Gram Positive Cocci

• In Groups

1. Staphylococcus aureus
2. Staphylococcus epidermidis
3. Staphylococcus saprophyticus

• In Chains
  

1. Streptococcus pyogenes (A)
2. Streptococcus agalactae
3. Streptococcus equi
4. Streptococcus bovis
5. Group G Streptococcus
6. Viridans streptococci
7. Streptococcus pneumoniae
   

Gram Positive Rods

1. Bacillus anthracis
2. Bacillus cereus
3. Corynebacterium diphtheriae
4. Clostridium difficile
5. Clostridium perfringens
6. Clostridium tetani
7. Clostridium botulinum
8. Listeria Monocytogenes
   

Gram Variable

• Enterococcus fecaelis

Gram Negative Cocci

1. Neisseria gonorrhea
2. Neisseria meningitidis
   

Gram Negative Rods

1. Brucella (abortus, melitensis, suis, canis)
2. Campylobacter fetus
3. Campylobacter jejuni
4. Escherichia coli
5. Francesella tualarenesis
6. Helicobacter pylori
7. Hemophilus ducreyi
8. Kleibsiella pneumoniae
9. Legionella pneumoniae
10. Proteus vulgaris
11. Proteus mirabilis
12. Pseudomonas aeruginosa
13. Salmonella enterica
14. Salmonella cholerasuis
15. Salmonella typhii
16. Shigella boydii, dysenteriae, flexneri, sonnei
17. Yersinia enterolytica
18. Yersinia pestis

Halophilic

1. Vibrio cholerae
2. Vibrio parahaemolyticus

Pleiomorphic

1. Bacteroides fragilis
2. Bordatella pertussis
3. Haemophilus influenzae

Acid Fast

1. Mycobacterium tuberculosis/bovis
2. Mycobacterium kansasii
3. Mycobacterium marinum
4. Mycobacterium scrofulaceum
5. Mycobacterium avium-intracellulare complex (MAC)
6. Mycobacterium fortuitum
7. Mycobacterium chelonei
8. Mycobacterium leprae
   

Spirochetes


1. Treponema pallidum
   
2. Leptospira interrogans
3. Borrelia recurrentis
4. Borrelia burgdorferi
   

Rickettsiaceae

1. Erlichia
2. Coxiella burnetii
3. Rickettsia rickettsiae
4. Rickettsia akari
5. Rickettsia (typhus)
   

Chlamydiaceae

1. Chlamydia trachomatis
2. Chlamydia psittaci
3. Chlamydia pneumoniae
   

Mycoplasmaceae

1. Mycoplasma pneumoniae
2. Ureaplasma urealyticum



Tags: bacteria, staphylococcus, strptococcus, mycobacteria, listeria, mycoplasma

• Virulent, nonmotile, nonsporeforming, facultative anaerobe,
  
• Gm +ve cocci in grapes/clusters
• Catalase +ve
• Coagulase +ve
• Ubiquitous in environment; normal flora of skin/nose
• Spread through lesions, fomites

• Enterotoxin- vomiting, diarrhea, heat resistant, (actually released in gut)
• TSST-1 – tampon use, wounds, superantigen
• Exfoliatin- scalded skin

TISSUE SPREAD:

• Alpha toxin(lechthinase)- skin necrosis;hemolysis
• Hyaluronidase- degrades proteoglycans
• Fibrinolysin- lysis fibrin clots

IMMUNE EVASION:

• Protein A- binds IgG-Fc, blocks opsonization and complement fixation
• Coagulase- activates prothrombin
• Hemolysin- destroys RBCs, PMNs, M0s, platelets
• Leukocidin- destroys WBCs

• Skin infections: impetigo, cellulitis, erysipelas, abcess, furuncle, carbuncle
  

• Bacteremia/sepsis: hematogenous spread
  

• Acute endocarditis: DESTRUCTIVE (compare to S.viridans and S.faecalis)

• Pneumonia –damaging process, cavitations, empyema, effusions

• Osteomyelitis/septic arthritis- hematogenous and traumatic spread

• Food poisoning – 1-8 hr onset, vomiting, preformed toxin

• Toxic shock syndrome- fever, vomiting, diarrhea, diffuse erythematous rash

• Gm + cocci in grapes,
• Catalase differentiates from Strep.
• S.aureus: Beta hemolysis, coagulase, Yellow (Au) pigment
  

1. (coagulase causes coagulation!)
   

Coagulase neg:
S. epidermidis: novobiocin sensitive

1. “sensitive skin”

S. saprophyticus: Novobiocin resistant

Treatment

• Beta lactamase production is common! Use methicillin, nafcillin, dicloxacillin
• MRSA: (Methicillin resistant S. aureus) : vancomycin
  

STREPTOCOCCI

In the upper respiratory tract, there is one genus of bacteria that cause 90% of infections (pharyngitis) Group A Streptococcus (aka S. pyogenes).

