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MCD > Pathology > Flashcards

Pathology Flashcards

1
Q

Define R0

A

R0 = the number of secondary cases arising from each primary case - it relates to the contagiousness of the disease, the higher the R0 the more likely a pathogen is to cause an epidemic

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2
Q

Name the two major Fungi groups - give some examples

A

Yeast

  • Candida (causes thrush and disseminated candiditis)
  • Cryptococcus (causes meningitis)
  • Histoplasma (this is a dimorphic yeast)

Mould

  • Aspergillis (causes infections in immunocompromised patients)
  • Dematophytes (causes ringworm)
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3
Q

Define a parasite

A

A parasite is an organism which exploits another for the purpose of staying alive - parasites do not form symbiotic relationships because they do not contribute to the other organism, instead they depend on them for food/energy.

Parasitic infections can be harmless or pathogenic

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4
Q

What is the difference between an ectoparasite and an endoparasite? Give examples

A

Ectoparasite

  • Lives on (not within) the host
  • Eg: ticks, mites, lice etc.

Endoparasite

  • Lives inside the host
  • Eg: parasitic worms (cestodes, nematodes, trematodes)
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5
Q

(a) What two hosts can schistoma species infect?
(b) How do schistoma spread?
(c) What disease do they cause?

A

(a) Freshwater snails & humans
(b) Contaminated water
(c) Schistomaniasis

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6
Q

(a) What disease do onchocerciasis cause?
(b) What type of parasite is onchocerciasis?
(c) What is the intermediate host?

A

(a) River blindness
(b) Parasitic Worm - nematode
(c) blackfly

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7
Q

(a) Name one of the major soil transmitted helminths?
(b) What diseases to STHs cause?

A

(a) Hookworm
(b) Intestinal Worms

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8
Q

(a) What are the two hosts of tapeworm?
(b) How is tapeworm transmitted?

A

(a) Human & Pig
(b) Via contaminated, undercooked pork & through human stool

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9
Q

What is the major causative pathogen of UK cases of malaria?

A

Falciparum malaria

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10
Q

What are the risk factors for developing malaria in the UK?

A
  • Tourists
  • Those from endemic regions
  • Over 65 years old
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11
Q

What causes malaria?

A

Plasmodium (a protozoan parasite)

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12
Q

How is malaria transmitted?

A

Female anopholes (mosquito)

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13
Q

Outline the lifecycle of plasmodium

A

*Human Host = asexual phase, Mosquito Host = sexual *

  1. Female anopheles takes blood meal from human injecting sporozoites into human blood stream
  2. Sporozoites migrate to liver & invade hepatocytes
  3. Parasitic differentiation produces merozoites
  4. Merozoites released from liver and infect RBCs (form schizonts)
  5. Merozoites are released ffrom schiznts as male or female gametocytes
  6. Second mosquito takes a blood meal, ingesting the gametocytes
  7. In mosquito, gametocytes fertilise (in the gut) producing sporozoites
  8. Sporozoites rest in the salivary glands to be injected at the next blood meal
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14
Q

Outline the major diagnostic points for malaria

A

History

  • Travel
  • Origin

Signs & Symptoms

  • Non-specific symptoms of infection (fever etc.)
  • Rapid progression

**Investigations **

  • Blood films

Confirmation

  • Parasite count
  • Peripheral schizonts analysis
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15
Q

Describe the treatment of malaria

A

Treatment varies depending on whether it is falciparum or non-falciparum malaria

  • Non-falciparum
    • Out-patient treatment
    • Chloroquine + Primaquine
  • Falciparum
    • In-patient treatment
    • Mild = oral quinine/malorone/riamet
    • Severe = quinine + artemisinins
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16
Q

Define viruses

A

Virsues are infectious obligate intracellualr parasites

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17
Q

What are two key features of viruses?

