplasma and as such it is the oldest and largest genus of the class with about half of the class' species (107 validly described), each usually limited to a specific host and with many hosts harboring more than one species, some pathogenic and some commensal. In later studies, many of these species were found to be phylogenetically distributed among at least three separate orders. A limiting criterion for inclusion within the genus Mycoplasma is that the organism have a vertebrate host. In fact, the type species, M. mycoides, along with other significant mycoplasma species like M. capricolum, is evolutionarily more closely related to the genus Spiroplasma in the order Entomoplasmatales than to the other members of the Mycoplasma genus. This and other discrepancies will likely remain unresolved because of the extreme confusion that change could engender among the medical and agricultural communities. The remaining species in the genus Mycoplasma are divided into three non-taxonomic groups, hominis, pneumoniae and fermentans, based on 16S rRNA gene sequences. The hominis group contains the phylogenetic clusters of M. bovis, M. pulmonis, and M. hominis, among others. M. hyopneumoniae is a primary bacterial agent of the porcine respiratory disease complex. The pneumoniae group contains the clusters of M. muris, M. fastidiosum, U. urealyticum, the currently unculturable haemotrophic mollicutes, informally referred to as haemoplasmas (recently transferred from the genera Haemobartonella and Eperythrozoon), and the M. pneumoniae cluster. This cluster contains the species (and the usual or likely host) M. alvi (bovine), M. amphoriforme (human), M. gallisepticum (avian), M. genitalium (human), M. imitans (avian), M. pirum (uncertain/human), M. testudinis (tortoises), and M. pneumoniae (human). Most if not all of these species share some otherwise unique characteristics including an attachment organelle, homologs of the M. pneumoniae cytadherence-accessory proteins, and specialized modifications of the cell division apparatus. A study of 143 genes in 15 species of Mycoplasma suggests that the genus can be grouped into four clades: the M. hyopneumoniae group, the M. mycoides group, the M. pneumoniae group and a Bacillus-Phytoplasma group.[11] The M. hyopneumoniae group is more closely related to the M. pneumoniae group than the M. mycoides group. [edit] Laboratory contaminant Mycoplasma species are often found in research laboratories as contaminants in cell culture. Mycoplasmal cell culture contamination occurs due to contamination from individuals or contaminated cell culture medium ingredients[clarification needed][citation needed]. Mycoplasma cells are physically small – less than 1 µm – and they are therefore difficult to detect with a conventional microscope. Mycoplasmas may induce cellular changes, including chromosome aberrations, changes in metabolism and cell growth. Severe Mycoplasma infections may destroy a cell line. Detection techniques include DNA Probe, enzyme immunoassays, PCR, plating on sensitive agar and staining with a DNA stain including DAPI or Hoechst. It has been estimated that at least 11 to 15% of U.S. laboratory cell cultures are contaminated with mycoplasma. [12] A Corning study showed that half of U.S. scientists did not test for mycoplasma contamination in their cell cultures. The study also stated that, in former Czechoslovakia, 100% of cell cultures that were not routinely tested were contaminated while only 2% of those routinely tested were contaminated (study page 6). Since the U.S. contamination rate was based on a study of companies that routinely checked for mycoplasma, the actual contamination rate may be higher. European contamination rates are higher and that of other countries are higher still (up to 80% of Japanese cell cultures).[13] About 1% of published Gene Expression Omnibus data may have been compromised.[14][15] Several antibiotic based formulation of anti-mycoplasma reagents have been developed over the years.[16] [edit] Synthetic mycoplasma genome A chemically synthesized genome of a mycoplasmal cell based entirely on synthetic DNA which can self-replicate has been referred to as Mycoplasma laboratorium.[17] Pathogenicity Several Mycoplasma species can cause disease, including M. pneumoniae, which is an important cause of atypical pneumonia (formerly known as "walking pneumonia"), and M. genitalium, which has been associated with pelvic inflammatory diseases. Mycoplasma infections in humans are associated with skin eruptions in 17% of cases.