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CMBM Exam 3 > Bacteria > Flashcards

Bacteria Flashcards

1
Q

General characteristics of staphylococci

A
  • Gram (+) cocci, arranged as grape-like clusters
  • Facultative anaerobes
  • Catalase (+)

*differentiates it from strep

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2
Q

General features of staphylococci in regard to infection

A
  • Pyogenic
  • Commonly found on skin and mucus membranes of humans
  • Prolonged survival on inanimate objects under various conditions
  • Common cause of community acquired and healthcare-assoc. infections
  • Antibiotic resistance a problem (e.g. MRSA)
  • Metastatic infections

*spread facilitated by elaboration of serine proteases, hyaluronidases, lipases, DNases

*usually requires implantation and previous damage to tissues

*abscesses in bones (osteomyelitis), joints, lungs and kidneys

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3
Q

Staphylococcus aureus

A
  • Most pathogenic species of the genus
  • Causes more varied diseases than any other pathogen
  • Causes disease through direct invasion and destruction of tissue, or through the production of toxins
  • Unique lab characteristics

* Coagulase (bound and free): converts fibrinogen to fibrin > formation of a clot

*bound: aka clumping factor (a MSCRAMM)

  • Golden colonies and Beta-hemolytic on blood agar
  • Protein A: binds Fc portion of IgG
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4
Q

Staphylococci epidemiology

A
  • Ubiquitous; humans a major reservoir

*anterior nares of 30-90% of healthy

*transient colonization: skin, oropharynx, vagina, GI tract

  • Carriage rate higher in hospitals, persons w/ skin diseases, or those who use needles regularly (e.g. diabetics)
  • A leading cause of community-acquired and health-care assoc. infections
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5
Q

Staphylococci community acquired (CA) infections

A
  • CA infections:

*skin and soft tissue infections (abcess)

*osteomyelitis; septic arthritis

*respiratory infections (e.g. aspiration pneumonia)

*infective endocarditis

*bacteremia

  • CA-methicillin resistant s. aureus

*assoc. w/ cutaneous infections in young, healthy individuals w/ no recent healthcare exposure

*risk factors include: skin trauma (e.g. abrasions, tattoos, injection drug use), incarceration, HIV infection, and sharing of contaminated equipement or articls

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6
Q

Compare and contrast S. aureus and CoNS flow chart

A
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7
Q

Immune response to staphylococci infection

A
  • Pyogenic disease: abscess formation at local and/or metastatic sites

*anti-capsular and anti-MSCRAMM facilitate opsonization and protect against infection

  • Primary immune response: intense; PMN’s w/ influx of macrophages and fibroblasts
  • Immune response will contain infection or infection can spread to adjoining tissue or blood
  • Patients w/ congenital defects in chemotactic or phagocytic response are more susceptible to staphylococcal disease
  • Toxigenic disease: may or may not involve viable bacteria
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8
Q

Virulence factors of S. aureus

A
  • Protein A

*binds to Fc moiety of IgG, exerting an antiphagocytic effect

  • Fibronectin-binding protein

*promote binding to mucosal cells and tissue matrices

  • Cytolytic exotoxins

*attack mammalian cell (including red blood cells) membranes and are often referred to as hemolysins

  • Superantigen exotoxins

*have an affinity for the T-cell receptor-MHC class II antigen complex

* stimulate an enhanced T lymphocyte response

* T cell activation can cause toxic shock by release of large amounts of T cell cytokines

  • Enzymes

*Coagulase, catalase, hyaluronidase, fibrinolysin

  • Polysaccharide capsule
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9
Q

Staphylococci infection of skin and mucus membranes is mediated by…

A
  • MSCRAMM’s

*fibronectin-binding proteins

*CNA’s (collagen adhesin): mediates binding to collagen in connective tissue, bones and joints

*clumping factors A and B

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10
Q

Staphylococcus spread/transmission

A
  • Through direct contact w/ carrier or aerosols assoc. w/ respiratory infections
  • Facilitated by people more prone to be colonized or carriers (e.g. hospital workers, diabetics, IV drug users)
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11
Q

