When you're in a bad mood and have your nose to the grindstone, all you see is the task at hand. But a good mood lets you see how the task fits into the bigger picture.
This isn't a motivational motto, it's the finding from five psychology experiments by marketing researchers Aparna A. Labroo, PhD, MBA, of the University of Chicago, and Vanessa M. Patrick, PhD, MBA, of the University of Georgia.
Research shows that a good mood broadens your attention and lets you see future opportunities. A bad mood, however, tends to make you focus on where you are right now. But how does your mood affect the kinds of choices you make?
Let's say you're at the fridge and see that picture of your smiling children. It makes you happy, thus giving you a broader perspective. Will your ability to look toward the future mean you'll put off dieting until later and indulge in unhealthy food later? Or will your foresight prompt you to ensure your future health by eating healthy food now?
Good Mood, Bad Mood Experiments
Labroo and Patrick first looked at whether feel-good cues prompted people to take things more broadly, and whether feel-bad cues prompt a more literal focus.
In their first study, they asked 58 college students to describe a list of 10 activities. Next to each activity (painting a room, for example) was a little smiley face, a little frowny face, or a little neutral face.
Sure enough, students used more abstract terms to describe the task if it was marked with a smiley face, and use more concrete terms for the frowny-face tasks.
Going beyond smiley faces, the researchers actually put 129 students into a good or bad mood by having them focus on either the best or worst day of their lives. Those in a good mood saw tasks in the abstract (painting beautifies the environment, for example). Those in a bad mood saw tasks more concretely (painting lets me choose my favorite paint color, for example).
In a third experiment, 40 students reported how good they felt. Half were given an abstract task -- they were asked to focus on why they study for exams. The other half got a concrete task -- they focused on how they study for exams. Then they were asked how important academic goals were to them.
Students in a good mood were more likely to find academic goals important when they focused on the abstract why question. Students in a bad mood were more likely to find academic goals important when the focused on the concrete how question.
Next, 90 students were asked to free associate to 10 positive words, 10 neutral words, or 10 negative words -- a task known to put people in a good, neutral, or bad mood. Then the students watched one of two orange juice ads. One ad said you should drink orange juice because it's an investment in your future health. The other ad said you should drink orange juice because it would ensure your health today.
Sure enough, students in a good mood were more likely to say they'd buy orange juice after seeing the future-benefit ad. Those in a bad mood were more likely to buy based on the immediate-benefit ad.
Finally, the researchers asked 69 students to focus on either academic goals or friendship goals. Then the students were asked to re-experience the best or worst day of their lives. After undergoing a free-association task, the students were given a scenario in which a person must decide between studying for an exam the next day or seeing an old friend who is passing through town on the way out of the country.
When cued to think about academic goals, students in a good mood were more likely than bad-mood students to choose studying for the exam. But when cued to think about friendship goals, students in a good mood were more likely than bad-mood students to choose seeing their old pal.
Good Mood, Big Picture
Taken together, Labroo and Patrick say, the findings show that a good mood makes people see things in more abstract terms. A good mood will lead people to adopt general, long-term goals -- but only those long-term goals seen as accessible.
"We propose that a positive mood, by signaling that a situation is benign, might allow people to step back and take in the big picture," they write. "In contrast, a negative mood, by signaling not only danger but its imminence, might focus attention on immediate and proximal concerns and reduce the adoption of abstract future goals."
Sunday, November 23, 2008
Babies born four months before the peak cold and flu season have a 30 percent higher risk of developing asthma, U.S. researchers said on Friday, suggesting that these common infections may trigger asthma.
"All infants are exposed to this and it is potentially preventable," said Dr. Tina Hartert, director of the center for Asthma Research at Vanderbilt University, whose study appears in the American Journal of Respiratory and Critical Care Medicine.
She said it has been known for some time that infants in the Northern Hemisphere born in the fall are at higher risk of developing asthma, but the study is the first to tie this trend to peak viral activity in the winter months.
Hartert and colleagues studied the medical records of 95,000 infants and their mothers in the state of Tennessee.
They found that all babies in the study were at increased risk if they had bronchiolitis, a lung infection usually caused by respiratory syncytial virus or RSV. But autumn babies were at the highest risk.
"What we were able to show was the timing of birth and the risk of developing asthma moves in time almost to the day with the peak of these viral infections each winter," she said.
While genetic risk factors predispose a child to develop asthma, Hartert thinks environmental exposure such as winter viral infection, and particularly RSV infection, may activate those genes.
Nearly every child is infected with RSV early in life, with infections occurring most often between the ages of 3 and 6 months. The virus usually clears up without serious complications.
Hartert said the task now is to prove that preventing such infections could keep infants from developing asthma. "That is where we are now. We need to prove that preventing this infection prevents this lifelong chronic disease," she said.
The easiest way to do that would be a vaccine, but so far, none exists. Vaccine makers GenVec Inc, AstraZeneca's MedImmune unit and others are working on RSV vaccines.
"It's in the pipeline. We just don't have one yet," Hartert said
Tuesday, November 11, 2008
AIDS
Acquired immune deficiency syndrome or acquired immunodeficiency syndrome (AIDS or Aids) is a set of symptoms and infections resulting from the damage to the human immune system caused by the human immunodeficiency virus (HIV).[1] This condition progressively reduces the effectiveness of the immune system and leaves individuals susceptible to opportunistic infections and tumors. HIV is transmitted through direct contact of a mucous membrane or the bloodstream with a bodily fluid containing HIV, such as blood, semen, vaginal fluid, preseminal fluid, and breast milk.[2][3] This transmission can involve anal, vaginal or oral sex, blood transfusion, contaminated hypodermic needles, exchange between mother and baby during pregnancy, childbirth, or breastfeeding, or other exposure to one of the above bodily fluids.
AIDS is now a pandemic.[4] In 2007, an estimated 33.2 million people lived with the disease worldwide, and it killed an estimated 2.1 million people, including 330,000 children.[5] Over three-quarters of these deaths occurred in sub-Saharan Africa,[5] retarding economic growth and destroying human capital.[6] Most researchers believe that HIV originated in sub-Saharan Africa during the twentieth century.[7] AIDS was first recognized by the U.S. Centers for Disease Control and Prevention in 1981 and its cause, HIV, identified by American and French scientists in the early 1980s.[8]
Although treatments for AIDS and HIV can slow the course of the disease, there is currently no vaccine or cure. Antiretroviral treatment reduces both the mortality and the morbidity of HIV infection, but these drugs are expensive and routine access to antiretroviral medication is not available in all countries.[9] Due to the difficulty in treating HIV infection, preventing infection is a key aim in controlling the AIDS epidemic, with health organizations promoting safe sex and needle-exchange programmes in attempts to slow the spread of the virus.
Contents
AIDS is now a pandemic.[4] In 2007, an estimated 33.2 million people lived with the disease worldwide, and it killed an estimated 2.1 million people, including 330,000 children.[5] Over three-quarters of these deaths occurred in sub-Saharan Africa,[5] retarding economic growth and destroying human capital.[6] Most researchers believe that HIV originated in sub-Saharan Africa during the twentieth century.[7] AIDS was first recognized by the U.S. Centers for Disease Control and Prevention in 1981 and its cause, HIV, identified by American and French scientists in the early 1980s.[8]
Although treatments for AIDS and HIV can slow the course of the disease, there is currently no vaccine or cure. Antiretroviral treatment reduces both the mortality and the morbidity of HIV infection, but these drugs are expensive and routine access to antiretroviral medication is not available in all countries.[9] Due to the difficulty in treating HIV infection, preventing infection is a key aim in controlling the AIDS epidemic, with health organizations promoting safe sex and needle-exchange programmes in attempts to slow the spread of the virus.
Contents
1 Symptoms
1.1 Pulmonary infections
1.2 Gastrointestinal infections
1.3 Neurological and psychiatric involvement
1.4 Tumors and malignancies
1.5 Other opportunistic infections
2 Cause
2.1 Sexual transmission
2.2 Exposure to blood-borne pathogens
2.3 Perinatal transmission
2.4 Misconceptions
3 Pathophysiology
3.1 Cells affected
3.2 The effect
3.3 Molecular basis
4 Diagnosis
4.1 WHO disease staging system
4.2 CDC classification system
4.3 HIV test
5 Prevention
5.1 Sexual contact
5.2 Exposure to infected body fluids
5.3 Mother-to-child transmission (MTCT)
6 Treatment
6.1 Antiviral therapy
6.2 Future research
6.3 Alternative medicine
7 Prognosis
8 Epidemiology
9 History
10 Society and culture
10.1 Stigma
10.2 Economic impact
10.3 AIDS denialism
11 Notes and references
12 Further reading
13 External links
Symptoms
A generalized graph of the relationship between HIV copies (viral load) and CD4 counts over the average course of untreated HIV infection; any particular individual's disease course may vary considerably.
CD4+ T Lymphocyte count (cells/mm³)
HIV RNA copies per mL of plasmaThe symptoms of AIDS are primarily the result of conditions that do not normally develop in individuals with healthy immune systems. Most of these conditions are infections caused by bacteria, viruses, fungi and parasites that are normally controlled by the elements of the immune system that HIV damages. Opportunistic infections are common in people with AIDS.[10] HIV affects nearly every organ system. People with AIDS also have an increased risk of developing various cancers such as Kaposi's sarcoma, cervical cancer and cancers of the immune system known as lymphomas. Additionally, people with AIDS often have systemic symptoms of infection like fevers, sweats (particularly at night), swollen glands, chills, weakness, and weight loss.[11][12] The specific opportunistic infections that AIDS patients develop depend in part on the prevalence of these infections in the geographic area in which the patient lives.
Main symptoms of AIDS.
Pulmonary infections
X-ray of Pneumocystis jirovecii caused pneumonia. There is increased white (opacity) in the lower lungs on both sides, characteristic of Pneumocystis pneumoniaPneumocystis pneumonia (originally known as Pneumocystis carinii pneumonia, and still abbreviated as PCP, which now stands for Pneumocystis pneumonia) is relatively rare in healthy, immunocompetent people, but common among HIV-infected individuals. It is caused by Pneumocystis jirovecii. Before the advent of effective diagnosis, treatment and routine prophylaxis in Western countries, it was a common immediate cause of death. In developing countries, it is still one of the first indications of AIDS in untested individuals, although it does not generally occur unless the CD4 count is less than 200 cells per µL of blood.[13]
Tuberculosis (TB) is unique among infections associated with HIV because it is transmissible to immunocompetent people via the respiratory route, is easily treatable once identified, may occur in early-stage HIV disease, and is preventable with drug therapy. However, multidrug resistance is a potentially serious problem. Even though its incidence has declined because of the use of directly observed therapy and other improved practices in Western countries, this is not the case in developing countries where HIV is most prevalent. In early-stage HIV infection (CD4 count >300 cells per µL), TB typically presents as a pulmonary disease. In advanced HIV infection, TB often presents atypically with extrapulmonary (systemic) disease a common feature. Symptoms are usually constitutional and are not localized to one particular site, often affecting bone marrow, bone, urinary and gastrointestinal tracts, liver, regional lymph nodes, and the central nervous system.[14]
Gastrointestinal infections
Esophagitis is an inflammation of the lining of the lower end of the esophagus (gullet or swallowing tube leading to the stomach). In HIV infected individuals, this is normally due to fungal (candidiasis) or viral (herpes simplex-1 or cytomegalovirus) infections. In rare cases, it could be due to mycobacteria.[15]
Unexplained chronic diarrhea in HIV infection is due to many possible causes, including common bacterial (Salmonella, Shigella, Listeria or Campylobacter) and parasitic infections; and uncommon opportunistic infections such as cryptosporidiosis, microsporidiosis, Mycobacterium avium complex (MAC) and viruses,[16] astrovirus, adenovirus, rotavirus and cytomegalovirus, (the latter as a course of colitis). In some cases, diarrhea may be a side effect of several drugs used to treat HIV, or it may simply accompany HIV infection, particularly during primary HIV infection. It may also be a side effect of antibiotics used to treat bacterial causes of diarrhea (common for Clostridium difficile). In the later stages of HIV infection, diarrhea is thought to be a reflection of changes in the way the intestinal tract absorbs nutrients, and may be an important component of HIV-related wasting.[17]
Neurological and psychiatric involvement
HIV infection may lead to a variety of neuropsychiatric sequelae, either by infection of the now susceptible nervous system by organisms, or as a direct consequence of the illness itself.
Toxoplasmosis is a disease caused by the single-celled parasite called Toxoplasma gondii; it usually infects the brain, causing toxoplasma encephalitis, but it can also infect and cause disease in the eyes and lungs.[18] Cryptococcal meningitis is an infection of the meninx (the membrane covering the brain and spinal cord) by the fungus Cryptococcus neoformans. It can cause fevers, headache, fatigue, nausea, and vomiting. Patients may also develop seizures and confusion; left untreated, it can be lethal.
Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease, in which the gradual destruction of the myelin sheath covering the axons of nerve cells impairs the transmission of nerve impulses. It is caused by a virus called JC virus which occurs in 70% of the population in latent form, causing disease only when the immune system has been severely weakened, as is the case for AIDS patients. It progresses rapidly, usually causing death within months of diagnosis.[19]
AIDS dementia complex (ADC) is a metabolic encephalopathy induced by HIV infection and fueled by immune activation of HIV infected brain macrophages and microglia. These cells are productively infected by HIV and secrete neurotoxins of both host and viral origin.[20] Specific neurological impairments are manifested by cognitive, behavioral, and motor abnormalities that occur after years of HIV infection and are associated with low CD4+ T cell levels and high plasma viral loads. Prevalence is 10–20% in Western countries[21] but only 1–2% of HIV infections in India.[22][23] This difference is possibly due to the HIV subtype in India. AIDS related mania is sometimes seen in patients with advanced HIV illness; it presents with more irritability and cognitive impairment and less euphoria than a manic episode associated with true bipolar disorder. Unlike the latter condition, it may have a more chronic course. This syndrome is less often seen with the advent of multi-drug therapy.
Tumors and malignancies
Kaposi's sarcomaPatients with HIV infection have substantially increased incidence of several cancers. This is primarily due to co-infection with an oncogenic DNA virus, especially Epstein-Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus (KSHV), and human papillomavirus (HPV).[24][25]
Kaposi's sarcoma (KS) is the most common tumor in HIV-infected patients. The appearance of this tumor in young homosexual men in 1981 was one of the first signals of the AIDS epidemic. Caused by a gammaherpes virus called Kaposi's sarcoma-associated herpes virus (KSHV), it often appears as purplish nodules on the skin, but can affect other organs, especially the mouth, gastrointestinal tract, and lungs.
High-grade B cell lymphomas such as Burkitt's lymphoma, Burkitt's-like lymphoma, diffuse large B-cell lymphoma (DLBCL), and primary central nervous system lymphoma present more often in HIV-infected patients. These particular cancers often foreshadow a poor prognosis. In some cases these lymphomas are AIDS-defining. Epstein-Barr virus (EBV) or KSHV cause many of these lymphomas.
Cervical cancer in HIV-infected women is considered AIDS-defining. It is caused by human papillomavirus (HPV).[26]
In addition to the AIDS-defining tumors listed above, HIV-infected patients are at increased risk of certain other tumors, such as Hodgkin's disease and anal and rectal carcinomas. However, the incidence of many common tumors, such as breast cancer or colon cancer, does not increase in HIV-infected patients. In areas where HAART is extensively used to treat AIDS, the incidence of many AIDS-related malignancies has decreased, but at the same time malignant cancers overall have become the most common cause of death of HIV-infected patients.[27]
Other opportunistic infections
AIDS patients often develop opportunistic infections that present with non-specific symptoms, especially low-grade fevers and weight loss. These include infection with Mycobacterium avium-intracellulare and cytomegalovirus (CMV). CMV can cause colitis, as described above, and CMV retinitis can cause blindness. Penicilliosis due to Penicillium marneffei is now the third most common opportunistic infection (after extrapulmonary tuberculosis and cryptococcosis) in HIV-positive individuals within the endemic area of Southeast Asia.[28]
Cause
For more details on this topic, see HIV.
