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AIDS

 

Definition


Acquired immune deficiency syndrome (AIDS) is an infectious disease caused by the human immunodeficiency virus (HIV). There are two variants of the HIV virus, HIV-1 and HIV-2, both of which ultimately cause AIDS.

Description


AIDS was first recognized in the United States 1981 in homosexual men. Today is seen in both homosexual and heterosexual men and women. AIDS is the advanced form of infection with HIV virus. This virus may not cause recognizable symptoms for a long period after the initial exposure (latent period). As of early 2009, no vaccine was available to prevent HIV infection. Until such a vaccine is developed, all forms of HIV/AIDS therapy are focused on improving the quality and length of life for people who are infected by slowing or halting the replication of the virus and treating or preventing infections and cancers that often develop in people with AIDS.
AIDS is one of the most devastating worldwide public health problems in recent history. The United States Centers for Disease Control and Prevention (CDC) estimated that in 2006 944,000 people in the United States had been diagnosed with AIDS since the disease was identified in 1981. In 2006, an additional 1-1.2 million Americans were diagnosed as infected with HIV but not yet showing symptoms (HIV positive). However, in early 2009, the CDC issued a statement that they now thought that earlier the HIV-positive estimates were too low, as many more people than were originally estimated are living with unreported or undiagnosed HIV infection.
According to the August 2008 report issued by the Joint United Nations Programme on HIV/AIDS (UNAIDS), as of 2007, approximately 33 million people worldwide are HIV positive. Over half of the 33 million are women and this statistic has remained stable for several years. The highest number of cases is found in sub-Saharan Africa and Southeast Asia.
More than 70% of HIV infections are transmitted through sexual contact. Traditionally in the United States, the majority of cases were found in homosexual or bisexual men. In 2007, about half of new HIV cases were acquired by men having sex with other men. Fewer than 20% of HIV-positive Americans were women. However, this is not the case worldwide, where transmission by heterosexual individuals is common.
Risk of acquiring HIV infection by entry siteEntry siteRisk virus reaches entry siteRisk virus entersRisk inoculatedConjuntivaModerateModerateVery lowOral mucosaModerateModerateLowNasal mucosaLowLowVery lowLower respiratoryVery lowVery lowVery lowAnusVery highVery highVery highSkin, intactVery lowVery lowVery lowSkin, brokenLowHighHighSexual:VaginaPenisUlcers (STD)LowHighHighLowLowHighMediumLowVery highBlood:ProductsShared needles Accidental needleHighHighLowHighHighHighHigh Very High LowTraumatic woundModestHighHighPerinatalHighHighHigh

Risk factors


AIDS can be transmitted in several ways. The risk factors for HIV transmission vary according to the method of transmission.
  • Sexual contact. People at greatest risk are those who do not practice safer sex by always using a condom, those who have multiple sexual partners, those who participate in anal intercourse, and those who have sex with a partner who has HIV infection and/or other sexually transmitted diseases (STDs). In the United States and Europe, most cases of sexually transmitted HIV infection result from homosexual contact, whereas in Africa, the disease is spread primarily through sexual intercourse among heterosexuals. Most people with AIDS in the United States are between 25 and 44 years of age.

  • Transmission in pregnancy. High-risk mothers include women sexually active with bisexual men, intravenous drug users, and women living in neighborhoods with a high rate of HIV infection among heterosexuals. The chances of transmitting the disease to the child are higher in women in advanced stages of the disease. Breast feeding increases the risk of HIV transmission as HIV passes into breast milk. The rate of pediatric HIV transmission in the United States had decreased substantially because of HIV testing and improved drug treatment for infected mothers, so fewer than 1% of AIDS cases now occur in children under age 15. In the developing world, mother to infant transmission remains epidemic. In 2006, AIDS was the single most common cause of death in children under age 5 in South Africa, while worldwide children account for about 10% of all AIDS cases.

  • Exposure to contaminated blood. Risk of HIV transmission among intravenous drug users increases with the frequency and duration of intravenous use, frequency of needle sharing, number of people sharing a needle, and the rate of HIV infection in the local population. In 2006, about 19% of men with AIDS and 25% of women with AIDS contracted the disease through sharing needles during intravenous drug injection. With the introduction of new blood product screening in the mid-1980s, HIV transmission through blood transfusions became rare in the developed world. However, contaminated blood is still a significant source of infection in the developing world.

  • Needle sticks or body fluid splashes among health care professionals. Transmission through theses sources accounts for fewer than 0.3% of all HIV infections in the United States. This rate reflects the emphasis on universal safety precautions (e.g., use of gloves, face shields, proper disposal of needles) among health care professionals and first responders.

HIV is not transmitted by handshakes or other casual non-sexual contact, coughing or sneezing, or by bloodsucking insects such as mosquitoes.

AIDS in women


Women exposed to HIV infection through heterosexual contact are the most rapidly growing risk group in the United States. The percentage of AIDS cases diagnosed in American women has risen from 7% in 1985 to about 25% in 2006. According to the CDC, in 2006 approximately 278,400 women in the United States were living with HIV/AIDS. The rate was highest among black women and lowest among white women. About 75% of these women contracted HIV through high-risk heterosexual activity; almost all of the remainder acquired the infection through needle sharing.
The prevalence of women with HIV in the United States is low compared to the rate in many countries in the developing world. Worldwide about half the people living with HIV are women. According to the United Nations, in 2005 about 59% of women living in sub-Saharan Africa are infected with HIV. The vast majority of them were infected through sex with an infected male partner.

AIDS in children


Since AIDS can be transmitted from an infected mother to a fetus during pregnancy or to an infant during the birth process or through breastfeeding, all infants born to HIV-positive mothers are considered a high-risk group. However, prenatal drug treatment of HIV-positive mothers in developed countries has reduced the number of children born infected with HIV. In the developing world, drug treatment is either not available or not affordable. According to the United Nations Children's Fund (UNICEF) worldwide 2.3 million children under age 13 were living with HIV in 2006. The previous year, about 380,000 children died of AIDS and more than half a million children were newly infected. UNICEF estimates that at least 15 million children have lost at least one parent to AIDS.
AIDS is the leading causes of death in children under age five many parts of Africa and Southeast Asia. The interval between exposure to HIV and the development of AIDS is shorter in children than in adults. Infants infected with HIV have a high chance of developing AIDS within one year and dying before age three. In the remainder, AIDS progresses more slowly; the average child patient survives to about seven years of age. Some survive into early adolescence.

Causes and symptoms


AIDS is a disease that can damage any of the body's major organ systems because HIV destroys immune system cells. HIV attacks the body through three disease processes: immunodeficiency, autoimmunity, and nervous system dysfunction.
Immunodeficiency describes the condition in which the body's immune response is damaged, weakened, or is not functioning properly. In AIDS, immunodeficiency results from the way that the virus binds to a protein called CD4, which is primarily found on the surface of certain subtypes of white blood cells. After the virus has attached to the cell's CD4 receptor, the virus-CD4 complex refolds to uncover another receptor called a chemokine receptor that helps mediate entry of the virus into the cell. One chemokine receptor in particular, CCR5, has been the focus of recent research after studies showed that defects in its structure (caused by genetic mutations) result in a slowing or stopping of the progression of AIDS. Scientists hope that this discovery will lead to the development of drugs that trigger an artificial mutation of the CCR5 gene or target the CCR5 receptor.
Once HIV has entered the cell, it can replicate intracellularly and kill the cell in ways that are still not completely understood. In addition to killing some lymphocytes directly, the AIDS virus disrupts the functioning of the remaining immune system cells. Because the immune system cells are destroyed, a wide variety of infections and cancers can take advantage of a person's weakened immune system (opportunistic infections/diseases).
The course of AIDS generally progresses through three stages, although not all patients will follow this progression precisely:

Acute retroviral syndrome


Acute retroviral syndrome describes a group of symptoms that can resemble mononucleosis and that may be the first sign of HIV infection in 50-70% of all patients and 45-90% of women. Most patients are not recognized as HIV positive during this phase and may not seek medical attention. The symptoms are similar to those of many other diseases and may include fever, fatigue, muscle aches, loss of appetite, digestive disturbances, weight loss, skin rashes, headache, and chronically swollen lymph nodes (lymphadenopathy). Some patients will experience a form of meningitis during this phase in which the membranes that cover the brain and spinal cord become inflamed. Acute retroviral syndrome develops between one and six weeks after infection and lasts for two to three weeks. Blood tests during this period will indicate the presence of HIV virus (viremia) and the appearance of the viral p24 antigen in the blood.

Latency period


After the virus enters a person's lymph nodes during the acute retroviral syndrome stage, the disease becomes latent for 10 years or more before symptoms of advanced disease develop. During latency, the virus continues to replicate in the lymph nodes, where it may cause one or more of the following conditions:

Persistent generalized lymphadenopathy (PGL)


Persistent generalized lymphadenopathy, or PGL, is a condition in which HIV continues to produce chronic, painless swellings in the lymph nodes during the latent period. The lymph nodes that are most frequently affected by PGL are those in the areas of the neck, jaw, groin, and armpits. PGL affects between 50-70% of patients during latency.

Constitutional symptoms


Many patients develop low-grade fevers, chronic fatigue, and general weakness. HIV also may cause a combination of food malabsorption, loss of appetite, and increased metabolism that contribute to AIDS wasting syndrome.

Other organ systems


At any time during the course of HIV infection, patients may develop a yeast infection in the mouth called thrush, open sores or ulcers, or other infections of the mouth; diarrhea and other gastrointestinal symptoms that cause malnutrition and weight loss; diseases of the lungs and kidneys; and degeneration of the nerve fibers in the arms and legs. HIV infection of the nervous system leads to general loss of strength, loss of reflexes, and feelings of numbness or burning sensations in the feet or lower legs.

