Gram Positive and Negative Cocci

Flashcards reviewing key concepts related to gram-positive and gram-negative cocci.

Staphylococcus

Genus of bacteria including important human pathogens S. aureus, S. epidermidis, and S. saprophyticus.

Staphylococcus aureus

Important human pathogen causing minor and serious diseases; can survive on dry surfaces and is heat-resistant. Gram positive and in grape clusters. Facultative anaerobic

Staphylococcus epidermidis

Present in normal flora, usually benign except when introduced via catheters, causing hospital-acquired infections.

Staphylococcus saprophyticus

Causes urinary tract infections.

Capsule and slime layer: Virulence factor of S.aureus

Mediates attachment to medical devices and inhibits chemotaxis and phagocytosis.

Protein A: Virulence factor of S.aureus

Specific affinity for Fc of IgGs, avoiding antibody clearance.

Teichoic acids: Virulence factor of S.aureus

Mediate attachment to fibronectin on mucosal membranes.

Peptidoglycan: Virulence factor of S.aureus

Inhibits phagocytosis and confers osmotic resistance.

Coagulase: Virulence factor of S.aureus

Binds to fibrinogen, making insoluble fibrin, aggregating bacterial cells.

Fibrinolysin (staphylokinase): Virulence factor of S.aureus

Dissolves fibrin clots.

Hyaluronidase: Virulence factor of S.aureus

Degrades connective tissues, facilitating spread (present in 90% of S. aureus strains).

Lipases: Virulence factor of S.aureus

Required for invasion into cutaneous and subcutaneous tissues.

Nuclease: Virulence factor of S.aureus

Hydrolyzes viscous DNA.

Penicilase: Virulence factor of S.aureus

Breaks the β-lactamic ring, providing resistance to penicillin.

Cytolytic toxins: Virulence factor of S.aureus

Membrane-damaging toxins that cause lysis of neutrophils, leading to lysosomal enzyme secretion.

– Alpha, beta, delta, gamma, leukocidin
– All cause lysis of neutrophils leading to massive lysosomal enzyme
secretion. Aditionally:
– Alpha is also toxic for red blood cells, hepatocites and platelets
– Beta is toxic for rbc, fibroblasts, and macrophages
– Delta is toxic for rbc and many other cells

Exfoliative toxins (A and B): Virulence factor of S.aureus

Separates the epidermal layer from the dermis, causing blistering and peeling of the skin; also known as exfoliative or epidermolytic toxin.

Toxic Shock Syndrome Toxin-1 (TSST-1)

Ultra absorbing tampons bind mg2+. Low mg2+ triggers TSST-1. Stimulates IL-1 by macrophagesand promotes massive cytokine release, leading to severe systemic effects including fever and shock.

Enterotoxins (A-E, G-I): Virulence factor of S.aureus

Resistant to gastric and jejunal enzymes; stable to heating; stimulate intestinal peristalsis and cause intense vomiting.

Folliculitis

Inflammation of hair follicle.

Furuncle (boil)

Inflammation of hair follicle or sebaceous gland progressing into abscess or pustule.

Carbuncle

Larger and deeper lesion created by aggregation and interconnection of a cluster of furuncles.

Impetigo

Bubble-like swellings that can break and peel away, commonly seen in newborns.

Food intoxication

Ingestion of heat-stable enterotoxins causing gastroenteritis.

Staphylococcal scalded skin syndrome

Toxin induces bright red flush, blisters, then desquamation of the epidermis.

Toxic shock syndrome

Toxemia leading to shock and organ failure.

Osteomyelitis

Infection established in the metaphysis, forming an abscess.

Bacteremia

Bacteria arrive in the bloodstream from another infected site or medical devices, potentially leading to endocarditis.

Methicillin, oxacillin, nafcillin, dicloxacillin

Semisynthetic penicillins resistant to ß-lactam hydrolysis, used to treat S. aureus.

MRSA

Methicillin-Resistant Staphylococcus aureus; resistant to synthetic penicillin methicillin.

Vancomycin

Acts by interfering with cell wall construction; side effects include hearing loss and nephrotoxicity.

Linezolid

Protein synthesis inhibitor used against MRSA.

Daptomycin

Causes membrane depolarization in bacteria, interrupting membrane transport.

Oritavancin

New glycopeptide similar to vancomycin, approved by the FDA in 2014 with fewer secondary effects.

Tigecyclin

Glycylcycline not affected by efflux pump or ribosomal protection mechanisms of resistance.

Dalbavancin

Semisynthetic lipoglycopeptide designed to improve vancomycin's effect.

StaphVAX®

Polysaccharide conjugate vaccine against S. aureus infections, not yet FDA approved.

Streptococcus

Gram-positive cocci in chains, facultative anaerobic, sensitive to penicillin.

Lancefield antigens

Classification criteria based on antigens (A, B, C, F, G).

Alpha hemolysis

Iron in haemoglobin oxidised, greenish color.

Beta hemolysis

Complete disruption of red cells, clear zone around colonies.

Gamma hemolysis

Non-hemolytic streptococci.

Streptococcus pyogenes

Group A beta-hemolytic streptococcus.

