Bacteria
Causal organism Staphylococcus aureus
Commensal
S. epidermidis – most common cause of endocarditis, prosthetic joint infection, CNS shunt infection & newborn sepsis (coagulase- & catalase+)
S. saprophyticus – UTI & cystitis
Other gram+ cocci includes: -
➢ Enterococcus
➢ Peptostreptococcus
➢ Streptococcus
Disease Skin infections (impetigo, cellulitis, abscesses), pneumonia, Ritter disease (SSSS), osteomyelitis, endocarditis, toxic shock syndrome, food poisoning
Morphology Gram+ cocci in cluster (in grape shaped)
Non-sporing, non-motile, non-capsulated & non-spore forming
Facultative anaerobes (can grow w/o O2)
Catalase+
Low G + C
2 important gram+ cocci include Staphylococcus & Streptococcus
Virulence factor Peptidoglycan, teichoic acid, protein A, clumping factor, alpha, beta lysin, gamma lysin, epidermolytic/exfoliative toxin (Type A & B), cytolytic toxin, Toxic
shock syndrome toxin (TSST), enterotoxin (type A-E & G-J), catalase, coagulase, hyaluronidase, nucleases, staphylokinase, lipase, beta-lactamase
Epidemiology One of the most common cause of hospital-acquired pneumonia
MRSA is the most common cause of skin abscess in the US
MOT Human nose is the main site of S. aureus colonization
Direct contact & air-borne
RF ➢ Immunocompromised
➢ Burn victim
➢ Indwelling catheters
Pathogenesis Entry & colonization
➢ Peptidoglycan – stimulate TLR → inflammation &
➢ Teichoic acid – promote adherence to mucosal
➢ Clumping factor – binds to fibrinogen promote aggregation
Immune evasion
➢ Protein A – binds to IgG preventing phagocytosis
➢ Coagulase – form fibrin to create clot around bacteria
➢ Staphylokinase – dissolve clot when need to escape
➢ Beta-lactamase
Tissue invasion & spread
➢ Hyaluronidase – facilitate further bacterial spread
➢ Lipase – promote survival in fatty environment
➢ Nuclease – ↓viscosity in pus enabling movement
Toxin mediated damage
➢ Alpha, beta & gamma lysin – lyse cell & impair immune
➢ Exfoliative toxin – cleave desmoglein → SSS
➢ TSST – superAg overstimulate T-cell → cytokine storm → systemic inflammation
➢ Enterotoxin – food poisoning acting as superAg
Stages of disease Local infection
➢ Skin & soft tissue involvement – boils & cellulitis
Invasive infection
➢ Bacteremia/endocarditis
Systemic infection
➢ SSSS/TSST
S&S Pyogenic
➢ Skin & soft tissue infection
➢ Abscess
➢ Conjunctivitis
➢ Mastitis
Toxin mediated
➢ Gastroenteritis
➢ TSS
Fever, hypotension, diffuse macular & sunburn like rash
➢ SSS
Fever, large bullae & erythematous macular rash. Large area of skin slough, serous fluid exude & electrolyte imbalance
Kawasaki syndrome (unknown etiology)
➢ Suspected to be due to certain strain of S. aureus
Complication Systemic infection
➢ Toxic shock syndrome
➢ Bacteremia
➢ Endocarditis
➢ Pneumonia
➢ Osteomyelitis
Lab diagnosis Specimen from: -
➢ Abscess, wound & burns pus – use swab
➢ Sputum
➢ Vomit/feces
➢ Blood
➢ Midstream urine
➢ Nasal/perineal swab
Mannitol salt agar
➢ S. aureus grows & ferment mannitol
➢ Yellow colonies (due to pH change)
Blood agar
➢ Light – golden yellow pigment
Catalase+
Coagulase+
PCR for mecA in SA
Differential diagnosis Streptococcus pyogenes – skin infection
Pseudomonas aeruginosa – wound infection
Clostridium perfringens – necrotizing infection
Treatment & management Methicillin (now has MRSA)
