<p><i>Fulvia fulva</i>, which causes tomato leaf mold, has developed resistance to fungicides with several modes of action, including quinone outside inhibitor (QoI) fungicides, making it difficult to control the spread of this disease in Japan. Although cross-resistance to QoI fungicides has been confirmed in many plant pathogens, a few QoI fungicides, including pyribencarb, are effective against resistant isolates. In this study, the efficacy of pyribencarb against sensitive and resistant isolates of <i>F. fulva</i> was evaluated. Fungicides with different modes of action were also identified. QoI resistant isolates with the F129L mutation in the cytochrome b gene were prevalent (86.5%; 45/52 isolates) in Nara Prefecture, Japan. In vitro evaluation revealed that the minimum inhibitory concentrations of pyribencarb and azoxystrobin were &lt; 0.1&#xa0;μg/mL in sensitive isolates and 1 or 10&#xa0;μg/mL in resistant ones with the F129L mutation. In an efficacy trial using tomato plants, spraying with pyribencarb and azoxystrobin did not reduce leaf mold development. In the field, difenoconazole, chlorothalonil, and mancozeb effectively controlled leaf mold. When fungicides were applied once 3&#xa0;days after inoculation, difenoconazole was more effective than other C14 demethylation inhibitor fungicides myclobutanil and triflumizole. Our results demonstrate that cross-resistance exists between pyribencarb and azoxystrobin and suggest that the effective fungicides evaluated in this study must be mainly applied in rotation programs to control tomato leaf mold.</p>