Scanning electron micrograph of HIV-1, colored green, budding from a cultured lymphocyte.AIDS is the most severe acceleration of infection with HIV. HIV is a retrovirus that primarily infects vital organs of the human immune system such as CD4+ T cells (a subset of T cells), macrophages and dendritic cells. It directly and indirectly destroys CD4+ T cells.[29] Once HIV has killed so many CD4+ T cells that there are fewer than 200 of these cells per microliter (µL) of blood, cellular immunity is lost. Acute HIV infection progresses over time to clinical latent HIV infection and then to early symptomatic HIV infection and later to AIDS, which is identified either on the basis of the amount of CD4+ T cells remaining in the blood, and/or the presence of certain infections, as noted above.[30]
In the absence of antiretroviral therapy, the median time of progression from HIV infection to AIDS is nine to ten years, and the median survival time after developing AIDS is only 9.2 months.[31] However, the rate of clinical disease progression varies widely between individuals, from two weeks up to 20 years. Many factors affect the rate of progression. These include factors that influence the body's ability to defend against HIV such as the infected person's general immune function.[32][33] Older people have weaker immune systems, and therefore have a greater risk of rapid disease progression than younger people. Poor access to health care and the existence of coexisting infections such as tuberculosis also may predispose people to faster disease progression.[31][34][35] The infected person's genetic inheritance plays an important role and some people are resistant to certain strains of HIV. An example of this is people with the homozygous CCR5-Δ32 variation are resistant to infection with certain strains of HIV.[36] HIV is genetically variable and exists as different strains, which cause different rates of clinical disease progression.[37][38][39]
Sexual transmission
Sexual transmission occurs with the contact between sexual secretions of one person with the rectal, genital or oral mucous membranes of another. Unprotected receptive sexual acts are riskier than unprotected insertive sexual acts, and the risk for transmitting HIV through unprotected anal intercourse is greater than the risk from vaginal intercourse or oral sex. However, oral sex is not entirely safe, as HIV can be transmitted through both insertive and receptive oral sex.[40][41] Sexual assault greatly increases the risk of HIV transmission as protection is rarely employed and physical trauma to the vagina frequently occurs, facilitating the transmission of HIV.[42]
Other sexually transmitted infections (STI) increase the risk of HIV transmission and infection, because they cause the disruption of the normal epithelial barrier by genital ulceration and/or microulceration; and by accumulation of pools of HIV-susceptible or HIV-infected cells (lymphocytes and macrophages) in semen and vaginal secretions. Epidemiological studies from sub-Saharan Africa, Europe and North America suggest that genital ulcers, such as those caused by syphilis and/or chancroid, increase the risk of becoming infected with HIV by about four-fold. There is also a significant although lesser increase in risk from STIs such as gonorrhea, Chlamydial infection and trichomoniasis, which all cause local accumulations of lymphocytes and macrophages.[43]
Transmission of HIV depends on the infectiousness of the index case and the susceptibility of the uninfected partner. Infectivity seems to vary during the course of illness and is not constant between individuals. An undetectable plasma viral load does not necessarily indicate a low viral load in the seminal liquid or genital secretions. However, each 10-fold increase in the level of HIV in the blood is associated with an 81% increased rate of HIV transmission.[43][44] Women are more susceptible to HIV-1 infection due to hormonal changes, vaginal microbial ecology and physiology, and a higher prevalence of sexually transmitted diseases.[45][46] People who have been infected with one strain of HIV can still be infected later on in their lives by other, more virulent strains.
Infection is unlikely in a single encounter. High rates of infection have been linked to a pattern of overlapping long-term romantic relationships. This allows the virus to quickly spread to multiple partners who in turn infect their partners. A pattern of serial monogamy or occasional casual encounters is associated with lower rates of infection.[47]
HIV spreads readily through heterosexual sex in Africa, but less so elsewhere. One possibility being researched is that schistosomiasis, which affects up to 50 per cent of women in parts of Africa, damages the lining of the vagina.[48][49]
Exposure to blood-borne pathogens
CDC poster from 1989 highlighting the threat of AIDS associated with drug useThis transmission route is particularly relevant to intravenous drug users, hemophiliacs and recipients of blood transfusions and blood products. Sharing and reusing syringes contaminated with HIV-infected blood represents a major risk for infection with HIV. Needle sharing is the cause of one third of all new HIV-infections in North America, China, and Eastern Europe. The risk of being infected with HIV from a single prick with a needle that has been used on an HIV-infected person is thought to be about 1 in 150 (see table above). Post-exposure prophylaxis with anti-HIV drugs can further reduce this risk.[50] This route can also affect people who give and receive tattoos and piercings. Universal precautions are frequently not followed in both sub-Saharan Africa and much of Asia because of both a shortage of supplies and inadequate training. The WHO estimates that approximately 2.5% of all HIV infections in sub-Saharan Africa are transmitted through unsafe healthcare injections.[51] Because of this, the United Nations General Assembly has urged the nations of the world to implement precautions to prevent HIV transmission by health workers.[52]
The risk of transmitting HIV to blood transfusion recipients is extremely low in developed countries where improved donor selection and HIV screening is performed. However, according to the WHO, the overwhelming majority of the world's population does not have access to safe blood and between 5% and 10% of the world's HIV infections come from transfusion of infected blood and blood products.[53]
Perinatal transmission
The transmission of the virus from the mother to the child can occur in utero during the last weeks of pregnancy and at childbirth. In the absence of treatment, the transmission rate between a mother and her child during pregnancy, labor and delivery is 25%. However, when the mother takes antiretroviral therapy and gives birth by caesarean section, the rate of transmission is just 1%.[54] The risk of infection is influenced by the viral load of the mother at birth, with the higher the viral load, the higher the risk. Breastfeeding also increases the risk of transmission by about 4 %.[55]
Misconceptions
Main article: HIV and AIDS misconceptions
A number of misconceptions have arisen surrounding HIV/AIDS. Three of the most common are that AIDS can spread through casual contact, that sexual intercourse with a virgin will cure AIDS, and that HIV can infect only homosexual men and drug users. Other misconceptions are that any act of anal intercourse between gay men can lead to AIDS infection, and that open discussion of homosexuality and HIV in schools will lead to increased rates of homosexuality and AIDS.[56]
Pathophysiology
This section may require cleanup to meet Wikipedia's quality standards.
Please improve this article if you can. (April 2008)
The pathophysiology of AIDS is complex, as is the case with all syndromes.[57] Ultimately, HIV causes AIDS by depleting CD4+ T helper lymphocytes. This weakens the immune system and allows opportunistic infections. T lymphocytes are essential to the immune response and without them, the body cannot fight infections or kill cancerous cells. The mechanism of CD4+ T cell depletion differs in the acute and chronic phases.[58] During the acute phase, HIV-induced cell lysis and killing of infected cells by cytotoxic T cells accounts for CD4+ T cell depletion, although apoptosis may also be a factor. During the chronic phase, the consequences of generalized immune activation coupled with the gradual loss of the ability of the immune system to generate new T cells appear to account for the slow decline in CD4+ T cell numbers.
Although the symptoms of immune deficiency characteristic of AIDS do not appear for years after a person is infected, the bulk of CD4+ T cell loss occurs during the first weeks of infection, especially in the intestinal mucosa, which harbors the majority of the lymphocytes found in the body. [59] The reason for the preferential loss of mucosal CD4+ T cells is that a majority of mucosal CD4+ T cells express the CCR5 coreceptor, whereas a small fraction of CD4+ T cells in the bloodstream do so.[60] HIV seeks out and destroys CCR5 expressing CD4+ cells during acute infection. A vigorous immune response eventually controls the infection and initiates the clinically latent phase. However, CD4+ T cells in mucosal tissues remain depleted throughout the infection, although enough remain to initially ward off life-threatening infections.
Continuous HIV replication results in a state of generalized immune activation persisting throughout the chronic phase. [61] Immune activation, which is reflected by the increased activation state of immune cells and release of proinflammatory cytokines, results from the activity of several HIV gene products and the immune response to ongoing HIV replication. Another cause is the breakdown of the immune surveillance system of the mucosal barrier caused by the depletion of mucosal CD4+ T cells during the acute phase of disease.[62] This results in the systemic exposure of the immune system to microbial components of the gut’s normal flora, which in a healthy person is kept in check by the mucosal immune system. The activation and proliferation of T cells that results from immune activation provides fresh targets for HIV infection. However, direct killing by HIV alone cannot account for the observed depletion of CD4+ T cells since only 0.01-0.10% of CD4+ T cells in the blood are infected. A major cause of CD4+ T cell loss appears to result from their heightened susceptibility to apoptosis when the immune system remains activated. Although new T cells are continuously produced by the thymus to replace the ones lost, the regenerative capacity of the thymus is slowly destroyed by direct infection of its thymocytes by HIV. Eventually, the minimal number of CD4+ T cells necessary to maintain a sufficient immune response is lost, leading to AIDS
Cells affected
The virus, entering through which ever route, acts primarily on the following cells:[63]
Lymphoreticular system:
CD4+ T-Helper cells
CD4+ Macrophages
CD4+ Monocytes
B-lymphocytes
Certain endothelial cells
Central nervous system:
Microglia of the nervous system
Astrocytes
Oligodendrocytes
Neurones - indirectly by the action of cytokines and the gp-120
The effect
The virus has cytopathic effects but how it does it is still not quite clear. It can remain inactive in these cells for long periods, though. This effect is hypothesized to be due to the CD4-gp120 interaction.[64]
The most prominent effect of the HIV virus is its T-helper cell suppression and lysis. The cell is simply killed off or deranged to the point of being function-less (they do not respond to foreign antigens). The infected B-cells can not produce enough antibodies either. Thus the immune system collapses leading to the familiar AIDS complications, like infections and neoplasms (vide supra).
Infection of the cells of the CNS cause acute aseptic meningitis, subacute encephalitis, vacuolar myelopathy and peripheral neuropathy. Later it leads to even AIDS dementia complex.
The CD4-gp120 interaction (vide supra) is also permissive to other viruses like Cytomegalovirus, Hepatitis virus, Herpes simplex virus, etc. These viruses lead to further cell damage i.e. cytopathy.
Molecular basis
For details, see:
Structure and genome of HIV
HIV replication cycle
HIV tropism
Diagnosis
The diagnosis of AIDS in a person infected with HIV is based on the presence of certain signs or symptoms. Since June 5, 1981, many definitions have been developed for epidemiological surveillance such as the Bangui definition and the 1994 expanded World Health Organization AIDS case definition. However, clinical staging of patients was not an intended use for these systems as they are neither sensitive, nor specific. In developing countries, the World Health Organization staging system for HIV infection and disease, using clinical and laboratory data, is used and in developed countries, the Centers for Disease Control (CDC) Classification System is used.
WHO disease staging system
Main article: WHO Disease Staging System for HIV Infection and Disease
In 1990, the World Health Organization (WHO) grouped these infections and conditions together by introducing a staging system for patients infected with HIV-1.[65] An update took place in September 2005. Most of these conditions are opportunistic infections that are easily treatable in healthy people.
Stage I: HIV infection is asymptomatic and not categorized as AIDS
Stage II: includes minor mucocutaneous manifestations and recurrent upper respiratory tract infections
Stage III: includes unexplained chronic diarrhea for longer than a month, severe bacterial infections and pulmonary tuberculosis
Stage IV: includes toxoplasmosis of the brain, candidiasis of the esophagus, trachea, bronchi or lungs and Kaposi's sarcoma; these diseases are indicators of AIDS.
CDC classification system
Main article: CDC Classification System for HIV Infection
There are two main definitions for AIDS, both produced by the Centers for Disease Control and Prevention (CDC). The older definition is to referring to AIDS using the diseases that were associated with it, for example, lymphadenopathy, the disease after which the discoverers of HIV originally named the virus.[66][67] In 1993, the CDC expanded their definition of AIDS to include all HIV positive people with a CD4+ T cell count below 200 per µL of blood or 14% of all lymphocytes.[68] The majority of new AIDS cases in developed countries use either this definition or the pre-1993 CDC definition. The AIDS diagnosis still stands even if, after treatment, the CD4+ T cell count rises to above 200 per µL of blood or other AIDS-defining illnesses are cured.
HIV test
Main article: HIV test
Many people are unaware that they are infected with HIV.[69] Less than 1% of the sexually active urban population in Africa has been tested, and this proportion is even lower in rural populations. Furthermore, only 0.5% of pregnant women attending urban health facilities are counseled, tested or receive their test results. Again, this proportion is even lower in rural health facilities.[69] Therefore, donor blood and blood products used in medicine and medical research are screened for HIV.
HIV tests are usually performed on venous blood. Many laboratories use fourth generation screening tests which detect anti-HIV antibody (IgG and IgM) and the HIV p24 antigen. The detection of HIV antibody or antigen in a patient previously known to be negative is evidence of HIV infection. Individuals whose first specimen indicates evidence of HIV infection will have a repeat test on a second blood sample to confirm the results. The window period (the time between initial infection and the development of detectable antibodies against the infection) can vary since it can take 3–6 months to seroconvert and to test positive. Detection of the virus using polymerase chain reaction (PCR) during the window period is possible, and evidence suggests that an infection may often be detected earlier than when using a fourth generation EIA screening test. Positive results obtained by PCR are confirmed by antibody tests.[70] Routinely used HIV tests for infection in neonates, born to HIV-positive mothers, have no value because of the presence of maternal antibody to HIV in the child's blood. HIV infection can only be diagnosed by PCR, testing for HIV pro-viral DNA in the children's lymphocytes.[71]
Prevention
Estimated per act risk for acquisition
of HIV by exposure route[72] Exposure Route Estimated infections
per 10,000 exposures
to an infected source
Blood Transfusion 9,000[73]
Childbirth 2,500[54]
Needle-sharing injection drug use 67[74]
Percutaneous needle stick 30[75]
Receptive anal intercourse* 50[76][77]
Insertive anal intercourse* 6.5[76][77]
Receptive penile-vaginal intercourse* 10[76][77][78]
Insertive penile-vaginal intercourse* 5[76][77]
Receptive oral intercourse*§ 1[77]
Insertive oral intercourse*§ 0.5[77]
* assuming no condom use
§ source refers to oral intercourse
performed on a man
The three main transmission routes of HIV are sexual contact, exposure to infected body fluids or tissues, and from mother to fetus or child during perinatal period. It is possible to find HIV in the saliva, tears, and urine of infected individuals, but there are no recorded cases of infection by these secretions, and the risk of infection is negligible.[79]
Sexual contact
The majority of HIV infections are acquired through unprotected sexual relations between partners, one of whom has HIV. The primary mode of HIV infection worldwide is through sexual contact between members of the opposite sex.[80][81][82] During a sexual act, only male or female condoms can reduce the chances of infection with HIV and other STDs and the chances of becoming pregnant. The best evidence to date indicates that typical condom use reduces the risk of heterosexual HIV transmission by approximately 80% over the long-term, though the benefit is likely to be higher if condoms are used correctly on every occasion.[83] The male latex condom, if used correctly without oil-based lubricants, is the single most effective available technology to reduce the sexual transmission of HIV and other sexually transmitted infections. Manufacturers recommend that oil-based lubricants such as petroleum jelly, butter, and lard not be used with latex condoms, because they dissolve the latex, making the condoms porous. If necessary, manufacturers recommend using water-based lubricants. Oil-based lubricants can however be used with polyurethane condoms.[84]
The female condom is an alternative to the male condom and is made from polyurethane, which allows it to be used in the presence of oil-based lubricants. They are larger than male condoms and have a stiffened ring-shaped opening, and are designed to be inserted into the vagina. The female condom contains an inner ring, which keeps the condom in place inside the vagina – inserting the female condom requires squeezing this ring. However, at present availability of female condoms is very low and the price remains prohibitive for many women. Preliminary studies suggest that, where female condoms are available, overall protected sexual acts increase relative to unprotected sexual acts, making them an important HIV prevention strategy.[85]
Studies on couples where one partner is infected show that with consistent condom use, HIV infection rates for the uninfected partner are below 1% per year.[86] Prevention strategies are well-known in developed countries, however, recent epidemiological and behavioral studies in Europe and North America have suggested that a substantial minority of young people continue to engage in high-risk practices and that despite HIV/AIDS knowledge, young people underestimate their own risk of becoming infected with HIV.[87]
Randomized controlled trials have shown that male circumcision lowers the risk of HIV infection among heterosexual men by up to 60%.[88] It is expected that this procedure will be actively promoted in many of the countries affected by HIV, although doing so will involve confronting a number of practical, cultural and attitudinal issues. Some experts fear that a lower perception of vulnerability among circumcised men may result in more sexual risk-taking behavior, thus negating its preventive effects.[89]
Exposure to infected body fluids
Health care workers can reduce exposure to HIV by employing precautions to reduce the risk of exposure to contaminated blood. These precautions include barriers such as gloves, masks, protective eyeware or shields, and gowns or aprons which prevent exposure of the skin or mucous membranes to blood borne pathogens. Frequent and thorough washing of the skin immediately after being contaminated with blood or other bodily fluids can reduce the chance of infection. Finally, sharp objects like needles, scalpels and glass, are carefully disposed of to prevent needlestick injuries with contaminated items.[90] Since intravenous drug use is an important factor in HIV transmission in developed countries, harm reduction strategies such as needle-exchange programmes are used in attempts to reduce the infections caused by drug abuse.[91][92]
Mother-to-child transmission (MTCT)
Current recommendations state that when replacement feeding is acceptable, feasible, affordable, sustainable and safe, HIV-infected mothers should avoid breast-feeding their infant. However, if this is not the case, exclusive breast-feeding is recommended during the first months of life and discontinued as soon as possible.[93]
Treatment
See also HIV Treatment and Antiretroviral drug.
