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GSSE Pathology > Infection & Antibiotics > Flashcards

Infection & Antibiotics Flashcards

1
Q

Describe the characteristics of suppurative inflammation.

A
  • increased vascular permeability and neutrophil recruitment

- caused by extracellular gram + cocci and gram - bacilli

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2
Q

Describe the characteristics of granulomatous inflammation.

A
  • viruses, intracellular bacteria, spirochetes, intracellular parasites and helminths
  • plasma cells/lymphocytes/macrophages accumulate usually evoked by resistant organisms that evoke a strong T cell response
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3
Q

Describe the characteristics of a Cytopathic-cytoproliferative reaction

A
  • viral infection
  • proliferation and necrosis with sparse inflammation
  • may show inclusion bodies, polykaryons, blisters or warts
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4
Q

What are the bacterial families found in the mouth and what are their susceptibilities?

A

oral anaerobes are members of the porphyromonas, prevotella and peptostreptococcus genera (usually suseptible to ADF)

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5
Q

Where is E. Faecalis a commensal?

A

e. faecalis is found in the upper GI tract

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6
Q

Is the microbial flora predominantly aerobic or anaerobic?

A

Anaerobic

Found predominantly in the large bowel, but can be altered significantly by hospitalization

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7
Q

What are 3 factors that make the skin an unsatisfactory environment?

A
  • resident microbial flora
  • dryness
  • acidic pH (5.5)
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8
Q

What are the 3 important regions of the gram negative lipid bilayer?
Where are the pores?

A
  1. Lipid A : endotoxin responsible for toxicity
  2. Polysaccharide core
  3. Terminal repeating O units

proteinacous pores on outer membrane allow passage of LMW solutes (Eg. antibiotics)

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9
Q

What are the 2 important features of a gram positive bacterial wall?

A
  1. peptidoglycan containing strands of teichoic acid, proteins, and CHO (depending on species)
  2. not protected by an outer membrane so susceptible to degradation by lysozyme
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10
Q

What is the body’s reaction when LPS complexes are injected IV?

A
  1. produce arteriolar dilatation
  2. activate complement through the alternate pathway
  3. injure endothelial cell membrane
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11
Q

What are the 3 ways that genes can be transferred between cells?

A
  1. TRANSFORMATION: recipient takes DNA from donor cell
  2. TRANSDUCTION: DNA transferred via a virus vector
  3. CONJUGATION: via fertility factor, usually plasmid or transposon
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12
Q

Name 5 bacteria that secrete exotoxins.

A
  1. Corynebacterium diphtheria
  2. Clostridium difficile
  3. Staph aureus
  4. Pseudomonas aeruginosa
  5. Tetanus
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13
Q

What are the 3 factors that contribute to gram negative septicaemic shock?

A
  • exotoxins
  • LPS (endotoxins)
  • products of complement activation
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14
Q

Describe the characteristics of necrotising inflammation.

A
  • usually uncontrolled viral infection or secreted bacterial toxins
  • contact mediated cytolysis of host cells
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15
Q

What are some of the virulence factors associated with staph aureus?

A
  • coagulase enzyme
  • surface receptors that bind them to host cells
  • enterotoxins (superantigens)
  • lytic enzymes (lysins)
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16
Q

What is the empiric therapy for MRSA? What are some therapeutically effective agents against community acquired MRSA? (4)

A

VANCOMYCIN

  • fusidic acid and rifampicin
  • linezolid
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17
Q

Name 5 streptococcal virulence factors.

A

o Rod-like surface M-proteins and a polysaccharide capsule that prevent bacteria from being phagocytosed
o A pneumolysin that lyses host cells and wastes host complement
o Exotoxins that produce rash in scarlet fever
o Proteases that degrade chemotactic peptides and immunoglobulins
o Lactic acid that demineralizes tooth enamel

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18
Q

What are 3 resistance mechanisms that are characteristic of enterococci?Which (Faecium vs faecalis) is responsible for VRE?

A

o Contain penicillin-binding proteins, hence resistant to beta-lactam Abx (pencillin, cephalosporin, macrolides)
o Have pre-formed folic acid which allows them to bypass inhibition of folate synthesis (resistant to Bactrim)
o Acquired resistance to many Abx

Faecium = VRE

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19
Q

What are 3 manifestations of E. coli?

A
  1. haemorrhagic colitis
  2. bacteraemic episodes in the early stages of peritonitis
  3. osteomyelitis of IV drug abusers
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20
Q

What are some virulence factors associated with pseudomonas?

