|
INFECTIOUS DISEASES
LYME DISEASE
MAD COW DISEASE
HEPATITIS
HERPES
WEST NILE VIRUS
STD'S
AIDS
Microwave kills germs on sponges
Two minutes in a microwave oven can sterilize most household sponges, U.S. researchers reported on Monday.
A team of engineering researchers at the University of Florida found that two minutes of microwaving on full power killed or inactivated more than 99 percent of bacteria, viruses or parasites, as well as spores, on a kitchen sponge.
"People often put their sponges and scrubbers in the dishwasher, but if they really want to decontaminate them and not just clean them, they should use the microwave," said Gabriel Bitton, a professor of environmental engineering who led the study.
Writing in the Journal of Environmental Health, Bitton and colleagues said they soaked sponges and scrubbing pads in raw wastewater containing fecal bacteria such as E. coli, viruses, protozoan parasites and bacterial spores.
Then they used a common household microwave oven to heat up the sponges. It took four to 10 minutes to kill all the spores but everything else was killed after two, they said.
"The microwave is a very powerful and an inexpensive tool for sterilization," Bitton said.
At least 76 million Americans get sick from food borne microbes every year, according to the U.S. Centers for Disease Control and Prevention, and 5,000 people die from them.
Kitchens are a common source of these illnesses.
 |
Want to prevent colds? Start exercising
|
 |
A long-term moderate exercise programme can reduce the risk of colds among older women, United States researchers said on Thursday.
In the first randomised clinical trial to investigate the impact of moderate physical activity on the common cold, researchers from the Fred Hutchinson Cancer Research Centre found that post-menopausal women who worked out regularly had about half the risk of colds as those who did not exercise.
"There has always been this anecdotal evidence, and some small studies, suggesting that with moderate exercise you can improve your immunity," said Cornelia Ulrich, lead author of the study published in the American Journal of Medicine.
"Our study ... is the first time that a rigorous trial showed that the number of colds can be affected by exercise," she said in an interview.
The study involved 115 overweight, post-menopausal women who had not been exercising before the trial.
The group was divided in two, with half the women assigned to undertake a moderate exercise programme of 45 minutes a day, five days a week. The other half were told to take part in once-weekly, 45-minute stretching sessions.
The exercisers were told to do moderate physical activity such as walking on a treadmill, cycling on a stationary bicycle or rapid walking outside.
Over the course of a year, the women filled out questionnaires every three months to report the number of times they had allergies, colds or other problems.
The study found that over 12 months, the risk of colds decreased modestly in exercisers and increased modestly in the group of stretchers.
The researchers found that the ability of moderate exercise to ward off colds seemed to increase over time. In the last three months of the study, the group of women who were only stretching were three times as likely to catch a cold as those who were exercising regularly.
The study did not reach any conclusions about the benefit of stretching but said that regular cardiovascular exercise was most beneficial.
"With regards to preventing colds, it seems you really have to stick with exercise long term," Ulrich said.
The results were seen as important in understanding the health benefits of exercise, Ulrich said.
"It may apply also to other age groups, it may apply to men," she said. "In the past, immune studies have been quite consistent among men and women. I wouldn't expect that to be different." - Reuters
|
 |
Medical Encyclopedia: Impetigo
URL of this page: http://www.nlm.nih.gov/medlineplus/ency/article/000860.htm
Definition
Impetigo is a skin disorder caused by bacterial infection and characterized by crusting skin lesions.
Causes, incidence, and risk factors
Impetigo is a common skin infection. It is most common in children, particularly children in unhealthy living conditions. In adults, it may follow other skin disorders. Impetigo may follow a recent upper respiratory infection such as a cold or other viral infection. It is similar to cellulitis, but is more superficial, involving infection of the top layers of the skin with streptococcus (strep), staphylococcus (staph), or both.
The skin normally has many types of bacteria on it, but intact skin is an effective barrier that keeps bacteria from entering and growing within the body. When there is a break in the skin, bacteria can enter the body and grow there, causing inflammation and infection. Breaks in the skin may occur with insect bites, animal bites, or human bites, or other injury or trauma to the skin. Impetigo may occur on skin where there is no visible break.
Impetigo begins as an itchy, red sore that blisters, oozes and finally becomes covered with a tightly adherent crust. It tends to grow and spread. Impetigo is contagious. The infection is carried in the fluid that oozes from the blisters. Rarely, impetigo may form deeper skin ulcers.
Symptoms
* Skin lesion on the face or lips, or on the arms or legs, spreading to other areas. Typically this lesion begins as a cluster of tiny blisters which burst, followed by oozing and the formation of a thick honey- or brown-colored crust that is firmly stuck to the skin.
* Itching blister:
o Filled with yellow or honey-colored fluid
o Oozing and crusting over
* Rash (may begin as a single spot, but if person scrathes it, it may spread to other areas).
* In infants, a single or possibly multiple blisters filled with pus, easy to pop and -- when broken -- leave a reddish raw-looking base.
* Lymphadenopathy -- local lymph nodes near the infection may be swollen.
Signs and tests
Diagnosis is based primarily on the appearance of the skin lesion. A culture of the skin or mucosal lesion usually grows streptococcus or staphylococcus.
Treatment
The goal is to cure the infection and relieve the symptoms.
A mild infection is typically treated with a prescription antibacterial cream such as mupirocin. Oral antibiotics such as erythromycin or dicloxacillin are also frequently prescribed, and result in rapid clearing of the lesions.
Wash the skin several times a day, preferably with an antibacterial soap, to remove crusts and drainage.
Prevent the spread of infection. Use a clean washcloth and towel each time. Do not share towels, clothing, razors, and so on with other family members. Wash the hands thoroughly after touching the skin lesions.
Expectations (prognosis)
The sores of impetigo heal slowly and seldom scar. The cure rate is extremely high, but they often come back in young children.
Complications
* The infection could spread to other parts of the body. This is common.
* Children often have multiple patches of impetigo.
* A systemic infection could lead to kidney failure (post-streptococcal glomerulonephritis). This is a rare occurrence.
* Permanent skin damage and scarring may occur (also extremely rare).
Calling your health care provider
Call for an appointment with your health care provider if symptoms indicating impetigo are present.
Prevention
Good general health and hygiene help to prevent infection. Minor abrasions or areas of damaged skin should be thoroughly cleansed with soap and clean water. A mild antibacterial agent may be applied if desired.
Impetigo is contagious, so avoid skin contact with drainage from impetigo lesions.
Human Genome Sciences Hepatitis C Drug
EW YORK (Reuters) - Human Genome Sciences Inc. on Thursday said its experimental drug for hepatitis C met its primary goal in a mid-stage trial of patients who had not previously been treated for the liver-damaging virus.
The Rockville, Maryland-based company said the favorable results were seen in a trial of 56 patients with the genotype 1 strain of hepatitis C, the hardest to treat of three main strains, who were given varying doses of its Albuferon injectable drug. The patients had never previously been treated for their condition.
Albuferon is a laboratory-altered form of interferon-alpha, a standard treatment for hepatitis C. But unlike standard interferon treatments that must be injected once weekly, researchers said the Phase II trial indicated Albuferon is highly effective with injections only every two to four weeks.
Patients taking the two highest doses of the drug saw their levels of virus decline by over 99.9 percent 28 days after treatment began. That satisfied the trial's primary goal of showing at least a 99 percent reduction in virus, meaning a reduction to undetectable levels, after four weeks.
The company said 69 percent of patients in those two high-dose groups achieved the 99 percent reduction of virus after four weeks. Undetectable virus levels after 42 days were seen in 23 percent of the same patients.
Swiss drugmaker Roche sells the most popular interferon, called Pegasys, which is taken with a pill called ribavirin to treat the often-deadly virus. Schering-Plough Corp.'s interferon, called Peg-Intron, is also taken alongside ribavirin.
Those standard combo treatments are considered the best available therapies for the virus, but use of them for up to 48 weeks only knocks down the virus to undetectable levels in about 42 percent of patients with genotype 1, Human Genome Sciences said.
Based on the promising results of its Phase II trial, Human Genome Sciences said it plans to conduct a larger 48-week mid-stage trial pairing Albuferon with ribavirin. The trial will pit the combo treatment against either the Roche or Schering-Plough combination therapy in patients with genotype 1.
David Stump, head of drug development for Human Genome Sciences, told Reuters he hopes Albuferon, when paired with ribavirin, will supercede the Roche or Schering-Plough combo in effectiveness as well as tolerability.
"If we show superiority in the head-to-head trial, we would become the new gold standard of treatment," he said.
' Morning After' Treatment Advised to Prevent AIDS
WASHINGTON (Reuters) - A "morning after" treatment for the AIDS (news - web sites) virus can help prevent infection after a rape, contact with a contaminated needle or even a night of passion without a condom, U.S. health officials said on Thursday.
Taking drug cocktails for four weeks seems to greatly reduce the risk of becoming infected with the virus, which is transmitted through sex -- heterosexual and homosexual -- drug use and shared needles, the Centers for Disease Control and Prevention (news - web sites) said.
These drug cocktails, called highly active antiretroviral therapy or HAART, are routinely taken for life by HIV (news - web sites)-infected patients who can afford it and have access. HAART can keep a patient healthy despite infection with the deadly and incurable virus.