[18]:293 [edit] Links to cancer Several species of mycoplasma are frequently detected in different types of cancer cells. [19][20][21] These species are: M. fermentans [22][19][23][20][21][24] M. genitalium [25] M. hyorhinis [26][19][25] M. penetrans [22][19][20][21][24] The majority of these mycoplasma have shown a strong correlation to malignant transformation in mammalian cells in vitro. [edit] Mycoplasma infection and host cell transformation The presence of mycoplasma was first reported in samples of cancer tissue in the 1960s. [21] Since then there have been several studies trying to find and prove the connection between mycoplasma and cancer, as well as how the bacterium might be involved in the formation of cancer. [20] Several studies have shown that cells that are chronically infected with the bacteria go through a multistep transformation. The changes caused by chronic mycoplasmal infections occur gradually and are both morphological and genetic. [20] The first visual sign of infection is when the cells gradually shift from their normal form to sickle shaped. They also become hyperchromatic due to an increase of DNA in the nucleus of the cells. In later stages, the cells lose the need for a solid support in order to grow and proliferate as well as the normal contact dependent inhibition. [21] [edit] Possible intracellular mechanisms of mycoplasmal malignant transformation Karyotypic changes related to mycoplasma infections Cells infected with mycoplasma for an extended period of time show significant chromosomal abnormalities. These include the addition of chromosomes, the loss of entire chromosomes, partial loss of chromosomes and chromosomal translocation. All of these genetic abnormalities may contribute to the process of malignant transformation. Chromosomal translocation and extra chromosomes help create abnormally high activity of certain proto-oncogenes. Proto-oncogenes with increased activity caused by these genetic abnormalities include those encoding c-myc, HRAS, [22] and vav. [20] The activity of proto-oncogenes is not the only cellular function that is affected; tumour suppressor genes are affected by the chromosomal changes induced by mycoplasma as well. Partial or complete loss of chromosomes causes the loss of important genes involved in the regulation of cell proliferation. [21] Two genes whose activities are markedly decreased during chronic infections with mycoplasma are the Rb and the p53 tumour suppressor genes. [20] A major feature that differentiates mycoplasmas from other carcinogenic pathogens is that the mycoplasmas do not cause the cellular changes by insertion of their own genetic material into the host cell. [22] The exact mechanism by which the bacterium causes the changes is not yet known. Partial reversibility of malignant transformations The malignant transformation induced by mycoplasma is also different from that caused by other pathogens in that the process is reversible. The state of reversal is, however, only possible up to a certain point during the infection. The window of time that reversibility is possible varies greatly; it depends primarily on the mycoplasma involved. In the case of M. fermentans, the transformation is reversible up until around week 11 of infection and starts to become irreversible between week 11 and 18. [21] If the bacteria are killed using antibiotics [21] (i.e. ciprofloxacin [20] or Clarithromycin [27]) before the irreversible stage, the infected cells should return to normal. [edit] Connections to cancer in vivo and future research Though mycoplasmas are confirmed to be carcinogenic in vitro, it is not yet confirmed whether mycoplasma might be an actual cause of cancer in vivo. [25] The uncertainties regarding the bacteria’s potential to cause malignancies is mostly due to the fact that the cells used for the studies are most often from immortalised cell lines like the BEAS-2B cells. These are essentially cells on the verge of becoming cancer cells. One big problem with using these cells to confirm carcinogenic properties is that they will transform spontaneously after 32 passagings (when a small number of cells are transferred into a new vessel to extend culture duration). [25] This, and the fact that no malignant transformation has been detected in non-immortalised “normal” cells that have been infected, might be an indication that mycoplasmas accelerates a cell’s progression towards malignancy, rather than actually causing it. No mycoplasma-generated cancer has yet to be documented in in vivo cultures. It might, however, be possible that very long, chronic infections of mycoplasma are able to cause cancer in non-immortalised cells. This is not yet known since non-immortalised cells can only divide for a limited number of times, and therefore it has not been possible to keep culturing them long enough to develop cancer. [25] More research is needed to confirm that mycoplasma infections cause cancer or initiate malignancies in human cells. This might be an important step to treat and prevent cancer. [25] [edit] Types of cancer associated with mycoplasma Colon cancer: In a study to understand the effects of mycoplasma contamination on the quality of cultured human colon cancer cells, it was found that there is a positive