Microbiology: STAPH AND STREP – Dr.

Salandanan MORPHOLOGY & IDENTIFICATION:

 1 μm in diameter, irregular clusters
 Single cocci, pairs, tetrads & chains are also seen in liquid cultures
 Young cocci stain strongly G+; when aging, many cells become G-
 Staph are non-motile & do not form spores
 MICROCOCCUS Sp. Often resemble staphylococci.
 Found free living in the environment & form regular packets

CULTURE:
 Grow readily on most bacteriologic media under aerobic or
microaerophilic conditions
 Colonies on solid media are round, smooth, raised & glistening.
 S. epidermis – gray to white on primary isolation
 No pigment is produced anaerobically or in broth
 PEPTOSTREPTOCOCCUS & PEPTONIPHILUS – anaerobic cocci, often
resemble staphylococci in morphology
 S. saccharolyticus & S. aureus subsp. anaerobius – initially grow only
under anaerobic conditions but become more aerotolerant on
subcultures

GROWTH CHARACTERISTICS :
 Staph are relatively resistant to drying, heat & 9% NaCl but are
readily inhibitied by certain chemicals, e.g. 3%
hexachlorophene
 RESISTANCE:
CATALASE TEST – differentiate staph from strep using hydrogen peroxide. 1. β-lactamase – e.g. pen G, ampicillin, ticarcillin, piperacillin, &
You form bubbles because similar drugs
you liberate oxygen and water. 2. Nafcillin, methicillin & oxacillin – independent of β-lactamase
 (+) Staph; (-) Strep production production

OVERLAPPING STREAKING – isolate pure colonies STAPHYLOCOCCAL CASSETTE CHROMOSOME MEC (SCCmec)
o resistance to nafcillin
STAPHYLOCOCCUS :
CHARACTERISTICS: - mecA – encodes a low-affinity penicillin binding protein
 G+, ―grape like‖ (PBP2a) that is responsible for the resistance.
 Facultative anaerobe - SCCmec TYPE 1, 2, 3 – assoc with hospital acquired
 Catalase (+) infections
 active metabolically, fermenting carbohydrates & producing - SCCmec TYPE 4 – community acquired MRSA (CA-MRSA);
pigments that vary from white to deep yellow less resistant, more transmissible
o E.g. members of normal flora of skin & mucous
membranes 3. Vancomycin –S. aureus & S, lugdunensis
 Others cause suppuration, abscess formation, variety of o if the MIC is ≤2μg/mL – susceptible
pyogenic infection & even fatal septicemia o 4-8 μg/mL – Intermediate susceptibility
 PATHOGENIC STAPHYLOCOCCI often hemolyze blood, o ≥16 μg/mL – resistant
coagulate plasma & produce a variety of extracellular
enzymes & toxins VANCOMYCIN INTERMEDIATE S. AUREUS (VISA)
 Has at least 40 species o generally have been isolated from patients with
complex infections who have received prolonged
vancomycin therapy
MEDICALLY IMPORTANT SPECIES:
o The mechanism of resistance is associated with ↑ cell
1. S. aureus – major pathogen for humans
wall synthesis & alterations in the cell wall & is not
2. S. epidermidis – 75% of these infections caused by (-) due to the van genes found in enterococci
coagulase staphylococci are due to S. epidermidis; o S. aureus strains of intermediate susceptibility to
o infections due to S. lugdunensis, S. warneri, S. hominis vancomycin usually are nafcillin-resistant but
& other other species are less common generally are susceptible to oxazolidinones & to
3. S. saprophyticus – relatively common cause of UTI in quinupristin/dalfopristin
young women, although it rarely causes infections in 4. Vancomycin-resistant S. aureus strains – isolates contained the
hospitalized patients vancomycin resistance gene vanA from enterococci & the
nafcillin resistance gene mecA
PROPERTIES S. aureus S. epidermidis S. saprophyticus 5. Plasmid mediated resistance to tetracyclines, erythromycins,
Coagulase + - - aminoglycosides, & other drugs is frequent in staphylococci
Mannitol + - - 6. ―Tolerance‖ – implies that staphylococci are inhibited by a
Novobiocin S S R drug but not killed by it – ie, there is great difference between
Yellow pigment + - - minimal inhibitory & minimal lethal concentrations of an
Hemolysis + - - antimicrobial drug. Tolerance can at times be attributed to lack
COAGULASE TEST – clotting forms of activation of autolytic enzymes in the cell wall
MANNITOL – red to yellow
VARIATION
MOST COMMON CAUSE OF UTI:
 G- : E. coli ANTIGENIC STRUCTURE
 Staph contain antigenic polysaccharides & proteins as well as
 G+ : S. saprophyticus
other substances important in cell wall structure

S. aureus is very virulent. 1. PEPTIDOGLYCAN – polysaccharide polymer containing linked

S. epidermidis though a normal flora, can also be a pathogen subunits, provides the rigid exoskeleton of the cell wall. It is
destroyed by strong acid or exposure to lysozyme. It is
important in the pathogenesis of infection. It elicits production
of IL-1 (endogenous pyrogen) & opsonic antibodies by

