Disposal of Hazardous materials

Surface impoundment (placing liquid or semiliquid wastes in unlined pits) keeps waste in long-term storage, but it is not considered a method of final disposal. About 8 percent of hazardous waste is injected into deep wells; 21 percent enters landfills (large, unlined pits into which solid wastes are placed) as its ultimate resting place.

Abandoned and particularly serious waste sites may qualify as “Superfund” sites, eligible for cleanup with government funding under legislation passed in 1980. In 1993, of about 38,000 hazardous-waste sites inventoried by the Environmental Protection Agency (EPA), 1407 sites were listed on or proposed for the National Priority List (NPL) for waste cleanup.

In 1995 the EPA estimated that 73 million people lived within 4 miles of a Superfund site in the United States. Before 1995, 3300 emergency removals—urgent cleanups of hazardous wastes because of the immediate hazard they present—were conducted.

The serious problem of underground plumes of hazardous materials leaving the original disposal sites has only partial solutions at this time. The typical method of handling this problem is the drilling of wells around a plume's perimeter.

Hazardous materials are then removed from some wells, and water may be injected into other wells to produce a barrier to the plume's motion. Drilling wells and monitoring holes near a toxic site carries risks; a plume originally confined between strata (horizontal layers of rock) may penetrate vertically through a drilled hole and escape confinement.

A recent method of treatment for shallow plumes of chlorinated solvents depends on their chemical reactivity. A trench is dug around the leaking waste site and filled with a mixture of soil and powdered iron. The iron then reacts with the chlorinated solvents, turning them into simple hydrocarbons, which are less hazardous.

Medical Wastes

Hospitals use special care in disposing of wastes contaminated with blood and tissue, separating these hazardous wastes from ordinary waste. Hospitals and doctors' offices must be especially careful with needles, scalpels, and glassware, called “sharps.” Pharmacies discard outdated and unused drugs; testing laboratories dispose of chemical wastes. Medicine also makes use of significant amounts of radioactive isotopes for diagnosis and treatment, and these substances must be tracked and disposed of carefully.

The best way to eliminate hazardous wastes is not to generate them in the first place. For example, improvements have been made in the production of integrated circuits: The toxic chlorinated hydrocarbons commonly used in the 1970s were replaced in the 1980s by less toxic glycol ethers and in the 1990s by low-toxicity esters and alcohols.

Recycling is the recovery or reuse of usable materials from waste. About 5 percent of hazardous waste in the United States is recycled as solvents; a similar amount is recovered as metals.
For example, approximately 15 percent of sulfuric acid is recycled in chemical manufacturing. In the past, most sulfur used for sulfuric acid production was mined; now the amount of sulfur recovered from smelters (facilities that remove metals from ores), refineries (facilities that purify substances), and manufacturers is more than double that produced by mining.

In the United States, the practice of using industrial wastes, which often contain hazardous wastes, as ingredients in commercial fertilizers is encouraged as a means of recycling hazardous wastes. The safety of this practice has recently been called into question, however, and some states are starting to regulate it.

Progress in the basic sciences and clinical research

Future Directions
Progress in the basic sciences and clinical research is moving scientists closer to identifying vaccine candidates suitable for large-scale HIV vaccine trials. Researchers continue to design and test novel ways to present HIV proteins to the immune system, as well as develop new antigen-adjuvant vaccine formulations.

Although the challenges are daunting, scientists remain hopeful that they can develop safe and effective HIV vaccines. A growing number and variety of experimental vaccines are entering clinical tests in primates and humans, and more trials are exploring whether changing immunization schedules, increasing booster doses, or using a combination vaccine strategy can stimulate stronger, more durable immune responses.

Currently, about 30 NIAID-sponsored preventive HIV vaccine clinical trials are underway or planned for various stages of testing in the United States and internationally. More vaccines will be studied in the next 2 years than in the last 5 years combined, and thousands of additional healthy volunteers from all populations will be needed in the coming years.

Therapeutic AIDS Vaccines

Clinical Trials of Therapeutic AIDS Vaccines
Currently, there are no approved therapeutic vaccines for people infected with HIV. To date, scientists have conducted more than 30 NIAID-funded therapeutic vaccine clinical trials. Additionally, new vaccine candidates are being tested as both potential therapeutic and preventive vaccines.

Therapeutic vaccine research started in the early 1990s with several trials in the United States and Europe in volunteers on antiretroviral therapy (ART). In June 1992, AVEG began its first therapeutic vaccine trial, enrolling 55 HIV-infected men and women. The experimental gp160 vaccine was found to be safe. The first therapeutic vaccine trial enrolling asymptomatic HIV-infected children and HIV-infected pregnant women began in 1993.

The current NIAID-funded network conducting therapeutic vaccine studies is the AIDS Clinical Trials Group (ACTG). The group was created in 1987 as a network of domestic clinical sites to develop therapeutic agents to treat HIV and opportunistic infections and malignancies. By 1991, ACTG was divided to create the Adult ACTG (AACTG) and the Pediatric ACTG (PACTG). As the largest network of its kind in the world, ACTG carries out a broad scientific, therapeutic, and pathogenesis-based research agenda.

Preventive HIV Vaccines

Clinical Trials of Preventive HIV Vaccines
Currently, there are no approved preventive vaccines for HIV infection. Since the first HIV vaccine trial opened in 1987, researchers have studied more than 50 different preventive vaccine candidates in more than 100 NIAID-funded clinical trials.

The first HIV vaccine clinical trial opened in August 1987 at the National Institutes of Health Clinical Center in Bethesda, Maryland. This Phase I trial enrolled 138 healthy, uninfected volunteers. The gp160 subunit candidate vaccine tested caused no serious adverse effects.

Six months later, the NIAID AIDS Vaccine Evaluation Group (AVEG), the first U.S. cooperative HIV vaccine clinical trials group, began enrolling volunteers in its first trial.
In December 1992, NIAID launched its first Phase II HIV vaccine clinical trial.

This trial included uninfected volunteers with a history of high-risk behavior-injection drug use, multiple sex partners, or sexually transmitted infections. Participants were counseled repeatedly to avoid any behaviors that put them at risk of HIV infection.

Created in May 2000, the NIAID-funded HIV Vaccine Trials Network (HVTN) is a network of clinical sites in the United States and abroad dedicated to developing a preventive HIV vaccine by testing and evaluating candidate vaccines in all phases of clinical trials.

The network includes more than 25 sites in the United States, Africa, Asia, South America, and the Caribbean. HVTN's global capacity allows for rapid expansion as more vaccine candidates enter the pipeline for testing and development, and for carrying out large-scale studies of suitable vaccines.

