I entered NYU Medical School in 1974 and in 1978 started my four year training in Psychiatry at Belleveue Hospital in New York. Bellevue is the oldest public hospital in America and was ground zero for the AIDS epidemic. In the late 1970s, a growing number of Gay men were being diagnosed with an unusual lung infection, Pneumocystis carinii pneumonia, and were found to have severely depressed immune systems. The disorder was labeled GRID (Gay Related Immune Deficiency) and later, when it was recognized that the causative agent was transmissible, the name was changed to AIDS (Acquired Immune Deficiency Syndrome.) Wikipedia has some of the history:
Author Randy Shilts mentioned that what was later called AIDS became evident in the gay community in the Fire Island, New York area in the four years after the 1976 Bicentennial celebrations. The infection tended to double in numbers about every nine to ten months. It therefore took a couple of years before a new disease was suspected because there were at first not enough symptomatic individuals to be noticed.
The official date for the beginning of the AIDS epidemic is marked as June 5, 1981, when the US Centers for Disease Control and Prevention reported in its Morbidity and Mortality Weekly Report newsletter that unusual clusters of Pneumocystis carinii pneumonia had been discovered in gay men in Los Angeles in the early 1980s. Over the next eighteen months, more PCP clusters were discovered among otherwise healthy men in cities throughout the country, along with other opportunistic diseases (such as Kaposi's sarcoma and persistent, generalized lymphadenopathy), common in immunosuppressed patients.
By 1983 the virus had been isolated and identified by two different research groups (in New York and Paris) and our understanding of the disease and its interactions with the human immune system has been progressing ever since. The AIDS epidemic shows some significant differences from typical historical epidemics. This relates to its mode of transmission and length of incubation.
Consider mankind's typical experience of epidemics. The "Black Death" of Bubonic Plague spread rapidly in two phases.
The initial ("index") cases were caused by the bite of infected fleas which lived primarily on rats. Symptoms appear 3-8 days later and include fever, chills, head aches, and the painful, swollen lymph nodes known as Bubos. The mortality of the bubonic form in the pre-antibiotic days was 50-80%. The ease of transmission from person to person of the bubonic from of the plague is uncertain. On occasion the Yersinia Pestis bacteria would make its way into the bloodstream and the person would rapidly die of a massive system wide infection, the septicemic form of the illness. The third form of the disease was the most problematic for our ancestors and occurred when an unfortunate victim developed the pneumonic form of the plague, where the bacteria infects the lungs. In these cases, the infected person would easily spread the disease to anyone in the vicinity by coughing who would develop the pneumonic form in their turn. The death rate from the pneumonic form was on the order of 95% and the spread was exponential until it burned itself out.
The hallmarks of the "Black Death" were ease of transmission, brief incubation period, high mortality, and the tendency for the disease to progress from a slightly less virulent form (Bubonic) to an extremely virulent form (Pneumonic) in an unpredictable fashion.
With the advent of modern medicine, Bubonic Plague has gone from a WMD to a nuisance. This probably relates to three major developments. First, our understanding of its routes of transmission has empowered our public health efforts in diminishing the rodent host population's proximity to, and ability to transmit, the fleas that carry the bacteria. Further, we can, if necessary, enforce more powerful public health measures, such as quarantine in any future epidemic. Second, the advent of antibiotics effective against the plague bacillus allows us to remove infected patients from the population and render them non-infectious in short order. And third, it is highly likely that the combination of better health and nutrition, along with the natural co-evolution of our immune systems and the bacillus have created conditions in which the Yersinia Pestis bacteria is less virulent than in the Middle Ages.
