Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
94 Cards in this Set
- Front
- Back
What are the names for different arrangements and numbers of flagella? |
Monotrichous - single flagellum Lophotrichous - multiple, at same spot Amphitrichous- single flagellum on opposite ends Peritrichous - project in all directions, E.Coli |
|
What is VBNC? |
Viable but non-culturable Some die, releasing nutrients |
|
What is specific growth rate? |
meangrowth rate the number ofgenerations per unit time u = 1/g |
|
What is the doubling time? |
Mean generation time
Time for all cells to double g = 1/u |
|
What is a mesophile? |
Optimum growth between 20-45oC |
|
What are osmophiles? |
Able to live in high osmotic pressures - high sugar |
|
What are halophiles? |
Thrive in high salt |
|
What are psychrophiles? |
Optimum 15-20. OK at 0 |
|
What are psychrotrophs? |
Optimum room temp. OK at 5 |
|
What are thermophiles?
|
Grow 50-80
Survive in higher temps. |
|
How are ROS generated? |
O2 + e− → O2·−
O2·− + e− + 2H+ → H2O2 H2O2 + e− + H+ → H2O + ·OH |
|
How are ROS removed? |
Superoxide Dismutase (SOD)2O2·− + 2H+→ H2O2+ O2 Catalase 2H2O2 → 2H2O + O2 |
|
How can species be separated based on oxygen-tolerance? |
Presence of SOD and Catalase - anaerobes have neither Where does it grow in anaerobic tube? At top, aerobic, etc. |
|
What are microaerophiles? |
Grow best in low 2-10% O2 Helicobacter pylori |
|
What is convalescence? |
Time spent recovering from an illness |
|
What are microbes that cause disease in healthy hosts called? |
Pathogens |
|
What are microbes that cause disease in immuno-compromised hosts called? |
Opportunistic pathogens e.g. S. aureus |
|
What is ID50? |
Numberof cells administered that result in disease for 50 % of the population Measure of pathogenicity |
|
What is the name for bacteria circulating in blood? |
Bacteremia |
|
What is the name for toxins circulating in blood? |
Toxemia |
|
What is septicemia? |
Whenthe concentration of the bloodborneagent increases to a life-threatening level |
|
What is type III secretion system? |
Appendage found in several Gram-negative bacteria. Used as a sensory probe to detect present of host and secrete proteins to help infect them. |
|
What are M cells? |
Gut epithelial cells Transport antigens from gut lumen by trancytosis to basolateral side - APCs Subverted by Salmonella. |
|
What are invasins? Example |
enzymesthat break down host tissues
Staphylokinase - activates plasminogen to form plasmin - digests fibrin clots. Cleaves IgG and C3b - inhibits phagocytosis |
|
What are Siderophores |
small, high-affinity iron chelating compounds Main classes: hydroxamatesand catechols |
|
How can lysozyme action be overcome? |
S.aureus protein OatA - acetylates NAM |
|
How does coagulase aid evasion? |
Reacts with prothrombin in blood - causes clotting by fibrinogen to fibrin
|
|
What factors affect transmission? |
Stability in environment
Environmental conditions ID50 Sanitation Host factors - normal flora |
|
What is vertical transmission? |
From parents to offspring
Through sperm, ovum, placenta, milk and blood |
|
What is antigenic shift? |
Exchange of homologous genes between different strains of a virus
Pathogen not recognised by host |
|
What is antigenic drift? |
natural mutation over time of known strains of influenza Reduced response by immune system |
|
What is epidemiology the study of? |
patterns, causes, and effects of health and disease conditions in defined populations. |
|
What is an endemic? |
The habitual presence of a disease withina given geographic area |
|
What is an epidermic? |
•The occurrence in a community or regionof a group of illnesses of similar nature, clearly in excess of normalexpectancy, and derived from a common or from a propagated source |
|
What is a pandemic? |
•A worldwide epidemic |
|
What is infectivity? |
thepropensityfor transmission |
|
What is pathogenicity? |
• the propensityfor an agent to cause disease or clinical symptoms. Canbe measured byID50 |
|
What is virulence?
