Kaul - Gram+ And Gram- Cocci Flashcards
Virulence factors of staph aureus
Cytotoxins - Hemolysins and Leukocidins (PVL)
Super antigen toxins - TSST-1, enterotoxin, exfoliatin
Protein A, Microcapsule, Adhesins
Invasins
How do the Staph Aureus super antigens work?
They non-specifically crosslink MHC to TCR –> activates T cells that shouldn’t be activated–> overproduction of cytokines
What does Protein A do?
Anti-opsonin effect by binding Fc region of antibodies
Most common clinical presentations of Steph aureus infections
Skin and Soft tissue infections (SSTIs)
- furuncles, carbuncles, impetigo, cellulitis
Osteomyelitis, septic arthritis, Pnemonia, and acute endocarditis
Toxinoses - Toxic Shock syndrome (TSST-1), food poisoning (enterotoxin), and scalded skin syndrome (exfoliatin)
Staph epidermis
- produces cell surface polysaccharide “slime” that adheres to bioprosthetic materials.
- major component of normal skin flora
- cause wound infections throug broken skin
- frequently involve in catheter infections, medical device infections, and IV live infections
Staph saprophyticus
- normal vaginal flora
- causes UTI, cystitis in women
- resistant to novobiocin
- sensitive to penicillin G
Between strep and staph which are in clusters and which are in chains
Staph = clusters Strep = chains
Between strep and staph which is catalase positive?
Staph
Of the staphs, which are coagulase positive and which negative?
Aureus = positive
Epidermidis and saprophyticus = negative
What are two ways you can distinguish strep organisms from each other?
Hemolysis pattern and lancefield group
Lancefield group
Based on antigenic cell wall polysaccharide called C-substance
- groups A-U
- tested in a slide agglutination assay
- common ones are A, B, D, and none
What is the breakdown of which strep is in which lancefield group and which hemolysis pattern?
Strep Pyogenes - Group A strep and beta hemolysis
Strep agalactiae - Group B strep, beta hemolysis
Strep neumo and Virdans group - no lancefield group and alpha hemolysis
Strep bovis - group D lancefield group and gamma hemolysis
Strep Pyogenes virulence factors
M protein - inhibits complement
Strepyolysin O and S - lyses RBCs
Streptokinase
Clinical manifestations of Strep Pyogenes (Group A Strep)
- Sore throat, pharyngitis, scarlet fever
- skin infections - impetigo, cellulitis, necrotizing fasciitis
- toxic shock syndrome
Post infection - rheumatic fever - myocarditis, arthritis, chorea, fever (JONES)
- acute glomerulonephritis
How is strep Pyogenes (GAS) spread?
Contact, droplets, food - it usually inhabits the nasopharynx, throat, and sometimes skin.
Strep agalactiae
Group B strep
- female reproductive tract
- causes neonatal sepsis
WHat test can be done to seperate strep Pyogenes from strep agalactiae?
Bacitracin
- Pyogenes = bacitracin sensitive
- agalactiae - bacitracin resistant
Virdans group strep
Live in the oral cavity
- usually not invasive but dental or oral surgical procedures facilitate entrance into the bloodstream
- causes dental cavities
- causes subacute endocarditis
What does strep Pneumo look like under microscope
Lancet shaped cells arranged in chains
Strep Pneumo virulence factors
- polysaccharide capsule that prevents phagocytosis. It is antigenic
Where is strep Pneumo usually found?
Nasopharynx - so infections are usually endogenous
Clinical manifestations of strep Pneumo
Meningitis, Otitis media, pneumonia, Sepsis
What tests can differentiate between strep Pneumo and strep Virdans?
Optochin test - Pneumo is optochin sensitive
Bile acids - Pneumo is bile sensitive
Quellung - strep Pneumo has a capsule so it will have a border around it.
Strep Pneumo treatment
Cephalosporins such as ceftriaxone or cefotaxamine
Strep Pneumo vaccine
Adults take PPV, which is a 23-valent polysaccharide for adults 65 and up or high risk people over 2
Children take PCV13 - given to children under 5 and immunocomprimised adults over 65
Strep Boviss
Component of gastrointestinal flora
- can grow on bile but not in NaCl
- gamma or sometimes alpha hemolysis
- Group D strep
Enterococci
Considered a Group D antigen
- gamma hemolysis (or sometimes alpha and even less sometimes beta)
- E. faecalis and E. Faecium are most summon types
- component of GI floria
- opportunistic infections that leads to endocarditis and bacteremia/sepsi
- also causes binary tract infections and urinary tract infections
What is a frequent resistance for enterococci?
Vancomycin
- called VRE
How to identify enterococci?
They grow on bile salts and also grow in NaCl
Treatment for enterococci?
Ampicillin + Gentamycin/Penicllin +streptomycin
Vancomycin
Linezolid for VRE
Neisseria
Gram negative Diplococci Often seen with PMNs IgA protease is virulence factor Pilli demonstrates phase variation
N. Gonorrhoeae
Unencapsulated Pili Opa LOS IgA protease Require iron, so they express proteins that can extract iron from host iron proteins such as transferrin and lactoferrin.
Clinical manifestations of N. Gonorrhoeae
Genitourinary infections - PID, urethritis
Ophthalmia neonatorum
Septic arthritis
Diagnosis of N. Gonorrhoeae
Gram stain from specimen or smear
Culture - must be cultured on Thayer-Martin medium, which suppresses normal flora.
- oxidase positive
NAATs
Treatment for N. Gonorrhoeae
IM ceftriaxone
- also give athromycin or doxycycline to cover possible concomitant chlamydia
N. Meningitidis virulence factors
Antigenic capsule Pilli LOS Opa IgA protease Iron extraction system
Where is N. Meningitidis usually carried?
Nasopharynx
Clinical manifestation of meningitidis
Petechial rash
Headache
Stiff neck
Sensitivity to light
Septic shock (LOS)
Disseminated intravascular coagulation (DIC)
Adrenal collapse (Waterhouse-Friedrichsen Syndrome)
Treatment for meningococcus
Ceftriaxone/cefotaxime
Prophylactic rifampin treatment for family members and close contact persons
Clinical diagnosis of meningitis
Gram stain CSF, blood, skin or nasopharyngeal samples
- oxidase positive
- culture for differentiation
- meningitidis ferments maltose whereas Gonorrhoeae doesn’t
- you can do a rapid latex agglutination test to test for capsular antigen
