Staphylococci Flashcards
(157 cards)
1
Q
What are the three types of gram positive pathogens?
A
- Staphylococci
- Streptococci
- Enterococci
2
Q
Describe the microscopic appearance of the gram positive pathogens:
A
- Staph→tend to form grape-like clusters
- Strep→Usually form chains, some form diplococci
- Entero→tend to form diplococci or very short chains (look very much like streptococci)
3
Q
Why do staphylococci form clusters?
A
Bacteria remain linked due to incomplete separation of daughter cells and clusters form simply due to the specific way in which cell division occurs in staph.
4
Q
Why do streptococci from chains and not clusters? What type of bacteria forms reasonably long chains?
A
Their cell division is different than that of staph and causes formation of chains.
Group A Strep such as S. Pyogenes form reasonably long chains.
5
Q
What are diplococci? What types of bacteria are more likely to form diplococci?
A
Diplococci chains that hardly ever get longer than just two cocci. Strep Pneumoniae tends to form diplococci. Enterococci also tend to form diplococci (or very short chains).
6
Q
What are some examples of staphylococci?
A
Staph aureus, S. epidermis, and S. saprophyticus
7
Q
What are some examples of Streptococci?
A
Strep pyogenes, S. agalactiae, S. mutans (and other viridians strep), and S. pneumoniae
8
Q
What are two examples of Enterococci?
A
E. faecalis and E. faecium
9
Q
How do Gram positive (G+) and Gram negative (G-) bacteria differ?
A
- They differ in coloration on gram stain
- They differ in cell wall thickness and structure/composition
- They have different numbers of cell membranes
- The presence or absence periplasm space
- Peptidoglycan exposure to innate immune system
- Their pathogenic toxins and the effects they cause
10
Q
How do G+ and G- bacteria differ on gram stains? Why?
A
In gram stain, G+ (staph and strep) are dark blue due to MUCH THICKER CELL WALL.
G- stains red due to thinner cell wall.
11
Q
What is the cell wall of G+ and G- bacteria composed of?
A
The cell wall is composed mostly of a thick peptidoglycan layer, but there are other components within the cell wall region as well. There are some structural differences in the peptidoglycan molecules of G+ vs G- cell walls.
12
Q
How do the membranes of G+ and G- bacteria differ? What is the result of this?
A
G+ (staph and strep) have ONLY ONE cell membrane, whereas G- (E coli, Klebsiella, etc) have INNER and OUTER membranes (2 total) separated by a PERIPLASM.
13
Q
Describe the cell wall of G- bacteria?
A
The peptidoglycan layer is much thinner than in G+, and it is located in the periplasm. There are some structural differences between in peptidoglycan molecules of G+ vs G- cell walls as well.
14
Q
When bacterial cells die and disintegrate, cells of the innate immune system are exposed to what? Is there more exposure to this in G+ or G- Infections? Why?
A
When bacteria die/disintegrate, cells of the innate immune system are exposed to peptidoglycan/cell wall fragments. Because G+’s have much more cell wall, there is much more exposure to peptidoglycan in G+ infections?
15
Q
In G+ infections, what type of antibiotics cause increased exposure of the immune system to peptidoglycan fragments?
A
When G+ infections are treated with cell wall-active antibiotics (penicillin), there is a lot more exposure of the immune system to peptidoglycan fragments than when protein synthesis inhibitors are used therapeutically.
16
Q
What is Lipopolysaccharide? Do G- or G+’s have it? Where is it located?
A
The outer membrane of G-‘s has has Lipopolysaccharide (LPS), aka Endotoxin. LPS is a VERY POTENT Toll-like Receptor Agonist.
17
Q
What is the counterpart to LPS in G+’s? How does it compare to LPS?
A
G+’s have Teichoic and Lipotechoic Acids. These molecules stimulate the immune system but are not nearly as potent as LPS.
18
Q
What does overstimulation of the immune system cause?
A
It is a key factor in Septic Shock
19
Q
Can LPS or TA/LTA cause septic shock?
A
LPS can cause shock by itself. Lipoteichoic acid does not cause shock.
20
Q
Why do G+’s need a very thick and strong cell wall?
A
To protect them from the high turgor pressure, as the intracellular pressures in G+ bacteria are very high. So, one little defect in the cell wall will allow them to explode.
21
Q
What is the basic structure of Peptidoglycan?
A
Long polymers of N-acetyl glucosamine (NAG) and N-acetlymuramic acid (NAM) that are cross-linked by peptides. The peptide structures are quite similar among the different G+ species, but they can vary.