|
•Thepropensity for an agent to cause severe disease. Measured by the case fatality ratio,can also be examined in the lab as Lethal Dose 50 (LD50) –the number of cells administered that result in deathfor 50 % of the population |
|
What is an incubation period? |
•Theperiod between exposure to the agent and onset of infection (with symptoms orsigns of infection) |
|
What is a A noncommunicable disease? |
non-infectious and non-transmissible among people
|
|
iron uptake |
siderophores are excreted intothe medium and then the iron-siderophorecomplexis takenupby specificreceptors onceinside the cell they arecleaved torelease the iron molecule |
|
iron acquisition - other methods |
somebacteria can also import siderophores made by other bacteria some bacteria produce toxins only when iron concentrations are low - killhuman cells,releasing stored iron for uptake |
|
iron abstinence |
replacedits small number of iron-sulphur clusterenzymes with those that use manganese instead |
|
What are biofilms? Name a gram-negative pathogen with a propensity to form biofilms |
theyexist within an extracellular polysaccharide slime thathelps glue them together and bind them to different surfaces Pseudomonas aeruginosa |
|
Advantage of biofilms |
biofilmsoffer protection from phagocytes, disinfectants and antibiotics motile bacteria recognize asurface and aggregate together more readily than non-motilebacteria |
|
Mechanism for switching surface proteins |
1. genetic recombination - RecA-mediatedstrand exchange 2. DNA inversion - occurs between two inverted repeatsites which the recombinase binds 3. strand slippage |
|
Natural transformation advantages
|
DNA for: Genetic diversity, repair and as food |
|
What is the source of DNA for transformation |
free DNA is abundant in theenvironment as it is released by dead organisms some bacteria secrete DNA or lysetheir cells |
|
mechanismof DNA uptake |
setof competence (com) genes are involved in transformationCompetenceis a specialised physiological state where bacteria become able to take up DNA |
|
Which enzyme improves accuracy of DNA replication? |
proof-reading (3’-5’exonuclease) activity |
|
Polymerase involved |
DNAPIII - alpha subunit with Pol, e - proofreading DNAPI - both |
|
What can defects in MMR encourage? |
horizontal gene transfer blocks interspecies recombinationbecause mismatches in heteroduplex DNA are recognised and the exchange aborted by MutHLS |
|
Are RNA viruses stable? |
No - RNA copying enzymes lack proof-reading capacity |
|
Retroviruses replication |
e.g. HIV. Convert RNA genome into DNA for integration. |
|
Can + or - function as mRNA? |
+strand (mRNA) functions as mRNA –strand (complementary to mRNA) must be copied to make mRNA |
|
HIV genetic information conversions |
RNAgenome into dsDNA RdDp DNA strand synthesised first and then RNA degraded by RNaseH before second DNA strandmade for transport to the nucleus |
|
What is HIVreverse transcriptase extremely tolerant of? |
non-standard base pairs |
|
What is the source of individual variation in retroviruses?
|
env gene |
|
Example of a HIV drug |
AZT - nucleoside drug inhibitor Resembles thymidine but blocks DNA synthesis N3 rather than 3' OH |
|
Resistance to AZT |
block binding of the AZT nucleoside in the polymerase active site |
|
Different oxygen enzymes in organisms |
SOD Catalase Obligate aerobe Yes Yes Facultative anaerobe Yes Yes Aerotolerant anaerobe Yes No Strict anaerobe No No Microaerophile Yes Maybe |
|
Biofilm steps |
Cell deposition cell absorption Desorption Cell-to-cell signalling and onset of exopolymer production Convective and diffusive transport of O2 and nutrients Replication and growth Secretion of polysaccharide matrix Detachment, erosion and sloughing |
|
What do biofilms contain? |
micro-environments Oxygen-nutrient gradient Cell-cell signals positively charger antimicrobial binds to negatively charged slime |
|
Three phases response to infection |
Innate - Early-induced innate - recruit of effector cells, recognition of PAMPs Adaptive - Ag to lymphoid tissue, T/B cell recognition - clonal expansion and differentiation |
|
innate immunity |
. Lysozymes. Cleavesβ1-4 glycosidic Lactoferrin - sequesters free Fe, binds LPS and produces peroxides - disrupts membrane permeability and causes lysis Cathelicidins -•Destroysbacterial membranes in phagosomes,following fusion with lysosomes of macrophage.•Insertinto bacterial membrane Defensins -•Inmucus, produced by epithelial cells and phagocytic cell. •Amphipathicproteins that cause pores to form in bacterial membranes. Ion leaves and waterfollows down the osmotic gradient |