The CDC said there was no ethical way to do a random trial comparing post-exposure prevention to a placebo or dummy pill.
But trials on animals and studies of rape victims and of people at high risk of HIV infection because of their behavior have shown that taking a two- or three-drug cocktail after the possible exposure does prevent infection.
"A 28-day course of HAART is recommended for persons who have had nonoccupational exposure to blood, genital secretions, or other potentially infected body fluids of a person known to be HIV infected when that exposure represents a substantial risk for HIV transmission," the CDC said.
The quicker, the better, it said.
In its report, the CDC pointed to a study of needlestick injuries to health-care workers. "In this study, the prompt initiation of zidovudine (AZT) was associated with an 81 percent decrease in the risk for acquiring HIV."
In another trial of 200 gay and bisexual Brazilians at high risk of HIV infection, doctors gave out "starter packs" of AZT and another AIDS drug called lamivudine.
In the group that used the drugs after having unprotected sex, one person became infected, while 11 people in the group that did not take the drugs became infected.
South African rape victims got a similar treatment and none of the women who started the drugs within 48 to 72 hours became infected.
"Although 400,000 new HIV infections occur in the United States each year, relatively few exposed persons seek care after nonoccupational exposure," the CDC said.
"Preferred regimens include efavirenz and lamivudine or emtricitabine with zidovudine or tenofovir and lopinavir/ritonavir (coformulated in one tablet as Kaletra) and zidovudine with either lamivudine or emtricitabine. Different alternative regimens are possible."
statins may be good for AIDS
Statins Inhibit HIV-1 Infection by Down-regulating Rho Activity
J. Exp. Med. 200: 541-547; published online before print as 10.1084/jem.20040061
Gustavo del Real1, Sonia Jiménez-Baranda1, Emilia Mira1, Rosa Ana Lacalle1, Pilar Lucas1, Concepción Gómez-Moutón1, Marta Alegret2, Jose María Peña3, Manuel Rodríguez-Zapata4, Melchor Alvarez-Mon4, Carlos Martínez-A.1, and Santos Mañes1
1 Department of Immunology and Oncology, Centro Nacional de Biotecnología/Spanish Council for Scientific Research (CSIC), E-28049 Madrid, Spain
2 Department of Pharmacology and Therapeutical Chemistry, Facultad de Farmacia, Universidad de Barcelona, E-08028 Barcelona, Spain
3 Department de Medicina, Servicio de Medicina Interna, Hospital La Paz, E-28046 Madrid, Spain
4 Department of Diseases of the Immune System, School of Medicine, Hospital Principe de Asturias, Universidad de Alcalá de Henares, E-28801 Madrid, Spain
Address correspondence to Carlos Martínez-A., Dept. of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, UAM Campus de Cantoblanco, E-28049 Madrid, Spain. Phone: 34-91-585-4850; Fax: 34-91-372-0493; email: cmartineza@cnb.uam.es; or Santos Mañes, Dept. of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, UAM Campus de Cantoblanco, E-28049 Madrid, Spain. Phone: 34-91-585-4850; Fax: 34-91-372-0493; email: smanes@cnb.uam.es
Human immunodeficiency virus (HIV)-1 infectivity requires actin-dependent clustering of host lipid raft–associated receptors, a process that might be linked to Rho guanosine triphosphatase (GTPase) activation. Rho GTPase activity can be negatively regulated by statins, a family of drugs used to treat hypercholesterolemia in man. Statins mediate inhibition of Rho GTPases by impeding prenylation of small G proteins through blockade of 3-hydroxy-3-methylglutaryl coenzyme A reductase. We show that statins decreased viral load and increased CD4+ cell counts in acute infection models and in chronically HIV-1–infected patients. Viral entry and exit was reduced in statin-treated cells, and inhibition was blocked by the addition of L-mevalonate or of geranylgeranylpyrophosphate, but not by cholesterol. Cell treatment with a geranylgeranyl transferase inhibitor, but not a farnesyl transferase inhibitor, specifically inhibited entry of HIV-1–pseudotyped viruses. Statins blocked Rho-A activation induced by HIV-1 binding to target cells, and expression of the dominant negative mutant RhoN19 inhibited HIV-1 envelope fusion with target cell membranes, reducing cell infection rates. We suggest that statins have direct anti–HIV-1 effects by targeting Rho.
Key Words: cholesterol • actin cytoskeleton • small GTPases • lipid rafts • prenylation
G. del Real and S. Jiménez-Baranda contributed equally to this work.
G. del Real's present address is Centro de Investigación en Sanidad Animal (CISA-INIA), Valdeolmos, E-28130 Madrid, Spain.
statins may be good for AIDS_EXPLANATION
A study of six AIDS patients has revealed that statins can reduce levels of HIV and boost immune cell numbers. If the results can be repeated in large-scale trials, it's hoped that statins could provide an alternative to standard HIV treatments.
Statins are taken by millions of people to lower cholesterol levels and help protect against heart disease. And studies have shown that cultured cells with low levels of cholesterol in their membranes are less likely to succumb to HIV infection.
So, Carlos Martínez from the Spanish Council for Scientific Research and colleagues decided to study the effects of cholesterol-lowering statin drugs on HIV patients. Their results are reported in the Journal of Experimental Medicine1.
A one-month course of statin treatment caused the virus levels of human patients to drop by up to 20-fold. Levels began to rise when patients stopped taking the drug.
When mice, injected with HIV-infected human cells, were given the drugs, their virus levels fell, in some cases to undetectable levels.
Together, these results suggest that statins may prove useful against HIV in human patients, says Martínez.
Killer virus
HIV suppresses the immune system by infecting and killing the cells of which it consists. Martínez believes that statins prevent the virus from entering healthy cells in the first place.
It is hoped that the drugs could offer an alternative to the standard AIDS treatment, highly active antiretroviral therapy (HAART). This therapy is becoming less effective as drug-resistant HIV strains continue to emerge.
Resistant strains have limited the options for many HIV-infected patients, explains HIV researcher Eric Freed of the HIV Drug Resistance Program at the National Cancer Institute in Frederick, Maryland. "This makes the development of alternative treatments especially urgent."
Statins could also prove safer than antiretrovirals. HAART can trigger serious side-effects, such as liver damage, but statins are relatively free of such problems.
Martínez hopes that statins could also be used preventatively. His study shows that white blood cells taken from patients on statins are less likely to succumb to HIV infection.
Larger clinical trials should be forthcoming, says Martínez. But he cautions that such studies are difficult to set up. It is hard to find HIV-positive patients who are not already taking anti-HIV medication, he points out. One solution may be to concentrate on patients who have already become resistant to the standard treatments.
Hepatitis Drug May Fight Anthrax
MONDAY, Feb. 16 (HealthDayNews) -- Not only has Wei-Jen Tang shown that a drug for hepatitis blocks the action of the anthrax bacteria in the lab, but he thanks the media for making the discovery possible.
In January 2002, Tang, an associate professor at the University of Chicago's Ben May Institute for Cancer Research, published a paper that described the structure of edema factor, one of three major toxins secreted by the anthrax bacteria. His report also showed how it worked.
Soon after, a pharmaceutical company researcher who had read of Tang's exploits in the newspaper contacted him about testing adefovir dipivoxil (brand name Hepsera) for anthrax. Adefovir had been approved in 2002 to treat chronic hepatitis B virus infection and the scientist thought it might work on the pathway Tang had described in his research.
"That's how things started," says Tang, whose findings appear in this week's issue of the Proceedings of the National Academy of Sciences (news - web sites). "It was a major quantum leap to advance our studies because it usually takes two to three years to get a [drug] lead and then it has to be approved."
Even so, this research is in its infancy. "This is a demonstration in principle that this drug may work in anthrax. I think there's a long way to go to show that it's useful clinically," says Dr. Adrian Di Bisceglie, a professor of internal medicine at St. Louis University and an expert in the treatment of hepatitis B.
Anthrax started appearing in mail rooms and post offices in the fall of 2001, killing nearly half of those who breathed in the deadly spores. Many survivors have lingering health problems such as fatigue, shortness of breath and memory loss, report the authors.
About the only defense doctors have against anthrax are antibiotics, but these work only in the early stages of infection. Scientists have been eager to find more effective treatments.
In addition to edema factor, the anthrax bacteria actually secretes two other major toxins, lethal factor and protective antigen (this latter toxin actually acts as an escort, helping the other toxins enter the cells).
Edema factor interferes with the host's immune response in the first stages of infection. This gives the bacteria a chance to multiply, spread and produce yet more deadly toxins. Later on in the infection, this same edema factor causes massive tissue damage.
In test tubes, adefovir blocked the action of edema factor.
Further examination revealed exactly how the drug worked: Adefovir binds onto the surface of edema factor and stops it from mimicking an enzyme called adenylyl cyclase, which helps regulate signaling between cells.
"In tissue culture cells, adefovir also prevented edema factor from interfering with normal communications between blood cells that are vital for us to defend bacterial pathogens," Tang explains. "Consequently, adefovir will likely allow our body to mount more effective and direct defenses against anthrax bacteria. Adefovir could also block the damages of vital organs caused by edema factor or the combination of edema factor and lethal factor."
