BIOCIDE COMPOSITIONS FOR APPLICATION TO BIOLOGICAL OR NON- BIOLOGICAL SURFACES AND USE THEREOF RELATED APPLICATIONS This application claims priority under applicable laws to US provisional application No.63/377.388 filed on September 28, 2022, US provisional application No.63/377.389 filed on September 28, 2022, US provisional application No. 63/377.388 filed on September 28, 2022, US provisional application No.63/501.539 filed on May 11, 2023, and US provisional application No. 63/501.560 filed on May 11, 2023, the contents of which are incorporated herein by reference in their entirety for all purposes. TECHNICAL FIELD The technical field generally relates to biocide compositions, and more particularly to biocide combinations and compositions comprising an alkylated chelating agent for the treatment of biological or non-biological surfaces. BACKGROUND Many types of biocide compositions are used to control microbial, biofilm and/or insect pests. Nevertheless, common biocides typically have several disadvantages, such as toxicity to humans, animals or plant, limited efficacy, possibility of developing microbial, biofilm and/or insect resistance, high cost or potentially causing harm to the environment. Accordingly, there is still a need for compounds, formulations, compositions and/or combinations to kill or suppress the activities of pests for application to biological or non- biological surfaces. SUMMARY In one aspect, a biocide composition is provided. The biocide composition comprises an EDTA derivative and a photosensitizer, wherein the EDTA derivative is of Formula (I): Formula (I) or a salt thereof, wherein: Z is NH or O; and R1 is selected from the group consisting of an optionally substituted C8-C18alkyl group, an optionally substituted C8-C18alkenyl group, an optionally substituted C8-C18alkynyl group and an optionally substituted steroidyl group. In some implementations, the EDTA derivative of Formula (I) is: or a salt thereof. In some implementations, the EDTA derivative of Formula (I) is: or a salt thereof. In some implementations, the photosensitizer is a macrocyclic tetrapyrrole compound selected from the group consisting of a porphyrin, a reduced porphyrin, and a mixture of at least two thereof. In some implementations, the macrocyclic tetrapyrrole compound is complexed with a metal to form a metallated macrocyclic tetrapyrrole compound. In some implementations, the macrocyclic tetrapyrrole compound comprises chlorophyllin, Chlorophyll a, chlorin e6, protoporphyrin IX, tetraphenylporphyrin, or Ce6- mix-DMAE ^15,17 amide. In some implementations, the macrocyclic tetrapyrrole compound comprises protoporphyrin IX. In some other implementations, the photosensitizer is an isoquinoline derivative, such as berberine. In some other implementations, the photosensitizer is a diarylheptanoid, such as curcumin. In some implementations, the biocide composition further comprises at least one of an oil, a base, an essential oil, a biosurfactant, a surfactant, a solvent, a biocompatible polymer, or an additional chelating agent. In some implementations, the biocide composition is an antimicrobial, an antibiofilm, or an insecticide composition. In another aspect, a method for inhibiting microbial pathogen and biofilm formation on a surface, disrupting pre-existing microbial pathogens and biofilms on a surface, or controlling insect pests on a surface is provided. The method comprises applying a biocide composition as defined herein to the surface. In some implementations, the surface is a biological surface or a non-biological surface. In some implementations, the biological surface is a plant. In some implementations, the method further comprises exposing the surface to illumination to induce photodynamic inactivation. In another aspect, a method for inhibiting microbial pathogens or disrupting pre- existing microbial pathogens on a wound on or in a subject, on a skin, or on a device in contact with a subject is provided. The method comprises applying the biocide composition as defined herein to the wound, the skin, or the device. In some implementations, the method further comprises exposing the wound to illumination to induce photodynamic inactivation. In another aspect, a use of a biocide composition as defined herein for inhibiting microbial pathogen and biofilm formation on a surface, disrupting pre-existing microbial pathogens and biofilms on a surface, or controlling insect pests on a surface is provided. In another aspect, a use of a biocide composition as defined herein for inhibiting microbial pathogens or disrupting pre-existing microbial pathogens on a wound on or in a subject, on a skin, or on a device in contact with a subject is provided. In another aspect, a biocide composition is provided. The biocide composition comprises an EDTA derivative and a liquid carrier, wherein the EDTA derivative is of Formula (I): Formula (I) or a salt thereof, wherein: Z is NH; and R ₁ is an unsubstituted C ₁₂ -C ₁₅ alkyl group or a substituted C ₁₂ -C ₁₅ alkyl group. BRIEF DESCRIPTION OF THE DRAWINGS Figure 1 is a schematic representation of a mode of action of an EDTA derivative disturbing bacteria membrane according to one implementation. Figure 2 is a quadrupole time-of-flight-mass spectrometry (qTOF-MS) spectrum of EDTA-mono-C8-amide, as described in Example 1(a). Figure 3 is a qTOF-MS spectrum of EDTA-mono-C12-amide, as described in Example 1(a). Figure 4 is a qTOF-MS spectrum of EDTA-mono-C14-amide, as described in Example 1(a). Figure 5 is a qTOF-MS spectrum of EDTA-mono-C15-amide, as described in Example 1(a). Figure 6 is a qTOF-MS spectrum of EDTA-mono-C16-amide, as described in Example 1(a). Figure 7 is a qTOF-MS spectrum of EDTA-mono-C18-amide, as described in Example 1(a). Figure 8 shows in (a) a plot of fluorescence intensity as a function of concentration of protoporphyrin IX (PPIX) in dimethyl sulfoxide (DMSO); in (b) a plot of fluorescence intensity as a function of the pH of three identical concentrations of PPIX; in (c) a graph of size distribution of three different concentrations of PPIX in water, measured by dynamic light scattering (DLS); in (d) a bar graph of Staphylococcus aureus (S.au) colony forming units per milliliter (CFU/mL) (log 10) after photodynamic inhibition (PDI) for various PPIX concentrations; and in (e) scanning electron microscope (SEM) back-scattering electron images of PPIX particles. Data are expressed as mean ± standard deviation. The size of the population n = 3. **P < 0.01, ****P < 0.0001. Figure 9 shows efficacy results of PPIX-mediated PDI alkylated ethylenediaminetetraacetic acid (EDTA) enhancers in eliminating planktonic S.au pathogens. Efficacy results are shown for exponentially growing S.au of optical density (OD ₆₀₀ ) of 0.3 preincubated with 10 μg mL ^-1 PPIX and 0.5 mM non-alkylated EDTA or 0.05 mM EDTA-mono-C8, C12, C14, C15, C16, or C18-amide in 96-well plate for 1h, followed by illumination in (a) for 1 hour; in (b) for 2 hours; and (c) 3 hours. Efficacy results after a serial dilution of the treated bacteria solutions and spreading on a Luria-Bertani (LB) plate, the bacteria viability was determined by counting bacterial colonies after 24 hours incubation at a temperature of 37°C. Data are presented as mean ± standard deviation (n = 3). ****P < 0.0001, ***P < 0.001, **P < 0.01, *P < 0.1 Figure 10 shows efficacy results of PPIX-mediated PDI alkylated EDTA enhancers. Efficacy results are shown for 5 μg mL ^-1 PPIX with non-alkylated EDTA or EDTA-mono- C12, C14, or C15-amide after 1 hour, 2 hours and 3 hours. Figure 11 shows efficacy results of PPIX-mediated PDI alkylated EDTA enhancers. Efficacy results are shown for 100 μg mL ^-1 PPIX with non-alkylated EDTA or EDTA-mono- C12, C14, or C15-amide after 1 hour, 2 hours and 3 hours. Figure 12 shows efficacy results of Mg-chlorophyllin-mediated PDI alkylated EDTA enhancers against S.au. Efficacy results are shown for Mg-chlorophyllin (64 ppm, 256 ppm, 512 ppm) with EDTA-mono-C14-ester (0.05 mM) after 1 hour. Figure 13 shows efficacy results of Mg-chlorophyllin-mediated PDI alkylated EDTA enhancers against Pseudomonas syringae pv. tomato (Pst). Efficacy results are shown for Mg-chlorophyllin (64 ppm, 256 ppm, 512 ppm) with EDTA-mono-C14-ester (0.05 mM) after 1 hour. Figure 14 shows efficacy results of Mg-chlorophyllin-mediated PDI alkylated EDTA enhancers against Pst. Efficacy results are shown for Mg-chlorophyllin (512 ppm) with EDTA-mono-C10-ester (0.05 mM) after 1 hour. Figure 15 shows efficacy results of berberine-mediated PDI alkylated EDTA enhancers against S.au. Efficacy results are shown for berberine (50 ppm) with EDTA- mono-C14-amine (0.05 mM) after 1 hour. Figure 16 shows efficacy results of curcurmin-mediated PDI alkylated EDTA enhancers against S.au. Efficacy results are shown for curcurmin (256 ppm) with EDTA- mono-C10-ester (0.05 mM) after 1 hour. Figure 17 shows S.au biofilm viability assay results. Mature S.au biofilms were treated with PPIX (5 μg mL ^-1 , 10 μg mL ^-1 , 50 μg mL ^-1 ) with non-alkylated EDTA (0 mM, 0.05 mM, 0.1 mM, and 0.5 mM) and, illuminated in (a) for 1 hour and in (b) for 2 hours, the remaining biofilms were then incubated with 0.5 mg/mL 3-(4,5-Dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide (MTT) for 4 hours at 37°C, formazan was dissolved in DMSO and optical density at 490 nm (OD490) was measured. The 0 mM EDTA cases were only treated with PPIX, all values were proportioned to the untreated group. The same method was employed on biofilms treated with the three concentrations of PPIX with EDTA-mono-C14-amide (0 mM, 0.05 mM, 0.1 mM, and 0.5 mM), illuminated in (c) for 1 hour and in (d) for 2 hours. Figure 18 shows S. au biofilm eradication assay results. Mature S. au biofilms were treated with the combination of PPIX (10 μg mL ^-1 ) and non-alkylated EDTA or EDTA- mono-C14-amide (0.05 mM, 0.1 mM, and 0.5 mM), followed by illumination for (a) 1 hour and (b) 2 hours. Figure 18 shows confocal laser scanning microscopy (CLSM) S.au biofilm eradication results showing in (d) a 3-dimensional z-stack reconstruction of S.au biofilms post illumination; in (e) cross-sections of the reconstructed biofilms shown in (d); and in (c) statistical analysis of the remaining biofilms obtained by Image J. observation. (Width 212.13 μm, Depth 20.00 μm). The biofilms were treated with 10 μg mL ^-1 PPIX with 0.1 mM non-alkylated EDTA or EDTA-mono-C14-amide, then illuminated for 1 hour, 2 hours, and 3 hours. The biofilms were then stained using the Live/Dead™ BacLight™ Bacterial Viability Kit with Syto9 (green), propidium iodide (red), and PPIX (blue) before observation. Data are presented as mean ± standard deviation (n = 3). ****P < 0.0001, ***P < 0.001, **P < 0.01. Figure 19 shows in (a) reactive oxygen species (ROS) detection results of S.au obtained by flow cytometry; in (b) the calculated ROS positive percentage; and in (c) the mean fluorescence intensity. The bacteria solutions were treated with 10 μg mL ^-1 PPIX with non-alkylated EDTA or EDTA-mono-C14-amide and incubated for 1 hour, then cultured with a dichlorodihydrofluorescein diacetate (DCFH-DA) detector for 15 minutes and irradiated for 30 minutes. Figure 19(d) shows ROS detection results of PPIX (10 μg mL ^-1 ) combinations in aqueous solution in the absence of bacteria. DCFH-DA was added into each well and incubated for 15 minutes. After illumination for 30 minutes, the fluorescence intensity was detected by spectrophotometer. Figure 19(e) shows size distribution of different PPIX combinations measured by DLS after 1 hour of incubation. Figure 19(f) presents SEM images of the PPIX particles incubated with non-alkylated EDTA or EDTA-mono-C14-amide. Data are presented as mean ± standard deviation (n = 3). ****P < 0.0001, ***P < 0.001. Figure 20 shows ROS detection results obtained for different PPIX combinations. 5 μg mL ^-1 PPIX was mixed with non-alkylated EDTA (0.5 mM) or EDTA-mono-C14-amide (0.5 mM, 0.05 mM) or sodium lauryl sulfonate (SDS) (0.5 mM) in saline for 1 hour in a 24- well plate. DCFH-DA was added in each well and incubated for 15 minutes and illuminated for 30 minutes. The fluorescence intensity was detected by spectrophotometry. Data are presented as mean ± standard deviation (n = 3). Figure 21 shows in (a) bacterial viability assay results obtained for different PPIX combinations. S.au bacteria were treated with 100 μg mL ^-1 PPIX and 0.5 mM non-alkylated EDTA, Wang-EDTA or non-alkylated EDTA with 0.5 mM CaCl2 for 1 hour, the CFU were counted after 24 hours of incubation; and in (b) inductively coupled plasma mass spectrometry (ICP-MS) results analyzing the element content of Wang-EDTA after culturing with S.au overnight. Data are presented as mean ± standard deviation (n = 3). **P < 0.01. Figure 22 shows size distribution results obtained for different PPIX combinations, in (a) S.au bacteria were treated with combinations of 100 μg mL ^-1 PPIX with different concentrations of EDTA-mono-C14-amide, and in (b) with combinations of 100 μg mL ^-1 PPIX with different concentrations of SDS (0.01 mM, 0.05 mM, 0.1 mM and 0.5 mM), particle size was measured by DLS after 1 hour of incubation. Figure 23 shows accumulation results of PPIX in S.au. Bacteria solutions of OD600 0.3 preincubated with 10 μg mL ^-1 PPIX and non-alkylated EDTA or EDTA-mono-C14- amide for 1 hour, the accumulation percentage was measured by flow cytometry after 1 hour of illumination. Figure 23 shows in (a) an overlap of data in different treated groups; and in (b) mean fluorescence intensity analysis of each group. Data are presented as mean ± standard deviation (n = 3). ****P < 0.0001. Figure 24 shows the minimum inhibitory concentrations (MICs) of 4 different alkylated chelators (comparative examples) in (a) against S.au; and in (b) against Escherichia coli (E. coli), as described in Example 1(b). Figure 25 shows the MICs of EDTA-mono-C8, C12, C14, C15, C16, and C18- amide, SDS and Vancomycin against S.au, as described in Example 1(b). Figure 26 shows time-dependent antibacterial effect of EDTA-mono-C14-amide and Vancomycin against S.au, as described in Example 1(c). Figure 27 CLSM images showing the time-dependent antibacterial effect of EDTA- mono-C14-amide and Vancomycin against S.au, as described in Example 1(d). Figure 28 shows the antibacterial effect of EDTA-mono-C14-amide and Vancomycin against various concentrations of S.au, as described in Example 1(d). Figures 28(a)-(d) show bar graphs of S.au CFU/mL (log 10) after being treated with different concentrations of EDTA-mono-C14-amide and Vancomycin. CFU was calculated (a) 2 x 10 ⁸ /well; (b) 2 x 10 ⁷ /well; (c) 2 x 10 ⁶ /well; and (d) 2 x 10 ⁵ /well. Figures 28(e)-(h) show graphs of the viability of S.au (%) as a function of the concentration of EDTA-mono- C14-amide and Vancomycin (e) 2 x 10 ⁸ /well; (f) 2 x 10 ⁷ /well; (g) 2 x 10 ⁶ /well; and (d) 2 x 10 ⁵ /well. Figure 29 shows a graph of the viability of S.au biofilms (%) as a function of the concentration of EDTA-mono-C14-amide, Vancomycin, SDS and potassium sorbate (PS) as described in Example 1(e). Figure 30 shows CLSM images obtained for S.au biofilms treated with EDTA- mono-C14-amide or Vancomycin at different times, as described in Example 1(e). Figure 31 shows cross-sections CLSM images of the reconstructed biofilms shown in Figure 30, and statistical analysis of the remaining biofilms obtained by Image J. observation. (Width 212.13 μm, Depth 20.00 μm), as described in Example 1(e). Figure 32 shows viability results of different kinds of bacteria treated with EDTA- mono-C14-amide, as described in Example 1(f). Figure 33 shows viability results of different kinds of bacteria biofilms treated with EDTA-mono-C14-amide, as described in Example 1(f). Figure 34 shows scanning electron microscope (SEM) images of EDTA-mono- C14-amide and Vancomycin treated S.au, as described in Example 1(g). Figure 35 shows the colorimetric aldehyde assay results, as described in Example 1(h). Figure 36 shows fluorescence spectra and confocal images of S.au and glutaraldehyde (top) and S.au, EDTA-mono-C14-amide and glutaraldehyde (bottom), as described in Example 1(i). Figure 37 shows MIC values of EDTA-mono-C12, C14 and C15-amide and Ceftazidime against E. coli, as described in Example 1(j). Figure 38 shows MIC values of methicillin against S.au and methicillin-resistant Staphylococcus aureus (MRSA), as described in Example 1(k). Figure 39 shows MIC values of EDTA-mono-C14-amide, SDS, PS, and sodium benzoate (SB) against S.au, as described in Example 1(l). Figure 40 shows critical micelle concentration (CMC) of EDTA-mono-C12, C14, C15, and C18-amide, C12-ester, and C18-ester determined using fluorescence. Figure 41 shows photodynamic inactivation results against Erwinia amylovora obtained for Ce6-mono-DMAE ¹⁵ amide (B17-mono) (1 µm, 10 µm, and 100 µm) with EDTA-mono-C16-amide (1 mM) (with 120 minutes of incubation; 15 minutes 50 seconds of illumination at 395 nm and 28 mW/cm ² ; 26.6 J/cm ² radiant exposure; and n = 2). Figure 42 shows photodynamic inactivation results against Erwinia amylovora obtained for chlorophyllin (Chl) (1 µm, 10 µm, and 100 µm) with EDTA-mono-C16-amide (1 mM) (with 120 minutes of incubation; 15 minutes 50 seconds of illumination at 395 nm and 28 mW/cm ² ; 26.6 J/cm ² radiant exposure; and n = 2). Figure 43 shows photodynamic inactivation results against Erwinia amylovora obtained for Cu-chlorophyllin (CuChl) (100 µm) and Cu-Ce6-mix-DMAE ^15,17 amide (CuB17) (100 µm) with EDTA-mono-C16-amide (5 mM) or BAYPURE™ DS 100 (1.2%) (with 30 minutes of incubation; and 72 minutes of illumination at 6.2 mW/cm ² ; 26.6 J/cm ² radiant exposure (except dark controls denoted as PS controls)). Figure 44 shows photodynamic inactivation results against Erwinia amylovora obtained for Ce6-mono-DMAE ¹⁵ amide (B17-mono) (10 µm and 100 µm) and Ce6-bis- DMAE ^15,17 amide (B17-0024) (10 µm and 100 µm) with EDTA-mono-C16-amide (1 mM) (with 30 minutes of incubation; and 26.6 J/cm ² radiant exposure (except dark controls denoted as PS controls)). Figure 45 shows a time-series images of ulcers after different treatments (control, PPIX, PPIX with non-alkylated EDTA (0.5 mM), and PPIX with EDTA-mono-C14-amide (0.5 mM)) in vivo on an animal model of infected ulcers. Figure 46 shows the average ulcer area after the different treatments (control, PPIX, PPIX with non-alkylated EDTA (0.5 mM), and PPIX with EDTA-mono-C14-amide (0.5 mM)) in vivo on an animal model of infected ulcers as a function of time. Data are presented as mean ± standard deviation (n = 3). ****P < 0.0001, ***P < 0.001. Figure 47 shows the amount of bacteria collected at the ulcer lesions after the different treatments (control, PPIX, PPIX with non-alkylated EDTA (0.5 mM), and PPIX with EDTA-mono-C14-amide (0.5 mM)) in vivo on an animal model of infected ulcers after 3, 5 and 7 days. Data are presented as mean ± standard deviation (n = 3). ****P < 0.0001, ***P < 0.001, **P < 0.01. Figure 48 shows a time-series images of ulcers after nine different treatments (PBS, PPIX, PPIX with non-alkylated EDTA (0.5 mM), and PPIX with EDTA-mono-C8, C12, C14, C15, C16, and C18-amide (0.5 mM)) in vivo on an animal model of infected ulcers. Figure 49 shows the average ulcer area after five different treatments (PBS, PPIX, PPIX with non-alkylated EDTA (0.5 mM), and PPIX with EDTA-mono-C15 and C18-amide (0.5 mM)) in vivo on an animal model of infected ulcers as a function of time. Data are presented as mean ± standard deviation (n = 3). Figure 50 shows the amount of bacteria collected at the ulcer lesions after the nine different treatments (PBS, PPIX, PPIX with non-alkylated EDTA (0.5 mM), and PPIX with EDTA-mono-C8, C12, C14, C15, C16, and C18-amide (0.5 mM)) in vivo on an animal model of infected ulcers after 3, 5 and 7 days. Data are presented as mean ± standard deviation (n = 3). Figure 51 shows a time-series images of ulcers after five different treatments (PBS, PPIX, PPIX with EDTA-mono-C10-amide (0.5 mM), and PPIX with EDTA-mono-C14 and C16-ester (0.5 mM)) in vivo on an animal model of infected ulcers. Figure 52 shows the average ulcer area after six different treatments (PBS, PPIX, PPIX with EDTA-mono-C10 and C14-amide (0.5 mM), and PPIX with EDTA-mono-C14 and C16-ester (0.5 mM)) in vivo on an animal model of infected ulcers as a function of time. Data are presented as mean ± standard deviation (n = 3). Figure 53 shows a time-series of catheter implanted areas on muscle wounds (Barlb/c mice), the catheter is coated with a biocide composition comprising EDTA-mono- C14-amide and the negative control corresponds to an uncoated catheter. Catheters have been pre-incubated with S.au bacteria. Figure 54 shows the determination of viable bacteria by plate counting method on the coated and uncoated catheters and the muscles. Figure 55 shows the determination of the duration of the coating’s antibacterial efficacies over time (PS stands for polystyrene and PLC for polycaprolactone / (PS or PLC)-C14-20, -C14-50 and -C14-100 refer to the final concentration of EDTA-mono-C14- amide: 20, 50 and 100 µg / mL). Figure 56 shows photodynamic inactivation results against Candida auris (C. auris) on porcine skin model obtained for Ce6-mix-DMAE ^15,17 amide (10 µM, 50 µM, and 100 µM) with EDTA-mono-C14-amide (0.5 mM) (after 15 minutes of incubation; illumination at 395 nm; and 25 J/cm ² radiant exposure). Figure 57 shows photodynamic inactivation results against C. auris on porcine skin model obtained for Ce6-mix-DMAE ^15,17 amide (100 µM) with and without EDTA-mono- C14-amide (0.5 mM) (no incubation; illumination at 395 nm; 100 J/cm ² radiant exposure; and n = 1). DETAILED DESCRIPTION The following detailed description and examples are illustrative and should not be interpreted as further limiting the scope of the claims. On the contrary, the present description is intended to cover all alternatives, modifications and equivalents that can be included as defined by the present description. The objects, advantages and other features of the present biocide compositions, methods of applying such compositions, and their uses will be more apparent and better understood upon reading the following non- restrictive description and references made to the accompanying drawings. When a range of values is mentioned herein, the lower and upper limits of the range are, unless otherwise indicated, always included in the definition. When a range of values is mentioned in the present application, then all intermediate ranges and subranges, as well as individual values within the ranges, are intended to be included. The chemical structures described herein are drawn according to conventional standards. Also, when an atom, such as a carbon atom as drawn, seems to include an incomplete valency, then the valency is assumed to be satisfied by one or more hydrogen atoms even if they are not necessarily explicitly drawn. The term “approximately” or its equivalent term “about”, as used herein, mean around or in the region of. When the terms “approximately” or “about” are used in relation to a numerical value, it is understood to encompass a variation of 10% above and below the numerical value. These terms can also take into account the rounding of a number or the probability of random errors in experimental measurements, for instance, due to equipment limitations. It is worth mentioning that throughout the following description when the article “a” or “an” is used to introduce an element, the article “a” or “an” does not have the meaning of “only one” and rather means “one or more” unless otherwise indicated. It is to be understood that where the specification states that a step, component, feature, or characteristic “may”, “might”, “can” or “could” be included, that particular component, feature or characteristic is not required to be included in all alternatives. When trade names are used herein, it is intended to independently include the tradename product and the active ingredient(s) of the tradename product. All technical and scientific terms and expressions used herein have the same definitions as those commonly understood by the person skilled in the art when relating to the present technology. The definition of some terms and expressions used herein is nevertheless provided below for clarity purposes. The term “pest”, as used herein, refers to an invasive species that can cause harm to humans, animals and/or plants. For example, the term pest can encompass microbial pathogens, biofilm and/or insects. The term “biocide”, as used herein, refers to a compound or a composition that kills and/or suppresses the activities of pests. The term biocide encompasses antimicrobials when the pest is a microorganism, including, but not limited to bacteria, archaea, fungi (yeasts and molds), algae, protozoa, and viruses. The term biocide encompasses antibiofilms when the pest is a biofilm. The term biocide encompasses insecticides when the pest is an insect. The term biocide encompasses pesticides when the pest to be killed and/or controlled is on a plant (i.e., when the surface to be treated with the biocide composition is a plant). The term biocide also encompasses disinfectants, for example, when the surface is a non-biological surface (or an inert surface). The term “antimicrobial”, as used herein, refers to a compound or a composition that kills, inhibits and/or stops the growth of microorganisms, including, but not limited to bacteria, archaea, fungi (yeasts and molds), algae, protozoa, and viruses. The term “antibiofilm”, as used herein, refers to inhibition of biofilm formation and/or to disruption or dispersal of preformed biofilms. The antibiofilm compositions of the present description can be applied to a surface, to prevent microorganisms from adhering to the surface, or to remove the microorganisms that have adhered to the surface. In other words, the surface can be coated or impregnated with the antibiofilm composition prior to a possible infection. Alternatively, the surface can be treated with the antibiofilm composition to control, reduce, or eradicate the microorganisms adhering to the surface. The term “microorganisms”, as used herein, refers to bacteria, archaea, fungi (yeasts and molds), algae, protozoa, and viruses. The term “insecticide”, as used herein, refers to a compound or a composition that kills, inhibits and/or control the population of insect pest. The term insecticide can also encompass ovicides and larvicides used against insect eggs and larvae, respectively. The term “biofilm”, as used herein, refers to a community of microorganism that is matrix-enclosed in a self-produced extracellular polymeric matrix, and attached to a biological or non-biological surface. Bacteria in a biofilm can be up to 1000 times more resistant to antibiotics/antimicrobials compared to their planktonic (free living) counterparts. The term “biofilm formation”, as used herein, refers to the attachment of microorganisms to surfaces and the subsequent development of multiple layers of cells. The term “biofilm formation” is intended to include the formation, growth and modification of the microbial colonies contained within the biofilm, as well as the synthesis and maintenance of the extracellular polymeric matrix of the biofilm. The term “insect pest”, as used herein, refers to adult insects and/or their larvae or nymphs, which are known to or have the potential to cause damages or negatively impact the health of humans, animal and/or plants. Non-limiting examples of insect pests can include insect pests from the orders of Hemiptera (groups of aphids, whiteflies, scales, mealybugs, stink bugs), Coleoptera (groups of beetles), Lepidoptera (groups of butterflies, moths), Diptera (groups of flies, mosquitoes), Thysanoptera (groups of thrips), Orthoptera (groups of grasshoppers, locusts), Hymenoptera (groups of wasps, ants) and mite pests (spider mites). The term “surface” or “surfaces”, as used herein, refers to biological