MicroPirated: Staph & Strep – Lil Wayne ft. Drake Page 1

 monocytes, & it can be a chemoattractant for
polymorphonuclear leukocytes, have endotoxin-like activity, &
activate complement.
2. TEICHOIC ACIDS – polymers of lycerol or ribitol phosphate, are
linked to the peptidoglycan & can be antigenic.
ANTITEICHOIC ACID ANTIBODIES – may be found in patients
with active endocarditis due to S. aureus
3. PROTEIN A – cell wall component of S. aureus strains; bacterial
surface protein that has been characterized among a group of
adhesins called microbial surface components recognizing
adhesice matrix molecules. It binds to the Fc portion of IgG
molecules except IgG3. Fab portion of the IgG bound to
protein A is free to combine with a specific antigen.
COAGGLUTINATION – protein A with attached IgG molecules
directed against a specific bacterial antigen will agglutinate
bacteria that have that antigen
4. CAPSULES – inhibit phagocytosis by polymorphonuclear
leukocytes unless specific antibodies are present.
COAGULASE (Clumping Factor) – present on the cell wall surface;
binds nonenzymatically to fibrinogen, yielding aggregation of the
bacteria
5. SEROLOGIC TESTS – limited usefulness
ENZYMES & TOXINS
1. CATALASE – converts hydrogen peroxide into water & oxygen.
Staph – (+); Strep (-)
2. COAGULASE – enzyme-like protein that clots oxalated or
citrated plasma. It binds to prothrombin; together they become
enzymatically active & initiate fibrin polymerization. It may
deposit fibrin on the surface of staphylococci, perhaps altering
their ingestion by phagocytic cells or their destruction within
such cells.
CLUMPING FACTOR – another example of an MSCRAMM that is
responsible for adherence of the organisms to fibrinogen &
fibrin.when mixed with plasma, S aureus forms clumps. It
induces a strong immunogenic response in the host, it has been
the focus of recent vaccine efforts
3. HYALURONIDASE (Spreading factor) – staphylokinase resulting in
fibrinolysis but acting much more slowly than streptokinase
4. Proteinases
5. Lipases
6. β-lactamase
EXOTOXIN
 α-TOXIN – heterogenous protein that acts on a broad spectrum
of eukaryotic cell membranes. It is a potent hemolysin.
 β-TOXIN – degrades sphingomyelin & therefore is toxic for many
kinds of cells, including human RBC
 δ-TOXIN – heterogenous & dissociates into subunits in nonionic
detergents. It disrupts biologic membranes & may have a role
in S. aureus diarrheal diseases.
 γ-HEMOLYSIN – refers to three proteins that interact with the 2
proteins comprising the Panton-Valentine leukocidin to form 6
potential 2 component toxins.
 All 6 of these protein toxins are capable of efficiently lysing
WBC by causing pore formation in the cellular membranes that
↑ cation permeability.
 These leads to massive release of inflammatory mediators such
as IL8, leukotriene & histamine which are responsible for
necrosis & severe inflammation
PANTON-VALENTINE LEUKOCIDIN :
 toxin of S. aureus has 2 components. It can kill WBC of humans
& rabbits.
 S & F act synergistically on the WBC membranes as described
for γ toxin. This toxin is an important virulence factor in CA-MRSA
infections.
MicroPirated: Staph & Strep – Lil Wayne ft. Drake
EXFOLIATIVE TOXINS
EPIDERMOLYTIC TOXIN A – chromosomal gene product & is heat stable
EPIDERMOLYTIC TOXIN B – plasmid mediated & heat labile
 Both of these are superantigens which yield the generalized
desquamation of the staphylococcal scalded skin syndrome by
dissolving the mucopolysaccharide matrix of the epidermis.
TOXIC SHOCK SYNDROME TOXIN
 TSST-1 – same as enterotoxin F.
 Prototypical superantigen.
 Binds to MHC Class II yielding T cell stimulation which promotes
the protean manifestations of the TSS
 Associated with fever, shock, & multisystem involvement,
including a desquamative skin rash.
 The gene for TSST-1 is found in about 20% of S aureus isolates,
including MRSA.
ENTEROTOXIN – (A-E, G-J, K-R & U, V) are also superantigens.
 heat stable & resistant to the action of gut enzymes
 produced when S aureus grows in carbohydrate & protein
foods
 25 μg of enterotoxin B – vomiting & diarrhea
 TSST 1 & enterotoxin genese are on chromosomal element
called PATHOGENECITY ISLAND. It interacts with accessory
genetic elements – bacteriophages – to produce toxins
PATHOLOGY
 The prototype of staphylococcal lesion is the furuncle or other
localized abscess.
 OSTEOMYELITIS – the primary focus of S. aureus growth is
typically in a terminal blood vessel of the metaphysic of a long
bone, leading to necrosis of bone & chronic suppuration.
 S. aureus may cause pneumonia, meningitis, empyema,
endocarditis or sepsis with suppuration in any organ.
 Staphylococci of low invasiveness are involved in many skin
infections (eg, acne, pyoderma or impetigo).
 Anaerobic cocci (Peptostreptococcus) participate in mixed
anaerobic infections.
 Staphylococci also cause disease through the elaboration of
toxins, without apparent invasive infection.
 Bullous exfoliation, the scalded skin syndrome, is caused by the
production of exfoliative toxins. TSS is associated with TSST-1.
CLINICAL FINDINGS
 A localized staph infection appears as a ―pimple‖, hair follicle
infection, or abscess.
 There is usually an intense, localized, painful inflammatory
reaction that undergoes central suppuration & heals quickly
when the pus is drained.
 S. aureus infection can also result from direct contamination of
a wound or infection following trauma.
 The clinical presentations resemble those seen with other
bloodstream infections.
 Secondary localization within an organ or system is
accompanied by the symptoms & signs of organ dysfunction &
intense focal suppuration
 TSS is manifested by an abrupt onset of high fever, vomiting,
diarrhea, myalgias, a scarlatiniform rash, & hypotension with
cardiac & renal failure in the most severe cases.
DIAGNOSTIC LABORATORY TESTS :
1. SPECIMENS – surface swab pus, blood, tracheal aspirate, or
spinal fluid for culture
2. SMEARS – although it is not possible to distinguish saprophytic (S.
epidermidis) from pathogenic (S. aureus) organisms on smears.
3. CULTURE
4. CATALASE TEST – used to detect presence of cytochrome
oxidase enzymes. Hydrogen peroxide is placed on a slide, & a
small amount of bacterial growth is placed in the solution.
Formation of bubbles indicates a (+) test.
5. COAGULASE TEST – a tube of plasma mixed with sterile broth is
included as a control. If it clots  (+)
6. SUSCEPTIBILITY TESTING
 Resistance to penG can be predicted by a (+) test for β-
lactamase. 90% of S aureus produce β-lactamase.
Page 2
  Resistance to nafcillin (oxacillin & methicillin) occurs in 65% of S. STREPTOCOCCUS
aureus & 75% of S. epidermidis.  G+, spherical or ovoid
 Chains or pairs
TREATMENT:  Catalase (-)
 S. epidermidis are difficult to cure because they occur in  Heterogenous group of bacteria
prosthetic devices where the bacteria can sequester
themselves in a biofilm. Catheter associated G+ cocci - ENTEROCOCCUS
 S. epidermidis is more often resistant to antimicrobial drugs than
is S. aureus; approximately 75% of S epidermidis strains are
nafcillin resistant

