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Steptococcus Flashcards

1
Q

Which streptococci species are beta hemolytic?

A

• Groups A - C + G are all beta-hemolytic (clear zone of hemolysis)

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2
Q

What differentiates types A-U streptococci?

A

Lancefield groups based on differences in the carbohydrate located in the cell wall

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3
Q

Staphylococci species are catalase _______________, while streptococci species are catalase ____________. **This is an important distinction to make.

A

Staphylococci species are catalase POSTIVIE, while streptococci species are catalase NEGATIVE. **This is an important distinction to make.

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4
Q

What are the most important stains in group A-D strep?

A

GAS => Strep. pyogenes
GBS => Strep. agalactiae
GCS (and G) => Strep. dysgalactiae subspecies equilsimilis
GDS => Strep. bovis, Enterococcus faecailis, Enterococcus faecium

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5
Q

What diseases are causes by streptococcus pyogenes (GAS)?

A
  • *P**haryngitis, Puerperal sepsis
  • *E**ndometritis
  • *R**heumatic fever
  • *G**lomerulonephritis
  • *S**carlet fever
  • *Nec.** rotizing fasciitis
  • *C**ellulitis/impetigo/erysipelas
  • *T**oxic Shock syndrome
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6
Q

Group A Streptococcus is part of the normal flora. Where do we find it?

A

• Found in skin and oropharynx in small numbers

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7
Q

What are 3 mechanisms that GAS uses to cause disease?

A

• Pyogenic inflammation
• Exotoxin production
• Immunologic(type II - direct human tissue cross reaction and Type III - immune complex hypersensitivity)

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8
Q

What features of strep are shown here?

A

• Gram positive cocci in chains

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9
Q

What anti-phagocytic virulence factors are found on GAS?
• Give a brief description of each of these.

A

M-protein
• hangs off the side of the cell and interferes with phagocyte ingestion, but antibodies that bind to this promote opsonization. There are over 200 emm types, this is why we see the ability of GAS to cause multiple infections.

Antiphagocytic Capsule
• Made of hyaluronic acid - this composition makes it antiphagocytic b/c humans have been desensitized to hyaluronic acid because we make it ourselves

(side note: B-cells that would react with hyaluronic acid (a long chain polysaccharide would be a B1 B-cell acting under a T-cell independent response (type II = TI2). this doesn’t happen because B cells are negatively selected the moment RAG rearrangments are done and the receptor goes to the cell surface in the bone marrow)

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10
Q

What GAS enzymes are responsible for inducing inflammation?

A

SSSS DCH

  • Streptokinase
  • Streptococcal chemokine protease
  • Streptolysin O
  • Streptolysin S
  • DNAase (streptodornase)
  • C5a peptidase
  • Hyaluronidase
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11
Q

Hyaluronidase
• function?

A

Inflammatory virulence factor of GAS that is aka SPREADING FACTOR that facillitates the spread of GAS in celluitis and other skin infections

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12
Q

Streptokinase
• Function?

A

Inflammatory virulence factor of GAS has an unclear role in GAS infections but it activates plasminogen to plasmin to dissolve fibrin clots (works like alteplase)

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13
Q

DNase (strepodornase)
• Function?

A

Inflammatory virulence factor of GAS that degrades DNA in exudates and necrotic tissue. This prevents Streptococci from getting trapped in neturophil NETs (neutrophil extracellular traps)

**Note: the MOA of this toxin is the same at dornase alpha that is given to Cystic fibrosis patients (∆F508) that get excess necrotic neutrophil debris in lungs**

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14
Q

C5a peptidase
• function?

A

Inflammatory virulence factor of GAS that minimizes the influx of neutrophils in early infection by cleaving C5a

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15
Q

Streptococcal Chemokine Protease
• function?

A

Inflammatory virulence factor of GAS that prevents migration of neutrophils into site of infection by degrading chemokine IL-8 (neutrophil chemoattractant)

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16
Q

Streptolysin O
• Function?

A

Inflammatory virulence factor of GAS that acts as an OXYGEN LABILE HEMOLYSIN. (so it only produces beta-hemolysis when the colonies grow under the surface of the blood agar plate)

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17
Q

Streptolysin S
• function?

A

Inflammatory virulence factor of GAS that is STABLE in the presence of oxygen and causes hemolysis on the Surface of the plate

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18
Q

Erythrogenic Toxin
• Function?