The drug actually binds 10,000 times better than the natural enzyme does. Not only does that make it effective, it also indicates it may be able to be given in such small amounts that there will be few, if any, side effects.
"We were surprised at how well it works," Tang says. "We were pleasantly surprised to find it has about a 10,000-fold higher affinity. That's a shocker to me."
Because the drug is already approved, it can immediately go into animal testing. It will never be tested in humans for ethical reasons.
"The problem with anthrax is that you can't do any clinical trials in advance because there are so few people and when you have them, it's an emergency," Di Bisceglie says. Animal studies will answer some questions, but not all.
Will it work in humans? "It's hard to tell," Tang says. "There's an outside chance it will work based on our understanding, but that doesn't mean it will work. Having said that, I will wait until we have other data."
Adefovir may also have applications beyond anthrax, specifically on Bordetella pertussis, which causes whooping cough, Yersinia pestis, which causes plague, and Pseudomonas aeruginosa, which causes many hospital-acquired infections.
"Potentially this can be used in those settings," Tang says. "We understand much less and therefore the applications may be significantly further away.
Although all three of these pathogens are considered potential bioterror agents, according to the study, Tang makes the point that whooping cough has been largely eradicated and plague is rarely seen. "The only thing that may have a clinical implication is hospital-acquired infections, and we've yet to find out how effective this is even in a tissue-culture setting," he says.
Viral Hepatitis: A Through E and Beyond
Hepatitis is inflammation of the liver.
|
Hepatitis is inflammation of the liver. Several different viruses cause viral hepatitis. They are named the hepatitis A, B, C, D, and E viruses.
All of these viruses cause acute, or short-term, viral hepatitis. The hepatitis B, C, and D viruses can also cause chronic hepatitis, in which the infection is prolonged, sometimes lifelong.
Other viruses may also cause hepatitis, but they have yet to be discovered and they are obviously rare causes of the disease.
Symptoms of Viral Hepatitis
Symptoms include
 jaundice (yellowing of the skin and eyes)
 fatigue
 abdominal pain
 loss of appetite
 nausea
 vomiting
 diarrhea
 low grade fever
 headache
|
However, some people do not have symptoms.
|
Hepatitis A
Disease Spread
Primarily through food or water contaminated by feces from an infected person. Rarely, it spreads through contact with infected blood.
People at Risk
International travelers; people living in areas where hepatitis A outbreaks are common; people who live with or have sex with an infected person; and, during outbreaks, day care children and employees, men who have sex with men, and injection drug users.
Prevention
The hepatitis A vaccine; also, avoiding tap water when traveling internationally and practicing good hygiene and sanitation.
Treatment
Hepatitis A usually resolves on its own over several weeks.
Hepatitis B
Disease Spread
Through contact with infected blood, through sex with an infected person, and from mother to child during childbirth.
People at Risk
People who have sex with an infected person, men who have sex with men, injection drug users, children of immigrants from disease-endemic areas, infants born to infected mothers, people who live with an infected person, health care workers, hemodialysis patients, people who received a transfusion of blood or blood products before July 1992 or clotting factors made before 1987, and international travelers.
Prevention
The hepatitis B vaccine.
Treatment
For chronic hepatitis B: drug treatment with alpha interferon, peginterferon, lamivudine, or adefovir dipivoxil.
Acute hepatitis B usually resolves on its own. Very severe cases can be treated with lamivudine.
Hepatitis C
Disease Spread
Primarily through contact with infected blood; less commonly, through sexual contact and childbirth.
People at Risk
Injection drug users, people who have sex with an infected person, people who have multiple sex partners, health care workers, infants born to infected women, hemodialysis patients, and people who received a transfusion of blood or blood products before July 1992 or clotting factors made before 1987.
Prevention
There is no vaccine for hepatitis C; the only way to prevent the disease is to reduce the risk of exposure to the virus. This means avoiding behaviors like sharing drug needles or sharing personal items like toothbrushes, razors, and nail clippers with an infected person.
Treatment
Chronic hepatitis C: drug treatment with peginterferon alone or combination treatment with peginterferon and the drug ribavirin.
Acute hepatitis C: treatment is recommended if it does not resolve within 2 to 3 months.
Hepatitis D
Disease Spread
Through contact with infected blood. This disease occurs only in people who are already infected with hepatitis B.
People at Risk
Anyone infected with hepatitis B: Injection drug users who have hepatitis B have the highest risk. People who have hepatitis B are also at risk if they have sex with a person infected with hepatitis D or if they live with an infected person. Also at risk are people who received a transfusion of blood or blood products before July 1992 or clotting factors made before 1987.
Prevention
Immunization against hepatitis B for those not already infected; also, avoiding exposure to infected blood, contaminated needles, and an infected person's personal items (toothbrush, razor, nail clippers).
Treatment
Chronic hepatitis D: drug treatment with alpha interferon.
Hepatitis E
Disease Spread
Through food or water contaminated by feces from an infected person. This disease is uncommon in the United States.
People at Risk
International travelers; people living in areas where hepatitis E outbreaks are common; and people who live or have sex with an infected person.
Prevention
There is no vaccine for hepatitis E; the only way to prevent the disease is to reduce the risk of exposure to the virus. This means avoiding tap water when traveling internationally and practicing good hygiene and sanitation.
Treatment
Hepatitis E usually resolves on its own over several weeks to months.
Other Causes of Viral Hepatitis
Some cases of viral hepatitis cannot be attributed to the hepatitis A, B, C, D, or E viruses. This is called non A-E hepatitis. Scientists continue to study the causes of non A-E hepatitis.
Hope Through Research
The National Institute of Diabetes and Digestive and Kidney Diseases, through its Division of Digestive Diseases and Nutrition, supports basic and clinical research into the nature and transmission of the hepatitis viruses, and the activation and mechanisms of the immune system. Results from these studies are used in developing new treatments and methods of prevention.
For More Information
American Liver Foundation (ALF)
75 Maiden Lane, Suite 603
New York, NY 10038-4810
24-hour helpline (7 days/week): 1-800-465-4837 or 1-888-443-7222
Phone: 1-800-676-9340 or (212) 668-1000
Fax: (212) 483-8179
Email: info@liverfoundation.org
Internet: www.liverfoundation.org
Centers for Disease Control and Prevention (CDC)
Division of Viral Hepatitis
1600 Clifton Road
Mail Stop C-14
Atlanta, GA 30333
Phone: 1-800-443-7232 or (404) 371-5900
Email: ncid@cdc.gov
Internet: www.cdc.gov/hepatitis
Hepatitis Foundation International (HFI)
504 Blick Drive
Silver Spring, MD 20904-2901
Phone: 1-800-891-0707 or (301) 622-4200
Fax: (301) 622-4702
Email: hfi@comcast.net
Internet: www.hepatitisfoundation.org
National Digestive Diseases Information Clearinghouse
2 Information Way
Bethesda, MD 20892-3570
Email: nddic@info.niddk.nih.gov
The National Digestive Diseases Information Clearinghouse (NDDIC) is a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). The NIDDK is part of the National Institutes of Health under the U.S. Department of Health and Human Services. Established in 1980, the clearinghouse provides information about digestive diseases to people with digestive disorders and to their families, health care professionals, and the public. NDDIC answers inquiries, develops and distributes publications, and works closely with professional and patient organizations and Government agencies to coordinate resources about digestive diseases.
Hepatitis C Infection Early in Life Rarely Serious
Tue Jan 27, 5:24 PM ET Add Health - Reuters to My Yahoo!
NEW YORK (Reuters Health) - Hepatitis C (HCV) infection acquired early in life rarely, if ever, progresses to the liver-scarring disease cirrhosis, new research suggests.
HCV infection during adulthood is associated with a higher risk of progression to cirrhosis within 20 years than that acquired earlier in life, senior investigator Dr. Alessandro Remo Zanetti and colleagues note in medical journal Hepatology. However, most studies of disease progression rarely encompassed more than 20 years of follow-up.
To gain further insight into outcomes of HCV infection, Zanetti, at the University of Milan in Italy, and his group identified 31 individuals who, as children in 1968, had received blood from donors later found to be infected with HCV.
The researchers obtained blood samples from these subjects in 1998, and found that only 18 had any evidence of infection. Although mild liver damage was noted in a few subjects on follow-up 5 years later, none had cirrhosis.
"Taking into account the limited study sample," the authors conclude, "these findings suggest that HCV infection acquired early in life shows a slow progression and mild outcome during the first 35 years of infection."
SOURCE: Hepatology, January 2004.
UV Lamps Could Reduce Worker Sickness
By EMMA ROSS, AP Medical Writer
LONDON - Sickness among office workers in industrialized countries could be reduced by using ultraviolet lamps to kill germs in ventilation systems, new research indicates.
Ultraviolet germicidal irradiation, or UVGI, is sometimes used in hospital ventilation systems to disinfect the air but is rarely incorporated into office or other building ducts because there has been little evidence of a bnefit.
About 70 percent of the work force in North America and Western Europe work indoors, and frequently have unexplained health problems such as irritation of the eyes, throat and nose, as well as respiratory illnesses.
In a study published this week in The Lancet medical journal, Canadian scientists found that the technique reduced overall worker sickness by about 20 percent, including a 40 percent drop in breathing problems.