22
Q
What provides strength to the overall cell wall?
A
NAM molecules are cross-linked in three dimensions by peptide cross-bridges which provide strength to the overall cell wall.
23
Q
If bacteria can’t synthesize the peptide cross-bridges, what happens? What is this the basis of? How is the important?
A
If they can't synthesize the cross-bridges, the cell wall cant form and DIVIDING bacteria explode. This is the basis for many antibiotics (ie penicllin), and this is the reason that class of antibiotics cant work if the bacteria are not dividing.
24
Q
How do cell wall-active antibiotics work?
A
They block the synthesis of one or another part of the peptide cross-bridge formation.
25
Under what circumstances would many standard antibiotics such as Penicllin and Vancomycin not work?
If the bacteria aren't growing, as in BIOFILMS.
26
What is a class of therapeutics being developed that can kill bacteria whether or not they are growing? How do they work?
```
Phage Lysins (PlyC)→a lysin derived from a bacteriophage.
Bacteriophages have to inject their DNA into bacteria and then whole phages have to get out, so they produce this cell wall lytic enzyme. PlyC degrades the cross-bridge by cleaving b/t the lactyl moiety of NAM and the L-Ala of the pentapeptide.
```
27
Describe two important characteristics of phage lysins:
Phage lysins are VERY SPECIFIC. For instance, a phage that can infect Strep pyogenes couldn't affect group B strep or staph. But, they are VERY POTENT and the organisms do not have to be growing.
28
What is another widespread and important component of G+ cell walls? Subtypes?
Techoic Acids: there are two basic types
1. Lipotechoic acid (LTA)
2. Wall techoic acid (WTA)
29
What is the important structural characteristic of techoic acids in general? How is this neutralized? Why is this important?
They have long poly-glycerolphosphate chains that are negatively charged due to phosphate.
This is neutralized in a regulated way by the addition of D-Ala which carries a positive charge.
Thus, TA's have a major effect on overall surface charge, which subsequently affects a great many processes.
30
What is the importance of TA structure/neutralization therapeutically?
If bacteria become unable to add D-Ala to LTA, they are much less virulent. So, this process is a potential target for antimicrobials.
31
What is the specific structure of LTA?
LTA possesses a diglucosyldiacylglycerol moiety on one end that is embedded in the cell wall. There are then a couple of hexoses and the long poly-glycerolphosphate moiety that extends out into the cell wall. The glycerolphosphate polymer can be different lengths in G+ species (up to 50-70 units long).
32
What is the specific structure of WTA?
WTA is is poly-glycerolphosphate without the diacylglycerol. These negatively charged polymers are attached to one of the ends of the cell wall peptide crossbridges. (WTA cant be attached to too many of the peptides bc each one eliminates one peptide that could have been used to cross-link saccharide polymers.)
33
What are the three most common staphylococci that infect humans?
Staph aureus, S. epidermis, S. saprophyticus
34
What should come to mind when you think Staph aureus? Staph epidermis? Staph saprophyticus?
S. Aureus→a. PUSS-FILLED ABSCESSES b.It can infect almost ANY niche of the body, and thus it's a very challenging pathogen
S. Epidermis→think infection of INDWELLING MEDICAL DEVICES
S. Saprophyticus→URINARY TRACT INFECTIONS
35
What are 4 general characteristics of staphylococci?
1. They are Facultative Aerobes→so they grow in air (O2) and they prefer reduced O2
2. Staph are VERY HARDY organisms so they can survive days or weeks on things like bed linnens
3. Staph are part of the NORMAL MICROBIOTA (normal flora), so they are usually on our skin either some or all of the time.
4. They are mainly EXTRACELLULAR PATHOGENS, so they dont invade cells like intracellular bacteria.
36
Where are the 3 most common human-infecting staphylococci usually found on humans? With what frequency?
S aureus→frequently colonizes the nasal cavity and niches such as the axilla and perineum
S epidermis→ALWAYS present on the skin (it helps prevent the colonization of skin by more pathogenic species)
S saprophyticus→almost always in the GI tract and perineum
37
What are staphylococci able to produce? Are these considered virulence factors (VF)? Why?
