One of the primary concerns is that the virus could quickly spread across countries as various birds follow their migration routes. In response, countries have begun planning in anticipation of an outbreak. While short-term strategies to deal with an outbreak focus on limiting travel and culling and vaccinating poultry, long-term strategies require substantial changes in the lifestyles of the most at-risk populations.
WHO announced on November, 16, 2005 that an outbreak is most likely to hit the Hong Kong Special Administrative issue by mid-December of this year. “If it were to hit in a highly residential area like Tin Hau, it would be sure to spread like wildfire.” Dr. N Column, Head of Epidemic Prevention announced.
The WHO divides a pandemic into six phases, ranging from minimal risk of an outbreak to full scale pandemic. Most health authorities categorize the situation as of 2005 at Phase 3, by which is meant that human infections of a new sub-type has occurred but there is little evidence of sustained human-to-human transmission.
Avian Influenza (Bird Flu)
Avian influenza, or �bird flu�, is a contagious disease of animals caused by viruses that normally infect only birds and, less commonly, pigs. Avian influenza viruses are highly species-specific, but have, on rare occasions, crossed the species barrier to infect humans.
In domestic poultry, infection with avian influenza viruses causes two main forms of disease. The so-called �low pathogenic� form commonly causes only mild symptoms (ruffled feathers, a drop in egg production) and may easily go undetected. The highly pathogenic form is far more dramatic. It spreads very rapidly through poultry flocks, causes disease affecting multiple internal organs, and has a mortality that can approach 100%, often within 48 hours.
Influenza A viruses have 16 H subtypes and 9 N subtypes. Only viruses of the H5 and H7 subtypes are known to cause the highly pathogenic form of the disease. On present understanding, H5 and H7 viruses may circulate and infect poultry flocks in their low pathogenic form. The viruses can then mutate, usually within a few months, into the highly pathogenic form. This is why the presence of an H5 or H7 virus in poultry is always cause for concern, even when the initial signs of infection are mild. Read more »
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Posted in medicalmatrix | February 13, 2010 | 
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Background
Malaria, which predominantly occurs in tropical areas, is a potentially life-threatening disease caused by infection with Plasmodium protozoa transmitted by an infective female Anopheles mosquito vector. Individuals with malaria may present with fever and a wide range of symptoms.
The 4 Plasmodium species known to cause malaria include Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, and Plasmodium malariae. A fifth species, Plasmodium knowlesi, has recently been identified as a clinically significant pathogen in humans. Timely identification of the infecting species is extremely important, as P falciparum infection can be fatal and is often resistant to standard chloroquine treatment. In some cases, individuals with malaria are infected with multiple Plasmodium species. P falciparum and P vivax are responsible for most new infections. Each Plasmodium species has a defined area of endemicity, although geographic overlap is common. Species can usually be distinguished by morphology on a blood smear. P falciparum is distinguished from the rest of plasmodia by its high level of parasitemia and the banana shape of its gametocytes.
Malaria in travelers typically manifests weeks after the individual leaves the endemic area. Presentation more than 4 weeks after returning from the endemic area is unusual. In some individuals, disease manifests months or years later, usually due to the presence of P vivax or P ovale hypnozoites, which can remain dormant in the liver and reactivate years after infection. Relapse with P vivax or P ovale infection is rare more than 5 years after initial infection. Because symptomatic delay is common, history of even a remote exposure to an endemic area should be elicited. Symptoms of malaria are nonspecific, and, because timely diagnosis and treatment are necessary, malaria should be considered in all patients from tropical areas who present with fever. Read more »
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Background
Rabies is a viral disease that affects the CNS. The genus Lyssavirus contains more than 80 viruses. Classic rabies, the focus of this article, is the prototypical human Lyssavirus pathogen. Ten viruses are in the rabies serogroup, most of which only rarely cause human disease. The genus Lyssavirus, rabies serogroup, includes the classic rabies virus, Mokola virus, Duvenhage virus, Obodhiang virus, Kotonkan virus, Rochambeau virus, European bat Lyssavirus types 1 and 2, and Australian bat Lyssavirus. In 1997, an unusual bat Lyssavirus caused a brief outbreak of a rabieslike illness in Australia.
The fatal madness of rabies has been described throughout recorded history, and its association with rabid canines is well known. For centuries, dog bites were treated prophylactically with cautery, unfortunately, with predictable results. In the 19th century, Pasteur developed a vaccine that successfully prevented rabies after inoculation and launched a new era of hope in the management of this uniformly fatal disease. Rabies is recognized as a zoonosis worldwide. Animal-control and vaccination strategies currently supersede postexposure prophylaxis in preventing the spread of rabies. Through such programs, rabies has been eliminated in several nations and some areas in the US territories.
Human rabies reflects the prevalence of animal infection and the extent of contact this population has with humans. Less than 5% of cases in developed nations occur in domesticated dogs; however, unvaccinated dogs serve as the main reservoir worldwide. Undomesticated canines, such as coyotes, wolves, jackals, and foxes, are most prone to rabies and serve as reservoirs. These reservoirs allow rabies to remain an indefinite public health concern, and ongoing public health measures are critical to its control. Raccoons, skunks, and insect-eating bats remain the prime vectors in the United States, followed by cats and cattle. Increasingly in the United States, the source of exposures cannot be identified, but the risk of death from rabies is exceedingly low, with fewer than 5 cases documented per year. Opossums are rarely infected and are not considered a likely risk for exposure. Read more »
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Background
The word tetanus comes from the Greek tetanos, which is derived from the term teinein, meaning to stretch. Tetanus appears in military medical documents throughout the ages. Slapping infected dung on the umbilical cords of newborns (ie, as part of ritualistic ceremonies) caused rampant tetanus neonatorum or trismus nascentium in the West Indies and in Africa. Osler’s textbook describes the “eight days sickness” caused by umbilical sepsis, which killed 84 of 125 children within a fortnight of birth in St. Kilda, Scotland. During World War I, tetanus occurred in 1.47 per 1000 British wounded and in 12.5 per 1000 persons involved in the Peninsular campaign. Nicolaier discovered the anaerobic bacillus Clostridium tetani in 1885. In 1889, Koch’s pupil, Kitasato, obtained the bacillus of tetanus in pure culture and associated the disease to animals.
Although rare, the disease has not been eradicated, and early diagnosis and intervention are life saving. Prevention is the ultimate management strategy for tetanus. The 4 clinical types of tetanus are generalized, local, cephalic, and neonatal.
Neonatal tetanus is a major cause of infant mortality in underdeveloped countries, but this form is rare in the United States. Infection results from cord contamination during unsanitary delivery conditions, coupled with a lack of maternal immunization. At the end of the first week of life, infected infants become irritable, feed poorly, and develop rigidity with spasms. This form of tetanus has a very poor prognosis for survival.
Cephalic tetanus is uncommon and usually occurs following head trauma or otitis media. Patients with this form present with cranial nerve palsies. The infection may be localized or may become generalized.
Patients with local tetanus present with persistent rigidity in the muscle group close to the injury site. The muscular rigidity is caused by a dysfunction in the interneurons that inhibit the alpha motor neurons of the affected muscles. No further CNS involvement occurs, and this form has very low mortality rates. 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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