7: corynebacterium & listeria

8/10/2019 7: Corynebacterium & Listeria

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Transcribed by Erica Manion 11/14/2014

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Infectious Diseases Lecture 7 Gram-Positive Rods (second hour) by Dr. Boylan

[29] [Pathogenesis C. perfringens][Dr. Boylan] -Hereis another beaut. Another really beautiful one. Called Clostridium

perfringens, causes gas gangrene. Virulence factors, spores out there in nature, and soil, andairborne, etc. Many, look at the complement of toxins and enzymes as well that this bacteria

can produce to cause gas gangrene. Gangrene means sore essentially, in some language orother, I think Greek. Or maybe Latin. And gas of course means the gas that is formed as this

tissue, the muscle tissue is destroyed and fermented. Gas, acids and gas are formed as we

will see in the beautiful lesions coming up in these slides. So, lecithinases, membrane

lecithin, hemolysins, red blood cells. Collagenases, collagen is destroyed, proteases, these

are what destroy proteins, our muscle protein. Break it down and fermenting it. And then

lipases as well, lipids are affected. So a whole complement of exotoxins.

[30] [Gas gangrene causes massive tissue damage]Massive tissue damage. Gangrene sore, really. Blood flow stops, dry, shrunken purple or

black blotches appear. Enzymes destroy cells, lecithinases and others. Fermenting muscle.

Putrefying proteins. Gas gangrene. You can see the gas is formed in some of the lesions,

especially the one in the middle there. As the protein is fermented and putrefied, very, and

some of these proteins that are fermented, you smell all the sulfur amino acids that are

there. So it has a very foul odor as well when these amino acids that have sulfur are

produced by the tissue as muscle is destroyed [that sentence was hard to hear, 1:01:44 left

in podcast]. So gas gangrene, intense pain, swelling, foul smells, skin turns dull red, green,

and black. And you can see concurrent gangrene here on the foot and toes here on this

individual on the right. Okay, so thats gas gangrene. C. perfringens, many virulence factors,

enzymes, and toxins.

[31] [Pathogenesis C. difficile (C. diff)]The third, another Clostridium, I guess the fourth one , is C. difficile - C. diff. Responsible for

pseudomembranous colitis. So colitis, inflammation of the colon, a pseudomembrane, as it

grows in our gut, it kind of coats our intestinal tissue in our gut with what looks like a

membrane, a clear coating. But its not really a membrane,its not that adherent. So it lookslike a membrane, a pseudomembrane that coats our intestinal cells and affects of course

therefore water absorption by our intestinal cells and less absorption of water and maybe

an outpouring of water in the cells that are already there, lead to diarrhea. Results as the

consequence of elimination of normal intestinal flora, the microbiota is the preferred term,through antibiotic therapy, most commonly Clindamycin. And most commonly, once again,

in a hospital or healthcare setting, we have this particular condition, although it can occur

outside the hospital too. So what happens is a patient in a hospital has an infection and

maybe they are there for the infection, maybe they picked up the infection in the hospital or

maybe they are there for some surgery. You get an infection, and they say, Ok lets treatwith an antibiotic. And often their first choice is Clindamycin. Youll use Clindamycin a lot

yourself in your practice. It is a very effective antibiotic. Usually, not many side effects.


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What happens when you use Clindamycin, it upsets the normal microbiota of the gut. It

starts to kill cells in our gut that are vegetative cells that line our gut, E. coli and all those

others. And it starts to destroy them at the same time it is trying to kill the bacteria causing

the infection in that patient, whatever it may be, Staph, Strep aureus. So it upsets the

microbiota and the normal composition of the microbial population in the gut.

However, in the gut we also have this bacterium, C. diff, a spore former. It is resistant to

Clindamycin. But all of a sudden, here is a spore, residing in the gut as a spore, not doing

any harm. But it recognizes somehow that all its neighbors of the gut are being destroyed

for some unknown reason, but it is because they were given an antibiotic that killed them

as well as the bacterium causing the infection. So C. diffspores are there, that now no

neighbors to contend with, or fewer neighbors, other bacteria bacteria. And then they say

ok now we can germinate. They are spores so youll see them germinate. Vegetative cellscome out, and they begin to grow and flourish in the gut as a result of suppression of bugs

by the antibiotics. They take over and they grow. And they can cause colitis, they can also

cause pores to be formed in the intestine, and a pseudomembrane as well, leading to

diarrhea, but also even more serious conditions later if it continues.

The virulence factors are a couple exotoxins called A and B. Different enterotoxins.

