and Enterococcal Infections Streptococcal
General (Murray 3rd (Ed pp 189
.to cause dramatic and life threatening diseases Unlike Staph, these are catalase negative and recently have a tendency .anaerobes, whilst species that are aerobes, capnophilic (CO2) also exist a capsule present in actively growing cells. Most species are facultative streptococci are gram positive organisms are non-motile, and there is ,Like Staphylococcus genus
:is quite difficult as there are three different types available namely The classification of Streptococci
(serological properties) Lancefield groupings
(alpha, beta, and gamma) Haemolytic properties
(physiological) Biochemical properties
.notes, and group them according to their haemolytic patterns These notes follow the lecture
If haemolysis is complete ? then we call it beta-haemolytic
If haemolysis is incomplete ? then we call it alpha-haemolytic
If there is no haemolysis ? then we call it gamma-haemolytic
Pathogenesis
.(appearing in cell free filtrates (i.e.: endo wall of the bacteria – and they affect intracellularly rather than produce endotoxins – these are heat stable toxins, found in the cell cytokines that mediate the shock and organ failure that results. Pneumococci themselves, acting on macrophages, and helper T cells – which release toxins called: pyrogenic exotoxins, these toxins act as antigens in capsule that protects it against phagocytosis. Streptococci produce Group A Streptococci has a
– haemolytic Streptococci Alpha
salivarius, S. Mitis .S. mutans, S. sanguis, S
.endocarditis, suppurative intraabdominal infections, brain abscesses tract. These organisms are mostly associated with dental caries, infective Streptococci have been isolated in the oropharynx, GIT, and genitourinary the production of green pigment on the blood agar plate. The Viridans and non-haemolytic Streptococci – and their name derives because of This group contains the alpha-haemolytic
Diagnosis
the infection/wound, blood agar, blood culture Diagnosis is achieved by swab ? .determine if alpha-haemolytic
Treatment
.is preferable observed in 10% pf the species. A combination of penicillin + gentamicin are susceptible to penicillin – although moderate resistance has been Most strains of viridans streptococci
Murray 3) Streptococcus Pneumoniaerd (Ed pp 200
.if incubated anaerobically are alpha haemolytic if incubated aerobically, and may appear beta haemolytic dissolve – leaving a dimpled appearance on the blood agar plate. Colonies and round. Autolysis is common when aging occurs; the central colonies gram positive coccus. The cells are lancet shaped, colonies are large ,This organism is an encapsulated
Pathogenesis
activate alternate complement pathway cells to the focus of infection. Teichoic acid and peptidoglycan fragments cells – if movement occurs, there is a net migration of inflammatory respiratory tract can be avoided if removed by mucus and ciliated epithelial by means of attachment to the epithelial cells – movement into the Isolates itself in the oropharynx ? C5a produced ? furthermore, pneumolysin ? (activates classic complement pathway (C3a & C5a ? activated leukocytes produce cytokines ? .migration of further inflammatory cells
Clinical Manifestations
.Meningitis, Bacteraemia, Septic arthritis, Osteomyelitis ,Lobar bronchopneumonia, Sinusitis
Diagnosis
.growth – if incubated overnight of the agar plate with growth – then see ring of inhibited bacterial sensitivity can also be identified, place an optochin disc in the middle whilst other alpha – haemolytic bacteria remain unchanged. Optochin ,Pneumoniae bacteria. Add a drop of bile to see if bacteria dissolve autolysins are activated – resulting in autolysis of the Streptococcus After exposure to bile, the
Treatment
.the drug to the penicillin binding proteins on the bacterial wall chloramphenicol. Resistance is spreading due to decreased affinity of ,agent. If allergic to penicillin use: ethrythromycin, cephalosporins after the advent of antibiotics, penicillin became the main therapeutic that it will opsonise the bacteria for efficient phagocytosis. However was available, type specific antibodies will be passively infused so Before antimicrobial therapy
.cell disease, HIV +, young + the elderly but does not work effectively in patients that are asplenic, have sickle ,of a pneumococcal vaccine – which is immunogenic in well patients Prevention is by the development
Murray 3) Beta-Haemolytic Streptococcird (Ed pp 189
.are used for this group of Streptococci – based on C antigen The Lancefield method of groupings
(S. pyogenes) Group A Streptococci
.bacteria” infections arise from Group A Streptococci. Often called “flesh eating Almost 90% of human streptococcal
Pathogenesis/Virulence Factors
phagocytosis Capsule: protects cell against
therefore protects against phagocytosis ,to beta-globulin factor H, this destabilises C3b responsible for opsinisation M Protein: Binds prefentially
