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FDN3 By Nathan and Minnie > Gram Positive Bacteria > Flashcards

Gram Positive Bacteria Flashcards

1
Q

What is a superantigen?

What biological and physiological effects does a superantigen have?

A

A substance that causes proliferation of entire subsets of T cells (those w/ T cell receptors w/ specific Vß domains)

Large amounts of cytokines such as IL-1 and TNF are released

Cytokines cause fever, shock, and organ failure

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2
Q

What are the steps in pathogenesis?

A
  1. Enter the host
  2. Adhere to the host
  3. Multiple, persist, damage the host (invade into cells, secrete toxins, evade immune response)
  4. Spread to next host sometimes
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3
Q

What are Staphylococci?

A

Gram-positive cocci that grow in grape-like clusters

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4
Q

What are the three medically important staphylococci?

A
  • Staphylococcus aureus
  • Staphylococcus epidermidis
  • Staphyloccocus saprophyticus
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5
Q

What is important about Staphylococcus saprophyticus?

A

Staphylococcus saprophyticus is a common cause of UTIs in young women

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6
Q

What is important about Staphylococcus epidermidis?

A

Staphylococcus epidermidis is adept at attaching to and growing on prosthetic devices

(normal inhabitant of skin, nose, and mouth of humans; less virulent than S. aureus)

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7
Q

Staphylococcus aureus is a [Gram, shape, description, metabolic]

A

Gram-positive cocci that grows in grape-like structures and is a facultative anaerobe

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8
Q

What is the most virulent of the staphylococci?

A

Staphylococcus aureus

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9
Q

Which compounds determine the pathogenicity of Staphylococcus aureus?

A
  • Toxic shock syndrome toxin 1 (TSST-1)
  • Staphylococcal enterotoxins A-E, G-I
  • Exfoliatin (exfoliative toxin)
  • Alpha toxin (alpha-hemolysin)
  • Panton-Valentine leukocidin (PVL)
  • Coagulase
  • Protein A
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10
Q

Why is TSST-1 from Staphylococcus aureus relevant?

How does TSST-1 exert systemic effects?

What sort of antigen is TSST-1?

A

Cause of most cases of bacterial toxic shock syndrome

May be produced by staphylococci growing at an isolated site, reach the bloodstream, and cause systemic effects without bacteremia

Superantigen

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11
Q

Why are Staphylococcal enterotoxins A-E and G-I relevant?

How do they exert their effects?

Why are they hard to kill?

A

Cause staphylococcal food poisoning and toxic shock syndrome

Superantigens

Act directly on neural receptors in upper GI tract, stimulating vomiting center in brain to cause vomiting 2-5 hrs after ingestion

Resistant to boiling for 30 minutes and digestive enzymes

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12
Q

What condition does exfoliatin from Staphylococcus aureus cause?

How does it do that?

A

Scalded skin syndrome

Disrupts intercellular junctions in the skin, leading to splitting of epidermis between stratum spinosum and stratum granulosum

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13
Q

What kind of toxin is alpha-toxin from Staphylococcus aureus?

What kind of factor alpha-toxin an example of?

A

Pore-forming toxin

(inserts into lipid bilayers of mammalian cells, forms pores, causes cell death and tissue destruction)

Hemolysin

(lyses RBCs when bacteria are grown on blood agar plates, thought to lyse other types of cells during infections or disrupt intercellular junctions in epithelial barriers)

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14
Q

What kind of toxin is Panton-Valentine leukocidin from Staphylococcus aureus?

What sort of Staphylococcus aureus infection is it associated with?

How does it work?

What is the gene for PVL carried by?

A

Pore-forming toxin

Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA)

Contributes to cell lysis, causing severe necrotic infections associated w/ many CA-MRSA strains

Bacteriophage

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15
Q

What is the function of coagulase from Staphylococcus aureus?

How does it work?

A

Helps create a mechanical barrier that blocks off neutrophils

  1. Binds to prothrombin to form a complex
  2. Complex initiates polymerization of fibrin to form a clot
  3. Fibrin contributes to fibrin capsule surrounding many abscesses
  4. Mechnical barrier prevents neutrophils from entering abscesses
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16
Q

What is the function of Protein A from Staphylococcus aureus?

How does it work?

A

Prevents antibody-mediated immune clearance

Binds to Fc portion of IgG molecules

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17
Q

What clinical diseases does Staphylococcus aureus cause?

A
  • Joint and bone infections
  • Endocarditis
  • Toxic shock syndrome
  • Staphylococcal food poisoning
  • Scalded skin syndrome
  • Skin and soft tissue infections
  • Hospital-acquired infections (nosocomial)
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18
Q

How does Staphylococcus aureus cause joint and bone infections?

A

Gains access to bloodstream and causes infections at distant sites such as joints (septic arthritis) and bones (osteomyelitis)

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19
Q

How does Staphylococcus aureus cause endocarditis?

Why does this often lead to death?

Which population is this especially common in?

What are the clinical signs?

A

Staphylococcus aureus goes to the bloodstream and causes localized infection of valves of the heart

Bacteria form biofilms on heart valves and a very difficult to eradicate with antibiotics

IV drug users

Osler’s nodes, Janeway lesions, conjunctivital hemorrhages, heart murmurs

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20
Q

What are the symptoms of toxic shock syndrome from Staphylococcus aureus?

What tends to occur upon resolution of toxic shock syndrome?

What is this illness most associated with?

What is this illness also associated with?

Are blood cultures positive or negative?

A

High fever, vomiting, diarrhea, sore throat, muscle pain, rash, hypotension or shock that can lead to organ failure

Desquamation of skin, especially digits

Most common cause: tampon use (strains that colonize vagina and produce TSST-1)

Wound infections (S. aureus enterotoxins or TSST-1 are the cause)

Blood cultures are negative

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21
Q

Which toxin is the cause of food poisoning in Staphylococcus aureus?

Describe food poisoning due to Staphylococcus aureus

A

Enterotoxin

A self-limited episode of vomiting and diarrhea that begins 2-5 hrs after ingestion of food contaminated w/ enterotoxins

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22
Q

Which toxin is the cause of scalded skin syndrome due to Staphylococcus aureus?

What is the main symptom?

Which age groups are primarily affected?

