I hypothesized cattle and Gulf Coast ticks (GCT), Amblyomma maculatum, may be involved in epidemiology of Rickettsia parkeri infection. I demonstrated transient rickettsemia by polymerase chain reaction (PCR) for the 17 kilodalton (kDa) gene in 33% (2/6) of calves experimentally exposed to R. parkeri either by direct inoculation or by placement of R. parkeri-infected GCT on calves’ ears. Calves (4/4) receiving GCT developed lesions at attachment sites consistent with a pathologic condition known as “gotch” ear whether or not GCT were infected with R. parkeri, suggesting the condition is related to GCT attachment and not to rickettsial infection. In calves exposed to R. parkeri, biopsy of injection sites and attachment sites revealed rickettsial organism by immunohistochemistry. Unexposed calves were seronegative, whereas, exposed calves seroconverted (produced antibodies). In a cross-section of Mississippi sale barn cattle, I did not demonstrate rickettsemia, although 7.1% (13/183) were GCT-infested and 49.5% (91/183) were immunofluorescent antibody (IFA) positive for SFG rickettsiae (1:32 dilution). In addition, 21.7% (5/23) and 4.3% (1/23) of GCT from cattle were PCR positive for the 17 kDa gene and rompA gene, respectively. I sequenced a rompA amplicon from one GCT and found it was 100% identical to a R. parkeri sequence in GenBank (U43802). I compared the distribution of SFG rickettsiae by IFA in salivary glands, midgut, ovaries, and Malpighian tubules from laboratory-reared and field-collected GCT and documented my approach to successful and consistent dissection of tick tissues. Since R. parkeri is transmitted by GCT, these ticks are significant cattle pests, and at least some GCT from cattle are naturally-infected with R. parkeri, cattle with R. parkeri-infected ticks may increase exposure of people and wildlife to the organism, and the ticks themselves may serve as invertebrate reservoirs of the pathogen. This study is the first to my knowledge to outline a clear case definition of “gotch” ear, and document experimentally the role of GCT in its pathology. Also, I demonstrated rickettsemia in calves experimentally exposed to R. parkeri, presence of GCT on Mississippi sale barn cattle, natural R. parkeri infection in GCT from cattle, and distribution of SFG rickettsiae in GCT.