HVTN built upon the many accomplishments of the HIV Prevention Trials Network and AVEG, two former NIAID networks that conducted preparedness and HIV vaccine studies. Scientific creativity, along with collaboration among private industry, academia, and government, are key aspects of HVTN's design.

In addition, NIAID's Dale and Betty Bumpers Vaccine Research Center (VRC) conducts research that facilitates the development of effective vaccines for human disease, with the primary focus of research being the development of vaccines for AIDS. Established in 1997 by former President Bill Clinton as part of an initiative to develop an AIDS vaccine and located in Bethesda,

VRC develops and tests vaccine candidates in all phases of clinical testing.
VRC works with scientists in academic, clinical, and industrial laboratories through a program of national and international collaborations. The center actively seeks industrial partners for the development, efficacy testing, and marketing of vaccines, and focuses on the development of new methodologies and training opportunities that will benefit all HIV vaccine researchers.

Phases of Clinical Trials

Clinical Trials
A Phase I trial is the first setting in which an experimental HIV vaccine is given to people. The trial, which can last up to 2 years, may enroll between 20 to 100 HIV-uninfected volunteers at low risk for HIV infection.

A Phase I trial primarily seeks information on safety, particularly looking for any vaccine-related side effects. The trial can also provide data on the dose and administration schedule needed to achieve the optimal immune responses.

If the vaccine elicits neutralizing antibodies or cytotoxic T lymphocytes (CTLs), scientists can study whether these responses are broadly protective against a wide variety of HIV strains that scientists refer to as subtypes or clades.

Once Phase I trials show the experimental HIV vaccine is safe, well tolerated, and appears promising, it can advance into Phase II. These trials, which can last longer than 2 years, enroll between 100 to 300 volunteers at high and low risk for acquiring HIV.
In these trials researchers gather more data on safety and immunogenicity.

Investigators supported by the National Institute of Allergy and Infectious Diseases (NIAID) investigators are also developing designs for intermediate trials that can provide preliminary answers about a candidate vaccine's efficacy, and determine if the vaccine candidate should move forward into large Phase III, or efficacy, trials.

A Phase IIb trial, also known as a "proof-of-concept" trial, is smaller, requiring 2,000 to 5,000 volunteers, is less expensive than Phase III trials, and may provide clues about the immune responses that can protect against disease.

The most promising vaccine candidates move into Phase III, enrolling 10,000 or more HIV-uninfected people at high risk for exposure to the virus. A Phase III trial, which can last up to 4 years, is typically designed to ensure enough data are collected on safety and effectiveness to support a license application to FDA.

AIDS

The 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.

AIDS stands for acquired immunodeficiency syndrome. AIDS is the final stage of HIV infection. It can take years for a person infected with HIV, even without treatment, to reach this stage. Having AIDS means that the virus has weakened the immune system to the point at which the body has a difficult time fighting infection. When someone has one or more specific infections, certain cancers, or a very low number of T cells, he or she is considered to have AIDS.

Origin of HIV

Scientists identified a type of chimpanzee in West Africa as the source of HIV infection in humans. The virus most likely jumped to humans when humans hunted these chimpanzees for meat and came into contact with their infected blood. Over several years, the virus slowly spread across Africa and later into other parts of the world

HIV was first identified in the United States in 1981.

It took several years for scientists to develop a test for the virus, to understand how HIV was transmitted between humans, and to determine what people could do to protect themselves.

In 2008, CDC adjusted its estimate of new HIV infections because of new technology and developed by the agency. Before this time, CDC estimated there were roughly 40,000 new HIV infections each year. New results shows there were dramatic declines in the number of new HIV infections from a peak of about 130,000 in the mid 1980s to a low of roughly 50,000 in the early 1990s.

Results also shows that new infections increased in the late 1990s, followed by a leveling off since 2000 at about 55,000 per year. In 2006, an estimated 56,300 individuals were infected with HIV.

AIDS cases began to fall dramatically in 1996, when new drugs became available. Today, more people than ever before are living with HIV/AIDS. CDC estimates that about 1 million people are living with HIV or AIDS. About one quarter of these people do not know that they are infected: not knowing puts them and others at risk.

Source: National Institutes of Health

How HIV Is and Is Not Transmitted

HIV is a fragile virus. It cannot live for very long outside the body. As a result, the virus is not transmitted through day-to-day activities such as shaking hands, hugging, or a casual kiss. You cannot become infected from a toilet seat, drinking fountain, doorknob, dishes, drinking glasses, food, or pets. You also cannot get HIV from mosquitoes.


HIV is primarily found in the blood, semen, or vaginal fluid of an infected person. HIV is transmitted in 3 main ways:

• Having sex (anal, vaginal, or oral) with someone infected with HIV


• Sharing needles and syringes with someone infected with HIV


• Being exposed (fetus or infant) to HIV before or during birth or through breast feeding.

HIV also can be transmitted through blood infected with HIV. However, since 1985, all donated blood in the United States has been tested for HIV. Therefore, the risk for HIV infection through the transfusion of blood or blood products is extremely low. The U.S. blood supply is considered among the safest in the world.

Risk Factors for HIV Transmission

You may be at increased risk for infection if you have :

• injected drugs or steroids, during which equipment (such as needles, syringes, cotton, water) and blood were shared with others


• had unprotected vaginal, anal, or oral sex (that is, sex without using condoms) with men who have sex with men, multiple partners, or anonymous partners


• exchanged sex for drugs or money


• been given a diagnosis of, or been treated for, hepatitis, tuberculosis (TB), or a sexually transmitted disease (STD) such as syphilis


• received a blood transfusion or clotting factor during 1978–1985


• had unprotected sex with someone who has any of the risk factors listed above

Preventing Transmission

Your risk of getting HIV or passing it to someone else depends on several things. Do you know what they are? You might want to talk to someone who knows about HIV. You can also do the following:

1. Abstain from sex (do not have oral, anal, or vaginal sex) until you are in a relationship with only one person, are having sex with only each other, and each of you knows the other’s HIV status.

• If both you and your partner have HIV, use condoms to prevent other sexually transmitted diseases (STDs) and possible infection with a different strain of HIV.


• If only one of you has HIV, use a latex condom and lubricant every time you have sex.

2. If you have, or plan to have, more than one sex partner, consider the following:

• Get tested for HIV


• If you are a man who has had sex with other men, get tested at least once a year.


• If you are a woman who is planning to get pregnant or who is pregnant, get tested as soon as possible, before you have your baby.


• Talk about HIV and other STDs with each partner before you have sex.


• Learn as much as you can about each partner’s past behavior (sex and drug use), and consider the risks to your health before you have sex.


• Ask your partners if they have recently been tested for HIV; encourage those who have not been tested to do so.


• Use a latex condom and lubricant every time you have sex.