Late-stage disease (AIDS)


AIDS is usually marked by a very low number of CD4+ lymphocytes, followed by a rise in the frequency of opportunistic infections and cancers. Doctors monitor the number and proportion of CD4+ lymphocytes in the patient's blood in order to assess the progression of the disease and the effectiveness of different medications. About 10% of infected individuals never progress to this overt stage of the disease.

Opportunistic infections


Once the patient's CD4+ lymphocyte count falls below 200 cells/mm 3, he or she is at risk for a variety of opportunistic infections. The infectious organisms may include the following:
  • Fungi. The most common fungal disease associated with AIDS is Pneumocystis carinii pneumonia (PCP). PCP is the immediate cause of death in 15-20% of AIDS patients. It is an important measure of a patient's prognosis. Other fungal infections include a yeast infection of the mouth (candidiasis or thrush) and cryptococcal meningitis.

  • Protozoa. Toxoplasmosis is a common opportunistic infection in AIDS patients that is caused by a protozoan. Other diseases in this category include isoporiasis and cryptosporidiosis.

  • Mycobacteria. AIDS patients may develop tuberculosis or mycobacterium avium complex (MAC) infections. MAC infections are caused by Mycobacterium avium-intracellulare and occur in about 40% of AIDS patients. This infection rarely develops until the CD4+ counts falls below 50 cells/mm3.

  • Bacteria. AIDS patients are likely to develop bacterial infections of the skin and digestive tract.

  • Viruses. AIDS patients are highly vulnerable to cytomegalovirus (CMV), herpes simplex virus (HSV), varicella zoster virus (VZV), and Epstein-Barr virus (EBV) infections. Another virus, JC virus, causes progressive destruction of brain tissue in the brain stem, cerebrum, and cerebellum (multifocal leukoencephalopathy or PML), which is regarded as an AIDS-defining illness by the CDC.

AIDS dementia complex and neurologic complications


AIDS dementia complex is usually a late complication of the disease. It is unclear whether it is caused by the direct effects of the virus on the brain or by intermediate causes. Loss of reasoning ability, loss of memory, inability to concentrate, apathy and loss of initiative, and unsteadiness or weakness in walking mark AIDS dementia complex. Some patients also develop seizures. There are no specific treatments for AIDS dementia complex.

Musculoskeletal complications


Patients in late-stage AIDS may develop inflammations of the muscles, particularly in the hip area, and may have arthritis-like pains in the joints.

Oral symptoms


In addition to thrush and painful ulcers in the mouth, patients may develop a condition called hairy leukoplakia. The CDC also regards this condition as an indicator of full-blown AIDS. Hairy leukoplakia is a white area of diseased tissue on the tongue that may be flat or slightly raised. It is associated with infection by the Epstein-Barr virus.

AIDS-related cancers


Patients with late-stage AIDS may develop Kaposi's sarcoma (KS), a skin tumor that primarily affects homosexual men. KS is the most common AIDS-related malignancy. It is characterized by reddish-purple blotches or patches (brownish in people with dark skin) on the skin or in the mouth. About 40% of patients with KS develop symptoms in the digestive tract or lungs. KS may be caused by a herpes virus-like sexually transmitted disease agent rather than HIV.
The second most common form of cancer in AIDS patients is a tumor of the lymphatic system (lymphoma). AIDS-related lymphomas often affect the central nervous system and develop very aggressively.
Invasive cancer of the cervix (related to certain types of human papilloma virus [HPV]) is an important diagnostic marker of AIDS in women.
While incidence of AIDS-defining cancers such as Kaposi's sarcoma and cervical cancer have decreased since increase use of antiretroviral therapy, other cancers have increased in AIDS patients. People with HIV have shown an increased incidence of lung cancer, head and neck cancers, Hodgkin's lymphoma, melanoma, and anorectal cancer.

Diagnosis


Because HIV infection produces a wide range of symptoms, the CDC has compiled a list of conditions regarded as defining AIDS. The physician will use the CDC list to decide whether the patient falls into one of these three groups:
  • definitive diagnoses with or without laboratory evidence of HIV infection

  • definitive diagnoses with laboratory evidence of HIV infection

  • presumptive diagnoses with laboratory evidence of HIV infection.

Almost all the symptoms of AIDS can occur with other diseases. The general physical examination may range from normal findings to symptoms that are closely associated with AIDS. These symptoms are hairy leukoplakia of the tongue and Kaposi's sarcoma. During an examination, the doctor will look for an overall pattern of symptoms rather than any one definitive finding.

Laboratory tests for HIV infection

Blood tests (serology)


Diagnostic blood tests for AIDS are given to individuals in high-risk populations, pregnant women, health care and public service workers who have been exposed to HIV, those who have symptoms associated with AIDS, or others who fear they may have been exposed to the virus. The first blood test for AIDS was developed in 1985. Patients who are being tested for HIV infection are usually given an enzyme-linked immunosorbent assay (ELISA) test for the presence of HIV antibody in their blood. Positive ELISA results are then tested with a Western blot or immunofluorescence (IFA) assay for confirmation. The combination of the ELISA and Western blot tests is more than 99.9% accurate in detecting HIV infection within four to eight weeks following exposure. The polymerase chain reaction (PCR) test can be used to detect the presence of viral nucleic acids in the very small number of HIV patients who have false-negative results on the ELISA and Western blot tests. These tests are also used to detect viruses and bacteria other than HIV and AIDS.

Other laboratory tests


In addition to diagnostic blood tests, other blood tests are used to track the course of AIDS in patients that have already been diagnosed. These include blood counts, viral load tests, p24 antigen assays, and measurements of 2-microglobulin (2M).
Doctors will use a wide variety of tests to diagnose the presence of opportunistic infections, cancers, or other disease conditions in AIDS patients. Tissue biopsies, samples of cerebrospinal fluid, and sophisticated imaging techniques, such as magnetic resonance imaging (MRI) and computed tomography scans (CT) are used to diagnose AIDS-related cancers, some opportunistic infections, damage to the central nervous system, and wasting of the muscles. Urine and stool samples are used to diagnose infections caused by parasites. AIDS patients are also given blood tests for syphilis and other sexually transmitted diseases.

Diagnosis in children


The CDC recommends HIV testing as a part of standard prenatal care for all pregnant women. When a pregnant woman tests positive for HIV, testing of her infant ideally begins within 48 hours of birth. Testing is repeated at between 1 and 2 months of age and again at age 3-6 months. Testing of infants uses a different technique to detect the presence of HIV virus. Infants can be diagnosed by direct culture of the HIV virus, PCR testing, and p24 antigen testing. By one month of age, results are highly accurate. Diagnostic blood testing in children older than 18 months is similar to adult testing, with ELISA screening confirmed by Western blot.
In terms of symptoms, children are less likely than adults to have an early acute syndrome. They are, however, likely to have delayed growth, a history of frequent illness, recurrent ear infections, a low white blood cell count, failure to gain weight, and unexplained fevers. Children with AIDS are more likely to develop bacterial infections, inflammation of the lungs, and AIDS-related brain disorders than are HIV-positive adults.

Treatment


Drug treatment guidelines for HIV/AIDS change frequently as new drugs are approved and new drug regimens developed. Two principles currently guide doctors in developing drug regimens for AIDS patients: using combinations of drugs rather than one medication alone; and basing treatment decisions on the results of the patient's viral load tests. Current information on United States Food and Drug Administration-(FDA)approved drugs by class can be found at the United States Department of Health and Human Services Aids Info Website at <http://www.aidsinfo.nih.gov/DrugsNew/Default.aspx?MenuItem=Drugs>. Individuals interested in participating in a trial of new HIV/AIDS drugs under development can find a list of clinical trials currently accepting volunteers at <http://www.clinicaltrial.gov>. There is not cost to volunteers to participate and some medical care and testing is provided.

Treatment of opportunistic infections and malignancies


Most AIDS patients require complex long-term treatment with medications for infectious diseases. This treatment is often complicated by the development of resistance in the disease organisms. AIDS-related malignancies in the central nervous system are usually treated with radiation therapy. Cancers elsewhere in the body are treated with chemotherapy.

Prophylactic treatment for opportunistic infections


Prophylactic treatment is treatment that is given to prevent disease. AIDS patients with a history of Pneumocystis pneumonia, with CD4+ counts below 200 cells/mm3 or 14% of lymphocytes, weight loss, or thrush should be given prophylactic medications. Drugs that may be given include antibiotics such as trimethoprim-sulfamethoxazole (Bactrim) or pentamidine (Pentam-300, Pentacarinat) and anti-fungals such as amphotericin B (AmBisome), flucytosine (Ancobon), and clotrimazole (Lotrim AF, Mycelex, Femizole-7). All these drugs can have undesirable side effects.

Anti-viral treatments


In recent years researchers have developed drugs that suppress HIV replication, as distinct from treating its effects on the body. These drugs fall into several classes:
  • Nucleotide reverse transcriptase inhibitors (also called nucleoside analogues). These drugs work by interfering with the action of HIV reverse transcriptase inside infected cells, thus ending the virus's replication process. These drugs include zidovudine (Retrovir), lamivudine (Epivir), and abacavir (Ziagen) and many others. They are often used in used in multi-drug combinations.

  • Non-nucleoside reverse transcriptase inhibitors. This class of drugs binds to an enzyme that is necessary for the HIV virus to reproduce. Examples of drugs in this class are viramune, delavirdine (Rescriptor), and efavirenz (Sustiva) and others.