Abacavir – a nucleoside analog reverse transcriptase inhibitor (NARTI or NRTI)
The chemical structure of AbacavirThere is currently no vaccine or cure for HIV or AIDS. The only known methods of prevention are based on avoiding exposure to the virus or, failing that, an antiretroviral treatment directly after a highly significant exposure, called post-exposure prophylaxis (PEP).[94] PEP has a very demanding four week schedule of dosage. It also has very unpleasant side effects including diarrhea, malaise, nausea and fatigue.[95]
Antiviral therapy
Current treatment for HIV infection consists of highly active antiretroviral therapy, or HAART.[96] This has been highly beneficial to many HIV-infected individuals since its introduction in 1996 when the protease inhibitor-based HAART initially became available.[9] Current optimal HAART options consist of combinations (or "cocktails") consisting of at least three drugs belonging to at least two types, or "classes," of antiretroviral agents. Typical regimens consist of two nucleoside analogue reverse transcriptase inhibitors (NARTIs or NRTIs) plus either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor (NNRTI). Because HIV disease progression in children is more rapid than in adults, and laboratory parameters are less predictive of risk for disease progression, particularly for young infants, treatment recommendations are more aggressive for children than for adults.[97] In developed countries where HAART is available, doctors assess the viral load, rapidity in CD4 decline, and patient readiness while deciding when to recommend initiating treatment.[98]
HAART allows the stabilization of the patient’s symptoms and viremia, but it neither cures the patient of HIV, nor alleviates the symptoms, and high levels of HIV-1, often HAART resistant, return once treatment is stopped.[99][100] Moreover, it would take more than the lifetime of an individual to be cleared of HIV infection using HAART.[101] Despite this, many HIV-infected individuals have experienced remarkable improvements in their general health and quality of life, which has led to the plummeting of HIV-associated morbidity and mortality.[102][103][104] In the absence of HAART, progression from HIV infection to AIDS occurs at a median of between nine to ten years and the median survival time after developing AIDS is only 9.2 months.[31] HAART is thought to increase survival time by between 4 and 12 years.[105][106]
For some patients, which can be more than fifty percent of patients, HAART achieves far less than optimal results, due to medication intolerance/side effects, prior ineffective antiretroviral therapy and infection with a drug-resistant strain of HIV. Non-adherence and non-persistence with therapy are the major reasons why some people do not benefit from HAART.[107] The reasons for non-adherence and non-persistence are varied. Major psychosocial issues include poor access to medical care, inadequate social supports, psychiatric disease and drug abuse. HAART regimens can also be complex and thus hard to follow, with large numbers of pills taken frequently.[108][109][110] Side effects can also deter people from persisting with HAART, these include lipodystrophy, dyslipidaemia, diarrhoea, insulin resistance, an increase in cardiovascular risks and birth defects.[111] Anti-retroviral drugs are expensive, and the majority of the world's infected individuals do not have access to medications and treatments for HIV and AIDS.
Future research
It has been postulated that only a vaccine can halt the pandemic because a vaccine would possibly cost less, thus being affordable for developing countries, and would not require daily treatments. However, even after almost 30 years of research, HIV-1 remains a difficult target for a vaccine.[112]
Research to improve current treatments includes decreasing side effects of current drugs, further simplifying drug regimens to improve adherence, and determining the best sequence of regimens to manage drug resistance. A number of studies have shown that measures to prevent opportunistic infections can be beneficial when treating patients with HIV infection or AIDS. Vaccination against hepatitis A and B is advised for patients who are not infected with these viruses and are at risk of becoming infected.[113] Patients with substantial immunosuppression are also advised to receive prophylactic therapy for Pneumocystis jiroveci pneumonia (PCP), and many patients may benefit from prophylactic therapy for toxoplasmosis and Cryptococcus meningitis as well.[95]
Researchers have discovered an abzyme that can destroy the protein gp120 CD4 binding site. This protein is common to all HIV variants as it is the attachment point for B lymphocytes and subsequent compromising of the immune system.[114]
Alternative medicine
Various forms of alternative medicine have been used to treat symptoms or alter the course of the disease.[115] Acupuncture has been used to alleviate some symptoms, such peripheral neuropathy, but cannot cure the HIV infection.[116] Several randomized clinical trials testing the effect of herbal medicines have shown that there is no evidence that these herbs have any effect on the progression of the disease, but may instead produce serious side-effects.[117]
Some data suggest that multivitamin and mineral supplements might reduce HIV disease progression in adults, although there is no conclusive evidence on if they reduce mortality among people with good nutritional status.[118] Vitamin A supplementation in children probably has some benefit.[118] Daily doses of selenium can suppress HIV viral burden with an associated improvement of the CD4 count. Selenium can be used as an adjunct therapy to standard antiviral treatments, but cannot itself reduce mortality and morbidity.[119]
Current studies indicate that that alternative medicine therapies have little effect on the mortality or morbidity of the disease, but may improve the quality of life of individuals afflicted with AIDS. The psychological benefits of these therapies are the most important use.[115]
Prognosis
Without treatment, the net median survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype,[5] and the median survival rate after diagnosis of AIDS in resource-limited settings where treatment is not available ranges between 6 and 19 months, depending on the study.[120] In areas where it is widely available, the development of HAART as effective therapy for HIV infection and AIDS reduced the death rate from this disease by 80%, and raised the life expectancy for a newly diagnosed HIV-infected person to about 20 years.[121]
As new treatments continue to be developed and because HIV continues to evolve resistance to treatments, estimates of survival time are likely to continue to change. Without antiretroviral therapy, death normally occurs within a year.[31] Most patients die from opportunistic infections or malignancies associated with the progressive failure of the immune system.[122] The rate of clinical disease progression varies widely between individuals and has been shown to be affected by many factors such as host susceptibility and immune function[32][33][36] health care and co-infections,[31][122] as well as which particular strain of the virus is involved.[38][123][124]
Epidemiology
Main article: AIDS pandemic
Estimated prevalence of HIV among young adults (15-49) per country at the end of 2005The AIDS pandemic can also be seen as several epidemics of separate subtypes; the major factors in its spread are sexual transmission and vertical transmission from mother to child at birth and through breast milk.[4] Despite recent, improved access to antiretroviral treatment and care in many regions of the world, the AIDS pandemic claimed an estimated 2.1 million (range 1.9–2.4 million) lives in 2007 of which an estimated 330,000 were children under 15 years.[5] Globally, an estimated 33.2 million people lived with HIV in 2007, including 2.5 million children. An estimated 2.5 million (range 1.8–4.1 million) people were newly infected in 2007, including 420,000 children.[5]
Sub-Saharan Africa remains by far the worst affected region. In 2007 it contained an estimated 68% of all people living with AIDS and 76% of all AIDS deaths, with 1.7 million new infections bringing the number of people living with HIV to 22.5 million, and with 11.4 million AIDS orphans living in the region. Unlike other regions, most people living with HIV in sub-Saharan Africa in 2007 (61%) were women. Adult prevalence in 2007 was an estimated 5.0%, and AIDS continued to be the single largest cause of mortality in this region.[5] South Africa has the largest population of HIV patients in the world, followed by Nigeria and India.[125] South & South East Asia are second worst affected; in 2007 this region contained an estimated 18% of all people living with AIDS, and an estimated 300,000 deaths from AIDS.[5] India has an estimated 2.5 million infections and an estimated adult prevalence of 0.36%.[5] Life expectancy has fallen dramatically in the worst-affected countries; for example, in 2006 it was estimated that it had dropped from 65 to 35 years in Botswana.[4]
History
Main article: AIDS origin
AIDS was first reported June 5, 1981, when the U.S. Centers for Disease Control and Prevention recorded a cluster of Pneumocystis carinii pneumonia (now still classified as PCP but known to be caused by Pneumocystis jirovecii) in five homosexual men in Los Angeles.[126] In the beginning, the Centers for Disease Control and Prevention (CDC) did not have an official name for the disease, often referring to it by way of the diseases that were associated with it, for example, lymphadenopathy, the disease after which the discoverers of HIV originally named the virus.[66][67] They also used Kaposi's Sarcoma and Opportunistic Infections, the name by which a task force had been set up in 1981.[127] In the general press, the term GRID, which stood for Gay-related immune deficiency, had been coined.[128] The CDC, in search of a name, and looking at the infected communities coined “the 4H disease,” as it seemed to single out Haitians, homosexuals, hemophiliacs, and heroin users.[129] However, after determining that AIDS was not isolated to the homosexual community,[127] the term GRID became misleading and AIDS was introduced at a meeting in July 1982.[130] By September 1982 the CDC started using the name AIDS, and properly defined the illness.[131]
A more controversial theory known as the OPV AIDS hypothesis suggests that the AIDS epidemic was inadvertently started in the late 1950s in the Belgian Congo by Hilary Koprowski's research into a poliomyelitis vaccine.[132][133] According to scientific consensus, this scenario is not supported by the available evidence.[134][135][136]
A recent study states that HIV probably moved from Africa to Haiti and then entered the United States around 1969.[137]
Also see AIDS origins opposed to scientific consensus
Society and culture
Stigma
Ryan White became a poster child for HIV after being expelled from school because of his infection.AIDS stigma exists around the world in a variety of ways, including ostracism, rejection, discrimination and avoidance of HIV infected people; compulsory HIV testing without prior consent or protection of confidentiality; violence against HIV infected individuals or people who are perceived to be infected with HIV; and the quarantine of HIV infected individuals.[138] Stigma-related violence or the fear of violence prevents many people from seeking HIV testing, returning for their results, or securing treatment, possibly turning what could be a manageable chronic illness into a death sentence and perpetuating the spread of HIV.[139]
AIDS stigma has been further divided into the following three categories:
Instrumental AIDS stigma—a reflection of the fear and apprehension that are likely to be associated with any deadly and transmissible illness.[140]
Symbolic AIDS stigma—the use of HIV/AIDS to express attitudes toward the social groups or lifestyles perceived to be associated with the disease.[140]
Courtesy AIDS stigma—stigmatization of people connected to the issue of HIV/AIDS or HIV- positive people.[141]
Often, AIDS stigma is expressed in conjunction with one or more other stigmas, particularly those associated with homosexuality, bisexuality, promiscuity, and intravenous drug use.
In many developed countries, there is an association between AIDS and homosexuality or bisexuality, and this association is correlated with higher levels of sexual prejudice such as anti-homosexual attitudes.[142] There is also a perceived association between AIDS and all male-male sexual behavior, including sex between uninfected men.[140]
Economic impact
Main article: Economic impact of AIDS
Changes in life expectancy in some hard-hit African countries.
Botswana
Zimbabwe
Kenya
South Africa
UgandaHIV and AIDS affects economic growth by reducing the availability of human capital.[6] Without proper nutrition, health care and medicine that is available in developed countries, large numbers of people are falling victim to AIDS. They will not only be unable to work, but will also require significant medical care. The forecast is that this will likely cause a collapse of economies and societies in countries with a significant AIDS population. In some heavily infected areas, the epidemic has left behind many orphans cared for by elderly grandparents.[143]
The increased mortality in this region will result in a smaller skilled population and labor force. This smaller labor force will be predominantly young people, with reduced knowledge and work experience leading to reduced productivity. An increase in workers’ time off to look after sick family members or for sick leave will also lower productivity. Increased mortality will also weaken the mechanisms that generate human capital and investment in people, through loss of income and the death of parents. By killing off mainly young adults, AIDS seriously weakens the taxable population, reducing the resources available for public expenditures such as education and health services not related to AIDS resulting in increasing pressure for the state's finances and slower growth of the economy. This results in a slower growth of the tax base, an effect that will be reinforced if there are growing expenditures on treating the sick, training (to replace sick workers), sick pay and caring for AIDS orphans. This is especially true if the sharp increase in adult mortality shifts the responsibility and blame from the family to the government in caring for these orphans.[143]
On the level of the household, AIDS results in both the loss of income and increased spending on healthcare by the household. The income effects of this lead to spending reduction as well as a substitution effect away from education and towards healthcare and funeral spending. A study in Côte d'Ivoire showed that households with an HIV/AIDS patient spent twice as much on medical expenses as other households.[144]
AIDS denialism
Main article: AIDS denialism
A small group of activists, including several scientists who do not study HIV/AIDS, question the connection between HIV and AIDS,[145] the existence of HIV itself,[146] or the validity of current testing and treatment methods. Though these claims have been examined and thoroughly rejected by the scientific community,[147] they continue to be promulgated through the Internet[148] and have had a significant political impact, particularly in South Africa, where former President Thabo Mbeki's embrace of AIDS denialism has been blamed for an ineffective response to that country's AIDS epidemic.[
1.1 Pulmonary infections
1.2 Gastrointestinal infections
1.3 Neurological and psychiatric involvement
1.4 Tumors and malignancies
1.5 Other opportunistic infections
2 Cause
2.1 Sexual transmission
2.2 Exposure to blood-borne pathogens
2.3 Perinatal transmission
2.4 Misconceptions
3 Pathophysiology
3.1 Cells affected
3.2 The effect
3.3 Molecular basis
4 Diagnosis
4.1 WHO disease staging system
4.2 CDC classification system
4.3 HIV test
5 Prevention
5.1 Sexual contact
5.2 Exposure to infected body fluids
5.3 Mother-to-child transmission (MTCT)
6 Treatment
6.1 Antiviral therapy
6.2 Future research
6.3 Alternative medicine
7 Prognosis
8 Epidemiology
9 History
10 Society and culture
10.1 Stigma
10.2 Economic impact
10.3 AIDS denialism
11 Notes and references
12 Further reading
13 External links
Symptoms
A generalized graph of the relationship between HIV copies (viral load) and CD4 counts over the average course of untreated HIV infection; any particular individual's disease course may vary considerably.
CD4+ T Lymphocyte count (cells/mm³)
HIV RNA copies per mL of plasmaThe symptoms of AIDS are primarily the result of conditions that do not normally develop in individuals with healthy immune systems. Most of these conditions are infections caused by bacteria, viruses, fungi and parasites that are normally controlled by the elements of the immune system that HIV damages. Opportunistic infections are common in people with AIDS.[10] HIV affects nearly every organ system. People with AIDS also have an increased risk of developing various cancers such as Kaposi's sarcoma, cervical cancer and cancers of the immune system known as lymphomas. Additionally, people with AIDS often have systemic symptoms of infection like fevers, sweats (particularly at night), swollen glands, chills, weakness, and weight loss.[11][12] The specific opportunistic infections that AIDS patients develop depend in part on the prevalence of these infections in the geographic area in which the patient lives.