Staph are able to produce a POLYSACCHARIDE CAPSULE. Capsules are almost always considered a virulence factor when present. Reasons:
1. The major reason it's an important VF is bc it can sterically block phagocytosis by phagocytic cells. The capsular material forms a physical barrier preventing interaction b/t FcR/CR of phagocytes and deposited proteins on bacteria
2. Also, Capsular material can act as an adhesive factor.
3. It can be shed from the bacteria and may activate the immune system to secrete cytokines.
38
Describe the capsule of Staph Aureus. What is the main virulence factor produced by S aureus?
The S. aureus capsule is usually relatively minor and not as important in virulence as other factors of this bacteria.
The main VFs they make are prominent extracellular toxins.
39
Describe the capsule produced by S. epidermis. What is it called? What is a major and a minor virulence factor of S epidermis?
The capsule of S epidermis is usually very heavy, so much so that is called SLIME.
Slime is a major virulence factor of S epidermis, and extracellular toxins are more minor.
40
What do you call bacteria that cause pus formation? Example?
Suppurative, Pyogenic, or Purulent.
| S aureus is a pyogenic cocci bc it forms pus-filled abscesses.
41
How can Staph be distinguished from Strep?
Catalase Test→ ALL Staph produce an enzyme called Catalase, while Strep (and enterococci) do not.
Thus, Catalase Positive=Staph
42
What catalase do and how do this help staph bacteria?
Catalase causes the breakdown of hydrogen peroxide into water and oxygen. So, it degrades ones of the molecules that phagocytes use to kill bacteria.
43
How does the catalase test work?
In the catalase test, you mix bacteria with hydrogen peroxide (H2O2) and if it bubbles it is catalase positive and therefore a Staph bacteria.
44
How do you distinguish Staph aureus from other staph species (S. epidermis, S. saprophyticus)? How does it work?
The Coagulase Test:
Of the staphylococci, only S aureus makes Coagulase. So, Positive Coag Test= S.aureus. Coagulase is an enzyme that activates prothrombin and causes plasma to clot (it's a clotting factor).
S epidermis and S saprophyticus are coagulase negative staph (CoaggNS)
45
What is the colonization frequency of Staph Aureus in humans?
20% of the human population is persistently colonized with S aureus, while 30% is intermittently colonized by it, and 90% or more of the population is colonized with it at one point or another.
46
What are its common sites of staph aureus colonization in humans?
Colonization is most common in the NASAL cavity, but other sites such as axilla, perineum/groin, and GI tract are also commonly colonized.
47
Under what conditions is the carriage rate of Staph aureus higher than in the general population?
Carriage rates in hospital personnel may be higher than in the general population.
48
What should you think when you hear Staph Aureus?
A very challenging pathogen that can colonize just about anywhere in the body. It causes PUS-FILLED ABSCESSES.
49
What is the carriage rate of Staph epidermis?
carriage rate of S epidermis are 100% on the skin
50
Individuals with staph aureus infection are commonly infected with what type of strain? Why is this important?
Individuals with S aureus infection are commonly infected with their own colonizing strain. Disease in carriers are probably less severe due to some degree of adaptive immunity.
51
In staph aureus infection of carriers by a pathogenic strain, why isn't there a always a symptomatic infection from the beginning?
It isn't exclusively the properties of the bacteria that lead to infection, there are a number of host factors that play a role. Symptoms experienced by carriers are usually less severe than in non-carriers who are infected, perhaps due to the acquisition of some level of adaptive immunity.
52
How is staph aureus spread?
From the nose, S aureus can spread to skin or clothing of carrier or to other people contacted.
53
Where does most Community-Aquired (CA) S.aureus infections come from? What strains are involved? What is another way these infections are spread?
Most CA S aureus infections are from carriers being infected with the strain they carry or infecting other people they come in contact with. These infections are usually due to a variety of different strains. Some of the spread by contact is due to poor hygiene.
54
What causes most Healthcare-Acquired (HA) S aureus infections? What do HA S aureus infections usually follow?
Most HA S aureus infections are caused by a SINGLE strain that passes around thru the facility.
These infections usually follow some sort of invasive procedure where the skin is breached in some way.
55
What are the important virulence factors (VF) of S aureus? Examples?
S aureus makes quite a few different extracellular toxins that are important VF's.
Examples:
1. α-toxin
2. PVL (Panton-Valentine Leukocidin)
56
What type of VF is α-toxin made by S aureud? How does it work?
α-toxin is a good example of a CYOLYTIC toxin. It is the prototype of the PORE-FORMING beta-barrel toxin family. The subunits of α-toxin are secreted and then form multimers in the eukaryotic cell membrane. Cells die because they lose critical monovalent and divalent ions thru these large pores.
