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Thread: Smallpox - Background info....arm yourself with knowledge.

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    Elite Member ghost's Avatar
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    Smallpox - Background info....arm yourself with knowledge.

    Before reading this, you should know that smallpox is the only virus that can be treated by the vaccine AFTER exposure to it. Problem is, routine vaccinations in the US for it ceased 25 years ago, so we're now susceptible and immunization stocks are very, very low. Mortaltiy rate among those not immunized is 30%.

    Okay, here we go. I read it, and found it extremely interesting. The best way to cope with these potential threats is to be armed with good information - takes the mystery out of it, and therefore, the fear, IMO. If you choose not to read this at all, then that's of course your choice, but I'd rather have hard facts and know with what I'm dealing, rather than rely on the media to tell me what I should think and do. [Thank you to SGTMAJRET for the inspiration to post this information.]

    The following is from the Journals of the AMA, so it gets deep easily, IYKWIM. Figure references are linked for your convenience.







    HISTORY AND POTENTIAL AS A BIOWEAPON



    Smallpox probably was first used as a biological weapon during the French and Indian Wars (1754-1767) by British forces in North America. Soldiers distributed blankets that had been used by smallpox patients with the intent of initiating outbreaks among American Indians. Epidemics occurred, killing more than 50% of many affected tribes. With Edward Jenner's demonstration in 1796 that an infection caused by cowpox protected against smallpox and the rapid diffusion worldwide of the practice of cowpox inoculation (ie, vaccination), the potential threat of smallpox as a bioweapon was greatly diminished.

    A global campaign, begun in 1967 under the aegis of the World Health Organization (WHO), succeeded in eradicating smallpox in 1977. In 1980, the World Health Assembly recommended that all countries cease vaccination. A WHO expert committee recommended that all laboratories destroy their stocks of variola virus or transfer them to 1 of 2 WHO reference laboratoriesthe Institute of Virus Preparations in Moscow, Russia, or the Centers for Disease Control and Prevention (CDC) in Atlanta, Ga. All countries reported compliance. The WHO committee later recommended that all virus stocks be destroyed in June 1999, and the 1996 World Health Assembly concurred. In 1998, possible research uses for variola virus were reviewed by a committee of the Institute of Medicine (IOM). The IOM committee concluded, as did the preceding WHO committee, that there were research questions that might be addressed if the virus were to be retained. However, the IOM committee did not explore the costs or relative priority to be assigned to such an effort, and that committee was not asked to weigh the possible benefits resulting from such research activities contrasted with the possible benefits resulting from an international decision to destroy all virus stocks. These considerations will be weighed and decided by the 1999 World Health Assembly.

    Recent allegations from Ken Alibek, a former deputy director of the Soviet Union's civilian bioweapons program, have heightened concern that smallpox might be used as a bioweapon. Alibek8 reported that beginning in 1980, the Soviet government embarked on a successful program to produce the smallpox virus in large quantities and adapt it for use in bombs and intercontinental ballistic missiles; the program had an industrial capacity capable of producing many tons of smallpox virus annually. Furthermore, Alibek reports that Russia even now has a research program that seeks to produce more virulent and contagious recombinant strains. Because financial support for laboratories in Russia has sharply declined in recent years, there are increasing concerns that existing expertise and equipment might fall into non-Russian hands.

    The deliberate reintroduction of smallpox as an epidemic disease would be an international crime of unprecedented proportions, but it is now regarded as a possibility. An aerosol release of variola virus would disseminate widely, given the considerable stability of the orthopoxviruses in aerosol form and the likelihood that the infectious dose is very small. Moreover, during the 1960s and 1970s in Europe, when smallpox was imported during the December to April period of high transmission, as many as 10 to 20 second-generation cases were often infected from a single case. Widespread concern and, sometimes, panic occurred, even with outbreaks of fewer than 100 cases, resulting in extensive emergency control measures.