correlation between the amount of M. hyorhinis present in the sample and the percentage of CD133 positive cells (a glycoprotein with an unknown function). Further tests and analysis are required to determine the exact reason for this phenomenon. [28] Gastric cancer: There are strong indications that the infection of M. hyorhinis contributes to the development of cancer within the stomach and increases the likelihood of malignant cancer cell development. [29] Lung cancer: Studies on lung cancer have supported the belief that there is more than a coincidental positive correlation between the appearance of Mycoplasma strains in patients and the infection with tumorigenesis. Because this is a such a new area of research, more studies must be performed to further understand the correlation and determine possible preventative steps for lung cancer involving mycoplasma. [30] Prostate cancer: p37, a protein encoded for by M. hyorhinis, has been found to promote the invasiveness of prostate cancer cells. The protein also causes the growth, morphology, and the gene expression of the cells to change, causing them to become a more aggressive phenotype. [31] Renal Cancer: Patients with renal cell carcinoma (RCC) exhibited a significantly high amount of Mycoplasma sp. compared with the healthy control group. This suggests that mycoplasma may play a role in the development of RCC. [27] [edit] References ^ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 409–12. ISBN 0-8385-8529-9. ^ Krass CJ, Gardner MW (January 1973). "Etymology of the Term Mycoplasma". Int. J. Of Syst. Bact. 23 (1): 62–64. doi:10.1099/00207713-23-1-62. ^ Edward DG, Freundt EA (February 1956). "The classification and nomenclature of organisms of the pleuropneumonia group". J. Gen. Microbiol. 14 (1): 197–207. PMID 13306904. ^ a b Nocard EIE , Roux E (1990). "The microbe of pleuropneumonia. 1896". Rev. Infect. Dis. 12 (2): 354–8. doi:10.1093/clinids/12.2.354. PMID 2184501. "translation of Le microbe de la péripneumonie. Ann Inst Pasteur 12, 240-262, 1898" ^ Hayflick L, Chanock RM (June 1965). "Mycoplasma Species of Man". Bacteriol Rev 29 (2): 185–221. PMC 441270. PMID 14304038. ^ Fraser CM, Gocayne JD, White O, Adams MD, Clayton RA, Fleischmann RD, Bult CJ, Kerlavage AR, Sutton G, Kelley JM, Fritchman RD, Weidman JF, Small KV, Sandusky M, Fuhrmann J, Nguyen D, Utterback TR, Saudek DM, Phillips CA, Merrick JM, Tomb JF, Dougherty BA, Bott KF, Hu PC, Lucier TS, Peterson SN, Smith HO, Hutchison CA, Venter JC (October 1995). "The minimal gene complement of Mycoplasma genitalium". Science 270 (5235): 397–403. doi:10.1126/science.270.5235.397. PMID 7569993. UREAPLASMA Ureaplasma urealyticum is a bacterium belonging to the family Mycoplasmataceae. Its type strain is T960. Contents 1 Clinical significance 2 Classification 3 Treatment 4 References 5 External links Clinical significance U. urealyticum is part of the normal genital flora of both men and women.[citation needed] It is found in about 70% of sexually active humans.[citation needed] It had also been associated with a number of diseases in humans, including non-specific urethritis (NSU), infertility, chorioamnionitis, stillbirth, premature birth, and, in the perinatal period, pneumonia, bronchopulmonary dysplasia[1] and meningitis. However, given the relatively low pathogenicity of the organism its role in some of these diseases remains contentious. U. urealyticum has been noted as one of the infectious causes of sterile pyuria.[2] Classification There are six recognised Ureaplasma species, They have a GC content of 27–30%, and a genome size ranging between 0.76–1.17 Mbp, and cholesterol is required for growth. A defining characteristic of the genus is that they perform urea hydrolysis. It is now recommended that some strains originally classified as Ureaplasma urealyticum should be treated as a new species, U. parvum. Treatment Doxycycline is the drug of choice but Azithromycin is also used as a 5 day course rather than a single dose that would be used to treat Chlamydia;[3] streptomycin is an alternative but is less popular because it must be injected. Penicillins are ineffective — U. urealyticum does not have a cell wall,[4] which is the drug's main target.