Define the terms: Normal flora; Opportunistic pathogen; pathogen; pathogenesis; virulence; colonisation and normal flora; asymptomatic carriage; infection.
pathogen- a bacterium, virus, or other microorganism that can cause disease.
pathogenesis- the origination and development of a disease
virulence- the severity
look the rest up if dont know
List the natural defence mechanisms of the host that protect against bacterial infection
barriers, ciliary elevators, mucous membranes, hair etc.
List examples of bacterial virulence determinants: - e.g. adhesins, capsules, exotoxins
Describe the main stages of a bacterial infection from adherence, immune evasion, transmission to clearance
Describe the direct and indirect effects of bacterial infection that cause tissue damage
Explain mechanism of action of type 1 bacterial toxins and how this results in disease
act at cell membrane but not transported in.
Define Koch’s postulates
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.
bit out of date.
Explain their mechanism of action of type 2 bacterial toxins and how this results in disease
forms pores in the membrane or facilitates enzymatic disruption.
Explain their mechanism of action of type 3 toxins and how this results in disease
translocated into the cell.
e.g cholera causes ATP-cAMP–> GTP-> cGTP which opens Cl channels and electrolyte loss.
dysentery cleaves r28s from ribosome- prevents protein formation
Describe mechanisms of disease pathogenesis as a consequence of bacterial infections
Describe the role of acute inflammatory changes in disease pathogenesis as a consequence of bacterial infections
inflammation is the weapon of the host.
it accumulates phagocytes + white blood cells
can cause a pyogenic infection if met by certain bacteria - leukocidin from staphylococci
Identify the role of bacterial enzymes, bacterial exotoxins.
what secreted exotoxins?
exotoxins are secreted by bacteria
can enact enzymatic lysis/ pore formation/ inhibition of protein synthesis.
exotoxins are made by gram + and -.
endotoxins only made by gram -ve.
Describe the mechanism of disease in Toxic Shock Syndrome- SUPERANTIGENS
toxins produced by staphlococcus aureius and streptococcus pyogenes.
able to act simultaneously on MHC2 and T lymphocites.
causes IL-1,6, TNF-a, inteferon gamma.
results in approx 20-30% of all cells being recruited- very large amounts of inflammation generated.
Outline immunopathology as a consequence of infection including immune complex related disease, molecular mimicry, autoimmunity and infection.
type 3 hypersensitivity reaction-
immune complexes formed by interaction of antibody and antigen.
antibodies can cross react with host cell as they are simalar
e.g rheumatic fever group A carb on strep + structural glycoprotein on heart valve.
or M protein of strep and cardiac muscle
discuss the actions of endotoxins.
part of the cell wall of gram -ve bacteria
activate macophage/ monocite cells. they release IL-1,6,8 TNF-A
cytokines act variously- including liver, clotting cascade, endothelium
activate compliment via alternate path.
can trigger clotting cascade.
results in inc vasc permeability, hypotension, fever, disseminated intravascular coagulation, multiple organ failure.
discuss type IV hypersensitivity reactions
T helper cells bind to specific antigens - release cytokines (inc TNF-a- activates macrophages)
can cause tissue damage greater than the pathogen would.
Define the term antibiotic, and discuss their microbiological origins and natural functions
Antibiotic- natural product of fungi and bacteria, kill or inhibit other microorganism. aid in natural selection and selective advantage.
mostly derived from fermentation, and altered chemically by us to change properties.
Describe the considerations for the choice of an antibiotic
spectrum of activity- broad vs narrow
bacteriocidal vs bacteriostatic (immune suppression etc)
route of administration
active dose vs toxic effect.
age/ renal capacity/ excretion
Explain the microbiological principles of the following terms: therapeutic index, selective toxicity, spectrum of activity.
therapeutic index- active dose vs toxic effects. avoid damage whilst doing rx, no safe drug.
selective toxicity- have effects on microbes but not on humans- i.g folic acid metabolism.
spectrum of activity- how many microorganisms that antibiotic is sensitive to
Outline the main sites of action of antibiotics in the bacteria
focus on cell wall action
Outline the components of the bacteria cell wall and describe their roles in antibiotic action
peptidoglycan found in gram +/-. much more in gram +ve.
penicillin prevent wall development.
