Mycoplasma has no cell wall and is the smallest free-living bacteria, being 1/5 to 1/25 the size of other bacteria. It is strictly anaerobic and has a special characteristic of metabolizing glucose. Like the virus, it is very dependent upon its host for survival. It was originally classified as a virus due to its small size and as a pleuro-pneumoniae organism because it was first found to be related to pneumonia.
There are many different species of Mycoplasma. Mycoplasma pneumonia as well as at least 7 other mycoplasma species have been linked as a direct cause or significant co-factor to many chronic diseases. These include Mycoplasma pneumonia, incognitos, penetrans, pirum, genitalium, fermentans, salivarium, hominis and Ureaplasma urealyticum. Scientists have been studying the relationship between Mycoplasma and different diseases for several decades. A list of such conditions includes cancer, auto-immune diseases (arthritis, lupus, scleroderma, multiple sclerosis) ALS, chronic fatigue syndrome and candidiasis. Mycoplasma are found to infect females 4 times more often than males, which just happens to be similar to the incidence rate in rheumatoid arthritis, fibromyalgia, Chronic Fatigue and other related disorders.
Due to the small size and the lack of a cell wall, this microorganism is capable of infecting a great number of cells in any part of the body and live as a parasite on the surface of the cells. Mycoplasmas can become a parasite in plants, insects, animals, and humans, and can trigger different diseases. Once the Mycoplasma becomes a parasite in the cell, morphologic and physiologic changes are developed and it takes on the appearance of various diseases such as pneumonia, urethritis, pyelonephritis, as well as arthritis, lupus and other immune diseases. In cancer, the tumor cells infected by Mycoplasma are more susceptible to spreading which contributes to metastases in different parts of the body. This is also true with Chronic Fatigue Syndrome (especially when the symptoms are severe), Multiple Sclerosis, and ALS (Amyotrophic Lateral Sclerosis).
A list of conditions which may be caused or influenced by Mycoplasma or for which Mycoplasma becomes an opportunistic infection include:
- AIDS/HIV
- ALS
- arthritis
- asthma
- bronchitis
- Cancer
- chronic fatigue syndrome
- chronic nongonococcal urethritis
- chronic pelvic inflammatory disease
- Crohn’s
- diabetes
- endocrine disorders
- eye and ear disorders and infections
- Fibromyalgia
- gingivitis and periodontal disease
- heart disease
- infertility
- irritable bowel syndrome
- leukemia
- lupus
- multiple sclerosis
- pneumonia
- psoriasis
- scleroderma
- TMJ disorders
- urinary tract infections
Further research is necessary to confirm these connections.
Since mycoplasma have no cell wall, immune cells can not ‘see’ them. Infected white blood cells (leukocytes) are not killed, but disabled. This results in the immune system being under the false impression that there are enough white cells in circulation. Both under activity (anergia) and over activity (hyperergia) of the immune system have been reported as a result of mycoplasma infections.
Mycoplasma is spread through contact with droplets from the nose and throat of infected people especially when they cough and sneeze. Transmission is thought to require prolonged close contact with an infected person. Spread in families, schools and institutions occurs slowly. The contagious period is probably fewer than 10 days and occasionally longer. In Mycoplasma pneumoniae infection, symptoms generally begin 15 to 25 days after exposure. The symptoms generally develop slowly, over a period of two to four days.
Signs, symptoms & indicators of Mycoplasma Infection
Fatigue of recent onset
Having a slight/having a moderate/having a high fever
Recent/chronic nonproductive cough
Conditions that suggest Mycoplasma Infection
Scleroderma
By Alan Cantwell, Jr., M.D. © 2000
Ask most doctors what causes scleroderma and they will tell you the cause is unknown. Furthermore, they will claim that no infectious agent has ever been shown in scleroderma. However, for more than 50 years scientific evidence has been accumulating in the medical journals showing that bacteria are indeed associated with scleroderma, and with closely allied diseases, such as lupus and rheumatoid arthritis.
In the past decade many chronic diseases once believed to be non-infectious are now thought to be caused by viruses, bacteria, or by tiny mycoplasma-like organisms which have characteristics of both bacteria and viruses. Even certain forms of cancer are now considered infectious.