A

**Structural Simplicity **

Intracellular Parasitism

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18
Q

Briefly name and describe the categories of the Baltimore Classification

A
  1. Class I - dsDNA viruses
  2. Class II - **+ **ssDNA viruses
  3. Class III - dsRNA viruses
  4. Class IV - + ssRNA viruses
  5. Class V - - ssRNA viruses
  6. Class VI - + ssRNA w/ DNA intermediate viruses
  7. Class VII - dsDNA w/ RNA intermediate viruses
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19
Q

Outline the general stages of the viral lifecycle

A
  1. Attachment
    • ​specific interactions facilitate viral attachment to the host cell
  2. Entry
    • ​​the virus genome enters the cell either by fusion or penetration
  3. Translation
    • ​​translation of viral mRNA to proteins by host cell machinery
  4. Replication
    • ​​replication of viral genome
  5. Assembly
    • ​​assembly of viral particle
  6. Exit
    • ​​maturation and release of viral particle from host cell
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20
Q

Outline how viral entry differs for enveloped and non-enveloped viruses

A
  • Viral entry is a specific process based on attachment and entry into the host cell
  • It requires receptor engagement, fusion and penetration of the cell
  • Enveloped virsues (eg: HIV, influenza)
    • penetration of the cell via fusion between the virus and cell membrane
  • Non-enveloped virsues (eg: polio)
    • penetration of the cell via disruption of the cell membrane
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21
Q

What kind of virus is influenza?

A

Class V = enveloped negative sense, segmented RNA

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22
Q

What is unique about the lifecycle of influenza?

A

Influenza encodes two proteins - sialic acid (binds to host membrane) and haemagglutinin (facilitates fusion and entry) which re importnt for entry into the host cell

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23
Q

Define the following terms:

  • Pathogenesis
  • Virulence
  • Transmission
  • Tropism
A
  • Pathogenesis - process by which viruses cause disease
  • Virulence - pathogenicity; the capacity of a virus to cause disease
  • Transmission - viral entry, spread, invasion and shedding
  • Tropism - site of viral replication
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24
Q

What are the major routes of transmission

A
  • Respiratory
  • Faecal-Oral
  • Blood
  • Sexual contact
  • Materno-foetal
  • Contact (lesion, saliva, formites)
  • Zoonosis
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25
Q

What 4 factors affect viral transmission

A
  1. Particle stability (of the virus) - enveloped viruses are less stable
  2. Duration of viral shedding - the shorter the shedding duration, the larger the viral load required
  3. Virus concentration - viral load per infection
  4. Availability of new hosts
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26
Q

Outline the difference between a local and systemic infection

A
  • Local infection
    • Shorter incubation period prior to symptom onset
  • Systemic Infection
    • Multiple replication phases resulting in longer and more spread incubation periods perior to symptom onset
    • Usually means severe infections
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27
Q

What are the two general outcomes of viral infection?

A
  • Acute Infection
    • Cleared within a matter or days/weeks
  • Peristent Infection
    • Smoldering = consistent viral load with diminished immune response
    • Latent = multiple “acute/quiescent/reactivation” cycles
    • Slow = constant low level infection with initial and final acute peaks
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28
Q

What are the general characteristics of an acute viral infection?

A
  • There is rapid production of the infectious virus
  • This is followed by rapid resolution and elimination
  • Infection is followed by viral clearance
  • Infection is controlled by the adaptive immune response
  • Transmission occurs before symptom onset
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29
Q

What are the general characteristics of a persistent viral infection?

A
  • Characterised by latent, slow or transforming infections
  • Long incubaton periods
  • Can be:
    • Chronic - low levels of replicating virus
    • Latent - viral genome is consistently maintained but there are episodes of viral reactivation
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30
Q

Define antigentic drift/shift

A

Antigenic shift is the ability of a virus to change its antigens so that it can re-infect hosts (i.e. there is no immunological memory)

Influenza is capable of this (antigenic drift accounts for seasonal infections, antigenic shift accounts for epidemics)

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31
Q

Why was the eradication of small pox possible?

