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Fundamentals of Pathology > W12 Principles of infection > Flashcards

W12 Principles of infection Flashcards

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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
Defences of tissue and blood
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
26
Local
surface infection; wound
27
Invasive
penetrate barriers - spread
28
Systemic
via blood to other sites
29
Effects at different site from colonisation
toxins | endotoxins
30
Immunopathology
- inflammation causes tissue damage - cross reactive antigens e.g. Streptococci and rheumatic heart disease - granuloma e.g. Tuberculosis
31
Local symptoms (inflammation)
Redness, swelling, warmth, pain | Pus – pyogenic infection
32
Systemic symptoms
Fever, rigors, chills, tachycardia, tachypnoea
33
Inflammation
Response to tissue injury - | functions to bring serum molecules and cells to site of infection
34
Changes caused by inflammation
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
Pyogenic Infection
Pus cell (neutrophil) Streptococci
36
Acute Infection
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
Chronic Infection
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
Asymptomatic Infection
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
Asymptomatic Infection examples
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
Chronic Infection examples
``` e.g. TB (Mycobacterium tuberculosis) Chronic osteomyelitis (Staphylococcus aureus) ```
41
Virulence Factors
Promote Colonisation and adhesion To establish infection e.g. adhesins Promote Tissue Damage Growth and transmission? e.g. toxins
42
M protein of Streptococcus pyogenes
M protein of Streptococcus pyogenes acts as adhesin and structural component of cell wall Electron micrograph 1 micron dia M-protein fibrills
43
Stages of Infection
``` 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
Spread of Infection
DIRECT CONTACT INDIRECT CONTACT AIRBORNE BLOOD PRODUCTS
45
HUMAN SOURCES
``` 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
Adherence
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
Neisseria gonorrhoeae
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
Whooping Cough: a toxin mediated disease
``` Bordetella pertussis Invasive adenylate cyclase lethal toxin (dermonecrotic toxin) - superantigen tracheal cytotoxin pertussis toxin, PTx ```
49
Whooping Cough: a toxin mediated disease - NET EFFECT?
permits multiplication at mucosal surface prevents localised immune activation and attack promotes survival and transmission
50
Multiplication
This occurs after internalisation of the microbe | Multiplication results in a focus of infection
51
Counter non-specific & specific defences
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
Local surface infection only
Vibrio cholera | Some strains of N. gonorrhoeae
53
Local Invasion
Shigella, some Staph aureus
54
Deeper Invasion
Through blood, lymph, (nerves) | S. typhi, N. meningitidis, Staph aureus
55
Multipliation may be critical for transmission
Respiratory, faeco-oral or sexual contact
56
Evasion of host defences
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
Intracellular pathogens:-
e.g. Mycobacterium tuberculosis Listeria Salmonella hidden from serum killing, complement, antibodies
58
Direct damage by microbe or toxins
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
Over-activity of immune defences
Endotoxin – all Gram-negative bacteria leading to SEPSIS
60
types of “hypersensitivity”
e.g. Type 4 – granuloma in TB
61
Cross-reaction of antibodies (damage by immune defences)
Cross-reaction of antibodies against streptococcal antigens with host antigens myocardium, synovium, brain Streptococcus pyogenes in Rheumatic Fever
62
Tuberculosis: cellular pathology
Cell-mediated delayed type hypersensitivity response (Type IV)
63
TB granuloma
spherical collection of lymphocytes, macrophages and epithelioid cells with a small area of central caseation necrosis
64
Shedding of infection
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
Mucosal contact
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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