    EPIDEMIOLOGY



    Smallpox was once worldwide in scope, and before vaccination was practiced, almost everyone eventually contracted the disease. There were 2 principal forms of the disease, variola major and a much milder form, variola minor (or alastrim). Before eradication took place, these forms could be differentiated clinically only when occurring in outbreaks; virological differentiation is now possible. Through the end of the 19th century, variola major predominated throughout the world. However, at the turn of the century, variola minor was first detected in South Africa and later in Florida, from whence it spread across the United States and into Latin America and Europe. Typical variola major epidemics such as those that occurred in Asia resulted in case-fatality rates of 30% or higher among the unvaccinated, whereas variola minor case-fatality rates were customarily 1% or less.

    Smallpox spreads from person to person, primarily by droplet nuclei or aerosols expelled from the oropharynx of infected persons and by direct contact. Contaminated clothing or bed linens can also spread the virus. There are no known animal or insect reservoirs or vectors.

    Historically, the rapidity of smallpox transmission throughout the population was generally slower than for such diseases as measles or chickenpox. Patients spread smallpox primarily to household members and friends; large outbreaks in schools, for example, were uncommon. This finding was accounted for in part by the fact that transmission of smallpox virus did not occur until onset of rash. By then, many patients had been confined to bed because of the high fever and malaise of the prodromal illness. Secondary cases were thus usually restricted to those who came into contact with patients, usually in the household or hospital.

    The seasonal occurrence of smallpox was similar to that of chickenpox and measlesits incidence was highest during winter and early spring. This pattern was consonant with the observation that the duration of survival of orthopoxviruses in the aerosolized form was inversely proportional to both temperature and humidity.9 Likewise, when imported cases occurred in Europe, large outbreaks sometimes developed during the winter months, rarely during the summer.

    The patient was most infectious from onset of rash through the first 7 to 10 days of rash (Figure 1). As scabs formed, infectivity waned rapidly. Although the scabs contained large amounts of viable virus, epidemiological and laboratory studies indicate that they were not especially infectious, presumably because the virions were bound tightly in the fibrin matrix.

    The age distribution of cases depended primarily on the degree of smallpox susceptibility in the population. In most areas, cases predominated among children because adults were protected by immunity induced by vaccination or previous smallpox infection. In rural areas that had seen little vaccination or smallpox, the age distribution of cases was similar to the age distribution of the population. The age distribution pattern of cases in the United States presumably would be such if smallpox were to occur now because vaccination immunity in the population has waned so substantially.




    MICROBIOLOGY



    Smallpox, a DNA virus, is a member of the genus orthopoxvirus. The orthopoxviruses are among the largest and most complex of all viruses. The virion is characteristically a brick-shaped structure with a diameter of about 200 nm. Three other members of this genus (monkeypox, vaccinia, and cowpox) can also infect humans, causing cutaneous lesions, but only smallpox is readily transmitted from person to person. Monkeypox, a zoonotic disease, presently is found only in tropical rain forest areas of central and western Africa and is not readily transmitted among humans. Vaccinia and cowpox seldom spread from person to person.




    PATHOGENESIS AND CLINICAL PRESENTATION



    Natural infection occurs following implantation of the virus on the oropharyngeal or respiratory mucosa. The infectious dose is unknown but is believed to be only a few virions. After the migration of virus to and multiplication in regional lymph nodes, an asymptomatic viremia develops on about the third or fourth day, followed by multiplication of virus in the spleen, bone marrow, and lymph nodes. A secondary viremia begins on about the eighth day and is followed by fever and toxemia. The virus, contained in leukocytes, then localizes in small blood vessels of the dermis and beneath the oral and pharyngeal mucosa and subsequently infects adjacent cells.

    At the end of the 12- to 14-day incubation period (range, 7-17 days), the patient typically experiences high fever, malaise, and prostration with headache and backache. Severe abdominal pain and delirium are sometimes present. A maculopapular rash then appears on the mucosa of the mouth and pharynx, face, and forearms, and spreads to the trunk and legs (Figure 2) (NOTE FROM ghost: WARNING! GRAPHIC!). Within 1 to 2 days, the rash becomes vesicular and, later, pustular. The pustules are characteristically round, tense, and deeply embedded in the dermis; crusts begin to form on about the eighth or ninth day of rash. As the patient recovers, the scabs separate and characteristic pitted scarring gradually develops. The scars are most evident on the face and result from the destruction of sebaceous glands followed by shrinking of granulation tissue and fibrosis.

