L3- medically important gram positive cocci

describe the stages of infection

1. transmission to new host through environmental contamination or through a vector or a reservoir

2. adherence by sticking to hosts epethelium→ may be cleared by the hosts innate immune system

3. colonization→ may be cleared by adaptive immune system

4. through toxic production may cause disease

5. may invade

6. immune evasion

7. will cause disease immedietly or be latent (establish site and replicate slowly to not be recognised by immune response)

how to differentiate between gram-positive strept vs straphylo coccus

through catalase reaction

• which involves the breakdown of hydrogen peroxide inot water and oxygen

• this is catalysed by the catalase enzyme which is present in staphylococcus

• therefore if it the microbe being tested is straph it will bubble and froth up => this is called catalase +ve

• while if its strept there will be no change=> catalase -ve

what are the two main groups of staphylococcus (gram +)

coagulase + (s. aureus) and - (s. epidermidis, s. saprophyticus)

how do you test for coagulase + vs - in staphylococcus?

1. add sample of bacteria to some blood plasma

2. coagulase enzyme will cause clotting factors so plasma will clot up

describe coagulase negative staphylococci

• most are members of normal skin flora of humans

• examples to know: S. epidermidis, S. saprophyticus. S. lugdunensis

• are usually lowvirulence

• are pathogenic in some settings

when are coagulase negative cocci pathogenic?

• typically when skin barrier has been breached. eg by invasive devices or premature infants

• eg intravenous catheter staphylococci can spread from opening of catheter→ catheter related infection

• eg in infants their skin barrier is not yet mature as they dont have stratified epithelium

pathogenic potential of S. lugdunensis

produces tissue destructive enzymes and can cause serious infection of heart valves- uncommon-, bones and prosthetic joint

pathogenic potential of S. saprophyticus

causes urinary tract infections in young sexually active women

describe staphylococcus aureus

• is coagulase positive

• beta hameolytic

• 20-40% are carriers

• usually carried in anterior nares and skin of the axilla and groin

• it may cause localised or disseminated infections

• can cause pyogenic (pus forming, eg abscess) infections in almost any organ

• abscess: pocket of pus contained by a surrounding area of fibrosis and coagulation. this is to wall of infection => lytic enzymes destroy tissue

• coagulase toxin walls off infection while lytic toxins (hemolysins, proteases) destroy tissue

S. aureus: what determines colonization vs disease

Quorum sensing GS

• chemical communication between bacteria that depends on the surrounding environmental conditions, including sensing bacterial density

• it influences bacterial behaviour, allowing bacteria to collaborate in response to environmental conditions

• the quorum sensing system in the qourum sensing system in aureus works through the accessory gene regulator,, agr,,

• agr contributes to S.aureus pathogenicity in several infection types. inc: subcutaneous abscesses, endocarditis and arthritis

what are the types of infections that S aureus causes?

• skin infections

• other localised infections

• some toxin producing strains of S. aureus can cause non pyogenic disease

skin infections due to S aureus

• folliculitis

• furuncles,,boils,,

• carbuncles- bigger boils

• impetigo

• cellulitis

• wound infections

what are some other s. aureus infections that occur

• lung or brain abscess

• mastitis in lactating women

disseminated infection- bacteraemia

• S. aureus circulating in the bloodstream

• may progress to infection of a heart valve; endocarditis- infection in the inner layer of the heart

non-pyogenic disease caused by S. aureus

non-pyogenic means non pus producing

examples

• staphylococcal scalded skin syndrome SSSS

• staphylococcal toxic shock syndrome STSS- associated with hyper absorbent tampons

• Staphylococcal food poisoning

staphylococcal scalded skin syndrome SSSS

• caused by an enterotoxin, the gene which originated in a bacteriophage- acquired by transduction

• the enterotoxin is a superantigen

• superantigen bypass normal antigen presentation by directly crosslinking T cells receptor and MCH II

• causes polyclonal activation of T cells and an inflammatory cascade=> inappropriate immune response

• characterised by the superficial layers of the skin peeling

what are the tree classes of streptococcus?

alpha, beta and gamma

how to differentiate bw the three classes of streptocooci

they are classified by the way they haemolyse blood agar

1. beta haemolysis, has enzymes that break down RBCs, blood is dissolved, agar is transparent

