Hantavirus pulmonary syndrome

Korean hemorrhagic fever, a problem during the Korean War. Named for the Hantaan River in South Korea, the virus infected 2,500 U.S. troops and killed between 5 and 10 percent of its victims. The related Seoul virus infects domestic rats, and causes a similar (but less deadly) type of fever. Because it is carried by rats, it is more common. Puumala virus affects the bank vole and is found most often in Scandinavia and western Europe.

Deer mice carry the United States strains.

hantavirus pulmonary syndrome A respiratory illness caused by a new strain of HANTAVIRUS (a group of viruses carried by rodents) that causes its victims to gasp for air as their lungs fill with fluid. It kills about half the people it infects, usually within a week. The syndrome was first diagnosed in this country in 1993 at a Navajo reservation in the Four Corners area of New Mexico, Colorado, Utah, and Arizona.

Hantaviruses can be found throughout the world, where more than 170 names have been given to the hantavirus infections, including the often-fatal hemorrhagic fever. Until 1993, hantaviruses had been linked to the development of hemorrhagic fever. But the strain that was discovered in Four Corners caused a new disease, with debilitating flulike symptoms and respiratory failure.

Today, the number of infections with the hantavirus in the United States is rising, reaching 131; almost half have been fatal, according to the Centers for Disease Control and Prevention. More than 50 of the 131 cases occurred before the Navajo reservation outbreak. Since the Navajo outbreak, more than 100 cases of hantavirus pulmonary syndrome have been reported in 21 states (including New York), with more than half of them fatal. In addition, seven cases have been diagnosed in Canada and four in Brazil.

Cause HPS is caused by a hantavirus first named Muerto Canyon (Valley of Death) virus for the spot on a New Mexico Navajo reservation where it was isolated. Because this name offended the Navajo, the virus was renamed SIN NOMBRE (or "no name") virus. The disease can be spread by several common rodent species (deer mice, white-footed mice, and cotton rats) and has been found in 23 states; it is most common in New Mexico, which has had 28 cases; in Arizona, with 21 cases; and in California, with 13 cases. Doctors believe victims become infected by breathing in the dried urine or feces of infected deer mice; about 30 percent of the deer mice in the Four Corners area carry the Sin Nombre agent. Infected rodents have been found in other parts of the country as well.

Oddly enough, some victims have contracted the illness after little or no contact with rodents. Studies have also shown that the virus does not trigger infection in everyone it infects. In fact, the CDC acknowledges that the link between rodents and victims is unclear. Scientists don't know why some people become infected and others don't.

Even more worrying, some people have exhibited symptoms of hantavirus pulmonary syndrome but don't have the virus. In fact, there were half a dozen recent incidents in California where young and healthy people died suddenly of acute respiratory failure, yet did not test positive for hantavirus or any other microbe.

Scientists believe the U.S. outbreak was triggered by climate irregularities associated with the most recent El Nino (the occasional warming of waters in the tropical Pacific). While it is believed that the mice who carry the virus were probably infected for years, the climate-induced explosion in the deer mouse population may have fueled the spread of the disease in humans.

In addition to contact with contaminated urine or droppings, people can become infected with the virus after being bitten by rodents. Many people who have developed the disease live in mice-infested homes. One woman who developed the disease was exposed to rodents her cat dragged into the house, and another died after cleaning a rodent-infested barn.

Researchers don't know why some people are susceptible to the infection while others are not. The hantavirus does not appear to be highly infectious, and it is almost always found in isolated cases. There were only four instances in which more than one case occurred at the same time and place.

Symptoms Hantavirus pulmonary syndrome begins as a flulike illness with fever and chills, muscle aches, and cough; it can be easily misdiagnosed as HEPATITIS or an inflamed pancreas. The virus goes on to damage the kidneys and lungs, causing an accumulation of fluid that can drown the victim. The disease is fatal in almost half of all cases.

Treatment There is no treatment approved specifically for hantavirus, but researchers are currently studying the effectiveness of the antiviral drug Virazole (ribavirin) for HPS.

Prevention Army scientists developed a vaccine against hantavirus infection in 1995. While it is experimental, it is available to protect military personnel in South Korea and other areas of the world where the infection is common, according to the army's Medical Research Institute of Infectious Diseases in Ft. Detrick, Maryland. Such a vaccine does not need the approval of the Food and Drug Administration to be used among military personnel, if they give informed consent.

The CDC cautions homeowners to be cautious around rodent excretion, even though hantavirus is a rare disease. People should assume that all rodent excretions are infected, and should handle the droppings only after spraying them with disinfectant and wearing gloves.

Haverhill fever A febrile disease transmitted by rat bite, first diagnosed in Haverhill, Massachusetts, in 1925.

Cause The disease is caused by the bacterium streptobacillus moniliformis. This spirochete-like bacterium is normally found in rat saliva.

Symptoms Within 10 days of a rat bite, the patient experiences fever, chills, vomiting, headache, muscle and joint pain, and a rash appears.

Diagnosis Lab analysis of blood or pus can reveal the bacteria that cause the disease.

Treatment Antibiotics are effective against Haverhill fever.

head lice See LICE.

hearing loss and infectious disease Hearing loss affects about three and a half percent of children up to age 17. Although ear infections are the most common cause of hearing loss in the United States, there are other infectious causes—many of which can be treated successfully. The most common of these are bacterial MENINGITIS and CYTOMEGALOVIRUS INFECTION, but there is a long list of other infectious agents—viruses, bacteria, and parasites—that can lead to hearing problems. Hearing loss can also be a side effect of antibiotics (such as the aminoglycosides).

Bacterial meningitis Hearing loss related to this disease can be caused by streptococcus pneumoniae (18 to 30 percent), Neisseria meningitidis (10 percent), and Haemophilus influenzae (6 percent). In pneumococcal meningitis, the incidence and severity of hearing loss is strongly linked to the length of time the disease lasts. Because of vaccination, H. influenzae is no longer a major cause of meningitis in the United States, although it remains a serious problem in other parts of the world.

The hearing loss with this disease is related either because of direct damage to the eighth cranial nerve (the hearing nerve) or to inflammation of the interior parts of the hearing mechanism itself.

Recent studies have shown that steroids can prevent hearing loss related to H. influenzae, but steroids do not help prevent hearing loss in meningitis caused by S. pneumoniae or N. meningitidis.

