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2. Foundations of Medicine PoD > Pathogens and Hosts > Flashcards

Pathogens and Hosts Flashcards

1
Q

What signs/symptoms characterise clinical infection

A
  • inflammation
  • pain
  • pyrexia
  • tachycardia
  • rigors
  • increased white cell cound
  • increased C reactive protein (CRP)

note: infection can be latent or sub-clinical

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2
Q

Pathogen

A

organism that can cause disease

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3
Q

Commensal

A

organism which is part of normal flora (e.g. E.coli in gut, S.aureus in nose, axilla)

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4
Q

What is fighting during pathogen/host interactions

A

host defence (immune system) vs organism pathogenicity

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5
Q

Pathogenicity (infectivty and virulence)

A

Capacity of microorganism to cause an infection
Requirements:
* infectivity; ability to becoem established
* virulence; ability to cause harmful effects once established

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6
Q

Infectivity

A

Ability to become established on or within a host
Needs:
* Attachment; E.Coli
* Acid resistance; helicobacter pylori

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7
Q

Virulence

A

Capacity to cause harmful effects (disease) once established
Conferred by virulence factors: genetically determined microbial components:
* Invasivness
* Toxin Production
* Evasion of immune system by microorganism

Specific to strains, not species

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8
Q

Invasiveness

give example and what it does

A

Streptococcus pyogenes (Group A streptococci)
* Necrotising fasciitis
* Cellulitis
* CT breakdown (through enzymes/toxins)
* Fibrinolysis

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9
Q

Toxins

A
  • Exotoxins are released extracellularly by the microorganism
  • Enterotoxins are exotoxins which act on the GI tract
  • Endotoxins is structurally part of the G-ve cell wall
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10
Q

Explain the Exotoxin: tetanus

A
  • Clostridium.tetani
  • Infection of dirty wounds
    * Toxin production: binds to nerve synapses, inhibits release of inhibitory neurotransmitters
  • Death caused by respiratory paralysis
  • Treatment by debridement, antibiotics and antitoxin
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11
Q

Explain the enterotoxin: cholera

A
  • Toxin affecting the intestines (e.g. cholera)
  • Vibrio cholerae (colonises small intestine)
  • Enterotoxin production: Inc cAMP levels: (inhibits uptake of Na+ and Cl- ions, stimulates secretion of Cl- and HCO3- ions. Passive, large outflow of H2O from gut.
  • Causes death by dehydration
  • Treated by rehydration
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12
Q

Superantigens

A
  • certain exotocins of s.pyogenes and s.aureus
  • able to stimulate division of T cells in absence of specific antigen
  • Overwhelming cytokine production causes “toxic shock”
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13
Q

Endotoxin

A
  • Componet fo G-ve bacterial cell wall: LPS: Lipid A, Oligosaccharide core, spicific polysacchariide chain
  • e.coli and other G-ve bacilli
  • Induces severe uncontrolled host response: cytokine production, fever/rigors/hypotension/tachycardia/collapse
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14
Q

what form of MRSA is easier to treat

A

community required MRSA as opposed to hospital required MRSA

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15
Q

bacillus anthracis

A

human infections associated with exposure to infected animals or contaminated animal products
Can often be cutaneous and is rarely fatal with treatment

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16
Q

what are pathogenic bacteria

A

those capable of causing disease

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16
Q

what are pathogenic bacteria

A

those capable of causing disease

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17
Q

Requirements of pathogenicity

2

A

infectivity and virulence

18
Q

What is virulence conferred by

A

invasiveness, toxin production and immune evasion

19
Q

What can harmful effects from bacterial infection be caused by

2 things

A
  • The bacterium
  • the host response

often both

20
Q

Virus pathogenic mechanisms

3

A
  • Cell destruction following virus infection
  • Virus-induced changes to cellular gene expression (e.g. tumor viruses)
  • Immonopathogenic disease (e.g. Influenza A)
21
Q

Sites of viral entry

A
  • Conjunctiva
  • Capillary
  • Skin
  • Respiratory tract
  • Alimentary tract
  • Urinogenital tract
22
Q

What is the case with the majority of viral infections

A

Most is unarrparant (either dormant or infection doesn’t show) - like iceberg: only small portion shows

