Micro Bacteria Flashcards
Gram+ Cocci lab algorithm
Cocci --> Catalase test Catalase -: Streptococcus Catalase +: Staph Staph --> Coagulase test Coagulase +: S aureus Coagulase -: Do Novobiocin test "NO StRESs at the staph retreat" Novobiocin sensitive: S epidermidis Novobiocin resistant: S saprophyticus
Gram+ rods
Clostridium (anaerobe) Corynebacterium Listeria Bacillus (aerobe) Mycobacterium (acid fast)
Gram+ with branching filaments
Anaerobe, not acid fast: Actinomyces
Aerobe, acid fast: Nocardia
Streptococcus algorithm
Hemolysis test
Partial hemolysis –> green on blood agar–> α
Complete hemolysis –> clear on blood agar –> β
No hemolysis on blood agar –> γ
α Hemolytic Strep Algorithm
“OVRPS”
Capsule, +Quellung, Optochin sensitive –> Strep pneumoniae
No capsule, Optochin resistant –> Viridans streptococci (S mutans)
β Hemolytic Strep Algorithm
“B-BRAS”
Group A: Bacitracin sensitive –> S pyogenes
Group B: Bacitracin resistent –> S agalactiae
γ Hemolytic Strep Algorithm
Group D (Enterococcus): Growth in bile and 6.5% NaCl (E faecalis) Nonenterococcus: Growth in bile, not 6.5% NaCl (S bovis)
β-Hemolytic Bacteria
Staphlococcus aureus (catalase+, coagulase+) Streptococcus pyogenes (GAS: Catalase-, Bacitracin sensitive) Streptococcus agalactiae (GBS: Catalase-, Bacitracin resistent) Listeria Monocytogenes (tumbling motility, meningitis in newborns, unpasteurized milk)
Staphyloccus aureus
Gram, Shape, Arrangement, Marker
Weapon
Diseases it causes?
Gram+ Cocci in Clusters, Catalase+, Coagulase+
Protein A binds FcIgG and inhibits complement fixation and phagocytosis
TSST –> fever, vomiting, rash, desquamation, shock, end organ failure
Skin infection, Organ abscess (coagulase forms fibrin clot around self), Pneumonia, Endocarditis, Osteomyelitis, Food poisoning (preformed toxins), TSS, Scalded skin syndrome (exfoliative toxin)
MRSA
What is it?
Resistent to…
Methicillin Resistent Staph Aureus
Resistent to β-lactams because of altered penicillin binding protein
Staphylococcus epidermidis
Where is it normally located
Contaminates what?
What does it infect?
Part of normal skin flora
Contaminates blood cultures
Infects prosthetic devices and IV catheters by producing adherent biofilms
Streptococcus pneumoniae Gram, Shape, Arrangement Weapons Markers Most common cause of... Presentation
Gram+, Lancet Shaped, Diplococci
Encapsulated, IgA protease
α hemolytic, Optochin sensitive
“MOPS are Most OPtochin Sensitive”
Meningitis, Otitis media (in children), Pneumonia, Sinusitis
Rusty sputum, sepsis in sickle cell anemia and splenectomy
Viridans Group Streptococci Markers Where are they normally What do they cause? What does it adhere to?
α hemolytic, Optochin Resistent, Produces Dextran from Sucrose
Normal flora of oropharynx
Dental caries (S mutans) and Subacute bacterial endocarditis (S sanguis) - stick to prosthetic valve via glycocalyx
Adheres to Fibrin-Platelet Aggregates
Streptococcus pyogenes Markers Versions w/ diseases Diagnosis Significant protein marker
Gram+ Cocci, β-Hemolytic, bacitracin sensitive
Pyogenic: pharyngitis, cellulitis, impetigo
Toxigenic: scarlet fever, TSLS, Necrotizing fasciitis
Immunologic: Rheumatic fever, acute glomerulonephritis
ASO titers
M protein enhances host defense but gives rise to rheumatic fever
Diagnosis of RF
What causes it?
GAS "JONES" Joints - polyaarthritis Carditis Nodules (subcutaneous) Erythema marginatum Sydenham's chorea
Scarlet Fever Presentation
Scarlet rash sparing face, Strawberry (scarlet) tongue, Scarlet throat
What GAS presentations can lead to other problems?