Syphilis Scientists have known for a long time that congenital syphilis is a cause of hearing loss, but only recently has it been understood that syphilis acquired at any time can lead to hearing problems. There are no controlled studies on treatment, but benzathine penicillin in combination with steroids offers the best hope for improvement.

Borrelia burgdorferi The agent that causes LYME DISEASE has been linked to hearing loss in about 2 percent of patients with the disease, usually involving low-frequency sound waves. The reason behind the deafness is not clear, but researchers suspect the loss occurs as a result of damage to the auditory center or the hearing nerve. Doxycycline or amoxicillin can be given to patients over age nine; younger children should receive amoxicillin or penicillin V. Those with hearing loss in the high frequencies are more likely to see improvement with antibiotic treatment.

Mycobacterium tuberculosis While it is uncommon to find TB infecting the middle ear, it may sometimes be the first symptom of the disease. Such infection causes multiple perforations of the eardrum and chronic ear inflammation Anti-TB drugs should be given to treat this condition.

Cytomegalovirus Of all children born with CMV, 95 percent do not show any symptoms. Among those who do, 60 percent will develop hearing loss. Those who don't have the symptoms rarely develop neurologic problems, but 10 percent of these infants remain at risk for hearing loss. Each year in the United States, about 4,000 children acquire hearing loss linked to CMV. It is suggested that the virus may interfere with the fetal development of the ear. The hearing loss usually centers in the high-frequency sounds, with equal loss in both ears. There is no known treatment.

Measles About 1 in every 1,000 cases of measles leads to hearing loss. Sensorineural hearing loss associated with measles is usually sudden and occurs in both ears, primarily of the higher frequencies; there may also be vertigo and ringing in the ears. This hearing loss tends to be permanent.

Mumps Hearing loss as a result of mumps occurs in about 5 of every 10,000 cases; there have been a few cases in the United States since vaccination was introduced in 1967. While scientists don't fully understand the link between mumps and deafness, they suspect the virus may cause the atrophy of the organ of Corti (part of the hearing mechanism) as well as a loss of hair cells within the hearing mechanism.

The onset of hearing loss is quick and occurs in only one ear in 80 percent of the cases; the deafness is usually profound and permanent and usually occurs in the higher frequencies. There may also be ringing of the ears, sensation of fullness in the ear, vertigo, nausea, and vomiting.

Rubella In the United States, rubella among pregnant women is rare; when it does occur it often leads to deafness (between 25 percent and 51 percent of the time). Hearing loss related to rubella is profound in 55 percent of the cases; severe in 30 percent; and mild to moderate in 15 percent. The hearing loss affects all frequencies, but the middle frequencies cause the most problems.

Recent research suggests that congenital rubella is progressive and continues to damage the ears even after infancy.

Varicella-zoster Infection with this virus can lead to a syndrome involving facial palsy, herpes of the ear, and hearing loss, first described in 1907. This Ramsay-Hunt syndrome (also called herpes zoster oticus) can produce several patterns of hearing loss, together with ringing of the ears in 48 percent of cases. A patient who also experiences vertigo is not likely to recover from the hearing loss. Prompt treatment with acyclovir seems to be effective.

HIV Studies have reported up to 49 percent of HIV-infected patients have some degree of sensorineural hearing loss, as a possible result of infection of the cochlea, hearing center in the brain, or both. Patients with HIV-associated hearing loss also may experience vertigo and facial nerve palsy. Drug treatment does not seem to affect the hearing loss.

Fungal infections Fungal infections of the ear can cause either a conductive or sensorineural hearing loss. The most common organisms responsible for the loss include the Candida and Aspergillus species. Among those with impaired immune systems, Cryptococcus neoformans and Zygomycetes are a particular problem. A variety of antifungal drugs can be used to treat the problem, but there are no studies that prove their efficacy.

Toxoplasma gondii Congenital infection with this organism has been related to hearing loss, although the reason behind the problem is not well understood. Treatment with pyrimethamine, sulfadiazine, or spiramycin is effective.

Visceral leishmaniasis While this is not common in the United States, it is endemic in many other areas of the world, where it causes a type of hearing loss, probably by affecting the covering (myelin) of the hearing nerve. Treatment with stibogluconate sodium is effective and can frequently cure the hearing loss.

Flukes Infestation with the intestinal FLUKE Fasciola hepatica can produce hearing loss. While rarely seen in the United States, it is more common in Latin America, Asia, and Africa. A patient is infected by eating raw aquatic plants contained with the flukes. Bithionol is the treatment of choice.

Helicobacter pylori The bacterium that may cause most stomach ulcers and almost all duodenal ulcers and one of the most common chronic infections in humans. The bacteria infect people around the world, ranging up to 40 percent in developed countries and up to 80 percent in developing countries.

Since the 1950s doctors knew that family members of ulcer patients were three times more likely than the general population to have ulcers as well. But the link wasn't firmly established until 1983, when Australian gas-troenterologist Barry J. Marshall identified the bacterium in stomach tissue of ulcer patients, when it was first called Campylobacter pylori. In an attempt to prove the link between bacteria and ulcers, he swallowed the bacteria and developed an ulcer. Before that time, physicians had believed that ulcers were a noninfectious disease.

In 1994, a conference sponsored by the National Institutes of Health declared that ulcer is an infectious disease and recommended that doctors stop treating symptoms with antacids and, instead, utilize antibiotics to cure the infection.

Ulcers are found in 1 out of every 10 Americans, and H. pylori is implicated in 90 percent of those cases. Virtually everyone with the bacteria has chronic gastritis (a mild inflammation of the stomach lining).

Cause Despite that the human stomach is filled with acids, this bacterium manages to thrive there. The bacteria can survive the hostile environment of the stomach by nestling into the stomach's mucous lining. How the bacteria spread is unclear, but groups living in close quarters are particularly vulnerable.

Studies suggest the bacteria are passed via person-to-person contact but are probably not sexually transmitted. If one family member is infected, it is likely that the rest of the family also harbor the bacteria. It is also common in areas of poor sanitation and crowded living conditions and in families with multiple children (especially where children share beds). Scientists suspect the infection may be spread by swallowing infected food or water in addition to person-to-person contact. H. pylori is not naturally found in animals.