    The lesions that first appear in the mouth and pharynx ulcerate quickly because of the absence of a stratum corneum, releasing large amounts of virus into the saliva. Virus titers in saliva are highest during the first week of illness, corresponding with the period during which patients are most infectious. Although the virus in some instances can be detected in swabs taken from the oropharynx as many as 5 to 6 days before the rash develops, transmission does not occur during this period.

    Except for the lesions in the skin and mucous membranes and reticulum cell hyperplasia, other organs are seldom involved. Secondary bacterial infection is not common, and death, which usually occurs during the second week of illness, most likely results from the toxemia associated with circulating immune complexes and soluble variola antigens. Encephalitis sometimes ensues that is indistinguishable from the acute perivascular demyelination observed as a complication of infection due to vaccinia, measles, or varicella.

    Neutralizing antibodies can be detected by the sixth day of rash and remain at high titers for many years. Hemagglutinin-inhibiting antibodies can be detected on about the sixth day of rash, or about 21 days after infection, and complement-fixing antibodies appear approximately 2 days later. Within 5 years, hemagglutinin-inhibiting antibodies decline to low levels and complement-fixing antibodies rarely persist for longer than 6 months.

    Although at least 90% of smallpox cases are clinically characteristic and readily diagnosed in endemic areas, 2 other forms of smallpox are difficult to recognizehemorrhagic and malignant. Hemorrhagic cases are uniformly fatal and occur among all ages and in both sexes, but pregnant women appear to be unusually susceptible. Illness usually begins with a somewhat shorter incubation period and is characterized by a severely prostrating prodromal illness with high fever and head, back, and abdominal pain. Soon thereafter, a dusky erythema develops, followed by petechiae and frank hemorrhages into the skin and mucous membranes. Death usually occurs by the fifth or sixth day after onset of rash.

    In the frequently fatal malignant form, the abrupt onset and prostrating constitutional symptoms are similar. The confluent lesions develop slowly, never progressing to the pustular stage but remaining soft, flattened, and velvety to the touch. The skin has the appearance of a fine-grained, reddish-colored crepe rubber, sometimes with hemorrhages. If the patient survives, the lesions gradually disappear without forming scabs or, in severe cases, large amounts of epidermis might peel away.

    The illness associated with variola minor is generally less severe, with fewer constitutional symptoms and a more sparse rash. A milder form of disease is also seen among those who have residual immunity from previous vaccination. In partially immune persons, the rash tends to be atypical and more scant and the evolution of the lesions more rapid.

    There is little information about how individuals with different types of immune deficiency responded to natural smallpox infection. Smallpox was eradicated before human immunodeficiency virus (HIV) was identified and before suitable techniques became available for measuring cell-mediated immunity. However, it is probable that the underlying cause of some cases of malignant and hemorrhagic smallpox resulted from defective immune responses. Vaccination of immune-deficient persons sometimes resulted in a continually spreading primary lesion, persistent viremia, and secondary viral infection of many organs. One such case is documented to have occurred in a vaccinated soldier who had HIV infection.




    DIAGNOSIS



    The discovery of a single suspected case of smallpox must be treated as an international health emergency and be brought immediately to the attention of national officials through local and state health authorities.

    The majority of smallpox cases present with a characteristic rash that is centrifugal in distribution, ie, most dense on the face and extremities. The lesions appear during a 1- to 2-day period and evolve at the same rate. On any given part of the body, they are generally at the same stage of development. In varicella (chickenpox), the disease most frequently confused with smallpox, new lesions appear in crops every few days and lesions at very different stages of maturation (ie, vesicles, pustules, and scabs) are found in adjacent areas of skin. Varicella lesions are much more superficial and are almost never found on the palms and soles. The distribution of varicella lesions is centripetal, with a greater concentration of lesions on the trunk than on the face and extremities.

    The signs and symptoms of both hemorrhagic and malignant smallpox were such that smallpox was seldom suspected until more typical cases were seen and it was recognized that a smallpox outbreak was in progress. Hemorrhagic cases were most often initially identified as meningococcemia or severe acute leukemia. Malignant cases likewise posed diagnostic problems, most often being mistaken for hemorrhagic chickenpox or prompting surgery because of severe abdominal pain.

