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2. STAPHYLOCOCCUS: AUREUS, EPIDERMIDIS, SAPROPHYTICUS

Staphylococcus: Aureus, Epidermidis, Saprophyticus Medical Editor: Abigail S. Xu, RPh

OUTLINE (B) SPECIES AND LOCATION IN BODY

(1) Staphylococcus aureus
I) OVERVIEW
II) PATHOLOGY Natural skin flora
III) DISEASES AND INFECTIONS o Armpits
IV) TREATMENT o Ears
V) REFERENCES o Pharynx
VI) REVIEW QUESTIONS o Groin
o Perineum
o Nares (15% of S. aureus are found here)
(2) Staphylococcus epidermidis
I) OVERVIEW Natural skin flora
o More frequently found in skin than S. aureus
(A) BACKGROUND
(3) Staphylococcus saprophyticus
(1) Etymology
Thrive in decaying organic material (i.e., meat)
Staph: cluster
Scenario: eating steak
Cocci: round/ spherical
o Steak may contain decaying organic material
Staphylococcus: cluster of spheres
o S. saprophyticus survive on decaying material
(2) Characteristics o Eat meat containing S. saprophyticus
o Digestion
Gram (+) o Fecal matter containing S. saprophyticus pass though
o Gram Stain: purple-like appearance
the GI tract
 retain crystal violet due to thick peptidoglycan
o S. saprophyticus colonize the perineum (area
layer
between anus and genitals)
 Staphylococcus look like a cluster of grapes
Females
Non-motile
o urogenital tract is close to perineal area and anus
o No flagella
o S. saprophyticus can easily spread to Urogenital
o No movement
tract of females, especially the urethra
Catalase (+)
Facultative anaerobes
o Survive in oxygen and no oxygen environments

Figure 1 Staphylococcus Bacteria

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(C) DIFFERENTIATING STAPHYLOCOCCUS SPECIES
(1) Catalase test
Staphylococcus species are catalase positive
When hydrogen peroxide (H2O2) is put into a petri dish
containing Staphylococcus bacteria, the solution will
bubble
The bacteria contain catalase
Catalase
o enzyme that converts H2O2 to oxygen and water
Production of oxygen causes the bubbling effect
(2) Coagulase test
Coagulase enzyme catalyzes conversion fibrinogen to
fibrin (prothrombin-like effect)
a colloid solution is added to a petri dish containing
bacteria
If bacteria produce coagulase → coagulase (+)
o Convert fibrinogen in the colloid to fibrin
o Clumping of colloid solution
o Only Staphylococcus aureus is coagulase (+)
among the three species discussed
If bacteria do not contain coagulase → coagulase (-)
o No clumping of colloid solution
o Staphylococcus epidermidis and Staphylococcus
saprophyticus are coagulase (-)
(3) Growth in Culture Media

(i) Mannitol Salt Agar

• S. aureus
• ferment mannitol and produce golden yellow
colonies
• Fun Fact: aureus means golden

(ii) Urea broth with Phenol Red AfraTafreeh.com

• S. epidermidis and S. saprophyticus
• Turn the Phenol Red indicator, which is red,
into pink
• Contain urease enzyme/ urease (+)
• Convert urea into ammonia, which is basic
• Phenol Red becomes pink in basic
environment
(4) Novobiocin sensitivity test
Differentiate S. epidermidis and S. saprophyticus Figure 2. Differentiation of Staphylococcus species
Novobiocin: antibiotic
Put novobiocin disk into petri dish with bacteria
Novobiocin sensitive
o Colonies die off around the antibiotic disk
o Produce a zone of inhibition
o S. epidermidis
Novobiocin resistant
o S. saprophyticus is resistant to novobiocin and can
survive
o No zone of inhibition since the antibiotic will not be
able to kill off the bacteria

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II) PATHOLOGY (iii) Exfoliative toxin

