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CAT 2 - MICRO/IMMUNO II
Terms in this set (46)
Epiglottitis, H infulenza B but is really rare, pneumococci which is generally due to an obstruction due to inflammation from another infection allowing colonisation within eustachian tube
What is the is the most conerning URTi? What causes it usually? What usually casues otitis media and how?
Will cause damage to nasal epithelia often resulting in ciliary stasis to increase chance of secondary infection, epiglottitis or some pharyngitis but is difficult in children
How does a cold become complicated? When do we investigate URTi?
Usually caused by descending URTi, pneumococci or H influenze, RSV or flu
What often causes acute bronchitis? Acute exacerbation of crhonic? Broncjiolitis?
Mixed anaerobes (staph or klebisella), S aureas if not from penumonia directly? Typical or atypical
What usually causes a lung abscess? Empyema? For pneumonia how can causative bacteria be categorised?
Strep pneu, S aureas and H influenzae, sudden onset, purulent bloody sputum and lobar spread
Top 3 causes of typical bac pneumonia? Three key features?
SLow onset and low grade fever, Non-productive cough, constitutional (headache) symptoms and non-lobar patterning, mycobacteria, legionella, chlamydiaophillia, interstitial inflammation only
Features of atypical pneumonia? Three causes? Histology?
Pertussis, TB or pseudomonas, Influenza, aspergillus/pneumocystis
Three bacter causing pneumonia neither typical/atyp? Key viral cause? Two fungal?
Gram-postiive Capsule to prevent immune recognition, survives intracellularly
How does S pneumonia (and what type of bac is it) manage to do so much damage before immunity helps? Mycobac/legionella?
Penicillin G or amoxy/doxy, cephalopsorin, cefepime for Pseudo/MSSA
Empirical treatment for CAP? HAP?
Lobar, bronchopneumonia/non-lobar, interstital, infection of lung parenchyma within airways or interstitium
Three patterns of pneumonia? Defn?
Congestion from extravasation and intra-alveolar fluid entry, red hepatisation from mass exudation contain neutrophils/RBC, grey hepatisation due to disintegration of RBC in alveoli and early organisation, resolution from breakdown of exudates and resorption, fibrous healing which can cause plugs
Four key stages of acute bac pneumonia? POssible problem at end?
Tissue destruction and necrosis leading to abscess, pleuritis/pleural effusion, empyema, Bacteriaemic dissemination
Complications of typical pneumonia?
Gram -ve bacilli usually pseudomonas or enterobacteria, +ve S aureas and often MSRA
Typical causative agnets of HAP?
Abnormal gag reflex from altered conciousness, stroke, esophagus issues, reflex, neurodegen, mix of both aerobes/anaerobes and often causes an abscess/necrosis
What causes aspiration of goodies from GI or URT into lung? Causative agents and typical outcome?
High fever, productive foul smelling sputum, prior pneumonia (usually aspiration) but can be septic embolism/obstruction from neoplasm
Two key symptoms of lung abscess pneumonia? Most common cause and two other seoncary?
Bacteria/fungi usually TB, localised infection in immunocomp patient, granulomatous inflam with some lymph node involvement
Typical causes of chronic pneumnia? How does it usually present?
Waxy cell wall with mycolic acid for acid fast protection, Type IV hypersensitivity and require T cells to clear it
What type of bacteria is TB? What type of response do we develop against it? What is needed to clear it?
MO absorb TB which blocks phagolysosome allow its multiplication, need PRRs to recognise TB to recruit adaptive response via release of IL-12 to recruit T-helper which releases IFN to allow killing of bacteria, macrophages form histiocytes to wall off infection and create a granuloma
How does TB initial stimulate an immune response/replicat? What is required after this to get an immune response and whats its initial two responses are (cytokine release causes 2X)?
Small grey-white consolodation with central caseous necrosis and granulomas called ghon focus, caseation at local lymph nodes which with focus is ghon complex, heal and clear, progresses to primary TB and disseminates into miliary, goes latent to cause seoncadry
What is the maker of an initial TB infection being fought? (Two features focus and complex)? Three outcomes from this?
Rexposure/reactivation, get immediate immune response due to sensitisation which often causes cavitation and healing with fibrosis, cavities grow and erode into airways/vessels and get whole pleural cavities, miliary TB which can lead to return of infection multifocally
What triggers secondary TB? Difference in response and what it procuces? If it is progressive what will happen? End stage of it?