    Laboratory confirmation of the diagnosis in a smallpox outbreak is important. Specimens should be collected by someone who has recently been vaccinated (or is vaccinated that day) and who wears gloves and a mask. To obtain vesicular or pustular fluid, it is often necessary to open lesions with the blunt edge of a scalpel. The fluid can then be harvested on a cotton swab. Scabs can be picked off with forceps. Specimens should be deposited in a container tube that should be sealed with adhesive tape at the juncture of stopper and tube. This tube, in turn, should be enclosed in a second durable, watertight container. State or local health department laboratories should immediately be contacted regarding the shipping of specimens. Laboratory examination requires high-containment (BL-4) facilities and should be undertaken only in designated laboratories with the appropriate training and equipment. Once it is established that the epidemic is caused by smallpox virus, clinically typical cases would not require further laboratory confirmation.

    Smallpox infection can be rapidly confirmed in the laboratory by electron microscopic examination of vesicular or pustular fluid or scabs. Although all orthopoxviruses exhibit identically appearing brick-shaped virions, history taking and clinical picture readily identify cowpox and vaccinia. Although smallpox and monkeypox virions may be indistinguishable, naturally occurring monkeypox is found only in tropical rain forest areas of Africa. Definitive laboratory identification and characterization of the virus involves growth of the virus in cell culture or on chorioallantoic egg membrane and characterization of strains by use of various biologic assays, including polymerase chain reaction techniques and restriction fragment-length polymorphisms. The latter studies can be completed within a few hours.




    PREEXPOSURE PREVENTIVE VACCINATION



    Before 1972, smallpox vaccination was recommended for all US children at age 1 year. Most states required that each child be vaccinated before school entry. The only other requirement for vaccination was for military recruits and tourists visiting foreign countries. Most countries required that the individual be successfully vaccinated within a 3-year period prior to entering the country. Routine vaccination in the United States stopped in 1972 and since then, few persons younger than 27 years have been vaccinated. The US Census Bureau reported that in 1998, approximately 114 million persons, or 42% of the US population, were aged 29 years or younger.

    In addition, the immune status of those who were vaccinated more than 27 years ago is not clear. The duration of immunity, based on the experience of naturally exposed susceptible persons, has never been satisfactorily measured. Neutralizing antibodies are reported to reflect levels of protection, although this has not been validated in the field. These antibodies have been shown to decline substantially during a 5- to 10-year period. Thus, even those who received the recommended single-dose vaccination as children do not have lifelong immunity. However, among a group who had been vaccinated at birth and at ages 8 and 18 years as part of a study, neutralizing antibody levels remained stable during a 30-year period. Because comparatively few persons today have been successfully vaccinated on more than 1 occasion, it must be assumed that the population at large is highly susceptible to infection.

    In the United States, a limited reserve supply of vaccine that was produced by Wyeth Laboratories, Lancaster, Pa, in the 1970s is in storage. This supply is believed to be sufficient to vaccinate between 6 and 7 million persons. This vaccine, now under the control of the CDC, consists of vaccine virus (New York Board of Health strain) grown on scarified calves. After purification, it was freeze-dried in rubber-stoppered vials that contain sufficient vaccine for at least 50 doses when a bifurcated needle is used. It is stored at -20C (James LeDuc, PhD, oral communication, 1998). Although quantities of vaccine have also been retained by a number of other countries, none have reserves large enough to meet more than their own potential emergency needs. WHO has 500,000 doses.

    There are no manufacturers now equipped to produce smallpox vaccine in large quantities. The development and licensure of a tissue cell culture vaccine and the establishment of a new vaccine production facility is estimated to require at least 36 months (Thomas Monath, MD, unpublished data, 1999).

    Because of the small amounts of vaccine available, a preventive vaccination program to protect individuals such as emergency and health care personnel is not an option at this time. When additional supplies of vaccine are procured, a decision to undertake preventive vaccination of some portion of the population will have to weigh the relative risk of vaccination complications against the threat of contracting smallpox.