A

Virulence factor of GAS that is a SUPERANTIGEN that causes the rash of scarlet fever

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19
Q

Pyrogenic (fever inducing) Exotoxin A
• Function

A

Virulence factor of GAS that causes most cases of TSS, this is a superantigen that causes large amounts of cytokines to be released

**Note: since this is called pyrogenic (fever inducing) toxin it probably causes the release of a lot of IL-6 and TNF-alpha)

(Note on superantigens: bind alpha chain of MHC II and beta chain of TCR to cause polyclonal activation of T cells leading to tons of cytokines getting released)

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20
Q 
Exotoxin B (extracellular cystein protease)
• function?
A

Protease that rapidly destroys tissue and is produced in large amounts by the necrotizing strains of GAS

**Note that necrotizing strains also secrete Exotoxins A and C too)

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21
Q

Which virulence factors of GAS act specifically against the neutrophilic response that we typically see to bacteria?

A
  • *DNase** - breaks down NETs secreted by neutrophils
  • *C5a petidase** - prevents chemoattraction of neutrophils by complement early in infection
  • *Streptococcal chemokine protease** - prevents migration of neutrophils into site of infection by degrading IL-8
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22
Q

T or F: Humans make antibodies to Streptolysin S.

A

False, In general streptolysin S is considered non-antigenic/immunogenic (Shane’s research may prove otherwise)

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23
Q

Which is more important to virulence of GAS: hemolysin O or hemolysin S?

A

Hemolysin O is a more important determinant of GAS virulence

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24
Q

How do you expect a patient with GAS pharyngitis to present to you?
• Clinical Findings

A

Presentation:
This will be someone with a sore throat and a fever that may also be experiencing nausea and vomitting. Importantly they WILL NOT complain of URI symptoms (runny nose, congestion, etc.)

Physical:
• Tonsils may be inflamed with pharyngeal exudate and there will be cervical lymphadenopathy.