STAPHYLOCOCCUS AUREUS
 OPTIMAL pH: 7.0-7.5
 Grows in 6.5-10% NaCl
 Some have capsule or slime layer
 Produces beta hemolysis
 Energy obtained via respiratory & fermentative pathways
 COLONY: entire edge, mucoid, white to
gold/golden/whitish/yellowish

GASTROENTERITIS
 ETIOLOGIC AGENT: S. aureus
 MOT: Fecal-oral route
 Possibly acquired by ingestion of toxin from contaminated
foods
 CLINICAL MANIFESTATION: vomiting, diarrhea
 TREATMENT:
o Local infection
o Antimicrobials MORPHOLOGY & IDENTIFICATION :
 Penicillin
 Cloxalcillin / Oxacillin TYPICAL ORGANISMS
 Nafcillin  As a culture ages & the bacteria die, they lose their gram-
 Vancomycin positivity & appear to be gram negative
 PREVENTION  Most grp A, B & C strains produce capsules composed of
o Proper hygiene hyaluronic acid
o Handwashing  STREPTOCOCCAL CELL WALL:
o Contains proteins (M, T, R antigens)
COAGULASE NEGATIVE STAPHYLOCOCCUS (CoNS) o Carbohydrates (group specific)
o Peptidoglycans
STAPHYLOCOCCUS EPIDERMIDIS  GRP A STREPTOCOCCI
 Normal flora of the skin o PILI: projects through the capsule, consist partly of M
 Opportunistic, low virulence protein, covered with LIPOTEICHOIC ACID (for
 Single most common isolate from infections associated with: attachment of streptococci to epithelial cells)
o Artificial cardiac valve
o Prosthetic joints (THR) CULTURE
o CNS Shunts  Most grow in solid media as discoid colonies
 TREATMENT  1-2 mm in diameter
o Antibiotic e.g. aminoglycosides  PEPTOSTREPTOCOCCUS – an obligate anaerobe

STAPHYLOCOCCUS SAPROPHYTICUS
GROWTH CHARACTERISTICS :
 Opportunistic
 ENERGY – from the utilization of sugars
 Causes UTI in sexually active young female
 Grows poorly on solid media or in broth unless enriched with
 Exfoliative toxins
blood or tissue fluids
o Epidermolysis
 Growth & hemolysis are aided by incubation in 10% CO2
o Cause SSS
 Most pathogenic hemolytic streptococci grow best at 37°C
 Toxic Shock Syndrome
 RESERVOIR: Skin, nasopharynx
Grp D ENTEROCOCCI – grow well at between 15°C
 DISEASES:
o Grow in high (6.5%) NaCl, 0.1% methylene blue or in
1. Cutaneous infections
bile esculin sugar
o Folliculitis, Furunculosis, Carbuncles, Impetigo
 Most streptococci are facultative anaerobes
o Wound infection
o Staphylococcal Scalded Skin Syndrome (SSSS)
VARIATION
 Bullous exfoliative dermatitis
 Group A – matte or glossy colonies
2. Toxic Shock Syndrome (TSS)
 MATTE: organisms that produce much M protein, virulent and
o Tampons
relatively insusceptible to phagocytosis by human leukocytes
3. Food Poisoning
 GLOSSY: produce little M protein and are often nonvirulent
o Food products
o INCUBATION – 4 hrs (COURSE: 24 hrs)
HEMOLYTIC PROPERTY VARIES BY SPECIES:
4. Endocarditis
1. β – clear
5. Bone & Joint infections
2. α – partial (green)
6. Pneumonia & empyema
3. γ – non-hemolytic
 LABORATORY DIAGNOSIS
o Smear
o Culture SEROGROUPED USING ANTIBODIES TO CELL WALL CARBOHYDRATES:
 BAP – medium of choice  Lancefield’s Group A-O (Rebecca Lancefield) – group specific
o Biochemical tests substance
 This carbohydrate is contained in the cell wall of many
streptococci & forms the basis of serologic grouping into
Lancefield groups A-H & K-U.
 (you only live once, life is too short to bother from A-U)