Vancomycin (but now ↑risk of VRSA)
, Daptomycin/quinupristin-dalfoprinstin
Surgical drainage for pus collection
IV fluid to prevent multi-organ failure in TSS
S. epidermidis – vancomycin (+rifampicin for CNS infection)
S. saprophyticus – trimethoprim/fluoroquinolone
Prevention Resistant to dry condition & ↑salt []
Hand antiseptic
Proper cleaning of wound
Aseptic catheter use
Causal organism Streptococcus pyogenes
Commensal
Lancefield & hemolysis classification
Group A – S. pyogenes
Group B – S. agalactide (both A & B is beta-hemolytic)
Group D – Enterococcus (gamma-hemolytic)
Viridans group streptococci – most common for endocarditis (alpha hemolysis)
S. pneumonia – alpha-hemolytic
Disease Phayngitis, scarlet fever, necrotizing fasciitis, rheumatic fever & acute glomerulonephritis
Morphology Gram+ in chain/pairs
Non-spore, non-motile
Facultative anaerobes
Catalase-
Group A lancefield group
Virulence factor Adhesion, hemolysin, M protein, capsule, C5a peptidase, streptolysin (O & S) – hemolysin, pyrogenic exotoxins, hyaluronidase, streptokinase,
lipoproteinase, DNAases
Epidemiology Leading cause of pharyngitis & cellulitis
MOT Wound inoculation, respiratory droplets, direct contact
RF ➢ Immune suppression
➢ Poor hygiene
➢ Skin injuries
Pathogenesis Entry & colonization
➢ Lipoteichoic acid & M protein – aid in adhesion
Immune evasion
➢ M protein – interfere w complement activation preventing opsonization
➢ C5a peptidase – no recruitment of neutrophil
➢ Capsule – hyaluronic acid mimic CT to evade immune
Tissue invasion
➢ Streptolysin O – lyses RBC → tissue necrosis
➢ Streptolysin S – beta-hemolysis
➢ Hyaluronidase – allow bacteria spread to deeper tissue
➢ Streptokinase – plasminogen → fibrin which break fibrin clot
➢ Lipoproteinase – aid in skin colonization
➢ DNAases - ↓viscosity allow spread
Toxin production & systemic spread
➢ Pyrogenic exotoxin – superAg → overstimulate T-cells → cytokine storm → systemic inflammation → shock
Persistent infection
➢ M protein – autoimmune reaction due to molecular mimicry → rheumatic fever & post-streptococcal GN
Stages of disease Localized infection
Toxin mediated disease
Immune mediated sequelae
S&S Pyogenic
➢ Pharyngitis
➢ Cellulitis
➢ Necrotizing fasciitis
Toxigenic
➢ Scarlet fever
➢ TSS
Immunologic
➢ Rheumatic fever
➢ AGN
Complication Rheumatic heart disease, endocarditis, post-streptococcal GN, necrotizing fasciitis, toxic shock-like syndrome
Lab diagnosis Blood agar with beta-hemolysis
Bactracin susceptibility test – is bacitracin sensitive
Elevated ASO titer for sequelae
Differential diagnosis Staphylococcus aureus – skin infection
Cornebacterium diphtheriae – pharyngitis
EPV – mononucleosis
Treatment & management Group A use penicillin G/amoxicillin
Erythromycin/clindamycin for penicillin allergy
S. pyogene has not been resistant to penicillin
Prevention Rheumatic fever can be prevented by treatment of bacteria w penicillin G
Prevention of streptococcal infection w benzathine penicillin
Causal organism Streptococcus agalactiae
Disease Neonatal sepsis, meningitis, pneumonia, postpartum infection, UTI & soft tissue infection
Morphology Gram+ cocci in chain
Virulence factor Capsule, C5a peptidase, adhesin, beta-hemolysin & hyaluronidase
Epidemiology
MOT Vertical, sexual transmission & direct contact
RF ➢ IC
➢ DM