• If you think you may have been exposed to another STD such as gonorrhea, syphilis, or Chlamydia trachomatis infection, get treatment. These diseases can increase your risk of getting HIV.


• Get vaccinated against hepatitis B virus.

3. Even if you think you have low risk for HIV infection, get tested whenever you have a regular medical check-up.
4. Do not inject illicit drugs (drugs not prescribed by your doctor). You can get HIV through needles, syringes, and other works if they are contaminated with the blood of someone who has HIV. Drugs also cloud your mind, which may result in riskier sex.

5. If you do inject drugs, do the following:

• Use only clean needles, syringes, and other works.


• Never share needles, syringes, or other works.


• Be careful not to expose yourself to another person's blood.


• Get tested for HIV test at least once a year.


• Consider getting counseling and treatment for your drug use.


• Get vaccinated against hepatitis A and B viruses.

6. Do not have sex when you are taking drugs or drinking alcohol because being high can make you more likely to take risks.


To protect yourself, remember these ABCs:
A=Abstinence
B=Be Faithful
C=Condoms

Symptoms of HIV Infection

The only way to know whether you are infected is to be tested for HIV.

You cannot rely on symptoms alone because many people who are infected with HIV do not have symptoms for many years.

Someone can look and feel healthy but can still be infected. In fact, one quarter of the HIV-infected persons in the United States do not know that they are infected.

HIV Testing

Once HIV enters the body, the body starts to produce antibodies—substances the immune system creates after infection.

Most HIV tests look for these antibodies rather than the virus itself. There are many different kinds of HIV tests, including rapid tests and home test kits.

All HIV tests approved by the US government are very good at finding HIV.

HIV Epidemiology

Introduction and Goals
Identifying and understanding the risk factors associated with HIV acquisition and transmission, and the development and progression of AIDS in men, women, and adolescents are critical aspects in the fight against this disease. Using epidemiological methods, NIAID-supported investigators are able to address key scientific questions by studying and comparing the effects of HIV in different human populations. Scientific findings gathered from these epidemiological studies help to provide insight on how to prevent the spread of HIV and also improve the quality of life for those already infected.


Clinical Trials and Cohort Studies
One major area of investigation involves studying the patterns of use and the efficacy/effectiveness of therapies in clinical trials and in cohort studies. The dramatic impact of highly active antiretroviral therapy (HAART) on HIV infection has prompted researchers to study the long-term clinical course of HIV infection in persons using HAART. While to date there have been no signs of a decrease in the effectiveness of HAART therapy, widespread drug resistance remains a concern. Furthermore, as people living with HIV continue to live longer, many of these immunocompromised individuals, who will naturally have a higher prevalence of other disease risk factors due to age, may develop other life threatening morbidities, such as heart disease or cancer, at a younger age than their HIV-negative peers. These types of scientific questions are now being investigated through epidemiological research.


International Research
Internationally, research opportunities have been expanding and accelerating in parts of the world that have been severely affected by the epidemic, including Africa, Asia and the Caribbean. Research has expanded as a result of dramatic cost reductions of HAART in many countries and the introduction of the Presidents Emergency Plan for HIV/AIDS Relief (PEPFAR), aimed at expanding access of antiretroviral therapy worldwide. The global availability of HAART has opened doors for studying the best use of therapy in different populations, which is important given that therapeutic regimens for HIV may differ in populations due to other health stressors such as other infectious diseases and nutritional deficits. Research on the availability, use and success of HAART in developing economy nations is now underway and additional research in these settings is being planned.


Goals of NIAID’s HIV/AIDS epidemiology research

• Identifying the proportion of the population affected by HIV and the rate at which new infections are occurring, as well as developing profiles on vital baseline information for HIV-infected populations and populations at risk, in order to evaluate vaccine efficacy and therapeutic clinical trials


• Describing the changing manifestations of the clinical and laboratory course of HIV infection, the changing frequency with which various complications occur, and the impact of therapy on modulating changes in HIV-related survival and clinical outcomes


• Investigating the clinical course of HIV infection among persons with other co-morbidities (i.e., HBV, HCV, tuberculosis, malaria, heart disease, diabetes) to better understand the natural and treated history of the disease in those with other chronic conditions


• Evaluating the patterns of adherence to HAART in populations around the world, the predictors of disease progression, and the efficacy of HAART in populations exposed to a variety of other concomitant infections and under nutritional and other health stressors


• Studying the biological, clinical, and epidemiological characteristics of people who are at high risk for HIV infection but do not become infected and those who are long-term non-progressors.

Source: National Institutes of Health

HIV/AIDS Connections

The HIV-AIDS
The acquired immunodeficiency syndrome (AIDS) was first recognized in 1981 and has since become a major worldwide pandemic. Abundant evidence indicates that AIDS is caused by the human immunodeficiency virus (HIV) , which was discovered in 1983. By leading to the destruction and/or functional impairment of cells of the immune system, notably CD4+ T cells, HIV progressively destroys the body's ability to fight infections and certain cancers.

Why is there overwhelming scientific consensus that HIV causes AIDS?
Before HIV infection became widespread in the human population, AIDS-like syndromes occurred extremely rarely, and almost exclusively in individuals with known causes of immune suppression, such as chemotherapy and underlying cancers of certain types.


A marked increase in unusual infections and cancers characteristic of severe immune suppression was first recognized in the early 1980s in homosexual men who had been otherwise healthy and had no recognized cause for immune suppression.


An infectious cause of AIDS was suggested by geographic clustering of cases, links among cases by sexual contact, mother-to-infant transmission, and transmission by blood transfusion. Isolation of the HIV from patients with AIDS strongly suggested that this virus was the cause of AIDS.


Since the early 1980s, HIV and AIDS have been repeatedly linked in time, place and population group; the appearance of HIV in the blood supply has preceded or coincided with the occurrence of AIDS cases in every country and region where AIDS has been noted.


Individuals of all ages from many risk groups – including men who have sex with men, infants born to HIV-infected mothers, heterosexual women and men, hemophiliacs, recipients of blood and blood products, healthcare workers and others occupationally exposed to HIV-tainted blood, and male and female injection drug users – have all developed AIDS with only one common denominator: infection with HIV.

HIV destroys CD4+ T cells, which are crucial to the normal function of the human immune system.

In fact, depletion of CD4+ T cells in HIV-infected individuals is an extremely powerful predictor of the development of AIDS.


Studies of thousands of individuals have revealed that most HIV-infected people carry the virus for years before enough damage is done to the immune system for AIDS to develop; however, with time, a near-perfect correlation has been found between infection with HIV and the subsequent development of AIDS.


Recently developed, sensitive tests have shown a strong correlation between the amount of HIV in the blood and the subsequent decline in CD4+ T cell numbers and development of AIDS. Furthermore, reducing the amount of virus in the body with anti-HIV drugs can slow this immune destruction.

