Micro G+ Quiz 2 Flashcards
Staphylococcus metabolism
Facultative anaerobe
Staphylococcus catalase test
positive
Staphylococcus optimal temperature
30º C (18º-40ºC)
Staphylococcus environmentally resists:
Drying, Salt (Mannitol Salt Agar used)
Staphylococcus aureus virulence factors
Peptidoglycan Teichoic acids – (ID species/strain) Protein A Coagulase Slime Layer Capsule (stop phagocytosis)
Staphylococcus aureus toxins
Alpha – cell lysis, tissue damage Beta – cell lysis, tissue destruction Gamma – rbc lysis Delta – detergent on rbc’s PV – leukocidin Exfoliative toxins (ETA and ETB) Enterotoxins Superantigens (A, B, etc.) – stimulate T-cells non-specifically Catalase-H2O2 breakdown (ALL Staphylococcus!!) Hyaluronidase -spreading in CT Staphylokinase -(fibrinolysin) dissolves clots Penicillinase
Diseases caused by Staphylococcus aureus
SOFT PAINS
SKIN (colonization)- folliculitis (hair follicule), furuncle/carbuncle (sebaceous gland), impetigo (superficial, children).
(exo/entero)TOXINS -food poisoning, scalded skin (exfoliative toxin), toxic shock (superantigen).
INTERNAL -bacteremia, endocarditis, osteomyelitis, pneumonia
Staphylococcus aureus hemolysis test
beta
clear
Staphylococcus epidermidis hemolysis test
Gamma or alpha (none or incomplete)
Staphylococcus aureus coagulase test
positive!!
Staphylococcus lugdunensis coagulase test
negative
Staphylococcus saprophyticus coagulase test
negative
Staphylococcus hemolyticus coagulase test
negative
Streptococcus coagulase test
negative
Two most important coagulase negative staphylococcus species
Staphylococcus epidermidis & Staphylococcus lugdunensis
What diseases do Staphylococcus epidermidis & Staphylococcus lugdunensis cause
Infections of catheters, prosthetic valves & joints
Diseases caused by Staphylococcus epidermidis
Bacteremia, endocarditis, surgical wound infections, UTI
Diseases caused by Staphylococcus lugdunensis
Arthritis, bacteremia, endocarditis, UTI
Diseases caused by Staphylococcus saprophyticus
UTI and other opportunistic infections
Diseases caused by Staphylococcus hemolyticus
Bacteremia, bone/joint, endocarditis, UTI, wound infection
Streptococcus metabolism
Facultative anaerobe
Streptococcus environmentally resists:
Some drying, salt
Streptococcus pyogenes Serological Grouping
GAS
Streptococcus agalactiae Serological Grouping
GBS
Streptococcus bovis Serological Grouping
GDS (enterococcus)
Streptococcus pneumoniae Serological Grouping
None
Streptococcus mutans Serological Grouping
None, viridans group
Streptococcus mitas Serological Grouping
None, viridans group
Streptococcus salivarius Serological Grouping
None, viridans group
Streptococcus pyogenes virulence factors
1) Capsule
2) Adhesins
- Lipoteichoic acid
- M-protein family
- F-protein – binds epithelial cells
Streptococcus pneumoniae virulence factors
HUGE capsule (resist phagocytosis)
IgA proteases
pnuemolysin to destroy ciliated cells
Streptococcus mutans virulence factors/metabolism
Acidogenic/acidouric
Streptococcus pyogenes toxins
Pyrogenic exotoxins - mitogens for T-cells/inflamm/rash/fever pus –SpeA, SpeB, SpeC
passed between bacteria by phage conversion
Streptolysin S – lyse wbc’s, platelets, rbc’s
Streptolysin O – lyses wbc’s, platelets, rbc’s (ASO test = recent strep infection)
Streptokinase – lyse blood clots allows spread
Hyaluronidase – spreading
DNase/streptodornase
C5a peptidase
Name the 2 post-Streptococcal infection Diseases
- Rheumatic fever: 2 week post effect (cross-reactive antibody, ASO test) age 5-15, aschoff body —> dental prophylaxis to prevent endocarditis
- Post-streptococcal glomerulonephritis (from antibodies to streptococcus clogging kidneys, ASO test)
Suppurative Streptococcus pyogenes Diseases
- *Necrotizing fasciitis: SUPERANTIGENS deeper infection (fascia)
- *Pyoderma/impetigo: purulent skin infection – hot climates, young kids
- *Erysipelas: acute skin infection – larger area
- *Cellulitis: deeper skin infection
- *Toxic Shock syndrome: superantigens – usually bacteremic/systemic
- *Endocarditis: infection of a heart valve
- *pharyngitis
Other disease caused by Streptococcus pyogenes
Scarlet fever: rash/skin peeling
Disease caused by Streptococcus agalactiae
S. agalactiae is GBS – most serious disease of neonate, cause septicemia/meniningitis/
-bacteremia in newborns (screen moms, 10-30% women carry, 60% babies get sick)
Disease caused by Streptococcus bovis