Describe the localization of the infection

A

Exfoliatin

Desquamation

Infants and children under 5 years old

Infection is usually localized, such as conjunctivitis, but exfoliatin reaches bloodstream and may cause exfoliation at remote sites

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23
Q

What is the difference between a furuncle and a carbuncle?

A

Furuncles are boils, most of which begin with the blockage of hair follicle or sweat gland that subsequently becomes infected

Carbuncles are multiple abscesses formed after infection spreads from a furuncle

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24
Q

What types of skin and soft tissue infections does Staphylococcus aureus cause?

A
  • Furuncle and carbuncle
  • Cellulitis (also folliculitis, other soft tissue infections)
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25
Q

Which two types of bacteria tend to cause skin infections?

A

Staphylococcus aureus, group A streptococci

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26
Q

What is a nosocomial infection?

A

An infection acquired after people are admitted to the hospital and have undergone procedures

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27
Q

Describe the diagnostic laboratory test findings for Staphylococcus aureus

A
  • Easily culturable on blood agar plates and seen on Gram-stain of tissue specimens
  • Colonies have a gold color
  • Catalase positive
  • Coagulase positive
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28
Q

How can you differentiate Staphylococcus aureus from streptococci using a lab test?

A

Staphylococcus aureus is catalase positive

Streptococci are catalase negative

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29
Q

How can you differentiate Staphylococcus aureus from Staphylococcus epidermidis and Staphylococcus saprophyticus on a lab test?

A

Staphylococcus aureus is coagulase positive

Staphylococcus epidermidis and Staphylococcus saprophyticus are coagulase negative

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30
Q

How is Staphylococcus aureus infection treated?

Why is treatment difficult?

A

Drainage of all collections of pus and antibiotics

Almost all isolates produce a beta-lactamase that degrades penicillin

Antistaphylococcal penicillins (methicillin, nafcillin, oxacillin) and cephalosporins are resistant to beta-lactamases but MRSA is resistant to the antistaphylococcal penicillins

VRSA is resistant to vancomycin

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31
Q

Why is MRSA resistant to antistaphylococcal penicillins?

A

MRSA contains a variant penicillin-binding protein called PBP2’ encoded by the mecA gene that does not bind beta-lactam antibiotics

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32
Q

How can MRSA be prevented?

A
  • Isolation of colonized or infected patients
  • Meticulous hand-washing and glove-wearing by healthcare personnel
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33
Q

Enterococci are [Gram, shape]

A

Enterococci are Gram-positive cocci

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34
Q

Which species of Enterococci are medically important?

Which is more common?

Which is more resistant to antimicrobials?

A

Enterococcus faecalis and E. faecium

E. faecalis is more common

E. faecium is more resistant to antimicrobials

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35
Q

Where are E. faecalis and E. faecium normally found?

A

GI tract

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36
Q

Why are Enterococci of medical concern?

A

Enterococci have antibiotic resistance especially to vancomycin

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37
Q

What carries the gene for vancomycin resistance in enterococci?

What biochemical change does the vancomycin resistance gene cause?

How does this make enterococci resistant to vancomycin?

A

Carried by a transposon that is carried by a self-transferrable plasmid

Encodes side chains that allow for synthesis and substitution of D-Ala-D-lactate for D-Ala-D-Ala in the peptide side chains of peptidoglycan

Vancomycin cannot bind to D-Ala-D-lactate

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38
Q

Where are Enterococci infections commonly acquired?

Where in the body do Enterocci infections occur?

A

Hospital (nosocomial)

UTIs, wounds, biliary tract, intra-abdomen, blood (intravascular catheters, endocarditis)

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39
Q

Describe the treatment strategy for Enteroccoci

A
  • Penicillin/ampicillin (usually w/ aminoglycosides)
  • If resistant to penicillin/ampicillin, use vancomycin
  • If resistant to vancomycin, use linezolid or daptomycin
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40
Q

Why are amigolycosides added to penicillin/ampicillin in the treatment of Enterococci?

A

Pencillin/ampicillin are bacteriostatic against Enterococci

When aminoglycosides are added, the combo is bacteriacidal

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41
Q

Why would you not want to overuse vancomycin?

A

Overuse of vancomycin predisposes to vancomycin-resistant Enterococci (VRE) colonization/infection

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42
Q

Who commonly transmits VRE from patient to patient?

How can VRE be prevented?

A

Healthcare workers

Hand washing and contact precautions, judicious use of vancomycin

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43
Q

What procedure is important to order after Streptococcus gallolyticus infection? Why?

A

Colonoscopy to rule out colon cancer

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44
Q

Which skin infection can be associated w/ coronary bypass surgery involving veins removed from the leg?

Which bacteria causes this?

A

Cellulitis

Streptococcus pyogenes

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45
Q

How are streptococci grouped?

A

By hemolysis

Alpha hemolysis: partial hemolysis, greenish tint

Beta hemolysis: complete hemolysis, clear color; Group A, Group B, Group D (Note: Group D usually has gamma hemolysis)

Gamma hemolysis: Group D; no hemolysis

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46
Q

List the relevant alpha-hemolytic streptococci

A

Viridans streptococci

Streptococcus pneumoniae

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47
Q

List the relevant beta-hemolytic streptococci

A

Group A: Streptococcus pyogenes

Group B: Streptococcus agalactiae

Group D: Streptococcus gallolyticus (usually gamma or alpha hemolytic)

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48
Q

What determines the groupings for beta-hemolytic streptococci?

A

Groupings (A, B, D) ar based on the carbohydrate antigens in the cell wall

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49
Q

Describe viridans streptococci

A
  • Alpha-hemolytic
  • Generally nongroupable (20+ species)
  • Includes S. mutans, S. sanguis, S. intermedius, S. anginosus
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50
Q

Describe Streptococcus pneumoniae

(Hemolysis, growth, clinical significance)

A
  • Alpha-hemolytic
  • Grows as diplococii on gram-stained specimen
  • Causes pneumonia, other respiratory tract infections
  • Virulence factors
    • Capsule: Prevents phagocytosis
    • Pneumolysin: degrades hemoglobin to a green pigment
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51
Q

What is the most clinically relevant group B streptococcus?