Pharyngitis –> RF and Glomerulonephritis
Impetigo more commonly precedes glomerulonephritis than pharyngitis
Streptococcus agalacgtiae Markers What does it produce? Colonizes where? What diseases does it cause? In whom? Screen Treatment
“GBS: B is for babies”
Gram+ Cocci, β-Hemolytic, bacitracin resistent, Hippurate test +
Produces CAMP factor which enlarges area of hemolysis formed by S aureus
Vagina
Pneumonia, Meningitis, and Sepsis in babies
Screen pregnant women at 35-37 weeks
Pt’s with + cultures receive intrapartum penicillin prophylaxis
Enterococcus Names Markers Where are they normally? Resistant to? What do they cause? Bad version?
GDS: E. faecalis and E. faecium
Gram+ cocci Non-hemolytic and growth in bile and 6.5% NaCl
Normally in colonic flora
Penicillin G resistent
UTI, Biliary tract infections, Subacute endocarditis
VRE important in nosocomial infection
Lancefield Grouping based on?
Difference in C carbohydrate in cell wall
Streptococcus bovis
Markers
Where does it colonize
What can it cause?
GDS: S bovis
Gram+ cocci Non-hemolytic and growth in bile but not 6.5% NaCl
Colonizes the gut
Bacteremia and subacute endocarditis in colon cancer patients
GDS
S bovis, E. faecalis, E. faecium
Corynebacterium diphtheriae Markers Plating Toxin test? Stains Diseases it causes? How? Symptoms Vaccine
Gram+ rods with metachromatic (blue and red) granules
Black colonies on Cystine-Tellurite agar
Elek’s test for toxins
+ Aniline dyes
Diphtheria via exotoxin encoded by β prophage. Inhibits protein synthesis by ADP-ribosylation of EF2
Pseudomembranous pharyngitis (gray-white membrane), lymphadenopathy, myocarditis, arrhythmias
Toxoid vaccine prevents diphtheria
Spores
What do have in their core?
How do you kill spores?
Dipicolinic acid in the core
Autoclave @ 121 degrees C for 15 minutes
Clostridia
Markers
What do they form?
Types
Gram+ rods that are obligate anaerobes. Spore forming
Tetani, Botulinum, Perfringens, Difficile
Clostridium tetani
Markers
Toxin
Presentation
Gram+ rods that are obligate anaerobes. Spore forming
Tetanospasmin is an exotoxin. Cleaves SNARE protein required for NT release of GABA and Gly neurons (Renshaw cells in spinal cord)
Muscle rigidity, lock jaw, Risus sardonicus
Clostridium botulinum
Markers
Toxin
Presentation
Gram+ rods that are obligate anaerobes. Spore forming
Botulinum toxin
Cleaves SNARE protein required for NT release of ACh from neurons
Baby who ate honey has Flaccid paralysis (floppy baby)
Clostridium perfringens
Markers
Toxin
Presentation
Gram+ rods that are obligate anaerobes. Spore forming
Alpha toxin (lecithinase)
Phospholipase that degrades tissues and cell membranes
Degradation of phospholipid C –> myonecrosis (gas gangrene) and hemolysis (double zone of hemolysis on blood agar)
Gas Gangrenous Leg
Clostridium difficile Markers Toxin Presentation Diagnosis Treatment
Gram+ rods that are obligate anaerobes. Spore forming
Toxin A (enterotoxin) binds brush border of gut
Toxin B (cytotoxin) destroys cytoskeletal structure of enterocytes causing pseudomembranous colitis
Diarrhea after antibiotic use (clindamycin or ampicillin)
Detection of toxin in stool
Metronidazole or oral vancomycin
Anthrax Markers What is special about it? What does it produce? Types
Gram+ spore forming rod
Only bacteria with polypeptide capsule (with D-glutamate)
Antrax toxin
Cutaneous vs Pulmonary
Cutaneous Anthrax
Contact –> black eschar (painless ulcer); can progress to bacteremia and death
Black skin lesion - black eschar (necrosis) surrounded by edematous ring
Caused by Lethal factor and Edema factor (Mimics AC and increases cAMP)
Pulmonary Anthrax
Inhalation of spores –> flu-like symptoms that rapidly progresses to fever, pulmonary hemorrhage, mediastinitis, and shock
Woolsorters’ Disease
Inhalation of Anthrax spores from contaminated wool
Bacillus cereus
Markers
How is it contracted
Types with presentation
Gram+ aerobic rods
Food poisoning. Spores survive cooking rice and keeping it warm results in germination of spores and enterotoxin formation
Emetic type: Rice and pasta. Nausea and vomiting for 1-5 hours caused by cereulide (a preformed toxin)
Diarrheal type causes watery non-bloody diarrhea and GI pain for 8-18 hours
Listeria Monocytogenes Markers Where can it live? How is it acquired? How do they travel?
