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Medical Forum / General / General / January 2006Avian Flu and "The Black Death" of the Middle Ages
I had a serious "ah-ha" moment. I previously watched a show on "The Black Death" and a scientist risked his reputation by publicly stating that he did not think the cause of the plague was the Bubonic bacteria. Some of his reasons why were: 1.) No samples from the victims exist to prove it was conclusively so. 2.) The Bubonic Bacteria is alive an well and can be found around the world (including the US) with no reappearing outbreaks of the magnitude needed in order to explain such devestation. 3.) Cemmetary records have survived from at least one town decimated by "The Black Death" and the information obtained there-in is suggestive to the scientist that from initial infection to death only took 3 weeks and both the nature and speed of transmission was indicative of a virus and not any known bacteria. 4.) The records and speed of transmission are also indicative of being transmitted by human-to-human contact and not from parasite-to-human. 5.) The scientist also stated that the symptom of the plauge most closely resembled modern hemoragic diseases such as Ebola. So I kept the above information in the back of my head. Tonight I watched a program on "The Bird Flu" and it mentioned one thing that I found amazing. If in fact the virus mutates so that it can spread from person to person, then the symptoms experienced by the infected will not be anywhere near the normal symptoms of the yearly flu. How do we know this? Detailed records of the 1918 pandemic showed that this was so. These records indicated that the infected people had symptoms such as: Full-Body Swelling Blackening of the Skin (In some cases Caucasions were mistaken for African-Americans) Bleeding from the Eyes, Ears, Nose, & Mouth Contortion of the Body As soon as I heard this I immediately connected it to the above information. All of these symptoms were identical to the plauge of the middle ages. In fact "The Black Death" was called such because of the Blackening of the Skin. I am seriously thinking that the true cause of "The Black Death" was none other than a Super-Flu pandemic, spread by human-to-human contact and not from the Bubonic Bacteria carried by flea infested rats. I am currently trying to track down an epidemiologist and see if my theory is unique and if it has any weight. I will keep you all informed. (If there are any Epidemiologists here in this NG, feel free to reply with your thoughts and opinions as well.) -Jason Here is a copy from "The Merck Manual" - an encyclopaedia of current medical practice. PLAGUE (Bubonic Plague; Pestis; Black Death) An acute, severe infection appearing most commonly in a bubonic or pneumonic form, caused by the bacillus Yersinia pestis. *Etiology and Epidemiology Yersiniapestis (formerlyPasteurellapestis) is a short bacillus that often shows bipolar staining (especially with Giemsa stain) and may resemble safety pins. Plague occurs primarily in wild rodents (eg, rats, mice, squirrels, prairie dogs); it may be acute, subacute, or chronic, and urban (mainly murine) or sylvatic. Massive human epidemics have occurred (eg, the Black Death of the Middle Ages); more recently, plague has occurred sporadically or in limited outbreaks. In the USA, > 90 % of human plague occurs in the southwestern states, especially New Mexico, Arizona, California, and Colorado. Bubonic plague is the most common form. Plague is transmitted from rodent to humans by the bite of an infected flea vector. Human-to-human transmission occurs by inhaling droplet nuclei through the cough of patients with bubonic or septicemic plague who have pulmonary lesions (primary pneumonic plague). In endemic areas in the USA, a number of cases have been associated with household pets, especially cats. Transmission from cats can be by bite, or, if the cat has pneumonic plague, by inhalation of infected droplets. *Symptoms and Signs In bubonic plague, the incubation period is usually 2 to 5 days but varies from a few hours to 12 days. Onset is abrupt and often associated with chills; the temperature rises to 39.5 to 41° C (103 to 106° F). The pulse may be rapid and thready; hypotension may occur. Enlarged lymph nodes (buboes) appear with or shortly before the fever. The femoral or inguinal lymph nodes are most commonly involved (50%), followed by axillary (22%), cervical (10%), or multiple (13%) nodes. Typically, the nodes are extremely tender and firm, surrounded by considerable edema; they may suppurate in the 2nd wk. The overlying skin is smooth and reddened but often not warm. A primary cutaneous lesion, varying from a small vesicle with slight local lymphangitis to an eschar, occasionally appears at the bite. The patient may be restless, delirious, confused, and uncoordinated. The liver and spleen may be palpable. The-WBC count is usually 10,000 to 20,000/p.L with a predominance of immature and mature neutrophils. The nodes may suppurate in the 2nd wk. Primary pneumonic plague has a 2- to 3day incubation period, followed by abrupt onset of high fever, chills, tachycardia, and headache, often severe. Cough, not prominent initially, develops within 20 to 24 h; sputum is mucoid at first, rapidly shows blood specks, and then becomes uniformly pink or bright red (resembling raspberry syrup) and foamy. Tachypnea and dyspnea are present, but pleurisy is not. Signs of consolidation are rare, and rales may be absent. Chest x-rays show a rapidly progressing pneumonia. Septicemic plague usually occurs with the bubonic form as an acute, fulminant illness. Abdominal pain, presumably due to mesenteric lymphadenopathy, occurs in 40% of patients. Pharyngeal plague and plague meningitis are less common forms. Pestis minor, a benign form of bubonic plague, usually occurs only in endemic areas. Lymphadenitis, fever, headache, and prostration subside within a week. *Diagnosis and Prognosis Diagnosis is based on recovery of the organism, which may be cultured from blood, sputum, or lymph node aspirate. Because surgical drainage may disseminate the organism, needle aspiration of a bubo is preferred. Y. pestis can grow on ordinary culture media or be isolated by animal (especially guinea pig) inoculation. Serologic tests include complement fixation, passive hemagglutination, and immunofluorescent staining of a node or tissue biopsy or secretions. Prior vaccination does not exclude plague in the differential diagnosis, since clinical illness may occur in vaccinated persons. The mortality rate for untreated patients with bubonic plague is about 60%, with most deaths occurring from sepsis in 3 to 5 days. Most untreated patients with