Stomach ulcers were definitely thought to be non-infectious for most of the last century, and physicians and microbiologists insisted bacteria could not grow in the acid environment of the stomach. The ultimate proof that certain bacteria could cause stomach ulcer disease was obtained when a physician-researcher drank a culture of the ulcer-producing bacteria and produced the disease in himself.
It is unthinkable (but true) that decades of research showing organisms in scleroderma and arthritis would be ignored by the medical establishment. Especially now that antibiotics appear to have a beneficial effect in these diseases, it is imperative for physicians to be aware of this research and to stop pretending it does not exist.
Before reviewing the case for bacteria in scleroderma and RA, it is important to acknowledge the role of mycoplasma-like organisms in these diseases. For most of the twentieth century, medical science has regarded these bacteria-like and virus-like microbes as laboratory curiosities of little import. But mycoplasmas can invade cells and even the cell nucleus, thereby promoting chronic infection difficult to eradicate.
Mycoplasma (also known as cell-wall deficient bacteria) are derived from bacteria which have shed all or part of their cell wall. Many chronic diseases may prove to be due to infectious bacteria which transform into the mycoplasma state in order to better adapt to the body. In recent years, mycoplasmas have been discovered in such diverse diseases as Gulf War Illness, AIDS, and certain forms of cancer.
Mycoplasmas may all look and act similarly when in the cell-wall deficient phase – and if a particular mycoplasma becomes stuck in this phase and does not revert back to its original “parent” bacteria, it is impossible to determine the exact bacterial origin of the mysoplasma in question.
Mycoplasma are notoriously difficult to detect and to culture. Thus, they frequently go unrecognized in disease states. Mycoplasma research is still in its infancy, and most experts in the field are microbiologists, rather than practicing medical doctors. Nevertheless, there is a wealth of research implicating mycoplasmas in human disease. The best book on this subject is Cell Wall Deficient Forms: Stealth Pathogens, by mycoplasma expert and Professor Emeritus Lida Holmes Mattman of the Department of Biology at Wayne State University in Detroit.
The Road Back Foundation advocates the use of antibiotic therapy for scleroderma and RA, based on the mycoplasma research first undertaken in the 1940s by Thomas McPherson Brown, M.D., and his microbiologist co-worker Harold W. Clark, Ph.D., currently the Director of the Mycoplasma Research Institute of Beverly Hills, Florida.
The scientific evidence linking mycoplasma to these diseases is simply explained in Dr. Brown’s book, The Road Back: Rheumatoid Arthritis, Its Cause and Treatment, [now out of print] and in Clark’s Why Arthritis?: Searching for the Cause and the Cure of Rheumatoid Disease. Medical writer Henry Scammell has also authored two books based on Brown’s research: The New Arthritis Breakthrough, and Scleroderma: The Proven Therapy That Can Save Your Life.
The first report of “acid-fast” bacteria (similar to the kind of microbes that cause tuberculosis) in scleroderma was published by Virginia Wuerthele-Caspe Livingston, M.D. in 1947. These unusual microbes were discovered in skin scrapings from a woman with ulcerations of the fingers. In later collaboration with pathologists, dermatologists, and microbiologists, she further characterized the peculiar and multi-shaped (pleomorphic) bacteria she consistently isolated from scleroderma cases. Her scleroderma research progressed into microbiologic studies showing similar-appearing acid-fast bacteria in various forms of cancer. Until her death in 1990 at the age of 84, Livingston constantly studied and published her findings on the various aspects of the ‘sclero-bacillus’ she isolated from scleroderma and the ‘cancer microbes’ associated with cancer. Despite the furor and controversy that her papers elicited from the cancer establishment, she never wavered in her belief that microbes were at the root of ‘autoimmune’ and cancerous diseases.
Livingston wrote two books about her lifelong research: Cancer: A New Breakthrough (1972), and The Conquest of Cancer (1984). Her major scientific publications (including the original scleroderma papers) and confirmatory papers by other leading scientists are collected and reprinted in Livingston’s The Microbiology of Cancer, available from the Livingston-Wheeler Foundation in San Diego, California.