Main symptoms of AIDS.
Pulmonary infections
X-ray of Pneumocystis jirovecii caused pneumonia. There is increased white (opacity) in the lower lungs on both sides, characteristic of Pneumocystis pneumoniaPneumocystis pneumonia (originally known as Pneumocystis carinii pneumonia, and still abbreviated as PCP, which now stands for Pneumocystis pneumonia) is relatively rare in healthy, immunocompetent people, but common among HIV-infected individuals. It is caused by Pneumocystis jirovecii. Before the advent of effective diagnosis, treatment and routine prophylaxis in Western countries, it was a common immediate cause of death. In developing countries, it is still one of the first indications of AIDS in untested individuals, although it does not generally occur unless the CD4 count is less than 200 cells per µL of blood.[13]
Tuberculosis (TB) is unique among infections associated with HIV because it is transmissible to immunocompetent people via the respiratory route, is easily treatable once identified, may occur in early-stage HIV disease, and is preventable with drug therapy. However, multidrug resistance is a potentially serious problem. Even though its incidence has declined because of the use of directly observed therapy and other improved practices in Western countries, this is not the case in developing countries where HIV is most prevalent. In early-stage HIV infection (CD4 count >300 cells per µL), TB typically presents as a pulmonary disease. In advanced HIV infection, TB often presents atypically with extrapulmonary (systemic) disease a common feature. Symptoms are usually constitutional and are not localized to one particular site, often affecting bone marrow, bone, urinary and gastrointestinal tracts, liver, regional lymph nodes, and the central nervous system.[14]
Gastrointestinal infections
Esophagitis is an inflammation of the lining of the lower end of the esophagus (gullet or swallowing tube leading to the stomach). In HIV infected individuals, this is normally due to fungal (candidiasis) or viral (herpes simplex-1 or cytomegalovirus) infections. In rare cases, it could be due to mycobacteria.[15]
Unexplained chronic diarrhea in HIV infection is due to many possible causes, including common bacterial (Salmonella, Shigella, Listeria or Campylobacter) and parasitic infections; and uncommon opportunistic infections such as cryptosporidiosis, microsporidiosis, Mycobacterium avium complex (MAC) and viruses,[16] astrovirus, adenovirus, rotavirus and cytomegalovirus, (the latter as a course of colitis). In some cases, diarrhea may be a side effect of several drugs used to treat HIV, or it may simply accompany HIV infection, particularly during primary HIV infection. It may also be a side effect of antibiotics used to treat bacterial causes of diarrhea (common for Clostridium difficile). In the later stages of HIV infection, diarrhea is thought to be a reflection of changes in the way the intestinal tract absorbs nutrients, and may be an important component of HIV-related wasting.[17]
Neurological and psychiatric involvement
HIV infection may lead to a variety of neuropsychiatric sequelae, either by infection of the now susceptible nervous system by organisms, or as a direct consequence of the illness itself.
Toxoplasmosis is a disease caused by the single-celled parasite called Toxoplasma gondii; it usually infects the brain, causing toxoplasma encephalitis, but it can also infect and cause disease in the eyes and lungs.[18] Cryptococcal meningitis is an infection of the meninx (the membrane covering the brain and spinal cord) by the fungus Cryptococcus neoformans. It can cause fevers, headache, fatigue, nausea, and vomiting. Patients may also develop seizures and confusion; left untreated, it can be lethal.
Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease, in which the gradual destruction of the myelin sheath covering the axons of nerve cells impairs the transmission of nerve impulses. It is caused by a virus called JC virus which occurs in 70% of the population in latent form, causing disease only when the immune system has been severely weakened, as is the case for AIDS patients. It progresses rapidly, usually causing death within months of diagnosis.[19]
AIDS dementia complex (ADC) is a metabolic encephalopathy induced by HIV infection and fueled by immune activation of HIV infected brain macrophages and microglia. These cells are productively infected by HIV and secrete neurotoxins of both host and viral origin.[20] Specific neurological impairments are manifested by cognitive, behavioral, and motor abnormalities that occur after years of HIV infection and are associated with low CD4+ T cell levels and high plasma viral loads. Prevalence is 10–20% in Western countries[21] but only 1–2% of HIV infections in India.[22][23] This difference is possibly due to the HIV subtype in India. AIDS related mania is sometimes seen in patients with advanced HIV illness; it presents with more irritability and cognitive impairment and less euphoria than a manic episode associated with true bipolar disorder. Unlike the latter condition, it may have a more chronic course. This syndrome is less often seen with the advent of multi-drug therapy.
Tumors and malignancies
Kaposi's sarcomaPatients with HIV infection have substantially increased incidence of several cancers. This is primarily due to co-infection with an oncogenic DNA virus, especially Epstein-Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus (KSHV), and human papillomavirus (HPV).[24][25]
Kaposi's sarcoma (KS) is the most common tumor in HIV-infected patients. The appearance of this tumor in young homosexual men in 1981 was one of the first signals of the AIDS epidemic. Caused by a gammaherpes virus called Kaposi's sarcoma-associated herpes virus (KSHV), it often appears as purplish nodules on the skin, but can affect other organs, especially the mouth, gastrointestinal tract, and lungs.
High-grade B cell lymphomas such as Burkitt's lymphoma, Burkitt's-like lymphoma, diffuse large B-cell lymphoma (DLBCL), and primary central nervous system lymphoma present more often in HIV-infected patients. These particular cancers often foreshadow a poor prognosis. In some cases these lymphomas are AIDS-defining. Epstein-Barr virus (EBV) or KSHV cause many of these lymphomas.
Cervical cancer in HIV-infected women is considered AIDS-defining. It is caused by human papillomavirus (HPV).[26]
In addition to the AIDS-defining tumors listed above, HIV-infected patients are at increased risk of certain other tumors, such as Hodgkin's disease and anal and rectal carcinomas. However, the incidence of many common tumors, such as breast cancer or colon cancer, does not increase in HIV-infected patients. In areas where HAART is extensively used to treat AIDS, the incidence of many AIDS-related malignancies has decreased, but at the same time malignant cancers overall have become the most common cause of death of HIV-infected patients.[27]
Other opportunistic infections
AIDS patients often develop opportunistic infections that present with non-specific symptoms, especially low-grade fevers and weight loss. These include infection with Mycobacterium avium-intracellulare and cytomegalovirus (CMV). CMV can cause colitis, as described above, and CMV retinitis can cause blindness. Penicilliosis due to Penicillium marneffei is now the third most common opportunistic infection (after extrapulmonary tuberculosis and cryptococcosis) in HIV-positive individuals within the endemic area of Southeast Asia.[28]
Cause
For more details on this topic, see HIV.
Scanning electron micrograph of HIV-1, colored green, budding from a cultured lymphocyte.AIDS is the most severe acceleration of infection with HIV. HIV is a retrovirus that primarily infects vital organs of the human immune system such as CD4+ T cells (a subset of T cells), macrophages and dendritic cells. It directly and indirectly destroys CD4+ T cells.[29] Once HIV has killed so many CD4+ T cells that there are fewer than 200 of these cells per microliter (µL) of blood, cellular immunity is lost. Acute HIV infection progresses over time to clinical latent HIV infection and then to early symptomatic HIV infection and later to AIDS, which is identified either on the basis of the amount of CD4+ T cells remaining in the blood, and/or the presence of certain infections, as noted above.[30]
In the absence of antiretroviral therapy, the median time of progression from HIV infection to AIDS is nine to ten years, and the median survival time after developing AIDS is only 9.2 months.[31] However, the rate of clinical disease progression varies widely between individuals, from two weeks up to 20 years. Many factors affect the rate of progression. These include factors that influence the body's ability to defend against HIV such as the infected person's general immune function.[32][33] Older people have weaker immune systems, and therefore have a greater risk of rapid disease progression than younger people. Poor access to health care and the existence of coexisting infections such as tuberculosis also may predispose people to faster disease progression.[31][34][35] The infected person's genetic inheritance plays an important role and some people are resistant to certain strains of HIV. An example of this is people with the homozygous CCR5-Δ32 variation are resistant to infection with certain strains of HIV.[36] HIV is genetically variable and exists as different strains, which cause different rates of clinical disease progression.[37][38][39]
Sexual transmission
Sexual transmission occurs with the contact between sexual secretions of one person with the rectal, genital or oral mucous membranes of another. Unprotected receptive sexual acts are riskier than unprotected insertive sexual acts, and the risk for transmitting HIV through unprotected anal intercourse is greater than the risk from vaginal intercourse or oral sex. However, oral sex is not entirely safe, as HIV can be transmitted through both insertive and receptive oral sex.[40][41] Sexual assault greatly increases the risk of HIV transmission as protection is rarely employed and physical trauma to the vagina frequently occurs, facilitating the transmission of HIV.[42]
Other sexually transmitted infections (STI) increase the risk of HIV transmission and infection, because they cause the disruption of the normal epithelial barrier by genital ulceration and/or microulceration; and by accumulation of pools of HIV-susceptible or HIV-infected cells (lymphocytes and macrophages) in semen and vaginal secretions. Epidemiological studies from sub-Saharan Africa, Europe and North America suggest that genital ulcers, such as those caused by syphilis and/or chancroid, increase the risk of becoming infected with HIV by about four-fold. There is also a significant although lesser increase in risk from STIs such as gonorrhea, Chlamydial infection and trichomoniasis, which all cause local accumulations of lymphocytes and macrophages.[43]
Transmission of HIV depends on the infectiousness of the index case and the susceptibility of the uninfected partner. Infectivity seems to vary during the course of illness and is not constant between individuals. An undetectable plasma viral load does not necessarily indicate a low viral load in the seminal liquid or genital secretions. However, each 10-fold increase in the level of HIV in the blood is associated with an 81% increased rate of HIV transmission.[43][44] Women are more susceptible to HIV-1 infection due to hormonal changes, vaginal microbial ecology and physiology, and a higher prevalence of sexually transmitted diseases.[45][46] People who have been infected with one strain of HIV can still be infected later on in their lives by other, more virulent strains.
Infection is unlikely in a single encounter. High rates of infection have been linked to a pattern of overlapping long-term romantic relationships. This allows the virus to quickly spread to multiple partners who in turn infect their partners. A pattern of serial monogamy or occasional casual encounters is associated with lower rates of infection.[47]
HIV spreads readily through heterosexual sex in Africa, but less so elsewhere. One possibility being researched is that schistosomiasis, which affects up to 50 per cent of women in parts of Africa, damages the lining of the vagina.[48][49]
Exposure to blood-borne pathogens
CDC poster from 1989 highlighting the threat of AIDS associated with drug useThis transmission route is particularly relevant to intravenous drug users, hemophiliacs and recipients of blood transfusions and blood products. Sharing and reusing syringes contaminated with HIV-infected blood represents a major risk for infection with HIV. Needle sharing is the cause of one third of all new HIV-infections in North America, China, and Eastern Europe. The risk of being infected with HIV from a single prick with a needle that has been used on an HIV-infected person is thought to be about 1 in 150 (see table above). Post-exposure prophylaxis with anti-HIV drugs can further reduce this risk.[50] This route can also affect people who give and receive tattoos and piercings. Universal precautions are frequently not followed in both sub-Saharan Africa and much of Asia because of both a shortage of supplies and inadequate training. The WHO estimates that approximately 2.5% of all HIV infections in sub-Saharan Africa are transmitted through unsafe healthcare injections.[51] Because of this, the United Nations General Assembly has urged the nations of the world to implement precautions to prevent HIV transmission by health workers.[52]
The risk of transmitting HIV to blood transfusion recipients is extremely low in developed countries where improved donor selection and HIV screening is performed. However, according to the WHO, the overwhelming majority of the world's population does not have access to safe blood and between 5% and 10% of the world's HIV infections come from transfusion of infected blood and blood products.[53]
Perinatal transmission
The transmission of the virus from the mother to the child can occur in utero during the last weeks of pregnancy and at childbirth. In the absence of treatment, the transmission rate between a mother and her child during pregnancy, labor and delivery is 25%. However, when the mother takes antiretroviral therapy and gives birth by caesarean section, the rate of transmission is just 1%.[54] The risk of infection is influenced by the viral load of the mother at birth, with the higher the viral load, the higher the risk. Breastfeeding also increases the risk of transmission by about 4 %.[55]
Misconceptions
Main article: HIV and AIDS misconceptions
A number of misconceptions have arisen surrounding HIV/AIDS. Three of the most common are that AIDS can spread through casual contact, that sexual intercourse with a virgin will cure AIDS, and that HIV can infect only homosexual men and drug users. Other misconceptions are that any act of anal intercourse between gay men can lead to AIDS infection, and that open discussion of homosexuality and HIV in schools will lead to increased rates of homosexuality and AIDS.[56]
Pathophysiology
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Please improve this article if you can. (April 2008)
The pathophysiology of AIDS is complex, as is the case with all syndromes.[57] Ultimately, HIV causes AIDS by depleting CD4+ T helper lymphocytes. This weakens the immune system and allows opportunistic infections. T lymphocytes are essential to the immune response and without them, the body cannot fight infections or kill cancerous cells. The mechanism of CD4+ T cell depletion differs in the acute and chronic phases.[58] During the acute phase, HIV-induced cell lysis and killing of infected cells by cytotoxic T cells accounts for CD4+ T cell depletion, although apoptosis may also be a factor. During the chronic phase, the consequences of generalized immune activation coupled with the gradual loss of the ability of the immune system to generate new T cells appear to account for the slow decline in CD4+ T cell numbers.
Although the symptoms of immune deficiency characteristic of AIDS do not appear for years after a person is infected, the bulk of CD4+ T cell loss occurs during the first weeks of infection, especially in the intestinal mucosa, which harbors the majority of the lymphocytes found in the body. [59] The reason for the preferential loss of mucosal CD4+ T cells is that a majority of mucosal CD4+ T cells express the CCR5 coreceptor, whereas a small fraction of CD4+ T cells in the bloodstream do so.[60] HIV seeks out and destroys CCR5 expressing CD4+ cells during acute infection. A vigorous immune response eventually controls the infection and initiates the clinically latent phase. However, CD4+ T cells in mucosal tissues remain depleted throughout the infection, although enough remain to initially ward off life-threatening infections.
Continuous HIV replication results in a state of generalized immune activation persisting throughout the chronic phase. [61] Immune activation, which is reflected by the increased activation state of immune cells and release of proinflammatory cytokines, results from the activity of several HIV gene products and the immune response to ongoing HIV replication. Another cause is the breakdown of the immune surveillance system of the mucosal barrier caused by the depletion of mucosal CD4+ T cells during the acute phase of disease.[62] This results in the systemic exposure of the immune system to microbial components of the gut’s normal flora, which in a healthy person is kept in check by the mucosal immune system. The activation and proliferation of T cells that results from immune activation provides fresh targets for HIV infection. However, direct killing by HIV alone cannot account for the observed depletion of CD4+ T cells since only 0.01-0.10% of CD4+ T cells in the blood are infected. A major cause of CD4+ T cell loss appears to result from their heightened susceptibility to apoptosis when the immune system remains activated. Although new T cells are continuously produced by the thymus to replace the ones lost, the regenerative capacity of the thymus is slowly destroyed by direct infection of its thymocytes by HIV. Eventually, the minimal number of CD4+ T cells necessary to maintain a sufficient immune response is lost, leading to AIDS
Cells affected
The virus, entering through which ever route, acts primarily on the following cells:[63]
Lymphoreticular system:
CD4+ T-Helper cells
CD4+ Macrophages
CD4+ Monocytes
B-lymphocytes
Certain endothelial cells
Central nervous system:
Microglia of the nervous system
Astrocytes
Oligodendrocytes
Neurones - indirectly by the action of cytokines and the gp-120
The effect
The virus has cytopathic effects but how it does it is still not quite clear. It can remain inactive in these cells for long periods, though. This effect is hypothesized to be due to the CD4-gp120 interaction.[64]
The most prominent effect of the HIV virus is its T-helper cell suppression and lysis. The cell is simply killed off or deranged to the point of being function-less (they do not respond to foreign antigens). The infected B-cells can not produce enough antibodies either. Thus the immune system collapses leading to the familiar AIDS complications, like infections and neoplasms (vide supra).
