View Full Version : H5N1, thoughts ?
Letters and numbers, but not an RC...
this "some for all thread" isn't an attempt to be alarmist or to go all necromantic on you...
Yet I was just wondering what are some of the fine minds we have around here have to say as to how the crisis will be dealt with, if the virus does mutate to allow interhuman transmission ( process which has probably began, as indicated by the recent mutations found in the analysis of turkish contaminations) and leads to pandemia.
Was reading some material on the 1918 crisis, pretty frightening issues.
Now of course medecine and general technicity has evolved a lot, but efficiency of the currently available antivirals is still being questioned, so we humans might have some pretty rough times ahead in the coming months.
any thoughts ?
b
SARS
Severe acute respiratory syndrome (SARS) is a new infectious disease first identified in humans in early 2003.
SARS is caused by a newly described coronavirus, called SARS-associated coronavirus (SARS-CoV). Previously identified human coronaviruses (named for their spiky, crown-like appearance) were known to cause only mild respiratory infections.
SARS typically begins with flu-like symptoms, including high fever that may be accompanied by headache and muscle aches, cough, and shortness of breath. Up to 20 percent of infected people may develop diarrhea. Most people with SARS subsequently develop pneumonia.
In the 2003 outbreak, there were more than 8,000 probable cases of SARS and 774 deaths (approximately 9 percent mortality), according to the World Health Organization. Eight confirmed cases were identified in the United States, with no deaths. Of the 774 deaths attributed to SARS, more than 50 percent occurred in people 65 years of age or older. Susceptibility decreased significantly with age, with children the least likely to acquire the disease. For current information about SARS, visit the Centers for Disease Control and Prevention (CDC) Web site at http://www.cdc.gov/ncidod/sars/.
The virus spreads primarily by close human contact. SARS-CoV-containing droplets can be released into the air when an infected person coughs or sneezes. Some specific medical procedures performed on SARS patients also can release virus-containing droplets into the air. Touching a SARS-CoV-infected surface and subsequently touching the eyes, nose, or mouth also may lead to infection.
Intensive and supportive medical care is the primary therapy, as no specific treatment has yet been shown to consistently improve the outcome of the ill person.
NIAID RESEARCH ON SARS AND CORONAVIRUSES
The prompt recognition that SARS is caused by a new type of coronavirus is a tribute to the dedication of and collaboration by the world's medical researchers and public health experts. Much more research is needed, however, to develop ways to identify, treat, and prevent this deadly illness. NIAID scientists, grantees, and industry partners are working to better understand the different aspects of SARS and the virus that causes it. Below are some recent accomplishments and goals for future efforts.
Understanding the virus and how it spreads
Using high-powered microscopes, blood tests, and other standard laboratory techniques, NIAID-supported scientists in Hong Kong were the first to show that SARS was caused by a virus. Within a few days, these scientists and others from CDC showed that the virus was a new and deadly type of coronavirus. These efforts subsequently sparked worldwide efforts to rapidly develop SARS-CoV diagnostic tests, drugs, and vaccines.
The genetic material, RNA, contained in the SARS-CoV is very difficult to manipulate in the lab. NIAID-funded researchers generated a form of SARS-CoV that is easier to work with. Researchers will be able to use it to study the structure and function of viral proteins, and use the information to develop vaccine candidates.
An ongoing NIAID-funded program for conducting influenza surveillance in the live bird markets of Hong Kong was expanded to search for animal carriers of SARS-CoV. Researchers traveled to live animal markets in China and determined that some of the samples taken from two animals, the palm civet and the raccoon-dog, were positive for SARS-CoV. These results were the first report of isolation of a SARS-like CoV from animals. Although it is not known if these animals are a natural reservoir for SARS-CoV, live animal markets provide opportunities for animal viruses to spread directly to humans.
In the area of basic immunological research, NIAID is supporting work to determine how the immune system responds to SARS-CoV and if there are human genetic variations that affect how susceptible a person is to SARS.
NIAID is supporting analyses of genes from human and animal coronaviruses, including many strains taken from SARS patients. This work could lead to a better understanding of where the virus came from, how it jumped from animals to humans, and how it causes disease, including the immune system response.
NIAID is encouraging grant applications on the immunopathology of SARS, including studies on inflammation and airway hypersensitivity, and the ways in which SARS-CoV may evade destruction by immune system cells.
NIAID scientists and collaborators at CDC have developed several animal models for SARS, including mouse, hamster, and non-human primate models. These models, will allow researchers to study the course of SARS infection, potential vaccines against the disease, and the safety and efficacy of experimental therapies.
Studying SARS in the clinic
NIAID has developed a project to study and treat SARS patients, contacts, and health care workers. Should the disease return, these clinical trials would take place at the NIH Clinical Center in Bethesda, Maryland, and would include researching the disease as well as evaluating antiviral and immune-based therapies.
NIAID, using its Collaborative Antiviral Study Group network of clinical trial sites, is taking the lead in a collaborative effort with the NIH National Heart, Lung, and Blood Institute, CDC, and academic and clinical investigators from the United States and Canada to study experimental SARS therapies. One experimental drug to be evaluated for efficacy is alpha interferon, a drug already approved by the Food and Drug Administration for treating hepatitis B and C infections.
Developing drug treatments
NIAID is participating in a project to screen up to 100,000 antiviral drugs and other compounds for activity against SARS-CoV. While several compounds have shown antiviral activity, only alpha interferon is suitable for immediate clinical evaluation. Several compounds that act by inhibiting the coronavirus cysteine protease enzyme showed a dramatic amount of antiviral activity. These compounds are undergoing preclinical safety evaluations to allow selection of a single candidate for clinical study. Experimental compounds are being provided by large and small pharmaceutical firms, foreign and domestic academic scientists, and members of the lay community.
As more is learned about the mechanisms of SARS-CoV infection, NIAID-supported researchers are beginning to design drugs specifically aimed at its weak points. One such project is developing an "entry inhibitor" that prevents SARS-CoV from infecting human cells.
In 2003, NIAID awarded a contract to develop humanized antibodies against SARS-CoV. Researchers hope that one of these antibodies could be used to prevent infection from gaining hold in health care workers and others who are exposed to SARS patients.
Developing diagnostic tests
Because the symptoms of SARS are similar to those of influenza, clinicians must have fast, accurate tests to identify and, if necessary, isolate people with SARS. NIAID-supported scientists in Hong Kong developed a test that is able to detect the virus in respiratory aspirates (material taken from the lungs and bronchial passages) and in fecal samples. Research is continuing to improve the accuracy of this test.
Developing vaccines
Since it is not known which type of vaccine will be most effective against the SARS-CoV, NIAID scientists and grantees are pursuing several parallel approaches in the search for a vaccine.
In 2003, NIAID awarded contracts to Baxter Healthcare and Sanofi Pasteur to produce experimental inactivated whole virus SARS vaccines and awarded a contract to Protein Sciences Corporation to produce a recombinant subunit vaccine. Once these experimental vaccines are ready, NIAID plans to test them in clinical trials conducted by its Vaccine and Treatment Evaluation Units.
Scientists at NIAID's Vaccine Research Center developed an experimental SARS vaccine that prevents the SARS-CoV from replicating in laboratory mice. The vaccine was tested on 10 healthy volunteers to determine if it is safe in people and to examine the immune response stimulated (immunogenicity). (For details on the study, see the December 13, 2004, press release: http://www3.niaid.nih.gov/news/newsreleases/2004/sarstrial.htm)
Through a grant to China's Center for Disease Control, NIAID plans to help support the development of several separate vaccine programs, including a protein vaccine made from select SARS-CoV proteins and a recombinant protein vaccine.
Scientists in NIAID's Laboratory of Infectious Diseases have developed mouse, hamster and non-human primate models for replication of SARS-CoV. Researchers found the magnitude of SARS virus replication in hamsters to be much higher than that detected in other models, making it easier to measure the effectiveness of candidate vaccines. Studies in mice demonstrated that antibodies produced by the mice block replication of SARS-CoV. These findings will help researchers working on SARS vaccines. NIAID scientists continue to work on other animal models, including rodents and non-human primates, to evaluate vaccine candidates and strategies for immunotherapy.
NIAID and foreign scientists are collaborating to develop and test a variety of vaccines including standard killed virus vaccines and molecularly designed vaccines, some of which can be administered intranasally.
Providing resources to researchers
To help the world's research community develop an agenda leading to effective control measures for SARS, NIAID convened an international meeting of experts in May 2003. (http://www.niaid.nih.gov/sars_meeting.htm)
Soon after the genetic code for SARS-CoV was determined, NIAID provided interested researchers with free SARS "gene chips" embedded with a reference strain of the virus. With the chip, researchers can rapidly detect genetic variations among SARS strains and could eventually determine which strains are the most dangerous as well as gain other information useful in developing antiviral drugs. (http://www.niaid.nih.gov/newsroom/releases/SARSChip.htm)
NIAID has also developed synthetic fragments of key SARS-CoV proteins that are available to SARS researchers. These protein fragments can be used to help understand the immune response to the SARS-CoV.