[5] Long Term Effects of Ureaplasma The main cause of ureaplasma is a minute bacterium that enters the body and later on acts as a virus. Ureaplasma lives in the body for a very long period of time without causing any discomfort whatsoever. In addition, ureaplasma can exist without the knowledge of the person infected by it. The spread of ureaplasma is aided by bodily fluids that are mucus like. Ureaplasma is curable and can as well be treated by using antibiotics. It is important to note that in case ureaplasma goes for several days, months or years without being treated can bring about meningitis, pneumonia as well as infertility. Ureaplasma can be transmitted by having unprotected sexual contact facilitates the spread of the causal bacteria. Having said this, here are the long term effects of ureaplasma. Firstly, ureaplasma can result in fertility problems. This is simply because ureaplasma is largely linked to tubal infection as well as decreased sperm motility. This plays a major role in causing infertility. It has been discovered that a majority of women who end up having miscarriages may be suffering from this condition. The most daunting aspect about ureaplasma is that a person who is infected does not experience any symptoms thus cannot be able to know all about ureaplasma. Another long term effect of ureaplasma is complications on the urinary tract. If left untreated, this can as well cause damage to the kidney. Additionally, if ureaplasma is left untreated, it can penetrate through the blood stream thus resulting to a condition that is fatal. This can lead to sepsis which takes place when the immune system destroys the body tissues in direct response to the ureaplasma infection. Long Term Complications If ureaplasma is left untreated for a long period of time, it can cause urethritis in both men and women. This condition comes about when the urethra becomes inflamed. In most cases, those infected will tend to have symptoms such as burning sensation while urinating, smelly discharge and some blood spotting in the urine. In case the ureaplasma condition is left untreated for a long period of time, ureaplasma can affect the bladder as well as other reproductive organs which can be fatal in the long run. Ureaplasma can cause long term effect in terms on the chronic urinary tract. A majority of patients will tend to have chronic urinary tract diseases that are caused by ureaplasma bacteria. The best thing about ureaplasma is that, qualified physicians can easily remove the bacteria through the use of antibiotics. However, for all those suffering from these tract diseases, they can be prescribed for antibiotic and at the same time undergo retests to determine the presence of ureaplasma bacteria. In case there is presence of ureaplasma bacteria, the physician will be prompted to prescribe the patient with a different antibiotic that will help in treating the condition. Most of the people who have this type of ureaplasma condition tend to urinate more often with no result at all, pain in the pelvic, pain while urinating, have urine that is cloudy and some blood traces in the urine. What is ureaplasma? Ureaplasma is a particularly small bacterium belonging to the family Mycoplasmataceae (commonly known as mycoplasma). There are seventeen identified species, most usually found in the respiratory and urogenital tracts. U. urealyticum is commonly found in the genital flora of sexually active men and women. It is found in about 70% of sexually active humans, and is usually commensal (harmless and symptom-free). You have a high chance of being infected with it if you have unprotected sex with someone who has had other sexual partners, and your chances of infection increase dramatically with the number of different partners. Even if you have no symptoms, you can still pass the microorganisms in your genitals to your partner(s). This is why so many adults are infected - the infected source person has no symptoms, and usually the person they infect also shows no symptoms. You are STRONGLY advised to have a pathology test if you have any symptoms, because there is a chance you may have, and be passing on, another more serious disease to your partner(s). Possible symptoms of ureaplasma • For most people, Ureaplasma remains in the genitals and has no effect or symptoms. • A continual dull ache or pain around the genitals. • Burning or pain when urinating. • Ureaplasma has been associated with a number of diseases such as non-specific urethritis (NSU) and sterile pyuria. • Whether Ureaplasma can cause infertility, chorioamnionitis, stillbirth, premature birth, and, in the perinatal period, pneumonia, bronchopulmonary dysplasia and meningitis is contentious. Risk of having symptoms • The older you are when you get your initial ureaplasma infection, the more likely that you will suffer a mild pain, an NSU or some other symptoms. • If your immune system is weak, there is an increased chance of suffering from the above symptoms. Treatment If you are suffering any symptoms, it is important to provide a urine sample for testing by a pathology lab. This will rule out the possibility of infection by a more dangerous bacteria / protozoa. Conventional medicine usually treats a u. urealyticum infection with antibiotic doxycycline or streptomycin. Of course both partners must be treated, and outside of a strictly monogamous relationship there is a high chance of re-infection. It requires a strong course of antibiotics, and there is a possibility that your digestive and other beneficial bacteria will be devastated, with a risk of development