Staph & Strep

Claffification of G+ Cocci

Staphylococci habitat

Skin, mucosa of anterior nares, vagina, and inanimate objects

S. aureus habitat

Nares, ears, groin.

10-30% of healthy people carry staph
5-10% vaginal carriage (increases during menses

S. aureus Virulence factors

• MSCRAMMs - Binds many ECM proteins

  • Clumping factors A&B (Bound Coagulase) - Bind fibrinogen and platelets → Aggregates *Important for UB

  • Fibronectin-binding proteins A&B (Fnbp A&B) - Helps in invasion (Attachment to exposed fibronectin in open wounds)

  • Collagen-binding adhesins (CNAs) → Invasion of CT, bones, joints

• Teichoic acid - Promotes colonizattion

• S layer - Antiphagocytic

• Protein A

• Coagulase

• Staphylokinase

• Hyaluronidase

• Lipase

• Nuclease

• Catalse

• Beta-lactamase

*Note: Staphylokinase coagulase are synthesized at different times (Invasion vs spread)

S. aureus toxins

Cytolytic axotoxins:

• Alpha hemolysin → Membrane-damaging toxin → Septic shock

• Beta hemolysin → Sphingomyelinase

• Panton-Valentine Leucocidin (PVL) → Lyses leukocytes → Maaive inflammation (Important in MRSA)

Superantigen exotoxins:

• Enterotoxins: A,B,C(1/2/3),D,E,H

• TSST

• Exfoliatin (SSSS)

S. aureus diseases (Everything)

Skin: Folliculitis, furuncle, carbuncle, abscess, wound infection, impetigo, paronychia, cellulitis

Soft tissue: Osteomyelitis, arthritis

RT: Bronchopneumonia, tonsillitis, pharyngitis, sinusitis, lung abscess, pneumonia

CNS: Brain abscess, meningitis, tntracranial thrombophlebitis

Endovascular: Bacteremia, septicemia, endocarditis

UT: Implants and catheters

Nosocomial infections (MRSA)

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• Staphylococcal food poisoning: Fast-acting, heat-resistant, preformed toxins. Mainly type A enterotoxin no more than 1 day - Sliced meat, puddings, pastries, milk, cheese

• STTS: Mainly caused by TSST-1 - Vaginal tampons→ Fever, vomitting, diarrhea, rash, desquamation, shock, end-organ failure, and high AST/ALT/bilirubin

• SSSS: Outer layer of the epidermis is separated from underlying tissue,

  • Newborns: Ritters’ Disease

  • Older patients: Toxic epidermal necrolysis

  • Milder forms: Pamphigus neonatorum/ Bullous impetigo

• Kawasaki: Inflammatory disease with potential heart

S. aureus biochemistry and selective characteristics

• OX -

• CAT +

• Coagulase + (free and bound)

• Mannitol +

• PYR A -

• Phosphatase +

• Tnase + (thormostable DNase)

Seletive stuff:

• Can grow in 10-15% NaCl

• Penicillin-resistant

S. aureus treatment

Drain abscess

If deep infection, need:

• Advanced penicillins

• Cephalosporins

• Erythromycin

• Clindamycin

If endocarditis:

• NODs + an AG

Life-threatening → Vancomycin

Choose based on sensitivity testing

Describe S. aureus resistance

First, penicillinases, then chromosomally encoded modified PBP, and also plasmid-borne resistance to erythromycin, tetracyclines, AGs, and almost all antibiotics

Describe CAMRSA. Reservoirs/ resistance mechanism/ virulence/ treatment

Reservoir: Healthy people and people who’ve had medical procedures, specifically: damaged skin, groin, oropharynx.