, ➢ Maternal infection
➢ Newborn
Pathogenesis Adhesion
➢ Attach to epithelial cell allow colonization
Evasion of immune system
➢ Capsule – prevent phagocytosis as it mimic host molecules
➢ C5a peptidase – impair neutrophils recruitment
Tissue invasion
➢ Hyaluronidase – facilitate spread through deeper tissue
➢ Beta-hemolysin – lysis of RBC
Systemic spread
➢ Bacteremia & cross BBB
Stages of disease Early onset disease – symptoms within 7 days of life
Late onset disease – symptoms btw 7 days – 3 months
S&S Neonate: -
➢ Respiratory distress
➢ Lethargy
➢ Poor feeding
➢ Fever
➢ Irritability
Adult
➢ Fever
➢ Pelvic pain
➢ Dysuria
➢ Sepsis
Complication Neonatal meningitis, pneumonia, septicemia, septic arthritis, endocarditis, stillbirth & postpartum endometritis
Lab diagnosis Gram stain w gram+
Blood agar shows beta-hemolytic buttery area (smaller)
Bacitracin susceptibility test – bacitracin resistant
PCR for GBS DNA
Serology test in CSF
Differential diagnosis Streptococcus pneumoniae – pneumonia & meningitis
Escherichia coli – neonatal sepsis
Listeria monocytogenes – neonatal meningitis
Treatment & management Penicillin G/ampicillin
Allergic to penicillin – cephalosporin/vancomycin
Prevention Routine GBS screening for pregnant women
Prophylactic intrapartum antibiotic
Causal organism Streptococcus pneumoniae
Commensal in mouth & pharynx
Disease Pneumococcal pneumonia/meningitis, sinusitis, otitis media & bacteremia
Morphology Gram+ cocci in pair/chains/lancet-shaped
Virulence factor Phosphorycholine, polysaccharide capsule, adhesin, IgA protease, pneumolysin, C-substance
Epidemiology Common in children & elderly
Most common cause of community-acquired pneumonia & meningitis
MOT Respiratory droplets
RF ➢ Children
➢ Head trauma – spinal fluid leak to nose predispose to pneumococcal meningitis
Pathogenesis Entry into upper respiratory tract
➢ IgA protease – allow colonization
Spread to alveoli
➢ Outpouring of RBC & WBC → lung consolidation
➢ Capsular polysaccharides & anticapsular Ab – protective
➢ Lipoteichoic acid – activates complements & cytokine production
➢ Pneumolysin – causes alpha-hemolysis
S&S Pneumonia
➢ Fever
➢ Sudden chills
➢ Cough
➢ Pleuritic pain
Complication Pneumococcal pneumonia/meningitis & bacteremia
Lab diagnosis Gram stain of sputum – red/brown rusty color
Blood agar w unpigmented alpha-hemolysis
Optochin susceptibility test – sensitive
Bile soluble
Quellung reaction+ – anti-capsular Ab causes bacteria’s capsule to swell
CSF culture – if meningitis+
Latex agglutination test
Treatment & management Penicillin G (DOC)/erythromycin
Vancomycin for penicillin resistant pneumococci
Prognosis Spontaneous recovery can occur within 5-10 days + anticapsular Ab
➢ When pneumococci are phagocytized leading to recovery of consolidation
Prevention 2 pneumococcal vaccine
➢ 13-valent conjugate vaccine
➢ 23-valent conjugate vaccine
Purified capsular vaccine – long-term immunity
Causal organism Viridans group of Streptococcus
mutans & sanguis
Disease Dental caries & dental plaque
Morphology Gram+ cocci
Lack group-specific carbs to be grouped into Lancefield
No capsule
MOT Inhabitant in mucosal areas
Complication Bacteremia → meningitis & endocarditis
Lab diagnosis Blood agar w alpha hemolysis
Not bile soluble
Optochin susceptibility test – resistant
Quellung test- no capsule
