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65 Cards in this Set
- Front
- Back
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what are the general features of viruses?
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nucleic acid genome surrounded by capsid (protein coat) & sometimes encased in lipid membrane
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what size are viruses & how are they visualised
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20-300nm
need electron microscope unless they form inclusion bodies which can sometimes be seen on light micro |
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what are the general features of bacteria?
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prokaryotes
cell membrane but no membrane bound nuclei or organelles |
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what are the cell wall features of bacteria/
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peptidoglycan - sugar polymer - cell wall
gram +ves - thich wall which retains crystal violet stain gram -ves - thin wall sandwiched between 2 peptidoglycan layers |
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what is the difference between facultative & obligate intracellular bacteria?
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facultative can survive and replicate either in or out of host cells vs obligate - only in host cells (eg chlamydia (epithelial), rickettsia (endothelial))
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what characterises fungi?
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eukaryotes which are either round or filamentous (hyphae - septate or aseptate)
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what is thermal dimorphism in fungi?
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hyphae at room temp
yeast at body temp |
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what are dermatophytes?
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fungi which are limited to superficial skin layers ie tinea
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when are deep fungal infections dangerous?
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in the immunocompromised
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what are protozoa and where are they important?
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single celled eukaryotes
major cause of M&M in developing world |
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where do protozoa replicate?
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intracellularly (eg plasmodium in RBCs, leishmaniasis in macrophage)
or extracellularly urogenital/intestine/blood |
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what are the 2 commonest enteric protozoae?
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G lamblia
entamoeba histolytica |
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what are the mechanisms for protozoal invasion?
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1. motile trophozoites attach +/- invade epithelial wall
2. immobile cysts resistant to stomach acid & infectious when ingested |
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what are helminths?
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complex parasitic worms
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what is the general pattern of helminth life cycle?
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usually alternate between sexual reproduction in definitive host & asexual reproduction in intermediary host
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what features of helminths cause disease
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usually proportional to number of worms but can be caused by inflammatory reaction rather than worm itself eg shistosomiasis
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what features of intact skin prevent infection?
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physical barrier
growth of non flora inhibited by pH 5.5 fatty acids |
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when can intact skin become infected?
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dermatophytes
schistosomae release collagenase/elastase & others to dissolve skin |
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when does most skin become infected?
give some examples (6) |
when there is a break
superficial pricks -> fungal wounds -> staph burns -> pseudomonas ulcers -> multi animal bites -> rabies virus/bact insect bites - many eg malaria, leishmaniasis, arbovirus (yellow fever), rickettsiae (rocky mountain) |
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how do microbes gain access to urogenital tract?
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almost always from exterior (ie urethra, vagina)
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what is the feature of successful urinary tract pathogens?
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adhere to epithelium
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what is the major preventable cause of renal failure?
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acute/chronic pyelonephritis
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what are the protective mechanisms in the vagina & how can they be compromised?
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low pH protects pathogens from puberty to menopause
- lactobacilli catabolyse glycogen in N epithelium if antibiotics kill lactobacilli -> increased suscetibility to infection |
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what features of the GI tract defend against infection? (5)
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gastric acid
mucous lytic pancreatic enzymes & bile detergents defensins (mucosal antimicrobial peptides) N flora IgA antibodies secreted by MALT |
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what conditions are required for GI infection (4)
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local defence weakened
- decreased acid - antibiotics alter N flora - obstruction/stalled paralysis or organisms can overcome defences |
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what are the mechanisms used by enteropathogenic bacteria? (3)
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1. toxin release (eg staph)
2. invade & damage intestinal mucosa/lamina propria -> ulcers -> dysentry eg shigella/salmonella/campylobacter 3. S typhi bpasses through damaged mucosa -> lymphatics -> systemic effect |
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how do intestinal protozoae cause disease?
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cysts resist acid
converted to mobile trophozoites in gut attach to gut sugars - giardia - brush border - crypto taken up by enterocytes - entamoeba - contact mediated cytolysis |
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how do helminths cause disease?
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when numbers are so great they cause mass effect eg obstruction or erosion
OR if nutrients sucke out eg hookworms & anaemia; fish tapeworm & B12 deficiency |
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what is the rule with pathogen size and entry into the respiratory tract?
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distance gained into the respiratory tract is inversely proportional to size
<5micrometres go straight to alveoli where they are phagocytosed everything else caught up in mucous |
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what are the characteristics of successful respiratory pathogens
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have specific mechanisms to overcome either mucociliary defence or alveolar macrophages
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how does influenza cause disease?
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attaches to epithelium & host cell tricked into engulfing -> viral entry and replication in cell
second protein allows viral release from cells, lowers viscosity of mucous & allows viral transit |
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which microbes impair ciliary activity & how?
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H influenzae/B pertussis -> paralyse mucosal cilia
P aeurignosa/M pneumonia produce ciliostatic substance |
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which microbes superimpose infection once viral infection causes reduced ciliated epithelia?
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S pneumonia
staph |
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where do microbes go?
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remain superficial/confined to hollow viscera
OR penetrate epithelium & spread via blood/lymphatics/nerves |
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what general pattern does microbe spread follow?
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path of least resistance -> lymphatics
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give examples of where major manifestations appear distal from entry site
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chickenpox/measles - entry respiratory but manifest skin
polio - enters intestine but affects motor neurones |
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when is the placental-foetal route important?