"Instllation of UVGI in most North American offices could resolve work-related symptoms in about 4 million employees, caused by (germ) contamination of heating, ventilation, and air conditioning systems," said the study's leader, Dr. Dick Menzies from the Montreal Chest Institute at McGill University in Montreal, Canada.
"The cost of UVGI installation could in the long run prove cost-effective compared with the yearly losses from absence because of building-related illness," he added.
A total of 771 employees from three different office buildings in Montreal were involved with the study.
The ultraviolet lamps were aimed at the cooling coils and drip pans in the ventilation systems of the buildings. The lights were turned on for four weeks, then turned off for 12 weeks. The cycle was repeated three times for almost a year.
The use of the lights resulted in a 99 percent reduction of the concentration of germs on irradiated surfaces within the ventilation systems.
Some weeks, use of the lamps resulted in a 20 percent overall reduction in all symptoms for some workers; a 40 percent reduction in respiratory symptoms and a 30 percent reduction in mucous problems. The benefits were greatest for workers with allergies and for people who had never smoked.
With the lights switched on, the frequency of muscle complaints among nonsmokers halved and the incidence of work-related breathing problems among them dropped by 60 percent.
Wladyslaw Jan Kowalski, an architectural engineer at Pennsylvania State University's Indoor Environment Center, said the study may be a landmark in proving that the technique could be cost-effective in commercial office buildings.
Kowalski, who was not involved with the research, also said the approach could be useful in the broader effort to combat contagious diseases such as flu, SARS (news - web sites), tuberculosis and cold viruses.
"Theoretically, if a large number of schools, office buildings and residences were modified, a number of airborne respiratory diseases could be eradicated by interrupting the transmission cycle," Kowalski said. "Reducing the transmission rate sufficiently would ... halt epidemics in their path."
However, Roy Anderson, an infectious diseases expert at Imperial College in London, said disinfecting ventilation systems by itself would not stamp out outbreaks of contagious respiratory diseases.
"Transport is particularly important — buses, subways, trains and airplanes," said Anderson, who was not connected with study. Disease also spreads through personal contact.
"You've got multiple methods of transmission and for control, you need to address all of them. It's an interesting new approach worth pursuing, but it needs detailed investigation," Anderson said.
Fall is Prime Lyme Disease Time
"In the spring and summer months, humans and animals are threatened by the nymphal stage of black-legged (or deer) ticks infected with Lyme disease. But it's the adult stage of these ticks that's active from October through May -- any time the temperature rises above 30 degrees," David Weld, executive director of the foundation, says in a prepared statement.
He notes the percentage of infected adult deer ticks at this time of year is twice that of spring and summer tick nymphs. In the northeast United States, that means that 50 percent to 60 percent of adult deer ticks may be infected with Lyme disease.
"Adults, especially the females, are mighty hungry. Fall is the time of year they're looking for meals to feed their eggs. They're sitting on vegetation 10 inches to 2 feet off the ground, waiting for a good host to walk by. Deer and dogs are favorite targets," Weld says.
The majority of Lyme disease cases in the United States have occurred in the northeast, mid-Atlantic and north-central states. But it's also an emerging threat to people and pets in many other areas of the country.
Southern and western states such as Florida, the Carolinas, Texas and California are among the national leaders in percentage growth of reported Lyme disease cases in recent years.
"The Centers for Disease Control and Prevention (news - web sites) [CDC] in Atlanta recently announced that 2002 witnesses the highest number of reported incidents of Lyme disease on record. Over the past year, 23,763 new cases of the disease were reported and an estimated 100,000 to 200,000 may have gone unreported to the CDC. That's an increase of nearly 25 per cent from 2000, the previous record infection year," Weld says.
Beat the Flu This Year With Nasal Spray
WASHINGTON - Starting next week, it's time to line up for flu vaccine again, and this year some Americans will get to choose a squirt up the nose instead of a shot in the arm.
But the new nasal-spray vaccine, called FluMist, will cost well more than twice as much as a shot. It also cannot be used by those who need protection against influenza the most: babies and toddlers, people 50 or older and those with asthma or other chronic illnesses.
Still, FluMist's expected advertising blitz could generate new interest in flu protection at a pivotal time. Specialists say far too few Americans get vaccinated, including healthy people who may not be at risk of dying but spread around influenza's misery.
In addition, fearing a winter return of the deadly new SARS (news - web sites) virus, the World Health Organization (news - web sites) is urging more flu vaccination. While flu vaccine won't prevent SARS, both diseases have similar symptoms, and WHO contends that holding down the number of serious influenza cases will mean less chance of doctors mistaking flu for SARS.
The U.S. Centers for Disease Control and Prevention (news - web sites) doesn't want to make that connection, cautioning that other respiratory viruses circulate during the winter that could be confused with SARS, too.
There's reason enough to get flu vaccine, stresses CDC's Dr. Scott Harper: Influenza kills 36,000 Americans in an average year, hospitalizes 114,000 and infects up to 20 percent of the population.
Roughly 70 million people get a flu vaccination every year, less than half the number especially urged to get it, Harper laments. Among the highest-risk patients, only a third of adults with asthma are vaccinated, and fewer than two-thirds of the elderly, even though flu shots are free under Medicare.
Vaccine experts think that's partly due to complacency — the last two flu seasons have been mild — and partly due to two years of manufacturing delays that had doctors rationing the season's earliest inoculations.
The manufacturing problems appear solved: CDC says plenty, 85.5 million doses, are becoming available, and early-October inoculations are open to everyone.
For the complacent, "it would be very unusual to have three mild seasons in a row," warns Dr. William Schaffner of the National Foundation for Infectious Diseases.
The following high-risk people need flu shots, CDC says:
_Everyone over age 50.
_Anyone with chronic medical conditions such as heart or lung disorders including asthma, diabetes, kidney disease or weak immune systems.
_Children aged 6 months to 2 years.
_Residents of nursing homes or other long-term care facilities.
_Women who will be more than three months pregnant during the flu season.
_Children of any age on long-term aspirin therapy.
Caregivers of high-risk people need vaccination as well.
FluMist, the new nasal spray, is an option for healthy people ages 5 to 49.
FluMist's maker and marketer, MedImmune Inc. and Wyeth Vaccines, hope to sell 5 million doses in this first season of sales. Even for the healthy, flu's misery is a major disruption, they argue, that causes 70 million missed workdays and 38 million missed schooldays a year.
But FluMist has an average wholesale price of $46 a dose — not counting the cost of administering the spray, which could add at least another $10. A flu shot typically costs $15 to $20.
Most healthy people pay for flu vaccine out-of-pocket at walk-in programs offered by drugstores or employers. Patients hoping for insurance coverage will have to check with their carriers; some have agreed to cover FluMist, sometimes with higher co-pays, although Wyeth won't reveal how many.
Why is FluMist only for the healthy? First, FluMist is made of live but weakened flu virus considered too risky for people with compromised immune systems; the shot is made of killed virus. The spray's safety hasn't been proved in older people or those with chronic illnesses. As for youngsters, a study found those under 5 were at increased risk of suffering asthma-like attacks after FluMist had been squirted up their noses.
For the healthy, FluMist's convenience likely will prove attractive — and whatever it takes, getting more people protected is the goal, says Schaffner, preventive medicine chairman at Vanderbilt University.
"I would hope that 10 years from now, we are recommending annual influenza immunization for everybody," he says
Aids link throws spotlight on Acambis vaccine
Annie Lawson Saturday September 13, 2003 The Guardian
A smallpox vaccine produced by Acambis, the biotechnology group based in Cambridge, could offer protection against the Aids virus, US researchers have found.
Although the company was quick to point out that the research is at a very early stage and based on limited testing, the news captured the imagination of the stock market. Acambis shares rose 15p to close at 381.5p even though it will be at least seven years before the smallpox vaccine can be used in the fight against Aids, assuming it receives the requisite approvals.
The company, considered a world leader in vaccine production, said yesterday it was discussing the findings with researchers at Virginia's George Mason University.
Laboratory tests showed that blood samples from people vaccinated against smallpox were fives times less likely to become infected by the Aids virus.
Even though a different smallpox vaccine was used in the experiment, Acambis' new Acam-2000 version is likely to be the focus of future studies.
The company has a £260m contract to supply 209m doses of smallpox vaccine to the US government.
The threat of a smallpox attack by bioterrorists prompted Washington to build a stockpile before the vaccine had received regulatory approval.
The company said of the research: "Acambis considers these findings to be very interesting and that they warrant further investigation. Discussions are ongoing with GMU concerning collaborative work to corroborate the data they have produced."
Professor Ken Alibek, director of the university's centre for biodefence, said it was not known why the vaccine appeared to boost immunity to the Aids virus. "There is a strange connection between the discontinuation of the smallpox vaccine in Africa and the emergence of the HIV infection."
Scientists had discussed the possibility of a link but it had not been scientifically tested.
Sam Fazeli, analyst at Nomura, warned that it could take up to seven years before the vaccine received the necessary clearance.
"Even if successful, we do not believe smallpox vaccine sales for this indication are likely until at least 2009-10," he added.