• Causes Staphylococcal scalded skin
(A) STAPHYLOCOCCUS AUREUS
syndrome or Ritter disease
(1) Biofilms • damage Desmoglein-1 that connects
Keratinocytes
Exopolysaccharide (EPS)
• Keratinocytes not able to stick to each other
Scenario: Venipuncture
o Need to get through skin before vein • Form blisters that slough off
o S. aureus is part of the normal skin flora • Scalded skin syndrome is usually seen in
o When needle punctures the skin, some bacteria can children <6-year-old
adhere to the needle (iv) Β-Hemolysin
o Bacteria can get introduced into the bloodstream
when the needle enters vein • Destroys red blood cell (RBC) membrane
o Bacteria secrete loose polysaccharide layer around • Release of hemoglobin from RBC
them • Test
o Put Staphylococcus aureus into blood
Polysaccharide layer allows the bacteria to pass on
agar plate (BAP)
genetic materials and cell-signaling mechanisms with
o S. aureus release β-hemolysin that
each other
destroys RBC in (BAP)
Immune cells and antibiotics may not be able to
o Empty spots in the BAP signify
penetrate the polysaccharide layer and kill the bacteria
destroyed RBC
o Commonly seen in intravenous catheter-associated
infections (v) Enterotoxin
(2) Exotoxins • Target enterocyte on epithelial lining within GI
tract
(i) Toxic Shock Syndrome Toxin type 1 (TSST-1) • Create pores and destroy cell membrane
• Released by S. aureus in the body • Sodium and water in the cells leak out
• Toxin binds to super-antigen • Intestinal cells won’t be able to function
• Antigen presenting cells have MHC-2 • ↓absorption of nutrients, water, electrolytes
complexes that interact with T cells • Electrolyte shift
• TSST-1 form bridging interaction between • Diarrhea
the T-cell and antigen presenting cell • Inflammation due to damage in GI lining →
• Hyperstimulate immune response gastroenteritis
• Massive release of cytokines o Symptoms felt < 6 hours after eating
o Interleukin-1 (IL-1) contaminated food
o IL-2 o Test tip: mayonnaise-containing food
o TNF-α
o Interferon-ɣ
• Massive inflammatory reaction
• Toxic Shock Syndrome
o Rash
 Skin inflammation
o Hypotension
 Increase capillary permeability
 Vasodilation
o Fever
 Act on hypothalamus
 Increase Prostaglandin E2 (PGE2)
release
• Commonly occur when bacteria thrive on
things that stay in the body for a long time
o Tampons left for too long
o Nasal packing with no antibiotic
o Lap pad left in body during surgery

(ii) Leukocidin
• Panton-Valentine leukocidin toxin
• Creates pores in leukocytes (WBC)
• Ions move in and out of WBC
• WBC necrosis
• Inflammation
• Common in lungs
o Damage to parenchymal lung tissue
o Necrotizing pneumonia

Figure 3. Pathology of S. aureus

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 (B) STAPHYLOCOCCUS EPIDERMIDIS
(1) Biofilms
Part of natural skin flora
Main pathological mechanism is through formation of
biofilms
Release extrapolysaccharide that make bacteria
resistant to antibiotics and evade immune system
Form biofilms in different locations:
(i) Vascular devices
• When a device needs to be inserted into the
vein, it needs to pass through the skin
• S. epidermidis can adhere to the device and
be introduced into the bloodstream
(ii) Urinary catheters
• When a Foley catheter or urinary catheter is
inserted into the bladder, it needs to pass
through the skin near the urinary tract
• S. epidermidis near the area can get
introduced into the body
(iii) Prosthetic Valves
• When a prosthetic device needs to be put into
the body, the skin needs to be opened to
access the area
• Allows introduction of device that is potentially
covered with Staphylococcus epidermidis
(iv) Prosthetic Joints
Once inside the body, S. epidermidis can create biofilms
that allow it to produce disease and infections, evade
immune cells, and resist antibiotics
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Figure 4. Pathology of S. epidermidis
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(C) STAPHYLOCOCCUS SAPROPHYTICUS
(1) Biofilms
Produce extrapolysaccharide
When a Foley catheter or urinary catheter is inserted into
the bladder, it needs to pass through the skin near the
urinary tract
S. saprophyticus near that area can get introduced
Produce biofilm and EPS leading to antibiotic
resistance and evade immune system
(2) Urease enzyme
Cause problematic issues
S. epidermidis also produce urease
S. saprophyticus can get introduced into the genitourinary
tract during catheter insertion
pH of urine is low (acidic)
o bacteria do not thrive in acidic environment
o protons cause denaturation of enzymes and DNA
S. saprophyticus releases urease that breaks down
urea in the urine into carbon dioxide and 2 molecules of
ammonia
Ammonia is basic
o ↑pH
o ↑bacterial growth
Ammonia combines with Mg2+ and SO42- in the urine
o Struvite crystals
o Stones obstruct urinary tract
o Urinary outflow obstruction
Modes of introduction of S. saprophyticus into
genitourinary tract
o Foley catheter insertion
o Females: back-to-front wiper
 Bacteria from the perineum can get introduced into
the genitourinary tract
 Bacteria can get into the urethra and bladder
Figure 5. Pathology of S. saprophyticus
Staphylococcus: Aureus, Epidermidis, Saprophyticus
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III) DISEASES AND INFECTIONS (iv) Infective endocarditis

