Field management practices for anthracnose include planting disease-free seed material, deep plowing of crop residue immediately after harvest, crop rotation with non-cucurbit crops for a minimum of 1 year (2 to 3 years is optimum), avoiding usage of farm machinery among fields when the foliage is wet, fungicide applications with effective active ingredients such as quinone outside inhibitors (QoIs), and resistant plant cultivars ^[1][4]. To reduce fruit damage by anthracnose, growers are recommended to avoid mechanical injury to fruits, inspect for infected fruits during harvest and discard them, disinfect the fruit surface with chlorinated water, and refrigerate the fruit after harvest to prevent or delay anthracnose development postharvest ^[1][4].

Host resistance screening was conducted either on cotyledons ^[2][15] or the two- to four-true-leaf stage ^{[3][4][5][6][7][8]}[52,53,54,55,56,57]. The disease inoculum used for the seedling screening varied from 2.5 × 10^{3 [8]}[57] to 5 × 10^{5 [5]}[54] conidial spores/mL. The incubation time also varied from 3 to 14 days post-inoculation (DPI). A recent study reported the optimum inoculum concentration and DPI for screening two- to four-leaf-stage seedlings for race 2 anthracnose resistance ^[4][53].

In 1937, Layton started breeding for anthracnose resistance and identified sources of resistance to develop commercial cultivars. Five cultivars from Africa with high resistance to anthracnose were identified, out of which three had edible fruit and desired horticultural traits ^[9][5]. The three cultivars were named Africa 8, 9, and 13, and were further used as parents. Homozygous anthracnose-resistant selections from Africa 8, 9, and 13 were crossed with commercial cultivars Iowa Belle and Iowa King and a few other cultivars ^[9][5]. The commercial Iowa cultivars were wilt-resistant, large-fruited, and crisp-fleshed. The first widely accepted anthracnose-resistant watermelon cultivars were ‘Congo’ (1949), ‘Fairfax’ (1953), and ‘Charleston Gray’ (1955), released by Andrus ^[8][10][57,58]. Charleston Gray, Congo, and Fairfax are resistant to races 1 and 3 but susceptible to race 2 ^[11][48]. Cultivars resistant to race 1 were also resistant to race 3 ^[8][12][57,59].

Resistance to race 2 was first found in a citron, W695, which was also resistant to races 1 and 3 ^[8][57]. PI 326515 was the first PI reported to have resistance only to race 2 ^[7][56]. More resistance sources to race 2 including PI 189225, 271775, 271778, and 512385 were identified ^[3][6][52,55]. Resistance to anthracnose race 2 was also identified in Citrullus colocynthis, designated as R309 ^[13][60]. Interestingly, two studies found that resistance in Citrullus colocynthis, R309, did not follow the single gene inheritance and was suggested to be multigenic ^[13][60]. These studies suggested that a dominant single gene confers major resistance, but there are other genes contributing to the phenotype. R309 has been the only source of multigenic resistance; no other multigenic resistance sources have been reported.

The first inheritance work on anthracnose resistance was performed in 1937 ^[9][5]. Resistance to race 1 is dominant over susceptibility and segregates as a single gene. Resistance to races 1 and 3 is controlled by the same gene, Ar-1 ^[8][57]. Inheritance of race 2 resistance is like race 1 resistance, dominant and segregating as a single gene ^[7][56]. In Korea, Jang et al. used a biparental population, ‘DrHS7250’ (female parent, resistant breeding line) and ‘Oto9491’ (male parent, susceptible breeding line), to identify a C. orbiculare race 1-resistance quantitative trait locus (QTL) on chromosome 8 and further conducted transcriptomics via RNAseq on the parents to identify a coiled-coil (CC)–nucleotide-binding site (NBS)–leucine-rich repeat (LRR) gene in the QTL region that conferred resistance to the disease ^[14][61]. They hypothesized that residue 18 of a conserved motif, IxxLPxSxxxLYNLQTLxL, could govern resistance in ‘DrHs7250’. An independent study conducted in the U.S. using a biparental mapping population, ‘Charleston Gray’ (female parent, resistant) and ‘New Hampshire Midget’ (male parent, susceptible), found a major C. orbiculare race 1-resistance QTL in the same region on chromosome 8 ^[15][62]. A PACE SNP marker designed from the SNP marker CL 14-27-9, identified earlier ^[14][61], was also the diagnostic marker for the QTL (LOD = 14.06) in the study. Even though the resistance source for the breeding line ‘DrHS7250’ was not reported, it seemed that both ‘DrHS7250’ and ‘Charleston Gray’ may have the same resistance gene for C. orbiculare race 1. Both studies in different watermelon resistance sources validated that the race 1 anthracnose resistance is governed by a single dominant gene. Even today, anthracnose is a problem and a major research priority in watermelon ^[16][17]. Most of the current commercial cultivars with anthracnose resistance were developed by private industry (Table 1). These commercial cultivars have intermediate to high levels of resistance to anthracnose race 1, and some descriptions do not specify the race. Many hybrid watermelon cultivars are resistant to races 1 and 2B and susceptible to race 2 ^[1][4]. The SNP marker CL 14-27-9 could be utilized as a diagnostic marker to develop race 1-resistant cultivars via marker-assisted selection in watermelon breeding programs.

Growers often use fungicides to manage watermelon anthracnose throughout the growing season. Fungicides can be applied preventatively if cost-effective, or application should be started with the occurrence of the symptoms in a 5-to-10-day interval. If disease severity is high or environmental conditions are conducive to disease (wet weather), growers will use the shorter application interval. Effective fungicide active ingredients for managing watermelon anthracnose include compounds in group 11: trifloxystrobin, azoxystrobin, pyraclostrobin, fluoxastrobin; group 7: boscalid, fluxapyroxad; group 3: difenoconazole; group M05: chlorothalonil; and group M03: mancozeb ^[17][18][63,64]. Group 11 fungicides correspond to quinone outside inhibitors (Q_oIs), group 7 fungicides correspond to succinate dehydrogenase inhibitors (SDHIs), group 3 fungicides correspond to demethylation inhibitors (DMIs), and M05 and M03 have multi-site contact activity. Products commonly recommended for watermelon anthracnose control include ‘Kocide 3000’ (Copper Hydroxide), ‘Pristine’ (pyraclostrobin, boscalid), ‘Cabrio’ (pyraclostrobin), ‘Quadris Top’ (azoxystrobin, difenoconazole), ‘Bravo WeatherStik’ (chlorothalonil), and ‘TopGuard EQ’ (azoxystrobin) ^{[17][19][20][21]}[63,65,66,67].