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How is Mycoplasma gallisepticum Spread?
How is Mycoplasma gallisepticum Spread?
As noted in the Fischer EID
Article, it is still not known how MG
is spread among finches. Like any infectious organism, MG might be spread
by one or a number of different manners. These possibilities include physical
contact between an infected bird and a noninfected one, ingestion or inhalation
of the MG organism, that is, for example, by eating contaminated food or
seeds or by inhaling it somehow. Even eye secretions may play a role. In
poultry, MG can even be spread vertically, from mother through the shell
before the egg is laid. Some feel this may be true with the finch strain
as well. There may be other mechanisms involved beyond these possibilities.
[Avian pox, for example, can be spread via insect bites, though I have seen
no discussion of this being considered in the spread of MG. The Michigan
Dept. of Agriculture Dec. 9, 1996 News Release mentioned previously, also
states " MG does not pose a threat to human health, but people can spread
the disease on shoes and clothing." I suspect here, however, this statement
is based on knowledge of transmission of poultry strains of MG, not necessarily
the finch strain.] (Copies of both the Fischer EID Article and the Michigan
DA News Release can be found on the "Web Links and
Other Resources" page.)
According to the authors of the Fischer EID article, bird feeders are seen
to play a significant role in the spread of the disease either by becoming
contaminated directly (examples might include via droppings or eye secretions
rubbed onto a feeder), or acting as important congregation points where many
finches come together in close proximity, making spread of the disease more
likely.
It has been suspected for some time that tube feeder portals might play a
role in the transmission of MG. If the wet eye secretions of infected finches
carry the MG organism, conceivably as an infected finch reaches into a tube
feeder to get seed, it might rub its eye secretions onto the sides of the
feeder portals where, before the MG organism dies, the next finch to use
that same portal might come in contact with the secretions left there, thus
in turn contracting the disease. Below, a female house finch with visible
symptoms of MG reaches into a tube feeder portal. As can be seen, there is
little room for it to avoid contacting the portal's sides.
Such groupings make spread of infectious diseases more likely, particularly
if the disease can be spread by casual contact, ingestions of seed contaminated
by droppings, and inhaling airborne organisms. Thus, if MG is in fact spread
in any of these manners, then it would seem likely that tray and platform
type feeders would encourage the spread of the disease more than other types,
simply by accommodating more birds closer together at the same time, resulting
in more frequent casual contact or by encouraging greater concentrations
of contaminated droppings.
However, when
it comes to disease transmission, contact at bird feeders, specifically,
may be a question of degree and kind. In some respects, there may be more
harmful physical contact between finches at certain tube and perch feeders
than even at crowded tray and platform feeders. Those who have such feeders
and have house finches visiting them regularly are probably very familiar
with the close contact, beak-to-beak, fighting and arguing that can go on
over competition for perch space. [The photo at right shows a goldfinch and
house finch fighting at a common thistle-type feeder.] In such cases, it
is possible that tube and perch feeders may be encouraging much closer and
more aggressive contact, in the form of nudging battles and arguments over
perch space, than might occur at even crowded tray and platform feeders.
Again, we know blue jays can contract MG, yet it does not seem to be a problem
for them even at feeders with rampant irruptions of MG in house finches visiting
the same feeders. Nor has it shown to be a problem with other larger birds
- grackles, mourning doves, even cardinals. Why? Perhaps because they do
not get involved in fighting with house finches, as goldfinches or other
small birds (including other house finches) do on occasion. When these larger
birds show up - regardless of the type of feeder - house finches either scatter
or they back off and give them room. There is rarely physical contact.
Yet, despite all of this, there remains the issue of the blue jays which
came down with symptoms - one of which was confirmed to have had MG - while
in captivity at a wildlife center that had been receiving finches with
conjunctivitis about the same time, back in 1994. According to one member
of the center's staff at the time, the blue jays and house finches were never
in direct physical contact. In their case, that leaves only a few avenues
whereby MG might have spread to them: among these are ingestion of or exposure
to some contaminated source, or by inhalation of particles or dust carrying
the organism. If either of these were the cause, then once again this raises
the possibility that direct contact with an infected bird is not needed to
spread this disease, and if that is true, then perhaps any bird feeder may
yet remain capable of helping spread MG.
