GENEVA (Reuters) - The H5N1 birdflu virus mutated somewhat among Indonesians in the largest known human cluster, but did not evolve into a more transmissible form, the World Health Organization (WHO) said on Friday.

A spokeswoman for the U.N. agency, Maria Cheng, said the result had come from its investigation into a recent cluster of cases in northern Sumatra, where seven members of a single family were killed in May.

“There was a mutation found, it was in a report recently given to the (Indonesian) government. It was the summary of the investigation into the northern Sumatra case,” she told Reuters in Geneva, in response to a query.

“But it did not mutate into a form that is more transmissible because it didn’t seem to go beyond the cluster,” she added.

Indonesian and WHO officials closely monitored more than 50 contacts of the victims, keeping them in voluntary home quarantine for several weeks following the outbreak, but none developed symptoms, according to the Geneva-based agency.

The H5N1 strain of avian influenza has spread rapidly out of eastern Asia in recent months. It almost exclusively infects birds but has killed 130 people since 2003, mostly in Asia.

Experts believe it poses the greatest threat yet of a pandemic, a global epidemic of flu that could kill millions, if it acquires the ability to pass easily from human to human.10,000 dollar loansloans 100k schoolloan amortizeloans 100 home financingvegas loans las home 100loan calculator 20 80instant $500 loanloan rules 401khome 1st loan time buyerloans home accredited

Reuters Health Information 2006. © 2006 Reuters Ltd.

By Maggie Fox

WASHINGTON (Reuters) Jun 14 - U.S. emergency rooms are understaffed, overwhelmed and could not cope with a crisis, whether a pandemic, attack or natural disaster, according to three reports released on Wednesday.

Americans rely heavily on emergency departments and emergency medical services to save their lives when sudden illness or disaster strikes, yet these services are not properly funded and often do not live up to expectations, the reports from the Institute of Medicine found.

“We are definitely not prepared for the onslaught we would receive today in the event of an emergency (such as) a hurricane, bioterrorist attack…or a pandemic,” Dr. Brent Eastman, Chief Medical Officer of Scripps Health in San Diego, told a news conference.

“We hope that this report will astonish the nation.”

The Institute, an independent body that advises the federal government on health matters, issued three reports on the fragile status of emergency care in the United States. It noted that emergency services are the primary source of health care for many uninsured and on evenings and weekends when clinics are closed.

“Each year in the United States approximately 114 million visits to emergency department occur, and 16 million of these patients arrive by ambulance. In 2002, 43 percent of all hospital admissions in the United States entered through the emergency department,” one of the reports stated.

LACK OF TRAINING, SUPPLIES

Despite increasing attention placed on emergency and disaster preparedness in the United States after the September 11 attacks, emergency services received only 4 percent of $3.38 billion distributed by the Homeland Security Department for emergency preparedness in 2002 and 2003, the Institute said. The report did not give figures for 2004 or 2005.

“The result is that few hospital and EMS professionals have had even minimal disaster preparedness training,” one report said.

“Even fewer have access to personal protective equipment; hospitals, many already stretched to the limit, lack the ability to absorb any significant surge in casualties; and supplies of critical hospital equipment, such as decontamination showers…ventilators, and intensive care unit beds, are wholly inadequate.”

Experts say none of the complaints are new and yet little has been done to address the problem, perhaps because the U.S. healthcare system relies heavily on private enterprise.

“Hospitals must be reimbursed for the significant amounts of uncompensated emergency and trauma care they provide. To do otherwise threatens to destroy the critical emergency care infrastructure that all Americans depend on,” said Dr. Rick Blum, president of the American College of Emergency Physicians.

The reports call for a pool of $50 million to pay for this.

State and federal governments must also work to ensure that hospitals and emergency medical services can communicate with police, fire departments and other emergency responders — something many cannot do now.

Some of the nation’s emergency medical services are municipally managed, others are privately owned. Some are organized under fire departments, while others are operated by hospitals or other medical organizations and they all need to coordinate better, the panel said.

It recommended that Congress allocate $88 million for projects to find ways to do this.