57
What type of VF is the Panton-Valentine Leukocidin (PVL) produced by S aureus? How does it work?
PVL is a pore-forming beta-toxin that also kills cells by forming pores in the cell membrane.
58
How was PVL transferred to S aureus? Why is this important?
PVL is a prophage that was transferred to S aureus by a bacteriophage and was incorporated into the S aureus chromosome.
Importance: PVL is thought to contribute to enhanced virulence characteristics of Community-Aquired Methicillin-Resistant Staph Aureus (CA-MRSA)
59
The prevalence of PVL is low in what types of S aureus and is high in what type of S aureus?
Prevalence of PVL is low in methicillin-sensitive SA and healthcare-associated MRSA. But, it is high in CA-MRSA.
60
What S aureus toxins cause Scolded Skin Syndrome (SSS)?
SSS is an infection caused by Exfoliatin, an epidermolytic exotoxin (chromosome-Exfoliative Toxin A; Plasmid-Exfol B) produced by S aureus.
61
Does staph aureus have to infect the skin to cause SSS?
No, the exofiative toxins are produced by the SA wherever the infected tissue is located, and the toxins disperse all over the body, but they are not active until they reach the skin.
62
How does exfoliatin cause skin problems in SSS?
Once they becomes active at the skin, they cause skin problems by degrading Desmoglein-1, a cadherin involved in holding desmosomes together.
63
What is the common type of skin problem caused by S aureus in SSS?
In most cases, the skin separates at a relatively superficial layer b/t stratum granulosum and and stratum spinosum.
64
How does SSS affect children younger than 5 compared to older children? In which age is SSS most common?
In more extensive infections, extensive amounts of fluid can be lost, so SSS can lead to death in very young children.
In older children the reaction is usually less severe and may only cause Bullous Impetigo (blisters).
SSS most commonly occurs in children under 5, and can cause death.
65
How does the skin protect us from infections?
In addition, to the anatomical/mechanical barriers of the epidermis, there are also commensal bacteria whose almost constant presence inhibits the ability of pathogens to adhere and grow. Normally the mechanical or bacterial barriers must be disrupted for before pathogens can gain a foothold.
66
What are some common factors that disrupt the protective barriers of skin?
Burns, insect or animal bites, abrasions, foreign bodies (splinters), primary dermatologic disorders, , surgery, pressure ulcers, etc.
These disruptions are common.
67
What are the natural breaches to the skin barriers that can become the focus of infection?
Natural breaches are caused by ducts and pores of sweat glands, hair follicles and associated sebaceuos glands, which are normally protected but can become the focus of infection.
68
Where are skin infections less severe? More severe? Why?
Infections confined to the most superior layers (impetigo, erysipelas) are generally less severe and systemic symptoms usually do not develop.
If infection spreads to the deeper layers of the dermis, they become more and more severe bc of access to the capillaries and lymphatics which subject them to macrophages and immune cells but also provide nutrients and a pathway for hematogenous spread to other areas.
69
What is another group of exotoxins made by S aureus? Do all S aureus produce these? Example?
A relatively small percentage of SA produce SUPERANTIGENS (SAg's), but when they do, they usually make more than one.
Example: Toxic Shock Syndrome Toxin 1 (TSST-1).
70
How do superantigens work and what do they cause?
The SAg has less specific binding sites for both MHC2 (on APCs) and TCR that is outside of the Ag-binding pocket. It interacts with AA sequences on these proteins that are present on many APCs and T cells (less specific interaction), so results in widespread activation of T cells.
71
What happens when the superantigen bridges the interaction b/t MHC2 on APCs and TCR on T cells?
There is polyclonal activation of up to 20% of all T cells (normal Ag <1%) leading to a massive release of cytokines called a CYTOKINE STORM which can rapidly lead to multiple organ failure and death.
72
What are Staph Aureus Enterotoxins (SEA, SEB)? What do they cause?
SEA and SEB are the subdivision of exotoxins that cause FOOD POISONING, leading to emesis (vomiting) and intestinal cramping. They are not often fatal.
73
What type of SA enterotoxin most commonly causes food poisoning?
SEB
74
What are characteristics of SAE?
They are EXTREMELY STABLE proteins that can be produced by bacteria that are dead.
75
What is the timing of the food poisoning caused by SE? What mediates it?
Usually 2-3 hours after ingesting via a GI reflex transmitted to medullary emetic centers via Vagus N.
76
Are SE's superantigens?
