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Fundamentals of Pathology > W12 Principles of infection > Flashcards

W12 Principles of infection Flashcards

1
Q

Infections and Host-Microbe interactions

A

Symbiosis → commensalism + mutualism + parasitism

Commensalism → normal flora

Parasitism → pathogen

Colonisation → asymptomatic (no symptoms) carriage → infection

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2
Q

Parasite

A

harmless/beneficial in healthy people (immunocompromised)
Conditional (from commensal to opportunist) (and from pathogen
Full pathogen (initiates infection via natural route, despite immune defences)

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3
Q

Saprophyte

A
  • free living organism
  • host-dependent
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4
Q

AIDS defining infections

A 
Pneumocystis carinii 
Cryptococcus
Toxoplasma
Herpes simplex infections
Cryptosporidia
Histoplasma
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5
Q

Opportunistic infections associated

with the declining CD4 cell counts in HIV infection

A

Bacterial skin infections
Oral candidiasis

Multidermal
Herpes zooster

Oral hairy leucoplakia
(EBV reactivation)

Tuberculosis

Cytomegalovirus
Disseminated mycobacteriosis

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6
Q

Commensals can sometimes be pathogens

A

In healthy individuals, the commensal microbes (normal flora) will do no harm
Colonisation (not infection)
BUT
If the host’s defenses are weakened (immunocompromised) infection may occur;
This is called opportunistic infection

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7
Q

Pathogen short definition

A

A microbe that causes disease

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8
Q

Commensals and Pathogens

A

Infection implies - harm is done to the host i.e. causes disease

Usually the host will manifest an inflammatory response to a pathogen, but not to a coloniser (commensal) at a normally non-sterile site

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9
Q

Staphylococcus aureus (commensal v pathogen)

A

Staphylococcus aureus in the nose (commensal)

Staphylococcus aureus in a post-operative wound infection (pathogen)

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10
Q

Escherichia coli (commensal v pathogen)

A

Escherichia coli in GI tract (commensal)

Escherichia coli in urinary tract causing UTI (pathogen)

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11
Q

Staphylococcus epidermidis (commensal v pathogen)

A

Staphylococcus epidermidis on skin (commensal)

Staphylococcus epidermidis bloodstream infection following infection of an intravenous line (pathogen)

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12
Q

Commensals can sometimes be pathogens - basic reasons

A

At another site
Due to immunosuppression
By-passing defences

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13
Q

Normally Sterile Body Sites

A

Sites without a normal flora are sterile

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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14
Q

Pathogen

A

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

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15
Q

Some organisms are strict pathogens

A

Some organisms are strict pathogens

i. e. will always cause disease
	e. g. Bacillus anthracis (anthrax)

Some are conditional pathogens

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16
Q

Virulent

A

Highly pathogenic microbes are said to be virulent

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17
Q

Virulence

A

degree to which it causes disease

	- virulent strains
	- gene content alters phenotype
	- host suceptibility
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18
Q

Koch’s Postulates

A

Robert Koch 1843 – 1910
1st to show a specific organism as cause of a disease – anthrax
Then for tuberculosis (Mycobacterium tuberculosis) and cholera (Vibrio cholerae)

“GERM THEORY”

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19
Q

A microorganism has to: (Koch’s Postulates)

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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20
Q

Koch’s Postulates changes

A

We now know not all organisms can be cultured e.g. M.leprae; Treponema pallidum; some viruses

Can detect their DNA or RNA genomes by PCR

Not universally applicable to all diseases
e.g. cancers associated with viruses (HepB; EBV)

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21
Q

Balance between the microbe and the host

A 
Properties of the microbe
(Pathogenic mechanisms):
Adhesins
Toxins
Capsule
Etc.
Properties of the host
Defensive mechanisms:
Natural barriers
Defensive cells
Complement
Immune response

Leads to Genome evolution

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22
Q

Natural Barriers

A 
Skin
Lungs
Gut
GU tract
Eyes
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23
Q

non-specific:

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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24
Q

adaptive:

A

MALT, SALT, GALT, associated lymphoid tissue, secretory IgA

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25
Q

Defences of tissue and blood

A

usually involves tissue damage and controlled by feedback mechanisms

non-specific:
transferrin, complement, acute phase proteins (released by liver)
phagocytes- monocytes and macrophages, PMN’s –neutrophils
macrophage activation

adaptive:
antibodies
T cells

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26
Q

Local

A

surface infection; wound

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27
Q

Invasive

A

penetrate barriers - spread

28
Q

Systemic

A

via blood to other sites

29
Q

Effects at different site from colonisation

A

toxins

endotoxins

30
Q

Immunopathology

A
  • inflammation causes tissue damage
  • cross reactive antigens e.g. Streptococci and rheumatic heart disease
  • granuloma e.g. Tuberculosis
31
Q

Local symptoms (inflammation)

A

Redness, swelling, warmth, pain

Pus – pyogenic infection

32
Q

Systemic symptoms

A

Fever, rigors, chills, tachycardia, tachypnoea

33
Q

Inflammation

A

Response to tissue injury -

functions to bring serum molecules and cells to site of infection

34
Q

Changes caused by inflammation

A

increase in blood supply
increase in capillary permeability
Migration of cells from blood to tissue
(Polymorphs, macrophages)