Hospitals also have to stop diverting patients to the emergency room, get patients out of the ER and into hospital rooms so they do not clog up the system, the committee said.

Human malaria is a parasitic disease transmitted through the bite of an infected female Anopheles mosquito. Most malaria cases in the United States occur in travelers who recently visited areas where malaria is endemic without taking adequate chemoprophylaxis (1). This report describes five cases of Plasmodium falciparum malaria that occurred in a family residing near Chicago, Illinois, during 2006. These cases underscore the importance of malaria-prevention measures (e.g., avoidance of mosquito bites and appropriate chemoprophylaxis) for travelers to malaria-endemic areas. In February 2006, three boys aged 10, 6, and 4 years (patients 1, 2, and 3, respectively [Table]) were hospitalized for complicated P. falciparum malaria (i.e., malaria with potentially life-threatening manifestations). They were members of a family of seven, including the two parents, the three male patients, and two girls aged 11 and 2 years (patients 4 and 5, respectively), all of whom had traveled in 2005 and early 2006 to Nigeria, the native country of the parents and their oldest daughter. The four youngest children, including the three boys and the girl aged 2 years, were born in the United States, where the family had lived for 10 years. Before the trip to Nigeria, the parents had asked their local health department about malaria medications. They were told that antimalarial drugs were available. However, they assumed incorrectly that the drugs were to be taken for treatment only and did not realize that the drugs could also be used for chemoprophylaxis; therefore, they did not request a prescription. The mother and the three youngest children spent 3 months in Nigeria; the father and the two oldest children stayed 5 weeks. The family visited friends and relatives in various locations of Nigeria (e.g., Abuja, Ilorin, Kano, and Lagos) without taking malaria chemoprophylaxis. During their travel, three of the children (patients 2, 3, and 5) had onset of separate febrile episodes that were treated uneventfully with antibiotics, ibuprofen, and sulfadoxine-pyrimethamine (Fansidar®), all recommended by a local physician. All family members returned to the United States in January 2006. Two weeks after their return, the four oldest children (the three boys and the girl aged 11 years) had onset of influenza-like symptoms, including fever and headaches, and were treated at a local clinic with antipyretics and amoxicillin. Three days later, the parents noticed that the eyes of the three boys (patients 1, 2, and 3) had yellow scleras and took them to the hospital. On examination, all three were febrile and jaundiced, and the boy aged 10 years (patient 1) appeared ill and had pallor and severe back pain. Blood smears confirmed the diagnosis of P. falciparum malaria in all three patients; the boy aged 4 years (patient 3) had a high parasitemia at 4.8%. Other abnormal laboratory findings for all three patients included anemia, thrombocytopenia, hyperbilirubinemia, and elevated aminotransferase levels. The boy aged 10 years (patient 1) had severe metabolic acidosis and hypoglycemia (glucose: 25 mg/dL; blood pH: 7.1; base excess: -15 mEq/L). Because patients 1, 2, and 3 each had at least one manifestation of complicated malaria (e.g., acidosis, hypoglycemia, severe anemia, or jaundice) (2), all three were admitted to the pediatric intensive care unit and treated with intravenous quinidine combined with doxycycline (patient 1) or clindamycin (patients 2 and 3, in whom doxycycline was contraindicated because they were aged <8 years) (3). The boy aged 10 years (patient 1) had a hyperhemolytic syndrome with markedly decreased hemoglobin concentration, severe metabolic acidosis, and hypoglycemia and therefore required intubation, dextrose infusion, transfusions of red blood cells