How HIV Causes AIDS

HIV destroys CD4 positive (CD4+) T cells, which are white blood cells crucial to maintaining the function of the human immune system.


As the virus attacks those cells, the person infected with HIV is less equipped to fight off infection and disease ultimately resulting in the development of AIDS.

Most people who are infected with HIV can carry the virus for years before sufficient damage to the immune system results in the development of AIDS.


However, there is a strong connection between high levels of HIV in the blood and the decline in CD4+ T cells and the development of AIDS.


Antiretroviral medicines can reduce the amount of virus in the body, preserve CD4+ T cells and dramatically slow the destruction of the immune system.

HIV Transmission

Transmission
HIV is primarily found in the blood, semen, or vaginal fluid of someone who is infected with the virus and is transmitted in four ways:

• Having unprotected sex (anal, oral or vaginal) with someone infected with HIV


• Sharing needles and syringes with someone infected with HIV


• Being exposed to the virus as a fetus or infant before or during birth or through breastfeeding from an HIV-infected mother


• Receiving a transfusion of HIV-infected blood or blood products. In the United States, all donated blood and blood products have been screened for HIV since 1985; therefore, the risk of transmission in this way is extremely low in the U.S.
  

HIV cannot survive for very long outside of the body. The virus cannot be transmitted through routine daily activities such as using a toilet seat, sharing food utensils or drinking glasses, shaking hands, or through kissing. The virus also cannot be spread by bloodsucking insects, such as mosquitoes.

HIV Symptoms

Early Symptoms

Many people will not have any symptoms when they first become infected with HIV. They may, however, have a flu-like illness within a month or two after exposure to the virus. This illness may include

• Fever


• Headache


• Tiredness


• Enlarged lymph nodes (glands of the immune system easily felt in the neck and groin)
  

These symptoms usually disappear within a week to a month and are often mistaken for those of another viral infection. During this period, people are very infectious, and HIV is present in large quantities in genital fluids.

Later symptoms
More persistent or severe symptoms may not appear for 10 years or more after HIV first enters the body in adults, or within 2 years in children born with HIV infection. This period of asymptomatic infection varies greatly in each person. Some people may begin to have symptoms within a few months, while others may be symptom-free for more than 10 years.

Even during the asymptomatic period, the virus is actively multiplying, infecting and killing cells of the immune system. The virus can also hide within infected cells and be inactive. The most obvious effect of HIV infection is a decline in the number of CD4 positive T (CD4+) cells found in the blood—the immune system’s key infection fighters. The virus slowly disables or destroys these cells without causing symptoms.

As the immune system becomes more debilitated, a variety of complications start to take over. For many people, the first signs of infection are large lymph nodes, or swollen glands, that may be enlarged for more than 3 months. Other symptoms often experienced months to years before the onset of AIDS include

• Lack of energy


• Weight loss


• Frequent fevers and sweats


• Persistent or frequent yeast infections (oral or vaginal)


• Persistent skin rashes or flaky skin


• Pelvic inflammatory disease in women that does not respond to treatment


• Short-term memory loss
  

Some people develop frequent and severe herpes infections that cause mouth, genital, or anal sores, or a painful nerve disease called shingles. Children may grow slowly or get sick frequently.

HIV Diagnosis

Because early HIV infection often causes no symptoms, a healthcare provider usually can diagnose it by testing blood for the presence of antibodies (disease-fighting proteins) to HIV.

HIV antibodies generally do not reach noticeable levels in the blood for 1 to 3 months after infection. It may take the antibodies as long as 6 months to be produced in quantities large enough to show up in standard blood tests.


Hence, to determine whether a person has been recently infected (acute infection), a healthcare provider can screen blood for the presence of HIV genetic material. Direct screening of HIV is extremely critical to prevent transmission of HIV from recently infected individuals.

Anyone who has been exposed to the virus should get an HIV test as soon as the immune system is likely to develop antibodies to the virus—within 6 weeks to 12 months after possible exposure to the virus.


By getting tested early, a healthcare provider can give advice to an infected person about when to start treatment to help the immune system combat HIV and help prevent the emergence of certain opportunistic infections (see section on treatment). Early testing also alerts an infected person to avoid high-risk behaviors that could spread the virus to others.

Most healthcare providers can do HIV testing and will usually offer counseling at the same time. Of course, testing can be done anonymously at many sites if a person is concerned about confidentiality.

Healthcare providers diagnose HIV infection by using two different types of antibody tests: ELISA (enzyme-linked immunosorbent assay) and Western blot. If a person is highly likely to be infected with HIV but has tested negative for both tests, a healthcare provider may request additional tests.


A person also may be told to repeat antibody testing at a later date, when antibodies to HIV are more likely to have developed.

Diagnosis in Babies
Babies born to mothers infected with HIV may or may not be infected with the virus, but all carry their mothers’ antibodies to HIV for several months. If these babies lack symptoms, healthcare providers cannot make a definitive diagnosis of HIV infection using standard antibody tests. Instead, they are using new technologies to detect HIV and more accurately determine HIV infection in infants between ages 3 months and 15 months. Researchers are evaluating a number of blood tests to determine which ones are best for diagnosing HIV infection in babies younger than 3 months.

HIV Infection

In the early 1980s when the HIV/AIDS epidemic began, people with AIDS were not likely to live longer than a few years. With the development of safe and effective drugs, however, people infected with HIV now have longer and healthier lives.


The discovery and development of new therapeutic strategies against HIV is a high priority for the National Institute of Allergy and Infectious Diseases (NIAID). Research supported by NIAID has already greatly advanced our understanding of HIV and how it causes disease.

This knowledge provides the foundation for NIAID's HIV/AIDS research effort and continues to support studies designed to further extend and improve the quality of life of those infected with HIV.

Drugs for HIV/AIDS

Currently, there are 30 antiretroviral drugs approved by the Food and Drug Administration to treat people infected with HIV. These drugs fall into four major classes.

1. Reverse transcriptase (RT) inhibitors interfere with the critical step during the HIV life cycle known as reverse transcription. During this step, RT, an HIV enzyme, converts HIV RNA to HIV DNA. There are two main types of RT inhibitors.

• Nucleoside/nucleotide RT inhibitors are faulty DNA building blocks. When these faulty pieces are incorporated into the HIV DNA (during the process when the HIV RNA is converted to HIV DNA), the DNA chain cannot be completed, thereby blocking HIV from replicating in a cell.



• Non-nucleoside RT inhibitors bind to RT, interfering with its ability to convert the HIV RNA into HIV DNA.
  

2. Protease inhibitors interfere with the protease enzyme that HIV uses to produce infectious viral particles.

3. Entry and fusion inhibitors interfere with the virus' ability to fuse with the cellular membrane, thereby blocking entry into the host cell.