Cytotoxins, enterotoxins that they form. Result in elimination of the normal intestinal

microbiota through antibiotic therapy. Clindamycin is the one most commonly associated

with this condition, but other drugs may do the same thing. If the gut bacteria are sensitive

to this antibiotic, and C. diffis not, spores germinate, grow, even in the presence of that

antibiotic they grow because they are resistant to them, and cause damage.

[32] [C. diff Diagnosis]

Abdominal pain and watery diarrhea. Laboratory indications, you can isolate the bacteria,you can do tests to look for the cytotoxins and enterotoxins that they produce, so there are

tests that can be done. But ordinarily it is the history of the patient, the therapy, did they

receive therapy or not? Do they have diarrhea, do they have cramping, do they have pain?

And then you put those things together, and oh, it is C. diff. C. diff infection, becoming more

and more prevalent. These bacteria were always there, it is one of the conditions that occur

as a result of advances in medicine, really. We have drugs to treat infections, but as a result

and they do! They treat the infectious agent, but they also upset the normal bacteria and

that leads to other bacteria who are there, not doing any damage before, to flourish and

cause damage, colitis and other abdominal problems as well. They get very, very sick.

[33] [Clostridium infections Treatment, Prevention, Control]So what is the - ok. Overall, Ill get back to one more thing about the C. diff on the bottom of

the next slide. Overall with Clostridium, infections or intoxications. We know there is a

vaccine for Tetanus, the DPT, it is shown there, for Diphtheria, Pertussis, that is whooping

cough, and Tetanus. And that is the one we give all the time to our children, DPT. Ok, a

very important point Ive mentioned many times before, is that in this vaccine we have the

toxoid. So in Tetanus, the tetanospasmin, that is the toxin. Remember you can heat it a bit


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or there are different ways to treat this toxin to make it non-toxic, but retain its

antigenicity. Thats a toxoid. A weakened toxin. It is no longer toxic, but still antigeniclyactive so that is what we have in the DPT. 3 doses required, booster immunizations every 5

years. No vaccines for gas gangrene. But if we have gas gangrene, or we have botulinum

toxin, the best treatment would be to neutralize the toxin. Antibiotics wont do any good

once the symptoms of intoxication occur like that. So the toxin is in the patients body, givethem anti-toxin, which are really antibodies against the toxin. You can inject them with

anti-toxin, they will seek out the toxin and bind it and neutralize it. So botulinum, gas

gangrene, [mumbled something inaudible, 1:08:36 into podcast], we have different anti-

toxins that can neutralize the toxin, and then hopefully the patient will get better.

The patients withC.Diffinfections occur as a result of an antibiotic, particularly

Clindamycin. But lets say the patient still has an infection, what do you do? Well theyshould switch to some other antibiotic that would help the patient with the infection they

had but also help cure, or treat, at least, the infection caused by C diff. So you switch to

some other antibiotic. So you stop the one you had the patient on, like Clindamycin, and

you [? 1:09:09 into podcast] something they often use, Vancomycin to now help with theproblem caused by the C. diff. Vancomycin is used, so, and that often helps alleviate the

pseudomembranous colitis.

[34] [CORYNEBACTERIA, LISTERIA]

[Student Question: Can you prescribe a probiotic if a patient is on Clindamycin?]

[Dr. Boylan] - Probiotics? I dont know, the science on that is kind of iffy. Its not the first

line of defense, I dont think. Probiotics often are bacteria that help, well actually I should

mention this. The most recent type of therapy for C. diffis what they call, and I should have

that on a slide, so please remember this as well,fecal transplants. Youve hear of that? Itused to be, they want to restore the normal bugs in the gut to what they were before C. diff.

So what do they do? They give people fecal material from a normal, healthy person, andhelp, and get it down into the gut. Endoscopy is one way to do it, and hope that that and it

has been very effective and youre going to see more of that in the future. Now you can takepills of the bacteria, got them from the fecal matter of people and feces the people thathave recovered from the infection. Or people with healthy gut bacteria you know, you just

get their gut bacteria. So you have in these pills, these capsules, a whole mixture of

different bacteria, just bacteria themselves, not any of that other gunk you find in fecal

matter. And they take, and they get down in the gut, and you hope they establish

themselves in the gut. So thank you, because really I should have had a Fecal Transplants or

replenishing the bacteria that were being lost. It takes a while, even if you stop therapy

with Clindamycin and add something else, it is going to take a while. But if you take these

pills it might speed up the processes of re-establishment of a normal gut bacteria, as youcan now with fecal transplants. It is going to be used now more extensively, I think in the

future. They are doing studies on that and making the approach a bit more palatable to

people, I guess youd say, and effective. So I guess that is probiotics in a way, but probablyyou think before, prophylaxis as well, but this is another way to treat, even after damage

has occurred. Get back that normal, resident biota, and that is whats gonna help. Theyllprotect the gut, again.


