Integrated Pest Management and Spatial Structure

During long time pest control was associated only to insecticides. The formulations were produced as an attempt of improving the insect control. However, some undesirable effects emerged in this time, mainly the toxin action and resistance. Insecticides are substances produced from chemical or biological products to control insect pests. The most common mode of action for insecticides is to kill insects by blocking physiological or biochemical processes (Ware & Whitacre, 2004). Usually, insecticides act on the nervous system, resulting in high efficacy and rapid responses in pest-control programs. Insecticides can be classified as physical, protoplasmic, metabolic inhibitors, neurotoxins, and hormone agonists (Matsumura, 1985). Mineral oil is an example of a physical insecticide, and heavy metals are protoplasmic insecticides (Amiri-Besheli, 2008; Gallo et al, 2002). Some examples of metabolic inhibitors are the inhibitors of multi-function oxidases, carbohydrate and amino-acid metabolism inhibitors, and chitin-synthesis inhibitors (Krieger, 2001). The neurotoxins act through acetylcholinesterase, the neurotoxin that affects ion permeability, intervening in the nerve receptors of insects (Haynes, 1988), killing the arthropod by disrupting the membrane integrity (Gill et al, 1992). The main groups of insecticides can be studied using the following classification: neurotoxins, insect growth regulators, cellular respiration inhibitors, and others. Of the neurotoxins, the organophosphates and carbamates act on synaptic transmission, accumulating acetylcholine molecules in the synapse, which in insects can produce a cholinergic syndrome characterized by nerve hyperexcitation (Costa et al, 2008; Thacker, 2002). The acetylcholine agonists nicotines, neonicotinoids (the newest group of synthetic insecticides) and spinosines connect to the nicotine receptors of acetylcholine located in the pre-synaptic neuron (Thacker, 2002). In this case, the nerve impulses are continuously transmitted, also resulting in nerve hyper-excitation in the insect (Thacker, 2002). The acetylcholine antagonists avermectin and milbemycin block the nerve stimulus, immobilizing the insect. Cyclodienes and phenyl-pyrazoles act differently from avermectin and milbemycin, killing insects by inducing hyperexcitability (Thacker, 2002). DDT (dichlorodiphenyltrichloroethane) and pyrethroids are sodium-channel modulators, acting on sodium channels of nerve cells in insects (Thacker, 2002). Action potentials can be repetitive, 1