W5 Infectious Diseases Flashcards
Define infectious disease, epidemiology and microbiology
Infectious disease: The admission of disease carrying agent to the new host and colonisation of that host is a process called infection.
Epidemiology: The study of the distribution and determinates of health to control health problems. How, what? Who?
Microbiology: microbiology is the study of microorganisms, those being unicellular, multicellular, or acellular.
Explain why mortality from infectious disease declined over the past decades.
The study of epidemiology, community immunisations, improved hygiene practices
Distinguish between pathogens and parasites.
Some infections have no clincal manifestations.
Pathogen: prion, virus, bacterial or fungal organisim.
Parasite: if it is a protozoan or a worm (helminth)
Outline the main types of infectious agents
Cellular (living)
Acellular (non living)
Outline and describe infectious agents’ main modes of transmission.
- Infectious agent: bacteria, virus fungi, parasite, protozoa.
- Reservoir; (where germs live) surfaces, environment, soil, blood etc.
- Portal of exit: (how do they get out of organism infected).
- Mode of transmission: (how germs get around) contact, droplet, airborne.
- Portal of entry: how germs get in, respiratory tract, GIT, skin, mucous membranes.
- Susceptible host: immunosupressed person, wounds, burns, neonate, elderly
Describe the chain of infection and ways of breaking it.
- Airborne: droplets aspirtaed by the host.
- Contact (betwene the source and the new host)
- Vechile (formites)
- Vector bites
Refer to picture
Outline factors that contribute to infection and its spreading.
- Pathogen featuers. - Entry/exit strategies - Virulence factors - Dose - Incubation period
- Host features - Susceptibility to a specific pathogen - acquired immunity
- Active vs passive
- Natural vs vaccination
- Herd immunity
- General health status - Age - Genetics - Culture and awareness
- Environment - Reserviors - Vectors
Define pathogenicity and explain how it can be measured.
A measure of the pathogens ability to cause diease, determined by:
- Infectivity: how easy it colonieses host).
* Measured: Infectious doe 50 (ID50) can be measure → numbre of infctious agents per hot required to infect 50% of experimental hosts.* - AVirulence of the pathogen (level of harm causes by a pathogen.
The lethal dos 50% (LD50) can be measured → number of infectious agents per host required to kill 50% of an experimental group of hosts.
- The few microbes need to kill a hist the | the virulence
Describe the factors that contribute to pathogenicity.
Toxins: substances released by the infectious agent that harm the host.
Adhesion factors: proteins produced by infectious agents that help them stick to the body.
- Invasion factors: surfacr components that allow the organism to invade host.
- Evasive factors: mechanisims that help keep the immune system from killing infective agent
Describe the three different types of infection.
- Primary pathogens: are capable of causing disease in healthy hosts.
- Opportunistic pathogens: only cause disease when the infection coincides with conditions that compromise.
- Superinfection: a secondary infection in a patient having a pre-existing infection, following anti-microbial therapy.
Define prions and describe how they cause disease.
Prions: not living infectious particles transmitted to mammals.
Infective host cells concert normal host cell protein into dangerous proteins → clumping together and damaging cells → not recognised by the immune system.
- Soingiform encephalopathies.
- Creutz-Jakob disease
Define retrovirus and describe its life cycle.
Retrovirus contain an extra enzyme: reverse transcription.
RNA → DNA. Virus invades host cell as RNA. RNA → to DNA by reverse transciptase →→→ integrats in host DNA (hiv)
Describe what is encoded by viral genetic material.
Categorized on their host type of genetic material and life cycle. Whether it is DNA, RNA, or a retrovirus (such as HIV).
These are be reprogrammed by the virus to promote it’s own reproduction:
- Proteins that will encapsulate the new viruses produced in cell (caspid proteins
- Signal proteins to co-ordinate the assembly & release of the new encapsulated viral particle
- Reproducing the viral RNA to produce viral mRNA
- Reverse transcription (retrovirus) →→→ Possible drug targets
Describe the general lifecycle of a virus.
- Absorption - binding of virus via viral attachment proteins to cell surface receptors
- Entry - penetration of the host membrane by endosytosis, fusion of cell membrane with host or direct penetration.
3, Uncoating - of viral genome into hosts cytoplasm
- Replication - of viral genetic material
- Transcription - of DNA into mRNA for production of viral proteins or to replicate genetic material.