15-30% of all sore throats are caused by Group A, 40% by unknown causes, 30% by viruses. This means that only about 30% of sore throats require antibiotics, which you should remember when you’re a doctor and a kid comes to you with a sore throat.

There are three types of Strep based on what they look like on blood agar after 24 hours:

1. β Hemolytic  If you look at the blood agar, you will see a colony of bacteria surrounded by white space. This is because there is complete hemolysis of the RBCs. The hemolysins are mainly streptolysins S and O. Important members of this group includes Group A, and to a lesser extent B, C, and G. (90% vs. 5%).

2. α Hemolytic  These convert hemoglobin into methemoglobin, which is green, therefore on the plate you will see a colony surrounded by green stuff. This type includes S. viridans and S. pneumoniae.

3. γ Hemolysis  this is also called nonhemolytic Strep, because all you see is the colony with no hemolysis. This includes S. bovis and group D.

You might be wondering why all these bacteria are called Group A, B, C etc. It’s because a scientist in the 30’s, Rebecca Lancefield, decided to classify all the different kinds of strep. She extracted bacteria from throat swabs immunized rabbits with it  used the antisera to see if it reacted. If it didn’t, she did it again, and again, until she got tons of groups. But 90% of the bacteria reacted with the first group, which is called Group A or S. pyogenes. Both names are used in the literature, so remember both. The professor refers to it as GAS (Group A Streptococcus) and so will I from now on.

Ok, so we know that all of GAS is dangerous, why not make a vaccine?

Well there are problems. The groups were distinguished based on polysaccharides in their cell membranes, and antibodies can’t be made against polysaccharides. Antibodies can be made against proteins, and the protein on GAS is called M protein. There are at least 60 different epitopes of M protein in GAS, and all cause disease. This is a lot of antibodies to include in one vaccine!!

MORPHOLOGY

If you do a gram stain of GAS from agar you’ll see short chains of round things attached to each other. If you do it from a throat swab, you’ll see long chains. This is the only Strep with long chains, so it’s immediately recognizable under the microscope.

Strep produce adhesion pili on their surface. In cross section these look like fuzz going out of the bacteria and sticking to the cell. What is this fuzz layer?Polyglycerophosphate linked to fatty acid. There are many types of adhesins, such as LTA and F protein.

What makes GAS so virulent?

It has lots of virulent factors, including two anti-phagocyte factors, which is rare in a bacterium. These are:

1. Capsule  made up of polyhiuronic acid (a self-antigen). This means that the body can’t recognize it as foreign and eat it.

2. Protein M  prevents compliment from acting.

A summary of other virulence factors:

1) F protein  mediates adhesion to fibronectin on epithelial cells

2) Lipoteichoic acid (LTA)  mediates adhesion to many type of cells

3) Pyrogenic Exotoxins  responsible for scarlet fever (Spe A), and for Streptococcal septic shock. Enhances susceptibility to LPS, stimulates a subset of T lymphocytes bearing defined V beta elements, and suppresses B lymphocyte function.

4) Streptolysin S  Cytolytic pore forming toxin, lyses many type of cells including leukocytes and erythrocytes. Nonimmunogenic.

5) Streptolysin O  Nonactive in oxygen. Cytolytic pore forming toxin. Lyses many type of cells, including platelets and erythrocytes. When injected into animals there is preference for injury of the heart tissue.Immunogenic and determination of serum antibody titer is of diagnostic value.

6) Streptokinase  Lyses blood clots; facilitates spread of bacteria in tissues.

7) Dnase  Depolymerizes cell-free DNA in purulent material.

1. Droplet infection (this is a disease of winter and spring and is usually caused by M types 3,5,6,19, and 12. A DNase.)

   1. GAS adhere to cell

   2. Colonize upper respiratory tract (the major reservoir). ~20% of kids in winter are colonized without being sick. The bacteria can only live long enough outside the body to infect another person.

   3. Occasionally critical mass is reached

   4. Invade submucosa

   5. Tonsillitis, Pharyngitis, Otitis

   6. 95% of cases the infections are resolved with no further problems. Some strains make pyrogenic toxins which lead to scarlet fever

   7. Sometimes when the infection was caused by rheumatogenetic strain after the infection goes away ~ 3% of cases rheumatic fever, which can attack the joints and/or heart.

   8. Invasive strain can get into the blood and cause toxic shock syndrome.

2. Skin Infection (This is a disease of summer and fall and is caused by M types 49, 2, and 55, but they tend to lose their M antigens. ASLO & ADNase .)