In 1953, Livingston’s finding of bacteria in scleroderma was confirmed by scientists at the Pasteur Institute in Brussels. Additional confirmation was published in 1966 in the Archives of Dermatology, when my own research (co-authored with professors of dermatology and microbiology) showed acid-fast bacteria in the skin biopsy samples from scleroderma cases. During the 1970s and 80s nine additional papers also confirmed the presence of cell-wall deficient, mycoplasma-like microbes in the skin of scleroderma, as well as in multiple diseased organs at autopsy in a fatal case of scleroderma. Like Livingston’s bacteria, the organisms we cultured from various patients were pleomorphic. In some fatal cases, the organisms cultured near death were similar to acid-fast mycobacteria associated with tuberculosis, whereas in milder cases the microbes were identified as staphlococci or corynebacteria. Using a tissue stain designed by Lida Mattman to detect acid-fast bacteria and cell-wall deficient bacteria (mycoplasma), bacteria were identified in the skin biopsy material from all cases.
Following the lead of Livingston, my scleroderma research progressed to similar studies of lupus erythematosus (another autoimmune disease) and certain forms of cancer. These studies all showed that pleomorphic bacteria, most likely in a mycoplasma state of growth within the diseased tissue, could be cultured and identified from these diseases. The results of these studies performed over a quarter-century are contained in my book, The Cancer Microbe: The Hidden Killer in Cancer, AIDS, and Other Immune Diseases. In addition, abstracts of most of these Cantwell papers can be retrieved online at the PubMed website sponsored by the National Library of Medicine ( http://www.ncbi.nlm.gov/PubMed ).
The scleroderma research of Livingston and her colleagues that began in the 1940s is undoubtedly related to current research implicating mycoplasmas in human disease. Her papers published in the 1950s clearly show pleomorphic microbes consistent with what are now known s mycoplasmas or cell wall deficient bacteria.
For the first half-century Livingston’s microbiology of scleroderma and cancer has been clearly outside the mainstream of medical thought. Although ignored by the medical establishment, her discoveries have never been disproven.
Despite all this, there is a wealth of research pointing to bacteria as the cause of scleroderma. Ignoring this research is indeed [unfortunate], particularly when it is again fashionable to talk about infectious agents in cancer, and at a time when antibiotics seem to be of value in treating diseases like scleroderma and RA.
Sarcoidosis
From time to time there have been reports of autoimmune disease succumbing to tetracycline antibiotics, but many have assumed this was due to coincidence, or to some ill-defined ‘anti-inflammatory property’ of the tetracyclines. But now the inflammation of Sarcoidosis has succumbed to antibiotics in two independent studies. This review examines the Cell Wall Deficient (antibiotic resistant) bacteria which have been found in tissue from patients with Sarcoidosis. It examines how such bacteria can infect the phagocytes of the immune system, and how they may therefore be responsible for not only sarcoid inflammation, but also for other autoimmune disease.
Proof positive of a bacterial pathogenesis for Sarcoidosis includes not only the demonstrated ability of these studies to put the disease into remission, but also the severity of Jarisch-Herxheimer Shock resulting from endotoxin release as the microbes are killed. Studies delineating the hormone responsible for phagocyte differentiation in the Th1 immune response, 1,25-dihydroxyvitamin D, are discussed, and its utility as a marker of Th1 immune inflammation is reviewed. Finally, data showing that the behavior of this hormone is also aberrant in Rheumatoid Arthritis, Systemic Lupus Erythematosus, and Parkinson’s, raise the possibility that these diseases may also have a CWD bacterial pathogenesis. [Autoimmunity Reviews, Vol 3, No 4, pp 295-300]
Pneumonia
Mycoplasma pneumoniae is a common cause of community-acquired pneumonia, and the disease usually is of gradual onset. The prolonged paroxysmal cough seen in this disease is thought to be due to the inhibition of ciliary movement, since the organism has a filamentous end that allows it to slip between cilia within the respiratory epithelium.
The organism has a selective affinity for respiratory epithelial cells, and it produces hydrogen peroxide, which is thought to be responsible for much of the initial cell disruption in the respiratory tract and for damage to erythrocyte membranes.
Infections with Mycoplasma pneumoniae result in pneumonia in only 3% of cases yet 77% do involve the upper respiratory tract. Although mycoplasmal pneumonia can occur at any time of the year, outbreaks tend to occur in the fall.
Pyelonephritis
M.hominis has been found present in cases of pyelonephritis, kidney disease, and U.urealyticum which is more usually seen in urine samples, can be found in some types of bladder stones.