(Hemolysis, clinical significance)

A

Streptococcus agalactiae

Beta-hemolytic

  • Causes neonatal sepsis, meningitis
  • Colonizes the vagina; passed to the newborn during delivery
  • Women who are GBS (+) are treated with penicillin or vancomycin prior to delivery
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52
Q

What is the most clinically significant Group D streptococcus?

(Hemolysis, clinical significance)

A

Streptococcus Gallolyticus

Gamma-hemolytic

  • Rarely causes infections
  • Bloodstream infection caused by S. Gallolyticus is often associated with colon cancer
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53
Q

Describe the laboratory findings that would indicate Streptococcus pyogenes

[Gram, growth patern, hemolysis, catalase, titers]

A
  • Gram (+)
  • Grows in chains or pairs
  • Beta-hemolysis (group A)
  • Catalase (-)
  • ASL-O antibody titers
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54
Q

Describe the appropriate course of treatment for a Streptococcus pyogens infection

A
  • Penicillin = treatment of choice
    • Most strains are sensitive
  • If STSS
    • Treat with penicillin + clindamycin (inhibits SPE production)
    • Give IVIG: Contains aintbodies against toxins
  • If necrotizing fasciitis
    • Treat with penicillin + clindamycin (inhibits SPE production)
    • Surgical debridement necessary
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55
Q

List the relevant toxins associated with Streptococcus pyogenes

A
  • Streptolysin (SLO)
  • M Protein
  • Streptococcal pyogenic endotoxins (SPEs)
  • Streptokinase
  • C5a Peptidase
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56
Q

List the clinical diseases associated with Streptococcus pyogenes

A
  • Streptococcal pharyngitis
  • Scarlet Fever
  • Streptococcal Toxic Shock Syndrome (STSS)
  • Necrotizing fasciitis
  • Impetigo
  • Cellulitis
  • Rheumatic Fever
  • Post-streptococcal glomerulonephritis (PSGN)
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57
Q

Describe the mechanism of action of streptolysin (SLO)

A

Note: We generate antibodies to SLO; SLO antibodies are diagnostic of an Streptococcus pyogenes infection

SLO formes pores in the plasma membrane of human cells.

This transports virulence factors into the cell, leading to beta-hemolysis

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58
Q

List the clinical diseases associated with SLO toxin

A

Streptococcal pharyngitis

Post-streptococcal glomerulonephritis (PSGN)

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59
Q

Describe the relevant clinical findings for streptococcal pharyngitis

A

“Strep throat”

  • Frequently occurs in children
  • Sore throat
  • Fever
  • Headach
  • Swollen, erythmatous tonsils, sometimes with purulent exudates
  • Impossible to clinically differentiate from viral pharyngitis
  • May be accompanied by scarlet fever
  • Usually self-limiting (but routinely treated with antibiotics to reduce risk of rheumatic fever)
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60
Q

Describe the relevant clinical findings of post-streptococcal glomerulonephritis (PSGN)

A
  • Onset 2 weeks after the initial S. pyrogenes infection
    • Early treatment is does not prevent PSGN
  • Damage due to accumulation of SLO antibodies/antigens in the kidney
  • Can follow pharyngitis OR soft tissue infection
  • Associated with edema, hypertension, hematuria, proteinuria
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61
Q

Describe the structure and significance of M protein

A

M protein is associated with streptococcus pyogenes infection

  • M protein is made up of fibrillar molecules that extend past the bacterial surface
  • It is anchored in peptidoglycan
  • Used to serotype S. pyogenes
  • Prevents phagocytosis
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62
Q

What clinical disease is associated with M protein?

A

M protein is the virulence factor associated with rheumatic fever. (Streptococcus pyogenes produces M protein)

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63
Q

Describe the cause of rheumatic fever

A

Onset ~3 weeks after onset of streptococcal pharyngitis

M protein is antiphagocytic and triggers a humoral response; M protein mimicks myosin in the heart, causing the body to mount a repsonse and attack myosin

This leads to permanent heart valve damage (M protein leads to damage of the Mitral valve)

Early treatment of pharyngitis can prevent rheumatic fever

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64
Q

How is rheumatic fever diagnosed?

A

Use JONES criteria

  • J - Joints (polyarthritis)
  • O - Heart problems (think of the O as a heart shape)
  • N - Nodules (subcutaneous)
  • E - Erythema marginatum (rash w/thick red border)
  • S - Sydenham’s chorea (rapid involuntary movements, especially in hands and face)

Look for SLO antibodies as evidence of a recent Group S streptococcus infection

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65
Q

Why is it important to treat streptococcal pharyngitis with antibiotics?

A

Early treatment can reduce the risk of developing rheumatic fever

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66
Q

Describe the effects of streptococcal pyogenic endotoxins (SPEs)

A

SPEA, SPEC -> Scarlet Fever, STSS

SPEB -> Necrotizing fasciitis

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67
Q

Which virulence factor is associated with necrotizing fasciitis?

A

SPE B

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68
Q

Describe the Streptococcal pyogenic endotoxins (SPEs)

A

SPEA, SPEC

  • Superantigens
  • Genes are carried by phage
    • Only S. pyogene bacterium that are infected by a phage can produce SPEA and SPEC
  • Lead to STSS, Scarlet Fever

SPEB

  • Superantigen
  • A protease
  • Leads to necrotizing fasciitis
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69
Q

What are the causative virulence factors of scarlet fever?

A

SPEA, SPEC produced by streptococcus pyogenes infection

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70
Q

Describe the clinical findings associated with scarlet fever

A
  • Streptococcus pyogenes infection
    • Superantigens SPEA, SPEC
  • Pharyngitis
  • Erythmatous, sandpaper rash
  • Widespread rash that spares the face/area around the mouth
  • Accentuated in skin creases
  • Strawberry tongue
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71
Q

Describe the clinical findings associated with Streptococcal Toxic Shock Syndrome (STSS)

A

Similar to TSS caused by staph infection

  • Fever, hypotension, multi-organ failure
  • No rash
  • Not associated with tampon use
  • Most patients are bacteremic, have an associated soft tissue infection
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72
Q

How would you differentiate between TSS and STSS?