pneumonic plague die within 48 h of symptom onset. Septicemic plague may be fatal before bubonic or pulmonary manifestations predominate. *Prophylaxis and Treatment Rodents should be controlled and repellents used to minimize fleabites. Although immunization with standard killed plague vaccine gives protection, vaccination is not indicated for most travelers to countries reporting cases of plague. Travelers should consider prophylaxis with tetracycline 500 mg po q 6 h during exposure periods. Immediate treatment reduces mortality to < 5%. In septicemic or pneumonic plague, treatment must begin within 24 h with streptomycin 30 mg/kg/day IM in 4 divided doses q 6 h for 7 to 10 days. Many physicians give higher initial dosages, up to 0.5 g IM q 3 h for 48 h. Tetracycline 30 mg/kg IV or po in 4 divided doses is an alternative. Gentarrticit, is probably also effective, although no controlled clinical trials have been conducted. For plague meningitis, chloramphenicol should be given in a loading dose of 25 mg/ kg IV, followed by 50 mg/kg/day in 4 divided doses IV or po. A multidrug-resistant strain has been reported from Madagascar. Routine aseptic precautions are adequate for patients with bubonic plague. Those with primary or secondary pneumonic plague require strict (airborne agent) isolation. All pneumonic plague contacts should be under medical surveillance; their temperatures should be taken q 4 h for 6 days. If this is not possible, tetracycline 1 g/day po for 6 days can be given; however, this can produce drug-resistant strains. Here is a copy from "The Merck Manual" - an encyclopaedia of current medical practice. PLAGUE (Bubonic Plague; Pestis; Black Death) An acute, severe infection appearing most commonly in a bubonic or pneumonic form, caused by the bacillus Yersinia pestis. *Aetiology and Epidemiology Yersiniapestis (formerlyPasteurellapestis) is a short bacillus that often shows bipolar staining (especially with Giemsa stain) and may resemble safety pins. Plague occurs primarily in wild rodents (eg, rats, mice, squirrels, prairie dogs); it may be acute, subacute, or chronic, and urban (mainly murine) or sylvatic. Massive human epidemics have occurred (eg, the Black Death of the Middle Ages); more recently, plague has occurred sporadically or in limited outbreaks. In the USA, > 90 % of human plague occurs in the south-western states, especially New Mexico, Arizona, California, and Colorado. Bubonic plague is the most common form. Plague is transmitted from rodent to humans by the bite of an infected flea vector. Human-to-human transmission occurs by inhaling droplet nuclei through the cough of patients with bubonic or septicemic plague who have pulmonary lesions (primary pneumonic plague). In endemic areas in the USA, a number of cases have been associated with household pets, especially cats. Transmission from cats can be by bite, or, if the cat has pneumonic plague, by inhalation of infected droplets. *Symptoms and Signs In bubonic plague, the incubation period is usually 2 to 5 days but varies from a few hours to 12 days. Onset is abrupt and often associated with chills; the temperature rises to 39.5 to 41° C (103 to 106° F). The pulse may be rapid and thready; hypotension may occur. Enlarged lymph nodes (buboes) appear with or shortly before the fever. The femoral or inguinal lymph nodes are most commonly involved (50%), followed by axillary (22%), cervical (10%), or multiple (13%) nodes. Typically, the nodes are extremely tender and firm, surrounded by considerable oedema; they may suppurate in the 2nd wk. The overlying skin is smooth and reddened but often not warm. A primary cutaneous lesion, varying from a small vesicle with slight local lymphangitis to an eschar, occasionally appears at the bite. The patient may be restless, delirious, confused, and uncoordinated. The liver and spleen may be palpable. The-WBC count is usually 10,000 to 20,000/p.L with a predominance of immature and mature neutrophils. The nodes may suppurate in the 2nd wk. Primary pneumonic plague has a 2- to 3day incubation period, followed by abrupt onset of high fever, chills, tachycardia, and headache, often severe. Cough, not prominent initially, develops within 20 to 24 h; sputum is mucoid at first, rapidly shows blood specks, and then becomes uniformly pink or bright red (resembling raspberry syrup) and foamy. Tachypnea and dyspnea are present, but pleurisy is not. Signs of consolidation are rare, and rales may be absent. Chest x-rays show a rapidly progressing pneumonia. Septicemic plague usually occurs with the bubonic form as an acute, fulminant illness. Abdominal pain, presumably due to mesenteric lymphadenopathy, occurs in 40% of patients. Pharyngeal plague and plague meningitis are less common forms. Pestis minor, a benign form of bubonic plague, usually occurs only in endemic areas. Lymphadenitis, fever, headache, and prostration subside within a week. *Diagnosis and Prognosis Diagnosis is based on recovery of the organism, which may be cultured from blood, sputum, or lymph node aspirate. Because surgical drainage may disseminate the organism, needle aspiration of a bubo is preferred. Y. pestis can grow on ordinary culture media or be isolated by animal (especially guinea pig) inoculation. Serologic tests include complement fixation, passive hemagglutination, and immunofluorescent staining of a node or tissue biopsy or secretions. Prior vaccination does not exclude plague in the differential diagnosis, since clinical illness may occur in vaccinated persons. The mortality rate for untreated patients with bubonic plague is about 60%, with most deaths occurring from sepsis in 3 to 5 days. Most untreated patients with pneumonic plague die within 48 h of symptom onset. Septicemic plague may be fatal before bubonic or pulmonary manifestations predominate. *Prophylaxis and Treatment Rodents should be controlled and repellents used to minimize fleabites. Although immunization with standard killed plague vaccine gives protection, vaccination is not indicated for most travellers to countries reporting cases of plague. Travellers should consider prophylaxis with tetracycline 500 mg po q 6 h during exposure periods. Immediate treatment reduces mortality to < 5%. In septicemic or pneumonic plague, treatment must begin within 24 h with streptomycin 30 mg/kg/day IM in 4 divided doses q 6 h for 7 to 10 days. Many physicians give higher initial dosages, up to 0.5 g IM q 3 h for 48 h. Tetracycline 30 mg/kg IV or po in 4 divided doses is an alternative. Gentarrticit, is probably also effective, although no controlled clinical trials have been conducted. For plague meningitis, chloramphenicol should be given in a loading dose of 25 mg/ kg