Interstitial Cystitis
Ureaplasma and Mycoplasma as a group of organisms are the least investigated and are probably the greatest cause of more chronic urinary and gynaecological problems than any other class of bacteria. They should be considered as a cause of I.C. in women and nonspecific urethritis in men.
Vaginitis/Vaginal Infection
“They may also be a causative organism in bacterial vaginosis and vaginitis thought to be caused by candida. There are presently no routine culture facilities for identifying such bacteria in the British National Health Service. A high vaginal swab may yield ureaplasma even if the urine sample is shown negative. Culture facilities for M.genitalis, M. hominis and M.urealyticum should be introduced as a matter of urgency.” [Dr Fred Lim, Private Consultant in Genito-Urinary Medicine]
Urethritis / Urethral Syndrome
Chronic nongonococcal urethritis may be associated with Mycoplasma infection. In men, about 15-20% of cases show U.urealyticum as a cause for non-gonococcal urethritis
Mycoplasma Infection can lead to
Sarcoidosis
From time to time there have been reports of autoimmune disease succumbing to tetracycline antibiotics, but many have assumed this was due to coincidence, or to some ill-defined ‘anti-inflammatory property’ of the tetracyclines. But now the inflammation of Sarcoidosis has succumbed to antibiotics in two independent studies. This review examines the Cell Wall Deficient (antibiotic resistant) bacteria which have been found in tissue from patients with Sarcoidosis. It examines how such bacteria can infect the phagocytes of the immune system, and how they may therefore be responsible for not only sarcoid inflammation, but also for other autoimmune disease.
Proof positive of a bacterial pathogenesis for Sarcoidosis includes not only the demonstrated ability of these studies to put the disease into remission, but also the severity of Jarisch-Herxheimer Shock resulting from endotoxin release as the microbes are killed. Studies delineating the hormone responsible for phagocyte differentiation in the Th1 immune response, 1,25-dihydroxyvitamin D, are discussed, and its utility as a marker of Th1 immune inflammation is reviewed. Finally, data showing that the behavior of this hormone is also aberrant in Rheumatoid Arthritis, Systemic Lupus Erythematosus, and Parkinson’s, raise the possibility that these diseases may also have a CWD bacterial pathogenesis. [Autoimmunity Reviews, Vol 3, No 4, pp 295-300]
Scleroderma
By Alan Cantwell, Jr., M.D. © 2000
Ask most doctors what causes scleroderma and they will tell you the cause is unknown. Furthermore, they will claim that no infectious agent has ever been shown in scleroderma. However, for more than 50 years scientific evidence has been accumulating in the medical journals showing that bacteria are indeed associated with scleroderma, and with closely allied diseases, such as lupus and rheumatoid arthritis.
In the past decade many chronic diseases once believed to be non-infectious are now thought to be caused by viruses, bacteria, or by tiny mycoplasma-like organisms which have characteristics of both bacteria and viruses. Even certain forms of cancer are now considered infectious.
Stomach ulcers were definitely thought to be non-infectious for most of the last century, and physicians and microbiologists insisted bacteria could not grow in the acid environment of the stomach. The ultimate proof that certain bacteria could cause stomach ulcer disease was obtained when a physician-researcher drank a culture of the ulcer-producing bacteria and produced the disease in himself.
It is unthinkable (but true) that decades of research showing organisms in scleroderma and arthritis would be ignored by the medical establishment. Especially now that antibiotics appear to have a beneficial effect in these diseases, it is imperative for physicians to be aware of this research and to stop pretending it does not exist.
Before reviewing the case for bacteria in scleroderma and RA, it is important to acknowledge the role of mycoplasma-like organisms in these diseases. For most of the twentieth century, medical science has regarded these bacteria-like and virus-like microbes as laboratory curiosities of little import. But mycoplasmas can invade cells and even the cell nucleus, thereby promoting chronic infection difficult to eradicate.
Mycoplasma (also known as cell-wall deficient bacteria) are derived from bacteria which have shed all or part of their cell wall. Many chronic diseases may prove to be due to infectious bacteria which transform into the mycoplasma state in order to better adapt to the body. In recent years, mycoplasmas have been discovered in such diverse diseases as Gulf War Illness, AIDS, and certain forms of cancer.
Mycoplasmas may all look and act similarly when in the cell-wall deficient phase – and if a particular mycoplasma becomes stuck in this phase and does not revert back to its original “parent” bacteria, it is impossible to determine the exact bacterial origin of the mysoplasma in question.