A

Because there is no animal reservoir of the virus - therefore once it was eliminated from man, there was no living host for the disease to be reseeded

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32
Q

List the 3 major requirements all vaccines should have

A
  1. Induce an immune response
    • Vaccinated individuals must be protected from the causative agent
  2. Safe
    • There must be no risk of disease from the vaccine
    • Side effects must be minimal
  3. Practical
    • Stable (biologically)
    • Easy to administer
    • Cost effective
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33
Q

What are the 4 major types of vaccine?

A
  • Killed = chemical inactivation of the virus (either whole or specific epitopes)
  • Live attenuated = avirulent live virus
  • Subunit = isolation of genes of interest
  • Recombinated = DNA vaccine
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34
Q

List some of the problems faced when making antiviral drugs

A
  • It is difficult to produce safe antivirals - viruses invade host cells therefore damaging the virus but not the host is difficult
  • There are limited targets for the drugs action
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35
Q

Outline the origins of HIV

A
  1. SIV = simian version of the virus = origin of HIV
  2. HIV2 = interim virus = capable of zoonosis
  3. HIV1 = what we know as HIV
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36
Q

Briefly outline the clinical spectrum of HIV/AIDS

A
  • HIV is split into three stages - asymptomatic, symptomatic & AIDS
  • Asymptomatic phase
    • Potential for some minor infections (eg: skin diseases)
    • Occurs for up to 7 years after infection
    • Can increase the risk of yeast and other viral infections
  • Symptomatic phase
    • More significant direct effects (eg: wasting, fever)
    • Occurs for up to 10 years after infection
    • Increase in risk of multiple infections
  • AIDS phase
    • Multiple serious direct effects (eg: weight loss, dementia etc.)
    • Occurs over 5 years after infection
    • Increase risk of any opportunistic infection
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37
Q

What are the two key viral (HIV) surface proteins? Outline their role

A

GP120

  • Extracellular protein
  • Binds to CD4 receptors
  • Promotes co-receptor binding

GP41

  • Transmembrane protein
  • Undergoes conformational change (following co-receptor binding)
  • Enables unfolding & insertion into cell membrane
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38
Q

What three proteins are encoded for in the viral (HIV) genome?

A

Gag - viral core protein

**Pol **- polymerase protein (reverse transcriptase)

Env - envelope protein

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39
Q

Briefly outline the lifecycle of HIV

A
  1. Binds via specific interactions involving GP120 & GP41
  2. Nucleocapsid enters host cell, releasing viral RNA
  3. Reverse transcriptase converst viral RNA to viral DNA
  4. Viral DNA integrated into host DNA by transcriptase
  5. Host cell activates replication (replicating viral DNA)
  6. Protease cleaves viral DNA transcript into viral protein
  7. Immature viral particle fuses with host cell membrane
  8. Budding forms matture virus
  9. Virus exits the cell
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40
Q

Briefly outline the pathogenesis of HIV (split it into acute, spread, chronic & latent infection stages)

A

Acute Infection

  • Viral invasion
  • Concentration of virus around dendritic cells - they have a close association with CD4+ T cells
  • Infection of CD4+ cells
  • CCR5 and CXCR4 are secondary receptors

Spread of Infection

  • Dissemination of virus throughout lymph nodes
  • Causes rapid expansion of CD4+ cells

Chronic Infection

  • Initial immune response is successful
  • Later stages = complete destruction of CD4+ system

Latent Infection

  • Quiescent stages within lymph nodes
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41
Q

What is the difference between CCR5 and CXCR4 receptors in terms of HIV infections

A
  • CCR5 = first secondary receptor infected
    • Less serious infection
    • Slow growing
    • CCR5 -/- = immune to HIV infections
  • CXCR4 = second secondary receptor infected
    • More serious infection
    • Usually means AIDS onset
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42
Q

Briefly outline the prinicple of HAART therapy

A
  • HAART = highly active anti-retroviral therapy
  • “cocktail” of drugs with multiple targets
  • Drug regime altered to prevent resistant
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43
Q

What is the structure & function of the bacterial cytoplasmic membrane?

