ELECTRON MICROSCOPY OF ENTOMOPATHOGENIC FUNGAL INVASION ON THE CABBAGE-HEART CATERPILLAR CROCIDOLOMIA BINOTALIS ZELLER (LEPIDOPTERA: PYRALIDAE)

The infection on Crocidolomia binotalis Zeller by the entomopathogenic fungi Paecilomyces fumosoroseus (Wise) Brown and Smith, Beauveria bassiana (Bals.) Vuill, and Metarhizium anisopliae var. majus (Metsch.) Sorokin was studied histopathologically using electron microscopy. Conidia which landed on the cuticle germinated within four to six hours. In the case of B. basiana, shortly after landing, an appresorium was formed that attached itself fast onto the cuticle at the point of fungal entry. The infected larva then entered the moribund state 12 to 24 hours after inoculation. Death of the larva followed 24 to 48 hours later. By then the body cavity as well as the trachea were clogged with mycelia, and compacted masses conidiophores producing white conidia were found all over the larval cadaver one to two days later. P. fumosoroseus sporulated more abundantly on the surface of the cadaver compared to B. bassiana or M. anisopliae.

THE STRIPED LYNX SPIDER, OXYOPES SALTICUS HENTZ (ARANEAE: OXYOPIDAE), AS A VECTOR OF A NUCLEAR POLYHEDROSIS VIRUS IN ANTICARSIA GEMMATALIS HÜBNER (LEPIDOPTERA: NOCTUIDAE)1

The potential for transmission of a nuclear polyhedrosis virus of Anticarsia gemmatalis Hübner (AgNPV) by the striped lynx spider, Oxyopes salticus Hentz, was examined in the laboratory. Activity of the virus in excreta of O. salticus which had fed on an AgNPV - infected A. gemmatalis larva was bioassayed on alternate days over a 14 - day period. Oxyopes salticus excreta contained an average of 3.3 ± 2.2 × 104 polyhedral inclusion bodies per spider over the test period, with 95% of the active virus excreted within 24 hrs of ingestion. The amount of virus excreted was significant because only a mean of 1.2% of the total virus present in infected larva was consumed by the spider. The results suggest that O. salticus, and probably other spider predators in soybeans, may be important in dissemination of AgNPV in A. gemmatalis populations.

Tolypocladium cylindrosporum. [Descriptions of Fungi and Bacteria].

A description is provided for Tolypocladium cylindrosporum. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS AND SUBSTRATA: Diptera: Aedes sierrensis and A. australis (Culicidae); Plecia neararctica (Bibionidae). Experimental infection of A. aegypti, A. caspius, Anopheles stephansi and Culex pipiens was successful (Soares 1982). Also found on bracken debris, Eucalyptus sp. and in soil. GEOGRAPHICAL DISTRIBUTION: Soil in Europe (Czechoslovakia, the Netherlands, UK), Nepal, Canada; Diptera in USA (California, Florida), N.Z. ; Eucalyptus sp., Australia; Picea mariana, Canada. DISEASE: Natural infections of treehole populations of A. sierrensis cause over 70% mortality. Infection of mosquito larvae occurs both through the external cuticle and the gut, mostly the midgut (Soares, 1982). The fungus multiplies in the host by mycelial growth and by forming blastospores. In some hosts encapsulation of invading hyphae occurs, the host dying only after the haemocoel is extensively invaded. Conidia are formed enteroblastically only if the infected larva is at the water surface, when a small mycelial mat is produced which sporulates actively. Adult females spread the disease from tree holes to other tree holes when laying and are themselves susceptible to the fungus (Federici et al., 1980). Experimental infection of Culex molestus[Culex pipiens form molestus] followed the same pattern, first symptoms appearing 5 days after infection, all exposed larvae being dead within 7 days (Weiser & Pillai, 1982).

DISEASE OF THE LARVAE OF TENT CATERPILLARS CAUSED BY A SPOREFORMING BACTERIUM

A newly discovered bacterial disease of larvae of Malacosoma pluviale (Dyar) (Lep.) is caused by infection of the gut with a large, motile, sporeforming bacterium, Bacillus sp., that increases in size before sporulation and bears the spore without bulging. It has not been cultivated. The bacterium invades the host with the food and multiplies in the midgut and foregut, producing changes in the pH and causing dysentery in the host. Sporulation occurs in the gut and both rods and spores are passed in the faeces and spread the disease. The infected larva loses its appetite, regurgitates excessively, produces wet faeces, decreases markedly in length, and dies in a characteristic, short, dry, mummified condition after about a week. Small ingested doses of spores initiate infection in laboratory populations of M. pluviale in all instars. M. americana (F.) also is susceptible to the disease but M. disstria Hbn. is resistant, only a few individuals dying from it.