2. Bacteria Flashcards
Gram (+) | Rods | ?
Clostridium (anaerobe) Corynebacterium Listeria Bacillus
Gram (+) | Cocci | Catalase (+), in clusters (Staphylococcus) | Coagulase (+) | ?
Staphylococcus aureus
Gram (+) | Cocci | Catalase (+), in clusters (Staphylococcus) | Coagulase (-) | ?
Novobiocin sensitive: Staphylococcus epidermidis Nobobiocin resistant: Staphylococcus saprophyticus
Gram (+) | Cocci | Catalase (-), in chains (Streptococcus) | partial hemolysis (green - alpha hemolysis) | ?
(+) Quellung (has capsule), Optochin sensitive, Bile soluble: Streptococcus pneumoniae (-) Quellung (no capsule), Optochin resistant, not bile soluble: Streptococcus viridans
Gram (+) | Cocci | Catalase (-), in chains (Streptococcus) | Complete hemolysis (clear, beta-hemolysis) | ?
Bacitracin sensitive: Group A Strep (GAS) aka Streptoccus pyogenes Bacitracin resistant: Group B strep aka Streptococcus agalactiae
Gram (+) | Cocci | Catalase (-), in chains (Streptococcus) | No hemolysis (gamma hemolysis) | ?
Enterococcus (E. faecalis) Peptostreptococcus (anaerobe)
Identifying Staphylococci w/ Novobiocin (once you know it’s a G(+)/catalase(+) coccus in clusters)
NO vobiocin - S aprophyticus is R esistant; E pidermidis is S ensitive On the office’s staph retreat, there was NO S tRES
Identifying Streptococci (once you know it’s a G(+)/catalase(-) coccus in chains)
O ptochin: V iridans is R esistant P neumoniae is S ensitive (OVRPS = overpass) B acitracin: group B strep are R esistant group A strep are S ensitive (B-BRAS )
alpha-hemolytic bacteria
Form a green ring around colonies on blood agar. Include: 1.) Streptococcus pneumoniae (catalase (-) and optochin sensitive) 2.) viridans streptococci (catalase (-), optochin resistant)
Beta-hemolytic bacteria
Form a clear area of hemolysis on blood agar. Include: 1.) Staphylococcus aureus (catalase and coagulase positive) 2.) Streptococcus pyogenes - GAS (catalase negative and bacitracin sensitive) 3.) Streptococcus agalactiae - GBS (catalase negative and bacitracin resistant) 4.) Listeria monocytogenes (tumbling motility, meningitis in newborns, unpasteurized milk)
Catalase
Catalase degrades H2O2, an antimicrobial product of PMNs. H2O2 is a substrate for myeloperoxidase.
Catalase/Coagulase in G(+) cocci
Staphylococci make catalase, whereas Streptococci do not S. aureus makes coagulase, whereas S. epidermidis and S. saprophyticus do not. (Staph make catalase b/c they have more staff. Bad staph (aureus, b/c epidermidis is skin flora) make coagulase and toxins.)
Protein A (virulence factor)
Virulence factor of Staphylococcus aureus Binds Fc-IgG, inhibiting complement fixation and phagocytosis
TSST (@ molecular level)
In Staph aureus A superAg that binds MHCII and the TCR, resulting in polyclonal T-cell activation
Dzs caused by Staphylococcus aureus
1.) Inflammatory Dz - skin infxns, organ abcesses, pneumonia 2.) Toxin-mediated dz - Toxic shock syndrome (TSST-1), scalded skin syndrome (exfoliative toxin), rapid-onset food poisoning (pre-formed enterotoxins) 3.) MRSA (methicillin-resistant S. aureus) infxn: important cause of serious nosocomial and community-acquired infxns. Resistant to beta-lactams due to altered penicillin-binding proteins. 4.) Misc. - acute bacterial endocarditis, osteomyelitis
Staphylococcus epidermidis
Infects prosthetic devices and catheters. Component of normal skin flora. Contaminates blood cultures.
Streptococcus pneumoniae (the pneumococcus)
Encapsulated. Has IgA protease. Most common cause of: Meningitis Otitis media (in children) Pneumonia Sinusitis (S. pneumoniae MOPS are M ost OP tochin S ensitive) Associated w/ rusty sputum, sepsis in sickle cell anemia and splenectomy.
Viridans group Streptococci
Alpha-hemolytic. Normal flora of the oropharynx. Cause dental caries (S. mutans) and subacute bacterial endocarditis (S. sanguis). Resistant to optochin, differentiating them from S. pneumoniae, which is alpha-hemolytic but optochin sensitive. (Viridans group strep live in the mouth b/c they are not afraid of-the-chin <–op-to-chin resistant)
Diseases caused by Streptococcus pyogenes (GAS)
1.) Pyogenic - pharyngitis, cellulitis, impetigo 2.) Toxigenic - Scarlet fever, toxic shock syndrome 3.) Immunologic - rheumatic fever, acute glomerulonephritis PH aryngitis gives you rheumatic PH ever and glomerulonePH ritis No rheum for SPECCulation: Subcutaneous nodules, Polyarthritis Erythema marginatum Chorea Carditis
Ab’s and Streptococcus pyogenes (GAS)
Ab’s to M protein enhance host defenses againt GAS but can give rise to rheumatic fever. ASO titer detects recent GAS infxn.
Streptococcus agalactiae (GBS)
Bacitracin resistant Beta-hemolytic Causes: Pneumonia meningitis Sepsis (mainly in babies) B is for Babies!