NIAID is working to establish a SARS-CoV research reagent repository. Scientists throughout the world performing basic SARS research or testing candidate vaccines and drugs against SARS-CoV can access them as these reagents become available.
http://www.nlm.nih.gov/medlineplus/severeacuterespiratorysyndrome.html
The whole world was fed fear with SARS. The same shit is happening now with bird flue. It's the new millenium bug. Sorry, but I don't buy it. A mass amount of infectious diseases roam this earth. This has always been and will probably always be. Same shit, different day. Any of these deseases can be focussed on and pointed out as the next pest. It's the media needing something to scream about. Sensation sells. And what does this have to do with drugs?
from what I've been reading the pandemic risk of the H5N1 influenza virus ( avian influenza virus, now still epizootic ) is even worse than SRAS type epidemics because of virus mutation speed.
the 1918 influenza pandemia ( H1N1) is considered to have wiped out 20 to 40 million people, one of the worst pandemic episodes the world has know, along with the black plague.
Recent analysis seem to indicate that the virus was of avian origin, from birds and not from pigs as it was thought.
what I find interesting is that we're talking about influenza type viruses.
because of particular molecular characteristics that human influenza viruses lack, avian influenza viruses strike human cells more devastatingly.
the problem is when the virus will mutate to become humanly transmissible, but this might have already happened acoording to some analysis of the last turkish infections...
pretty scary stuff since available vaccines are not proved to be effective on new mutations of the virus.
http://crofsblogs.typepad.com/h5n1/
Ebola virus is one of at least 18 known viruses capable of causing the viral hemorrhagic fever syndrome. Although agents of the viral hemorrhagic fever syndrome constitute a geographically diverse group of viruses, to date, all are RNA viruses, all are considered zoonoses, all damage the microvasculature resulting in increased vascular permeability, and all are members of 1 of 4 families: Arenaviridae, Bunyaviridae, Flaviviridae, and Filoviridae.
The family Filoviridae resides in the order Mononegavirales and contains the largest genome within the order. Originally considered members of the family Rhabdoviridae, Ebola virus and the antigenically distinct Marburg virus now comprise the family Filoviridae.
Pathophysiology:
Epidemiology
Ebola and Marburg viruses are responsible for well-documented outbreaks of severe human hemorrhagic fever with resultant case mortality rates ranging from 23% for Marburg virus (Marburg, Germany; 1967) to 88% for Ebola virus (Yambuku, Democratic Republic of the Congo [DRC]; formerly Zaire; 1976). Ebola virus (Reston, Va; 1989) also has caused a highly lethal disease in cynomolgus macaques (Macaca fascicularis) imported into Reston, Va from the Philippines, but it caused no deaths in 4 infected employees who worked at the primate facility that housed these animals.
Ultrastructure and pathogenesis
The 4 distinguishable subtypes of Ebola and the single subtype of Marburg virus comprise the known members of the family Filoviridae. Controversy remains regarding the question of whether the 4 distinguishable Ebola viruses are subtypes or separate species.
Filoviruses share a characteristic filamentous form with a uniform diameter of approximately 80 nm but display a great variation in length. Filaments may be straight, but they are often folded on themselves. Ebola virus has a nonsegmented, negative-stranded, RNA genome containing 7 structural and regulatory genes. The Ebola genome codes for 4 virion structural proteins (VP30, VP35, nucleoprotein, and a polymerase protein [L]) and 3 membrane-associated proteins (VP40, glycoprotein [GP], and VP24). The GP gene is positioned fourth from the 3' end of the 7 linearly arranged genes.
Following infection, human and nonhuman primates experience an early period of rapid viral multiplication that, in lethal cases, is associated with an ineffective immunological response. Although a full understanding of Ebola must await further investigations, part of the pathogenesis has been elucidated. Most Filovirus proteins are encoded in single reading frames; the surface GP is encoded in 2 frames (open reading frame [ORF] I and ORF II). The ORF I (amino-terminal) of the gene encodes for a small (50-70 kd), soluble, nonstructural secretory glycoprotein (sGP) that is produced in large quantities early in Ebola infection.
The sGP binds to neutrophil CD16b, a neutrophil-specific Fc g receptor III, and inhibits early neutrophil activation. The sGP also may be responsible for the profound lymphopenia that characterizes Ebola infection. Thus, sGP is believed to play pivotal roles in the ability of Ebola to prevent an early and effective host immune response. One hypothesis is that the lack of sGP production by Marburg virus may explain the reduced virulence with this agent as compared to that of African-derived Ebola.
Recently, Leroy et al reported their observations of 24 close contacts of symptomatic patients actively infected with Ebola. Eleven of the 24 contacts developed evidence of asymptomatic infection associated with viral replication. Viral replication was proven by the authors' ability to amplify positive-stranded Ebola RNA from the blood of the asymptomatic contacts. A detailed study of these infected but asymptomatic individuals revealed that they had an early (4-6 d after infection) and vigorous immunologic response with production of interleukin-1beta, interleukin-6, and tumor necrosis factor, resulting in enhanced cell-mediated and humoral-mediated immunity. In patients who eventually died, proinflammatory cytokines were not detected even after 2-3 days of symptomatic infection.
A second glycoprotein of 120-150 kd, transmembrane glycoprotein, is incorporated into the Ebola virion and binds to endothelial cells but not to neutrophils. Ebola virus is known to invade, replicate in, and destroy endothelial cells. Destruction of endothelial surfaces is associated with disseminated intravascular coagulation, and this may contribute to the hemorrhagic manifestations that characterize many, but not all, Ebola infections.
Clinical infection in human and nonhuman primates is associated with rapid and extensive viral replication in all tissues. Viral replication is accompanied by widespread and severe focal necrosis. The most severe necrosis occurs in the liver, and this is associated with the formation of councilmanlike bodies similar to those seen in yellow fever. In fatal infections, the host's tissues and blood contain large numbers of Ebola virions, and their tissues and body fluids are highly infectious.
Presently, 4 distinct subtypes have been identified, each named for the location where it caused documented human or animal disease. Two Africa subtypes, Ebola virus Zaire (EBO-Z) and Ebola virus Sudan (EBO-S), have been responsible for most of the reported deaths caused by filoviruses. Clinical disease due to African-derived Ebola virus is severe and, with the exception of 2 patients infected with the Ebola virus Côte-d'Ivoire (EBO-C) subtype who survived, is associated with a mortality rate of 65% (Sudan, 1979) to 89% (DRC, Dec 2002 to Apr 2003). The fourth subtype is Ebola virus Reston (EBO-R), which was first isolated in 1989 in monkeys imported from a single Philippine exporter. A virtually identical isolate imported from the same Philippine exporter was detected in 1992 in Siena, Italy.
Between 1994 and 1997, a stable strain of Ebola caused 3 successive outbreaks of hemorrhagic fever in Gabon (mortality rates ranged from 60-74%). Because the Gabon strain has a greater than 99% homology of the nucleoprotein and GP gene regions with EBO-Z, it has not been considered a distinct subtype.
To date, no reservoir has been identified for any Filovirus. However, in 1996, members of the National Institute for Virology of South Africa went to Kikwit, Zaire (now the DRC) and evaluated the infectivity of Ebola for 24 species of plants and 19 species of vertebrates and invertebrates. Insectivorous bats, Tadarida pumila, and fruit bats, Epomophorus wahlbergi, were found to support Ebola virus replication without dying. Furthermore, serum Ebola titers in infected fruit bats reached as high as 10,000,000 fluorescent focus-forming units per milliliter, and feces contained viable Ebola virus.
Mechanisms of dispersion
African-derived Filovirus infections are characterized by transmission from an unknown host (possibly bats) to humans or nonhuman primates, presumably via direct contact with body fluids such as saliva or blood or other infected tissues. Evidence in nonhuman primates indicates that EBO-Z and EBO-S may be transmitted by contact with mucous membranes, conjunctiva, pharynx and gastrointestinal surfaces, small breaks in the skin, and, at least experimentally, by aerosol. Recently, dogs have been shown to acquire asymptomatic Ebola infections, possibly by contact with virus-laden droplets of urine, feces, or blood of unknown hosts. Of epidemiologic significance was the observation that seroprevalence rates in dogs rose in a linear fashion as sampling approached areas of human cases and reached as high as 31.8%. Thus, an increase in canine seroprevalence may serve as an indicator of increasing Ebola circulation in primary vectors within specific geographical areas.
Human infection with African-derived strains often has occurred in caregivers, either family or medical, or in family members who have prepared dead relatives for burial. Late stages of Ebola are associated with the presence of large numbers of virions in body fluids, tissues, and, especially, skin. Individuals who come into contact with patients infected with Ebola without proper barrier protection are at high risk of becoming infected.
The first recorded outbreak occurred in Yambuku, DRC in 1976, where 316 patients were infected. In the largest recorded urban outbreak to date (DRC, 1995; 318 cases), admission to a hospital acted to greatly amplify the frequency of transmission. The lack of proper barrier protection (gloves, fluid-resistant gowns, and proper sanitation) and the use and reuse of contaminated medical equipment, especially needles and syringes, resulted in rapid nosocomial spread of infection. Only after adequate barrier protection and alteration in burial rituals were implemented was the outbreak contained.
