A swine flu outbreak appears to have killed dozens of people in Mexico and caused mild illnesses in the United States.
The Atlanta-based federal Centers for Disease Control and Prevention and the New York City Department of Health are recommending several steps to prevent the spread of the virus.
- If you have flu symptoms, stay home from work or school to avoid spreading the disease. Do not return until two days after your symptoms are gone.
- Cover your nose and mouth when you cough or sneeze, and wash your hands frequently.
- Go to the hospital if you have severe symptoms such as difficulty breathing, but if your symptoms are mild stay home to avoid spreading the virus to others at the hospital. Read more »
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Posted in medicalmatrix | February 13, 2010 |
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It may seem a daunting task to keep yourself and your loved ones free of infections. Beyond the obvious—steering clear of runny noses and hacking coughs—you may be wondering about some other practical ways of staying infection-free. Your skin acts as a natural barrier against harmful microbes that cause infections, but smart “bugs” have found alternative routes to get into your body and cause infection. By making a few simple behavioral changes (which ultimately reduce their access into your body), you can easily prevent the spread of many infectious diseases.
- Wash your hands frequently. Did you know that microbes can live on inert surfaces anywhere from a few minutes to several months? Imagine these disease-causing microbes living on your computer keyboard, your light-switch, or even on the pedestrian-crossing button next to the crosswalk!Surprisingly, most people don’t know the best way to effectively wash their hands. The CDC recommends washing thoroughly and vigorously with soap and water for at least 20 seconds, followed by hand-drying with a paper towel. In the absence of running water, an alcohol-based hand gel or wipe will suffice, although nothing beats good ol’ soap and water. This takes about as long as it does to sing “Happy Birthday”, so some hospitals recommend washing your hands for the duration of this simple tune!
- Don’t share personal items. Toothbrushes, towels, razors, handkerchiefs, and nail clippers can all be sources of infectious agents (bacteria, viruses, and fungi). In kindergarten, you were taught to share your toys, but keep your hands to yourself. Now try to remember to keep personal items to yourself as well!
- Cover your mouth when you cough or sneeze. In a similar vein, good personal hygiene includes not only personal cleanliness, but also the age-old practice of covering your mouth when you cough or sneeze. Why is this important if you aren’t sick? For most infections, the disease-causing microbe has already started growing and dividing long before any symptoms begin to show. Coughing or sneezing can spread these germs through microscopic droplets in the air. The current recommendation is to cover your mouth with your arm, sleeve, or crook of the elbow, rather than using your hands. Read more »
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PHILADELPHIA – For the folks who promote vaccination, these are trying times. Recently, CNN hosted a segment titled: “Virus or Vaccine: Which is Worse?”
It’s enough to set Paul Offit to ranting, which he did this week at a meeting of the Infectious Diseases Society of America. Offit, a physician who heads the infectious disease division at Children’s Hospital of Philadelphia, has devoted a career to fighting illness. In his job, vaccines are often the most reliable weapon available, and cost-effective to boot. And although it’s astonishingly more dangerous to contract a disease than it is to get vaccinated for it, that message seems to have gotten lost somewhere along the way.
Offit traces this detour back to 1982, when DPT — the shot that prevents diphtheria, tetanus and pertussis – was (wrongly) linked to brain damage. “Three people believed their kids were harmed by the vaccine,” he says.
Offit has compassion for families who have a child who has suffered, whatever the cause may be, known or unknown. But since 1982, it’s been one accusation after another against vaccines. People tried to link the HIB vaccine to diabetes (no evidence), the hepatitis B vaccine to multiple sclerosis (all but one study found no link), and other vaccines to SIDS or autism. Recently, the HPV vaccine — which prevents cervical cancer – got linked to heart attacks and strokes (no proof).
And now the seasonal flu vaccine and H1N1 flu vaccine are being skipped by millions of people who somehow distrust the science that went into making them, even though the illnesses they cause can be fatal. Read more »
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Background
Acute rheumatic fever (ARF) is an autoimmune inflammatory process that develops as a sequela of streptococcal infection. ARF has extremely variable manifestations and remains a clinical syndrome for which no specific diagnostic test exists. Persons who have experienced an episode of ARF are predisposed to recurrence following subsequent (rheumatogenic) group A streptococcal infections. The most significant complication of ARF is rheumatic heart disease, which usually occurs after repeated bouts of acute illness.