About STDs and HPV
Many people believe they are not at risk for sexually transmitted diseases (STD). However, STDs are the nation's most common type of infection. Even people who have had only one sexual partner can have a STD. Anyone who has ever been sexually active can have a STD. This is especially true for people who:
Have had more than one sex partner
Have ever had unprotected sex
Don't know their partner's sexual history
Have had sexual intercourse before the age of 21
Have had an abnormal Pap smear
Have symptoms such as warts, sores, burning or redness in the genital area
The cause of one of the most common viral sexually transmitted disease (STD) in the United States today is Human Papillomavirus (HPV). As many as one in five American adults has a genital HPV infection.
 What is HPV?
 About HPV and Genital Warts
 How Common is HPV?
 About HPV, Genital Warts and Cervical Cancer
 About HPV, Genital Warts and Pregnancy
 How Do You Get HPV or Genital Warts?
 What Do Genital Warts Look Like?
 How Genital Warts are Diagnosed
 Do Genital Warts Need to Be Treated?
 Treatments
 How Can I Avoid Getting STDs Including Genital Warts
 If You Are Diagnosed With a STD
 It is Normal to Feel Emotional?
What Is HPV?
Human Papillomavirus is a group of more than 80 types of viruses. Certain types cause warts on the genital area (sex organs) and other types cause warts on hands and feet. Of the types that affect the genital area, some are linked with cervical cancer; these are usually called "high-risk" types. The types of HPV that cause raised external genital warts are not usually linked with cancer. These are called "low-risk" types.
About HPV and Genital Warts
Genital warts (condylomata acuminata or venereal warts) are caused by only a few of the many types of HPV. Other common types of HPVs, such as those that cause warts on the hands and soles of the feet, do not cause genital warts. Genital warts are spread by sexual contact with an infected partner and are very contagious. Approximately two-thirds of people who have sexual contact with a partner with genital warts will develop warts, usually within three months of contact. Scientists estimate that as many as 1 million new cases of genital warts are diagnosed in the United States each year.
In women, the warts occur on the outside and inside of the vagina, on the cervix (the opening to the uterus), or around the anus. In men, genital warts are less common. If present, they are seen on the tip of the penis; however, they also may be found on the shaft of the penis, on the scrotum, or around the anus. Rarely, genital warts also can develop in the mouth or throat of a person who has had oral sexual contact with an infected person. People who suspect that they have genital warts should be examined and treated by a health care provider.
How Common is HPV?
Human papillomavirus (HPV) is one of the most common causes of sexually transmitted disease (STD) in this country. Genital HPV infections are widespread among adults who have been sexually active and are estimated to have the highest incidence of any sexually transmitted disease (STD) in the U.S.
Top
About HPV, Genital Warts and Cervical Cancer
The types of HPV linked to cervical cancer usually are not the types that cause genital warts. But a woman with genital warts, like any other sexually active woman, should get yearly Pap smears. The Pap smear detects abnormal cells caused by HPV that can lead to cancer. With regular Pap smears and follow-up care, cervical cancer can almost always be prevented or cured.
About HPV, Genital Warts and Pregnancy
Genital warts sometimes cause problems during pregnancy and delivery. Because of hormone changes in the body during pregnancy, warts can grow in size and number, bleed, or make delivery more difficult. Very rarely, babies exposed to HPV during birth may develop warts in the throat. Despite these risks, a woman with genital warts does not need to have a cesarean-section delivery unless warts are blocking the birth canal.
It is important that a pregnant woman notify her doctor or clinic if she or her partner(s) has had HPV or genital warts.
How Do You Get HPV or Genital Warts?
HPV and genital warts are usually spread by direct, skin-to-skin contact during vaginal, anal, or oral sex with someone who has this infection. Warts on other parts of the body, such as the hands, are caused by different types of HPV. Contact with these warts does not seem to cause genital warts.
Top
What Do Genital Warts Look Like?
Genital warts often occur in clusters and can be very tiny or can spread into large masses on genital tissues. Genital warts often appear as small bumps or growths, but can appear as groups of warts and grow quite large. Left untreated, genital warts may cause discomfort and pain, interfere with sexual activity and eventually develop a fleshy, cauliflower-like appearance.
How Genital Warts are Diagnosed
Warts sometimes can be very difficult to see and it's also hard to tell the difference between a wart and other bumps or pimples. If you think you have warts or have been exposed to HPV, go to a health care provider or clinic. The health care provider will check more closely and may use a magnifying lens to find small warts.
Do Genital Warts Need to Be Treated?
Most people need some help in getting rid of the warts. Untreated warts may stay the same, grow larger, or multiply. The longer you have them, the harder they are to treat. So, it's important to have genital warts treated as soon as possible.
Find out more about the treatment options available.
Treatments
Though genital warts can be treated, none of the available treatments is a cure for HPV. The virus can remain in nearby skin after treatment. Because the virus can lie dormant in the cells, in some cases warts can return months or even years after treatment. In other cases, warts never recur.
How Can I Avoid Getting STDs Including Genital Warts
Certain ways to lower your risk of getting any sexually transmitted disease also may be effective with HPV or genital warts:
You can reduce your risk of getting HPV or genital warts by not having sex with anyone or by having sex only with one uninfected partner who has sex only with you. People who have many sexual partners are at higher risk of getting sexually transmitted infections.
Latex condoms, used properly from start to finish each time you have sex, provide some protection if they cover the area of the HPV infection. Condoms are recommended with all new or casual sexual partners.
Spermicidal foams, creams, and jellies are not proven to act against HPV and genital warts. They are best used along with condoms, not in place of condoms.
If You Are Diagnosed With An STD
Those STDs caused by bacteria (such as chlamydia or gonorrhea) can be cured with antibiotics. Those STDs caused by a virus (such as herpes or HPV) cannot be cured, but they can be treated to relieve symptoms.
Follow your provider's treatment directions.
Ask your provider about ways to avoid spreading the STD to a partner.
Tell your partner you have a STD. Ask your partner to get tested too.
Avoid sex until both you and your partner have been treated.
Return for follow-up care if your provider asks you to.
Top
Is it Normal To Feel Emotional and Upset About Having HPV or Genital Warts?
Yes. Some people feel very upset. They feel ashamed or less attractive or less interested in sex. They feel angry at their sexual partner(s), even though it is usually not possible to know exactly when or from whom the virus was spread. They're afraid that the infection could lead to cancer. It is normal to have all, some, or none of these feelings.
Treatment options include the following:
 Podofilox solution or gel is a patient-applied treatment for external genital warts.
 Cryotherapy freezes the wart(s) off with liquid nitrogen. This procedure must be performed by a trained health care provider.
 Podophyllin is a chemical compound that must also be applied by a health care provider.
 Trichlorocetic acid (TCA) is a chemical compound applied to the surface of the wart by a health care provider.
 Laser therapy (using an intense light to destroy the warts) or surgery (cutting off the warts) has the advantage of getting rid of warts in a single office visit. However, treatment can be expensive and the health care provider must be well-trained in these methods.
 ALDARA
Aldara
Topical Application Induces A Local Immune Response
 Cytokines activate dendritic cells:
 Process human papillomavirus (HPV) antigen
 Travel to lymph nodes
 Activate HPV-specific T cells to enter the bloodstream
 HPV-specific T cells travel to the wart to kill HPV-infected cells
 Monocytes and macrophages phagocytize the debris
Proven To Induce A Local Immune Response
 Induces production of interferon and other cytokines in human peripheral blood mononuclear cells in vitro
 Induces local production of interferon in patients applying ALDARA cream to external genital warts
Reduces HPV Viral Load
 Shown to reduce viral load of HPV-6 and HPV-11, the subtypes most commonly associated with external genital warts
 Significant correlations between increased cytokine production and reduced viral load were seen in patients treated with ALDARA cream
Clears External Genital And Perianal Warts
 Time to total clearance was as early as 4 weeks for females and 6 weeks for males
 Median time to complete clearance was 8 weeks for females and 12 weeks for males
 Of the patients who cleared, 83% exhibited a response to therapy within 4 weeks
 More than 90% of patients experienced reductions in target wart area.
Patients Who Cleared Tended To Remain Clear
Nonablative - And Well Tolerated
 Fewer than 2% of patients discontinued therapy due to application-site or local reactions
 Minimal impact was seen in healthy skin
Clinical Signs Of A Local Immune Response
 Local skin reactions may be a sign of local immune response
 Most local skin reactions were mild to moderate in intensity; however, severe skin reactions were reported in 4% of patients
 Redness, which is not usually painful, is often seen during treatment
Prescribe With Confidence
 Recommended by the CDC as first-line treatment for external genital warts
 Low incidence of side effects
 Minimal impact on healthy skin
 Designated as Pregnancy Category B
Easy For Patients To Apply In Private
 Apply a thin layer of cream to wart area at bedtime every other day (3 times a week), until warts are gone (or up to 16 weeks)
 Each single-use packet contains enough cream to cover a wart area of up to 20 cm 2
 The treated area should be washed with mild soap and water upon waking (6 to 10 hours after application)
Encourage Realistic Expectations
 As an immune response modifier, ALDARA cream clears warts gradually
 Of the patients who cleared, 83% exhibited a response to therapy within 4 weeks
 Clearance may occur as early as 4 weeks; patients should treat until clear (or up to 16 weeks)
ALDARA cream elicits a local immune response; redness, which is not usually painful, is frequently seen at the wart site
For more information on STDs call the CDC National STD Hotline 1-800-227-8922, or visit them at http://www.cdc.gov/std.