IV, followed by 50 mg/kg/day in 4 divided doses IV or po. A multidrug-resistant strain has been reported from Madagascar. Routine aseptic precautions are adequate for patients with bubonic plague. Those with primary or secondary pneumonic plague require strict (airborne agent) isolation. All pneumonic plague contacts should be under medical surveillance; their temperatures should be taken q 4 h for 6 days. If this is not possible, tetracycline 1 g/day po for 6 days can be given; however, this can produce drug-resistant strains. > Here is a copy from "The Merck Manual" - an > encyclopaedia of current medical practice. [quoted text clipped - 4 lines] > in a bubonic or pneumonic form, caused by the > bacillus Yersinia pestis. (snipped for space) I appreciate the effort, but unfortunately that did not address my post. -Jason > > Here is a copy from "The Merck Manual" - an > > encyclopaedia of current medical practice. [quoted text clipped - 11 lines] > > -Jason Jason, you need to read the info. It states the formation of buboes where it gets it's name. What viral infection do you see this associated with in which the lymph node busts open and weeps with bacteria? Have you seen this with HIV? The pneumonic form can cause transmission from person to person. The primary form is from vector to host. Bacteria evolve with increased or decreased virulence. This has happened with a variety of bacteria including scarlet fever. >Jason, you need to read the info. >It states the formation of buboes where it gets it's name. What viral [quoted text clipped - 4 lines] >Bacteria evolve with increased or decreased virulence. This has happened >with a variety of bacteria including scarlet fever Robert, I am much aware of the particuliar symptom you described above. I have contacted both my state's resident epidemiologist, as well as several other epidemiologists. Some dismissed this offhand, other found this theory intriguing and even brought up evidence which could support such. Also, the swelling and rupturing of the lymph nodes is indeed not just caused by "Bubonic Plauge". It is also apparant in many Hemoraghic Fevers, such as Ebola, and several other viral infections, although the reasons for such differ in bacterial pathogens vs.viral ones. Also, do consider that symptoms experienced by the infected during the 1918 Flue Pandemic. They are quite remarkably similiar to the symptoms of "The Black Death", not the bacteria we identify with said disease today, but the actual symptoms noted during that time in history. One epidemiologist even flat out told me thus: "Most of us (epidemioligists) are conservitive in our views in a professional sense. However we do toss around theories and hold personal opinions that often do not agree with the accepted answers people are most likely to hear. When it comes to the topic of "The Black Death", I am personaly convinced that it is quite similiar to "Biblical Leprosy". Biblical Leprosy was not limited to our modern disease named Leprosy. Instead, the "Biblical" version was a coglamoration of various diseases, disorders, conditions, birth deffects, often completely normal and temporary in nature. Most, if not all, of these were non-infectious." My response was "So you are saying that "The Black Death" was most likely caused by many diseases which were then lumped under one header?" "Yes, that is my personal theory. If this is indeed the case then I would most definatley include Influenza in the mix." So Robert, I think you were caught up with the pathogen responsible for the disease we know as "Bubonic Plauge" today, but my post was concerning an alternative proposal to the pathogen actualy responsible for "The Black Death". Also realize that most epidemiologists firmly believe that "The Black Death" was caused by the bacteria that we all were taught was responsible. However, this belief is lacking in sufficient proof to remove all doubt. Base upon my communication with the particuliar epidemiologist above, I have sence agreed and adopted that particuliar view point, that "The Black Death" was most likely not caused by one single pathogen spreading all over the known world. Since "The Plague" occured in waves seperated by years and decades, it is most likely that multiple pathogens were responsible and were only later lumped together under "The Black Death". -Jason > such. Also, the swelling and rupturing of the lymph nodes is indeed > not just caused by "Bubonic Plauge". This is a description from 1348 "... it began with swellings in the groin and armpit, in both men and women, some of which were as big as apples and some of which were shaped like eggs, some were small and others were large; the common people called these swellings gavoccioli. From these two parts of the body, the fatal gavaccioli would begin to spread and within a short while would appear over the entire body in various spots; the disease at this point began to take on the qualities of a deadly sickness, and the body would be covered with dark and livid spots, which would appear in great numbers on the arms, the thighs, and other parts of the body; some were large and widely spaced while some were small and bunched together. And just like the gavaciolli earlier, these were certain indications of coming death." >It is also apparant in many > Hemoraghic Fevers, such as Ebola, and several other viral infections, > although the reasons for such differ in bacterial pathogens vs.viral > ones. Heres a description of Ebola which is the opposite of dissolution and involution of lymph node centers and not enlargement. Filoviral Marburg and Ebola infections are severe hemorrhagic fevers. Damage to blood clotting and vessel permeability are the most prominent clinical features in humans. In fatal Marburg and Ebola infections, humans and monkeys generally die with no evidence of an immune response; however, details of immune system damage are poorly investigated [Peters et al., 1996]. Involution of lymphoid follicles developed in monkeys over the course of Marburg and Ebola infection. Rapid involution was manifested as a 69% reduction in the relative volume of the germinative centers of the follicles of the mesenteric lymph nodes during the first two days of Ebola infection. The reduction was mainly due to a decrease in the number of follicles and, to a lesser extent, in their size. The increasing lymphoid depletion became obvious from days 3-4 in both Marburg and Ebola infections. The lymphoid depletion was not caused by necrosis of lymphocytes. At the last days of infection, few visible follicles of lymph nodes and splenic white pulp had morphological appearances suggesting their waning function: small size, homogeneous germinal centers without