Unlike Asian-derived Ebola (ie, the Reston strain traced to a Philippine supplier of primates), African-derived strains appear to be spread more often by direct contact than by the respiratory route. However, the Reston strain has repeatedly been demonstrated to spread among nonhuman primates and possibly from primates to humans via the respiratory route. Fortunately, although the Reston subtype has been documented to cause infection in humans, it does not appear to be pathogenic to humans.
Frequency:
In the US: Ebola is not endemic in the United States. However, several human infections with the Reston strain of Ebola have been acquired by animal care workers at primate holding facilities within the United States. Fortunately, the Reston strain has not demonstrated pathogenic effects in humans. Others at potential risk are laboratory workers who work with infected animals or with the virus in tissue culture.
Internationally: Individuals considered at risk for Ebola hemorrhagic fever include persons with a travel history to sub-Saharan Africa, persons who have recently cared for infected patients, and animal workers who have worked with primates infected with African-derived Ebola subtypes.History: In patients who have Ebola infection, 2 types of exposure history are recognized, primary and secondary.
Primary exposure
These histories usually involve travel to or work in an Ebola-endemic area such as sub-Saharan Africa, especially the DRC (formerly Zaire), Sudan, Gabon, and Côte d'Ivoire.
Because the natural reservoir of Ebola has not been identified, the relationship between specific exposure to potential arthropod, animal, or plant vectors and disease remains unknown. However, a history of exposure to tropical African forests is more frequent in patients with Ebola than is a history of working within cities in the same region.
Secondary exposure
This refers to human-to-human or primate-to-human exposures.
In each major outbreak, medical personnel or family members who cared for patients or those who prepared deceased patients for burial were at very high risk.
Another group at risk for infection are animal care workers who provide care for primates. This latter group includes patients who developed infection with the Reston strain of Ebola but did not develop Ebola disease.
Physical: The findings upon physical examination depend on the stage of disease in which patients present. Early in the disease, patients may present with fever, pharyngitis, and severe constitutional signs and symptoms. A maculopapular rash, more easily seen on white skin than on dark skin, often is present, as is bilateral conjunctival injection. Late in the disease, patients often develop an expressionless hippocratic facies. At this point in the disease, bleeding from intravenous puncture sites and mucous membranes commonly occurs. Of interest is that in the 1976 Ebola outbreak, bleeding was seen in most cases, whereas in the 1995 Ebola outbreak, bleeding occurred in only half the patients. Myocarditis and pulmonary edema also are seen in the later stages of the disease. Terminally ill patients often die tachypneic, hypotensive, anuric, and in a coma.
Clinical course
Human infections with African-derived strains are characterized by an incubation period of 3-8 days in primary cases and slightly longer in secondary cases. However, cases with incubation periods of 19 and 21 days have been observed.
The onset of clinical symptoms is sudden. Severe headache (50-74%), arthralgias or myalgias (50-79%), fever with or without chills (95%), anorexia (45%), and asthenia (85-95%) occur early in the disease.
Gastrointestinal symptoms, including abdominal pain (65%), nausea and vomiting (68-73%), and diarrhea (85%), soon follow. Evidence of mucous membrane involvement includes conjunctivitis (45%), odynophagia or dysphagia (57%), and bleeding from multiple sites in the gastrointestinal tract. Bleeding from mucous membranes and puncture sites is reported in 40-50% of patients.
A cutaneous rash, which in survivors desquamates during convalescence, is seen in approximately 15% of patients. Terminally ill patients often are obtunded, anuric, tachypneic, normothermic, and in shock.
Although the mechanism is unclear, hiccups have been noted in fatal cases of Ebola in both the 1976 and the 1995 outbreaks in the DRC. In the 1995 Ebola outbreak in Kikwit, DRC, tachypnea was the single-most discriminating sign that separated survivors (0%) from patients who died (37%) (P = 0.027).
Causes:
Human Ebola hemorrhagic fever is caused by infection with 3 of the 4 presently known subtypes of Ebola: EBO-Z, EBO-S, and EBO-C. The fourth species, EBO-R, has caused human infection but, to date, has not been documented to cause human disease.History: In patients who have Ebola infection, 2 types of exposure history are recognized, primary and secondary.
Primary exposure
These histories usually involve travel to or work in an Ebola-endemic area such as sub-Saharan Africa, especially the DRC (formerly Zaire), Sudan, Gabon, and Côte d'Ivoire.
Because the natural reservoir of Ebola has not been identified, the relationship between specific exposure to potential arthropod, animal, or plant vectors and disease remains unknown. However, a history of exposure to tropical African forests is more frequent in patients with Ebola than is a history of working within cities in the same region.
Secondary exposure
This refers to human-to-human or primate-to-human exposures.
In each major outbreak, medical personnel or family members who cared for patients or those who prepared deceased patients for burial were at very high risk.
Another group at risk for infection are animal care workers who provide care for primates. This latter group includes patients who developed infection with the Reston strain of Ebola but did not develop Ebola disease.
Physical: The findings upon physical examination depend on the stage of disease in which patients present. Early in the disease, patients may present with fever, pharyngitis, and severe constitutional signs and symptoms. A maculopapular rash, more easily seen on white skin than on dark skin, often is present, as is bilateral conjunctival injection. Late in the disease, patients often develop an expressionless hippocratic facies. At this point in the disease, bleeding from intravenous puncture sites and mucous membranes commonly occurs. Of interest is that in the 1976 Ebola outbreak, bleeding was seen in most cases, whereas in the 1995 Ebola outbreak, bleeding occurred in only half the patients. Myocarditis and pulmonary edema also are seen in the later stages of the disease. Terminally ill patients often die tachypneic, hypotensive, anuric, and in a coma.
Clinical course
Human infections with African-derived strains are characterized by an incubation period of 3-8 days in primary cases and slightly longer in secondary cases. However, cases with incubation periods of 19 and 21 days have been observed.
The onset of clinical symptoms is sudden. Severe headache (50-74%), arthralgias or myalgias (50-79%), fever with or without chills (95%), anorexia (45%), and asthenia (85-95%) occur early in the disease.
Gastrointestinal symptoms, including abdominal pain (65%), nausea and vomiting (68-73%), and diarrhea (85%), soon follow. Evidence of mucous membrane involvement includes conjunctivitis (45%), odynophagia or dysphagia (57%), and bleeding from multiple sites in the gastrointestinal tract. Bleeding from mucous membranes and puncture sites is reported in 40-50% of patients.
A cutaneous rash, which in survivors desquamates during convalescence, is seen in approximately 15% of patients. Terminally ill patients often are obtunded, anuric, tachypneic, normothermic, and in shock.
Although the mechanism is unclear, hiccups have been noted in fatal cases of Ebola in both the 1976 and the 1995 outbreaks in the DRC. In the 1995 Ebola outbreak in Kikwit, DRC, tachypnea was the single-most discriminating sign that separated survivors (0%) from patients who died (37%) (P = 0.027).
Causes:
Human Ebola hemorrhagic fever is caused by infection with 3 of the 4 presently known subtypes of Ebola: EBO-Z, EBO-S, and EBO-C. The fourth species, EBO-R, has caused human infection but, to date, has not been documented to cause human disease.Last outbreak was in 2004, so it is reasonable to say that ebola is alive and will bpobably break out again. 81.3% of all people who get this die.
The whole world was fed fear with SARS. The same shit is happening now with bird flue. It's the new millenium bug. Sorry, but I don't buy it. A mass amount of infectious diseases roam this earth. This has always been and will probably always be. Same shit, different day. Any of these deseases can be focussed on and pointed out as the next pest. It's the media needing something to scream about. Sensation sells. And what does this have to do with drugs?
drugs ? tamiflu and anti-depressants ? just kidding ;)
well it was a "some for all" topic, so ok,it has *nothing* to do with drugs, I just though it was worth bringing up...there are other threads in this forum that have nothing to do with drugs (IQ, are you a racist, britain for americans, extreme sports etc) so I thought it was ok to share a few views on this, sorry if I was wasting posting space...
I agree with you don't really buy it either, the fear syndrome, and I do agree about the sensationalism. But I can't help getting a different feeling from this threat than from the former "millenium bugs"...
and then again what is happening in Turkey is more frightening than sensational.
and who's possibly getting money from this ? Roche and the lab lobby ? the media cartel ? evil governments greedy for more control ? I don't really buy that either.
what I find interesting about this particular situation, mutated *influenza* viruses, is the major historical precedents, which are pretty chilling, with 30 million deaths linked to an avian influenza virus in the last century, the "spanish flu". Ok, we've gone a long way since 1918, and almighty science will probably be able to counter this one now, at least faster, but it's still slightly worrying, much more than SRAS if you ask me, considering the yearly influenza epidemics in europe for instance, this particular strain...
you're probably right, nothing will happen, another hot air balloon will deflate... then again I can't help noting it when I hear that the virus has probably mutated already and reading about the growing rate of contaminations in Turkey, and the correlation with the coming yearly "traditional" influenza epidemic.
