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Infections > Bacteria Pt 1 > Flashcards

Bacteria Pt 1 Flashcards

1
Q

What are general characteristics of clostridia pathogens?

Why do we have so much C diff?

A

Gram positive
spore forming, anaerobic rods
all are obligate anaerobes, but oxygen tolerance varies
- if bug doesn’t make catalase, oxygen is toxic
- if bug doesn’t make superoxide dismutase, very sensitive to superoxide

spore are highly resistant to oxygen, which is reason for so many nosocomial C. diff infections

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2
Q

Which clostridia have neurotoxins and what are their symptoms?

A

Clostridia tetanii (tetatnospasm)

Clostridia botulinum (flaccid paralysis)

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3
Q

Which clostridia have tissue damaging toxins?

A

Clostridia perfigens have alpha toxin (causing cell lysis, massive destruction of muscle, soft tissue)

Clostridia difficile toxins cause ulceration of colon

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4
Q

Which clostridia cause pathology from toxins and which cauase pathology from infection?

A

Clostridia botulinum result from ingestion of toxin, there is no live bacteria consumed
- exception to infant botulism, and wound botulism
clostridia perfinges cause pathology from toxins (alpha toxin)

clostridia dificile produce tissue damaging toxin (pseudomembranous colitis)

Clostridia tetatni causing tetanus and C diff causing pseudomembranous colitis are caused by infections

Clostridia perfringes cause damage via toxin (alpha toxin, theta toxin, enterotoxin)

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5
Q

What is an exotoxin and what is the classic example?

A

Exotoxins are secreted proteins that directly interact with targets in host tissues to cause loss of function, altered function, or physical damage?

Botulinum toxin is the classic example

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6
Q

Which toxins do not fit the A-B model? Which do?

A

Do not- Pore forming toxins via assembly of a ring of protein subunits
Lipases that degrade lipids organizing the membrane (Clostridium perfringes)

Do- Botulism toxin, cholera toxin, bordatella pertussis toxin

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7
Q

Clostridium perfringens characteristics- Gram? Spore? Growth? Where is it found?

A

Gram positive, anaerobic, spore former, invasive,
- more aerotolerant than other clostridial pathogens

capable of VERY rapid growth (10 min generation time)

common in soil and intestines of many mammals
- risk of infection following wound contamination, abdominal surgery

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8
Q

How does Clostridium perfringens cause pathology? What type of pathology does it cause?

A

Produces many toxins
alpha toxin most important- phospholipase that hydrolyzes cell membrane proteins leading to lysis

q-toxin is a pore forming toxin causing lysis

enterotoxin- important in benign food poisoning

Pathology- anaerobic cellulitis, gas gangrene

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9
Q

What are characteristics of Clostridium dificile? Treatment?

A

Gram positive, spore former

antibiotic associated pseudomembranous colitis

treat with oral vancomycin or metronidazole

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10
Q

What are characteristics of Clostridium botulinum? Where is it commonly found? Treatment/Prevention?

A

Gram positive rod, anaerobe, spore-former

Encounter: commonly found in food/honey, and no live bacteria involved in transmission! just toxin

Mech: Has botulinum neruotoxin (AB) which inactivates synaptobrevin, blocks cholinergic synpases of peripheral nerves at motor end plates and cause descending flaccid paralysis (respiratory paralysis can be fatal)

Clinical: Presents with dysphagia

Infants and wound botulinum involve infections

  • infant- toxin produced by gut bacteria
  • wound- spores germinate in wound and result in similar Sx to botulism toxin

Prevent by heating to 80C before eating, polyvalent antitoxin

Sketch- Robutulism

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11
Q

What are characteristics of Clostridium tetanus?

A

Gram positive rod, o. anaerobe, spore former, non-invasive, MOTILE

Encounter: Wound contaminated with soil

Mech: TOXIN causes symptoms
Tetanospasm from zinc-dependent protease inactivating synaptobrevin/SNARE, utilizes zinc-dependent protease to move up motor neurons to CNS, prevents release of GABA and Glycine, resulting is spastic paralysis

Clinical: Lockjaw, respiratory paralysis, osiphotonus (back muscle rigidity) and facial muscle rigidity (Risus sardonicus)

Treatment: untreated mortality>50%, antitoxin, DPT vaccine, boosters, antibiotics

Sketchy: Risus Research Revolution

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12
Q

What are characteristics of Corynebacterium diptheriae?