Staphylococcus evasion of host response

A
  • Anti-phagocytic capsule
  • Protein A: binds Fc portion of IgG, prevents opsonophagocytosis by PMN’s
  • Coagulase: fibrin clots protects bugs from white blood cells
  • Intracellular survival of small colony variants in endothelial cells and macrophages
  • Cytolytic exotoxins

*alpha, beta, delta, gamma and Panton-Valentine (P-V) leukocidin (linked w/ severe pulmonary and cutaneous infections)

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12
Q

Toxins that mediate staphylococcal disease

A
  • Exfoliative toxins (ETA and ETB)

*superantigens

*mediates staphylococcal scalded skin syndrome (SSSS)

*serine protease that split desmoglein-1

  • Enterotoxins (A-X)

*superantigens

*stable to heating at 100 C for 30 min. and resistant hydrolysis by gastric and jejunal enzymes

*enterotoxin A most commonly assoc. w/ food poisoning

*enterotoxin B and C assoc. w/ 50% of non-menstruation assoc. TSS

  • Toxic Shock Syndrome Toxin (TSST-1)

*superantigen

*strains that carry gene responsible for 90% of menstruation assoc. TSS; also assoc. w/ 50% of other cases of TSS

*can penetrate mucosal barriers

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13
Q

Skin infections caused by S. aureus

A
  • Folliculitis: pyogenic infection in hair follicle; stye if in base of eyelid
  • Furuncle: extension of folliculitis, large, painful, underlying dead and necrotic tissue (abscess)
  • Carbuncles: multiple interconnected boils that extend into deeper tissues. Fever and chills point to systemic spread
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14
Q

Staphylococcal Scalded Skin Syndrome (SSSS)

A
  • Now called Ritter’s disease
  • Caused by strains that produce exfoliative toxins A and B

*tissue specific serine proteases that cause separation of the layers of the epidermis at the desmosomes

  • An exfoliative dermatitis: characterized by extensive sloughing of the skin remote from infection site
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15
Q

Toxic Shock Syndrome (TSS) cause and characterization

A
  • Caused by exotoxins that are superantigens

*toxic shock syndrom toxin-1 (TSST-1)

*staphylococcal enterotoxin serotypes B and C

*IL-1 > fever

*TNF-a and b > capillary leakage (hypotension)

*interferon-y and IL-2 > rash

  • Characterized by fever, skin rash, hypotension, and peeling of the skin on recovery

*originally assoc. w/ use of highly absorbent tampons

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16
Q

Staphylococcal food poisoning cause and characterization

A
  • An acute gastroenteritis (an intoxication)

*short incubation period (1-6 hrs)

  • Caused by ingestion of pre-formed staphylococcal enterotoxin serotypes A-X (SEA, SEB, SEC…)

*processed meats, custard filled pastries, potato salad, ice cream

*contamination by human carriers

  • Characterized by intensive intestinal peristalsis, diarrhea and vomiting
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17
Q

Staphylococcal infection treatment

A
  • Most (90%) S. aureus resistant to penicillin due to B-lactamase
  • Drain abscess and treat w/ B-lactamase resistant penicillins and cephalosporins (e.g. nafcillin). Effective for methicillin sensitive strains (MSSA)
  • Use vancomycin for MRSA. Treat VRSA with linezolid, Synercid and daptomycin
  • Anti-toxin antibodies protect against TSS, SSSS and staphylococcal food poisoning. Consider protein synthesis inhibiting antibiotics to treat toxin mediated disease.
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18
Q

Staphylococcal resistance factors

A
  • B-lactamase

*hydrolyzes classical penicillins

*plasmid encoded

* ~90% of strains

  • Penicillin-binding protein 2a (PBP2a)

*transpeptidase w/ an alteration in binding site that results in reduced affinity for penicillin and cephalosporin-class antibiotics

*MRSA makes this

  • PBP2a encoded on diff. cassettes on Staph chromosome
  • S. aureus strains that express PBP2a referred to as MRSA strains (HA- or CA-)
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19
Q

Methicillin

A
  • a B-lactamase resistant penicillin that binds transpeptidases (PBP’s) and prevents crosslinking of peptidoglycan. Get breakdown of cell wall and the bacteria goes through osmotic lysis and dies
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20
Q

Genetics of MRSA resistance

A
  • mecA encodes for PBP2a; on a pathogenicity island w/ other exotoxin genes

*staphylococcal cassette chromosome (SCCmec)

*10 diff. SCCmec types (1 to 10)???