of IBS and other problems. The natural home remedy approach to treating ureaplasma urealyticum is to leave them alone - in a healthy person they are a commensal - in other words, they should cause no problems, and most sexually active people have them. If your symptoms are serious AND a test has confirmed a u. urealyticum infection and no other infections or causes, a natural antibiotic such as colloidal silver may be able to contain the bacterial overgrowth. Usually the symptoms improve or resolve over a period of weeks or months, and an improvement in the strength of your immune system may also contain the infection. References ^ Kafetzis DA, Skevaki CL, Skouteri V, et al (October 2004). "Maternal genital colonization with Ureaplasma urealyticum promotes preterm delivery: association of the respiratory colonization of premature infants with chronic lung disease and increased mortality". Clin. Infect. Dis. 39 (8): 1113–22. doi:10.1086/424505. PMID 15486833. ^ Dieter RS (2000). "Sterile pyuria: a differential diagnosis". Compr Ther 26 (3): 150–2. doi:10.1007/s12019-000-0001-1. PMID 10984817. ^ ^ ^ UREAPLASMA & MYCOPLASMA (Also Called 'Mycoplasma & Ureaplasma Infections') What are ureaplasma and mycoplasma infections? Ureaplasma and mycoplasma are among the smallest free-living bacteria. Unlike other bacteria however, these organisms lack a cell wall and live inside cells. However, they can also live in cultures outside of cells, similar to the way viruses live. Unlike viruses, though, they can be killed by certain antibiotics. What symptoms do ureaplasma and mycoplasma cause? Symptoms can be "silent" or can cause noticeable symptoms such as discharge, burning, urinary frequency, urinary urgency, and pain. How are ureaplasma and mycoplasma diagnosed? Special laboratory tests and cultures (a method of multiplying the bacteria to better identify them) is required. The diagnosis and treatment of illnesses involving these organisms is particularly difficult due to the following reasons: These organisms require special tests and even when these special tests are conducted, it can still be very difficult to isolate the organisms and treat the patient. The tests are not something done by a typical general practitioner or gynecologist. Only a select few antibiotics kill these particular bacteria and the antibiotics have to be taken for many days, weeks, or even longer. Many patients do not take their medications as prescribed; do not take their medications long enough to be cured; or come in close contact with an infected person and become reinfected. It is important to note that the illnesses caused by these bacteria can be acquired in all kinds of ways. As an example, one of the ways ureaplasma can be acquired is through sexual relations. However, a diagnosis of ureaplasma in yourself or your partner does not imply that infidelity took place. There is no way of knowing for sure how or when the organism was actually transmitted to the first partner. What is known for sure is that both partners are treated to help prevent any possible spread and development of bladder problems between the two individuals. How are illnesses caused by ureaplasma and mycoplasma treated? Treatment usually consists of the use of certain antibiotics, out of a family of antibiotics called the tetracyclines or erythromycins. Be sure to inform the doctor if you are allergic to the medication before taking it. Do not engage in sexual activity while you are taking the antibiotic prescription. Take the antibiotic as prescribed and for the full length as directed on the prescription label. This is important to ensure that the organism is fully eliminated. Important. If you are sexually active, your partner will need to be prescribed antibiotics to treat the infection. First-line treatments are either: doxycycline 100 mg, 1 pill, taken by mouth twice daily for 14 days, or erythromycin 400 mg, 2 pills, taken by mouth four times a day for 7 days Ideally, the partner should be placed on the same antibiotic as the patient. You should be retested for the organism after finishing the course of antibiotics, which can be done at your local hospital, your local doctor's office, or a lab. At that time, a urine or vaginal specimen will be taken and recultured to determine if the bacteria is completely eliminated from your body. We advise that your partner be tested or retested for this organism. Sometime you may need another round of antibiotic to treat the infection again. MICROBIOLOGY OF BIOFIMS A biofilm is any group of microorganisms in which cells stick to each other on a surface. These adherent cells are frequently embedded within a self-produced matrix of extracellular polymeric substance (EPS). Biofilm EPS, which is also referred to as slime (although not everything described as slime is a biofilm), is a polymeric conglomeration generally composed of extracellular DNA, proteins, and polysaccharides. Biofilms may form on living or non-living surfaces and can be prevalent in natural, industrial and hospital settings.