A

Gram positive rod, F anaerobe, non spore former

Encounter: human throat, transmitted oral secretions

Mech: Diptheria toxin (AB), expressed only when organism is infected with a particular bacteriophage! in absence, only pharyngitis

Clinical: sore throat and pharyngitis, pseudomembrane in throat, BULL NECK due to cervical edema and lymphadenitis, asphyxiation, reversible neuro impairment (muscle paralysis)

Treatment: Antitoxin, DPT vaccine

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13
Q

What are characteristics of Bordatella pertussis? What is it commonly called in kids?

A

Gram negative coccobacillus, non motile, non-invasive fastidious slow grower, aerobe

Encounter: Aerosols, Human only host, colonizes on ciliated respiratory epithelium

Mech: toxin

  • Pertussis toxin (AB) exotoxin, causes ADP-ribosylation of G protein, causing increase in cAMP, increased mucosal secretions, high lymphocytosis
  • Filamentous hemagluttinin mediates adhesion to increase colonization
  • Adenylate cyclase (AB), exotoxin
  • Tracheal cytotoxin (TCT), an endotoxin, destroys ciliated epithelial cells

Clinical

  • Catarrahl phase (1-2 weeks) with mild fever and dry nonproductive cough, highly infectious
  • Paroxysmal phase (2-4 weeks) with explosive cough, danger of secondary pnemonia
  • Convalescent phase

Treatment: Antibiotics early- macrolides d
DTap/Tdap with toxoid in it, acellular vaccine
- purified proteins
- D for diptheria and T for tetanus

Sketchy- Disabled GI coughing with bowtie spilling popcorn with tracheal toxin (tractor) which cleaves grass (cilia)

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14
Q

What are the two most pyogenic organisms?

A

Streptococcus and staphylococcus

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15
Q

What are the classification methods and how can you differentiate different types of streptococcus? Group A specifically?

A

Hemolytic pattern on a blood agar plate

  • alpha hemolytic- partial clearing
  • beta hemolytic- complete clearing
  • gamma hemolytic- no clearing

For alpha and beta hemolytic streptococci you can use the Lancfield grouping according to major cell-wall carbohydrate antigens

Group A streptococcus has the M antigen, a major virulence protein allowing it to resist phagocytosis

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16
Q

What are the official names for Group A strep and Group B strep? Tests to differentiate the two?

A

Group A- Streptococcus pyogenes
Group B- Streptococcus agalactiae
Group A- bacitracin sensitive
Group B- Bacitracin resistant

17
Q

What are characteristics of Streptococcus pyogenes?

A 
Gram positive cocci in pairs or chains 
Beta hemolytic
Group A (Lancfield) 
Possess M antigen- evading phagocytosis 
Lots of genetic diversity due to horizontal genetic exchange

Encounter: Human reservoir, may be carried in nasopharynx, skin, GI tract asymptomatically. Air-born and food born, colonized on human skin/mucous membranes. Person to person transmission. Transmitted by M protein adhering to keritinocytes. Lopoteichoic acid binding fibronectin. F protein binding Fibronectin (stimulated by increased O2)

Mech: Enters by adhering to cells (M protein- to keratinocytes or lipoteichoic acid)

  • has multiple antiphagocytic mechanisms (M protein binds host complement control factors and has an antibody to M protein which is protective, Hyaluronic acid capsule- anti-phagocytic, diminished chemotaxis via C5a peptidase, kill phagocytes using streptolysin O
    • streptolysin O can be used diagnostically to see if we really had a strep infection
  • Damage caused by hydrolytic enzymes, inflammatory response, STSS

Clinical: sore throat, person to person transmission

  • Asymptomatic carrier
  • Suppurative disease
    • skin and mucous membrane infections leads to classic strep, impetigo, or erysupelas
    • deep tissue and blood leading to pneumonia, cellulitis, necrotizing fasciitis, myositis, puerperal fever
    • toxigenic manifestations leading to Scarlet fever with Pastias lines or Streptococcal toxic shock syndrome (TSS)
  • Non-suppurative complications
    • Acute rheumatic fever (triggered by pharyngitis)
    • Glomerulonephritis
    • endocarditis

Treatment: Penicillin, amoxicillin and other beta-lactam agents (Nafcillin), If allergic to penicillin use clindamycin, azithromycin, vancomycin if severe

Sketchy- Pie genies shop encapsulated hot apple pies (hyaluronic acid), bacitracin sensitive (basset hound)

18
Q

What are characteristics of Streptococcus agalactiae (Group B)?

A

Gram positive cocci in pairs or chains
Beta hemolytic

Encounter: Human reservoir, may be carried in nasopharynx, skin, genital tract asymptomatically.