blast cells. The B-zones were more affected than the T-zones in lymph nodes. However, the T-zones showed no signs of functional activity. Taken together, our studies revealed severe damage to lymphoid tissue in Marburg and Ebola viruses infected monkeys, which indicates that the function of immune system is greatly affected. http://www.asanltr.com/ASANews-97/Immunosuppression.html > Also, do consider that symptoms experienced by the infected during the > 1918 Flue Pandemic. They are quite remarkably similiar to the symptoms > of "The Black Death", not the bacteria we identify with said disease > today, but the actual symptoms noted during that time in history. Any descriptions that can be similar to the 1348 account? > One epidemiologist even flat out told me thus: > [quoted text clipped - 8 lines] > deffects, often completely normal and temporary in nature. Most, if > not all, of these were non-infectious." That's correct when you mention a name or refer to a disease by a name. When someone writes a detailed description then one can be more clear. > My response was "So you are saying that "The Black Death" was most > likely caused by many diseases which were then lumped under one > header?" I would imagine anyone who died at the time was labeled with dying from the black death but that does not negate that a large epidemic had not taken place. > "Yes, that is my personal theory. If this is indeed the case then I > would most definatley include Influenza in the mix." > > So Robert, I think you were caught up with the pathogen responsible for > the disease we know as "Bubonic Plauge" today, but my post was > concerning an alternative proposal to the pathogen actualy responsible > for "The Black Death". The flu does not resemble the black death except probably some form of pneumonic which is still pushing it. Also realize that most epidemiologists firmly > believe that "The Black Death" was caused by the bacteria that we all > were taught was responsible. However, this belief is lacking in > sufficient proof to remove all doubt. There's been many pandemic flu outbreaks and they don't resemble the black death. Sorry. Base upon my communication with > the particuliar epidemiologist above, I have sence agreed and adopted > that particuliar view point, that "The Black Death" was most likely not > caused by one single pathogen spreading all over the known world. The population of the earth was almost wiped out and not ordinary typical deaths. No problem as it makes good talk at parties just as saying that HIV does not cause AIDS. > Since "The Plague" occured in waves seperated by years and decades, it > is most likely that multiple pathogens were responsible and were only > later lumped together under "The Black Death". With the same classical descriptions? I doubt it. > -Jason >This is a description from 1348 >"... it began with swellings in the groin and armpit, in both men and women, >some of which were as big as apples and some of which were shaped like eggs, >some were small and others were large; the common people called these >swellings gavoccioli. Merely one written account from one area experiencing a Plague. It does in no way represent every Plague occuring prior or subsequent, especialy in other areas of Europe. >Filoviral Marburg and Ebola infections are severe hemorrhagic fevers. Damage >to blood clotting and vessel permeability are the most prominent clinical >features in humans. In fatal Marburg and Ebola infections, humans and >monkeys generally die with no evidence of an immune response; however, >details of immune system damage are poorly investigated [Peters et al., >1996]. ummm...I'm not sure about the accuracy of this source. Death from Hemorrhagic Fevors is normaly caused by "Cytokine Storm", or over-responce of the Immune system. BTW, this is also the main cause of death in Flu Pandemics. You should read up a bit more on Flu Pandemics in general since the pandemic of 1918 had symptoms not in anyway connected with the normal yearly Flu we are all familiar with. >Any descriptions that can be similar to the 1348 account? Faulty Logic, you are assuming one description covers hundreds of years of waves of Plauge. I am not denying that said source was not a description of Bubonic Plauge, merely informing you one description does not represent every Plague. >I would imagine anyone who died at the time was labeled with dying from the >black death but that does not negate that a large epidemic had not taken >place. I never implied it wasn't. You do realize the Flu is the deadliest disease known to man, don't you? >The flu does not resemble the black death except probably some form of >pneumonic which is still pushing it. I used to think the same thing before I saw a doccumentary on "The Bird Flu" in which they had a segment on the 1918 pandemic. An epidemiologist interviewed clearly said that any Flu pandemic we face with the Bird Flu may have symptoms not indicative of the yearly flu. She went on to say that we knew this because the symptoms of the 1918 pandemic included: Swelling of the Body Blackening of the skin Bleeding from the eye, ears, mouth, & nose (coughing up blood as well) Contortions of the Body Compare this infor to my original post where the scientist in question said in his opinion that the symptoms of "the Black Death" were most identical to Hemorrhagic Fevers. >There's been many pandemic flu outbreaks and they don't resemble the black >death. Sorry. Once again, you seem to be stuck on the symptoms of one particuliar pathogen. There have been Flu Pandemics where the symptoms have been extremely close to the ones described in "The Black Death". I have already informed you of the 1918 Pandemic and the symptoms associated with that particuliar strain. >The population of the earth was almost wiped out and not ordinary typical >deaths. Yes and the speed of it's travel is one of the problems that epidemiologists have not, IMO, properly addressed. Fast traveling diseases, such as those in "The Black Death", are most often caused by Viral Pathogens and not Bacterial ones. I could go on and on with this but I feel that no matter what I write, no information will sway you into admitting something that even the experts in this field have told me, that there is still doubt as to the true pathogen responsible for "The Black Death". >No problem as it makes good talk at parties just as saying that HIV does not >cause AIDS. At least we have samples from the infected to prove that said pathogen was in fact present. How many samples do we have from victims of "The Black Death"? -Jason "Lucky" <LuckyHoodoo@aol.com> wrote in message > I used to think the same thing before I saw a doccumentary on "The Bird > Flu" in