****Absence of Concurrent URI symptoms is VERY IMPORTANT****

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25
How do you diagnose GAS pharygitis? • how accurate are these methods? • how do they work?
_GAS pharyngitis Dx:_ Rapid antigen test works in 10 minutes, but it has a **very low sensitivity** with a **high specificity.** You do a throat swab and **extract antigens from the throat swab** and then **react them with Abs. that are bound to latex particles. Agglutination** of latex implies a **positive test** \*\*\*\*IF this test is negative but your clinical suspicion is high, do a throat culture\*\*\*\*\*
26
A patient comes in with a sore throat and a fever of 101, they complian that they've been vomitting. You do a Rapid antigen test that comes back negative. What should you do next?
Culture their pharynx and Start them on antibiotics IMMEDIATELY
27
A patient comes in with a sore throat and a fever of 101, they complian that they've been vomitting. You do a Rapid antigen test that comes back negative. • you started the patient on antibiotics, but the cultures came back negative. What do you do next?
• Discontinue therapy if cultures come back negative
28
What is the treatment for GAS pharyngitis?
**• Oral Penicillin, Amoxicillin, or Cephalexin for 10 DAYS** (500 mg, twice a day) IF the pt. is allergic to ß-lactams: • **Azithromycin (2-5 days), Clarithromycin (10 days), or Clinamycin (10 days)** can be used
29
Remind your patients that its vital that they complete their treatment even if they start feeling better. What are some complications that could happen if they don't? • Local extention? • Immune mediated?
Complications of Untreated Pharyngitis include: POSMM-R Local extention • **P**eritonsillar/retropharyngeal abscess • **O**titis Mmedia • **S**inusitis • **M**astoiditis - infection of the air spaces in the mastoid process behind the ear • **M**eningitis Immune Mediated: • **R**heumatic Fever
30
What is shown here? • key features?
**_Erysipelas_** - **rapidly spreading rash with well demarcated, serpigenous borders that may develope in a buffly distribution on the face.**
31
What organs does this GAS infection involve? • Is this a typical location or the rash?
Erysipelas - is typically **located on the face** and **involves the skin and lymphatics**
32
What is shown here? • Key features? • what is the progession of the skin pathology?
**Impetigo** - caused by GAS is shown here. • Most often it is located on the **FACE** (important in distinction from staph aureus) and begins as **papules =\> Vesicles =\> pustules =\> breakdown into a golden crust**
33
What is shown here? • what tissues are involved?
**Cellultis** is shown. This invovles the **dermis** and **subcutaneous fat**
34
What is this?
**Necrotizing fascitis** =\> the key feature being shown here is the fact that the outside appearance of the infection may appear mild but there is a lot of cell death going on in the inside (note the absence of purulence, this could be due to factors like DNase, C5a protease, and Strep. Chemokine protease)
35
What are some factors that may put you at a higher risk of getting Necrotizing Fascitis from GAS?
ANYONE can get GAS necrotizing Facsiitis but those at an elevated risk are: • Mothers that 1**just gave birth** via C-section (2**surgery**) use 3**IVDs**, get beat (4**blunt trauma**) and have 5**skin lacerations**
36
In cases were there is no clear portal of entry to GAS, what is believed to the be the mechanism by which necrotizing faciitis by GAS developes?
In these people its thought that the infection spreads from the **pharynx hematogenously after an asymptomatic infection** where it travels down to a site where there has been **muscle strain or blunt trauma has taken place.**
37
Once in deeper tissues are infected in GAS necrotizing faciitis, how does the bacteria spread? • why does it spread this way? • What KEY symptom are we looking for on exam?
Once deeper tissues are infected by GAS the infection **spreads along the fascia** that has a **poor blood supply** so that it can cause destruction of **more muscle fascia and overlying subcutaneous fat.** We are looking for **PAIN that is OUT OF PROPORTION TO THE EXAM.**
38
What strains are responsible for GAS necrotizing faciitis? • what allows them to do this? • Do you expect the infection site to be pyogenic? • Does this mean bacteria aren't present?
M-types **1 and 3 are most commonly implicated.** In order to produce necrotizing faciitis they must produce **extoxins A, B, or C.** There will be a remarkable **absence of neutrophils** from the infection site (Mostly due to Strep. Chemokine Protease (IL-8 cleavage), but C5a protease and DNase probably help too). Despite lack of purulence there can be a **billion microorganisms per gram of muscle.**
39
How will your patient with necrotizing faciitis progress if you fail to catch it? • how long does onset of the disease take after intitial bacterial seeding? • what do you need to do now?
NF by GAS is **very acute** and patients become symptomatic after **~2 days** of infection. This will start with some **inflammation over the affected area that is often shiny and exquisitley tender**. Over the next few days the overlying skin will go **Red =\> Purple =\> Blue =\> grey** and **crepitus** may develop. This can develop into **SHOCK.** **NF via GAS is a SURGICAL EMERGENCY - take them to the OR**
40
T or F: the majority of cases of GAS necrotizing fasciitis are not accompanied by shock.
False, around 50% of GAS necrotizing fasciitis cases are accompanied by shock so you should be on the lookout for this in your patients
41
After giving birth a woman develops abdominal pain and her blood pressure falls to 80/50 with a fever of 102. • what has happened here? • How fatal is this disease?
This is probably peurperal sepsis (given the shocky symptoms) but it could be endometritis in a less severe case. • Abdominal pain, HypoTN, and Fever are key • This disease is pretty rare but about 4% die