Clinical: Neonatal meningitis and sepsis, from mom during delivery, pneumonia
meningitidis bacteremia in adults

CAMP Test Positive

Sketchy- Space galactic baby (new born serious infections) with hippo stuffed animal, bacitracin resistant, with space camp and a space ship with pencil legs

19
Q

What causes acute rheumatic fever and what is its presentation?

A

Group A streptococcus (S pyogenes)

  • Triggered by pharyngitis and is delayed for weaks after strep throat
  • Often recurs, and predisposes one to endocarditis due to heart valve damage
  • Presents clinically with carditis, erytheema marginata
  • Caused by a specific subset of Group A strep, and it is decreasing in incidence
  • It is immune mediated, and treated with aspirin acutely and long term penicillin prophylaxis
20
Q

What causes of acute glomerulonephritis and what is its presentation/pathogenesis?

A

Caused by Streptococcus pyogenes
Associated with a few M types, and follows pharyngitis OR impetigo
- spread via immune complexes of IgG and complement in the glomerular basement membrane of the kidney

21
Q

What are characteristics of Enterococci, or Group D streptococci?

A

Gram positive cocci in pairs and short chains, catalase negative

Encounter: Normal fecal flora of humans/animals, has extended survival on surfacecs, resistant to cephalosporins, inhibited but not killed by vancomycin, often spread by healthcare workers

Mech: resistant to multiple antibiotics

Clinical: can cause UTI, endocarditis, bacteremia, catheter related infections, intra-abdominal/pelvic infections

Treatment: Not unless causing major infection

  • intravascular infection requires bactericidal, synergistic therapy (ampicillin and gentamicin) with a cell wall agent and an aminoglycoside
  • VRE are becoming a problem in hospitals
22
Q

What are common noscomial infections?

A

Enterococcus faecalis

  • in pts treated with broad spectrum antibiotics or immunocompromised patients
  • leads to same types of infections of enterococci (UTI, endocardits, bacteremia, etc)
23
Q

What are the characteristics of Streptococcal pneumoniae?

A

Gram positive diplococci, alpha hemolytic, positive P test (optochin sensitivity) and bile solubility, fastidious growth (difficult to grow), opaque and transparent colony morphologies

Encounter: Asymptomatic carriers, Air borne (preschool!) colonized in the nasopharynx

Mech: Acute inflammatory response, Cell wall components induce cytokines IL-1 and TNF, resulting in systemic manifestation

  • IgA Protease cleaves IgA antibodies from immune response
  • Capsule diminishes complement help, phagocytosis when capsule specific antibody is produced
  • Pneumolysin- pore forming toxin causes damage and may impair mucociliary clearance from lower respiratory tract, promotes auto lysis due “Autolysin” production
  • Subject to PHASE VARIATION
  • Spreads to lower respiratory tract due to loss of conscioussness, preceding viral infection, or immune defects

Clinical: MOPS- meningits, otitis media, pneumonia, strep throat, Fever and chills, pleuritic chest pain, crackles, productive cough, dullness at lung bases, egophony

  • complications include pleural effusion, recurrent otitis media, septic shock/death, meningitis, bacteremia with seeding or pericardial or peritoneal spaces
  • 5% fatality, 25% fatality for bacteremia, higher mortality for splenectomized individuals

Treatment: PCN resistant, need multivallent vaccine based on capsular polysaccharide, can use ceftriaxone

24
Q

What are the clinical phases of pneumococcal pneuonia?

A

Exudative phase
- alveoli fill in with exudate, bacteria–> lobar pneumonia
Early consolidation
- Chemotaxis causes infiltrate of RBC and PMNs into alveoli
Hepatization
- lung looks like liver
Resolution
- macrophages clear debris, lung architecture restored

25
Q

What are Koch’s postulates?

A

The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms.

The microorganism must be isolated from a diseased organism and grown in pure culture.

The cultured microorganism should cause disease when introduced into a healthy organism.

The microorganism must be reisolated from the inoculated, diseased experimental host and identified as being identical to the original specific causative agent.

26
Q

What was the first organism for transformation to be demonstrated in?

A

Streptococcal pneumoniae

27
Q

Virdans streptocci

A

alpha hemolytic

colonizes the orapharynx (normal flora)

low virulence

can cause subacute bacterial endocarditis, on the teeth

28
Q

What is a special part about streptococcus pneumoniae cell wall? What are some of the proteins that interact with this cell wall component?