You may also visit the American Social Health Association's (ASHA) website for information at www.ashastd.org.
Published at www.nejm.org April 7, 2003 (10.1056/NEJMoa030685)
A Major Outbreak of Severe Acute Respiratory Syndrome in Hong Kong
Nelson Lee, M.D., David Hui, M.D., Alan Wu, M.D., Paul Chan, M.D., Peter Cameron, M.D., Gavin M. Joynt, M.D., Anil Ahuja, M.D., Man Yee Yung, B.Sc., C.B. Leung, M.D., K.F. To, M.D., S.F. Lui, M.D., C.C. Szeto, M.D., Sydney Chung, M.D., and Joseph J.Y. Sung, M.D.
ABSTRACT
Background There has been an outbreak of the severe acute respiratory syndrome (SARS) worldwide. We report the clinical, laboratory, and radiologic features of 138 cases of suspected SARS during a hospital outbreak in Hong Kong.
Methods From March 11 to 25, 2003, all patients with suspected SARS after exposure to an index patient or ward were admitted to the isolation wards of the Prince of Wales Hospital. Their demographic, clinical, laboratory, and radiologic characteristics were analyzed. Clinical end points included the need for intensive care and death. Univariate and multivariate analyses were performed.
Results There were 66 male patients and 72 female patients in this cohort, 69 of whom were health care workers. The most common symptoms included fever (in 100 percent of the patients); chills, rigors, or both (73.2 percent); and myalgia (60.9 percent). Cough and headache were also reported in more than 50 percent of the patients. Other common findings were lymphopenia (in 69.6 percent), thrombocytopenia (44.8 percent), and elevated lactase dehydrogenase and creatine kinase levels (71.0 percent and 32.1 percent, respectively). Peripheral air-space consolidation was commonly observed on thoracic computed tomographic scanning. A total of 32 patients (23.2 percent) were admitted to the intensive care unit; 5 patients died, all of whom had coexisting conditions. In a multivariate analysis, the independent predictors of an adverse outcome were advanced age (odds ratio per decade of life, 1.80; 95 percent confidence interval, 1.16 to 2.81; P=0.009), a high peak lactate dehydrogenase level (odds ratio per 100 U per liter, 2.09; 95 percent confidence interval, 1.28 to 3.42; P=0.003), and a high absolute neutrophil count on presentation (odds ratio, 1.60; 95 percent confidence interval, 1.03 to 2.50; P=0.04).
Conclusions SARS is a serious respiratory illness that led to significant morbidity and mortality in our cohort.
Notice: Because of possible public health implications, this article has been published at www.nejm.org on April 7, 2003.
 West Nile Virus Infection in the United States: A Review and Update
Deborah S. Asnis, MD Infect Med 19(6):266-278, 2002. © 2002 Cliggott Publishing, Division of SCP Communications
Posted 08/14/2002 Abstract and Introduction
Abstract
In August 1999, a cluster of patients were admitted to medical ICUs in New York City with fever, confusion, GI complaints, muscle weakness, and a presumed diagnosis of encephalitis. A cooperative investigation was conducted by the city and state departments of health along with the CDC and ultimately determined that West Nile virus (WNV) was the causative agent; interagency cooperation was key in identifying the outbreak. It was the first time that WNV was found in the Western Hemisphere. In the following 2 years, cases appeared in areas near New York and then in states up and down the East Coast. The epidemiology this year will depend on weather and other factors.
Introduction
The first recognized arbovirus infection in New York City since yellow fever in the 1800s occurred in the city in the summer of 1999. On August 12, 1999, a 60-year-old man was admitted to Flushing Hospital Medical Center (FHMC) in New York City, complaining of fever, weakness, and nausea of 3 days' duration. The initial diagnosis was pneumonia, and he was treated with antibiotics. Within 4 days, he became confused and had proximal muscle weakness with depressed deep tendon reflexes, urinary retention, and respiratory difficulty. The patient was transferred to the medical ICU (MICU), where he underwent a lumbar puncture (LP) and required oxygen supplementation.
The patient was treated with intravenous ceftriaxone and acyclovir for presumed meningoencephalitis. Electromyogram/nerve conduction velocity (EMG/NCV) studies demonstrated axonal-type polyneuropathy consistent with Guillain-Barré syndrome (GBS), and plasmapheresis was started. He remained in the hospital for about 6 weeks and was transferred for rehabilitation, with gradual improvement of his mental status, muscle strength, and bladder control.[1]
A Cluster of Cases
In the following 2-week interval, 4 additional patients were admitted to the MICU with similar neurologic symptoms. On August 15, an 80-year-old man was brought by ambulance after paramedics found him unresponsive and in cardiac arrest. He was intubated and resuscitated. Before this event, he had suffered from fever, headache, weakness, and diarrhea for about a week. Within a few days, flaccid paralysis developed, and EMG/NCV studies showed motor axonopathy. He received intravenous ceftriaxone and clindamycin. He died after 3 weeks of hospitalization, with complications including myocardial infarction, hypotension, disseminated intravascular coagulation, and hepatic and renal insufficiency.[1]
On August 18, a 75-year-old man with prostate cancer presented with fever, confusion, tremors, and urinary incontinence. He required mechanical ventilation, and flaccid paralysis developed. EMG/NCV studies showed axonal-type polyneuropathy. He was given intravenous ampicillin, ceftriaxone, and acyclovir. He died after 3 weeks.[1]
On August 20, an 87-year-old woman with colon and breast cancer presented with headache, diarrhea, fever, mild dysarthria, and weakness. She was initially admitted to the medical service with dehydration. However, instead of improving, she became febrile, lethargic, confused, and diffusely weak. She was transferred to the MICU and was intubated. She was given intravenous ceftriaxone and acyclovir, and she underwent plasmapheresis for presumed GBS. EMG/NCV studies showed diffuse motor axonal polyneuropathy. She died on day 10.[1]
On August 23, the New York City Department of Health (NYCDOH) was notified about these patients. The differential diagnosis included viral meningoencephalitis, GBS, toxin exposure, and botulism. The health department physician thought the diagnosis was most likely viral encephalitis and helped expedite viral analysis of spinal fluid at the New York State Laboratories.
After the fourth patient entered the MICU, the NYCDOH was recalled on August 27; during the conversation, the attending neurologist mentioned that there was a similar case at a neighboring hospital. The CDC was called that afternoon. Investigators from the NYCDOH reviewed the charts at both hospitals on August 28. While they were conducting their investigation at FHMC, a fifth patient was admitted there. He was a 57-year-old man who had fever, confusion, and vomiting. He was not weak but was quite agitated. He was given intravenous ampicillin, ceftriaxone, and acyclovir and was discharged 2 weeks later.
The 5 MICU patients all had encephalitis, and each had an LP (Table 1).[1] All but patient 2 had pleocytosis. The patients with pleocytosis had lymphocyte predominance except for patient 3. He presented within 24 hours of onset of symptoms, and a repeated LP showed a change to lymphocyte predominance. All of the patients had a protein level above 40 mg/dL. None had a depressed glucose level. Four of the 5 patients had CT scans of the head; atrophy was demonstrated in 3. Four patients had severe muscle weakness and respiratory difficulty, a finding atypical for encephalitis but confirmed by EMG/NCV studies showing diffuse motor axonopathy.
All 5 patients had temperatures above 38.4°C (101.1°F), and 4 of the 5 had temperatures above 39°C (102.1°F). GI complaints, such as nausea, vomiting, and diarrhea, occurred in 4 of the 5 patients.[1] Three patients died, and the city medical examiner's office performed autopsies. Microglial nodules and perivascular inflammation were noted in the white and gray matter, with brain stem involvement, especially of the medulla. Focal mononuclear inflammation was present in the cranial nerve roots of the medulla. A positive immunohistochemical stain for flavivirus was eventually obtained, along with a polymerase chain reaction (PCR) test for West Nile virus (WNV).[1,2]
After the MICU cluster was detected, 3 more patients (1 with encephalitis, 2 with meningitis) were seen in the medical service. These patients were not as ill, were younger, and did not have severe muscle weakness. All 8 patients had a relative lymphocytopenia, defined as less than 20% lymphocytes on peripheral smear, and their white blood cell (WBC) counts ranged from 4.3 to 17.9/µL.[3]
This article reviews the epidemiology and medical history of WNV infection in the United States since this first outbreak, with an emphasis on the importance of cooperation among health agencies in recognizing and responding to the disease. It ends with a warning note on the likelihood of continued outbreaks and provides suggestions for monitoring for WNV infection.
