Composts are commonly used in agriculture to minimize losses from soil-borne plant pathogens such as Pythium aphanidermatum, the causal agent of seed and seedling rot in a wide range of host plants. Currently, there is a lack of understanding in how composts suppress pathogens and diseases, and the mechanisms by which suppression occur remain unclear. The goal of this study was to examine the developmental responses of Pythium aphanidermatum zoosporangia when exposed to compost to understand how suppression of Pythium seedling disease is expressed. Mature zoosporangia were exposed to liquid vermicompost extracts (VCE) and the developmental responses were monitored using time lapse photomicroscopy. Sterile and non-sterile VCEs inhibited viable zoospore production by inhibiting indirect germination and causing vesicles and zoospores to immediately lyse while at the same time stimulating direct germination and germ tube production. Additional treatments were tested to determine factors that stimulate direct germination or inhibit indirect germination. The pH (5-9 at 0.001 M) and ionic strength (0.1-0.0001 at pH 6) of potassium phosphate buffer did not alter zoosporogenesis compared to sterile water. However, decreasing the osmotic potential in glucose and sucrose from -248 to -2,712 kPa or in polyethylene glycol 8000 from -0.335 to -105 kPa caused indirect germination to decrease with a corresponding increase in direct germination. Significant infection was observed within 1 h when cucumber seeds exposed to zoosporangia germinating indirectly to produce zoospores in sterile water and directly to produce germ tubes in sucrose solution (0.5 M). Germ tube infection was suppressed after 1 h in treatments of VCE, but significant disease was observed after 2 h. Germ tube infection was greater in sucrose solutions than VCE at 1, 2, and 3 h of inoculum exposure. My data show that VCEs suppress zoosporogenesis and stimulate direct germination; however, this did not lead to long-term disease suppression.