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Year One: Pesky Things > Principles of Infection > Flashcards

Principles of Infection Flashcards

1
Q

Recall the types of host-microbe interactions

A
  1. Commensalism- normal flora
  2. Mutualism?
  3. Parasitism
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2
Q

Summarise some opportunistic infections associated with HIV

A

Oral candidiasis

  1. Herpes zooster
  2. Pneumocytosis carnii
  3. Cytomegalovirus
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3
Q

How can be commensals be pathogen sometimes?

A
  • At another site
  • Due to immunosuppression
  • By-passing defences
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4
Q

Give examples of commensals that turn into pathogens in different sites

A

Staphylococcus aureus in the nose (commensal)
• Staphylococcus aureus in a post-operative wound infection (pathogen)
Escherichia coli in GI tract (commensal)
• Escherichia coli in urinary tract causing UTI (pathogen)
Staphylococcus epidermidis on skin (commensal)
• Staphylococcus epidermidis bloodstream infection following infection of an intravenous line (pathogen)

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5
Q

Recall sterile body sites- no commensal organism

A
  • Lower respiratory tract
  • Blood
  • Bone, joint and subcutaneous connective tissue
  • Female upper genital tract
  • Urinary tract (not distal urethra)
  • CNS including CSF and eye
  • Other viscera e.g. liver, spleen, pancreas
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6
Q

What is a pathogen?

A

a microbe that can initiate infection, often with only small numbers, via natural routes, despite natural barriers and immune defences

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7
Q

Name a strict pathogen that will always cause disease

A

Bacillus anthracis (anthrax)

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8
Q

What are virulent microbes?

A

• Highly pathogenic microbes

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9
Q

What is virulence dependent on?

A
  • Virulence – degree to which it causes disease
    • virulent strains
    • gene content alters phenotype
    • host susceptibility
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10
Q

What is pathogenic potential?

A

potential to cause pathological disease

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11
Q

According to germ theory what does a microorganism have to do?

A
  • Be present in every case of the infection
  • Be cultured from cases in vitro
  • Reproduce disease in an animal
  • Be isolated from the infected animal
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12
Q

Describe the balance between pathogenic mechanisms and defensive mechanisms

A

Pathogenic mechanisms: adhesion, capsule, toxins

Defensive: neutral barriers, defensive cells, complement, immune response

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13
Q

Defences of tissue and blood

A

• usually involves tissue damage and controlled by feedback mechanisms

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14
Q

Natural non-specific barriers:

A
  • physical conditions (dry, acidic), sloughing, microflora, lysozyme,
  • toxic lipids, lactoferrin, lactoperoxidases, tight junctions, bile, mucin,
  • cilliated epithelia, bile, cryptdins, phagocytes, intraepithelial lymphocytes
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15
Q

Natural adaptive barriers:

A

MALT( mucosa-associated lymphoid tissue), SALT(skin), GALT(gut), associated lymphoid tissue, secretory IgA

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16
Q

Types of infection

A
  • Local surface infection; wound
  • Invasive penetrate barriers – local spread
  • Systemic via blood to other sites
  • Effects at different site from colonisation - toxinsspecific disease, endotoxins SEPSIS
17
Q

Recall local and systemic symptoms

A

Local symptoms (inflammation)
• Redness, swelling, warmth, pain
• Pus – pyogenic infection

Systemic symptoms
• Fever, rigors, chills, tachycardia(heart rhythm disorder), tachypnoea(rapid breathing)

18
Q

Acute inflammation pathogen examples:

A

• Acute inflammatory response e.g. infection with Streptococcus pyogenes or Staphylococcus aureus
• Toxin mediated e.g. diphtheria (Corynebacterium diphtheriae)
tetanus (Clostridium tetani)

19
Q

What is chronic infection?

A
  • Slower onset or post-acute
  • But may still have major local and systemic symptoms
  • Chronic inflammatory response
  • Results when host does not succumb immediately to infection, but cannot clear infection e.g. TB (Mycobacterium tuberculosis), Chronic osteomyelitis (Staphylococcus aureus)
20
Q

What is asymptomatic infection?