and fresh frozen plasma, erythrophoresis (exchange transfusion), and plasmapheresis. The boy aged 4 years (patient 3) required packed red blood cell transfusions for anemia. The boys aged 6 and 4 years (patients 2 and 3, respectively) had prolonged QT intervals on electrocardiogram, which resolved after discontinuation of the intravenous quinidine. Parasitemia in all three patients had resolved by the third day of hospitalization, and all three children were discharged in good condition after 1 week. The day after hospitalization of the three boys, their two sisters also were tested by blood smear and determined to be infected with P. falciparum, albeit at lower parasite densities. The girl aged 11 years (patient 4) had fever and headache; her sister aged 2 years (patient 5) was asymptomatic (Table). Both were hospitalized in a general pediatric unit and treated successfully with oral quinine combined with either doxycycline or clindamycin; parasitemia resolved by the third day of hospitalization. The parents reported that patients 1 and 5 had sickle cell disease. Subsequent hemoglobin electrophoresis indicated that all five children had either sickle cell disease (SS) or sickle cell trait (SA). Infection with P. falciparum was confirmed by polymerase chain reaction (PCR) performed at CDC on the pretreatment blood specimens of patients 1, 2, 3, and 4 (4). No pretreatment blood sample was available for patient 5; PCR results for a posttreatment specimen (obtained 1 day after completion of quinine therapy) were negative. Both parents were asymptomatic. They consulted their primary physician, who treated them presumptively with mefloquine, without taking a blood smear. Reported by: D Glikman, MD, JF Marcinak, MD, RS Daum, MD, Section of Infectious Diseases, CP Montgomery, MD, KS Hoehn, MD, Section of Critical Care Medicine, Dept of Pediatrics, J Anastasi, MD, Dept of Pathology, Univ of Chicago, Chicago, Illinois. HS Bishop, P Nguyen-Dinh, MD, Div of Parasitic Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases (proposed), CDC. Editorial Note:   The high attack rate reported in the family described in this report illustrates the elevated risk for malaria in travelers to sub-Saharan Africa. Among 1,190 imported cases of malaria reported in the United States during 2004 for which the region of acquisition was known, 68% were acquired in Africa, with the majority of cases attributed to P. falciparum (1), the species that most typically causes severe malaria in humans. Three of the five infected children described in this report had complicated malaria and required treatment in the intensive care unit. All five children had the sickle cell gene; two were SS homozygotes, and three were heterozygotes. The sickle cell gene is found more commonly in persons of African descent because the sickle cell trait confers a selective advantage, resistance to severe malaria (5). In a recent large cohort study of Kenyan children, the sickle cell trait was found to be approximately 50% protective against mild clinical malaria, 75% protective against admission to the hospital for malaria, and 90% protective against severe or complicated malaria (6). However, two of the three patients with sickle cell trait described in this report (patients 2 and 3) still had complicated malaria. Patient 1 had a low parasitemia but was severely ill, probably because of hyperhemolysis related to sickle cell disease. In a study from Nigeria, malaria was found to be an important risk factor for hyperhemolytic crisis in children with sickle cell disease (7). These five cases underscore the importance of preventive measures, including avoidance of mosquito bites and appropriate chemoprophylaxis, for travelers to malaria-endemic areas (8). The majority of cases of imported malaria occur in travelers who have not taken appropriate prophylaxis. Among U.S. civilians with imported malaria reported in 2004, approximately 76% had not taken any prophylaxis or had