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Trinity Term 1 > The Natural History of Infectious Disease I: Bacterial Diseases I > Flashcards

The Natural History of Infectious Disease I: Bacterial Diseases I Flashcards

1
Q

Describe Koch’s postulates

A

– microbe is found in all cases of disease and is absent in its absence
– microbe can be isolated and grown in pure culture
– cultured microbe can cause disease in a healthy host
– microbe can be re-isolated and cultured from this host

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2
Q

Describe the revisiting of Koch’s postulates

A

in the light of knowledge on molecular pathology and the microbiome.

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3
Q

Describe the multidisciplinary approach of infectious diseases

A
  • Microbiology (germs)
  • Epidemiology (spread)
  • Resistance (immunology)
  • Virulence (host-microbe-environment interactions)
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4
Q

What are the molecular Koch’s postulates interested in?

A

virulence genes and diseases

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5
Q

What are the ecological Koch’s postulates interested in?

A

dysbiotic microbiota

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6
Q

Describe the human microbiota

A

normally the body is colonised harmlessly and stably

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7
Q

When can dysbiotic disease occur?

A
  • microbes change host biology: cancer, immunological diseases
  • normal microbiota invade: ‘accidental’ pathogens;
  • other microorganisms invade
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8
Q

Describe the invasion of other microorganisms into the microbiota

A

– obligate ‘professional’ pathogens
– opportunistic pathogens

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9
Q

The same microbes can

A

play different roles, depending on circumstances, i.e. ecology, host immune responses etc.

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10
Q

Describe dysbiotic diseases

A
  • IBD
  • liver disease
  • chronic kidney disease
  • brain disorders
  • diabetes
  • respiratory disease
  • cancer
  • heart disease
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11
Q

Describe IBD

A
  • Crohn’s disease
  • ulcerative colitis
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12
Q

Describe liver disease

A
  • Cirrhosis
  • Hepatitis
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13
Q

Describe brain disorders

A
  • Parkinson’s disease
  • Alzheimer’s disease
  • depression
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14
Q

Describe diabetes

A
  • Type 1
  • Type 2
  • gestational
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15
Q

Describe respiratory disease

A
  • asthma
  • bronchitis
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16
Q

Describe cancer

A
  • lung cancer
  • colorectal cancer
  • pancreatic cancer
  • oral cancer
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17
Q

Describe heart disease

A
  • hypertension
  • atherosclerosis
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18
Q

Describe immunopathology

A

Host damage (pathology) can be due to host immune responses

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19
Q

List some host immune responses

A
  • Rheumatic fever.
  • Group A streptococcal (S. pyogenes) infections of the throat.
  • Bacterial molecular mimicry results in host damage by autoantibodies.
  • Haemolytic anaemia.
  • Mycoplasma pneumoniae, atypical pneumonia.
  • Autoantibodies against host cells.
  • Glomeronephritis.
  • Streptococcus pyogenes.
  • Circulating immune complexes settle in the glomeruli
  • Septic shock.
  • Inflammatory response.
  • Commonly Gram positive (Staphylococcus, Streptococcus) or Gram negative (Neisseria meningitidis).
  • Toxic shock syndrome (‘super antigen’ endotoxins).
  • Staphylococcus, Streptococcus.
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20
Q

Describe the basis of sepsis

A

excessive inflammation

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21
Q

Describe leukocytes and parenchymal cells in sepsis

A
  • release of pro-inflammatory mediators
  • cell injury with release of DAMPs
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22
Q

Describe endothelia in sepsis

A
  • release of pro-inflammatory mediators with adhesive and procoagulant properties
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23
Q

What is the function of the endothelium

A

barrier

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24
Q

Describe the platelets in sepsis

A
  • release of pro-inflammatory mediators
  • activation of neutrophils and the endothelium
  • microvascular thrombi
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25
Q

Describe the general effects of sepsis

A
  • coagulation activation (microvascular thrombosis)
  • complement activation
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26
Q

Describe immune suppression enactants

A
  • CD4+ cells
  • CD8+ cells
  • neutrophils
  • antigen-presenting cells
  • lymph node
    • others
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27
Q

