Micro Immuno Review

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Staphylococcus Gram + cocci Arranged in Bunches of Grapes produce Catalase (protection against killing by Neutrophil) Staphylococcus aureus Coagulase +, ferments Mannitol, -Haemolytic Surface components: o Protein A pathogenicity factor in cell wall, binds to Fc portion of IgG to prevent binding & activation of complement o Teichoic Acids adherence to mucosal cells o Microcapsule antiphagocytic o Peptidoglycan endotoxin-like properties (stimulate production of cytokines and activate complement and coagulase cascades (can manifest as septic shock) Transmission: in Vagina of 5% of women, human lesions o NF to anterior nares, nasopharynx, and axilla Pathogenesis: o Enterotoxins A-F acts as a Superantigen within GIT, releasing lots of IL-1 & 2, causing food poisoning o Toxic Shock Syndrome Toxin (TSST) produced in Vagina, Nose, or other infected site acts as a Superantigen releasing IL-1, IL-2 & TNF Tx: administer fluids, pressor drugs and inotropic drugs to BP, beta-lactamase-resistant drugs (Nafcillin), serum globulins containing anti-TSST antibodies may be useful in neutralizing toxin o Exfoliatin cleaves Desmoglein causing separation of epidermis at Granular cell layer (stratum granulosum) desquamation of the skin = Scaled Skin Syndrome (fever, large bullae, electrolyte imbalance) o Enzymes coagulase, fibrinolysin, hyaluronidase, proteases, nucleases, lipases, cytolytic enzymes (lyse any cell causing marked necrosis of skin and haemolysis) Coagulase walls off infection site by clotting plasma Fibrinolysin lyse thrombi

Hyaluronidase helps with movement/spread of infection through connective tissue Clinical findings: o Skin Infections Impetigo*, furuncles, carbuncles, cellulites, folliculitis, blepharitis, mastitis o Septicaemia active division of the organism within the bloodstream followed by colonization causes Fever, Purpura, DIC (may lead to formation of metastatic abscesses) o Infective Endocarditis infects normal heart valves & IV drug abusers (right-sided endocarditis MC bc IV drug users inject into veins RA/RV) Sudden onset of fever, heart murmur*, and leukocytosis o Osteomyelitis & Arthritis esp in Children; hematogenous spread; children with bone/joint pain, limp/gait abnormality o Pneumonia in postoperative patients (MC nosocomial pneumonia) following viral infection possible abscess formation and empyema o Food Poisoning more vomiting than diarrhea, short incubation period (4-8 hrs), pre-formed toxin within protein rich food (custard, eggs, ham, chocolate) o TSS Fever, Hypotension*, sunburn-like rash (maculopapular) that desquamates, involvement of 3 or more of Liver, Kidney, GIT, CNS, muscle, blood (no labs needed) Lab diagnosis: golden-yellow colonies, -haemolytic (clear haemolysis), Mannitol-Salt agar Treatment: Penicillins, Cephalosporons (inhibit cell wall synthesis - -lactams) bind PBP on bacteria (if modified = no binding and no cell wall synthesis inhibition) o 90% of strains are resistant to Penicillin due to plasmid containing beta-lactamase o 20% of strains are methicillin-resistant (MRSA) or nafcillinresistant (NRSA) DOC then is vancomycin + gentamicin o Synercid investigational drug currently o Abscesses requires drainage (mastitis, septic arthritis) Staphylococcus epidermidis Coagulase -, Non-Haemolytic

Diseases: usually hospital-acquired Endocarditis, Prosthetic joint infections Pathogenesis: pyogenic infection by eliciting Neutrophilic response o Glycocalyx (biofilm) for adherence Clinical findings: infections of IV catheters & prosthetic implants o neonatal sepsis, peritonitis (peritoneal dialysis due to kidney failure) & cerebrospinal shunts (hydrocephalus) Laboratory diagnosis: white colonies, non-haemolytic, Novobiocin-sensitive (zone of growth inhibition) Treatment: highly antibiotic-resistant, most produce betalactamase, methicillin and nafcillin resistant o Vancomycin (DOC) with rifampin or AG o Remove catheter or other prosthetic device

Staphylococcus saprophyticus Coagulase -, Non-Haemolytic Pathogenesis: pyogenic infection by eliciting Neutrophilic response Clinical findings: community-acquired, 2nd most common cause of UTIs after E. coli (Gm -) o Dysuria, urinary frequency, no fever, burning o Staph sap. can reduce nitrates nitrites (E. coli cannot) Laboratory diagnosis: white colonies, non-haemolytic, Novobiocin-insensitive Treatment: Quinolone (inhibit topoisomerase or DNA gyrase) or Trimethoprim-sulfamethoxazole (inhibit folic acid synthesis) Streptococcus Gram + cocci Arranged in chains or pairs Catalase negative (no protection from neutrophil killing/phagocytosis) -hemolysis = green zone formed around colonies on blood agar due to Incomplete lysis -hemolysis = clear zone formed around colonies on blood agar due to Complete lysis by Streptolysins O & S