Symptoms Following infection, patients experience nausea and stomach pain, vomiting and fever, which lasts between 3 and 14 days. If not treated, patients will develop chronic gastritis that can last for decades. While half the world's populations are believed to be infected (including an estimated 40 million Americans), for some reason it only causes ulcers in between 10 to 20 percent of its hosts. It does not always cause ulcers to form, but it almost always produces inflammation of the stomach lining. Some people with the infection don't have ulcers but do experience nausea, gas, bloating, and burning stomach pain. These symptoms occur twice as often in people with H. pylori compared to those without the bacteria.

Diagnosis Blood tests can determine the presence of antibodies to the bacteria. This test tells if a patient has ever had the infection, but can't determine if the infection is active. It is not 100 percent accurate, however. A punch biopsy of the stomach can be examined under a microscope for the presence of H. pylori.

The newest diagnostic method, breath tests that can detect the bacteria, were cleared for marketing in the fall of 1996 by the U.S. Food and Drug Administration. The simple new breath test—the first of its kind cleared by the FDA—is as good as biopsy in detecting the bacterium and can be administered in a doctor's office. In the 30-minute test, the patient drinks a new, nonradioactive diagnostic drug solution, then exhales into a collection kit. The solution contains the drug Pranactin, which determines the presence or absence of active H. pylori. The kit is then sent to the manufacturer, Meretek Diagnostics, Inc., in Nashville, Tennessee. Results are available within two days. In studies of 499 U.S. and Canadian patients with duodenal ulcer, the breath test detected the bacteria 95 percent of the time.

Treatment About 90 percent of H. pylori infections can be cured with a combination of anti-ulcer medication and specific antibiotics (Pepto Bismol, Biaxin, metronidazole, clarithromycin and omeprazole, tetracycline, or amoxicillin). Because the treatment may not be completely successful, follow-up testing at least four weeks after completing treatment may be needed to make sure the bacteria are no longer present. If tests reveal no bacteria, the patient is not likely to be reinfected ever again. Persistent infection may require a different medication for longer period of time.

The National Institutes of Health has recommended that all patients with stomach or duodenal ulcers who also have H. pylori be treated for both the ulcer and the infection. While there appears to be a relationship between the bacteria and stomach cancer, these cancers are becoming less common in the United States, and therapy for H. pylori has not been recommended as a preventive measure.

There is no solid evidence that diet affects H. pylori or ulcer healing. With proper medical treatment, ulcers heal as well on a regular diet as with a bland diet. Still, it is wise to avoid smoking, nonsteroidal antiinflammatory drugs (NSAIDs), aspirin, excessive alcohol, and caffeine.

Complications The organism has also been found in a disproportionately large number of patients with certain kinds of stomach cancer. Some scientists suggest the infection may triple the risk of this rare cancer.

Prevention In 1996, the National Institutes of Health has urged U.S. doctors to test all ulcer patients for the bacterium and to treat the infected with antibiotics for two weeks. However, the treatment is not easy; it involves taking 12 to 16 pills for two weeks and carries the risk of some side effects, such as fatigue and dizziness.

Careful personal hygiene (thorough handwashing, using separate personal items such as glasses and toothbrushes) is probably the best way to prevent person-to-person spread.

Since scientists have succeeded in immunizing mice, a human vaccine may be developed in the future.

For more information about Helicobacter pylori, contact the International Research Foundation for Helicobacter and Intestinal Immunology, P.O. Box 7965, Charlottesville, VA 22906.

helminth A suffix meaning "worm."

helminthiasis An infestation by any species of parasitic worms. Ascariasis, FILARIASIS, HOOKWORM DISEASE, and TRICHINOSIS are all common types of worm disease.

hemolytic uremic syndrome (HUS) This serious disorder—once considered to be a rare form of kidney disease—has in recent years become more common as a complication of food-borne infection of ESCHERICHIA COLI 0157:H7, characterized by the destruction of red blood cells and failing kidneys.

Between 2 and 7 percent of ESCHERICHIA COLI 0157:H7 infections lead to this complication in certain high-risk people (such as the very young or old). In the United States, HUS is the main cause of kidney failure in children. Most cases are caused by infection with this type of E. coli.

Symptoms As the bacteria enter the kidneys, causing bleeding and destroying red blood cells, the victim becomes pale and tired, with a fever and rising blood pressure. The kidneys shut down and urine is no longer produced.

Treatment This is a life-threatening condition that must be treated in a hospital intensive care unit, where the patient receives blood transfusions and is placed on kidney dialysis to maintain life until the organs recover. Most patients do recover at this point, but a small percentage (about 15 percent) do not, and require permanent dialysis or a kidney transplant.

Prognosis With intensive care, the death rate from this syndrome is still between 3 and

5 percent. One third of the survivors will have abnormal kidney function years later and a few need long-term dialysis. Another 8 percent suffer with other complications, including high blood pressure, seizures, blindness, and paralysis, for the rest of their lives. See also ESCHERICHIA COLL

hepatitis The description for any inflammation of the liver. It is generally caused by a virus, but alcoholism or certain drugs can also damage the liver and lead to hepatitis. When the liver is damaged, it can't excrete the blood breakdown substance called bilirubin, which then builds up in the blood. This causes a yellow tinge to skin and eyes (called jaundice). The appearance of jaundice is more or less a warning sign that the liver is no longer able to cleanse the blood. In severe cases of hepatitis, the liver fails altogether, resulting in death unless a liver transplant is done.

Hippocrates was the first to mention epidemics of jaundice, and the disease went on to become a factor in many large military campaigns. During the Civil War, for example, hepatitis struck more than 70,000 soldiers. By the time World War II began, scientists were able to differentiate between two types of hepatitis—"infectious" hepatitis, spread by contaminated food or water, and "serum," spread by infected blood.

By the 1960s, scientists were beginning to learn that the disease was caused by specific unrelated viruses and gave them alphabetical names to distinguish them. The alphabet of hepatitis viruses all belong to different genuses. An international team has reported finding a hepatitis F virus recently, although others have not yet confirmed the finding. Now, a cluster of viruses dubbed HEPATITIS G has recently been found.

