Eimeria funduli, a coccidium infecting the liver and pancreas of killifishes and requiring an intermediate host, was allowed to develop at 22±2 °C for 5, 10, 15 or 20 days (schizont through zygote stages) in Fundulus grandis and was then exposed to 10·0±0·5 °C for 20 days or to 7·0±0·5 °C for 5 or 20 days. Both low temperature treatments inhibited all developmental stages, except for the case of fish infected for 5 days before exposure to 7 °C in which infections were eliminated. Returning fish back to a temperature of 22 °C for 20 days resulted in resumed development of all stages at the same or somewhat reduced rate. In all cases, intensity of infections was greatly reduced during exposure to low temperatures. Many organisms exhibited abnormalities. Gamonts and zygotes were atrophied or disintegrated within their parasitophorous vacuoles in all exposures and, in fish exposed to 7 °C for 20 but not 5 days, about 30% of the oocysts were abnormal, with from 1–8 sporoblasts. Areas of degeneration or necrosis incorporated aggregates and single parasites in both the pancreas and the hepatic parenchyma. The granulocytic inflammatory response, which at 22 °C was normally restricted to the period spanning development of gamonts and formation of the oocyst wall, was inhibited or delayed from infiltrating infected, diseased areas at low temperatures. The response intensified after cold-exposed fish were returned to 22 °C. A fibroid, non-granulocytic response occurred in fish introduced 5 days post-infection to 10°C before being returned to warm water. Two other types of lesion occurred in the pancreas. The first could develop into necrosis and was associated with low temperature; it did not always involve infected tissue. The other, a degenerating focal alteration, was not necessarily associated with infections or low temperatures.