Yes, they are also SAg's but they don't get into the bloodstream and pretty much stay in the GI tract, so they don't cause the same symptoms as other SAg's.
77
Why is SE induced food poisoning considered and intoxication rather than an infection?
Since you can kill the food and kill the bacteria, but the toxin can remain and cause the illness
78
What are VF's of Staph Aureus that are not secreted?
Surface bound proteins called Adhesins
79
What are Adhesins? Why are Adhesins on Staph aureus surfaces VFs?
Bacteria usually must adhere to host cells/tissues in order to survive and cause an infection (and not get flushed into stomach and get killed). To adhere to host cells, bacteria (S Aureus) use cell surface molecules called Adhesins which bind specifically to host receptor molecules.
80
What are some of the host receptors bound by bacterial adhesins?
Extracellular matrix proteins such as fibronectin, collagen, laminin, etc.
81
What is a clinical term that describes most G+ adhesins?
MSCRAMM→Microbial Surface Components Recognizing Adhesive Matrix Molecules
82
How are many MSCRAMM's anchored to the bacterial cell wall?
By a special mechanism involving an enzyme called SORTASE
83
Describe the process of sortase anchoring of bacterial surface proteins to the bacterial cell surface?
a. The signal sequence of a surface protein initiates protein travel thru the cell membrane. b. All surface proteins anchored this way have a LPXTG AA sequence near C-terminus, and sortase clips between T and G.
c. Sortase then covalently anchors the T of the protein to a G of a peptidoglycan crossbridge (using up a few more peptide crossbridges).
84
Why is sortase anchoring important?
Because anchored surface proteins are often VF's and/or vaccine targets
85
What type of S aureus VF are more like virulence enhancers than virulence factors?
Hyaluronidase
86
What is Hyaluronidase and how does it work?
It is a secreted virulence factor/enhancer that aids the spread of infection by degrading hyaluronic acid in connective tissue spaces.
87
What other virulence factors have a similar effect to Hyaluronidase and facilitate the spread of infecting organisms?
Lipases, Proteases, DNAses
88
What are Pathogen-Associated Molecular Patterns (PAMPs)? Examples?
Another group of virulence factors used by S aureus. They are generally cell wall components such as peptidoglycan, LTA, and TA that are shed in deep tissue infections.
89
How do PAMPs work as virulence factors?
They are potent stimulators of Toll-like receptors on monocytes/macrophages and other cells of the innate immune system.
Combinations of these PAMPs can cause excessive cytokine secretion→ cytokine storm leading to septic shock
90
What is an important characteristic of VF expression?
VF expression is HIGHLY REGULATED. They produce adhesins early and cytolysins and toxins later after they have adhered.
91
How are biofilms formed?
After bacteria have attached to host components, they switch on production of extracellular polysaccharides for biofilm formation.
92
Why is gene regulation very important?
so that valuable energy reserves are not wasted doing something unnecessary
93
What is an important mechanism of gene regulation? How does it work?
Quorum Sensing (QS). This mechanism alerts bacteria to the mass/density they have accumulated thru cell division. Everything that happens in the environment is a signal for the organisms to change gene expression. Amassing a certain quorum of organisms is a very important signal for major changes.
94
What is the best studied QS mechanism? How does it work? (low yield)
The agrABCD Operon. Accumulation of autoinducing peptide (AIP) → P of surface sensor AgrC→P's AgrA (cytoplasmic response regulator) which together with SarA activates expression of P3 promoter→formation of major regulatory mRNA, RNAIII, the downstream effector of Agr system which activates or suppresses downstream target genes
95
What is the most important function of QS mechanisms?
They are very important in the development and dispersal of biofilms.
96
Why is biofilm formation very important?
Biofilm formation protects bacteria and this leads to big medical problems
97
Why is there reduced antibiotic susceptibility of bacteria in biofilms?
Several reasons:
1. Abx can't penetrate the extracellular polysaccharide and protein materials that are secreted by the bacteria and gelled around the colonies.
2. Growth within the biofilm slows (or stops), so cell wall-active Abx won't work.
98
What are the stages of biofilm development? (5)
1. First, there's Adhesion of a bacteria to a mucosal surface or plastic tube (catheter).
2. Colonization: stable colony forms due to cell division
3. Microcolony Formation and accretion of other bacteria: when QS factors tell the bacteria they've reached a certain number, they turn prod of extracellular materials to help them stick together and protect the colony in the biofilm
4. Maturation: it matures producing more of same or other components and/or accumulating other bacteria that can adhere
5. Dispersal: fragments detach. This is a specific process when a gene(s) is induced that begins to break down the biofilm. This begins the dispersal phase in which the fragments may attach elsewhere and form a new nidus infection.
