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56 Cards in this Set
- Front
- Back
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The likelihood of an infection developing depends upon the balance between...
Think, though I think you'll just skip! |
...the microbial virulence factors of the infecting agent and the host defence mechanisms
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What are the six superficial, mechanical and biochemical host defence?
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Skin
Stomach acid Motility Cilial action Normal flora Secretions |
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Acts as a mechanical barrier and, if breached can be a portal of entry for organisms
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Skin (Superficial, mechanical and biochemical protection)
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The pH of 1.5 is bactericidal - bacterial overgrowth can occur if the acid is neutralised
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Stomach acid (Superficial, mechanical and biochemical protection)
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Maintains normal commensal flora. In cases of an intestinal 'blind loop' bacterial overgrowth occurs
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Motility (Superficial, mechanical and biochemical protection)
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Mechanical removal of trapped matter in the respiratory tract
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Cilial action (Superficial, mechanical and biochemical protection)
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Provides colonisation resistance by preventing foreign bacteria from establishing e.g. hydrogen peroxide produced by oral streptococci can kill coliforms
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Normal flora
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Given an example of normal flora effects in the mouth
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Hydrogen peroxide is produced by oral streptococci, which can kill coliforms
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What are the two innate mechanisms of host defence?
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Phagocytosis
Complement |
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What are the two adaptive cells used in adaptive mechanisms of host defence?
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B cells
T cells |
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Produce IgM in the primary response, IgG in the secondary and IgA antibodies on mucosal surfaces
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B cells
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Mediate killing of infected cells
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T cells
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Motility is a necessary virulence factor for all bacteria T/F
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FALSE. However, it is true for some as non-motile variations of some bacteria are non pathogenic
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Can fimbriae be an adhesin?
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Yes
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What is special about enteropahtogenic (residing in the GI tract) E. coli?
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EPEC lack fimbriae, ST and LT toxins, but they utilize an adhesin known as intimin to bind host intestinal cells
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The cell wall of bacteria and many epithelial surfaces are both negatively charged. How is this overcome when the bacteria needs to adhere to the surface?
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Forces of attraction (e.g. hydrophobicity) counteract the electrostatic repulsive forces for a sufficient length of time for covalent links to be formed between the surface polymers of the bacterial cell and the substrate
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Bacteria move towards a surface by organised/random motion
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Random (however, they are attracted along a nutrient gradient (chemotaxis)
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The organ of locomation for bacteria is the...
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...bacterial flagellum
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What happens when a bacterium adheres to the epithelium?
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They create micro-colonies and become covered in a glycocalyx, which traps nutrients and protects the bacteria from adverse environmental insults
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What are the five possible consequences to the host of bacterial adhesion?
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No effect
Altered morphology Cytokine release Apoptosis Invasion |
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How might a bacteria evade host defences once attached? (4)
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Bacterial capsules can inhibit phagocytosis
Bacterium can become coated in host proteins Bacterium can undergo antigenic variation of its outer surface Can invade a host cell |
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What are the three main ways bacteria are pathogenic?
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Exotoxins
Invasion Immunopathology |
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Give four examples of bacteria that release toxins that give rise to a specific illness
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V. cholerae --> Cholera
C. diptheriae --> Diptheria Cl. tetani --> Tetanus Cl. botulinum --> Botulism |
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How does V. cholerae cause cholera?
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Inhibits regulation of salt and water transport in enterocytes (involved in water transport), leading to massive fluid loss
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How does C. diptheriae cause diptheria?
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Inhibits protein synthesis in cells
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How dos Cl. tetani cause tetanus
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Inhibits inhibitory synapses in the spinal cord leading to muscle spasticity
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How does Cl. botulinum cause botulism?
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Inhibits transmission of acetylcholine at neuromuscular junctions, leading to flaccid paralysis ( weakness or paralysis and reduced muscle tone without other obvious cause)
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Where is V. cholerae found?
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Gut
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Where is C. diptheriae found?