The various hepatitis viruses differ in their likelihood of producing chronic infection. Almost everyone, for example, who is infected with HEPATITIS C becomes a carrier of the virus. HEPATITIS A causes only temporary liver damage, which is reversed as the body produces antibodies. HEPATITIS B or HEPATITIS C, however, can cause long-term complications. Delta, or D, virus, is always a coinfec-tion with hepatitis B; HEPATITIS E does not occur in North America. Although the viruses are unrelated to each other, they act in similar ways, attacking and damaging only the liver.

For some reason, hepatitis B and C may quickly develop into fulminant hepatitis, in which the liver cells are completely destroyed. As the liver function stops, toxic substances build up and affect the brain, causing lethargy, confusion, combativeness, stupor, and coma. This can often lead to death, although with aggressive treatment the patient may live. If the victim does not die, the liver is often able to regenerate and resume function, and the brain recovers.

hepatitis A The most common and least dangerous type of hepatitis, this is the first virus that scientists were able to identify. A food-borne virus, it looks much like a poliovirus with just one bare strand of RNA within a 20-sided shell that can replicate only in the liver. It infects only humans and a few primates, primarily via contaminated feces. Formerly known as "infectious hepatitis," hepatitis A is fairly common; in 1994, 22,000 Americans were reported to have hepatitis A, but thousands of cases go unreported; about 100 people die each year.

While there is not a typical "season" for hepatitis A, it occurs in cycles. In the United States, cases peaked from 1961 to 1971, declined, and then peaked again from 1983 to 1991; numbers dropped again after 1992. Foods have been implicated in more than 30 outbreaks since 1983. The most recent include imported lettuce in Louisville in 1987; ice-slush beverages in Alaska, restaurant iced-tea in North Carolina, and raw oysters in Florida—all during 1988; unidentified food in a Washington restaurant chain in 1989; north

Georgia frozen strawberries, Montana frozen strawberries, and Baltimore shellfish—all in 1990.

The illness is a disease of filth and occurs most often among school-age children and young adults. In overcrowded areas in developed countries and many developing countries, it is so common that 90 percent or more of 10 year olds are healthy carriers and immune as adults. It is estimated that 40 percent of healthy adults in the United States are immune to hepatitis A as a result of previous infection and have lifelong immunity.

The virus dates from 400 B.C., when it afflicted armies in every war; it is believed to have played a role in Napoleon's defeat.

Other former names for hepatitis A include epidemic hepatitis, epidemic jaundice, catarrhal jaundice, infectious icterus, Botkins disease, and MS-1 hepatitis.

Cause Hepatitis A belongs to the ENTEROVIRUS GROUP of the picornaviruses, which include poliovirus, COXSACKIEVIRUS, ECHOVIRUS, and RHINOVIRUS. Hepatitis A is spread by eating food or drinking water contaminated with the hepatitis A virus (HAV), which is shed in the stool.

The virus enters through the mouth, multiplies in the body, and is passed in the feces; it can then be carried on an infected person's hands and spread by direct contact, or by eating food or drink handled by that person. Anyone can get hepatitis A, but it occurs most often among children. Most people get it either from close personal contact between family members, sex partners (especially homosexual men), and in nursery schools or child care centers.

The virus is hardy and spread easily. Unlike many other viruses, it can live for more than a month at room temperature on kitchen countertops, children's toys, and other surfaces. It can be maintained indefinitely in frozen foods and ice. To inactivate the virus, food must be heated at 185 degrees F for one minute.

A food handler with hepatitis A can spread the disease if he or she touches food that isn't cooked before it is eaten (usually sandwiches or salads). Well water contaminated by improperly treated sewage has also been implicated, since hepatitis A can live for a long time in water. It is difficult to test water for hepatitis A. People who drink treated municipal or county water supplies are not at risk.

It's possible to get hepatitis A from eating raw or undercooked foods, such as shellfish (especially oysters). When they eat, shellfish filter large amounts of water and if it is contaminated with hepatitis A, it will be concentrated in the shellfish. In Florida in 1988, 61 people caught hepatitis A after eating raw oysters illegally taken from contaminated waters. Even though federal regulations and posting of contaminated waters offer some protection, there is still a risk of contracting viruses when eating raw shellfish. In 1990, an infected Missouri dish washer who prepared lettuce infected 110 people who had eaten at the restaurant; two died.

Symptoms One quarter of all people with hepatitis A won't have any symptoms. Infants and young children tend to have very mild cases; three quarters of children have no symptoms and the rest have low fever and achiness, but rarely jaundice. However, children do serve as the primary source of contagion for adults.

The disease in older patients can be more serious, characterized by fever (100 to 104 degrees F), extreme tiredness, weakness, nausea, stomach upset, pain in the upper right side of the stomach, and loss of appetite. Within a few days, a yellowish tinge appears in the skin and the whites of the eyes. Urine will be darker than usual, and the stool is light colored. Anyone over age 12 may become quite sick for a week or two. Once the jaundice appears, patients begin to feel better. The disease is rarely fatal, and most people recover in a few weeks without any complications.

The incubation period ranges from 15 to 50 days. Patients are most infectious in the two weeks before symptoms develop. Food handlers who know they are infected should not work until they are past the infectious stages, which ends one week after first becoming jaundiced.

Diagnosis Blood tests showing antibodies to hepatitis A are the best diagnosis. Symptoms of hepatitis A are so similar to other diseases that a doctor needs a test to make the correct diagnosis.

Treatment There is no drug treatment for hepatitis A. While symptoms appear, patients should rest and eat well—low-fat, high-carbo-hydrate, easily digested foods in small amounts are good choices. These could include crackers, noodles, rice, or soup. Antinausea medicine can be prescribed for severe nausea. Headaches or body aches may respond to acetaminophen. Normal activities may be resumed when the acute illness is over.

Complications Very rarely, hepatitis A can also develop into fulminant hepatitis in which the liver cells are completely destroyed. As the liver function stops, toxic substances build up and affect the brain, causing lethargy, confusion, combativeness, stupor, and coma. This can often lead to death, although the patient may live with aggressive treatment. If the victim does not die, the liver is able to regenerate and resume function, and the brain recovers.

Prevention A new vaccine said to be 100 percent effective after a single primary dose became available in 1996 in the United States. In earlier vaccines, more than 99 percent of people in the vaccine studies became immune after two doses; a booster is recommended for this vaccine between 6 and 12 months after the first dose.