[1][2] The microbial cells growing in a biofilm are physiologically distinct from planktonic cells of the same organism, which, by contrast, are single-cells that may float or swim in a liquid medium. Microbes form a biofilm in response to many factors, which may include cellular recognition of specific or non-specific attachment sites on a surface, nutritional cues, or in some cases, by exposure of planktonic cells to sub-inhibitory concentrations of antibiotics.[3][4] When a cell switches to the biofilm mode of growth, it undergoes a phenotypic shift in behavior in which large suites of genes are differentially regulated.[ Formation Formation of a biofilm begins with the attachment of free-floating microorganisms to a surface. These first colonists adhere to the surface initially through weak, reversible adhesion via van der Waals forces. If the colonists are not immediately separated from the surface, they can anchor themselves more permanently using cell adhesion structures such as pili.[6] Hydrophobicity also plays an important role in determining the ability of bacteria to form biofilms, as those with increased hydrophobicity have reduced repulsion between the extracellular matrix and the bacterium.[7] Some species are not able to attach to a surface on their own but are sometimes able to anchor themselves to the matrix or directly to earlier colonists. It is during this colonization that the cells are able to communicate via quorum sensing using products such as AHL. Some bacteria are unable to form biofilms as successfully due to their limited motility. Nonmotile bacteria cannot recognize the surface or aggregate together as easily as motile bacteria.[8] Once colonization has begun, the biofilm grows through a combination of cell division and recruitment. Polysaccharide matrices typically enclose bacterial biofilms. In addition to the polysaccharides, these matrices may also contain material from the surrounding environment, including but not limited to minerals, soil particles, and blood components, such as erythrocytes and fibrin.[9] The final stage of biofilm formation is known as dispersion, and is the stage in which the biofilm is established and may only change in shape and size. The development of a biofilm may allow for an aggregate cell colony (or colonies) to be increasingly antibiotic resistant. [edit] Development There are five stages of biofilm development (see illustration at right): Initial attachment: Irreversible attachment: Maturation I: Maturation II: Dispersion: [edit] Dispersal Dispersal of cells from the biofilm colony is an essential stage of the biofilm life cycle. Dispersal enables biofilms to spread and colonize new surfaces. Enzymes that degrade the biofilm extracellular matrix, such as dispersin B and deoxyribonuclease, may play a role in biofilm dispersal.[10][11] Biofilm matrix degrading enzymes may be useful as anti-biofilm agents.[12][13] Recent evidence has shown that a fatty acid messenger, cis-2-decenoic acid, is capable of inducing dispersion and inhibiting growth of biofilm colonies. Secreted by Pseudomonas aeruginosa, this compound induces cyclo heteromorphic cells in several species of bacteria and the yeast Candida albicans.[14] Nitric oxide has also been shown to trigger the dispersal of biofilms of several bacteria species [15][16] at sub-toxic concentrations. Nitric oxide has the potential for the treatment of patients that suffer from chronic infections caused by biofilms.[17] [edit] Properties Biofilms are usually found on solid substrates submerged in or exposed to an aqueous solution, although they can form as floating mats on liquid surfaces and also on the surface of leaves, particularly in high humidity climates. Given sufficient resources for growth, a biofilm will quickly grow to be macroscopic (visible to the naked eye). Biofilms can contain many different types of microorganism, e.g. bacteria, archaea, protozoa, fungi and algae; each group performs specialized metabolic functions. However, some organisms will form single-species films under certain conditions. The social structure (cooperation, competition) within a biofilm highly depends on the different species present.[18] [edit] Extracellular matrix The biofilm is held together and protected by a matrix of secreted polymeric compounds called EPS. EPS is an abbreviation for either extracellular polymeric substance or exopolysaccharide. This matrix protects the cells within it and facilitates communication among them through biochemical signals. Some biofilms have been found to contain water channels that help distribute nutrients and signalling molecules.