A
  • Composed of proteins and phospholipids
  • Functions:
    • Synthesis of cell wall componenets
    • Respiration
    • Secretion of enzymes
    • Uptake of nurtients
    • Helps confer resistance
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44
Q

What is the structure & function of the bacterial cell wall?

A
  • Repeating polymers of NAM & NAG
  • Functions
    • Protective
    • Structural support
    • Shape maintenance
    • Important for virulence (contains antigens)
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45
Q

What is the structure & function of the bacterial capsule?

A
  • Mucoid polysaccharide
  • Functions
    • Anti-phagocytic
    • Addhesion
    • Confers resistance
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46
Q

Describe the structure & function of bacterial pili

A
  • Protein (pilin)
  • Functions
    • Sex pili transfer
    • Attachement
    • Anti-phagocytic
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47
Q

Describe the structure & function of flagella

A
  • Protein (flagellin)
  • Motility
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48
Q

How do bacteria replicate?

A

Via binary fission - this can either be balanced (all required nutrients are supplied) or unbalanced (nutrients not supplied)

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49
Q

Outline the principle of Gram staining

A
  • Gram staining is a way of determining if a bacteria is Gram-positive or Gram-negative
  • When stained, gram-posistive organisms appear purple as the stain is trapped by the peptidoglycan component of the membrane
  • When stained, gram-negative organisms appear pink as the violet stain cannot reach the peptidoglycan layer therefore must be counter-stained
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50
Q

Outline the differences between the cell walls of Gram-positive and -negative bacteria

A
  • Negative = thin
    • 3 layers thick
      • Plasma membrane
      • Peptidolycan layer (thin)
      • Outer membrane (OMP + LPS)
  • Positive = thick
    • 2 layers
      • Plasma membrane
      • Peptidoglycan + teichoic acids (thick)
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51
Q

In Gram-negative bacteria what is the function of LPS?

A
  • LPS = lipopolysaccharide
  • It consists of:
    • Lipid A - toxic component of endotoxin
    • Polysaccharide - core component
    • O Antigen - major surface antigen
  • It is very toxic to humans (confers bacterial virulence)
  • LPS is responsible for endotoxic shock (fever)
52
Q

Outline the difference between (a) endotoxins and (b) exotoxins

A

(a) Endotoxins

  • Integral parts of the cell wall
  • Heat stable
  • Antigenic
  • eg: LPS (negatives) and teichoic acid (positives)

(b) Exotoxins

  • Released for the cell
  • Heat labile
  • Antigenic + immunogenic
53
Q

What are the three major morphological groups of Gram-negative bacteria?

A
  • Cocci
  • Bacilli (rods)
  • Coccobacilli
54
Q

Give some examples of lactose and non-lactose fermenters (Gram-negative bacilli)

A

Lactose Fermenters

  • E. coli
  • Klebsiella
  • Enterobacter

Non-Lactose Fermenters

  • Pseudomonas
  • Salmonella
  • Shigella
55
Q

What are the major Gram-negative infection sites?

A
  • CNS
  • Lower resp. tract
  • Bloodstream
  • GI tract
  • Urinary tract
56
Q

Concerning E. coli:

(a) What kind of bacteria is E. coli?
(b) Where is is found physiologically?
(c) What pathologies can it cause?

A

(a) Gram-negative rod (bacilli), lactose fermenter
(b) E. coli is a gut commensal
(c) Enteritis, UTI, community sepsis, meningitis etc.

57
Q

Concerning Klebsiella:

(a) What kind of bacteria is klebsiella?
(b) Where is is found physiologically?
(c) What pathologies can it cause?

A

(a) Gram-negative rod (bacilli), lactose fermenter
(b) It is a gut commensal
(c) Abscesses (eps. gut), HAIs, VAP/HAP

58
Q

Concerning pseudomonas:

(a) What kind of bacteria is pseudomonas?
(b) Where does it colonise?
(c) What pathologies can it cause?
(d) What is unique about pesudomonas?