A
  • pili and adherence proteins for epithelial cells and lung mucin
  • Endotoxin causing sepsis and DIC
  • Exotoxin A simlar to diphtheria toxin
  • phospholipase C: lyses red cells and degrades surfactant
  • elastase that degrades IgG and ECM
  • iron containing compounds that are toxic to endothelium
  • expolysaccharide secreted in CF patients which forms biofilm
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21
Q

Summarise the GI pathogenicity for the following organisms.

  • staph aureus
  • vib cholerae/e.coli
  • shigella/salmonella/campylobacter
  • salmonella typhi
A

STAPH AUREUS = contaminate and grow in food, releases exotoxins that cause food poisoning without bacterial multiplication
CHOLERA AND E COLI = bind to intestinal epithelium, multiply and release exotoxins that causes secretory diarrhea
SHIGELLA/SALMONELLA/CAMPYLOBACTER = invades & damage intestinal mucosa; causes ulceration & haemorrhage (dysentery)
SALMONELLA TYPHY= passes from damaged mucosa through Peyer’s patches into the blood (systemic infection)

22
Q

What are the most common causes of vaginitis?

A

T. vaginalis and Candida albicans

23
Q

What are the most common aetiologic agents for osteomyelitis?

A
  • Staphylococcus aureus = most frequent causative organism
  • E. coli & group B strep = important causes in neonates and ?IV drug users
  • Salmonella = especially common in patients with sickle cell disease
  • TB
24
Q

What are the 3 types of peritonitis?

A 
o Primary (spontaneous) – don’t know the source of infection eg. cirrhosis, ascites o Secondary – leakage of microbes from an injured or ruptured viscus
-> Initial phase – diffuse peritonitis, bacteraemia with or without shock (usually GNB eg. E. coli, Pseudomonas)
-> Second phase – infection is localized into abscesses
o Tertiary – persistent peritonitis in seriously ill patients (generalized sepsis with shock)
25
Q

What are the characteristics and virulence factors associated with bacteroides fragilis?

A

Anaerobic GRAM NEG

  • production of β-lactamase
  • capsule allows abscess formation

Predominantly found in intra-abdominal abscesses

26
Q

What antibiotics would form an empiric regimen for necrotising fasciitis?

A

o Penicillin, amoxicillin, flucloxacillin, clindamycin, ceftriaxone or cefuroxime (GPCs eg. Staph and Strep)
o 3rd gen cephalosporin eg. ceftriaxone or ciprofloxacin (anti-Gram negative bacilli)
o Clindamycin or metronidazole (for anaerobes)

27
Q

List examples of and the generalised structure of herpesviruses.

A

HSV1 HSV2
EBV
CMV
VZV

All herpesviruses are composed of relatively large double stranded, linear DNA encased in an isosahedral protein cage (capsid)

28
Q

What are the two key mechanisms by which herpesviruses evade the immune system?

A

o Encoding a protein that mimics human IL-10 (hIL-10)
 Viral human IL-10 homologue has been found to inhibit pro-inflammatory cytokine synthesis
 down regulates IFN-γ, IL-1α, GM-CSF, IL-6 and TNF-α
 able to down-regulate MHC I & II
 suppresses cell-mediated immune response and NK cell response

o Down-regulation of MHCI
 Viruses encode proteins that detain newly formed MHC in the ER (therefore cannot activate T-cell response)
 The MHCs can also be targeted for destruction in the proteasome or lysomsome
 HLA-G is often up-regulated which prevents the natural killer cell response

29
Q

What are the clinical, radiographic and histological features of pneumocystis jirovecii (carinii)

A

o Fever, dry cough and SOB occur in 90% of patients
o Hypoxia is frequent; RFTs demonstrate a restrictive lung defect
o Radiographic changes show bilateral perihilar and basilar infiltrates

FUNGUS
o Microscopically, involved areas of the lung demonstrate a characteristic intra-alveolar foamy, pink-staining exudate
o The septa are thickened by oedema with a minimal mononuclear infiltrate

30
Q

What are the histological characteristics of a granuloma due to TB?

A

epithelioid histiocytes & multinucleate giant cells

31
Q

What is the histological morphology of candida albicans?

A

o C. albicans demonstrates yeast-like forms, pseudohyphae and true hypae
o Pseudohyphae are an important diagnostic clue; it represents budding yeast cells joined end to end at constrictions

32
Q

What are the factors that delay wound contraction?