Investigation
The investigation that was led by the NYCDOH identified 8 patients who were relatively healthy, active, older persons aged between 58 and 87 years who lived in a 4-square-mile radius of one another in northern Queens, a section of the city. All had a prodromal illness with fever and GI symptoms followed by an acute change in mentation, severe muscle weakness with flaccid paralysis and/or EMG evidence of axonal neuropathy, cerebrospinal fluid (CSF) and blood parameters consistent with viral causation, and the risk factor of spending time outdoors in the evening hours in the 2 weeks before the onset of illness.[4]
On September 3, 1999, serologic testing of blood and CSF confirmed St Louis encephalitis (SLE) virus, and emergency mosquito control with both ground and aerial spraying was implemented. SLE had been reported in New York State but never in New York City. About 400,000 cans of mosquito repellent were distributed by local firehouses, and the NYCDOH printed brochures about the disease in 8 languages, with daily updates faxed to city hospitals. The NYCDOH telephone hot line, which was staffed around the clock, received more than 150,000 calls during a 2-month period.[5] That summer, officials estimated that the state, city, and 4 counties involved spent more than $14 million on mosquito control measures, including aerial and ground spraying of pesticides, application of a biologic larvicide to stagnant water, and a public health campaign for personal protection against mosquito bites from August until October.[6]
Disease in Birds
Concurrent with the human outbreak was a separate veterinary event that, together with additional data from the clinical cases, pointed away from SLE and toward an infectious cause new to this hemisphere. In early June, a veterinarian at an animal health clinic in Queens examined several birds that had nervous system disorders. During July and August, there were increased reports of dead birds. Dead birds were sent to the wildlife pathologist at the state department of environmental conservation, but no clear cause was identified. Several exotic birds died at the Bronx Zoo soon after the human outbreak of SLE was announced. Autopsy of the birds demonstrated hemorrhage and inflammation, not only in the brain but also in the heart and GI tract. The chief pathologist at the Bronx Zoo did not think the birds were dying as a result of SLE, because this disease normally does not sicken its host.
Samples were sent to the US Department of Agriculture's National Veterinary Service Laboratory in Ames, Iowa, where a flavivirus was suspected but could not be identified. The pathologist pursued this by sending her samples to the US Army Medical Research Institute of Infectious Diseases as well as the CDC arbovirus laboratory at Fort Collins, Colo. On September 23, the CDC confirmed that "a West Nile-like virus" was found in the birds.[6]
The Correct Diagnosis
At the same time, specimens from the brains of the 3 encephalitis patients were sent to the University of California at Irvine, and these were found to be positive for West Nile-like virus too.[7] On September 27, the CDC confirmed that a West Nile-like virus was found in both the animal and human outbreaks.[6] This was the first time WNV was found in the Western Hemisphere. The strain's DNA, which belongs to lineage I of the 2 possible evolutionary lineages, was more than 99.8% identical to a WNV strain found in the brain of a dead goose in Israel. Lineage I includes primarily West Africa, the Middle East, Eastern Europe, and Australia and is associated with human or equine outbreaks.[8]
Patient Characteristics
By the end of 1999, 62 people had become ill with WNV infection, and 7 of these had died. The geographic distribution included 46 in New York City, 9 in Westchester County, and 6 in Nassau County (both adjacent to the city). One patient was a Canadian tourist visiting Queens. Among the New York City cases, 32 were in Queens, 10 in the Bronx, 3 in Brooklyn, and 1 in Manhattan (Table 2). It is worth mentioning that no cases occurred in Staten Island during 1999.[4]
The median age of the hospitalized patients was 71 years; the majority were older than 50. The older patients were more likely to have severe neurologic disease.[9] There were only 2 pediatric cases, one in a 5-year-old with aseptic meningitis and the other in a 15-year-old with encephalitis. (Children are not at higher risk for WNV infection.[10]) One third of the patients recalled a mosquito bite in the month preceding the illness. Coexistent medical conditions included hypertension (in 42%), diabetes mellitus (in 20%), coronary artery disease (in 20%), and immunosuppression (in 14%). There were 8 immunosuppressed patients, including 5 with cancer, 1 with HIV infection, 1 receiving prednisone therapy for asthma, and 1 with alcoholism.[9]
Avian or mosquito surveillance demonstrated that WNV extended into 4 states: New York, New Jersey, Connecticut, and Maryland.[11] The source of this outbreak is not exactly known but could have been an infected bird that either migrated or was imported, infected mosquitoes, or a viremic person.
A study showed that the virus could overwinter in mosquitoes and return the next summer.[12] A serosurvey of 677 persons conducted in northern Queens, the epicenter, in October 1999 showed a seroprevalence of 2.6%. Four hundred fifty-nine households were surveyed, and residents interviewed had to be at least 5 years old. About 1 in 5 persons infected with WNV had had a mild nonspecific febrile illness. For every patient with West Nile meningoencephalitis, there were 140 patients with subclinical or mildly symptomatic infections. Applying this ratio to the 59 hospitalized meningoencephalitis patients in 1999, it is estimated that about 8200 WNV infections (1700 with febrile illnesses) occurred in the greater New York City metropolitan area.[13]
Seroprevalence was studied in healthy horses, dogs, and cats in the city as well. Two (3%) of 73 horses, 10 (5%) of 189 dogs, and 0 (0%) of 12 cats were positive for WNV-neutralizing antibodies.[14] A seroprevalence study of WNV in wild birds in 5 city areas showed that 50% of sampled birds in Queens, 11% in Westchester County, 6% in Nassau County, 5% in Brooklyn, and 2% in Staten Island had evidence of flavivirus-neutralizing antibody.[15] In addition to humans, horses can also succumb to WNV infection with fever, ataxia, muscle fasciculations, and tremors. During 1999, WNV infection developed in about 25 (20 definite, 5 probable) horses, with a 20% (4 of 20) mortality. Infection in horses occurs later in the season than that in humans and may be carried by a different mosquito vector.[16]
The NYCDOH has conducted a long-term study of the city's hospitalized patients who survived to measure persistent symptoms and long-term sequelae. After 1 year of follow-up, the following symptoms were reported: fatigue (67%), memory loss (50%), difficulty in walking (49%), muscle weakness (44%), and depression (38%). These complaints were found more frequently in patients older than 65 years and in those in whom encephalitis was originally diagnosed.[17]
Characteristics of WNV Infection
Classification and Natural History
WNV is a member of the Flaviviridae, a family of single-stranded RNA viruses, which is subdivided into 2 genera: flavivirus and pestivirus. WNV is a flavivirus, and transmission of disease occurs by mosquitoes.[18] WNV has been isolated from ticks, but it is unclear how important ticks are to the natural transmission cycle.[19] The virus belongs to the Japanese encephalitis complex and shares this category with Japanese, St Louis, and Murray Valley encephalitis viruses; Kunjin virus; and other pathogens.[18] It was first isolated in 1937 from the blood of a febrile, but otherwise asymptomatic, Ugandan woman.[20] WNV is found throughout Africa and the Middle East and in parts of Europe, Russia, India, and Indonesia. The incubation period of WNV is 5 to 15 days.[4] Wild birds are the primary reservoir; the mosquito, specifically, several Culex species, is the main vector.
Clinical Infection
The majority of infections are clinically silent. Symptoms typically include fever, headache, myalgias, pharyngitis, conjunctivitis, and diarrhea. A nonpruritic roseolar or maculopapular rash on the chest, back, and arms reportedly develops in about half of patients,[18] although only 19% of patients had this sign in the New York City outbreak.[9] Lymphadenopathy is also seen. Encephalitis or meningitis is seen rarely, in fewer than 1%.[13]
Laboratory studies can reveal either leukocytosis[3,9] or leukopenia,[9,18] as well as relative lymphocytopenia.[1,9,21] Examination of CSF demonstrates leukocytosis or an elevated protein level. Diagnosis is made by isolating WNV from or showing viral antigen in tissues or blood, CSF, or other body fluid; demonstrating IgM antibody to WNV in CSF by enzyme-linked immunosorbent assay (ELISA); demonstrating a 4-fold serial change in results of plaque reduction neutralization test (PRNT) for WNV in paired, acute, and convalescent serum samples taken at least 2 weeks apart; or obtaining both WNV IgM and IgG antibody in a single serum specimen applying both ELISA and PRNT.[17] IgM-capture ELISA for serum and CSF is the preferred and most sensitive method.[17]
A PRNT is then done to rule out cross-reactions with other flaviviruses. Viral culture from CSF or brain tissue in humans has not been successful.[9] In 1999 and 2000, almost all patients (95%) had positive results for WNV on IgM-capture ELISA in CSF. IgM was found within 8 days of onset of symptoms in 90% of patients. Viral RNA by real-time PCR assay was identified in CSF of only 57% of patients and in serum of 14% in 1999 and in CSF of 8% of patients in 2000.[17]
Reappearance in 2000
WNV reappeared in 2000, either through wintering or reintroduction. In February, the virus was found in a red-tailed hawk, a nonmigratory bird, before the mosquito season in Connecticut and again in April in another hawk in Suffolk County, New York.[22] Twenty-one persons contracted WNV, 19 of whom were hospitalized with encephalitis or meningitis: 14 in New York, 6 in New Jersey, and 1 in Connecticut. Of the 14 cases in New York, 10 were located in Staten Island -- the new epicenter -- 2 in Brooklyn, 1 in Queens, and 1 in Manhatten.[23] There were 2 deaths (Table 2).