A

(a) Gram-negative rod (bacilli), non-lactose fermenter
(b) It is an opportunistic organism that colonises moist areas
(c) Major HAIs (eg: HAP/VAP, catheter associated UTIs) etc.
(d) It forms a biofilm enabling anaerobic growth and conferring resistance

59
Q

Concerning salmonella:

(a) What kind of bacteria is salmonella?
(b) Where does it colonise?
(c) What pathologies can it cause?
(d) What is unique about salmonella?

A

(a) Gram-negative rod (bacilli), non-lactose fermenter
(b) Human GI tract
(c) Gastroenteritis, bacteraemia, arthritis
(d) It is a motile organism therefore is quickly spread - carriage is asymptomatic. It is a notifiable disease

60
Q

Concerning neisseria:

(a) What kind of bacteria is neisseria?
(b) What three major sub-species are there?
(c) What pathologies do they cause?
(d) Which sugars are each type able to metabolise?

A

(a) Gram-negative (diplo)cocci
(b) N. meningitidis, N. gonorrhoeae & N. lactamica
(c) Meningitis, gonorrhoeae, normal upper resp. tract commensal
(d) Maltose, glucose, lactose

61
Q

Concerning helicobacter pylori:

(a) What kind of bacteria is h. pylori?
(b) What pathologies can it cause?
(d) What is unique about it?

A

(a) Gram-negative coccibacilli
(b) Peptic ulcers + increased risk of stomach cancer
(c) Produces urease

62
Q

Concerning virbrio cholerae:

(a) What kind of bacteria is v. cholerae?
(b) What pathologies can it cause?
(d) How is it transmitted

A

(a) Gram-negative coccibacilli
(b) Cholera
(c) Faecal-oral route via contaminated water

63
Q

Concerning legionella:

(a) What kind of bacteria is legionella?
(b) What pathologies can it cause?

A

(a) Gram-negative, fastidious - rod
(b) Legionnaires disease

64
Q

What are the two major morphological groups of Gram-positive bacteria?

A

**Cocci **& Bacilli

65
Q

What are the two types of Gram-positive cocci?

A

Catalase positive (staph) & Catalase negative (strep)

66
Q

How can you differentiate between staphylococcal species?

A

Coagulase test

S. aureus = coagulase +

S. epidermidis = coagulase -

67
Q

How can you differentiate between streptococcal species?

A

Haemolysis

Group A = S. pyogenes

Group B = S. aggalactoae

Group D = Enterococcus

68
Q

What proteins help Gram-positive bacteria colonise and invade the host?

A
  • Adhesins = assist with colonisation, part of the cell wall
  • Invasins = assist with penetration through epithelial layers
69
Q

What are the major sites of Gram-positive infection?

A
  • Resp. tract
  • NS
  • Skin
  • GI tract
  • Urinary tract
70
Q

Concerning Staph. aureus:

(a) What kind of bacteria is s. aureus?
(b) Name some of the virulence factors
(c) What are the major sites of colonisation?

A

(a) Gram-positive cocci
(b) Enterotoxin, TSS toxin (toxic shock), coagulase, DNase
(c) Nose & Skin

71
Q

Concerning Strep. pyogenes

(a) What kind of bacteria is s. pyogenes?
(b) Name some of the virulence factors
(c) What pathologies does it cause?

A

(a) Gram-positive cocci, Group A strep
(b) exotoxins, M-protein, C5a peptidase, DNase
(c) Impetigo, sarlet fever, necrotising fascitis

72
Q

Concerning Strep. pneumonia

(a) What kind of bacteria is S. pneumonia?
(b) Name some of the risk factors for S. pneumonia infection
(c) What pathologies does it cause?

A

(a) Gram-positive cocci, Group A strep
(b) Chronic condition, immun deficiency, HIV, viral resp. infection
(c) Pneumonia, meningitis, otis media

73
Q

Concerning bacillus anthracis

(a) What kind of bacteria is B. anthracis
(b) Name some of the virulene factors
(c) What is the role of the spores?

A

(a) Gram-positive bacilli, spore forming
(b) Capsid, tripartite toxin, oedema factor, lethal factor
(c) Highly virulent, taken up by macrophages and germinate - eventually inactive the immune system

74
Q

Concerning Clostridium difficile:

(a) What kind of bacteria is C. diff?
(b) Name some of the viruelnce factors
(c) What pathologies does it cause?