MicroPirated: Staph & Strep – Lil Wayne ft. Drake Page 3

  It is determined by an amino sugar: CLASSIFICATION OF STREPTOCOCCI:
o Grp A – rhamnose-N-acetylglucosamine Based on:
o Grp B – rhamnose-glucosamine polysaccharide 1. colony morphology and hemolytic reactions on blood agar
o Grp C – rhamnose-N-acetylgalactosamine 2. serologic specificity of the cell wall group-specific substance
o Grp D – glycerol teichoic acid containing d-alanine (Lancefield classification) and other cell wall or capsular
& glucose antigens
o Grp F – glucopyranosyl-N-galactosamine o to classify S pneumoniae
 Typing is generally done only for grps A, B, C, F & G which o to typify the group B streptococci (S agalactiae).
cause disease in humans & for which there are reagents that 3. biochemical reactions and resistance to physical and chemical
allow typing using simple agglutination or color reactions factors
 Aside from the colonies, you look for hemolysis: o sugar fermentation reactions
o α – partial hemolysis; green o tests for the presence of enzymes
o β – complete hemolysis; clear o tests for susceptibility or resistance to certain
o γ – no hemolysis; red (color of the BAP) chemical agents
o used for species that typically do not react with the
M PROTEIN commonly used antibody preparations for the
 major virulence factor of group A S pyogenes group-specific substances, groups A, B, C, F, and G.
 hair-like projections of the streptococcal cell wall 4. ecologic features
 two major structural classes of M protein, classes I and II
 M protein and perhaps other streptococcal cell wall antigens SEROGROUPED USING KNOWN ANTIBODIES:
have an important role in the pathogenesis of rheumatic fever  Capsules for S. pneumonia
 M-protein for S. pyogenes
T SUBSTANCE
 no relationship to virulence of streptococci MEDICALLY IMPORTANT STREPTOCOCCI
 acid-labile and heat-labile SPECIES LANCEFIELD HEMOLYSIS LAB CHARAC
 permits differentiation of certain types of streptococci by S. pyogenes A β Bacitracin – S
agglutination with specific antisera PYR test (+)
S. agalactiae B β Bacitracin – R
NUCLEOPROTEINS Hippurate utilized
 P SUBSTANCES: mixtures of proteins and other substances of little CAMP (+)
serologic specificity E. faecalis D α,β or none Growth in 6.5% NaCl
PYR test (+)
TOXINS & ENZYMES: S. bovis D α or none No growth in 6.5% NaCl
1. STREPTOKINASE (FIBRINOLYSIN) S. pneumonia Not α Bile soluble
o produced by many strains of group A β-hemolytic grouped Optochin – S
streptococci Viridans group Not α Not bile soluble
o transforms the plasminogen of human plasma into grouped Optochin - R
plasmin
o treatment of pulmonary emboli and of coronary PYR TEST demonstrates the presence of pyrrolidonyl arylamidase
artery and venous thromboses.
NOT GROUPABLE – lack the carbohydrate cell wall antigens
2. STREPTODORNASE
STREPTOCOCCUS PYOGENES (GABS)
o depolymerizes DNA
 CHARACTERISTICS:
o Mixtures of streptodornase and streptokinase are
o β-hemolytic colonies
used in "enzymatic debridement
o Bacitracin sensitive
o PYR (+) – hydrolysis of L-pyrrolidonyl-2-
3. HYALURONIDASE
naphthylamide)
o splits hyaluronic acid
o contain the group A antigen
o antigenic and specific for each bacterial or tissue
 RESERVOIR: Human throat & skin
source
 TRANSMISSION: Spread by respiratory droplets or by direct
contact
4. PYROGENIC EXOTOXINS (Erythrogenic Toxin)
 PATHOGENESIS:
o elaborated by group A streptococci
o Hyaluronic acid capsule (a polysaccharide) is non-
o streptococcal pyrogenic exotoxins: A, B, and C
immunogenic; inhibits phagocytic uptake
o EXOTOXIN A – produced by group A streptococci
o M-protein; virulence factor, antiphagocytic, used to
that carry a lysogenic phage
type group A strep; M12 strains – associated with
o superantigen
acute glomerulonephritis
o streptococcal pyrogenic exotoxins have been
 TOXINS:
associated with streptococcal toxic shock syndrome
o Streptolysin O: immunogenic, hemolysin/cytolysin
and scarlet fever
o Streptolysin S: non-immunogenic, hemolysin/cytolysin
5. DIPHOSPHOPYRIDINE NUCLEOTIDASE
GABS
o related to the organism's ability to kill leukocytes.
 SPREADING FACTORS:
o STREPTOKINASE – breaks down fibrin clot
6. HEMOLYSINS
o Streptococcal DNAse liquefies pus, extension of
o α HEMOLYSIS - Incomplete lysis of erythrocytes with
lesion
the formation of green pigment
o HYALURONIDASE: hydrolyzes the ground substances
o β HEMOLYSIS - disruption of erythrocytes with release
of connective tissues; important to spread in cellulitis
of hemoglobin
o STREPTOLYSIN O – hemolytically active in the
EXOTOXINS A-C
reduced state (available –SH groups)
 Pyrogenic or erythrogenic
o inactivated in the presence of oxygen
 Phage-coded
o combines quantitatively with antistreptolysin O, an
 Association to Scarlet fever
antibody that appears in humans following infection
 Inhibit liver activity to endotoxins
with any streptococci that produce streptolysin O
 ACTIVATE:
o STREPTOLYSIN S – agent responsible for the hemolytic
o Th-cells
zones around streptococcal colonies growing on the
o MHC Class II antigens
surface of blood agar plates
o elaborated in the presence of serum
o not antigenic