  • Hospital acquired strains

*carry large SCCmec types 1 to 3

*extensively drug resistant

  • Community acquired strains

*type 4 SCC mecA

*resistance to meth and other B-lactams and not other classes of antibiotics

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21
Q

Staphylococcal immunity/prevention

A
  • Immune clearance is mediated by opsonizing IgG which allows for more efficient phagocytosis
  • Immunity short live and incomplete so individuals can be re-infected
  • Good hand washing is best prevention
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22
Q

Coagulase negative staphylococci

A
  • Staphylococcus epidermidis
  • Staphylococcus saprophyticus
  • Staphylococcus lugdunensis
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23
Q

Coagulase negative staphylococci effects

A
  • Infect prosthetic and native heart valves (less common)
  • Major cause of endocarditis of artificial heart valves
  • Cause more than 50% of all infections of catheters and shunts. Major problem b/c devices are commonly used to manage critically ill patients
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24
Q

S. epidermidis general features

A
  • Coagulase (-)
  • Novobiocin sensitive
  • Normal flora; most abundant species on skin
  • Virulence: slime/biofilm formation allowing adhesion to plastic surfaces and protection from antibiotics and immune cells
  • Clinical disease: nosocomial infections assoc. w/ plastic prosthetic devices, shunts, grafts, and catheters
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25
Q

S. saprophyticus

A
  • Coagulase (-)
  • Genitourinary mucosa flora
  • Novobiocin resistant
  • Virulence: epithelial adhesions
  • Clinical disease: outpatient urinary tract infections in women
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26
Q

S. lugdunensis and S. schleiferi

A
  • Coagulase (-)
  • Novobiocin sensitive
  • Produce more serious infections than other CoNS
  • Clinical disease: native-valve endocarditis and osteomyelitis (but more commonly assoc. w/ endocarditis of artificial valves)
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27
Q

Streptococci general characteristics

A
  • Gram (+), occurs in chains or pairs
  • Catalase (-)
  • Beta hemolytic
  • Usually encapsulated
  • Normal flora: respiratory tract, genitourinary tract, gastrointestinal tract
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28
Q

Classification of Streptococci

A
  • Serologic properties (Lancefield groupings)
  • Hemolytic patterns
  • Biochemical (physiological) properties
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29
Q

Lancefield grouping

A
  • Used to classify Streptococci serologically
  • Based on major cell wall carbohydrates (A-W)
  • Diagnostic tests based on detection of these antigens
  • Originally developed to differentiate beta-hemolytic strains
  • Currently used to classify a few medically important strains (A, B, C, F, G)
30
Q

Medically important Streptococci

A
  • Group A: Streptococcus pyogenes
  • Group B: Streptococcus agalactiae
  • Group C and G: S. milleri, S. dysgalactiae
  • Group D: Enterococcus: a seperate genus but has group D antigen
  • Viridans streptococci

*heterogenous group

*several species: S. salivarius, S. mitis, S. sanquis and S. mutans

  • Anaerobic streptococci

*peptostreptococci

31
Q

Classification by hemolysis

A
  • Alpha: incomplete hemolysis, colony surrounded by a green halo
  • Beta: complete hemolysis, colony surrounded by a clear zone
  • Gamma: no hemolysis (non-hemolytic)
32
Q

Streptococcus pyogenes general characteristics

A
  • aka GAS, GABHS (Group A Beta Hemolytic Strep)
  • Expresses Group A antigen in cell wall
  • M protein: major type-specific protein assoc. w/ virulent strains

*M protein is an MSCRAMM

  • Hyaluronic acid capsule (some strains)
  • Causes suppurative and non-suppurative disease

*most common cause of bacterial pharyngitis

*life threatening myonecrosis

*acute rheumatic fever; post-strep. glomerulonephritis

33
Q

Streptococcus pyogenes virulence factors

A
  • Structural components

*M protein: blocks C3b binding; anti-phagocytic; invasion

*M-like proteins: bind Fc portion of antibody

*Hyaluronic acid capsule (some strains): weak immunogen; anti-phagocytic

*C5a peptidase; protecting from chemotaxis

*Adhesion proteins: LTA, M protein, F protein

*Invasion of epithelial cells: M and Sfbl

  • Extracellular products

*Spreading factors (what enable it to eat flesh): streptokinases (break up clots), DNases, proteases (break up ECM)