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the bacteria produce the toxin AB, and the B part is the part that binds to our cells, in the

epithelium of the throat, upper respiratory tract. The B binds, it has to bind, then the toxin,

the whole toxin is taken inside of the cells, one of our cells. The AB components separate

from each other, and the A is the toxin. What does A toxin do now, Diphtheria, to destroy

those cells? Its toxic, its going to kill the cells. Well, it acts as a - here is the toxin, you see it

on the left there, here is the diptheria toxin. Specifically, how does it work? It breaks apartNAD to form nicotinomide and ADP ribose. What the ADP does, it causes ADP-ribosylation,

remember that, of this protein, EF-2. So, the ADP ribose is produced as a result of this

toxin, breaks down NAD, ADP ribose, one of the two components of it, it binds to Elongation

Factor 2, EF2, the protein in our cell. Thats a protein involved in the initiation of protein

synthesis. So it blocks protein syntheses. So, toxin, diphtheria toxin, many toxins do this as I

mentioned before. They carry out this reaction where NAD is broken down into

Nicotinamide and ADP ribose. It is called ADP-ribosylation of the protein, and the protein

here is Elongation Factor 2. Blocks protein synthesis, cells die. ADP-ribosylation happens

with a lot of different toxins but as I mentioned before, the target of this ADP ribose varies,

depending upon the toxin. Sometimes it stops EF-2, and other proteins in the cell are

affected by ADP-ribosylation, depending upon the toxin. Diphtheria, botulinum, whatever.But in diphtheria, it is specifically causes the binding of ADP-ribose, ADP-ribosylation of the

EF-2 protein, the protein involved in protein synthesis.

[38] [Diphtheriae- Diagnosis]

Diphtheria diagnosis, muscle weakness, sore throat, fever, you have a pseudomembrane,

here is an example of a pseudomembrane on the tonsils and throat. And the child has after

a while, difficulty breathing, and it can lead to suffocation. Thats a problem of course. It

used to be called the great strangler, the strangler because the child, it was often a

child and before vaccines this was a rampant infection in children. A hundred years ago, ahundred and ten years ago in New York City, it was tough for a child to survive to the age of

5 because of Diphtheria, measles and mumps, and other things that they were exposed to,typhoid fever. But once vaccinations came along, such as diphtheria, instance went way

down. So the vaccination is key. We saw that recently, after the fall of the Berlin wall. 25

years ago now, in Germany and also in Russia after some events of that time, as a result of

that, of the health care system was affected dramatically. As democracy sort of you know,

things changed, and the health care system broke down. All of a sudden, people were not

being vaccinated, their children were not being vaccinated with DPT, and a lot of cases of

diphtheria, and death due to these childhood infections.

[39] [DiphtheriaTreatment, Prevention, Control]Immunization, if the child has it. Once again, passive immunization does give them

antitoxin antibodies that neutralize the toxin. Penicillin will treat the infection. DPT. SoDPT, once again, and also the component for the prevention of Diphtheria is the toxoid.

This toxin we are talking about here, Diphtheria toxin. The toxoid of it, heated, treated,

loses its toxicity but still is antigenic.

[40] [Listeria]Ok, lets talk about Listeria. And it is the last one in this group. Listeria, Aerobic, gram

positive rod, widespread in nature, especially in animal populations, so its out there, its


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not just a human disease. Animals, floating around in nature in soils and streams. The only

human pathogen, the only species, isListeria monocytogenesthat causes infection in

humans. This is the bug, the main one that we talked about that has the ability, it is called

psychrophylic, remember what that means? It is shown there, it grows very well at 4

degrees, in refrigerator temperatures. It grows better in the cold, at 4 degrees, then it does

at 37, our body temperature, or our room temperature, it thrives there. So if our food iscontaminated with these bacteria, as a result of being meats or cheeses or dairy foods we

eat, these bacteria somehow landing on them, they are present in the food in our

refrigerator, they continue to grow, and we eat this contaminated food, we get infection

caused by this bacterium. The disease is listeriosis, especially effected, you should

remember this also, who is mainly at risk? Pregnant women, newborns, and as

always, immunocompromised adults. This is zoonosis because it comes primarily from

animals, primarily cattle, dairy foods, but after a while, as a lot of people do become

infected with it, they, some humans do carry it. It is a very low - would say it is a zoonosis

really. But we find even some people who have this infection do carry it for the rest of their

lives, are carriers. But it is a very low percentage, so I would say that we dont even get it

from other people. It is a zoonosis. Contaminated food. Can cause septicemia andmeningitis.