A

TSS: Caused by Staphylococcus aureus

  • Rash
  • Associated with tampon use

STSS: Caused by Streptococcus pyogenes

  • No rash
  • Not associated with tampon use
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73
Q

Describe the clinical findings associated with necrotizing fasciitis

A
  • Streptococcus pyogenes infection
    • Protease: SPEB
  • Necrossi of superficial and/or deep fascia of muscles
  • Infection site is minor break in skin or surgical wound
  • Abrupt onset
  • Pain sensitivity, fever, malaise, with minimal physical findings
  • Tissue damage progresses rapidly
  • Buliae on surface
  • Mottled, dusky skin over necrosis
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74
Q

What is streptokinase?

Why is it significant?

A

Streptokinase is virulence factor associated with streptococcus pyogenes

It causes lysis of fibrilin clots by converting plasminogen to plasmin

  • Bad: causes bacteria to spread
  • Good: Therapeutic uses in lysing coronary artery clots in acute myocardial infarction
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75
Q

Which streptococcus pyogenes-associated virulence factor has a therapeutic use?

A

Streptokinase; it is used to lyse coronary artery clots in acute myocardial infarction

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76
Q

What is C5a peptidase?

What does it do?

A

A virulence factor associated with Streptococcus pyogenes

It is an extracellular enzyme that cleaves C5a (a complement component)

  • This prevents the recruitment of phagocytes to bacteria
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77
Q

Describe the clinical findings associated with impetigo

A

Infection by Streptococcus Pyogenes

  • Infection of the epidermis
  • Seen in children
  • Associated with poor hygiene
  • Small vescicles on exposed skin enlarge and become pustular
  • Vescicles rupture -> yellow crust
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78
Q

Describe the clinical findings associated with cellulitis

A

Infection by Streptococcus Pyogenes

  • Infection of the dermis, subcutaneous tissue
  • Fever, lymphangitis
  • Located at sites wtih compromised lymph drainage
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79
Q

List the soft tissue infections associated with Streptococcus pyogenes

A
  • Impetigo
  • Cellulitis and Erysipelas
  • Necrotizing fasciitis
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80
Q

List the nonsupprative sequale associated with S**treptococcus pyogenes infection

A
  • Post-streptococcal glomerulonephritis
    • Follows soft tissue infection of pharyngitis
    • 2 weeks initial infection
    • Early treatment of the initial infection cannot prevent
  • Rheumatic fever
    • Follows pharyngitis only
    • 3 weeks after initial infection
    • Early treatmetn of the initial infection can prevent
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81
Q

Straberry tongue is associated with [disease], caused by [bacteria]

A

Straberry tongue is associated with scarlet fever, caused by streptococcus pyogenes

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82
Q

What condition is caused by streptococcal pyogenic enterotoxin B?

A

Necrotizing fasciitis

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83
Q

What bacteria causes impetigo and cellulitis?

A

Staphylococcus aureus or streptococcus pyogenes

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84
Q

Bacillus spp. are [metabolic, Gram stain, shape, important characteristc]

A

Bacillus spp. are aerobic Gram-positive rods that form spores

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85
Q

Which Bacillus bacteria are of medical importance?

A
  • Bacillus anthracis (anthrax)
  • Bacillus cereus (food-poisoning)
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86
Q

Bacillus anthracis is a [metabolic, Gram stain, shape, feature of growth, important characteristic]

A

Bacillus anthracis is aerobic Gram-positive rods that grows in chains (bamboo rods/box cars) and forms spores

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87
Q

How are humans exposed to Bacillus anthracis?

Who is most at risk?

A

Handling of contaminated meats and hides

Agricultural workers and veterinary personnel

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88
Q

Where are virulence factors for Bacillus anthracis carried?

89
Q

What are the determinants of pathogenicity of Bacillus anthracis?

Where are they found?

A
  • Anthrax toxin
  • Capsule composed of poly-D-glutamic acid

Both found on a plasmid

90
Q

What sort of toxin is anthrax toxin?

91
Q

How do A-B toxins work?

A

Fragment B (binding) binds to surface of cells and transports Fragment A into cells

Fragment A (active) has activity that damages cell

92
Q

What kind of toxin is anthrax toxin?

Describe the structure of anthrax toxin

A

A-B toxin

Actually two toxins that share the same B subunit

B subunit: edeme factor and lethal factor

A subunit: protective antigen

93
Q

How does the edema factor portion of the anthrax toxin exert its effects?

A
  1. Has adenylate cyclase activity
  2. Increases intracellular cAMP levels
  3. Causes edema and inhibition of neutrophil phagocytosis
94
Q

How does the lethal factor portion of anthrax toxin exerts its effects?

A
  1. Zinc metalloprotease that cleaves host cell kinases
  2. Causes lysis or inactivation of macrophages, dendritic cells, and suppressor T cells
95
Q

What does protective antigen (PA) do?

A

Forms a pore that binds to cells and facilitates entry of edema factor and lethal factor

96
Q

What is the capsule of Bacillus anthracis composed of?

Where is it encoded?

How does this protect Bacillus anthracis?

A

Poly-D-glutamic acid

Encoded on plasmid

Has antiphagocytic properties

97
Q

What clinical diseases does Bacillus anthracis cause?

A
  • Cutaneous anthrax
  • Inhalation anthrax (Woolsorters’ disease)
  • Gastrointestinal anthrax
98
Q

List the types of diseases caused by Bacillus anthracis in order of decreasing mortality

A

Inhalation anthrax > GI anthrax > cutaneous anthrax

99
Q

How does cutaneous anthrax occur?

Describe the symptoms of cutaneous anthrax

How does cutaneous anthrax resolve?

A

Spores introduced into skin through cuts or abrasion exposed to contaminated carcasses or through fly bights

Small red papule enlarges to form an ulcer w/ blackened necrotic eschar surrounded by expanding zone of edema, painless, may be surrounded by small satellite vesicles

Spontaneously resolves

100
Q

How does inhalation anthrax (Woolsorters’ disease) occur?

Describe the symptoms of inhalation anthrax

What disease does inhalation anthrax resemble?

How does inhalation anthrax resolve?

A

Spores inhaled often during handling of contaminated hides, hair, or wool

Fever, shortness of breath, hypotension

Resembles the flu

Death

(large hemorrhagic mediastinal lymph nodes are common, organisms sometimes seen on blood smear)

101
Q

What is a telltale symptom of inhalation anthrax on xray?

A

Widened mediastinum

102
Q

How does gastrointestinal anthrax occur?