which they had a segment on the 1918 pandemic. There were diagnostic tests for the flu and very little by way of labs. They called it the flu based on symptoms and they were right with present day technology. The clinical diagnosis based on symptoms was upheld. An > epidemiologist interviewed clearly said that any Flu pandemic we face > with the Bird Flu may have symptoms not indicative of the yearly flu. [quoted text clipped - 5 lines] > Bleeding from the eye, ears, mouth, & nose (coughing up blood as well) > Contortions of the Body And yet they knew it was the flu. They did not say it was hemorrhagic fever or the black death or typhoid or typhus epidemics of old. The people knew back then and they know now to look for distinguishing features that may be diagnostic for a particular infection. It was a flu that presented as the flu and was very bad. > Compare this infor to my original post where the scientist in question > said in his opinion that the symptoms of "the Black Death" were most > identical to Hemorrhagic Fevers. You mean out of all the bubonic cases in which buboes predominated and people wrote on there might have been the one plague that you mention. That is possible. Does he also believe that the flu of 1918 was hemorrhagic fever based on your description? It was possible until evidence showed that the clinical diagnosis was correct. > >There's been many pandemic flu outbreaks and they don't resemble the black > >death. Sorry. [quoted text clipped - 4 lines] > already informed you of the 1918 Pandemic and the symptoms associated > with that particuliar strain. And nobody seems to be confusing it with anything else as it was called a flu long before diagnostic tests were employed back in 1918 or earlier years. Influenza outbreak in 1732-33 and even 1775-6 How do they know that? 1657 Boston: Measles 1687 Boston: Measles 1690 New York: Yellow Fever 1713 Boston: Measles 1729 Boston: Measles 1732-33 Worldwide: Influenza 1738 South Carolina: Smallpox 1739-40 Boston: Measles 1747 Connecticut, New York, Pennsylvania & South Carolina: Measles 1759 North America (areas inhabited by white people): Measles 1761-61 North America & West Indies: Influenza 1772 North America: Measles 1775 North America (especially hard in New England): Epidemic (unknown) 1775-76 Worldwide: Influenza 1781-82 Worldwide: Influenza (one of worst flu epidemics) 1788 Philadelphia & New York: Measles 1793 Vermont: Influenza and a "putrid fever" 1793 Virginia: Influenza (kills 500 people in 5 counties in 4 weeks) 1793 Philadelphia: Yellow fever (one of worst) 1783 Delaware (Dover): "extremely fatal" bilious disorder 1793 Pennsylvania (Harrisburg & Middletown): many unexplained deaths 1794 Philadelphia: Yellow fever 1796-97 Philadelphia: Yellow Fever 1798 Philadelphia: Yellow Fever (one of worst) 1803 New York: Yellow Fever 1820-23 Nationwide: "fever" (starts on Schuylkill River, PA & spreads 1831-32 Nationwide: Asiatic Cholera (brought by English emigrants) 1832 New York & other major cities: Cholera 1837 Philadelphia: Typhus http://www.bacteriamuseum.org/niches/features/diseasehistory.shtml The people knew the difference between the plague and influenza "Between 1550 and 1566, when Bubonic plague and Influenza were sweeping through the country, (The population of England probably fell by at least 6% between 1556 and 1560) 15 the average burial rate in Loughborough dropped to 37.16 As Griffin points out, this lower than anticipated figure may have been the result of a large epidemic striking the town in the years in which the Parish Register was not kept (1548-58, during the reign of Queen Mary), therefore possibly reducing the population and the subsequent death rate. However, analysis of the burial figures for 1550-53 indicates an annual average burial rate of 27, whilst 1560-66 was 42, thus invalidating the hypothesis." http://www.loughborough.co.uk/plague/ The people knew the difference between the plague and influenza. > >The population of the earth was almost wiped out and not ordinary typical > >deaths. [quoted text clipped - 3 lines] > diseases, such as those in "The Black Death", are most often caused by > Viral Pathogens and not Bacterial ones. That would go against then the theory that it was viral as there were no airplanes or fast travel in old europe. The infection would have died out as the person wouldn't get very far. With vector infection and human transmission you have both ways of transmision and a reservoir. That's the arguement with Ebola as people infected die within a small radius and don't get very far and so the infection dies out to the point they have not found the reservoir but it reappears again. I could go on and on with this > but I feel that no matter what I write, no information will sway you > into admitting something that even the experts in this field have told > me, that there is still doubt as to the true pathogen responsible for > "The Black Death". There will always be doubt but the burden lies on those proposing alternatives. We have flesh eating bacteria in which people can die within a day or two without treatment and have O157 E.coli that can also kill rapidly along strep. They don't know why. > >No problem as it makes good talk at parties just as saying that HIV does not > >cause AIDS. > > At least we have samples from the infected to prove that said pathogen > was in fact present. How many samples do we have from victims of "The > Black Death"? None. They usually rely on experienced observations by doctors at the time. > -Jason >None. They usually rely on experienced observations by doctors at the time. You made a large reply, but unfortunately it is flawed. You claim that the people alive in the middle ages were sophisticated enough to be able to specificly identify and diagnose the Flu from other said diseases, even when said "experts" of the time had no clue that pathogens existed and believed illness to be caused by "bad air", bathing, and the negative influence of the stars (Influenza "Influence" in Latin). You even claim that these same people would interprett the different symptoms associated with a Flu pandemic as being associated with the ordinary Flu, even though the symptoms are so widely different from any of those experienced with the yearly Flu. None of this makes sense. I recieved a reply from the HMMI (Howard Memorial Medical Institute) on this topic. I was told that my theory was interesting and they admitted that their is technicaly no proof what pathogen was responsible for "The Black Death". Of course they are of conservative opinion and therefore would not embrace my theory without sufficient proof, but at least they did not shoot it down entirely. -Jason > >None. They