[41] [L. monocytogenes]

Heres a very unusual feature of this bacterium, Listerium monocytogenes. What it is

phagocytized, you know, our immune system comes into play, recognizes this bacterium

should not be in our body, it wants to phagocytize it, our neutrophils, macrophages, etc.

Lets engulf this bacterium and digest it, spit it out, present the antigens on the surface,

etc. But it is not degraded. So this bacterium has the ability to produce this toxin called

Listeriolysin O. Thats its first major virulence factor. What does that do? Well, themacrophages actually do ingest these bacteria. They bind to them, they engulf them, they

take them inside. And once these bacteria are inside of our neutrophils, they produce thisListeriolysin O, and they dissolve the vacuole. The vacuole that takes the bacteria into the

cells, in macrophages comes from the cell membrane, Listeriolysin O is produced by the

bacterium inside the phagosome, lysing the phagosome, destroying the phagosome. What

does that mean? It is good for the bacteria because now the lysosome can not bind the

phagosome, where digestion and destruction of the bacteria really occurs. So Listeriolysin

O helps the bacteria get out of the phagosome, it dissolves that membrane. Ok, now we

have the bacteria free in the neutrophil.

So what happens next? Very unusual feature of this bacterium. It replicates in the

macrophages and it can move from cell to cell. It forms a comet-like tail, shown here. Here

are the bacterium, they are engulfed, they break free of the phagosome, now the cell isthere, and it begins to replicate. And what it does, it uses some of the material inside the

cell to make a tail of actin, actin. And this actin tail produced by the bacteria helps propel

the bacteria around in the cell, and finally the bacteria pushes up against this membrane of

the cell, and goes on and infects an adjacent, neighboring cell, and repeats the process over

and over again. So, what is the goal of this process? If it goes from cell to cell to cell, it is

evading our immune system. The rest of the components of our immune system are out

here, blood vessels are in other parts of our tissue, and fluids and they are looking for


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bacteria out here, but these bacteria are sneaking from one cell to another by this tail of

actin propelling it through one cell into another. It evades the immune system. There are a

couple of others that do this, a very unusual virulence factor. Its kind of like youre in here,

and you brought some food, coffee or dessert and pie in, and the guards are out there

looking for you, but they are going to wait until you come out with your food, then theyll

arrest you or grab you or take you here or there, but if you can escape youre going topunch a hole through the wall in the back and go to the room next to you, youre going to

evade the police! You dont get caught, so you can survive and grow from day to day. So this

is essentially what some of these bacteria do. They evade the immune system, they dontexpose themselves to the immune system, they progress from one cell to another and

continue to grow and divide and do damage in that way. This is how eventually they cause

a lot of problems in us and cause the food poisoning, as they destroy more and more of our

cells.

[42] [L. monocytogenes]

These can be treated with antibiotics, peniciilin, sulfa drugs. No vaccine. Prevention,

proper food handling. Let me just go on. I think I lied about stopping here. But it is so earlyand I have to cover a couple more (opens Acinomyces and Nocardia ppt), but these are kind

of interesting ones I think, because, at least this first one, causes some serious infections in

the oral cavity.

Actinomycesand Nocardiapowerpoint

[1] [Actinomycesand Nocardia, Other Gram-positive Rods]

Ok, so-called other gram-positive rods in addition to the ones weve already discussed.

Actinomyces and Nocardia. ParticularlyActinomyces is the more important one of the two,

so well see how far we go. Ill stop afterActinomyces today.

[2] [Actinomyces]Actinomyces, means ray now these two are bacteria. Actinomycesand Nocardia, they are

true prokaryotes, bacteria. They are not fungi. Actinomyces, the name means ray fungusin Greek. What property does it have in common with fungi, molds, we are going to talk

about later. These two bacterium,Actinomyes and Nocardiacan both branch. They have

branching. Instead of nice, long chains or pairs, you can see a chain branching off there, X,

Y, etc. This is a very unusual feature of bacteria, and it is like fungi, so the branching is why

its given its name that indicates its something aboutActinomycesthat indicates a ray

fungus, sort of like fungi which are eukaryotes.