A

(a) Gram-positive bacilli, spore forming
(b) Enterotoxin (toxin A) and Cytotoxin (toxin B)
(c) Major cause of HAIs

75
Q

Concerning C. diptheria

(a) What kind of bacteria is C. diptheria
(b) Name some of the virulenec factors
(c) How does it invade?

A

(a) Gram-positive bacilli, non-spore forming aerobe
(b) Toxin - subunit A and B
(c) Invasion and colonisation in the throat

76
Q

Concerning Actinomyces:

(a) What kind of bacteria is actinomyces?
(b) Where is it normally found?
(c) What pathologies does it cause?

A

(a) Gram-positive bacilli, non-spore forming aerobe
(b) Part of normal oral flora
(c) When it leaves the oral cavity it causes infection in the jaw, thorax, abdo & pelvis

77
Q

What pathogen causes TB? What kind of bacteria is it?

A

M. tuberculosis - bacilli

78
Q

What is unique about M. tuberculosis?

A

It cannot be Gram-stained therefore is an acid-fast bacillus

79
Q

How is TB transmitted?

A

TB can only be transmitted when the infection is an active pulmonary TB - transmission is via aerosol droplets

80
Q

Outline the epidemiology of TB

A

1/3 of the world have TB - 90% latent, 10% active

81
Q

List the various risk factors for TB infection

A
  • Ethnicity
  • Travel
  • Exposure
  • Poverty
  • Living Conditions
  • Immunosuppression (esp. HIV+)
  • Previous history of TB
82
Q

What infection route does TB infect?

A

Respiratory route (esp. small airways)

83
Q

Outline the pathogenesis of TB

A
  1. Inhalation of aerosol droplets into small airways
  2. Phagocytosis of M.tuberculosis by alveloar macrophages and resident (lung) dendritic cells
  3. Bacteria arrests phagosome maturation preventing phagocytosis
  4. Rapid spread of bacteria (to adjacent alveoli and the contralateral lung and systemically)
84
Q

Name the following types of TB:

(a) pleura + lymph nodes
(b) millet-seet deposits (systemic)
(c) brain + meninges
(d) bones + joints
(e) pericardium
(f) peritoneal cavity

A
  • Pulmonary TB
  • Milliary TB
  • Central (meningitis) TB
  • Skeletal TB
  • Cardiac TB
  • Peritoneal TB
85
Q

Outline the immune response to TB

A
  • ​There is no antibacterial response due to the high lipid component of the bacterial cell wall
  • There is a classical TH1 immune response
    • Adaptive
    • Stimulated by antigens presented by alveolar macrophages
    • Invovles CD4+ T cells
    • Results in the production of cytokines - INF-y & TNF=a
    • Production of ROS causes phagosome maturation
86
Q

Outline how granulomas form in TB

A
  • ROS (produced by cytokines) limit the dissemination of TB however, it does not combat the curent infection sites - highly organised granulomas develop at these sites.
  • Granulomas often become casseating
    • Giant cells form from epitheliod (infected) macrophages
    • Some become langhans cells (characteristic + specific to TB)
    • Internal portion of the granuloma becomes necrotic destroying the host tissue also
    • Fibrosis and calcficiation causes irreversible damage to the lungs
87
Q

Outline the signs & symptoms of TB

A

General

  • Fever
  • Weight loss
  • Night sweats

Specific

  • Chronic, productive cough
  • SOB
  • Haemoptysis
88
Q

How is pulmonary TB diagnosed?

A

CXR - shows scarring/fibrosis/tissue destruction in upper lobe (most common) of lungs

+ Culture

89
Q

Outline the treatment of TB

A
  • 2 months of: rifampicin, isoniazid, ethambutol, pyrazinamide
  • 4 months of: rifampicin, isoniazid
90
Q

What is the BCG?