Resistance: mecA gene product: PBP2a

Virulence: PVL

Treatment: Vancomycin and teicoplanin - GLYCOPEPTIDES

Coagulase-negative Staph infection risk factors

Implants

Coagulase-negative Staph lab characteristics

Similar to S. aureus but white colonies and coagulase-negative

Clinical picture of Coagulase-negative Staph

Infect prosthetic valves → Endocarditis
Contaminate blood cultures (Mainly S. epidermidis)
UTIs in pregnant women (S. Saprophyticus)

Coagulase-negative Staph treatment

Beta-lactams/ Vancomycin

S. saprophyticus treatment

TMP-SMX/ Quinolones

Biochem differences among Staphylococci (Coagulase / Mannitol / Phosphatase / Novobiocin sensitivity)

Treatment of Coagulase-negative staph

Bacitracin

Chlorohexidine (locally)

Vancomycin

Sreptococcus geus characteristics

G+, Non-motile, FA, fermentative metabolism of carbohydrates

Penicillin-sensitive

Commensals, parasites, saprophytes

GAS habitat

Pharynx (mainly) and skin
→ Obligate human pathogen, but it can be carried asymptomatically

S. pyogenes virulence factors and exotoxins

Virulence factors:

• Streptolysin O - SLO (O2-labile) → Damages cardiac cells (Ca2+ influx)

  • Note: Highly antigenic: Anti-SLO (ASLO) titer is a marker for infection recency

• Streptolysin S - SLS → Oxygen stable, non-antigenic

• Hyaluronic acid capsule - Immune mimicry

• M-like proteins: Bind IgM and IgG - STRUCTURALLY SIMILAR TO MYOSIN

• LM-Protein: Adhesins and antiphagocytics

• F-Protein: Adherence

• Phage lysogeny → Steptococcal Pyrogenic Exotoxin

Exotoxins:

• Streptococcal Pyrogenic Exotoxin (SPEs) → SCARLET FEVER

• Exoenzymes: Streptokinase/ Streptodornase (DNase) → ASDOR/ Hyaluronidase

Sterptococcus pyogenes diseases

• Pharyngitis & tonsilitis

  • If lysogenized → Scarlet fever: Sand-paper-like upper body rash + Strawberry tongue

• Otitis media

• Sinusitis

• Pneumonia

How can you differentiate Streptococcal pharygitis from viral

In strep infection, symptoms will also include: headache, nausea, vomiting, and abdominal pain. In viral, it’s common-cold like only.

Strep: Tonsillar eudates. None in viral

Strep: Painful cervical adenopathy, in viral, adenopathy can occur but it’s painless

Streptococcus pyogenes Cutenous and soft tissue infections

Impetigo (Contagious pyoderma - honey-crusted lesions)

Erysipelas (Upper dermis + superficial lymphatics)

Cellulitis (Deep dermis and subcutaneous fat)

Necrotizing fasciitis (Subcutaneous fat + fascia → Destruction of muscle and fat)

• (May or not progress from erysipelas to cellulitis to NF)

Wound infections

Lymphangitis (Inflammation of

Describe the clinical appearance of Erysipelas

You will find Erythema + Bullae (It’s only seen in Strep, not staph)

Streptococcal pyogenes systemic disease

Streptococcal toxic shock-like syndrome
Bacteremia

Sequelae of Strep infections

Acute rheumatic fever (ARF) - T2HS, Follows pharyngitis

Rheumatic heart disese (RHD) - T2HS, Follows pharyngitis

Acute glomerulonephritis (AG) - T3HS, usually follows pyoderma

S. pyogenes diagnosis

Rapid antigen test (95% Specificity, but only 70-90% sensitive)

Culture: Done in 5-10% CO2, on BA + NA → Produce B-hemolytic colonies, HOWEVER, some strains are ALPHA-HEMOLYTIC
*Note, their capsules make the colony appearances look mucoid

ASLO/ASDOR titer: Helps us to diagnose Strep complications

S. pyogenes biochemistry

• Ox -

• Cat -

• Bacitracin S

GBS habitat

Low GIT (normal flora)
Female genital tract (Newborns at ris if females have it)

GBS pathognicity

• Neonatal disease and obstetrics complications

• Neonatal meningitis

• Puerperal sepsis

• Pneumonia

• Systemic, cutenous, and urinary infections

GBS specimen and culture

Specimen: CNS, blood, vagina/rectal smears, urine

Culture: 5-10% CO2 on BA + Colistin (inhibit G- enterics)+ NA (inhibit G+ cocci)