So gram-positive, anaerobic. Filaments in a branching rod, filaments means very thin rods,part of our normal microbiota, particularly in the subgingival plaque, we have to be

concerned about those. Now,Actinomycescan form four or five different types of serious

infections in the body, but we are going to focus on the one in the oral cavity. Theres anormal population, these bacteria are also in our gut, but its an anaerobe. Its an anaerobe.

And it is also part of our oral microbiota. So where is it commonly found? In the

supragingival plaque on our teeth? No, thats more aerobic. They are down there in the sub-


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gingival plaque. The high population ofActinomyces, this particular genus, because

anaerobic environment, maybe down in the gingival sulcus as well, anaerobe.

Here are the species we have to be concerned about, but lets just rememberActinomyces

israelii, some features of it our shown here, unusual, branching, intertwining, filamentous

bacteria. But on the yellow there, this is a characteristic feature of the type of colonies that

it forms when it grows on a media. It is one of the things that almost gives it away that theculture you are working with is your bacteria, when it forms these types of colonies on

plates isActinomyces. A characteristic of the colony looks like either or molars or

breadcrumbs, they have that appearance the colonies do, on plates. When they grow,colonies will form these So thats unusual. You know, molar tooth or breadcrumb

appearance on agar as shown there on the yellow. The one in the middle there is

microscopic observation of the filamentous bacteria themselves.

[3] [Actinomycosis]

Actinomycosis is the infection. Five major types, we arent going to talk about the other

four. We are going to focus more on the cervicofacial actinomycosis. It is the most common

actinomycosis.

In the face and neck region, it causes what is often referred to as a lumpy jaw, and we see

that in these figures here, in the neck and the cheek on this woman here. It forms this

lumpy jaw and abscess. Slowly, enlarging, hard, red, although not always red but usually

red, lump. Lumpy jaw. It is a result of, when these bacteria are there in our mouth, a

number of different reasons can cause this infection to begin. Poor oral hygiene, not

brushing or flossing or doing anything, a lot of patients youll see dont bother to do good

oral hygiene, tooth extraction, ok to extract the teeth, bloody area, bacteria are there, they

can spread from that site into adjacent tissue, root canal, endodontic therapy, and trauma.

Any trauma can give these bacteria that are there, not doing any harm at all, an ability to

grow and spread in the adjacent tissue. Jaw surgery as well. SoActinomyces,the bacteriaenter the subcutaneous tissue following injury, and that can be anything from an abscess to

a granuloma, and they have draining sinus tracts. So the infection occurs inside, of course,

near the gingiva, but then it can spread through these channels that form, sinus tracts that

you are probably familiar with, channels that form from where the infection is inside,

through the tissue to the outside of the cheek. And that is when the abscess appears, the

lump appears, hard lump. Draining sinus tracts.

[4] [Actinomycosis cont]

Forget about these others, but I just wanted to point out there are other types of

actinomycosis. We wont bother with this slide of the four other types of actinomycosis that

can occur.

[5] [Actinomycosis The Infection]

It could be pyogenic, a lot of pus when you see these lesions as well. More common as a

chronic infection, more suppurative and granulomatous. Abscesses, sinus tracts and

channels form, bring the bacteria out to the surface, lumpy jaw. Characteristically, this is

another term you will hear associated with this infection.


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Sulfur granules. What color is sulfur? Remember? It has a yellow color of all the elements, it

is kind of yellow-ish. So, granules, sulfur granules. If you got some of the pus or the

abscess material from the lumpy jaw or the sinus tracts even, and you looked at it

microscopically and there are a lot ofActinomycesthere, they look yellow-ish, they look like

sulfur. So they are clumps of this bacteria. Clumps ofActinomycesfrom the pus you

sampled, put on the slide, microscopically it looked like yellow, a bit yellowish. So they arecalled sulfur granules, and that is indicative of this infection. An actinomycosis. I remember

years ago when I had a lab upstairs, a former student who graduated maybe 25 years ago,

would come by once a year to give a lecture in one of the clinical courses. And she would

often drop by. And she would say You know, I have this infection, and whenever I stand on

my head and blow my nose, I get this yellowish stuff comes out. And I would say Oh what

is it? I dont know! I said, Sulfur granules? It is probably actinomycosis Oh! Shed

come back the next year, you know, when I stand on my head.. And I blow my nose, I getthese yellow, what could it be? Sulfur granules, maybe actinomycosis? Oh. Third time

she came back, I said, Dont tell me. You should know by now what you have! But

characteristic pathignomic (?) feature of these things are the yellow color of the granules

which are really tissue but also the bacteria, theActinomycesyou see. The sulfur granules.Suppuration, pus, you know fibrotic walling off the lesion, you are trying to prevent it from

getting any further into your body if you wall off this fibrotic granuloma, you dont let these

bacteria get any further into the blood. Ultimately there could be bone involvement and

destruction of the bone.