A
  • Infection with a pathogenic microbe (not a commensal or part of the normal flora)
  • Inflammatory response is mild or none at all
  • Damage to the host is mild or not at all

Example: No symptoms present e.g. Chlamydia trachomatis
(urethral infection in men, cervical infection in women)
50% males are asymptomatic
80% females are asymptomatic
e.g. herpesvirus shedding post-acute infection

21
Q

What is reactivation of latent infection?

A

The virus never goes away it’s always in the body

  • When you get older, the virus may be reactivated and this causes shingles or herpes Zoster
22
Q

Stages of infection

A
  • Acquisition from spread – 9Fs
  • Colonisation – adherence
  • Penetration and Spread – local or general
  • Immune evasion
  • Tissue damage
  • Shedding and transmission
  • Resolution
  • Not all microbes need all stages
23
Q

F-List:

A
  • Fingers
  • Fresh Air
  • Fomites – (objects or materials which are likely to carry infection)
  • Fluids (blood etc.)
  • Faeces
  • Flies
  • Food
  • Foetus
  • Fornication
24
Q

Examples of mucosal contact:

A
  • genital tract – gonorrhea, chlamydia, HIV, HepB, syphilis
  • Saliva – Herpes, CMV, EBV
  • Skin – Staphylococci, VZV, HPV,
    • fungal infections
25
Q

Describe adherence of pathogens

A

• Surface adhesion structures of bacteria and viruses
• Host mucosal surfaces
• Specific receptors on host cells
e.g. Influenza A virus – hemagglutinin and sialy-oligosaccharides
• HIV and CD4 + CXCR5 surface proteins of CD4 cells– specific cell entry

26
Q

How does Neisseria gonorrhoeae allow bacterium to adhere to blood group?

A

Fimbriae of Neisseria gonorrhoeae allow the bacterium to adhere to the P blood group antigen of uroepithelial cells

27
Q

What are the virulence factors?

A
  • Promote Colonisation and adhesion To establish infection e.g. adhesins
  • Promote Tissue Damage Growth and transmission e.g. toxins, tissue degrading enzymes
28
Q

What is whopping cough?

A

a toxin mediated disease Bordetella pertussis

• Invasive adenylate cyclase lethal toxin (dermonecrotic toxin) - superantigen tracheal cytotoxin pertussis toxin adheres to ciliated epithelial cells, PTx

29
Q

What is the net effect of whopping cough pathogen?

A

• Net effect - permits multiplication at mucosal surface prevents localised immune activation and attack promotes survival and transmission

30
Q

Give examples of intracellular pathogens

A

Mycobacterium tuberculosis Listeria Salmonella hidden from serum killing, complement, antibodies

31
Q

Describe some evasion mechanisms of pathogens

A

Antigenic variation (e.g. N gonorrhoeae)
- Capsules can stop contact with phagocyte
o S. pneumoniae or B anthracis
- Inhibit phagolysosome formation
o M tuberculosis, Listeria monocytogenes
- Immunosuppress host
o Some bacterial toxins; some viruses block antigen presentation – Herpes

32
Q

How do pathogens cause tissue damage?

A

DIRECT: cytolysis of infected cells

INDIRECT VIA NATURAL IMMUNE RESPONSE:• Over-activity of immune defences
– Endotoxin – all Gram-negative bacteria SEPSIS

INDIRECT VIA ADAPTIVE RESPONSE: IL-4, IgE, cytotoxicity

33
Q

Describe TB pathology

A

• Cell-mediated delayed type hypersensitivity response (Type IV)
TB granuloma spherical collection of lymphocytes, macrophages and epithelioid cells with a small area of central caseation necrosis and tissue becomes destroyed

34
Q

What is shedding of infection

A

o In order to perpetuate, microbe must find a new host
o Host damage not always linked to transmission
o Humans ‘dead-end’ host in some pathogen evolution
o Some symptoms facilitate transmission

35
Q

How do microbes cause host damage?

A 
Direct damage by ​microbes or toxins
o Systematically
▪ Exotoxins – ​C diphtheriae C tetani
o Locally
▪ Enzymes; ​Staph aureus
▪ Toxins; ​Clostridium perfringens, V cholera
  • Caused by ​host’s immune response
    o Immunopathology

Year One: Pesky Things (20 decks)

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