or non- biological surface(s). The term “surface” or “surfaces” also refers to the surface of devices for contacting a biological surface or for implantation and/or insertion in the body. Non- limiting examples of biological surfaces include plants, grass, trees, and animal body part, such as a mammal body part, including a human body part. For example, and without being limiting, the human or animal body part can be wounds (including chronic and acute wounds), skin lesions, skin, mucous membranes, mucous membrane lesions, internal organs, breast tissue, nipples, body cavity, oral cavity, bone tissue, muscle tissue, nerve tissue, ocular tissue, urinary tract tissue, lung and trachea tissue, sinus tissue, ear tissue, dental tissue, gum tissue, nasal tissue, vascular tissue, cardiac tissue, epithelium, and epithelial lesions, and peritoneal tissue. For example, and without being limiting, the wound is on a subject. For example, and without being limiting, the subject is a mammal such as a human. Non-limiting examples of a device for implantation or insertion in the body include medical, veterinary, or agricultural devices. Non-limiting examples of such medical devices include tubes and catheters. For example, and without being limiting, the medical device is for implantation into tissues. For example, and without being limiting, the catheter can be contacting a mucous membrane, a muscle, or other tissues. For example, and without being limiting, the catheter can be inserted through the skin. For example, and without being limiting, the catheter can be inserted through a blood vessel. For example, and without being limiting, the catheter can be an intravascular catheter, a urinary catheter, a brain catheter, a soaker catheter, a nephrostomy tube, or a drain catheter. For example, and without being limiting, the agricultural devices include apparatus to milk livestock. Non-limiting examples of non-biological surfaces include the surface of an article of manufacture such as a veterinary and human medical device, pipes, filters, walls, floors, table-tops or toilets. The surfaces can be porous, soft, hard, semi-soft, semi-hard, regenerating, or non-regenerating. These surfaces include, but are not limited to, polyurethane, metal, alloy, or polymeric surfaces in veterinary and human medical devices. The term “applying”, as used herein, refers to contacting at least one part of the surface to be treated with at least one composition of the present description, by any means known in the art (e.g., spraying, pouring, coating, immersing, dipping, soaking, and wiping). The term applying encompasses manual, automatic, and/or machined application of the composition of the present description to the at least one part of the surface to be treated. The term “salt”, as used herein, refers to salts that exhibit biocide activity (e.g., pesticidal activity, antimicrobial activity, antibiofilm activity and/or insecticidal activity). When the surface is a plant, the term salt also encompasses agriculturally acceptable salts that are or can be converted in plants, water or soil to a compound or salt that exhibits biocide activity (e.g., pesticidal activity, antimicrobial activity, antibiofilm activity and/or insecticidal activity). The “agriculturally acceptable salt” can be an agriculturally acceptable cation or agriculturally acceptable anion. Non-limiting examples of agriculturally acceptable cations can include cations derived from alkali or alkaline earth metals and cations derived from ammonia and amines. For example, agriculturally acceptable cations can include sodium, potassium, magnesium, alkylammonium and ammonium cations. Non-limiting examples of agriculturally acceptable anions can include halide, phosphate, alkylsulfate, and carboxylate anions. For example, agriculturally acceptable anions can include chloride, bromide, methylsulfate, ethylsulfate, acetate, lactate, dimethyl phosphate, or polyalkoxylated phosphate anions. When the surface is a human or an animal body part, the term salt also encompasses pharmaceutically acceptable salts. The term “pharmaceutically acceptable salt” means a salt that is pharmaceutically acceptable and that possesses the desired biocide activity (e.g., pesticidal activity, antimicrobial activity, antibiofilm activity, and/or insecticidal activity). As used herein, the phrase “a compound of Formula (I)” means a compound of Formula (I) or a salt thereof. With respect to isolatable intermediates, the phrase “a compound of Formula (number)” means a compound of that formula and salts thereof. The term “Alkyl”, as used herein, means a hydrocarbon containing primary, ^{secondary, tertiary, or cyclic carbon atoms.} _{The term “Cm-Cn alkyl” refers to an alkyl group} having from the indicated “m” number of carbon atoms to the indicated “n” number of _{carbon atoms.} Examples of suitable alkyl groups include, but are not limited to, methyl (Me, -CH3), ethyl (Et, -CH2CH3), 1-propyl (n-Pr, n-propyl, -CH2CH2CH3), 2-propyl (i-Pr, i-propyl, -CH(CH3)2), 1-butyl (n-Bu, n-butyl, -CH2CH2CH2CH3), 2-methyl-1-propyl (i-Bu, i- butyl, -CH2CH(CH3)2), 2-butyl (s-Bu, s-butyl, -CH(CH3)CH2CH3), 2-methyl-2-propyl (t-Bu, t-butyl, -C(CH3)3), 1-pentyl (n-pentyl, -CH2CH2CH2CH2CH3), 2-pentyl (-CH(CH3)CH2CH2CH3), 3-pentyl (-CH(CH2CH3)2), 2-methyl-2-butyl (-C(CH3)2CH2CH3), 3-methyl-2-butyl (-CH(CH3)CH(CH3)2), 3-methyl-1-butyl (-CH2CH2CH(CH3)2), 2-methyl-1- butyl (-CH2CH(CH3)CH2CH3), 1-hexyl (-CH2CH2CH2CH2CH2CH3), 2-hexyl (-CH(CH3)CH2CH2CH2CH3), 3-hexyl (-CH(CH2CH3)(CH2CH2CH3)), 2-methyl-2-pentyl (-C(CH3)2CH2CH2CH3), 3-methyl-2-pentyl (-CH(CH3)CH(CH3)CH2CH3), 4-methyl-2-pentyl (-CH(CH3)CH2CH(CH3)2), 3-methyl-3-pentyl (-C(CH3)(CH2CH3)2), 2-methyl-3-pentyl (- CH(CH2CH3)CH(CH3)2), 2,3-dimethyl-2-butyl (-C(CH3)2CH(CH3)2), 3,3-dimethyl-2-butyl (- CH(CH3)C(CH3)3, n-heptyl (-(CH2)6CH3), n-octyl (-(CH2)7CH3), n-nonyl (-(CH2)8CH3), n- decyl (-(CH2)9CH3), n-undecyl (-(CH2)10CH3), n-dodecyl (-(CH2)11CH3), n-tridecyl (-(CH2)12CH3), n-tetradecyl (-(CH2)13CH3), n-pentadecyl (-(CH2)14CH3), n-hexadecyl (-(CH ₂ ) ₁₅ CH ₃ ), n-heptadecyl (-(CH ₂ ) ₁₆ CH ₃ ), n-octadecyl (-(CH ₂ ) ₁₇ CH ₃ ), and the like _. The term “Alkenyl”, as used herein, means a hydrocarbon containing primary, secondary, tertiary, or cyclic carbon atoms with at least one site of unsaturation, i.e., a ^{carbon-carbon sp2 double bond.} _{The term “Cm-Cnalkenyl” refers to an alkenyl group having} from the indicated “m” number of carbon atoms to the indicated “n” number of carbon _atoms. Examples of suitable alkenyl groups include, but are not limited to, ethylene or vinyl (-CH ^CH2), allyl (-CH2CH ^CH2), cyclopentenyl (-C5H7), 5-hexenyl (-CH ₂ CH ₂ CH ₂ CH ₂ CH ^CH ₂ ) and 9-octadecenyl (-CH ₂ -(CH ₂ ) ₇ -CH=CH-(CH ₂ ) ₇ -CH ₃ ). It is understood that the term “alkenyl” also includes terpenyl radicals. Terpenyl radicals are derived from terpenes which are of general formula (C5H8)n where n is 2, 3, 4 or more. As used herein, the terms “terpene” and “terpenyl” extend to compounds which are known as “terpenoids”, involving the loss or shift of a fragment, generally a methyl group. As a non- limiting example, sesquiterpenes (where n is 3) can contain 14 rather than 15 carbon atoms – and are then considered to be terpenoids (or more specifically sesquiterpenoids). Terpene or terpenyl radicals can be cyclic or acyclic. Non-limiting examples of sub-classes of terpenes are carotenes or carotenoids, also referred to as tetraterpenes or tetraterpenoids. The term “Alkynyl”, as used herein, means a hydrocarbon containing primary, secondary, tertiary or cyclic carbon atoms with at least one site of unsaturation, i.e., a ^{carbon-carbon, sp triple bond.} _{The term “Cm-Cnalkynyl” refers to an alkynyl group having} from the indicated “m” number of carbon atoms to the indicated “n” number of carbon _atoms. Examples of suitable alkynyl groups include, but are not limited to, acetylenic (-C ^CH), propargyl (-CH2C ^CH), and hexadecynyl (-(CH2)14-C ^CH). The term “Alkoxy”, as used herein, is interchangeable with the term “O(Alkyl)”, in which an “Alkyl” group as defined above is attached to the parent molecule via an oxygen atom. For example, and without being limiting, the alkyl portion of an O(Alkyl) group can have 1 to 24 carbon atoms (i.e., C ₁ -C ₂₄ alkyl), 4 to 18 carbon atoms (i.e., C ₄ -C ₁₈ alkyl), 8 to 16 carbon atoms (i.e., C ₈ -C ₁₆ alkyl) or 12 to 16 carbon atoms (i.e., C ₁₂ -C ₁₆ alkyl). _Examples of suitable Alkoxy or O(Alkyl) groups include, but are not limited to, methoxy (-OCH ₃ or - OMe), ethoxy (-OCH ₂ CH ₃ or -OEt) and t-butoxy (-O-C(CH ₃ ) ₃ or -OtBu). Similarly, “O(alkenyl)”, “O(alkynyl)”, and the corresponding substituted groups will be understood by a person skilled in the art. The term “Acyl”, as used herein, is meant to encompass several functional moieties such as “C=O(Alkyl)”, “C=O(Alkenyl)”, “C=O(Alkynyl)” and their corresponding substituted groups, in which an “Alkyl”, “Alkenyl” and “Alkynyl” groups are as defined above and attached to an O, N, S of a parent molecule via a C=O group. For example, and without being limiting, the alkyl portion of a C=O(Alkyl) group can have 1 to 24 carbon atoms (i.e., C ₁ -C ₂₄ alkyl), 1 to 8 carbon atoms (i.e., C ₁ -C ₈ alkyl), 1 to 6 carbon atoms (i.e., C ₁ -C ₆ alkyl) ^{or 1 to 4 carbon atoms (i.e., C} 1 ^-C 4 ^alkyl). _{Examples of suitable Acyl groups include, but are} not limited to, formyl (i.e., a carboxyaldehyde group), acetyl, trifluoroacetyl, propionyl, and butanoyl. A person skilled in the art will understand that a corresponding definition applies for “C=O(Alkenyl)” and “C=O(Alkynyl)” moieties. In the present description, ^{“C=O(Alkyl)”,} “C=O(Alkenyl)”, “C=O(Alkynyl)” can also be written as “CO(Alkyl)”, “CO(Alkenyl) and “CO(Alkynyl)”, respectively. It is understood that the term “(C ₁ -C ₂₄ )acyl, as used herein, refers to “C=O((C ₁ -C ₂₄ )Alkyl), C=O(((C ₁ -C ₂₄ )Alkenyl), or C=O(((C ₁ -C ₂₄ )Alkynyl)”. The term “Alkylene”, as used herein, means a saturated, branched or straight chain or cyclic hydrocarbon radical having two monovalent radical centers derived by the removal of two hydrogen atoms from the same or two different carbon atoms of a parent alkane. For example, and without being limiting, an alkylene group can have 1 to 24 carbon atoms, 1 to 18 carbon atoms, 1 to 10 carbon atoms, 1 to 6 carbon atoms, 1 to 4 carbon atoms, 8 to 24 carbon atoms or 8 to 18 carbon atoms. Typical alkylene radicals include, but are not limited to, methylene (-CH2-), 1,1-ethyl (-CH(CH3)-), 1,2-ethyl (-CH2CH2-), 1,1- propyl (-CH(CH2CH3)-), 1,2-propyl (-CH2CH(CH3)-), 1,3-propyl (-CH2CH2CH2-) and 1,4- butyl (-CH2CH2CH2CH2-). The term “Alkenylene”, as used herein, means an unsaturated, branched or straight chain or cyclic hydrocarbon radical having two monovalent radical centers derived by the removal of two hydrogen atoms from the same or two different carbon atoms of a parent alkene. For example, and without being limiting, and alkenylene group can have 2 to 24 carbon atoms, 2 to 18 carbon atoms, 2 to 10 carbon atoms, 2 to 6 carbon atoms, 2 to 4 carbon atoms, 8 to 24 carbon atoms, or 8 to 18 carbon atoms. Typical alkenylene radicals include, but are not limited to, 1,2-ethylene (-CH ^CH-). The term “Alkynylene”, as used herein, means an unsaturated, branched or straight chain or cyclic hydrocarbon radical having two monovalent radical centers derived by the removal of two hydrogen atoms from the same or two different carbon atoms of a parent alkyne. For example, and without being limiting, an alkynylene group can have 2 to 24 carbon atoms, 2 to 18 carbon atoms, 2 to 10 carbon atoms, 2 to 6 carbon atoms or 2 to 4 carbon atoms, 8 to 24 carbon atoms or 8 to 18 carbon atoms. Typical alkynylene radicals include, but are not limited to, acetylene (-C ^C-), propargyl (-CH ₂ C ^C-), and 4- pentynyl (-CH2CH2CH2C ^C-). The term “Aryl”, as used herein, means an aromatic hydrocarbon radical derived by the removal of one hydrogen atom from a single carbon atom of a parent aromatic ring system. For example, and without being limiting, an aryl group can have 6 to 20 carbon atoms, 6 to 14 carbon atoms, or 6 to 10 carbon atoms. Typical aryl groups include, but are not limited to, radicals derived from benzene (e.g., phenyl), substituted benzene, naphthalene, anthracene, and biphenyl. It is understood that the term “aryl” encompasses polyaromatic radicals, such as naphtalenyl, biphenyl, fluorenyl, anthracenyl, phenanthrenyl, and phenalenyl. The polyaromatic radicals can be substituted or unsubstituted. The term “Arylalkyl”, as used herein, means an acyclic alkyl radical in which one of the hydrogen atoms bonded to a carbon atom, typically a terminal or sp ³ carbon atom, is replaced with an aryl radical. Typical arylalkyl groups include, but are not limited to, benzyl, 2-phenylethan-1-yl, naphthylmethyl, 2-naphthylethan-1-yl, naphthobenzyl, 2-naphthophenylethan-1-yl and the like. For example, and without being limiting, the arylalkyl group can include 7 to 20 carbon atoms, e.g., the alkyl moiety is 1 to 6 carbon atoms, and the aryl moiety is 6 to 14 carbon atoms. The term “Arylalkenyl”, as used herein, means an acyclic alkenyl radical in which one of the hydrogen atoms bonded to a carbon atom, typically a terminal or sp ³ carbon atom, but also a sp ² carbon atom, is replaced with an aryl radical. The aryl portion of the arylalkenyl can include, for example, any of the aryl groups described herein, and the alkenyl portion of the arylalkenyl can include, for example, any of the alkenyl groups described herein. The arylalkenyl group can include 8 to 20 carbon atoms, e.g., the alkenyl moiety is 2 to 6 carbon atoms, and the aryl moiety is 6 to 14 carbon atoms. The term “Arylalkynyl”, as used herein, means an acyclic alkynyl radical in which one of the hydrogen atoms bonded to a carbon atom, typically a terminal or sp ³ carbon atom, but also a sp carbon atom, is replaced with an aryl radical. The aryl portion of the arylalkynyl can include, for example, any of the aryl groups disclosed herein, and the alkynyl portion of the arylalkynyl can include, for example, any of the alkynyl groups disclosed herein. For example, and without being limiting, the arylalkynyl group can include 8 to 20 carbon atoms, e.g., the alkynyl moiety is 2 to 6 carbon atoms, and the aryl moiety is 6 to 14 carbon atoms. The term “steroidyl group”, as used herein, refers to a steroid fused ring system which can be covalently bound to the EDTA derivative. Non-limiting examples of steroids include cholesterol, cholic acid, lanosterol and chenodeoxycholic acid. Is should be understood that the steroidyl group can be attached to the EDTA derivative in various ways and via an oxygen, nitrogen, sulfur, or carbon atom of the streroidyl group. The term “substituted”, as used herein in reference to alkyl, alkylene, alkoxy, alkenyl, alkynyl, alkenylene, aryl, alkynylene, etc., for example “substituted alkyl”, “substituted alkylene”, “substituted alkoxy” – “or substituted O(Alkyl)”, “substituted alkenyl”, “substituted alkynyl”, “substituted alkenylene”, “substituted aryl” and “substituted alkynylene”, unless otherwise indicated, means alkyl, alkylene, alkoxy, alkenyl, alkynyl, alkenylene, aryl and alkynylene, respectively, in which one or more hydrogen atoms are each independently replaced with a non-hydrogen substituent. Typical non-hydrogen substituents include, but are not limited to, -X, -R ^B , -O-, =O, -OR ^B , -SR ^B , -S-, -NR ^B 2, Si(R ^C )3, -N ⁺ R ^B 3, -NR ^b -(Alk)-NR ^B 2, -NR ^B -(Alk)-N ⁺ R ^B 3, -NR ^B - (Alk)-OR ^B , -NR ^B -(Alk)-OP(=O)(OR ^B )(O-), -NR ^B -(Alk)-OP(=O)(OR ^B )2, -NR ^B -(Alk)-Si(R ^C )3, -NR ^B -(Alk)-SR ^B , -O-(Alk)-NR ^B 2, -O-(Alk)-N ⁺ R ^B 3, -O-(Alk)-OR ^B , -O-(Alk)-OP(=O)(OR ^B )(O-),_-O-(Alk)-OP(=O)(OR ^B )2, -O-(Alk)-Si(R ^C )3, -O-(Alk)-SR ^B , =NR ^B , -CX3, -CN, -OCN, -SCN, -N=C=O, -NCS, -NO, -NO2, =N2, -N3, -NHC(=O)R ^B , -OC(=O)R ^B , -NHC(=O)NR ^B 2, -S(=O)2-, -S(=O)2OH, -S(=O)2R ^B , -OS(=O)2OR ^B , -S(=O)2NR ^B 2, -S(=O)R ^B , -OP(=O)(OR ^B )(O-), -OP(=O)(OR ^B )2, -P(=O)(OR ^B )2, -P(=O)(O-)2, -P(=O)(OH)2, -P(O)(OR ^B )(O-), -C(=O)R ^B , -C(=O)X, -C(S)R ^B , -C(O)OR ^B , -C(O)O-, -C(S)OR ^B , -C(O)SR ^B , -C(S)SR ^B , -C(O)NR ^B 2, -C(S)NR ^B 2 or -C(=NR ^B )NR ^B 2 where each X is independently a halogen: F, Cl, Br, or I; each R ^B is independently H, alkyl, aryl, arylalkyl, a heterocycle, an alkyloxy group such as poly(ethyleneoxy), PEG or poly(methyleneoxy), or a protecting group; each R ^C is independently alkyl, O(alkyl) or O(tri-substituted silyl); and each Alk is independently alkylene, substituted alkylene, alkenylene, substituted alkenylene, alkynylene, or substituted alkynylene. Unless otherwise indicated, when the term “substituted” is used in conjunction with groups such as arylalkyl, which have two or more moieties capable of substitutions, the substituents can be attached to the aryl moiety, the alkyl moiety, or both. The term “PEG” or “poly(ethylene glycol)”, as used herein, is meant to encompass any water-soluble poly(ethylene oxide). Typically, substantially all, or all monomeric subunits are ethylene oxide subunits, though the PEG can contain distinct end capping moieties or functional groups. PEG chains of the present description can include one of the following structures: -(CH ₂ CH ₂ O) _m - or -(CH ₂ CH ₂ O) _m-1 CH ₂ CH ₂ -, depending on if the terminal oxygen has been displaced, where m is a number, optionally selected from 1 to 100, 1 to 50, 1 to 30, 5 to 30, 5 to 20 or 5 to 15. The PEG can be capped with an “end capping group” that is generally a non-reactive carbon-containing group attached to a terminal oxygen or other terminal atom of the PEG. Non-limiting examples of end capping groups can include alkyl, substituted alkyl, aryl, substituted aryl, alkenyl, substituted alkenyl, alkynyl, substituted alkynyl, CO(alkyl), CO(substituted alkyl), CO(alkenyl), CO(substituted alkenyl), CO(alkynyl) or CO(substituted alkynyl). In the present description, it is understood that “(EO)t” means “-(CH2CH2O)t-” . Similarly, the term “(PO)w1” means “-(CH(CH3)CH2O)w1-”. It is also understood that the numbers t and w1 can be integers or non-integers. It is understood that when t and/or w1 are non-integers, several compounds are present in a mixture, and the value of t and w1 represents a mean value. The term “minimum inhibitory concentration (MIC)”, as used herein, refers to the lowest concentration of an antimicrobial agent expressed in mg/L (μg/mL) which, under strictly controlled in vitro conditions will inhibit the visible growth of a microorganism after overnight incubation. The term “critical micelle concentration (CMC)”, as used herein, refers to the concentration of surfactants above which micelles form and all additional surfactants added to the system will form micelles. A person skilled in the art will recognize that substituents and other moieties of the compounds of the present description should be selected in order to provide a useful compound which can be formulated into an acceptably stable biocide composition, that can be applied to surfaces. The definitions and substituents for various genus and subgenus of the compounds of the present description are described and illustrated herein. It should be understood by a person skilled in the art that any combination of the definitions and substituents described herein should not result in an inoperable species or compound. It should also be understood that the phrase “inoperable species or compound” means compound structures that violate relevant scientific principles (such as, for example, a carbon atom connecting to more than four covalent bonds) or compounds too unstable to permit isolation and composition into acceptable biocide compositions. Selected substituents of the compounds of the present description can be present to a recursive degree. In this context, “recursive substituent” means that a substituent can recite another instance of itself. Because of the recursive nature of such substituents, theoretically, a large number of compounds can be present in any given implementation. For example, R ^x includes a R ^y substituent. R ^y can be R. R can be W ³ . W ³ can be W ⁴ and W ⁴ can be R or include substituents including R ^y . A person skilled in the art of organic chemistry understands that the total number of such substituents is to be reasonably limited by the desired properties of the compound intended. Such properties include, by way of example and not limitation, physical properties such as molecular weight, solubility or log P, application properties such as activity against the intended target, possibility of application in biocide compositions, surface tension, foamability, and practical properties such as ease of synthesis. Typically, each recursive substituent can independently occur 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, 1, or 0, times in a given implementation. For example, each recursive substituent can independently occur 3 or fewer times in a given implementation. Recursive substituents are an intended aspect of the compounds of the present description. A person skilled in the art of organic chemistry understands the versatility of such substituents. The term “optionally substituted”, as used herein in reference to a particular moiety of the compounds of the present description, means a moiety wherein all substituents are hydrogen or wherein one or more of the hydrogens of the moiety can be replaced by substituents such as those listed under the definition of the term “substituted” or as otherwise indicated. It will be understood that all enantiomers, diastereomers, and racemic mixtures, tautomers, polymorphs, and pseudopolymorphs of compounds within the scope of the formulae and compositions described herein and their agriculturally acceptable salts, are embraced by the present description. All mixtures of such enantiomers and diastereomers are also within the scope of the present description. Various to biocide compositions and methods for the inhibition of microbial pathogens, microbial biofilms and/or insect pests on surfaces are described herein. More particularly, the biocide compositions as described herein include an EDTA derivative that includes a hydrophobic moiety that is covalently bound to the EDTA. In some implementations, the biocide compositions as described herein are biocide compositions and methods for the photodynamic inhibition of microbial pathogens, microbial biofilms and/or insect pests on surfaces. The compositions as described herein can further include at least one photosensitizer compound. In some implementations, the composition can be free of a photosensitizer compound (i.e., the EDTA derivative act as a photodynamic inhibitor and the composition is free of other photosensitizer compounds). It should be understood that the biocide composition can be used alone and the EDTA derivative can act as a biocide active component. Alternatively, the biocide composition can be used in combination with a light source and the EDTA derivative can act as a photodynamic inhibitor and/or as a photodynamic inhibition enhancer. In some preferred implementations, the biocide composition is used alone and the EDTA derivative acts as a biocide active component. The biocide composition is an antimicrobial composition, an antibiofilm composition, and/or an insecticide composition. When the surface is a plant and a combination of EDTA derivative and any other optional photosensitizers, essential oils, biosurfactants, additives, and adjuvants is described herein, an agriculturally effective amount of each one of the components of the combination can be used so as to provide the biocide activity (e.g., pesticidal, antimicrobial, antibiofilm and/or insecticidal activity) while being minimally or non-toxic to humans, minimally or non-toxic to animals, and/or minimally or non-phytotoxic to the host plant, depending on the surface to be treated. When the surface is another biological surface or the surface of devices for contacting a biological surface or for implantation and/or insertion in the body, and a combination of EDTA derivative and a photosensitizer is described herein, a pharmaceutically effective amount of each one of the components of the combination can be used so as to provide the biocide activity (e.g., antimicrobial activity). The use of an EDTA derivative that includes a hydrophobic moiety can provide substantially improved inhibition or photodynamic inhibition of microbial pathogens, microbial biofilms and/or insect pests on surfaces compared to unmodified EDTA. The combined use of an EDTA derivative that includes a hydrophobic moiety, and a photosensitizer compound can provide substantially improved photodynamic inhibition of microbial pathogens, microbial biofilms and/or insect pests on surfaces compared to each used individually. In some implementations, the biocide compositions as described herein are biocide compositions that include an EDTA derivative and a polymer. More details regarding the EDTA derivative and other liquid carriers, additional chelating agents, polymers, photosensitizer compounds, essential oils, biosurfactants, additives, and adjuvants are provided in the present description. EDTA derivatives The EDTA derivative can provide the microbial, biofilm and/or insect pest eradication activities or can substantially enhance the microbial, biofilm and/or insect pest eradication activities of the photosensitizer (if present). Without wishing to be bound by theory, these EDTA derivatives can anchor on and destabilize the bacterial outer membrane, thus facilitating the entry of the photosensitizer in the bacteria and enhance the PDI activity. For a more detailed understanding of the disclosure, reference is first made to Figure 1, which provides a schematic representation a mode of action of an EDTA derivative disturbing bacteria membrane according to a possible implementation. The EDTA derivative can be a compound Formula (I): Formula (I) or a salt thereof, wherein: Z is NH or O; and R ₁ is selected from the group consisting of an optionally substituted C ₄ -C ₂₄ alkyl group, an optionally substituted C ₄ -C ₂₄ alkenyl group, an optionally substituted C ₄ -C ₂₄ alkynyl group, and an optionally substituted steroidyl group. For example, the EDTA derivative can be a compound Formula (IA) or Formula (IB): Formula (IA) Formula (IB) or a salt thereof, wherein: R1 is selected from the group consisting of an optionally substituted C4-C24alkyl group, an optionally substituted C4-C24alkenyl group, an optionally substituted C4-C24alkynyl group, and an optionally substituted steroidyl group. In some implementations, R1 is an optionally substituted C5-C18alkyl, C6-C18alkyl, C7-C18alkyl, C8-C18alkyl, C8-C17alkyl, C8-C16alkyl, C8-C15alkyl, C9-C15alkyl, C10-C15alkyl, C11-C15alkyl, C12-C15alkyl, or C14-C15alkyl group. In some implementations of interest, R1 is an optionally substituted C12-C15alkyl group, and preferably an optionally substituted C14-C15alkyl group. In some other implementations, R1 is an optionally substituted C5-C18alkenyl, C6- C18alkenyl, C7-C18alkenyl, C8-C18alkenyl, C8-C17alkenyl, C8-C16alkenyl, C8-C15alkenyl, C9- C15alkenyl, C10-C15alkenyl, C11-C15alkenyl, C12-C15alkenyl, or C14-C15alkenyl group. In some implementations of interest, R1 is an optionally substituted C12-C15alkenyl group, and preferably an optionally substituted C14-C15alkenyl group. In some other implementations, R1 is an optionally substituted C5-C18alkynyl, C6- C18alkynyl, C7-C18alkynyl, C8-C18alkynyl, C8-C17alkynyl, C8-C16alkynyl, C8-C15alkynyl, C9- C ₁₅ alkynyl, C ₁₀ -C ₁₅ alkynyl, C ₁₁ -C ₁₅ alkynyl, C ₁₂ -C ₁₅ alkynyl, or C ₁₄ -C ₁₅ alkynyl group. In some implementations, R1 is an optionally substituted C14-C15alkynyl group, and preferably is an optionally substituted C14-C15alkynyl group. In some implementations, the steroidyl group is: Non-limiting examples of compounds of Formula (IA) include:

5 or a salt thereof. In some implementations, the compound of Formula (IA) is:

or a salt thereof. In some implementations, the compound of Formula (IA) is:

or a salt thereof. In some implementations, the compound of Formula (IA) is: or a salt thereof. Non-limiting examples of compounds of Formula (IB) include:

or a salt thereof. In some implementations, the compound of Formula (IB) is:

or a salt thereof. In some implementations, the compound of Formula (IB) is: or a salt thereof. In some implementations, the compound of Formula (IB) is: or a salt thereof. Liquid carrier As mentioned above, the biocide compositions of the present description can include a liquid carrier. In some implementations, the liquid carrier can be an aqueous carrier. It is understood that the term “liquid carrier”, as used herein, refers to a liquid that can solubilize and/or disperse the components of the biocide compositions of the present description. In some scenarios, the liquid carrier can include water. In other scenarios, the liquid carrier can be free of water. In some implementations, the liquid carrier can include an organic solvent that can be partially or fully water-soluble, such as tetrahydrofuran, methanol, ethanol, propanol, butanol, or a polyol such as a glycol (e.g., glycerol, propylene glycol, and polypropylene glycol). In some implementations, the liquid carrier can include a nontoxic and/or biodegradable compound that can solubilize and/or disperse the components of the biocide compositions described herein. It is understood that the term “aqueous carrier” means a composition including greater than or equal to 50 wt.% of water and optionally one or more water-soluble compound(s), and/or non-water-soluble solvent(s) that can form an emulsion with water and/or that can be dispersed in water. The aqueous carrier can solubilize and/or disperse the components of the biocide compositions of the present description. Suitable water-soluble compounds (including partially water-soluble compounds) can include, for example, methanol, ethanol, acetone, methyl acetate, dimethyl sulfoxide, or a combination of at least two thereof. In some implementations, the aqueous carrier includes equal to or greater than 80 wt.% of water, or equal to or greater than 90 wt.% of water, or equal to or greater than 95 wt.% of water, or equal to or greater than 99 wt.% of water, based on the total amount of the aqueous carrier. In some scenarios and depending on the components of the biocide composition, making use of a water-soluble compound can help solubilize or disperse the components of the biocide composition in the aqueous carrier. In some implementations, the aqueous carrier can include a compound that is non- water-soluble such as an oil. The oil can be dispersed in the water or can form an oil-in- water emulsion. The oil can be selected from the group consisting of a mineral oil (e.g., paraffinic oil), a vegetable oil, an essential oil, and a mixture thereof. In some scenarios and depending on the components of the biocide composition, making use of an oil can help solubilize or disperse the components of the biocide composition in the aqueous carrier. In other implementations, the aqueous carrier is free of oil. Non-limiting examples of vegetable oils include oils that contain medium chain triglycerides (MCT), or oils extracted from nuts. Other non-limiting examples of vegetable oils include coconut oil, canola oil, soybean oil, rapeseed oil, sunflower oil, safflower oil, peanut oil, cottonseed oil, palm oil, rice bran oil, and a mixture of at least two thereof. Non- limiting examples of mineral oils include paraffinic oils, branched paraffinic oils, naphthenic oils, aromatic oils, and a mixture of at least two thereof. Non-limiting examples of paraffinic oils include various grades of poly-alpha-olefin (PAO). For example, the paraffinic oil can include HT60 ^TM , HT100 ^TM , High Flash Jet, LSRD ^TM , and N65DW ^TM . The paraffinic oil can include a paraffin having a number of carbon atoms ranging from about 12 to about 50, or from about 16 to 35. In some scenarios, the paraffin can have an average number of carbon atoms of about 23. In some implementations, the paraffinic oil can have a paraffin content of at least 80 wt.%, or at least 90 wt.%, or at least 99 wt.%. As used herein, the term “oil-in-water emulsion” refers to a mixture in which the oil is dispersed as droplets in the water. In some implementations, the oil-in-water emulsion is prepared by a process that includes combining the oil, water, and any other components and applying shear until an emulsion is obtained. It should be understood that the liquid carrier typically allows obtaining a stable solution, suspension, and/or emulsion of the components of the biocide composition. Chelating agents The compositions of the present description can further include an additional chelating agent. The additional chelating agent can be an alkylated chelating agent or a non-alkylated chelating agent. For example, the additional chelating agent can be a non- alkylated EDTA. In some implementations, the compositions as defined herein can further include a non-alkylated chelating agent (e.g., a non-alkylated EDTA). In some implementations, the compositions as defined herein can be substantially or completely free (or exempt) of an additional chelating agent. It is to be understood that, in these implementations, the EDTA derivative as defined herein is the only chelating agent present in the compositions as defined herein. In some other implementations, the compositions as defined herein can be substantially or completely free (or exempt) of an additional non-alkylated chelating agent. It is to be understood that, in these implementations, the compositions as defined herein can comprise one or more EDTA derivative(s) as defined herein but cannot include an additional non-alkylated chelating agent. Photosensitizer compounds As mentioned above, the compositions of the present description can further include at least one photosensitizer compound. The photosensitizer compound can be any known compatible photosensitizer compound. The photosensitizer compounds can be used to enable photodynamic inhibition of microbial pathogens, microbial biofilms and/or insect pests on a surface. The photosensitizer compounds react to light by generating ROS. The photosensitizer compounds can also be referred to as ROS generators. Depending on the type of ROS generated, photosensitizers can be classified into two classes, namely Type I photosensitizers, and Type II photosensitizers. On the one hand, Type I photosensitizers form short-lived free radicals through electron abstraction or transfer from a substrate when excited at an appropriate wavelength in the presence of oxygen. On the other hand, Type II photosensitizers form a highly reactive oxygen state known as “singlet oxygen”, also referred to herein as “reactive singlet oxygen species”. Singlet oxygen species are generally relatively long lived and can have a large radius of action. It should be understood that the photosensitizer compound can be metallated or non-metallated. When metallated, as can be the case for various nitrogen-bearing macrocyclic compounds that are complexed with a metal, the metal can be selected to generate either a Type I or a Type II photosensitizer in response to light exposure. For example, when chlorin photosensitizer compounds are metallated with copper, the ROS that are generated are generally Type I photosensitizers. When the same chlorin photosensitizer compounds are metallated with magnesium, the ROS that are generated are typically Type II photosensitizers. Both Type I and Type II photosensitizers can be used to enable photodynamic suppression of microbial pathogens, biofilms, and/or insect pests that can be present on the surface. In some scenarios, the photosensitizer compound is a Type I photosensitizer. In other scenarios, the photosensitizer compound is a Type II photosensitizer. It should be understood that the term “singlet oxygen photosensitizer”, as used herein, refers to a compound that produces reactive singlet oxygen species when excited by light. In other words, the term “singlet oxygen photosensitizer” refers to a photosensitizer in which the Type II process defined above is dominant compared to the Type I process. In some implementations, the photosensitizer compound is a photosensitive nitrogen-bearing macrocyclic compound that can include four nitrogen-bearing heterocyclic rings linked together. In some implementations, the nitrogen-bearing heterocyclic rings are selected from the group consisting of pyrroles and pyrrolines, and are linked together by methine groups (i.e., =CH- groups) to form tetrapyrroles. The nitrogen-bearing macrocyclic compound can, for example, include a porphyrin compound (four pyrrole groups linked together by methine groups), a chlorin compound (three pyrrole groups and one pyrroline group linked together by methine groups), a bacteriochlorin compound or an isobacteriochlorin compound (two pyrrole groups and two pyrroline groups linked together by methine groups), or porphyrinoids (such as texaphrins or subporphyrins), or a functional equivalent thereof having a heterocyclic aromatic ring core or a partially aromatic ring core (i.e., a ring core which is not aromatic through the entire circumference of the ring), or again multi-pyrrole compounds (such as boron- dipyrromethene). It should also be understood that the term “nitrogen-bearing macrocyclic compound” can be one of the compounds listed herein or can be a combination of the compounds listed herein. The nitrogen-bearing macrocyclic compound can therefore include a porphyrin, a reduced porphyrin, or a mixture of at least two thereof. Such nitrogen-bearing macrocyclic compounds can also be referred to as “multi-pyrrole macrocyclic compounds” (e.g., tetra-pyrrole macrocyclic compounds). It should be understood that the term “reduced porphyrin” as used herein, refers to the group consisting of chlorin, bacteriochlorin, isobacteriochlorin, and other types of reduced porphyrins such as corrin and corphin. It should be understood that the nitrogen-bearing macrocyclic compound can be a non-metal macrocycle (e.g., chlorin e6, PPIX, or tetraphenylporphyrin (TPP)) or a metal macrocyclic complex (e.g., Chlorophyll a, Mg-porphyrin, Mg-chlorophyllin, Cu- chlorophyllin, or Fe-protoporphyrin IX etc.). The nitrogen-bearing macrocyclic compound can be an extracted naturally occurring compound, or a synthetic compound. In implementations where the porphyrin or the reduced porphyrin compound is metallated, the metal can be selected such that the metallated nitrogen-bearing macrocyclic compound is a Type I photosensitizer or a Type II photosensitizer that generates reactive singlet oxygen species. For, example in the case of chlorins and porphyrins, non-limiting examples of metals that generally enable generation of reactive singlet oxygen species through the formation of a Type II photosensitizer are Mg, Zn, Pd, Sn, Al, Pt, Si, Ge, Ga, and In. Similarly, non-limiting examples of metals that are known to form Type I photosensitizers when complexed with chlorins and/or porphyrins are Cu, Co, Fe, Ni, and Mn. It should be understood that when a metal species is mentioned without its degree of oxidation, all suitable oxidation states of the metal species are to be considered, as would be understood by a person skilled in the art. In other implementations, the metal species can be selected from the group consisting of Mg(II), Zn(II), Pd(II), Sn(IV), Al(III), Pt(II), Si(IV), Ge(IV), Ga(III), and In(III). In other implementations, the metal species can be selected from the group consisting of Cu(II), Co(II), Fe(II), and Mn(II). In other implementations, the metal species can be selected from the group consisting of Co(III), Fe(III), Fe(IV), and Mn(III). It should also be understood that the specific metals that can lead to the formation of Type II photosensitizers versus the specific metals that lead to the formation of Type I photosensitizers can vary depending on the type of nitrogen-bearing macrocyclic compound to which it is to be bound. It should also be understood that non-metallated nitrogen-bearing macrocyclic compounds can be Type I photosensitizers or Type II photosensitizers. For example, chlorin e6 and protoporphyrin IX are both Type II photosensitizers. It should be understood that the nitrogen-bearing macrocyclic compound to be used in the methods and compositions of the present description can also be selected based on their toxicity to humans or based on their impact on the environment. For example, porphyrins and reduced porphyrins tend to have a lower toxicity to humans as well as enhanced environmental biodegradability properties when compared to other types of nitrogen-bearing macrocyclic compounds such as phthalocyanines. The following formulae illustrate several non-limiting examples of nitrogen-bearing macrocyclic compounds that can be used in the methods and compositions described herein: Porphyrin Chlorin

Protoporphyrin IX (PPIX) Metallated protoporphyrin IX (PPIX) Chlorin e6 Metallated chlorin e6 Tetraphenylporphyrin (TPP) Metallated tetraphenylporphyrin (TPP)

Ce6-mono-DMAE ¹⁵ amide Ce6-bis-DMAE ^15,17 amide Various nitrogen-bearing macrocyclic compounds such as Zn-TPP and Mg- chlorophyllin can be obtained from chemical suppliers such as Organic Herb Inc., Sigma Aldrich or Frontier Scientific. In some scenarios, the nitrogen-bearing macrocyclic compounds are not 100% pure and can include other components such as organic acids and carotenes. In other scenarios, the nitrogen-bearing macrocyclic compounds can have a high level of purity. In some implementations, the photosensitizer compound is: Protoporphyrin IX (PPIX) In some other implementations, the photosensitizer compound is: Mg-chlorophyllin In some other implementations, the photosensitizer compound is: Chlorophyll a In some other implementations, the photosensitizer compound is:

Berberine In some implementations, the photosensitizer compound is selected from the group consisting of a macrocyclic tetrapyrrole compound such as porphyrin or a reduced porphyrin (e.g., chlorin, bacteriochlorin, isobacteriochlorin, corrin, corphin), a diarylheptanoid (e.g., curcumin), a phenothiazinium (e.g., methylene blue, toluidine blue), a squaraine compound, a boron dipyrromethene (BODIPY), an anthraquinone or anthraquinone derivative (e.g., a naphthodianthrone such as hypericin), isoquinoline derivative (e.g., berberine), and a flavin (e.g., riboflavin). Polymer The compositions of the present description can include at least one polymer. In some implementations, the polymer is a biocompatible polymer. The term “biocompatible polymer”, as used herein refers to a polymer that does not alter the body normal functioning and/or does not trigger allergies or other side effects. A biocompatible polymer to be coated on a device to be implanted or inserted in the body may come into contact with blood and should have the capacity to resist protein adsorption and blood cell adhesion. In some implementations, the biocompatible polymer is selected from the group consisting of polyglycolic acid, polylactic-co-glycolic acid, polycaprolactone, polylactic acid, poly(3-hydroxybutyrate-co-3-hydroxyvalerate), chitosan, cellulose and poly(2- methoxyethyl acrylate). In some implementations, moderate biocompatible polymers can be used, such as polystyrene. In some implementations, the biocompatible polymer is selected from the group consisting of polystyrene and polycaprolactone. Bases The compositions of the present description can include at least one base. In some implementations, the EDTA derivative can be combined with a base, such as a weak base, for improved aqueous solubility. Non-limiting examples of bases that can be used include triethanolamine (N(CH ₂ CH ₂ OH) ₃ ), TRIS-buffer ((2-Amino-2-(hydroxymethyl)propane-1,3- diol), sodium bicarbonate (NaHCO ₃ ), potassium bicarbonate (KHCO ₃ ), sodium carbonate (Na ₂ CO ₃ ), or potassium carbonate (K ₂ CO ₃ ). Essential oils The compositions of the present description can include at least one essential oil. The term “essential oil”, as used herein, refers to volatile liquids that can be extracted from plant material. Essential oils are often concentrated hydrophobic liquids containing volatile aroma compounds. Essential oil chemical constituents can fall within several classes of chemical compounds, such as terpenes (e.g., p-cymene, limonene, sabinene, α-pinene, γ-terpinene, β-caryophyllene), and terpenoids (e.g., cinnamaldehyde, eugenol, vanillin, safrole). The essential oil can be natural (i.e., derived from plants), or synthetic. Non- limiting examples of essential oils can include one or more of the following oils: African basil, bishop’s weed, cinnamon, clove, coriander, cumin, garlic, kaffir lime, lime, lemongrass, mustard oil, menthol, oregano, rosemary, savory, Spanish oregano, thyme, anise, ginger, bay leaf, sage, bergamot, eucalyptus, melaleuca, peppermint, spearmint, wintergreen, cannibus, marjoram, orange, rose, and a combination of at least two thereof. In some implementations, the essential oil includes at least one of thymol, eugenol, geranial, nerol, citral, carvacrol, cinnamaldehyde, terpinol, α-terpinene, citronella, citronellal, citronellol, geraniol, geranyl acetate, limonene, lavender oil, orange oil, methyl isoeugenol, and a mixture of at least two thereof. In some implementations, the essential oil includes thymol, carvacrol, or α-terpinene, preferably the essential oil includes thymol. Biosurfactants The compositions of the present description can include at least one biosurfactant selected from the group consisting of an alkyl polyglycoside, a rhamnolipid, a sophorolipid, and a combination of at least two thereof. It is understood that the biosurfactant can be natural or synthetic. The biosurfactant can include an alkyl polyglycoside. The term “alkyl polyglycoside”, as used herein, refers to a non-ionic surfactant, which can be alkoxylated with one or more alkylene oxide groups (e.g., C ₂ -C ₄ alkylene oxide groups). In some implementations, the biosurfactant is an alkyl polyglycoside. In some implementations, the alkyl polyglycoside can be represented by Formula (II): R ₂ O-(R ₃ O) _x (G) _DP Formula (II) wherein: R ₂ is a substituted or unsubstituted C ₆ -C ₂₄ alkyl, C ₆ -C ₂₄ alkenyl or C ₆ -C ₂₄ alkynyl, or an alkylaryl group including a linear or branched C6-C24alkyl group; R3 is an alkylene group comprising from 2 to 4 carbon atoms; G is a saccharide unit comprising from 5 to 6 carbon atoms; x is a value between 0 and 10, or between 0 and 4; and DP is a value ranging from 1 to 15. In some implementations, R2 is a C8-C18alkyl, C8-C18alkenyl or C8-C18alkynyl, which is substituted or unsubstituted. Preferably, R2 is a C8-C18alkyl. Non-limiting examples of substituents for R2 include halogen, -OH, -O-C1-C4alkyl, CF3, and -CN. In some implementations, G is glucose, fructose, or galactose. Preferably, G is glucose. In some implementations, x is between 0 and 3. In some implementations, x = 0. The degree of polymerization of the alkyl polkyglycoside is represented by DP in formula (II) and ranges on average from 1 to 15, or from 1 to 4. Preferably, DP ranges from 1 to 2, or from about 1.1 to about 1.5. The glycoside bonds between the saccharide units can be of 1-6 or 1-4 type. Non-limiting examples of alkyl polyglycosides include the Plantacare ^TM , Glucopon ^TM , NaturalAPG ^TM , APG™ 325 N, and Atlox ^TM products. In some implementations, the biosurfactant is APG™ 325 N or Atlox ^TM . In some implementations, the alkyl polyglycoside is a C ₈ -C ₁₀ alkyl polyglycoside, a C ₉ -C ₁₁ alkyl polyglycoside, a C ₈ -C ₁₆ alkylpolyglycoside, a C ₁₂ -C ₁₆ alkyl polyglycoside, or a C ₁₂ -C ₁₄ alkyl polyglycoside. In some implementations, the alkyl polyglycoside can be added in combination with additives such as sodium sulfate, sodium silicate, sodium coco sulfate, alcohol ethoxylate, and a mixture of at least two thereof. In some implementations, the biosurfactant can include a rhamnolipid. The term “rhamnolipid”, as used herein, implies indistinctively crude or highly purified rhamnolipids. Rhamnolipids are a class of glycolipid produced by microorganisms such as Pseudomonas aeruginosa. Rhamnolipids have a glycosyl head group, such as a rhamnose moiety, and a 3-(hydroxyalkanoyloxy)alkanoic acid (HAA) fatty acid tail, such as 3-hydroxydecanoic acid. Rhamnolipids include mono-rhamnolipids and di- rhamnolipids, which include of one or two rhamnose groups respectively. Rhamnolipids are also typically heterogeneous in the length and degree of branching of the HAA moiety, which varies with the growth media used and the environmental conditions. In some implementations, the rhamnolipid is a compound represented by the following general Formula (III): Formula (III) In some implementations, the compound of Formula (III) is selected such that: r = 0, 1 or 2; q = 0 or 1; R ₄ and R ₅ are each independently a C ₁ -C ₂₄ alkyl, a C ₂ -C ₂₄ alkenyl, or a C ₂ -C ₂₄ alkynyl, preferably a C ₈ -C ₁₈ alkyl, a C ₈ -C ₁₈ alkenyl, or a C ₈ -C ₁₈ alkynyl, wherein R ₄ and R ₅ are each independently optionally branched, optionally substituted with at least one of a halogen, - OH, -O-C ₁ -C ₄ alkyl, CF ₃ , and -CN, and preferably substituted with at least one -OH. In some implementations, the biosurfactant can include a sophorolipid. The term “sophorolipid”, as used herein, refers to a surface-active glycolipid compound that can be synthesized by a number of yeast species. The term “sophorolipid” refers to a compound comprising a residue of sophorose (i.e., the disaccharide consisting of two glucose residues linked by a β-1,2’ bond, and a fatty acid as an aglycone. The sophorolipid can be acetylated on the 6 and/or 6’-positions of the sophorose residue. One terminal or subterminal hydroxylated fatty acid is β-glycosidically linked to the sophorose moiety. The hydroxy fatty acid residue can have one or more unsaturated bonds. The carboxlic group of the fatty acid is either free (acidic or open form) or internally esterified (lactonic form). It is understood that sophorolipids can exist in the form of lactones, either or both in monomeric and in dimeric forms. In some implementations, the sophorolipid is a compound represented by the following general Formula (IV): Formula (IV) In some implementations, the compound of Formula (IV) is selected such that: R6 and R7 are each independently selected from a hydrogen atom and an acetyl (Ac) group; R8 is a hydrogen atom or a methyl group; A is a C8-C24alkylene, a C8-C24alkenylene, or a C8-C24alkynylene which is optionally branched, optionally substituted with at least one of a halogen, -OH, -O-C1-C4alkyl, CF3, and -CN. Additives and adjuvants The compositions of the present description can include at least one additives or adjuvants. In some implementations, a second oil can be added to the composition. The second oil can be selected from the group consisting of a mineral oil (e.g., paraffinic oil) or a vegetable oil, and a mixture of at least two thereof. Non-limiting examples of vegetable oils include oils that contain medium chain triglycerides (MCT), or oils extracted from nuts. Other non-limiting examples of vegetable oils include coconut oil, canola oil, soybean oil, rapeseed oil, sunflower oil, safflower oil, peanut oil, cottonseed oil, palm oil, rice bran oil, and a mixture of at least two thereof. Non- limiting examples of mineral oils include paraffinic oils, branched paraffinic oils, naphthenic oils, aromatic oils, and a mixture of at least two thereof. Non-limiting examples of paraffinic oils include various grades of poly-alpha-olefin (PAO). For example, the paraffinic oil can include HT60 ^TM , HT100 ^TM , High Flash Jet, LSRD ^TM , and N65DW ^TM . The paraffinic oil can include a paraffin having a number of carbon atoms ranging from about 12 to about 50, or from about 16 to 35. In some scenarios, the paraffin can have an average number of carbon atoms of about 23. In some implementations, the oil can have a paraffin content of at least 80 wt.%, or at least 90 wt.%, or at least 99 wt.%. In some implementations, the only oil in the composition is an essential oil (i.e., the composition is free of paraffinic oil or vegetable oil). In some implementations, an additional surfactant can be added to the compositions of the present description. The additional surfactant can be a non-ionic surfactant, a cationic surfactant, an anionic surfactant, a zwitterionic surfactant, or a combination of at least two thereof. Non-limiting examples of non-ionic surfactants include ethoxylated alcohol, a polymeric surfactant, a fatty acid ester, a poly(ethylene glycol), an ethoxylated alkyl alcohol, a monoglyceride, an alkyl monoglyceride, a polysorbate, and a mixture of at least two thereof. For example, the fatty acid ester can be a sorbitan fatty acid ester. The additional surfactant can include a plant-derived glycoside such as a saponin. The additional surfactant can be a polysorbate type surfactant (e.g., Tween™ 80), a silicone polyether copolymer surfactant (e.g., Xiameter™ OFX-0309 silicone surfactant), or another suitable non-ionic surfactant. In some implementations, the poly(ethylene glycol) can include a poly(ethylene glycol) of Formula R ⁹ -O-(EO) _f -R ¹⁰ , wherein: each R ⁹ and R ¹⁰ is each, independently, a hydrogen atom, an alkyl, a substituted alkyl, an aryl, a substituted aryl, a CO(alkyl), or a CO(substituted alkyl); and f is an integer selected from 1 to 100; wherein the substituted alkyl groups are, independently, substituted with one or more of F, Cl, Br, I, hydroxy, alkenyl, CN, and N3. Non-limiting examples of anionic surfactants include sulfate, sulfonate, phosphate, and carboxylates anionic surfactants. Non-limiting examples of anionic surfactants include ammonium lauryl sulfate, sodium lauryl sulfate, SDS, sodium dodecylbenzene sulfonate, sodium lauryl ether sulfate, dioctyl sodium sulfosuccinate, perfluorooctane sulfonate, alkyl-aryl ether phosphates, alkyl ether phosphates, and sodium stearate. The additional surfactant can be a sodium alkylnaphthalene sulfonate condensate (NSC) (e.g., Morwet™ D-400) or another suitable anionic surfactant. Non-limiting examples of cationic surfactants include primary, secondary, or tertiary amines that become positively charged at a pH lower than about 10, such as octenidine dihydrochloride. Another non-limiting example of a cationic surfactant includes permanently charged quaternary ammonium salts such as cetrimonium bromide (CTAB), cetylpyridinium chloride (CPC), benzalkonium chloride (BAC), benzethonium chloride (BZT), dimethyldioctadecylammonium chloride, and dioctadecyldimethylammonium bromide (DODAB). Non-limiting examples of zwitterionic surfactants include sultaines such as 3-[(3- cholamidopropyl)dimethylammonio]-1-propanesulfonate or betaines such as cocamidopropyl betaine. Solvents The compositions of the present description can include at least one solvent. In some implementations, the composition further includes an aqueous solvent such as water or an aqueous solution of phosphate-buffered saline (PBS). In some implementations, the composition includes a non-aqueous solvent. In some implementations, the composition includes water and a non-aqueous solvent. In some implementations, the non-aqueous solvent is at least partially soluble in water. Non- limiting examples of non-aqueous solvents include ethanol, acetone, isopropanol, ethylene glycol, pyrrolidone, propylene glycol, and a mixture of at least two thereof. The composition can include between about 0.1 wt.% and about 50 wt.%, or between about 0.1 wt.% and about 20 wt.%, or between about 0.1 wt.% and about 15 wt.%, or between about 0.1 wt.% and about 10 wt.%, or between about 0.1 wt.% and about 5 wt.% of a non- aqueous solvent, based on a total weight of the composition. In other implementations, the composition is free of a non-aqueous solvent. Biocide compositions It should be understood that the components of the biocide combination can be provided together as part of a biocide composition. In some implementations, the components of the biocide composition can be packaged in a concentrated form, without water or with little water, and water can be added to form the composition directly by the operator that can then apply the biocide composition to the surface. The biocide composition can be provided as a single-pack system or as a multiple-pack system (e.g., a 2-pack system in which each one of the two packs includes at least one separate component of the biocide composition). For example, the EDTA derivative can be provided as in a first pack and another component of the biocide composition (e.g., the optional photosensitizers, bases, essential oils, biosurfactants, additives or adjuvants, and/or the optional solvents described herein) can be provided in a second pack. The optional photosensitizers described herein, the optional bases described herein, the optional essential oils described herein, the optional biosurfactants described herein, the optional additives or adjuvants, and/or the optional solvents described herein could also be provided by a user. For example, a user can combine the single-pack system or each pack of the multiple-pack system with water (or an appropriate solvent) prior to use. Properties of the biocide compositions In some scenarios, the antimicrobial compositions of the present description can have antibacterial, anti-fungi and/or anti-viral properties. In some scenarios, the antimicrobial compositions of the present description are effective against biofilms comprising at least one of gram-negative bacteria and gram-positive bacteria. In some scenarios, the antimicrobial compositions of the present description are effective against biofilms comprising gram-negative bacteria and gram-positive bacteria. In some scenarios, the biocide compositions of the present description are effective against fungal biofilms comprising at least one fungus (e.g., C. auris). In some scenarios, the insecticide compositions of the present description can be used to increase mortality of insect pests. Concentrations of the component of the biocide composition In some scenarios, the components of the biocide composition are provided as part of a single composition and the ready-to-use composition can be provided to have certain concentrations. For example, the ready-to-use composition can include of the EDTA derivative at a concentration between about 3 µg/mL and about 130 µg/mL, or between about 3 µg/mL and about 120 µg/mL, or between about 3 µg/mL and about 110 µg/mL, or between about 3 µg/mL and about 100 µg/mL, or between about 3 µg/mL and about 90 µg/mL, or between about 3 µg/mL and about 80 µg/mL, or between about 3 µg/mL and about 70 µg/mL, or between about 3 µg/mL and about 60 µg/mL, or between about 3 µg/mL and about 50 µg/mL, or between about 3 µg/mL and about 40 µg/mL, or between about 3 µg/mL and about 30 µg/mL, or between about 3 µg/mL and about 20 µg/mL, or between about 3 µg/mL and about 10 µg/mL, or between about 3 µg/mL and about 5 µg/mL, limits included. In some preferred implementations, the ready-to-use composition can include of the EDTA derivative at a concentration between about 3 µg/mL and about 10 µg/mL, limits included. Concentrations of the component of the biocide composition when used in combination with light (PDI biocide composition) In some scenarios, the biocide composition is used in combination with light and the components are provided as part of a single composition. The ready-to-use composition can be provided to have certain concentrations and relative proportions of components. The ready-to-use composition can include between about 0.005 wt.% and about 2 wt.%, or between about 0.01 wt.% and about 1.5 wt.%, or between about 0.01 wt.% and about 1 wt.%, or between about 0.01 wt.% and about 0.9 wt.%, or between about 0.01 wt.% and about 0.8 wt.%, or between about 0.01 wt.% and about 0.7 wt.%, or between about 0.01 wt.% and about 0.6 wt.%, or between about 0.01 wt.% and about 0.6 wt.% of the EDTA derivative, based on a total weight of the composition. When the components are provided as part of a single composition, the ready-to- use composition can be provided to have certain concentrations and relative proportions of components. The ready-to-use composition can include between about 0.001 wt.% and about 1 wt.%, or between about 0.01 wt.% and about 0.9 wt.%, or between about 0.01 wt.% and about 0.8 wt.%, or between about 0.01 wt.% and about 0.7 wt.%, or between about 0.01 wt.% and about 0.6 wt.%, or between about 0.01 wt.% and about 0.5 wt.%, or between about 0.01 wt.% and about 0.4 wt.%, or between about 0.01 wt.% and about 0.3 wt.% of the photosensitizer compound, based on a total weight of the composition. The ready-to-use composition can include between about 0.05 wt.% and about 2.5 wt.%, between about 0.05 wt.% and about 2 wt.%, or between about 0.05 wt.% and about 1.5 wt.%, or between about 0.05 wt.% and about 1 wt.%, or between about 0.05 wt.% and about 0.5 wt.%, or between about 0.1 wt.% and about 0.5 wt.% of biosurfactant, based on a total weight of the composition. The ready-to-use composition can include between about 0.01 wt.% and about 4.5 wt.%, between about 0.01 wt.% and about 3 wt.%, or between about 0.01 wt.% and about 2 wt.%, or between about 0.01 wt.% and about 1 wt.%, or between about 0.01 wt.% and about 0.5 wt.%, or between about 0.01 wt.% and about 0.1 wt.% of essential oil, based on a total weight of the composition, if present in the ready-to-use composition. The ready-to-use composition can include between about 0.01 wt.% and about 1 wt.%, or between about 0.01 wt.% and about 0.9 wt.%, or between about 0.01 wt.% and about 0.8 wt.%, or between about 0.01 wt.% and about 0.7 wt.%, or between about 0.01 wt.% and about 0.6 wt.%, or between about 0.01 wt.% and about 0.5 wt.%, or between about 0.01 wt.% and about 0.4 wt.%, or between about 0.01 wt.% and about 0.3 wt.%, or between about 0.01 wt.% and about 0.2 wt.% of the base, if present in the ready-to-use composition. In some scenarios where the surface is another biological surface or the surface of devices for contacting a biological surface or for implantation and/or insertion in the body, the biocide composition can comprise a polymer and between about 0.1 wt.% and about 10 wt.%, or between 1 wt.% and about 8 wt.%, or between 2 wt.% and about 6 wt.%, or between 3 wt.% and about 5 wt.%, or between 0.1 wt.% and about 2 wt.%, or between 1 wt.% and about 2 wt.% of the EDTA derivative, based on a total weight of the composition. In some scenarios, the biocide composition comprising the EDTA derivative, the liquid carrier and the biocompatible polymer further comprises a solvent. The solvent refers to a liquid that can solubilize and/or disperse the components of the biocide compositions of the present description. In some scenarios, the solvent can include water. In other scenarios, the liquid carrier can be free of water. In some implementations, the solvent can include organic solvents that are partially or fully water-soluble, such as tetrahydrofuran, methanol, ethanol, propanol or butanol, or polyols such as glycols (e.g., glycerol, propylene glycol, polypropylene glycol). In some implementations, the solvent refers to a nontoxic and biodegradable solvent that can solubilize and/or disperse the components of the biocide compositions described herein. Synergistic effect of the combinations In some scenarios, the components of the biocide compositions of the present description can exhibit a synergistic response for inhibiting the formation of microbial pathogens and/or biofilms and/or for disrupting or killing existing microbial pathogens, preformed biofilms or insect pests. It should be understood that the terms “synergy” or “synergistic”, as used herein, refer to the interaction of two or more components of a combination (or composition) so that their combined effect is greater than the sum of their individual effects. This can include, in the context of the present description, the action of the EDTA derivative and at least one of the optional photosensitizer compounds, essential oils, biosurfactants and additives or adjuvants, if present. In some scenarios, the EDTA derivative and the photosensitizer compound can be present in synergistically effective amounts. In some scenarios, the EDTA derivative and the photosensitizer compound and optionally at least one of the essential oil, the biosurfactant and the additive or adjuvant can be present in synergistically effective amounts. Treatment It is also noted that the biocide compositions described herein can have various inhibitory effects on the microbial pathogens, biofilms and/or insect pests depending on the type of surface and microbial pathogens, biofilms, and/or insect pests as well as the state of microbial, biofilm and/or insect pest infection. While herein it is described that the biocide composition can inhibit microbial pathogen and/or biofilm growth and/or control insect population on a surface, such expressions should not be limiting but should be understood to include suppression of microbial pathogens and/or biofilms, prevention against microbial pathogens, biofilms and/or insect pests, destruction of microbial pathogens and/or biofilms, killing insect pests or generally increasing toxicity toward microbial pathogens, biofilms and/or insect pests. Preventive treatment The present description also relates to a method for inhibiting microbial pathogen, biofilm formation and/or controlling insect pest population on a surface. The method includes applying the biocide composition as described herein to a surface. Any compatible method to apply the biocide composition to the surface is contemplated. For instance, the biocide composition can be applied to the surface under conditions that provide a substantially uniform coverage of the biocide composition on the surface. In some scenarios where the surface is a plant, the biocide composition can be applied to plant, for example, using track sprayer. In some implementations, the method for inhibiting microbial pathogen, biofilm formation and/or controlling insect pest population on a surface can also include exposing the treated surface to illumination to induce PDI. Disinfection or curative treatment The present description also relates to a method for disrupting or killing pre-existing microbial pathogens, biofilms and/or insect pests on a surface. The method includes applying the biocide composition as described herein to a surface infected with a microbial pathogen, a biofilm and/or insect pests. Any compatible method to apply the biocide composition to the infected surface is contemplated. For instance, the biocide composition can be applied to the infected surface under conditions that provide a substantially uniform coverage of the biocide composition on the infected surface. In some scenarios where the surface is a plant, the biocide composition can be applied to the infected plant, for example, using a track sprayer. For instance, the biocide composition can be applied to the infected plant under conditions that provide a substantially uniform coverage of the biocide composition on the infected plant. The method for disrupting or killing pre-existing microbial pathogens, biofilms and/or insect pests on a surface can further include exposing the treated surface to illumination to induce PDI. Wound treatment It is also noted that the biocide compositions described herein can have various inhibitory effects on the microbial pathogens depending on the type of biological surface and microbial pathogens as well as the state of microbial infection. While herein it is described that the biocide composition can inhibit microbial pathogen on a biological surface, such expressions should not be limiting but should be understood to include suppression of microbial pathogens, prevention against microbial pathogens, destruction of microbial pathogens or generally increasing toxicity toward microbial pathogens. The present description also relates to biocide compositions for the treatment of wounds, wherein the treatment of wounds consists in healing the wound, and / or inhibiting or preventing microbial pathogen activity in the wound. In some implementations, healing the wound consists in tissue regeneration and / or wound closing and / or wound contraction (i.e., a healing response involving the reduction of the size of the tissue defect and subsequent decrease of the amount of damaged tissue that needs repair). In some implementations, inhibiting or preventing microbial pathogen activity includes suppression of microbial pathogens, prevention against microbial pathogens, destruction of microbial pathogens or generally increasing toxicity toward microbial pathogens. In some implementations, the biocide compositions are used for the treatment of wounds and infections resulting from mastitis. Mastitis is an inflammation of the breast that occurs most often in mammals who are breastfeeding. Mastitis can be caused by poor milk flow from the breast. When milk builds up in a breast, the milk leaks into the nearby breast tissue. Infection can also develop when a nipple of a mammal becomes cracked and/or irritated. The tissue can then become infected with bacteria. The treatment of wounds and infections resulting from mastitis includes healing the wound, and / or inhibiting or preventing microbial pathogen activity in the wound. Applications The biocide compositions of the present description can be used on any compatible surface. Any compatible use of the biocide compositions of the present description is contemplated. In some scenarios, the biocide composition of the present description is used in the agricultural industry or the health care industry. For example, the biocide compositions of the present description can be used in the medical or veterinary sector. In some scenarios where the surface is a plant, the biocide compositions described herein can have various inhibitory effects on the microbial pathogens, biofilms and/or insect pests depending on the type of plant and pathogens or insect pests as well as the state of microbial, biofilm and/or pest infection. While herein it is described that the biocide composition can inhibit microbial pathogen and/or biofilm growth and/or control insect population on a plant, such expressions should not be limiting but should be understood to include suppression of microbial pathogens and/or biofilms, prevention against microbial pathogens, biofilms and/or insect pests, destruction of microbial pathogens and/or biofilms, killing insect pests or generally increasing toxicity toward microbial pathogens, biofilms and/or insect pests. In some scenarios, the biocide compositions are used for the treatment of wounds and infections resulting from mastitis. Any compatible use of the biocide compositions of the present description is contemplated. For example, the biocide compositions of the present description can be used in the medical or veterinary sector and more particularly in the agricultural sector such as to treat mammals used in dairy production. For example, the biocide compositions of the present description can be applied to the teats of dairy livestock. In some scenarios, the biocide compositions are used to coat medical devices for implantation or insertion into the body. For example, the biocide compositions of the present description can be used to coat tubes and catheters. For example, the biocide compositions of the present description are applied to the apparatus used to milk dairy livestock. EXAMPLES The following non-limiting examples are illustrative and should not be construed as further limiting the scope of the claims. These examples will be better understood in combination with the accompanying Figures. Unless otherwise indicated, all numbers expressing quantities of components, preparation conditions, concentrations, properties, and so forth used herein are to be understood as being modified in all instances by the term “about.” At the very least, each numerical parameter should be construed in light of the number of reported significant digits and by applying ordinary rounding techniques. Accordingly, unless indicated to the contrary, the numerical parameters set forth herein are approximations that can vary depending upon the properties sought to be obtained. Notwithstanding that the numerical ranges and parameters setting forth the broad scope of embodiments are approximations, the numerical values set forth in the following examples are reported as precisely as possible. Any numerical value, however, inherently contains certain errors resulting from variations in experiments, testing measurements, statistical analyses, etc. Example 1 – Biological or non-biological surface applications Example 1(a) – PPIX-based photosensitizer composition including an alkylated EDTA enhancer Synthesis of alkylated EDTA derivatives Synthesis of alkylated EDTA derivatives were carried out by a process as illustrated in Scheme 1 below: Scheme 1 Synthesis of alkylated EDTA derivatives were performed as previously reported (see Jaeger, D. A., et al. "A surfactant transition metal chelate." Langmuir 19.11 (2003): 4859- 4862). Ethylenediaminetetraacetic dianhydride (EDTAD) (16.73 g, 65.3 mmol) was dissolved in dry N,N-dimethylformamide (DMF) (80 mL) in a round-bottom flask at a temperature of about 70°C. Then water (0.94 mL, 52.2 mmol) diluted in 10 mL of dry DMF was added dropwise into the flask in about 30 minutes. Subsequently, the reaction mixture was stirred for about 2 hours at a temperature of about 70°C and cooled to room temperature to give ethylenediaminetetraacetic monoanhydride (Intermediate 1) as a precipitate. The solid was filtered, washed with 50 mL of dry DMF and dried under vacuum. Then Intermediate 1 (17.92 g, 65.3 mmol) and alkylamine (58.8 mmol) were added into 70 mL of dry DMF and stirred for about 10 hours at a temperature of about 70°C. Afterwards, the reaction mixture was cooled to room temperature and poured into water (400 mL). The precipitate was collected by centrifugation and washed with 50 mL of water. The EDTA derivatives were obtained after lyophilization. The molecular weights of alkylated EDTA derivatives were validated by qTOF-MS (Figures 2 to 7) and presented in Table 1 below. Table 1. Calculated and determined molecular weights of EDTA-mono-C8, C12, C14, C15, C16, and C18-amide Bacterial strains S.au was purchased from China General Microbiological Culture Collection Center, the sequence analysis identified it originated from Staphylococcus aureus strain ATCC 12600™, the identical percentage was 99.57%. The bacteria were grown on LB cultural agarose media dish and sealed well. Preparation of bacteria Bacterial strains were thawed in an ultra-low temperature freezer, shake overnight in LB broth medium for at least 16 hours at a temperature of 37°C in an atmosphere containing 5% of CO ₂ . The bacteria suspension was diluted with fresh broth to an optical density measured at a wavelength of 600 nm (OD ₆₀₀ ) of 0.3, which contains approximately 1×10 ⁹ CFU/mL bacteria, the antibacterial assays against planktonic S.au were conducted at this concentration. Photosensitizer and illuminator PPIX (purchased from MACKLIN corporation) was dissolved to 1 mg/mL with ultrapure water. 0.1 mM NaOH was used to adjust the pH to a value of about 10.0 to completely dissolve the PPIX. The solution was stored at 4°C in the dark. The illuminator (purchased from Youke Instrument & Equipment Corporation) was fitted with an LED light source and added with an extra 640 nm red light. The distance between the light source and the sample was about 30 cm, and the maximum illumination intensity at this position was approximately 10000 lux, equivalent to 20 µmol/m ² /s, 10 mW/cm ² , 0.01 J/cm ² ·s. All experiments conducted under illumination were carried out at the maximum intensity. Bacterial viability assay for different drug combinations The conventional plate counting method was used to measure the antimicrobial ability of PPIX in the presence and absence of light. The light-treated groups were illuminated under the illuminator described above at different times. S.au bacterial fluid of OD600 = 0.3 was added to a 96-well plate, 80 µL (approximately 1x10 ⁸ CFU) per well.10 µL PPIX and 10 µL non-alkylated EDTA or alkylated EDTA were added into the well to reach a final volume of 100 µL. The final concentration of PPIX was 5/10/100 μg mL ^-1 , the final concentration of non-alkylated EDTA was 0.5 mM, and final concentration of alkylated EDTA was 0.05 mM. The well was preincubated under dark conditions at room temperature (from about 20°C to about 30°C) for 1 hour, then illuminated for 1 hour, 2 hours, or 3 hours, followed by a broth dilution method to test the antimicrobial activities of the drugs. Biofilm eradication assay The MTT method was employed to assess the biofilm eradication ability of the compounds. Briefly, exponentially growing S.au bacterial suspension containing 1x10 ⁹ CFU S.au per mL in LB medium was prepared as mentioned above, added to a 96-well plate (200 µL/well) to form a mature biofilm after incubating the plate at 37°C for 24 hours. The mature biofilm was then rinsed 3 times with saline to remove the unbound planktonic bacteria.100 µL of PPIX of different concentrations (5 μg mL ^-1 , 10 μg mL ^-1 , 100 μg mL ^-1 ) combined with non-alkylated EDTA or EDTA-mono-C14-amide having a concentration of 0.05 mM, 0.1 mM, and 0.5 mM were mixed in saline and treated on the biofilms. The PPIX treated group was used for comparison, and untreated biofilm was used as a negative control. The plate was placed at a temperature of 37°C under static conditions. The supernatant which consisted of floating bacteria and destructed biofilm debris was removed after 24 hours of incubation. The biofilm residual was gently rinsed 3 times with saline and subjected to a 200 µL MTT solution (containing 20 µL 5 mg/mL of MTT and 180 µL of LB broth medium). Formazan sediments indicated the number of bacteria alive in the biofilms after 2~4 hours of incubation at a temperature of 37°C. Then the formazan was solubilized in DMSO (150 µL/well) for 15 minutes. The absorbance at an optical density measured at a wavelength of 490 nm (OD490) was measured, and the biofilm viability was proportioned by comparing it with the untreated group. Biofilm live/dead staining assay Mature biofilms were created by incubating 1x10 ⁷ CFU bacteria on a sterile confocal plate for 24 hours, removing the unbound floating bacteria then rinsing the biofilm with saline 3 times.10 μg mL ^-1 PPIX, or 10 μg mL ^-1 PPIX + 0.1 mM non-alkylated EDTA or alkylated EDTA were employed and illuminated for 1 hour, 2 hours, and 3 hours. After washing with saline adequately, the residual biofilms were stained with SYTO 9 dye (10 µg.mL ^-1 ) and propidium iodide (10 µg.mL ^-1 ) for 15 minutes. Afterward, the plates bearing biofilms on them were observed using a confocal laser scanning microscope (CLSM). Reactive oxygen species (ROS) detection A DCFH-DA detector was used to detect the ROS generation efficiency. DCFH- DA was dissolved in DMSO to obtain a stock having a concentration of 10 mM and stored at a temperature of -20°C in the dark. S.au were incubated overnight with shaking to reach an exponentially growing state. PPIX (10 μg mL ^-1 ), PPIX with non-alkylated EDTA (0.5 mM, 0.05 mM) or EDTA-mono-C14-amide (0.05 mM) were mixed with a S.au solution (approximately 1x10 ⁹ CFU) to obtain a total volume of 500 µL in a 24-well plate. A final concentration of 0.01 mM DCFH-DA was added to the mixed solution after being kept for 1 hour in the dark and incubated for another 15 minutes at room temperature. The plate was illuminated for 30 minutes, and the bacteria solutions in the wells were transferred to tubes. The bacteria sediments were collected by centrifugation and washed 3 times with saline. ROS fluorescent signal (Ex:488; Em:525) was detected by flow cytometry. Statistical analysis All experiments were repeated three times, and the quantitative data were presented as means ± standard deviation. Student’s T-tests was used to analyze the significance of differences between the two groups. The results were considered to be of significant difference when P < 0.05 (*),P < 0.01 (**), P < 0.001 (***), and P < 0.0001 (****). Evaluation of the concentration of PPIX in PDI antibacterial performance Generally, a photosensitizer will have a weak fluorescence if it produces singlet oxygen effectively. Nonetheless, for PPIX, the poor water solubility and readily aggregation quench its fluorescence as well as singlet oxygen production. The relationships between the concentration of PPIX, fluorescence intensity, and PPIX particle size were investigated to assess the correlation with the inactivation efficacy of bacteria. The fluorescence intensity of PPIX in DMSO at different concentrations (Figure 8(a)) was measured first. The fluorescence intensity increased with increasing PPIX concentration, reached the maximum at around 10 μg mL ^-1 , then decreased thereafter. Then, PPIX in water at three representative concentrations (5 μg mL ^-1 , 10 μg mL ^-1 , 100 μg mL ^-1 ) at pH ranging from 7 to 11 were tested (Figure 8(b)). A similar trend was found, where 10 μg mL ^-1 PPIX had the highest fluorescence intensity, but 100 μg mL ^-1 gave weak fluorescence. The higher fluorescence intensity at 10 μg mL ^-1 PPIX is indicative of smaller particle sizes or a weaker tendency to aggregate at this concentration. Indeed, the DLS measurement showed that PPIX at 10 μg mL ^-1 had a primary peak at 30 nm and a secondary peak at 150 nm, whereas 5 and 100 μg mL ^-1 yielded larger particles, even including aggregates of 5500 nm (Figure 8(c)). Scanning electron microscope back- scattering electron images examination further confirmed this observation (Figure 8(e)). The antibacterial PDI activity of PPIX at the three concentrations mentioned above was evaluated using the plate counting assay of the viability of planktonic S.au pathogens, a Gram-positive model microbial, in terms of the CFU after 2 hours of illumination. Compared with the control group, the treatment with 10 μg mL ^-1 or 5 μg mL ^-1 PPIX decreased the bacterial viability by 2 or 1.5, whereas the treatment with 100 μg mL ^-1 had no effects on bacterial proliferation (Figure 8(d)). This result validates the critical role of concentration-dependent aggregation in the PDI activity of PPIX. Non-alkylated EDTA and alkylated EDTA improved PPIX photoinactivation on planktonic S.au. We then sought to validate whether alkylated EDTA derivatives could enhance the PDI activity of PPIX. The alkylated EDTA with different alkyl chains (EDTA-mono-C8, C12, C14, C15, C16, or C18-amide) were synthesized as described above and characterized by proton nuclear magnetic resonance ( ¹ H NMR) and liquid chromatography–mass spectrometry (LC–MS) for mass and structure confirmation. The conventional plate counting method was used to identify the PPIX-mediated PDI enhancement by non- alkylated EDTA and alkylated EDTA. EDTA alkylated with different alkyl chain lengths were synthesized and compared with non-alkylated EDTA as enhancers in PDI of PPIX. S.au solution of OD600 = 0.3 (approximately 1 x 10 ⁸ CFU) was treated with 10 μg mL ^-1 PPIX with non-alkylated