Listeria monocytogenes is a gram-positive, rod-shaped bacterium. It can be found in the environment as a soil inhabitant. However, it also can be a frequent contaminant of our food supply. As the latter, the bacterium is a significant public health concern, as it is capable of causing serious infections. Listeriosis (infection with Listeria) causes ~2500 serious illnesses and 500 deaths each year in the United States, and the hardest-hit are those with poor immune systems due to age (the very young and old), other immunocompromsing conditions (such as chemotherapy, organ transplant, or AIDS), and pregnant women. Once ingested, the bacterium is able to cross the intestine and spread throughout the body via the bloodstream, where it can attack organs and cause serious damage.

The very fact that it’s typically an environmental organism (rather than a solely pathogenic agent) likely accounts for some of its virulence and transmission. It’s able to survive a number of environmental stresses, including low temperature and high salt concentrations. Indeed, its ability to grow at relatively low temperatures is one way it evades our efforts to control it: it can grow in food even at refrigeration temperatures.

Listeria is particularly insidious as a cause of fetal death or other complications during pregnancy. Intrauterine infection can lead to preterm labor, spontaneous abortion, stillbirth, or serious–and potentially deadly–infection of the neonate. However, fairly little is known regarding exactly how this condition develops, or the mechanisms that lead to infection of the fetus. It has been thought that the increased susceptibility to infection with Listeria during pregnancy is largely due to a decrease in cell-mediated immunity that occurs as a result of pregnancy. This is a particularly attractive hypothesis for Listeria, which is an intracellular pathogen. A new paper in PLoS Pathogens examines this phenomenon in greater detail, using a guinea pig model of infection.

Initial studies examined the effect of pregnancy on bacterial load in different maternal organs, comparing pregnant to non-pregnant guinea pigs. They found that pregnant animals were unable to clear the bacterium from the liver and spleen, and had more sustained bacteremia (the presence of bacteria in the blood) than nonpregnant animals, and that levels of bacteria in the placenta increased substantially, and steadily, over 72 hours.

The authors state this increase could be due to 3 factors: bacterial replication, decreased clearance of bacteria by the immune system, or influx of bacteria from maternal organs to the placenta. They tested the impact of trafficking by inoculating mice with a 1:1 ratio of two different, equally virulent, isolates of L. monocytogenes, one of which was resistant, and the other susceptible, to erythromycin. After 24 hours of infection, they found that in 13/14 animals, pure cultures of one strain were collected–suggesting that cases of placental infection were clonal (that is, even a single bacterium could have been sufficient to cause placental infection). In animals harvested later in the infection (72 hours), the majority of animals were found to have mixed cultures both strains, leading the authors to conclude that the bacterium traffics from other organs to the placenta; however, by comparing the observed numbers of bacteria per organ and the changes in ratios of the strains, they estimated that fewer than 10 bacteria trafficked from the placenta to other organs between 24 and 48 hours post-infection. Therefore, they concluded that most of the bacteria in the placenta was due to growth in that organ, following initial colonization by only a few Listeria organisms. In other words, the placenta was largely protected from bacterial colonization, but when they got a foothold, they grew like crazy.

This still left the question of whether this increase in growth was due to enhanced bacterial replication or decreased clearance (for example, due to decreased cell-mediated immunity resulting from pregnancy). To examine this, they input data into a mathematical model, taking into account initial seeding of bacteria into an organ, bacterial replication within that organ, clearance of the bacteria, as well as influx and efflux of bacteria in and out of the organ. From this, they determined that it wasn’t necessarily either replication nor clearance that made the biggest difference; but instead, it was the rate of bacterial clearance relative to bacterial replication in the placenta that led to an increase in growth. If you tweaked either even slightly, you could get significant bacterial growth.

