Chloridea virescens

The tobacco budworm goes through 4 life stages: egg, larval, pupal, and adult. The life cycle generally occurs during the warmer months of late spring to early fall, depending on the region that the budworm is found. During this time, Chloridea virescens can undergo around 4 to 5 generations depending on the region. For larval, pupal, and adult stages, warmer temperatures encourage faster maturation but also faster senescence, while colder climates allow the budworm to mature at a slower rate. Chloridea virescens moths emerge between March and May in the southern United States.[1]

Larval form on petunia buds

Females generally produce 300 to 500 eggs in the wild but have been seen to produce 1000 to 1500 eggs on an artificial diet consisting of primarily water, wheat germ, casein, and sucrose at cool temperatures in an Arizona study.[4] Eggs are deposited on the blossoms, fruit, or terminal growths of host plants. They are initially whitish or yellowish and turn grey as they age. With a radius of 0.5 to 0.6 millimeters, eggs are generally spherical with a flattened base where they are attached to the plant. There are 18 to 25 ridges that radiate from the top of the egg. Tobacco budworm eggs are almost indistinguishable from the eggs of the corn earworm. In tobacco budworm eggs, primary ribs terminate before they reach the cells surrounding micropyle, a small pore opening at the top of the egg. On the other hand, corn earworm ridges extend to the rosette.[1]

Chloridea virescens larvae usually have 5 to 6 instars or moultings, but there have been instances where 7 instars are necessary to reach the pupal stage. Head width of the larvae starts from 0.26 mm and grows to 2.87 mm by the last instar. Larval length ranges from 1.4 mm in the first instar and grows to 36 mm by the fifth instar. Larvae are a yellow or yellowish green upon hatching, with a yellowish brown head capsule. During later instars, larvae have variable colors ranging from greenish to pinkish, or even a dark red or maroon with a broad brown head capsule. Whitish dorsal and ventral bands run down the length of its body, along with a broad lateral band that is generally brown in color. Larvae also have black thorn-like microspines. Starting from the third or fourth instar, cannibalistic behavior can be observed. Similar to the eggs, early instar C. virescens larvae are difficult to distinguish from corn earworm larvae, with minor differences such as missing or differing lengths of microspines.[1]

Pupation, or the process of transforming from an immature stage to an adult, occurs in the soil. Pupae start off a shiny reddish-brown that progresses to a dark brown color. The size of a pupa averages 18.2 mm to 4.7 mm in width. The budworm overwinters in the pupal stage, and diapause or dormancy can be initiated by either short days or low temperatures.[1]

Development time and lifespan show a negative correlation with temperature. Higher temperatures result in shorter development times in studies conducted on Chloridea virescens raised in a temperature controlled laboratory environment.[4]

In the larval stages, development time for the instars required anywhere between 2.6 and 10.1 days at 20 °C. When the temperature was increased to 25 °C instar development times ranged between 1.9 and 5.7 days. Most notably, the later instar development times were nearly halved. The duration of the pupal stage also decreases with increasing temperature: on average, 22 days were required to hatch at 20 °C, while only 13 days were needed at 25 °C, and 11.2 days at 30 °C. Adulthood longevity ranges from 25 days at 20 °C but drops to 15 days at 30 °C.[4]

Chloridea virescens larvae attack C. nigriceps females that approach with an oral exudate that causes C. nigriceps to become agitated and groom themselves, allowing the budworm to escape. C. nigriceps also avoid budworms painted with this exudate. It is hypothesized that this exudate may function by overloading the wasp's sensory receptors.[11]

Winthemia rufopicta eggs are sometimes laid on C. virescens larvae, but upon hatching and trying to penetrate its host, caterpillars react by biting, crushing, puncturing, or trying to eat the parasitoid eggs. This kills off many of the maggots.[11]

In Chloridea virescens, juvenile hormone (JH, which regulates many aspects of insect development) is necessary for the deposition of nutrients into the female germ cell, or yolk formation (vitellogenesis). It is thought that mating can enhance egg maturation, increase egg production, and induce oviposition due to stimulation of JH production. Mating was correlated with a surge in JH production by the corpus allatum in females - a 5 to 15 fold increase compared to virgin females, an allototropic effect. Juvenile hormone released by mated females increased 2.5 fold. The profile of the juvenile hormone produced also changed - synthesis of JH II exhibited significant increases, JH I increases but not significantly, and JH III remained the same. In males, juvenile hormone is synthesized in small quantities by accessory sex glands. At birth, males synthesize around 1.5 nanograms of JH I and II; this quantity increases by 12 hours after emergence and remains steady for up to 54 hours after emergence. While mating, males also transfer the juvenile hormone they synthesize to the females they copulate with. By 6 hours, levels on the female bursa copulatrix decrease dramatically.[14]

