Morphology & Incubation Period

Figure 4: Life cycle of R. seeberi (Garcia et al.)

Although the organism has not been able to be replicated in vitro, much has been uncovered about the life cycle of R. seeberi. Endospores ("esporoblastos en tejido" above) develop into trophocytes ("trophocito temprano" above), which are juvenile forms of sporangia that do not contain endospores. They average 10-100 microns and have a cell wall made of a single layer of cells that is 2-3 microns thick. They also generally contain a granular cytoplasm. Trophocytes mature into intermediate sporangia ("trofocito tardio" above), which differ from trophocytes in their larger size and their lack of a nucleus. They also tend to have thicker, bilamellar walls. Mature sporangia ("esporangio" above), the stage that commonly is most illustrative of the presence of R. seeberi, measure approximately 100-300 microns. They are round structures and are typically associated with cells of the immune system, including lymphocytes, monocytes, and plasma cells (Arora et al 2001). They are filled with large numbers of daughter cells that are called endospores. Watery substances stimulate the sporangia to extrude the endospores through an apical pore in the cell wall. The endospores ("esporoblastos liberados" above) subsequently mature into sporangia via the intermediate trophocyte stage.

Figure 5: A mature sporangium that is extruding its endospores to the surface of the skin. A watery environment induces the release. A trophocyte can be seen in the lower right corner (bottom half cut off slide). The granular nature of its cytoplasm is observable in the slide (image from Blanchard 1998).

Figure 6: PAS stain of a biopsied polyp that shows trophocytes. The thick walls of the trophocytes are stained pink (image from Fredricks et al. 2000)

After the endospores have been extruded from the sporangia, it takes approximately 10 days for them to mature into sporangia. After initial infection with the organism, replication proceeds rapidly in the mucosa of the main site of infection, with host tissue growing rapidly around it (hyperplasia) and simultaneous accompaniment by a local immune response (Hospenthal 2002). The precise time period of this interval is unknown.