4. Integrase inhibitors block integrase, the enzyme HIV uses to integrate genetic material of the virus into its target host cell.

5. Multidrug combination products combine drugs from more than one class into a single product.

Currently available drugs do not cure HIV infection or AIDS. They can suppress the virus, even to undetectable levels, but they cannot eliminate HIV from the body. Hence, people with HIV need to continuously take antiretroviral drugs.

Highly Active Antiretroviral Therapy (HAART)

Counters Drug Resistance
As HIV reproduces itself, variants of the virus emerge, including some that are resistant to antiretroviral drugs. Therefore, health care providers recommend that people infected with HIV take a combination of antiretroviral drugs known as highly active antiretroviral therapy, or HAART.

This strategy, which typically combines drugs from at least two different classes of antiretroviral drugs, has been shown to effectively suppress the virus when used properly. Developed by NIAID-supported researchers, HAART has revolutionalized how people infected with HIV are treated.

HAART works by suppressing the virus and decreasing the rate of opportunistic infections. HIV Transmission and Antiretroviral DrugsAlthough the use of HAART has greatly reduced the number of deaths due to HIV/AIDS, and possibly the transmission of HIV/AIDS as well, this powerful combination of drugs cannot suppress the virus completely.

Therefore, people infected with HIV who take antiretroviral drugs can still transmit HIV to others through unprotected sex and needle-sharing.

Antiretroviral Drug

Opportunistic Infections and AIDS-associated Co-infections
People infected with HIV have impaired immune systems that can leave them susceptible to opportunistic infections (OIs) and AIDS-associated co-infections, caused by a wide range of microorganisms such as protozoa, viruses, fungi, and bacteria. One example of an associated co-infection is hepatitis C virus infection, which can lead to liver cancer.

Potent HIV therapies such as HAART, however, have produced dramatic responses in patients. These therapies often allow the immune system to recover, sustain, and protect the body from other infections.

Hence, antiretroviral drugs provide a way for the immune system to remain effective, thereby improving the quality and length of life for people with HIV.

Antiretroviral Drugs

Antiretroviral Drugs
People taking antiretroviral drugs may have low adherence to complicated drug regimens. Current recommended regimens involve taking several antiretroviral drugs each day from at least two different classes, some of which may cause unpleasant side effects such as nausea and vomiting.
In addition, antiretroviral drugs may cause more serious medical problems, including metabolic changes such as abnormal fat distribution, abnormal lipid and glucose metabolism, and bone loss.
Therefore, NIAID is investigating simpler, less toxic, and more effective drug regimens.

Effective Antiretroviral Drugs

Development of New Safe and Effective Antiretroviral Drugs
NIAID supports the development and testing of new therapeutic agents, classes, and combinations of antiretroviral drugs that can continuously suppress the virus with few side effects.

Through human clinical trials, NIAID-supported studies provide accurate and extensive information about the safety and efficacy of drug candidates and combinations, and identify potential uncommon but important toxicities of newly approved agents. Studies are also under way to assess rare toxicities of older approved agents, especially as a result of long-term use.

Through the Multicenter AIDS Cohort Study and Women's Interagency HIV Study, NIAID supports long-term studies of HIV infection and its treatment in both men and women. Since their inception, these cohort studies have enrolled and collected data from more than 10,000 people.

In addition, NIAID supports treatment studies conducted through three HIV/AIDS clinical trials networks: the AIDS Clinical Trials Group, the International Maternal Pediatric Adolescent AIDS Clinical Trials Group, and the International Network for Strategic Initiatives in Global HIV Trials.

Complications of Antiretroviral Drugs

NIAID Research on the Complications of Antiretroviral Drugs
NIAID supports studies aimed at understanding the side effects of antiretroviral drugs as well as strategies to reduce exposure to potentially toxic drug regimens, such as:

• Structured treatment interruption (STI) protocols.


• Use of immune-based therapies with HAART


• Studies to compare different drug dosing schedules or combinations


• Studies to compare early versus delayed treatment
  

NIAID also supports projects evaluating regimens containing agents associated with toxicities. For example, NIAID-funded researchers are conducting studies to evaluate treatments for several drug-associated metabolic complications, including fat redistribution, lipid and glucose abnormalities, and bone loss. In addition, researchers are studying the long-term metabolic effects of various antiretroviral regimens in pregnant women and their infants and in HIV-infected children and adolescents.

New Drugs in the Pipeline

Down the Road:
The Pharmaceutical Research and Manufacturers Association of America maintains a database of new drugs in development to treat HIV infection. They include new protease inhibitors and more potent, less toxic RT inhibitors, as well as other drugs that interfere with entirely different steps in the virus' lifecycle. These new categories of drugs include:

• Entry inhibitors that interfere with HIV's ability to enter cells


• Integrase inhibitors that interfere with HIV's ability to insert its genes into a cell's normal DNA


• Assembly and budding inhibitors that interfere with the final stage of the HIV life cycle, when new virus particles are released into the bloodstream.


• Cellular metabolism modulators that interfere with the cellular processes needed for HIV replication


• Gene therapy that uses modified genes inserted directly into cells to suppress HIV replication. These cells are designed to produce T cells that are genetically resistant to HIV infection.

In addition, scientists are exploring whether immune modulators help boost the immune response to the virus and may make existing anti-HIV drugs more effective. Therapeutic vaccines also are being evaluated for this purpose and could help reduce the number of anti-HIV drugs needed or the duration of treatment.

HIV/AIDS Prevention

Because there is no vaccine for HIV, the only way people can prevent infection with the virus is to avoid behaviors putting them at risk of infection, such as sharing needles and having unprotected sex.


Many people infected with HIV have no symptoms. Therefore, there is no way of knowing with certainty whether a sexual partner is infected unless he or she has repeatedly tested negative for the virus and has not engaged in any risky behavior.

Abstaining from having sex or using male latex condoms or female polyurethane condoms may offer partial protection, during oral, anal, or vaginal sex. Only water-based lubricants should be used with male latex condoms.

Although some laboratory evidence shows that spermicides can kill HIV, researchers have not found that these products can prevent a person from getting HIV.

Recently, NIAID-supported two studies that found adult male medical circumcision reduces a man’s risk of acquiring HIV infection by approximately 50 percent. The studies, conducted in Uganda and Kenya, pertain only to heterosexual transmission.

As with most prevention strategies, adult male medical circumcision is not completely effective at preventing HIV transmission. Circumcision will be most effective when it is part of a more complete prevention strategy, including the ABCs (Abstinence, Be Faithful, Use Condoms) of HIV prevention.