  • Protease inhibitors. Protease inhibitors work by disabling protease, an enzyme necessary for HIV reproduction. Protease inhibitors include saquinavir (Invirase), ritonavir (Norvire), indinavir (Crixivan), nelfinavir (Viracept), amprenavir (Agenerase), kaletra, and many others.

  • Integrase inhibitors. Integrase inhibitors prevent the virus from inserting its own genetic material into the DNA of the infected cell. This stops the virus from replicating. Integrase was the only FDA-approved drug in this class as of early 2009. Several investigational drugs in this category were in clinical trials at that time.

  • Fusion inhibitors and entry inhibitors. Fusion inhibitors block specific proteins on the surface of the virus or the CD4+ cell. These proteins help the virus gain entry into the cell. The only FDA-approved fusion inhibitor as of early 2009 was enfuvirtide (Fuzeon). Entry inhibitors block HIV from entering cells. The only FDA-approved fusion inhibitor as of early 2009 was maraviroc (Selzentry). Several drugs in this class are, as of 2009, in pre-approval clinical trials.

Stimulation of blood cell production


Because many patients with AIDS have abnormally low levels of both red and white blood cells, they may be given medications to stimulate blood cell production. Epoetin alfa (erythropoietin) may be given to anemic patients. Patients with low white blood cell counts may be given filgrastim or sargramostim.

Alternative treatment


Alternative treatments for AIDS can be grouped into two categories: those intended to help the immune system and those aimed at pain control. Treatments that may enhance the function of the immune system include Chinese herbal medicine and western herbal medicine, macrobiotic and other special diets, guided imagery and creative visualization, homeopathy, and vitamin therapy. Pain control therapies include hydrotherapy, reiki, acupuncture, meditation, chiropractic treatments, and therapeutic massage. Alternative therapies also can be used to help with side effects of the medications used in the treatment of AIDS.

Prognosis


As of early 2009, there was no cure for AIDS and no vaccine to prevent infection. Treatment stresses aggressive combination drug therapy for those patients with access to the expensive medications and who tolerate them adequately. The use of these multi-drug therapies has significantly improved and prolonged the life of HIV/AIDS patients in the United States.
Researchers are actively working on producing preventative and therapeutic vaccines for HIV. Preventative vaccines immunize an individual against a disease, so that he or she does not become infected. A therapeutic vaccine, also called a treatment vaccine, does not keep someone from getting a disease the way a preventative vaccine does. Instead, therapeutic vaccines are used to boost the body's immune system in order to help control infection. The potential exists to prolong life indefinitely using these and other drug therapies to boost the immune system, keep the virus from replicating, and ward off opportunistic infections and malignancies.

Prevention


As there is no cure for AIDS, prevention of HIV infection becomes extremely important in controlling the disease. Efforts to prevent the spread of AIDS include:
  • Restricting sexual activity to a single partner and practicing safer sex (i.e., always using a condom). Besides avoiding the risk of HIV infection, condoms are successful in reducing other sexually transmitted diseases and unwanted pregnancies. Before engaging in a sexual relationship with someone, getting tested for HIV infection is recommended.

  • Avoiding needle sharing among intravenous drug users.

  • Donating one's own blood before planned major surgery to prevent risk of infection from a blood transfusion, although blood supplies are extremely safe in the developed world.

  • Practicing universal safety precautions when handling body fluids or needles. Healthcare professionals, first responders, and teachers, for example, are now trained in these precautions.

  • Testing for HIV infection by anyone how suspects infection. If treated aggressively and early, the development of AIDS may be postponed. If HIV infection is confirmed, it is also vital to let past sexual partners know so that they can be tested and receive medical attention.

Key Terms


Acute retroviral syndrome
A group of symptoms resembling mononucleosis that often are the first sign of HIV infection.

AIDS dementia complex
A type of brain dysfunction caused by HIV infection that causes difficulty thinking, confusion, and loss of muscular coordination.

Antibody
A protein produced by the immune system in response to a foreign protein or toxin called an antigen. Each different antigen stimulates the production of a different antibody.

Antigen
Any substance that stimulates the body to produce antibody.

Autoimmunity
A condition in which the body's immune system produces antibodies in response to its own tissues or blood components instead of foreign particles or microorganisms.

CCR5
A chemokine receptor; defects in its structure caused by genetic mutation cause the progression of AIDS to be prevented or slowed.

CD4
A type of protein molecule in human blood, sometimes called the T4 antigen, that is present on the surface of 65% of immune cells. The HIV virus infects cells with CD4 surface proteins, and as a result, depletes the number of immune system cells (T cells, B cells, natural killer cells, monocytes) in the individual's blood. Most of the damage to an AIDS patient's immune system is done by the virus' destruction of CD4+ lymphocytes.

Chemokine receptor
A receptor on the surface of some types of immune cells that helps to mediate entry of HIV into the cell.

Hairy leukoplakia of the tongue
A white area of diseased tissue on the tongue that may be flat or slightly raised. It is caused by the Epstein-Barr virus and is an important diagnostic sign of AIDS.

Hemophilia
Any of several hereditary blood coagulation disorders occurring almost exclusively in males. Because blood does not clot properly, even minor injuries can cause significant blood loss that may require a blood transfusion, with its associated minor risk of infection.

Human immunodeficiency virus (HIV)
A transmissible retrovirus that causes AIDS in humans. Two forms of HIV are now recognized: HIV-1, which causes most cases of AIDS in Europe, North and South America, and most parts of Africa; and HIV-2, which is chiefly found in West African patients. HIV-2, discovered in 1986, appears to be less virulent than HIV-1 and may also have a longer latency period.

Immunodeficient
A condition in which the body's immune response is damaged, weakened, or is not functioning properly.

Kaposi's sarcoma
A cancer of the connective tissue that produces painless purplish red (in people with light skin) or brown (in people with dark skin) blotches on the skin. It is a major diagnostic marker of AIDS.

Latent period
Also called incubation period, the time between infection with a disease-causing agent and the development of disease.

Lymphocyte
A type of white blood cell that is important in the formation of antibodies and that can be used to monitor the health of AIDS patients.

Lymphoma
A cancerous tumor in the lymphatic system that is associated with a poor prognosis in AIDS patients.

Macrophage
A large white blood cell, found primarily in the bloodstream and connective tissue, that helps the body fight off infections by ingesting the disease-causing organism. HIV can infect and kill macrophages.

Monocyte
A large white blood cell that is formed in the bone marrow and spleen. About 4% of the white blood cells in normal adults are monocytes.

(MAC) infection
A type of opportunistic infection that occurs in about 40% of AIDS patients and is regarded as an AIDS-defining disease.

Non-nucleoside reverse transcriptase inhibitors
The newest class of antiretroviral drugs that work by inhibiting the reverse transcriptase enzyme necessary for HIV replication.

Nucleoside analogues
The first group of effective anti-retroviral medications. They work by interfering with the AIDS virus' synthesis of DNA.

Opportunistic infection
An infection by organisms that usually do not cause infection in people whose immune systems are working normally.

Persistent generalized lymphadenopathy (PGL)
A condition in which HIV continues to produce chronic painless swellings in the lymph nodes during the latency period.

pneumonia (PCP)
An opportunistic infection caused by a fungus that is a major cause of death in patients with late-stage AIDS.

Progressive multifocal leukoencephalopathy (PML)
A disease caused by a virus that destroys white matter in localized areas of the brain. It is regarded as an AIDS-defining illness.

Protease inhibitors
The second major category of drug used to treat AIDS that works by suppressing the replication of the HIV virus.

Protozoan
A single-celled, usually microscopic organism that is eukaryotic and, therefore, different from bacteria (prokaryotic).

Retrovirus
A virus that contains a unique enzyme called reverse transcriptase that allows it to replicate within new host cells.

T cells
Lymphocytes that originate in the thymus gland. T cells regulate the immune system's response to infections, including HIV. CD4 lymphocytes are a subset of T lymphocytes.

Thrush
A yeast infection of the mouth characterized by white patches on the inside of the mouth and cheeks.

Viremia
The measurable presence of virus in the bloodstream that is a characteristic of acute retroviral syndrome.

Wasting syndrome
A progressive loss of weight and muscle tissue caused by the AIDS virus.

For Your Information

Resources


Books

  • Silverstein, Alvin and Virginia Silverstein, and Laura Silverstein Nunn. The AIDS Update. Berkeley Heights, NJ: Enslow, 2008.

Organizations

  • Gay Men's Health Crisis, Inc., 129 West 20th Street, New York, NY 10011-0022. (212) 807-6655.

Websites

  • "Aids." MedlinePlus. January 9, 2009 [cited January 13, 2009]. http://www.nlm.nih.gov/medlineplus/aids.html.

  • "AIDS Info." National Institutes of Health. January 9, 2009 [cited January 13, 2009]. http://www.aidsinfo.nih.gov .

  • "U.S. National AIDS Hotlines & Resources." The Body.com. undated [cited January 13, 2009]. http://www.thebody.com/index/hotlines/national.html.