2. Alpha haemolysis, partial haemolysis of agar with a olive green tinge

3. Gamma haemolysis, no haemolysis

describe Beta- haemolytic streptococci

• it is further classified according to antigenic differences in cell wall carbohydrates

• there is a lancefield grouping system; 20 groups(A-H. K-V)

• two lancefeild groups to know: A and

Lancefield Group A:

• strep A

• Also known by its species name, streptococcus pyogenes

Lancefeild group B

• Also known by its species name: Streptococcus agalactiae

• colonises the urogenital tracts and rectum of women, transmitted to infants during or after brith

• causes severe infections,, meningitis and bloodstream infections,, in neonates

what are the types of primary infections of Lancefeild Group A beta- haemolytic streptococcus

throat

• pharyngitis or tonsilitis→ abscess, can spread to local extension in the sinus or mastoid

skin

• cellulitis or impetigo

• can become necrotizing fasciitis which can has suppurative complications

throat infections caused by strep A

• pharyngitis/tonsilitis ie strep throat

• peritonsillar abscess or quinsy

skin and soft tissue infections caused by strep A

• impertigo which is very common looks like a bunch of scabs

• necrotising fasciitis , rapidly spreading destructive infection into muscle requiring amputation

non-suppurative complications of strep A infection

acute rheumatic fever→ rheumatic disease

acute glomerulonephritis

acute rheumatic fever

• common in areas of poverty

• syndrome including arthritis, rash. writhing movements and carditis

• carditis: damage to heart valves and muscles

• recurrant rheumatic fever leads to rheumatic heart disease years later

• results in chronic stiffness or narrowing of heart valves

pathogenesis of acute rheumatic fever

some of the proteins that Strep A produces on it cell wall are very similar to protein found on human heart tissue

so when the immune system produces antibody against those proteins a cross reaction occurs attacking heart tissue

antigenic mimicry

what are the two types of alpha haemolytic streptococci

are common commensals of the oropharynx, nasopharynx, gut and genital tract

1. viridans group of streptococci: exist in upper GIT, eg. streptococcus mutans group which causes dental caries or decay

2. streptococcus pneumoniae

pathogenesis of dental caries

1. Continuous intake of sucrose (sugar) favours the growth of S. mutans.

2. S. mutans secretes glycosyltransferases (GTFs) which adsorb onto the enamel.

3. GTFs catabolize sucrose to produce large amounts of glucans, which contribute to the buildup of extracellular polysaccharide matrix which serves as a scaffold for biofilm.

4. Organic acids (eg lactic acid) are produced by bacteria in the biofilm, decreasing pH.

5. The low-pH leads to demineralization of enamel and initiates the carious process.

The introduction of fermented foods into the human diet (due to agricultural practices and food preservation methods) put lactic acid bacteria, such as Lactobacillus and Leuconostoc, in contact with oral Streptococci. Streptococci acquired the gtf gene via horizontal gene transfer from these lactic acid bacilli. Selective pressure (eating sugar) resulted in selection for Streptococcal strains with multiple copies of the gtf gene

streptococcus pneumoniae

pneumococcus

• leading bacterial cause of pneumonia

• also causes meningitis

• gram positive diplococcus

• has a polysaccharide capsule

• there are over 94 capsular types

• it is important as a pathogenic factor for invasive disease, prevents phagocytosis

• protection is specific to capsular type(serotypes) vaccine protects against specific serotypes

how is S. pneumoniae carried

• Nasopharyngeal carriage of S. pneumoniae is necessary for transmission of bacteria and precedes invasive disease

• Carriage is age-dependent (more common in children)

what are conjugate vaccines ***need to learn what it is

• Polysaccharide vaccines (based on bacterial capsules) do not induce a strong or persistent immune response in young children • Polysaccharides become very immunogenic when linked to a carrier protein (e.g, tetanus toxoid) = conjugate vaccine • Importantly, conjugate vaccines induce memory responses and reduce nasopharyngeal carriage of bacteria, impacting on transmission • Conjugate vaccines against Haemophilus influenzae type b (Hib), pneumococcus and meningococcus serogroups C, A, W, and Y have contributed to the virtual elimination of bacterial meningitis caused by these bacteria and prevent more than a million deaths annually