Maybe i'm just being too gullible and it's just a big bucks conspiracy.
here is the World Health Org. fact sheet on H5N1, dating for last october, which can be seen as alarmist or sensational, judge for yourself :
------------
http://www.who.int/csr/disease/influenza/pandemic10things/en/print.html
Ten things you need to know about pandemic influenza
14 October 2005
1. Pandemic influenza is different from avian influenza.
Avian influenza refers to a large group of different influenza viruses that primarily affect birds. On rare occasions, these bird viruses can infect other species, including pigs and humans. The vast majority of avian influenza viruses do not infect humans. An influenza pandemic happens when a new subtype emerges that has not previously circulated in humans.
For this reason, avian H5N1 is a strain with pandemic potential, since it might ultimately adapt into a strain that is contagious among humans. Once this adaptation occurs, it will no longer be a bird virus--it will be a human influenza virus. Influenza pandemics are caused by new influenza viruses that have adapted to humans.
2. Influenza pandemics are recurring events.
An influenza pandemic is a rare but recurrent event. Three pandemics occurred in the previous century: “Spanish influenza” in 1918, “Asian influenza” in 1957, and “Hong Kong influenza” in 1968. The 1918 pandemic killed an estimated 40–50 million people worldwide. That pandemic, which was exceptional, is considered one of the deadliest disease events in human history. Subsequent pandemics were much milder, with an estimated 2 million deaths in 1957 and 1 million deaths in 1968.
A pandemic occurs when a new influenza virus emerges and starts spreading as easily as normal influenza – by coughing and sneezing. Because the virus is new, the human immune system will have no pre-existing immunity. This makes it likely that people who contract pandemic influenza will experience more serious disease than that caused by normal influenza.
3. The world may be on the brink of another pandemic.
Health experts have been monitoring a new and extremely severe influenza virus – the H5N1 strain – for almost eight years. The H5N1 strain first infected humans in Hong Kong in 1997, causing 18 cases, including six deaths. Since mid-2003, this virus has caused the largest and most severe outbreaks in poultry on record. In December 2003, infections in people exposed to sick birds were identified.
Since then, over 100 human cases have been laboratory confirmed in four Asian countries (Cambodia, Indonesia, Thailand, and Viet Nam), and more than half of these people have died. Most cases have occurred in previously healthy children and young adults. Fortunately, the virus does not jump easily from birds to humans or spread readily and sustainably among humans. Should H5N1 evolve to a form as contagious as normal influenza, a pandemic could begin.
4. All countries will be affected.
Once a fully contagious virus emerges, its global spread is considered inevitable. Countries might, through measures such as border closures and travel restrictions, delay arrival of the virus, but cannot stop it. The pandemics of the previous century encircled the globe in 6 to 9 months, even when most international travel was by ship. Given the speed and volume of international air travel today, the virus could spread more rapidly, possibly reaching all continents in less than 3 months.
5. Widespread illness will occur.
Because most people will have no immunity to the pandemic virus, infection and illness rates are expected to be higher than during seasonal epidemics of normal influenza. Current projections for the next pandemic estimate that a substantial percentage of the world’s population will require some form of medical care. Few countries have the staff, facilities, equipment, and hospital beds needed to cope with large numbers of people who suddenly fall ill.
6. Medical supplies will be inadequate.
Supplies of vaccines and antiviral drugs – the two most important medical interventions for reducing illness and deaths during a pandemic – will be inadequate in all countries at the start of a pandemic and for many months thereafter. Inadequate supplies of vaccines are of particular concern, as vaccines are considered the first line of defence for protecting populations. On present trends, many developing countries will have no access to vaccines throughout the duration of a pandemic.
7. Large numbers of deaths will occur.
Historically, the number of deaths during a pandemic has varied greatly. Death rates are largely determined by four factors: the number of people who become infected, the virulence of the virus, the underlying characteristics and vulnerability of affected populations, and the effectiveness of preventive measures. Accurate predictions of mortality cannot be made before the pandemic virus emerges and begins to spread. All estimates of the number of deaths are purely speculative.
WHO has used a relatively conservative estimate – from 2 million to 7.4 million deaths – because it provides a useful and plausible planning target. This estimate is based on the comparatively mild 1957 pandemic. Estimates based on a more virulent virus, closer to the one seen in 1918, have been made and are much higher. However, the 1918 pandemic was considered exceptional.
8. Economic and social disruption will be great.
High rates of illness and worker absenteeism are expected, and these will contribute to social and economic disruption. Past pandemics have spread globally in two and sometimes three waves. Not all parts of the world or of a single country are expected to be severely affected at the same time. Social and economic disruptions could be temporary, but may be amplified in today’s closely interrelated and interdependent systems of trade and commerce. Social disruption may be greatest when rates of absenteeism impair essential services, such as power, transportation, and communications.
9. Every country must be prepared.
WHO has issued a series of recommended strategic actions [pdf 113kb] for responding to the influenza pandemic threat. The actions are designed to provide different layers of defence that reflect the complexity of the evolving situation. Recommended actions are different for the present phase of pandemic alert, the emergence of a pandemic virus, and the declaration of a pandemic and its subsequent international spread.
10. WHO will alert the world when the pandemic threat increases.
WHO works closely with ministries of health and various public health organizations to support countries' surveillance of circulating influenza strains. A sensitive surveillance system that can detect emerging influenza strains is essential for the rapid detection of a pandemic virus.
Six distinct phases have been defined to facilitate pandemic preparedness planning, with roles defined for governments, industry, and WHO. The present situation is categorized as phase 3: a virus new to humans is causing infections, but does not spread easily from one person to another.
HANTAVIRUS:
Significance
Hantavirus Pulmonary Syndrome (HPS) is a respiratory disease caused by a virus known as Sin Nombre Virus. The virus is carried by wild rodents, especially deer mice. The virus produces no clinical signs in the deer mice, but can produce a deadly infection in man - over 50% of human cases have been fatal.
Biology
Sin Nombre belongs a family of viruses known as Hantaviruses. Deer mice (genus Peromyscus) and other wild rodents can carry the virus without ill effect and can shed the virus in their urine, feces, and saliva. Sin Nombre virus is not associated with laboratory mice or with ordinary house mice or laboratory mice (genus Mus). Deer mice, in general, inhabit wild areas and rural rather than urban or suburban areas; you won’t find them in your kitchen in a city, but you might in a mountain cabin.
Humans become infected with the hantavirus when they inhale dust which has been contaminated with rodent urine. Most individuals who have become infected have lived or worked in areas that were heavily contaminated with rodent droppings. Campgrounds, abandoned cabins, and other areas that have become infested with high populations of wild rodents should be considered risky. Digging up a rodent nest, trapping wild rodents or performing necropsies on wild rodents would also be considered risky activities.
If a human being becomes infected, signs of illness usually appear about two weeks after exposure, although the time can range from a few days to as long as six weeks. The first signs are fever, headache, and pain in the abdomen, joints, and back. Afterwards the patient’s lungs begin to fill with fluid and breathing becomes extremely difficult. A high proportion of the patients die, but early treatment offers the best chance of survival.
If you develop symptoms that are suspicious of HPS, and you have worked with or been around wild rodents within the last six weeks, report this information to your physician immediately.
Relative Risks
Most individuals who have contracted HPS have acquired the disease by living and sleeping in areas where there are large populations of rodents and copious quantities of dust contaminated with their feces. Confined spaces, such as rodent nests, abandoned cabins, or empty barns or pump houses that have been overrun with deer mice are the greatest potential risks.
In a research setting, there is also risk associated with individuals that work with wild rodents.
Prevention
Laboratory reared colonies of deer mice on campus must be tested for the virus and shown negative. These animals can be worked with as though they were ordinary mice. These colonies should be re-tested periodically (consult your facility's veterinarian for information).
Never introduce wild caught deer mice into laboratory reared colonies of deer mice.
Wild caught deer mice must be contained in isolation facilities until testing establishes their health status. Those caring for these animals must wear fitted HEPA filtered respirators when changing cages.
Wildlife biologists who work with wild caught deer mice in field conditions must treat all wild deer mice as though they were potentially infected. Individuals who will handle the animals or empty the traps must be fitted with HEPA filtered respirators by EH&S, and the respirators must be worn when handling the animals and cleaning the traps.
Equipment and surfaces potentially contaminated with Peromyscus urine or feces should be sprayed down with a 10% solution of household bleach before cleaning.
If you must clean out a rodent infested structure, do the following:
Wear a fitted respirator with a HEPA filter. Contact EH&S (Phone: 2-1493) to arrange to be fitted for a respirator.
Open the building up first and let it air out for a day.
Spray all surfaces to wetness with a 10% solution of household bleach before beginning the cleanup. Wet things down rather than sweeping so that dust is not stirred up.
Wear study rubber sturdy latex gloves when cleaning up, and disinfect them with 10% bleach before taking them off.
Don't sleep in a building or camp in an area that is obviously contaminated with rodent feces.
OK, here's more mayhem to worry about:
Dengue Fever
OVERVIEW
Dengue fever is an infectious disease carried by mosquitoes and caused by any of four related dengue viruses. This disease used to be called break-bone fever because it sometimes causes severe joint and muscle pain that feels like bones are breaking, hence the name. Health experts have known about dengue fever for more than 200 years.
