Comparative Efficacy of Residual Insecticides against the Turkestan Cockroach,  Blatta lateralis , (Blattodea: Blattidae) on Different Substrates

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Abstract

The Turkestan cockroach, Blatta lateralis (Walker) is an invasive urban pest prevalent throughout the Southwestern United States. Despite the presence of this cockroach in peridomestic areas, there is limited information on strategies that can be utilized by pest management professionals (PMPs) to effectively manage populations of this pest. We evaluated the efficacy of dry residues of liquid insecticides commonly used for household and structural insect pest control: Tandem (0.10% thiamethoxam, 0.03% lambda-cyhalothrin), Transport GHP (0.05% acetamiprid, 0.06% bifenthrin), Temprid SC (0.10% imidacloprid, 0.05% beta-cyfluthrin), Demand CS (0.06% lambda-cyhalothrin), Talstar P (0.06% bifenthrin), and Phantom (0.5% chlorfenapyr) on three different substrates against Turkestan cockroach nymphs. Except for Phantom and Talstar P, all insecticide formulations killed 100% of the cockroaches on concrete, 89–100% on tile, and 77–100% on wood within 4 days. The rate of cockroach mortality varied according to the substrates to which they were exposed. Temprid SC and Transport GHP killed cockroaches faster on tile than wood. Tandem provided a faster mortality rate than Transport GHP and Temprid SC on concrete. Demand CS and Tandem killed cockroaches at similar rates on the three substrates. This study provides information to guide PMPs in their selection of insecticide formulations for the management of Turkestan cockroach infestations.

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Systemic insecticides (neonicotinoids and fipronil): trends, uses, mode of action and metabolites

N. Simon-Delso, V. Amaral-Rogers, L P Belzunces … (2014)

Since their discovery in the late 1980s, neonicotinoid pesticides have become the most widely used class of insecticides worldwide, with large-scale applications ranging from plant protection (crops, vegetables, fruits), veterinary products, and biocides to invertebrate pest control in fish farming. In this review, we address the phenyl-pyrazole fipronil together with neonicotinoids because of similarities in their toxicity, physicochemical profiles, and presence in the environment. Neonicotinoids and fipronil currently account for approximately one third of the world insecticide market; the annual world production of the archetype neonicotinoid, imidacloprid, was estimated to be ca. 20,000 tonnes active substance in 2010. There were several reasons for the initial success of neonicotinoids and fipronil: (1) there was no known pesticide resistance in target pests, mainly because of their recent development, (2) their physicochemical properties included many advantages over previous generations of insecticides (i.e., organophosphates, carbamates, pyrethroids, etc.), and (3) they shared an assumed reduced operator and consumer risk. Due to their systemic nature, they are taken up by the roots or leaves and translocated to all parts of the plant, which, in turn, makes them effectively toxic to herbivorous insects. The toxicity persists for a variable period of time—depending on the plant, its growth stage, and the amount of pesticide applied. A wide variety of applications are available, including the most common prophylactic non-Good Agricultural Practices (GAP) application by seed coating. As a result of their extensive use and physicochemical properties, these substances can be found in all environmental compartments including soil, water, and air. Neonicotinoids and fipronil operate by disrupting neural transmission in the central nervous system of invertebrates. Neonicotinoids mimic the action of neurotransmitters, while fipronil inhibits neuronal receptors. In doing so, they continuously stimulate neurons leading ultimately to death of target invertebrates. Like virtually all insecticides, they can also have lethal and sublethal impacts on non-target organisms, including insect predators and vertebrates. Furthermore, a range of synergistic effects with other stressors have been documented. Here, we review extensively their metabolic pathways, showing how they form both compound-specific and common metabolites which can themselves be toxic. These may result in prolonged toxicity. Considering their wide commercial expansion, mode of action, the systemic properties in plants, persistence and environmental fate, coupled with limited information about the toxicity profiles of these compounds and their metabolites, neonicotinoids and fipronil may entail significant risks to the environment. A global evaluation of the potential collateral effects of their use is therefore timely. The present paper and subsequent chapters in this review of the global literature explore these risks and show a growing body of evidence that persistent, low concentrations of these insecticides pose serious risks of undesirable environmental impacts.

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Overlapping confidence intervals or standard error intervals: What do they mean in terms of statistical significance?