(cant be detected now) portion of IgG, IgA – therefore coating bacteria with host antigen M-like Proteins: Can bind Fc
bacterial attachment to the epithelial cells of the oropharynx F protein: major adhesin for
Streptolysins S & O: S ? cell. O release of lysosomal contenst after phagocytosis therefore killing phagocytic can lysis red blood cells, leukocytes, and platelets, can stimulate ? .(ASO test) antibodies easily formed, therefore good detection of recent infection
.clots, therefore are responsible for easy spread of the Group A Streptococci Streptokinases: can lyse blood
occurs free DNA present in pus, dilution of pus – spreading of infection Deoxyribonuclease: depolymerise
.which is responsible for recruitment and activation of phagocytic cells ,C5a peptidase: disrupts C5a
Clinical Manifestations
:and non-suppurative conditions This can be divided into suppurative
Suppurative
Pharyngitis
Scarlet Fever
infection of skin Pyoderma: purulent
infection of skin Erysipelas: acute
of deep subcutaneous tissues Cellulitis: infection
occurs infection begins deep in subcutaneous tissues, muscle and fat necrosis :Necrotizing Fasciitis
.failure, affects multiple organ systems local infections spread to affect organs, leading to shock and organ :Toxic shock syndrome
Non-suppurative
(is a non-suppurative sequelae of pharyngitis Rhematic fever (this
(this is a non-suppurative sequalae of Skin infections) Acute Glomerularnephritis
(S. agalactiae) Group B Streptococci
.(another infant ,bacteraemia and meningitis (acquired from exogenous source eg: mother Early onset causes bacteraemia, pneumonia, meningitis. Late onset causes .more due to lack of complement, which is required of bactericidal activity insufficient levels of maternal antibodies. Also neonates are affected the human vagina. It is rather pathogenic in neonates, due to their This is common commensal in
(Streptococci (S.milleri Other beta-haemolytic
:Groups C,F,G. Two species associated with human disease in Group C The most common ones here are .S anginosus & S equisimilis .associated with abcess formation sequelae to acute glomerulonephritis but never rheumatic fever. Former ,Produce large colonies with beta haemolyis, latter can cause pharyngitis
.bacteria is by penicillin and erthyromycin of Group A achieved by bacitracin sensitivity. Treatment of this group & G. Group A also part of S. milleri group. Tentative identification ,Former also part of Group F
(Streptococci (Both are same thing Enterococci and Group D
common enterococcus is Group D Streptococci that were not part of the Enterococci. The most to be classified as Enterococci, in simple terms. But there were some Group D Streptococci were found .E. faecium, & E. facaelis
General
.species of PYR etc) are required for further differentiation of the enterococcal organisms. Other phenotypic tests such as (motility, fermentation, hydrolysis distinguish enterococci from other catalase negative, gram positive salts, and can hydrolise esculin. These basic properties are used to They appear as white colonies, grow in 6.5% NaCl, tolerate 40% bile .cocci, facultative anaerobes, and grow readily on blood agar media The enterococci are gram positive
Pathogenesis and Immunity
.survival of the organisms despite antimicrobial therapy They possess several genes that encode resistance, and can also permit .cause serious disease. Can cause UTIs, nosocomial infections, endocarditis potential for causing serious disease but the right combination can Usually commensal, have limited
Diagnosis
.(other phenotypic tests (motility, pigment production etc optochin, do not dissolve when exposed to bile, hydrolysis of PYR) and from other organisms by simple biochemical tests (eg: resistance to agar, and chocolate agar (heated agar plates). They can be readily differentiated They readily grow on blood
Treatment and Prevention
.by plasmids, resistance is transferable to other bacteria Because these resistance to aminoglycosides and vancomycin are mediated .50% resistant to ampicillin, and further 25% reports resistance to vancomycin ,resistance has made is difficult to treat. 25% resistant to aminoglycoside penicillin, aminoglycosides, and vancomycin but recently high level Traditionally, therapy uses
.colonisation of bacteria careful use of antibiotics – strict infection control, can reduce Prevention is complex, but
S. bovis
.case, along with Bile dissolvation being negative this is the exception to that rule. PYR hydrolysis is negative in this D Streptococci. Remember I mentioned that Group D = Enterococci – This is nonenteroccocal group
Anaerobic Streptococci
.(it is a anaerobe :.abscesses, and epyema. Treatment is by penicillin and Flagyl (i.e Can infection already divitalised tissue such as wounds etc. Cause brain .This is a commensal organism