Causal organism Staphylococcus aureus
Commensal
S. epidermidis – most common cause of endocarditis, prosthetic joint infection, CNS shunt infection & newborn sepsis (coagulase- & catalase+)
S. saprophyticus – UTI & cystitis
Other gram+ cocci includes: -
➢ Enterococcus
➢ Peptostreptococcus
➢ Streptococcus
Disease Skin infections (impetigo, cellulitis, abscesses), pneumonia, Ritter disease (SSSS), osteomyelitis, endocarditis, toxic shock syndrome, food poisoning
Morphology Gram+ cocci in cluster (in grape shaped)
Non-sporing, non-motile, non-capsulated & non-spore forming
Facultative anaerobes (can grow w/o O2)
Catalase+
Low G + C
2 important gram+ cocci include Staphylococcus & Streptococcus
Virulence factor Peptidoglycan, teichoic acid, protein A, clumping factor, alpha, beta lysin, gamma lysin, epidermolytic/exfoliative toxin (Type A & B), cytolytic toxin, Toxic
shock syndrome toxin (TSST), enterotoxin (type A-E & G-J), catalase, coagulase, hyaluronidase, nucleases, staphylokinase, lipase, beta-lactamase
Epidemiology One of the most common cause of hospital-acquired pneumonia
MRSA is the most common cause of skin abscess in the US
MOT Human nose is the main site of S. aureus colonization
Direct contact & air-borne
RF ➢ Immunocompromised
➢ Burn victim
➢ Indwelling catheters
Pathogenesis Entry & colonization
➢ Peptidoglycan – stimulate TLR → inflammation &
➢ Teichoic acid – promote adherence to mucosal
➢ Clumping factor – binds to fibrinogen promote aggregation
Immune evasion
➢ Protein A – binds to IgG preventing phagocytosis
➢ Coagulase – form fibrin to create clot around bacteria
➢ Staphylokinase – dissolve clot when need to escape
➢ Beta-lactamase
Tissue invasion & spread
➢ Hyaluronidase – facilitate further bacterial spread
➢ Lipase – promote survival in fatty environment
➢ Nuclease – ↓viscosity in pus enabling movement
Toxin mediated damage
➢ Alpha, beta & gamma lysin – lyse cell & impair immune
➢ Exfoliative toxin – cleave desmoglein → SSS
➢ TSST – superAg overstimulate T-cell → cytokine storm → systemic inflammation
➢ Enterotoxin – food poisoning acting as superAg
Stages of disease Local infection
➢ Skin & soft tissue involvement – boils & cellulitis
Invasive infection
➢ Bacteremia/endocarditis
Systemic infection
➢ SSSS/TSST
S&S Pyogenic
➢ Skin & soft tissue infection
➢ Abscess
➢ Conjunctivitis
➢ Mastitis
Toxin mediated
➢ Gastroenteritis
➢ TSS
Fever, hypotension, diffuse macular & sunburn like rash
➢ SSS
Fever, large bullae & erythematous macular rash. Large area of skin slough, serous fluid exude & electrolyte imbalance
Kawasaki syndrome (unknown etiology)
➢ Suspected to be due to certain strain of S. aureus
Complication Systemic infection
➢ Toxic shock syndrome
➢ Bacteremia
➢ Endocarditis
➢ Pneumonia
➢ Osteomyelitis
Lab diagnosis Specimen from: -
➢ Abscess, wound & burns pus – use swab
➢ Sputum
➢ Vomit/feces
➢ Blood
➢ Midstream urine
➢ Nasal/perineal swab
Mannitol salt agar
➢ S. aureus grows & ferment mannitol
➢ Yellow colonies (due to pH change)
Blood agar
➢ Light – golden yellow pigment
Catalase+
Coagulase+
PCR for mecA in SA
Differential diagnosis Streptococcus pyogenes – skin infection
Pseudomonas aeruginosa – wound infection
Clostridium perfringens – necrotizing infection
Treatment & management Methicillin (now has MRSA)
