Tag Archives: microbiology

An ounce of prevention: A microbiology extra credit opportunity

Most flu shots are administered  I.M. (intra muscularly), therefore, at a 90 degree angle relative to the skin.

Most flu shots are administered I.M. (intra muscularly), therefore, at a 90 degree angle relative to the skin.

Bob and Sally go to get their annual Flu vaccine at the public clinic. Every year, the two go together and neither have contracted Influenza since they began five years ago.

This time, while he was getting his shot, he says to his nurse, “These shots are great. I haven’t been infected with the Flu for years, despite at least some of my co-workers getting sick every year.”

His nurse finishes his injection and then says, “Well, you might have gotten infected, but you’ve didn’t get sick.”

“What do you mean? Isn’t that the same thing?”

“Actually,” says the nurse, ” it’s not.”

Explain what the nurse means by ‘infection’ and ‘getting sick’ being different things. Include, in your explanation, why it is that a vaccine might not prevent organisms from getting into your body and even into your cells, but that they can still fail to make you ill. What cells and molecules are involved in protecting you in this way?

Leave a comment

Posted by on May 1, 2015 in Uncategorized


Tags: , , ,

Invitation to Submit Questions for Microbiology (Mini) Exam II

infectious_diseaseMy microbiology class is having a special mini-exam on the Tuesday after we come back from Spring Break. This exam will cover chapters 11 and 12 of the Cowen Microbiology text, which is basically ‘how do we kill microbes outside of the body’ and ‘how do we kill microbes inside the body?’ This exam will also have elements taken directly from Exam I presented as an opportunity to retain that material and be sure that we keep these core ideas in mind.

That said, I will be happy to entertain any questions proposed by students (or non-students) on these topics.

Leave a comment

Posted by on March 12, 2015 in Uncategorized


Tags: , , , , , ,

A Pointer

For my Microbiology students….

Screen Shot 2014-11-21 at 11.53.01 AM

“I feel kinda sick”

As we finish up the year dividing out time between Immunology and Epidemiology, you may find it useful or just interesting to take a look at the online Epidemiology course offered at Coursera. It is a six-part course taught by Lorraine Alexander and Karin Yeatts of the University of North Carolina, Chapel Hill.

As all Coursera classes, this is 100% free unless you would like to receive a signed certificate of completion.


Leave a comment

Posted by on November 21, 2014 in Uncategorized


Tags: , , ,

It’s a Wide World

Have you ever asked yourself, “how is it that our immune system can fight off almost everything?”33707699

It’s one of those things that is easily ignored.

 It works. That’s all I care about.

If that’s not a good enough answer, then read on…

The answer lies somewhere between biology and statistics. And I want to  start with an analogy.

Think of a website that makes you log in when you visit (Google’s gmail, for instance). You come up with a password when you join and then use it every time you log in. Some annoying websites make you cycle your passwords regularly for security purposes. (I’m not saying there’s anything wrong with that, but it can be taxing to those who don’t use a password storage program. – by the way, I use Dashlane  and love it)

But every time you use a password, it’s off the list – you can’t use it again. So after about three changes, you start to sweat because you think your head is filling with all those old passwords and you can’t remember the latest one any more. As an analogy for the immune system, imagine a simple program that creates random passwords for you and ensures that they’re not repeats of any that you’ve used before.

Your immune system has no idea what you’ll come up against in the world. All it can do is make a vast repertoire of immune cells with the hope that it will be sufficient to react to anything. For simplicity, let’s just consider how cells make antibodies. To do this, your cells have a way of randomizing the protein sequence responsible for making these proteins.

The problem with this system, if it’s just a random grab-bag, is that sometimes those antibodies might bind to your proteins causing big problems. So, after the random process that generates antibodies, there is a second, non-random selection process that eliminates any that bind to you.

In my analogy, imagine that a random password is generated (the antibody), but then it checks to be sure it’s not the same as a previous password (no self – reactivity).

If you do any programming you can imagine outlining your code:

(let’s say passwords are 4-digit numbers from 0-9)


  1. generate a random number from 0001 – 9999
  2. cycle through old passwords
    1. check that the new password is not equal to the old password.
    2. If it matches, discard that password and go back to step I
    3. If it does not match, cycle to next old password
    4. Repeat until all old passwords have been checked
    5. Present new password to user

Now that I look at it this way, it is very much like evolution by natural selection. Random process à non-random selection.