Describe the symptoms of gastrointestinal anthrax

A

Ingestion of contaminated meat

Ulcers form at site of infection (mouth, esophagus, intestine)

103
Q

What diagnostic lab tests are used for Bacillus anthracis?

A
  • Gram-staining
  • Grow from pus, blood, or sputum streaked on blood agar plates
  • Serologic tests
104
Q

What is notable about Gram-staining of cutaneous lesions of someone with cutaneous anthrax?

A

Large number of Bacillus anthracis organisms will be seen

105
Q

How is Bacillus anthracis treated?

A
  • Sensitive to penicillin
  • Ciprofloxacin and doxycycline are recommended due to concerns about weaponized strains resistant to penicillin
  • Second agent added for inhalational anthrax (rifampin, vancomycin, pencillin, clarithromycin)
  • Raxibacumab and oblitoxaximab for inhalational anthrax
106
Q

How do raxibacumab and obiltoxaximab work?

A

Monoclonal antibodies that bind to host cell receptor of PA and prevent binding of PA to the receptor

107
Q

How can anthrax infection be prevented?

A
  • Nonliving vaccine (PA active component) used in humans
  • Live-attenuated vaccine containing spores used in domestic animals
  • 60 day course of ciprofloxacin recommended after presumed exposure to aerosolized spores
108
Q

Listeria are [Gram stain, metabolic, shape]

A

Listeria are Gram-positive facultatively anaerobic rod-shaped bacteria

109
Q

Which species of Listeria is medically important?

A

Listeria monocytogenes

110
Q

Listeria monocytogenes are [Gram stain, metabolic, shape, intra/extracellular]

A

Listeria monocytogenes are Gram-positive facultatively anaerobic rod-shaped bacteria that are facultatively intracellular

111
Q

At what temperatures do Listeria monocytogenes grow well in?

A

Refrigeration temperatures

112
Q

What route of transmission is important for Listeria monocytogenes?

A

Foodborne transmission (unpasteurized milk, cheeses, coleslaw, raw meat)

113
Q

Name a common case of Listeria monocytogenes infection

A

Person infected after eating at a delicatessen

114
Q

What does it mean that Listeria monocyotgenes is a facultative intracellular pathogen?

A

Can grow and replicate in environment (not obligate intracellular)

Ability to invade eukaryotic cells is essential step in its pathogenesis

115
Q

What are adhesins?

A

Factors that mediate adherence of bacteria to eukaryotic cells

116
Q

What does internalin do for Listeria monocytogenes?

A

Mediates attachment and invasion of mammalian cells (a type of adhesin)

117
Q

What happens when Listeria monocytogenes bacteria enter a cell?

A
  1. Briefly reside inside intracellular vacuoles
  2. Escape via listeriolysin O
  3. Propel themselves around cytoplasm by forming and pushing against actin tails
  4. Form protrusions into neighboring epithelial cells using ActA
  5. Membranes around protrusions lysed
  6. Bacteria enter cytoplasm of adjacent epithelial cells without exposure to external environment
118
Q

What kind of toxin is listeriolysin O?

What other toxins is listeriolysin analogous to?

A

Pore-forming toxin

Analogous to streptolysin O of Streptococcus pyogenes and pneumolysin of Streptococcus pneumoniae

119
Q

What bacterial protein does Listeria monocytogenes use to propel around the cytoplasm by forming and pushing against actin tails and then form protrusions to neighboring epithelial cells?

120
Q

What is the purpose of protrusions formed by Listeria monocytogenes?

A

Protrusions allow Listeria monocytogenes to enter cytoplasm of adjacent epithelial cell without exposure to external environment or humoral immune system)

121
Q

What clinical diseases does Listeria monocytogenes cause?

A
  • Asymptomatic or influenza-like illness in pregnant women (but can cause abortion, premature delivery, bacteremia)
  • Neonatal disease (early or late onset)
  • Mengitis in elderly or immunocompromised individuals
122
Q

How is early onset neonatal disease due to Listeria monocytogenes acquired?

What is it characterized by?

A

Transmission across placenta from infected mother

Disseminated abscesses and granulomas

123
Q

What can late onset neonatal disease due to Listeria monocytogenes cause?

A

Meningitis

124
Q

How is Listeria monocytogenes infection usually diagnosed in diagnostic lab tests?

What are the important characterisrtics?

A
  • Growing organism from CSF, blood, amniotic fluid
  • Small smooth colonies surrounded by narrow rim of beta-hemolysis when grown on blood agar plates
  • Catalase positive
  • Characteristic tumbling motility in fluid media at 25ºC
125
Q

Listeria monocytogenes is [type of hemolysis, reaction to catalase, and type of motility]

A

Listeria monocytogenes is beta-hemolytic, catalase positive, and has tumbling motility

126
Q

How is Listeria monocytogenes treated?

A
  • Ampicillin (may be used in combo with aminoglycoside for synergy)
  • Trimethoprim-sulfamethoxazole is bactericidal and recommended for those with penicillin allergies
127
Q

How can Listeria monocytogenes infection be prevented?

A
  • Avoiding raw meat and unpasteurized milk and cheese especially during pregnancy
  • Washing raw vegetables
128
Q

Cornyebacteria are [metabolic, Gram stain, shape, distinctive morphology]

A

Corynebacteria are aerobic Gram-positive bacilli that can have an irregular swelling (club shape) on one end under certain growth conditions

129
Q

Which species of Corynebacteria is best known?

A

Corynebacteria diptheriae

130
Q

Corynebacteria diptheriae is a [metabolic, Gram stain, shape, distinctive morphology]

A

Corynebacteria diptheriae are aerobic Gram-positive bacilli that can have an irregular swelling at one end (club shape) under certain growth conditions

131
Q

What is disease does Corynebacteria diptheriae cause?

A

Diphtheria

132
Q

How is Corynebacteria diptheriae maintained in humans?

What are the hosts for Corynebacteria diptheriae?

A

Asymptomatic carriage in immune humans

Humans are the only host

133
Q

How is Corynebacteria diptheriae transmitted from person to person?

A

Direct contact or droplets

134
Q

What is the determinant of pathogenicity of Corynebacteria diptheriae?

A

Diphtheria toxin

135
Q

What type of toxin is diphtheria toxin?

What carries diphtheria toxin?