Dengue fever is found mostly during and shortly after the rainy season in tropical and subtropical areas of
Africa
Southeast Asia and China
India
Middle East
Caribbean and Central and South America
Australia and the South and Central PacificAn epidemic in Hawaii in 2001 is a reminder that many states in the United States are susceptible to dengue epidemics because they harbor the particular types of mosquitoes that transmit it.
The World Health Organization estimates 50 to 100 million cases of dengue infection occur each year. This includes 100 to 200 cases reported annually to the Centers for Disease Control and Prevention (CDC), mostly in people who have recently traveled abroad. Many more cases likely go unreported because some doctors do not recognize the disease.
During the last part of the 20th century, cases of dengue began increasing in many tropical regions of the world. Epidemics also began occurring more frequently and with more severity. In addition to typical dengue, dengue hemorrhagic fever and dengue shock syndrome also have increased in many parts of the world.
VIRUSES THAT CAUSE DENGUE FEVER
Dengue fever can be caused by any one of four types of dengue virus: DEN-1, DEN-2, DEN-3, and DEN-4. A person can be infected by at least two, if not all four types at different times during a life span, but only once by the same type.
TRANSMISSION
People get dengue virus infections from the bite of an infected Aedes mosquito. Mosquitoes become infected when they bite infected humans, and later transmit infection to other people they bite. The two main species of mosquito, Aedes aegypti and Aedes albopictus, have been responsible for all cases of dengue transmitted in this country. Dengue is not contagious from person to person.
SYMPTOMS
Symptoms of typical uncomplicated (classic) dengue usually start with fever within 5 to 6 days after you have been bitten by an infected mosquito and include
High fever, up to 105 degrees Fahrenheit
Severe headache
Retro-orbital (behind the eye) pain
Severe joint and muscle pain
Nausea and vomiting
RashThe rash may appear over most of your body 3 to 4 days after the fever begins. A second rash may appear later in the disease.
Symptoms of dengue hemorrhagic fever include all of the symptoms of classic dengue plus
Marked damage to blood and lymph vessels
Bleeding from the nose, gums, or under the skin, causing purplish bruisesThis form of dengue disease causes some deaths .
Symptoms of dengue shock syndrome—the most severe form of dengue disease—include all of the symptoms of classic dengue and dengue hemorrhagic fever, plus
Fluids leaking outside of blood vessels
Massive bleeding
ShockThis form of the disease usually occurs in children (sometimes adults) experiencing their second dengue infection. The fatality rate is 5 to 15 percent.
DIAGNOSIS
Your health care provider can diagnose dengue fever by doing two blood tests, 2 to 3 weeks apart. The tests can show whether a sample of your blood contains antibodies to the virus. In epidemics, a health care provider often can diagnose dengue by typical signs and symptoms.
TREATMENT
There is no specific treatment for classic dengue fever, and like most people you will recover completely within 2 weeks. To help with recovery, health care experts recommend
Getting plenty of bed rest
Drinking lots of fluids
Taking medicine to reduce feverCDC advises people with dengue fever not to take aspirin. Acetaminophen or other over-the-counter pain-reducing medicines are safe for most people.
For severe dengue symptoms, including shock and coma, early and aggressive emergency treatment with fluid and electrolyte replacement can be lifesaving.
PREVENTION
The best way to prevent dengue fever is to take special precautions to avoid contact with mosquitoes. Several dengue vaccines are being developed, but none is likely to be licensed by the Food and Drug Administration in the next few years.
When outdoors in an area where dengue fever has been found
Use a mosquito repellant containing DEET, picaridin, or oil of lemon eucalyptus
Dress in protective clothing—long-sleeved shirts, long pants, socks, and shoesBecause Aedes mosquitoes usually bite during the day, be sure to use precautions especially during early morning hours before daybreak and in the late afternoon before dark.
Other precautions include
Keeping unscreened windows and doors closed
Keeping window and door screens repaired
Getting rid of areas where mosquitoes breed, such as standing water in flower pots, containers, birdbaths, discarded tires, etc.COMPLICATIONS
Most people who develop dengue fever recover completely within 2 weeks. Some, however, may go through several weeks to months of feeling tired and/or depressed. Others develop severe bleeding problems. This complication, dengue hemorrhagic fever, is a very serious illness which can lead to shock (very low blood pressure) and is sometimes fatal, especially in children and young adults.
NIAID RESEARCH
Scientists supported by the National Institute of Allergy and Infectious Diseases (NIAID) are trying various approaches to develop vaccines against dengue. Researchers in NIAID laboratories in Bethesda, Maryland, are using weakened and harmless versions of dengue viruses as potential vaccine candidates against dengue and related viruses.
Other researchers supported by NIAID are investigating ways to prevent dengue viruses from reproducing inside mosquitoes. Although dengue virus has emerged as a growing global threat, scientists know little about how the virus infects cells and causes disease. New research is beginning to shed light on how the virus interacts with humans—how it damages cells and how the human immune system responds to dengue virus invasion.
Micklemouse
27-01-2006, 23:57
A good friend of mine had Dengue in Thailand. He doesn't recommend it.
Here's another rodent related goodie...
Weil's disease
Also known as icteric leptospirosis. Infection with the spirochaete Leptospira interrogans (the most virulent serogroup of which is L. icterohaemorrhagiae).
Epidemiology reported1,2 (http://www.patient.co.uk/showdoc/40000444/#Notes) to be the most widespread zoonosis in the world (having an incidence greater in warm-climate areas than in temperate regions).
Prevalence A large proportion of the population is antibody positive in areas such as rural Belize and Vietnam. A significant human disease in eastern and southern Europe, Australia and New Zealand.
Risk Factors Sewage workers (17% were seropositive in Glasgow)3 (http://www.patient.co.uk/showdoc/40000444/#Notes), travellers (eg swimming in contaminated water), farmers, veterinarians, abattoir workers, rodent control workers, and other occupations with animals.
Incubation period 7-12 days (range 2-20)
The spirochaetes nest in the renal tubules of mammalian hosts. Different serotypes (referred to as serovars) prefer different hosts with the variety causing Weils's disease preferring rats. They are shed from the urine and can survive in the environment for several months in moist, warm conditions. They enter the bloodstream through abraded skin or the mucosa from contaminated water or soil. Water-borne transmission has been documented.
Presentation Many infections are mild (non specific fever etc.) without jaundice - and patients may not seek medical attention. Medical personnel generally become involved in the ~10% of patients who become jaundiced (http://www.patient.co.uk/showhtml.asp?ID=40024562) (with hepatocellular necrosis) - a severe and rapidly progressive form of the disease. The jaundice appears during days 5-9 of illness and is most intense 4-5 days later, continuing for about 1 month. The degree of jaundice itself is not indicative of prognosis (although leptospirosis without jaundice is very rarely fatal).
Other symptoms include fever, vomiting, abdominal pain, skin rashes, conjunctival haemorrhage (characteristic, particularly with suffusion and scleral yellowing), uveitis. There is often a severe headache, retro-orbital pain, and photophobia; and a severe myalgia (lower back, and legs) is common. Leptospirosis may present as aseptic meningitis.
Pulmonary symptoms vary from cough, dyspnoea, and haemoptysis (http://www.patient.co.uk/showhtml.asp?ID=40001826) to adult respiratory distress syndrome and massive pulmonary haemorrhage.
Examination may reveal hepatomegaly (http://www.patient.co.uk/showhtml.asp?ID=40000092) - with hepatic percussion tenderness a useful indicator of continuing disease activity. 4 (http://www.patient.co.uk/showdoc/40000444/#notes)
Purpura, petechiae, epistaxis, minor haemoptysis and other signs of bleeding are common.
Kidney dysfunction (Leptospiral nephropathy) is usual, sometimes with life threatening renal failure with signs of uraemia, ±disturbance of consciousness.
Differential Diagnosis Viral hepatitis, malaria, typhoid fever, relapsing fever, scrub typhus, Hantaan virus infection, Dengue fever.
Investigations Serum bilirubin (raised), prothrombin time (prolonged), WBC - leucocytosis (15,000-30,000/mm3). FBC, U&E and creatinine - anaemia and uraemia. MSU usually shows sediment and proteinuria. Serum amylase levels are raised (in acute renal failure).
Diagnosis based on serology (paired) - using either microscopic slide agglutination test or new rapid sero-diagnostic kits.
Management In mild cases – oral doxycycline (100 mg twice a day for 7 days) reduces length of symptoms by 2 days. If jaundiced - admit to ITU for rehydration and management of possible complications (multi-organ failure). Patients may need dialysis. In severe disease or with vomiting – IV penicillin G. is often used
Complications Acute renal failure, massive haemorrhage, CVA ± subarachnoid bleed, myocarditis. Rarely Guillain-Barré syndrome, Erythema nodosum, Kawasaki disease, acute cholecystitis, cerebral arteritis.
Prevention In high risk patients for short period, doxycycline 200mg po. once a week.
Prognosis Most cases without jaundice recover spontaneously. Leptospirosis with jaundice is fatal in 5-15%.