42
Which of the GAS exotoxins is most important in necrotizing fasciitis? • which is important in GAS TSS?
**Exotoxin B** is most important in necrotizing fasciitis from GAS. It is a cysteine protease that gives strains 1 and 3 their flesh-eating properties. (remember there is a large amount of cysteine in skin, hair and nails) Exotoxin **A** is the most important factor in GAS TSS. It is a super**A**ntigen that causes the release of cytokines.
43
What stain of strep is most often responsible for TSS?
GAS
44
How will your patient with streptococcal TSS likely present? • what are some common portals of entry?
_Most Common portals of entry:_ • **Skin, vagina, and pharynx** _Presentation:_ Patients often present with **fever, chills, myalgias, n/v/d, that progresses to shock** (_hypotermia, hypoTN, altered mental status, DIC, acute kidney injury)_ and _ARDS_. **Diffuse erythema** is also possible (10%).
45
Where does the infection that causes TSS develop and how? • is there any chance of this progressing to necrotizing fasciitis? \*note that this is different than the portal of entry.
The portal of entry in TSS is typically the skin, vagina, or pharynx. From here the GAS moves to a **soft tissue in an extremity** that has experienced some **minor trauma** and it grows there for **48-72 hours** before you start to experience symptoms of infection. \*\*\*YES, 75% TSS cases produce necrotizing fasciitis\*\*\*
46
How do we diagnose TSS for GAS? • how does this differ from S. aureus TSS/ how will you know which protocol to use?
Dx of GAS TSS requires that you **isolate GAS from a sterile site like blood, CSF, or tissue.** Typically its pretty obvious where the infection is that the toxins are being secreted from in GAS TSS so isolating and culturing is reasonable. In S. aureus TSS there will be nothing physically abnormal with the patients other than a tampon, nasal packing, or surgical packing that you think might be seeding the growth so in S. aureus TSS no culture is required.
47
How do we treat GAS TSS? • Why? • How does this compare to the treatment for necrotizing fasciitis?
**GAS TSS** is treated with **Penicillin + Clindamyci**n **GAS Necrotizing Fasciiits** is treated with **Penicillin + Clindamycin + debridement** We use **Clindamycin** (or linezolid) to **prevent toxin synthesis** by the bacteria (50s ribosome inhibition)
48
Who typically presents to you with scarlet fever and how do they present?
A child between **3 and 15** will present with a history of **sore throat** and **strawberry tongue** that progressed to **diffuse erythema on the head and neck** (hence scarlet fever). This **SAND-PAPERY** rash then **spreads to involve the trunk.** Over the next few days the rash **desquamates.**
49
What toxin causes Scarlet fever? • what is the initial infection that most often leads to this disease?
Scarlet fever (like TSS) is a toxin mediated complication of GAS infection. The toxin involved is **Erythrogenic toxin.** Typically GAS infections occur in association with **pharyngitis** (hence the sore throat at the beginning of infection)
50
What GAS infection does this kid have?
**Scarlet Fever** • Sandpaper rash • Strawberry tongue • Desquamation of skin
51
What diseases are caused by GAS toxin production?
Toxic Shock Syndrome Scarlet Fever
52
What Immunologic conditions are caused by GAS?
* Post-strep glomerulonephritis * Acute Rheumatic Fever
53
A patient with PSGN (post-streptococcal glomerular nephritis) is most likely to present to you _________ weeks after ___________ or less likely they will present __________ weeks after \_\_\_\_\_\_\_\_\_.
A patient with PSGN (post-streptococcal glomerular nephritis) is most likely to present to you **3-6 weeks** after **a skin infection** or less likely they will present **1-3 weeks** after **pharyngitis.** \*\*\*PSGN most often follows skins infection
54
John presented to you 3 weeks ago with erysipelas and now has elevated blood pressure and coke colored urine. • What is wrong with him? • What else could he have presented to you with 3 weeks ago?
He has **PSGN**, this typically follows GAS skin infections like **erysipelas, impetigo, or cellulitis.**
55
John presented to you 3 weeks ago with erysipelas and now has elevated blood pressure and coke colored urine. • what type of immune reaction is this? • what other signs and symptoms could he have presented with?
PSGN is a type III immune reaction PSGN is characterized by: **• HTN • Facial edema (often periorbital) • Lower Extremity Edema • Dark urine (with RBCs)**
56
John presented to you 3 weeks ago with erysipelas and now has elevated blood pressure and coke colored urine. • What would you see on H and E if you biopsied his kidney? • what would you see on EM? • what is his prognosis if he's a kid? adult?
H and E would show hypercellularity and EM would show subepithelial humps Prognosis is usually good and recovery is complete, but 1% or children and 25% of adults progress RPGN (rapidly progressive glomerularnephritis)
57
What is the JONES critieria for acute rheumatic fever?
58
It typically take acute rheumatic fever __________ weeks to develop following \_\_\_\_\_\_\_\_\_. • what do you do to help with the diagnosis?
It typically take acute rheumatic fever **2** weeks to develop following **PHARYNGITIS.** In addition to the JONES criteria you may want to do an **ASO titer to aid in diagnosis.** (ASO = antistreptolysin O) \*\*\*REMEMBER CULTURES ARE USELESS, THESE PEOPLE HAVE ALREADY CLEARED THE INFECTION\*\*\*
59
Despite the fact that there is no bacteria in the blood of patients that have suffered from ARF we still treat them. • how?
A **FULL course of abx.** is recommended to erradicate any left over GAS. We also want to **prophylax** these patients with **IM penicillin monthly for many years.**
60