taken prophylaxis that did not conform to CDC recommendations (1). Failure to take prophylaxis is a major contributing factor to malaria cases and deaths in U.S. travelers (9). Especially low compliance rates are reported among U.S. residents born in malaria-endemic areas who return to their country of origin to visit friends and relatives, a situation derived from various cultural and economic factors, such as misperception that malaria is not a serious illness or lack of adequate insurance coverage (10). Acquired immunity to malaria is never complete and persists only through continual reexposure to malaria. Persons born in a malaria-endemic country who move to a nonendemic area are at risk for symptomatic and severe malaria upon return to their native country, unless they take preventive measures. Travelers who have onset of malaria while visiting a malaria-endemic country might receive a treatment that does not adhere to CDC guidelines; for example, the drug used to treat presumed malaria in three of the children during their travel (sulfadoxine-pyrimethamine) is no longer recommended by CDC because of drug resistance and adverse drug effects (3). Prophylaxis recommendations should be based on risk for malaria acquisition, occurrence of drug resistance in the areas to be visited, and traveler characteristics (e.g., age, reproductive status, and medical history). For example, chloroquine-resistant malaria is widespread in sub-Saharan Africa, including Nigeria, and resistance to sulfadoxine-pyrimethamine also occurs in this region. Malaria can affect both adults and children. Among 732 cases of malaria in U.S. civilians of known age reported in the United States during 2004, approximately 11% were in children aged <15 years. Detailed recommendations for preventing malaria in traveling infants and children are available from CDC.* In addition, recommendations for prevention of malaria in travelers of all ages are available.† Finally, CDC biannually publishes recommendations in Health Information for International Travel (i.e., “The Yellow Book”) (8), which is available for purchase (telephone, 800-545-2522) and available and updated more frequently on the CDC website.§ * Available at http://www.cdc.gov/travel/mal_kids_hc.htm. † Available at http://www.cdc.gov/travel/diseases.htm#malaria and http://www.cdc.gov/malaria/travel/index.htm. § Available at http://www.cdc.gov/travel. References   CDC. Malaria surveillance—United States, 2004. MMWR 2006;55 (No. SS-04):23–37. World Health Organization. Management of severe malaria—a practical handbook. 2nd ed. Geneva, Switzerland: World Health Organization; 2000. Available at http://www.who.int/malaria/docs/hbsm_toc.htm. CDC. Treatment of malaria (guidelines for clinicians). Atlanta, GA: US Department of Health and Human Services, CDC; 2006. Available at http://www.cdc.gov/malaria/diagnosis_treatment/tx_clinicians.htm. Johnston SP, Pieniazek NJ, Xayavong MV, Slemenda SB, Wilkins PP, da Silva AJ. PCR as a confirmatory technique for laboratory diagnosis of malaria. J Clin Microbiol 2006;44:1087–9. Allison AC. Protection afforded by sickle-cell trait against subtertian malarial infection. Br Med J 1954;1:290–4. Williams TN, Mwangi TW, Wambua S, et al. Sickle cell trait and the risk of Plasmodium falciparum malaria and other childhood diseases. J Infect Dis 2005;192:178–86. Juwah AI, Nlemadim EU, Kaine W. Types of anaemic crises in paediatric patients with sickle cell anaemia seen in Enugu, Nigeria. Arch Dis Child 2004;89:572–6. CDC. Health information for international travel, 2005–2006. Atlanta, GA: US Department of Health and Human Services, Public Health Service, CDC; 2005. Available at http://www.cdc.gov/travel. Newman RD, Parise ME, Barber AM, Steketee RW. Malaria-related deaths among U.S. travelers, 1963–2001. Ann Intern Med 2004;141: 547–55. Angell SY, Cetron MS. Health disparities among travelers visiting friends and relatives abroad. Ann Intern Med 2005;142:67–72.

