Pathogenicity of the Fungus, Aspergillus clavatus, Isolated from the Locust, Oedaleus senegalensis, Against Larvae of the Mosquitoes Aedes aegypti, Anopheles gambiae and Culex quinquefasciatus

The use of insect pathogenic fungi is a promising alternative to chemical control against mosquitoes. Among the Hyphomycetes isolated from insects for mosquito control, the genus Aspergillus remains the least studied. In September 2005, four fungi were isolated from the Senegalese locust, Oedaleus senegalensis Kraus (Orthoptera: Acrididae), collected in Dakar, Senegal. One of these fungi, identified as Aspergillus clavatus, Desmazières (Eurotiales: Trichocomaceae) was highly pathogenic against larvae of the mosquitoes Aedes aegypti L., Anopheles gambiae s.l. Giles and Culex quinquefasciatus Say (Diptera: Culicidae). An application of 1.2 mg/ml dry conidia yielded 100% mortality after 24 hours against both Ae. aegypti and Cx. quinquefasciatus while with An. gambiae it was 95%. With unidentified species in the genus Aspergillus, mortality after 24 h was <5% against all the larval species. Application of A. clavatus produced in a wheat powder medium using doses ranging between 4.3 to 21×107 spores/ml, caused 11 to 68% mortality against Cx. quinquefasciatus at 24h, and 37 to 100% against Ae. aegypti. Microscopic observations showed fungal germination on both Ae. aegypti and Cx. quinquefasciatus larvae. Histological studies revealed that A. clavatus penetrated the cuticle, invaded the gut and disintegrated its cells. Some Cx. quinquefasciatus larvae, treated with A. clavatus reached the pupal stage and produced infected adults. However, the infection was mainly located on the extremity of their abdomen. These results suggest that A. clavatus could be an effective tool to manage mosquito proliferation

Metarhizium anisopliae Pathogenesis of Mosquito Larvae: A Verdict of Accidental Death

Metarhizium anisopliae, a fungal pathogen of terrestrial arthropods, kills the aquatic larvae of Aedes aegypti, the vector of dengue and yellow fever. The fungus kills without adhering to the host cuticle. Ingested conidia also fail to germinate and are expelled in fecal pellets. This study investigates the mechanism by which this fungus adapted to terrestrial hosts kills aquatic mosquito larvae. Genes associated with the M. anisopliae early pathogenic response (proteinases Pr1 and Pr2, and adhesins, Mad1 and Mad2) are upregulated in the presence of larvae, but the established infection process observed in terrestrial hosts does not progress and insecticidal destruxins were not detected. Protease inhibitors reduce larval mortality indicating the importance of proteases in the host interaction. The Ae. aegypti immune response to M. anisopliae appears limited, whilst the oxidative stress response gene encoding for thiol peroxidase is upregulated. Cecropin and Hsp70 genes are downregulated as larval death occurs, and insect mortality appears to be linked to autolysis through caspase activity regulated by Hsp70 and inhibited, in infected larvae, by protease inhibitors. Evidence is presented that a traditional host-pathogen response does not occur as the species have not evolved to interact. M. anisopliae retains pre-formed pathogenic determinants which mediate host mortality, but unlike true aquatic fungal pathogens, does not recognise and colonise the larval host