Outline the role of penicillin binding proteins (transpeptidases) in the synthesis of peptidoglycan and the action of penicillin’s and cephalosporins
both beta Lactam antibiotics.
PBP usually forms peptidoglycan dimers, which then form the wall.
betalactams bond to PBP and prevent wall maturation
- Explain the microbiological principles and clinical relevance of the following terms: disc diffusion test; MIC; serum bactericidal test
disc diffusion test- diameter of zone of exclusion measured- categorised as resistant/ intermediate/ susceptible
minimum inhibitory concentration- exact concentration of antibiotic needed to inhibit growth. can guide treatment dose/ length.
- Discuss why antibiotic blood levels sometimes need to be measured and how this might be accomplished
ensure has gotten concentrations higher than the minimum inhibitory concentration.
can guide more effective treatment strategies- spiking high can cause more effectivenss in some abs.
measure at the peak (1-2hrs post administration) and at the trough (immediately before next dose)
- Distinguish between a bactericidal and a bacteriostatic antibiotic. Explain why both types of antibiotics are useful
bacteriocidal antibiotics- kill bacteria- used in serious infection.
bacteriostatic- cause a stasis of the bacteria. - relies on host mechanisms, not good in immuno suppressed.
- Explain how to detect drug resistant bacteria
take sample of bacteria
expose to different types of drug, if continues to grow then resistant.
may take 16-20 hours
Recognize the cardinal signs and symptoms of meningitis and meningococcal septicaemia, relating each to the underlying pathophysiological mechanisms
headache- swelling and possibly increased CSF
non-blanching rash- small bleeds around the skin
neck pain (arched back and extended neck posture)- inflamed meninges
dislike of lights- inflamed meninges
high temperature- sign of infection
reduced feeding in infants/ babies
Demonstrate an understanding of the importance of early intervention in a case of suspected bacterial meningitis
it can quickly cause sepsis and cause irreparable damage to the brain and spinal cord.
List the tests performed on blood and CSF in a case of suspected meningitis
csf cell count- lymphocytes/ neutrophils etc.
csf fluid culture
csf gram stain
Describe which tests are most useful in the immediate management of a suspected case of meningitis
lumber puncture- facilitate CSF cell count. CSF glucose testing
PCR amplification of cultures
swabs (throat, nasopharngeal, faeces) to detect for enteroviruses
Name 4 bacteria that cause meningitis
haemofolous influenzae type b
group B beta-haemolytic streptococcus
Describe the changes in the CSF glucose, protein and white cell count in the cases of bacterial and viral meningitis
Explain why and when antigen detection assays are useful
detects bacteria specific DNA - can then facilitate accurate antibiotic therapy.
can take a longer time than latex agglutination asseys
Explain the value of serotyping of meningococci in terms of Public Health
can monitor the effectiveness of vaccine campaigns.
can monitor levels within the community and its spread.
Give an example of each of the following mechanisms of drug resistance: Antibiotic inactivating enzymes, altered target, by-pass metabolic routes, altered transport of drug
List 3 ways Gram negative bacteria may be penicillin resistant
alteration of porins
alternative forms/ mutations in efflux pumps
Penicillin binding protein mutates and so is no longer a fit for the molecule
Discuss the role of bacterial plasmids in drug resistance
exchange of genetic material between bacteria (plasmids) can transfer the information for antibiotic resistance.
Demonstrate recognition of the role of antibiotic misuse in the emergence of bacterial resistance
most resistance occurs in countries where use is heaviest.
resistance increases with use.
Explain the concepts behind antibiotic treatment strategies to prevent bacterial drug resistance
stop feeding it routinely to animals
complete course of ABx + directly observed therapy in TB
infection prevention measures (ward, society, personal)
Describe the history of methicillin resistant Staphylococcus aureus (MRSA)
Explain why Gram positive and Gram negative bacteria have different sensitivities to antibiotics
different structures of the cell wall mean different binding sites and molecules available.
gram +ve membrane is highly porous and lets things in
gram -ve much more barrier resistance.
need different mechanisms to target the different physiologies.