Describe the CD4+ cells in immune suppression

A
  • enhanced apoptosis
  • exhaustion
  • TH2 cell polarisation
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28
Q

Describe the CD8+ cells in immune suppression

A
  • enhanced apoptosis
  • exhaustion
  • decreased cytotoxic function
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29
Q

Describe the neutrophils in immune suppression

A
  • down regulated apoptosis
  • enhanced immature cells with decreased antimicrobial functions
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30
Q

Describe the antigen-presenting cells in immune suppression

A
  • reprogramming of macrophages to an M2 phenotypes
  • reduced HLA-DR expression
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31
Q

Describe the lymph node in immune suppression

A

apoptosis of B cells and follicular DCs

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32
Q

Describe other functions in immune suppression

A

expansion of T-regs and MDSC populations

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33
Q

Describe protective immunity

A
  • localised innate immune response
  • local repair mechanisms
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34
Q

Describe the localised innate immune response

A
  • release of pro-inflammatory mediators
  • leukocyte recruitment
  • complement activation
  • coagulation activation
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35
Q

Describe the local repair mechanisms

A
  • inhibition and resolution of inflammation
  • tissue repair
  • return to homeostasis
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36
Q

Describe the microbiome and cancer

A
  • microbes can promote cancers by a number of specific mechanisms
  • macrobiont, can become perturbed
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37
Q

Describe the microbial promotion of cancers

A
  • promotion of inflammation by Helicobacter pylori.
  • immune responses
  • dysbiosis
  • genotoxicity
  • metabolism
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38
Q

Describe quantitative changes in the microbiome in cancer

A
  • bacterial overgrowth
  • occurs in some locations only
  • qualitative and meta genomic changes
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39
Q

Describe the qualitative and metagenomic changes occurring in the microbiome during cancer

A
  • suppression of health-promoting symbionts
  • enhancement of invasive and inflammation-inducing bacteria
  • enhancement of genotoxic bacteria
  • enhancement of cancer-promoting metabolites
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40
Q

Give an example of a cancer-promoting metabolite

A

DCA

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41
Q

Describe macrobiotic inflammation associated with cancer

A
  • MAMP or PRR signalling
  • TH17 cytokines
  • NF-kappaB
  • IL6, TNF, EREG
  • survival and proliferation
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42
Q

Describe the barrier failure associated with cancer

A
  • antibacterial peptides
  • IgA
  • low pH
  • mucous layer
  • tight junctions
  • GALT
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43
Q

Describe the Natural History of the Meningococcus

A
  • ordinarily a commensal, causing disease rarely.
  • invasion plays no role in transmission
  • accidental pathogen
  • acquisition/colonisation; invasion; disease; shedding; clearance
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44
Q

Define accidental

A

not essential to the existence of a thing; not necessarily present; incidental; secondary; subsidiary

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45
Q

Describe Meningococcal transmission, carriage, invasion and virulence factors

A
  • transmission competent meningococci express pili and capsules
  • some meningococci are acapsulate, or cnl
  • adhesion to the epithelium requires pili, then other outer membrane proteins
  • down-regulation of capsule expression is required
  • growth in the bloodstream usually requires expression of a capsule, which is necessary for immune evasion
  • acquisition of nutrients also important
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46
Q

capsule null

A

cnl

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47
Q

Describe the acquisition of nutrients in infectious diseases

A

iron obtained from host tissues.

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48
Q

Describe the transmission of N. meningitidis

A

oropharynx

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49
Q

Describe the role of capsules in colonisation and disease

A
  • anti-phagocytic
  • host-mimicry
  • antigenic diversity
  • adhesion and biofilm formation
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50
Q

Describe anti-phagocytic capsules

A

serogroup A capsules of Neisseria meningitidis

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51
Q

Describe host-mimetic capsules

A

serogoup B capsules of Neisseria meningitidis

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52
Q

Describe antigenic diversity in capsules

A

Streptococcus pneumoniae; >100 capsular types

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53
Q

Describe adhesion and biofilm formation in capsules

A

Klebsiella pneumoniae

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54
Q

Most bactertial capsules are … but Borrelia burgdorferi…

A
  • carbohydrates
  • which causes Lyme Disease, has a protein capsule: Osp.
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55
Q

