Gram positive staphylococci and streptococci l.jpg
This presentation is the property of its rightful owner.
Sponsored Links
1 / 40

Gram-positive: Staphylococci and Streptococci PowerPoint PPT Presentation


  • 197 Views
  • Uploaded on
  • Presentation posted in: General

Gram-positive: Staphylococci and Streptococci. Medical Microbiology SBM 2044. Staphylococcus aureus. The most common pus-forming (pyogenic) bacteria Can produce focal abscess, from the skin (furuncles, boils) to the lungs, osteomyelitis, kidneys and endocarditis

Download Presentation

Gram-positive: Staphylococci and Streptococci

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -

Presentation Transcript


Gram positive staphylococci and streptococci l.jpg

Gram-positive: Staphylococci and Streptococci

Medical Microbiology

SBM 2044


Staphylococcus aureus l.jpg

Staphylococcus aureus

  • The most common pus-forming (pyogenic) bacteria

  • Can produce focal abscess, from the skin (furuncles, boils) to the lungs, osteomyelitis, kidneys and endocarditis

  • Include S. aureus, S. epidermidis, S. saprohyticus (UTI)

  • S. aureus can persist in the body because they have numerous cell surface virulence, exotoxins and enzymes


S aureus l.jpg

S. aureus

  • Staphylo = grape clusters (Greek)

  • A large 1µm Gram-positive coccus growing in cluster-of-grapes shape.

  • Can survive in long period of dry, on inanimate object. Heat resistant.

  • Identification: large, creamy colonies on nutrient agar; catalase +


Staphylococci l.jpg

Staphylococci


S aureus5 l.jpg

S. aureus

Encounter

  • Major reservoirs = humans

  • Live on skin – grow at high salt and lipid concentrations because they make lipases and glycerol ester hydrolases, that degrade skin lipids

  • Colonise skin and mucosal surfaces using MSCRAMMs:

    • Fibronectin–binding proteins (FnbpA, FnbpB)

    • Collagen-binding

    • Clumping factors A and B

  • Spread person-to-person by direct contact or airborne


S aureus pathogenesis l.jpg

S. aureus pathogenesis

  • Entry

  • Tissue penetration upon skin or mucosal membrane damaged by cut

  • Spread and Multiplication

  • Survival in tissues dependon

    • no. of entering microorganisms

    • site involved

    • speed of body’s inflammatory responses

    • immunological history of the host


S aureus pathogenesis7 l.jpg

S. aureus pathogenesis

  • Damage

  • Local infections  pus collection, i.e. abscess

  • Staphylococci can spread into subcutaneous and submucosal tissues and caused cellulitis

  • Activate acute inflammatory reaction, pouring in chemotactic factors

  • Damaged area are usually localised by the formation of thick-walled fibrin capsule : center of abscess is necrotic with debris of dead cells

  • Why many virulence factors?


Slide8 l.jpg

  • Surface structures:

  • Capsules – inhibit phagocytosis

  • Peptidoglycan – interacts with TLR-2, activate alternative pathway

  • Teichoic acid – C’ activation and adherence to mucosal cells

  • Protein A – binds to Fc terminus of IgG

  • Secreted factors:

  • Catalase – H2O2 H2O

  • Coagulases – fibrinogen  fibrin

  • Pore-forming toxins – create channels to disturb cellular homeostasis

  • Haemolysins –

  • Leukocidin

  • Hyaluronidase – hydrolyse matrix of connective tissues

  • Β-lactamase – hydrolyse penicillin

  • Penicillin-binding protein (PBP2a)


S epidermidis l.jpg

S. epidermidis

  • Normal flora, rarely caused disease

  • Infections of S. epidermidis with other catalase-negative staphylococci in patients implanted with artificial devices e.g. prosthetic joints or IV catheters

  • Results in septicaemia and endocarditis

  • Possibly peptidoglycan or slime layer allows the organisms to stick to the surface of plastics


S saprophyticus l.jpg

S. saprophyticus

  • Caused cystitis in young women


Staphylococcal toxin diseases l.jpg

Staphylococcal toxin diseases

  • Staphylococcal scalded skin syndrome (SSSS)

    • Exfoliative toxins A and B – highly tissue specificserine proteases that causes separation of the layers of the epidermis at the desmosomes

  • Staphylococcal toxic shock syndrome (TSS)

    • characterised by fever, skin rash, hypotension, peeling of the skin

    • use tampons – oxygenated vagina and stimulate toxin production

    • TSST-1, staphylococcal enterotoxins AE

  • Virulence gene regulation – two-component regulatory systems

    • Accessory gene regulator (Agr), staphylococcal respiratory response (Srr)


Slide12 l.jpg

  • Diagnosis

  • Gram stain and culture

  • Treatment

  • Methicillin-sensitive S. aureus – Rx: semi-synthetic penicillins and cephalosporins

