On a couple of occasions this year and last, I have
been asked if it is possible that diseases can be transmitted from
adult Saturniidae moths to the eggs they produce.
My original answer was, "I don't know, but I do remember reading
somewhere that Louis Pasteur is credited with saving the silkworm
industry by discovering/identifying the causative agent of pebrine,
a microbial disease of silkworms." Pasteur examined adult moths under
a microscope and advocated destruction of all eggs
deposited by infected females.
I recently learned "In the culture of Antheraea mylitta Drury,
a semi-domesticated Tasar Silk Moth, eggs of mother moths infected with
Nosema sp., (microsporidian) must be discarded to avert any
catastrophe on crops caused by this pathogen. The infected mother
moths (pebrine diseased) are detected by a method derived from that
used in sericulture (Pasteur, 1870). In this method, the abdomen of
an adult is severed with scissors, placed in a small mortar, mixed
with water and crushed with pestle. A drop of the smear is placed on
a clean slide and examined under a microscope for Nosema sp., spores."
It is now clear to me that Microsporidia can be transmitted from an
infected Saturniidae female to her offspring in what is called
"vertical transmission".
On November 9, 2002, I received an article from Karen Perizzolo. The
article (2001 Microbes and Infection 3, 381-388) was written by
Dr. Alison Dunn and
Dr. Judith E Smith
Short excerpts from Dr. Smith's article appear in red
text below.
The report was highly technical and dealt with many animal phyla.
I have tried to explain implications for rearing Saturniidae.
I have written in black text
my comments/understandings/explanations.
Senior Lecturer
School of Biology
Leeds University
Leeds LS2 9JT
UK
The following is offered in CancerWEB's On-line Medical Dictionary:
"Common name for members of the protozoan phylum Microspora. It includes some 80 genera
parasitizing all classes of vertebrates and many invertebrates,
especially the insects. Several genera, such as Encephalitozoon,
Enterocytozoon, Nosema, Pleistophora, and Septata have been
implicated in the infection of immunocompromised humans."
Here are the excerpts from Dr. Smith's article:
Within the microsporidian lifecycle there are two basic morphological forms, the meront or proliferative stage and the spore or transmission stage (Canning and Lom 1986).
The meront develops from a spore,
usually ingested by a caterpillar, possibly from the foliage it eats
and/or possibly from ingestion of the egg shell when it first emerges,
and takes nutrients internally from caterpillar cells. The meronts
develop and reproduce at varying rates. Since these organisms are
deriving nutrients and energy from their hosts, infected caterpillars
usually do not grow as rapidly as non-infected caterpillars.
In some cases the meronts reproduce at an amazing rate and seem to
exist in sufficient numbers to result in the sudden death of larvae,
usually in the fourth and fifth instars.
Like most spores, the microsporidan spore has a thick, resistant wall
which enables it to survive for extensive periods of time, possibly
years, outside the body of any potential host.
Creepy, but, it seems the ingested spores have the ablitiy to invade
host cells via an extrusion apparatus which literally bores its way
through cells membranes, creating a conduit for the movement of
sporoplasm from the inside of the spore directly into the
living matter of the host cell.
Microsporidian outbreaks may be responsible for the seasonal
population crashes associated with many lepidopteran species.
It is also possible that some microsporidia may have indirect
life cycles where different stages have to utilize different hosts.
Horizontal parasite transmission can occur between related or
unrelated hosts of the same or different generations and between
hosts from the same or different species.
Parasites may be transmitted per os, venereally and by direct
invasion through the host epithelium. It is likely that the most common type of
transmission is by ingestion of spores on foliage. Inside the
caterpillar gut, the spores infect the cells, the meronts develop and
reproduce, spreading to other cells. Fatty tissues are probably the
first to be invaded (hence slower growth), with invasion of critical
organs to follow.
If a healthy caterpillar does not become infected until the later
stages of its life, it may well pupate and emerge as a moth (since
there has been insufficient development of/damage by meronts) carrying
spores in and on its body. Colder temperatures (diapausing moth
pupae) may well have arrested the growth of meronts, causing them to
form spores.