Infection of the cells of the CNS cause acute aseptic meningitis, subacute encephalitis, vacuolar myelopathy and peripheral neuropathy. Later it leads to even AIDS dementia complex.
The CD4-gp120 interaction (vide supra) is also permissive to other viruses like Cytomegalovirus, Hepatitis virus, Herpes simplex virus, etc. These viruses lead to further cell damage i.e. cytopathy.
Molecular basis
For details, see:
Structure and genome of HIV
HIV replication cycle
HIV tropism
Diagnosis
The diagnosis of AIDS in a person infected with HIV is based on the presence of certain signs or symptoms. Since June 5, 1981, many definitions have been developed for epidemiological surveillance such as the Bangui definition and the 1994 expanded World Health Organization AIDS case definition. However, clinical staging of patients was not an intended use for these systems as they are neither sensitive, nor specific. In developing countries, the World Health Organization staging system for HIV infection and disease, using clinical and laboratory data, is used and in developed countries, the Centers for Disease Control (CDC) Classification System is used.
WHO disease staging system
Main article: WHO Disease Staging System for HIV Infection and Disease
In 1990, the World Health Organization (WHO) grouped these infections and conditions together by introducing a staging system for patients infected with HIV-1.[65] An update took place in September 2005. Most of these conditions are opportunistic infections that are easily treatable in healthy people.
Stage I: HIV infection is asymptomatic and not categorized as AIDS
Stage II: includes minor mucocutaneous manifestations and recurrent upper respiratory tract infections
Stage III: includes unexplained chronic diarrhea for longer than a month, severe bacterial infections and pulmonary tuberculosis
Stage IV: includes toxoplasmosis of the brain, candidiasis of the esophagus, trachea, bronchi or lungs and Kaposi's sarcoma; these diseases are indicators of AIDS.
CDC classification system
Main article: CDC Classification System for HIV Infection
There are two main definitions for AIDS, both produced by the Centers for Disease Control and Prevention (CDC). The older definition is to referring to AIDS using the diseases that were associated with it, for example, lymphadenopathy, the disease after which the discoverers of HIV originally named the virus.[66][67] In 1993, the CDC expanded their definition of AIDS to include all HIV positive people with a CD4+ T cell count below 200 per µL of blood or 14% of all lymphocytes.[68] The majority of new AIDS cases in developed countries use either this definition or the pre-1993 CDC definition. The AIDS diagnosis still stands even if, after treatment, the CD4+ T cell count rises to above 200 per µL of blood or other AIDS-defining illnesses are cured.
HIV test
Main article: HIV test
Many people are unaware that they are infected with HIV.[69] Less than 1% of the sexually active urban population in Africa has been tested, and this proportion is even lower in rural populations. Furthermore, only 0.5% of pregnant women attending urban health facilities are counseled, tested or receive their test results. Again, this proportion is even lower in rural health facilities.[69] Therefore, donor blood and blood products used in medicine and medical research are screened for HIV.
HIV tests are usually performed on venous blood. Many laboratories use fourth generation screening tests which detect anti-HIV antibody (IgG and IgM) and the HIV p24 antigen. The detection of HIV antibody or antigen in a patient previously known to be negative is evidence of HIV infection. Individuals whose first specimen indicates evidence of HIV infection will have a repeat test on a second blood sample to confirm the results. The window period (the time between initial infection and the development of detectable antibodies against the infection) can vary since it can take 3–6 months to seroconvert and to test positive. Detection of the virus using polymerase chain reaction (PCR) during the window period is possible, and evidence suggests that an infection may often be detected earlier than when using a fourth generation EIA screening test. Positive results obtained by PCR are confirmed by antibody tests.[70] Routinely used HIV tests for infection in neonates, born to HIV-positive mothers, have no value because of the presence of maternal antibody to HIV in the child's blood. HIV infection can only be diagnosed by PCR, testing for HIV pro-viral DNA in the children's lymphocytes.[71]
Prevention
Estimated per act risk for acquisition
of HIV by exposure route[72] Exposure Route Estimated infections
per 10,000 exposures
to an infected source
Blood Transfusion 9,000[73]
Childbirth 2,500[54]
Needle-sharing injection drug use 67[74]
Percutaneous needle stick 30[75]
Receptive anal intercourse* 50[76][77]
Insertive anal intercourse* 6.5[76][77]
Receptive penile-vaginal intercourse* 10[76][77][78]
Insertive penile-vaginal intercourse* 5[76][77]
Receptive oral intercourse*§ 1[77]
Insertive oral intercourse*§ 0.5[77]
* assuming no condom use
§ source refers to oral intercourse
performed on a man
The three main transmission routes of HIV are sexual contact, exposure to infected body fluids or tissues, and from mother to fetus or child during perinatal period. It is possible to find HIV in the saliva, tears, and urine of infected individuals, but there are no recorded cases of infection by these secretions, and the risk of infection is negligible.[79]
Sexual contact
The majority of HIV infections are acquired through unprotected sexual relations between partners, one of whom has HIV. The primary mode of HIV infection worldwide is through sexual contact between members of the opposite sex.[80][81][82] During a sexual act, only male or female condoms can reduce the chances of infection with HIV and other STDs and the chances of becoming pregnant. The best evidence to date indicates that typical condom use reduces the risk of heterosexual HIV transmission by approximately 80% over the long-term, though the benefit is likely to be higher if condoms are used correctly on every occasion.[83] The male latex condom, if used correctly without oil-based lubricants, is the single most effective available technology to reduce the sexual transmission of HIV and other sexually transmitted infections. Manufacturers recommend that oil-based lubricants such as petroleum jelly, butter, and lard not be used with latex condoms, because they dissolve the latex, making the condoms porous. If necessary, manufacturers recommend using water-based lubricants. Oil-based lubricants can however be used with polyurethane condoms.[84]
The female condom is an alternative to the male condom and is made from polyurethane, which allows it to be used in the presence of oil-based lubricants. They are larger than male condoms and have a stiffened ring-shaped opening, and are designed to be inserted into the vagina. The female condom contains an inner ring, which keeps the condom in place inside the vagina – inserting the female condom requires squeezing this ring. However, at present availability of female condoms is very low and the price remains prohibitive for many women. Preliminary studies suggest that, where female condoms are available, overall protected sexual acts increase relative to unprotected sexual acts, making them an important HIV prevention strategy.[85]
Studies on couples where one partner is infected show that with consistent condom use, HIV infection rates for the uninfected partner are below 1% per year.[86] Prevention strategies are well-known in developed countries, however, recent epidemiological and behavioral studies in Europe and North America have suggested that a substantial minority of young people continue to engage in high-risk practices and that despite HIV/AIDS knowledge, young people underestimate their own risk of becoming infected with HIV.[87]
Randomized controlled trials have shown that male circumcision lowers the risk of HIV infection among heterosexual men by up to 60%.[88] It is expected that this procedure will be actively promoted in many of the countries affected by HIV, although doing so will involve confronting a number of practical, cultural and attitudinal issues. Some experts fear that a lower perception of vulnerability among circumcised men may result in more sexual risk-taking behavior, thus negating its preventive effects.[89]
Exposure to infected body fluids
Health care workers can reduce exposure to HIV by employing precautions to reduce the risk of exposure to contaminated blood. These precautions include barriers such as gloves, masks, protective eyeware or shields, and gowns or aprons which prevent exposure of the skin or mucous membranes to blood borne pathogens. Frequent and thorough washing of the skin immediately after being contaminated with blood or other bodily fluids can reduce the chance of infection. Finally, sharp objects like needles, scalpels and glass, are carefully disposed of to prevent needlestick injuries with contaminated items.[90] Since intravenous drug use is an important factor in HIV transmission in developed countries, harm reduction strategies such as needle-exchange programmes are used in attempts to reduce the infections caused by drug abuse.[91][92]
Mother-to-child transmission (MTCT)
Current recommendations state that when replacement feeding is acceptable, feasible, affordable, sustainable and safe, HIV-infected mothers should avoid breast-feeding their infant. However, if this is not the case, exclusive breast-feeding is recommended during the first months of life and discontinued as soon as possible.[93]
Treatment
See also HIV Treatment and Antiretroviral drug.
Abacavir – a nucleoside analog reverse transcriptase inhibitor (NARTI or NRTI)
The chemical structure of AbacavirThere is currently no vaccine or cure for HIV or AIDS. The only known methods of prevention are based on avoiding exposure to the virus or, failing that, an antiretroviral treatment directly after a highly significant exposure, called post-exposure prophylaxis (PEP).[94] PEP has a very demanding four week schedule of dosage. It also has very unpleasant side effects including diarrhea, malaise, nausea and fatigue.[95]
Antiviral therapy
Current treatment for HIV infection consists of highly active antiretroviral therapy, or HAART.[96] This has been highly beneficial to many HIV-infected individuals since its introduction in 1996 when the protease inhibitor-based HAART initially became available.[9] Current optimal HAART options consist of combinations (or "cocktails") consisting of at least three drugs belonging to at least two types, or "classes," of antiretroviral agents. Typical regimens consist of two nucleoside analogue reverse transcriptase inhibitors (NARTIs or NRTIs) plus either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor (NNRTI). Because HIV disease progression in children is more rapid than in adults, and laboratory parameters are less predictive of risk for disease progression, particularly for young infants, treatment recommendations are more aggressive for children than for adults.[97] In developed countries where HAART is available, doctors assess the viral load, rapidity in CD4 decline, and patient readiness while deciding when to recommend initiating treatment.[98]
HAART allows the stabilization of the patient’s symptoms and viremia, but it neither cures the patient of HIV, nor alleviates the symptoms, and high levels of HIV-1, often HAART resistant, return once treatment is stopped.[99][100] Moreover, it would take more than the lifetime of an individual to be cleared of HIV infection using HAART.[101] Despite this, many HIV-infected individuals have experienced remarkable improvements in their general health and quality of life, which has led to the plummeting of HIV-associated morbidity and mortality.[102][103][104] In the absence of HAART, progression from HIV infection to AIDS occurs at a median of between nine to ten years and the median survival time after developing AIDS is only 9.2 months.[31] HAART is thought to increase survival time by between 4 and 12 years.[105][106]
For some patients, which can be more than fifty percent of patients, HAART achieves far less than optimal results, due to medication intolerance/side effects, prior ineffective antiretroviral therapy and infection with a drug-resistant strain of HIV. Non-adherence and non-persistence with therapy are the major reasons why some people do not benefit from HAART.[107] The reasons for non-adherence and non-persistence are varied. Major psychosocial issues include poor access to medical care, inadequate social supports, psychiatric disease and drug abuse. HAART regimens can also be complex and thus hard to follow, with large numbers of pills taken frequently.[108][109][110] Side effects can also deter people from persisting with HAART, these include lipodystrophy, dyslipidaemia, diarrhoea, insulin resistance, an increase in cardiovascular risks and birth defects.[111] Anti-retroviral drugs are expensive, and the majority of the world's infected individuals do not have access to medications and treatments for HIV and AIDS.
Future research
It has been postulated that only a vaccine can halt the pandemic because a vaccine would possibly cost less, thus being affordable for developing countries, and would not require daily treatments. However, even after almost 30 years of research, HIV-1 remains a difficult target for a vaccine.[112]
Research to improve current treatments includes decreasing side effects of current drugs, further simplifying drug regimens to improve adherence, and determining the best sequence of regimens to manage drug resistance. A number of studies have shown that measures to prevent opportunistic infections can be beneficial when treating patients with HIV infection or AIDS. Vaccination against hepatitis A and B is advised for patients who are not infected with these viruses and are at risk of becoming infected.[113] Patients with substantial immunosuppression are also advised to receive prophylactic therapy for Pneumocystis jiroveci pneumonia (PCP), and many patients may benefit from prophylactic therapy for toxoplasmosis and Cryptococcus meningitis as well.[95]
Researchers have discovered an abzyme that can destroy the protein gp120 CD4 binding site. This protein is common to all HIV variants as it is the attachment point for B lymphocytes and subsequent compromising of the immune system.[114]
Alternative medicine
Various forms of alternative medicine have been used to treat symptoms or alter the course of the disease.[115] Acupuncture has been used to alleviate some symptoms, such peripheral neuropathy, but cannot cure the HIV infection.[116] Several randomized clinical trials testing the effect of herbal medicines have shown that there is no evidence that these herbs have any effect on the progression of the disease, but may instead produce serious side-effects.[117]
Some data suggest that multivitamin and mineral supplements might reduce HIV disease progression in adults, although there is no conclusive evidence on if they reduce mortality among people with good nutritional status.[118] Vitamin A supplementation in children probably has some benefit.[118] Daily doses of selenium can suppress HIV viral burden with an associated improvement of the CD4 count. Selenium can be used as an adjunct therapy to standard antiviral treatments, but cannot itself reduce mortality and morbidity.[119]
Current studies indicate that that alternative medicine therapies have little effect on the mortality or morbidity of the disease, but may improve the quality of life of individuals afflicted with AIDS. The psychological benefits of these therapies are the most important use.[115]
Prognosis
Without treatment, the net median survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype,[5] and the median survival rate after diagnosis of AIDS in resource-limited settings where treatment is not available ranges between 6 and 19 months, depending on the study.[120] In areas where it is widely available, the development of HAART as effective therapy for HIV infection and AIDS reduced the death rate from this disease by 80%, and raised the life expectancy for a newly diagnosed HIV-infected person to about 20 years.[121]
As new treatments continue to be developed and because HIV continues to evolve resistance to treatments, estimates of survival time are likely to continue to change. Without antiretroviral therapy, death normally occurs within a year.[31] Most patients die from opportunistic infections or malignancies associated with the progressive failure of the immune system.[122] The rate of clinical disease progression varies widely between individuals and has been shown to be affected by many factors such as host susceptibility and immune function[32][33][36] health care and co-infections,[31][122] as well as which particular strain of the virus is involved.[38][123][124]
Epidemiology
Main article: AIDS pandemic
Estimated prevalence of HIV among young adults (15-49) per country at the end of 2005The AIDS pandemic can also be seen as several epidemics of separate subtypes; the major factors in its spread are sexual transmission and vertical transmission from mother to child at birth and through breast milk.[4] Despite recent, improved access to antiretroviral treatment and care in many regions of the world, the AIDS pandemic claimed an estimated 2.1 million (range 1.9–2.4 million) lives in 2007 of which an estimated 330,000 were children under 15 years.[5] Globally, an estimated 33.2 million people lived with HIV in 2007, including 2.5 million children. An estimated 2.5 million (range 1.8–4.1 million) people were newly infected in 2007, including 420,000 children.[5]
Sub-Saharan Africa remains by far the worst affected region. In 2007 it contained an estimated 68% of all people living with AIDS and 76% of all AIDS deaths, with 1.7 million new infections bringing the number of people living with HIV to 22.5 million, and with 11.4 million AIDS orphans living in the region. Unlike other regions, most people living with HIV in sub-Saharan Africa in 2007 (61%) were women. Adult prevalence in 2007 was an estimated 5.0%, and AIDS continued to be the single largest cause of mortality in this region.[5] South Africa has the largest population of HIV patients in the world, followed by Nigeria and India.[125] South & South East Asia are second worst affected; in 2007 this region contained an estimated 18% of all people living with AIDS, and an estimated 300,000 deaths from AIDS.[5] India has an estimated 2.5 million infections and an estimated adult prevalence of 0.36%.[5] Life expectancy has fallen dramatically in the worst-affected countries; for example, in 2006 it was estimated that it had dropped from 65 to 35 years in Botswana.[4]
History
Main article: AIDS origin
AIDS was first reported June 5, 1981, when the U.S. Centers for Disease Control and Prevention recorded a cluster of Pneumocystis carinii pneumonia (now still classified as PCP but known to be caused by Pneumocystis jirovecii) in five homosexual men in Los Angeles.[126] In the beginning, the Centers for Disease Control and Prevention (CDC) did not have an official name for the disease, often referring to it by way of the diseases that were associated with it, for example, lymphadenopathy, the disease after which the discoverers of HIV originally named the virus.[66][67] They also used Kaposi's Sarcoma and Opportunistic Infections, the name by which a task force had been set up in 1981.[127] In the general press, the term GRID, which stood for Gay-related immune deficiency, had been coined.[128] The CDC, in search of a name, and looking at the infected communities coined “the 4H disease,” as it seemed to single out Haitians, homosexuals, hemophiliacs, and heroin users.[129] However, after determining that AIDS was not isolated to the homosexual community,[127] the term GRID became misleading and AIDS was introduced at a meeting in July 1982.[130] By September 1982 the CDC started using the name AIDS, and properly defined the illness.[131]
A more controversial theory known as the OPV AIDS hypothesis suggests that the AIDS epidemic was inadvertently started in the late 1950s in the Belgian Congo by Hilary Koprowski's research into a poliomyelitis vaccine.[132][133] According to scientific consensus, this scenario is not supported by the available evidence.[134][135][136]
A recent study states that HIV probably moved from Africa to Haiti and then entered the United States around 1969.[137]
Also see AIDS origins opposed to scientific consensus
Society and culture
Stigma
Ryan White became a poster child for HIV after being expelled from school because of his infection.AIDS stigma exists around the world in a variety of ways, including ostracism, rejection, discrimination and avoidance of HIV infected people; compulsory HIV testing without prior consent or protection of confidentiality; violence against HIV infected individuals or people who are perceived to be infected with HIV; and the quarantine of HIV infected individuals.[138] Stigma-related violence or the fear of violence prevents many people from seeking HIV testing, returning for their results, or securing treatment, possibly turning what could be a manageable chronic illness into a death sentence and perpetuating the spread of HIV.[139]
AIDS stigma has been further divided into the following three categories:
Instrumental AIDS stigma—a reflection of the fear and apprehension that are likely to be associated with any deadly and transmissible illness.[140]
Symbolic AIDS stigma—the use of HIV/AIDS to express attitudes toward the social groups or lifestyles perceived to be associated with the disease.[140]
Courtesy AIDS stigma—stigmatization of people connected to the issue of HIV/AIDS or HIV- positive people.[141]
Often, AIDS stigma is expressed in conjunction with one or more other stigmas, particularly those associated with homosexuality, bisexuality, promiscuity, and intravenous drug use.