    A further deterrent to extensive vaccination is the fact that presently available supplies of vaccinia immune globulin (VIG), also maintained by the CDC, are very limited in quantity. The working group recommends VIG for the treatment of severe cutaneous reactions occurring as a complication of vaccination. Vaccinia immune globulin has also been given along with vaccination to protect those who needed vaccination but who were at risk of experiencing vaccine-related complications. It has been estimated that if 1 million persons were vaccinated, as many as 250 persons would experience adverse reactions of a type that would require administration of VIG (James LeDuc, PhD, oral communication, 1998). How much VIG would be needed to administer with vaccine to those at risk is unknown.




    POSTEXPOSURE THERAPY



    At this time, the best that can be offered to the patient infected with smallpox is supportive therapy plus antibiotics as indicated for treatment of occasional secondary bacterial infections. No antiviral substances have yet proved effective for the treatment of smallpox, and the working group is not aware of any reports that suggest any antiviral product is therapeutic. Encouraging initial reports in the 1960s describing the therapeutic benefits of the thiosemicarbazones, cytosine arabinoside, and adenine arabinoside proved questionable on further study.

    Recent studies on tissue culture, mice, and a small number of monkeys have suggested the possibility that cidofovir, a nucleoside analog DNA polymerase inhibitor, might prove useful in preventing smallpox infection if administered within 1 or 2 days after exposure (John Huggins, PhD, oral communication, 1998). At this time, there is no evidence that cidofovir is more effective than vaccination in this early period. Moreover, the potential utility of this drug is limited, given the fact that it must be administered intravenously and its use is often accompanied by serious renal toxicity.





    ...



    VACCINE ADMINISTRATION AND COMPLICATIONS



    Smallpox vaccine is currently approved by the US Food and Drug Administration (FDA) for use only in persons in special-risk categories, including laboratory workers directly involved with smallpox or closely related orthopoxviruses. Under epidemic circumstances, widespread vaccination would be indicated, as recommended by the working group.

    Vaccination has been successfully and safely administered to persons of all ages, from birth onward. However, there are certain groups for whom elective vaccination has not been recommended because of the risk of complications. Under epidemic circumstances, however, such contraindications will have to be weighed against the grave risks posed by smallpox. If available, VIG can be administered concomitantly with vaccination to minimize the risk of complications in these persons.

    Vaccination is normally performed using the bifurcated needle (Figure 3). A sterile needle is inserted into an ampoule of reconstituted vaccine and, on withdrawal, a droplet of vaccine sufficient for vaccination is held by capillarity between the 2 tines. The needle is held at right angles to the skin; the wrist of the vaccinator rests against the arm. Fifteen perpendicular strokes of the needle are rapidly made in an area of about 5 mm in diameter. The strokes should be sufficiently vigorous so that a trace of blood appears at the vaccination site after 15 to 30 seconds. After vaccination, excess vaccine should be wiped from the site with gauze that should be discarded in a hazardous waste receptacle. The site should be covered with a loose, nonocclusive bandage to deter the individual from touching the site and perhaps transferring virus to other parts of the body.

    After about 3 days, a red papule appears at the vaccination site and becomes vesicular on about the fifth day (Figure 4). By the seventh day, it becomes the typical Jennerian pustulewhitish, umbilicated, multilocular, containing turbid lymph and surrounded by an erythematous areola that may continue to expand for 3 more days. Regional lymphadenopathy and fever is not uncommon. As many as 70% of children have 1 or more days of temperature higher than 39C (100F) between days 4 and 14. The pustule gradually dries, leaving a dark crust, which normally falls off after about 3 weeks.

    A successful vaccination for those with partial immunity may manifest a gradient of responses. These range from what appears to be a primary take (as described herein) to an accelerated reaction in which there may be little more than a papule surrounded by erythema that reaches a peak between 3 and 7 days. A response that reaches a peak in erythema within 48 hours represents a hypersensitivity reaction and does not signify that growth of the vaccinia virus has occurred. Persons exhibiting such a reaction should be revaccinated.