MicroPirated: Staph & Strep – Lil Wayne ft. Drake Page 4

PATHOGENESIS & CLINICAL FINDINGS
INFECTIONS CAN BE DIVIDED INTO SEVERAL CATEGORIES:
 DISEASES ATTRIBUTABLE TO INVASION BY Β-HEMOLYTIC GROUP A
STREPTOCOCCI (S PYOGENES)
o a. ERYSIPELAS
 If the portal of entry is the skin, erysipelas
results, with massive brawny edema and a
rapidly advancing margin of infection
o b. CELLULITIS
 acute, rapidly spreading infection of the
skin and subcutaneous tissues
 Pain, tenderness, swelling, and erythema
occur.
 Cellulitis is differentiated from erysipelas by
two clinical findings: In cellulitis, the lesion
is not raised and the line between the
involved and uninvolved tissue is indistinct
o c. NECROTIZING FASCIITIS (Streptococcal Gangrene)
 infection of the subcutaneous tissues and
fascia
 group A streptococci that cause
necrotizing fasciitis have sometimes been
termed "flesh- eating bacteria."
o d. PUERPERAL FEVER
 streptococci enter the uterus after
delivery, puerperal fever develops, which
is essentially a septicemia originating in
the infected wound (endometritis)
o e. SEPSIS
 Infection of traumatic or surgical wounds
with streptococci results in sepsis or
surgical scarlet fever.
 DISEASES ATTRIBUTABLE to LOCAL INFECTION WITH β-HEMOLYTIC
GROUP A S pyogenes and Their By-Products:
o a. STREPTOCOCCAL SORE THROAT
 The most common infection due to β-
hemolytic streptococci is streptococcal
sore throat
 Virulent group A streptococci adhere to
the pharyngeal epithelium by means of
lipoteichoic acid-covered surface pili. The
glycoprotein fibronectin (MW 440,000) on
epithelial cells probably serves as
lipoteichoic acid ligand.
 Pneumonia due to β-hemolytic
streptococci is rapidly progressive and
severe and is most commonly a sequela
to viral infections, eg, influenza or measles,
which seem to enhance susceptibility
greatly
o b. STREPTOCOCCAL PYODERMA
 Local infection of superficial layers of skin,
especially in children, is called IMPETIGO
 It consists of superficial blisters that break
down and eroded areas whose denuded
surface is covered with pus or crusts
INFECTIVE ENDOCARDITIS
ACUTE ENDOCARDITIS
 Patients with prosthetic heart valves are at special risk
SUBACUTE ENDOCARDITIS
 involves abnormal valves (congenital deformities and
rheumatic of atherosclerotic lesions)
 group D streptococci also are common causes of subacute
endocarditis
GROUP B STREPTOCOCCI
 part of the normal vaginal flora in 5-25% of women
 Group B streptococcal infection during the first month of life
may present as fulminant sepsis, meningitis, or respiratory
distress syndrome
 Intrapartum intravenous ampicillin appears to prevent
colonization of infants whose mothers carry group B
streptococci
MicroPirated: Staph & Strep – Lil Wayne ft. Drake
POSTSTREPTOCOCCAL DISEASES (RHEUMATIC FEVER, GLOMERULONEPHRITIS)
A. ACUTE GLOMERULONEPHRITIS
 This sometimes develops 3 weeks after streptococcal
infection, particularly with M types 12, 4, 2, and 49
 Glomerulonephritis may be initiated by antigen-antibody
complexes on the glomerular basement membrane
 The most important antigen is probably in the
streptococcal protoplast membrane
B. RHEUMATIC FEVER
 most serious sequela of hemolytic streptococcal infection
because it results in damage to heart muscle and valves
 The onset of rheumatic fever is often preceded by a
group A streptococcal infection 1–4 weeks earlier,
although the infection may be mild and may not be
detected.
 Typical symptoms and signs: fever, malaise, a migratory
nonsuppurative polyarthritis, and evidence of
inflammation of all parts of the heart (endocardium,
myocardium, pericardium)
 Erythrocyte sedimentation rates, serum transaminase
levels, electrocardiograms, and other tests are used to
estimate rheumatic activity.
 has a marked tendency to be reactivated by recurrent
streptococcal infections, whereas nephritis does not
DIAGNOSTIC LABORATORY TESTS
1. SPECIMENS – throat swab, pus, or blood is obtained for culture
 Serum is obtained for antibody determinations.
2. SMEARS – Smears from pus often show single cocci or pairs
rather than definite chains. If smears of pus show streptococci
but cultures fail to grow, anaerobic organisms must be
suspected
 Smears of throat swabs are rarely contributory
3. CULTURE – on blood agar plates.
 Oxygen inactivates streptolysin O.
 Blood cultures will grow hemolytic group A
streptococci
 Group A streptococci can be rapidly identified by a
fluorescent antibody test, the PYR test, and by rapid
tests specific for the presence of the group A-
specific antigen.
 Streptococci belonging to group A may be
presumptively identified by inhibition of growth by
bacitracin
ANTIGEN DETECTION TESTS
 use enzymatic or chemical methods to extract the antigen
from the swab, then use EIA or agglutination tests to
demonstrate the presence of the antigen.
SEROLOGIC TESTS
 antibodies include antistreptolysin O (ASO), particularly in
respiratory disease
 anti-DNase and antihyaluronidase, particularly in skin infections
 antistreptokinase
 anti-M type-specific antibodies
IMMUNITY
 Resistance against streptococcal diseases is type-specific
 M protein interferes with phagocytosis, but in the presence of
type-specific antibody to M protein, streptococci are killed by
human leukocytes.
TREATMENT
 All β-hemolytic group A streptococci are sensitive to penicillin G
 most are sensitive to erythromycin
 Some are resistant to tetracyclines. Aminoglycosides often
enhance the rate of bactericidal action of penicillin on
streptococci, particularly enterococci.
 Antimicrobial drugs are also very useful in preventing
reinfection with β-hemolytic group A streptococci in rheumatic
fever patients
EPIDEMIOLOGY, PREVENTION, & CONTROL
 Many streptococci (viridans streptococci, enterococci, etc)
are members of the normal flora of the human body
 They produce disease only when established in parts of the
body where they do not normally occur (eg, heart valves).
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  ultimate source of group A streptococci is a person harboring  TREATMENT
these organisms. o Ampicillin, cefoxatime with gentamycin