Pathophysiology
ARF is characterized by nonsuppurative inflammatory lesions of the joints, heart, subcutaneous tissue, and central nervous system. An extensive literature search has shown that, at least in developed countries, rheumatic fever follows pharyngeal infection with rheumatogenic group A streptococci. The risk of developing rheumatic fever after an episode of streptococcal pharyngitis has been estimated at 0.3-3%. More recent investigations of rheumatic fever occurring in the aboriginal populations of Australia suggest that streptococcal skin infections might also be associated with the development of rheumatic fever. In Oceania and Hawaii, streptococcal strains that are not typically associated with rheumatic fever have been found to cause the disease.
Molecular mimicry accounts for the tissue injury that occurs in rheumatic fever. Both the humoral and cellular host defenses of a genetically vulnerable host are involved. In this process, the patient’s immune responses (both B- and T-cell mediated) are unable to distinguish between the invading microbe and certain host tissues.The resultant inflammation may persist well beyond the acute infection and produces the protean manifestations of rheumatic fever.
Frequency
United States
The incidence of ARF has declined markedly in the past 50 years in both the United States and Western Europe. Most Western physicians see only the late sequelae of rheumatic heart disease; the diagnosis of an acute case is usually reason enough for a ground rounds presentation. This remarkable decline of rheumatic fever likely reflects improved socioeconomic conditions, as well the decline in prevalence of the classically described rheumatogenic strains of group A streptococci.
Following two decades of almost total absence, a resurgence of ARF occurred in the 1980s among middle-class white children in Salt Lake City, Utah. Clusters were also reported in US Army and Navy training camps during the same period. These limited outbreaks were associated with mucoid rheumatogenic strains that were rarely seen in the preceding 20 years. Today, ARF remains a rarity in most of the United States, although Hawaii and American Samoa continue to see a significant number of cases, many of which are caused by streptococcal strains not usually associated with rheumatic fever in persons of Polynesian descent. Read more »
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Background
Typhus refers to a group of infectious diseases that are caused by rickettsial organisms and that result in an acute febrile illness. Arthropod vectors transmit the etiologic agents to humans. The principle diseases of this group are epidemic or louse-borne typhus and its recrudescent form known as Brill-Zinsser disease, murine typhus, and scrub typhus. (For more information on pediatric scrub typhus, see the eMedicine article Scrub Typhus in the Pediatric: General Medicine volume.)
Pathophysiology
Epidemic typhus is the prototypical infection of the typhus group of diseases, and the pathophysiology of this illness is representative of the entire category. The arthropod vector of epidemic typhus is the body louse (Pediculus corporis). This is the only vector of the typhus group in which humans are the usual host. Rickettsia prowazekii, which is the etiologic agent of typhus, lives in the alimentary tract of the louse. A Rickettsia- harboring louse bites a human to engage in a blood meal and causes a pruritic reaction on the host’s skin. The louse defecates as it eats; when the host scratches the site, the lice are crushed, and the Rickettsia- laden excrement is inoculated into the bite wound. The Rickettsia travel to the bloodstream and rickettsemia develops.
Rickettsia parasitize the endothelial cells of the small venous, arterial, and capillary vessels. The organisms proliferate and cause endothelial cellular enlargement with resultant multiorgan vasculitis. This process may cause thrombosis, and the deposition of leukocytes, macrophages, and platelets may result in small nodules. Thrombosis of supplying blood vessels may cause gangrene of the distal portions of the extremities, nose, ear lobes, and genitalia. This vasculitic process may also result in loss of intravascular colloid with subsequent hypovolemia and decreased tissue perfusion and, possibly, organ failure. Loss of electrolytes is common.
Some people with a history of typhus may develop a recrudescent type of typhus known as Brill-Zinsser disease. After a patient with typhus is treated with antibiotics and the disease appears to be cured, Rickettsia may linger in the body tissues. Months, years, or even decades after treatment, organisms may reemerge and cause a recurrence of typhus. How the Rickettsia organisms linger silently in a person and by what mechanism recrudescence is mediated are unknown. The presentation of Brill-Zinsser disease is less severe than epidemic typhus, and the associated mortality rate is much lower. Risk factors that may predispose to recrudescent typhus include improper or incomplete antibiotic therapy and malnutrition.
Murine typhus and scrub typhus share the same pathophysiology as epidemic typhus, although they are somewhat milder. The incubation period is approximately 12 days for the typhus group. Prior infection with Rickettsia typhi provides subsequent and long-lasting immunity to reinfection. Read more »
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