In addition, workers in child care centers where there are diapered children must maintain strict rules about frequent hand washing and procedures for diaper changing.

Cooking tainted food kills the virus. Shellfish from contaminated areas must be cooked (boiled) for at least eight minutes to be considered safe for eating.

Those who are exposed to hepatitis A can prevent infection by getting a shot of immune globulin (IG), which is pooled human blood plasma that contains protective antibodies against the disease. People who need a shot of IG include the following:

• all household members and sex partners of hepatitis A patients

• close friends of an infected school-age child

• restaurant staffers where one food handler has hepatitis A; patrons of the restaurant need IG within two weeks of exposure only if the infected food handler handles uncooked food and has poor hygienic practices, or has diarrhea

• staff and residents of prisons, institutions, homes, when two or more residents have hepatitis A

• all staff in child care centers or homes where one ore more children or employees have hepatitis A; if three or more children or their families have hepatitis A, family members of the other children need IG as well

• unimmunized travelers to developing countries hepatitis B Formerly known as serum hepatitis, this is the most common preventable infectious disease in the United States. The virus, which is far more complex than HEPATITIS A, can destroy the liver and is 100 times more transmissible than the AIDS virus. It is believed that there are 300,000 cases a year in the United States, of which only about 15,000 are reported; about 1.25 million Americans are carriers, which means they are infectious for all their lives.

Almost 6,000 Americans each year die from acute hepatitis B or complications of the infection; around the world, the fatality rate is 2 million per year. It can be prevented by vac cine, but of the group who accounts for most infections—those aged 15 to 39—only about 5 percent ever get vaccinated.

Cause The hepatitis B virus (HBV) is carried in the blood and is also found in saliva, semen, and other bodily fluids. It is transmitted much the same as the AIDS virus, but hepatitis B is even easier to catch: One drop of blood infected with hepatitis B contains millions of viral particles. Still, hepatitis B is not spread by casual contact. The virus must get into a person's blood to cause infection; it enters the blood via sexual contact, blood transfusions, dirty needles, or by sharing toothbrushes, razors, or utensils. Unfortunately, the virus is very stable and can survive on dried surfaces (even thorns or stones) for days. More than half of all cases are linked to sexual intercourse with infected partners.

Many health care workers have become infected from needle sticks, lab accidents, or splashing blood; dentists have caught the infection from patients and gone on to infect other patients. A health care worker with a needle stick from a patient with hepatitis B has between a 6 percent and 30 percent chance of becoming infected. By comparison, the chance of contracting AIDS this way is only about 0.5 percent.

It is possible for infected mothers to pass the virus to their babies during the final three months of pregnancy, during delivery, or during nursing. There is less danger of passing on the infection if the mother contracts the disease in the early stages of pregnancy. All pregnant women should be tested for hepatitis B.

Many millions of people around the world are chronically infected with hepatitis B, and can give the virus to others (unlike those who have had hepatitis A). Because the germ can induce liver cancer, it is believed to be the world's most common viral cause of cancer.

Symptoms It can take up to six months after exposure before symptoms of hepatitis B

appear, as compared to only six weeks for hepatitis A. Many people have few symptoms. If they do appear, they appear gradually and include tiredness, nausea, joint and muscle aches, mild abdominal pain in upper right side, poor appetite, hives or rash, and mild diarrhea for three to ten days. This may be followed by jaundice in about half of those who become infected. Nausea is usually not associated with hepatitis B (it is more common with hepatitis A). Other symptoms may include light-colored stools, dark urine, and itchy skin. After jaundice appears, symptoms may improve. Infants infected by their mothers may have no symptoms at first, but they are at high risk for developing cirrhosis and liver cancer in the second decade of life.

In about one third of cases, people aren't terribly sick; another third have no symptoms at all. In fact, the chance of becoming a carrier are greater if the symptoms don't develop. About 25 percent of carriers do suffer chronic symptoms and are at greatest risk of developing cirrhosis. A few may be quite ill for several weeks. Those over age 40 may be more severely ill; children have few symptoms.

The virus can be found in blood and body fluids several weeks before symptoms appear and several months after. The appearance of certain antibodies indicate resolution of disease. People who are chronic carriers (about 10 percent of those infected) are always infectious, although they do not appear to be ill. Those who recover are immune for life.

Diagnosis Hepatitis B can be diagnosed by blood tests; other tests (that look for markers) can differentiate hepatitis B from other types of hepatitis. Liver function tests can measure enzymes produced by the liver that will be elevated in all forms of hepatitis.

Treatment Chronic active hepatitis B is treated with alpha-interferons. Many people report short-term side effects from interferon, such as fever, chills, appetite loss, vomiting, muscle aches, and sleep problems that disappear after a few weeks.

For acute hepatitis, there is no treatment beyond bed rest and a high carbohydrate, low-fat diet. After recovery, patients need a blood test to see if they have retained the E antigen. Those who do are extremely infectious and are at higher risk of developing complications. About 10 percent of these chronic carriers lose the antigen each year. A high percentage of patients go on to develop chronic hepatitis, leading to chronically poor liver function.

Complications Most people recover from the infection entirely and are not at risk for long-term complications. On the other hand, babies, children, and the 5 percent of adult carriers are of more concern.

Between 10 and 85 percent of babies born to infected mothers will develop hepatitis themselves; of those, 90 percent develop chronic hepatitis, at high risk for eventually developing cirrhosis or liver cancer as adults. Twenty-five percent of them will die of liver disease as adults.

Prevention While hepatitis B is com--pletely preventable, thousands continue to come down with the disease each year. The vaccine introduced in 1983 was made from blood plasma; a few years later a vaccine from synthetic products was introduced; a third synthetic vaccine was produced in 1991. The last two vaccines are given in three doses. Anyone at risk for the disease, including all medical and nursing personnel, should have the vaccine. As of November 1991, the vaccine was recommended for all infants; boosters are not currently recommended.

Unlike some vaccines, there is no apparent risk of serious side effects from the hepatitis B vaccine. If any, reactions seem to be limited to a sore arm at the site of injection or a slight fever.

Those who are not immunized but have been exposed may receive immune globulin HBIG for 90 percent protection if they receive the dose within seven days of exposure and begin the hepatitis B vaccine series at the same time.

