The probable cause of "sweet itch" in England.
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Burgeoning consumer interest in organically produced foods has made organic farming one of the fastest growing segments of agriculture. This growth has not been supported adequately by rigorous research to address challenges such as arthropod pest management. The research that has been conducted, however, is complemented by research in aspects of conventional agriculture that may have applicability in organic systems, as well as by research in underpinning fields such as applied ecology. This article synthesizes the available literature in relation to a conceptual model of arthropod pest management strategies suitable for organic systems. The present work uses the four phases of the model to review the strategies in an agroecological context and provides a synthesis of the factors that influence the success of each phase. Rather than constituting a fringe science, pest management research for organic systems draws on cutting edge science in fields such as landscape and chemical ecology and has a bright future.
Push-pull strategies involve the behavioral manipulation of insect pests and their natural enemies via the integration of stimuli that act to make the protected resource unattractive or unsuitable to the pests (push) while luring them toward an attractive source (pull) from where the pests are subsequently removed. The push and pull components are generally nontoxic. Therefore, the strategies are usually integrated with methods for population reduction, preferably biological control. Push-pull strategies maximize efficacy of behavior-manipulating stimuli through the additive and synergistic effects of integrating their use. By orchestrating a predictable distribution of pests, efficiency of population-reducing components can also be increased. The strategy is a useful tool for integrated pest management programs reducing pesticide input. We describe the principles of the strategy, list the potential components, and present case studies reviewing work on the development and use of push-pull strategies in each of the major areas of pest control.
Contact with insects may induce cutaneous or systemic reactions, ranging from little more than annoying to life threatening. The diagnosis depends on maintaining a high index of suspicion and being familiar with the insect fauna of the patient's environment and area of travel.
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This is a case report of central nervous system toxicity associated with paradichlorobenzene (PDCB) ingestion. The patient had ingested mothballs composed of 99.99% PDCB for a period of 7 months. She was admitted for depression and had no neurologic symptoms. Later she developed an acute cerebellar syndrome followed by stupor and coma. An extensive workup was negative except for decreasing levels of PDCB in her serum. Imaging revealed a diffuse leukoencephalopathy. Her clinical picture was attributed to PDCB toxicity.
Sunscreen use can reduce the incidence of certain skin cancers. However, a number of commercially available formulations have been shown to enhance the transdermal penetration of the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D). Most of the active ingredients used in these compounds can individually act as penetration enhancers. Commercial sunscreens frequently contain multiple active ingredients in order to provide broad sunscreen protection. The purpose of this study was therefore to examine the effect of these active ingredient combinations on the transdermal absorption of 2,4-D in vitro. All six of the combinations tested resulted in increased cumulative penetration (P <0.01) and faster lag times (P <0.05). The 2,4-D cumulative penetration in the presence of the OFF! Deepwoods combination was significantly greater than the absorption with either the individual ingredients or their average (P <0.05). A systematic study designed to isolate the chemicals responsible for this enhancement demonstrated that with UV absorbers DEET synergistically increased the 2,4-D penetration and that DEET's cumulative enhancement properties correlate with its concentration. By contrast, octocrylene significantly slowed the lag time when used in combinations and was the only active ingredient that showed any antagonistic effects on 2,4-D penetration. Because none of the active ingredient combinations were able to inhibit dermal uptake of 2,4-D, it seems that proper selection of inert ingredients may be the most feasible solution for reducing penetration enhancement.
Recently, a dimeticone formulation has been shown to be effective at preventing Schistosoma cercariae infecting skin, while DEET (N,N-diethyl-m-toluamide), a highly effective insecticide, has been shown to have activity against cercariae. Seven formulations, 3 containing DEET, were prepared and applied to excised human skin in Franz cells for 1 h. Schistosoma cercariae were applied for 30 min at 1 and 24 h, and the number that penetrated the skin calculated (n = 9). DEET could not be incorporated into the dimeticone formulation, yet it remained the most effective at preventing cercarial penetration, both 1 and 24 h after application. The ointments that contained DEET did prevent penetration but their mode of action was due to the toxicity of DEET against the cercariae. The persistence of the protection afforded by the dimeticone formulation after washing suggests that the formulation may be interacting with the stratum corneum to prevent cercarial recognition of skin.