*Streptolysin (hemolysin) S and O: damage cell membranes and accounts for hemolysis

*Streptococcal pyrogenic exotoxins (SpeA, SpeB, SpeC and SpeF); super antigens

34
Q

Streptococcal pyrogenic exotoxins

A
  • SpeA, SpeB, SpeC and SpeF
  • Produced by lysogenic strains

*not every strain has the genes that produce these toxins; acquired from bacteriophage

  • Act as superantigens
  • Responsible for rash assoc. w/ scarlet fever
  • Linked to severe invasive infections
35
Q

Suppurative infections

A
  • Caused by streptococcus pyogenes
  • Upper Respiratory Tract Infection

*Pharnyngitis: most common bacterial cause of exudative pharyngitis in children (5-15)

>Nonsuppurative complications: ARF and PSGN

>Scarlet fever exanthem assoc. w/expression of Spe A, B or C

  • Skin and soft-tissue infections

*Impetigo (pyoderma): superficial infection of the skin

*Erysipelas: acute skin infection, invovles skin and subcutaneous tissue and includes systemic signs (usually preceded by resp. or skin infection w/ S. pyogenes

*Cellulitis

*Necrotizing fasciitis: streptococcal gangrene

>strep implicated in 60% of necrotizing fasciitis cases

36
Q

Streptococcal Toxic Shock Syndrome

A
  • Staphylococcal toxic shock syndrome the organism is in a localized spot and the toxin spreads into the blood-w/ Streptococcal toxic shock syndrome its not just the toxin but is the organism itself that spread so, it tends to be also assoc. w/bacteremia and necrotizing fasciitis
  • Assoc. w/strains producing: Spe A or C; M serotypes 1 or 3; very mucoid capsule
  • Freq. assoc. w/bacteremia and necrotizing fasciitis
  • Risk factors: HIV (+), cancer, diabetes, IV drug use…
37
Q

Acute Rheumatic Fever (ARF)

A
  • An autoimmune reaction to infection w/Group A strep.
  • Most common in children in developing countries; usually follows a severe respiratory infection
  • Characterized by inflammatory changes involving heart, joints, blood vessels and subcutaneous tissues (e.g. pancarditis, polyarthritis)
38
Q

Post-Streptococcal Glomerulonephritis (PSGN)

A
  • Antibodies that are specific for the M-protein on strep bind in the glomeruli and when complement comes in you get destruction of the tissue in the kidneys
  • Acute inflammation of renal glomeruli w/edema hypertension, dark urine and proteinuria
  • May follow respiratory or skin infection
39
Q

Streptococci Group A Diagnosis

A
  • Rapid tests for strep throat
  • Gram (+) cocci in pairs and chains assoc. w/leukocytes can be diagnostic for skin infections
  • Beta-hemolytic on blood agar
  • Bacitracin sensitive; seperates it from Group B
  • PYR (+): presence of L-pyrrolidonyl arylamidase (all other strep negative)
  • Streptolysin-O (ASO test): titer detects recent respiratory S. pyogene infection; Anti-DNase B for recent cutaneous infection
40
Q

Streptococci Non-suppurative complications

A
  • Sometimes when children come down w/pharyngitis and theyre not treated w/antibiotics, they can be more susceptible to these non-suppurative complications and these non-suppurative complications are actually autoimmune reactions that occur b/c the M-protein may be having some cross-reactivity w/some of the antigens that are found in our cardiac and also some of the antigens that are found in the kidneys
  • Acute Rheumatic Fever (ARF)
  • Post-Streptococcal Glomerulonephritis (PSGN)
41
Q

Streptococcus agalactiae (GBS) characteristics

A
  • GBS; Group B strep assoc. w/neonatal disease
  • Colonize the lower GI and GU tract; transient vaginal carriage
  • Major virulence factor: Anti-phagocytic polysaccharide
  • Most common cause of sepsis and meningitis in newborns
  • Early onset (endogenous): sepsis (80%), pneumonia or meningitis
  • Late onset (exogenous): bacteremia w/meningits
42
Q