23
Q

4 different types of viral infections

name and breifly describe each

A
  • Acute infection: arise and then goes away
  • Latent infection: arises, lies dormant, (stimulus) arises again
  • Chronic infection: arises, small dec but remains
  • Tumor virus infection: small inc, stable, suddenly shoots up in late diesease stage
24
Q

Examples of acute viral infections

A
  • Influenza A -respiratory infection
  • Enterovirus - enteric (GI) and neurological infections
25
Q

Summarise process of acute virus infection

A
  • Viral infection
  • Multiplies and inc exponentially
  • Reaches peak (symptoms worst)
  • Host immune system activated and begins to fight back
  • host develped enough antibodies, and viral numbers dec
  • Reduce to 0
26
Q

2 features of acute virus infections

A

Localised to specific site of body (e.g. infulenza in resp. tract)
Development of viraemia with widespread infection of tissues

27
Q

Explain Influenza A virus infection

A
  • Virus infects cells of respiratory tract
  • Destruction of respiratory epithelium: (secondary bacterial infections)
  • Altered cytokine expression leading to fever
28
Q

Explain Influenza A virus infection

A
  • Virus infects cells of respiratory tract
  • Destruction of respiratory epithelium: (secondary bacterial infections)
  • Altered cytokine expression leading to fever
29
Q

Explain Influenza A virus infection

A
  • Virus infects cells of respiratory tract
  • Destruction of respiratory epithelium: (secondary bacterial infections)
  • Altered cytokine expression leading to fever
30
Q

How are novel influenza viruses generated?

2 mechanisms

A
  • Antigenic drift: minor changes (natural mutations) in genes of virus occur gradually over time to generate antigenic varients
  • Antigenic shift: abrupt major changes in virus antigenic structure
31
Q

Give some commone enterovirus infections

A
  • Poliomyelitis (poliovirus)
  • Aseptic meningitis (many enteroviruses)
  • Myocarditis (coxsackie B viruses)
  • Pancreatitis (coxsackie B virus)
  • Respiratory infections (many enteroviruses)
32
Q

Breifly describbe process of enterovirus infection

A
  • oral —> GI system (gut)
  • Viraemia: non-neuronal tissues, neuronal tissues (e.g. CNS) —> paralysis
  • Virus also extreted in faeces
33
Q

Where do enteroviruses live/infect initially

A

The Gut/intestines (GI tract)

34
Q

Give example of a latent virus infection

A

Herpes simplex virus (cold sores = type 1, genital lesions = type 2)

35
Q

Give brief overview of herpes virus infection and latancy

A
  1. Primary infection:
    * Virus infection of epithelium (e.g. cold sore)
    * Virus migrates to ganglia
    * Virus latent in nucleus
  2. Reactivation:
    * Stimulus occurs (e.g. neurological, phycological, immunocompromised)
    * Virus migrates to epithelium leading to virus replication
    * Cold sore again
    * Viral release
36
Q

Give 2 examples of virus-induced tumors

A
  • Papillomaviruses (HPV) - cervical carcinoma
  • Retroviruses - lymphomas and leukemias
37
Q

Summarise the retrovirus replication cycle

A
  1. Attachment
  2. Membrane fusion
  3. Uncoating of viral RNA in cytoplasm
  4. Reverse transcriptase acts and converts to viral DNA
  5. Virus DNA integration into nucleus
38
Q

Summarise retrovirus-induced tumours

A
  • Virus infects cell
  • Virus nucleic acid, as DNA, integrates into ceullular genome
  • Virus causes changes in cellular gene expression
  • Uncontrolled cell multiplication and tumor formation
39
Q

Colonisation

A

presence of a microorganism on/in a host, with growth and multiplication of the organism, but without interaction between host and organism

40
Q

Latent

A

the time interval between when an individual or host is infected by a pathogen and when they become infectious, i.e. capable of transmitting

41
Q

Asymptomatic infection

A

An infection without symptoms

42
Q

Example of tumor causing virus

A

Human T-lymphotropic virus-1 (HTLV-1): causes abnormal gene expression

43
Q

features of viral pathogenesis

A

Pathogenesis is the process by which an infection leads to disease. Pathogenic mechanisms of viral disease include:
1. implantation of virus at the portal of entry
2. local replication
3. spread to target organs (disease sites)
4. spread to sites of shedding of virus into the environment.

2. Foundations of Medicine PoD (28 decks)

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