  • Methicillin-resistant S. aureus – Rx: vancomycin

  • vancomycin-resistant S. aureus –acquired the genes of resistance from vancomycin-resistant Enterococcus species


Streptococci l.jpg

Streptococci

  • Classification

    • Haemolytic pattern – in blood agar media, colonies formed may be surrounded by a clear zone of haemolysis (α,β, γ)

    • Group-specific antigens (Lancefield classification) – by serological reactivity of extracted cell wall antigens (A  U)

    • Species – biochemical tests


Slide14 l.jpg

  • Homofermentative

[Glucoselactic acid]

Streptococcus

  • Gram-positive

  • Grow in chains

  • Non-motile

  • Facultative anaerobes

  • Early studies distinguished 3 broad groups on blood agar

  • a-haemolytic

  • non-haemolytic

  • b-haemolytic


Slide15 l.jpg

  • Streptococci


Slide16 l.jpg

  • GAS diseases – changing patterns

  • Changes in virulence of prevailing GAS strains ?

  • Changes in social conditions – less crowding?

  • Changes in herd immunity to prevailing virulent strains?

  • Reemergence of severe invasive infections

  • Sporadic cases since mid-1980s – new virulent strains?

  • Streptococcal toxic shock

  • Some cases associated with obviously severe tissue infections

  • Many others – shock following mild or unapparent infections

  • Sporadic – implies predisposing factors


Group a streptococci l.jpg

Group A Streptococci

  • Epidemiology

    • Ubiquitous worldwide

    • Common diseases are acute pharyngitis or pyoderma infections (skin and soft tissues)

  • Encounter

    • Carriers appear asymptomatic

    • Person-to-person spread is mediated by respiratory droplets or by direct contact to skin

  • Entry

    • For pyodermal infections, streptococci need to gain entry into deeper layers of skin

    • In pharyngeal infections, to prevent from being swept away, GAS must lipoteichoic acid (LTA),protein F and M protein


Slide18 l.jpg

  • Spread and multiplication

    • Most GAS remain localised to the site of initial infection

    • In pharynx and tonsils, may result in erythema and exudate associated with strep throat

    • Peritonsillar abscess (quinsy) or spread to adjacent structures (mastoid and middle ear)

    • Impetigo in skin

    • Erysipelas and cellulitis in deeper layers of skin

    • GAS may spread laterally in deep tissues, by secreting enzymes

      • necrotizing fasciitis and myositis


Slide20 l.jpg

GAS virulence factors – Excreted products

  • Both lyse wide range of cells, including PMNs

  • suppuration and/or necrosis

  • Cytolytic toxins

  • Streptolyxin O (SLO)

Produced by all strains

  • Streptolysin S (SLS)

  • Various subtle effects at sub-lytic concentrations

  • SLO – ‘sensitive’ to O2

  • SLS – stable in O2

b-haemolysis

“Thiol-activated” toxin

(NB: Salyers & Whitt misleading - neither are “enzymes” )


Slide21 l.jpg

SLO- and SLS-defective mutants

  • murine s.c. model - weight loss at 24h post infection

Sterile

~3 x 108 cfu

~3 x 106 cfu

+ 0.5

~3 x 107 cfu

~3 x 105 cfu

~3 x 109 cfu

0.0

- 0.5

- 1.0

Weight gain (grams)

- 1.5

- 2.0

- 2.5

sloΔ1-

sagBΔ1

sagBΔ1

sloΔ1

WT

PBS


M protein l.jpg

M protein

  • Important for cell adherence to keratinocytes

  • Prevent opsonization by complement

    • bind to fibrinogen and interferes with the alternative pathway

    • bind with host complement control proteins and inhibit opsonins formation

  • Hypervariable regions of M protein are antigenic, but there are > 100 M protein serotypes


Hyaluronic acid capsule l.jpg

Hyaluronic acid capsule

  • Antiphagocytic structure on bacterial surface

  • Hyaluronic acid is abundant in human connective tissue - hence GAS can camouflaged themselves

  • But capsule may interfere with the adherence of GAS to epithelial cells

    • so GAS shed the capsule during the early stages of infection using hyaluronidase


Damage l.jpg

Damage

  • GAS can evoke an intense inflammatory responses in tissues

  • Streptococcal pyrogenic exotoxins (SPE)

    • SPE A, B and C cause rash, a characteristic of scarlet fever

    • SPE A and C are bacterial superantigens that activate a large subset of T cells

  • Immunologically mediated disease (nonsuppurative sequelae)

    • acute rheumatic fever (ARF)

    • acute post-streptococcal glomerulonephritis


Diagnosis l.jpg

Diagnosis

  • Impetigo – a cluster of small vesicles on a pink base that breaks down to honey-coloured crusts