In the AIDS epidemic, the slowness of progression of the illness along with its difficulty in transmission caused the epidemic to build slowly and insidiously. In the early days, the illness was considered close to 100% fatal. The virus disables the immune system, multiplies undetected, and then proceeds to infect its next host through intimate contact and the exchange of bodily fluids. The close contact and relatively poor transmissibility means that it takes many close contacts to cause a new infection and an infected individual has a long period of time during which he can continue to infect intimate contacts without any of the participants being aware of their risk. Modern medicine has learned a great deal about the illness and can now intervene at many steps along the way. Public Health campaigns designed to encourage safe sex, and increase the awareness of high risk behavior, are the equivalent of clearing trash piles to discourage rodent vectors of Bubonic Plague; the increasing availability of retrovirals is the equivalent of antibiotics; and there are some suggestions that the human immune system and the HIV virus are co-evolving in ways which will increase the ability of the host to survive the pathogen, beginning the evolutionary process of diminished virulence which all infectious diseases eventually track.
I would propose that Islamic fundamentalist fascism shows a great many facets that are in common with infectious disease. This is not a novel idea, but is worth exploring. Islamic expansionism, Jihad, has traditionally spread in very similar fashion to an infectious disease. It has traditionally killed a significant part of the population and taken up residence in the survivor populations, often in an uneasy, chronic truce/illness. When the invaded population finally mobilizes its immune system, the invading pathogen has been forced into quiescence, as at the Gates of Vienna in 1683. This is a model of an epidemic that consisted solely of a host pathogen interaction. In this model, in which Islam has colonized great swaths of the planet, the host's immune system has been weak (when there is a novel pathogen, our immune systems must first identify the pathogen and then mount a response; by its nature an initial presentation of a pathogen is when it is most virulent). Further, prior to 1683, in Europe, there was no equivalent to a Public Health or antibiotic approach to Expansionist Islam. Essentially, we had a naive population exposed to a virulent agent, which expanded until the host managed to mount an adequate immune response.
Please note, the immune system has several levels of defense; disease occurs when a pathogen becomes more virulent (via mutation), a new pathogen enters the biome, or the immune system becoems weakened.
Once the West responded with an adequate immune response, the fever of Jihad lessened (the Earth does have a fever but it is not the one Al Gore imagines) and for four hundred years Islam and the West coexisted in a relatively peaceful accommodation, with occasional outbreaks of minor infections when a naive host came into contact with the world of Islam (the shores of Tripoli.)
In the 1920s Islam mutated. Hassan al-Banna created the Muslim Brotherhood, a Sunni Jihad group dedicated to restoration of Islam's past glories and the re-establishment of the Caliphate. It gained further virulence through the efforts of Sayyid Qutb. It remained endemic in the Arab world until Osama bin Laden, alarmed by the increasing ability of the West to introduce a new virus, modernity, into the heart of the Arab world. On 9/11, the infection became symptomatic.
Since that time, the virus of Expansionist Islam has taken a traditional path similar to AIDS. It is spread by close, frequent contact, it relies on disabling the host's immune system (the early warning cells in the Media that, were they properly doing their jobs, would be informing people throughout the West of the danger they face) and mobilizing its forces whenever it appears the West's immune system is likely to mount a significant response (Iraq).
There is now evidence that the West's immune system has evolved in ways which have facilitated the virus's spread but also offers novel approaches to inoculate against the virus. The Blogophere and new media are both agents of spread and the venue form which new antibiotics may yet emerge. Fruthermore, Jihad has not yet mutated to acquire the virulence of a Pneumonic Plague and remains at the level of virulence of AIDS. The great danger is that a weak immune response and some further unpredictable mutation, perhaps facilitated by the easy routes of transmission newly opened to it, will creat conditions conducive to such a transition.
Islamism shows all the signs of being a mental virus, a meme. It disables the critical functions of the infected host, it attacks the host population in which it thrives, it destroys the productive capabilities of its hosts, and it insists on spreading wherever possible. Imagining Expansionary Islam as an illness to be combated, occasionally with military force, offers a way to conceptualize the problems we are facing in ways that might be useful in mobilizing support for our immune response and in suggesting further steps to take to strengthen that response. This is something, that if properly understood, could allow the left and right to come to a better working agreement on the future approach to Islamofascim.
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