A

Has a c- cell wall susbtance

  • the polysaccharide residue of teichoic acid has a phosphorylcholine residue
  • the choline anchors certain proteins important in pathogenesis like autolysins, PspA, CbpA
  • – PspA- decreases complement activation, binds lactoferrin
  • choline can bind to C-reactive protein and activate complement
29
Q

What is the main pathogenic mechanism of S pneumoniae?

A

Capsular polysaccharide- 90 different types

30
Q

What are examples of pneumococcal phase variation?

A

Opaque colonies have:
low peptidoglycan/choline
high capsule
invade blood stream

Transparent colonies have:
high phosphoryl choline
low capsule
colonize nasopharynx better

31
Q

What is phase variation and how is it useful for microbes? Mechanisms of phase variation include…

A

Phase variation results in phenotypic heterogeneity in an organism to evade host defenses

  • can take on a capsule to get into blood, but has difficulty attaching to endothelial cells with capsule
  • uncapsulated bugs establish niches in nasopharynx better in S pneumo, N meningitidis and H influenzae

Mechanisms:
Slipped strain mispairing
Site specific homologous recombination
Epigenetic regulation mediated by DNA methylation

32
Q

What are characteristics of haemophilus influenzae?

A

Small pleomorphic, gram negative rods, can be encapsulated or nonencapsulated, encodes pili for adhesion and flagellae for movement

  • encapsulated– Hib
  • nonencapsulated- common cause of otitis media in kids

Encounter: human only known host, mucosal colonization in the nasopharynx (Attachment, IgA protease, LPS), areosol spread

Spread: Local or Systemic (invasion into blood, polysaccharide capsule promotes systemic infection)

Mech: damage caused by LPS (endotoxin) and is proinflammatory and causes endothelial leakage

Clinical: Subdural effusion due to H. flu meningitis (capsular type B)
Epiglotitis (drooling and inspiratory stridor)
Otitis media

Treatment: Anticapsular antibodies
- polysaccharide antigen requires a T-INDEPENDENT response
- 3 m to 3 y/o major vulnerability
- ceftriaxone
- rifampin propylaxes
Sketchy- Phylises chocolate (agar) covered cherries (cherry red tounge) with kid screaming with huge epiglottis

33
Q

What are pneumococcal vaccines targetting?

A

Polysaccharide capsule (23-valent vaccine with no t-cell memory and limited efficacy, then a 7 valent conjugate vaccine for kids, and now a 13 valent conjugate vaccine),

34
Q

What are similarities between encapsulated pneumococcus and haemophilus?

A

Humans are only host and asymptomatic carriers are key to transmission

Nasopharyngeal colonization
- IgA protease, phosphoryl choline

Invasive disease due to capsule

Anti-capsular antibody critical for protection

Underlying conditions that diminish bloodstream clearance increase risk for infection

35
Q

What are the characteristis of Clostridum difficile?

A

Gram + anaerobe, spore former
Colonizes the intestinal flora
Antibiotic-associated pseudomembranous colitis
Relapse common
Stop antibiotics, treat with oral vancomycin or metronidazole

36
Q

What are some differences between Strep pneumo and Strep viridans?

A

Both are alpha hemolytic
Pneumo- optochin sensitive, bile soluble, capsule
Viridans- optochin resistant, bile insoluble, no capsule

37
Q

What type of organisms and why are some individuals more susceptible to infection if they have had a splenectomy?

A

Encapsulated organisms, spleen plays a major role in removing encapsulated organisms from the body (sickle cell patients)

38
Q

What are major characteristics of Streptococcus viridans?

A

alpha hemolytic, colonizes the oropharynx (normal flora), low virulence, and commony associated with dental carries and subacute bacterial endocarditis

39
Q

What are Klebsiellae characteristics?

A

Gram - rods, important cause of nosocomial infections, lactose fermenter (like E. coli), capsule, grow pink on McConkey Agar, immotile, urease positive

3 As of Klebsiellae-alcoholics, abcesses, aspiration

Encounter: colonize GI tract, skin, pharynx (which serve as important pathogenic reservoirs)

Risk: diminished host immune defense AND/OR antibiotic use (Klebsiellae are often resistant to multiple antibiotics)

Virulence: K antigen- prominent polysaccharide capsule which is antiphagocytic and antigenically diverse

Clinical Presentation:

  1. Respiratory infection, introduced potentially via respiratory support equipment, causes lobar pneumonia with destructive changes (necrosis, inflammation, hemorrhage within lung tissue sometimes producing a thick, bloody, mucoid sputum- Currant jelly sputum)
  2. UTIs, risk factor if using urinary catheter

Treatment: Carbapenem

Infections (6 decks)

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