2. Infection: it's acquisition and its spread

Describe the host, pathogen and environmental factors that influence susceptibility to infection, Explain how Koch's postulates establish a causal link between a microorganism and disease, and outline their limitations (e.g. asymptomatic carriage, unculturable organisms, polymicrobial and opportunistic infection). Describe the principal bacterial virulence factors (e.g. adhesins, capsules, toxins, immune-evasion mechanisms) and how they contribute to disease. Discuss antimicrobial resistance, how it affects the management of infection and methods of tackling it. Describe the chain of infection, including routes of transmission (contact, droplet, airborne, faecal–oral, vector-borne, bloodborne) and the distinction between horizontal and vertical transmission. Distinguish colonisation from infection, endogenous from exogenous sources, and community-acquired from healthcare-associated (hospital-acquired) infection.

What do Koch’s postulates do

They establish that a specific microbe causes a specific disease.

what are 4 of Kock’s postulates

1. the microbe is present in every case of the disease, and absent from healthy hosts

2. it can be isolated from a diseased host and grown in pure culture

3. the pure culture causes disease when introduced into a healthy host

4. the same microbe is re-isolated from the new host, and matches the original agent.

What are the pathogen factors varying the disease result between any two hosts and a pathogen?

virulence

inoculum

route of entry

What are the host factors varying the disease result between any two hosts and a pathogen?

immunity

physiological reserve

why are some bacteria more virulent than others? in terms of proximate- 3 things

adhesisns & pill

immune evasion

toxins

how can adhesins and pili make bacteria more virulent

they help the baccy attach to host surfaces, establishing colonisation and resisting clearance more

how can immune evasion make bacteria more virulent

antigenic variation, IgA proteases, complement resistance, intracellular survival, antiphagotic capsule

what’s antigenic variation?

pathogens altering their surface proteins to avoid immune responses

what are IgA proteases

bacterial enzyme that cleaves matching antibodies in order to avoid immune responses

what’s complement resistance

when a pathogen deactivates a body’s complement system- a system of blood proteins that will tag and destroy them.

what’s an antiphagotic capsule

protective outer layer surrounding the bacteria, preventing immune cells from eating and destroying them.

how do toxins make bacteria more virulent?

they target host cells, and drive the inflammatory cascade.

why are some bacteria more virulent than others? evolutionary terms (why the trait exists)

virulence can be favoured by selection when disease aids transmission. but much damage is an accidental by-product, not an adaption.

what is inoculum

inoculum is the no. organisms exposed to the host. there’s usually a threshold dose and it varies widely (handful for 1, millions for others)

below the dose?

defences clear the organism before it establishes

What’s route of entry and why’s it matter

which way it goes in. this decides which defences are met or bypassed.

what does immunity decide

whether infection takes hold.

innate components affecting immunity

barriers like skin and mucosa

ciliary escalator (clears the airways)

phagocytes

microbiota

adaptive components affecting immunity

antibodies and T-cells.

why’s physiological reserve important

it decides whether the patient can withstand the infection/how much they can absorb before dying :)

components impacting physiological reserve

age, frailty, comorbidity and nutrition.

3 catergories for external factors deciding if a pathogen survives, spreads and reaches a host

physical

social

biological

physical examples

climate, water, sanitation, air

social examples

crowding, housing, travel, access to care

biological examples

vectors, animal reservoirs

colonisation vs infection

present, but no host response or damage vs present w host response and damage

why’s colonisation vs infection matter

a positive culture’s not automatically infection. colonisation isn’t treated.

endogeneous vs exogeneous

from patient’s own flora vs from outside: ppl, environment, devices

why’s endogenous vs exogeneous matter

they way to prevent it differs. if endo, keep the patient upright to reduce aspiration and remove cannulae and catheters when no longer needed.

community acquired vs healthcare associated

acquired outside healthcare vs in care.

why’s community acq vs healthcare acq matter

there are different likely organisms and resistance, so a different empirical cover in each area.

chain of infection (6 bits)

1. infectious agent

2. reservoir

3. portal of exit

4. transmission

5. portal of entry

6. susceptible host

reservoir meaning

where the organism normally lives and multiplies.

portal of exit meaning

how the organism leaves the reservoir to spread

2 types of transmission

horizontal (between individuals) and vertical (passed from mother to child)

examples of horizontal transmissions

contact, respiratory, sexual, faecal-oral, vector-borne, bloodborne

examples of vertical transmission

transplacental (in utero), perinatal (during birth), breast milk

how do healthcare teams break the chain of infection?

with policies, procedures, practices

especially important ppl in infection control

hospital and community infection control team

cleaners

medical microbiologists

local health protection team

environmental health officer

why’s it matter so much in healthcare environments?

there are way more vulnerable patients, shared surfaces and devices, and antibiotic selection pressure. stuff’s easily spread.

standard prevention precautions

handwashing, PPE, handling waste well, safe shaps

precautions for preventing transmission via contact

single room gloves + apron. dedicated/decontaminated equipment

precautions for preventing transmission via enteric

single room gloves + apron.

precautions for preventing transmission via respiration

droplets can be stopped w single room, fluid resistant surgical masks, and goggles.

airborne can be stopped with fit-tested FFP3 masks.

Notifiable diseases. who resports, to whom, where and why?

the attending doctor reports it to the proper officer of the local authority within 3 days (in 1 day if urgent), so public health can act.

does one need to worry about carriers?

yes, as they’ll pass it to someone who may get infected.

why antimicrobial resistance matters (when the usual drugs stop working)

1. initial treatment no must anticipate local resistance patterns

2. last line drugs are more toxic/expensive/IV only

3. more chance of treatment failure & longer admissions

4. some infections become less treatable as antibiotics dwindle

5. modern medicine depends heavily of effective antibiotics.

How does the lab check the antibiotic’ll work

1. spread a ‘law’ of bacteria across the plate

2. add paper discs, each holding a set amount of 1 antibiotic

3. where the drug inhibits growth, a clear zone forms around the disc

4. there’s a cut-off to zone size, calibrated to blood levels at a normal dose.

what’s antimicrobial stewardship

the right antibiotic, for the right patient, only when needed, no longer than needed

system-wide measures for antimicrobial stewardship

• prventing w IPC or vaccine

• audit, feedback, education