In many developed countries, there is an association between AIDS and homosexuality or bisexuality, and this association is correlated with higher levels of sexual prejudice such as anti-homosexual attitudes.[142] There is also a perceived association between AIDS and all male-male sexual behavior, including sex between uninfected men.[140]
Economic impact
Main article: Economic impact of AIDS
Changes in life expectancy in some hard-hit African countries.
Botswana
Zimbabwe
Kenya
South Africa
UgandaHIV and AIDS affects economic growth by reducing the availability of human capital.[6] Without proper nutrition, health care and medicine that is available in developed countries, large numbers of people are falling victim to AIDS. They will not only be unable to work, but will also require significant medical care. The forecast is that this will likely cause a collapse of economies and societies in countries with a significant AIDS population. In some heavily infected areas, the epidemic has left behind many orphans cared for by elderly grandparents.[143]
The increased mortality in this region will result in a smaller skilled population and labor force. This smaller labor force will be predominantly young people, with reduced knowledge and work experience leading to reduced productivity. An increase in workers’ time off to look after sick family members or for sick leave will also lower productivity. Increased mortality will also weaken the mechanisms that generate human capital and investment in people, through loss of income and the death of parents. By killing off mainly young adults, AIDS seriously weakens the taxable population, reducing the resources available for public expenditures such as education and health services not related to AIDS resulting in increasing pressure for the state's finances and slower growth of the economy. This results in a slower growth of the tax base, an effect that will be reinforced if there are growing expenditures on treating the sick, training (to replace sick workers), sick pay and caring for AIDS orphans. This is especially true if the sharp increase in adult mortality shifts the responsibility and blame from the family to the government in caring for these orphans.[143]
On the level of the household, AIDS results in both the loss of income and increased spending on healthcare by the household. The income effects of this lead to spending reduction as well as a substitution effect away from education and towards healthcare and funeral spending. A study in Côte d'Ivoire showed that households with an HIV/AIDS patient spent twice as much on medical expenses as other households.[144]
AIDS denialism
Main article: AIDS denialism
A small group of activists, including several scientists who do not study HIV/AIDS, question the connection between HIV and AIDS,[145] the existence of HIV itself,[146] or the validity of current testing and treatment methods. Though these claims have been examined and thoroughly rejected by the scientific community,[147] they continue to be promulgated through the Internet[148] and have had a significant political impact, particularly in South Africa, where former President Thabo Mbeki's embrace of AIDS denialism has been blamed for an ineffective response to that country's AIDS epidemic.[
Tuberculosis
Tuberculosis (abbreviated as TB for tubercle bacillus or Tuberculosis) is a common and often deadly infectious disease caused by mycobacteria, mainly Mycobacterium tuberculosis [1]. Tuberculosis usually attacks the lungs (as pulmonary TB) but can also affect the central nervous system, the lymphatic system, the circulatory system, the genitourinary system, the gastrointestinal system, bones, joints, and even the skin. Other mycobacteria such as Mycobacterium bovis, Mycobacterium africanum, Mycobacterium canetti, and Mycobacterium microti also cause tuberculosis, but these species are less common.
The typical symptoms of tuberculosis are a chronic cough with blood-tinged sputum, fever, night sweats, and weight loss. Infection of other organs causes a wide range of symptoms. The diagnosis relies on radiology (commonly chest X-rays), a tuberculin skin test, blood tests, as well as microscopic examination and microbiological culture of bodily fluids. Tuberculosis treatment is difficult and requires long courses of multiple antibiotics. Contacts are also screened and treated if necessary. Antibiotic resistance is a growing problem in (extensively) multi-drug-resistant tuberculosis. Prevention relies on screening programs and vaccination, usually with Bacillus Calmette-Guérin (BCG vaccine).
Tuberculosis is spread through the air, when people who have the disease cough, sneeze, or spit. One third of the world's current population have been infected with M. tuberculosis, and new infections occur at a rate of one per second.[2] However, most of these cases will not develop the full-blown disease; asymptomatic, latent infection is most common. About one in ten of these latent infections will eventually progress to active disease, which, if left untreated, kills more than half of its victims. In 2004, mortality and morbidity statistics included 14.6 million chronic active cases, 8.9 million new cases, and 1.6 million deaths, mostly in developing countries.[2] In addition, a rising number of people in the developed world are contracting tuberculosis because their immune systems are compromised by immunosuppressive drugs, substance abuse, or AIDS. The distribution of tuberculosis is not uniform across the globe with about 80% of the population in many Asian and African countries testing positive in tuberculin tests, while only 5-10% of the US population testing positive.[1] It is estimated that the US has 25,000 new cases of tuberculosis each year, 40% of which occur in immigrants from countries where tuberculosis is endemic.[1]
Contents
1 Other names
2 Symptoms
3 Bacterial species
3.1 Evolution
4 Transmission
5 Pathogenesis
6 Diagnosis
7 Progression
8 Treatment
9 Prevention
9.1 Vaccines
10 Epidemiology
11 History
11.1 Folklore
11.2 Study and treatment
12 Infection of other animals
13 See also
14 References
14.1 Notes
14.2 Further reading
15 External links
[ Other names
In the past, tuberculosis has been called consumption, because it seemed to consume people from within, with a bloody cough, fever, pallor, and long relentless wasting. Other names included phthisis (Greek for consumption) and phthisis pulmonalis; scrofula (in adults), affecting the lymphatic system and resulting in swollen neck glands; tabes mesenterica, TB of the abdomen and lupus vulgaris, TB of the skin; wasting disease; white plague, because sufferers appear markedly pale; king's evil, because it was believed that a king's touch would heal scrofula; and Pott's disease, or gibbus of the spine and joints.[3][4] Miliary tuberculosis—now commonly known as disseminated TB—occurs when the infection invades the circulatory system resulting in lesions which have the appearance of millet seeds on X-ray.[3][5] TB is also called Koch's disease after the scientist Robert Koch.[6]
Symptoms
Further information: Tuberculosis classification
When the disease becomes active, 75% of the cases are pulmonary TB. Symptoms include chest pain, coughing up blood, and a productive, prolonged cough for more than three weeks. Systemic symptoms include fever, chills, night sweats, appetite loss, weight loss, pallor, and often a tendency to fatigue very easily.[2]
In the other 25% of active cases, the infection moves from the lungs, causing other kinds of TB, collectively denoted extrapulmonary tuberculosis[7]. This occurs more commonly in immunosuppressed persons and young children. Extrapulmonary infection sites include the pleura in tuberculosis pleurisy, the central nervous system in meningitis, the lymphatic system in scrofula of the neck, the genitourinary system in urogenital tuberculosis, and bones and joints in Pott's disease of the spine. An especially serious form is disseminated TB, more commonly known as miliary tuberculosis. Although extrapulmonary TB is not contagious, it may co-exist with pulmonary TB, which is contagious.[8]
Bacterial species
Main article: Mycobacterium tuberculosis
Scanning electron micrograph of Mycobacterium tuberculosisThe primary cause of TB, Mycobacterium tuberculosis, is an aerobic bacterium that divides every 16 to 20 hours, an extremely slow rate compared with other bacteria, which usually divide in less than an hour.[9] (For example, one of the fastest-growing bacteria is a strain of E. coli that can divide roughly every 20 minutes.) Since MTB has a cell wall but lacks a phospholipid outer membrane, it is classified as a Gram-positive bacterium. However, if a Gram stain is performed, MTB either stains very weakly Gram-positive or does not retain dye due to the high lipid & mycolic acid content of its cell wall.[10] MTB is a small rod-like bacillus that can withstand weak disinfectants and survive in a dry state for weeks. In nature, the bacterium can grow only within the cells of a host organism, but M. tuberculosis can be cultured in vitro.[11]
Using histological stains on expectorate samples from phlegm (also called sputum), scientists can identify MTB under a regular microscope. Since MTB retains certain stains after being treated with acidic solution, it is classified as an acid-fast bacillus (AFB).[1][10] The most common acid-fast staining technique, the Ziehl-Neelsen stain, dyes AFBs a bright red that stands out clearly against a blue background. Other ways to visualize AFBs include an auramine-rhodamine stain and fluorescent microscopy.
The M. tuberculosis complex includes three other TB-causing mycobacteria: M. bovis, M. africanum and M. microti. M. africanum is not widespread, but in parts of Africa it is a significant cause of tuberculosis.[12][13] M. bovis was once a common cause of tuberculosis, but the introduction of pasteurized milk has largely eliminated this as a public health problem in developed countries.[1][14] M. microti is mostly seen in immunodeficient people, although it is possible that the prevalence of this pathogen has been underestimated.[15]
Other known pathogenic mycobacteria include Mycobacterium leprae, Mycobacterium avium and M. kansasii. The last two are part of the nontuberculous mycobacteria (NTM) group. Nontuberculous mycobacteria cause neither TB nor leprosy, but they do cause pulmonary diseases resembling TB.[16]
Phylogenetic tree of the genus Mycobacterium.
[edit] Evolution
Tuberculosis has co-evolved with humans for many thousands of years, and perhaps as much as several million years,[17] but the oldest human remains are 9,000 years old.[18] During this evolution, M. tuberculosis has lost numerous coding and non-coding regions in its genome, losses that can be used to distinguish between strains of the bacteria. The implication is that M. tuberculosis strains differ geographically, so their genetic differences can be used to track the origins and movement of each strain.[19]
Transmission
Further information: Transmission (medicine)
When people suffering from active pulmonary TB cough, sneeze, speak, or spit, they expel infectious aerosol droplets 0.5 to 5 µm in diameter. A single sneeze can release up to 40,000 droplets.[20] Each one of these droplets may transmit the disease, since the infectious dose of tuberculosis is very low and the inhalation of just a single bacterium can cause a new infection.[21]
People with prolonged, frequent, or intense contact are at particularly high risk of becoming infected, with an estimated 22% infection rate. A person with active but untreated tuberculosis can infect 10–15 other people per year.[2] Others at risk include people in areas where TB is common, people who inject drugs using unsanitary needles, residents and employees of high-risk congregate settings, medically under-served and low-income populations, high-risk racial or ethnic minority populations, children exposed to adults in high-risk categories, patients immunocompromised by conditions such as HIV/AIDS, people who take immunosuppressant drugs, and health care workers serving these high-risk clients.[22]
Transmission can only occur from people with active — not latent — TB [1]. The probability of transmission from one person to another depends upon the number of infectious droplets expelled by a carrier, the effectiveness of ventilation, the duration of exposure, and the virulence of the M. tuberculosis strain.[8] The chain of transmission can, therefore, be broken by isolating patients with active disease and starting effective anti-tuberculous therapy. After two weeks of such treatment, people with non-resistant active TB generally cease to be contagious. If someone does become infected, then it will take at least 21 days, or three to four weeks, before the newly infected person can transmit the disease to others.[23] TB can also be transmitted by eating meat infected with TB. Mycobacterium bovis causes TB in cattle. (See details below.)
Pathogenesis
Mycobacterium tuberculosis (stained red) in sputumAbout 90% of those infected with Mycobacterium tuberculosis have asymptomatic, latent TB infection (sometimes called LTBI), with only a 10% lifetime chance that a latent infection will progress to TB disease.[1] However, if untreated, the death rate for these active TB cases is more than 50%.[24]
TB infection begins when the mycobacteria reach the pulmonary alveoli, where they invade and replicate within the endosomes of alveolar macrophages.[1][25] The primary site of infection in the lungs is called the Ghon focus, and is generally located in either the upper part of the lower lobe, or the lower part of the upper lobe[1]. Bacteria are picked up by dendritic cells, which do not allow replication, although these cells can transport the bacilli to local (mediastinal) lymph nodes. Further spread is through the bloodstream to other tissues and organs where secondary TB lesions can develop in other parts of the lung (particularly the apex of the upper lobes), peripheral lymph nodes, kidneys, brain, and bone.[1][26] All parts of the body can be affected by the disease, though it rarely affects the heart, skeletal muscles, pancreas and thyroid.[27]
Tuberculosis is classified as one of the granulomatous inflammatory conditions. Macrophages, T lymphocytes, B lymphocytes and fibroblasts are among the cells that aggregate to form a granuloma, with lymphocytes surrounding the infected macrophages. The granuloma functions not only to prevent dissemination of the mycobacteria, but also provides a local environment for communication of cells of the immune system. Within the granuloma, T lymphocytes (CD4+) secrete cytokines such as interferon gamma, which activates macrophages to destroy the bacteria with which they are infected.[28] T lymphocytes (CD8+) can also directly kill infected cells.[25]
Importantly, bacteria are not always eliminated within the granuloma, but can become dormant, resulting in a latent infection.[1] Another feature of the granulomas of human tuberculosis is the development of cell death, also called necrosis, in the center of tubercles. To the naked eye this has the texture of soft white cheese and was termed caseous necrosis.[29]
If TB bacteria gain entry to the bloodstream from an area of damaged tissue they spread through the body and set up many foci of infection, all appearing as tiny white tubercles in the tissues. This severe form of TB disease is most common in infants and the elderly and is called miliary tuberculosis. Patients with this disseminated TB have a fatality rate of approximately 20%, even with intensive treatment.[30]
In many patients the infection waxes and wanes. Tissue destruction and necrosis are balanced by healing and fibrosis.[29] Affected tissue is replaced by scarring and cavities filled with cheese-like white necrotic material. During active disease, some of these cavities are joined to the air passages bronchi and this material can be coughed up. It contains living bacteria and can therefore pass on infection. Treatment with appropriate antibiotics kills bacteria and allows healing to take place. Upon cure, affected areas are eventually replaced by scar tissue.[29]
Diagnosis
For more details on this topic, see Tuberculosis diagnosis.
Mantoux tuberculin skin testTuberculosis is diagnosed definitively by identifying the causative organism (Mycobacterium tuberculosis) in a clinical sample (for example, sputum or pus). When this is not possible, a probable diagnosis may be made using imaging (X-rays or scans) and/or a tuberculin skin test.