[6] [Periodontal Disease and Dental Caries]

Ok, heres something that might be a little controversial, Im not sure but.. Ok. Association

between Heres another species.Actinomyces viscosus. Involved in gingivitis, possibly in

mild cases of periodontitis. That is probably true. How does it promote periodontitis?

Infection, inflammation, loss of teeth. The tissue around the tooth. Periodontitis. Well, this

bacteria promotes adhesion to the periodontal pathogen,Porphyromonas gingivalis todental plaque, thereby maybe set the stage for development of periodontitis. P. gingivalis.

Porphyromonas gingivalis,probably the main culprit, not the only culprit but the main

culprit often these bacteria work in teams, but this is definitely associated withperiodontal disease. P. gingivalis. So what does it want to do? Ok, if it is going to cause

periodontitis, it wants to stick to the tissue there. Stick to there, to adhere, and one of the

things it adheres to is another bacteria,Actinomyces. In this way,Actinomycesmight play a

role in the development of periodontal disease. It may not cause damage itself in

periodontal disease, but it serves as a nitis (?) or point of attachment of the main culprit in

periodontal disease to it, thereby enabling it to survive and grow, and youll see what kindof damage it does when we give the lecture on periodontal disease. Also produces

succinate, which stimulates the growth of P. gingivalis, so it seems to be a real pal of thisother bacterium that causes periodontal disease.

Ok, caries, root surface caries. I dont know if youve had any lectures on that yet, but weknow that its Mutans streptococci, and that family of mutans, group of mutans, so-called

Mutans streptococci, Strep mutans, Strep sobrinus, Strep oralis, Dr. Caufield probably talked

to you about that already. The culprit. How about in the root surface? Not coronal but the

root surface? Are there other bacteria that cause caries there? And for a while there it was


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thought that yeah,Actinomyces. The species we just were talking about, maybe other

species, maybe viscosus, a couple others, butActinomyces, maybe they might be involved in

root surface caries. Because we often find them there, once we see the caries in the root, we

see we isolateActinomyces[hard to hear, 1:38:46 into podcast], so that must be one of the

agents that cause it. Well I can, through some controversy, thats why Iput the reference

down here where now they think that is not actually true.Actinomycesare always there,even, they are there in healthy subgingival plaques, in the healthy, no periodontal disease.

They are there also when there is periodontal disease, but their numbers really do not

increase that much. So youll find them in healthy and diseased states, subgingival plaqueand gingival sulcus, but no big increase in numbers. So they dont really think you still

need those other bacteria to cause caries, even in the root surface like the Mutans strep. You

need bacteria that are acidogenic and acidurgic like Strep mutans and lactobacilli. Not

Actinomyces. So if someone says You have root surface caries? Oh, you haveActinomyces.Well say maybe not, because some of the studies recently have shown that may not be the

case and Ive given you the reference in case you need to back up what you say if someone

doesnt believe you.

[7] [Laboratory Identification]Sulfur granules, look for these in filamentous bacteria.

[8] [Laboratory Identification]

Prevention, treatment, removal of tissue, long term, you need long term therapy. Penicillin

Actinomycesare very susceptible to Penicillin. You need I.V. administration of Penicillin

for up to 6 weeks, chronic infection. If there is a granuloma forming, you know it is going to

be tough for the blood system, the blood vessels to get to that granuloma. So even if you

have drugs and Penicillin in the blood stream, to get to the site with the bacteria may be

difficult. The fibrin wall, and around the bacteria, around this mass, forming the granuloma.

So you need long term therapy, you need surgery to get rid of as much of the lump that youcan, to provide better access of the blood vessels and blood stream to that area, so the

antibiotics in the blood can get to the bacteria. And good oral hygiene will hopefully help

prevent it.

So lets stop there, well talk about Nocardiamaybe next time, ok? Thanks for showing uptoday. Any questions? Email me, write me, send me love letters, whatever. Flowers. I will

respond. No hate mail! Thank you!!

7: corynebacterium & listeria

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