- Translation - to produce viral proteins (functional and structural)
- Assembly - of proteins and nucleic acid to produce viral particles.
- Release - of mature infectious virions by budding or cell lysis
Explain how viruses may harm their host.
Direct cell damage and death from viral infection may result from.
- Cell Lysis
- Diversion of the cells energy
- Shutoff or competitive re-diretion of a hot cell DNA, RNA and protein systhesis
- Viral inclusions
- Indirect cell damage can result integration of the viral genome, induction of mutation in the host genome, inflammation and host immune response
Explain and distinguish between antigenic drift and antigenic shift.
Antigenic drift: minor changes in viral structures (due to small mutation in genome) - may cause epidemic
Antigenic shift: occurs when there is a major genetic change (less theen antigenic drift)
- Can enable virus to jump from on species to another or dramatically ↑ severity. - May cause pandemic
Discuss why the development of successful viral drugs is challenging.
- Development of antiviral drugs have been limited because:
- viruses do not have their own metabolic processes to target therapy.
- the enzymes involved in viral replication in a host cell are also required by the host cell.
- virsues are simple so less things to target.
- Successful use of antiviral drugs are limited because they are often subclinical until viral reproduction present
- Immunisation and prevention remains as the most effective mans of disease control.
Outline the 5 main types of antiviral (non-retroviral) drugs and exemplify.
- Attachmnt.fusion
- Uncoating
- Replication- different drugs are used to target different methods of replications (DNA or RNA, and retrovirus).
- Viral synthsis and assmbly - target at level of transcription, translation or proteolytic processing,
- Release - cut free from host
Outline the 2 main types of anti-retroviral drugs and explain their mechanism of action.
Drugs used to treat hiv.
NRTI - nucleoside analogue rverse transcription inhibitors : incorporatd into DNA rplication but terminate the extention reaction (lack 3’OD).
NNRTI - non-nucleoside analogue reverse transcription inhibitors: inhibit rplication machinery by binding to proteins
Define Bacteria and describe its structure.
Prokaryotes are uniceellular organisms.
- Their cell lack membrane-bound organelles and a nuclear envelope.
- They can live independently or in colonies.
- Cell membrane: selectivly permable phospholipid bilayer containing embeddd transport molecules.
- Cell wall: peptidoglycan
- Glycocalynx: slime that helps bacterial invasion.
- Plasmids: replicate
- Phili: enable exchange + attachment to surfaces
- Ribosomes: protein synthesis
Explain how bacteria may be classified and why this is useful
Identification in case of pathology in clinical sample.
Cause and effect = tx management.
- Cell shape
- colony morphology
- reaction with specific stains
- growth requirements
- genetics
Explain the importance of bacterial staining and culturing methods.
Gram + thick pepdidoglycan (blue) Cell wall specifically targeted by some antibiotics
Gram - thin pepdidgoglycan (pink). Plasma membrane easier to break with disinfectants/antiseptics.
The staining helps distinguish different strains
Acid-fast staining: mycobacterium are an important bacteria that does not stain with th gram technique because of a thicker wall and hydropohic properties. Can be based on growth
Describe the two categories of bacterial toxins.
Bacterial Endotoxins: Lypopolisaccarides contained in a layer outside the cell wall of a gram + bacteria.
↑ bacterial virulence.
Gram - septic shock is the result of endotoxin release.
Bacterial Exotoxins: Proteins released during bacterial growth. Damages cell membranes, inhibits protein synthesis.Causes production of antibodies
Define disinfectant, antiseptic and antimicrobial antibioc agents.
Disinfectant: agents that kill microbial organisms in an environment.
Antiseptic: agents kill microbes on the host skin but cannot be ingested.
Antimicrobial antibiotic agents: are chemicals that specifically kill microbial organisims in the body without harming the host
Describe the general characteristics of antibiotics.
Oral administration: most stable in gastric environmenet and able to absorb.
Distribution: mostly highly permeable, can cross cell-membranes, blood-brain barrier They either destroy the micro-organisim or Suppress the growth of micro-organisim
Define MIC and MIB and explain why they are important to determine dosing regime.
MIC: minimum inhibitory concentration for bacteriostatic drugs. Minimal bactericidal concentration for bactericidal drugs,
MIB: for a period of time to have an effect; but remain below a concentration that can cause toxicity to the human cells.
Explain how antibiotic resistance develops.
The ability of the bacterial to rapidly adapt, and the overuse of antibiotics.