usually rely on experienced observations by doctors at the time. > [quoted text clipped - 4 lines] > pathogens existed and believed illness to be caused by "bad air", > bathing, and the negative influence of the stars (Influenza "Influence" You are confusing their beliefs in the origins with disease with their detailed descriptions of disease. They did not know the origins of malaria and called it "bad air" but they obviously knew the symtoms. "Cocoliztli was a swift and highly lethal disease. Francisco Hernandez, the Proto-Medico of New Spain, former personal physician of King Phillip II and one of the most qualified physicians of the day, witnessed the symptoms of the 1576 cocoliztli infections. Hernandez described the gruesome cocoliztli symptoms with clinical accuracy (4,5). The symptoms included high fever, severe headache, vertigo, black tongue, dark urine, dysentery, severe abdominal and thoracic pain, large nodules behind the ears that often invaded the neck and face, acute neurologic disorders, and profuse bleeding from the nose, eyes, and mouth with death frequently occurring in 3 to 4 days. These symptoms are not consistent with known European or African diseases present in Mexico during the 16th century." http://www.cdc.gov/ncidod/EID/vol8no4/01-0175.htm Dr Hernandez did not call it the black death. > in Latin). You even claim that these same people would interprett the > different symptoms associated with a Flu pandemic as being associated > with the ordinary Flu, They observed symptoms and wrote them down and detailed enough for present scientists to be able to call them the flu and what the people at the time called it is not relevent. There were doctors at the time who looked at signs and symtoms. even though the symptoms are so widely different > from any of those experienced with the yearly Flu. The 1918 flu was a bird flu like no other or your super flu that you interpret to mean it would have completely different symptoms for one not to be able to diagnose it as the flu. That is not the case. People had suspected it was a lethal flu and probably bird in origin and so they searched for evidence. None of this makes > sense. People are making guess as to what the detailed descriptions mean noted in the past. Are those observations accurate is a valid question. Granted it's difficult to study something that is not with us but centuries later. There was a plague outbreak in India and the signs and symptoms were not identical to the past infections of record, but if you read the accounts in the last century in which the last outbreak occured they were stating that it was being cured and one doctor even said he success rate was 50%. There was a wipe out of populations of the most susceptible and those that lived had a genetic advantage making them less susceptible. The disease was already changing back then. There are people immune to HIV and the origins of that is in the genes that seem to have spread greatly during the years of the plaque. You couple that with the infectious agent toning down it's virulence. A good parasite is one that does not kill it's host in order to be able to transmitted to others. A poor parasite is one in which it kills it's host swiftly and not allow transmission. We now have a problem on trying to figure out what happened back then. I recieved a reply from the HMMI (Howard Memorial Medical > Institute) on this topic. I was told that my theory was interesting > and they admitted that their is technicaly no proof what pathogen was [quoted text clipped - 3 lines] > > -Jason I am not really sure where you get descriptions that the plague was hemorrhagic or that Ebola has a prominent lymphadopathy. Histologic Findings: Although capable of involving many tissues, the virus has a predilection for endothelial cells, hepatocytes, and mononuclear phagocytes. Viral replication is associated with extensive focal necrosis and is most severe in the liver, spleen, lymph nodes, kidney, lung, and gonads. In the liver, councilmanlike bodies of focal necrosis similar to those seen in yellow fever are prevalent. However, the focal necrosis associated with Ebola replication results in a minimal effective inflammatory response. Late in the disease, the intestinal mucosa may separate from the lamina propria and slough. http://www.emedicine.com/MED/topic626.htm Ebola-Poe: A Modern-Day Parallel of the Red Death? Possible Models for the Red Death Even though a fictional product of Poe's fertile and bizarre imagination, the red death is likely modeled after a disease within the author's lifetime and experience. Some have speculated that Poe's family history of tuberculosis (his mother, his adoptive mother, his wife, and possibly his brother died of the disease) may have prompted him to write about a similar disease in Life in Death-a story about a painter and his dying wife, who incidentally resembled Poe's wife (5). Along the same lines, Poe's experience of nursing his wife through her bouts of exsanguinating hemoptysis, cradling her head for hours, and wiping away the blood from her face may well have been on his mind when he mused about "the scarlet stains upon the face" of the afflicted in Masque of the Red Death. As described by Poe, the red death seems to be some type of a viral hemorrhagic fever. Epidemics of yellow fever killed 100,000-150,000 in the United States from 1693 to 1905 (6). Northern ports (Boston, New York, Philadelphia, Baltimore), where Poe lived at various times in his life, were affected by yellow fever until 1822. He could have been inspired by a nationwide, severe epidemic of yellow fever in 1841 (a year before he wrote The Masque of Red Death), but yellow fever was a commonplace disease without any mystery attached to it. Like red death, yellow fever causes high body temperatures; body ache; damage to capillaries, which can result in bleeding from the nose and mouth; stools stained dark with blood; and (the most dreaded symptom) copious black vomit caused by gastric bleeding. Poe's red death, however, has a much higher death rate and communicability. Besides, the eponymous jaundice of yellow fever is not described as a feature of red death. Poe named his fictional disease "red" death, probably to differentiate it from "black" death, otherwise known as the plague. "Red" death is also descriptive of the profuse bleeding characteristic of this fictional disease. Poe maximizes the horror of the disease by intentionally making it mysterious and universally fatal. By alluding to the black death, he invokes memories of the vast plague epidemics that ravaged the world. http://www.cdc.gov/ncidod/EID/vol8no12/02-0176.htm >From the Howard Hughes Medical Institute: "This is an interesting