Challenges in Designing HIV Vaccines

Designing HIV Vaccines
Vaccines teach the immune system to recognize a specific harmful organism and fight off the disease when the body faces the real thing. Despite extraordinary advances in understanding both HIV and the human immune system, a fully successful HIV vaccine continues to elude researchers.
The most difficult challenges today for HIV vaccine researchers are:

• HIV attacks CD4+ T cells, the most important part of the immune system that coordinates and directs the activities of other types of immune cells that combat intruding microbes. For a vaccine to be effective, it will need to be able to activate these cells-a difficult feat if they're being infected and destroyed by the virus.

• Scientists have not identified the correlates of immunity, or protection, for HIV and are still trying to design vaccines to induce the appropriate immune responses necessary for protection. Unlike other viral diseases for which investigators have made successful vaccines, there are no documented cases of complete recovery from HIV infection. Therefore, HIV vaccine researchers have no human model of recovery from infection and subsequent protection from re-infection to guide them.

• In an infected person, HIV continually mutates and recombines to evolve into new strains of virus that differ slightly from the original infecting virus. This extensive diversity of HIV poses a challenge to vaccine design as an HIV vaccine would need to protect against many different strains of the virus circulating throughout the world. Conventional vaccines have had to protect against one or a limited number of strains.

• Ideally, an HIV vaccine will marshal two kinds of immune responses to fight HIV: T cells and antibodies secreted by B cells. These immune responses would prevent the establishment and spread of the virus from the original site of infection and decrease the effects of the disease in those who do become infected. However, scientists have not yet been able to stimulate both types of responses. To date, researchers have only stimulated T cell responses weakly with experimental HIV vaccines, and have had difficulty stimulating the production of antibodies that protect against a broad range of HIV strains.

• Researchers lack the knowledge about which HIV immunogens, pieces of HIV used to construct an experimental HIV vaccine, will get the immune system to recognize HIV during an actual encounter and protect against disease.
  



• Lack of a practical animal model to predict the effectiveness of an HIV vaccine in people hampers HIV vaccine development. Currently, researchers rely on experiments using non-human primate models infected with the simian cousin of HIV, known as SIV, and an engineered combination of SIV and HIV, known as SHIV, to somewhat mimic disease progression. Evaluating experimental vaccines in these animals requires a SIV or SHIV analog instead of the actual HIV vaccine candidate used in clinical trials in humans.

Epidemiology of Meningitis

Epidemiology of Meningitis Caused by Neisseria meningitidis,
Streptococcus pneumoniae and Haemophilus influenzae
The procedures described in this manual are not new; most have been used for many years. Even though they require an array of laboratory capabilities, these procedures were selected because of their utility, ease of performance, and ability to give reproducible results. The diversity of laboratory capabilities, the availability of materials and supplies, and their cost, were taken into account.

Bacterial menigitis, an infection of the membranes (meninges) and cerebrospinal fluid (CSF) surrounding the brain and spinal cord, is a major cause of death and disability world-wide.

Beyond the perinatal period, three organisms, transmitted from person to person through the exchange of respiratory secretions, are responsible for most cases of bacterial meningitis:
Neisseria meningitidis, Haemophilus influenzae, and Streptococcus pneumoniae.

The etiology of bacterial meningitis varies by age group and region of the world. Worldwide, without epidemics one million cases of bacterial meningitis are estimated to occur and 200,000 of these die annually.

Case-fatality rates vary with age at the time of illness and the species of bacterium causing infection, but typically range from 3 to 19% in developed countries. Higher case-fatality rates (37-60%) have been reported in developing countries.

Up to 54% of survivors are left with disability due to bacterial meningitis, including deafness, mental retardation, and neurological sequelae.

Two clinically overlapping syndromes – meningitis and bloodstream infection (meningococcaemia) - are caused by infection with N. meningitidis (meningococcal disease).

While the two syndromes may occur simultaneously, meningitis alone occurs most frequently. N. meningitidis is classified into serogroups based on the immunological reactivity of the capsular polysaccharide.

Although 13 serogroups have been identified, the three serogroups A, B and C account for over 90% of meningococcal disease.

Meningococcal disease differs from other leading causes of bacterial meningitis because of its potential to cause large-scale epidemics.

A region of sub-Saharan Africa extending from Ethiopia in the East to The Gambia in the West and containing fifteen countries and over 260 million people is known as the “meningitis belt” because of its high endemic rate of disease with superimposed, periodic, large epidemics caused by serogroup A, and to a lesser extent, serogroup C.

During epidemics, children and young adults are most commonly affected, with attack rates as high as 1,000/100,000 population, or 100 times the rate of sporadic disease. The highest rates of endemic or sporadic disease occur in children less than 2 years of age.

In developed countries, endemic disease is generally caused by serogroups B and C. Epidemics in developed countries are typically caused by serogroup C although epidemics due to serogroup B have also occurred in Brazil, Chile, Cuba, Norway and more recently in New Zealand.

Meningitis caused by H. influenzae occurs mostly in children under the age of 5 years, and most cases are caused by organisms with the type b polysaccharide capsule (H. influenzae type b, Hib).

While most children are colonized with a species of H. influenzae, only 2-15% harbour Hib. The organism is acquired through the respiratory route. It adheres to the upper respiratory tract epithelial cells and colonizes the nasopharynx. Following acquisition of Hib, illness results when the organism is able to penetrate the respiratory mucosa and enters the blood stream.

This is the result of a combination of factors, and subsequently the organism gains access to the CSF, where infection is established and inflammation occurs. An essential virulence factor which plays a major role in determining the invasive potential of an organism is the polysaccharide capsule of Hib.

Meningitis is the most severe form of Hib disease; in most countries, however more cases and deaths are due to pneumonia than to meningitis. Meningitis in individuals at the extremes of age infants, young children and the elderly is commonly caused by S. pneumoniae.

Younger adults with anatomic or functional asplenia, haemoglobinopathies, such as sickle cell disease, or who are otherwise immunocompromised, also have an increased susceptibility to S. pneumoniae infection. S. pneumoniae, like Hib, is acquired through the respiratory route.

Following the establishment of nasopharyngeal colonization, illness results once bacteria evade the mucosal defences, thus accessing the bloodstream, and eventually reaching the meninges and CSF.

As is the case with Hib, many more cases and deaths are due to Pneumococcal pneumonia, even though pneumococcal meningitis is the more severe presentation of pneumococcal disease.

The risk of secondary cases of meningococcal disease among close contacts (i.e. household members, day-care centre contacts, or anyone directly exposed to the patient’s oral secretions) is high.

Antimicrobial chemoprophylaxis with a short course of oral rifampin, a single oral dose of ciprofloxacin, or a single injection of ceftriaxone is effective in eradicating nasopharyngeal carriage of N. meningitidis.