Other

  • GHMC Web Peer Counseling. hotline@gmhc.org

HIV infections
HIV tests
AIDS treatment
Opportunistic infections
AIDS (Disease)

AIDS

(ādz),
A deficiency of cellular immunity induced by infection with the human immunodeficiency virus (HIV-1) and characterized by opportunistic diseases, including Pneumocystis jiroveci (formerly carinii) pneumonia, Kaposi sarcoma, oral hairy leukoplakia, cytomegalovirus disease, tuberculosis, Mycobacterium avium complex (MAC) disease, candidal esophagitis, cryptosporidiosis, isoporiasis, cryptococcosis, non-Hodgkin lymphoma, progressive multifocal leukoencephalopathy (PML), herpes zoster, and lymphoma. HIV is transmitted from person to person in cell-rich body fluids (notably blood and semen) through sexual contact, sharing of contaminated needles (as by IV drug abusers), or other contact with infected blood (as in accidental needlesticks among health care workers). Maternal-fetal transmission also occurs. The primary targets of HIV are cells with the CD4 surface protein, including principally helper T lymphocytes. Antibody to HIV, which appears in the serum 6 weeks to 6 months after infection, serves as a reliable diagnostic marker but does not bind or inactivate HIV. Gradual decline in the CD4 lymphocyte count, typically occurring over a period of 10-12 years, culminates in loss of ability to resist opportunistic infections. The appearance of one or more of these infections defines the onset of AIDS. In some patients, generalized lymphadenopathy, fever, weight loss, dementia, or chronic diarrhea occurs much earlier in the course of the infection. Untreated AIDS is uniformly lethal within 2-5 years after the first appearance of an opportunistic infection. Besides prophylaxis against opportunistic infection, standard therapy of HIV infection includes use of nucleoside analogues (for example, didanosine, lamivudine, ribavirin, stavudine, zipovudine), nonnucleoside reverse transcriptase inhibitors (for example, delavirine, efavirenz, nevirapine) and protease inhibitors (for example, atazanavir, crixivan, indinavir, ritonavir, saquinavir).
See also: human immunodeficiency virus, plasma viral load.
[acronym, acquired immunodeficiency syndrome]

Each year about 5 million people contract AIDS worldwide, and 3 million die of it. Some 40-50 million are estimated to be living with the disease. The gender incidence is approximately equal. The highest prevalence is in some African countries, where as many as 25% of the adult population may test HIV positive; about 70% of the world's infected population lives in sub-Saharan Africa. The first cases of AIDS were reported in the U.S. in June 1981. During the succeeding 2 decades an estimated 1.4 million people in this country were infected with HIV and 816,149 cases of AIDS and 467,910 deaths were reported to the U.S. Centers for Disease Control and Prevention (CDC). The numbers of new AIDS cases and deaths declined substantially after introduction of combination antiretroviral therapy in the late 1990s. The annual number of new cases of AIDS in the U.S. has remained stable at about 40,000, with 16,000 deaths since 1998. The number of people infected with HIV continues to increase, and of an estimated 1 million, one fourth are unaware that they are infected. In the U.S., AIDS is the leading cause of death among men 25-44 years old, and the fourth leading cause of death among women in the same age group. The development of effective antiretroviral agents (for example, reverse transcriptase inhibitors and protease inhibitors) and of quantitative plasma HIV RNA assays that can monitor progression of disease and response to treatment has shifted the goal of management in AIDS from prophylaxis and treatment of opportunistic infections to achievement of remission through suppressive therapy. Immune compromise is monitored by serial CD4 counts, viral replication by plasma HIV RNA assay (that is, plasma viral load, PVL). Indications for starting antiretroviral therapy are the appearance of symptoms of opportunistic infection, decline of the CD4 count below 350/mm3, or viral load exceeding 30,000 copies/mL. The CD4 count is considered a more sensitive predictor of disease progression than viral load. Empiric treatment may be begun early (within 6 months after conversion to HIV-positive status) in an effort to preserve immune function and mobilize the patient's own defenses against the virus. But current guidelines advise deferring treatment as long as possible so as to limit induction of drug resistance. Protease inhibitors have been shown to be highly effective antiretroviral agents and standard treatment regimens combining 2 reverse transcriptase inhibitors with 1 protease inhibitor ("triple therapy") have clearly demonstrated superiority over monotherapy. These drugs are expensive. Regimens are often complex, with varying requirements for fasting and timing of doses, and adverse effects and drug interactions are common. Protease inhibitors have been associated with elevation of cholesterol and triglycerides, insulin resistance, and disfiguring lipodystrophy. In one large study, more than one half of HIV-infected adults under treatment were found to be infected with strains of virus resistant to one or more antiretroviral drugs, and strains of HIV that are resistant to all available protease inhibitors have appeared. The rationale for current AIDS regimens is an effort to eradicate HIV infection by inhibiting spread of virus to new cells until all infected cells have died. However, actual cure seldom if ever occurs. A small number of resting CD4 memory cells in treated patients with undetectable plasma HIV RNA levels harbor HIV proviral DNA capable of replication, and these cells may survive for months or years. Macrophages and CNS neurons may serve as an anatomic sanctuary for HIV into which antretroviral drugs cannot penetrate in adequate concentration. When antiretroviral therapy is initiated early, CD4 helper cell counts rise, CD4 cell activity is preserved, and HIV RNA levels may remain undetectable for long periods. But in about 50% of patients with advanced disease, even multidrug regimens fail to suppress plasma viral RNA to undetectable levels. Many treatment failures result from poor compliance with multidrug regimens. Failure of one therapeutic regimen often precludes success with others because of the high degree of cross-resistance among antiretroviral drugs. After failure of an initial regimen, genotypic testing can be used to identify mutations in the HIV genome that confer resistance to one or more classes of HIV drugs. Many patients remain vulnerable to opportunistic infections despite restoration of CD4 counts to normal, probably because some subpopulations of T cells have been annihilated and cannot be recovered even after HIV has been suppressed. Moreover, even HIV-infected patients with undetectable viral loads must still be considered infectious. In a small set of those infected with HIV, impairment of immunity progresses to AIDS slowly or not at all. CD8 T-cells from such nonprogressors have been found to produce proteins called α-defensins. Evolving standards of treatment in HIV disease include aggressive prophylaxis in pregnancy and after accidental needle stick and sexual assault. Administration of antiretroviral agents to HIV-positive mothers before birth and during labor and delivery, and to newborns for the first 6 weeks of life, markedly decrease the risk of vertical transmission of HIV infection. The risk of HIV infection after occupational parenteral exposure to blood from an HIV-infected patient is approximately 0.3%. Postexposure prophylaxis with antiretroviral agents continued for 28 days have been shown to reduce the risk by 80%. The selection of agents depends on the source patient's therapeutic history. Efforts to develop a vaccine against HIV have been hampered by the unique properties of the virus and the long incubation period of AIDS. Early in the 21st century, public health authorities sought to make HIV testing a routine part of medical care, to facilitate diagnosis outside formal clinical settings, to prevent new infections by educating people and their sexual partners, and to decrease perinatal HIV transmission through routine HIV testing of pregnant women and of infants whose mothers were not screened.

AIDS

acquired immunodeficiency syndrome.

AIDS

(ādz)
n.
A severe immunological disorder caused by the retrovirus HIV, resulting in a defect in cell-mediated immune response that is manifested by increased susceptibility to opportunistic infections and to certain rare cancers, especially Kaposi's sarcoma. It is transmitted primarily by exposure to infected body fluids, especially blood and semen.

AIDS

[ādz]

AIDS

Acquired Immunodeficiency Syndrome. An immunosuppressing condition which is intimately linked to infection by a retrovirus, human immunodeficiency virus (HIV-1). 
Bangui definition A points-based system used to define AIDS in countries where HIV testing is not available. It was developed by workers from the CDC and WHO at a conference held in Bangui, Central African Republic, in 1985, and gives the most points for severe weight loss, protracted asthenia, recalcitrant fever and diarrhoea. AIDS is diagnosed with scores of 12 or more.
Clinical findings Weight loss exceeding 10% of body weight, protracted asthenia, continuous fever for >1 month, diarrhoea >1 month, persistent cough, oropharyngeal candidiasis, relapsing cutaneous herpes, generalised pruritic dermatosis, generalised lymphadenopathy, Kaposi's sarcoma.
Management Long-term survival after HIV infection is possible, but requires aggressive multi-agent therapy; once clinical AIDS develops, it is fatal, despite temporary response to various therapies.
AIDS is also an abbreviation for:
Academy of International Dental Studies
Accident/Incident Data System
Accretive Industrial Development Syndrome. A non-medical term used in real estate.
All Individuals Deserve Support. A slogan used by an AIDS support group.

AIDS

Acquired immunodeficiency syndrome A condition defined by CDC criteria, which is intimately linked to infection by a retrovirus, human immunodeficiency virus–HIV-1; long-term survival after HIV infection is possible; once clinical AIDS develops, it is fatal, despite temporary response to various therapies. See ARC, 'Dominant dozen. ', gp120, gp160, Hairy leukoplakia, HIV-1, HIV-2, Isospora belli, Nonprogressive HIV infection Patient zero, Pneumocystis carinii, VLIA–virus-like infectious agent, Walter Reed classification.
AIDS CDC Surveillance Case Definition
AIDS diagnosed definitively w/o need to confirm HIV infection
Candidiasis of esophagus, trachea, bronchi, lungs Cryptococcosis, extrapulmonary Cryptosporidiosis > 1 month duration CMV infection of any organ EXCEPT liver, spleen, or lymph nodes in Pts > 1 month of age Herpes simplex infection, mucocutaneous > 1 month duration and/or of esophagus, bronchi, lungs Kaposi sarcoma < age 60 Primary CNS lymphoma < age 60 Lymphoid interstital pneumonitis and/or pulmonary lymphoid hyperplasia < age 13 Mycobacterium avium complex or M kansasiidisseminated Pneumocystis cariniipneumonia Progressive multifocal leukoencephalopathy Toxoplasmosis of the brain in Pts > 1 month of age
AIDS diagnosed definitively with confirmation of HIV infection
or recurrent pyogenic bacterial infections Coccidioidomycosis, disseminated Histoplasmosis, disseminated Isoporaspp infection, > 1 month duration Kaposi sarcoma, any age Mycobacterium (not M tuberculosis), disseminated Mycobacterium tuberculosis–extrapulmonary Non-Hodgkin's lymphoma (small noncleaved cell, Burkitt or non-Burkitt, immunoblastic sarcoma) Primary CNS lymphoma, any age Salmonella septicemia, recurrent
AIDS diagnosed presumptively with confirmation of HIV infection
Candidiasis of esophagus CMV retinitis Disseminated mycobacterial infection–culture not required HIV encephalopathy HIV wasting syndrome Kaposi sarcoma Lymphoid interstital pneumonitis and/or pulmonary lymphoid hyperplasia < age 13 Pneumocystis cariniipneumonia Toxoplasmosis of the brain in Pts > 1 month of age
.