hypothesis. You are correct that it is not absolutely certain what caused the Black Death." The statement then went on to say that most conservitive scientists do hold that it was Yersinia Pestis, however this view is by "educated guess" only and not any actual proof. You can reply all you want but this topic will always remain open for debate as long as no sufficient evidence is obtained to definatively rule in one direction or another. -Jason > >From the Howard Hughes Medical Institute: > [quoted text clipped - 5 lines] > hold that it was Yersinia Pestis, however this view is by "educated > guess" only and not any actual proof. Here is a quote of old and some of the animals it infected and the symptoms. "Neither physicians nor medicines were effective. Whether because these illnesses were previously unknown or because physicians had not previously studied them, there seemed to be no cure. There was such a fear that no one seemed to know what to do. When it took hold in a house it often happened that no one remained who had not died. And it was not just that men and women died, but even sentient animals died. Dogs, cats, chickens, oxen, donkeys sheep showed the same symptoms and died of the same disease. And almost none, or very few, who showed these symptoms, were cured. The symptoms were the following: a bubo in the groin, where the thigh meets the trunk; or a small swelling under the armpit; sudden fever; spitting blood and saliva (and no one who spit blood survived it). It was such a frightful thing that when it got into a house, as was said, no one remained. Frightened people abandoned the house and fled to another." The bacteria was isolated in 1898 from patients during one of the epidemics. This was the first time it was done so only after thousands died with the same China origin as before. Fundamental Works: The fundamental but separate works by Yersin and Kitasato in 1894 on the discovery of the etiologic agent of plague in Hong Kong opened the way for investigating the disease and how it is spread. Kitasato and Yersin described, within days of each other's findings, the presence of bipolar staining organisms in the swollen lymph node (bubo), blood, lungs, liver and spleen of dead patients (Bibel et al., 1976). Cultures isolated from patient specimens were inoculated into a variety of laboratory animals, including mice. These animals died within days after injection, and the same bacilli as those found in patient specimens were present in the animal organs. Though both investigators reported their findings, there were a series of confusing and contradictory statements by Kitasato that eventually led to the acceptance of Yersin as the primary discoverer of the organism now named after him, Yersinia pestis (Bibel et al., 1976). Yersin had recorded that rats were affected by plague not only during plague epidemics but also often preceding such epidemics in humans. In fact, plague was designated, in local languages, as a disease of the rats: villagers in China, India and Formosa (Taiwan) described that when hundreds and thousands of rats lie dead in and out of houses, plague outbreaks in people soon followed (Gross, 1995). The transmission of plague was described by Simond in 1898. He noted that persons who became ill did not have to be in close contact with each other to acquire the disease. In Yunnan, China, inhabitants would run away from their homes as soon as they saw dead rats. On the island of Formosa, residents considered handling dead rats a risk for developing plague. These observations led Simond to suspect that the flea might be an intermediary factor in the transmission of plague since people acquired plague only if they were in contact with recently dead rats and were not affected if they touched rats that were dead for more than 24 hours. Simond demonstrated that the rat flea (Xenopsylla cheopis) transmitted the disease in a now classic experiment in which a healthy rat, separated from direct contact with a recently plague-killed rat, died of plague after the infected fleas jumped from the first rat to the second. > You can reply all you want but this topic will always remain open for > debate as long as no sufficient evidence is obtained to definatively > rule in one direction or another. > > -Jason No problem why not Anthrax. Lets be different here. Twigg concludes that it would have been nearly impossible for Y. pestis to have been the causative agent of the beginning of the plague, let alone its explosive spread across all of Europe and England. Twigg also shows that the common theory of entirely pneumonic spread does not hold up. He proposes, based on a reexamination of the evidence and symptoms, that the Black Death may actually have been an epidemic of pulmonary anthrax caused by Bacillus anthracis. In a similar vein, historian Norman F. Cantor, in his 2001 book In the Wake of the Plague, suggests the Black Death might have been a combination of pandemics including a form of anthrax, a cattle murrain. He cites many forms of evidence including: reported disease symptoms not in keeping with the known effects of either bubonic or pneumonic plague, the discovery of anthrax spores in a plague pit in Counterarguments There is still a thriving majority of historians that support the bubonic plague as cause, and so counterarguments have been drawn in defense of the bubonic plague theory. The uncharacteristically rapid spread of the plague could be due to low levels of immunity in that period's European population. Historical examples of pandemics of other diseases in populations without previous exposure, such as smallpox and tuberculosis amongst American Indians, show that the low levels of inherited adaptation to the disease cause the first epidemic to spread faster and to be far more virulent than later epidemics among the descendants of survivors. Also, the plague returned again and again and was regarded as the same disease through succeeding centuries into modern times when the Yersinia bacterium was identified. In addition, it was previously argued that tooth pulp tissue from a 14th-century plague cemetery in Montpellier tested positive for Y. pestis DNA. However, such a finding was never confirmed in any other cemetery. In September 2003, a team of researchers from Oxford University tested 121 teeth from 66 skeletons found in 14th-century mass graves. The remains showed no genetic trace of Yersinia pestis, and the researchers suspect that the Montpellier study was flawed. I forgot to mention the Comet theory something you really can't rule out also. "The weakest part of Cantor's book is his roundup, at the end, of the various theories of the Black Death that have accumulated over the