Ordered Process – regulated

vasodilation, oedema, complement activation, mast cell degranulation, PMNs recruitment, clotting

35
Q

Pyogenic Infection

A

Pus cell
(neutrophil)

Streptococci

36
Q

Acute Infection

A

Rapid onset
Major local and systemic symptoms
Acute inflammatory response
e.g. infection with Streptococcus pyogenes or Staphylococcus aureus

Toxin mediated
e.g. diphtheria (Corynebacterium diphtheriae)
tetanus (Clostridium tetani)

37
Q

Chronic Infection

A

Slower onset or post-acute
But may still have major local and systemic symptoms
Chronic inflammatory response
Results when host doses not succumb immediately to infection, but cannot clear infection

38
Q

Asymptomatic Infection

A

Infection with a pathogenic microbe (not a commensal or part of the normal flora)
Inflammatory response in mild or none at all
Damage to the host is mild or not at all
No symptoms present

39
Q

Asymptomatic Infection examples

A

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

40
Q

Chronic Infection examples

A 
e.g.	TB (Mycobacterium tuberculosis)
		Chronic osteomyelitis (Staphylococcus aureus)
41
Q

Virulence Factors

A

Promote
Colonisation and adhesion
To establish infection
e.g. adhesins

Promote
Tissue Damage
Growth and transmission?
e.g. toxins

42
Q

M protein of Streptococcus pyogenes

A

M protein of Streptococcus pyogenes
acts as adhesin and
structural component of cell wall

Electron micrograph
1 micron dia
M-protein fibrills

43
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

44
Q

Spread of Infection

A

DIRECT CONTACT
INDIRECT CONTACT
AIRBORNE
BLOOD PRODUCTS

45
Q

HUMAN SOURCES

A 
Go to toilet
Bugs on fingers, toilet seat, etc
Direct spread to others 
Contamination of food
Contamination of drinking water by sewage
Contamination of vegetables by sewage
Breathing air – flu, TB,
46
Q

Adherence

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

47
Q

Neisseria gonorrhoeae

A

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

Adhesins in bacterial CW

Adhesin receptor on host CM

48
Q

Whooping Cough: a toxin mediated disease

A 
Bordetella pertussis
Invasive adenylate cyclase	
lethal toxin (dermonecrotic toxin) -  superantigen
tracheal cytotoxin		
pertussis toxin, PTx
49
Q

Whooping Cough: a toxin mediated disease - NET EFFECT?

A

permits multiplication at mucosal surface
prevents localised immune activation and attack
promotes survival and transmission

50
Q

Multiplication

A

This occurs after internalisation of the microbe

Multiplication results in a focus of infection

51
Q

Counter non-specific & specific defences

A

Gastric pH
e.g. gut infections - Salmonella spp

“colonisation resistance” of normal flora

Continuing adherence prevents physical removal by micturition, peristalsis

IgA proteases in Neisseria gonorrhoeae
avoids mucosal immune defence

52
Q

Local surface infection only

A

Vibrio cholera

Some strains of N. gonorrhoeae

53
Q

Local Invasion

A

Shigella, some Staph aureus

54
Q

Deeper Invasion

A

Through blood, lymph, (nerves)

S. typhi, N. meningitidis, Staph aureus

55
Q

Multipliation may be critical for transmission

A

Respiratory, faeco-oral or sexual contact

56
Q

Evasion of host defences

A

Each step in specific and nonspecific immunity
– multiple specific mechanisms

Antigenic variation (e.g. N. gonorrhoeae)

Capsules can stop contact with phagocyte
S. pneumoniae or B. anthracis

Inhibit phagolysosome formation
M. tuberculosis, Listeria monocytogenes

Immunosuppress host
some bacterial toxins;
some viruses block antigen presentation - Herpes

57
Q

Intracellular pathogens:-

A

e.g. Mycobacterium tuberculosis
Listeria
Salmonella

hidden from serum killing, complement, antibodies

58
Q

Direct damage by microbe or toxins

A

Direct damage by microbe or toxins
Systemically:
Exotoxins – C. diphtheriae C. tetani

Locally;
Enzymes; Staph aureus
Toxins; Clostridium perfringens, V. cholera

Caused by host’s immune response
immunopathology

59
Q

Over-activity of immune defences

A

Endotoxin – all Gram-negative bacteria leading to SEPSIS

60
Q

types of “hypersensitivity”

A

e.g. Type 4 – granuloma in TB

61
Q

Cross-reaction of antibodies (damage by immune defences)

A

Cross-reaction of antibodies against streptococcal antigens with host antigens
myocardium, synovium, brain
Streptococcus pyogenes in Rheumatic Fever

62
Q

Tuberculosis: cellular pathology

A

Cell-mediated delayed type hypersensitivity response (Type IV)

63
Q

TB granuloma

A

spherical collection of lymphocytes,
macrophages and epithelioid cells
with a small area of central
caseation necrosis

64
Q

Shedding of infection

A

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

65
Q

Mucosal contact

A

genital tract – gonorrhea, chlamydia, HIV, HepB, syphilis

Saliva – Herpes, CMV, EBV

Skin – Staphylococci, VZV, HPV,
fungal infections

Fundamentals of Pathology (23 decks)

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