SAQs - Parasitology, Bacteriology, Virology, Mycology Flashcards
Trematode
(Fluke) Adult morphology:
- Two suckers (oral and ventral).
- Blind-ended gut, no anus (one opening).
- All hermaphrodites (no M/F) apart from schistosomes (blood flukes).
- Leaf-shaped.
Cestode
(Tapeworm) Adult general features:
- Flat, segmented.
- No gut - nutrients diffuse directly through the integument.
- Always parasitic - adults rarely pathogenic e.g. in intestine, juveniles usually pathogenic - cysts in organs.
Life cycle:
•Eggs - eternal environment —> juveniles - intermediate host —> adults - definitive host
Nematode
(Roundworm)
- Most are free-living in the soil.
- All are dioecious - separate M + F
Development: egg —> 1st stage = L1 –(1st moult)—> L2 –(2nd moult)–> L2 –(3rd moult)–> L4 –(4th moult)–> adult
Astigmatid mite life cycle (9)
Tick life cycle (3)
Lice - adaptations and life cycle
Flea adaptations to parasitic life (6)
Flea - life cycle (7)
Beneficial uses of bacteria (5)
How one health implementation is achieved (7)
Koch’s postulates (4)
Weaknesses of Koch’s postulates (6)
Bacterial strategies to evade host defences (5)
Role of bacteria in gut health (5)
Mechanisms of gene transfer (3)
- 1). Conjugation - two living bacteria come in direct contact - one bacterium transfers its DNA (plasmid) to the other.
- Occurs primarily between closely-related strains or species, can occur between distantly-related species.
- Donor needs to possess the capacity to create a conjugating pili.
- 2). Transformation - when a bacterium dies, its DNA is released into the environment where it can be taken up by another living (competent) bacteria (free DNA).
- 3). Transduction - A phage (virus infecting bacteria) takes some DNA from one bacteria and transfers it to another (acting as a vector).
- Mediated by a bacteriophage - virus specific to bacteria (can kill the bacteria).
How antibiotics work + examples
Mechanisms of bacterial resistance (6)
- Altered target site e.g. altered ribosomal protein, altered cell wall stem peptide, ribosomal RNA methylation.
- Antibiotic destroying mechanisms - aminoglycosides, beta-lactamases, chloramphenicol.
- Decreased uptake - beta-lactamases = alteration in bacterial permeability.
Virus infection of a cell (5)
- 1). Entry - incoming virus particle ‘suicide’ - once virus is uncoded + released viral genome it is no longer infectious, ready to start replication.
- Attachment - to receptor om surface of cell.
- Adsorption - into cell.
- Penetration - virion within cytoplasm.
- Uncoating of envelope (if has one) - release genome - used for protein synthesis.
- 2). Protein synthesis of structural and non-structural viral proteins.
- Transcription - in cytoplasm or nucleus (depends on virus).
- Translation.
- Viral protein synthesis - always in the cytoplasm using cell machinery.
- Virus that replicates in the nucleus, the proteins are made in the cytoplasm and transported back to the nucleus.
- Only viruses that replicate in the nucleus can use the cellular replication enzymes.
- Processing (glycosylation) - post-modification.
- 3). Genome replication.
- 4). Particle assembly - requires hot cell machinery, each capsid must include genome and the structural proteins, some need to acquire envelope (target to plasma membrane).
- 5). Exit and release:
- Lysis: consequence to cell e.g. cytolytic viruses - break open + destroy cell on released, causes damage + more of effect on immune system.
- Budding - enveloped, cytopathic viruses.
- Exocytosis.
Virus replication in the nucleus vs cytoplasm (adv + disadv) (4)
Nucleus:
+ive:
- May be able to use the host enzymes for replication, transcription and modification.
- Latency easier to establish.
-ive:
- Needs to cross the nucleus membrane.
- Could trigger apoptosis.
Cytoplasm:
+ive:
- No need to enter nucleus.
- Less risk to cause apoptosis.
-ive
•Cannot use any of the host enzymes.
•Need to bring/synthesis own
How viruses avoid the host immune defences in the cell (4)
- Non-structural proteins.
- Multiple actions on many cellular defence mechanisms - blocks interferon signalling + apoptosis.
- Time delay to enable viral replication.
- Success depends on whether cell responds quickly enough - recognises virus genome in its cytoplasm, protein synthesis machinery overtaken, proteins being produced
Virus dissemination in the host (3)
- 1). Passive viraemia - virus directly enters blood without any viral replication.
- 2). Primary viraemia - small amounts of replication @ site of inoculation.
- 3). Secondary viraemia - in organs, higher amount of virus.