Vancomycin (but now ↑risk of VRSA)
, Daptomycin/quinupristin-dalfoprinstin
Surgical drainage for pus collection
IV fluid to prevent multi-organ failure in TSS
S. epidermidis – vancomycin (+rifampicin for CNS infection)
S. saprophyticus – trimethoprim/fluoroquinolone
Prevention Resistant to dry condition & ↑salt []
Hand antiseptic
Proper cleaning of wound
Aseptic catheter use
Causal organism Streptococcus pyogenes
Commensal
Lancefield & hemolysis classification
Group A – S. pyogenes
Group B – S. agalactide (both A & B is beta-hemolytic)
Group D – Enterococcus (gamma-hemolytic)
Viridans group streptococci – most common for endocarditis (alpha hemolysis)
S. pneumonia – alpha-hemolytic
Disease Phayngitis, scarlet fever, necrotizing fasciitis, rheumatic fever & acute glomerulonephritis
Morphology Gram+ in chain/pairs
Non-spore, non-motile
Facultative anaerobes
Catalase-
Group A lancefield group
Virulence factor Adhesion, hemolysin, M protein, capsule, C5a peptidase, streptolysin (O & S) – hemolysin, pyrogenic exotoxins, hyaluronidase, streptokinase,
lipoproteinase, DNAases
Epidemiology Leading cause of pharyngitis & cellulitis
MOT Wound inoculation, respiratory droplets, direct contact
RF ➢ Immune suppression
➢ Poor hygiene
➢ Skin injuries
Pathogenesis Entry & colonization
➢ Lipoteichoic acid & M protein – aid in adhesion
Immune evasion
➢ M protein – interfere w complement activation preventing opsonization
➢ C5a peptidase – no recruitment of neutrophil
➢ Capsule – hyaluronic acid mimic CT to evade immune
Tissue invasion
➢ Streptolysin O – lyses RBC → tissue necrosis
➢ Streptolysin S – beta-hemolysis
➢ Hyaluronidase – allow bacteria spread to deeper tissue
➢ Streptokinase – plasminogen → fibrin which break fibrin clot
➢ Lipoproteinase – aid in skin colonization
➢ DNAases - ↓viscosity allow spread
Toxin production & systemic spread
➢ Pyrogenic exotoxin – superAg → overstimulate T-cells → cytokine storm → systemic inflammation → shock
Persistent infection
➢ M protein – autoimmune reaction due to molecular mimicry → rheumatic fever & post-streptococcal GN
Stages of disease Localized infection
Toxin mediated disease
Immune mediated sequelae
S&S Pyogenic
➢ Pharyngitis
➢ Cellulitis
➢ Necrotizing fasciitis
Toxigenic
➢ Scarlet fever
➢ TSS
Immunologic
➢ Rheumatic fever
➢ AGN
Complication Rheumatic heart disease, endocarditis, post-streptococcal GN, necrotizing fasciitis, toxic shock-like syndrome
Lab diagnosis Blood agar with beta-hemolysis
Bactracin susceptibility test – is bacitracin sensitive
Elevated ASO titer for sequelae
Differential diagnosis Staphylococcus aureus – skin infection
Cornebacterium diphtheriae – pharyngitis
EPV – mononucleosis
Treatment & management Group A use penicillin G/amoxicillin
Erythromycin/clindamycin for penicillin allergy
S. pyogene has not been resistant to penicillin
Prevention Rheumatic fever can be prevented by treatment of bacteria w penicillin G
Prevention of streptococcal infection w benzathine penicillin
Causal organism Streptococcus agalactiae
Disease Neonatal sepsis, meningitis, pneumonia, postpartum infection, UTI & soft tissue infection
Morphology Gram+ cocci in chain
Virulence factor Capsule, C5a peptidase, adhesin, beta-hemolysin & hyaluronidase
Epidemiology
MOT Vertical, sexual transmission & direct contact
RF ➢ IC
➢ DM
, ➢ Maternal infection