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Oropharynx
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Where is Cl. tetani found?
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Ear/wound
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Where is Cl. botulinum found?
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Gut
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What are two examples of extracellular toxins secreted by bacteria?
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Hyaluronidase, lipase (locally destructive action)
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What is an example of a localised and superficial infection?
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Cellulitis
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What is an example of a localised and deep infection?
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Abscess
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What is an example of a disseminated (Spread throughout an organ or the body) infection?
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Septicaemia
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Superficial or deep pyogenic infection e.g. boils, pneumonia, septicaemia
Scalded skin syndrome - epidermolytic toxins Food poisoning - enterotoxins Toxic shock syndrome toxin |
Staphylococcus aureus (illnesses and exotoxins associated with commonly occurring pathogens)
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Superficial skin infection
Scarlet fever - erythrogenic toxin Septicaemia Immunological complications, e.g. rheumatic fever |
Streptococcus pyogenes (illnesses and exotoxins associated with commonly occurring pathogens)
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Superficial locally destructive infection, e.g. eye, ear - elastase, exotoxin A septicaemia, pneumonia, urinary tract infection
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Pseud. aeruginosa (illnesses and exotoxins associated with commonly occurring pathogens)
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IgA protease, fimbriae
Gonorrhoea, meningitis |
Neisseria sp (illnesses and exotoxins associated with commonly occurring pathogens)
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Urinary tract infection -fimbriae, haemolysin
Gastroenteritis - entertoxins Septicaemia |
Escherichia coli (illnesses and exotoxins associated with commonly occurring pathogens)
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What is an enterotoxin?
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A toxin produced in or affecting the intestines, such as those causing food poisoning or cholera
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Bacteria can invade epithelial but not endothelial cells, T/F
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False, they can invade both
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Some bacteria can survive in macrophages T/F
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True - M. TB is an example
1647191110 |
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Why do some cells HAVE to invade body cells to survive? Give an example of such a pathogen
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They are obligate intracellular pathogens, e.g. Chlamydia
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What are the two ways for pathogens to avoid the host defence mechanisms?
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Cause tissue necrosis or subvert (Undermine the power and authority of) the normal phagocytic process
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Many invasive bacteria possess genes that allow them to invade cells. Where are these located?
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On plasmids or PATHOGENICITY ISLANDS on the bacterial chromosome
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What is a pathogenicity island?
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An area of the bacterial chromosome responsible for carrying genes that allow bacteria to invade cells
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Give the process of bacterial invasion
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Adhesion
Subversion of eukaryotic intra-cellular signalling Re-arrangement of microfilaments or microtubules Pseudopodia formation or membrane ruffling Uptake of bacteria into endocytic vesicle May ermain or escape from vesicle |
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Adhesion
Subversion of eukaryotic intra-cellular signalling Re-arrangement of microfilaments or microtubules Pseudopodia formation or membrane ruffling Uptake of bacteria into endocytic vesicle May ermain or escape from vesicle |
The process of bacterial invasion
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If a bacteria is taken up into a macrophage, what are the three things a bacterium can do? Give examples of each case
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Survive the hostile environment of phagolysosome (e.g. Coxiella)
Inhibit acidification of the vacuole (e.g. Legionella) Inhibit phagolysosome fusion (e.g. Chlamydia, M. TB, Salmonella) |
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Which dastardly bacteria activate host defence mechanisms in such a manner to cause tissue injury?
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Gram negative bacteria that have lipopolysaccharide components
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What is LPS and what kind of bacteria produces it?
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Lipopolysaccharide, gram negative bacteria produce it
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LPS is bound to LPS-binding protein found in the plasma, T/F
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T
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The LPS to LPS-binding protein complex binds to CD14 on macrophage cell membranes, which activates it, T/F
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T
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Activation of macrophages by The LPS complex and CD14 causes what cytokines to be released?
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TNF and IL-1
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LPS activates coagulation and complement, but not kallikrein cascades T/F
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F, it activates all 3
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