DNA damage in the germline is a double-edged sword. Induced double-strand breaks establish the foundation for meiotic recombination and proper chromosome segregation but can also pose a significant challenge for genome stability. Within the germline, transposable elements are powerful agents of double-strand break formation. How different types of DNA damage are resolved within the germline is poorly understood. For example, little is known about the relationship between the frequency of double-stranded breaks, both endogenous and exogenous, and the decision to repair DNA through one of the many pathways, including crossing over and gene conversion. Here we use the Drosophila virilis hybrid dysgenesis model to determine how recombination landscapes change under transposable element activation. In this system, a cross between two strains of D. virilis with divergent transposable element profiles results in the hybrid dysgenesis phenotype, which includes the germline activation of diverse transposable elements, reduced fertility, and male recombination. However, only one direction of the cross results in hybrid dysgenesis. This allows the study of recombination in genetically identical F1 females; those with baseline levels of programmed DNA damage and those with an increased level of DNA damage resulting from transposable element proliferation. Using multiplexed shotgun genotyping to map crossover events, we compared the recombination landscapes of hybrid dysgenic and non-hybrid dysgenic individuals. The frequency and distribution of meiotic recombination appears to be robust during hybrid dysgenesis. However, hybrid dysgenesis is also associated with occasional clusters of recombination derived from single dysgenic F1 mothers. The clusters of recombination are hypothesized to be the result of mitotic crossovers during early germline development. Overall, these results show that meiotic recombination in D. virilis is robust to the damage caused by transposable elements during early development.