The following characteristics describe what bacteria? =\> point why each of these is important • gram positive cocci in chains, narrow zone of hemolysis, does not hydrozyse bile esculin agar, but does hydrolyze hippurate, and is resistant to bacitracin.
**Streptococcus agalactiae (GBS)**
61
Describe streptococcus agalactiae.
• gram positive cocci in chains, narrow zone of hemolysis, does not hydrozyse bile esculin agar, but does hydrolyze hippurate, and is resistant to bacitracin.
62
The following characteristics describe what bacteria? =\> point why each of these is important • Gram + cocci in chains, gamma hemolytic, hydrolyzes esculin in the present of bile
Group D strep **Hydrolyzing esculin in the presence of bile contrasts GDS from GBS** \*\*Note that only GDS enterococcus is shown in the picture\*\*
63
What are the key characteristics of GDS from other types? • how can we group bacteria are found in GDS?
**Hydroysis of esculin in the presence of bile to produce black pigement on the bile-esculin agar** There are two subtypes of GDS enterococci (**E. faecalis and E. Faecium**) and one non-enterococci (**Strep. bovis**), the enterococci are differentiated on their ability to grow in hypertonic saline
64
The following characteristics describe what bacteria? =\> point why each of these is important • gram positive cocci in chains that are alpha hemolytic, that can grow in, bile and hypertonic saline
This describes **enterococcus group D strep** (**E. faecalis and E. faecium**)
65
The following characteristics describe what bacteria? =\> point why each of these is important • gram positive cocci in chains, alpha hemolytic, resistant to lysis by bile, optochin resistant
**S. viridans**
66
Characterize GDS enterococci.
67
Characterize GBS.
\*\*\***note the GBS also has an antiphagocytic polysaccharide capsule\*\*\***
68
Characterizee GAS.
69
Characterize Viridans group Strep.
70
Characterize S. bovis.
71
What is the CAMP test and how does GBS respond in this test?
CAMP test: There is **protein produced by GBS that enhances hemolysis on sheep blood agar when combined with beta-hemolysin from S. aureus (see below for picture)**
72
Where do we find GBS strep (strep aglactiae) and why is it important? • who gets in infected? when? disease(s)? • What are some risk factors of getting this infection?
GBS is often found in the **colon but it colonizes the genital tract of some women** and **babies get infections in utero or during passage through the vagina** infection can cause **neonatal sepsis, meningitis, and pneumonia.** **\*\***The most important risk factor here is Pre-mature rupture of membranes, babies born prior to 37 weeks, and children whose mothers lack antibodies\*\*\*
73
Why are babies born prior to 37 weeks at a higher risk of getting GBS (strep agalactiae) infection?
**ALL pregnant women are screened for GBS between 35 and 37 weeks and if they are positive we give them Penicillin G/Ampicllin IV at the time the baby is born.** \*\*\*Babies born before 37 weeks may be coming from mothers who have not yet been screened.
74
What kind of adult would you expect to see getting a Strep aglactiae (GBS) infection? • what type of infection are they likely to get? • How is GBS diagnosed
People with dia**B**tes and **B**reast cancer are predisposed to G**B**S infections. \*\*Infections: • **Septic arthritis** • **Cellulitis • Ostomyelitis (multiple joints)** **DX: Gram stain and culture** or Rapid Vaginal/rectal test that **detects DNA**
75
Contrast Group D and Group B strep with respect to the ability to produce toxins and enzymes. • do they have capsules?
**Group D strep** • can produce enzymes that can injure host tissue. • Has a capsule **Group B strep** • does not have enzymes or toxins. • Has a capsule
76
You encounter streptococcus that is VRE. • what strain is it most likely to be? • how do you treat it?
Since we're talking about an enterococcus (GDS), its most likely to be **E. faecium** than E. faecalis VRE is treated with Linezolid or Daptomycin
77
GDS - **E. faecalis/faecium** • where does it typically live? • Comment on its virulence • What infections does it give you? • How do you treat?
78
GDS- Streptococcus bovis (galolyticus) • What infections does it cause? in who? • How do you differentiate it from GDS enterococci?
**Strep bovis** causes **endocarditis** and is VERY strongly associated with colon cancer so if you find this in someone's blood you need to **go look for colon cancer.** **•** Unlike the enterococci species of GDS, strep bovis **will not grow on hypertonic saline** (tx. PCN, ceftriaxone, or Vanc)
79
**Viridans group strep** • Where is it normal flora? • what enzymes or toxins does it produce? • What is the mechanism that is uses to cause endocarditis?
**Viridans** is normal flora in the **mouth and colon**. It often enters the blood after a _dental surgery or in patients with cavities or poor dentition._ Viridans **doesn't produce any enzymes or exotoxins,** instead it produces **endocarditis by producing a glycocalyx that allows it so attach the damaged heart valves.**
80
**Virdidans group strep** • What species are in the group? • Which one causes dental caries?
Viridans Group: **• anginosus, milleri, intermedius, mutans, sanguis** **Strep Mutans** causes **dental caries** and also makes the polysaccharides in dental plaque
81
**Viridans Group Strep** • Asside from endocarditis and dental caries, what other infections can this group do?
Viridans Group can cause: • Brain abscesses • Liver and Abdominal Abscesses
82
**Viridans Group Strep** • treatment?
Treatment for Viridans Group strep depends on susceptibilities but most often its done with Penicillin or Ceftriaxone • If susceptibility to penicillin is weak add Gentimicin
83
84
Peptostreptococcus • metabolism • Where does it live? • Infections caused • Tx?
85

Dermatology - Microbiology (7 decks)

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