Mycoplasma are notoriously difficult to detect and to culture. Thus, they frequently go unrecognized in disease states. Mycoplasma research is still in its infancy, and most experts in the field are microbiologists, rather than practicing medical doctors. Nevertheless, there is a wealth of research implicating mycoplasmas in human disease. The best book on this subject is Cell Wall Deficient Forms: Stealth Pathogens, by mycoplasma expert and Professor Emeritus Lida Holmes Mattman of the Department of Biology at Wayne State University in Detroit.
The Road Back Foundation advocates the use of antibiotic therapy for scleroderma and RA, based on the mycoplasma research first undertaken in the 1940s by Thomas McPherson Brown, M.D., and his microbiologist co-worker Harold W. Clark, Ph.D., currently the Director of the Mycoplasma Research Institute of Beverly Hills, Florida.
The scientific evidence linking mycoplasma to these diseases is simply explained in Dr. Brown’s book, The Road Back: Rheumatoid Arthritis, Its Cause and Treatment, [now out of print] and in Clark’s Why Arthritis?: Searching for the Cause and the Cure of Rheumatoid Disease. Medical writer Henry Scammell has also authored two books based on Brown’s research: The New Arthritis Breakthrough, and Scleroderma: The Proven Therapy That Can Save Your Life.
The first report of “acid-fast” bacteria (similar to the kind of microbes that cause tuberculosis) in scleroderma was published by Virginia Wuerthele-Caspe Livingston, M.D. in 1947. These unusual microbes were discovered in skin scrapings from a woman with ulcerations of the fingers. In later collaboration with pathologists, dermatologists, and microbiologists, she further characterized the peculiar and multi-shaped (pleomorphic) bacteria she consistently isolated from scleroderma cases. Her scleroderma research progressed into microbiologic studies showing similar-appearing acid-fast bacteria in various forms of cancer. Until her death in 1990 at the age of 84, Livingston constantly studied and published her findings on the various aspects of the ‘sclero-bacillus’ she isolated from scleroderma and the ‘cancer microbes’ associated with cancer. Despite the furor and controversy that her papers elicited from the cancer establishment, she never wavered in her belief that microbes were at the root of ‘autoimmune’ and cancerous diseases.
Livingston wrote two books about her lifelong research: Cancer: A New Breakthrough (1972), and The Conquest of Cancer (1984). Her major scientific publications (including the original scleroderma papers) and confirmatory papers by other leading scientists are collected and reprinted in Livingston’s The Microbiology of Cancer, available from the Livingston-Wheeler Foundation in San Diego, California.
In 1953, Livingston’s finding of bacteria in scleroderma was confirmed by scientists at the Pasteur Institute in Brussels. Additional confirmation was published in 1966 in the Archives of Dermatology, when my own research (co-authored with professors of dermatology and microbiology) showed acid-fast bacteria in the skin biopsy samples from scleroderma cases. During the 1970s and 80s nine additional papers also confirmed the presence of cell-wall deficient, mycoplasma-like microbes in the skin of scleroderma, as well as in multiple diseased organs at autopsy in a fatal case of scleroderma. Like Livingston’s bacteria, the organisms we cultured from various patients were pleomorphic. In some fatal cases, the organisms cultured near death were similar to acid-fast mycobacteria associated with tuberculosis, whereas in milder cases the microbes were identified as staphlococci or corynebacteria. Using a tissue stain designed by Lida Mattman to detect acid-fast bacteria and cell-wall deficient bacteria (mycoplasma), bacteria were identified in the skin biopsy material from all cases.
Following the lead of Livingston, my scleroderma research progressed to similar studies of lupus erythematosus (another autoimmune disease) and certain forms of cancer. These studies all showed that pleomorphic bacteria, most likely in a mycoplasma state of growth within the diseased tissue, could be cultured and identified from these diseases. The results of these studies performed over a quarter-century are contained in my book, The Cancer Microbe: The Hidden Killer in Cancer, AIDS, and Other Immune Diseases. In addition, abstracts of most of these Cantwell papers can be retrieved online at the PubMed website sponsored by the National Library of Medicine ( http://www.ncbi.nlm.gov/PubMed ).
