No abstract

Since 1991, a new disease of cucurbits in central Texas and Oklahoma, designated yellow vine, has resulted in the decline and plant death of watermelon, cantaloupe, squash, and pumpkin. Affected plants are characterized by leaf yellowing, phloem discoloration, and plant collapse. Year-to-year variation in disease incidence has ranged from spotty outbreaks to complete crop loss in early-planted watermelon fields. A systematic investigation to determine the causal agent of the disease included pathogen isolation attempts, transmission tests, serological assays with various antisera (enzyme-linked immunosorbent assay and Western blotting), and DNA hybridizations with selected probes (dot and Southern blots). None of these tests revealed a consistent relationship between the expression of yellow vine symptoms and the presence of a particular microorganism or virus in the plant. However, transmission electron microscopic examination showed the consistent presence of a bacterium in the phloem sieve elements of symptomatic plants. The rod-shaped bacteria, observed only in symptomatic cucurbits, measured 0.25 to 0.5 μm in width and 1.0 to 3.0 μm in length and were surrounded by a triple-layered cell envelope.

When cat fleas, Ctenocephalides felis (Bouché), were fed concentrations of lufenuron in cattle blood ranging from 0.5 to 4 ppm, adult mortality increased in a dose-dependent manner to a maximum of approximately 24% over a period of 10 d. Fleas treated with 0.5 ppm produced abnormal endocuticle consisting of protein globules embedded in an amorphous chitin matrix. At concentrations of 1.0 ppm or greater, endocuticle formation was inhibited. Ultrastructural studies demonstrated that inhibition of chitin synthesis was associated with degeneration of the epidermal cells. The amount of epidermal cytoplasm decreased and cytoplasmic organelles including mitochondria, ribosomes, and golgi showed lytic changes. At least some mortality of treated fleas was likely the result of a weakened endocuticle and the corresponding decrease in resiliency of the cuticle to expansion during blood-feeding and egg production. An unexpected result of lufenuron treatment was the inhibition of midgut epithelial cell differentiation. At concentrations of 0.5 and 1.0 ppm, partially differentiated epithelial cells were seen in the midgut of bloodfed fleas along with fully differentiated cells.

Adult cat fleas, Ctenocephalides felis (Bouché), were fed suboptimal in vitro concentrations of lufenuron in blood to allow hatching of flea larvae for cytological study. At concentrations of 0.125, 0.25, and 0.5 ppm, larval hatch was 64, 15, and 4%, respectively. Larvae hatching from eggs laid by adults fed lufenuron at concentrations of 0.025, 0.08, or 0.125 ppm did not differ significantly from the control. However, many larvae from the 0.08-ppm group and higher concentrations died during the 1st instar. Examination of these larvae revealed that they were dying from desiccation caused by bleeding from microscopic lesions in the cuticle or the inability to complete the molt to the next instar. Electron micrographs showed that lufenuron often disrupted formation of the endocuticle resulting in the deposition of an amorphous mass of randomly oriented chitin microfibrils. Other larvae formed normal endocuticle but were unable to digest the old endocuticle or produce new procuticle after apolysis. Failure of larvae to digest old cuticle or form new cuticle was caused by degeneration of the epidermal cells needed for the synthesis of molting fluid and chitin.

An antiserum raised against the peptide, culetachykinin II, immunocytochemically detected a group of neurosecretory cells in the first flagellar segment of the antennae of both males and females of the mosquito, Culex salinarius. This is the first insect species in which neurosecretory cells have been found in the antennae. The ultrastructure of these antennal neurosecretory cells (ANC) is described, as well as their relationship to other neurons in the antennae and antennal lobe of the mosquito. These tachykinin-reactive cells contain relatively small (140-220 nm) elementary neurosecretory granules. Not only do the ANC have axons that terminate on specific glomeruli of the deutocerebrum, but these neurons also have collaterals that form neurohemal terminals in the receptor lymph channels of the dendrites of the sensory neurons. Thus, the ANC not only influence higher centers of the brain that interpret signals from the antennal sensillae, but also modulate the response of the sensory receptors. To our knowledge, this is the first report of neurosecretory cells directly affecting the signal reception of sensory neurons.