It is possible that these spores may then be transmitted from one
generation to the next in what is called vertical transmission where
the infection is transmitted from parent to offspring.
I do not know for sure, but here there seem to be several
possibilities, none of them very nice:
The spores may be inside the eggs, even while in the female's body;
the spores may be on the eggshells inside the female's body;
the spores may be transmitted during pairing from males to females;
the spores may be transmitted from female body hairs/scales during
ovipositing.
Vertical transmission is mainly uniparental and there
will be strong selective pressures for low virulence in the host sex
which transmits the infection (females). However, parasites in male
hosts are not subjected to the same selective pressures, as male hosts
do not transmit the infection vertically (Bandi et al 2000).
Selection may favour parasites which are more virulent in male hosts
if this causes an increase in parasite prevalence. Two different
strategies of sex-specific virulence occur in the microsporidia.
Male killers are benign in female hosts but kill males to release
spores for horizontal transmission (Kellen et al 1965).
Feminisers are also
benign in female hosts but convert genetic male hosts into
functional, phenotypic females which go on to transmit the parasite
vertically to the next generation of hosts (Dunn et al 1995).
Crafty little devils, aren't they?? The previous paragraphs suggest that if you are getting mostly female cocoons instead of a healthy 50-50 split, you may have microsporidia which are less virulent (deadly) to females, or the microsporidia may actually be converting the males to females instead of Killing them.
Horizontal transmission.
Horizontal transmission of microsporidian parasites is strongly
dependent on parasite burden as spores are released into the
environment where they are ingested by the next host. The greater the
number of spores produced, the more opportunities of infecting a new
host. Meronts divide in these cells
and, after 48, hours some differentiate to form early spores
characterised by a short polar filament and thin spore wall. The
early spores germinate spontaneously to infect adjacent host cells.
Other meronts divide and differentiate to form high numbers of thick
walled, binucleate spores which have a polar filament with many coils.
Massive spore production of binucleatecauses destruction of the host
cells to release spores for transmission via the faeces. The high
metabolic load and pathogenicity of this parasite lead to reduced
host fitness and survival (de Graaf 1994; Canning 1993).
Vertical transmission.
In contrast to horizontal selection is predicted to favour reduced
virulence in vertically transmitted parasites (Ewald 1987; Smith &
Dunn 1991; Dunn et al 1995).
The mechanism of feminisation is unkown. However, breeding studies have
shown that 80% of the offspring of infected hosts become female.
Although these parasites cause low pathogenicity in the individual
host (Terry et al 1997), feminisers have severe implications for the
ecology and evolution of the host. Theoretical models show that
feminisers may spread through the host population causing sex ratio
distortion and even have the potential to drive the population
extinct due to lack of males (Hatcher et al. 1999)
In microsporidia with alternate transmission routes, horizontal
transmission is associated with high virulence, vertical transmission
with low virulence.
Microsporidia with alternating transmission cycles also provide clear
evidence for male killing. Male killing parasites cause sex-specific
mortality in their hosts. They cause a benign infection in female
hosts, but are highly pathogenic in male hosts and lead to mortality
during host development (Kellen et al 1965)
Sporogony leads to the production of vertical type spores which infect the gametes. Most females of this
F1 generation also have benign infections. However, in F1
generation male hosts (i.e. infected vertically) a horizontal type sporulation
sequence occurs. Massive parasite replication in the fat body
results in death during the 4th larval instar and subsequent release
of spores into the environment for horizontal transmission . Male
hosts do not transmit the parasites vertically. Sex specific
virulence maximises the opportunities for both vertical (through
females) and horizontal (through males) transmission (Hurst 1991).
Conclusions
The role of horizontal transmission is uncontroversial for
microsporidia infecting both vertebrate and invertebrate hosts, and
this transmission route is associated with massive spore
proliferation and pathogenicity to the host. However, there is
growing evidence for the importance of vertical transmission in
microsporidia which infect invertebrates. This transmission route is
associated with spore polymorphism and modified virulence in the form
of feminisation and male killing.
