Common Bacterial Pathogens 1 Flashcards

1
Q

Which bacteria are gram + cocci?

A

Staphylococcus
S. aureus
SSNA (e.g. S. epidermidis)

Streptococcus
	S. pyogenes (Group A Strep)
	S. pneumoniae
	Enterococcus faecalis, E. faecium
	“Viridans” streptococci
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2
Q

Where do people usually have S. aureus

A

Anterior nares and perineum

Asymptomatic carriage in 30% of healthy individuals

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3
Q

Are cutaneous S. aureus infections usually systemic or local?

A

Local infections like boils, folliculitis, focal abscesses, often associated with foreign body

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4
Q

What is the mechanism of S. aureus cutaneous infections? What are the major virulence factors?

A

Localized abscess → formation of capsule → walls off infection → interferes with host defense

Coagulase:
-helps form fibrin capsule →interferes with phagocytosis 

Alpha toxin:
-major cytotoxic agent → invasiveness and virulence

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5
Q

What are the three Staphylococcal toxinogenic diseases?

A
  1. Staphylococcal Scalded Skin Syndrome (SSSS)
  2. Toxic Shock Syndrome- TSST
  3. Staphylococcal Food poisoning
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6
Q

What happens in Staphylococcal Scalded Skin Syndrome?

A

epidermis falls off

Toxins are produced which attack desmosones

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7
Q

What cells do superantigens target?

A

Sags cause non-specific activation and proliferation of T-cells which release IL-2, INF-gamma, TNF-alpha

**Picture the little cofactor that grabs onto the side of MHC class II and forces APC to stay connected with T cell

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8
Q

What population is most common to get Toxic shock syndrome?

A

Menstruating women => tampons

1/3 of the cases are men

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9
Q

What microbiological property is different with Staph. Epidermis than Staph. Aureus?

A

Coagulase negative

  • hence the nickname Coagulase Negative Staph (CNS)
  • not to confused with catalase (all staph are positive)

Also called SSNA (staph species not aureus)

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10
Q

If Staph. epidermidis is normally on your skin flora, how can it be a pathogen?

A

Extracellular glycocalyx “slime” allows biofilm formation

=> adherence to foreign bodies, e.g., catheters, shunts, hip prostheses, artificial (or damaged) heart valves (*Endocarditis)

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11
Q

Describe microbio properties of Strep. pyrogenes

A

Gram + cocci (all strep)
Catalase negative (like all strep)
B-hemolytic

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12
Q

What causes streptococcal pharyngitis (strep throat)?

A

Strep. pyrogenes/ Group A strep

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13
Q

Why is strep concerning?

A

Pharyngitis can result in rheumatic “Phever” and glomerulonePhritis

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14
Q

What’s a key virulence factor in pharyngitis?

A

M protein

involved with adherence and has antiphagocytic properties (binds factor H and reduces C3b and C5a)

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15
Q

How does strep lead to glomerulonephritis?

A

Type 3 immunopathology:
-immune complexes get stuck in kidney

*Coke colored urine

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16
Q

Why can rheumatic fever follow Group A Strep pharyngitis?

A

You can produce antibodies → recognize bacterial antigens AND host antigens of myocardium and heart valves → progressive antibody mediated tissue damage

17
Q

How is endocarditis different from RF?

A

endocarditis is bacteria attacking tissue

RF is antibodies attacking tissue

18
Q

What are symptoms of rheumatic fever?

A

F J♥NES

i. Fever
ii. Joints - polyarthritis 
iii. ♥ - carditis
iv. Nodules (subcutaneous) 
v. Erythema marginatum 
    vi. Sydenham Chorea
19
Q

Microbio characteristics of S. pneumonia?

A
  • Gram +
  • Diplococci (pairs are also called pneumococcus)
  • Catalase negative (all strep)
  • Normal flora in UR tract of up to 40% of healthy people
20
Q

What are some invasive and non-invasive diseases caused by streptococcus pneumonia?

A
Non invasive:
       Pneumonia (~60% of bacterial pneumonia)
       Sinusitis
       otitis media
       bronchitis 

Invasive:
Meningitis
Bacteremia/septicemia

*BS MOPS

21
Q

What is the underlying cause of the pathogenesis of S. pneumonia?

A

=Ability to grow and evade host defenses

22
Q

How does S. pneumonia grow and evade host defenses?

A

ANTIPHAGOCYTIC POLYSACCHARIDE CAPSULE!
-MULTIPLE antigenic types of capsule (at least 91 distinct antigenic types)

Recovery/immunity due to development of anti capsular antibody

23
Q

What are predisposing factors to pneumococcal disease?

A

Young or old
Alcoholism (e.g., mucocillary defect)
Respiratory viral infection

24
Q

Who would you give the 23-valent pneumovax vaccine to?

A

=Adults (23 yr olds)

  • IgM response
  • protection against INVASIVE disease in elderly and immunocompromised adults. Ironically, does NOT provide protection against pneumonia.
25
Q

Who would you give the 7 and 13-valent Prevnar vaccine to?

A

=Kids

  • Conjugate vaccines
  • 7 valent is IgG response
  • Confers herd immunity
26
Q

Where do you usually find enterococcus faecalis and faecium? (hint: entero)

Where do infections occur?

A

-Normal flora in intestines

  • infections: Urinary tract, surgical wounds, biliary tract, endocarditis
  • Hospital acquired infection from patient to patient encounter on hands or medical devices
27
Q

Why is it important to distinguish Enterococcus faceless from other “streptococci”?

A
  • because of its intrinsic and emerging acquired antibiotic resistance including vancomycin!
  • It is selected by therapy with cephalosporins (to kill streptococci and keep enterococci
28
Q

What bacteria causes cavities and can spread to bloodstream after dental extractions?

A

Viridans Streptococci
“you have Very Strapping teeth”

*Spreading into blood can lead to endocarditis!

29
Q

What is the major virulence trait of Viridians Streptococci?

A

Dextrans

-adherence to teeth, oral tissue, or to fibrin and platelets on damaged heart valves→ tissue damage/function