99
S. Aureus shows a predilection for attaching to what? What about Staph epidermis? What do these infections often form?
Things going thru the skin (catheters, sutures, splinters, etc).
S epidermis is an even bigger problem for IV catheters and other indwelling medical devices
In these cases, biofilms often form around the plastic tubing, etc.
100
How do you eradicate staph infections on indwelling medical devices once a biofilm is formed?
It is frequently necessary to remove the device. If it is still necessary in the treatment of the patient, one would have to start over again in a different spot with better care of the site.
101
What diseases can staph aureus cause? Where in the body can S aureus cause an infection?
Staph aureus can cause a very wide variety of diseases. Basically, it can cause an infection in the body in any location "where the blood goes."
102
What are some of the specific diseases caused by S aureus? (Think PUS-FILLED ABSCESSES anywhere in the body)
A. Skin and Soft Tissue→BACTEREMIA, Furuncles/Carbuncles, wound infections, Folliculitis, Styes, Bullous Impetigo,SSS
B. CNS→meningitis, brain and epidural abscesses,etc
C. Endocarditis
D. Pulmonary→ embolic, pneumonia
E. GU tract→renal carbuncle, etc
F. Musculoskeletal→osteomyelitis, etc
103
What is folliculitis? Where is the infection located? What can cause it?
Folliculitis is a common S aureus skin infection (other bacteria can also cause it), in which the infection is in HAIR FOLLICLES, which serve as the portal of entry. (PUS-FILLED Abscesses if S aureus)
104
What is the most common cause of localized folliculitis?
S aureus
105
Why are sebaceous cysts often formed in Folliculits?
Sebaceous glands empty into hair follicles an their ducts may become blocked, forming sebaceous cysts.
106
What are the symptoms in a typical case of folliculitis?
There are usually no or very few systemic symptoms, if the infection is kept under control.
107
What are Faruncles and what bacteria causes them? How do they develop?
Faruncles are boils caused by S aureus infection. They have PUS just beneath the epidermis. They perhaps began as an infected hair follicle or an area of abrasion that became infected, and then the infection and inflammation have spread beyond the boundaries of the initial focal infection.
108
What symptoms are usually seen with Faruncles?
In the case of faruncles, few if any systemic symptoms will be seen if the infection is controlled. Those few possible symptoms include fever and chills.
109
What are Carbuncles? Where do they occur? What type of bacteria can cause them?
Carbuncles are numerous boils in one area (BUNCHES of BOILS). They can be the result of S aureus infection. They can occur anywhere, but are very common on the BACK OF THE NECK.
110
How do carbuncles develop? What is pus?
A progression of faruncles. The S aureus skin infection has probably invaded deeper layers of the skin and there are more bacteria (either dead or alive).
Pus is mainly dead bacteria, dead white blood cells, and coagulate tissue fluid.
111
Does a patient with carbuncles have any systemic symptoms?
The patient likely does have systemic symptoms such ad fever and chills in this case.
112
What is a Stye (aka Hordeoleum)? What type of bacteria cause it? What are the two types? Are there usually systemic symptoms?
Styes/Hordeoleums are infections of the eyelid at the base of the eyelash or in sweat glands most often caused by S aureus.
They can be external or internal.
Patients usually have no systemic symptoms.
113
What areas are infected in a stye/hordeoleum?
Different morphologic areas are usually infected:
1. External Stye→infection of the sebaceous glands of Zeiss or sweat glands of Moll
2. Internal Stye→infection of the Meibomian (Tarsal) glands (located in the deep surface of the tarsal plates)
114
What is a Chalazion?
A cyst of the eyelid caused by inflammation due to blockage of the Meibomian gland.
115
What is Bullous Impetigo? What bacteria-caused disease is associated with bullae?
Bullous impetigo are skin blisters that eventually burst and a crust forms over them. Bullae are blisters that frequently form in SSS due to S aureus infection and production of exfoliatin, but they also form in Impetigo and other superficial infections caused by S aureus or other bacteria.
116
What happens to the skin of infants vs older children w/ Bullous Impetigo/SSS?
In infants, the superficial part of the skin comes off, while in older children bullae are more common. They eventually burst and a crust forms over them.