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bacterial/mycoplasmal placentitis -> still birth/prem
viral -> maldevelopment (eg rubella) congenital syphilis |
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when are respiratory diseases infectious?
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when lesion open to airwways
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what water borne viruses are commonly implicated in epidemic outbreaks?
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hep A & E
polio rotavirus |
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what are the innate host defences BEFORE infection sets in? (5)
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physical barriers
phagocytes natural killer cells proteins eg complement/inflammatory mediators adaptive immunity (T/B cells) |
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what are the 3 main mechanisms by which microbes can cause disease?
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- contact/enter cells & directly cause cell death
- release toxins to kill at a distance/release degrading enymes/damage vessels -> ischaemic necrosis - induce damaging host response |
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draw the general mechanisms by which viruses can cause disease
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robbins 8-5
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what is tropism?
what determines it? |
prediliction for viruses to enter certain cells & not others
determined by - viral receptors on cells #1 - presence of transcription factors that recognise virus - anatomical barriers - local conditions (pH, temp, host defence) |
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what are "pathogenicity islands"
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groups of genes which lie together on bacterial genomes & confer disease causing properties
differences in small # of these determine pathogenicity ie non pathogenic into pathogenic |
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what is quorum sensing?
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regulation of gene expresion in a large population of bacteria which allows some to behave in different ways ie starts to behave like a multicellular organism
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what are biofilms and where do we see them?
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organisms live in a viscous polysaccharide layer which adheres to host surfaces
seen in relapsing/persistant infections eg endocarditis, artificial joint infections, resp infections in CF |
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how do bacteria adhere?
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adhesins - surface molecules bind to host cells eg S pyogenes & protein F/teichoic acid
pili - filamentous projections with variable tips specific for binding |
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how can bacteria use intracellular replication to evade host response?
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enters cell & then either evades macrophage response from proceeding properly or escapes by manipulating cytoskeleton
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what defines a toxin?
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any bacterial substance that contributes to illness
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what is the difference between endo & exotoxins?
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endo - component of bacterial cell
exo - protein secreted by bacteria |
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where are endotoxins seen & how do they work?
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in gram -ve bacteria
lipopolysaccharide in outer membrane w variable carb chain which can be used to discriminate different bact strains activates protective immunity in several ways but high levels thought to induce excessive cytokines -> DIC/septic shock/ARDS |
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what are the classes of exotoxins?
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- enzymes
- toxins that change signalling/regulation - neurotoxins (clostridia) - superantigens - stimulate huge T cell response -> cytokines -> capillary leak & shock (eg toxic shock) |
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give 3 examples of when host immunity causes the disease rather than the bacteria
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- M tuberculosis - delayed hypersensitivity manifests as granulomatous inflammation
- cytotoxic T cells in HBV/HCV - S pyogenes - antibodies to strep M protein cross react w cardiac protein -> rheumatic fever or antistrep antibodies form immune complexes in the kidneys |
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what are the 4 main mechanisms used by pathogens to evade immune response?
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1. growth in niches inaccessible to host immune system
2. antigenic variation 3. resist innate immune defences 4. impair T cell response by immunosuppression |
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give examples of microbes that replicate in inaccessible sites (4)
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those that replicate in lumen of intestine (C difficile) or gallbladder (S typhi)
those that enter cells rapidly eg malaria to liver large parasites forming cysts with an inaccessibly dense capsule viral latency hides antigens from the immune system |
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give examples of microbes which use antigenic variation to escape the immune system
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lyme disease borrelia organisms vary their outer membrane proteins
mainly viruses which either mutate or reassort (influenza does both) some have large diversity of serotypes eg rhinoviruses, S. pneumoniae |
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?? how much detail do we need re mechanisms for immune evasion??
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.
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what kind of bacteria are those w no spleen susceptible to?
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encapsulated bacteria eg S pneumoniae as these are normally opsonized & phagocytosed by splenic macrophages
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how do the number of morphological patterns of tissue responses compare to the diversity of microbes?
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vast number of microbes
only 5 major histologic patterns of tissue reaction in infections |
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what are the 5 major histologic patterns of tissue reaction in infection?
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suppurative (purulent) inflammation
mononuclear/granulomatous inflam cytopathic-cytoproliferative tissue necrosis chronic inflam/scarring |
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what are main features of suppurative inflam in infection
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neutrophils attracted to chemoattractants from pyogenic bacteria
(usually extracellular gram +ve cocci & gram -ve rods) lots of neutrophils + liquefactive necrosis = pus |
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what are the main features of mononuclear inflammation?
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diffuse, mononuclear (type depends on host immune response) interstitial infiltrates in ALL chronic inflammatory processes but can develop in actue viral, intracellular bacterial or intracellular parasite
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what is granulomatous inflammation?
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a subset of mononuclear inflammation where infectious agent resist eradication & stimulate strong cell mediated immunity - characterised by accumulation of activated macrophages & may also see caseous necrosis
eg tb |
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what characterises cytopathic/cytoproliferative reactions?
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usually viral
cells necrose (HSV - skin cells damaged & detach) or proliferate (eg HPV, MC) sparse inflammation |
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what are features of tissue necrosis in infections?
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rapid and severe necrosis by toxins (eg C perfringens) w few inflam cells - can look like infarcts
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