Babies born to infected mothers receive HBIG within 12 hours after birth. The vaccine series must be started at the same time.

Carriers should follow standard hygienic procedures to make sure their close contacts are not directly contaminated. Carriers must not share razors, toothbrushes, or any other object that may become contaminated with blood. In addition, household members (especially sexual partners) should be immunized with hepatitis B vaccine. It is important for carriers to inform their dentist and health care providers of their status.

hepatitis C A mysterious blood-borne type of hepatitis that can live quietly in the body for years, hepatitis C was identified in 1988 and called non-A, non-B hepatitis.

Until the virus starts to attack the liver, most people don't know they are infected. Many don't know how they got the disease, and even after it is diagnosed, virtually nothing will get rid of it. The disease can be far more deadly than its cousins hepatitis A and B, both of which can be avoided with a vaccine.

In the United States, hepatitis C virus is linked to 20 percent of all clinical hepatitis cases and is the leading cause of chronic hepatitis. It is also the number-one reason for liver transplants in this country. Hepatitis C can lead to liver cancer, killing up to 10,000 Americans a year and causing almost half of all deaths from liver failure, according to the National Center for Infectious Diseases. Mickey Mantle had hepatitis C, as well as liver cancer and liver damage from excessive drinking.

Not everyone with hepatitis C will get sick; however, about a third of those with chronic hepatitis C will develop either cirrhosis or cancer of the liver. More than half of all patients exposed to the virus become carriers, and up to 20 percent of these carriers develop cirrhosis (a severe liver disease).

While the actual number of patients is not known, it is believed to be the most common form of viral hepatitis in the United States and may affect as many as 4 million Americans (1 out of every 60 people). The Centers for Disease Control estimates that 150,000 Americans are newly infected each year; long-term liver damage in chronic patients kills between 8,000 to 10,000 Americans a year.

The number of newly diagnosed patients (those who were infected years ago and are just now being diagnosed) is clearly rising, especially among baby boomers who were IV-drug abusers. Intravenous-drug users make up about 30 percent of the HCV-infected population; experts believe that almost all such users are ultimately infected by the lethal virus.

Cause Hepatitis C is spread primarily through blood-related sources, such as IV-drug use, transfusions, and kidney dialysis. It is the cause of most cases of post-transfusion hepatitis. The risk of sexual transmission appears to be small. There is no evidence that this type of hepatitis can be spread by casual contact, by eating tainted food, or by coughing or sneezing. In rare cases, an infected mother can pass the disease to a newborn. Some people carry the virus in their bloodstream and may remain contagious for years.

Before 1989, the infection was spread through transfusions; about 300,000 patients may have contracted the disease this way, before the nation's blood banks began testing for the virus in 1990.

Oddly enough, in about half of cases the patients have done nothing that would put themselves at risk, and the source of the infection cannot be identified.

The virus is related to the YELLOW FEVER virus.

Symptoms About 25 percent of those infected with the virus will become sick with symptoms, including appetite loss, fatigue, nausea and vomiting, stomach pain, and jaundice within two weeks to six months after exposure. Usually, symptoms appear by two months. Fifty percent of these patients may go on to develop chronic liver disease.

Diagnosis People who have no symptoms usually find out they have hepatitis C when they give blood or get a liver function test when applying for life insurance. Many patients are model citizens who had experimented with heroin in the 1960s and 1970s. A variety of liver function tests, plus liver biopsy, can detect the disease.

Treatment There is no known cure for hepatitis C, but the FDA has approved a drug called recombinant alpha-interferon for treating those with chronic hepatitis C. Alpha-inter-feron eliminates the virus for between 10 and 25 percent of patients. The drug can temporarily reduce the virus levels in about 50 percent, but these patients then experience relapse. Combining interferon with the antiviral drug ribavirin may improve response to treatment.

However, alpha-interferon has serious side effects. It causes flulike symptoms and makes many patients feel depressed. It is also expensive, costing about $6,000 per year.

Research published in October 1996 identified the structure of a protein that the virus needs to reproduce; scientists hope they may be able to design a drug that can disable the protein, rendering the virus unable to destroy liver cells.

Prevention At the present time, there is no hepatitis C vaccine. Hope for such a vaccine faded, according to the National Institute of Allergy and Infectious Diseases, when their studies showed that exposure to the virus does not protect against reinfection.

Since 1990, U.S. blood donation centers have routinely used a blood-donor-screening test for hepatitis C. Widespread use of this test has significantly reduced the number of transfusion-associated cases of hepatitis C. People who have had hepatitis C should understand that their blood and possibly other body fluids are potential sources of infection. They should avoid sharing toothbrushes, razors, needles, and the like.

In addition, infected patients should not donate blood and should inform health care workers. Limits on sexual activity with steady partners may not be needed; however, those with acute illness and multiple sex partners may be at higher risk and should use condoms to reduce the risk of acquiring or transmitting hepatitis C as well as other infections.

hepatitis D An uncommon version of the hepatitis virus in the United States, HDV infects about 15 million people around the world. Because the virus requires the presence of HEPATITIS B virus (HBV) to produce infection, the frequency of hepatitis D closely parallels HBV. In southern Italy, parts of Russia, and Romania, more than 20 percent of HBV carriers with no symptoms and more than 60 percent of those with chronic liver disease due to HBV are also infected with hepatitis D.

Cause The major way hepatitis D is spread is through contaminated needles (primarily IV-drug abuse and exposure to blood products). Sexual transmission of hepatitis D is less efficient than for hepatitis B, but non-IV-drug-using male homosexuals, female prostitutes, and institutionalized mentally retarded people are at higher risk for developing hepatitis D.

Transmission from mother to child has not been documented in the United States.

Symptoms Hepatitis D can't be distinguished from other causes of hepatitis. The development of a new episode of acute hepatitis in a patient with known chronic hepatitis B infection should prompt a search for evidence of a new hepatitis D infection.

Diagnosis In patients with acute hepatitis D infection, anti-HDV antibody may be detected. The disease can be diagnosed by detecting HDV antigen in liver biopsies or antibodies in blood.

Treatment There is no reliable treatment for hepatitis D.