- Alter the target site for the antibiotic
- changes in target site may ↓ affinity for antibiotic
- emergence of alternatives to target enzymes.
- Alter their uptake of the antibiotic.
- ↓ permeability to the drug.
- development of pumping mechanisim which remove drug from bacterial cell.
- They can produce antibiotic-inactivating enzymes, particularly again penicllins, cephalosportin, aminglycosides
Explain how antibiotic resistance develops.
The ability of the bacterial to rapidly adapt, and the overuse of antibiotics.
- Alter the target site for the antibiotic
- changes in target site may ↓ affinity for antibiotic
- emergence of alternatives to target enzymes.
- Alter their uptake of the antibiotic.
- ↓ permeability to the drug.
- development of pumping mechanisim which remove drug from bacterial cell.
- They can produce antibiotic-inactivating enzymes, particularly again penicllins, cephalosportin, aminglycosides Antimicrobial selection pressure Transmission resistance microbes,
Describe the most common adverse reaction to antibiotics.
Diahaea, nausea, vomiting, headache, oral and vaginal candidiasis, allrgy, hives, pruritis, anaphylaxis, rash, joint pain, fever. Reactions to penicillin.
Antibody or immune cell mediated: penicillin metabolite inc indices antibody production → histamine is released from mast cells. *Reaction is not dose dependant.
Explain the difficulty of treating small and intracellular bacteria.
Histological stainings because they are very small, challenging to idenitfy.
Mycoplasmal diseases: no cell wall
Chlamydial diseases: intracellular pathogen, Tickettsiea (intracellular pathogen)
Explain how vaccines may be developed.
Administration of a dead/weakened infectious agent or its components to an individual with the purpose of inducing an immune response and forming memory cells that are sensitive to this infectious agent.
Describe the characteristics of Fungi organisms and exemplify fungal pathogens.
Molds, yeast, and higher fungi. Most are multicellular, yeasst in unicellular.
Gram +mand eukaryotic
- Cell structures include a membrane bound mucleus
- Cell wall present
- Cell membrane present .
A fungal infection is termed mycosis, superficial eg. skin mouth and external genitalia. This may cause pneumona is immunocompromised people.
Describe the mechanism of action of the main antifungal drug groups.
- Inhibitors of nucleic acid and protein synthesis.
- Inhibitors of fungal cell membrane → target ergosterol.
- Inhibitors of fungal cell wall → echinocandins
Explain the term parasite and outline the main types of human “parasites”.
Is a form of symbiotic interaction, where they both benefits at the expense of the other organisims.
- Protozoa
- Helminths (worms)
3, Arthropods: tickets, lice, fleas
Describe the characteristics of protozoans and exemplify protozoan parasites.
Are single cell eukaryotes that exist everywhere. Very serious. Can be found in drinking water.
Explain how protozoan drugs are classified and exemplify.
Malaria:
sexual (mosiquitos).
Asxual cycle (humans)
Classified according to their site of action.
- Luminal drugs act in bowel lumen and are ineffective on amoeba that have moved into tissues,
- Extra luminal drugs act on those tissue, So combination therapy is used from the Azole drug group
Describe the characteristics of worms (helminths) and exemplify helminthic parasites.
Simple, invertebrae animals, can be infectious parasites. 0 mechanical injury such as obstruction
- release of toxic products damaging tissue.
Multicellular with physiology similiar to humans, making it difficult to treat, Can cause pneumonia. - Round worm - Flukes - Tape worms
Describe the mechanism of action of the main anthelmintic drugs.
Aim to starve them to daeth or paralysing them,
- Drugs that block glucose uptake (kill by starvation) → benzimisazoles.
- Act in the gut lumem → poorly absorbd from gut.
- Vermicidal (kills words) and ovicidal (kills worm eggs).
- Drugs that paralyse the worm.
- Pyrantel (luminal drug): depolarises the action potential in nerves and muscles causing contraction and paralysis.
- Ivermectin (luminal and extra-luminal) : dirupts transmission by opening chloride channels causing muscle paralysis.
- Praziquantal (extra luminal → well absorbed from the gut): penetrates cell membranes ↑ permeability and loss of cellular calcium = worm paralysis, ↑ susceptibility to phagocytes
Describe the characteristics of arthropod parasites and how they are treated.
Colonise the host. Infect and colonise host and transmissible from person to person. Causes disease by secondary infection and initiating inflammatory repsonse.