Streptococcus agalactiae

Group B beta-hemolytic streptococcus.

Streptococcus pneumoniae

Alpha hemolytic streptococcus.

Virulence factors of Streptococcus pyogenes to avoid phagocytosis

Capsule, M protein, F protein, lipoteichoic acid.

Streptolysin O

O2-labile toxin that causes hemolysis.

Streptolysin S

O2-stable toxin that causes hemolysis and is produced in the presence of serum.

Streptococcal pyrogenic exotoxins (A, B, C, and F)

Also known as erythrogenic toxins; mediators of red rash in scarlet fever and shock.

Streptokinases (A and B)

Anticlotting properties by degrading plasminogen, fibrin, and fibrinogen.

DNases (A to D)

Depolymerize free DNA in pus abscesses, increasing microorganism dissemination.

Strep throat

Acute bacterial pharyngitis/tonsillitis.

Scarlet fever

Complication of pharyngitis causing rash on trunk and extremities, mediated by pyrogenic toxin.

Impetigo (pyoderma)

Superficial lesions that break and form highly contagious crust.

Erysipelas

Acute skin infection with localized pain, inflammation, lymph node enlargement, and fever.

Cellulitis

Pathogen enters through a break in the skin and spreads to the dermis and subcutaneous tissues.

Necrotizing fasciitis

Infection of deep areas of subcutaneous tissue, destroying muscle and adipose tissues.

Streptococcal toxic shock like syndrome (TSLS)

Initial infection may have been pharyngitis, cellulitis, or peritonitis; leads to rapid shock and organ failure.

Rheumatic fever

Nonsuppurative complication of pharyngeal infections causing inflammation of heart, joints, blood vessels, and subcutaneous tissues.

Acute glomerulonephritis (AGN)

Antigen-antibody complexes deposit in the glomerulus, causing kidney damage.

Penicillin

Drug of choice for S. pyogenes treatment; erythromycin if patient is allergic.

Streptococcus agalactiae

Colonizes the urogenital tract of pregnant women and can cause premature rupture of membranes and premature delivery.

Early-onset infection of S. agalactiae

Occurs in neonates younger than 7 days; vertical transmission from mother, manifests as pneumonia or meningitis with bacteremia.

Late-onset infection of S. agalactiae

Occurs between 1 week and 3 months after birth, usually in the form of meningitis.

Streptococcus pneumoniae

Inhibits the nasopharyngeal areas of healthy individuals

Pneumonia

Most common cause of bacterial pneumonia.

Otitis media

Most common cause of otitis media in children < 3 years.

Enterococci

Gram-positive cocci in short chains, part of the normal bowel flora, common cause of nosocomial infections.

Associated infections of Enterococcus

Bacteremia, urinary tract infections, wound infections, nosocomial infections, and endocarditis.

Virulence factors of Enterococcus

Surface adhesins, cytolysin, pheromone, gelatinase, multiple plasmid and antibiotic resistance.

Genus Neisseria

Gram-negative cocci often arranged in pairs with adjacent sides flattened.

Growth conditions of N. gonorrhoeae

Requires complex media pre-warmed to 35-37C, soluble starch, and moist atmosphere with CO2.

Gonococcal virulence factor

Only fimbriated cells are virulent.

Por (porin protein)

Prevents phagolysosome fusion, promoting intracellular survival.

Opa (opacity protein)

Mediates firm attachment to epithelial cells and subsequent invasion.

Rmp (reduction-modifiable protein)

Protects other surface antigens from bactericidal antibodies.

Lipooligosaccharide (LOS)

Incomplete Lipopolysaccharide that still retains endotoxin activity.

Chromosomally-mediated changes in cellular permeability

Inhibits entry of penicillin, tetracycline, erythromycin, aminoglucosides.

Epidemiology of gonorrhea

Major reservoirs, lack of protective immunity, higher risk of disseminated disease with late complement deficiencies.

Pathogenesis of N. gonorrhoeae

Microorganism invades intact mucous membranes or skin with abrasions, penetrates, multiplies, and establishes infection in the sub-epithelial layer.

Gonorrhea in men

Urethritis, epididymitis.

Gonorrhea in women

Cervicitis, vaginitis, Pelvic Inflammatory Disease (PID) Disseminated Gonococcal Infection (DGI)

Disseminated Gonococcal Infection (DGI)

Skin lesions, arthralgias, tenosynovitis, septic arthritis.

Opthalmia neonatorum

Chemoprophylaxis with silver nitrate, tetracycline, or erythromycin eye ointments; treatment with ceftriaxone.

Neisseria meningitidis virulence factor

Pili-mediated, receptor-specific colonization of nonciliated cells of nasopharynx.

Antiphagocytic polysaccharide capsule

Spreads in the absence of specific immunity.

Toxic effects of N. meningitidis

Effects mediated by hyperproduction of lipooligosaccharide.

Highest incidence for Neisseria meningitidis

Children younger than 5 years.

Treatment of N. meningitidis

Penicillin along with supportive therapy for meningeal symptoms; chloramphenicol or cephalosporins as alternatives.