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N-allyl (NAOx) and N-propyl (NPOx) oxamates were designed as inhibitors of alpha-hydroxyacid dehydrogenase (HADH) isozyme II from Trypanosoma cruzi. The kinetic studies showed that NAOx and NPOx were competitive inhibitors of HADH-isozyme II (Ki = 72 microM, IC50 = 0.33 mM and 70 microM, IC50 = 0.32 mM, respectively). The attachment of the allylic and propylic chains to nitrogen of the competitive inhibitor oxamate (Ki = 0.91 mM, IC50 = 4.25 mM), increased 12.6 and 13-folds respectively, the affinity for T. cruzi HADH-isozyme II. NAOx and NPOx were selective inhibitors of HADH-isozyme II, because other T. cruzi dehydrogenases were not inhibited by these substances. Since HADH-isozyme II participates in the energy metabolism of T. cruzi, a trypanocidal effect can be expected with these inhibitors. However, we were not able to detect any trypanocidal activity with these oxamates. When the corresponding ethyl esters of N-allyl (Et-NAOx) and N-propyl (Et-NPOx) oxamates were tested as a possible trypanocidal prodrugs, in comparison with nifurtimox and benznidazole, the expected trypanocidal effects were obtained.
Laboratory bioassays were conducted to evaluate neem oil and neem extract for the management of key honey bee (Apis mellifera L.) pests. Neem pesticides inhibited the growth of Paenibacillus larvae (Ash, Priest & Collins) in vitro but had no effect on the growth of Ascophaera apis (Olive & Spiltoir). Azadirachtin-rich extract (neem-aza) was 10 times more potent than crude neem oil (neem oil) against P. larvae suggesting that azadirachtin is a main antibiotic component in neem. Neem-aza, however, was ineffective at controlling the honey bee mite parasites Varroa jacobsoni (Ouduemans) and Acarapis woodi (Rennie). Honey bees also were deterred from feeding on sucrose syrup containing > 0.01 mg/ml of neem-aza. However, neem oil applied topically to infested bees in the laboratory proved highly effective against both mite species. Approximately 50-90% V. jacobsoni mortality was observed 48 h after treatment with associated bee mortality lower than 10%. Although topically applied neem oil did not result in direct A. woodi mortality, it offered significant protection of bees from infestation by A. woodi. Other vegetable and petroleum-based oils also offered selective control of honey bee mites, suggesting neem oil has both a physical and a toxicological mode of action. Although oils are not as selective as the V. jacobsoni acaricide tau-fluvalinate, they nonetheless hold promise for the simultaneous management of several honey bee pests.
Many photoactive dyes are relatively nontoxic to vertebrates despite their insecticidal properties. Several photoactive dyes known to be toxic to some groups of insects were evaluated at various concentrations for toxicity to American and migratory grasshoppers in laboratory and field studies. Rose bengal and phloxine B were effective at inducing mortality of grasshoppers when applied at 2 and 5% to bran bait, though erythrosin B and uranine were ineffective. Partial replacement of phloxine with uranine in dye mixtures resulted in no significant loss of efficacy. Some indication of feeding inhibition was observed at high dye concentrations, so minimum effective dosages, probably 2%, are optimal. Phloxine B and rose bengal appeared to be stable upon exposure to sunlight, and able to withstand at least 24 h of sunlight without significant degradation. Dyes such as phloxine B could be a viable grasshopper control agent for small or medium-sized grasshopper species because mortality can be induced by consumption of a single flake dusted with 5% dye, and yet pose little hazard to vertebrates. Large species such as American grasshopper must consume several flakes before mortality is induced.
Experiments were conducted to determine whether subterranean termites, Reticuliternes virginicus (Banks), previously exposed to sublethal doses of imidacloprid (Premise), and allowed to recover for 1 wk, demonstrated behavioral aversion to a subsequent exposure. Worker termites experiencing a previous sublethal but debilitating exposure to imidacloprid-treated sand (either 10 or 100 ppm for 4 h) showed no apparent aversion to a second encounter with imidacloprid-treated sand under conditions of this experiment. If these laboratory results hold in the field and termites traveling through a zone of soil treated with imidacloprid are impaired but subsequently recover, they will be just as likely as their naive nestmates to reenter the treated area if their travels take them through the nonrepellent application a second time. Our results also indicate that a sublethal exposure to imidacloprid can affect termite tunneling behavior. Many worker termites that received an initial 4-h exposure to 100 ppm imidacloprid-treated sand died, but those that survived tunneled significantly less than did their naive nestmates, as did some termites exposed to 10 ppm imidacloprid.