[19] This matrix is strong enough that under certain conditions, biofilms can become fossilized (Stromatolites). Bacteria living in a biofilm usually have significantly different properties from free-floating bacteria of the same species, as the dense and protected environment of the film allows them to cooperate and interact in various ways. One benefit of this environment is increased resistance to detergents and antibiotics, as the dense extracellular matrix and the outer layer of cells protect the interior of the community. In some cases antibiotic resistance can be increased a thousandfold.[20] Lateral gene transfer is greatly facilitated in biofilms and leads to a more stable biofilm structure.[21] However, biofilms are not always less susceptible to antibiotics. For instance, the biofilm form of Pseudomonas aeruginosa has no greater resistance to antimicrobials than do stationary-phase planktonic cells, although when the biofilm is compared to logarithmic phase planktonic cells, the biofilm does have greater resistance to antimicrobials. This resistance to antibiotics in both stationary phase cells and biofilms may be due to the presence of persister cells.[22] [edit] Examples Biofilms are ubiquitous. Nearly every species of microorganism, not only bacteria and archaea, have mechanisms by which they can adhere to surfaces and to each other. Biofilms will form on virtually every non-shedding surface in a non-sterile aqueous (or very humid) environment. • Biofilms can be found on rocks and pebbles at the bottom of most streams or rivers and often form on the surface of stagnant pools of water. In fact, biofilms are important components of food chains in rivers and streams and are grazed by the aquatic invertebrates upon which many fish feed. • Biofilms can grow in the most extreme environments: from, for example, the extremely hot, briny waters of hot springs ranging from very acidic to very alkaline, to frozen glaciers. • In the human environment, biofilms can grow in showers very easily since they provide a moist and warm environment for the biofilm to thrive. Biofilms can form inside water and sewage pipes and cause clogging and corrosion. Biofilms on floors and counters can make sanitation difficult in food preparation areas. • Biofilms in cooling- or heating-water systems are known to reduce heat transfer.[23] • Biofilms in marine engineering systems, such as pipelines of the offshore oil and gas industry,[24] can lead to substantial corrosion problems. Corrosion is mainly due to abiotic factors; however, at least 20% of corrosion is caused by microorganisms that are attached to the metal subsurface (i.e., microbially influenced corrosion). • Bacterial adhesion to boat hulls serves as the foundation for biofouling of seagoing vessels. Once a film of bacteria forms, it is easier for other marine organisms such as barnacles to attach. Such fouling can reduce maximum vessel speed by up to 20%, prolonging voyages and consuming fuel. Time in dry dock for refitting and repainting reduces the productivity of shipping assets, and the useful life of ships is also reduced due to corrosion and mechanical removal (scraping) of marine organisms from ships' hulls. • Biofilms can also be harnessed for constructive purposes. For example, many sewage treatment plants include a treatment stage in which waste water passes over biofilms grown on filters, which extract and digest organic compounds. In such biofilms, bacteria are mainly responsible for removal of organic matter (BOD), while protozoa and rotifers are mainly responsible for removal of suspended solids (SS), including pathogens and other microorganisms. Slow sand filters rely on biofilm development in the same way to filter surface water from lake, spring or river sources for drinking purposes. What we regard as clean water is effectively a waste material to these microcellular organisms. • Biofilms can help eliminate petroleum oil from contaminated oceans or marine systems. The oil is eliminated by the hydrocarbon-degrading activities of microbial communities, in particular by a remarkable recently discovered group of specialists, the so-called hydrocarbonoclastic bacteria (HCB).[25] • Stromatolites are layered accretionary structures formed in shallow water by the trapping, binding and cementation of sedimentary grains by microbial biofilms, especially of cyanobacteria. Stromatolites include some of the most ancient records of life on Earth, and are still forming today. • Biofilms are present on the teeth of most animals as dental plaque, where they may cause tooth decay and gum disease. • Biofilms are found on the surface of and inside plants. They can either contribute to crop disease or, as in the case of nitrogen-fixing Rhizobium on roots, exist symbiotically with the plant.[26] Examples of crop diseases related to biofilms include Citrus Canker, Pierce's Disease of grapes, and Bacterial Spot of plants such as peppers and tomatoes.[27] • Biofilms are used in microbial fuel cells (MFCs) to generate electricity from a variety of starting materials, including complex organic waste and renewable biomass.