CONTROL PROCEDURES ARE DIRECTED MAINLY AT THE HUMAN SOURCE:  PREVENTION

1. Detection and early antimicrobial therapy of respiratory and
skin infections with group A streptococci.
2. Antistreptococcal chemoprophylaxis in persons who have
suffered an attack of rheumatic fever.
3. Eradication of group A streptococci from carriers.
4. Dust control, ventilation, air filtration, ultraviolet light, and
aerosol mists are all of doubtful efficacy in the control of
streptococcal transmission. Milk should always be pasteurized.
5. Group B streptococci account for most cases of neonatal
sepsis at present.
o Treat mother prior to delivery if
 Had preious baby with sepsis (GBS)
 Documented GBS colonization
 PROM
GROUPS C AND G
 occur sometimes in the nasopharynx
 cause sinusitis, bacteremia, or endocarditis
 β – hemolytic
 identified by reactions with specific antisera for groups C or G.

GABS STREPTOCOCCUS PNEUMONIA (Pneumococcus)

 DISEASES  CHARACTERISTICS:
TABLE 2: ACUTE (SUPPURATIVE) S. PYOGENES INFECTIONS: o Alpha-hemolytic
Diseases Clinical Manifestations o Optochin (ethylhydrocupreine hydrochloride)
Pharyngitis Sore throat, fever, malaise, headache sensitive
tonsillar abscesses & tender anterior o Lancet shaped diplococcic
cervical lymph nodes o Bile soluble/lyzed by bile
Scarlet fever As above followed by blanching, o Lancet shaped
“sand paper rash”, circumoral pallor,  RESERVOIR:
palms & soles sparing; strawberry o Human upper respiratory tract
tongue; n/v  TRANSMISSION: Respiratory droplets
Pyoderma / Impetigo Pus-producing skin infection (honey-  PREDISPOSING CONDITION FOR PNEUMONIA
crusted lesions) o Influenza or measles
Cellulitis / Necrotizing fasciitis Flesh eating bacteria o COPD
o CHF
 Other diseases o Alcoholism
o Pneumonia o Asplenia
o Toxic shock like syndrome  PATHOGENESIS :
o IgA PROTEASE: colonization
TABLE 3: NON-SUPPURATIVE SEQUELAE o TEICHOIC ACID: attachment
o POLYSACCHARIDE CAPSULE: major virulence factor;
Disease Sequelae Mechanism
retards phagocytosis
Rheumatic fever Pharyngitis Ab to heart tissue
o Peptidoglycan/Teichoic acid highly inflammatory in
mean =19.1
CNS
AGN (MI2 serotype) Pharyngitis / cutaneous Immune complex
o PNEUMOLYSIN O: hemolysin/cytolysin
deposits on GBM
 Damages respiratory epithelium
o RUSTY SPUTUM – pneumococcus stimulates release of
LABORATORY fluid & RBC, WBC
 Rapid antigen Test  DISEASES
 Throat swab culture 1. BACTERIAL PNEUMONIA – most common cause (>65 y/o)
 ASO titer for rheumatic fever (>200) 2. ADULT MENINGITIS – most common cause
3. OTITIS MEDIA & SINUSITIS (in children) – most common cause
TREATMENT 4. Septicemia in splenectomized patients
 PENICILLIN G – drug of choice
 ERYTHROMYCIN – alternative  TREATMENT
 Other Beta lactam antibiotics o Penicillin G
o Alternative
PREVENTION
 Penicillin injection  Some penicillin-resistant strains are resistant to ceftizoxime.
 Resistance to tetracycline and erythromycin occurs also.
STREPTOCOCCUS AGALACTIAE (GBS)  Pneumococci remain susceptible to vancomycin.
 CHARACTERISTICS:  PREVENTION
o β-hemolytic, bacitracin resistant o Pneumovaccine (23 serotypes)
o hydrolyzes hippurate
o Camp test (+) - Christie, Atkins, Munch-Peterson  MORPHOLOGY & IDENTIFICATION
o group B streptococci o TYPICAL ORGANISMS
o normal flora of the female genital tract  Autolysis of pneumococci is greatly enhanced
o important cause of neonatal sepsis and meningitis. by surface-active agents
o produce zones of hemolysis that are only slightly  Lysis of pneumococci occurs in a few minutes
larger than the colonies (1–2 mm in diameter) when ox bile (10%) or sodium deoxycholate
 RESERVOIR : (2%) is added to a broth culture or suspension
o Human vagina (15-20% of women) of organisms at neutral pH.
 Viridans streptococci do not lyse and are thus
 TRANSMISSION : easily differentiated from pneumococci.
o During birth – newborn  On solid media, the growth of pneumococci is
 PROM - ↑ risk inhibited around a disk of optochin; viridans
streptococci are not inhibited by optochin.
GBS
 PATHOGENESIS  CULTURE
o Capsule o Pneumococci form a small round colony, at first
o β-hemolysin & cAMP factor (incomplete hemolysin) dome-shaped and later developing a central
plateau with an elevated rim.
 DISEASES o Pneumococci are α-hemolytic on blood agar.
o Neonatal septicemia o Growth is enhanced by 5–10% CO2.
o Meningitis