→ Should get Beta-hemolytic colonies, but some strains are gamma-hemolytic

GBS screening

Screen pregnant women at 35-37 weeks of gestation with vaginal and rectal swabs, if + → Give prophylaxis

GBS biochemistry

• Ox -

• Cat -

• Esculin -

• Hippurate +

• Bacitracin R

• CAMP test +

What’s S. pneumoniae among strep, and what is its habitat

It’s an alpha-hemolytic streptococcus

Inhabitant of URT of 40-70% of people

S. pneumoniae types distribution, and. general epidemiology

Pneumococci types 1-8 → adults
Pneumococci types 6 + anything above 8 = Children

They are responsible for 60% of all bacterial pneumonias

Risk factors for S. pneumoniae pneumonia

• Viral and other infections OF URT

• Alcohol or drug intoxication

• Circulatory system pathologies

• Malnutrition

• Sickle cell

• Hyposplenia and asplenia (Encapsulated pathogens)

• Nephrosis

• Complement deficency

S. pneumoniae virulence factors

• Capsule

• Choline-binding protein A → Adhesin

• Neuraminidases → Help invade nasopharynx

• Proteases → Degrades IgG, IgM, IgA

• Pneumolysin O → Cytolytic to eukaryotic cells

• H2O2 → Damage host cells and competing microbiota (NHS (S here is S. aureus)

Pneumococal diseases (10)

• Acute lobar pneumonia

• Pneumococcal pneumonia → Rusty sputum

• Bacteremia

• Bacterial meningitis in children

• AOM

• Sinusitis

• Peicarditis

• Conjuctivitis

• Arthritis

• Peritonitis

S. pneumoniae morphological characteristics

G + diplococci

Capsulated

S. pneumoniae culture

Sputum is gold standard:

• 5-10% CO2

• Choline

• BA + NA → Alpha hemolytic colonies

• Enrich with defibrinated blood

S. pneumoniae

• Ox -

• Cat -

• Optichin S

• Bile soluble

S. pneumoniae serology

• Detection of pneumococcal antibodies and capsular polysaccharide Ag in urine or CSF

• PCR

Note: Non-beta hemolytic strep are called: Non-lancefield Group streptococci

S. pneumoniae treatment

Based on sensitivity testing

Penicillin, 3rd gen cephalosporins, imipenem, vancomycin

S. pneumoniae vaccine

Conjugate or polysaccharide pneumococcal vaccines

Describe the Viridans

They’re normal oral/nasopharyngeal flora
Include: S .mutant/sanguis/salivarius/mitis

Common post-tooth axtraction bacteremia → They implant on damaged or prosthetic heart valves

*S. sanguis specifically is the most common cause of subacute bacterial endocaditis

Prior to tooth extraction procedure, must always give antibiotics 2 days prior

Lab diagnosis of viridans

Hemoculture

Growth on BA + NA + Colistin in 5-10% CO2

→ Alpha hemolytic, but can be gamma

Viridans biochem

Optichin R

PYRA -

Group D enterococcus and their infections

E. faecalis and E. faecium

Nosocomial infections (VREs):
UTIs/Wound infections/ bacteremia/ endocarditis/ Intrabdominal abscesses

Enterococci culture

5-10% CO2

BA + NA + Colistin → Alpha/beta/gamma (wow)

OE

BEA - Bile esculin agar (Enterococci degrade esculin in the presence of iron and give off a black coloration)

Enterococci labs

Non-enterococcus Group D strep

S. gallolyticus → Alpha-hemolytic

NOTE: Patients with S. gallolyticus endocarditis have a higher incidence of colon cancer

Group G streptococcus

S. anginosus / S. constellatus/ S. intermidius

Can cause deep pyogenic abscesses

Culture on: BA + NA + Colistin → alpha/beta/gamma
→ Caramel odor due to diacetyl metabolite