[2] [edit] Biofilms and infectious diseases Biofilms have been found to be involved in a wide variety of microbial infections in the body, by one estimate 80% of all infections.[28] Infectious processes in which biofilms have been implicated include common problems such as urinary tract infections, catheter infections, middle-ear infections, formation of dental plaque,[29] gingivitis,[29] coating contact lenses,[30] and less common but more lethal processes such as endocarditis, infections in cystic fibrosis, and infections of permanent indwelling devices such as joint prostheses and heart valves.[31][32] More recently it has been noted that bacterial biofilms may impair cutaneous wound healing and reduce topical antibacterial efficiency in healing or treating infected skin wounds.[33] It has recently been shown that biofilms are present on the removed tissue of 80% of patients undergoing surgery for chronic sinusitis. The patients with biofilms were shown to have been denuded of cilia and goblet cells, unlike the controls without biofilms who had normal cilia and goblet cell morphology.[34] Biofilms were also found on samples from two of 10 healthy controls mentioned. The species of bacteria from interoperative cultures did not correspond to the bacteria species in the biofilm on the respective patient's tissue. In other words, the cultures were negative though the bacteria were present.[35] Biofilms can also be formed on the inert surfaces of implanted devices such as catheters, prosthetic cardiac valves and intrauterine devices. [36] New staining techniques are being developed to differentiate bacterial cells growing in living animals, e.g. from tissues with allergy-inflammations .[37] Research has shown that sub-therapeutic levels of β-lactam antibiotics induce biofilm formation in Staphylococcus aureus. This sub-therapeutic level of antibiotic may result from the use of antibiotics as growth promoters in agriculture, or during the normal course of antibiotic therapy. The biofilm formation induced by low-level methicillin was inhibited by DNase, suggesting that the sub-therapeutic levels of antibiotic also induce extracellular DNA release. [38] [edit] Dental plaque Dental plaque is the material that adheres to the teeth and consists of bacterial cells (mainly Streptococcus mutans and Streptococcus sanguinis), salivary polymers and bacterial extracellular products. Plaque is a biofilm on the surfaces of the teeth. This accumulation of microorganisms subject the teeth and gingival tissues to high concentrations of bacterial metabolites which results in dental disease.[29][39] [edit] Legionellosis Legionella bacteria are known to grow under certain conditions in biofilms, in which they are protected against disinfectants. Workers in cooling towers, persons working in air conditioned rooms and people taking a shower are exposed to Legionella by inhalation when the systems are not well designed, constructed, or maintained.[40] [edit] References ^ Hall-Stoodley L, Costerton JW, Stoodley P (February 2004). "Bacterial biofilms: from the natural environment to infectious diseases". Nature Reviews. Microbiology 2 (2): 95–108. doi:10.1038/nrmicro821. PMID 15040259. ^ a b Lear, G; Lewis, GD (editor) (2012). Microbial Biofilms: Current Research and Applications. Caister Academic Press. ISBN 978-1-904455-96-7. ^ Karatan E, Watnick P (June 2009). "Signals, regulatory networks, and materials that build and break bacterial biofilms". Microbiology and Molecular Biology Reviews 73 (2): 310–47. doi:10.1128/MMBR.00041-08. PMC 2698413. PMID 19487730. ^ Hoffman LR, D'Argenio DA, MacCoss MJ, Zhang Z, Jones RA, Miller SI (August 2005). "Aminoglycoside antibiotics induce bacterial biofilm formation". Nature 436 (7054): 1171–5. doi:10.1038/nature03912. PMID 16121184. (primary source) ^ An D, Parsek MR (June 2007). "The promise and peril of transcriptional profiling in biofilm communities". Current Opinion in Microbiology 10 (3): 292–6. doi:10.1016/j.mib.2007.05.011. PMID 17573234. ^ JPG Images: ^ Donlan, Rodney M. 2002. Biofilms: Microbial Life on Surfaces. Emerging Infectious Diseases. Vol. 8, No. 9: pg. 881-890. ^ Ibid. ^ Ibid. ^ Kaplan JB, Ragunath C, Ramasubbu N, Fine DH (August 2003). "Detachment of Actinobacillus actinomycetemcomitans biofilm cells by an endogenous beta-hexosaminidase activity". Journal of Bacteriology 185 (16): 4693–8. doi:10.1128/JB.185.16.4693-4698.2003. PMC 166467. PMID 12896987. ^ Izano EA, Amarante MA, Kher WB, Kaplan JB (January 2008). "Differential roles of poly-N-acetylglucosamine surface polysaccharide and extracellular DNA in Staphylococcus aureus and Staphylococcus epidermidis biofilms". Applied and Environmental Microbiology 74 (2): 470–6. doi:10.1128/AEM.02073-07. PMC 2223269. PMID 18039822.

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