117
What is characteristic of Pneumonia caused by S aureus? How does S aureus pneumonia compare with the strep pneumoniae pneumonia (most common cause)?
S aureus can cause pneumonia, and when it does, the disease is usually a very severe necrotizing pneumonia with a poor prognosis and high mortality. Pneumonia due to Strep pnemo is more common, but if it is treated, the lung usually returns to good health. This is not the case with S aureus pneumonia b/c there are frequently NECROTIC AREAS (ABSCESSES) WHERE TISSUE IS DESTROYED.
118
Pneumonia due to S aureus and Strep pneumo are frequently secondary to what? What does this sometimes cause? Which is more common? Which is worse and why?
S aureus pneumonia and Strep pneumo pneumonia are frequently secondary to influenza infections. Secondary bacterial infection following flu is one of the main causes of death from flu.
S Pneumo infections following flu are more common, but the prognosis is better because it does not produce as many toxins and there isn't the tissue destruction seen in S aureus.
119
What are risk factors that increase the risk of bacterial pneumonia following influenza? What about risk factors for most kinds of infections?
1. Preceding Influenza infection
2. Cystic Fibrosis
3. Alcoholism
4. Diabetes
These are also the risk factors for almost any kind of infection
120
What is infective endocarditis? What are the two types of infective endocarditis? How do they differ?
Infective endocarditis is an infection of the lining of the heart, particularly the valves.
1. Acute Infective endocarditis→rapid onset and short duration
2. Subacute infective endocarditis→slow onset and long duration
121
What is the most common cause of acute infective endocarditis (AIE)?
Staph aureus
122
Where does S Aureus AIE infections occur? What do they form?
They can occur on previously normal valves, where it forms large bulky VEGETATIONS, the term used to describe bacterial growth on heart valves.
123
What does a S aureus vegetation ultimately form? Why?
The vegetations enlarge both because the number of bacteria increases and also because platelets attach and fibrinogen is converted to fibrin and plasma proteins bind to these components. Thus, a vegetation is a complex BIOFILM.
124
What bacteria is associated with subacute IE? What is characteristic of these infections? Can S aureus cause SIE?
Strep viridans is the most common cause of SIE, and S aureus is NOT a cause of SIE.
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Describe the infections of SIE?
These infections usually form on valves previously damaged in some way, such as by Rheumatic Fever or Prosthetic heart valves. The vegetations are much smaller, they grow slower, and there is much slower onset of symptoms.
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What symptoms are associated with AIE? What are major risk factors for AIE?
Symptoms: rapid onset of fever or sepsis, associated with splenomegaly and embolic events.
Risk factors: IV drug use is a major risk factor (esp w/ Tricuspid involvement), as well as other intravascular devices.
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What are vegetations?
Infections of heart valves (bacterial growth on heart valves)
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Staphylococcal toxic shock syndrome was first associated with what?
the usage of a particular brand of tampon
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What causes Staph TSS? Where does this come from? How does it cause shock?
It is caused by Toxic Shock Syndrome Toxin-1 (TSST-1). The gene for TSST-1 is located within a PATHOGENICITY ISLAND in the S aureus chromosome. It causes shock b/c it is a Superantigen (SAg)
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What is a Pathogenicity Island? What does this mean about TSST-1?
It is an example of a mobile genetic element. This means that the TSST-1 gene can theoretically spread to other bacteria.
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Do all S aureus genes have the TSST-1 gene?
No, it is estimated that 5-25% of S aureus isolates have the gene
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How does TSST-1 cause shock? What are the symptoms of staph TSS? What are two common factors that lead to S aureus infection causing TSS?
It causes a cytokine storm like other SAg's.
Symptoms: high fever, vomiting, diarrhea, sore throat, and a skin rash that blanches when pressure is applied.
Common Factors: tampon usage, surgical wound infection
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Where is the rash located? Is that where the infection is located?
The rash may cover wide areas of the body, but the bacteria secreting the toxin are not necessarily present everywhere the rash is present.
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Is Staph or Strep TSS worse?
The prognosis of patients with staph TSS is NOT AS BAD as for strep TSS, which is also caused by superantigens.
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What is the diagnostic definition of Staph TSS?
A. Fever w/ T equal/greater than 38.9C (102F)
B. HTN: BP equal/less than 90 mmHg
C. Diffuse macular rash
D. Multisystem involvment: Hepatic (bilirubin or TA more than 2x normal), Hematologic (plt's2x normal), Mucosa (hyperemia/redness), GI (v/d), Muscular (myalgias), CNS (disorientationw/out focal neurologic sign)
E. Negative for measles, leptospirosis, and Rocky Mtn Spotted Fever
F. Negative blood and CSF cultures for organisms other than S aureus
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What is an important characteristic of Staph aureusFood Poisoning? How is it caused?