Finally, using an antibiotic challenge, they determined that the bacterial burden in the placenta was significantly decreased after treatment. This may seem obvious, but with Listeria and other intracellular bacteria, administering an antibiotic doesn’t necessarily cure the infection, because antibiotics are unable to penetrate the host cells–and therefore, intracellular bacteria are protected. However, bacteria associated with the placenta are extracellular (and therefore, susceptible to antibiotic treatment); therefore, the results were consistent with their hypothesis that the placenta was the nidus of infection, and that the trafficking of the bacterium from the placenta to other organs alone was sufficient to explain the difference in disease seen in pregnant versus non-pregnant animals.

This infection model, emphasizing growth in–and dissemination from–the placenta, also partially explains the pathology of listeriosis in pregnant women. Expulsion of the placenta interrupts the infection; therefore, pre-term labor or spontaneous abortion can be seen as a protective mechanism on the part of the mother. As they note, it also has implications for the control of Listeria, especially in environmental settings where the aborted placenta can act as an environmental reservoir of infection.

It should be noted that, while the results are interesting and consistent with what we see in human Listeria infections that occur during pregnancy, any animal model has its own strengths and limitations, and this is no exception. Still, it provides insight into an infection that is still largely mysterious, and that can result in not only loss of life but also severe mental anguish on the part of the family that has suffered the tragedy of a Listeria-induced stillbirth or abortion.

References

Bakardjiev et al. 2006. Listeria monocytogenes Traffics from Maternal Organs to the Placenta and Back. PLoS Pathogens. 2:623-31. Link.

Comments

  1. #1 Monado
    July 17, 2006

    So it’s possible that spontaneous abortion of an infected placenta is approximately equivalent to vomiting and diarrhea during a gut infection. Interesting. Nature does have that “lighten ship” reaction.

  2. #2 LS.
    July 18, 2006

    Yo Tara,

    sorry to post this on the wrong thread, but you keep shutting down discussions!

    So, I asked Kristjen Wagner a couple questions, and she said, I believe it was… “fuck off”. (is that a technical response? Hmmm)

    Chris the Noblest of all said that I was a creationist.

    Nobody asked me if I believed a guy in the sky created the world in six days (and had a barbeque on the 7th).

    I don’t believe that of course, but then again, nobody asked. Just ass-u-med. Hey! Look at that.

    So, I’ll repost my original query to Kristjen Wagner, minus the “minx” comment that got her so angry that she refused to answer any of my points, and told me to “fuck off” (I believe that’s the correct spelling).

    Here goes:

    Hi Kristjan

    That’s a lovely name. I bet you’re a[silly noun deleted]

    You say:

    This is like when Creationists demand “the evidence” for evolution. We can show them the fossil record, the evidence of evolution going on at the moment, and many other pieces of evidence, yet they keep demanding more.

    Which evolution are you talking about, specifically?

    The Punctuated Equlibrium evolution? The acquired genomes of Margullis, et al?

    The morphological resonance of Sheldrake?

    The unnamed impetus of Darwin?

    Survival of the fittest?

    What makes one ‘fit?’ Just the ability to [tawdry word, also used by K.Wagner, replaced with}:procreate? And produce more than others, I suppose...

    So, Ugandese are more "fit" than Americans, as they have a stronger population growth.

    What is the impetus for evolution? Accidental gene drift? Gene-shuffling via transposable elements? Exposure to chemicals in utero (the plastic stage of existence?)

    Which theory, exactly, is exactly like the theory that you seem to think is being debated here,

    [made-up adverb deleted],

    Liam

  3. #3 Stephen Uitti
    July 18, 2006

    All analogies break down. If an analogy doesn’t break down, then it isn’t an analogy – it’s the thing you wanted to talk about.

    Animal models also break down. If it doesn’t, then you’re using the animal that was the goal of the study.

    OK, so the later isn’t necessarily a tautology. The difference between theory and practice is that, in theory, they’re the same.

  4. #4 Eric
    July 18, 2006

    Hopefully dragging the thread back toward the actual article…

    That’s really very interesting. A difficult infection, combined with an already stressed and weaker system due to pregnancy. It makes sense to “jettison” the infective tissue…sadly killing the fetus…to save the mother for future procreation attempts.