Osp

A

outer surface protein

56
Q

Neisseria

A

grows on agar

57
Q

Describe the highly variable surface structures of Neisseria meningitidis

A
  • interact with host cells
  • phase variation (on/off);
  • multiple copies (antigenic variation).
  • evolved to promote commensalism;
  • can promote pathogenesis
58
Q

Describe how surface structures promoting pathogenesis

A

including tropism to particular tissues and the evasion of immune responses

59
Q

Give examples of pathogens with surface structures

A

– Bordetella pertussis fimbriae
– Escherchia coli P fimbriae
– Streptococcus mutans glycan

60
Q

Describe secreted toxins

A
  • especially proteinous
  • attack and damage the host or act to modulate and control signalling systems
  • downregulate the host immune response
61
Q

Describe pathogens with secreting toxins

A
  • AB exotoxins
    – Diphtheria toxin, Corynebacterium
    diphtheriae
    – Tetanus toxin, Clostridium tetani
    – Anthrax toxin, Bacillus anthraces
    – Cholera toxin, Vibrio cholerae
    – YOPS
    – Cytotoxins, e.g. Salmonella sp and Clostridium perfringens
62
Q

YOPS

A

Yersinia outer proteins

63
Q

Describe diphtheria pathology

A
  • bull neck: enlarged lymph nodes
  • thick pseudomembrane in posterior pharynx
  • cutaneous legion
64
Q

Describe diphtheria

A
  • Corynebacterium diphtheriae
  • carrying toxin-encoding phage (tox+)
65
Q

Describe diphtheria vaccine

A
  • immunisation with toxoid
  • protects against disease and transmission of tox+ bacteria.
  • vaccine-induced herd immunity can eradicate disease
  • does not eradicate Corynebacterium diphtheriae
66
Q

toxoid

A

inactive toxin

67
Q

Describe M. tuberculosis

A
  • a ‘professional pathogen’
  • obligate parasite of man and animals
  • pulmonary tuberculosis necessary for spread via aerosol droplets
  • chronic infections are established: asymptomatic
68
Q

Describe the pathogenesis of tuberculosis

A
  • primary or secondary infection
  • innate immune phase
  • delayed onset of CD4+ and CD8+ cell responses
  • immunological equilibrium: latency
  • reactivation
  • transmission
  • inflammatory lung tissue damage
69
Q

Describe immunological equilibrium

A
  • equilibrium between effector Ts and T-regs
  • latency
70
Q

Describe the contributing mechanisms to tuberculosis pathogenesis

A
  • defective CD4+ T cells as in HIV+ individuals
  • TNF blockage, glucocorticoids
  • T cell exhaustion
  • imbalance between T-effectors and T-regs
  • altered antigen expression
  • altered cell trafficking
71
Q

Decsribe inactive TB

A

spontaneous immunological control or bacterial switch to dormancy

72
Q

Describe the two transmission types of TB

A
  • high level
  • low level
73
Q

Describe high level transmission of TB

A
  • cavitary; high bacterial burden in lungs
  • non-cavitary; low bacterial burden in lungs
74
Q

Describe what happens on primary or secondary infection of TB

A
  • intracellular growth
  • modification of PAMPs to limit inflammation
75
Q

Give the general pathogenesis of TB

A

Stage 1: Infection
Stage 2: Symbiotic phase
Stage 3: Host mounts a delayed-type hypersensitivity reaction.
Stage 4: Calcified lesions formed, infected tissue surrounded by macrophages latent infection.
Stage 5: Reactivation.