Prevention The hepatitis B vaccine can prevent hepatitis D, since hepatitis B infection is required for hepatitis D infection to occur.

hepatitis E A form of hepatitis that is clinically indistinguishable from HEPATITIS A disease and that occurs primarily in underdeveloped countries. The disease exists in both epidemic and sporadic forms and is usually associated with contaminated drinking water. Major waterborne epidemics have occurred in Asia, North Africa, and East Africa. To date, no U.S. outbreaks have been reported, although imported cases were identified in Los Angeles in 1987. There is no evidence for immunity against this virus in the American population, so in theory it could become a problem in this country.

The disease is most often seen in young to middle-aged adults between ages of 15 and 40. Pregnant women appear to be extremely susceptible to severe disease, and high rates of death have been reported in this group.

Also known as enterically transmitted non-A, non-B hepatitis (ET-NANBH), it is also called fecal-oral non-A, non-B hepatitis or A-like non-A non-B hepatitis. It should not be confused with HEPATITIS C, also called par-enterally transmitted non-A non-B (PT-NANBH) or B-like non-A non-B hepatitis.

Major outbreaks have occurred in India (1955 and 1975-76), the USSR (1955-56), Nepal (1973), Burma (1976-77), Algeria (1980-81), the Ivory Cost (1983-84), in refugee camps in Eastern Sudan and Somalia (1985-86), and most recently in Borneo (1987).

Cause The hepatitis E virus is transmitted by the fecal-oral route. The virus has been transmitted via water and person-to-person; the potential exists for transmission via contaminated food.

Symptoms Between two to nine weeks after infection, symptoms of malaise, anorexia, abdominal pain, and fever appear. The disease is usually mild and fades away within two weeks. The fatality rate is very low; less than one percent of nonpregnant patients progress to fatal fulminant hepatitis, but in pregnant women the fatality rate rises to 20 percent.

Diagnosis Symptoms and epidemiological characteristics of the disease, and by excluding hepatitis A and B by blood tests. Confirmation requires identification of certain viruslike particles by immune electron microscope in the feces of acutely ill patients.

Treatment No antiviral treatment has been proven effective against hepatitis E, although preliminary studies suggest ribavirin and alpha-interferon may work.

Prevention Good sanitation and personal hygiene are the best preventive measures. There is no current vaccine, and it is not yet clear whether infection with hepatitis E confers lifelong immunity. Several recombinant HEV vaccines are being tested, but none are currently available for commercial use.

hepatitis F The HFV has been described in France in a handful of cases, and scientists have succeeded in transmitting the infection to primates. There is very little else known about this virus.

hepatitis G One of the "alphabet" hepatitis viruses, hepatitis G was first identified in 1996. It apparently causes a mild acute hepatitis but is not a clinically significant chronic disease. However, the precise effects on the liver and an individual's health over time remain unknown. Very similar to hepatitis C, hepatitis G is also called hepatitis GB virus C or HGBV-C; hepatitis G is a flavivirus. Coin-fection with hepatitis B or C—or both—is common. However, hepatitis G infection doesn't seem to worsen coinfection with hepatitis B or C.

Hepatitis G has at least five subtypes, depending on the part of the country where it occurs. It appears to be primarily a monkey virus that was transferred from one monkey to another until it infected humans via conta-

minated blood. Researchers have found the virus in blood in the United States, Canada, Peru, Egypt, West Africa, and Europe. About 1.5 percent of Japanese hepatitis patients who don't have the A through E varieties are infected with the G virus. About 18 percent of similar West African patients have the same virus in their blood.

Healthy people in the United States may carry the G virus since research suggests it was present in the nation's blood supply 25 years ago. And experts suggests that between 1 and 2 percent of the nation's blood donors have a previously undetected hepatitis G infection— higher than the rate for either hepatitis B or C.

Cause In 0.3 percent of cases of community-acquired acute viral hepatitis, hepatitis G is the only identified virus. This strain of viral hepatitis was previously thought to be transmitted only through infected blood; now it is known to be transmitted sexually as well. Researchers in Sweden and Honduras found a surprisingly high rate of infection with the virus in healthy individuals without known risk factors (such as injection drug use and treatment for hemophilia). It was the high rates of infection in homosexual men and in healthy volunteers that led the authors to question the possibility of transmission via sexual contacts. It is known that HGV can be transmitted from an infected mother to her infant during childbirth, but now they believe HGV might be transmitted by "other routes yet to be defined."

There is an increased prevalence of hepatitis G genetic material among groups with frequent exposure to blood or blood products (such as people with hemophilia, patients on hemodialysis, and injection drug users). Other modes of transmission are possible but have not been well documented.

About 10 percent to 20 percent of cases of community-acquired hepatitis and transfusion-associated hepatitis are not associated with the known major hepatitis viruses (A, B, C, D, or E). The fairly recent identification from patients with hepatitis G, which is about 25 percent identical to the hepatitis C virus, has implicated it as a cause of non-A-E hepatitis.

Symptoms After a brief attack, the virus may remain in the body for years, scientists speculate. They believe the virus may replicate in the liver for years, eventually revealing liver damage. Japanese studies suggest that some hepatitis patients whose liver failed were indeed infected with hepatitis G.

Diagnosis At this time, HGV infection can be identified only through special liver function tests that indicate current infection. An antibody test for HGV is under development and, when available, should explain the origins of infection more fully than HGV RNA testing can.

It appears that once antibodies are found, the virus is usually no longer present in the blood.

Prognosis The nature and frequency of HGV infection are unclear; there is also uncertainty about risk factors and means of prevention. Although caution and vigilance must be maintained, there is a growing consensus that HGV is "a virus looking for a disease" and may in fact prove not to be a cause of viral hepatitis. Acute HGV infection is generally reported to be clinically and biochemically mild and transient. Although the viral genetic material can be detected for years after infection in perhaps a minority of people who have been infected, there is no compelling evidence that HGV infection can lead to serious consequences. However, the role of HGV in a more virulent form of hepatitis (fulminant hepatitis) is unknown.

Treatment There is no proven treatment for HGV infection; at this point, guidelines for its investigation and management cannot be developed.