Although very effective in preventing secondary cases, antimicrobial chemoprophylaxis is not an effective intervention for altering the course of an outbreak. In epidemics, mass chemoprophylaxis is not recommended.

Vaccines have an important role in the control and prevention of bacterial meningitis. Vaccines against N. meningitidis, H. influenzae, and S. pneumoniae are currently available, but the protection afforded by each vaccine is specific to each bacterium and restricted to some of the serogroups or serotypes of each bacterium.

For example, vaccines are currently available to prevent H. influenzae infections due to
serotype b (Hib) but not those infections due to other serotypes or unencapsulated organisms (i.e. nontypeable H. influenzae).

In addition to establishing a diagnosis, an important role for the laboratory, therefore, is to determine the bacteria and serogroups/serotypes that are causing meningitis in a community.

In industrialized countries, routine use of polysaccharide-protein Hib conjugate vaccines for immunization of infants has almost eliminated Hib meningitis and other forms of severe Hib disease. Several studies in developing countries have corroborated these finding.

Pneumococcal polysaccharide vaccines have been used to prevent disease in the elderly and in persons with chronic illnesses that may impair their natural immunity to pneumococcal disease.

Meningococcal polysaccharide vaccines are generally used in response to epidemics and for the prevention of disease in overseas travellers although other uses are currently under investigation.

In addition to the existing armamentarium of vaccines, new generation vaccines against meningococcal and pneumococcal disease are under development and evaluation.

These vaccines may provide a high degree of protection and broad coverage in all age groups. Until these vaccines become widely available, the current vaccines should be used appropriately and efficiently.

Use of any of these vaccines will require laboratory identification of the agents causing disease in addition to epidemiological information about the age and risk groups that are most affected.

Source: National Institutes of Health

Can I get viral meningitis if I’m around someone who has it?

The viruses that cause viral meningitis are contagious. Enteroviruses, for example, are very common during the summer and early fall, and many people are exposed to them.

However, most infected persons either have no symptoms or develop only a cold or rash with low-grade fever.

Only a small proportion of infected persons actually develop meningitis.

Therefore, if you are around someone who has viral meningitis, you have a moderate chance of becoming infected, but a very small chance of developing meningitis.

Are there vaccines against meningitis?

Yes, there are vaccines against Hib, against some serogroups of N. meningitidis and many types of Streptococcus pneumoniae.
The vaccines against Hib are very safe and highly effective.
There are two vaccines against N. meningitidis available in the U.S. Meningococcal polysaccharide vaccine (MPSV4 or Menomune®) has been approved by the Food and Drug Administration (FDA) and available since 1981.

Meningococcal conjugate vaccine (MCV4 or MenactraT) was licensed in 2005.
Both vaccines can prevent 4 types of meningococcal disease, including 2 of the 3 types most common in the U.S. (serogroup C, Y, and W-135) and a type that causes epidemics in Africa (serogroup A).

Meningococcal vaccines cannot prevent all types of the disease. But they do protect many people who might become sick if they didn't get the vaccine. Meningitis cases should be reported to state or local health departments to assure follow-up of close contacts and recognize outbreaks.
MCV4 is recommended for all children at their routine preadolescent visit (11 to 12 years of age).

For those who have never gotten MCV4 previously, a dose is recommended at high school entry. Other adolescents who want to decrease their risk of meningococcal disease can also get the vaccine.

Other people at increased risk for whom routine vaccination is recommended are college freshmen living in dormitories, microbiologists who are routinely exposed to meningococcal bacteria, U.S. military recruits, anyone who has a damaged spleen or whose spleen has been removed; anyone who has terminal complement component deficiency (an immune system disorder), anyone who is traveling to the countries which have an outbreak of meningococcal disease, and those who might have been exposed to meningitis during an outbreak.

MCV4 is the preferred vaccine for people 11 to 55 years of age in these risk groups, but MPSV4 can be used if MCV4 is not available.
MPSV4 should be used for children 2 to 10 years old, and adults over 55, who are at risk.

Although large epidemics of meningococcal meningitis do not occur in the United States, some countries experience large, periodic epidemics.

Overseas travelers should check to see if meningococcal vaccine is recommended for their destination.

Travelers should receive the vaccine at least 1 week before departure, if possible. Information on areas for which meningococcal vaccine is recommended can be obtained by calling the Centers for Disease Control and Prevention at (404)-332-4565.

There are vaccines to prevent meningitis due to S. pneumoniae (also called pneumococcal meningitis) which can also prevent other forms of infection due to S. pneumoniae.

The pneumococcal polysaccharide vaccine is recommended for all persons over 65 years of age and younger persons at least 2 years old with certain chronic medical problems.

There is a newly licensed vaccine (pneumococcal conjugate vaccine) that appears to be effective in infants for the prevention of pneumococcal infections and is routinely recommended for all children younger than 2 years of age.


Vaccines are also available against some of the bacteria that can cause meningitis. A vaccine against one strain of Haemophilus influenzae, once the most common cause of bacterial meningitis, was introduced during the 1980s and has been a part of routine childhood immunization in the United States since 1990.

This vaccine has dramatically reduced the number of cases of bacterial meningitis. Vaccines also exist for certain strains of Neisseria meningitidis and Streptococcus pneumoniae but are not a part of routine immunization.

The Neisseria meningitidis vaccine is given to military recruits and people who are planning travel to areas of the world where outbreaks of meningococcal meningitis are common. The Streptococcus pneumoniae vaccine is recommended for people over age 65.

Is meningitis contagious?

Yes, some forms of bacterial meningitis are contagious. The bacteria are spread through the exchange of respiratory and throat secretions (i.e., coughing, kissing). Fortunately, none of the bacteria that cause meningitis are as contagious as things like the common cold or the flu, and they are not spread by casual contact or by simply breathing the air where a person with meningitis has been.

However, sometimes the bacteria that cause meningitis have spread to other people who have had close or prolonged contact with a patient with meningitis caused by Neisseria meningitidis (also called meningococcal meningitis) or Hib.

People in the same household or day-care center, or anyone with direct contact with a patient's oral secretions (such as a boyfriend or girlfriend) would be considered at increased risk of acquiring the infection.

People who qualify as close contacts of a person with meningitis caused by N. meningitidis should receive antibiotics to prevent them from getting the disease. Antibiotics for contacts of a person with Hib meningitis disease are no longer recommended if all contacts 4 years of age or younger are fully vaccinated against Hib disease.

Can meningitis be treated?

Early diagnosis and treatment are very important. If symptoms occur, the patient should see a doctor immediately. The diagnosis is usually made by growing bacteria from a sample of spinal fluid.


The spinal fluid is obtained by performing a spinal tap, in which a needle is inserted into an area in the lower back where fluid in the spinal canal is readily accessible. Identification of the type of bacteria responsible is important for selection of correct antibiotics.