The main problem with tuberculosis diagnosis is the difficulty in culturing this slow-growing organism in the laboratory (it may take 4 to 12 weeks for blood or sputum culture). A complete medical evaluation for TB must include a medical history, a physical examination, a chest X-ray, microbiological smears and cultures. It may also include a tuberculin skin test, a serological test. The interpretation of the tuberculin skin test depends upon the person's risk factors for infection and progression to TB disease, such as exposure to other cases of TB or immunosuppression.[8]
Currently, latent infection is diagnosed in a non-immunized person by a tuberculin skin test, which yields a delayed hypersensitivity type response to an extract made from M. tuberculosis.[1] Those immunized for TB or with past-cleared infection will respond with delayed hypersensitivity parallel to those currently in a state of infection, so the test must be used with caution, particularly with regard to persons from countries where TB immunization is common.[31] Tuberculin tests have the disadvantage in that they may produce false negatives, especially when the patient is co-morbid with sarcoidosis, Hodgkins lymphoma, malnutrition, or most notably active tuberculosis disease.[1] New TB tests are being developed that offer the hope of cheap, fast and more accurate TB testing. These use polymerase chain reaction detection of bacterial DNA and antibody assays to detect the release of interferon gamma in response to mycobacteria.[32] These tests are not affected by immunization, so generate fewer false positive results.[33] The development of a rapid and inexpensive diagnosis would be particularly valuable in the developing world.
Progression
Progression from TB infection to TB disease occurs when the TB bacilli overcome the immune system defenses and begin to multiply. In primary TB disease—1–5% of cases—this occurs soon after infection.[1] However, in the majority of cases, a latent infection occurs that has no obvious symptoms[1]. These dormant bacilli can produce tuberculosis in 2–23% of these latent cases, often many years after infection.[34] The risk of reactivation increases with immunosuppression, such as that caused by infection with HIV. In patients co-infected with M. tuberculosis and HIV, the risk of reactivation increases to 10% per year.[1][24]
Patients with diabetes mellitus are at increased risk of contracting tuberculosis,[35] and they have a poorer response to treatment, possibly due to poorer drug absorption[36]
Other conditions that increase risk include IV drug abuse; recent TB infection or a history of inadequately treated TB; chest X-ray suggestive of previous TB, showing fibrotic lesions and nodules; silicosis; prolonged corticosteroid therapy and other immunosuppressive therapy; head and neck cancers; hematologic and reticuloendothelial diseases, such as leukemia and Hodgkin's disease; end-stage kidney disease; intestinal bypass or gastrectomy; chronic malabsorption syndromes; vitamin D deficiency;[37] and low body weight.[1][8]
Twin studies in the 1940s showed that susceptibility to TB was heritable. If one of a pair of twins got TB, then and the other was more likely to get TB if he was identical than if he was not.[38] Since then, specific gene polymorphisms in IL12B have been linked to tuberculosis susceptibility.[39]
Some drugs, including rheumatoid arthritis drugs that work by blocking tumor necrosis factor-alpha (an inflammation-causing cytokine), raise the risk of activating a latent infection due to the importance of this cytokine in the immune defense against TB.[40]
Treatment
For more details on this topic, see Tuberculosis treatment.
Treatment for TB uses antibiotics to kill the bacteria. The two antibiotics most commonly used are rifampicin and isoniazid. However, instead of the short course of antibiotics typically used to cure other bacterial infections, TB requires much longer periods of treatment (around 6 to 12 months) to entirely eliminate mycobacteria from the body.[8] Latent TB treatment usually uses a single antibiotic, while active TB disease is best treated with combinations of several antibiotics, to reduce the risk of the bacteria developing antibiotic resistance.[41] People with latent infections are treated to prevent them from progressing to active TB disease later in life. However, treatment using Rifampin and Pyrazinamide is not risk-free. The Centers for Disease Control and Prevention (CDC) notified healthcare professionals of revised recommendations against the use of rifampin plus pyrazinamide for treatment of latent tuberculosis infection, due to high rates of hospitalization and death from liver injury associated with the combined use of these drugs.[
Drug resistant tuberculosis is transmitted in the same way as regular TB. Primary resistance occurs in persons who are infected with a resistant strain of TB. A patient with fully-susceptible TB develops secondary resistance (acquired resistance) during TB therapy because of inadequate treatment, not taking the prescribed regimen appropriately, or using low quality medication.[41] Drug-resistant TB is a public health issue in many developing countries, as treatment is longer and requires more expensive drugs. Multi-drug resistant TB (MDR-TB) is defined as resistance to the two most effective first line TB drugs: rifampicin and isoniazid. Extensively drug-resistant TB (XDR-TB) is also resistant to three or more of the six classes of second-line drugs.[43]
Prevention
TB prevention and control takes two parallel approaches. In the first, people with TB and their contacts are identified and then treated. Identification of infections often involves testing high-risk groups for TB. In the second approach, children are vaccinated to protect them from TB. Unfortunately, no vaccine is available that provides reliable protection for adults. However, in tropical areas where the levels of other species of mycobacteria are high, exposure to nontuberculous mycobacteria gives some protection against TB.[44]
The World Health Organization (W.H.O.) declared TB a global health emergency in 1993, and the Stop TB Partnership developed a Global Plan to Stop Tuberculosis that aims to save 14 million lives between 2006 and 2015.[45] Since humans are the only host of Mycobacterium tuberculosis, eradication would be possible: a goal that would be helped greatly by an effective vaccine.[46]
Vaccines
Many countries use Bacillus Calmette-Guérin (BCG) vaccine as part of their TB control programs, especially for infants. According to the W.H.O., this is the most often used vaccine worldwide, with 85% of infants in 172 countries immunized in 1993.[47] This was the first vaccine for TB and developed at the Pasteur Institute in France between 1905 and 1921.[48] However, mass vaccination with BCG did not start until after World War II.[49] The protective efficacy of BCG for preventing serious forms of TB (e.g. meningitis) in children is greater than 80%; its protective efficacy for preventing pulmonary TB in adolescents and adults is variable, ranging from 0 to 80%.[50]
In South Africa, the country with the highest prevalence of TB, BCG is given to all children under age three.[51] However, BCG is less effective in areas where mycobacteria are less prevalent; therefore BCG is not given to the entire population in these countries. In the USA, for example, BCG vaccine is not recommended except for people who meet specific criteria:[8]
Infants or children with negative skin test results who are continually exposed to untreated or ineffectively treated patients or will be continually exposed to multidrug-resistant TB.
Healthcare workers considered on an individual basis in settings in which a high percentage of MDR-TB patients has been found, transmission of MDR-TB is likely, and TB control precautions have been implemented and were not successful.
BCG provides some protection against severe forms of pediatric TB, but has been shown to be unreliable against adult pulmonary TB, which accounts for most of the disease burden worldwide. Currently, there are more cases of TB on the planet than at any other time in history and most agree there is an urgent need for a newer, more effective vaccine that would prevent all forms of TB—including drug resistant strains—in all age groups and among people with HIV.[52]
Several new vaccines to prevent TB infection are being developed. The first recombinant tuberculosis vaccine entered clinical trials in the United States in 2004, sponsored by the National Institute of Allergy and Infectious Diseases (NIAID).[53] A 2005 study showed that a DNA TB vaccine given with conventional chemotherapy can accelerate the disappearance of bacteria as well as protect against re-infection in mice; it may take four to five years to be available in humans.[54] A very promising TB vaccine, MVA85A, is currently in phase II trials in South Africa by a group led by Oxford University,[55] and is based on a genetically modified vaccinia virus. Many other strategies are also being used to develop novel vaccines. In order to encourage further discovery, researchers and policymakers are promoting new economic models of vaccine development including prizes, tax incentives and advance market commitments.[56][57]
The Bill and Melinda Gates Foundation has been a strong supporter of new TB vaccine development. Most recently, they announced a $200 million grant to the Aeras Global TB Vaccine Foundation for clinical trials on up to six different TB vaccine candidates currently in the pipeline.[58]
Epidemiology
Annual number of new reported TB cases. Data from WHO.[59]
World TB incidence. Cases per 100,000; Red => 300, orange = 200–300, yellow = 100–200, green = 50–100, blue =< grey =" n/a.">
Skin care: Top 5 habits for healthy skin
Proactive skin care, from skin protection to proper shaving technique, will help you keep your skin youthful and healthy.
Your busy lifestyle leaves little time for pampering skin care. The result: Your skin isn't the baby-soft body glove you were born with. As you age, your skin gradually becomes thinner and finely wrinkled. Oil-producing (sebaceous) glands grow less active, leaving your skin drier. The number of blood vessels in your skin decreases, your skin becomes more fragile, and you lose your youthful color and glow.
Good skin care — such as avoiding the sun, washing your skin gently and applying moisturizer regularly — can help delay the natural aging process and prevent many skin problems. These simple skin-care habits will help you protect your skin to keep it healthy and glowing for years to come.
1. Protect yourself from the sun
The most important way to take care of your skin is to protect it from the sun. Ultraviolet light — the invisible but intense rays from the sun — damages your skin, causing deep wrinkles, dry, rough skin, liver spots, and more serious disorders, such as noncancerous (benign) and cancerous (malignant) skin tumors. In fact, most of the changes seen in aging skin are actually caused by a lifetime of sun exposure.
For the most complete sun protection, use all three of these methods:
Avoid the sun during high-intensity hours. The sun's rays are most damaging from 10 a.m. to 4 p.m. Reduce the time you spend outdoors during these hours.
Wear protective clothing. Cover your skin with clothing, such as long-sleeved shirts, long pants and wide-brimmed hats. Also, keep in mind that certain clothing styles and fabrics offer better protection from the sun than do others. For example, long-sleeved shirts offer better protection than short-sleeved shirts do. And tightly woven fabrics such as denim are better than are loosely woven fabrics such as knits. Several companies now make sun protective clothing (SPF clothing), which is specifically designed to block out ultraviolet rays while keeping you cool and comfortable.
Use sunscreen. Choose a broad-spectrum sunscreen with a sun protection factor (SPF) greater than 15. Apply liberally 20 minutes before going outdoors and reapply every two hours, after heavy sweating or after being in water.
MORE ON THIS TOPIC
Sunscreen: Answers to your burning questions
Sunburn
Age spots (liver spots)
2. Don't smoke
Smoking accelerates aging of your skin and increases wrinkles. Skin changes from smoking can appear in young adults after 10 years of smoking.
Smoking causes narrowing of the tiny blood vessels in the outermost layers of skin. This decreases blood flow, depleting the skin of oxygen and nutrients, such as vitamin A, that are important to skin health. All of these factors increase damage to the elastic fibers (elastin) and collagen, which give your skin strength and elasticity.
In addition, the repetitive facial expressions you make when smoking — such as pursing your lips when inhaling and squinting your eyes to keep out smoke — may contribute to wrinkles. It's also possible that repeated exposure to the heat from burning cigarettes may damage your facial skin over time.
3. Wash your skin gently
Cleansing is an essential part of caring for your skin. The key is to treat your skin gently.
Use warm water and limit bath time. Hot water and long showers or baths remove oils from your skin. Limit your bath or shower time to about 15 minutes or less, and use warm, rather than hot, water.
Avoid strong soaps. Strong soaps — those most capable of stripping oil from your skin — can leave your skin dry. Instead, choose mild soaps or detergent substitutes with added oils and fats. Good choices include Dove, Vanicream, Cetaphil and Purpose.
Avoid irritating additives. If your skin is sensitive, avoid products containing perfumes or dyes. These can irritate your skin and may trigger an allergic response.
Remove eye makeup carefully. Use a soft sponge, cotton cloth or cotton balls when removing eye makeup to avoid damaging the delicate tissue around your eyes. If you wear heavy, waterproof makeup, you may need to use an oil-based product, such as Eucerin, Aquaphor or petroleum jelly, to remove makeup.
Pat dry. After washing or bathing, gently pat or blot your skin dry with a towel so that some moisture remains on the skin. Immediately moisturize your skin with an oil or cream.
4. Moisturize regularly
Moisturizers help maintain your skin's natural moisture levels. They work by providing a seal over your skin — to keep water from escaping — or by slowly releasing water into your skin.
The moisturizer that's best for you and the frequency with which you need to moisturize depend on many factors, including your skin type, your age and whether you have specific conditions such as acne. A good way to test if you need a moisturizer is to wait 20 minutes after bathing. If your skin feels tight, you should apply a moisturizer.
Select a moisturizer with an SPF of at least 15 to help protect your skin from damaging ultraviolet rays. If you have sensitive skin, look for products free of heavy dyes, perfumes or other additives. If your skin is very dry, you may want to apply an oil, such as baby oil, while your skin is still moist. Oil has more staying power than moisturizers do and prevents the evaporation of water from the surface of your skin. If your skin is oily, you may want to skip moisturizing.
MORE ON THIS TOPIC
Moisturizers 101: The basics of softer skin
Dry skin
5. Shave carefully
Shaving is a common and inexpensive way to remove unwanted hair. But shaving can cause skin irritations, especially if your skin is thin, dry or very sensitive. For a smooth shave:
Press a warm wash cloth on your skin before shaving to soften the hair. Or shave after a warm bath or shower.
Don't shave dry skin, which can cause razor burn. Apply shaving cream, lotion or gel before shaving to protect and lubricate your skin.
Use a clean, sharp razor. If using an electric razor, don't use the closest setting, which can aggravate the skin.
Shave in the direction of hair growth, not against it.
Rinse your skin afterward with warm water.
If irritation does occur, apply a lotion that doesn't contain ethyl or isopropyl alcohol. Though alcohol and alcohol-based products may feel cooling, they don't really soothe irritated skin because the alcohol evaporates rapidly from the skin.
Your busy lifestyle leaves little time for pampering skin care. The result: Your skin isn't the baby-soft body glove you were born with. As you age, your skin gradually becomes thinner and finely wrinkled. Oil-producing (sebaceous) glands grow less active, leaving your skin drier. The number of blood vessels in your skin decreases, your skin becomes more fragile, and you lose your youthful color and glow.
Good skin care — such as avoiding the sun, washing your skin gently and applying moisturizer regularly — can help delay the natural aging process and prevent many skin problems. These simple skin-care habits will help you protect your skin to keep it healthy and glowing for years to come.
1. Protect yourself from the sun
The most important way to take care of your skin is to protect it from the sun. Ultraviolet light — the invisible but intense rays from the sun — damages your skin, causing deep wrinkles, dry, rough skin, liver spots, and more serious disorders, such as noncancerous (benign) and cancerous (malignant) skin tumors. In fact, most of the changes seen in aging skin are actually caused by a lifetime of sun exposure.
For the most complete sun protection, use all three of these methods:
Avoid the sun during high-intensity hours. The sun's rays are most damaging from 10 a.m. to 4 p.m. Reduce the time you spend outdoors during these hours.
Wear protective clothing. Cover your skin with clothing, such as long-sleeved shirts, long pants and wide-brimmed hats. Also, keep in mind that certain clothing styles and fabrics offer better protection from the sun than do others. For example, long-sleeved shirts offer better protection than short-sleeved shirts do. And tightly woven fabrics such as denim are better than are loosely woven fabrics such as knits. Several companies now make sun protective clothing (SPF clothing), which is specifically designed to block out ultraviolet rays while keeping you cool and comfortable.
Use sunscreen. Choose a broad-spectrum sunscreen with a sun protection factor (SPF) greater than 15. Apply liberally 20 minutes before going outdoors and reapply every two hours, after heavy sweating or after being in water.
Sunscreen: Answers to your burning questions
Sunburn
Age spots (liver spots)
2. Don't smoke
Smoking accelerates aging of your skin and increases wrinkles. Skin changes from smoking can appear in young adults after 10 years of smoking.
Smoking causes narrowing of the tiny blood vessels in the outermost layers of skin. This decreases blood flow, depleting the skin of oxygen and nutrients, such as vitamin A, that are important to skin health. All of these factors increase damage to the elastic fibers (elastin) and collagen, which give your skin strength and elasticity.
In addition, the repetitive facial expressions you make when smoking — such as pursing your lips when inhaling and squinting your eyes to keep out smoke — may contribute to wrinkles. It's also possible that repeated exposure to the heat from burning cigarettes may damage your facial skin over time.