    Complications

    The frequency of complications associated with use of the New York Board of Health strain (the strain used throughout the United States and Canada for vaccine) is the lowest for any established vaccinia virus strain, but the risks are not inconsequential. Data on complications gathered by the CDC in 1968 are shown in Table 1. Complications occurred most frequently among primary vaccinees.

    Postvaccinial Encephalitis.
    Postvaccinial encephalitis occurred at a rate of 1 case per 300,000 vaccinations and was observed only in primary vaccinees; one fourth of these cases were fatal and several had permanent neurological residua. Between 8 and 15 days after vaccination, encephalitic symptoms developedfever, headache, vomiting, drowsiness, and, sometimes, spastic paralysis, meningitic signs, coma, and convulsions. Cerebrospinal fluid usually showed a pleocytosis. Recovery was either complete or associated with residual paralysis and other central nervous system symptoms and, sometimes, death. There was no treatment.

    Progressive Vaccinia (Vaccinia Gangrenosa).
    Cases of progressive vaccinia occurred both among primary vaccinees and revaccinees. It was a frequently fatal complication among those with immune deficiency disorders. The vaccinial lesion failed to heal and progressed to involve adjacent skin with necrosis of tissue, spreading to other parts of the skin, to bones, and to viscera. Vaccinia immune globulin was used for this problem. One case in a soldier with acquired immunodeficiency syndrome was successfully treated with VIG and ribavirin. These treatment strategies were off-label and would be considered experimental.

    Eczema Vaccinatum.
    A sometimes serious complication, eczema vaccinatum occurred in some vaccinees and contacts with either active or healed eczema. Vaccinial skin lesions extended to cover all or most of the area once or currently afflicted with eczema. Vaccinia immune globulin was therapeutic.

    Generalized Vaccinia.
    A secondary eruption almost always following primary vaccination, generalized vaccinia resulted from blood-borne dissemination of virus. Lesions emerged between 6 and 9 days after vaccination and were either few in number or generalized. This complication was usually self-limited. In severe cases, VIG was indicated.

    Inadvertent Inoculation.
    Transmission to close contacts or autoinoculation to sites such as face, eyelid, mouth, and genitalia sometimes occurred. Most lesions healed without incident, although VIG was useful in some cases of periocular implantation.

    Miscellaneous.
    Many different rashes have been associated with vaccination. Most common are erythema multiforme and variously distributed urticarial, maculopapular, and blotchy erythematous eruptions, which normally clear without therapy.

    Groups at Special Risk for Complications

    Consensus recommendations for special-risk groups as set forth herein reflect the best clinical and science-based judgment of the working group and do not necessarily correspond to FDA-approved uses.

    Five groups of persons are ordinarily considered at special risk of smallpox vaccine complications: (1) persons with eczema or other significant exfoliative skin conditions; (2) patients with leukemia, lymphoma, or generalized malignancy who are receiving therapy with alkylating agents, antimetabolites, radiation, or large doses of corticosteroids; (3) patients with HIV infection; (4) persons with hereditary immune deficiency disorders; and (5) pregnant women. If persons with contraindications have been in close contact with a smallpox patient or the individual is at risk for occupational reasons, VIG, if available, may be given simultaneously with vaccination in a dose of 0.3 mL/kg of body weight to prevent complications. This does not alter vaccine efficacy. If VIG is not available, vaccine administration may still be warranted, given the far higher risk of an adverse outcome from smallpox infection than from vaccination.

    VIG Therapy for Complications

    Vaccinia immune globulin is valuable in treating patients with progressive vaccinia, eczema vaccinatum, severe generalized vaccinia, and periocular infections resulting from inadvertent inoculation. It is administered intramuscularly in a dose of 0.6 mL/kg of body weight. Because the dose is large (eg, 42 mL for a person weighing 70 kg), the product is given intramuscularly in divided doses over a 24- to 36-hour period and may be repeated, if necessary, after 2 to 3 days if improvement is not occurring. Because the availability of VIG is so limited, its use should be reserved for the most serious cases. Vaccinia immune globulin, as well as vaccinia vaccine, is made available by the CDC through state health departments. Consultative assistance in the diagnosis and management of patients with complications can be obtained through state health departments.