What are the signs and symptoms of meningitis?

No matter what the cause, the symptoms of meningitis are always similar and usually develop rapidly, often over the course of a few hours. Nearly all patients with meningitis experience vomiting, high fever, and a stiff neck.

Meningitis may also cause severe headache, back pain, muscle aches, sensitivity of the eyes to light, drowsiness, confusion, and even loss of consciousness. Some children have convulsions. In infants, the symptoms of meningitis are often more difficult to detect and may include irritability, lethargy, and loss of appetite.

Most patients with meningococcal meningitis develop a rash of red, pinprick spots on the skin. The spots do not turn white when pressed, and they quickly grow to look like purple bruises.


High fever, headache, and stiff neck are common symptoms of meningitis in anyone over the age of 2 years. These symptoms can develop over several hours, or they may take 1 to 2 days. Other symptoms may include nausea, vomiting, discomfort looking into bright lights, confusion, and sleepiness.

In newborns and small infants, the classic symptoms of fever, headache, and neck stiffness may be absent or difficult to detect, and the infant may only appear slow or inactive, or be irritable, have vomiting, or be feeding poorly. As the disease progresses, patients of any age may have seizures.

What is meningitis?

Meningitis is an infection of the fluid of a person's spinal cord and the fluid that surrounds the brain. People sometimes refer to it as spinal meningitis.

Meningitis is usually caused by a viral or bacterial infection. Knowing whether meningitis is caused by a virus or bacterium is important because the severity of illness and the treatment differ.

Viral meningitis is generally less severe and resolves without specific treatment, while bacterial meningitis can be quite severe and may result in brain damage, hearing loss, or learning disability.

For bacterial meningitis, it is also important to know which type of bacteria is causing the meningitis because antibiotics can prevent some types from spreading and infecting other people. Before the 1990s,

Haemophilus influenzae type b (Hib) was the leading cause of bacterial meningitis, but new vaccines being given to all children as part of their routine immunizations have reduced the occurrence of invasive disease due to H. influenzae.

Today, Streptococcus pneumoniae and Neisseria meningitidis are the leading causes of bacterial meningitis.

Reduce chances of becoming infected, and prevent it?

The viruses that cause viral meningitis are contagious. Enteroviruses, for example, are very common during the summer and early fall, and many people are exposed to them. However, most infected persons either have no symptoms or develop only a cold or rash with low-grade fever.

Only a small proportion of infected persons actually develop meningitis. Therefore, if you are around someone who has viral meningitis, you have a moderate chance of becoming infected, but a very small chance of developing meningitis.

Good hygiene to prevent the spread of viruses is the only method of preventing viral meningitis. To help prevent the spread of bacterial meningitis, antibiotics are sometimes given to family members and other people who have had close contact with patients who develop the disease.

How is the virus spread?

Enteroviruses, the most common cause of viral meningitis, are most often spread through direct contact with respiratory secretions (e.g., saliva, sputum, or nasal mucus) of an infected person. This usually happens by shaking hands with an infected person or touching something they have handled, and then rubbing your own nose or mouth.

The virus can also be found in the stool of persons who are infected. The virus is spread through this route mainly among small children who are not yet toilet trained. It can also be spread this way to adults changing the diapers of an infected infant. The incubation period for enteroviruses is usually between 3 and 7 days from the time you are infected until you develop symptoms. You can usually spread the virus to someone else beginning about 3 days after you are infected until about 10 days after you develop symptoms.


Although the viruses and bacteria that cause meningitis are contagious, not everyone who comes in contact with someone with meningitis will develop the disease. In fact, meningitis typically occurs in isolated cases. Occasionally outbreaks of meningitis caused by Neisseria meningitidis, also known as meningococcal meningitis, occur in group living situations, such as day-care centers, college dormitories, or military barracks.

A child whose immune system is weakened—due to a disease or genetic disorder, for instance—is at increased risk for developing meningitis. In general, however, scientists do not know why microorganisms that are usually harmless are able to cross into the CSF and cause meningitis in some people but not others.

How is viral meningitis treated?

It is imperative to seek immediate medical attention if the symptoms of meningitis develop in order to determine whether the meningitis is viral or bacterial. Any delays in treating bacterial meningitis can lead to stroke, severe brain damage, and even death. Patients with bacterial meningitis are usually hospitalized and given large doses of intravenous antibiotics. The specific antibiotic used depends on the bacterium responsible for the infection. Antibiotic therapy is very effective, and if treatment begins in time, the risk of dying from bacterial meningitis today is less than 15 percent.

With bed rest, plenty of fluids, and medicine to reduce fever and control headache, most patients recover from viral meningitis within a week or two and suffer no lasting effects.


No specific treatment for viral meningitis exists at this time. Most patients completely recover on their own. Doctors often will recommend bed rest, plenty of fluids, and medicine to relieve fever and headache.

How is viral meningitis diagnosed?

Viral meningitis is usually diagnosed by laboratory tests of spinal fluid obtained with a spinal tap. The specific cause of viral meningitis can be determined by tests that identify the virus in specimens collected from the patient, but these tests are rarely done.


Meningitis is diagnosed by a lumbar puncture, or spinal tap, in which a doctor inserts a needle into the lower back to obtain a sample of CSF. The fluid is then tested for the presence of bacteria and other cells, as well as certain chemical changes that are characteristic of meningitis.

What causes viral meningitis?

Many different viruses can cause meningitis. About 90% of cases of viral meningitis are caused by members of a group of viruses known as enteroviruses, such as coxsackieviruses and echoviruses. These viruses are more common during summer and fall months. Herpesviruses and the mumps virus can also cause viral meningitis.


The most common causes of viral meningitis are coxsackie viruses and echoviruses, although herpesviruses, the mumps virus, and many other viruses can also cause the disease. Viral meningitis is rarely fatal, and most patients recover from the disease completely.


Most cases of bacterial meningitis are caused by one of three species of bacteria—Haemophilus influenzae, Streptococcus pneumoniae, and Neisseria meningitidis. Many other bacteria, including Escherichia coli and the bacteria that are responsible for tuberculosis and syphilis, can also cause the disease. Bacterial meningitis can be fatal if not treated promptly. Some children who survive the infection are left with permanent neurological impairments, such as hearing loss or learning disabilities.

Is viral meningitis a serious disease?

Viral ("aseptic") meningitis is serious but rarely fatal in persons with normal immune systems. Usually, the symptoms last from 7 to 10 days and the patient recovers completely. Bacterial meningitis, on the other hand, can be very serious and result in disability or death if not treated promptly. Often, the symptoms of viral meningitis and bacterial meningitis are the same. For this reason, if you think you or your child has meningitis, see your doctor as soon as possible.