A

Both A-B toxin and ADP-ribosylating toxin

Carried on integrated bacteriophage

136
Q

How does Diphtheria toxin work as an A-B toxin and ADP-ribosylating toxin?

A
  1. Fragment A inhibits peptide chain elongation during protein translation by ADP-ribosylating EF-2
  2. Inhibits protein synthesis in pharyngeal epithelial cells, leading to necrosis
137
Q

What is an ADP-ribosylating toxin?

A

Toxin that transfers ADP-rubose from NAD to host cell proteins, altering the activity of these proteins

138
Q

List examples of ADP-ribosylating toxins

A
  • Diphtheria toxin of Corynebacteria diptheriae
  • Exotoxin A of Pseudomonas aeruginosa
  • Cholera toxin of Vibrio cholerae
  • Heat labile toxin of Escherichia coli
  • Pertussis toxin of Bordetella pertussis
139
Q

Describe the clinical disease caused by Corynebacteria diptheriae

A
  • Usually affects kids
  • Sore throat, fever, difficulty swallowing, cough, hoarseness, rhinorrhea
  • Thick grey adherent pseudomembrane on mucosa of the oropharynx, palate, nasopharynx, nose, or larynx that may lead to airway obstruction
  • Damage to heart causing cardiac arrhythmias
  • Nerve damage causing paralysis of eye muscles, soft palate, extremities
  • Adrenal damage causing hypoadrenalism
  • Skin infections
140
Q

What is a prominent indicator of diphtheria?

A

Thick grey adherent pseudomembrane observed on mucosa of oropharynx, palate, nasopharynx, nose, or larynx

(composed of necrotic cell debris, fibrin, and blood cells that accumulate after cell damage caused by diphtheria toxin)

141
Q

How is Corynebacteria diptheriae diagnosed on lab test?

A
  • Gram stain of smears: bacteria lie in clusters at acute angles (Chinese letter) or parallel groups (palisade)
  • Gray to black colony on specialized medium containing tellurite that inhibits growth of most upper respiratory bacteria
142
Q

What is notable about definitive laboratory tests for Corynebacteria diptheriae?

A

Require at least a week

143
Q

How is Corynebacteria diptheriae treated?

A
  • Horse antisera against diphtheria toxin
  • Patients monitored for respiratory or cardiac failure
  • Antibiotics given to prevent spread of infection, not to increase rate of healing in people who have receive antitoxin (macrolides, penicillin G, rifampicin, clindamycin)
  • Close contacts should be cultured and given vaccination booster if required
144
Q

Why are antibiotics used in people who have received the antitoxin for diphtheria toxin?

A

To prevent spread of the infection

Do not increase rate of healing in people who have received antitoxin

145
Q

How can Corynebacteria diptheriae be prevented?

A

A diphtheria toxin toxoid vaccine (produced after DT treated with formaldehyde)

146
Q

What is a toxoid?

A

A chemically treated toxin that is no longer toxic but retains immunogenicity

147
Q

Why can individuals vaccinated with the diphtheria toxin toxoid vaccine still spread disease to unvaccinated individuals?

A

Vaccinated individuals are protected from disease but can be colonized by Corynebacteria diptheriae

148
Q

What caracteristics initially distinguish necrotizing fascitis from other skin infections?

A
  • Very painful upon palpation
  • Dark spots indicating air in deep fascia/muscle upon CT scan
  • Rash itself might not look too bad on the surface of the skin
149
Q

Why does necrotizing fasciitis spread so quickly?

A

SPE B breaks down tissue quickly, causing the necrotizing fasciitis to spread.

150
Q

How would you treat a furuncle?

A

Incision and Drainage

May follow with antibiotics

151
Q

If you don’t see any pus, which organism is likely causing an erythmatous skin legion?

A

Strep spp (especially S. pyogenes)

152
Q

What organism usually causes an infection where a pus-filled abscess or furuncle is present?

A

Staphylococcus spp.

(Especially S. aureus)

Staph is coagulase (+). Coagulase converts fibrinogen to fibrin, which forms a barrier around the furuncle

153
Q

How would you treat necrotizing fasciitis?

A

Surgical debridement

IV antibiotics (Penicillin + Clindamycin)

Note: Penicillin acts on cell wall, clindamycin inhibits SPE production

Most Strep spp are penicillin sensitive; If S. aureus is causing abscess, be aware of MRSA

154
Q

A 36-week pregnant woman comes into your outpaitent OB/Gyn office. Your preceptor orders a vaginal swab

Why?

What do you do if she tests positive?

A

Screen for Group B strep, caused by Strep**. agalactiae

If she tests positive, administer intrapartum antibiotics (penicillin = first choice; ampicillin also works)

155
Q

What bacterium has this appearance when grown on tellurite agar?

A

Corynebacterium Diphtheriae

156
Q

Which gram-positive bacteria have available vaccines?

A
  • Corynebacterium diphtheriae
  • Bacillus anthraces
  • Clostridium tetani
157
Q

Which bacteria is this?

A

Bacillus anthracis

Gram (+), rod-shaped bacteria that grows in chains

158
Q

Which bacteria have a capsule made from Poly-D-glutamic acid?

A

Bacillus Anthracis

159
Q

Growth of this pseudomembrane in the oropharynx is associated with which bacteria?

A

Corynebacterium diphtheriae; seen in diphtheria patients

160
Q

Clostridium tetani is a [Gram stain, metabolic, shape distinctive morphology]

A

Clostridium tetani is a gram (+), obligate anaerobe bacillus that forms terminal spores that exist in large reservoirs in soil

161
Q

What are the 4 medically relevant clostridia spp?

A
  • C. tetani*
  • C. botulinum*
  • C. perfringens*
  • C. difficile*
162
Q

What clinical disease is associated with Clostridium tetani?

163
Q

Which organism forms these spores?

A

Clostridium tetani

Forms terminal spores - club/drumstick shaped

reservoir in soil

164
Q

What kind of toxin is tetanus toxin?

165
Q

Describe the structure and action of tetanus toxin

A

Tetanus toxin is an A-B toxin

  • Synthesized as a single polypeptide chain, which is cleaved and linked via disulfide bonds
  • B = heavy chain
  • A = light chain
    • A protease that cleaves SNARE proteins in neuronal synapses
    • Acts on Renshaw cells to inhibit the release of GABA and glycine
    • This decreases inhibitory signaling, resulting in rapid firing of motor neurons, leading to rigidity/increased tone
166
Q

What cells does tetanus toxin act on?