Thus, the issue comes full circle: researchers studying this disease do not
yet know how MG is being spread. And until more is known about how, exactly,
it is being spread among house finches and goldfinches, whether via
eye secretions, physical contact, ingestion, inhalation, or some other means
(or combination of means) - then the potential role of bird feeders in the
spread of this disease remains a matter of speculation. [Perhaps more on
this question may yet come out of the Cornell Labs' House Finch Study, if
it is possible for them to query their data to see if there is any correlation
between the incidence of reports of diseased birds and the types of feeders
observers report using.] Until then, this question ultimately falls
on the shoulders of each individual bird feeder to assess for themselves,
based on each persons situation.
[See section entitled "What To DO" for further
information. This section also discusses the possibility that MG might
one day be spread by infected birds nesting in artificial nest housing; see
section entitled: Nest Box and Purple Martin House Precautions.]
The Summer, 1996, issue of the Cornell Labs' newsletter Birdscope noted there were indeed seasonal changes in the numbers of finches
observed by participants in their House Finch Study, changes paralleled in
the findings of the bird bander, mentioned previously -- and changes I had
noticed in my own finches as well. What this bird bander found, which Cornell
noted correlated highly with their House Finch Study data, was that "disease
symptoms increased in the spring [sic] of 1995 [note: their diagram
shows the increase occurring from January through March, not during the spring],
declined over the breeding season and as young birds dispersed in late summer,
increased dramatically in the fall and winter, then decreased again in the
spring of 1996."
While, again, this is all entirely speculation on my part, I had noticed
this same pattern followed very nicely house finches' flocking behavior -
and thus also reflects the changes in numbers of house finches foraging at
specific bird feeders, if my feeders are typical. (More obviously, it also
follows what one might expect to be the annual peak and low point in finch
populations as well, with their lowest numbers occurring at the end of winter
and early spring, while their largest number would be at the end of breeding
season. And it also reflects the relative abundances of bird feeders themselves,
with more people putting out feeders during the winter months than at any
other time of year while often them down as spring arrives.) At the end of
winter, house finch flocks disperse and individual pairs scatter to find
nest sites. MG sightings at my feeders - and the numbers of house finches
visiting my feeders - are at their lowest at this time of year. In late summer,
the smaller groups of juveniles and adults in local areas begin merging into
larger groups, perhaps traveling together over larger areas. At this point,
MG being carried by any of these individuals can spread rapidly among these
newly formed flocks, triggering an outbreak of MG seen in the larger numbers
of finches by then showing up at feeders.
Both the Cornell and the bird bander's data found that the highest incidence
of disease in finches occurred (as of their study dates) in the late fall,
1995, through the early winter months of 1996. I have also noted myself a
number of smaller irruptions of MG over the past three years following major
winter storms or severe cold spells (as was true of all three instances where
I observed conjunctivitis in goldfinches, as mentioned previously), and the
data found in these studies may, alternatively, reflect this as well:
the winter of 1995-96, especially in January, 1996, where both show their
highest reports of diseased finches, was a time of major, record-breaking
blizzards in the mid-Atlantic region and perhaps elsewhere in the eastern
US. (Recall that diseased finches originally began appearing in the dead
of winter, early 1994.)
Again, this raises the question of what role, if any, bird feeders may be
playing in the spread of MG? With much of their natural food sources occasionally
buried in snow, does the Cornell and bird bander data reflect that finches
were forced to forage more exclusively at feeders during such winter episodes,
thus increasing the chances of MG's spread? Or does winter stress weaken
their immune systems, making them more susceptible to catching MG as they
flock or visit feeders together? Or might not this be evidence that MG can
be harbored in a dormant state, as some theorize - a condition found in many
avian diseases - only to be activated by such great stress as severe winter
weather, triggering symptoms in large numbers of finches at the same time,
over wide areas, independent ly of feeders? Furthermore, if the MG organism
is itself very fragile, without so much as a cell wall to protect it, one
would think it would be most vulnerable outside its host under harsh
environmental conditions -- such as the extreme cold of winter, perhaps not
living very long in such circumstances. Yet paradoxically, this seems to
be when cases of finches with symptoms of MG seems to be at their absolute
highest. One possible scenario, again entirely speculative, that might explain
this is if, possibly, MG is contracted earlier in time (by whatever mechanism),
but perhaps not all of finches come down with symptoms immediately. In these
others, perhaps it lies dormant, only to be activated when these birds fall
under great stress, such as in winter? Ironically, if this is true, bird
feeders in such harsh situations, might actually help reduce
stress by providing abundant ready food sources, thereby reducing
the expenditure of much needed energy needed to stay warm that might have
been lost in foraging?
© 1997 James Cook
All Rights Reserved