Vitellogenin (VG), an egg yolk precursor protein, is dependent on juvenile hormone levels. Mated females exhibit higher levels of VG than virgin females 48 hours after emergence; mated females also exhibit significantly higher egg production rates than virgin females at 48–120 hours post emergence.[15]

The tobacco budworm has a long record of attempted management. Records dating back to the early 1800s have descriptions of pest damage and control measures that match the damage caused by Chloridea virescens; the USDA has records dating to around 100 years ago describing significant losses to tobacco agriculture totaling around US$2000 per hectare.[16] C. virescens was misidentified up until the 1920s as Heliothis zea, both of which are still referred to as heliothines or the “bollworm complex." The bollworm complex was described by the Ecological Society of America as “the nation’s most destructive and ecologically disruptive insect pest problem, costing the country over $1 billion dollars for their damage."[16]

This damage occurs because larvae tunnel into buds and blossoms, tender terminal growth, leaf petioles, and stalks of their host plant. Larvae will also burrow into fruit, but this increased the frequency of plant disease. If there is no reproductive tissue available, Chloridea virescens will readily feed on leaves. Injury of the crop presents very similar patterns and at similar levels as the corn earworm.[1]

Previously, insecticides such as Paris Green or arsenates were used in high enough doses that affected not only the insects they were meant to kill, but also the plants that the insecticides were supposed to be protecting.[16]

Part of the reason Chloridea virescens has proved so difficult to control is because of its ability to rapidly evolve insecticide and pesticide resistance. C. virescens acquired resistance to DDT a mere 14 years after widespread use, carbaryl within 10 years, pyrethroids in 7, and methomyl in less than 5 years of intensive use.[16]

When insecticides are implemented, foliar insecticides are used, but this often also hurts beneficial organisms that control Chloridea virescens populations, further exacerbating the damage.[1]

Large cone-shaped wire traps are baited with sex pheromone lures are able to capture adult moths. Smaller bucket traps are also widely used but not as effective as the larger wire traps.[1]

Mowing or killing weeds with herbicide early in the spring can reduce budworm population size later in the year. Killing larvae already on the weeds is also effective.[1]

Heliothis nuclear polyhedrosis virus have been used to suppress populations on field crops and early season weed hosts. Release of Trichogamma egg parasitoids is beneficial in some vegetable crops.[1]

Around the 1980s, a multi-tactic approach was developed, including destruction of weed hosts, biological insecticides, and release of sterile Chloridea virescens crosses. While these tactics had no immediate effect on the tobacco budworm population, much of the data collected during these control efforts was valuable in control efforts for other pests.[16]

Studies have been done on the usage of reserpine and subsequently exposing the moth with gamma irradiation (treatments ranged from 0 to 25 krad).[17]

No level of radiation treatments completely sterilized the adult males, but fecundity was reduced to 33-40%. Fertility (percentage hatched) was dramatically reduced, and greater doses of radiation resulted in a sex imbalance that lowered the proportion of female progeny. Females were completely sterilized at the 25 krad treatment. It was also observed that sterility could be inherited; the fecundity of F1 females, born from treated females, was still markedly reduced. There was a high female pupal mortality rate that increased with doses of irradiation treatment. Hatching rates decreased at lower levels of radiation; above 20 krad treatments, eggs ceased to hatch.[17]

Cotton has been genetically engineered to express insecticidal proteins (specifically Cry1Ac and Cry1Ab, d-endotoxin proteins of Bacillus thuringiensis) to resist the budworm.[16] These transgenic cotton plants are remarkably effective, especially considering previous lack of success with insecticides. In cage studies where larvae were placed with cotton expressing Cry1ab for 10 days, less than 2% survived.[18] Transgenic cotton that has been genetically engineered to express Bacillus thuringiensis toxins have proved incredibly effective for controlling Chloridea virescens populations.[1]

The limiting factor to long term usage of transgenic cottons as a method of population control is the development of resistant pest populations. A study in North Carolina collected wild Chloridea virescens populations and fed some diets containing Bacillus thuringiensis toxins. After just 12 selection episodes, survivors were already 7-fold more resistant to the toxins. It is estimated that the frequency of the resistant allele may be as high as 0.001 in the population.[18]

There have been strategies proposed to delay the rate of resistance development. One strategy proposes mixing transgenic and nontransgenic seeds before packaging them for sale, resulting in a mixed field population. However, studies modeling this situation suggest that Chloridea virescens larvae will simply ingest sublethal doses of toxin, then move to a nontransgenic plant and recover. Therefore, this strategy may actually hasten the rate of resistance development.[18]