Serosurveys were conducted to determine the prevalence of WNV in 3 separate areas: Staten Island, New York (0.46%); Fairfield County, Connecticut (0.0%); and Suffolk County, New York (0.12%) during October and November 2000. These 3 areas were selected because of the high WNV activity found in dead birds and through mosquito surveillance. The seroprevalence found in Staten Island may have been lower than the prevalence in 1999 in Queens because the epizootic disease in Queens in 1999 was more intense (house sparrows in Queens had 6 times higher neutralizing antibody than those in Staten Island); the 1999 survey covered a more concentrated area of 3 square miles, whereas the Staten Island survey was evenly spread over 56 square miles; the prevention measures initiated by the NYCDOH included public health campaigns, application of larvicide before the season, and reduction of breeding sites for mosquitoes; or the nature of WNV outbreaks was sporadic.[24]
WNV was also isolated from 480 pools of mosquitoes comprising 14 species, of which 90% were Culex[17]; more than 4000 birds from more than 75 species (80% were crows)[17]; 63 horses[17]; and a few small mammals, such as bats, rodents, rabbits, cats, and skunks.[9] The geographic distribution of WNV rapidly expanded to include 12 states (Connecticut, Delaware, Maryland, Massachusetts, New Hampshire, New Jersey, New York, North Carolina, Pennsylvania, Rhode Island, Vermont, Virginia) and the District of Columbia (Table 2).[23]
Year 2001
As of March 4, 2002, 66 cases of WNV infection (64 with encephalitis or meningitis and 2 with fever but without neurologic illness) had been reported as occuring in 2001, spanning 10 states: New York (15), Florida (12), New Jersey (12), Connecticut (6), Maryland (6), Pennsylvania (3), Massachusetts (3), Georgia (6), Louisiana (1), and Alabama (2). Nine of the cases were in New York City (2 in Staten Island, 2 in Queens, 2 in Brooklyn, and 3 in Manhattan). Infected birds were reported in 27 states and the District of Columbia, 679 horses from 19 states were infected, and 904 mosquito pools were found in 16 states and the District of Columbia (Figure). Infected birds were also found in the area of Windsor, Toronto, and London in southeast Ontario (A. A. Marfin, CDC, personal communication). The first person infected with WNV was reported in the Cayman Islands.
Figure. Areas reporting West Nile virus (WNV) activity in the United States as of November 20, 2001. (From Marfin A. West Nile Virus 2001: Southern and Western Expansion. 2002.[35]) Dark Purple: Human West Nile encephalitis or meningitis and animal WNV activity. Light Purple: Animal WNV activity only.
One of the 2 Queens patients was admitted to FHMC; this time, WNV was considered early in the hospital stay. The patient, a 75-year-old man from Uruguay, had been in the United States for 3 months. He presented with fever, chills, decreased mentation, and weakness. He admitted to early morning walks to improve his cardiac function. On examination, his temperature was 39.8°C (103.6°F), his affect was dull, and his reflexes were normal, but he could not move his legs well. An LP was done and the CSF showed a WBC count of 429/µL, mostly lymphocytes; red blood cell count of 10/µL; protein level of 215 mg/dL; and glucose level of 62 mg/dL. The peripheral WBC count was 8.1/µL, but the percentage of lymphocytes was 8.3. This time, WNV was confirmed quickly, and the patient was discharged to a rehabilitation facility.
2002 and Beyond
Case Reporting and Diagnosis
A multistate surveillance program known as ArboNET was started in 1999 to help identify animal and human infections and devise strategies for prevention (Box, page 276). Physicians should report all cases of viral encephalitis, aseptic meningitis in those aged 17 and older, and GBS to their local health departments.
Clues that should raise suspicion for West Nile encephalitis are listed in Table 3.[25] Serologic testing for IgM-capture antibody by ELISA should be ordered on both blood and CSF, and PCR testing can also be done if needed. (The specificity of the PCR test approaches 100%, but the sensitivity is less than that of the IGM-capture ELISA. A negative PCR result on CSF or tissue does not rule out WNV infection; it may be due either to clearance from the spinal fluid at the time of the procedure or to the limit of the sensitivity threshold of the test.[17]) Two tubes of CSF, minimum 1 mL, must be frozen at 270°C and forwarded to the health department laboratory. A red-top tube with 5 to 10 mL of serum must be centrifuged and refrigerated.[17] PCR assays for other causes of encephalitis, such as herpes simplex virus, varicella-zoster virus, enteroviruses, cytomegalovirus, and Epstein-Barr virus, can be requested depending on your state laboratory.
Three potential problems can occur with testing for WNV and cause false-positive viral IgM and IgG ELISA results: previous yellow fever vaccination; previous or current infection with other related flaviviruses, such as dengue or St Louis encephalitis virus; and residence in areas where WNV is endemic.[17] The NYCDOH and the CDC studied survivors of the 1999 WNV outbreak and found that WNV IgM antibody can persist for months after the initial illness. About two thirds of the survivors continued to have antibody at 6 months; this decreased to one third after 1 year. Results of a single IgM test could thus be misleading in a patient from a community where the virus has appeared, especially if he or she is asymptomatic. In all these instances, a WNV-specific PRNT on sera obtained during both the acute and convalescent stage of illness would help clarify possible errors.[17]
Treatment for WNV infection is supportive; experimental trials with ribavirin,[26] interferon,[27] and other antivirals[28] are ongoing. One study in Israel successfully used intravenous gamma globulin with high titers of WNV in a seriously ill patient.[29] The development of a vaccine is being attempted, using either the yellow fever vaccine[30] or the dengue virus chimera[31] as the backbone.
How Great a Threat This Year?
Although climate and weather may influence mosquito populations, predictions based on weather may be too simplistic in forecasting WNV epidemics.[32] Despite this, one cannot forget that New York City in 1999 had a mild winter followed by a hot, dry summer.[32] This particular scenario is conducive to arboviral outbreaks such as West Nile or St Louis encephalitis. In hot, dry weather, water in city drains and catch basins becomes richer in organic material that the Culex pipiens mosquito thrives in; there are fewer mosquito predators, such as frogs and dragonflies; and birds that spread WNV congregate at fewer watering holes, where the virus can circulate more easily. Extremely high temperatures also speed viral production within the mosquito.[33] These specific climatic events were not present in 2000, which had a cool, wet summer. This can be one reason fewer WNV infection cases were seen. So the number of WNV infections this year will depend at least in part on the weather but also on other complex factors, including density and age of both vector and human population.
Since the inception of this outbreak, certain lessons continue to be reemphasized. We must work to foster strong relationships between health departments, community physicians, veterinarians, and entomologists along with improving our laboratory capacity and capability to diagnose unusual pathogens. Only with such cooperation will we be able to meet the next challenge.
Clues to West Nile encephalitis
Unexplained bird or horse deaths
Mosquito season
Age > 50 years
Muscle weakness and/or flaccid paralysis
Hyporeflexia
EMG/NCV showing axonal neuropathy
Lymphocytopenia
MRI showing enhancement of leptomeninges and/or periventricular area
Dr Asnis is clinical assistant professor in medicine, Weill Medical College of Cornell University, New York, and director of infectious diseases, department of internal medicine, Flushing Hospital Medical Center, Flushing, NY.
--------------------------------------------------------------------------------
Reprinted from ScienceDaily Magazine ...
Source: NIH/National Institute Of Allergy And Infectious Diseases
Date Posted: Thursday, June 21, 2001
Web Address: http://www.sciencedaily.com/releases/2001/06/010619073530.htm
NIAID Collaboration Yields New Test For Lyme Disease
A new test developed with funding from the National Institute of Allergy and Infectious Diseases (NIAID) has been shown to be highly accurate and sensitive for detecting antibodies to Lyme disease. Produced by Immunetics, Inc. of Cambridge, Massachusetts, the new assay recently won approval from the Food and Drug Administration (FDA) for use as a diagnostic test for Lyme disease.
It is the first diagnostic tool to use a synthetic product called C6, a hybrid chemical marker based on components derived from the surface of Borrelia burgdorferi, the tick-borne bacterium that causes Lyme disease. The C6 test is sensitive only to antibodies generated during an active infection.
Lyme disease can be difficult to diagnose, especially in later stages of infection when an individual’s antibodies can fall to very low levels. Laboratory testing showed the C6 approach resulted in a high rate of sensitivity to antibodies from both the early and late stages of Lyme disease. The kit also resulted in fewer false positive readings when compared with current screening methods. Significantly, no false positive readings were obtained when the kit was used to test people who had previously received Lymerix®, the Lyme disease vaccine. Another advantage is the test’s ability to detect antibodies specific to both U.S. and European strains of Borrelia.
“The C6 test is the result of years of collaboration in an ongoing effort to improve our ability to diagnose Lyme disease,” explains microbiologist Phillip Baker, Ph.D., NIAID’s Lyme disease program officer. “This new approach is an important first step in that direction.”
NIAID is a component of the National Institutes of Health (NIH). NIAID supports basic and applied research to prevent, diagnose, and treat infectious and immune-mediated illnesses, including HIV/AIDS and other sexually transmitted diseases, tuberculosis, malaria, autoimmune disorders, asthma and allergies.
Press releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at http://www.niaid.nih.gov.
The National Institute of Allergy and Infectious Diseases is a component of the National Institutes of Health, U.S. Department of Health and Human Services
Copyright © 1995-2001 ScienceDaily Magazine | Email: editor@sciencedaily.com
|