   1. Through direct contact with mosquitoes

   2. Occasionally critical mass is reached

   3. Invade dermis

   4. Pyoderma inflamed skin infection,

   5. Impetigo skin lesions,

   6. if it spreads subcutaneously it can cause Erysipelas acute superficial cellulitis, hot red and sharply defined bumps

   7. Usually cured

   8. Sometimes, if nephritogenic strain is the cause of the infection glomerulonephritis. It occurs 10-14 days after the infection and can also be caused by throat infections.

   9. If necrotizing strain (aka flesh eating bacteria) causes the infection, it can lead to a soft tissue infection called necrotizing fascitis. If it gets into the blood it can lead to toxic shock syndrome. Once this strain gets in the tissue there is a 30% death rate, even with antibiotics. The penicillin window is only the first 3 days. By day 4 it is too late because the bacteria are already in the blood.

NONGROUP A β- HEMOLYTIC STREP

These bacteria also cause disease, but not as much, even though they are commonly found in the throat. It is associated with food consumption. Groups C and G are the most prevalent. The infection is usually short, but long infections are seen in poor people.

Other bacteria that don’t cause disease very often include diphtheria, which is mostly caused by the toxin, and Borditella pertussis, which causes whooping cough.

S. pneumoniae causes alpha hemolysis, but don’t confuse it with normal flora. A quick test to distinguish it from normal flora would be to look under a microscope. It always comes in two and so is sometimes called diplococci.

So how does the infection happen?

1. Well it starts as a droplet infection

2. Goes into the upper respiratory tract (S. pneumoniae live only in humans and their favorite place to live is the URT, they’re often found there with absolutely no harm to the host, for example after being a while in a military camp ~ 60% of soldiers test positive, but they aren’t sick.)

3. Can stay there for a while

4. Someone has a predisposing factor. (skull fracture , otitis, obstruction of eustacian tube , sinusitis. S. pneumoniae is the leading cause of ear infections in kids.) Flu or viral infection can also be a predisposing factor and brings the bacteria to the lungs {that’s why the flu is dangerous}

5. Invade tissue and initiate inflammation (inflammation is caused by the acidic capsule which the bacteria usually lose so the antibodies the body built up for the capsule are no good)

6. Lobar pneumonia: this has a very typical lesion that can be diagnosed by a radiologist looking at an x-ray

7. Most cases cured even without antibiotics, but

   1. Can get to pleural cavity

• Cause emphysema and even death if not treated.

2. If a person has a splenectomy, sickle cell anemia, or a defect in phagocyte formation the bacteria can get to the bloodstream and lead to endocarditis, meningitis, or arthritis.

Now onto assorted facts about the bacteria itself

1. These bacteria actually where the ones used to discover that DNA is the genetic material in 1943.

2. When bacteria react with capsular antibodies and water there is a quellung reaction – the capsule swells.

3. The most typical test for S. pneumoniae is adding detergents. These activate autolytic enzymes and make the live cells lyse, so if you look at the plate there will be a clear zone.

4. The bacteria bind to an acute phase protein (C Reactive Protein, CRP) produced by the liver because of inflammation, also used to diagnose inflammation. CRP activates compliment so bacteria can be eaten.

5. Capsular Polysaccharide There are 83 different serotypes, and this is how the bacteria can be distinguished. FAVORITE USMLE QUESTION  what antigen allows you to serotype what bacteria? REMEMBER S. pyogenes  M protein, S. pneumoniae  capsule.

6. The huge number of serotypes is a problem, how do we vaccinate? Well there are only 22 that actually cause disease, so we vaccinate against these serotypes. #’s 10 and 22 cause 85% of cases. The vaccine’s been around for 45 years and it protects from pneumonia and complications.

What are S. pneumoniae’s virulence factors

Teichoic Acid, LTA, and peptidoglycan fragments are released when the cell lyses. They activate compliment and trigger cytokine release by the cells of the immune system. Pneumolysin is a cytolytic toxin. The capsule is antiphagocytic and prevents C3b from attaching and causing opsonization.

S. viridans

Although they mostly stick to teeth, they also adhere to the tongue and cheek. If they get into blood because lets say someone got a tooth pulled, and that person has damaged heart valves, you can see subacute endocarditis. This is very rare nowadays because dentists give antibiotics when they pull teeth and ask if you have heart disease in the family so they know they have to be careful. This is an example where the predisposing factors are known so the disease is eliminated.

The oral cavity is home to >500 different species of bacteria that have been found so far. >90% of these are not found anywhere else, only 30 can live in other places. Why is the mouth such a popular place? Well it’s nice and moist all the time, and there is lots of food there.

Bacteria need to stick to survive, and this is a big problem in the mouth. The bacteria are subject to shear forces but still have to manage to hold on. The tooth is a great place for bacteria to grow because it is never shed. When you clean your teeth, you give a nice smooth surface for bacteria to stick on to; these are called the early colonizers. Other bacteria stick to that bacteria and eventually you get a biofilm unique to the mouth.