What does all this mean?
Naturally occuring microsporidians, infecting
Saturniidae, can be transmitted vertically from parents to their
offspring via the egg. The microsporidians may be ingested when the
emerging larvae consume part of the eggshell and thereby
ingest spores, or the microsporidians may already be inside the
developing embryos, or both.
Microsporidians may also be transmitted horizontally from one
caterpillar to another by contact with feces and by ingesting foliage
harbouring spores.
I am not trained in the detection of microsporidians, but they can be
seen under a microscope if you know what to look for. Additional
information here would be appreciated.
Live moths not sufficiently infected to cause their own demise,
apparently survive and can transmit the disease to subsequent
generations.
Spores are long lived and can exist outside the caterpillar and moth
bodies. It is therefore essential that diseased caterpillars be
discarded properly. Letting them fall to ground or re-using rearing
cages, jars, tubs, sleeves, etc., that have been exposed to an
outbreak is not a good idea, without a thorough scrubbing.
Diseased caterpillars probably should be flushed down a toilet. If
you are in the fields or woods and encounter disease, then you
probably should have a covered bucket of bleach with you, and
infected larvae should be dropped into the bucket. Hands should be
washed to avoid contamination of healthy larvae.
I am aware that other breeders have actually used antibiotics to
"control" or at least reduce the incidence of "disease". Last year
I believe their was an article in Lep. Soc. publication about the
use of CIPRO, an antibiotic, to help reduce problems besetting
Saturniidae. It is my understanding that you cannot obtain CIPRO
legally in Canada without a prescription, and that it is expensive.
I do not know laws in the states regarding its availability.
In principle, however, I am against the use of antibiotics because
I feel their too frequent use does two things:
1) Aids in successful development of weaker strains of Saturniidae
stock;
I advocate proper disposal of infected larvae, thorough cleaning of
rearing materials, possible washing of eggs, and maintenance of rearing
compartments that are frequently changed/cleaned and are not
overcrowded.
I will let you know if I "learn" anything this coming summer.
Thanks to Karen for forwarding the response from Dr. Smith. Help
from other members would be appreciated.
Hope this doesn't provoke an unwarranted alarm. I suspect major
outbreaks are relatively uncommon, probably not as often as bouts of
Nuclear Polyhedrosis Virus. Sanitation, proper disposal of diseased
insects and avoidance of overcrowding are all good pre-emptive measures.
I asked several people to critique my summary/notes and
appreciate the email that came back from Chris Conlan:
Bill, I have no doubt that it could occur with Saturniids as
well. It was also very common for vertical transmission to occur
that almost certainly was coming from within the egg. We sterilized
the crap out of all our eggs and still an occasional disease would
get in and stay put at a low but detectable level. When nosema
showed up I believe we used to maintain as sanitary conditions as
possible and treat with a drug called Fumadil(sp.?). I am not certain
of the name of the drug as it has been many years (I know it started
with an F!). However, it usually took a few generations of treatment
to finally push the disease to undetectable levels.
Obviously, if one has the luxury of discarding all stock and starting
over that is the best way to go but these things can be lurking in
many colonies and show up the minute conditions go sub-optimal.
Antibiotics in rearing do work very well but they must be used from
the very start or their value drops off quick. Waiting until symptoms
appear to treat will usually still result in heavy losses.
A disease that takes out Hyalophora quickly and efficiently
is usually NPV (at least in my experience). Since that is viral,
antibiotics would
have little effect other than to keep them healthy enough that their
resistance to infection or secondary infection would be greater. In
my personal rearing I tend to avoid antibiotics unless I have
something that I really want/need to get through or a species that
is notoriously disease prone. Don't know if this helped at all but
if you have other questions just let me know!
Chris
2) Encourages development of resistant strains of bacteria and
possibly viruses and microsporidians.
I am a bit out of my league here to comment on much of this article.
What I can tell you is based on my experience working in large scale
private insectaries. Both vertical and horizontal transmission occur
and it seemed to be more of a problem in some Lep colonies than
others.