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The effect of a soil application of salicylic acid (SA) and a biocontrol agent, Trichoderma harzianum (TH) on the induction of phenolic accumulation content and defense enzymes in tomato plants infected with Fusarium oxysporum f. sp. lycopersici (F. oxysporum) was investigated. The phenolic content was recorded to be higher in all the treatments viz. F. oxysporum, F. oxysporum + TH, F. oxysporum + SA and F. oxysporum + TH + SA than that of the healthy plants and reached its maximum level in the plants treated with F. oxysporum + TH + SA. Tomato plants treated with different concentrations of SA (0.5, 1.0, 1.5, 2.0, 2.5 and 3.0 mM) showed significant increases in the activities of both peroxidase and polyphenol oxidase where a prominent enhancement was observed at a 1.5 mM concentration of SA. F. oxysporum infection resulted in the induction of both of the enzyme activities but at a lower level. The activities of both peroxidase and polyphenol oxidase reached their maximum on the 28th day, when the plants were treated with F. oxysporum and SA (1.5 mM). The combined application of SA (1.5 mM) and TH in Fusarium infected tomato plants, also enhanced the activities of both of the enzymes.

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Biological control of wilt of egg plant (Solanum melongena L.) caused by Fusarium solani was made with the application of five Trichoderma species, T. harzianum, T. viride, T. lignorum, T. hamatum and T. reesei. The effect of volatile and non-volatile antibiotics of Trichoderma origin on growth inhibition of the wilt pathogen was studied. T. harzianum showed maximum growth inhibition (86.44 %) of the pathogen through mycoparasitism. The nonvolatiles produced by the Trichoderma species exhibited 100 % growth inhibition of the pathogen under in vitro condition. Production of siderophores and fungal cell wall degrading enzymes, chitinase and β-1,3-glucanase were found. Treatments with two most efficient Trichoderma species, T. harzianum and T. viride resulted in the decreasing population of Fusarium solani in soil thereby deterring disease incidence in field condition.

This study was designed to determine the role of a new temperate DNA phage BcP15 in relation to drug resistance. The multidrug resistant Shigella flexneri NK1925 was isolated from a patient of Infectious Diseases Hospital, Kolkata, India. This strain contained five plasmids ranging in size from 3 to 212 kb. After curing of five plasmids, this strain became sensitive to antibiotics. A plasmidless multidrug-resistant strain Burkholderia cepacia DR11 was isolated during the survey of microorganisms from coastal waters of deltaic Sunderbans. This strain always released a temperate phage BcP15 into culture supernatant. Turbid plaque formation was observed on the lawn of a plasmidless version (Pl(-)35) of Shigella flexneri NK1925. A few distinct clones (Pl(-)35R) appeared within the region of each plaque after 18 h incubation. S. flexneri NK1925, Pl(-)35, and Pl(-)35R clones showed the same PFGE band pattern of XbaI-digested chromosomal DNA. However, Pl(-)35R clones were resistant to co-trimoxazole, trimethoprim, and eryth- romycin, to which B. cepacia DR11 was also resistant. Southern hybridization results indicated that these three antibiotic resistances in Pl(-)35R clones were due to a BcP15 phage lysogen in the Pl(-)35 version of S. flexneri NK1925.