Streptococcus agalactiae clinical considerations

A
  • Colonizes female genitourinary tract

*all pregnant women screen at 35-37 weeks gestation

  • 50% of infants born to colonized mothers become colonized
  • Pregnant women

*postpartum endometritis, wound infections, UTI’s

  • Non pregnant women and men

*opportunistic infections (HIV, diabetics, cancer); skin and soft tissue infectins, bacteremia, urosepsis

43
Q

Streptococcus agalactiae diagnosis techniques

A
  • Gram stain of CSF
  • CAMP test: increased hemolysis on blood plates when grown w/S. aureus
  • PCR-based amplification assay
44
Q

Viridan Streptococci general characteristics

A
  • Heterogenous collection of alpha and non-hemolytic strep
  • Constitute main facultative oral flora
  • Diseases include:

*dental caries

*sub-acute bacterial endocarditis in patients w/abnormal heart valves, dental caries, and intra-abdominal infections

  • Bacteremia
  • Abscesses in brain, oropharnyx or peritoneal cavity
45
Q

Streptococcus pneumoniae general characteristics

A
  • Gram pos. diplococci, lancet shaped in short chains
  • Alpha-hemolytic on blood agar
  • Optochin sensitive, lysed by bile
  • Encapsulated, quite a few serotypes, most isolated serotypes included in polyvalent vaccine (e.g. Prevnar 13); encapsulation is necessary for the virulence-protects them from phagocytes
  • Normal flora of throat and nasopharynx, infection can be endogenous or exogenous
  • Highest incidence of infection in children and the elderly b/c of low levels of protective antibodies
46
Q

Streptococcus pneumoniae virulence factors

A
  • Capsule (basis for vaccine)
  • Surface protein adhesions
  • Release of cell wall components>inflammatory response
  • Pneumolysin

*exotoxin that creates pores in ciliated epithelial cells and phagocytes; activates complement>migration of inflammatory cells>tissue damage

  • Secretory IgA protease
47
Q

Streptococcus pneumoniae clinical diseases

A
  • Typical lobar pneumonia: leading cause; often referred to as pneumococcal pneumonia

- Meningitis: most common cause in children and young adults

  • Otitis media
  • Sinusitis
  • Bacteremia
48
Q

Streptococcus pneumoniae laboratory diagnosis

A
  • Lancet-shaped diplococcus
  • Optochin sensitive
  • Bile soluble (dissolves in bile)

- Quelling reaction to detect capsule

  • Pneumococcal C polysaccharide can be detected in urine (immunoassay detection)
49
Q

Streptococcus pneumoniae treatment and prevention

A
  • Antibiotics: will be discussed in systems
  • Polyvalent vaccines for young children and for 55+ available (e.g. Prevnar 13)
50
Q

Enterococci general characteristics

A
  • For the most part patients must be compromised one way or another to be infected by; so must worry about hospitalized patients getting a nosocomial infection
  • Gram pos. cocci, usually in pairs
  • Variable hemolysis
  • Normal intestinal flora (as name implies)

*due to its antibiotic resistance, this organism doesn’t die so when the flora gets knocked out by a broad-spectrum antibiotic it will no longer have resistance from the other bacteria being around and it can overgrow

  • Virulence: resistance to commonly used antibiotics
  • One of the most common causes of nosocomial infections
51
Q

Enterococci clinical considerations

A
  • Infections in patients

*elderly or debilitated

*mucosal or epithelial layer has been disrupted (e.g. catheterization)

*treated w/broad spectrum antibiotics

52
Q

Enterococci clinical manifestations

A
  • UTI

*one of the #1 types of infection cause by this organism

  • Nosocomial bacteremia

*assoc. w/localized infection or endocarditis; can start in UTI and gain access to blood

  • Bacterial endocarditis

*10-20% of cases on both native and prosthetic valves

  • Peritonitis

*typically polymicrobial

53
Q

Enterococci laboratory identification

A
  • Growth in 6.5% salt
  • Grows at 42 C
  • Grows in the presence of 40% bile salts
  • PYR (+): produces L-pyrrolidonyl-arylamidase
54
Q

