...more microbiology

Let's pick up...sort of where we left off. Oh yikes, you can see my reflection.

Anyway...here's some cell shapes.

...and here are the groupings/arrangements of cocci and bacilli cells.

Take note on the Neisseria gonorrhoeae which is a diplococcus!

Here we have the UGLIEST bacterial cell ever drawn. I've labeled stuff, too. You've got the capsule on the outsides. Need to talk a bit about capsules at some point...

Then comes the cell wall, followed by the cytoplasmic membrane and the cytoplasm on the inside.

{I'll talk a very tiny bit about glycocalyx (capsules and slime layers) before we go onto lipid bilayers. Glycocalyx is the protective outer layer. Not all bacteria have it. It can either be a capsule or a slime layer. Capsules are thick while slime layers are thin and diffuse. The glycocalyx also helps bacteria stick to surfaces of things.}

Luckily since I took orgo, I'm quite familiar with lipid bilayers. Hydrophobic insides and hydrophilic (water-loving) on the outside and within. These make up cytoplasmic membranes in cells.

Here's a more (only sadly slightly more..) 3-D version of the plasma membrane. It has proteins in it that typically enable the passing of material that can't pass through the membrane itself.If you somehow destroy a bacterium's plasma membrane, you effectively kill the bacterium. Shit's important. Bacteria and archaea have the same structural features in the plasma membrane but the lipids differ (duh). 

Things that can and can't pass through the lipid bilayer.

A horrible rendition of transport proteins. They change shape apparently, when letting things pass through them.

I want to switch gears for a sec and talk about Cell Walls and the peptidoglycan that makes them up. I talked in the last post about N-acetylmuramic acid and N-acetylglucosamine and how they're the structural components of peptidoglycan...Here's how the structure is laid out. Ugh the photo is AWEFUL but bear (bare?) with me here. There's chains of ...NAM-NAG-NAM-NAG... and they're attached by layers of tetrapeptide (four peptides..) chains in between. In G+ cells, there's peptide interbridges that are not present in G- cells. There's an enzyme in our saliva and tears called Lysozyme, which has the capacity to break the bond in peptidoglycan between the NAM and NAG units..This messes with the structural integrity of the cell wall. Antibiotics like penicillin have acting mechanisms similar to this.

Here's a visual and slightly better idea of G- cells than what I had in the last post...Ehh...sort of. The lipopolysaccharide is on the outside, part of the outer membrane. The outer membrane is a protective lipid bilayer. It has porin proteins that let small molecules into the periplasmic space...then comes the periplasmic space where the thin layer of peptidoglycan is, and finally the plasma membrane (phospholipid bilayer) with integral proteins. When people first get to the end of orgo 2/beginning of biochem they're like: "ugh phospholipid bilayers like THAT matters"....well it does. Just sayin'. In G - cells, the plasma membrane regulates what goes in/out of the cell. It has transporters (those proteins) to regulate movement of shit that doesn't pass through the bilayer on its own. 

It might also be a good idea to talk about the growth curve in laboratory conditions. This is produced by batch cultures, which are closed systems - meaning you don't renew nutrients or remove waste from the plates/flasks. In open systems, you would need to add nutrients and remove waste to ensure continuous growth.

But this curve is for closed systems. Initially we have the lag phase, in which the cells are figuring out their environment, turning on whatever genes are needed, and feeling out their surroundings. Next is the log or exponential growth phase. Cells grow rapidly and there's almost no variability in their activities. Following that is the stationary phase. Cell death and cell replication are in equilibrium; there is variation/heterogeneous activity. The death phase soon follow as cells run out of nutrients, followed by the phase of prolonged decline.

Cells are most sensitive to antibiotics in the log phase when they're actively replicating. Endospores are formed in the stationary phase, when cells are kind of realizing that they are running low on nutrients. If you're testing enzyme activity, you want to do it in the log phase since there's little to no variation in what the cells are doing. To calculate growth rate, you have:

N(t) = No x 2^n

# cells at time (t) = initial number of cells x 2^number of cell divisions

Some things to leave myself off with before I try to fall asleep..

Prokaryotes naturally have no nuclear membrane. 

Only bacteria have peptidoglycan in their cell walls.

Protozoa is the only group in Eukaryotes that have only single-celled members...they're also bigger than Prokaryotic cells by about 50-100 times.

Antibiotics are intended to target the cell walls of gram positive cells, fucking with the peptidoglycan in there. Some shit may not be effective for gram negative cells since 

a) the peptidoglycan is UNDERNEATH the outer membrane and

b) the peptidoglycan is a significantly thinner layer

Gram positive cells have techoic acids and lipotechoic acids intermingling with the peptidoglycan layer.

Gram negative cells have an outer membrane, whose outside layer is lipopolysaccharide and their cell wall is in between the outer membrane and cytoplasmic membrane. The LPS is important when considering pathogens since our immune systems see the LPS of bacterial cells first. Some pathogens can fuck with our immune system and modify the LPS.

Only gram positive bacteria is sensitive to penicillin and lysozyme. 

Bacillus and Clostridium are infamous for forming endospores. Fuck that shit.

Mycoplasma refers to a genus of bacteria that lacks a cell wall.

Mycobacteria are acid-fast Gram positive bacteria that have a very thick, protective, waxy cell wall.

^That is thanks to : http://ntmnews.blogspot.com/2012/08/mycobacteria-and-mycoplasma-what-is.html