• Attack heart valves
(A) S. AUREUS
• Infectious vegetations
(1) Skin and Soft Tissue Infections Risk factors for introducing S. aureus
S. aureus is a part of normal skin flora o IV drug users
Problems arise when there are big breaks in the skin and o Surgical procedures (dental, open surgery, etc.)
there are many S. aureus bacteria in the skin
(6) Toxic Shock Syndrome
Bacteria can invade through the breaks in the skin and
lead to: Signs and Symptoms
o Tissue damage o Rash
o White blood cells (WBCs) come into area o Hypotension
 Inflammation o Fever
 Pain Cause: Tampon used for long time
 Redness Due to TSST-1
(i) Furuncle (7) Staphylococcal Scalded Skin Syndrome
• Inflammation around hair follicle a.k.a. Ritter’s disease
Exfoliative toxin destroys Desmoglein
(ii) Carbuncle Separation of Keratinocyte
• Many furuncles that come together Manifestations
o Red rash
(iii) Impetigo o Progress to blisters
• Infect just the epidermis o (+) Nikolsky’s sign
 skin slough off when blister is rubbed
(iv) Cellulitis
(8) Gastroenteritis
• Infect epidermis and dermis
Enterotoxin destroys epithelial lining of GI tract
(v) Abscess Alters absorption and movement of electrolyte
Manifestation: diarrhea
• Infection spreads into dermis
Secondary to food poisoning
• Immune system wall-off the infection
o Usually due to mayonnaise-containing food
• Forming a pus that contains immune cells,
WBCs, bacteria, and broken-down cellular
debris
Bacteria from the epidermis can infiltrate the skin though
breaks and spread through the dermis, subcutaneous
tissues, and into the underlying tissues:
o Connective tissue
o Muscles
o Bones
o Joints
(2) Pyomyositis
Bacteria spread to muscle leading to inflammation and
infection
(3) Osteomyelitis
Destruction of bone tissue
(4) Septic arthritis
Infect joints leading to inflammation and infection
(5) Bacteremia
Bacteria in blood
If it causes disease and infection → septicemia
Can infect tissue via hematogenous route (by invading
bloodstream)

(i) Meningitis
• Infect meninges

(ii) Brain abscess

(iii) Pneumonia
• Inflammation and infection of lungs
• Test tip: Figure 6. Diseases caused by S. aureus
o usually seen in elderly after flu infection
o Previous influenza infection is a risk factor
in developing bacterial pneumonia

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 (B) S. EPIDERMIDIS IV) TREATMENT
(1) Catheter associated infections
(A) S. AUREUS
Part of normal skin flora
Antibiotic resistance
Adhere to foreign devices i.e., vascular devices
o Bacteria develop mechanisms to survive antibiotics
Central venous catheter
S. epidermidis like to form biofilms on catheter, leading to (1) Methicillin Sensitive S. aureus (M.S.S.A.)
infections
Can produce β-lactamase
High yield: Contaminant for blood cultures since it is a
o Enzyme that can inhibit β-lactam antibiotics
normal part of skin flora
o Resistant to β-lactam antibiotics
Treatment: remove device
Antibiotics that can be used
o Oxacillin
(2) Catheter associated urinary tract infections o Nafcillin
S. epidermidis like to form biofilms on catheter (2) Methicillin Resistant S. aureus (M.R.S.A.)
Lead to infection in urinary tract
Treatment: remove catheter Strain start becoming resistant to Methicillin; therefore,
oxacillin and nafcillin cannot be used for them
(3) Prosthetic valve infection Develop mecA gene that produce Penicillin Binding
Bacteria like to form biofilm on prosthetic valve Protein Type 2a (PBP2a)
Like an endocarditis PBP2a decreases efficacy of methicillin by changing the
Diagnosis structure of Penicillin Binding Protein (PBP)
o (+) blood culture Methicillin, nafcillin, oxacillin, and β-lactam antibiotics
o Evidence of infection (fever) cannot interact with PBP and cannot inhibit it
o Evidence of vegetations on esophageal transthoracic PBP
cardiogram o transpeptidase
o helps grow the bacterial cell wall
(4) Prosthetic joint infection
Inhibition of PBP
Manifestations → inhibit transpeptidation
o Pain, redness on joint → inhibit cell wall growth
o Pus from prosthetic joint area Types:
o Hospital Acquired MRSA
o Community Acquired MRSA
Antibiotics Treatment
o Hospital Acquired MRSA
 Vancomycin
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o Community Acquired MRSA
 Doxycycline
 Clindamycin
 Trimethoprim-Sulfamethoxazole (Bactrim)
(3) Vancomycin Resistant S. aureus (VRSA)
Vancomycin: powerful antibiotic
Develop VAN-A gene
Alter peptidoglycan cell wall
↓↓↓Vancomycin efficacy
o Vancomycin not able to inhibit cell wall process
Antibiotics Treatment
Figure 7. Diseases caused by S. Epidermidis o Linezolid
(C) S. SAPROPHYTICUS
(1) Urinary Tract Infections
Travel from perineum to genitourinary tract
Insertion of Foley catheter into urinary tract