|
Complement activation |
•ClassicalPathway - Antigen:antibody complexes detected on pathogen surface •MB-LectionPathway - Mannose-bindingprotein (a lectin) is upregulated in acute phase(inflammation). Binds bacterial cell walls, viral envelopes, antigen-antibodycomplexes •AlternativePathway - Complement proteins(like C3b) bind directly to repetitive pathogen surface structures such as LPS MAC, opsonisation, phagocyte recruitment |
|
How is infection detected? |
PRR (e.g. TLR) recognise PAMPs
•TLR3 –binds dsRNA •TLR4– binds LPS TLR5 - flagellin |
|
Role of phagocytic cells in innate immunity |
Respiratory burst Or oxygen independent; charged proteinsthat damage the membrane, lysozyme, lactoferrin, proteases and hydrolytic enzymes Extracellular ; nitric oxideis released and kills nearby microbes |
|
NK cells |
•NKcells contains granules in the cytoplasm, which contain –Perforin;makes pore in cells –Proteases, aka granzyme cells marked by MHCI •Cancerousand virus-infected cells lose MHCI, and are killed by NK cells •If acell is coated with antibodies, NK cells recognise this cell and kill it by antibody-dependentcell-mediatedcytoxicity (ADCC) |
|
Induced innate response |
TLR activation triggers cytokine and chemokine production |
|
Explain the Inflammatory Response |
bacteria trigger macrophages to release cytokines and chemokines Vasodilation and increased vascular permeabiltiy Inflammatory cell migrate into tissue - release inflammatory mediators |
|
What does the innate immune system result in that activates adaptive immunity? |
–Lymphcontaining antigen and antigen-presenting cells –Complementfragments on microbial surfaces –Releaseof cytokines and chemokines thatactivate T lymphocytes |
|
Adaptive immunity - T cell-mediated |
–Recognizeantigen on surface of dendritic cells–ActivatedT cells travel to the thymus to mature Differentiation |
|
Adaptive immunity - B cell antibody response |
•Whenantigen is detected –Bcell can act as an APC to activate T cells –Ifa corresponding Th cell is available, B cell matures in BM anddifferentiates •Plasmacells–Makeantibodies against antigens •MemoryB cells–Readyto initiate rapid response |
|
Consequences of antibody binding |
Neutralisation complement fixation Agglutination Opsonisation Ppt |
|
Overview of adaptive |
(>96 h) Infection Transport of antigen to lymphoidtissue Recognition by B and T cells Clonal expansion and differentiation Removal of infectious agent |
|
Example of microbes entering through skin q |
S. aureus Gram pos C. tetani - gram-pos. |
|
Which organism has type III secretion system? |
Gram-negative bacteria. sensory probe to detect the presence of eukaryotic organisms and secrete proteins that help the bacteria infect them. |
|
Where aretype III secretion systems encoded? |
Pathogenicityislands |
|
Mucosa entry site - which cells are involved? How is this function subverted? |
–Gutepithelia contains microfold (M)cells roleof M cells is to transport antigens from the gut lumen by transcytosis –antigenfrom one side of the cell to the other, where it is provided toAPCs on the basolateral side •Salmonellainduce ruffling in M cells |
|
respiratorytract entry |
- Adhesins - Inhibitingciliaryactivity |
|
Staphylokinase |
–Activatesplasminogen to form the protease plasmin, which digests fibrin clots and allowsmovement of bacterial cells –CleavesIgG andcomplement component C3b, inhibiting phagocytosis |
|
Hyaluronidase |
–Hyaluronicacid is a non-sulfated glycosaminoglycan distributed widely throughoutconnective, epithelial and neural tissues spreadingfactor |
|
How is CathelicidinLL-37 cleaved? |
metalloproteinase secreted from S.aureus |
|
Coagulase |
Coagulasereacts with prothrombin in the blood cause sblood to clot by converting fibrinogen to fibrin |
|
What does superantigen do? |
–Bridge the MHC class II protein onantigen presenting cells with the T cell receptor on the surface of T cells |
|
What is α-haemolysin? |
cytolytic toxin |
|
β-haemolysin |
sphingomyelinase targetsmembranes rich in this lipid |
|
How can O2 be removed in growing chamber |
2H2 + O2 ---> 2H2O Palladium pellets catalyse reaction |
|
Indole test;
|
•tryptophanase |
|
Kirby-Bauer Method |
•Canbe used to determine whether the bacterium is “susceptible”, “intermediate”, or“resistant” to the tested antibacterial |
|
Methods for MIC |
Etest strips |
|
Endospores |
Ccore is dehydrated - enables heat resistance, long-term dormancy Small acid-soluble spore proteins - protect DNA from UV radiation + carbon source Producing spores enables bacteria to endure extreme stress and spread easily |
|
Is TB gram-positive or neg |
Positive |