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thousand different probabilities calculated in the model There is no way to know the price until an investor places an offer As an option seller you can choose to sell for less, the same, or more; or as the buyer you can buy or not buy There is no physical price for the option until the buyer and seller nd a price together to trade the $20 fur ball call option Until an option writer agrees to take the risk at that price, there is no market for the option The difference between the practical function and the academic research of option pricing is liquidity, variables in pricing models, and the subjective risk assessment of the seller If an option trades at a particular price, that price is the option s tradable value, regardless of theoretical or fair value indicated by the option model If you are the one bidder on an option in a thin market, you may have to pay the seller s subjective price or not trade your option This is common in out-of-the-money deferred options in both equity and commodity markets When that trade hits the pricing model, the volatility may be completely out of line, and it may appear to be an overvalued option, but in reality that is the option s value, overvalued or undervalued That price will remain until the next seller and buyer come together on a price for the same option Experienced active option traders often have a different view of option pricing from those in research departments and classrooms An active option trader will view the option market as a uid pricing model in itself The vast capability of arbitrage traders to research and quickly identify variance in option pricing between the underlying asset and their respective options creates a system of active value for the retail market Unless an option market is thinly traded or the contracts are deferred, an active option market will have fair value versus the underlying given the volatility most of the time.

Ponka and Pettersson) Most are due to viral infections Of these, the most common are the enteroviral infections echovirus and Coxsackie virus These make up 80 percent of cases of aseptic meningitis in which a speci c viral cause can be established Mumps is perhaps next in frequency, followed by HSV-2, lymphocytic choriomeningitis (LCM), and adenovirus infections EBV (infectious mononucleosis), CMV, leptospirosis, HSV-1, and the bacterium Mycoplasma pneumoniae (see Chap 32) In uenza virus, adenoviruses, and numerous sporadic and otherwise innocuous agents have at times been isolated from the spinal uid in cases of aseptic meningitis The California and West Nile viruses, which are arthropod-borne viruses ( arboviruses ), are responsible for a small number of cases (usually the arboviruses cause an encephalitis or meningoencephalitis, as discussed further on) Rarely, the icteric stage of infectious hepatitis is preceded by mild meningitis, the nature of which becomes evident when the jaundice appears All these viral infections, particularly those due to the enteroviruses together with mycoplasmal infection, leptospirosis, and Lyme borreliosis account for the largest proportion of infectious cases of aseptic meningitis in which the etiology can be established, the remainder being due to tuberculosis, fungal infections and rarer organisms Chronic and recurrent meningitis constitutes a special problem, discussed below It is now well recognized that infection with HIV may present as an acute, self-limited aseptic meningitis with an infectious mononucleosis-like clinical picture While HIV has been obtained from the CSF in the acute phase of the illness, seroconversion occurs only later, during convalescence from the meningitis (see further on in this chapter) HSV-1 has been isolated from the CSF of patients with recurrent bouts of benign aseptic meningitis (so-called Mollaret meningitis), but this nding has not been consistent (Steel et al) As discussed in Chap 47, it is now believed that this virus also underlies many if not most cases of what has been traditionally considered idiopathic Bell s palsy Finally, two other aspects of the virology of aseptic meningitis should be noted; rst, in every published series of cases from virus isolation centers, a speci c cause cannot be established in one-third or more of cases of presumed viral origin; second, most agents capable of producing aseptic meningitis also sometimes cause encephalitis.

Clinical distinctions between the many viral causes of aseptic meningitis cannot be made with a high degree of reliability, but useful leads can be obtained by attention to certain details of the clinical history and physical examination It is important to inquire about recent respiratory or gastrointestinal symptoms, immunizations, past history of infectious disease, family outbreaks, insect bites, contact with animals, and areas of recent travel The presence of a local epidemic, the season during which the illness occurs, and the geographic location are other helpful data As already mentioned, the enteroviruses (echo, Coxsackie and, in underdeveloped countries, polio) are by far the commonest causes of viral meningitis Because these organisms grow in the intestinal tract and are spread mainly by the fecal-oral route, family outbreaks are usual and the infections are most common among children A number of echovirus and Coxsackie virus (particularly group A) infections are associated with exanthemata and may, in addition, be associated with the grayish vesicular lesions of oral

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