References Used
Watt G in Oxford Textbook of Medicine, 4th Edition. Eds; Warrell DA et al. OUP 2003.
Levett PN. (http://www.webmentorlibrary.com/gateway.asp?medline=http://www.ncbi.nlm.nih.gov/htbin-post/Enrez/query?db=m%26form=6%26uid=11292640%26dopt=r) Leptospirosis. Clin Microbiol Rev. 2001 Apr; 14(2):296-326. Review. [Free Full Text] (http://cmr.asm.org/cgi/content/full/14/2/296?view=full&pmid=11292640)
Stuart, R. D. Weil's disease in Glasgow sewer workers. BMJ 1939 i:324-326
Leblebicioglu H, Sencan I, Sunbul M, et al (http://www.webmentorlibrary.com/gateway.asp?medline=http://www.ncbi.nlm.nih.gov/htbin-post/Enrez/query?db=m%26form=6%26uid=9060072%26dopt=r); Weil's disease: report of 12 cases.;Scand J Infect Dis 1996;28(6):637-9.[abstract] Acknowledgements EMIS is grateful to doctoronline.nhs.uk for facilitating draft authoring of this article. The final copy has passed peer review of the independent Mentor GP authoring team. ©EMIS 2003.
Not what you want, but as with all the diseases listed rare and at one point the end of civilisation as we know it, if the media are to be believed.
The media might be right one of these days, but if you tell someone every day that they're going to die, then one day you'll be able to say 'I told you so.'
Basically what I think we're trying to say is - Don't Panic!! There's a lot of bad things in the world, and it's still a beautiful world!
(Wipes tear from eye and walks stage left, whistling...)
I get your points...yet i still believe the diseases you have listed have less pandemic potential than an influenza virus, SRAS included.
this is not a rare virus, it's just a particularly potent form of influenza. Influenza epidemics happen every year, no big deal, you get fever for 2 days and feel ill for 5... nothing much you can do about it, vaccines work as long as they can target on the right virus, and influenza viruses mutate fast.
This avian influenza is epizootic for now, only a handful of people have died from it and they were directy in contact with the infected birds.
But it's very likely that this virus will mutate to become humanly transmitable, just like regular influenza, since it *is* an influenza virus, only particulary destructive for the reasons mentioned above.
If this happens, and it is possible that it has already happened regarding the last turkish infection cases, there are two solutions : either the antivirals we have work, and then hurray, pandemia is stopped, or they don't, and then we have to wait until scientists come up with a solution and it's a mess.
In my opinion this is more serious than dengue, or even meningoccoal diseases or whatever deadly viruses you can dig up because of the particular nature of influenza viruses, and the historical precedent we have.
The last time we had an avian influenza pandemic crisis, roughly 30 million people ( Pasteur institute estimates) died. This was the worst pandemic since the black plague. Ok it was 1918, sure,it was exceptional, and science has gone a long way. Yet the particular nature of influenza viruses make things complicated... this is the type of scenario we're possibly facing, this historical precedent of 88 years ago.
Now the current WHO estimate for N5H1, is only 2 to 7 million deaths, so it's not that bad, and will probably be mostly in areas were people don't have access to treatment, read third-world countries.
don't get me wrong, I'm not panicking and stocking up on antivirals or masks or saying people should, it doesn't mess with my sleeping, and hell i don't even feel harrassed by the media on this issue...I don't have a tv mind you, so I don't know what people are seeing. I just read a national paper everyday and everyonce in while there is this article on recent evolutions, and emergency plans and funding allocated, that's all.
Personnally I don't think it's a media-government-laboratory-whatever conspiracy to gain more money, power, or publish sensational articles either...
To me it's just an potential influenza pandemic risk, and as such, in the light of historical precedents, a greater risk than recent threats...Risk of what, I don't know, let's just say of disturbance.
but since you all think it's all just sensationalist blown out of proportion propaganda, i'll just let it lie and keep my questionings to myself, i don't want to sound alarmist myself.
I was actually curious about what people here thought would happen in the worst case scenario of a pandemic influenza virus a la "spanish influenza", the way such a crisis would be dealt with, the north-south balance, drug access and control measures, influences such a situation might have on our daily lives etc...In that sense also the measures announced by WHO and local governments interest me, what this could lead to. Ok maybe i've read too much science-fiction, i rest my case...
sorry for bringing this up, i didn't want to sound like some gullible stressed out loony
... since you all think it's all just sensationalist blown out of proportion propaganda, i'll just let it lie and keep my questionings to myself, i don't want to sound alarmist myself.
sorry for bringing this up, i didn't want to sound like some gullible stressed out loony
Too late!
RABIES
INTRODUCTION
Rabies is an infectious disease of animals caused by a bullet-shaped, enveloped RNA virus, 180 x 75 nm. Man is occasionally infected, and once infection is established in the CNS, the outcome is almost invariably fatal.
HUMAN RABIES
Is acquired from virus in saliva entering a bite wound caused by an infected animal, usually a rabid dog. The severity of the bite determines the risk of infection. The disease does not usually spread from man to man.
Incubation
After inoculation, the virus enters small nerve endings at the site of the bite. The virus slowly travels up the nerve to reach the CNS where it replicates and then travels down nerves to the salivary glands where there is further replication. The time it takes to do this depends upon the length of the nerve - a bite on the foot will have a very much longer incubation period than a bite on the face. The incubation period may last from two weeks to six months. Very often the primary wound is healed and forgotten by the time of clinical presentation.
Clinical Presentation
A) Furious Rabies
When the virus reaches the CNS the patient presents with headache, fever, irritability, restlessness and anxiety. This may progress to muscle pains, salivation and vomiting. After a few days to a week the patient may experience a stage of excitement and be wracked with painful muscle spasms, triggered sometimes by swallowing of saliva or water. Hence they drool and learn to fear water (* Hydrophobia). The patients are also excessively sensitive to air blown on the face. The stage of excitement lasts only a few days before the patient lapses into coma and death.
Once clinical disease manifests, there is a rapid, relentless progression to invariable death, despite all treatment.
B) Dumb Rabies
Starts in the same way, but instead of progressing into excitement, the subject retreats steadily and quietly downhill, with some paralysis, to death. Rabies diagnosis may easily be missed.
ANIMAL RABIES
Very similar picture to human rabies. In the stage of excitement the animal may bite vigorously and viciously at anything: sticks, stones, grass, other animals and humans, without provocation.
Wild animals may be abnormally tame or appear sick - beware of approaching or picking up such an animal ("dumb rabies").
Epidemiology
1. The disease is endemic in wild animals in most parts of the world although some countries (UK, Australia) are rabies free through vigorous control. The wild animal cycle constitutes the natural reservoir.
2. Wild animals may bite and infect domestic animals (cattle, horses, pigs, dogs and cats) which in turn may infect man. Occasionally wild animals may infect man directly.
3. In recent decades, a separate form of dog rabies (spread from dog to dog) has been recognised as spreading from West Africa eastwards and southwards in Africa. Via Mozambique, it reached Natal Kwazulu in the late 1970's and early 80's. Semi-wild dogs in Natal have formed the highest endemic rabies reservoir and source for human cases in the whole of the RSA.
ANIMAL RESERVOIR
MONGOOSE (main reservoir in RSA in the wild)
SURICATE
JACKAL
BAT (some evidence to suggest carrier status and droplet infection)
FOX (in Europe)
SKUNKS, RACCOONS (in USA)
SEMI-WILD DOGS (in Natal)
Note: As in man, an infected animal becomes sick and dies. There is no substantial evidence of a true carrier status in apparently well animals, except perhaps in bats.
DIAGNOSIS
By assessment of:
1.Bite
Geographical area, type of animal, severity and site of bite.
2. Animal
Live - observe in cage:
If survives > 8 days, then NOT rabies.
Dead - brain sent to Onderstepoort
- Negri bodies
- IFA
- virus isolation
3. Man
Live - difficult diagnosis
- clinical picture, skin biopsy, corneal impression (antibodies only appear very late)
Dead - brain sent to Onderstepoort
"Negri bodies" in cytoplasm of brain cells;
immunofluorescence virus isolation
TREATMENT
1. Wash wound (soap, detergent and water)
2. Anti-rabies serum (human). Passive immunisation.
3. Vaccine (intensive course). Active immunisation.
RABIES VACCINE
A good but expensive killed virus vaccine (Human Diploid Cell Vaccine, HDCV) grown in human fibroblasts is available for safe use in man.
The unusually long incubation period of the virus permits the effective use of active immunisation with vaccine post-exposure. When used, vaccine has dramatically cut the rabies death rate. Supplied free by the State through district surgeons in South Africa.
(Older killed virus vaccines, made from infected neural tissues, were poorly immunogenic and had allergic encephalitic side effects, but are still used in developing countries.)
Prophylaxis
High-risk persons, eg. veterinarians, may be immunised before exposure, and then merely require one or two booster doses if they should be exposed to rabies.
Animal Vaccines
A range of live and killed virus vaccines are available for domestic animals (farm animals, cats and dogs).
Experimental vaccination of wildlife by using recombinant vaccinia vaccine (live) in bait for foxes in Europe and North America has been quite promising.