EDTA or EDTA-mono-C8, C12, C14, C15, C16, or C18-amide and illuminated for 1 hour, 2 hours, and 3 hours. The results are shown in Figure 9. The results demonstrated that both non-alkylated EDTA and alkylated EDTA significantly enhanced the PDI activity of PPIX, but alkylated EDTA had a substantially higher activity than non-alkylated EDTA. PPIX alone only reduced the CFU by 2 Log10- unit in 3 hours. PPIX with 0.05 mM or 0.5 mM non-alkylated EDTA reduced the CFU by 3 or 4.5 Log10-unit. By comparison, PPIX with 0.05 mM EDTA-mono-C12, C14 and C15- amide gave a reduction of 8 Log10-unit, all bacteria were eliminated in 3 hours. The alkyl chain length affected the sensitizing activity of alkylated EDTA. Short or long alkyl chains lowered the alkylated EDTA activity. It was determined that EDTA-mono- C8-amide, EDTA-mono-C16-amide, and EDTA-mono-C18-amide had the lowest sensitizing activity, and EDTA-mono-C14-amide performed the best, which enabled PPIX to eliminate all bacteria after 2 hours of illumination. EDTA-mono-C12-amide and EDTA- mono-C15-amide also exhibited potent sensitizing activities, whose combination with PPIX eliminated the bacteria after 3 hours of illumination. It was demonstrated that EDTA- mono-C12-amide, EDTA-mono-C14-amide and EDTA-mono-C15-amide had outstanding synergistic activity potentiating PPIX-mediated photo-inactivation on S.au. 5 μg mL ^-1 or 100 μg mL ^-1 PPIX PDI activity combined with non-alkylated EDTA or EDTA-mono-C12-amide, EDTA-mono-C14-amide and EDTA-mono-C15-amide were evaluated, and the results are shown in Figures 10 and 11, respectively. The results were the same with 10 μg mL ^-1 that alkylated EDTA significantly performed better than non- alkylated EDTA at the two PPIX concentrations. Also as expected, PPIX PDI activities enhanced by non-alkylated EDTA or alkylated EDTA were in accordance with its fluorescence intensity, it is to be understood that 10 μg mL ^-1 > 5 μg mL ^-1 > 100 μg mL ^-1 . For instance, EDTA-mono-C14-amide with 100 μg mL ^-1 or 5 μg mL ^-1 PPIX reduced 3 or 6 Log10-unit in 2 hours, in contrast with 8 Log10-unit at 10 μg mL ^-1 . It should be noted that such potent PDI activity of porphyrin derivatives is unusual. For example, Photogem™ a hematoporphyrin derivative used with success in many clinical cases such as skin cancer and inactivation of bacteria, could only reduce the S.au CFU by 6 logs at a concentration of 12 μg/mL and a light fluence of 60 J/cm ² (see GOIS, M. M., et al. "Susceptibility of Staphylococcus aureus to porphyrin-mediated photodynamic antimicrobial chemotherapy: an in vitro study." Lasers in medical science 25 (2010): 391- 395). In contrast, it was shown that the combination of 10 μg/mL of PPIX and 0.05 mM of EDTA-mono-C14-amide can substantially eradicate the same amount of S.au (> 8 logs) at the same light fluence. Alkylated EDTA improved Mg-chlorophyllin photoinactivation on S.au. The antibacterial PDI activity of Mg-chlorophyllin at three representative concentrations (64 ppm, 256 ppm, 512 ppm) was evaluated using the plate counting assay of the viability of S.au pathogens, in terms of the CFU after 1 hour of illumination. S.au bacterial fluid was adjusted to OD600 = 0.5, and then diluted 200 times.400 µL of the S.au bacterial fluid was then added to a 48-well plate (approximately 1x10 ⁹ CFU/mL) per well.100 µL of Mg-chlorophyllin (64 ppm, 256 ppm, 512 ppm) with EDTA- mono-C14-ester (0.05 mM) were added into the wells. The well was the incubated under dark conditions at room temperature for 0.5 hour, then illuminated for 1 hour. The fluid was then diluted (10-fold) in a 96-well plate.10 µL of the fluid was then coated on a solid LB medium. The colonies were counted after 24 hours of incubation at a temperature of 37°C. Figure 12 shows that the antibacterial effect of Mg-chlorophyllin with EDTA-mono- C14-ester is substantially superior to that of Mg-chlorophyllin alone at the three representative concentrations and to that of EDTA-mono-C14-ester alone. Alkylated EDTA improved Mg-chlorophyllin photoinactivation on Pst. The antibacterial PDI activity of Mg-chlorophyllin at three representative concentrations (64 ppm, 256 ppm, 512 ppm) was evaluated using the plate counting assay of the viability of Pst. pathogens, in terms of the CFU after 1 hour of illumination. Pst. bacterial fluid was adjusted to OD600 = 0.5, and then diluted 200 times.400 µL of the Pst. bacterial fluid was then added to a 48-well plate (approximately 1x10 ⁹ CFU/mL) per well.100 µL of Mg-chlorophyllin (64 ppm, 256 ppm, 512 ppm) with EDTA- mono-C14-ester (0.05 mM) were added into the wells. The well was the incubated under dark conditions at room temperature for 1 hour, then illuminated for 1 hour. The fluid was then diluted (10-fold) in a 96-well plate.10 µL of the fluid was then coated on a solid LB medium. The colonies were counted after 24 hours of incubation at a temperature of 37°C. Figure 13 shows that the antibacterial effect of Mg-chlorophyllin with EDTA-mono-C14-ester is substantially superior to that of Mg-chlorophyllin alone at the three representative concentrations and to that of EDTA-mono-C14-ester alone. Figure 14 shows efficacy results of Mg-chlorophyllin-mediated PDI alkylated EDTA enhancers against Pst. Efficacy results are shown for Mg-chlorophyllin (512 ppm) with EDTA-mono-C10-ester (0.05 mM) after 1 hour. The results were obtained by the method described in the present example. Figure 14 shows that the antibacterial effect of Mg- chlorophyllin with EDTA-mono-C10-ester is substantially superior to that of Mg- chlorophyllin alone and to that of EDTA-mono-C10-ester alone. Alkylated EDTA improved berberine photoinactivation on S.au. S.au bacterial fluid was adjusted to OD600 = 0.5, and then diluted to the appropriate bacterial concentration.400 µL of the S.au bacterial fluid was then added to a 48-well plate (approximately 1x10 ⁹ CFU/mL) per well.100 µL of berberine (50 ppm) with EDTA-mono-C14-amide (0.05 mM) were added into the wells. The well was the incubated under dark conditions at room temperature for 0.5 hour, then illuminated for 1 hour. The fluid was then diluted (10-fold) in a 96-well plate.10 µL of the fluid was then coated on a solid LB medium. The colonies were counted after 24 hours of incubation at a temperature of 37°C. Figure 15 shows that the antibacterial effect of berberine with EDTA-mono-C14- amide is substantially superior to that of berberine alone and to that of EDTA-mono-C14- amide alone. Alkylated EDTA improved curcurmin photoinactivation on S.au. S.au bacterial fluid was adjusted to OD600 = 0.5, and then diluted to the appropriate bacterial concentration.400 µL of the S.au bacterial fluid was then added to a 48-well plate (approximately 1x10 ⁹ CFU/mL) per well.100 µL of curcurmin (256 ppm) with EDTA-mono-C14-amide (0.05 mM) were added into the wells. The well was the incubated under dark conditions at room temperature for 1 hour, then illuminated for 1 hour. The fluid was then diluted (10-fold) in a 96-well plate.10 µL of the fluid was then coated on a solid LB medium. The colonies were counted after 24 hours of incubation at a temperature of 37°C. Figure 16 shows that the antibacterial effect of curcurmin with EDTA- mono-C14-amide is substantially superior to that of curcurmin alone and to that of EDTA- mono-C14-amide alone. PPIX with non-alkylated EDTA or alkylated EDTA eradicated biofilms Alkylated EDTA, especially EDTA-mono-C14-amide, exhibited excellent PPIX PDI efficacy against S.au planktonic pathogen lightened interest in further investigating its biofilm eradication capacity. The viability of biofilms was assessed by MTT assay. MTT could react with succinate dehydrogenase inside of mitochondrion in living cells, forming water-insoluble formazan sedimented at the bottom. The formazan could be dissolved in DMSO and the absorbance at 490 nm can be measured to quantify the number of live cells. The absorbance values determined in each group were proportioned to the untreated group. The viability of biofilms decreased with increasing PPIX concentrations. PPIX in combination with EDTA-mono-C14-amide had better biofilm eradication capacity than non-alkylated EDTA. For example, biofilms treated with 10 μg mL ^-1 PPIX remained 70% viable in 1 hour. 10 μg mL ^-1 PPIX with 0.05 mM and 0.5 mM non-alkylated EDTA eradicated 30% and 60% of the biofilms respectively (Figure 17(a)), while PPIX with EDTA-mono-C14-amide destroyed 50% and 80% at the same concentrations (Figure 17(c)). 2 hours of illumination on the biofilms was also conducted to achieve a better biofilm eradication effect. Almost 80% of eradication could be observed when 10 μg mL ^-1 PPIX was combined with 0.5 mM non-alkylated EDTA (Figure 17(b)), while more than 90% of the biofilm was eradicated when treated with 10 μg mL ^-1 PPIX and 0.05 mM EDTA- mono-C14-amide (Figure 17(d)). Demonstrating a combination of PPIX and EDTA-mono- C14-amide was highly effective at low concentrations in killing suspended or biofilm S.au. The biofilm eradication capacity of a combination of PPIX and EDTA-mono-C14- amide is presented in Figure 18. As opposed to planktonic bacteria, biofilms were reported to be 10 to 1000 times more resistant to antibiotics or other antimicrobial agents because of the formidable barrier to drug infiltration in biofilms (see Passerini, L., et al. "Biofilms on indwelling vascular catheters." Critical care medicine 20.5 (1992): 665-673). For instance, a 600-fold higher chlorine concentration was required to destroy S.au biofilms than that used for planktonic S.au (see Luppens, S. B., et al. "Development of a standard test to assess the resistance of Staphylococcus aureus biofilm cells to biocides." Applied and Environmental Microbiology 68.9 (2002): 4194-4200). Figure 13 shows similar results to Figure 17. More particularly, it was found that while treating the biofilm with 10 μg mL ^-1 of PPIX for 1 hour only decreased the bacterial viability by 27%, the combination with 0.05 mM and 0.5 mM non-alkylated EDTA enhanced the inhibitory effect to some extents, destroying 33% and 63% of biofilms, respectively (Figure 18(a)). More importantly, the combination of PPIX with EDTA-mono-C14-amide led to 47% and 81% of biofilms eradicated (Figure 18(a)). Prolonging the illumination time on biofilms achieved an even higher biofilm eradication effect, with more than 90% of the biofilms eradicated when treated with 10 μg mL ^-1 PPIX and 0.05 mM EDTA-mono-C14-amide for 2 hours (Figure 18(b)). To better visualize the biofilm eradication degree with time, CLSM was used to observe the z-stacked images of three-dimensionally structured biofilms of this process. The biofilms were stained using a LIVE/DEAD™ BacLight™ kit, including a green- fluorescent dye (Syto9) that can stain the total bacteria populations, and a specific dead cell nuclear staining dye (propidium iodide). All biofilms were treated with 10 μg mL ^-1 PPIX, 10 μg mL ^-1 PPIX and 0.1 mM non-alkylated EDTA or 10 μg mL ^-1 PPIX and 0.1 mM EDTA- mono-C14-amide and placed under light illumination for 1 hour, 2 hours, and 3 hours. It could be observed that the control consisting of an untreated biofilm (only saline) was stained green (live) only. The majority of biofilm in the case of PPIX illuminated for 1 hour was stained green, red-stained dead cells accounted for only a substantially small percentage. Biofilm treated with a PPIX and non-alkylated EDTA combination was stained with substantially strong red fluorescent but had an almost intact structure. Whereas all the three fluorescent dyes were seldom presented in the case of PPIX with EDTA-mono- C14-amide after 1 hour. This indicates that PPIX had little biofilm eradication effect (Figure 18(d)), PPIX with non-alkylated EDTA killed the bacteria in the biofilm, but barely had biofilm eradication capacity. While PPIX with EDTA-mono-C14-amide eradicated most of the biofilm in 1 hour of illumination. After being illuminated for 3 hours, PPIX or PPIX with non-alkylated EDTA groups remained fundamental biofilms at distance from the biofilm upper layer of 6.1 µm and 4.2 µm, respectively. After being illuminated for 3 hours, there was 0.4 µm remained in PPIX with EDTA-mono-C14-amide treated biofilm (Figure 18(c)). Figure 18(e) shows cross-sections of the 3D biofilms, facilitating a more intuitive observation of the biofilm mass and thicknesses. Mechanistic investigation of the non-alkylated EDTA or alkylated EDTA enhancement on PPIX-mediated photo-inactivation ROS generation of PPIX and non-alkylated EDTA or alkylated EDTA enhanced PPIX-mediated PDI were detected with the help of DCFH-DA ROS-specific fluorescence markers by flow cytometry. Once entering cells, dichlorofluorescein diacetate (DCFA-DA) could be cleaved by the intracellular nonspecific esterase into nonfluorescent dichlorodihydrofluorescein (DCFH) which would be oxidized by ROS and turn into dichlorofluorescein (DCF) with green fluorescence (Ex:488; Em:525). DCF could be easily detected by flow cytometry or fluorescence spectrophotometry. Illumination for 30 minutes sparked 23% of total cells generating ROS by 10 μg mL ^-1 PPIX with 0.05 mM EDTA-mono- C14-amide, compared to 5% ROS generation by the same concentration of PPIX with non-alkylated EDTA. Improving the concentration of non-alkylated EDTA by 10 times to 0.5 mM elevated the ROS generation to 10%, which still had a significant difference with the case of PPIX and EDTA-mono-C14-amide. While the PPIX treated and non-treated groups generated 2.3% and 2% ROS correspondingly (Figure 19(b)). The fluorescent intensity of DCF had the similar trend with the ROS positive percentage in each group (Figure 19(c)). ROS generation of PPIX with non-alkylated EDTA or EDTA-mono-C14- amide but without bacteria were also measured by fluorescence spectrophotometer. EDTA-mono-C14-amide promoted the ROS production of PPIX was then investigated. It was found that in the absence of bacteria, EDTA-mono-C14-amide itself could substantially boost the photo-activated ROS production of PPIX. As the ROS production of PPIX can mirror the aggregation degree, it was inferred that the presence of EDTA-mono-C14-amide can potentially alleviate the aggregation of PPIX, which had been confirmed by the DLS (Figure 19(e)) and SEM results (Figure 19(f)). Furthermore, EDTA- mono-C14-amide substantially facilitated the accumulation of PPIX in bacteria. Flow cytometry analysis demonstrated that bacteria treated with 10 μg mL ^-1 of PPIX gave a mean fluorescence intensity of 40 relative fluorescence units (RFU), while those co- treated with PPIX and EDTA-mono-C14-amide (0.05 mM) gave a corresponding value of 380 RFU. By contrast, while non-alkylated EDTA could mildly enhance the antibacterial activity of PPIX, it had little effect on the singlet oxygen production, regardless of the presence of bacteria. Nor did non-alkylated EDTA lessen the aggregation of PPIX or increase the accumulation in bacteria. In addition, when we used SDS, a common surfactant in molecular biology, instead of EDTA-mono-C14-amide, to interact with PPIX, no particle minimizing effect was observed, either. These results demonstrate that both the EDTA and alkyl chain parts are crucial for EDTA-mono-C14-amide to diminish PPIX aggregation. Figure 20 shows that the untreated group had a fluorescent intensity of 100 after illuminating for 30 minutes. PPIX at the concentration of 5 μg mL ^-1 gave a fluorescent intensity of 300, PPIX with 0.5 mM non-alkylated EDTA was slightly lower than PPIX alone at 250. The fluorescent intensity of the combination of PPIX and 0.05 mM EDTA-mono- C14-amide reached 6000, which was 24 times of PPIX with non-alkylated EDTA. Non-alkylated EDTA was connected to a large and unsoluble Wang-resin and synthesized into Wang-EDTA. S.au bacteria of OD600 = 0.3 were incubated with 0.5 mM non-alkylated EDTA or Wang-EDTA for 1 hour. The bacterial viability was assessed by the plate counting assay. The result demonstrated that 100 μg mL ^-1 PPIX had no antimicrobial effect on S.au. PPIX with 0.5 mM non-alkylated EDTA decreased by 1.5 Log10-unit of S.au in contrast to PPIX with Wang-EDTA which reduced only by 0.5 Log10- unit. Blocking the non-alkylated EDTA with equal moles of Ca ²⁺ , then PPIX with non- alkylated EDTA was deprived of the antibacterial capacity, exhibiting no difference with untreated groups (Figure 21(a)). The overnight cultured Wang-EDTA in the bacterial solution was also collected and analyzed of the chelated types of metal irons by ICP-MS (Figure 21(b)). It revealed that the dominantly attached metal ion Ca ²⁺ was more than 10 times more than the amount of the secondly attached Zn ²⁺ and Mg ²⁺ . The particle size of PPIX in the solution was measured by DLS after incubation with different concentrations of EDTA-mono-C14-amide. As shown in Figure 22(a), 100 μg mL ^-1 PPIX with 0.5 mM non-alkylated EDTA was of no difference in size distribution with PPIX. Increasing the concentration of EDTA-mono-C14-amide from 0.01 mM to 0.05 mM, the solution size became smaller, with the major peak was at 30 nm, and the size distribution of particles around 300 nm in the volume got narrower. Higher concentrations of EDTA-mono-C14-amide at 0.1 mM or 0.5 mM made peaks smaller and more stable, for the peaks were at 20 nm with higher volume percentage and peaks at 300 nm became flat. This indicates that 0.05 mM EDTA-mono-C14-amide successfully lowered the particle size of PPIX to 20 nm, coincidentally identical to the concentration applied in the planktonic antibacterial assay. Similar results were confirmed when PPIX was at the concentration of 5 μg mL ^-1 , only EDTA-mono-C14-amide minimized the PPIX particle size to lower than 100 nm, while other combinations maintained the size distribution with a peak between 100 nm and 1000 nm. Figure 22(b) shows comparative results obtained with SDS. The same concentrations of SDS from 0.01 mM to 0.5 mM were mixed with PPIX for 1 hour, and their sizes were measured. The peaks seemed to be of no difference and identically overlapped with two obvious peaks at about 300 nm and about 6000 nm. The results validated that SDS had no minimizing effect. It is to be understood that neither non- alkylated EDTA nor alkyl chains were found to exhibit noticeable enhancements in PPIX- mediated photo-inactivation. However, the conjunction of the two chemicals presents increased antibacterial activities. Accumulation of PPIX in bacteria was evaluated by Flow Cytometry. PPIX at the concentration of 10 μg mL ^-1 was preincubated with S.au and illuminated for 1 hour. As is shown in Figure 23(b), PPIX alone accumulated in S.au was with the mean fluorescence value of 40, which was similar to the value of PPIX with 0.5 mM non-alkylated EDTA. However, the combination of PPIX and EDTA-mono-C14-amide significantly enhanced the accumulation in bacteria, the fluorescent value was 10 times higher. Discussion PPIX has been known as a biocompatible photosensitizer, but its poor solubility caused aggregation and quenches PDI. Therefore, PPIX applied at low or high concentrations is not sufficiently effective. From the results of investigating the fluorescence intensity and size distribution of PPIX, 10 μg mL ^-1 was confirmed to be the most dispersed and balanced state of PPIX in water. But still, the major peak of size was distributed at 300 nm, which should be smaller. Therefore, the key factors to improve is PPIX water solubility and PDI activity. EDTA is a traditional enhancer potentiating various biocides or antibiotics (Finnegan, S., & Percival, S. L. "EDTA: an antimicrobial and antibiofilm agent for use in wound care." Advances in wound care 4.7 (2015): 415-421). Without wishing to be bound by theory, it was proposed that EDTA interacted with the divalent ions on the bacterial film and facilitated the entry of the antibacterial agents into the bacteria (see Walsh, S. E., et al. "Activity and mechanisms of action of selected biocidal agents on Gram‐positive and‐ negative bacteria." Journal of applied microbiology 94.2 (2003): 240-247; and Sharma, M., et al. "Toluidine blue-mediated photodynamic effects on staphylococcal biofilms." Antimicrobial agents and chemotherapy 52.1 (2008): 299-305). Introducing a long alkyl chain to EDTA could anchor EDTA into the bacterial membrane and thus further potentiate its activity. Thus, a series of alkylated EDTAs were synthesized and tested. It was shown that EDTA with a C ₈ -C ₁₅ alkyl chain increases the antimicrobial activities of PPIX against S.au (Figure 9). As can be observed in Figure 9, EDTA-mono-C14-amide was the most efficient of all tested alkylated EDTA, alkylated EDTA with shorter and longer chains were substantially less active than medium chains. Meanwhile, longer illumination time resulted in better elimination efficacy. More importantly, alkylated EDTA substantially improved the antibiofilm activity of PPIX. The biofilm was reported to be 10-1000 times more resistant to antibiotics or other antimicrobial agents than planktonic bacteria because of their inefficient infiltration in the biofilm (see Passerini, L., et al. "Biofilms on indwelling vascular catheters." Critical care medicine 20.5 (1992): 665-673). For instance, a 600-fold higher chlorine concentration was required to destroy S.au biofilms than that used for planktonic S.au (see Luppens, S. B., et al. "Development of a standard test to assess the resistance of Staphylococcus aureus biofilm cells to biocides." Applied and Environmental Microbiology 68.9 (2002): 4194-4200). In the presence of 0.1 mM EDTA-mono-C14-amide, 10 μg mL ^-1 PPIX was already able to substantially remove the biofilms in 2 hours. PPIX is known to generate ROS killing bacteria under the light (see Habermeyer, B., Chilingaryan, T., & Guilard, R. "Bactericidal efficiency of porphyrin systems." Journal of Porphyrins and Phthalocyanines 25.05n06 (2021): 359-381; and Carvalho, M. L., et al. "Biofilm formation by Candida albicans is inhibited by photodynamic antimicrobial chemotherapy (PACT), using chlorin e6: increase in both ROS production and membrane permeability." Lasers in Medical Science 33.3 (2018): 647-653). The mechanism that alkylated EDTA enhanced the PDI activity of PPIX was attributed to generating more ROS, as shown in Figure 19. The enhanced ROS generating ability can be attributed to the alkylated EDTA promoting PPIX to generate ROS and/or to the alkylated EDTA facilitating PPIX accumulation in the bacteria. To determine this hypothesis, accumulation of PPIX in bacteria and ROS generation of PPIX without bacteria were evaluated. The results in Fig.6 demonstrated that PPIX accumulation in S.au was significantly enhanced by EDTA-mono-C14-amide for 10 times by contrast to PPIX with non-alkylated EDTA (Figure 20). In the meantime, EDTA-mono-C14-amide greatly enhanced the ability of PPIX to generate ROS by 10 times Figure 19(c), indicating that the two factors contributed the enhanced ROS generation and PDI activity against the bacteria. the **(optimized/narrowed/reducted) dispersion of PPIX can account for the EDTA- mono-C14-amide enhanced ROS generation. EDTA-mono-C14-amide can be considered as an amphiphilic surfactant and can dissociate large PPIX particles into substantially smaller ones (Figure 22 (a)) and thus inhibited PPIX’s aggregation-induced quenching of PDI. The increased intra-bacterial PPIX concentration can result from the disturbed **(bacteria cell) membrane by EDTA-mono-C14-amide. EDTA was reported to destabilize the cell membrane by chelating the bivalent ions stabilizing the membrane (see Lefebvre, E., et al. "Synergistic antibiofilm efficacy of various commercial antiseptics, enzymes and EDTA: a study of Pseudomonas aeruginosa and Staphylococcus aureus biofilms." International journal of antimicrobial agents 48.2 (2016): 181-188). Indeed, the immobilized EDTA on Wang-resin sequestrated Ca ²⁺ and **( Mg ²⁺ Zn ²⁺ ) ions (Figure 21). Thus, alkylated EDTA was inferred to have the ability to disturb and insert into the bacteria cell membrane. Example 1(b) – Antibacterial activity of EDTA-mono-C8, C12, C14, C15, C16, and C18- amide MIC measurement protocol The MIC values of different drugs including EDTA-mono-C8, C12, C14, C15, C16, and C18-amide, SDS, Vancomycin and 4 other chelators (TPTD, DATD, OPTD and THTD) were determined by the broth dilution method. The lowest concentration of chelators that could inhibit bacterial growth was defined as MIC. The assay was carried out in a 96-well transparent round bottom plate. The MICs of TPTD, DATD, OPTD and THTD against S.au and E. coli treated were obtained as comparative examples. Bacteria solutions of OD600 = 0.5 were diluted by 1000 times, 90 µL of the bacteria solution (1 x 10 ⁶ CFU) were treated with 10 µL of the chelators in a well of a 96-well plate to reach a final concentration of from 1 µg/mL to 512 µg/mL. The MTT method was employed to assess the viability after 24 hours of incubation. The comparative results are shown in Figure 24. MICs of EDTA-mono-C8, C12, C14, C15, C16, and C18-amide, SDS and Vancomycin against S.au were obtained. Bacteria solutions of OD600 = 0.5 were diluted by 1000 times, 90 µL of the bacteria solution (1 x 10 ⁶ CFU) were treated with 10 µL of the chelators in a well of a 96-well plate to reach a final concentration of from 0.25 µg/mL to 768 µg/mL. The MTT method was employed to assess the viability after 24 hours of incubation. The results are shown in Figure 25 and presented in Table 2 below. Table 2. MICs of EDTA-mono-C8, C12, C14, C15, C16, and C18-amide, SDS and vancomycin against S.au Example 1(c) – Time-dependent antibacterial effect of EDTA-mono-C14-amide against S.au Figure 26 shows a bar graph presenting the time-dependent antibacterial effect of EDTA-mono-C14-amide and Vancomycin against S.au results. The corresponding CLSM images are shown in Figure 27. The time-dependent antibacterial effect results were obtained by treating 500 µL S.au inoculum of OD ₆₀₀ = 0.5 with 50µg/mL of EDTA-mono-C14-amide or Vancomycin for 5 minutes, 10 minutes, 20 minutes, 40 minutes, 1 hour, 2 hours, 3 hours and 24 hours.10 µL of the treated bacteria solutions were spread on a LB plate. The colonies were counted after 24 hours of incubation at a temperature of 37°C. Figures 26 and 27 show that the antibacterial effect of EDTA-mono-C14-amide with time is substantially superior to that of Vancomycin. Example 1(d) – Concentration-dependent antibacterial effect of EDTA-mono-C14-amide against S.au The antibacterial effect of EDTA-mono-C14-amide and Vancomycin against various concentrations of S.au was tested. S.au solution of OD600 = 0.5 (2 x 10 ⁹ CFU) was diluted to different final concentrations (2 x 10 ⁸ ; 2 x 10 ⁷ ; 2 x 10 ⁶ ; and 2 x 10 ⁵ CFU/well) and treated with various concentrations of EDTA-mono-C14-amide and Vancomycin (ranging from 0.25 µg/mL to 128 µg/mL). The viability was evaluated after 24 hours of incubation by spectrophotometer.10 µL of the treated bacteria solutions were spread on a LB plate. The colonies were counted after 24 hours of incubation at a temperature of 37°C. Results are shown in Figure 28. Example 1(e) – Biofilm eradication capacity of EDTA-mono-C14-amide Viability of S.au treated with EDTA-mono-C14-amide, Vancomycin, SDS and PS MIC measurement protocol The MIC values of different chelators including EDTA-mono-C14-amide, Vancomycin, SDS and PS were determined by the broth dilution method. The lowest concentration of chelators that could inhibit bacterial growth was defined as the MIC. The assay was conducted in a 96-well transparent round bottom plate.90 µL of inoculum was added with 10 µL of the tested chelator to reach a final volume of 100 µL.10 µL of PBS was used as the corresponding negative control. The chelators were tested in concentration ranging from 0.5 µg/mL to 256 µg/mL. Each well contained 2 × 10 ⁶ CFU exponentially growing S. au (S.au of OD600 = 0.5 was considered as 2 × 10 ⁹ CFU). The plate was then incubated at a temperature of 37°C for 24 hours in an atmosphere containing 5% of CO2 before determining the OD600 value of each triplicate well using a microplate reader. Finally, the viability percentage was generated by comparing the experimental value against the negative control value. Biofilm eradication protocol The MTT method was used to assess the biofilm eradication ability of the chelators. Bacterial suspension was prepared as mentioned above containing 1 × 10 ⁹ CFU of bacteria per mL in a LB broth medium and seeded on a 96-well plate (200 µL/well). A mature biofilm was formed after incubating the plate at a temperature of 37°C for 24 hours. The mature biofilm was then rinsed with PBS 3 times to remove the unbounded planktonic bacteria. Serial dilutions of the chelators (20 µL) were placed in the well (the concentration was ranging from 8 µg/mL to 512 µg/mL) mixed with 180 µL LB broth medium per well. Vancomycin was used for comparison and untreated biofilm was used as a negative control. The plate was then placed at a temperature of 37°C under static conditions. The supernatant consisting of floating bacteria and destructed biofilm debris was removed after 24 hours of incubation. The residual biofilm was rinsed gently 3 times with PBS and then subjected to 200 µL of MTT solution (containing 20 µL 5 mg/mL MTT and 180 µL LB broth medium). A blue purple sediment was formed indicating the number of bacteria alive in the biofilm after 2~4 hours of incubation at a temperature 37°C. The sediment was solubilized in DMSO (150 µL/well) for 15 minutes. The absorbance at OD ₄₉₀ was measured and the biofilm viability was calculated by comparing it with the untreated group. Viability results (%) as a function of the concentration of EDTA-mono-C14-amide, Vancomycin, SDS and PS are shown in Figure 29. Biofilm live/dead staining assay Mature S.au biofilms were obtained by incubating 1 mL 2×10 ⁷ CFU/mL of S.au bacteria on sterilized confocal plate for 24 hours, removing the unbounded floating bacteria then rinsing the biofilms 3 times. EDTA-mono-C14-amide (60 µg/mL) was then added to the mature S.au biofilms for different period of time (3, 4.5, 8, and 24 hours). Vancomycin was used as a positive control. The treated mature S.au biofilms were then adequately washed with saline. The residual biofilms were stained with Syto9 (10 µg/mL) (green) and propidium iodide (10 µg/mL) (red) for 15 minutes and then rinsed 3 times with PBS. CLSM images were obtained to visualize the state of the S.au biofilms. The CLSM images are shown in Figures 30 and 31. Example 1(f) – Antibacterial and/or antibiofilm activity of EDTA-mono-C14-amide against different kind of bacteria MIC values and antibiofilm activity of EDTA-mono-C14-amide against SP Gram- positive (SP G+), Escherichia coli Gram-negative (E. coli G-) and Pseudomonas Gram- negative (Pseu G-) were tested using the protocol described in Example 1(e). The results are shown in Figures 32 and 33. Figures 32 (a) to (c) show the viability (%) as a function of the concentration in (a) for SP G+ treated with EDTA-mono-C14-amide and Vancomycin; in (b) for E. coli G- treated with EDTA-mono-C14-amide and Ceftazidime, and in (c) for Pseu G- treated with EDTA-mono-C14-amide and Ceftazidime, respectively. Figures 33 (a) to (c) show the biofilm viability (%) as a function of the concentration in (a) for SP G+ biofilms treated with EDTA-mono-C14-amide and Vancomycin; in (b) for E. coli G- biofilms treated with EDTA-mono-C14-amide and Ceftazidime, and in (c) for Pseu G- biofilms treated with EDTA-mono-C14-amide and Ceftazidime, respectively. Example 1(g) – Morphological observation of S. au treated with EDTA-mono-C14-amide The morphology of EDTA-mono-C14-amide and Vancomycin treated S.au was observed by scanning electron microscopy (SEM). To do so, exponentially growing S.au were adjusted to OD ₆₀₀ = 0.5, 50 µg/mL of EDTA-mono-C14-amide or Vancomycin were then added to the bacteria solution for 1 hour, 3 hours, and 5 hours. The bacteria sediment was collected by centrifugation and fixed in 2.5 % glutaraldehyde. The bacteria were then dehydrated and sprayed with gold. The surface of the bacteria was then imaged by SEM after the dehydration and gold spraying treatment. Example 1(h) – Colorimetric aldehyde assay The detoxification (disappearance) of glutaraldehyde from the media was measured using the colorimetric aldehyde assay. The results are shown in Figure 35. As shown in Figure 35(A), EDTA-mono-C14-amide treated bacteria including E. coli, Pseu, SP, MRSA, S.au formed a pink-colored pellet after incubation with glutaraldehyde. However, no change of color was observed when bacteria were treated with SDS, which has a structure similar to EDTA-mono-C14-amide. Figures 35(B) and 35(C) show photographs of a solution comprising a high concentration of EDTA-mono-C14-amide (10 mM, 500 µL) and glutaraldehyde (2.5% in PBS, 1 mL) after 30 minutes and overnight, respectively. As can be observed, after 30 minutes the solution was pink and became a darker shade of pink overnight. Figure 35(C) is a photograph of a solution comprising a high concentration of non-alkylated EDTA and glutaraldehyde showing no visible change of color. Example 1(i) – Fluorescence induced by glutaraldehyde fixation assay S.au was treated with 50 µg/mL of EDTA-mono-C14-amide for 1 hour. The supernatant was discarded after centrifugation. The sediment was resuspended with 1 mL glutaraldehyde (2.5%). Pink bacteria sediment formed after overnight culturing. Images of the sediment were captured and fluorescence spectra were recorded (Figure 36), it could be observed the pink sediment emitted fluorescence amid the wavelength between 570 nm and 620 nm, when excited at 543nm. Example 1(j) – Viability of E. Coli treated with EDTA-mono-C12, C14 and C15-amide MIC values of EDTA-mono-C12, C14 and C15-amide and Ceftazidime against E. coli were tested using the protocol described in Example 1(e). The results are shown in Figure 37. Example 1(k) – Viability of S.au and MRSA treated with methicillin MIC values of methicillin against S.au and MRSA were tested using the protocol described in Example 1(e). The results are shown in Figure 38. As can be observed, MRSA was indeed substantially more resistant to Methicillin than S.au. Example 1(m) – Viability of S.au treated with EDTA-mono-C14-amide, SDS, PS and SB MIC values of EDTA-mono-C14-amide, SDS, PS and SB against S.au and MRSA were tested using the protocol described in Example 1(e). The results are shown in Figure 39. As can be observed, EDTA-mono-C14-amide was more effective against S.au than SDS, PS and SB. Example 1(n) – Alkylated EDTA improved Ce6-mono-DMAE ¹⁵ amide (B17-mono) photoinactivation on Erwinia amylovora Relative photoinactivation results on Erwinia amylovora were obtained for Ce6- mono-DMAE ¹⁵ amide with EDTA-mono-C16-amide (1 mM). Ce6-mono-DMAE ¹⁵ amide (1 µm, 10 µm, and 100 µm) with EDTA-mono-C16-amide (1 mM) were added to samples containing Erwinia amylovora. The samples were incubated for about 120 minutes. The samples were then illuminated (except for dark controls) for about 15 minutes and 50 seconds using appropriate light irradiation conditions (395 nm and 28 mW/cm ² ). Radiant exposure: 26.6 J/cm ² . The relative photoinactivation results are presented in Figure 41. Example 1(o) – Alkylated EDTA improved chlorophyllin (Chl) photoinactivation on Erwinia amylovora Relative photoinactivation results on Erwinia amylovora were obtained for chlorophyllin with EDTA-mono-C16-amide (1 mM). Chlorophyllin (1 µm, 10 µm, and 100 µm) with EDTA-mono-C16-amide (1 mM) were added to samples containing Erwinia amylovora. The samples were incubated for about 120 minutes. The samples were then illuminated (except dark controls) for about 15 minutes and 50 seconds using appropriate light irradiation conditions (395 nm and 28 mW/cm ² ). Radiant exposure: 26.6 J/cm ² . The relative photoinactivation results are presented in Figure 42. Example 1(p) – Alkylated EDTA improved Cu-chlorophyllin (CuChl) and Cu-Ce6-mix- DMAE ^15,17 amide (CuB17) photoinactivation on Erwinia amylovora Relative photoinactivation results on Erwinia amylovora were obtained for Cu- chlorophyllin (CuChl) (100 µm) and Cu-Ce6-mix-DMAE ^15,17 amide (CuB17) (100 µm) with EDTA-mono-C16-amide (5 mM). The results were compared to samples in which the EDTA-mono-C16-amide (5 mM) was replaced by BAYPURE™ DS 100 a polyaspartic acid sodium salt dispersant (1.2%). The samples were incubated for about 30 minutes. The samples were then illuminated (except dark controls) for about 72 minutes using appropriate light irradiation conditions (6.2 mW/cm ² ). Radiant exposure: 26.6 J/cm ² . The relative photoinactivation results are presented in Figure 43. Figure 43 shows an increase in the relative inactivation for the samples comprising EDTA-mono-C16-amide (5 mM) compared to those comprising BAYPURE™ DS 100 (1.2%). Example 1(q) – Alkylated EDTA improved Ce6-mono-DMAE ¹⁵ amide (B17-mono) and Ce6-bis-DMAE ^15,17 amide (B17-0024) photoinactivation on Erwinia amylovora Relative photoinactivation results on Erwinia amylovora were obtained for Ce6- mono-DMAE ¹⁵ amide (B17-mono) (10 µm and 100 µm) and Ce6-bis-DMAE ^15,17 amide (B17-0024) (10 µm and 100 µm) with EDTA-mono-C16-amide (1 mM). The samples were incubated for about 30 minutes. The samples were then illuminated (except dark controls). Radiant exposure: 26.6 J/cm ² . The relative photoinactivation results are presented in Figure 44. Figure 44 shows substantial relative inactivation for the samples comprising Ce6-mono-DMAE ¹⁵ amide and Ce6-bis-DMAE ^15,17 amide with EDTA-mono-C16-amide. Example 2 – Agricultural applications Example 2(a) – Fungal pathogen Colletotrichum orbiculare (Cgm) - PDI assay protocols and results (host plants - Nicotiana benthamiana (NB) - growth room conditions: 24°C) NB plants preparation NB seeds were planted into potting soil, allowed to germinate, and grown until two true leaves have developed (~14 days). The NB plants thus obtained were transferred into 4” pots containing potting soil and allowed to grow for an additional 14 days (6-8 leaves stage, ~3-4 weeks old). The NB plants were maintained until the they have developed 5- 6 leaves or until the size of the lower true leaves have reached approximately 4-5 cm in diameter. Preventative assays and results of fungal pathogen Cgm on the NB host plants In this example, control of the fungal pathogen Cgm on host NB plants following the treatment was assessed. Treatments were applied to NB plants 1 hour or 48 hours prior to inoculation with a spore suspension of Cgm (2.0 x 10 ⁶ spores per ml). The treated plants were then exposed to LED light LED illumination for 12 hours light followed by 12 hours of dark incubation for 2 days, followed by dark incubation until disease symptoms were evident on the water treated control plants. Once disease symptoms were evident, lesions were counted, and leaf area measured to determine the number of lesions/cm ² leaf area. Six replicate plants were used per treatment and plants were randomized under the light source. Illumination was provided by LED lights emitting about 350 µmol/m ² /s photosynthetically active radiation (PAR). Treatment (preventative application) The plants were sprayed with the solutions using a track sprayer. Two passes with track sprayer at standard settings of 45 speed and 55 psi (spray volume approximately 380 L/ha or 40 g/acre) were carried out to provide a substantially uniform coverage on the plants. Water was used for untreated control treatment. Immediately after being sprayed the treated plants were randomly placed on a light rack and exposed to LED illumination (LED lights emitting about 350 µmol/m ² /s PAR) for 12 hours of light followed by 12 hours of dark incubation. The cycle was repeated for 2 days. Inoculum preparation Spores of Cgm (ATC20767) were transferred from -80°C glycerol stocks to two SYAS media and allowed to grow for four days (master plate). Plugs were transferred from the master plate to fresh SYAS plates, the plugs were streaked to spread the spores and hyphae across the new plates and the pathogens were grown for 7 days. Spores from the 7-day-old plates were washed with 10 mL of deionized (DI) water. The spore suspension was then centrifuged (500xg for 3 minutes) to obtain pellets. The pellets were then re- suspended in DI water and centrifuged again (500xg for 3 min) to obtain a pellet. The supernatant was poured off and the pellets were collected in 1 mL of DI water. The concentrated spore suspension thus obtained was diluted to a concentration of 2.0 x 10 ⁶ spores per mL. Inoculation The two most fully expanded leaves of each plant were marked, and the plant was inoculated by misting inoculum on the plant using an artist’s spray brush and a compressor at 25 psi. NB plants were inoculated with the 2.0 x 10 ⁶ spores per mL spore suspension of Cgm. Immediately after inoculation the plants were randomly placed on an illuminated shelf, the plants were covered with transparent plastic domes to provide humidity and exposed to light for 12 hours and then kept in the dark for 4 days. Disease evaluation The disease was assessed 5 days after inoculation. The number of lesions on the marked leaves were counted and the leaf area was measured using Image J to determine the number of lesions/cm ² leaf area. Results The preventative assays and results of fungal pathogen Cgm on the NB host plant are presented in Tables 3 to 7 below. Table 3. Preventative treatments 48 hours prior inoculation: evaluation of EDTA-mono- C16-amide as a Mg-Chlorophyllin-mediated PDI enhancer

