Soil-borne pathogenic fungi (SBPF) and root-knot nematodes (RKN) co-exist in the rhizosphere and are major pathogens causing root diseases in cucurbits. Current knowledge on soil-borne pathogens of cucurbit crops grown under protected cultivation, their host-pathogen interactions, and mechanisms of resistance has been reviewed. Plant resistance is an effective and sustainable method to control soil-borne diseases and the available resistant cultivars and rootstocks to key soil-borne pathogens are reported. The importance of proper pathogen diagnosis in the right choice of cultivar or rootstock is highlighted because of the specificity in the response of the cucurbit crops to fungal and nematode species and races. Plants protect themselves through common mechanisms of resistance against SBPF and RKN including hardening of their cell walls, pathogenesis-related (PR) proteins, and production of antimicrobial molecules. The activity of some enzymes, such as peroxidases and phenylalanine lyase, is increased after pathogen infection and is higher on SBPF and RKN resistant than susceptible cucurbits. Plant hormones such as salicylic acid, jasmonic acid, and ethylene are involved in the response of cucurbits to SBPF. Most mechanisms of resistance to RKN affect post-infection development of the nematode, which results in a delay or disruption of the life cycle. Traditional and biotechnological tools used for breeding for resistance in cucurbits are described. Grafting is an effective non-host resistance method to control primarily Fusarium wilt but not to control RKN. However, new rootstocks with resistance to both pathogens have been developed recently and their effects on fruit quality and yield stability need additional studies. The impact of grafting on yield in pathogen-infested soils is discussed.

Losses caused by phytoparasitic nematodes in crops depend directly on their soil densities at the start of the crop, so reducing their populations before planting is the main aim of nematological management. Efficacies in reducing Meloidogyne soil populations of soil disinfestation methods, such as agrochemicals, botanicals, or biosolarization were estimated on multiple field trials conducted over fourteen years in intensive horticultural crops. Soil nematode populations were reduced by 87 to 78% after fumigation with 1,3-dichloropropene + chloropicrin and dimethyl-disulphide, respectively. Non-fumigant nematicides such as azadirachtin, dazomet, fenamiphos, fluopyram, fosthiazate, metam-sodium, and oxamyl showed efficacies ranging from 51 to 64%, whereas the efficacy of natural products, such as abamectin, garlic extracts, or essential oils was 41 to 48%. Biosolarization with chicken manure had an efficacy of 73%. An economic cost-benefit study of nematode management methods was performed for seven vegetable–M. incognita pathosystems. Fumigation with 1,3-dichloropropene + chloropicrin and biosolarization with chicken manure were the only treatments able to reduce RKN populations above 1000 and 750 J2 per 100 cm³ of soil, respectively, to levels below the nematode economic damage threshold, keeping profitability. Fumigation was able to manage RKN soil densities up to 350 J2 per 100 cm³ of soil in most susceptible crops as aubergine or cucumber and up to 1000 J2 per 100 cm³ of soil for more tolerant crops, such as other cucurbits, pepper, or tomato. Other nematicidal treatments were not able to reduce RKN populations above 200–300 J2/100 cm³ of soil below the economic thresholds but were profitable when RKN densities were below the limits of 200–300 J2/100 cm³ of soil.

The nematicidal efficacy of milbemectin and its commercial formulate Milbeknock^® on (i) egg hatching, (ii) juvenile motility and (iii) infective capacity of root-knot nematodes was evaluated in vitro and in planta assays. Serial dilutions of pure milbemectin were tested against nematode eggs and juveniles and lethal concentrations LC50 and LC90 calculated. Exposure of egg masses to milbemectin at a concentration of 30 μg/mL for 72 h reduced egg hatching by 52%. The increase in exposure time to 240 h did not increase the egg hatching inhibition at the highest concentration 30 μg/mL (53%) but reduced egg hatching at 15 and 7 μg/mL by 35 and 24%, respectively, when compared to untreated controls. The inhibitory effect of milbemectin on juvenile motility ranged from 41 to 87% depending on its concentration, and this effect was persistent after rinsing the juveniles in water. The probabilistic dose–response model indicated that lethal concentrations of milbemectin for juvenile motility were LC50: 7.4 μg/mL and LC90: 29.9 μg/mL. The pre-plant application of Milbeknock^® to soils infested with the nematode reduced its infective capacity by 98–99% compared to untreated soils in pot experiments. Milbeknock^® reduced nematode soil population densities by 50–60% in natural infestations under field conditions. Milbemectin shows a high level of efficacy against root-knot nematodes as it reduces egg hatching, persistently immobilizes nematode juveniles, and reduces tomato root infection.

Commercial tomatoes are usually complex F1 hybrids with multiple resistances genes from different wild Solanum species. The response of tomato cultivars with resistance to root-knot nematodes (RKN) and Tomato yellow leaf curl virus (TYLCV) as infected by Meloidogyne javanica was determined in a controlled environment and field conditions. Four treatments were tested, viz. tomato cultivars with (i) RKN resistance alone; (ii) combination of RKN and TYLCV resistance (RKN + TYLCV); (iii) TYLCV resistance alone; and (iv) control (susceptible to the nematode and virus). The RKN-resistant plants effectively suppressed nematode infection and reproduction both in a controlled environment and in field conditions. The RKN + TYLC-resistant plants were less effective (p < 0.001) than the RKN plants in a controlled environment, and their resistance levels were significantly reduced in the field. Nonetheless, the RKN + TYLCV plants supported lower (p < 0.001) nematode infection and reproduction than the susceptible control plants. The TYLCV-resistant plants reduced (p < 0.001) nematode infection and reproduction compared to the susceptible control in a controlled environment and in field conditions. The divergent response of tomato cultivars with resistance to TYLCV via infection by M. javanica can be attributed to the genetic background of the cultivars.