MicroPirated: Staph & Strep – Lil Wayne ft. Drake Page 6

  GROWTH CHARACTERISTICS
o Most energy is obtained from fermentation of
glucose; this is accompanied by the rapid
production of lactic acid, which limits growth.
o Neutralization of broth cultures with alkali at intervals
results in massive growth
o Variation
o Pneumococcal isolates that produce large amounts
of capsules produce large mucoid colonies.
o Capsule production is not essential for growth on
agar medium, and capsular production
 ANTIGENIC STRUCTURE
o COMPONENT STRUCTURES :
 The pneumococcal cell wall has
peptidoglycan and teichoic acid
 QUELLUNG REACTION
o When pneumococci of a certain type are mixed
with specific antipolysaccharide serum of the same
type—or with polyvalent antiserum—on a
microscope slide, the capsule swells markedly, and
the organisms agglutinate by cross-linking of the
antibodies.
o polyvalent antiserum, which contains antibody to all
of the types ("omniserum"), is a good reagent for
rapid microscopic determination of whether or not
pneumococci are present in fresh sputum
 PATHOGENESIS
o TYPES OF PNEUMOCOCCI
 adults, types 1–8 are responsible for about
75% of cases of pneumococcal
pneumonia
 in children, types 6, 14, 19, and 23 are
frequent causes.
 PRODUCTION OF DISEASE
o Pneumococci produce disease through their ability
to multiply in the tissues.
o produce no toxins of significance.
o virulence of the organism is a function of its capsule,
which prevents or delays ingestion by phagocytes.
 LOSS OF NATURAL RESISTANCE
o factors that probably lower resistance and thus
predispose to pneumococcal infection are the
following:
1. Viral and other respiratory tract infections that damage surface
cells; abnormal accumulations of mucus (eg, allergy), which
protect pneumococci from phagocytosis; bronchial
obstruction (eg, atelectasis); and respiratory tract injury due to
irritants disturbing its mucociliary function.
2. Alcohol or drug intoxication, which depresses phagocytic
activity, depresses the cough reflex, and facilitates aspiration of
foreign material.
3. Abnormal circulatory dynamics (eg, pulmonary congestion,
heart failure).
4. Other mechanisms, eg, malnutrition, general debility, sickle cell
anemia, hyposplenism, nephrosis, or complement deficiency.
 PATHOLOGY
o Pneumococcal infection causes an outpouring of
fibrinous edema fluid into the alveoli, followed by red
cells and leukocytes, which results in consolidation of
portions of the lung. Many pneumococci are found
throughout this exudate, and they may reach the
bloodstream via the lymphatic drainage of the
lungs. The alveolar walls remain normally intact
during the infection. Later, mononuclear cells
actively phagocytose the debris, and this liquid
phase is gradually reabsorbed. The pneumococci
are taken up by phagocytes and digested
intracellularly.
 CLINICAL FINDINGS
o The onset is usually sudden, with fever, chills, and
sharp pleural pain.
MicroPirated: Staph & Strep – Lil Wayne ft. Drake
 DIAGNOSTIC LABORATORY TESTS
1. Stained Smears
 Gram-stained film of rusty-red sputum shows typical
organisms, many polymorphonuclear neutrophils,
and many red cells
2. Capsule Swelling Tests
 Fresh emulsified sputum mixed with antiserum gives
capsule swelling (the quellung reaction) for
identification of pneumococci and possible typing
 Peritoneal exudate
3. Culture
 Sputum cultured on blood agar and incubated in
CO2 or a candle jar. Blood culture.
PNEUMOCOCCAL MENINGITIS
 Prompt examination and culture of cerebrospinal fluid will
make this diagnosis.
IMMUNITY
 Immunity is type-specific and depends both on antibodies to
capsular polysaccharide and on intact phagocytic function.
Vaccines can induce production of antibodies to capsular
polysaccharides
VIRIDANS (S. sanguis, S. mutans, S. salivarius)
 CHARACTERISTICS
o Alpha hemolytic but may be non hemolytic
o Bile & optochin resistant
o include S mitis, S mutans, S salivarius, S sanguis
o growth is not inhibited by optochin
o colonies are not soluble in bile (deoxycholate)
o most prevalent members of the normal flora of the
upper respiratory tract
 VIRIDANS
o may reach the bloodstream as a result of trauma
and are a principal cause of endocarditis on
abnormal heart valves.
o Some viridans streptococci (eg, S mutans) synthesize
large polysaccharides such as dextrans or levans
from sucrose and contribute importantly to the
genesis of dental caries.
 RESERVOIR
o Normal flora of human oropharynx
 DISEASES:
1. DENTAL CARIES
o S. mutans
2. INFECTIVE ENDOCARDITIS
o PREDISPOSING CONDITIONS
 Damaged or prosthetic valves
 Dental work without prophylaxis
 Poor oral hygiene
 PATHOGENESIS
o Dextran (biofilm)
o Growth in vegetation protects organism from
immune system
 TREATMENT
o Penicillin G with aminoglycosides for IE
 PREVENTION
o Prophylactic penicillin
ENTEROCOCCUS (Enterococcus/Streptococcus faecalis)
 CHARACTERISTICS
o Group D
o Hydrolyzes ecculin in 40% bile and 6.5% NaCl
o PYR (+)
o part of the normal enteric flora
o nonhemolytic and occasionally α-hemolytic
o more resistant to penicillin G than the streptococci
o plasmids that encode for β-lactamase
o Many isolates are vancomycin-resistant
o ENTEROCOCCUS FAECALIS: most common
o ENTEROCOCCUS FAECIUM causes 5–10%.
o most frequent causes of nosocomial infections,
particularly in intensive care units, and are selected
by therapy with cephalosporins and other antibiotics
to which they are resistant.
o transmitted from one patient to another primarily on
the hands of hospital personnel.
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  RESERVOIR: human colon, urethra & female genital tract
 PATHOGENESIS & PREDISPOSING CONDITIONS:
o Bile/salt tolerance allow survival in bowel & GB
o During medical procedures on GI or GU tract
o E. faecalis  bloodstream damaged heart valves
 SBE
 DISEASES :
o Urinary & Biliary tract infections
o SBE (elderly)
 TREATMENT
o Drug resistant
 Vancomycin
 PREVENTION
o Use of penicillin & gentamicin