ImageTo illustrate how this works with the actual proteins, it’s best to go to good old Janeway:

The top two panels show something more like the actual structure of the antibody. The bottom panel shows a simplified cartoon, highlighting the variable region and the constant region of antibodies. Think of the constant region as the backbone of the molecule – it comes in a few models, but doesn’t change.

The variable region is where the antibody binds its target. This is the region that gets scrambled up so the antibody will have a unique binding region.

The variable region is actually composed of several parts (V, D and J) that get pieced together, one of each sort. This accounts for some variability, but could only result in a handful of different types.

In addition to this mix-and-match, the joining of segments is also imperfect. Recall that DNA is ‘read’ in three-base codons. Because of this, adding one extra base in joining the elements will result in a frame-shift that creates even greater diversity. It also admits the real possibility that the protein made will be entirely unstable and useless. To account for this, each cell is positively selected for only ones that make stable receptors. It has two shots* at making this work. Once for each of the two chromosomes (one from your mom, and one from your dad) bearing this gene. If it succeeds, it goes on developing**; if it fails, it commits cellular suicide: apoptosis.


Another figure adapted from Janeway

The result is a pre-immune repertoire of about 1012 antibodies available to protect you from any nasty ‘bugs’ out there.


* There is data supporting additional receptor editing. 

**         Heavy Chain is rearranged and interrogated first, then Light Chain.


Leave a comment

Posted by on May 2, 2014 in Uncategorized


Tags: , , , , , ,

Another Puzzle – about the interaction of host and pathogen

Ok, I realize that some of the past puzzles I’ve made either had errors or were simply too obscure in their clues (again, I’m a crossword novice). I tried to be a little more clear with this puzzle and also did my best to force as many clues into actually ‘crossing’ as possible.

Let me know what you think and if you suspect any errors. The topic is: the host-pathogen interaction, our first chapter on immunology.





Leave a comment

Posted by on April 15, 2014 in Uncategorized


Tags: , , , , , , ,

A game for cramming micro students

Exam II in Microbiology happens this Tuesday. If only there was some less stressful way of studying for the exam. Perhaps a puzzle to kick back and contemplate …?

(As an aside, I really don’t like the way this puzzle turned out – for a crossword puzzle, there are very few words that cross. I may attempt to redo this later, but there’s an exam to write first)



Oh No!

Autocorrect strikes again – 1 Across = the DESTRUCTION of all microbial life.

I do apologize for my poor clue-writing. I’m only a recent adopter of crosswords and I’m not yet very good at writing them the way they should appear.

(I can only solve NYTimes’ Monday puzzles)


Leave a comment

Posted by on April 6, 2014 in Uncategorized


Tags: , , , , , , , , ,

“This blog is our last hope ”

“No, there is another.”

Exam I for Microbiology nears. Where will the extra credit questions come from? Will they all be found here? Perhaps. But there is A New Hope.

Leave a comment

Posted by on February 19, 2014 in Uncategorized


Tags: , , , , , , , , , , , , ,

Agriculture, emigration, deforestation and Malaria

ImageWhen malaria first began to infect humans is something of a mystery. It was a mystery that I hadn’t thought about much before now because … well, I don’t know, it just never occurred to me.

However, recently a colleague mentioned that there was a connection between it and the beginnings of agriculture. Despite the fact that I should know better, I dismissed the idea out of hand. That’s too recent, I thought. There’s no way that could be the case.

The idea of a connection was originally suggested by Frank Livingstone, who “suggested that Plasmodium falciparum (which is by far the deadliest of the several parasites that cause human malaria) had jumped into Homo sapiens from chimpanzees. He speculated that the rise of agriculture had led to human encroachment on wild forests, giving the chimp version of the bug, P. reichenowi, the chance to find a new host.” 1 

Despite my dismissal, the idea did come back to me late last night and I started to look into what was published on the subject. The first thing I found was one of Scientific American’s 60 second science podcasts on the possible connection between recent deforestation in South America and a resurgence in Malaria.  “Researchers looked at stats for 2006 …[and] compared those cases to deforestation in the same health districts over the previous 10 years. They found that a loss of just four percent of forest cover was associated with nearly 50 percent more malaria cases.”2

As always, correlation isn’t causation, but something is happening, and because Malaria is more common in open areas than forests, causation isn’t much of a stretch. And, if malaria does increase when land is cleared of forest, the connection to the advent of agriculture may not be far fetched at all.

Humans started domesticating animals and farming the land about 10,000 years ago , so we do have a date to shoot for in our estimate. The question is, ‘was malaria widespread prior to ~8000 B.C.E.?”