The scleroderma research of Livingston and her colleagues that began in the 1940s is undoubtedly related to current research implicating mycoplasmas in human disease. Her papers published in the 1950s clearly show pleomorphic microbes consistent with what are now known s mycoplasmas or cell wall deficient bacteria.
For the first half-century Livingston’s microbiology of scleroderma and cancer has been clearly outside the mainstream of medical thought. Although ignored by the medical establishment, her discoveries have never been disproven.
Despite all this, there is a wealth of research pointing to bacteria as the cause of scleroderma. Ignoring this research is indeed [unfortunate], particularly when it is again fashionable to talk about infectious agents in cancer, and at a time when antibiotics seem to be of value in treating diseases like scleroderma and RA.
Pneumonia
Mycoplasma pneumoniae is a common cause of community-acquired pneumonia, and the disease usually is of gradual onset. The prolonged paroxysmal cough seen in this disease is thought to be due to the inhibition of ciliary movement, since the organism has a filamentous end that allows it to slip between cilia within the respiratory epithelium.
The organism has a selective affinity for respiratory epithelial cells, and it produces hydrogen peroxide, which is thought to be responsible for much of the initial cell disruption in the respiratory tract and for damage to erythrocyte membranes.
Infections with Mycoplasma pneumoniae result in pneumonia in only 3% of cases yet 77% do involve the upper respiratory tract. Although mycoplasmal pneumonia can occur at any time of the year, outbreaks tend to occur in the fall.
Recommendations for Mycoplasma Infection
Antibiotics
Doxycycline, tetracycline, clindamycin, lincomycin, and ciprofloxacin were found to be effective against Mycoplasma incognitus. But erythromycin, the antibiotic most commonly used to treat mycoplasma infections, was not effective and penicillin, streptomycin, gentamicin, and others also had no effect. Treatment is very long term compared to the typical course of antibiotic use.
For other mycoplasmas, doxycycline at 600mg per day is needed and anything lower and the patient does seem to need repeated and unhelpful courses.
Your sexual partner must also take a high dose to stop future transmission and reinfection. Condoms are recommended when sex resumes. Circumcised men are less likely to carry it but even so, may carry the organism, too, if they were once
infected by an infected female. Repeat episodes between you must stop because doxycycline may eventually stop working.
Key
| Weak or unproven link |
| Strong or generally accepted link |
| Proven definite or direct link |
| Likely to help |
Glossary
Bacteria
Microscopic germs. Some bacteria are "harmful" and can cause disease, while other "friendly" bacteria protect the body from harmful invading organisms.
Anaerobic
Of, relating to, or being activity in which the body incurs an oxygen debt (for example weight training or resistive exercises) and does not immediately burn off a lot of calories and fat.
Metabolism
The chemical processes of living cells in which energy is produced in order to replace and repair tissues and maintain a healthy body. Responsible for the production of energy, biosynthesis of important substances, and degradation of various compounds.
Glucose
A sugar that is the simplest form of carbohydrate. It is commonly referred to as blood sugar. The body breaks down carbohydrates in foods into glucose, which serves as the primary fuel for the muscles and the brain.
Virus
Any of a vast group of minute structures composed of a protein coat and a core of DNA and/or RNA that reproduces in the cells of the infected host. Capable of infecting all animals and plants, causing devastating disease in immunocompromised individuals. Viruses are not affected by antibiotics, and are completely dependent upon the cells of the infected host for the ability to reproduce.
Chronic
Usually Chronic illness: Illness extending over a long period of time.
Cancer
Refers to the various types of malignant neoplasms that contain cells growing out of control and invading adjacent tissues, which may metastasize to distant tissues.
Arthritis
Inflammation of a joint, usually accompanied by pain, swelling, and stiffness, and resulting from infection, trauma, degenerative changes, metabolic disturbances, or other causes. It occurs in various forms, such as bacterial arthritis, osteoarthritis, or rheumatoid arthritis. Osteoarthritis, the most common form, is characterized by a gradual loss of cartilage and often an overgrowth of bone at the joints.
Multiple Sclerosis
Demyelinating disorder of the central nervous system, causing patches of sclerosis (plaques) in the brain and spinal cord, manifested by loss of normal neurological functions, e.g., muscle weakness, loss of vision, and mood alterations.