AIDS

(ādz)
Acronym for acquired immune deficiency (or immunodeficiency) syndrome; disorder of the immune system characterized by opportunistic diseases, including candidiasis, Pneumocystis jiroveci pneumonia, oral hairy leukoplakia, herpes zoster, Kaposi sarcoma, toxoplasmosis, isosporiasis, cryptococcosis, non-Hodgkin lymphoma, and tuberculosis. The syndrome is caused by the human immunodeficiency virus (HIV-1, groups M and O, and HIV-2), which is transmitted in body fluids (notably breast milk, blood, and semen) through sexual contact, sharing of contaminated needles (by IV drug abusers), accidental needle sticks, contact with contaminated blood, or transfusion of contaminated blood or blood products. Hallmark of the immunodeficiency is depletion of T4+ or CD4+ helper/inducer lymphocytes, primarily the result of selective tropism of the virus for the lymphocytes.
Synonym(s): acquired immunodeficiency syndrome.

AIDS

Acronym for the ACQUIRED IMMUNE DEFICIENCY SYNDROME.

AIDS

acronym for Acquired Immune Deficiency Syndrome, a serious disease caused by Human Immunodeficiency Virus (HIV) which debilitates the immune system. HIV 1 attaches to the CD4 receptor present on T LYMPHOCYTES and MACROPHAGES. The viral RNA enters the host cell and is transcribed by REVERSE TRANSCRIPTASE into DNA. This viral DNA becomes integrated into the chromosomal DNA of the host. There it may control the production of new HIV particles, which are budded off from the infected host cell. Alternatively, the integrated DNA may remain latent and not be detected by the immune system. HIV avoids the host's IMMUNE RESPONSE by remaining in vacuoles within macrophages. HIV also shows high rates of ANTIGENIC VARIATION, since errors during replication of HIV RNA to DNA cause numerous changes in the nature of the ENVELOPE PROTEINS of the virus. Not everyone who carries HIV develops AIDS, but all infected individuals can pass it on. There are three major routes of transmission:
  1. through sexual intercourse,
  2. by transfer of blood on needles shared by drug users or by transfusion of contaminated blood (only before 1985 in the USA), or accidentally by contaminated needles, or
  3. by mother to baby before or during birth or by means of the milk. Drug users and homosexuals are high-risk groups, but in central Africa it is now widespread amongst heterosexuals where a second virus, HIV 2 is also present. This is endemic throughout West Africa but does not appear to have resulted in an epidemic of the disease.

From the time of infection by HIV, AIDS normally develops within ten years, though there are now drugs which may be used to extend this time. The immune failure, which is characteristic of AIDS, occurs as a consequence of a gradual decline in the number of CD4 T lymphocytes. Eventually the infected person succumbs to a variety of infections by BACTERIA, FUNGI, protozoa or viruses and/or develops a cancer(s) such as Kaposi's Sarcoma.

In order for a person to be infected, HIV must be present in the transmitted body fluids, and its concentration (very high in blood) determines whether infection takes place. HIV must get into the blood stream and can only enter via an open cut or sore or by contact through the mucous membranes of the anus, rectum, genitalia, mouth or eyes. Outside the body HIV can live up to 15 days in a stable temperature and humidity, if it is in high concentration, but usually only for a short time (a few hours). It is not transmitted by insect bites, through saliva, tears, sweat, faeces or urine. There are documented cases of oral infection and male to female transmission is much more frequent than female to male. There are records of Simian immunodeficiency virus being transmitted to humans, but these have so far not given rise to the disease. The virus in chimpanzees can be transmitted but not similiar viruses from other animals.

There are difficulties in developing an effective VACCINE against HIV, because the virus is so adept at avoiding the host immune defence system. Research is in progress, using both conventional and very unconventional approaches, to develop such a vaccine. Various chemotherapeutic agents are being tested. AZT (azidothymidine), which inhibits virus replication, has been used, but it has side effects and only helps certain patients. Radiation has also been employed but again there are side effects. So far around 22 million people have died of AIDS and a further 40 million are living infected by HIV.

AIDS

acquired immune deficiency syndrome

syndrome

aggregated objective signs, subjective symptoms and specific pathologies that typify specific conditions
  • acquired immunodeficiency syndrome; AIDS severe reduction in numbers of T4 lymphocyte helper (CD4) cells (due to infection with human immunodeficiency virus [HIV]) and resultant compromise of humoral and cell-mediated immunity; patients show lymphadenopathy, opportunistic infections (e.g. tinea and verrucae) and unusual infections (e.g. histoplasmosis, gastrointestinal tract candidiasis, Pneumocystis carnii pneumonia [PCP]), unusual malignancies (e.g. Kaposi's sarcoma), wasting diseases and presenile dementia

  • acute compartment syndrome; ACS increased lower-limb intracompartmental pressure on exercise (exercise expands muscles, increases intracompartmental pressures, inducing pain); treated initially by rest, immobilization, non-steroidal anti-inflammatory drugs; severe cases may require surgical decompression (fasciotomy)

  • anterior tarsal syndrome; ATS deep peroneal nerve entrapment at anterior ankle/dorsal talonavicular joint, due to restriction of ankle dorsiflexion (e.g. tight boots; ski boots), or local soft-tissue trauma (e.g. dorsal tarsal exostoses); characterized by extensor hallucis longus weakness, dorsal foot paraesthesia and numbness of first intermetatarsal space (symptoms can be induced by deep peroneal nerve percussion as crosses the anterior aspect of the ankle joint, or by ankle joint plantarflexion whilst simultaneously dorsiflexing toes)

  • anterior tibial compartment syndrome ischaemic necrosis of anterior compartment muscle fibres, due to local arterial compression by engorged muscles, after unaccustomed exertion

  • anterior tibiotalar impingement syndrome anterior ankle pain at ankle dorsiflexion (e.g. at midstance, just before heel lift) due to inferior tibial/neck of talus exostosis

  • Apert's syndrome type Ia acrocephalosyndactyly, characterized by features of Carpenter's syndrome, with lesser digital (2-5) fusion into one mass, usually with a common mega-nail

  • Apert-Crouzon syndrome type IIa acrocephalosyndactyly characterized by features of Carpenter's syndrome with additional craniofacial dysostosis, maxillary hypoplasia, and 2-4 digit fusion

  • Bazex syndrome; acrokeratosis paraneoplastica keratoderma (i.e. erythema, scaling and irritation) of skin of ears, nose, hands and feet and later generalized hyperkeratosis in men with underlying internal malignancy; condition regresses when underlying malignancy is resolved

  • Behçet's syndrome chronic vasculitic disease of unknown cause; characterized by seronegative arthritis of knees and ankles, elbows and wrists, mouth ulcers, erythema nodosum, visual impairment and cerebrovascular accident

  • benign familial joint hypermobility syndrome; BFJHS generalized joint hypermobility, diagnosed as 2 major/1 major + 2 minor/4 minor criteria (see Table 1) in the absence of Ehlers-Danlos syndrome, Marfan's syndrome and osteogenesis imperfecta

  • Brocq-Lyell syndrome; toxic epidermal necrolysis severe, acute, systemic drug reaction characterized by hyperpigmented skin lesions and epidermal detachment

  • Brown-Séquard syndrome hemiparaplegia and hyperaesthesia, with ipsilateral loss of stereognosis and contralateral hemianaesthesia; due to unilateral spinal cord lesion

  • carpal tunnel syndrome pain, paraesthesia and loss of power of palmar muscles; associated with rheumatoid arthritis

  • Carpenter's syndrome; acrocephalopolysyndactyly oxycephaly, bradysyndactyly and polydactyly of the feet, with learning difficulties

  • Charcot's syndrome see intermittent claudication

  • chronic compartment syndrome; CCS; chronic exertional compartment syndrome exercise-induced fascial compartment pain; caused by compromised circulation and relative ischaemia of intracompartmental tissues, with long-term muscle and nerve dysfunction and damage; recalcitrant cases require surgical decompression through fasciotomy (see syndrome, acute compartment)

  • compartment syndrome see syndrome, acute compartment; syndrome, chronic compartment

  • complex regional pain syndrome; CRPS; chronic regional pain syndrome neuroinflammatory dysfunction, due to ion interaction of nociceptive C-fibre nerve endings, the sympathetic nervous system and spinal cord efferent motor nerves; characterized by vasomotor instability, hyperalgesia and impaired motor function; diagnosed from clinical presentation, symptoms reduction on administration of sympathetic nerve blockade, and intense, focal periarticular uptake of contrast medium in a delayed imaging-phase bone scan; treated by early, aggressive physical therapy to prevent contracture and muscle wasting, symptomatic relief by sympathetic nerve blockade, non-steroidal anti-inflammatory drugs, tricyclic antidepressants and anticonvulsant medication; immobilization is contraindicated

  • complex regional pain syndrome type 1; CRPS 1; reflex sympathetic dystrophy; Sudek's atrophy; allodynia sympathetic nervous system-mediated acute pain and vasomotor instability, triggered by minor or surgical trauma without obvious nerve injury; affects women more than men; pain is excessive and out of proportion to severity of initiating injury; diagnosis is based on clinical symptoms aided by bone scan, laser Doppler studies and thermography; patients may show anxiety, depression and disturbed sleep; condition is difficult to manage; patients suspected of CRPS 1 should have early referral to a pain clinic (see Table 2); presents in three stages:

    • stage 1 acute phase, lasting 2-3 months, with regional severe burning pain, warmth and swelling triggered by stress/light touch, bone demineralization, skin trophic changes

    • stage 2 dystrophic phase/Sudek's atrophy; lasting for several months; characterized by constant unrelenting pain, exacerbated by any stimulus, and tissue cyanosis, coolness and induration, and diffuse osteoporosis

    • stage 3 atrophic phase, characterized by reduced/absent/intractable pain, irreversible atrophy of skin/subcutaneous tissues, flexion contractures of foot, advanced osteoporosis with a 'ground-glass' appearance on X-ray of affected bone

  • complex regional pain syndrome, type 2; CRPS 2; causalgia; sympathetic pain syndrome persistent and severe skin paraesthesia/burning sensations; caused by trauma to peripheral sensory nerve fibres; symptoms, progress and treatment are similar to that of CRPS 1

  • Conn's syndrome primary aldosteronism; characterized by headaches, thirst, nocturia, polyuria, hypovolaemia, fatigue, hypertension, alkalosis, and potassium depletion

  • constrictive band syndrome intrauterine development of deep, tight, circumferential folds around leg/foot, and compromised limb development distal to band (e.g. autoamputation; marked oedema of distal tissues); thought to relate to strands of amniotic membrane enwrapping the developing limb

  • Cushing's syndrome raised blood cortisol (e.g. due to pituitary tumour; long-term steroid therapy); characterized by central obesity, moon-like facies, acne, skin striae, hypertension, decreased carbohydrate tolerance and tendency to diabetes, female amenorrhoea and hirsutism

  • Down's syndrome chromosomal disorder (trisomy 21) characterized by congenital short stature, broad short hands/feet, characteristic facies (pronounced epicanthic skin folds, flat hypoplastic face, short nose, enlarged tongue), transverse palmar crease, very dry skin, learning difficulties; formerly termed mongolism

    Edwards' syndrome trisomy 18, with congenital characteristic facies (micrognathia, low-set ears), rocker-bottom feet, severe learning difficulties; affected children often die in early childhood

  • Ehlers-Danlos syndrome; Ehlers-Danlos diseases I-X hereditary connective tissue disorder characterized by collagen abnormality, marked generalized skin and blood vessel laxity, and joint hypermobility; skin is readily traumatized and heals slowly; see syndrome, hypermobility

  • Franconi's syndrome a form of anaemia associated with renal tubule dysfunction; adult Franconi's syndrome shows synostosis with osteomalacia, and acquired Franconi's syndrome is associated with multiple myeloma

  • Giles de la Tourette syndrome motor incoordination characterized by verbal, facial or limbic tics

  • Gorlin's syndrome multiple naevus-like basal cell carcinomata, causing small pits and depressions of palmar and plantar skin

  • Guillain-Barré syndrome; acute inflammatory polyneuropathy; acute idiopathic polyneuritis; infectious polyneuritis; postinfective polyneuropathy sudden-onset, acute, postviral polyneuritis; presents as distal pain, muscular weakness/flaccidity, paraesthesia; spreads proximally over 14-21 days; severe cases show spinal nerve involvement, with respiratory failure and limb paralysis (patient will require life support and anticoagulation to prevent deep-vein thrombosis); spontaneous recovery occurs over several weeks/months; some residual neuromotor effects may persist

  • Haglund's syndrome prominence of posterior superior lateral area of calcaneum, retrocalcaneal bursitis, Achilles tendon thickening and Achilles tendinitis; diagnostic rearfoot radiographic features include positive parallel pitch lines, loss of retrocalcaneal recess (indicating retrocalcaneal bursitis), Achilles tendon thickening, loss of distinct interface between Achilles tendon and pre-Achilles fat pad

  • heel pain syndrome see heel pain

  • heel spur syndrome see heel spur

  • Howel-Evans syndrome familial palmoplantar keratoderma, with increased risk of oesophageal cancer

  • Hurler's syndrome; lipochondrodystrophy; dysostosis multiplex autosomal-recessive inherited generalized lipid disturbance and mucopolysaccharoidosis, affecting cartilage, bone, skin, subcutaneous tissues, brain, liver and spleen; characterized by short stature, shortness of neck, trunk and digits, kyphosis, reduced joint mobility, learning difficulties, characteristic facies (so-called gargoylism) and visual impairment

  • hypermobility syndrome; joint hypermobility syndrome disordered collagen (types 1 and 3) structure, with associated decreased tensile strength of skin/structural tissues; characterized by generalized joint hypermobility, easy bruising, impaired healing, increasing incidence of joint/soft-tissue pain, joint dislocation and osteoarthritis; a presenting feature of benign familial joint hypermobility syndrome (BFJHS) (see Table 3), Ehlers-Danlos syndrome, Marfan syndrome and osteogenesis imperfecta

  • iliotibial band syndrome; ITBS; iliotibial band friction syndrome; ITBFS overuse-associated, friction-induced inflammation of ITB and associated bursa, where ITB moves over lateral femoral condyle (Gerdy's tubercle); due to repeated knee flexion and extension, especially in athletes/cyclists; presents as ITB pain at heel strike progressing to constant ITB pain; early-stage treatment includes a daily stretching programme (see Table 4) and application of heat (pre-exercise) and ice (postexercise) (see Table 5)

  • joint hypermobility syndrome see syndrome, hypermobility

  • lobster-claw syndrome extreme form of ectrodactyly; characterized by absence of third and fourth rays

  • Korsakoff's syndrome confusion and severe memory impairment with confabulation and Wernicke's syndrome, associated with chronic alcoholism

  • Lyell's syndrome drug-induced, acute skin sensitivity reaction; characterized by acute erythema, urticaria, vasculitis, purpura, marked exfoliation (peeling), flaccid bullae formation, subepidermal separation/detachment

  • Marfan's syndrome familial, autosomal-dominant, congenital changes in mesodermal and ectodermal tissues; characterized variably by musculoskeletal changes (e.g. increased height, excessive limb length, arachnodactyly; generalized tissue laxity and joint hypermobility), visual effects, and cardiovascular effects (e.g. aortic aneurysm)

  • medial tibial stress syndrome; MTSS; tibial fasciitis; shin splint muscle fatigue, reduced shock absorption, traction enthesiopathy and periostitis along anterior and posterior medial lower one-third of tibia (see Table 6) secondary to overuse/underpreparation for exercise; exacerbated by exercising on hard surfaces, especially in individuals who pronate excessively; treated by muscle-strengthening exercises, pre-exercise flexibility programme, modification of overall sports exercise programme (see Table 7), in conjunction with gait analysis, orthoses and correct shoe selection

  • Morquio's syndrome; type IV mucopolysaccharoidosis severe skeletal dysplasia including spine/thorax deformity, irregular epiphyses but normal shaft length of long bones, enlarged joints, flaccid ligaments, waddling gait and urinary abnormalities, due to autosomal-recessive error of mucopolysaccharide metabolism

  • Morton's syndrome congenital shortening of first metatarsal with apparent shortening of hallux and associated metatarsalgia

  • Munchausen's syndrome repeated fabrication of illness/symptoms of illness

  • Munchausen's syndrome by proxy repeated reporting of spurious illness/symptoms of illness by one person about another

  • musculoskeletal pain syndrome see polymyalgia rheumatica

  • nail-patella syndrome; hereditary arthrodysplasia autosomal-dominant abnormality of finger/toenails, absent/hypoplastic patella, defects of head of radius and iliac horns, and iris discoloration

  • nephrotic syndrome peripheral oedema, albuminuria, reduced plasma albumin (hypoalbuminaemia), refractory bodies in urine and raised blood cholesterol

  • nerve entrapment syndromes local nerve trunk compression (e.g. tibial, medial calcaneal lateral, first lateral branch of calcaneal, lateral plantar, high tibial, popliteal, deep peroneal, superficial, saphenous, sural or medial common hallucal nerves), as in tarsal/carpal tunnel syndromes, plantar digital neuritis, Morton's neuroma; characterized by distressing distal dermatomal sensory (e.g. pain and paraesthesia) and/or motor symptoms (e.g. muscle atrophy) (see Table 8)

  • Nievergelt-Pearlman syndrome rare autosomal-dominant bone disease causing lower-limb 'rhomboidal' tibia/fibula (crura rhomboidei), joint dysplasias, genu valgum, club foot, deformed toes; more common in males

  • overlap syndromes see mixed connective tissue diseases

  • patellofemoral joint syndrome see syndrome, runner's-knee

  • peroneal cuboid syndrome loss of rearfoot eversion due to long-standing peroneal tendon dysfunction/tendinitis; characterized by plantar pain from cuboid to first metatarsal

  • polycystic ovary syndrome see syndrome, Stein-Leventhal

  • Raynaud's syndrome concomitant Raynaud's disease (always affecting hands, and frequently feet) in patients with connective tissue disorders, characterized by generalized digital cyanosis, localized painful vasculitic lesions of dorsal forefoot (30% of cases) and apices of toes (20-25% of cases); subcutaneous calcinosis (20% of cases) may masquerade as a seed corn

  • Reiter's syndrome urethritis, iridocyclitis, arthritis, plantar enthesiopathy and heel spur formation, often triggered by earlier gastrointestinal Escherichia coli infection or exposure to a sexually transmitted disease (e.g. Chlamydia trachomatis); more common in human leukocyte antigen (HLA) B27 tissue-type males; see keratoderma blenorrhagicum