ANTIBIOTIC RESISTANCE
 E faecium is usually much more antibiotic-resistant than E
faecalis

STREPTOCOCCUS BOVIS
 nonenterococcal group D streptococci.
 They are part of the enteric flora
 occasionally cause endocarditis, & sometimes cause
bacteremia in patients with colon carcinoma
 nonhemolytic
 PYR-negative
 grow in the presence of bile and hydrolyze esculin (bile esculin-
positive)
 do not grow in 6.5% NaCl.
 viridans streptococci

STREPTOCOCCUS ANGINOSUS GROUP

 other species names: S constellatus, S intermedius, and S milleri
 part of the normal flora
 May be α-β, or nonhemolytic.
 S anginosus group includes β-hemolytic streptococci that form
minute colonies (< 0.5 mm in diameter) and react with groups
A, C, or G antisera and all β-hemolytic group F streptococci
 Group A are PYR-negative.
 Voges-Proskauer test-positive
 may be classified as viridans streptococci.

GROUP N STREPTOCOCCI
 rarely found in human disease states
 produce normal coagulation ("souring") of milk
 GROUPS E, F, G, H, AND K–U STREPTOCOCCI
 occur primarily in animals

NUTRITIONALLY VARIANT STREPTOCOCCI

 ABIOTROPHIA ADJACENS, previously Streptococcus adjacens,
and Abiotrophia defectiva, previously Streptococcus
defectivus) have been known as "nutritionally deficient
streptococci," "pyridoxal-dependent streptococci," and by
other names.
 require pyridoxal or cysteine for growth on blood agar or grow
as satellite colonies around colonies of staphylococci and
other bacteria.
 α-hemolytic but may be nonhemolytic.
 They are part of the normal flora and occasionally cause
bacteremia or endocarditis and can be found in brain
abscesses and other infections

PEPTOSTREPTOCOCCUS (Many Species)

 grow only under anaerobic or microaerophilic conditions
 variably produce hemolysins
 part of the normal flora of the mouth, upper respiratory tract,
bowel, and female genital tract

“HONESTLY YOU READ THIS

SHIT? ITS SALANDANAN.
SAMPLEX THIS BITCH!!”
– Lil Wayne

MicroPirated: Staph & Strep – Lil Wayne ft. Drake Page 8