CONTROL OF RABIES (Government Department of Veterinary Services)
1. Education
2. Vaccination of dogs, cats and farm animals.
3. Notification
- animals (district vet officer, police, magistrate) - human (district surgeon)
[QUOTE=Woodman]Too late!
I don't really get your point in posting these diseases description lists in answer to what I've written.
Is your point just that many dangerous viruses exist and therefore any new annoucement is to be brushed off always look on the bright side of life-it's a wonderful world-don't worry be happy-I will survive ? Ok got that and I agree.
You think it's either sensationalist journalism, control aimed fear propangada or a big bucks scheme, ok, got that too and I don't agree.
ah but this particular thingie I mentioned might have immediate political and social consequences, as planned by governements around the world, in the emergency plans and measures, fundings allocated etc...As far as I know this situation make this possible influenza threat pretty different from dengue, rabies and other diseases for which efficient vaccines exist, paludism, meningoccol infections, hepatititis, yellow fever, leprosy, ebola, herpes, hay fever, jock itch or athlete's foot...
ok i give up before I go logorroic again, and i'll go back to watching Kobayashi Masaki's "Seppuku", great movie btw
now where was I...
b
I can play your game too, you never know, there could be a pandemic threat hidden in these dark corners :)
Now that I've made one of my most useless posts, i'll just try to downvote this thread in punishement for letting myself get carried away.
*kneels and proceeds to autoflagellation*
----------
Hemorrhoids
What are hemorrhoids?
Symptomatic hemorrhoids come from inflammation of the mucosa and interstitial tissue surrounding the normal veins of the anorectum. These veins provide the normal pathway for return of blood from the anus and rectum back through the circulation to the heart. Of importance is the fact that the veins in the rectum drain into the portal circulation and thus to the liver prior to returning to the heart, while the veins of the anus drain directly into the central circulation.
I am frequently asked questions by patients about internal versus external hemorrhoids. The distinction is somewhat artificial as external hemorrhoids are merely the external component of a hemorrhoid that originates internally. The dividing line between external and internal is called the dentate line, which is the point at which rectal mucosa changes to anal skin.
Who gets hemorrhoids?
Millions of people suffer with painful hemorrhoids chronically and regularly. In fact, the majority of people suffer from some hemorrhoid symptoms at least occasionally. Though there are certain groups of people who are at risk for development of hemorrhoids, most cases occur without specific cause. They do occur with greater frequency in people who have jobs that require them to sit for long periods of time such as office workers and taxi drivers.
Diet is also a major factor; people who eat foods low in fiber are prone to constipation and hemorrhoid symptoms. Also, people who eat spicy foods may have exacerbation of their symptoms. Some people who simply do not drink enough fluid may suffer from constipation and hemorrhoid symptoms.
Underlying medical conditions may contribute to hemorrhoid symptoms. Many women very typically develop hemorrhoids during pregnancy. This has to do with the large gravid uterus pressing on pelvic veins and altering circulation in those veins. In addition, pregnancy induces a state in which there is a greater circulating blood volume and general engorgement of blood vessels.
Cirrhosis of the liver is another medical condition which may underlie hemorrhoids. The hemorrhoidal veins are a natural path of collateral circulation for blood trying to return to the heart from the rectum. Under normal circumstances this blood first passes through the liver before entering the central circulation and returning to the heart. In cirrhotic patients, circulation through the liver is obstructed and blood needs to find alternative pathways to return to the central circulation. One of these is via the hemorrhoidal veins, resulting in swelling, inflammation and often bleeding from these hemorrhoids.
What are the symptoms of hemorrhoids?
Symptoms of hemorrhoids may vary but typically consist of pain and bleeding. The pain may be excruciating after defecation and may be associated with feeling a lump in or around the anus. Bleeding is usually only a few drops seen on the stool, in the toilet bowl or on the toilet paper. This may be caused by tearing of an engorged vein during defecation or by ulceration of the rectal mucosa.
Pain may be caused by simple inflammation of the hemorrhoidal tissue but may also be caused by thrombosis or prolapse of the hemorrhoid. When a hemorrhoid prolapses it may become very painful because of the constant irritation from clothing, sitting, or defecation. Often when the prolapse is reduced symptoms improve but may not disappear entirely. The worst pain and inflammation is often caused with extensive thrombosis within hemorrhoidal veins.
What is the treatment?
Treatment depends on the severity and nature of the hemorrhoids, whether or not there is thrombosis, and whether there is associated ano-rectal pathology.
Patients who present with a history of bleeding should undergo proctosigmoidoscopy to rule out the presence of a tumor, which may also cause bleeding and may be missed because of the presence of hemorrhoids and the assumption that they are the source of bleeding. Patients over 50 may require a full colonoscopy.
All patients presenting with symptomatic hemorrhoids should be started on a regimen of stool softeners and warm soaks called sitz baths. For some patients this may be all that is required for symptomatic relief. I prefer to use medications that are relatively natural such as Metamucil and mineral oil so as not to alter the normal motility of the gastrointestinal tract and to avoid over utilization of laxatives.
Patients who have thrombosed hemorrhoids will usually require incision and drainage of the thrombosed hemorrhoid. This is a minor procedure done in the office with local anesthesia and usually provides immediate relief of the exquisite pain caused by the thrombosed hemorrhoid. Additional treatment may subsequently be warranted for removal of the hemorrhoid.
Patients with low grade, non-thrombosed hemorrhoids are very easily treated with rubber band ligation in the office using local anesthesia. Patients with more extensive hemorrhoids or with hemorrhoids in association with a fistula or fissure may require surgery in the hospital setting.
Surgical Hemorrhoidectomy involves removal of the hemorrhoidal tissue in the operating room under spinal or general anesthesia. The tissue is removed with cautery or laser and the resulting defect is repaired with sutures. Patients usually go home the same day. I start all patients on an aggressive regimen to force soft but formed bowel movements to minimize pain with defecation. No narcotic pain medications are used so as to avoid the constipation that is frequently associated with use of these products.
What are Anal Fistula and Fissure?
Fistula in-ano
Other conditions which affect the ano-rectum and may be confused with or occur concomitant with hemorrhoids include anal fistula and anal fissures.
A fistula is an abnormal communication between the inside of a hollow organ and the skin. In the case of an anal fistula the communication is from inside the rectum to the skin outside the anus or on the buttock. The inciting cause is trauma of defecation which causes a break in the mucosa of the rectum. Bacteria track into the tissue under the mucosa and form an abscess. The abscess eventually finds its way to the skin where it ruptures and drains. The outer opening may heal but the inner opening remains and permits the cycle to repeat itself. Patients often present with years of repeated abscesses in this area which drain, heal and return again.
Surgical treatment involves opening the entire fistula from its outer opening to its inner opening and allowing the wound to heal from the inside out thus obliterating the fistula. If the fistula track runs deep to the anal sphincter muscle, the muscle will need to be divided; however, doing so carries a risk of causing fecal incontinence. Often, when this is the case, the procedure will be done in two stages. During the first stage, the fistula is opened to the level of the anal sphincter muscle including the overlying skin or mucosa, but the sphincter is left intact. A strip of cotton tape called a "Seton" is passed around the sphincter muscle in this area and tied tight. This causes the sphincter muscle in this area to scar down. A few weeks later, it is safe to cut the muscle as it will not retract and open up but instead just stays in place and the remainder of the fistula can heal. The risk of incontinence is greatly reduced performing the procedure in this way when the sphincter is involved.
Anal Fissure
A fissure is simply a crack or tear in the anal skin in the anal canal. The cause is also straining with bowel movement. They are often exquisitely painful. So much so, that when I see a patient in excruciating pain in the anus, the patient will not allow me to do a digital exam and I cannot see a thrombosed hemorrhoid, I will usually just treat for a fissure as the presumptive diagnosis. Surgical treatment involves doing a lateral sphincterotomy. The skin in the outer part of the anus is opened slightly to expose the sphincter muscle and the muscle is divided superficially. This does not carry the same risk of incontinence as when dividing the muscle for a fistula, because the location and degree of muscle division can be completely controlled by the surgeon. With a fistula, the area of muscle involvement is dictated by the disease.
Surgery for fissures can often be avoided with the use of topical Nitroglycerine applied directly to the anus. Nitroglycerine relaxes the muscles of the anal sphincter the same way it relaxes the smooth muscle of blood vessels when treating Coronary Artery Disease. It may cause a low blood pressure in normal patients even when applied to the anus in this manner and therefore, may not be suitable for everyone. It is; however, a good first line treatment option that often resolves the problem and avoids the need for surgery.
Surgical Hemorrhoidectomy may be combined with a Fistulotomy for concomitant anal fistula or with a sphincterotomy for concomitant anal fissure.
Marsofold
28-01-2006, 14:43
Is it true that only assholes get hemorrhoids? :p
Pubic Lice (Crabs)
Cause
Pubic Lice is caused by Phthirus pubis (the crab louse).
Symptoms
Symptoms include itchiness in the pubic hair and/or visible eggs or lice.
How do I know if I have it?
Diagnosis is usually made by observation. If you develop itching in the pubic area and are unsure if you have lice, see a doctor.