Enterococci treatment

A
  • Just know that antibiotic resistance is a problem for enterococci
55
Q

Enterobacteriaceae general characteristics

A
  • Facultative, gram negative, rod-shaped bacteria found as normal flora or pathogen in the GI tract of humans or animals
  • Ubiquitous organism

*present throughout the environment; soil, water, etc…

*normal intestinal flora in humans and animals

  • Opportunistic and primary infections
  • All ferment glucose
  • All are oxidase negative (no cytochorme C oxidase)

*important in seperating them from pseudomonas

  • Motility and ability to ferment lactose is speicies-specific
  • Some produce prominent capsules
  • Many possess common and sex pili
56
Q

Enterobacteriaceae clinical diseases

A
  • Sepsis (1/3)
  • UTI’s (70%)
  • GI’s
  • Pneumonias
  • Meningitis
  • Devices assoc. infections
  • Community and hospital-acquired by primary and opportunistic pathogens
57
Q

Enterobacteriaceae organisms

A
  • Escherichia
  • Shigella
  • Salmonella
  • Klebsiella
  • Proteus
  • Yersinia
58
Q

Escherichia coli diseases

A
  • Uropathogenic strains (UPEC) are the leading cause of UTI

*cause ~85% of UTI’s in females- in hopital case ~50% b/c when in dwelling catheter is placed is when the other opportunist pathogens come in

  • K1 strains are assoc. w/ neonatal meningitis

*along w/Group B strep

  • Most common Gram (-) isolated from patients w/sepsis
59
Q

Enterobacteriaceae opportunists

A
  • Opportunist organisms for the most part will only be found in patients found in long term healthcare facilities or hospitalized, have in dwelling catheters, debilitated or immuno compromised in one way or another
  • Salmonella
  • Klebsiella
  • Proteus
60
Q

Enterobacteriaceae serological classification

A
  • O, H, K antigens
  • O (somatic) antigen

*O side chains on LPS

*made of repeated sugars, hydrophilic, is very antigenic and can undergo variation; the antigenic variation can be responsible for diff. serotype in these species

  • H antigens

*flagella antigens

  • K antigens

*capsular antigens

*type specific polysaccharides

61
Q

Klebsiella diseases

A
  • Necrotic pneumonia (primary lobar)

*pneumonia produces a thick, bloody sputum referred to as “current jelly” sputum

  • Community and hospital acquired UTI’s
  • Multidrug resistant strains a problem
62
Q

Proteus mirabilis diseases

A
  • Produces large quantities of urease
  • Swarming motility
  • Community and hospital acquired UTI’s
63
Q

Pseudomonas and related bacteria general characteristics

A
  • Gram (-) bacilli
  • Oxidase (+)
  • Non-fermentative
  • Opportunistic
  • Antibiotic resistance a problem
  • Important nosocomial pathogens
64
Q

Pseudomonas aeruginosa

A
  • Most medically important strain of Pseudomonas
  • Ubiquitous, tolerate a wide range of temps

*can be found everywhere but, especially likes moist environments, can be found in some disinfectants, distilled water

  • Fast growing, requires minimal nutrients for growth which accounts for broad environmental distribution
  • Infections are primarily opportunistic

*e.g. important pathogen in individuals w/cancer, cystic fibrosis, neutropenic patients and burn victims

65
Q

Pseudomonas laboratory features

A
  • Gram (-) rods, in pairs, motile
  • Non-fermentative, aerobic or anaerobic
  • Growth on agar plates

*produces a blue/green luminescent colony

66
Q

Burkholderia species

A
  • B. cepacia and B. gladioli species: low virulence and morbidity except in CF patients or patients w/granulomatous disease
67
Q

Lipid A

A
  • Gram (-) endotoxin
  • Portion of LPS that can enduce endotoxic shock

*fever, shock, hypotension, disseminated intravascular coagulation (DIC)

68
Q

Acinetobacter baumannii

A
  • Pseudomonas related bacteria
  • Opportunist
69
Q

Moraxella catarrhalis

A
  • Pseudomonas related bacteria
  • Cause problems in patients w/ COPD, especially elderly and antibiotic resistance is not a major concern
70
Q

Stenotrophomonas maltophilia

A
  • Pseudomonas related bacteria
  • Major Opportunist

CMBM Exam 3 (7 decks)

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