Chronic Fatigue Syndrome
CFS (Chronic Fatigue Syndrome) is a disorder of unknown cause that lasts for prolonged periods and causes extreme and debilitating exhaustion as well as a wide range of other symptoms such as fever, headache, muscle ache and joint pain, often resembling flu and other viral infections. Also known as Chronic Fatigue and Immune Dysfunction Syndrome (CFIDS), Chronic Epstein-Barr Virus (CEBV), Myalgic Encephalomyelitis (ME), "Yuppy Flu" and other names, it is frequently misdiagnosed as hypochondria, psychosomatic illness, or depression, because routine medical tests do not detect any problems.
Candidiasis
Infection of the skin or mucous membrane with any species of candida, usually Candida albicans. The infection is usually localized to the skin, nails, mouth, vagina, bronchi, or lungs, but may invade the bloodstream. It is a common inhabitant of the GI tract, only becoming a problem when it multiplies excessively and invades local tissues. Growth is encouraged by a weakened immune system, as in AIDS, or with the prolonged administration of antibiotics. Vaginal symptoms include itching in the genital area, pain when urinating, and a thick odorless vaginal discharge.
Rheumatoid Arthritis
A long-term, destructive connective tissue disease that results from the body rejecting its own tissue cells (autoimmune reaction).
Fibromyalgia
(FMS): Originally named fibrositis, it is a mysteriously debilitating syndrome that attacks women more often than men. It is not physically damaging to the body in any way, but is characterized by the constant presence of widespread pain that often moves about the body. Fibromyalgia can be so severe that it is often incapacitating.
Parasite
An organism living in or on another organism.
Pyelonephritis
Inflammation of the renal pelvis.
HIV
Abbreviation for human immunodeficiency virus, a retrovirus associated with onset of advanced immunodeficiency syndrome (AIDS).
Asthma
A lung disorder marked by attacks of breathing difficulty, wheezing, coughing, and thick mucus coming from the lungs. The episodes may be triggered by breathing foreign substances (allergens) or pollutants, infection, vigorous exercise, or emotional stress.
Bronchitis
Inflammation of the mucous membrane of the bronchial tubes, frequently accompanied by cough, hypersecretion of mucus, and expectoration of sputum. Acute bronchitis is usually caused by an infectious agent and of short duration. Chronic bronchitis, generally the result of smoking, may also be known as Chronic Obstructive Pulmonary Disease (COPD) or Emphysema.
Pelvic Inflammatory Disease
(PID) A Purulent (pus-like) vaginal discharge with fever and lower abdominal pain.
Crohn's Disease
Chronic inflammatory disease of the gastrointestinal tract. The most common symptoms are abdominal pain, often in the lower right area, and diarrhea. Rectal bleeding, weight loss, and fever may also occur. Bleeding may be serious and persistent, leading to anemia.
Diabetes Mellitus
A disease with increased blood glucose levels due to lack or ineffectiveness of insulin. Diabetes is found in two forms; insulin-dependent diabetes (juvenile-onset) and non-insulin-dependent (adult-onset). Symptoms include increased thirst; increased urination; weight loss in spite of increased appetite; fatigue; nausea; vomiting; frequent infections including bladder, vaginal, and skin; blurred vision; impotence in men; bad breath; cessation of menses; diminished skin fullness. Other symptoms include bleeding gums; ear noise/buzzing; diarrhea; depression; confusion.
Gingivitis
Inflammation of the fibrous tissues that surround the teeth.
Irritable Bowel Syndrome
(IBS) A condition that causes upset intestines for a long period of time. It is very unpleasant to the sufferer but tends to be harmless and usually does not lead to more serious complaints. The symptoms vary from person to person and from day to day. In order to be diagnosed with IBS, a person must have at least three of the following symptoms: pain in the lower abdomen; bloating; constipation; diarrhea or alternating diarrhea and constipation; nausea; loss of appetite; tummy rumbling; flatulence; mucous in stools; indigestion; constant tiredness; frequent urination; low back pain; painful intercourse for women.
Leukemia
Cancer of the lymph glands and bone marrow resulting in overproduction of white blood cells (related to Hodgkin's disease).
Psoriasis
An inherited skin disorder in which there are red patches with thick, dry silvery scales. It is caused by the body making too-many skin cells. Sores may be anywhere on the body but are more common on the arms, scalp, ears, and the pubic area. A swelling of small joints may go along with the skin disease.
