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Malignant small cell tumor of the thoracopulmonary region (MSCT) was first described in 1979 and has been referred to as the Askin tumor. This malignant neoplasm is a member of the peripheral primitive neuroectodermal tumor (PPNET) family and typically involves the periosteum, soft tissue, and extrapulmonary tissue of the thoracic wall. MSCT may also involve the lung parenchyma by local extension or may arise de novo in peripheral lung tissue. Local recurrence, abdominal involvement by tumor extravasation across the diaphragm, and skeletal metastatic disease are relatively common. However, metastasis to the head and neck region and in particular to the oral cavity is extremely rare. We present a recurrent intrapulmonary MSCT with metastasis to the oral cavity in an adolescent Hispanic boy, and review the literature regarding this member of the PPNET family. Differentiation from neuroblastoma may be made based on immunoreactivity for beta 2 microglobulin and HBA71 and lack of immunoreactivity for chromogranin in PPNET and MSCT. Ultrastructural features commonly seen in MSCT and PPNET are round to ovoid tumor cells with occasional cytoplasmic processes with relatively few pleomorphic dense core granules. These tumors lack the gangliocytic and Schwann cell differentiation that is characteristic of neuroblastoma. MSCT and PPNET have a common reciprocal cytogenetic translocation [t(11;22)q(24;q12)], which is shared with Ewing's sarcoma. Prognosis in MSCT is quite dismal, with a 2-year survival of 38% and a 6-year survival of only 14%.

MZM~~~~~~~~~~~~CAL JOUm"A have found that different batches of the same brand of wool may yield significantly different survital patterns for most Gram-positive organisms. However, if we substitute serum swabs for the usual plain type then the first factor is automatically removed and the second becomes less critical. As a result, estimates of survival time on serum swabs may be accepted with greater confidence than those applying to untreated swabs.Assuming a moderately heavy contamination of a serum swab (this is an important variable impossible to control clinically), we suggest that an examination may be expected to yield a valid result when cultured within the following time limits: (1) (Table II), we do not recommend delaying plating longer than eight hours. In some clinical cases which we have examined [he organisms failed to survive 24 hours on serum swabs. Although autoclaved albumin-dipped swabs have not been studied so exhaustively the results were similar to those achieved with serum.We have attempted to discover how serum prolongs survival, but without success. For instance, it could not be shown that serum inactivated a toxic lipoid or water-soluble agent in the wool or that it acted as a substrate for growth. The effect of serum protein is probably a physico-chemical one acting on tie bacterial cells and prolonging their survival irrespective of the materials on which they are lodged.It is felt that these findings may have a broader significance than the somewhat restricted object of this investigation:. Two facts are worthy of consideration from an epidemiological point of view. The first is the rapidity with which enteric pathogens die off when dried in air, and the second is that organisms leaving their hosts in serous exudates will live longer than those discharged in secretions of low protein content. These two points may throw some light on factors determining the survival of pathogenic organisms outside their natural hosts. SummaryA study has been made of the survival patterns of a large number of organisms on plain swabs undet standard laboratory conditions. From this study the

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