Enterococci
include Enterococus faecalis and E. faecium) Penicillin G resistant. Cause UTI and subacute endocarditis. Enterococci are hardier than nonenterococcal group D, thus can grow in 6.5% NaCl. Variable hemolysis.
Lancefield group D
Includes enterococci and nonenterococcal group D streptococci. Lancefield grouping is based on differences in the C carbohydrate on the bacterial cell wall.
VRE
Vancomycin-resistant Enterococci: an important cause of nosocomial infxn.
Streptococcus bovis
Highly associated w/ colon cancer. One of the group D streptococci.
Diphtheria
Caused by Corynebacterium diphtheriae via an exotoxin encoded by beta-prophage. Potent exotoxin inhibits protein synthesis via ADP ribosylation of EF-2. Sx include: pseudomembranous pharyngitis (grayish-white membrane) w/ lymphadenopathy. Lab Dx based on G(+) rods w/ metachromatic granules. Corynebacterium diphtheriae grows on tellurite agar. ABCDEFG ADP ribosylation Beta-prophage Corynebacterium Diphtheriae Elongation Factor 2 Granules
Bacterial spores
Certain G(+) rods form spores when nutrients are limited (@ the end of stationary phase) Spores are highly resistant to destruction by heat and chemicals. Have dipiclonic acid in their core. Have no metabolic activity. Must autoclave to kill spores.
Important spore-forming bacteria
G (+) spores found in soil: Bacillus anthracis Clostridium perfringens C. tetani Other spore formers: B. cerus C. botulinum
Clostridia (generally)
G(+) Spore-forming Obligate anaerobic Bacilli
Clostridium tetani
produces the exotoxin that causes tetanus TETanus is TETanic paralysis (blocks glycine release [an inhibitory NT]) from Renshaw cells in spinal cord
Clostridium botulinum
produces preformed, heat-labile toxin that inhibits ACh release at the NMJ, causing botulism (flaccid paralysis). In adults, dz is caused by ingestion of preformed toxin. In babies, ingestion of bacterial spores in honey causes dz (floppy baby syndrome). BOTulinum is from bad BOTtles of food and honey.
Clostridium perfringens
Produces alpha-toxin (lecithinase) that can cause myonecrosis (gas gangrene) and hemolysis PERFringens PERForates a gangrenous leg
Clostridium dificile
Produces a cytotoxin, an exotoxin that kills enterocytes, causing pseudomembranous colitis. Often 2’ to ABX use, especially clindamycin or ampicillin. DI fficile causes DI arrhea Tx: metronidazole
Anthrax
Caused by Bacillus anthracis: Gram (+), spore-forming rod that produces anthrax toxin. Only bacterium w/ a protein capsule (contains D-glutamate)
Anthrax infxn via contact
Malignant pustules (painless ulcer) Can progress to bacteremia and death Black skin lesions - vesicular papules covered by black eschar *[I think these only occur via contact route of infxn]
Anthrax via inhalation of spores
Flulike Sx that rapidly progress to fever, pulmonary hemorrhage, mediastinitis, and shock
Woolsorter’s dz
Anthrax caused by inhalation of spores from contaminated wool
Listeria monocytogenes route of transmission
Acquired by ingestion of unpasteurized milk/cheese and deli meats, or by vaginal transmission during birth.
Listeria monocytogenes motility
Form actin rockets by which they move from cell to cell. Characteristic tumbling motility.
Listeria monocytogenes Diseases
Can cause: amnionitis septicemia spontaneous abortion granulomatosis infantiseptica neonatal meningitis meningitis in the immunocompromised mild gastroenteritis (healthy individuals) *Note: is the only G(+) organism w/ endotoxin*
Actinomyces and Nocardia
Both are G(+) rods forming long branching filaments, resembling fungi SNAP: S ulfa for N ocardia, A ctinomyces use P CN
Actinomyces israelii
G(+) anaerobe Causes oral/facial abscesses that may drain thru sinus tracts in skin. Forms yellow sulfur granules in sinus tracts. Normal oral flora.
Nocardia asteroides
G(+) and also weakly acid-fast aerobe found in soil. Causes pulmonary infxn in immunocompromised pts.
Primary TB
Mycobacterium infects nonimmune host (usu. child). 1’ TB causes hilar nodes and Ghon focus (usu. in lower lobes) -> together = Ghon Complex Several outcomes: Heals by fibrosis Progressive lung dz Severe bacteremia Preallergic lymphatic or hematogenous dissemination
Primary TB (Heals by fibrosis)
Immunity and hypersensitivity | Tuberculin (+)
Primary TB | Progressive Lung dz
(Seen in HIV, malnutrition) | Death (rare)
Primary TB (severe bacteremia)
Miliary TB | Death
Primary TB Preallergic lymphatic or hematogenous dissemination
Dormant tubercle bacilli in several organs | Reactivation in adult life | Extrapulmonary TB or Reactivation of TB in lungs
Extrapulmonary TB
CNS (parenchymal tuberculoma or meningitis) Vertebral body (Pott’s dz) Lymphadenitis Renal GI
Secondary TB
Due to re-infxn of partially immune hypersensitized host (usu. adult) or reactivation of dormant TB in the lungs Causes Fibrocaseous cavitary lesion (usu. in upper lobes)
PPD test and TB
PPD (+) w/ current infxn, past exposure, or BCG vaccinated PPD (-) if no infxn or anergic (steroids, malnutrition, immunocompromise, sarcoidosis)
Ghon complex
TB granulomas (Ghon focus) w/ lobar and perihilar lymph node involvement. Reflects primary infxn or exposure.
Mycobacterium tuberculosis
Causes TB (Sx: fever, night sweats, weight loss, and hemoptysis) Often resistant to multiple drugs