Mark E. Payton, Matthew Greenstone, Nathaniel Schenker (2003)

We investigate the procedure of checking for overlap between confidence intervals or standard error intervals to draw conclusions regarding hypotheses about differences between population parameters. Mathematical expressions and algebraic manipulations are given, and computer simulations are performed to assess the usefulness of confidence and standard error intervals in this manner. We make recommendations for their use in situations in which standard tests of hypotheses do not exist. An example is given that tests this methodology for comparing effective dose levels in independent probit regressions, an application that is also pertinent to derivations of LC50s for insect pathogens and of detectability half-lives for prey proteins or DNA sequences in predator gut analysis.

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Neurotoxic actions of pyrethroid insecticides.

D Söderlund, J Bloomquist (1988)

Pyrethroid insecticides interact with a variety of neurochemical processes, but not all of these actions are likely to be involved in the disruption of nerve function. Several lines of evidence suggest that the voltage-sensitive sodium channel is the single principal molecular target site for all pyrethroids and DDT analogs in both insects and mammals. The alterations of sodium channel functions identified in both biophysical and biochemical studies are directly related to the effects of these compounds on intact nerves. The pyrethroid recognition site of the sodium channel exhibits the stringent stereospecificity predicted by in vivo estimates of intrinsic neurotoxicity in both insects and mammals. Type I and Type II compounds produce qualitatively different effects on sodium channel tail currents, divergent actions on intact nerves, and different effects on the excitability of vertebrate skeletal muscle. Moreover, compounds that are defined as intermediate in the Type I/Type II classification scheme are also intermediate in their effects on sodium channel kinetics. The range of different actions on sensory and motor nerve pathways arising from these qualitatively different effects at the level of the sodium channel appear to be sufficient to explain the distinct poisoning syndromes that have been identified in both insects and mammals. Thus, it does not appear necessary to invoke different primary target sites for Type I and Type II compounds to explain their actions in whole animals. Although the voltage-sensitive sodium channel is likely to be the principal site of pyrethroid action, it is probably not the only site involved in intoxication. Insect neurosecretory neurons are sensitive to very low concentrations of pyrethroids, and disruption of the neuroendocrine system has been implicated as a factor contributing to the irreversible effects of pyrethroid intoxication in insects. Since action potentials in these nerves are carried by calcium ions through TTX-insensitive voltage-gated cation channels, these findings provide evidence that pyrethroids can alter neuronal excitability through an action on voltage-sensitive channels other than the sodium channel. Actions on voltage-sensitive calcium channels may also be involved in the effects of pyrethroids on neurotransmitter release in mammals. The proconvulsant actions of pyrethroids mediated through the peripheral-type benzodiazepine receptor may also contribute to pyrethroid intoxication. Both Type I and Type II compounds are potent proconvulsants in vivo at doses well below those required to produce pyrethroid-dependent intoxication.(ABSTRACT TRUNCATED AT 400 WORDS)

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Author and article information

Journal

Journal ID (nlm-ta): Insects

Journal ID (iso-abbrev): Insects

Journal ID (publisher-id): insects

Title: Insects

Publisher: MDPI

ISSN (Electronic): 2075-4450

Publication date (Electronic): 28 July 2020

Publication date Collection: August 2020

Volume: 11

Issue: 8

Electronic Location Identifier: 477

Affiliations

[1 ]Department of Entomology, University of Kentucky, Lexington, KY 40546, USA; sgaire@ 123456uky.edu

[2 ]Department of Entomology, Plant Pathology and Weed Science, New Mexico State University, Las Cruces, NM 88003, USA

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[* ]Correspondence: aromero2@ 123456nmsu.edu ; Tel.: +1-575-646-5550

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Publisher ID: insects-11-00477

DOI: 10.3390/insects11080477

PMC ID: 7469171

PubMed ID: 32731364

SO-VID: 55644fff-e5dd-4579-b811-f06416636d90

License:

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

Comparative Efficacy of Residual Insecticides against the Turkestan Cockroach, Blatta lateralis, (Blattodea: Blattidae) on Different Substrates

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Most cited references 31

Systemic insecticides (neonicotinoids and fipronil): trends, uses, mode of action and metabolites

Overlapping confidence intervals or standard error intervals: What do they mean in terms of statistical significance?

Neurotoxic actions of pyrethroid insecticides.

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