HOME  |  ABOUT MMWR  |  MMWR SEARCH  |  DOWNLOADS  |  CONTACT POLICY  |  DISCLAIMER  |  ACCESSIBILITY Morbidity and Mortality Weekly Report Centers for Disease Control and Prevention 1600 Clifton Rd, MailStop K-95, Atlanta, GA 30333, U.S.A Department of Health and Human Services

Here is another abstract I wrote recently.  Just an FYI:

Background: Linezolid is a new antibiotic from the oxazolidine class. It’s trade name is Zyvox. Both oral and intravenous varieties of the drug were approved by the US Food and Drug Administration in 2000. Its indications for use include: vancomycin-resistant Enterococcus faecium infections, nosocomial pneumonia caused by Staph aureus and St pneumoniae and commplicated skin and skin structure infections, such as a diabetic foot infection. So far, there has been no cross-resistance with other antibiotic classes and there have been only a limited number of cases of bacterial resistance. These features and the fact that it has a high oral bioavailability are making linezolid an attractive choice for inpatients, as well as, outpatients. However, linezolid exhibits weak reversible MAO-A and MAO-B effects. These are the enzymes that metabolize monoamine neurotransmitters (epinephrine, norepinephrine, serotonin, and dopamine.) Therefore, there is the risk that in advertently coupling linezolid therapy with adrug that can increase the CNS concentration of serotonin might expose the patient to serotonin toxicity. Objective: To quantify and examine the cases of patients who developed serotonin toxicity while receiving linezolid therapy in conjuction with medications that increase the CNS serotonin concentrations. Design: Retrospective review. Population: 29 cases. Interventions: The authors assessed all postmarketing adverse event reports from the FDA involving 1) linezolid, 2) the concurrent use of a drug or drugs that increased CNS seotonin and 3) the development of serotonin toxicity. Results: Twenty-nine cases (age range: 17-83 years) were classified as serotonin toxic. Proportion of males to females was the same. Over 40 drugs were reported that were serotonergic. The types of serotonergic drugs that were used in conjunction with linezolid in descending order were: 1) serotonin reuptake inhibitors [SSRIs] (26/43 patients), 2) tricyclic antidepressants (6/43), and 3) atypical antidepressants (4/43). Seven patients required initial or prolonged hospitalization, six required major intervention to prevent permanent impairment or death, and three died. Conclusion: Linezolid added to a drug that increases CNS serotonin may expose the patient to serotonin toxicity and its risk of causing permanent disability and death. Comment: While the hallmarks of serotonin toxicity are 1) cognitive/behavioral changes, 2) autonomic instability, and 3) neuromuscular excitability, the initial manifestations can be deceptively innocuous (agitation, diarrhea, sweats, tachycardia). It could go on to hyperthermai, seizures, and death if not recogized in time. {Spontaneous clonus is a characteristic of the syndrome.}

This is my abstract from the June, 2006 issue of Clinical Infectious Diseases 2006; 42:1527-1535.

West Nile Virus (WNV) is a flavivirus whose major manifestations include West Nile Fever, West Nile meningitis, West Nile encephalitis, and flaccid paralysis. Fortunately, most infections are asymtomatic. However, from 1999-2004 in the United States, there have been 16,706 cases of WNV disease (9268 cases of Fever, 7096 cases of neuroinvasive disease, and 666 deaths). These manifestations are logical since WNV is antigenically similar to Japanese encephalitis virus and St. Louis encephalitis virus. While these syndromes have received considerable attention in the English-speaking literature, little has been mentioned about hemorrhagic complications. The hemorrhagic syndrome may be due to the fact WNV shares some antigenic determinants with dengue virus, yellow fever virus, and Omsk hemorrhagic fever virus.  Rare cases have been reported in the Central African Republic and South Africa. The hemorrhagic fever caused by WNV, however, has not been documented previously in the Western Hemisphere, until now. The present article presents the first case of WNV Hemorrhagic Fever in the United States. The present case concerns a 59-year-old male in good health (except for diabetes, hypertriglyceridemia, and hypertension) who presented to an ED in Florida, July 2003. He presented with hypotension, metabolic acidosis, and acute renal failure. He had just returned from a 4 day visit to the Lake Okeechobee area where he received numerous mosquito bites. His travel history also included a trip to Cosat Rica 12 days earlier. Prior to coming to the ED, he complained of fatique, malaise, weakness, chills, nausea, vomiting, dark urine, and loose, blood-streaked stools. On exam, he was awake, alert with cool, pale skin. Vital signs included: Temp of 35.6 degrees C, Pulse of 126 bpm, respirations of 24 breaths/minute and a B/P of 94/59 mm Hg. He had petecchiae on his extremities and ecchymoses on his torso and thighs. Unusual labs included a normal WBC, but with a significant left shift, a platelet count of 84,000, elevated D-dimer, PT and PTT, low bicarbonate level, elevated BUN/Cr and LFTs. He was admitted to ICU in multiorgan failure and despite receiving pressor support, exotic antibiotic therapy, and other machinations, he remained hypotensive, acidotic, and died 24 hours later. Peri- and postmortem analysis ruled out all the usual suspects such as dengue fever, RMSF, and meningococcemia. The diagnosis of WNV was confimed by skin biopsies, serum and tissue analysis. Comment: Remember that other systemic manifestations of WNV have also been reported, albeit rarely. They include hepatitis, pancreatitis, and myocarditis.