(i) Cystitis
• Infection/ inflammation of bladder

(ii) Pyelonephritis
• Infection/ inflammation ureter and kidney

Figure 8. Disease caused by S. Saprophyticus Figure 9. Treatment of S. aureus infections

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(B) S. EPIDERMIDIS (C) S. SAPROPHYTICUS

(1) Methicillin Sensitive S. epidermidis (M.S.S.E.) Urinary Tract Infections
Cystitis (most common)
Can produce β-lactamase
o Enzyme that can inhibit β-lactam antibiotics (1) First line
o Resistant to β-lactam antibiotics Nitrofurantoin (Macrobid)
Antibiotics that can be used Trimethoprim-Sulfamethoxazole (Bactrim)
o Oxacillin Fosfomycin
o Nafcillin o One-time dose
(2) Methicillin Resistant S. epidermidis (M.R.S.E.) (2) Second line
Strain start becoming resistant to Methicillin; therefore, When first line cannot be given
oxacillin and nafcillin cannot be used for them o may be due to contraindications, ineffective, etc.
Develop mecA gene that produce Penicillin Binding Cephalexin
Protein Type 2a (PBP2a) o Not commonly prescribed
PBP2a change the structure of Penicillin Binding o 4 times a day
Protein (PBP) → ↓Methicillin efficacy o ↓compliance
Antibiotic
o Vancomycin Amoxicillin + Clavulanic acid (Augmentin)
Ciprofloxacin
(3) Catheter Associated Infections o Avoid giving
Remove device o Adverse effects
Bacteria mainly produce effect through biofilms, which  QT-prolongation
evade immune system  CYP 450 interactions
Removing the device will remove the infection  Achilles’ tendon rupture
o Reserved for resistant/ chronic cases

Figure 11. Treatment of S. saprophyticus infections

V) REFERENCES
● Le T, Bhushan V, Sochat M, Chavda Y, Zureick A. First Aid for
the USMLE Step 1 2018. New York, NY: McGraw-Hill Medical; 2017

Figure 10. Treatment of S. epidermidis infections

VI) REVIEW QUESTIONS

1) Which of the following is false regarding S. aureus? 6) Bacteria commonly found in the nares
a) Gram (+) a) S. aureus
b) Catalase (+) b) S. epidermidis
c) Golden yellow colonies on mannitol salt agar c) S. saprophyticus
d) Darting movement d) None of the above
2) Catalase (+), coagulase (-), Novobiocin sensitive 7) Treatment for VRSA
a) S. aureus a) Penicillin
b) S. epidermidis b) Linezolid
c) S. saprophyticus c) Doxycycline
d) All of the above d) Vancomycin
3) Causative agent of Ritter’s disease 8) Common contaminant of blood cultures
a) S. aureus a) S. aureus
b) S. epidermidis b) S. epidermidis
c) S. saprophyticus c) S. saprophyticus
d) None of the above d) None of the above
4) Enzyme that catalyzes the conversion of fibrinogen to fibrin 9) Drug of choice to treat hospital acquired MRSA
a) Catalase a) Doxycycline
b) Coagulase b) Vancomycin
c) Transpeptidase c) Clindamycin
d) Urease d) Bactrim
5) Characterized by rash, hypotension, and fever. Usually 10) Break down urea into ammonia
caused by leaving tampons for an extended period of time a) Catalase
a) Toxic shock syndrome b) Coagulase
b) carbuncle c) Transpeptidase
c) Ritter’s disease d) Urease
d) Abscess
CHECK YOUR ANSWERS

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