Prevention Blood banks don't have a way to screen for hepatitis G. The threat that HGV may pose to the nation's blood supply is an important issue. Some healthy blood donors may have hepatitis G, and transmission through transfusion has been documented. However, there is no commercial test available for screening; antibody testing, when it becomes available, may not be of particular value because it will not identify current infection. Donors already infected with hepatitis B or C will largely be excluded already; and the hepatitis G infection seems largely benign.

herpes Any of a variety of inflammatory skin diseases characterized by spreading or creeping small clustered blisters caused by the herpes simplex virus. Forms of the virus cause COLD SORES and the sexually transmitted disease genital herpes (see HERPES, GENITAL), characterized by blisters on the sex organs. The virus also causes many other conditions affecting the skin.

There are two forms of the herpes simplex virus—type 1 and type 2. Herpes simplex, type 1 (HSV1) is usually associated with infections of the lips, mouth, and face, whereas herpes simplex, type 2 (HSV2) is usually associated with infections of the genitals and in babies, who acquire the disease duriiig birth.

However, there is a certain amount of overlap between the two, and conditions usually caused by HSV2 may be caused by HSV1, and vice versa. Both types are highly infectious, spread by direct contact with the lesions or by the fluid inside the blisters.

Most people have been infected with HSV by the time they reach adulthood. While the first infection with this virus may cause no symptoms at all, there may be a flulike illness in addition to ulcers on the skin around the mouth; afterward, the virus remains in the nerve cells of the face. Many people experience recurrent reactivations of the virus, suffering with repeated attacks of cold sores, especially during a fever or prolonged sun exposure.

Sometimes the virus infects the finger, causing painful blisters called herpes whitlow. In patients with a preexisting skin condi tion (such as dermatitis), the virus may cause an extensive rash of blisters called ECZEMA HERPETICUM.

A person suffering an immunodeficiency disorder (such as AIDS) or someone taking immunosuppressant drugs who is exposed to the virus may experience a severe generalized infection that can be fatal.

A close cousin of the herpes simplex virus, the VARICELLA-ZOSTER VIRUS, is responsible for two other skin blistering disorders—CHICKEN POX and SHINGLES (herpes zoster). Like the herpes simplex virus, the varicella-zoster virus can affect the eyes or the brain, in addition to the skin. Herpes gestationis and dermatitis herpetiformis are among other conditions in which herpeslike groups of blisters may appear on the skin, but neither is related to the herpes simplex or varicella-zoster virus infections.

Treatment of HSV varies according to its site and severity. The antiviral drug acyclovir (taken internally or applied topically to the blisters) is effective in shortening the symptoms during a primary attack, and there is some indication the drug taken prophylacti-cally may lessen future attacks.

herpes, genital Until AIDS appeared, genital herpes was one of the most common sexually transmitted diseases in the country, striking young, single, and usually middle-class men and women. Despite the hysteria, the medical community has always considered genital herpes to be more of a discomfort rather than a dangerous or life-threatening situation. This nonlethal but incurable disease invades the body and remains for a lifetime, appearing often several times a year with painful sores in the genital area. It is estimated that there are more than 700,000 new cases each year and that the disease is responsible for more than 500,000 physician visits annually.

Cause Herpes simplex, type 2 causes most of the genital herpes cases. HSV1 causes most herpes infections above the waist. The virus can infect any skin or mucous membrane surface on the body. For example, a person with a cold sore who engages in oral sex can transmit herpes to a partner's genitals.

The infection is spread by contact with the genital secretions of a person with an active lesion. It is possible, however, for a person in the latent phase (with no active lesion) to shed virus and infect a sex partner. Genital herpes can also be acquired by infants as they pass through the birth canal of infected mothers. Neonatal herpes simplex infection can cause serious damage to the brain and many other organs; even with therapy, more than 20 percent of the 1,500 infants infected each year in the United States will die, and many of the survivors are seriously impaired. Because of this, thousands of women in the United States with a history of genital herpes are advised to undergo a Cesarean section when prenatal cultures or exams suggest an active infection near the time of delivery.

HSV2 infection can also lead to serious or fatal complications in adults who have a weakened immune system because of AIDS or who are undergoing drug therapy for organ transplants.

Symptoms Many people who are infected have no symptoms at all; only about 40 percent of victims ever have symptoms. When they do, the primary (or first) appearance of herpes lesions is the worst, with severe local symptoms and many painful lesions. These last up to 10 days, and it may take two to three weeks to completely recover from this first attack. When the sores fade away, the virus remains behind. The virus is now latent. During the first attack, some people have a generalized sick feeling, with swollen glands in the pelvic area and fever, fatigue, headache, muscle ache, and nausea. People with no antibodies to herpes (cold sores) usually will be sicker during a first attack. Women usually have lesions on the cervix or vulva. Recurrences may appear on the vulva, skin between vagina and anus, upper thighs, anal area, or buttocks. Men get lesions on the head or shaft of the penis and the anus.

Most people have a recurrence within six months of their first attack. This recurrence begins with a tingling, itching, or prickling sensation in the area where the virus entered the body. This is followed in a few days by a raised cluster of small painful blisters; there may be several groups of blisters. Eventually, the sores will crust over and dry up. Most people don't have the generalized sick feeling with recurrent infections.

Patients are infectious until the sores heal completely, usually up to 12 days; recurrent infections usually remain infectious for up to a week. Recent studies have shown that it is quite possible to shed virus without symptoms, which is how it is possible to infect a partner when no sores are present.

Neonatal herpes can take many different forms. About one third of babies will have skin, eyes, or mouth lesions before any other symptoms; another third will have a brain infection (ENCEPHALITIS), PNEUMONIA, or infection of other organs. The other third will have both. Respiratory distress, fever, skin lesions, or convulsions are common herpes symptoms in newborns.

Diagnosis Doctors may diagnose genital herpes by symptoms alone, but there are also several lab tests that can confirm the infection. A specimen from the base of a lesion can identify the type of cell called giant cells, which usually indicates a herpes virus. Herpes also grows rapidly in tissue culture; specimens from a new lesion can be identified within 48 hours in the lab. Blood tests can look for antibodies to herpes; the newest blood tests can tell the difference between type 1 and 2, but differentiation is not clinically important as they both behave and are treated in the same way.

Complications Rarely, herpes MENINGITIS (infection in the lining of the brain or spinal cord) or herpes encephalitis (infection in the brain) follows an initial infection. In the past, it was believed that there could be a link

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