Stressors and rearing diseases of Trichoplusia ni: evidence of vertical transmission of NPV and CPV.

Inability to consistently rear healthy Trichoplusia ni led to a study of its rearing diseases. Four diseases were designated after preliminary research which included electron microscopy: cytoplasmic polyhedrosis (due to cytoplasmic polyhedrosis virus, or CPV), nuclear polyhedrosis (due to nucleopolyhedrovirus, or NPV), "neonate death" syndrome (mortality in first or second instars), and "late-instar" syndrome (death in late instars accompanied by bacterial decomposition). Infectious agents were not detected by electron microscopy in insects with the latter two diseases. Prevalence of CPV and NPV, but not the neonate-death or late-instar diseases, in progeny was significantly associated with pairs of mating adults. In conjunction with egg-surface decontamination, this indicated that both viruses may be transmitted transovarially. Pupae killed by CPV had virions in the cytoplasm of infected cells, but polyhedra were empty, not occluding virions. None of the diseases had a consistent pattern of prevalence associated with the date on which eggs were laid after oviposition began. Prevalence rates of cytoplasmic polyhedrosis, nuclear polyhedrosis, and the late-instar disease were significantly greater at 95-100% relative humidity (RH) than at RH levels of 75% or below. These same three diseases killed significantly more insects in crowded rearing conditions (four or five larvae per cup with 10.2-cm(2) diet surface) than in uncrowded conditions (one to three larvae per cup). As a result of these experiments, healthy T. ni have been reared for 10 generations by use of a modified Pasteur method and rearing cups containing no more than two larvae.