years. Cantor was a famously argumentative man, and at times it seems as though his main criterion in judging a theory were its popularity. If it's unpopular, he likes it. In 1979, the astrophysicist Fred Hoyle and the mathematician Chandra Wickramasinghe published a book arguing that the organic matter from which the Black Death (and human life) developed came from outer space, via comets-a proposal that Cantor says was ignored by most historians. He thinks it makes some sense, and he points out that in the nineteen-eighties the Nobel laureate Francis Crick made a related argument. Cantor also looks kindly on the idea, advanced in 1984 by the zoologist Graham Twigg, that the cause of the Black Death was not the rat-disease bubonic plague, imported from Asia, but the cattle-disease anthrax, contracted from Europe's own herds. Most experts reject Twigg's argument. Cantor accepts it, halfway. He believes that the Black Death involved both bubonic plague and anthrax, simultaneously. " Robert, Conviently, the show that inspired me is airing several times today on The Discovery Times Channel. It's called "Return of the Black Death". Apparantly the scientific consensus is indeed switching, since many scientists were interviewd claiming the notion that Bubonic Plague was "The Black Death" is incorrect. The scientists interviewd then go through and disprove just how implausible Bubonic Plague is as a pausible explanation. Here are a couple: 1.) The Black Rat is the native species of Europe and Asia. It is quite lazy and is only spread from country to country by stowing aboard cargo ships. It does not spread out through the open country-side, nor does it travel beyond it's city homes. Therefore if rats were the carriers of fleas which spread the bacteria, then country dwellers would be safer from infection. This was not the case. "The Black Death" killed both city and country dweller indiscriminately. Also, in order for an epidemic to occur an rat population explosion would have to occure. The evidence gathered so far shows no population explosion in rat population. Also, if rat population did rise, then predator population would also increase. Scientists who study birds of prey that do feed on rats have found no increase of bird population during this time period. Lastly, buildings/constructions from the time of "The Black Death" show that people had no concern of rats as they built chicken houses and dove homes literaly inches off of the ground. In places where rats were a problem, great steps were taken to protect these and other similiar animals from predation by rats. 2.) One of the symptoms of "The Black Death" was not "Buboes". This notion results from twisting and tinkering of the discription of the diseas in order to make it fit "Bubonic Plague". The records only say "swellings of the body" and "Black and Bloody pustules over the entire body". Neither of these mention "Buboes" and the last one is definately not a symptom of Bubonic Plauge. Some of the other recorded "Black Death" symptoms were: Bleeding from the eyes,ears, mouth, coughing and vomitting blood, and prolonged fever. Again, not symptoms of Bubonic Plague. I would recommend, if you get a chance, you see the program that inspired me. Only one scientist interviewed was willing to offer a theory on the possible pathogen due to the actual reported symptoms of those infected with "The Black Death", and he said Hemorrhagic Fevers most fits the description. The show disproves rats, fleas, and "buboes" all-together. It is quite fascinating. Here is my favorite paraphrase of a quote from the show: "Many scientists are so obsessed with the notion that Bubonic Plague was "The Black Death" that they are willing to go to absurd and intricate lengths in an attempt to fill in the many holes of this blatantly incorrect theory." -Jason > Robert, > "Many scientists are so obsessed with the notion that Bubonic Plague [quoted text clipped - 3 lines] > > -Jason That's true that there are holes in the theory of bubonic plague. The implication being a change in susceptible host and evolving virulence factors. The problem with epidemiologist is that they look for present day models of a disease which may not be valid. The bird flu has not evolved in present day to allow person to person transmission but they are expecting it to. I'ts like saying the bird flu could not have been the source of the 1918 flu because man can not transmitt the bird flu. The rat theory is also in the same mode. In actuality rodents are one way reservoir for certain hemorrhagic fevers. "The geography of the 16th century cocoliztli epidemics supports the notion that they may have been indigenous fevers carried by rodents or other hosts native to the highlands of Mexico." You are looking at today and saying it couldn't be possible yesterday. Measles doesn't kill people today so therefore it couldn't have been measles that killed thousands of Indians yesterday. The same thing holds for symptomatology. They create their own holes. There has not been any big pandemic of Ebola even with todays mobile society. They have not found a reservoir host in non-primates for Ebola. The symptoms of bleeding along with hemorrhagic fever is consistent with DIC and multiple organ failure. Those symptoms are present in infectious and non-infectious and are not specific for any disease. The Black Death got it's name from the ecchymosis and not from the profuse bleeding from the eyes or open wounds. I quoted that epidemic of a hemorrhagic type disease in the new world in which they described the disease and no transmission from the new world to the old on ships to Spain. There are gaps in any theory and to overlook one in order to accept another then you must again overlook many things including the fact that the plague occured several times with evolution of symptoms and severity and host genetics. Good luck > > Robert, > > "Many scientists are so obsessed with the notion that Bubonic Plague [quoted text clipped - 3 lines] > > > > -Jason (Snipped) > There are gaps in any theory and to overlook one in order to accept another > then you must again overlook many things including the fact that the plague > occured several times with evolution of symptoms and severity and host > genetics. > > Good luck Robert, Do try to watch the show. You will be suprised when and how the theory "Bubonic Plague" IS "The Black Death" first came about. It was literaly a "Because I say so" moment, and science doesn't work that way. -Jason Robert, Here are some links you might visit as well: http://www.rense.com/general63/ebola.htm http://www.recombinomics.com/News/03080504/H5N1_Atypical_1918.html -Jason
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