76
Q

Describe infection with tuberculosis

A
  • small numbers of M. tuberculosis infect via the lung, invading macrophages & growing
  • host-to-host
77
Q

Describe the symbiotic phase of tuberculosis

A

Bacteria invade immature macrophages forming clusters of infection

78
Q

Describe the innate immune phase in response in response to TB infection

A
  • neutrophil
  • innate lymphocyte
79
Q

Describe the adaptive immune phase in response to TB infection

A

containment of infection in 90% of individuals

80
Q

Describe a caseated granuloma

A

encased in immune T and B cells

81
Q

Describe TB reactivation

A

+ dissemination occurs in 10% of infected individuals

82
Q

Describe the host immune response to TB

A
  • rapid TH1 cell response develops
  • interferon decreases the amount of fibrosis
83
Q

Describe blood-borne TB

A

spread 3 weeks after unimmunized individuals are first infected by aerosol

84
Q

Describe the characteristic symptoms of TB

A
  • weight loss
  • cavitation and fibrosis
  • progression to cavitary TB
85
Q

Describe the progression to cavitary TB

A

cavities open into the bronchi; allows the spread of TB by aerosols during coughing

86
Q

Describe some things that can reactivate TB

A
  • immunosuppression
  • HIV infection
  • smoking
87
Q

blood-borne

A

haematogenous

88
Q

Describe Treponema pallidum

A
  • causative agent of sexually transmitted syphilis
  • bacterium
  • grows poorly in vitro, slow generation times
  • derives most of its metabolites from the host
    – large number of transport systems
  • no porins
89
Q

Why does Treponema palladium grow poorly in vitro

A

– lack of metabolic capabilities
– limited stress response
– highly sensitive to raised body temperature

90
Q

Describe the genome of Treponema pallidum

A
  • small
  • 1.14Mbp
91
Q

Describe Tp0453

A

may perturb the outer membrane allowing nonselective diffusion of nutrients into the periplasm.

92
Q

Almost always, the metabolic capacity of a pathogen is

A

much more limited than the ancestral organism from which it evolved

93
Q

Describe the ecology of Vibrio cholerae

A
  • opportunistic pathogen
  • associated with reservoir
  • antagonistic organisms that shape its virulence potential
94
Q

List some reservoirs of V. cholerae

A
  • crustaceans
  • copepods
  • chironomid egg masses
  • phytoplankton
  • fish
  • turtles
  • aquatic birds
  • shellfish
  • protozoa
95
Q

Describe the antagonist interactions of V. cholerae

A
  • protists
  • bacteriophages
  • predatory bacteria
96
Q

Describe the pre-adaptation of V. cholerae to human infection

A

convergence of the aquatic environment and the human host

97
Q

List some factors involved in Vibrio cholerae colonisation, survival, and toxicity in the human host and the aquatic environment:

A
  • CT
  • MSHA
  • TCP
  • GbpA
  • VPI-2
  • VSP-1
  • HAP
  • PrtV
  • MARTXvc
  • T6SS
  • VSP-2
  • VBNC
98
Q

CT

A

cholera toxin

99
Q

MSHA

A

mannose-sensitive hemagglutinin

100
Q

TCP

A

toxin-coregulated pilus

101
Q

GbpA

A

N-acetylglucosamine-binding protein A

102
Q

VPI-2

A

Vibrio pathogenicity island 2

103
Q

VSP-1

A

Vibrio seventh pandemic island I

104
Q

HAP

A

hemagglutinin protease

105
Q

PrtV

A

Vibrio metalloprotease

106
Q

MARTXvc

A

multifunctional autoprocessing repeats-in-toxin

107
Q

T6SS

A

type VI secretion system

108
Q

VSP-2

A

Vibrio seventh pandemic island II

109
Q

Describe the factors involved in V. cholerae colonisation

A
  • TCP
  • GbpA
  • VPI-2
  • VSP-1
110
Q

Describe the factors involved in V. cholerae antibacterial activity

A
  • T6SS
  • VSP-2
111
Q

Describe the factors involved in V. cholerae quorum sensing

A
  • HapR
  • PrtV
  • HAP
112
Q

List some V. cholerae toxins

A
  • CT
  • cholix toxin
  • MARTXvc
113
Q

Describe the factor involved in V. cholerae bile resistance

A

OmpU

114
Q

Describe the factor involved in V. cholera biofilm formation

A

MSHA

115
Q

List some factors involved in aquatic V. cholera toxicity

A
  • T6SS
  • cholix toxin
  • MARTXvc
116
Q

List some factors involved in the interaction between V. cholerae and Protozoa

A
  • T6SS
  • ToxR
  • OmpU
117
Q

Describe the factor involved in V. cholerae chemotaxis

A

VSP-1

118
Q

Describe the factor involved in V. cholerae in microcolony formation

A

TCP

119
Q

Describe the factor involved in early attachment of V. cholerae

A

GbpA

120
Q

Describe the factor in V. cholerae phage predation

A

OmpU

121
Q

Describe Yersinia pestis

A
  • many key Y. pestis virulence factors are located on plasmids: accessory genome of Y. pestis ancestors, acquired in separate evolutionary events
  • virulent obligate pathogen of today is an ancestral clone, which successively acquired virulence genes on episomes.
122
Q

Describe the evolution of Yersinia

A
  • non-pathogenic Yersinia acquiries virulence plasmid and becomes pathogenic
  • acquires hms and HPI insect toxins from bacteria in soil or animal gut
  • Y. pseudotuberculosis
  • acquires pFra from Salmonella or other enterobacteria
  • acquires mutliple copies of pPst from bacteria in rat or flea gut
123
Q

hms

A

chromosomal gene in Yersinia for biofilm formation

124
Q

pFra

A
  • plasmid
  • encodes phospholipase D
  • allows for survival (but inefficient transmission) in the flea
125
Q

pPst

A
  • encodes plasminogen activator for dissemination of primary pneumonia in mammalian host
  • makes flea transmission more frequent
126
Q

Describe the effect of ymt on host range in Y. pestis

A
  • on pMT1/pFra
  • Ymt- can cycle between brown rats, black rats, fleas and humans
  • Ymt+ introduces other mammals such as mice
127
Q

Describe the pathology of the bubonic plague in humans

A
  • infected flea bite
  • pre-inflammatory phase
  • cytokine release
  • IL-1RA
  • efferocytosis by macrophages
  • free-floating and cell-borne Y. pestis via the lymph to subcapsular node
  • inflammatory phase
  • hijacks apoptosis, pyroptosis and necroptosis causing lysis and spreading
  • chemotaxis of effector cells and chemokines
  • septicaemia leads to multi-organ infection and failure
  • clinical signs and death
128
Q

Describe the pathogenesis of pneumonic plague in humans

A
  • Y. pestis established in permissive lung environment
  • alveolar phagocytosis, induced programmed death
  • biphasic role of attracted neutrophils
  • lung failure, septicaemia, cytokine storm and death
129
Q

Describe the innovation of the pneumonic plague

A

pneumonia secondary to bubonic plague releases aerosols infected with Y. pestis

130
Q

Describe the biphasic role of the neutrophils

A
  • control Y. pestis
  • cause necrosis
131
Q

Describe bacterial movement and pathogenicity

A
  • primary role for flagella is motility
  • movement between hosts (Vibrio cholerae)
  • movement within hosts (e.g. Helicobacter pylori)
  • formation of biofilms (e.g. Salmonella sp.)
  • attachment to host cells (e.g. Campylobacter jejuni)
132
Q

Infectious disease is the product of biological interactions at the

A

molecular, organismal, population, and ecological levels.

133
Q

Bacteria diseases can arise from the healthy microbiota:

A

– as a consequence of bacterial presence (cancer, immunopathology);
– when the bacteria gain virulence factors (e.g. diphtheria);
– by ‘accident’ – failed or dysfunctional host-pathogen interaction (e.g. meningococcal disease).
– host immune suppression (e.g. post-transplant infections).

134
Q

Explain some of the diversity of bacterial diseases in terms of duration, location, and effect on the host

A

– obligate opportunistic, and accidental pathogens
– respiratory, feacal/oral, sexual, zoonotic transmission

135
Q

Interactions modulated by specific bacterial components include

A

– attachment or movement in the host
– immune evasion, modulation
– host damage, both direct and indirect

Trinity Term 1 (38 decks)

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