➢ Newborn
Pathogenesis Adhesion
➢ Attach to epithelial cell allow colonization
Evasion of immune system
➢ Capsule – prevent phagocytosis as it mimic host molecules
➢ C5a peptidase – impair neutrophils recruitment
Tissue invasion
➢ Hyaluronidase – facilitate spread through deeper tissue
➢ Beta-hemolysin – lysis of RBC
Systemic spread
➢ Bacteremia & cross BBB
Stages of disease Early onset disease – symptoms within 7 days of life
Late onset disease – symptoms btw 7 days – 3 months
S&S Neonate: -
➢ Respiratory distress
➢ Lethargy
➢ Poor feeding
➢ Fever
➢ Irritability
Adult
➢ Fever
➢ Pelvic pain
➢ Dysuria
➢ Sepsis
Complication Neonatal meningitis, pneumonia, septicemia, septic arthritis, endocarditis, stillbirth & postpartum endometritis
Lab diagnosis Gram stain w gram+
Blood agar shows beta-hemolytic buttery area (smaller)
Bacitracin susceptibility test – bacitracin resistant
PCR for GBS DNA
Serology test in CSF
Differential diagnosis Streptococcus pneumoniae – pneumonia & meningitis
Escherichia coli – neonatal sepsis
Listeria monocytogenes – neonatal meningitis
Treatment & management Penicillin G/ampicillin
Allergic to penicillin – cephalosporin/vancomycin
Prevention Routine GBS screening for pregnant women
Prophylactic intrapartum antibiotic
Causal organism Streptococcus pneumoniae
Commensal in mouth & pharynx
Disease Pneumococcal pneumonia/meningitis, sinusitis, otitis media & bacteremia
Morphology Gram+ cocci in pair/chains/lancet-shaped
Virulence factor Phosphorycholine, polysaccharide capsule, adhesin, IgA protease, pneumolysin, C-substance
Epidemiology Common in children & elderly
Most common cause of community-acquired pneumonia & meningitis
MOT Respiratory droplets
RF ➢ Children
➢ Head trauma – spinal fluid leak to nose predispose to pneumococcal meningitis
Pathogenesis Entry into upper respiratory tract
➢ IgA protease – allow colonization
Spread to alveoli
➢ Outpouring of RBC & WBC → lung consolidation
➢ Capsular polysaccharides & anticapsular Ab – protective
➢ Lipoteichoic acid – activates complements & cytokine production
➢ Pneumolysin – causes alpha-hemolysis
S&S Pneumonia
➢ Fever
➢ Sudden chills
➢ Cough
➢ Pleuritic pain
Complication Pneumococcal pneumonia/meningitis & bacteremia
Lab diagnosis Gram stain of sputum – red/brown rusty color
Blood agar w unpigmented alpha-hemolysis
Optochin susceptibility test – sensitive
Bile soluble
Quellung reaction+ – anti-capsular Ab causes bacteria’s capsule to swell
CSF culture – if meningitis+
Latex agglutination test
Treatment & management Penicillin G (DOC)/erythromycin
Vancomycin for penicillin resistant pneumococci
Prognosis Spontaneous recovery can occur within 5-10 days + anticapsular Ab
➢ When pneumococci are phagocytized leading to recovery of consolidation
Prevention 2 pneumococcal vaccine
➢ 13-valent conjugate vaccine
➢ 23-valent conjugate vaccine
Purified capsular vaccine – long-term immunity
Causal organism Viridans group of Streptococcus
mutans & sanguis
Disease Dental caries & dental plaque
Morphology Gram+ cocci
Lack group-specific carbs to be grouped into Lancefield
No capsule
MOT Inhabitant in mucosal areas
Complication Bacteremia → meningitis & endocarditis
Lab diagnosis Blood agar w alpha hemolysis
Not bile soluble
Optochin susceptibility test – resistant
Quellung test- no capsule