What is the result?

A

Tetanus toxin acts on Renshaw cells (inhibitory neurons in the CNS) to prevent the release of GABA and glycine

The result is loss of inhibitory signaling -> rapid firing of motor neurons -> increased muscle tone

167
Q

What kind of wounds may become infected with Clostridium tetani?

A

Deep puncture wounds

The bacteria is an obligate anaerobe; the spores must reach a part of the body where the is no oxygen in order to germinate

168
Q

Describe the transport of tetanus toxin in the body

A

Retrograde transport from the site of inocculation to the neuron cell bodies in the CNS

169
Q

Describe the clinical manifestation of tetanus

A
  • Rigidity in…
    • Jaw (lockjaw)
    • Neck, shoulder, back (opisthotonus)
    • Abdominal and leg muscles
  • Spasms caused by minor stimuli
  • Sympathetic nervous system involvement
    • Hypotension
    • Tachycardia
    • Arrhythmia
    • Sweating
    • Vasoconstriction
170
Q

How is Tetanus diagnosed?

A

Consistent clinical findings

Tetanus toxin production

Note: Isolating spores is not indicative of disease; sometimes healthy people have spores, sometimes diseased people do not

171
Q

How is tetanus treated?

A
  • Penicillin or metronidazole (but antibiotics in general have unproven value)
  • Human tetanus immunoglobulin: Neutralizes unbound tetanus toxin
  • Other agents to control muscle spasm
172
Q

How can tetanus infection be prevented?

A

Vaccine of tetanus toxoid

Boosters to follow trauma

173
Q

This baby cannot relax their face.

What is this called?

What is most likely causing this condition?

What else would you look for to confirm your diagnosis?

How would you treat it?

A

This face is characteristic of lockjaw, also called risus sardonicus

It is most likely caused by Clostridium tetani infection

Also look for arching of the back, increased muscle tone in other muscles. Inquire about puncture wounds (more relevant in adults maybe)

It should be treated with penicillin or metronidaole, as well as human tetanus immunoglobulin to neutralize the unbound toxin

174
Q

Clostridium botulinum is a [Gram stain, metabolic, shape, distinctive morphology]

A

Clostridium botulinum is a Gram (+) obligate anaerobe bacillus that forms subterminal spores. It is found is soil, ponds, lakes, and on plants

175
Q

Where are C**lostridium tetani spores in the environment found?

A

Soil, rusty nails (construction sites)

176
Q

What disease is caused by Clostridium botulinum?

A

Botulism (Food borne, wound, or infant)

177
Q

Which organism forms these spores?

A

Clostridium botulinum

Forms Subterminal spores

178
Q

What is the difference between tetanus toxin and botulism toxin?

A

Their targets;

Tetanus toxin targets inhibitory neurons in the CNS (renshaw cells), inhibiting GABA and glycine release

Botulinum toxin targets motor neurons in the CNS, inhibiting ACh release

179
Q

What are the three diseases caused by C. botulinum?

A

Food-borne botulism

Wound botulism

Infant botulism

180
Q

What bacteria causes “floppy baby syndrome”

A

Clostridium botulinum

181
Q

Describe the structure and action of botulinum toxin

A

Botulinum toxin is an A-B toxin

  • B = Heavy chain
  • A = Light Chain
    • Protease
    • Cleaves SNARE proteins in motor neurons, inhibiting the release of ACh
    • This results in inhibition; muscles cannot contract, causing flaccid paralysis
182
Q

Where are people likely to contract food-borne botulism?

A

Canned foods; the spores germinate in the anaerobic environment of the can

Humans ingest the pre-formed toxin (toxin can survive boiling for 10+ minutes)

183
Q

Describe the clinical manifestation of food-borne botulism

A

Symmetric descending, flaccid paralysis

  • Diplopia, ptosis (droopy eyelids)
  • Dysarthria
  • Dysphagia
  • Respiratory failure
  • Nausea, vomiting, abdominal pain (fever unusua)
  • Look for groups presenting together (families, people who live together, anyone who may have eaten the same food)
184
Q

Describe the clinical manifestation of wound botulism

A

A wound contaminated by Clostridium botulinum spores

Symptoms same as food borne but no GI symptoms

  • Symmetric descending flaccid paralysis
    • Diplopia, ptosis
    • Dysarthria
    • Dysphagia
    • Respiratory failure
185
Q

Why is it recommended that children <12 months old do not consume honey?

A

Honey has a large concentration of Clostridium Botulinum spores

Unlike adults, these spores can germinate in the infant intestine, due to lack of natural flora

This predisposes infants to botulism from spore ingestion

186
Q

How is infant botulism different from food-borne botulism?

A

Infant botulism: ngestion of spores

Food-borne botulism: ingestion of the pre-formed toxin

Spores cannot germinate in the adult intestine, but they can germinate in the infant’s; this leads to toxin production and infant botulism

187
Q

Why dont Clostridium botulinum spores germinate in the adult intestine?

A

Natural flora prevents germination (and thus prevents botulinum toxin production)

188
Q

How is botulism diagnosed?

A
  • Compatible history and clinical symptoms (descending flaccid paralysis)
  • Isolation of the toxin or organis from vomit, stool, or wound
  • May be found in blood
189
Q

How is botulism treated?

A
  • Respiratory support
  • Trivalent equine antitoxin
  • Antibiotics to eliminate residual toxin are unproven
190
Q

How is botulism prevented?

A

No vaccine is available

Thoroughly cook canned foods/practice proper canning techniques

Don’t feed honey to infants <12 months

191
Q

What are the major differences between botulism and tetanus infetions?

A

Type of paralysis

  • Tetanus = increased muscle tone
  • Botulism = no muscle tone

Method of contracting the disease

  • Tetanus = puncture wound
  • Botulism = canned food, wound, honey (infant)

Treatment

  • Tetanus = Human tetanus immunoglobulin, penicillin or metronidazole
  • Botulism = Trivalent equine antitoxin, respiratory support
192
Q

What are the major differences between Clostridium tetani and Clostridium botulinum?