C Carbohydrate in cell wall, used to determine group of hemolytic streptococcus (ex. A, B, etc) determined by amino sugar o Lancefield groups groups A-U identification carried out by precipitin tests M Protein anti-phagocytic virulence factor protruding from cell surface and interferes with ingestion by phagocytes, determines serotype of group A (S. pyogenes) [~80 serotypes = multiple strep pyogenes infections] -hemolysis = non-hemolytic Groups can be grouped into those that cause primarily rheumatic fever and those that cause primarily nephritogenic (strain 12) on basis of M-protein Streptococcus pyogenes -hemolysis Group A Bacitracin sensitive Antiphagocytic hyaluronic acid capsule M-protein: major virulence factor (fimbriae for adherence to pharyngeal epithelium) further serotyping Pathogenesis: o Pyogenic Inflammation locally at site of multiplication in tissues Pharyngitis, cellulitis o Exotoxin Production (toxigenic) cause systemic symptoms where organisms are not present Scarlet fever (blanching rash), Toxic-shock-like syndrome (TSLS) o Immunological Damage cross-reaction of Ab (antigens/normal tissue share epitopes = autoimmune) against component of bacterium to normal tissue resulting in inflammation Rheumatic fever, acute Glomerulonephritis o Enzymes DNase = Streptodornase (reduce viscosity of pus antibodies to DNase B develop during pyoderma), Hyaluronidase (spreading factor), Streptokinase (fibrolysin activates plasminogen to dissolve clots) o Erythrogenic/Pyrogenic Toxin causes rash of Scarlet fever (difficult swallowing, sore throat + rash), SUPERANTIGEN, necessary to have Phage carrying the gene for the toxin (lysogenized strains)

o Streptolysin O antigenic, ASO (Ab) titer (>200) can be diagnostic in Rheumatic Fever (mitral stenosis), oxygenlabile o Streptolysin S non-antigenic, non-oxygen-labile betahaemolysis o Pyrogenic Exotoxin A causes most cases of TSLS,SUPERANTIGEN

o Exotoxin B rapidly destroys tissue necrotizing fasciitis (flesh-eating bacteria) Clinical findings: o Pharyngitis* (MC bacterial sore throat) spontaneous recovery within 10 days, OR may extend to Otitis, Sinusitis, Mastoiditis or Meningitis, Rheumatic fever (non-suppurative infection, auto-Ab), Scarlet fever (w/ Erythrogenic) Sore throat, difficulty in swallowing, lymphadenopathy, tender cervical LN, fever o Scarlet fever diffuse erythematous blanching rash, followed by desquamation (5-7 days); buccal mucosa is deep red except for circum-oral pallor around mouth & nose, palms and soles, punctate hemorrhages on hard/soft palates, yellowwhite exudates later sheds to reveal Strawberry tongue o Streptococcal toxic shock syndrome (TSLS) similar clinical findings to Staph. o Skin infections* cellulitis, pyoderma (Impetigo pus-filled lesions honey-crusted), erysipelas D/D: Staph (catalase +) o Other Necrotising fasciitis, Lymphangitis (red lymphatics, streaks), bacteraemia, Puerperal fever (vaginal infection ascends into endometrium [endometritis] after childbirth), Glomerulonephritis (non-suppurative infection, follows after skin infections like pyoderma), Rheumatic Fever (follows a sore throat) Post-streptococcal diseases: o Acute Glomerulonephritis (AGN) child - 2-3 weeks after skin infection, Ag-Ab complexes (medium-sized) on glomerular basement membrane (activate complement, recruit neutrophils, Type III hypersensitivty lose integrity

of BM hematuria/proteinuria), HTN, edema, Smoky urine = M12 Strain Early eradication of nephritogenic strep at sites of colonization in skin diseases o Acute Rheumatic Fever 2 weeks after pharyngitis (NOT skin infections!), cross-reaction Ab btw certain serotypes of M protein & antigens of Joint & Heart tissue (Type II Hypersensitivity), Migratory Polyarthritis, Pancarditis (involvement of all layers-valves murmur Mitral Stenosis), ASO titers elevated (>200), ESR o Tx for Group A Penicillin G (no benefit if symptoms of rheumatic fever or AGN have begun), oral penicillin V used to treat mild infections, allergic to penicillin erythromycin o Prevention - Benzathine (long acting penicillin given to prevent recurrence of rheumatic fever) Streptococcus agalactiae -hemolysis Group B Bacitracin resistant hydrolyse Hippurate polysaccharide Capsule Transmission: NF of Colon, genital tract of some women (infection to newborn thru birth canal = sepsis or meningitis) Pathogenesis: do NOT produce cytotoxic enzymes or exotoxins elicits Inflammatory response Clinical findings: o Neonatal sepsis & meningitis (#1 cause in neonate) due to colonization of mothers vaginal epithelium, Rupture of Membranes >18 hrs prior to delivery, premature birth (4cfu/dl is unacceptable) treat with chlorination Antibiotic Therapy: - Penicillins, Cephalosporons, AG, Sulphonamides - Frequent conjugation btwn strains and species spread of resistance via R-plasmids

Escherichia coliFacultative Anaerobe of colon (part of normal flora) reduces Nitrates to Nitrites Ferments Lactose pink colonies on MacConkeys, Oxidase (-)