  • Erysipelas – a raised, bright red patch of skin

  • More difficult to diagnose streptococcal pharyngitis

    • rapid strep tests

    • throat cultures (throat swab)


Treatment and prevention l.jpg

Treatment and Prevention

  • Penicillin – 10 day oral therapy

  • Erythromycin or other macrolide antibiotics for individuals allergic to penicillin


Slide27 l.jpg

  • M-type specific antigen was sensitive to proteases M proteins

Streptococcus pyogenes

  • Natural habitat: Humans

  • Strains distinguished by M serotyping

  • Devised by Lancefield in 1920s, using panels of absorbed sera

  • to hot-HCl extracted antigen, she called “M antigen”

  • > 100 distinct M types of GAS distinguished since then

  • - called M1, M2, M3, M4,……..etc.

  • Highly versatile pathogen

  • Suppurative infections

  • Toxinogenic diseases

  • Immunologically-mediated diseases


Slide28 l.jpg

Group A Streptococci

Principle sites

of infection:

Invasive infections

Local spread (e.g.)

Other tissues

Pharyngitis, tonsillitis,

otitis media, sinusitis.

Pharynx

Bacteraemia or septicaemia

Skinpyroderma, erysipelas

Occasionally

Streptococcal

Toxic Shock

Extensive necrosis

(necrotizing fasciitis)

Deep-seated

tissues

  • Puerperal fever (childbirth fever) in women – major killer in past


Slide29 l.jpg

Streptococcus pyogenes

Tonsillitis

Follicular tonsillitis


Slide30 l.jpg

Streptococcus pyogenes

Impetigo

Erysipleas

Cellulitis


Slide31 l.jpg

Streptococcus pyogenes

Necrotizing fasciitis

(< 24 hours post surgery)


Slide32 l.jpg

Streptococcus pyogenes


Slide33 l.jpg

Streptococcus pyogenes

Scarlet fever


Slide34 l.jpg

Toxic Shock

  • In past – probably linked to scarlet fever

  • Since mid-1980s – associated with ‘new’ highly virulent

    strains - rapidly fulminating

  • some cases in previously healthy young adults, no obvious

  • predisposing factors

  • Associated with production of superantigenic toxins, but

    other factors also involved


Slide35 l.jpg

Acute rheumatic fever (ARF)

  • autoimmune disease - triggered only by GAS pharyngitis

  • associated with strong immune response to GAS.

  • antibodies and/or T cells X-react with host antigens? (later)

  • Symptoms arise > 10days + after GAS infection

  • responsible GAS strain already ‘cleared’

  • Symptoms may include:

  • inflammation multiple sites, starting with major joints (arthritis)

  • neurological disorders (Sydenhams chorea)

  • rheumatic heart disease (RHD) (ca 50% cases)

  • - damage to heart valves, permanent scaring in survivors


Slide36 l.jpg

Acute rheumatic fever (ARF)

  • Initial attack rates low (3% in untreated pharyngitis)

  • High recurrence (up to 50%) - increasing in severity

Widespread prescription of penicillin for ‘sore throats’

Remarkably, GAS have not (yet ?) developed resistance to penicillins


Slide37 l.jpg

GAS infections - complications

Post-streptococcal acute glomerulonephritis (PSGN):

  • Common, but rarely life-treating - some GAS infections

  • of either pharynx or skin.

  • Symptoms arise some 10 days after infection

  • reflect kidney dysfunction, probably involving inflammation

  • of glomeruli

  • Pathogenesis:

  • Most probably entrapment of GAS antigen-host antibody

  • complexes at basement membranes of glomeruli

  • might also involve an ‘autoimmune’ response


Slide38 l.jpg

Normal glomerulus

Glomerulonephritis

Mesangial cell

Mesangial cell

intrusion

Endothelial

cell, has

100 nm

pores

PMN

Basement membrane

Inflammation

Too much large immune

complex entrapment ?

Small complexes diffuse thro’

basement membrane into urine,

but the occasional larger complex

can’t & is normally removed by

mesangial cell

Example: Sequel of some

S. pyogenes infections


Group b streptococci l.jpg

Group B streptococci

  • Streptococcusagalactiae are aerobic G+ diplococci that are β-haemolytic on blood agar plates

    • found in lower GIT and female genital tracts

    • GBS is a leading cause of neonatal sepsis and meningitis

    • prevent opsonization and phagocytosis with a polysaccharide capsule


Enterococci l.jpg

Enterococci

  • Enterococcusfaecalis cause UTI, wound infections, endocarditis, intraabdominal abscesses and bacteremia.

    • Normal flora of GIT and GUT

    • resistant to bile and high salt concentrations

    • nosocomial infections

    • resistance to many antibiotics, often bacteriostatic

    • bacterial killing must use a combination treatment of a β-lactam and an aminoglycoside


  • Login