Gram+ rods
Facultative intracellular microbe
Ingestion of unpasteurized milk/cheese or deli meats. Vaginal transmission during birth
Forms actin rockets to move from cell to cell with characteristic tumbling motility
Listeria Monocytogenes
Diseases caused by them?
Treatment
Amnionitis, Septicemia, and Spontaneous abortion in pregnant women
Granulomatosis infantiseptica, Neonatal meningitis
Meningitis in immunocompromised pts
Mild gastroenteritis in health individuals
Gastroenteritis is self limiting
Ampicillin for infants, immunocompromised and elderly
Actinomyces Markers Air? Acid Fast? Where is it found? Presentation Treatment
Gram+ branching filaments Anaerobic Not Acid Fast Normal oral flora Oral/facial abscesses that drain through sinus tracts forming yellow sulfur granules Penicillin
Nocardia Markers Air? Acid Fast? Where is it found? Presentation Treatment
Gram+ branching filaments
Aerobe
Acid Fast
Soil
Pulmonary infections in immunocompromised
Cutaneous infections after trauma in normals
Sulfonamides
PPD+ vs PPD-
+: Current infection, Past exposure, BCG vaccinated
-: No infection, anergic (steroids, malnutrition, immunocompromised), or Sarcoidosis
Mycobacteria
Stain
Names
Acid Fast Tuberculosis Kansaii (pulmonary TB-like symptoms) Avium-Intracellulare (disseminated nonTB disease in AIDS resistant to multiple drugs. Treat prophylactically with azithromycin) Leprae
Mycobacterium tuberculosis
Symptoms
Weapons
Histo
Fever, Night sweats, Wt loss, Hemoptysis
Cord Factor: inhibits macrophage maturation and induces release of TNFα
Sulfatides (surface glycolipids) inhibit phagosysosomal fusion
Caseating granuloma w/ multinuclear Langhan’s giant cells
Primary TB
Who is at risk?
Course
Non immune host (usually a child)
Hilar nodes + Ghon focus (usually in mid zone of lung) = Ghon Complex
Heals by fibrosis –> immunity and hypersensitivity –> Tuberculin+
Progressive disease
Bacteremia –> miliary TB
Preallergic lymphatic or hematogenous dissemination –> dormancy in several organs –> reactivation in adult life
Secondary TB
Who is at risk?
Initial Course
Reactivation
Partially immune hypersensitized host (adult)
Fibrocaseous cavitary lesion usually in upper lobes
Reactivation in the lungs
CNS (parenchymal tuberculoma or meningitis)
Vertebral body (Pott’s Disease)
Lymphadenitis, Renal, GI
Mycobacterium leparae Temperatures Growth in vitro Reservoir in US Forms Treatment
Likes cool temps: infects skin, superficial nerves (glove and stocking loss of sensation) Cannot be grown in vitro Armadillos Lepromatuous vs Tuberculoid Dapsone + Rifampin
Lepromatous Leprosy Presentation Communicable? Host response? Treatment
Presents diffusely over skin
Communicable
Low cell-mediated immunity with a humoral Th2 response
Dapsone + Rifampin + Clofazimine for 2-5 years
Tuberculoid Leprosy
Presentation
Host response?
Treatment
Limited to a few hypoesthetic hairless skin plaques
High cell-mediated immunity with Th1 cell response
Dapsone + Rifampin for 6 months