Curative assays and results of fungal pathogen Cgm on the NB host plant In this example, control of the fungal pathogen Cgm on the NB host plant following the treatment was assessed. Treatments were applied to NB plants 24 hours after inoculation with a spore suspension of Cgm (2.0x10 ⁶ spores per ml). The treated plants were then exposed to LED light illumination for 12 hours of light followed by 12 hours of dark incubation for 2 days, followed by dark incubation until disease symptoms were evident on the water treated control plants. Five days after inoculation, disease lesions were counted, and leaf area measured to determine the number of lesions/cm ² leaf area. Six replicate plants were used per treatment and plants were randomized under the light source. Illumination is provided by LED lights emitting about 350 µmol/m ² /s PAR. Results The curative assays and results of fungal pathogen Cgm on the NB host plant are presented in Tables 8 and 9 below. Table 8. Curative treatments: evaluation of EDTA-mono-C18-amide, EDTA-mono-C16- amide and EDTA-mono-C8-amide as Mg-Chlorophyllin-mediated PDI enhancers Example 2(b) – Bacterial pathogen Pseudomonas syringae pv. Tabaci (Pst) - PDI assay protocol (host plant - NB - growth room conditions: 24°C, 16 hours light/ 8 hours dark) NB plants preparation NB seeds were planted into potting soil, allowed to germinate, and grown until two true leaves have developed (~14 days). The NB plants thus obtained were transferred into 4” pots containing potting soil and allowed to grow for an additional 14 days (5-7 leaves stage, ~3-4 weeks old). The NB plants were maintained until the they have developed 5- 6 leaves or until the size of the lower true leaves have reached approximately 4-5 cm in diameter. Preventative assays of bacterial pathogen Pst on host NB plants In this example, control of the bacterial pathogen Pst on host NB plants following the treatment was assessed. Treatments were applied to NB plants 2 hours or 48 hours prior to inoculation with Pst culture (3x10 ⁸ CFU/mL). The treated plants were then exposed to LED light illumination for 12 hours light followed by 12 hours of dark incubation.7 days after inoculation the disease severity (% disease per plant) was assessed using a modified Horsfall-Barratte scale (0-100). Disease symptoms include yellow lesions, discoloration on foliage, leaf deformations and plants stunting. Six replicate plants were used per treatment and plants were randomized under the light source. Illumination is provided by LED lights emitting about 350 µmol/m ² /s PAR. Treatment (preventative application) The plants were sprayed with the solutions using a track sprayer. Two passes with the track sprayer at standard settings of 45 speed and 55 psi (spray volume approximately 380 L/ha or 40 g/acre) were carried out to provide a substantially uniform coverage on the plants. Water was used for untreated control treatment. Immediately after being sprayed the treated plants were randomly placed on a light rack and exposed to LED illumination (LED lights emitting about 350 µmol/m ² /s PAR) for 12 hours of light followed by 12 hours of dark incubation. The cycle was repeated for 2 days. Inoculum preparation Bacterial cells from a Pst pure culture stored in a 30% glycerol solution at a temperature of -80°C was streaked on Tryptic Soy Agar (TSA) plates and incubated at a temperature of 28°C for 24 hours. 10 mL of DI water was added to the Petri-dish to completely cover the plate. The bacteria were then gently scraped using an inoculation loop and then suspended in the water. Once all the bacteria have been scraped, the water and bacteria were poured from the Petri-dish into a 50 mL Falcon tube. The Falcon tube was then shaken to ensure that the bacteria were substantially well dispersed in the water. The optical density at 600 nm (OD600) measurements were then performed by adjusting the settings so that an OD600 = 1 is equivalent to 3x10 ⁸ CFU/mL. The blank samples for the OD600) measurements were consisting of DI water. From the OD600 = 1 (3x10 ⁸ CFU/mL) spectrum reading, the samples were diluted to 1.0 X 10 ⁸ CFU/mL and 0.02% Silwet™ L-77 was added. Inoculation 48 hours after the treatment the plants were inoculated by misting the Pst inoculum on the plant using an artist’s spray brush and a compressor at 25 psi. The entire plant was sprayed with Pst inoculum to ensure a substantially thorough coverage of the entire plant. Immediately after inoculation the wet inoculated plants were randomly placed in a plastic tray on a bench (photoperiod 16 hours of light and 12 hours of darkness, 180 µmol/m ² /s PAR) and covered with transparent domes to provide about 100% humidity. Disease assessment The disease severity (% disease per plant) was assessed 7 days after the inoculation using a modified Horsfall-Barratt scale (0-100). Disease symptoms included yellow lesions, discoloration on foliage, leaf deformations and plants stunting. Results Preventive assays of bacterial pathogen Pst on the NB host plant are presented in Tables 10 and 11 below.