3. Wash your skin gently
Cleansing is an essential part of caring for your skin. The key is to treat your skin gently.
Use warm water and limit bath time. Hot water and long showers or baths remove oils from your skin. Limit your bath or shower time to about 15 minutes or less, and use warm, rather than hot, water.
Avoid strong soaps. Strong soaps — those most capable of stripping oil from your skin — can leave your skin dry. Instead, choose mild soaps or detergent substitutes with added oils and fats. Good choices include Dove, Vanicream, Cetaphil and Purpose.
Avoid irritating additives. If your skin is sensitive, avoid products containing perfumes or dyes. These can irritate your skin and may trigger an allergic response.
Remove eye makeup carefully. Use a soft sponge, cotton cloth or cotton balls when removing eye makeup to avoid damaging the delicate tissue around your eyes. If you wear heavy, waterproof makeup, you may need to use an oil-based product, such as Eucerin, Aquaphor or petroleum jelly, to remove makeup.
Pat dry. After washing or bathing, gently pat or blot your skin dry with a towel so that some moisture remains on the skin. Immediately moisturize your skin with an oil or cream.
4. Moisturize regularly
Moisturizers help maintain your skin's natural moisture levels. They work by providing a seal over your skin — to keep water from escaping — or by slowly releasing water into your skin.
The moisturizer that's best for you and the frequency with which you need to moisturize depend on many factors, including your skin type, your age and whether you have specific conditions such as acne. A good way to test if you need a moisturizer is to wait 20 minutes after bathing. If your skin feels tight, you should apply a moisturizer.
Select a moisturizer with an SPF of at least 15 to help protect your skin from damaging ultraviolet rays. If you have sensitive skin, look for products free of heavy dyes, perfumes or other additives. If your skin is very dry, you may want to apply an oil, such as baby oil, while your skin is still moist. Oil has more staying power than moisturizers do and prevents the evaporation of water from the surface of your skin. If your skin is oily, you may want to skip moisturizing.
Moisturizers 101: The basics of softer skin
Dry skin
5. Shave carefully
Shaving is a common and inexpensive way to remove unwanted hair. But shaving can cause skin irritations, especially if your skin is thin, dry or very sensitive. For a smooth shave:
Press a warm wash cloth on your skin before shaving to soften the hair. Or shave after a warm bath or shower.
Don't shave dry skin, which can cause razor burn. Apply shaving cream, lotion or gel before shaving to protect and lubricate your skin.
Use a clean, sharp razor. If using an electric razor, don't use the closest setting, which can aggravate the skin.
Shave in the direction of hair growth, not against it.
Rinse your skin afterward with warm water.
If irritation does occur, apply a lotion that doesn't contain ethyl or isopropyl alcohol. Though alcohol and alcohol-based products may feel cooling, they don't really soothe irritated skin because the alcohol evaporates rapidly from the skin.
Dandruff
If dandruff is the only thing standing between you and a closet full of basic black, you're not alone. Many people have this chronic scalp disorder, which is marked by itching and excessive flaking of the scalp. Although dandruff isn't contagious and is rarely serious, it can be embarrassing and surprisingly persistent.
The good news is that dandruff can usually be controlled. Mild cases of dandruff may need nothing more than daily shampooing with a gentle cleanser. And stubborn flakes often respond to medicated shampoos. What's more, researchers have identified a yeast-like fungus that may cause or aggravate dandruff, a discovery that may lead to better treatments.
Symptoms
For most people, the signs and symptoms of dandruff are unmistakable: white, oily looking flakes of dead skin that dot your hair and shoulders and an itchy, scaling scalp. But it's not quite that simple — many conditions cause excessive skin scaling, including:
Dry skin. Simple dry skin — the kind you get in winter when the air is cold and rooms are overheated — is by far the most common cause of itchy, flaking skin. But flakes from dry skin are generally smaller and less oily than those caused by dandruff.
Seborrheic dermatitis. This condition, a frequent cause of dandruff, is marked by red, greasy skin covered with flaky white or yellow scales. Seborrheic dermatitis affects not only your scalp but also other areas rich in oil glands, such as your eyebrows, the sides of your nose and the backs of your ears, your breastbone, your groin area, and sometimes your armpits.
Psoriasis. This skin disorder causes an accumulation of dead skin cells that form thick silvery scales. Psoriasis commonly occurs on your knees, elbows and trunk, but it can also affect your scalp.
Cradle cap (seborrheic dermatitis of the scalp). This disorder, which causes a scaling, crusty scalp, is most common in newborns, but it can occur anytime during infancy. Although it can be alarming for parents, cradle cap isn't dangerous and usually clears up on its own by the time a baby is a year old.
Contact dermatitis. Sometimes sensitivities to certain hair-care products or hair dyes can cause a red, itchy, scaling scalp.
Causes
At one time or another, dandruff causes have been attributed to dry skin, oily skin, shampooing too often or not often enough, a poor diet, stress, and the use of too many fancy styling products. Although some of these factors may exacerbate or contribute to scalp flaking, the real culprit may be a fat-eating, yeast-like fungus called malassezia, formerly known as pityrosporum.
Malassezia lives on the scalps of most healthy adults without causing problems. But sometimes it grows out of control, feeding on the oils secreted by your hair follicles and causing irritation that leads to increased cell turnover. The result is a large number of dead skin cells. As the cells fall off, they tend to clump together with oil from your hair and scalp, making them appear white, flaky and all too visible.
Exactly what causes an overgrowth of these organisms isn't known, although increased oil production; hormonal fluctuations; stress; illness; neurological disorders, such as Parkinson's disease; a suppressed immune system; infrequent shampooing and extra sensitivity to the malassezia fungus may contribute to the development of dandruff.
Risk factors
Almost any adult is a candidate for dandruff, but certain factors can make you more susceptible:
Age. Dandruff usually begins in young adulthood and continues through middle age. That doesn't mean older adults don't get dandruff, however. For some people, the problem can be lifelong.
Sex. Because more men than women have dandruff, some researchers think male hormones may play a role in dandruff. Men also have larger sebaceous glands that produce an oil called sebum.
Oily hair and scalp. Malassezia feeds on oils in your scalp. For that reason, having excessively oily skin and hair makes you more prone to dandruff.
Certain illnesses. For reasons that aren't clear, adults with neurological diseases, such as Parkinson's disease, are more likely to develop seborrheic dermatitis and dandruff. So are people recovering from stressful conditions, particularly heart attack and stroke, and those with compromised immune systems.
Treatments and drugs
Dandruff is a chronic condition that can almost always be controlled, but dandruff treatment may take a little patience and persistence. In general, mild scaling can often be helped by daily cleansing with a gentle shampoo to reduce oiliness and cell buildup.
When regular shampoos fail, OTC dandruff shampoos may succeed. But dandruff shampoos aren't all alike, and you may need to experiment until you find one that works best for you. Dandruff shampoos are classified according to their active ingredient:
Zinc pyrithione shampoos (Selsun Salon, Head & Shoulders). These contain the antibacterial and antifungal agent zinc pyrithione, which has been shown to reduce the fungus that causes dandruff and seborrheic dermatitis.
Tar-based shampoos (Neutrogena T/Gel). Coal tar, a byproduct of the coal manufacturing process, helps conditions such as dandruff, seborrheic dermatitis and psoriasis by slowing cell turnover.
Shampoos containing salicylic acid (Ionil T). These "scalp scrubs" help eliminate scale, but they may leave your scalp dry, leading to more flaking. Using a conditioner after shampooing can help counter dryness.
Selenium sulfide shampoos (Selsun Blue). These shampoos help prevent cell turnover and may also reduce the number of malassezia. Because they can discolor blonde, gray or chemically colored hair, be sure to use them only as directed and to rinse well after shampooing.
Ketoconazole shampoos (Nizoral). The newest addition to the dandruff armamentarium, ketoconazole is a broad-spectrum antifungal agent that may work when other shampoos fail. It's available over-the-counter as well as by prescription.
Try using one of these shampoos daily until your dandruff is controlled, then cut back to two or three times a week. If one type of shampoo works for a time and then seems to lose its effectiveness, try alternating between two types of dandruff shampoos. Be sure to leave the shampoo on for at least five minutes — this allows the ingredients time to work.
If you've shampooed faithfully for several weeks and there's still a dusting of dandruff on your shoulders, talk to your doctor or dermatologist. You may need a prescription-strength shampoo or more aggressive treatment with a steroid lotion.
Lifestyle and home remedies
You can't prevent dandruff, but you can take steps to reduce your risk:
Learn to manage stress. Stress affects your overall health, making you susceptible to a number of conditions and diseases. It can even help trigger dandruff or exacerbate existing symptoms.
Shampoo often. If you tend to have an oily scalp, daily shampooing to remove the excess oil may help prevent dandruff.
Cut back on styling products. Hair sprays, styling gels, mousses and hair waxes can all build up on your hair and scalp, making them oilier.
Eat a healthy diet. A diet that provides enough zinc, B vitamins and essential fatty acid may help prevent dandruff.
Get a little sun. Sunlight may be good for dandruff. But because exposure to ultraviolet light damages your skin and increases your risk of skin cancer, don't sunbathe. Instead, just spend a little time outdoors. And be sure to wear sunscreen on your face and body.
Alternative medicine
While there are many purported home remedies for dandruff, one therapy that seems to be effective is daily shampooing with tea tree oil. Tea tree oil, which is extracted from the leaves of the Australian tea tree (Melaleuca alternifolia), has been used for centuries as an antiseptic, antibiotic and antifungal agent. It's now included in a number of shampoos found in natural foods stores. The oil is generally well tolerated but may cause allergic reactions in some people.
The good news is that dandruff can usually be controlled. Mild cases of dandruff may need nothing more than daily shampooing with a gentle cleanser. And stubborn flakes often respond to medicated shampoos. What's more, researchers have identified a yeast-like fungus that may cause or aggravate dandruff, a discovery that may lead to better treatments.
Symptoms
For most people, the signs and symptoms of dandruff are unmistakable: white, oily looking flakes of dead skin that dot your hair and shoulders and an itchy, scaling scalp. But it's not quite that simple — many conditions cause excessive skin scaling, including:
Dry skin. Simple dry skin — the kind you get in winter when the air is cold and rooms are overheated — is by far the most common cause of itchy, flaking skin. But flakes from dry skin are generally smaller and less oily than those caused by dandruff.
Seborrheic dermatitis. This condition, a frequent cause of dandruff, is marked by red, greasy skin covered with flaky white or yellow scales. Seborrheic dermatitis affects not only your scalp but also other areas rich in oil glands, such as your eyebrows, the sides of your nose and the backs of your ears, your breastbone, your groin area, and sometimes your armpits.
Psoriasis. This skin disorder causes an accumulation of dead skin cells that form thick silvery scales. Psoriasis commonly occurs on your knees, elbows and trunk, but it can also affect your scalp.
Cradle cap (seborrheic dermatitis of the scalp). This disorder, which causes a scaling, crusty scalp, is most common in newborns, but it can occur anytime during infancy. Although it can be alarming for parents, cradle cap isn't dangerous and usually clears up on its own by the time a baby is a year old.
Contact dermatitis. Sometimes sensitivities to certain hair-care products or hair dyes can cause a red, itchy, scaling scalp.
Causes
At one time or another, dandruff causes have been attributed to dry skin, oily skin, shampooing too often or not often enough, a poor diet, stress, and the use of too many fancy styling products. Although some of these factors may exacerbate or contribute to scalp flaking, the real culprit may be a fat-eating, yeast-like fungus called malassezia, formerly known as pityrosporum.
Malassezia lives on the scalps of most healthy adults without causing problems. But sometimes it grows out of control, feeding on the oils secreted by your hair follicles and causing irritation that leads to increased cell turnover. The result is a large number of dead skin cells. As the cells fall off, they tend to clump together with oil from your hair and scalp, making them appear white, flaky and all too visible.
Exactly what causes an overgrowth of these organisms isn't known, although increased oil production; hormonal fluctuations; stress; illness; neurological disorders, such as Parkinson's disease; a suppressed immune system; infrequent shampooing and extra sensitivity to the malassezia fungus may contribute to the development of dandruff.
Risk factors
Almost any adult is a candidate for dandruff, but certain factors can make you more susceptible:
Age. Dandruff usually begins in young adulthood and continues through middle age. That doesn't mean older adults don't get dandruff, however. For some people, the problem can be lifelong.
Sex. Because more men than women have dandruff, some researchers think male hormones may play a role in dandruff. Men also have larger sebaceous glands that produce an oil called sebum.
Oily hair and scalp. Malassezia feeds on oils in your scalp. For that reason, having excessively oily skin and hair makes you more prone to dandruff.
Certain illnesses. For reasons that aren't clear, adults with neurological diseases, such as Parkinson's disease, are more likely to develop seborrheic dermatitis and dandruff. So are people recovering from stressful conditions, particularly heart attack and stroke, and those with compromised immune systems.
Treatments and drugs
Dandruff is a chronic condition that can almost always be controlled, but dandruff treatment may take a little patience and persistence. In general, mild scaling can often be helped by daily cleansing with a gentle shampoo to reduce oiliness and cell buildup.
When regular shampoos fail, OTC dandruff shampoos may succeed. But dandruff shampoos aren't all alike, and you may need to experiment until you find one that works best for you. Dandruff shampoos are classified according to their active ingredient:
Zinc pyrithione shampoos (Selsun Salon, Head & Shoulders). These contain the antibacterial and antifungal agent zinc pyrithione, which has been shown to reduce the fungus that causes dandruff and seborrheic dermatitis.
Tar-based shampoos (Neutrogena T/Gel). Coal tar, a byproduct of the coal manufacturing process, helps conditions such as dandruff, seborrheic dermatitis and psoriasis by slowing cell turnover.
Shampoos containing salicylic acid (Ionil T). These "scalp scrubs" help eliminate scale, but they may leave your scalp dry, leading to more flaking. Using a conditioner after shampooing can help counter dryness.
Selenium sulfide shampoos (Selsun Blue). These shampoos help prevent cell turnover and may also reduce the number of malassezia. Because they can discolor blonde, gray or chemically colored hair, be sure to use them only as directed and to rinse well after shampooing.
Ketoconazole shampoos (Nizoral). The newest addition to the dandruff armamentarium, ketoconazole is a broad-spectrum antifungal agent that may work when other shampoos fail. It's available over-the-counter as well as by prescription.
Try using one of these shampoos daily until your dandruff is controlled, then cut back to two or three times a week. If one type of shampoo works for a time and then seems to lose its effectiveness, try alternating between two types of dandruff shampoos. Be sure to leave the shampoo on for at least five minutes — this allows the ingredients time to work.
If you've shampooed faithfully for several weeks and there's still a dusting of dandruff on your shoulders, talk to your doctor or dermatologist. You may need a prescription-strength shampoo or more aggressive treatment with a steroid lotion.
Lifestyle and home remedies
You can't prevent dandruff, but you can take steps to reduce your risk:
Learn to manage stress. Stress affects your overall health, making you susceptible to a number of conditions and diseases. It can even help trigger dandruff or exacerbate existing symptoms.
Shampoo often. If you tend to have an oily scalp, daily shampooing to remove the excess oil may help prevent dandruff.
Cut back on styling products. Hair sprays, styling gels, mousses and hair waxes can all build up on your hair and scalp, making them oilier.
Eat a healthy diet. A diet that provides enough zinc, B vitamins and essential fatty acid may help prevent dandruff.
Get a little sun. Sunlight may be good for dandruff. But because exposure to ultraviolet light damages your skin and increases your risk of skin cancer, don't sunbathe. Instead, just spend a little time outdoors. And be sure to wear sunscreen on your face and body.
Alternative medicine
While there are many purported home remedies for dandruff, one therapy that seems to be effective is daily shampooing with tea tree oil. Tea tree oil, which is extracted from the leaves of the Australian tea tree (Melaleuca alternifolia), has been used for centuries as an antiseptic, antibiotic and antifungal agent. It's now included in a number of shampoos found in natural foods stores. The oil is generally well tolerated but may cause allergic reactions in some people.
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