A

Site of action

  • C. tetani: Renshaw cells (inhibitory neurons in CNS)
  • C. botulinum: Motor neurons

Spore formation

  • C. tetani: Terminal spores
  • C. botulinum: Subterminal spores

Where it’s found

  • C. tetani: Soil, construction sites (rusty nails)
  • C. botulinum: Canned foods (found in soil, ponds, lakes, on plants, but adult humans only contract disease from pre-formed toxin, found typically in canned foods)
193
Q

What are the medically-important families of actinomycetes?

A

Nocardia spp.

Acinomyces israelii

194
Q

What is unique about the growth of Actinomycetes bacteria?

A

They are true growing bacteria, but from long, branchin filaments that resemble fungi

195
Q

This is a kinyoun stain of which bacteria?

A

Nocardia

Grows in long, branching filaments; stains partially acid fast

196
Q

Nocardia spp. are [Gram stain, metabolic, shape distinctive morphology]

A

Nocardia spp. are gram (+) obligate aerobes. They grow in long, branching filamentous rods with cells that remain conjoined after division

Catalase (+), Does not form spores,

197
Q

What is the main determinant of pathogenicity for Clostridium tetani?

A

Tetanus toxin

198
Q

What is the main determinant of pathogenicity for Clostridium botulinum

A

Botulinum Toxin

199
Q

What is the main determinant of pathogenicity for Nocardia?

A

It cannot be killed efficiently by neutrophils

  • Neutralizes oxidants
  • Prevents phagosome acidification
  • Inhibits phagosome-lysosome fusion

This means that cell-mediated immunity is needed to control the infection

200
Q

Which individuals are most likely to be infected with Nocardia?

A

Anyone with deficient cell-mediated immunity. This includes patients with…

  • Lymphoma
  • Transplants
  • Glucocorticoid use
  • Men (more sucesptible than women
201
Q

What are the 3 diseases caused by Nocardia?

A

Pulmonary nocardiosis

CNS nocardiosis

Transcutaneous nocardiosis

202
Q

Describe the clinical presentation of pulmonary nocardiosis

A
  • Subacute pneumonia
  • Forms nodules, cavitary lesions, abscesses
    • Ignores tissue planes
  • Empyma (pus in pleural space)
  • May disseminate to systemic circulation
    • Causes CNS nocardiosis w/brain abscesses
203
Q

Describe the clinical presentation of CNS nocardiosis

A

Brain abscesses

Preceded by pulmonary nocardiosis

204
Q

Describe the clinical presentation of transcutaneous nocardiosis

A
  • Inoculation of an open wound with nocardia spp
    • Usually foot tissue after local trauma associated with walking barefoot
  • Seen more often in developing countries
  • Induration (hardened mass) and inflammatory reaction
    • May forma a fistula with serous or purulent discharge
  • Spreads slowly
    • Ignores tissue planes
    • May involve skin, subcutaneous tissue, bone
    • May take years to spread
205
Q

How is a Nocardia infection diagnosed?

A
  • The organism is present in large numbers in lesions
  • Truly gram (+)
  • Stains partially acid-fast on Kinyoun or Carbol Fuchsin
  • Catalase (+)
  • Urease (+)
  • Organisms are culturalbe on blood agar
    • Grows as characteristic filamenous structures
    • But may take 2 weeks for colonies to be visible
206
Q

How is a Nocardia infection treated?

A

Choice: Trimethoprim/sulfamethoxazole

Alternative: Minocycline, amikacin

Brain abscesses may need to be drained, debridement may be necessary

207
Q

How can Nocardia infection be prevented?

A

It can’t really… No vaccine is available

208
Q

Acinomyces israelli is a [Gram stain, metabolic, shape distinctive morphology]

A

Actinomyces israelii is a gram (+), obligate anaerobe that grows in filamentous rods that resemble fungus

It is part of the normal flora of the mouth, GI tract, and female genital tract

209
Q

What are the major differences between Nocardia spp. and Actinomyces israelii?

A

Metabolism

  • Nocardia = obligate aerobe
  • A. israelii = obligate anaerobe

Staining

  • Nocardia stains partially acid fast
  • A. israelii does not
210
Q

What disesaes are caused by Actinomyces israelii?

A

Indolent, supprative infections

  • Indolent = painless
  • Supprative = pus-forming

Examples

  • Oral-cervicofacial actinomyces infection
  • Pulmonary/chest infection
  • Abdominal/pelvic infection
211
Q

How do people typically contract an Actinomyces israelii infection?

A

Usually through a jaw trauma or tissue injury that causes A. israelii to grow in a place where it doesn’t usually grow

Examples: Dental work or other injury

212
Q

Describe the clinical presentation of an oral-cervicofacial actinomyces infection

A

Slow!

  • Begins as a nontender lump
  • Turns into an abscess
  • Forms draning sinus tracts containing pus with yellow sulfur granules
213
Q

Describe the clinical presentation of a pulmonary/chest infection caused by Actinomyces israelii

A

Occurs if infectious contents in the mouth are aspirated

  • Infection fo pulmonary parenchyma and pleural space
  • May spread to involve bone and chest wall
214
Q

What might trigger an abdominal or pelvic infection of A. israelii?

A

Intestinal rupture or IUD use

215
Q

How is an Actinomyces israelii infection diagnosed?

A

Organism seen in gram-stained sulfur granules

  • The granules themselves are diagnostic of Actinomyces israelii infection
  • The organism will grow from cultures
  • If sulfur granules are not present, it may just be part of normal flora
  • Not acid fast (distinguishes from Nocardia)
216
Q

How is an Actinomyces israelii infection treated?

A

Choice: Penicillin

Alternative: Tetracycline

May need surgical drainage in complicated cases

217
Q

Describe Clostridioides difficile

[Gram stain, metabolism, shape]

A

Clostridioides difficile, aka C. diff is a gram-positive, anaerobic bacillus

Note: Spore forming, like other Clostridioides spp.

218
Q

What is the clinical manifestation of a C. difficile infection?

A

Diarrhea due to inflammation caused by toxigenic strains that disrupt the epithelial barrier of the large intestine, causing fluid leakage. Usually watery, may be bloody

  • Caused by antibiotic use that wipes out the normal flora of the gut or ingestion of C. diff spores
219
Q

Which bacterial infection is associated with antibiotic use?

A

C. difficile

FDN3 By Nathan and Minnie (14 decks)

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