TMJ
Tempero-mandibular joint - hinge of the jaw.
White Blood Cell
(WBC): A blood cell that does not contain hemoglobin: a blood corpuscle responsible for maintaining the body's immune surveillance system against invasion by foreign substances such as viruses or bacteria. White cells become specifically programmed against foreign invaders and work to inactivate and rid the body of a foreign substance. Also known as a leukocyte.
Leukocyte
A white blood cell which appears 5,000 to 10,000 times in each cubic millimeter of normal human blood. Among the most important functions are destroying bacteria, fungi and viruses and rendering harmless poisonous substances that may result from allergic reactions and cell injury.
Immune System
A complex that protects the body from disease organisms and other foreign bodies. The system includes the humoral immune response and the cell-mediated response. The immune system also protects the body from invasion by making local barriers and inflammation.
Stomach
A hollow, muscular, J-shaped pouch located in the upper part of the abdomen to the left of the midline. The upper end (fundus) is large and dome-shaped; the area just below the fundus is called the body of the stomach. The fundus and the body are often referred to as the cardiac portion of the stomach. The lower (pyloric) portion curves downward and to the right and includes the antrum and the pylorus. The function of the stomach is to begin digestion by physically breaking down food received from the esophagus. The tissues of the stomach wall are composed of three types of muscle fibers: circular, longitudinal and oblique. These fibers create structural elasticity and contractibility, both of which are needed for digestion. The stomach mucosa contains cells which secrete hydrochloric acid and this in turn activates the other gastric enzymes pepsin and rennin. To protect itself from being destroyed by its own enzymes, the stomach’s mucous lining must constantly regenerate itself.
Ulcer
Lesion on the skin or mucous membrane.
pH
A measure of an environment's acidity or alkalinity. The more acidic the solution, the lower the pH. For example, a pH of 1 is very acidic; a pH of 7 is neutral; a pH of 14 is very alkaline.
Rheumatism
General term applied to conditions of pain, or inability to articulate, various elements of the musculoskeletal system.
Tuberculosis
Also known as TB, Consumption or "The White Plague", tuberculosis is an infectious disease caused by a bacterium called Mycobacterium tuberculosis, usually affecting the lungs but possibly also the brain, kidneys and bones. Patients may at first be symptom-free or experience a flu-like illness. In the secondary stage, there might be a slight fever, night sweats, weight loss, fatigue and various other symptoms, depending on the part of the body affected. Tuberculosis of the lung is usually associated with a dry cough that eventually leads to a productive cough with blood-stained sputum. There might also be chest pain and shortness of breath.
Biopsy
Excision of tissue from a living being for diagnosis.
Autoimmune Disease
One of a large group of diseases in which the immune system turns against the body's own cells, tissues and organs, leading to chronic and often deadly conditions. Examples include multiple sclerosis, rheumatoid arthritis, systemic lupus, Bright's disease and diabetes.
Anti-inflammatory
Reducing inflammation by acting on body mechanisms, without directly acting on the cause of inflammation, e.g., glucocorticoids, aspirin.
Hormones
Chemical substances secreted by a variety of body organs that are carried by the bloodstream and usually influence cells some distance from the source of production. Hormones signal certain enzymes to perform their functions and, in this way, regulate such body functions as blood sugar levels, insulin levels, the menstrual cycle, and growth. These can be prescription, over-the-counter, synthetic or natural agents. Examples include adrenal hormones such as corticosteroids and aldosterone; glucagon, growth hormone, insulin, testosterone, estrogens, progestins, progesterone, DHEA, melatonin, and thyroid hormones such as thyroxine and calcitonin.
Cytokines
Cytokines are chemical messengers that control immune responses. They are secreted by white blood cells, T cells, epithelial cells and some other body cells. There are at least 17 different kinds of interleuken and 3 classes of interferon called alpha, beta and gamma and various subsets. Interleukens and interferons are called “cytokines” and there are two general groupings, Th1 and Th2. Th1 (T-cell Helper type 1) promote cell-mediated immunity (CMI) while Th2 (T-cell Helper type 2) induce humoral immunity (antibodies).
Ciliary
Often Ciliary activity: Activity of the eyelashes or any hairlike processes (cilia).
Peroxides
Free radicals that are by-products formed in our bodies when molecules of fat react with oxygen.