It is an INTOXICATION, not an infection. Staph grow in certain food products and secrete enterotoxins (SEA, SEB) that are so STABLE that cooking doesn't usually inactivate them.
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What is the onset of Staph food poisoning? Symptoms? Duration/Limit?
There is rapid onset of symptoms usually w/in 2-6 hours of eating contaminated food. It's generally self-limiting (when the toxin passes thru the body, the symptoms pass as well.
The patient experiences Violent Vomiting and diarrhea.
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What is staph food poisoning associated with? How does staph aureus usually get into the food?
It is associated with eating unrefrigerated foods and commonly contaminated foods such as pastries, potato salads and hamburgers.
It usually spreads into the food from a food handler who has a skin lesion infected with S Aureus.
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What techniques are used to dx staph aureus infections? Results?
1. Morphology in Gram stain→dark blue clusters
2. WBC count →high
3. Blood agar plate→Beta
4. Catalase/Coagulase tests→both are positive
5. Agglutination tests→positive with IgG or fibrinogen (coag test)
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What does S aureus look like in gram stain? What is the WBC count in S aureus infections?
They are gram+, so they are dark blue and in clusters/clumps.
They have a high WBC count
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What are the three basic types of hemolysis seen on a blood agar plate?
1. Alpha-hemolysis→incomplete hemolysis that turns agar GREEN as hemoglobin is converted to methemoglobin
2. Beta-hemolysis→Compete hemolysis as the agar around colonies CLEARS completely.
3. Gamma-hemolysis→essentially non-hemolytic
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What type of hemolysis does S aureus show on a blood agar plate?
They grow on a blood agar plate and most are Beta-hemolytic
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What is the appearance of S aureus when grown on a plate? Why? S epidermis?
Colonies have a golden appearance due to Carotenoid Pigment (S epidermis is pale)
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What type of Staph infections are hardest to diagnose?
Deep tissue infections that are difficult to access are harder to diagnose
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Describe the treatment process of S aureus:
Tx of S aureus is complicated due to increasing resistance to a variety of antibiotics. This mandates that antibiotic susceptibility tests must be ordered so you know what Abx will work. So it is very important to acquire samples from the infected site.
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What are some Abx that some S aureus strains have developed resistance against?
B-Lactams (penicillin) →B-lactamases
| Methicillin
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What are two important coagulase negative Staphylococci (CoagNS)?
1. S epidermis
2. S saprophyticus
All staph other than S aureus are CoagNS
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What are S epidermis infections associated with?
They are important HA infections b/c they are associated with use indwelling medical devices, especially implanted plastic catheters. Eradication is difficult unless the device is removed.
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Where is S epidermis usually located? At what frequency?
It is an ever-present normal commensal inhabiting the skin. It grows on most skin surfaces in a variety of temperatures, moist contents, pH, etc.
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What individuals are at high risk of S epi infections?
Infants and individuals with immune system problems
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Does S epi show resistance to any Abx?
Yes, most are resistant to Pencillin, 80% are resistant to oxacillin, but resistance to Vancomycin has not been yet in CoagNS.
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What are the primary virulence factors of S epi other than their ubiquitous presence on the skin?
1. Their ability to adhere to and colonize foreign bodies
| 2. Their ability to form biofilms→they make SLIME which is important for biofilm formation
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Can S epi cause endocarditis?
Yes, it causes 15-40% of prosthetic valve endocarditis cases
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What makes diagnosis of S epi infections difficult?
1. B/c they are always present on the skin, it is hard to know whether it is the infecting agent or merely a contaminant of the sample
2. So, you have to rely on things like # of CFU found in the sample, the number of sequential cultures that are positive, and the amount of time it takes for colonies to develop
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Is S saprophyticus part of the normal body flora? How do S sapro infections develop? What type of infection does it commonly cause?
Yes, it is a normal inhabitant of the GI tract. From this location, it can gain access to the urinary tract to cause UTI's.
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Is S sapro CA or HA?
It is a community-acquired infection
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Is E coli or S sapro a more common cause of UTI?
S sapro is 2nd to E coli in causing UTI in sexually active young women, but in most patient populations it is a very distant 2nd to E coli.