    SUMMARY



    The specter of resurgent smallpox is ominous, especially given the enormous efforts that have been made to eradicate what has been characterized as the most devastating of all the pestilential diseases. Unfortunately, the threat of an aerosol release of smallpox is real and the potential for a catastrophic scenario is great unless effective control measures can quickly be brought to bear.

    Early detection, isolation of infected individuals, surveillance of contacts, and a focused selective vaccination program are the essential items of a control program. Educating health care professionals about the diagnostic features of smallpox should permit early detection; advance regionwide planning for isolation and care of infected individuals in their homes as appropriate and in hospitals when home care is not an option will be critical to deter spread. Ultimately, success in controlling a burgeoning epidemic will depend on the availability of adequate supplies of vaccine and VIG. An adequate stockpile of those commodities would offer a relatively inexpensive safeguard against tragedy.

  2. #2
    Imperial Impotentate brembo's Avatar
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    Oh ****.

    I do not like smallpox at all.
    Tao_Jones Cult Member since 2004
    I gave Miss Manners a Dirty Sanchez, and she LIKED it.

  3. #3
    Moderator David's Avatar
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    I could never figure out why they stopped innoculating children for smallpox with the virus still in existence.

    Those who survive and they very likely to do so with present day antivirals will have disfigurements. Small pox scars up pretty bad.

    david

    Hell_Yes

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    Elite Member ghost's Avatar
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    Originally posted by Hell_Yes
    I could never figure out why they stopped innoculating children for smallpox with the virus still in existence.

    Those who survive and they very likely to do so with present day antivirals will have disfigurements. Small pox scars up pretty bad.

    david
    I think it was the risk of the vaccine vs. no known reports of the disease for X-number of years. There's some info on that in the article.

    God, take a look at Figure 2 in the article, then Figure 3. Ugh. Then again, don't look at 'em.

  5. #5
    Morterator Immortal's Avatar
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    is small pox the one where u get it once and u'll never get it again.. or is that chicken pox?

  6. #6
    Moderator David's Avatar
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    Originally posted by ghost


    I think it was the risk of the vaccine vs. no known reports of the disease for X-number of years. There's some info on that in the article.

    God, take a look at Figure 2 in the article, then Figure 3. Ugh. Then again, don't look at 'em.
    Not a good assumption to make. Unless the disease entity is completely eradicated, it would make a viable and dangerous weapon. It is not like scientists or lay folks have never accidently introduced a dangerous organism into an environment.


    david

    BTW. you only suffer from small pox once.
    Chicken pox can recur as shingles in later life (Varicella-Zoster virus)

    Hell_Yes

    Luck is where preparation meets opportunity - Seneca

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    Morterator Immortal's Avatar
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    so if I got small pox when I was small.. that means I can't get infected anymore?

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    Moderator David's Avatar
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    Originally posted by Immortal
    so if I got small pox when I was small.. that means I can't get infected anymore?
    The vaccine is a related virus call cow pox. Once innoculated, your carcass produces antibodies for the rest of your life.

    Hell_Yes

    Luck is where preparation meets opportunity - Seneca

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  9. #9
    SG Stud ColdFusion's Avatar
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    Ok, Im gonna read it so i can be armed with the info

  10. #10
    Elite Member ghost's Avatar
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    Originally posted by Hell_Yes
    Not a good assumption to make. Unless the disease entity is completely eradicated, it would make a viable and dangerous weapon. It is not like scientists or lay folks have never accidently introduced a dangerous organism into an environment.

    david
    That's true, no argument there.

    But how does one know if a disease has been eradicated? The only thing to go by is reports from the field all over the world. I realize that perhaps there may be a case or two in, say, a remote part of Africa where no medical facilities exist, but once those people die, so does that batch of smallpox. With no one to spread it to, it dies out. Apparently, that's what happened in real life here on earth, since there were no reported cases over a period of time. Therefore the vaccinations stopped.

    To debate whether or not the WHO made a good decision is a moot point. What we have to decide now is whether or not a real threat exists, and if so, should we start producing the vaccines once again. My opinion is "yes."

    But we'd better start RIGHT NOW. One report indicated that it would take 36 months to construct a suitable facility and make the required vaccines.

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