A
  • Vaccination conferring immunity to TB
  • Live attenuated strain of M. bovis (avirulent in humans)
  • Never given to HIV+ patients due to immunosuppression
91
Q

Discuss the issues posed by MDR and XDR TB

A
  • MDR = multi-drug resistant, in terms of TB = resistant to rifampicin, isoniazid
    • Mostly due to HIV co-infection
    • Requires 18+ months of treatment
  • XDR = extremely drug resistant, in terms of TB = resistant to almost all available treatments (inc. extreme injectable therapies)
    • Usually fatal
    • Virtually impossible to treat pharmacologically
92
Q

Define: antibiotic

A

An antibiotic is a substance produce by a micro-organism (or pharmacologically formed) that inhibits the growth of other micro-organisms

93
Q

Define selectiv toxicity

A

A property of drugs (esp. Abx) causing it to be harmful to the microbe but not the host - it is acheived by capitalising on fundamental differences between prokaryotes and eukaryoktes

94
Q

What are the 4 major target sites of antbiotics?

A
  • Cell wall
  • Protein synthesis (ribosomes)
  • Enzymes
  • Cell membrane
95
Q

Name the four classes of Abx that target bacterial cell wall synthesis (give an example for each class)

A
  • Beta-lactams (eg: penicillin, cephalosporins, carbapenems)
  • Glycopeptides (eg: vancomycin)
  • Cycloserine
  • Cyclic polypeptides
96
Q

Outline the general MOA of bacterial cell wall synthesis inhibitors

A
  • Seective toxicity through targetting PBPs (uniquely invovled in the synthesis of the bacterial cell wall)
  • Inhibition of PBPs, inhibits peptidoglycan synthesis
  • Causes reduced functionality of the cell wall
  • Causes osmotic lysis –> cell death
97
Q

Outline how beta-lactams work

A
  • B-lactam ring breaks between the C-N bond
  • C=O reacts with the serine residue in the PBP binding site
  • Binding = irreversible inhibition of PBP
98
Q

Name 5 classes of antibiotics that bacterial target protein synthesis

A
  • Tetracyclines
  • Aminoglycosides
  • Macrolides
  • Glycyclines
  • Oxazolidinones
99
Q

Outline the general MOA of Abx that target bacterial protein synthesis

A
  1. Alter bacterial ribosomes
    • Bind to 30S or
    • Bind to 50S
  2. Block translation
  3. Faulty protein synthesis
  4. Cell death
100
Q

Which ribosomal subunits do the following Abx bind to?

  • Tetracyclines
  • Aminoglycosides
  • Macrolides
  • Glycyclines
  • Oxazolidinones
A
  • 30S
  • 30S
  • 50S
  • 30S
  • 50S
101
Q

Name 4 antibitoic classes that block bacterial DNA synthesis

A
  • ​Floroquinolones
  • Rifamycins
  • Metronidazole
  • Nitrogurantoin
102
Q

Outline the general MOA of Abx that inhibit bacterial DNA synthesis

A
  1. Inhbiit key enzymes (topoisomerases)
  2. Block DNA replication
  3. Block transcription
  4. Cell Death
103
Q

Name two antibiotic classes that block metabolites

A
  • Sulfonamies
  • Trimethroprim
104
Q

Outline the general MOA of Abx that block metabolites

A
  1. Inhibition of metabolites (eg: folic acid)
  2. Block cell metabolism
  3. Lack of energy (i.e. no ATP production)
  4. Cell Death
105
Q

Name two antbiotic classes that target the bacterial cell membrane

A
  • Polymyxins
  • Lipopeptides
106
Q

Outline the general MOA of Abx that target the bacterial cell membrane

A
  1. Alteration or damage to cell membrane
  2. Osmotic pressure
  3. Cellular contents leak out
  4. Cell death
107
Q

What are the 4 major consequences of bacterial resistance to Abx

A
  • Mortality
  • Morbidity
  • Cost
  • Limited solutions
108
Q

Explain (briefly) how resistance to Abx has arisen

A
  • Overuse + misuse of Abx
  • Increased selection pressure on bacteria
  • Rapid evolutionary time of bacteria
109
Q

What are the three types of antibiotic resistance?