One way to ask this question was to question whether Malaria was with us before we (humans) left Africa, or more recently. This moves the timeframe back to about 50,000 years ago (a reasonable landmark prior to agriculture). One way to ask this question is to look at diversity of the parasite’s genes. Just as the greatest diversity among humans occurs in Africa with less diverse groups coming out from this population, the same should be true of the microbe.

“The researchers found that genetic diversity did indeed decrease at greater distances from Africa. The correlation is very strong, says lead author Francois Balloux of the MRC Centre for Outbreak Analysis and Modelling in London, and the pattern matches human migration out of Africa, which scientists believe started some 50,000 to 60,000 years ago.”3 ( See here and here

For a visual representation of the genetic argument for the origin of malaria, see the map below:


                                         Genetic Variation of Malaria                                                     (grey dots represent possible sites of origin)

Whether Livingstone’s idea may be correct or not probably has no bearing on the idea that human disease originated in chimps and does nothing to undermine the possibility of a connection between recent outbreaks of disease and clearing land for farms.



1. “The source of malaria” The Economist. Aug 4th 2009.

 2. “Plasmodium falciparum Accompanied the Human Expansion out of Africa “Kazuyuki Tanabe  et al. Current Biology, Volume 20, Issue 14, 1283-1289, 17 June 2010

 3. “When Humans Left Africa, Malaria Came Along” MARTIN ENSERINK. Science Now. 18 June 2010.


Leave a comment

Posted by on January 30, 2014 in Uncategorized


Tags: , , , , , , , , ,

A damn fine cup of coffee

I was looking through my next lecture for Microbiology (which I realize I still need to post online) and was reminded of an older post that I made pointing to a virtual lab on streak plating of bacteria.

I recommend my students check that out if they have not plated bacterial cultures in the past. You can find that post here.

Also, as always this time of year, I like to reflect on some of the great pleasures of life. And, because these things often become conversations in my classes, I’d like to share a short video that couples two of my favorite things: Coffee and Twin Peaks

Leave a comment

Posted by on January 15, 2014 in Uncategorized


Tags: , , , , , ,

Antigen Presentation #3: MHC Class I

Antigen Presentation

Presentation by Epithelial Cells

Consider: Under what circumstances would any cell in the body need to initiate an immune response?

Here, I’m using epithelial cells as an example, however, every cell in the body has the ability to present antigens on MHC Class I. In fact, it is a normal, continuous process that the cells cannot fail in without consequence.

While professional APCs process and present antigens that they have phagocytized, other cells divert a small amount of the total protein they make towards MHC I presentation. This allows the immune system to constantly observe these cells and ensure that they are not suffering gross mutations or infections. Most of the time, cells produce normal, ‘self’ proteins against which there are no T Cells (due to negative selection – see Lymphocyte Development).

In the event that MHC I expression is subverted, these cells are presumed to be infected and will be targeted for killing by special cells called Natural Killers, or NK Cells.

If a Non-Self antigen is presented by MHC I, these are recognized by CD8 T Cells. Like the reactions between APCs and CD4 T Cells, cells expressing MHC I + Non-Self Ag engage T Cells via their unique TCRs. The only difference is that these T Cell : Presenting-cell complexes are stabilized by CD8 molecules on CD8+ Killer T Cells.

ImageThe result of this binding is the activation and proliferation of Killer T Cells that will turn upon and kill the presenting cells by releasing perforin and granzymes that perforate target cells and trigger apoptosis (cellular suicide).

Keep in Mind the Big Picture!

To summarize with an example:

  1. Host cells are infected with a virus
  2. The virus replicates within the host cell, producing viral proteins in the process
  3. Some of these proteins are diverted to proteases that digest them and load the antigen fragments onto MHC I molecules
  4. The MHC I +Ag is transported to the plasma membrane to ‘present’ Ag
  5. MHC I +Ag is recognized by a T Cell bearing an TCR specific for the MHC+Ag complex. This interaction is stabilized by CD8 binding to MHC I.
  6. If a stable interaction is formed, the T Cell will become activated, meaning it will proliferate and secrete perforin and granzyme toward the presenting cell
  7. Perforin and Granzyme will lead to the apoptotic death of the presenting cell
  8. By killing the infected cells, the infection can be stopped before spreading farther in the body.

A CD8 T Cell (the smaller cell) killing a virally infected host cell:


Leave a comment

Posted by on December 8, 2013 in Uncategorized


Tags: , , , , , , , ,