Curative assays of bacterial pathogen Pst on host NB plants In this example, control of the bacterial pathogen Pst on host NB plants following the treatment was assessed. Treatments were applied to NB plants 24 hours after inoculation with the Pst culture (3x10 ⁸ CFU/mL). The treated plants were then exposed to LED light illumination for 12 hours light followed by 12 hours of dark incubation.7 days after inoculation the disease severity (% disease per plant) was assessed using a modified Horsfall-Barratte scale (0-100). Disease symptoms include yellow lesions, discoloration on foliage, leaf deformations and plants stunting. Six replicate plants were used per treatment and plants were randomized under the light source. Illumination is provided by LED lights emitting about 350 µmol/m ² /s PAR. Results Curative assays of fungal pathogen bacterial pathogen Pst on the NB host plant are presented in Tables 12 to 16 below.

Example 2(c) – Insect pests – Western Flower Thrips (WFT) – PDI assay protocol (conditions: 25°C, 12 hours light/ 12 hours dark) Ingestion assays using Insecticide Resistance Action Committee (IRAC) susceptibility test method 019 with normal fluorescent light (low light) and LED light (high light) conditions were carried out. Method Each trial included nine treatments with ten repetitions per treatment (n = 20). WFT practical resistance was tested using IRAC susceptibility test method 019. Ten adult female WFT enclosed in small shallow deli cups containing agar and a young cabbage leaf disk treated with an insecticide composition as a food source. To do so, agar was prepared in the small shallow deli cups and a young cabbage leaf disk was placed on top of the agar just before solidifying. The insecticide composition was sprayed onto the young cabbage leaves and the young cabbage leaves were then air dried. Once the young cabbage leaves were substantially dried, ten adult female WFT were released per container by aspirating them into the containers. The temperature was kept at 25°C ± 2°C and the relative humidity (RH) at 70% ± 5%. Fluorescence The abaxial side of the young cabbage leaves were exposed to fluorescent light at an average of 250 µmol/m ² /s PAR in 12 hours of light: 12 hours of dark photoperiod cycle. LED The abaxial side of the young cabbage leaves were exposed to LED lights at an average of 5000 µmol/m ² /s PAR in 12 hours of light: 12 hours of dark photoperiod cycle. Mortality Mortality was recorded on the fifth day. Results The mean percentage of mortality of the WFT was evaluated after feeding on young cabbage leaf disks treated with the insecticide composition for five days. Water was used for untreated control treatment. The ingestion assays and results are presented in Table 17 below. Example 2(d) – Green Mold - Penicillium digitatum (P. digitatum) - PDI assay protocol (growth room conditions: 22~24°C) Method Isolate of P. digitatum was purchased from GAGE Research Institute (UAMH Centre for Global Microfungal Biodiversity, UFT, Canada). Isolate of P. digitatum was isolated from rotting fruit of Citrus sinensis (Australia, Canberra) and deposited to GAGE collection. A single spore culture of P. digitatum isolate was growing on potato dextrose agar (PDA) (Difco™ Laboratory, USA) and stored in a 20% glycerol solution as mycelial PDA plugs and on PDA slants at a temperature of 4°C. 9 cm in diameter Petri dishes with PDA media were used in the assays. Mycelium growth inhibition test P. digitatum was cultured on fresh PDA media for five days in the dark at room temperature (~22-24°C). Plugs with freshly growing mycelium were cut from 5 days old P. digitatum colonies using a 5 mm diameter cork borer and placed into 6-well plates. 6 mL of the antimicrobial composition were added to each well, containing ~5-6 plugs. Plugs with mycelium were submerged into the antimicrobial composition and incubated for 5 minutes. During the incubation time, the plates were gently moved to provide a better contact between the mycelium and the antimicrobial composition. The antimicrobial composition was removed from the wells and plugs with mycelium were immediately exposed to Helios led light with a full-spectrum light and an intensity of 10344 PAR or dark conditions for 5 minutes. Immediately after light exposure plugs with mycelium (side-down) were transferred on PDA plates and maintained in dark conditions at room temperature. 5 or 6 replicates for each treatment were obtained for this assay. The diameter of each P. digitatum colony (including plug size – 5 mm) was measured using calipers 24 hours after treatment and the percentage of inhibition of the mycelial growth was calculated. The mycelium growth inhibition assays and results are presented in Table 18 below. Example 2(e) – Phytotoxicity assays Phytotoxicity assays were carried out. Data were obtained after 0, 7, 14, and 21, days. In comparison to the control samples, no detectable significant difference in leaf damage incidence rate, senescence, or overall plant development was observed in any of the treated plant samples. The phytotoxicity assays are presented in Table 19 below.

Example 3 – Veterinary applications Example 3(a) – Animal model of infected ulcers Wounds were produced with a punch of 8 mm in diameter on the skin of BALB/c mice (female, 8-10 weeks old, 18-22 g). Methotrexate (10 mg kg ^-1 ) was intraperitoneally injected into mice 1 day before and 2 days after the wound induction. S. aureus suspension (1.5×10 ⁷ CFU in 30 μL) was inoculated into the wound sites and the ulcers was then applied with sterile dressings. Mature biofilms were formed the next day. Treatments were performed on day 3, 5, and 7 by immersing the ulcer regions with PBS, 100 µg/mL PPIX in PBS, 100 µg/mL PPIX with non-alkylated EDTA (0.5 mM) in PBS, 100 µg/mL PPIX with EDTA-mono-C8, C10, C12, C14, C15, C16, or C18-amide (0.5 mM) in PBS, or 100 µg/mL PPIX with EDTA-mono-C14, or C16-ester (0.5 mM) in PBS for 1 hour, followed by illumination for 2 hours. Immediately after each treatment, sterile miniswabs were covered over the ulcer regions for 20 minutes, immersed into 1 mL of saline, and then sonicated for 2 minutes to allow for sufficient detachment of bacteria from the swab tips. The bacteria amount was determined by the standard plate count method. All animals were purchased from Shanghai SLAC Laboratory Animal Co., Ltd. and housed in a specific pathogen-free (SPF) animal facility at Zhejiang University. All animal experiments were carried out under the protocols approved by the Institutional Animal Care and Use Committee (IACUC) of Zhejiang University in accordance with the institutional guidelines. In vivo therapeutic effect of PPIX, PPIX with EDTA-mono-C8, C10, C12, C14, C15, C16, and C18-amide, and PPIX with EDTA-mono-C14, and C16-ester The in vivo therapeutic effect of the combination of PPIX and EDTA-mono-C8, C10, C12, C14, C15, C16, or C18-amide or EDTA-mono-C14, or C16-ester was investigated on an animal model of infected ulcers. The ulcers were produced by an 8- mm-diameter punch and infected with S. aureus locally (Figures 45, 48, and 51). As the ulcer lesions secrete a variety of proteins, cytokines and other components that may inactivate the treatment agents to some extents, the PPIX and non-alkylated EDTA/ EDTA-mono-C8, C10, C12, C14, C15, C16, or C18-amide/ EDTA-mono-C14, or C16- ester concentrations were increased to 100 μg mL ^-1 and 0.5 mM, respectively. The ulcer sites were treated with different PPIX combinations and then subjected to a light fluence of 60 J cm ^-2 . Compared with the control group, the individual PPIX treatment failed to promote the wound healing, leading to ulcer areas as large as ~33 mm ² after 9 days. In contrast, the different PPIX with non-alkylated or alkylated EDTA combinations reduced the ulcer area to ~18 mm ² . Of the most significant therapeutic efficacy were the combinations of PPIX with EDTA-mono-C14, and C15-amide, which almost healed the ulcers with an area of only ~1.3 mm ² and ~2.7 mm ² (Figures 46, 49, and 52). The plate count assay performed immediately after three different treatments (PPIX, PPIX with non- alkylated EDTA (0.5 mM), and PPIX with EDTA-mono-C14-amide (0.5 mM)) further validated the potent effectiveness of the PPIX with EDTA-mono-C14-amide combination, which reduced the S. aureus CFU by 5 logs after 7 days (Figure 47). Figure 50 shows the plate count assay performed immediately after nine different treatments (PBS, PPIX, PPIX with non-alkylated EDTA (0.5 mM), and PPIX with EDTA-mono-C8, C12, C14, C15, C16, and C18-amide (0.5 mM)). The results show the following trend: PPIX with EDTA-mono- C14-amide (0.5 mM) > PPIX with EDTA-mono-C15-amide (0.5 mM) > PPIX with EDTA- mono-C12-amide (0.5 mM) > PPIX with EDTA-mono-C16-amide (0.5 mM) > PPIX with EDTA-mono-C8-amide (0.5 mM) > PPIX with EDTA-mono-C18-amide (0.5 mM) > PPIX with non-alkylated EDTA (0.5 mM) > PPIX > PBS. Example 3(b) – Antimicrobial activity of EDTA-mono-C14-amide Catheter coating procedure Dissolving 1 mg of EDTA-mono-C14-amide in 100 μL of methanol, 10 mg of polystyrene in 100 μL of tetrahydrofuran, and mixing them. Cutting a catheter of 1 cm in length, immersing the catheter in the C14-polystyrene mixture for 5 min, then drying it in a dryer for 10 min, repeating the immersing-drying operation for 3 times. In vivo antifouling test In vivo antibacterial activity of EDTA-mono-C14-amide was assessed by a catheter antifouling model. Incisions of 8 cm diameter on the back of Barlb/c mice were cut carefully, and catheters coated or uncoated by C14-polystyrene were implanted in the muscles. The catheters were pre-incubated with 10 ⁸ CFU/mL S. au bacteria for 3 hours to enable the bacteria adhere on the surface adequately. The implanted site was observed, and a picture taken every day (Figure 53) until the yellow inflammatory hyperplasia obviously wrapped the uncoated catheter on the 5-7 days’ post-implantation. The mice were sacrificed by anesthetization and the implants or muscles excised around separately; the viable bacteria were determined by plate counting method (Figure 54). Except for the in vivo antifouling test, in vitro antifouling experiments were also conducted. The bottom of a 24-well plate was covered by the mixture C14-polystyrene or C14-polycaprolactone (EDTA-mono-C14-amide in methanol mixed with 10 times mass of PS or PCL in tetrahydrofuran, the final concentration of EDTA-mono-C14-amide is 20, 50, 100 μg/mL and the final volume is 1 mL). Then, 1*10 ⁶ CFU/mL concentration of S.au inoculum were inoculated (500μL) in each well and incubated at 37 °C overnight. The S.au inoculum was refreshed every 24 hours to determine the duration of the coatings’ antibacterial efficacy (Figure 55). Plate counting method The plate counting method refers to the Broth Dilution Method. In this method, microorganisms are tested for the ability to produce visible growth on agar plates. To be specific, the coated or uncoated catheters implanted under the muscles were transferred in 1 mL tubes of sterile PBS separately, then ultrasound was applied to detach the bacteria adequately into the PBS. Muscles around the catheters were excised for the same mass then put in the tubes and sonicated.10-fold dilution of the solution with fresh PBS serially in 96-well plate was performed, and 10 μL of solution of each well were applied on the agar plate evenly. After overnight incubation at 37°C, the agars were examined for visible bacterial growth and counted to evaluate the viability of microorganisms. Example 3(c) – Photodynamic inactivation treatment against C. auris on porcine skin model Standard operating protocol for photodynamic inactivation treatment Fresh raw abdominal skins from six-month-old female pigs were obtained from a local slaughterhouse. The skin was washed with distilled water, dabbed with 70% (volume/volume percentage; %v/v) ethanol to remove the present skin flora (or skin microbiota), and the bristles were cut with razor blades. Afterwards, the porcine skin samples were wrapped in freezer bags and stored at a temperature of about −20 °C until usage. The porcine skin samples were then carefully defrosted. The porcine skin samples were cut to obtain porcine skin samples of about 25 mm in diameter. The porcine skin samples were then washed with 70% (%v/v) ethanol and then with ultra-pure and sterile water (ddH2O). The porcine skin samples were then transferred to a 6-well plate, embedded in agar-agar (5%), and covered with 70% (%v/v) ethanol for about 3 minutes. 250 µL C. auris (OD = 0.1) were applied onto the surface of the porcine skin samples by pipetting. The porcine skin samples were incubated for about 5 minutes.250 µL of Ce6- mix-DMAE ^15,17 amide (10 µM, 50 µM, and 100 µM) with EDTA-mono-C14-amide (0.5 mM) were added by pipetting (with and without about 15 minutes incubation). The porcine skin samples were then illuminated (except dark controls) from above using a LED-array in the appropriate wavelength (i.e., 395 nm). Radiant exposure: 25 + 100 J/cm ² (except for double negative controls, Co −/− and dark controls). The samples were then carefully transferred into micro tubes containing Dulbecco's Phosphate-Buffered Saline (DPBS) using sterile cotton sticks, serially diluted, and plated on agar dishes. The CFU was determined by counting fungal colonies about 48 hours post illumination. A substantial increase in relative inactivation can be observed for the porcine skin samples treated with Ce6-mix-DMAE ^15,17 amide (10 µM, 50 µM, and 100 µM) with EDTA-mono-C14-amide (0.5 mM) compared to the different controls (Figures 56 and 57). Abbreviations Numerous modifications could be made to any of the implementations described above without distancing from the scope of the claims. Any references, patents or scientific literature documents referred to in the present application are incorporated herein by reference in their entirety for all purposes. *** In some of the implementations where the surface is a biological or non-biological surface described in the present description include the following items: Item 1. A biocide composition comprising an EDTA derivative and a liquid carrier, wherein the EDTA derivative is of Formula (I): Formula (I) or a salt thereof, wherein: Z is NH or O; and R1 is selected from the group consisting of an optionally substituted C8-C18alkyl group, an optionally substituted C8-C18alkenyl group, an optionally substituted C8-C18alkynyl group and an optionally substituted steroidyl group. Item 2. The biocide composition of item 1, wherein the steroidyl group is: . Item 3. The biocide composition of item 1 wherein R ₁ is selected from the group consisting of an optionally substituted C ₁₂ -C ₁₅ alkyl group, an optionally substituted C ₁₂ -C ₁₅ alkenyl group and an optionally substituted C ₁₂ -C ₁₅ alkynyl group. Item 4. The biocide composition of item 1, wherein R ₁ is an optionally substituted C ₁₂ -C ₁₅ alkyl group. Item 5. The biocide composition of item 1, wherein R ₁ is an unsubstituted C ₁₂ -C ₁₅ alkyl group. Item 6. The biocide composition of item 1, wherein the EDTA derivative of Formula (I) is:

or a salt thereof. Item 7. The biocide composition of item 6, wherein the EDTA derivative of Formula (I) is: or a salt thereof. Item 8. The biocide composition of item 7, wherein the EDTA derivative of Formula (I) is: or a salt thereof. Item 9. The biocide composition of item 1, wherein the EDTA derivative of Formula (I) is:

or a salt thereof. Item 10. The biocide composition of item 9, wherein the EDTA derivative of Formula (I) is: or a salt thereof. Item 11. The biocide composition of item 10, wherein the EDTA derivative of Formula (I) is: or a salt thereof. Item 12. The biocide composition of any one of items 1 to 11, wherein the liquid carrier is an aqueous carrier. Item 13. The biocide composition of item 12, wherein the aqueous carrier comprises an oil and is an oil-in-water emulsion. Item 14. The biocide composition of item 13, wherein the oil is selected from the group consisting of a mineral oil, a vegetable oil and a mixture thereof. Item 15. The biocide composition of item 14, wherein the oil comprises a vegetable oil selected from the group consisting of coconut oil, canola oil, soybean oil, rapeseed oil, sunflower oil, safflower oil, peanut oil, cottonseed oil, palm oil, rice bran oil and mixtures thereof. Item 16. The biocide composition of item 14 or 15, wherein the oil comprises a mineral oil selected from the group consisting of a paraffinic oil, a branched paraffinic oil, naphthenic oil, an aromatic oil and mixtures thereof. Item 17. The biocide composition of any one of items 14 to 16, wherein the oil comprises a poly-alpha-olefin (PAO). Item 18. The biocide composition of any one of items 1 to 17, further comprising at least one photosensitizer compound. Item 19. The biocide composition of item 18, wherein the photosensitizer is a macrocyclic tetrapyrrole compound selected from the group consisting of a porphyrin, a reduced porphyrin, and a mixture of at least two thereof. Item 20. The biocide composition of item 19, wherein the reduced porphyrin compound is selected from the group consisting of a chlorin, a bacteriochlorin, an isobacteriochlorin, a corrin, a corphin, and a mixture of at least two thereof. Item 21. The biocide composition of item 19 or 20, wherein the macrocyclic tetrapyrrole compound is complexed with a metal to form a metallated macrocyclic tetrapyrrole compound. Item 22. The biocide composition of item 21, wherein the metal is selected such that, in response to light exposure, the metallated photosensitive compound generates reactive oxygen species. Item 23. The biocide composition of item 22, wherein the metal is selected from the group consisting of Mg, Pd, Co, Al, Ni, Zn, Sn, and Si. Item 24. The biocide composition of item 21, wherein the metal is selected such that the metallated macrocyclic tetrapyrrole compound does not generate singlet oxygen. Item 25. The biocide composition of item 24, wherein the metal is selected from the group consisting of Cu, Co, Fe, and Mn. Item 26. The biocide composition of any one of items 19 to 25, wherein the macrocyclic tetrapyrrole compound comprises chlorophyllin. Item 27. The biocide composition of any one of items 19 to 26, wherein the macrocyclic tetrapyrrole compound comprises Chlorophyll a. Item 28. The biocide composition of any one of items 19 to 27, wherein the macrocyclic tetrapyrrole compound comprises chlorin e6. Item 29. The biocide composition of any one of items 19 to 28, wherein the macrocyclic tetrapyrrole compound comprises protoporphyrin IX. Item 30. The biocide composition of any one of items 19 to 29, wherein the macrocyclic tetrapyrrole compound comprises tetraphenylporphyrin. Item 31. The biocide composition of any one of items 19 to 30, wherein the macrocyclic tetrapyrrole compound comprises an extracted naturally-occurring macrocyclic tetrapyrrole compound. Item 32. The biocide composition of any one of items 19 to 31, wherein the macrocyclic tetrapyrrole compound comprises a synthetic macrocyclic tetrapyrrole compound. Item 33. The biocide composition of item 18, wherein the photosensitizer is an isoquinoline derivative, such as berberine. Item 34. The biocide composition of item 18, wherein the photosensitizer is a diarylheptanoid, such as curcumin. Item 35. The biocide composition of any one of items 1 to 34, further comprising at least one base. Item 36. The biocide composition of item 35, wherein the base is selected from the group consisting of triethanolamine (N(CH2CH2OH)3), TRIS-buffer ((2-Amino-2- (hydroxymethyl)propane-1,3-diol), sodium bicarbonate (NaHCO3), potassium bicarbonate (KHCO3), sodium carbonate (Na2CO3) and potassium carbonate (K2CO3). Item 37. The biocide composition of item 36, wherein the base is TRIS-buffer ((2- Amino-2-(hydroxymethyl)propane-1,3-diol). Item 38. The biocide composition of item 36, wherein the base is sodium carbonate (Na2CO3). Item 39. The biocide composition of any one of items 1 to 38, further comprising at least one essential oil. Item 40. The biocide composition of item 39, wherein the essential oil is selected from the group consisting of thymol, eugenol, geranial, nerol, citral, carvacrol, cinnamaldehyde, terpinol, α-terpinene, citronellal, citronellol, geraniol, geranyl acetate, limonene, lavender oil, methyl isoeugenol and mixtures thereof. Item 41. The biocide composition of item 40, wherein the essential oil comprises thymol, carvacrol, or α-terpinene. Item 42. The biocide composition of item 41, wherein the essential oil comprises thymol. Item 43. The biocide composition of any one of items 1 to 42, further comprising at least one biosurfactant. Item 44. The biocide composition of item 43, wherein the biosurfactant is selected from the group consisting of an alkyl polyglycoside, a rhamnolipid, a sophorolipid and a combination of at least two thereof. Item 45. The biocide composition of item 44, wherein the biosurfactant is an alkyl polyglycoside. Item 46. The biocide composition of any one of items 1 to 45, further comprising at least one oil selected from the group consisting of a mineral oil, a vegetable oil, and a mixture of at least two thereof. Item 47. The biocide composition of item 46, wherein the oil comprises a vegetable oil selected from the group consisting of coconut oil, canola oil, soybean oil, rapeseed oil, sunflower oil, safflower oil, peanut oil, cottonseed oil, palm oil, rice bran oil, and a mixture of at least two thereof. Item 48. The biocide composition of item 46 or 47, wherein the oil comprises a mineral oil selected from the group consisting of paraffinic oils, branched paraffinic oils, naphthenic oils, aromatic oils, and a mixture of at least two thereof. Item 49. The biocide composition of item 48, wherein the paraffinic oil is a poly- alpha-olefin (PAO). Item 50. The biocide composition of any one of items 1 to 49, further comprising at least one surfactant. Item 51. The biocide composition of item 50, wherein the surfactant is selected from the group consisting of a non-ionic surfactant, a cationic surfactant, an anionic surfactant, a zwitterionic surfactant or a combination of at least two thereof. Item 52. The biocide composition of item 51, wherein the surfactant comprises a non-ionic surfactant selected from the group consisting of ethoxylated alcohol, a polymeric surfactant, a fatty acid ester, a poly(ethylene glycol), an ethoxylated alkyl alcohol, a monoglyceride, an alkyl monoglyceride, a polysorbate, and a mixture of at least two thereof. Item 53. The biocide composition of any one of items 1 to 52, further comprising at least one solvent selected from an aqueous solvent, a non-aqueous, or a miscible mixture of at least two thereof. Item 54. The biocide composition of item 53, wherein the solvent comprises water. Item 55. The biocide composition of item 53 or 54, wherein the solvent comprises a non-aqueous solvent which is at least partially soluble in water. Item 56. The biocide composition of any one of items 53 to 55, wherein the solvent comprises a non-aqueous solvent selected from the group consisting of ethanol, acetone, isopropanol, ethylene glycol, propylene glycol and a miscible mixture of at least two thereof. Item 57. The biocide composition of any one of items 53 to 56, wherein the solvent comprises isopropanol. Item 58. The biocide composition of any one of items 1 to 57, further comprising at least one additional chelating agent. Item 59. The biocide composition of item 58, wherein the additional chelating agent is EDTA. Item 60. The biocide composition of any one of items 1 to 57, which is free of an additional chelating agent. Item 61. The biocide composition of any one of items 1 to 60, wherein the biocide composition is provided as a multiple-pack system comprising at least two packs, each one of the two packs comprising at least one separate component of the composition. Item 62. The biocide composition of any one of items 1 to 61, which is an antimicrobial composition. Item 63. The biocide composition of any one of items 1 to 61, which is an antibiofilm composition. Item 64. The biocide composition of any one of items 1 to 61, which is an insecticide composition. Item 65. A method for inhibiting microbial pathogen and biofilm formation on a surface, comprising applying the biocide composition of any one of items 1 to 64 to the surface. Item 66. A method for disrupting pre-existing microbial pathogens and biofilms on a surface, comprising applying the biocide composition of any one of items 1 to 64 to the surface. Item 67. A method for controlling insect pests on a surface, comprising applying the biocide composition of any one of items 1 to 64 to the surface. Item 68. The method of any one of items 65 to 67, wherein the surface is a biological surface. Item 69. The method of item 68, wherein the biological surface is a plant. Item 70. The method of item 69, wherein the salt of the EDTA derivative of Formula (I) is an agriculturally acceptable salt. Item 71. The method of item 68, wherein the biological surface is a human or animal body part. Item 72. The method of item 71, wherein the salt of the EDTA derivative of Formula (I) is a pharmaceutically acceptable salt. Item 73. The method of any one of items 65 to 67, wherein the surface is a non- biological surface. Item 74. The method of item 73, wherein the non-biological surface is the surface of an article of manufacture. Item 75. The method of item 74, wherein the article of manufacture is a veterinary and human medical device, a pipe, a filter, a wall, a floor, a table-tops or a toilet. Item 76. Use of a biocide composition as defined in any one of items 1 to 64 for inhibiting microbial pathogen and biofilm formation on a surface. Item 77. Use of a biocide composition as defined in any one of items 1 to 64 for disrupting pre-existing microbial pathogens and biofilms on a surface. Item 78. Use of a biocide composition as defined in any one of items 1 to 64 for controlling insect pests on a surface. *** In some of the implementations where the application is an agricultural application described in the present description include the following items: Item 1. A pesticidal composition for application to a plant, comprising a photosensitizer and an EDTA derivative comprising a hydrophobic moiety that is covalently bound to the EDTA. Item 2. The pesticidal composition of item 1, wherein the EDTA derivative is a compound Formula (I): Formula (I) or an agriculturally acceptable salt thereof, wherein: Z is NH or O; and R ₁ is selected from the group consisting of an optionally substituted C ₄ -C ₁₈ alkyl group, an optionally substituted C ₄ -C ₁₈ alkenyl group, an optionally substituted C ₄ -C ₁₈ alkynyl group and an optionally substituted steroidyl group. Item 3. The pesticidal composition of item 2, wherein the steroidyl group is: . Item 4. The pesticidal composition of item 2, wherein R ₁ is selected from the group consisting of an optionally substituted C ₈ -C ₁₅ alkyl group, an optionally substituted C ₈ - C ₁₅ alkenyl group and an optionally substituted C ₈ -C ₁₅ alkynyl group. Item 5. The pesticidal composition of item 2, wherein R ₁ is an optionally substituted C ₈ - C ₁₅ alkyl group. Item 6. The pesticidal composition of item 2, wherein R ₁ is an unsubstituted C ₈ -C ₁₅ alkyl group. Item 7. The pesticidal composition of item 2, wherein the compound of Formula (I) is:

or an agriculturally acceptable salt thereof. Item 8. The pesticidal composition of item 7, wherein the compound of Formula (I) is:

or an agriculturally acceptable salt thereof. Item 9. The pesticidal composition of item 2, wherein the compound of Formula (I) is:

or an agriculturally acceptable salt thereof. Item 10. The pesticidal composition of item 9, wherein the compound of Formula (I) is:

or an agriculturally acceptable salt thereof. Item 11. The pesticidal composition of any one of items 1 to 10, wherein the photosensitizer is a macrocyclic tetrapyrrole compound selected from the group consisting of a porphyrin, a reduced porphyrin and a mixture of at least two thereof. Item 12. The pesticidal composition of item 11, wherein the reduced porphyrin compound is selected from the group consisting of a chlorin, a bacteriochlorin, an isobacteriochlorin, a corrin, a corphin, and a mixture of at least two thereof. Item 13. The pesticidal composition of item 11 or 12, wherein the macrocyclic tetrapyrrole compound is complexed with a metal to form a metallated macrocyclic tetrapyrrole compound. Item 14. The pesticidal composition of item 13, wherein the metal is selected such that, in response to light exposure, the metallated photosensitive compound generates reactive oxygen species. Item 15. The pesticidal composition of item 14, wherein the metal is selected from the group consisting of Mg, Pd, Co, Al, Ni, Zn, Sn, and Si. Item 16. The pesticidal composition of item 13, wherein the metal is selected such that the metallated macrocyclic tetrapyrrole compound does not generate singlet oxygen. Item 17. The pesticidal composition of item 16, wherein the metal is selected from the group consisting of Cu, Co, Fe, and Mn. Item 18. The pesticidal composition of any one of items 11 to 17, wherein the macrocyclic tetrapyrrole compound comprises chlorophyllin. Item 19. The pesticidal composition of any one of items 11 to 18, wherein the macrocyclic tetrapyrrole compound comprises Chlorophyll a. Item 20. The pesticidal composition of any one of items 11 to 19, wherein the macrocyclic tetrapyrrole compound comprises chlorin e6. Item 21. The pesticidal composition of any one of items 11 to 20, wherein the macrocyclic tetrapyrrole compound comprises protoporphyrin IX. Item 22. The pesticidal composition of any one of items 11 to 21, wherein the macrocyclic tetrapyrrole compound comprises tetraphenylporphyrin. Item 23. The pesticidal composition of any one of items 11 to 22, wherein the macrocyclic tetrapyrrole compound comprises an extracted naturally-occurring macrocyclic tetrapyrrole compound. Item 24. The pesticidal composition of any one of items 11 to 23, wherein the macrocyclic tetrapyrrole compound comprises a synthetic macrocyclic tetrapyrrole compound. Item 25. The pesticidal composition of any one of items 1 to 10, wherein the photosensitizer is an isoquinoline derivative, such as berberine. Item 26. The pesticidal composition of any one of items 1 to 10, wherein the photosensitizer is a diarylheptanoid, such as curcumin. Item 27. The pesticidal composition of any one of items 1 to 26, further comprising at least one base. Item 28. The pesticidal composition of item 27, wherein the base is selected from the group consisting of triethanolamine (N(CH2CH2OH)3), TRIS-buffer ((2-Amino-2- (hydroxymethyl)propane-1,3-diol), sodium bicarbonate (NaHCO3), potassium bicarbonate (KHCO3), sodium carbonate (Na2CO3) and potassium carbonate (K2CO3). Item 29. The pesticidal composition of item 28, wherein the base is TRIS-buffer ((2- Amino-2-(hydroxymethyl)propane-1,3-diol). Item 30. The pesticidal composition of item 28, wherein the base is sodium carbonate (Na ₂ CO ₃ ). Item 31. The pesticidal composition of any one of items 1 to 30, further comprising at least one essential oil. Item 32. The pesticidal composition of item 31, wherein the essential oil is selected from the group consisting of thymol, eugenol, geranial, nerol, citral, carvacrol, cinnamaldehyde, terpinol, α-terpinene, citronellal, citronellol, geraniol, geranyl acetate, limonene, lavender oil, methyl isoeugenol and mixtures thereof. Item 33. The pesticidal composition of item 32, wherein the essential oil comprises thymol, carvacrol, or α-terpinene. Item 34. The pesticidal composition of item 33, wherein the essential oil comprises thymol. Item 35. The pesticidal composition of any one of items 1 to 34, further comprising at least one biosurfactant. Item 36. The pesticidal composition of item 35, wherein the biosurfactant is selected from the group consisting of an alkyl polyglycoside, a rhamnolipid, a sophorolipid and a combination of at least two thereof. Item 37. The pesticidal composition of item 36, wherein the biosurfactant is an alkyl polyglycoside. Item 38. The pesticidal composition of any one of items 1 to 37, further comprising at least one oil selected from the group consisting of a mineral oil, a vegetable oil, and a mixture of at least two thereof. Item 39. The pesticidal composition of item 38, wherein the oil comprises a vegetable oil selected from the group consisting of coconut oil, canola oil, soybean oil, rapeseed oil, sunflower oil, safflower oil, peanut oil, cottonseed oil, palm oil, rice bran oil, and a mixture of at least two thereof. Item 40. The pesticidal composition of item 38 or 39, wherein the oil comprises a mineral oil selected from the group consisting of paraffinic oils, branched paraffinic oils, naphthenic oils, aromatic oils, and a mixture of at least two thereof. Item 41. The pesticidal composition of item 40, wherein the paraffinic oil is a poly- alpha-olefin (PAO). Item 42. The pesticidal composition of any one of items 1 to 41, further comprising at least one surfactant. Item 43. The pesticidal composition of item 42, wherein the surfactant is selected from the group consisting of a non-ionic surfactant, a cationic surfactant, an anionic surfactant, a zwitterionic surfactant or a combination of at least two thereof. Item 44. The pesticidal composition of item 43, wherein the surfactant comprises a non-ionic surfactant selected from the group consisting of ethoxylated alcohol, a polymeric surfactant, a fatty acid ester, a poly(ethylene glycol), an ethoxylated alkyl alcohol, a monoglyceride, an alkyl monoglyceride, a polysorbate, and a mixture of at least two thereof. Item 45. The pesticidal composition of any one of items 1 to 44, further comprising at least one solvent selected from an aqueous solvent, a non-aqueous, or a miscible mixture of at least two thereof. Item 46. The pesticidal composition of item 45, wherein the solvent comprises water. Item 47. The pesticidal composition of item 45 or 46, wherein the solvent comprises a non-aqueous solvent which is at least partially soluble in water. Item 48. The pesticidal composition of any one of items 45 to 47, wherein the solvent comprises a non-aqueous solvent selected from the group consisting of ethanol, acetone, isopropanol, ethylene glycol, propylene glycol and a miscible mixture of at least two thereof. Item 49. The pesticidal composition of any one of items 45 to 48, wherein the solvent comprises isopropanol. Item 50. The pesticidal composition of any one of items 1 to 49, further comprising at least one additional chelating agent. Item 51. The pesticidal composition of item 50, wherein the additional chelating agent is EDTA. Item 52. The pesticidal composition of any one of items 1 to 49, which is free of an additional chelating agent. Item 53. The pesticidal composition of any one of items 1 to 52, wherein the pesticidal composition is provided as a multiple-pack system comprising at least two packs, each one of the two packs comprising at least one separate component of the composition. Item 54. The pesticidal composition of any one of items 1 to 53, which is an antimicrobial composition. Item 55. The pesticidal composition of any one of items 1 to 53, which is an antibiofilm composition. Item 56. The pesticidal composition of any one of items 1 to 53, which is an insecticide composition. Item 57. A method for inhibiting microbial pathogen and biofilm formation on a plant, comprising applying the pesticidal composition of any one of items 1 to 56 to the plant. Item 58. A method for disrupting pre-existing microbial pathogens and biofilms on a plant, comprising applying the pesticidal composition of any one of items 1 to 56 to the plant. Item 59. A method for controlling insect pests on a plant, comprising applying the pesticidal composition of any one of items 1 to 56 to the plant. Item 60. Use of a pesticidal composition as defined in any one of items 1 to 56 for inhibiting microbial pathogen and biofilm formation on a plant. Item 61. Use of a pesticidal composition as defined in any one of items 1 to 56 for disrupting pre-existing microbial pathogens and biofilms on a plant. Item 62. Use of a pesticidal composition as defined in any one of items 1 to 56 for controlling insect pests on a plant. *** In some of the implementations where the application is a veterinary application described in the present description include the following items: Item 1. A biocide composition comprising an EDTA derivative and a liquid carrier, wherein the EDTA derivative is of Formula (I): Formula (I) or a pharmaceutically acceptable salt thereof, wherein: Z is NH or O; and R1 is selected from the group consisting of an optionally substituted C8-C18alkyl group, an optionally substituted C8-C18alkenyl group, an optionally substituted C8-C18alkynyl group and an optionally substituted steroidyl group; wherein the biocide composition is an antimicrobial composition to be applied to a subject or to a device in contact with the subject. Item 2. The biocide composition of item 1, wherein the biocide composition is for use in treating a wound in the subject or for use in disinfecting the device in contact with the subject. Item 3. The biocide composition of item 1 or 2, wherein the subject is a mammal. Item 4. The biocide composition of item 2, wherein the wound is a chronic wound or an acute wound. Item 5. The biocide composition of any one of items 2 to 4, wherein the wound is caused by mastitis, burn wounds, wounds associated with surgery, wound associated with knee replacement, wound associated with hip replacement, skin damage, skin erosion and ulcers including diabetic foot, and bedsore. Item 6. The biocide composition of any one of items 2 to 5, wherein treating the wound comprises: (a) healing the wound, and / or (b) inhibiting or preventing microbial pathogen activity in the wound. Item 7. The biocide composition of any one of items 1-3, wherein the device in contact with the subject is in contact with skin or is inserted in tissues. Item 8. The biocide composition of any one of items 1 to 7, wherein the device is a medical device or an agricultural device. Item 9. The biocide composition of item 8, wherein the agricultural device is an apparatus to milk livestock. Item 10. The biocide composition of item 8, wherein the medical device is a tube or a catheter. Item 11. The biocide composition of any one of items 1 to 10, wherein disinfecting the device in contact with the subject comprises: preventing and/or inhibiting microbial pathogen activity on the device and / or in the subject. Item 12. The biocide composition of any one of items 1 to 11, wherein the steroidyl group is: . Item 13. The biocide composition of any one of items 1 to 11, wherein R ₁ is selected from the group consisting of an optionally substituted C ₁₂ -C ₁₅ alkyl group, an optionally substituted C ₁₂ -C ₁₅ alkenyl group and an optionally substituted C ₁₂ -C ₁₅ alkynyl group. Item 14. The biocide composition of any one of items 1 to 11, wherein R ₁ is an optionally substituted C ₁₂ -C ₁₅ alkyl group. Item 15. The biocide composition of any one of items 1 to 11, wherein R ₁ is an unsubstituted C ₁₂ -C ₁₅ alkyl group. Item 16. The biocide composition of any one of items 1 to 11, wherein the EDTA derivative of Formula (I) is:

or a salt thereof. Item 17. The biocide composition of any one of items 1 to 11, wherein the EDTA derivative of Formula (I) is: or a salt thereof. Item 18. The biocide composition of any one of items 1 to 11, wherein the EDTA derivative of Formula (I) is: or a salt thereof. Item 19. The biocide composition of any one of items 1 to 11, wherein the EDTA derivative of Formula (I) is:

or a salt thereof. Item 20. The biocide composition of any one of items 1 to 11, wherein the EDTA derivative of Formula (I) is: or a salt thereof. Item 21. The biocide composition of any one of items 1 to 11, wherein the EDTA derivative of Formula (I) is: or a salt thereof. Item 22. The biocide composition of any one of items 1 to 21, wherein the liquid carrier is selected from the group consisting of an aqueous carrier, methanol, ethanol and tetrahydrofuran. Item 23. The biocide composition of any one of items 1 to 22, further comprising at least one photosensitizer compound. Item 24. The biocide composition of item 23, wherein the at least one photosensitizer compound is a macrocyclic tetrapyrrole compound selected from the group consisting of a porphyrin, a reduced porphyrin, and a mixture of at least two thereof. Item 25. The biocide composition of item 24, wherein the reduced porphyrin compound is selected from the group consisting of a chlorin, a bacteriochlorin, an isobacteriochlorin, a corrin, a corphin, and a mixture of at least two thereof. Item 26. The biocide composition of item 24 or 25, wherein the macrocyclic tetrapyrrole compound is complexed with a metal to form a metallated macrocyclic tetrapyrrole compound. Item 27. The biocide composition of item 26, wherein the metal is selected such that, in response to light exposure, the metallated photosensitive compound generates reactive oxygen species. Item 28. The biocide composition of item 27, wherein the metal is selected from the group consisting of Mg, Pd, Co, Al, Ni, Zn, Sn, and Si. Item 29. The biocide composition of item 26, wherein the metal is selected such that the metallated macrocyclic tetrapyrrole compound does not generate singlet oxygen. Item 30. The biocide composition of item 29, wherein the metal is selected from the group consisting of Cu, Co, Fe, and Mn. Item 31. The biocide composition of any one of items 24 to 30, wherein the macrocyclic tetrapyrrole compound comprises chlorophyllin. Item 32. The biocide composition of any one of items 24 to 31, wherein the macrocyclic tetrapyrrole compound comprises Chlorophyll a. Item 33. The biocide composition of any one of items 24 to 32, wherein the macrocyclic tetrapyrrole compound comprises chlorin e6. Item 34. The biocide composition of any one of items 24 to 33, wherein the macrocyclic tetrapyrrole compound comprises protoporphyrin IX. Item 35. The biocide composition of any one of items 24 to 34, wherein the macrocyclic tetrapyrrole compound comprises tetraphenylporphyrin. Item 36. The biocide composition of any one of items 24 to 35, wherein the macrocyclic tetrapyrrole compound comprises an extracted naturally occurring macrocyclic tetrapyrrole compound. Item 37. The biocide composition of any one of items 1 to 36, wherein the macrocyclic tetrapyrrole compound comprises a synthetic macrocyclic tetrapyrrole compound. Item 38. The biocide composition of item 23, wherein the at least one photosensitizer compound is an isoquinoline derivative, such as berberine. Item 39. biocide composition of item 23, wherein the at least one photosensitizer compound is a diarylheptanoid, such as curcumin. Item 40. The biocide composition of any one of items 1 to 39, further comprising at least one biocompatible polymer. Item 41. The biocide composition of item 40, wherein the biocompatible polymer is selected from the group consisting of polystyrene and polycaprolactone. Item 42. The biocide composition of item 40 or 41, wherein the biocide composition further comprises a solvent selected from the group consisting of tetrahydrofuran and methanol. Item 43. The biocide composition of any one of items 1 to 42, further comprising at least one additional chelating agent. Item 44. The biocide composition of item 43, wherein the additional chelating agent is EDTA. Item 45. The biocide composition of any one of items 1 to 42, which is free of an additional chelating agent. Item 46. A method for treating a wound on or in a subject, comprising applying the biocide composition of any one of items 1 to 45 to the wound. Item 47. A method for inhibiting microbial pathogens on a wound on or in a subject, on a skin, or on a device in contact with a subject, comprising applying the biocide composition of any one of items 1 to 45 to the wound, the skin, or the device. Item 48. A method for disrupting pre-existing microbial pathogens on a wound on or in a subject, on a skin, or on a device in contact with a subject, comprising applying the biocide composition of any one of items 1 to 45 to the wound, the skin, or the device. Item 49. The method of any one of items 46 to 48, wherein the subject is a mammal. Item 50. The method of any one of items 46 to 48, wherein the wound is a chronic wound or an acute wound. Item 51. The method of any one of items 46 to 50, wherein the salt of the EDTA derivative of Formula (I) is a pharmaceutically acceptable salt. Item 52. The method of any one of items 46 to 51, further comprising exposing the wound to illumination to induce photodynamic inactivation (PDI). Item 53. Use of a biocide composition as defined in any one of items 1 to 45 for treating a wound on or in a subject. Item 54. Use of a biocide composition as defined in any one of items 1 to 45 for inhibiting microbial pathogens on a wound on or in a subject, on a skin, or on a device in contact with a subject. Item 55. Use of a biocide composition as defined in any one of items 1 to 45 for disrupting pre-existing microbial pathogens on a wound on or in a subject, on a skin, or on a device in contact with a subject.