The early colonizers at first have to survive in aerobic conditions, but as more and more bacteria stick to them, they have to learn to survive in anaerobic conditions. Bacteria also have to adjust to feast and famine situations. When you eat there’s lot of food, and when you don’t there’s no food (unless you’re like me and never stop eating).

The tongue is the most populated part of the body; it’s kinda like a shag carpet with lots of crevasses and hills. However, it rarely gets infections, so there must be a huge immune system going on there. The main source of bad breath is the back of the tongue.

When a baby is born, she is sterile until she is colonized by her parent’s bacteria. That’s right, you inherited your bad breath, BO, and all your other bacteria from your parents. Think of that the next time you see a mom hugging and kissing her baby – she’s really infecting the baby.

Cavities are because of the bacteria that likes refined sugar. People who don’t eat refined sugar don’t get so many cavities.

Saliva has lysozyme, antibodies, lactoperoxidase, and lactoferrin. It’s good because it clears the bacteria from the mouth, but the reason there is so much bacteria in the mouth is that saliva keeps it moist. Saliva is needed for talking, eating, swallowing, and spitting.

You can physically transmit your mouth bacteria by kissing, licking, sharing food and utensils, sneezing, coughing, biting, and oral sex. When you brush your teeth you get a transient bacteremia. Human bite wounds are worse than animal ones because the bacteria are already adapted to live in humans.

Gram + bacteria are vegetative and just secret acid and stuff. Gram – are proteolytic and cause tissue damage, periodontal cases, and bad breath.

Mutans Strep is a group of S. viridans made up of many species with certain things in common. They can take sucrose and produce acid that they are resistant to. They stick in pits and fissures and cause cavities on biting surfaces in kids. After they do the initial damage, the lactobacilli come. Mutans strep can cause SBE (subacute endocarditis).

Periodontal disease is caused by proteolytic anaerobic Gram – species. For example P. gingivalis and Fusobacteria nucleatum. The bacteria invade a crevice and cause inflammation and the tissue destroys itself and the gums recede and your teeth fall out. This has recently been associated with heart disease.

BAD BREATH

Bad breath usually originates in the mouth itself due to putrification. It rarely comes form the GI tract; so don’t send patients with bad breath to a GI doctor. A study in Belgium showed that 86% of bad breath was due to the oral cavity, 5% ENT, 3% tonsils, unknown 5%, so a very small proportion is due to all the diseases that can happen in your body.

Bacteria are the cause of most bad smells, like that dirty dishrag, fecal matter, bad breath, and body odor. The bacteria break down meat and tissue in the mouth and some of the gases that are released are the same as in shit. Potential sites for bad breath bacteria are the back of the tongue, dental plaque, under bridges, around crowns, and abscesses.

The back of the tongue is a good site because there is a high level of microorganisms, it is poorly cleaned by saliva, and , there is post-nasal drip that lands there which is yummy for bacteria to eat. Tongue brushing reduces bad breath by 68-77%.

The odor is worse when the mouth is dry and bad breath decreases right after eating something. Mouth breathing, fasting, medications, prolonged talking, insufficient fluids, and stress all cause mouth dryness, therefore they all cause bad breath.

When someone comes in with bad breath make sure they bring along someone because a lot of people have an irrational fear of having bad breath that just isn’t true. Tell them to come back in 2-3 hours and not to put anything in their mouths during this time. Take a history from them and compare nasal and oral odors. Do a spoon test – take a spoon and scoop at the back of the tongue and see if any green or yellow stuff comes on the spoon, this is post-nasal drip.

People come into the doctor complaining that they have little stones that drop onto their mouths and they smell really bad when squeezed. Most doctors don’t know what it is. All it is plaque falling from the tonsils, it is nothing to worry about and it does not cause bad breath. Now you will know what it is and you won’t scare your patients.

How do you alleviate bad breath? Dental care and oral hygiene, including flossing at night, drinking lots of water, chewing gum if the mouth is dry, deep gentle tongue cleaning with a plastic cleaner, stay away from coffee, gargle with mouthwash before bedtime, eat breakfast.

COMMUNITY:

typical

• 1. Strep. pneumonia
• 2. H. influenza
• 3. Klebsiella
• S. aureus
• atypical
• mycoplasm
• influenza
• chlamydia
• Legionella
  

LOBAR:

• Strep. pneumonia
  

BRONCHOPNEUMONIA:

• S. aureus
• H. influenza
• Klebsiella
• Strep. pyogenes
  

INTERSTITIAL:

• Mycoplasma
  

HOSPITAL AQUIRED:

• Klebsiella
• Pseudomonas
• E. coli