A
  • corticosteroid administration
  • burns
  • skin grafting
  • x-radiation
33
Q

What are some mechanisms of bacterial resistance against beta lactams?

A

1) Synthesise additional PBP
2) ↓membrane permeability (GNB) or mutate porin genes
3) Beta-lactamases

34
Q

What are 6 key side effects of cephalosporins?

A

1) thrombophlebitis (usually IV form)
2) allergy (cross-reactivity 10%)
3) ↑bleeding (↓vit K, plt dysfunction)
4) diarrhoea
5) sludge in GB and CBD
6) nephrotoxicty

35
Q

Why do we not use tetracyclines in children?

A

fucks up bone development and stains teeth brown

36
Q

Which antibiotic has the side effect of alcohol intolerance?

A

Metronidazole

37
Q

What is the mechanism of action and some examples of aminoglycosides?

A

Inhibits protein synthesis, bactericidal

Includes gentamicin, amikacin, tobramycin

38
Q

Which penicillins are resistant to the beta-lactamases of staph. aureus?

A

Flucloxacillin
Dicloxacillin
Methicillin

39
Q

What would be the treatment of choice for neisseria mengitidis meningitis? And the prophylaxis regime?

A

Penicillin (or chloramphenicol)

Rifampicin and polysaccharide vaccine

40
Q

What would be the treatment of choice for haemophilus meningitis?

A

Ampicillin, ceftriaxone or cefotaxime

41
Q

What is the empiric treatment for menigitis?

What is the regime for immunocompromised patients and why?

A

o Empirical treatment (immunocompetent) = ceftriaxone or vancomycin + ciprofloxacin/moxifloxacin

o Empirical treatment (immunocompromised) = ceftriaxone + benzylpenicillin (to cover Listeria)

42
Q

What are some agents aside from Vancomycin that are useful in MRSA?

A
  • cotrimoxazole
  • fusidic acid
  • rifampicin
  • gentamicin
  • ciprofloxacin
43
Q

What are the key agents for treating bacteroides fragilis?

A

metronidazole
imipenem/meropenem
chloramphenicol
co-amoxyclav

44
Q

Which antifungals target DNA/RNA synthesis and what are they used for?

A
  • > 5-FC can be used in yeast infections

- > Griseofulvin can be used for ringworm

45
Q

Which antifungals target membrane synthesis?

A
  • > The azole group of antifungals (eg. fluconazole) inhits the cytochrome P450 activity in the ergosterol pathway
  • > Polyenes (eg. amphotericin B) inhibit in some way the amount of ergosterol in the membrane
46
Q

What families of organisms should we think about covering in large bowel prophylaxis? What antibiotics would be suitable?

A

o Enteric coliforms eg. Escherichia coli
o Obligate anaerobes eg. Bacteroides fragilis
o Skin flora eg. Staphylococcus aureus (important skin wound pathogen in all invasive surgical settings)

  • cefoxitin
  • cefotetan
  • co-amoxyclav
47
Q

What are the common pathogens associated with IVC associated sepsis?

A
  • staph epidermidis
  • candida
  • staph aureus
  • GNB (E. coli, Pseudomonas, Klebsiella)
  • enterococcus
48
Q

What are the most common infective agents associated with post-splenectomy sepsis?

A

ENCAPSULATED ORGANISMS

Strep. pneumoniae, Haemophilius influenzae & Neisseria meningitides

49
Q

What are the main pathogens that cause infections of burn wounds?
What are the primary antibiotic agents used?

A

o Pseudomonas aeruginosa and other Gram-negative rods
o Staphylococcus aureus (most common)
o Streptococcus pyogenes
o Other streptococci
o Enterococci
o Candida and Aspergillus (account for 5% of infections)
o Anaerobes are rare in burn wound infections

aminoglycoside (gentamicin) with beta-lactam (azlocillin, ceftazidime)

50
Q

What are some effective topical agents to treat burn wound infections?

A

o Chlorhexidine gluconate = topical wash with bactericidal activity
o Silver sulfadiazine = prevention of infections from second- or third-degree burns (poor eschar penetration)
o Silver nitrate = removes granulation tissue; good against GP, GN and candida; poor eschar penetration
o Mafenide = topical sulfonamide; diffuses freely into the eschar, effective against GN including Pseudomonas
o Bactroban = good against MRSA

GSSE Pathology (6 decks)

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