STREPTOCOCCI AND ENTEROCOCCI
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| 🇬🇧 | 🇬🇧 |
| Entry and exit of S.pyogenes infective particles | Nose: sneezing and coughing |
| A gram positive spherical bacteria that forms pairs or chains during growth, is catalase and oxidase negative, with some strains possesing hyaluronic acid and others possessing polysaccharide capsule. ? | Streptococci. on blood agar, they can be alpha( green) beta (clear) and gama/non-haemolytic. |
| Lancefield classification of S.pyogenes | Pyogenes( means pus producing) group A, Beta hemolytic organism |
| Classification of S.pneumoniae | Alpha hemolytic organism |
| Cellular structure of S.pyogenes/ group A BETA- hemolytic streptococci | Contains A-polyssacharide. which makes up 10%(relatively high) of its dry weight. it consist of polymer of L-rhamnose and N acetyl-D-glucosamine in a 2:1 ratio. Antigenic components: linked by phosphate containing bridges to peptidoglycan which consist of N-glutamin acid, L-lysine and D and L- alanine. |
| Strepcoccos species that is the most common cause of acute pharyngitis | S. pyogenes; streptococcus species are part of the normal flora of the upper respiratory tract. |
| Antigenic components of S.Pyogenes. | Linked by phosphate containing bridges to peptidoglycan which consist of N-glutamin acid, L-lysine and D and L- alanine. |
| Both gram positive, what is the difference betwenn staphyloccoci and streptoccoci | 1) streptococci appear as chains or in pairs, staphylococci apear as clusters. 2) streptoccoci is catalase negative and staphylococci is catalase positive |
| The principle behind the catalase test? | Catalase is an enzyme that converts H2O2 to H20 and O2. when present, catalase organisms produce bubbles. |
| S. pyogenes cuases | Strep throat, scarlet fever, rheumatic fever and post streptococcal glomerulonephritis. |
| Two major classes of protiens in the S. pyogenes cell wall | M and T protiens. |
| Characteristics of the M proteins of S.pyogenes | They are the major virulent factor of the organism. They are fimbriae hair like extensions, that are acid and heat resistance and are trypsin sensitive. |
| Antigenic character of the C-carbohydrate of S. pyogenes | Lancefield antigen Group A |
| Major virulent factor S.pyogenes. | The M protien: it inhibits the activation of complement and protects the organism from phagocytosis. |
| The weakest point of S.pyogens defense | M protein: plasma B cells generate antibodies against M protein which binds and opsonizes the protein allowing destruction by macrophages and neutrophils. |
| T protein of S. pyogenes | Non virulent,heat, acid and trypsin resistant, it aid the organism to invade host tissues. T proteins are useful in epidemiological markings. |
| Minor S.pyogenes protein classes | Class F, R and M antigens |
| Virulence factors of S. pyogens | 1)Hemolysins/streptolysis O(antigenic) and S: lyses RBC and WBC 2) streptokinase: activates plasminogen to lyse fibrin clots 3) DNAases: hydrolyses DNA 4)NADases: hydrolyses NAD 5) Hyaluronidase: breaks down proteoglycans/ host connective tissue 6)pyrogenic exotoxins: consist of erthrogenic toxins A,B and C. stimulate Tcells to binding to class 2 MHC directly or non specifically. 7) proteases: soft tissue nercrosis or toxic shock syndrome |
| Why is ASO titre ordered. | Following pharyngeal or systemic S pyogenes infection, ASO antibidies develop thus ASO titre confirms infection. |
| F protein of S.pyogenes | Binds to fibrin |
| Capsular polysaccharide components | Contains hyaluronic acid |
| Importance Hyaluronic acid capsules of s.pyogenes | Non antigenic because it is made up of the same composition of the hose connective tissue thus it can hide its antigen and go unrecognised by the host. it also prevents opsonisation |
| The 3 types of adhesins of S.pyogenes | 3 types: lipoteichoic acids, M proteins, fibronectin- binding protiens, they help the organism bind to the host epithelium |
