Principles of Infection Flashcards
Describe commensalism.
- Commensalism is where the microbe (called a commensal) derives its food and shelter from the host after colonisation of the host; normally it’ll do no harm to the host. The host may even benefit from the presence of the microbe (called mutualism).
- Commensals are also sometimes referred to as the “normal flora”(microorganisms that live on other organisms without causing harm) which may vary at different sites of the body. For example, blood, the urinary tract and the lower respiratory tract don’t have normal flora and so are usually sterile.
PARASITES - Organisms that can cause damage but dependent on their hosts
INFECTION - when pathogen causes harm to host
PATHOGEN - Microbe that can initiate infection, often with only small numbers, via natural routes despite natural barriers and immune defences
SAPROPHYTE - Free living organisms that are host dependent
How can commensals sometimes be pathogens?
In healthy individuals, the commensal microbes (normal flora) will do no harm, but, if the host’s defences are weakened (immunocompromised), an infection may occur. This is called an opportunistic infection. Usually the host will manifest an inflammatory
response to a pathogen, but not to a coloniser (commensal) at a normally non-sterile site
e.g Staphylococcus aureus in the nose (commensal) and Staphylococcus aureus in a post-operative wound infection (pathogen)
An example would be a patient with leukaemia being infected with candida, which may be a commensal of the oral cavity in a normal healthy person. Another example would be that a person with HIV could be infected by an organism with low virulence. Virulence is a term used to describe the degree of pathogenicity and host susceptibility.
Virulence factors promote colonisation, adhesion and tissue damage. M protein of Streptococcus pyogenes acts as an adhesin
TWO TYPES OF PATHOGENS
- CONDITIONAL -Rely on preexposure
- FULL - Initiates infection via natural route despite immune defences
WAYS COMMENSAL CAN BECOME PATHOGENS
- if found at another site
- due to immunosuppression
- by by-passing defences
Expand on the balance between the microbe and the host.
Whether a microbe behaves as a pathogen i.e. causes disease depends on the properties of the microbe and defensive properties of the host, this can be viewed as a balance between the microbial and host properties.
If the balance is in favour of the microbe (e.g. good adhesion, toxins, capsule etc.) then infection will occur.
If the balance is in favour of the host (e.g. natural barriers, defensive cells, immune response, complement) then no infection will result.
What are the three types of infection?
LOCAL: surface infection, wound
INVASIVE: penetrate barriers e.g skin, lungs and eyes spread
SYSTEMIC: via blood to other sites - can cause fever, rigors
Immunopathology - inflammation causes tissue damage
- cross reactive antigens
e.g. Streptococci and rheumatic heart disease
- granuloma
e.g. Tuberculosis
Describe the role of inflammation in responding to infection.
It functions to bring serum molecules and cells to the site of infection.
- increases blood supply
- increases capillary permeability
- induced migration of cells from blood to tissue (polymorphs, macrophages)
- causes redness and pyogenic infections
- Causes vasodilation - may cause oedema
What is a pyogenic infection?
It is a pus-producing infection.
List some differences between acute and chronic infections.
ACUTE:
- rapid onset
- major local and systemic responses
- acute inflammatory response
- toxin-mediated
- EXAMPLE: dipththeria
CHRONIC:
- slower onset or post-acute
- may still have major local and systemic symptoms
- chronic inflammatory response
- results when the host doesn’t succumb immediately to infection but cannot clear it either
- EXAMPLE: TB
What is an asymptomatic infection or asymptomatic carriage?
It’s an infection with a pathogenic microbe, but not showing (visible) symptoms when infected.
- inflammatory response is mild/ none at all
- damage to the host is mild/ none at all
- no symptoms present
- EXAMPLE: Chlamydia trachomatis
‘reactivation from latent infection’
- You have cleared the disease once, but the pathogen remains latent in the body, and then its reactivated later when you may be immunocompromised i.e pathogen remains so considered asymptomatic
What are some ways in which an infection can spread?
- Direct contact
- Indirect contact
- Airborne
- Blood products
- Mucosal contact - genital, skin and saliva
A way to remember some is by the F-list:
- Fingers
- Fresh Air
- Fomites (touch)
- Fluids (blood, etc.)
- Flies
- Food i.e contamination
- Foetus
- Fornication
- 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
- Infection can resolve with no obvious detrimental effect to the host
Describe microbe multiplication.
Once microbes are internalised, either by an active process as in many virus infections or introduced passively as most bacterial infections, they will multiply locally to produce a focus of infection. During the process of multiplication, many microbes produce various tissue-destroying enzymes which allow invasion of surrounding tissues as well as deeper sites.
Some bacteria produce toxins and tissue destroying enzymes, these toxins are capable of local or systemic actions. Following multiplication, the infection may remain localised, e.g. abscess or spread to contiguous tissues e.g. cellulitis or spread via the blood – septicaemia.
Expand on how microbes adhere, enter the host cell, and evade the host’s defences.
In order to gain a foothold in the host, a microbe needs to adhere(i.e adhesion to structures of host tissue/cells) to the host’s tissue.
This is done by various mechanisms including attachment to tissue via fimbriae (pili), adhesins and other molecules present on the surface of some of these microbes (e.g. attaching to urethral epithelium).
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
EXAMPLE
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
Muco-cillary-clearance mechanism
- When the pathogen releases cytotoxins which specifically damages the cilli and then they can attach
EVADE DEFENCES BY:
- antigenic variation
- capsules can stop contact with a phagocyte
- they can inhibit phagolysosome formation
- they can immunosuppress the host
Describe the functions of toxins in infection.
- they promote the spread or survival of bacteria
- they damage or destroy cells
- they interfere with cell metabolism
- they affect nerves
What are Koch’s Postulates?
They are four criteria that were established by Robert Koch to identify the causative agent of a particular disease.
A microorganism has to:
- 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
Mostly hold up but not all microorganisms e.g Treponema pallidum can be cultured.
What are the 7 stages of infection?
- acquisition from spread (9Fs)
- colonisation (adherence)
- penetration and spread
- tissue damage
- shedding and transmission
- resolution
Not all microbes need all of these stages
Outline some of the host defences
NATURAL BARRIERS
- Skin, eyes, GU tract and the lungs
- Have bile, lysozyme, phagocytes, toxic lipids, cilia etc. as non-specific defences
- ADAPTIVE DEFENCES: Secretory IgA and lymphoid tissue, MALT
TISSSUE/BLOOD DEFENCES
- Non-specific defenses: Phagocytes, macrophages, transferrin, complement proteins
- Adaptive defences: antibodies, T cells
Some immune defences can cause further damage to host.
Tissue Damage - Damage by host’s immune
defences
* Over-activity of immune defences
– Endotoxin – all Gram-negative bacteria –> SEPSIS
* Types of “hypersensitivity”
e.g. Type 4 – granuloma in TB
* Cross-reaction of antibodies against streptococcal antigens with host antigens
– myocardium, synovium, brain
– Streptococcus pyogenes in Rheumatic Fever