How is it transmitted?
In most cases pubic lice are transmitted through sexual activity where pubic hair or other hair touches. Lice can also be spread through sharing towels, sheets or clothing, though this is less common as they do not live outside the body for very long.
Treatment/Management
Lotions to treat pubic lice are available over the counter at most pharmacies.
All clothes, towels and sheets should be washed in hot water at the time of treatment.
All sexual partners also need to be treated.
Prevention
Unfortunately condoms do not protect against pubic lice.
Woodman, it seems we have been exposed. lol.
Damn Benga, you beat me to the Hemoroids! Well of to the next one then:
Hansen's Disease (Leprosy)
Clinical FeaturesThis chronic infectious disease usually affects the skin and peripheral nerves but has a wide range of possible clinical manifestations. Patients are classified as having paucibacillary or multibacillary Hansen's disease. Paucibacillary Hansen's disease is milder and characterized by one or more hypopigmented skin macules. Multibacillary Hansen's disease is associated with symmetric skin lesions, nodules, plaques, thickened dermis, and frequent involvement of the nasal mucosa resulting in nasal congestion and epistaxis.
Etiologic AgentA bacillus, Mycobacterium leprae, that multiplies very slowly and mainly affects the skin, nerves, and mucous membranes. The organism has never been grown in bacteriologic media or cell culture, but has been grown in mouse foot pads.
IncidenceIn 2002, the number of new cases detected worldwide was 763,917. In 2002, 96 cases occurring in the United States were reported to CDC. In 2002, WHO listed Brazil, Madagascar, Mozambique, Tanzania, and Nepal as having 90% of cases.
SequelaeWorldwide, 1-2 million persons are permanently disabled as a result of Hansen's disease. However, persons receiving antibiotic treatment or having completed treatment are considered free of active infection.
TransmissionAlthough the mode of transmission of Hansen's disease remains uncertain, most investigators think that M. leprae is usually spread from person to person in respiratory droplets.
Risk GroupsClose contacts with patients with untreated, active, predominantly multibacillary disease, and persons living in countries with highly endemic disease.
SurveillanceHansen's disease is nationally notifiable in the United States.
TrendsPrevalence has remained relatively stable in the United States. Decreasing numbers of cases worldwide with pockets of high prevalence in certain countries.
ChallengesMulti-drug therapy has not been implemented in many endemic areas. Nerve damage must be recognized and managed. Relapse rate after completion of short course multi-drug therapy may rise.
OpportunitiesOpportunities exist for participation in Hansen's disease elimination activities in endemic-disease countries, and for Mycobacterium research in the Laboratory Research Branch of the National Hansen's Disease Program.
you guys remember Malthus?
i would like to say he was wrong, but over and over he proves US wrong.
the epidemics were, are and will bee with us until the end of the human race. however this doesnt mean that one of this epidemics actually wont be the end of the human race.
alfa dont be so smug when it comes to this matter, RNA viruses are probably the most terrifying forms of life that i know of, if we exclude humans, and are the candidate for the top of the food chain.
they mutate so easily, but 90% of those mutations, as in every species, prove to be fatal for the virus itself. so now i may sound crazy or paranoid or just like me, but i know that mutated ver of bird flu has to go through a 2nd or a 3rd generation in order to preserve its strain....and go to people.....and how the fuck did it go directly from china to turkey? w/out going through some of the more interesting grounds for breeding? there must be some great poultry trading routes b/w china and the turks. yeah right.
never liked chicken to start with..or meat....more of a fish person, i am. plus considering the world we live in along with all the emissions/imissions maybe we should consider the change in our vitamin diets...
they mutate so easily, but 90% of those mutations, as in every species, prove to be fatal for the virus itself. so now i may sound crazy or paranoid or just like me, but i know that mutated ver of bird flu has to go through a 2nd or a 3rd generation in order to preserve its strain....and go to people.....and how the fuck did it go directly from china to turkey? w/out going through some of the more interesting grounds for breeding? there must be some great poultry trading routes b/w china and the turks. yeah right.
never liked chicken to start with..or meat....more of a fish person, i am. plus considering the world we live in along with all the emissions/imissions maybe we should consider the change in our vitamin diets...
Daeron, the infection has spread from chicken and poultry to wild birds, and when it hit the birds it started spreading worldwide through regular to migrations routes. It has followed the main migratory routes of wild birds (north west route, Asia to Siberia), infected ducks have been found etc...which allowed scientists to predict the arrival of the virus wave to some extent. Migratory birds come in contact with poultry breeding compounds during stops ( open air ones and other ways, and then infection spreads).
here is an FAO article on the subject, dating back to august 2005.
http://www.fao.org/newsroom/en/news/2005/107405/
and here is a wild bird migratory route map (also from august 2005) and correlations with H5N1 infections.
http://www.fao.org/ag/againfo/subjects/en/health/diseases-cards/migrationmap.html
and a slightly more recent map ( december 2005), with proven and suspicious infections and bird deaths( slightly hard to decipher)
http://www.recombinomics.com/H5N1_Map_2005_QinghaiL.html
Now the virus as reached Turkey, and possibly eastern europe ( possible contaminations in Romania)
So the spreading has began, and the virus has mutated quite a lot already. The last turkish human deaths linked to H5N1 infections, still under analysis, suggest that there is a chance that it might might have mutated to a human transmissible form. nothing is sure yet, except that infections have been much quicker in Turkey, but so far only seem to have struck people (especially children) who have been in direct contact with infected birds ( farmers), so nothing is certain.
the main fear now in the scientific community are the coming seasonal influenza epidemics, which happen every year. If the virus mutates to a humanly transmissible form, there is a chance the regular influenza virus might couple with the mutated H5N1 form and be spread by the regular influenza epidemic, and because of its potency, lead to a pandemic situation
As for meat, if it stays epizootic, an avian virus only, apparently poultry is safe as long as it is cooked, heat destroying the virus.
As for hemorroids, there might be a link with overly comfortable toilet seats and fascinating litterature...
PEYROIES DISEASE
What is Peyronie's disease?
Peyronie's disease is characterized by a plaque, or hard lump, that forms on the erection tissue of the penis. The plaque often begins as an inflammation that may develop into a fibrous tissue.
Peyronie's disease was first described in 1743 by a French surgeon, François de la Peyronie. It was classified as a form of impotence. However, now impotence is recognized as one factor associated with Peyronie's disease, but is not always present.
What causes Peyronie's disease?
Some researchers believe Peyronie's disease develops following a trauma that causes bleeding inside the penis. This trauma may explain acute cases of Peyronie's disease, but does not explain why most cases develop slowly, or what causes the disease after no apparent traumatic event.
Generally, when the disease heals within a year or so, the plaque does not advance beyond an initial inflammatory phase. However, when the disease lasts for years, the plaque often becomes a tough, fibrous tissue, and calcium deposits may form.
What are the symptoms of Peyronie's disease?
The plaque in Peyronie's disease is benign, or non-cancerous. The following are the most common symptoms of Peyronie's disease. However, each individual may experience symptoms differently. Symptoms may include:
Plaque on the top of the shaft, which is the most common condition, causes the penis to bend upward.
Plaque on the underside causes the penis to bend downward.
In cases where the plaque develops on both top and bottom, indentation and shortening of the penis may occur.
Pain, bending, and emotional distress can prohibit sexual intercourse.
Painful erections may occur.
The symptoms of Peyronie's disease may resemble other conditions or medical problems. Always consult your physician for a diagnosis.
How is Peyronie's disease diagnosed?
A diagnosis of Peyronie's disease is usually made when men seek medical attention for painful erections and difficulty with intercourse. In addition to a complete medical history and physical examination, diagnostic procedures for Peyronie's disease may include the following:
ultrasound examination of the penis - a diagnostic technique which uses high-frequency sound waves to create an image of the internal organs.
color Doppler examination - a type of ultrasound that uses sound waves to measure the flow of blood through a blood vessel; waveforms of the blood flow are shown on the ultrasound screen (to evaluate erectile function, anatomy, and blood flow).
Treatment for Peyronie's disease:
Specific treatment for Peyronie's disease will be determined by your physician based on:
-your age, overall health, and medical history
-extent of the disease
-your tolerance for specific medications, procedures, or therapies
-expectations for the course of the disease
-your opinion or preference
In general, the goal of treatment is to keep the patient with Peyronie's disease sexually active. Providing education about the disease and its course is often included in the treatment plan. In some cases, treatment is not necessary, as Peyronie's disease often occurs in a mild form that heals without treatment in 6 to 15 months. Treatment may include:
-prescribing or continuing palliative methods
-surgery
vitamin E
Small studies have reported improvements with oral vitamin E prescribed by a physician, however, larger controlled studies have not been completed to establish the effectiveness of this treatment.
injections of various chemical agents into the plaques
Injections of various chemical agents into the plaques have been utilized in a small number of patients, and, for this reason, this intervention is considered unproven; unwanted side effects may occur.
radiation therapy
With this treatment approach, radiation is aimed at the plaque to reduce pain, but does not affect the plaque itself; unwanted side effects or worsening of the disease may occur.