| Function of lipoteichoic acid on the cell wall of S.pyogenes. | Lipoteichoic acids( avchored to protien on bactarial surface,supported by fimnria on cell wall and helps adherence to host epithelial cells) |
| Streptolysin S and streptolysin O leukocidin | Streptolysin s is oxigen stable leukocidin and streptolysin O is oxygen labile leukocidin |
| Types of specific proteins on S.pyogenes | M,T,F proteins, Lipoteichoic acid, and capsular polysaccharide |
| Virulent factors of s pyogenes | Hyaluronic acid capsule, adhesins, inavasins and exotoxins, and pryogenic exotoxins |
| Suppurative(pus forming) disease-processes of discharge and pus | Meningitis, otitis, sinusitis, tonsilitis and pharyngitis, adenitis, pneumonia, endocarditis, impetigo, erysipelas, scarlet fever, puerperal fever, myositis, fascilitis |
| Entry and exit of S.pyogenes infective particles | Upper respiratory tract: sneezing and coughing |
| Non suppurative sequelae of S.pyogenes infection/ post infection consequences of S. pyogenes infection | Results from over active immune response:Rheumatic fever, glomerulonephritis, scarlet fever and toxic shock syndrome |
| Specimen of choice for identification of S.pyogenes | Blood, tissue, pharyngeal exudates, bpdy fluid |
| Culture of S.pyogenes | Done of blood agar, show a clear Beta hymolysis. |
| Bacitracin sesitivty test of S.pyogenes | Zone of inhibition around colonies shows presence of S. pyogenes |
| Test to differentiate S.pyogenes from other B hemolytic strep | L-pyrolidonyl-beta-napthylamide test |
| Other test for S.pyogenes | DAD test and serodiagnosis test, and PCR. |
| Antibiotic sensitivity test for S.pyogens | Bacitraccin: sensitive optochin: resistance CAMP test: negative |
| Difference between S.pyogenes and S. agalactea | Bacitracin : s. pyogenes is sensitive, s agalctea is resistant. CAMP: S.pyogenes is negative, S. Agalactea is positive |
| Antimicrobial thereapy for S. pyogenes | Penicillin and ampicillin. high of doses of penicillin and clindamycin are recommended for toxic shock, necrotizing fascitis. |
| Drugs in prevention reinfection and of diseases caused by Group A strep. | Chemoprophylaxis and vaccines |
| Description of S. agalactiae | Group B strep with Beta helomysis. causes postpartum infection and most common cause of neonatal sepsis. colonises lower GI tract and genitourinary tract. |
| Serotypes of S. agalactia | 1a( most common in adults) 3 and 5. |
| Apearance of S agalactiae on culture plates | Buttery white colonies with Beta hemolysis |
| Serological markers for S. agalactiae | Rhamose, NAG (n-acytyl glucosamine) and galactose |
| Surface prtoein of S.Agalactiae | C-protein |
| Virulence factors of S. agalctiae | Polysaccharide toxins. thus antibiotics is effective on the capsular polyssacharide and is serotype specific |
| Most common cause of premature delivery | S. agalactiae |
| Immunity of S agalactiae | Achieved via the capsular polysaccharide of type 1a,1b and 2 which poses sialic acid that inihibits activation of alternative and complement pathway. |
| Spectrum of disease caused by S agalactiae | 1) early onset neonatal disease: bacteremia, pneumonia meningitis in 1st week of life 2) late onset :7days- 3months: via exposure to child: bactermia, late onset osteomylitis or septic arthritis |
| S. agalactiae lab ID samples | Blood, CSF, joint fluid, peritoneal fluid, plueral fluid, bone scarpping, throat and rectal swabs |
| Culture of S agalactiae | Nutrient rich agar |
| Lab test for s agalactiae: group specific antigen detection | Latex agglutination, enzyme immunoassay, indirect immunoflouresence |
| CAMP for agalactiae | CAMP positive |
| Hippurate test for agalactiae | Hydrolysis of hippaurate: purple color confirming hippurate hydrolysis |
| Most important test to identify S. agalactiea | It is CAMP positive. S. pyogenes is CAMP negative |
| Antimicrobial meds for S.agalactiae | Penicillin, ampicillin(+ aminoglycoside). Oral clindamycin to follow parenteral administration for bone, soft tissue and lung infections. due to resistance to clindamycin, vancomycin is the initial course of treatment when there is allergy to penicillin. |