A
  • Natural/intrinsic resistance
    • Existed prior to the exposure to Abx
  • Mutational acquired resistance
    • Genetic resistance developed on exposure
  • Extrachromosomal acquired resistance
    • Resistance developed on exposure
110
Q

What are the two main genetic processes that help spread resistance?

A
  • Horizontal eveolution - exchange of genes between strains and species
  • Vertical evolution - mutation and selection
111
Q

What are the three major mechanism employed bacteria in the spread of resistance?

(i.e. exchange mechanisms)

A
  • Conjugation
  • Transduction
  • Transformation
112
Q

Outline the process of Conjugation

A
  • The transfer of DNA mediated by plasmids or transposons
  • Plasmids = circular extrachromosomal DNA found in bacteria
    • Transferred via sex pili
    • Incorportated in adjacent bacterlal cell’s DNA
  • Transposons = sequences of DNA capable of moving around to different positions
113
Q

Outline the process of Transduction

A

The transfer of DNA by bacteriophages

114
Q

Outline the process of Transformation

A

The uptake of short, naked DNA fragments either from the environment or via recombination

115
Q

What are the 4 major mechanisms of resistance?

A
  • Inactivation of the drug
  • Alteration of the target site
  • Active drug efflux
  • Decreased permeability
116
Q

Outline how bacteria are capable of inactivating Abx - give some examples

A
  • Enzymes contributing to resistance destroy/inactivate the drug
  • B-lactamase
    • Produced by bacteria (eg: S. aureus)
    • Cleaves the b-lactam ring, inactivating Abx
    • Can either be simple or extended spectrum (ESBL) which affect multiple drugs
117
Q

Outline how bacteria are capable of altering the Abx target site - give some examples

A
  • Altering the target site of the antibiotic to either reduce or prevent binding
  • Altering PBP2a
    • MRSA
    • Abx cannot bind therefore drug cannot enter the cell
118
Q

Outline how bacteria are capable of active drug efflux - give some examples

A
  • Active efflux of the antibiotic out of the cell’s environment
  • Requires energy (therefore is a metabolic tradeoff)
  • Tet
    • Efflux gene of enterobacteria
  • Mef
    • Efflux gene of S. pyogenes + S. pneumoniae
119
Q

Outline how bacteria are capable decreasing their permeability to Abx

A
  • Preventing entry of the Abx into the cell
  • Usually occurs through altered carrier proteins
120
Q

Give an example of a bacteria that employs all 4 resistance mechanism

A

P. aeruginosa

121
Q

Name 4 mechanisms employed by bacteria to enable colonisation

A
  • non-specific eletrostatic interactions
  • tethering via projections
  • attachment to specific receptors
  • internalisation into epithelial cells
122
Q

What are the three ways in which bacteria can penetrate through the epithelial layer?

A
  • Artificial penetration
  • Through the cell membrane
  • Transit between cell layers
123
Q

Define SIRS

A

SIRS = systemic inflammatory response syndrome

It is a non-specific clinical response including two of:

  • Fever
  • Increased HR (90+ bpm)
  • Increased resp. rate
  • Increased WBC count
124
Q

Define sepsis

A

Sepsis = SIRS with a confirmed infectious process

125
Q

What is severe sepsis?

A

Sepsis + acute organ dysfunction (in at least one organ)

126
Q

Outline the pathogenesis of sepsis

A
  1. Infection
  2. Host immune response
    • WBC activation
    • Anti-inflammatory mediators
    • Pro-inflammatory mediators
  3. Mitochondrial dysfunction
  4. Microvascular flow redistribution
  5. Endothelial dysfunction
  6. Tissue injury
  7. Organ dysfunction (multi-organ = MODS)
  8. Death
127
Q

Outline the management of sepsis

A
  • Treat underlying infection
  • Oxygen support (maintains health of tissues)
  • Haemodynamic support (maintain effective BP)

MCD (13 decks)

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