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Malacosoma disstria J-Hibner. 3/3
1940, Blais et al. 1955, Witter et al. 1972, Hodson 1977). Unusually cold winter weather
is also sometimes responsible for population decline (Witter et al. 1975). Hodson (1941,
1977) found that starvation, often coupled with high pupal parasitism by Sarcophaga
aldrichi Parker, was a major contributor to population collapse. A large variety of insect
parasites attacks the forest tent caterpillar (Witter & Kulman 1972), but the most prevalent is
usually S. aldrichi, which often attacks over 90% of the pupae in the declining phases of
an outbreak (Hodson 1941, 1977). Predation by various birds (McAtee 1926, Hodson
1941, Witter & Kulman 1972) and invertebrate predators such as ants (Tot hill 1918,
Green & Sullivan 1950, Ayre & Hitchon 1968) has been observed on a number of occasions,
but it is usually unimportant.
Bacteria, fungi, microsporidia, and viruses all cause diseases in forest tent caterpillar
larvae and pupae (Bird 1971). The bacteria isolated from M. disstria larvae include
Bacillus cereus Frankland & Frankland, Clostridium brevifaciens Butcher, a Pseudomonas
species, and Serratia marcescens Bizio, but all were rare (Smimoff 1968). The
forest tent caterpillar is also susceptible to Bacillus thuringiensis Berliner (B.t.), although
this organism is not usually found under natural conditions. Several fungi have been
isolated from forest tent caterpillar larvae and pupae, but according to Stairs (1972) only
Beauveria bassiana (Balsamo) Vuillemin and Entomophthora sp. were of any importance,
and then only under humid conditions. A microsporidium, Nosema disstriae Thompson,
has killed up to 90% of early-instar larvae in some areas (Smirnoff 1968). It also causes a
reduction in the size of the insects and may affect their vigour, so that the full significance of
infection is hard to assess (Bird 1971).
Infection with a nuclear polyhedrosis virus (NPV) is often thought to be one of the
most important factors in terminating forest tent caterpillar outbreaks. For example,
Stairs (1966) stated that "Epizootics of nuclear polyhedrosis virus disease are known to
be associated with the rapid decline of tent caterpillar popUlations, Malacosoma spp."
Although this statement may be true for the tent-forming species, the evidence is
equivocal for the forest tent caterpillar. Of the references cited by Stairs (1966), the
following three deal with M. disstria. Bergold (1951) obtained high mortality among
larvae in cages when they were sprayed with the virus under experimental conditions.
Sippell (1952) demonstrated that a large percentage of egg bands collected in late fall
were infected with virus. Neither experiment attempted to show that the virus had an
effect on population trends. The third paper (Chapman & Glaser 1915) states: "Though
wilt disease was also reported to have occurred in many places in the forest tent
caterpillar, neither of us have seen more than a few typical cases from the field. Many
caterpillars were sent in by field men but only a few of them proved to have typical wilt."
Smimoff (1968) conducted a long-term study of M. disstria diseases in Quebec, and
found NPV to be unimportant. Similarly, population studies by Hodson (1941) showed
that the virus was responsible for less than 1 % mortality in Itasca State Park in 1936, and
Witter el al. (1972), on the basis of intensive sampling, considered the virus to be
unimportant in northern Minnesota during 1967-69.
Although NPV appears to be unimportant as a control agent under natural conditions,
it is possible that artificial dissemination of the virus into field populations might
increase the amount of virus infection, thus increasing its effectiveness. Stairs (1964)
used a small backpack mist blower to apply various dosages of virus to different larval
instars of the forest tent caterpillar in 1963. A concentration of 10' polyhedral inclusion
bodies (PIB) per millilitre applied to second- and third-instar larvae caused 92% mortality,
most of the larvae dying within 10 days of the application. Stairs (1965) found virusinfected
larvae in 1964 in both of the areas that had been sprayed in 1963, but not in an
unsprayed area. The virus also occurred at considerable distances from the sprayed
areas, and Stairs believed that he had been successful in artificially initiating an epizootic.