| Prevention and control of S agalactiae | Chemoprophylaxis. there may be antibiotic allergies, including anaphylaxis although rearely seen since there is a reduction in the rate o f S.agalactiae infection. also in the hospital, analphylaxis intervention is readily available. |
| Streptococcus pneumonea features | Normal inhabitant of the human respiratory tract in human. G pos alpha hemolytic, catalase negative, lancet shaped diplococci, glucose fermenting (to lactic acid) that is the leading cause of invasive bacterial disease in children and elderly |
| Structure of the cell of s.pneumonia | Very thick cell wall: both teichoic acid and lipoteicholic acid contain phorphrylcholine, an essential element in S. pneumonia since choline adheres to choline binding receptors located on human cells. it contains pilli which helps in colonization of the upper respiratory tract |
| Virulent factors of s. pneumonea | Pilli, capsule (disrupts phogocytosis and prevent opsonization), cell wall components, haemolysins, neuraminidase and Iga protease, choline binding protiens. |
| Lipoprotein on the cell wall of S pnuemonea | Pspa (protien antigen that prevents opsonization) Lyt A,B,C(autolysins responsible for lysis in stationary phase and in presence of antibiotics) CbpA (adhesion with * choline binding repeats) |
| Nature of pneumococcal pneumonia infections | Sudden onset with fever, chills and sharp pleural pain. sputum is characteristically bloody/ rusty coloured. mortality my be high with age of patient and underlyin medical conditions. |
| Specimen of choice for laboratory test of s. pnuemoniae | Blood, csf, sputum, bronchial washings and urine. |
| S. pnuemonia culture; | Blod agar, alpha hemolytic, mucoid colonies type 3 and 37, contain autolysin- autolysis which kills all the curlture. |
| Biochemical test for S pnuemonea | Inulin test, used to separate pneumococci from stretcococci: strep does nt ferment inulin sugar. bile solubility test and optochin sensitivity test: used to separate pneumococcus from strep viridans |
| Serotyping for S pneumonea | Done with capsular swelling/ quellung reaction; makes the capsule of the organism visible due to exposure of agglutinating anticapsular antibodies |
| Antigen detection of S pnuemonae | Pneumococcal polysaccharide is excreted in urine |
| Drugs in treating S pneumonea | Penicillin: also erythromycin, cephalosporin and chloramphenicol |
| Resistance to meds of S pneumo | To cephalosporin and pencillin: achieved by altering of binding sites on the cell wall |
| Prevention and control of Spneumonea | Via vaccinations (not to be given to those who have had adverse reactions of low grade fever and mild soreness at the site of administration) |
| Strep Viridans | Alpha hemolytic, optochin resistance, polysaccharide absent. insoluble bile fermentation and inulin negative. the most common cause of infective endocarditis |
| Site of location s viridans | Most common in the mouth and can later be introduced to the blood stream. it can synthesis dextrans from glucose which it uses to attach to damage heart valves |
| Antimicrobial medication of S. viridans | Penicillin ampicillin. clindamycin, erythromycin and vancomycin if allergic to penicillin |
| Prevention and control | Proper dental care and management of teeth and mouth infections |
| Enterococcus | Can grow in 6.5% salt solution and hydrolyze esculin in presence of 40% bile salt. |
| Most enterococcus infection are by two species | Enterococcus faecalis and feacium: they colonise the GI tract and selected for by ABX |
| Clinical manisfestation of Enterococcus | Bacteremia fellowed by infective endocariditis, UTI meningitis, skin and soft tissue infections,neonatal infections |
| Treatment of enterococcus | Highly resistance thus a multitherapy is required. resistance achieved due to acquisitions of genes that alter cell wall of biochmistry. |