  • restless-leg syndrome overwhelming need to move the lower limbs constantly; characteristic of chronic renal failure; thought to be triggered by accumulation of metabolites and uraemia

  • Reye's syndrome cerebral oedema and death (in 50% of cases, usually children), provoked by aspirin therapy; aspirin is proscribed for children less than 16 years old

  • Riley-Day syndrome; familial dysautonomia autosomal-dominant complete indifference to pain; also characterized by orthostatic hypotension, hyperhidrosis and hyporeflexic/absent deep tendon reflexes, pes cavus and trophic plantar ulceration

  • Roussy-Levy syndrome; hereditary areflexic dystasia; Charcot-Marie-Tooth (CMT) disease type II essential tremor, sensory ataxia, poor coordination and judgement of movement, kyphoscoliosis and distal muscle atrophy (especially peronei); autosomal-dominant inherited disease similar to CMT disease type 1, but developing in early childhood

  • runner's-knee syndrome mild lateral subluxation of patella in patellar groove; due to an increase in Q angle (i.e. >15°), often in association with excessive foot pronation, tibial varum, internal tibial torsion, weakened quadriceps group, malposition of vastus medialis, hard running surfaces or faulty sports shoes, leading to uneven pressure on anterolateral surface of femoral condyle and local pain; often affects female runners; treated by prescription orthoses to reduce torque, torsion and knee joint stress

  • scalded-skin syndrome scaled/peeling appearance of skin overlying areas of infection, or associated with adverse drug reactions

  • 'second-class travel' syndrome pulmonary thromboembolism due to prolonged periods of inactivity, e.g. passengers (who have been static for > 4 hours during long-haul intercontinental air flights) develop deep-vein thrombosis; the clot detaches, passing through venous circulation and heart, to block the pulmonary artery; characterized by sudden collapse and death; passengers on long-haul flights are advised to undertake leg muscle exercises regularly throughout the duration of the flight, wear 'antithrombotic' elasticated hosiery and consider medication with aspirin in the weeks before long-haul flight

  • sinus tarsi syndrome sensation of unsteadiness when walking on gravel/uneven ground and ongoing pain in lateral tarsal area just distal to and level with lateral malleolus, subsequent to inversion sprain/excess rearfoot pronation (e.g. as in rearfoot rheumatoid arthritis); local symptoms are exacerbated by heel inversion/eversion; treated by non-steroidal anti-inflammatory drugs, local immobilization, orthoses or steroid injection

  • SjÖgren's syndrome; sicca syndrome; keratoconjunctivitis sicca oral mucous membranes dryness, loss of lacrimal secretion, facial telangiectasias (i.e. butterfly rash), bilateral parathyroiditis (in younger women), strongly associated with rheumatoid arthritis and Raynaud's phenomenon

  • Stein-Leventhal syndrome; polycystic ovary syndrome multiple ovarian cyst formation, with associated menstrual abnormalities, infertility, enlarged ovaries, insulin resistance, obesity, acne, evidence of masculinization (e.g. hirsuitism) and increased tendency to type 2 diabetes mellitus; responds to treatment with oral contraceptive pill and/or metformin

  • Stevens-Johnson syndrome widespread bullous erythema multiforme of skin/mucous membranes; due to hypersensitivity/drug reaction

  • talar compression syndrome posterior ankle pain when foot is maximally plantarflexed at ankle joint; due to compression of posterior tubercle of talus on posterior margin of distal end of tibia; note: similar condition occurs with os trigonum, which impinges on posteroinferior margin of tibia (see Table 9)

  • tarsal tunnel syndrome; TTS pain, paraesthesia and numbness in sole of foot; due to tibial nerve compression within tarsal tunnel; associated with excess foot pronation or rearfoot rheumatoid arthritis; symptoms reproduced by tapping the skin overlying distal medial malleolar area (Tinel's sign positive); conservative treatment includes valgus filler pads, cobra pads and medial heel wedges, or control of excessive rearfoot pronation with moulded cushioned orthoses worn with bespoke shoes, together with non-steroidal anti-inflammatory drugs and/or disease-modifying antirheumatic drugs; surgical treatment includes decompression procedures to free posterior tibial nerve and excise local fibrous structures (see tarsal tunnel)

  • distal tarsal tunnel syndrome isolated entrapment of medial/lateral plantar nerves; medial plantar nerve is compressed between navicular tuberosity and belly of abductor hallucis longus, causing 'jogger's foot'; first branch of lateral plantar nerve (Baxter's nerve) may be entrapped as it courses laterally between bellies of abductor hallucis and quadratus plantae (flexor accessories) muscles (see Table 10)

  • proximal tarsal tunnel syndrome entrapment of posterior tibial nerve/its branches deep to flexor retinaculum; due to excessive subtalar joint pronation (with narrowing of tarsal tunnel, e.g. in rheumatoid foot) due to entrapment within attachments of flexor retinaculum, compression by an enlarged abductor hallucis muscle belly, enlarged navicular tuberosity, accessory navicular, presence of os tibialis externum, ischaemic compromise of posterior tibial nerve, or varicosities within tarsal tunnel

  • trisomy 21 syndrome see syndrome, Down's

  • Turner's syndrome sex-chromosome (XO) abnormality affecting 1:2500 females, with characteristic morphology (web neck, short stature), infantilism and amenorrhoea, coarctation of aorta and peripheral oedema; feet are oedematous, short and broad, show excess subtalar joint pronation and hyperextended halluces; nails tend to involution, and affected subjects are prone to ingrowing nails

  • Werner's syndrome autosomal-recessive condition characterized by scleroderma-like skin, cataracts, progeria (premature senility), hypogonadism and diabetes mellitus

  • Wernicke's syndrome; Wernicke-Korsakoff syndrome; Wernicke's encephalopathy brainstem ischaemia causing nystagmus and other ocular effects, tremors and ataxia, mental confusion, hypothermia and hypotension; more common in chronic alcoholics

  • Wolff-Parkinson-White syndrome congenital atrioventricular interconnection causing tachycardia and characteristic electrocardiogram pattern

  • yellow-nail syndrome see nail, yellow

Table 1: The major and minor diagnostic criteria of benign familial joint hypermobility syndrome (BFJHS)
Major criteria
Current/historic Brighton score of 4/9
Arthralgia for >3/12 in four or more joints
Minor criteria
Current/historic Brighton score of 1, 2 or 3/9 (0, 1, 2, 3/9 if >50 years old)
Arthralgia for minimum of 3 months in 1-3 joints, or back pain for minimum of 3 months, or spondylosis/spondylolysis/spondylolisthesis
Dislocation/subluxation of > one joint, or one episode of simultaneous dislocation/subluxation of more than one joint
Three or more lesions of soft-tissue rheumatism (e.g. spondylitis, tenosynovitis, bursitis)
Marfanoid habitus (i.e. tall, slim physique, span:height ratio >1.3, upper:lower segment ratio <0.89, arachnodactyly [+Steinberg/wrist signs])
Abnormal skin: striae, hyperextensibility, thin skin, papyraceous scarring
Eye signs: drooping eyelids, myopia, antimongoloid slant
Varicose veins or hernia or uterine/rectal prolapse

Note: BFJHS is diagnosed in the presence of two major criteria, or one major and two minor criteria, or four minor criteria (adapted from Grahame R, Bird HA, Child A, Dolan AL, Fowler-Edwards A, Ferrell W, Gurley-Green S, Keer R, Mansi E, Murray K, Smith E. The British Society Special Interest Group on Heritable Disorders of Connective Tissue Criteria for the Benign Joint Hypermobility Syndrome. "The Revised (Brighton 1998) Criteria for the Diagnosis of the BJHS". Journal of Rheumatology 2000; 27:1777-1779).

Table 2: Features of complex regional pain syndrome
PhaseFeatures
Acute phase (duration: 2-3 months)
Reversible
Severe burning pain, warmth, swelling and joint stiffness within a limb: not confined to a dermatome or myotome
Bone demineralization
Symptoms (exacerbated by limb dependence, contact or stress) persist for 2-3 months
Chronic phase (duration: several months)
Reversible
Pain continues
The limb becomes cool, firm and cyanotic
Radiographs show diffuse osteoporosis
Digits develop flexure contractures
Persists for several months
Atrophic phase
Irreversible
Pain diminishes or becomes intractable
Skin and subcutaneous tissues become atrophic
Flexion contractures in foot become fixed
Osteoporosis becomes advanced; bone has a 'ground-glass' appearance
Table 3: The major and minor diagnostic criteria of benign familial joint hypermobility syndrome (BFJHS)
Major criteria
Current/historic Brighton score of 4/9
Arthralgia for >3/12 in four or more joints
Minor criteria
Current/historic Brighton score of 1, 2 or 3/9 (0, 1, 2, 3/9 if >50 years old)
Arthralgia for minimum of 3 months in 1-3 joints, or back pain for minimum of 3 months, or spondylosis/spondylolysis/spondylolisthesis
Dislocation/subluxation of > one joint, or one episode of simultaneous dislocation/subluxation of more than one joint
Three or more lesions of soft-tissue rheumatism (e.g. spondylitis, tenosynovitis, bursitis)
Marfanoid habitus (i.e. tall, slim physique, span:height ratio >1.3, upper:lower segment ratio <0.89, arachnodactyly [+Steinberg/wrist signs])
Abnormal skin: striae, hyperextensibility, thin skin, papyraceous scarring
Eye signs: drooping eyelids, myopia, antimongoloid slant
Varicose veins or hernia or uterine/rectal prolapse

Note: BFJHS is diagnosed in the presence of two major criteria, or one major and two minor criteria, or four minor criteria (adapted from Grahame R, Bird HA, Child A, Dolan AL, Fowler-Edwards A, Ferrell W, Gurley-Green S, Keer R, Mansi E, Murray K, Smith E. The British Society Special Interest Group on Heritable Disorders of Connective Tissue Criteria for the Benign Joint Hypermobility Syndrome. "The Revised (Brighton 1998) Criteria for the Diagnosis of the BJHS". Journal of Rheumatology 2000; 27:1777-1779).