S. bovis = mystery:
15% of colon cancer patients have
Disease caused by Streptococcus pneumoniae
Lung infection, spread to sinuses & meninges, increase C-reactive protein
Disease caused by Streptococcus mutans
Dental caries
Treatment for Streptococcus pneumoniae infections
- Becoming penicillin resistant —> vancomycin
2. polysaccharide multi-strain vaccine given to under 2 yr & 65+
To prevent secondary Streptococcus pyogenes infections
Penicillin, cephalosporin, within 10 days
Diagnosis of Streptococcus pyogenes infection
- Elevated CRP
2. Cells lyse rapidly with bile
Streptococcus pyogenes hemolysis test
beta
Streptococcus agalactiae hemolysis test
beta
Streptococcus bovis hemolysis test
gamma (NON-hemolytic)
Streptococcus pneumoniae (Pnuemococcus, diplo) hemolysis test
alpha
Streptococcus mutans hemolysis test
alpha
Streptococcus mitas hemolysis test
alpha
Streptococcus salivarius hemolysis test
alpha
Two most common Streptococcus mutans species in humans
S. mutans, S. sobrinus (cariogenic)
mutans is a term used to describe not only Streptococcus mutans, but seven species including S. mutans, S. sobrinus, S. criceti, S. ferus, S. ratti, S. macacae and S. downei. S. sanguis (less acidogenic but lay groundwork)
Enterococcus metabolism
Facultative anaerobe
Enterococcus virulence factors
few, except SUPER drug resistant
Diseases caused by Enterococcus
Bacteremia, UTI, abdominal abscess, diverticulitis, endocarditis
Where is Enterococcus found?
Water supply, though resistant to drying and salt
Streptococcus catalase test
Negative
Two spore-forming bacteria
Bacillus + Clostridium
Bacillus metabolism
Facultative aerobe
Bacillus Virulence Factors
ENDOSPORES, can survive extreme conditions bc they contain dipicolinic acid and calcium, also bacterial DNA
Bacillus anthracis virulence factors
- Spores
* (no spores in clinical samples) - Capsule
- Toxins- all three on one plasmid (PA, EF and LF)
Bacillus cereus virulence factors
Spores & Enterotoxin- heat stable (food poisoning from rice)
Diseases caused by Bacillus anthracis
- Mostly cutaneous, contact with spores eschar = black (necrotic) scab (20% fatal), septicemia
- Inhalation: spreads via lymph node —> meningitis (95% fatal) (wool sorters)
- GI: grazing animals, 100% fatal
Bacillus stearothermophilus significance
autoclave indicator organism
Treatment for Bacillus anthracis
- Ciprofloxacin stops DNA/protein synthesis
- Doxycycline -penicillin resistance reported
3.Prevent with vaccine – available for military.
(vaccine for cows?)
Diagnosis of Bacillus anthracis
Can do DFA test to bind capsule
Diseases caused by Bacillus anthracis
Food poisoning, occasional eye infections
Emetic form – intoxication/enterotoxin rice)
Diarrheal form – longer reaction time, infection NOTintoxication - heat labile enterotoxin – (meat/veggies)
Ocular form less common, secondary to traumatic eye injury/post-op
Listeria Metabolism
Aerobe/Facultative anaerobe
Listeria general mode of pathology
facultative intracellular (CMI needed to clear/Anti-bodies not effective)
Listeria monocytogenes virulence factors
Actin rockets: propel into next cell without exposure to antibodies
(facultative intracellular pathogen)
Listeria monocytogenes toxin
Listerialysin: enzymes to escape cytoplasm
Disease caused by Listeria monocytogenes
Food poisoning (20-30% mortality) (50% for preg, transplant patients, cancer, etc… & increased meningitis) -deli meats, dairy, raw veggies
Treatment for Listeria monocytogenes
- penicillin
- gentamicin + penicillin
- ampicillin for serious infection
Corynebacterium virulence factors/pathogenicity
Often part of normal flora, -opportunistic, few pathogenic species othwewise
Corynebacterium metabolism
aerobic, or facultatively anaerobic
Corynebacterium diphtheriae toxins
A-B exotoxin inhibits translation in heart/nerve cells
(A for Action, B for Binding)
B subunit binds to the cell - specific for heart and nerve cells
A subunit goes into the cell and causes damage by stopping translation
Diseases caused by Corynebacterium diphtheriae
Diptheria: pseudomembrane block airway, also secondary cardiac and neurological damage
-Mortality 5-10% BUT 20% for under 5 and 40+
Cutaneous form toxic & can go systemic
Corynebacterium diphtheriae treatment
Antitoxin neutralizes exotoxin
Penicillin/erythromycin to remove bacteria
Toxoid vaccine (inactivated toxin) (DTP)
Where is Clostridium found?