  5. #5 W. Kevin Vicklund
    July 18, 2006

    BTW, Kristjan is a guy, from Denmark, if I recall correctly. You seem to be suffering from a common ailment known as foot-in-mouth disease, Liam.

  6. #6 ls.
    July 18, 2006

    Hi W. Kevin Vicklund,

    who asked you, you bloody crumb?

    Maybe I knew that! Maybe you’re a homophobe. Maybe I was looking for a date?

    No, you got me! I didn’t know it! I’m not sure I believe you’re correct. And even so, still a minxy name, isn’t it?

    Kristjen…

    But read Kristjen’s response to my original questions, and see if the call to feminism, against a sea of chauvanists doesn’t lead you to think, she’s a she?

    Even so, the questions were pre-eminent.

    Still no response, from Kristjen, the he-she, or from Tara, the cowardly libel.

    Stephen, I love what you said, sort of an extended haiku.

    Will have to consider it for merit, but it’s certainly fun.

  7. #7 Pinko Punko
    July 19, 2006

    Dear Liam,

    You are more annoying that Wilhelm. Thank you for ruining this thread.

    Nice post, Dr. Tara.

  8. #8 LS
    July 19, 2006

    Alright, sorry about posting on the wrong thread (I don’t know if that’ll go through, it’s being held for comment by moderator Tyrana, and as such, can be deleted). My fault! Too many windows open at once! Not enough attention paid. Lesson learned.

    So, punko, I don’t think this thread is ruined, child. You still managed to come in a sulk on it. But the truth is, all of this would’ve stayed on the originating thread, if Tara the cowardly libeler had stayed, answered her libel, and not shut it down, running away as quickly as she could.

    If Tara the tyrannical would like to open a dedicated thread to pick up where both “boredom” and “coming soon” left off, we’ll do it there.

    I asked one of your own (K.Wagner) very fair questions about her assertions (boy, you get a lot of those over here, don’t you?) re: aids and creationism, and she (or he) gave me the bird.

    I went to repost, the thread was bare.. shut down.

    Talk to the Tyrannical Tara. If you want this to be a private, invite-only blog, well – your S.O.L., because Seed is funding this, for open dialogue. If you want a ‘punko and Tara and friends ONLY! (boys stay out! except Dale) Blog, go and do it. Otherwise, shut the f up, and let’s have some honesty here.

    Get Tyrannasaurus Sororitus to stop having panic attacks, and to let these things run.

    Tell her to give clear warnings about what is allowable, and to be freaking consistent, instead of bugging the software to limit responses from some of us.

    Tell her to be clean, consistent and open in what can go on and what will be blocked, (she claims that a guy was blocked for invoking nazi-ism, I guess I understand, but she and many of you do it all the time (What’s a ‘denier?’).

    So, time for some clarity, Clara.

    Either get to Tara to open it up, clearly, with rules stably enforced, or admit she is a fraud.

  9. #9 Tara C. Smith
    July 19, 2006

    Liam, Seed is footing the bill, but we’re free to run things as we like. In 6 months, I’ve only closed down a handful of discussions that have gotten nasty (and that one, as you even point out, had insults from all sides). I’ve allowed insults to stand from you, Bialy, Michael, and many others, and allowed an open dialogue on issues even when I completely disagree with what’s being said. There have been some problems with the software lately because a new spam filter was installed (PZ has also mentioned this), so while you allege I’m being “cowardly” and “bugging the software,” I’ll tell you that the software doesn’t even allow us to ban people unless we move to requiring Typekey or another system. Thing is, there are still AIDS threads open, so you can post all your insults and accusations in one of those. I don’t need multiple threads running that have converged on the same topic.

  10. #10 Terry
    July 19, 2006

    Grabbed the paper to use in next semester as an example of compartmental modeling, thanks!

    Might be fun to see if the animal-to-animal variation can be explained with a stochastic model.