Table 4: Iliotibial band-stretching regime
Muscle groupAction (hold for 5-10 seconds; repeat ×5, three times a day)
Hip abductorStand erect, legs straight, feet together; stretch trunk (on frontal plane) towards the unaffected leg
Iliotibial bandLie on a bench on the unaffected side, with the unaffected hip and knee slightly flexed, in order to maintain balance; flex the affected hip and straighten the affected knee so that the affected leg hangs off the bench; allow the iliotibial band of the affected leg to be stretched by gravitational pull
Lie on a bench on the affected side with the affected leg in line with the body and the hip and knee locked; flex the unaffected (upper) leg; place the hands on the bench immediately under the shoulder and push the trunk upwards as far as possible to apply stretch to the lateral area of the affected leg
Upper iliotibial bandStand erect; with affected leg behind normal leg; stretch trunk (on frontal plane) towards unaffected side
Lower iliotibial bandStand erect as above, with the knee of the affected leg slightly flexed and hips rotated (on transverse plane) towards affected leg; stretch trunk (on frontal plane) towards the unaffected side
Iliotibial band and hamstringsStand erect, with the affected leg behind the normal leg so that the knee of the affected leg rests on the posterior aspect of the non-affected knee; rotate the trunk (on transverse plane) away from the affected leg and attempt to touch the heel of the affected leg
Table 5: Treatment regime for iliotibial band syndrome
VisitAction
1Examination
Including Nobel's and Ober's tests, and excluding other causes of knee joint pain
Gait analysis - walking and running
Check for presence of tibial varum, tibial torsion, uncompensated rearfoot varus and limb length discrepancy (include shoe wear pattern)
Instigate the iliotibial band stretching regime (see Table 11), with a quadriceps- and adductor-strengthening programme
Ice massage to painful area at lateral aspect of knee Advise reduction in athletic activity
2Commence physical therapies, e.g. cortisone iontorphoresis or ultrasound and ice massageStabilizing orthoses and/or foot and ankle taping, ± heel lift
Continue stretching programme ± massage
Non-steroidal anti-inflammatory (10-day course of 400 mg ibuprofen qds)
Stop all athletic activity if pain does not resolve
3Magnetic resonance imaging/computed tomographic scan to knee joint areaRefer to orthopaedics

Most cases will resolve with one treatment; more severe cases will require a second visit and some will require orthopaedic referral.

Table 6: Iliotibial band-stretching regime
Muscle groupAction (hold for 5-10 seconds; repeat ×5, three times a day)
Hip abductorStand erect, legs straight, feet together; stretch trunk (on frontal plane) towards the unaffected leg
Iliotibial bandLie on a bench on the unaffected side, with the unaffected hip and knee slightly flexed, in order to maintain balance; flex the affected hip and straighten the affected knee so that the affected leg hangs off the bench; allow the iliotibial band of the affected leg to be stretched by gravitational pull
Lie on a bench on the affected side with the affected leg in line with the body and the hip and knee locked; flex the unaffected (upper) leg; place the hands on the bench immediately under the shoulder and push the trunk upwards as far as possible to apply stretch to the lateral area of the affected leg
Upper iliotibial bandStand erect; with affected leg behind normal leg; stretch trunk (on frontal plane) towards unaffected side
Lower iliotibial bandStand erect as above, with the knee of the affected leg slightly flexed and hips rotated (on transverse plane) towards affected leg; stretch trunk (on frontal plane) towards the unaffected side
Iliotibial band and hamstringsStand erect, with the affected leg behind the normal leg so that the knee of the affected leg rests on the posterior aspect of the non-affected knee; rotate the trunk (on transverse plane) away from the affected leg and attempt to touch the heel of the affected leg
Table 7: Grades and characteristics of medial tibial stress syndrome (MTSS)
GradeCharacteristic
1Pain on palpation of the anteromedial (or posteromedial) area of tibial crest
No pain during activity or exercise
2Pain after activity or exercise
No pain during activity or exercise
3Pain during activity or exercise
Pain after activity or exercise
4Pain and discomfort during normal walking
Continual pain during activity or exercise
Table 8: Phased treatment approach to medial tibial stress syndrome (MTSS)
PresentationTreatment
Phase 1: acute phaseCessation of exercise activity until all pain resolves RICE(P)
Phase 2: rehabilitation phaseDeep compartment muscle exercise to strengthen the deep fascial-bone interface and reduce tension on the deep fascial insertion, in order to decrease pain and swelling and prevent fascial scarring
Phase 3: functional phaseUse of antipronatory/functional orthoses, strapping or taping in order to strengthen the fascial-bone interphase and prevent further excessive tension on the tibia
Phase 4: return to activityPhased and gradual return to normal levels of activity
Table 9: Presentations of nerve trunk irritation in the foot
Neuroma/lesionInvolved nerveLocation
Proximal tarsal tunnel syndromeBranches of the posterior tibial nerveMedial ankle area
Distal tarsal tunnel syndrome Jogger's footMedial plantar nerveBetween navicular tuberosity and belly of abductor hallucis
Distal tarsal tunnel syndrome Baxter's neuritisLateral plantar nerveBetween bellies of abductor hallucis, quadratus plantae and abductor digiti quinti minimi
Joplin's neuromaMedial plantar nerve properMedial area of first metatarsal head
Houser's neuromaFirst plantar intermetatarsal nerveBetween 1 and 2 metatarsals
Heuter's neuromaSecond plantar intermetatarsal nerveBetween 2 and 3 metatarsals
Morton's neuromaThird plantar intermetatarsal nerveBetween 3 and 4 metatarsals
Islen's neuromaFourth plantar intermetatarsal nerveBetween 4 and 5 metatarsals
Table 10: Accessory bones in the foot
Accessory bone in the footLocation
Os tibiale externum (accessory navicular)Within tibialis posterior tendon, adjacent to proximal part of navicular tuberosity
Os trigonumPosterior margin of talus
Os peroneumWithin peroneus longus tendon, adjacent to inferior lateral border of cuboid/calcaneocuboid joint
Os vesalianumAdjacent to fifth metatarsal base
Os intermetatarseumBetween bases of first and second metatarsals
Os interphalangeusWithin insertion of flexor hallucis longus tendon, adjacent to plantar area of hallux interphalangeal joint
Table 11: Presentations of nerve trunk irritation in the foot
Neuroma/lesionInvolved nerveLocation
Proximal tarsal tunnel syndromeBranches of the posterior tibial nerveMedial ankle area
Distal tarsal tunnel syndrome Jogger's footMedial plantar nerveBetween navicular tuberosity and belly of abductor hallucis
Distal tarsal tunnel syndrome Baxter's neuritisLateral plantar nerveBetween bellies of abductor hallucis, quadratus plantae and abductor digiti quinti minimi
Joplin's neuromaMedial plantar nerve properMedial area of first metatarsal head
Houser's neuromaFirst plantar intermetatarsal nerveBetween 1 and 2 metatarsals
Heuter's neuromaSecond plantar intermetatarsal nerveBetween 2 and 3 metatarsals
Morton's neuromaThird plantar intermetatarsal nerveBetween 3 and 4 metatarsals
Islen's neuromaFourth plantar intermetatarsal nerveBetween 4 and 5 metatarsals

AIDS (ādz),

n.pr See syndrome, acquired immune deficiency.

AIDS

(ādz)
Acronym for acquired immune deficiency (or immunodeficiency) syndrome; disorder of the immune system characterized by opportunistic diseases, including candidiasis, Pneumocystis jiroveci and others. Caused by the human immunodeficiency virus, which is transmitted in body fluids (notably breast milk, blood, and semen) through sexual contact, sharing of contaminated needles (by injecting drug abusers), accidental needle sticks, and contact with contaminated blood.

AIDS,

n the abbreviation for acquired immunodeficiency syndrome. See also human immunodeficiency virus (HIV).

AIDS

acquired immune deficiency syndrome of humans, caused by the lentivirus, human immunodeficiency virus 1 (HIV1), less commonly HIV2. The virus initially infects macrophages and then attacks and destroys T helper CD4 lymphocytes, thereby producing immunodeficiency and resulting in death, usually after a very prolonged incubation period followed by a very prolonged clinical course. A very similar virus SIV1 causes simian AIDS in captive macaque monkeys. A further similar virus SIV2 has been isolated from healthy green monkeys.

feline AIDS
see feline immunodeficiency virus.

Patient discussion about AIDS

Q. Why AID spred? and How?

A. if you mean AIDS- it spread mostly because people don't practice safe sex or sharing needles when injecting drugs. here is a nice tutorial about HIV, it is also specify the ways of infection-
http://www.nlm.nih.gov/medlineplus/tutorials/aids/htm/lesson.htm

Q. The HIV test came back POSITIVE! My very close friend 'Demonte'. One day in December as he was returning from a business trip, his wife met him at the airport with terrible news. During a routine pregnancy check up, her doctor had administered an HIV test along with other blood-work. The HIV test came back POSITIVE! The doctor wanted to begin administering drugs immediately but the cost of these drugs here when compared to their family income was prohibitive. I helped him with some of my savings. He already sold his favorite sentimental car to save his precious wife. Now i want to know is there any NATURAL medicine to cure this? Hope it costs less and available.

A. there are no effective natural remedy for HIV. the medications are very hard ones that try to control the virus from spreading (cannot eliminate it though). no herbal remedy or nutrition change will do that.

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