Soil, sewage, human GI tract
Clostridium metabolism
Anaerobic
mostly
Clostridium virulence factors
ENDOSPORES
contain dipicolinic acid and calcium, bacterial DNA
Clostridium toxins
Histolytic toxins, enterotoxins and neurotoxins
Clostridium perfringens toxins
12+ toxins, high mortality
Lecithinase – most important / alpha toxin
Histotoxin – hydrolyzes host cell membranes (rbc, wbc, platelets and endothelial cells).
Mediates massive hemolysis, increased vascular permeability/bleeding, tissue destruction, hepatic toxicity, myocardial dysfunction.
Diseases caused by Clostridium perfringens
- Gas gangrene, cut off blood supply & necrosis
- Gastroenterotitis
- Wound infection: necrosis, myonecrosis, ischemia
Clostridium perfringens treatment
Wound care + penicillin
Diseases caused by Clostridium tetani
Tetanus, wound infections (fatal in newborns)
Clostridium tetani treatment
Anti-toxin
Antibiotics (Metronidazole)
(DTP vaccine)
Clostridium tetani toxins
Tetanolysin: hemolysin
Tetanospasmin: A-B toxin: neurotoxin
Diseases caused by Clostridium botulinum
Food poisoning, wound & infant botulism: Muscle failure, 25% mortality
Clostridium botulinum treatment
Often no treatment
If in GI tract: metronidazole or penicillin
-use antitoxin
Prevention is best :
Destroy spores in food
Prevent germination – cold or acid
Destroy toxin – 60 degrees for 10 minutes
Clostridium botulinum toxins
A-B toxin: Most potent neurotoxins known
- blocks ACh release, - don’t need live organisms – toxin in food will cause botulism
Diseases caused by Clostridium difficile
In 5% of people: normal flora Pseudomembranous colitis (caused by clindamycin wiping out "probiotics")
Clostridium difficile treatment
Stop clindamycin, use metronidazole/vancomycin
Clostridium difficile metabolism
Obligate Anaerobe (makes sense, in gut)
Nocardia metabolism
Aerobe
Diseases caused by Nocardia
- Immunocompromised at risk for bronchopulmonary disease & cutaneous infection (ubiquitous)
- Dental: Nocardia in gingival pockets w/ Actinomyces, role unknown
Nocardia treatment
Wound care, sulfonamide
Where is Lactobacillus found?
Human mouth, GI & GU tract
Lactobacillus metabolism
Air tolerant anaerobe
Lactobacillus virulence factors
Acidogenic/Acidouric
Diseases caused by Lactobacillus
Dental Caries: acidogenic and acidouric
pit and fissure caries, often late colonizer (after S. mutans)
Actinomycetes metabolism
Facultative or strict anaerobe
Actinomycetes pathogenicity
Opportunistic pathogen, often part of normal flora
Diseases caused by Actinomycetes israelii
Post-Cranio Facial surgical actinomycosisi in jaw, hyphae seen
Caries at enamel/dentin surface
Sulfur granules
Actinomycetes israelii treatment
Removing infected tissue, penicilin
Mycobacterium gram stain
ACID FAST (sometimes weakly +)
Mycobacterium metabolism
Aerobic (makes sense, think lungs)
Mycobacterium toxins
few if any
Diseases caused byMycobacterium tuberculosis
Tuberculosis: Damage is from YOUR immune response, forming granulomas.
Primary infection: droplet/aerosolized transmission taken up by macrophage. Ghon’s complex formed, inflammation –> wbc/tissue destruction
Secondary infection: reactivation of infection - pulmonary TB or miliary TB (spreading), granulomas, inflammation, chronic fever, night sweats, weight loss, cough
Treatment for Mycobacterium tuberculosis
Prevent w/ BCG vaccine
Treatment is difficult & long term
Rifamycins – inhibit transcription – liver damage
Isoniazid – cell wall synthesis inhibitor – mycolic acid – liver toxicity
Pyrazinamide – unclear mode
Diagnosis of Mycobacterium tuberculosis
PPD test (aka Mantoux test). Newer Quantiferon-TB gold blood test
Mycobacterium leprae mode of pathogenicity
intracellular (cell mediated immunity needed)
Diseases caused by Mycobacterium leprae
Leprosy
- Lepromatous leprosy – most severe (Hansen’s disease)
- Highly infectious
- Lack of CMI
- Skin destruction
- Takes at least a year of treatment - Tuberculoid leprosy –milder form
- Hypopigmented skin lesions
- Nerve damage
- Low infectivity
Disease caused by Mycobacterium avium
Pulmonary disease or disseminated disease, especially in immunocompromised individuals
Treatment for Mycobacterium avium
Prophylaxis in HIV patients – azithromycin
Treat infections with rifampin or isoniazid