Usually asymptomatic from CMV, adenovirus can cause haemorrhagic cystitis
Most viral infections of the UT present as what? One really bad one?
E. coli or proteus species normally which are carried from GIT, staph saprophyticus most often from sex, gram -ves like klebisella, enterobacteria or pseudomanas
What are the most common causes of community UTI? Hospital?
Also anaerobic envrionment and transitional epithelia supports the bacteria well, short urethera in women, incomplete bladder emptying, cathertisatin, diabetes mellitus among others
Why do bacteria from GI tract like the UT? What host factors are important?
Adhesins to attach to epithelia, flagella allow swimming up urine, urease assists grwoth/development and can increase formation of stones, type I pili adhesin for bladder wall and PAP for kidneys and flagella
What are three key virulence features of bacteria in causing UTi? What does E. COli have?
Cystitis has dysuria with increased frequency/urgency and suprapubic pain, more systemic like fever, rigors from flank pain and potential sepsis, No can get both
Symptoms of cystitis? Pyelonephritis? Can these occur simultaneously?
Non-infectious conditions, partial treatment, difficult to grow bacteria
Why might we get sterile pyuria?
Alkalise urine, trimethoprime/cephalexin/amoxicillin, double treatment period from one week to two, pregnancy, men less than 60, cephalexin/amocy
What is the empirical treatment for UTi? How does cystitis treatment compared to pyelonephritis? When does asymptomatic bacteriuria occur? Treatment?
Provide metabolism pathways we cannot, immune system development and function, protection from enteropathogens
Three broad ways microbiota improve us?
Dietary folate in form of cellulose, 10% of energy, Vitamin B2, K and biotin/folate
What are bacteria really good at digesting that we cant do anything to? How much of our energy do they supply? Three other key things?
Short chain fatty acids, CHO and lipid metabolism, affect gluconeogenesis and lipogenesis in liver,
What are the key molecules that bacteria produce that affect us? How do they alter our GI metabolism? Systemic metabolism?
IL-22, enhance AM peptide release, epithelial repair and enhances barrier, within mucosa but must renter circulation, via M/golbet cell delivery
What is the key IL in the GI tract? What three things does it induce? What are the two ways DC sample antigens in GI tract?
DC will induce Tref and TH2 to maintain steady state or Th1 and Th17 to induce inflammation, IgA
How does the type of immune response change from sampling normal biota to unknown biota? Important Ig Class in GI?
GI DC will activate a4b7 on lymphocyte so it can bind MAdCAM-1 in GI vascular endothelium and also activates receptors for GI tract specific chemokines, although they can go anywhere once activated are more likely to come back to GI system
WHat is key to the GI tract activation of lymphocytes (it does two things)? Why is this quite important in this context?
Directly by lying on mucosal layer, produce own antimicrobials, interact with PRRs to maintain and enhance enterocytes, cause AM peptide release, cytokine release including IL-22, SCFA
How do microbiota directly aid mucos/gut layer defences? Indirectly? Something else that causes this activation?
Colistridium difficile which causes pseudomembranous colitis, gram positive anaerobes which can form spores which are activated when host is weak, faecal transplant
What is a common GI bug that overgrows but is otherwise normal and what it is said to cause? Type of bacteria and a feature of this which enhances this voergrowth function? If we get recurrent infections of this how do we treat?
Fimicutes and bacteroidetes, Actinobacteria, proteobacteria, all anaerobes
Generally speaking what phyla of bacteria is dominant in colon? Duodenum? Stomach? These are all mostly what type of bacteria?
Those with obesity, T1/2D diabetes have more bacteria that don't produce butyrate and enzymes involved in propionate and vitaminB6 synthesis) and less of those that do, also have more oppurtunistic bacteria
What evidence exists that microbiota is key to the onset of certain diseases (lack a particular set of biota products)>
Changes in fluid and electrolyte balance, lose energy through diarrhoea/vomiting/inflammation, reduced intake from malabsorption/anorexia, malnutrition leads to stunting of growth/illnesses
What are the ways the GI infections kill in short term (3)? In long term?
Frequent small passings, blood and tenesmus, less frequent but larger volume, minimal blood but is associated with malabsorption
What are the features of diarrhoea when issue is large bowel? Small bowel?
ETEC toxigenic which releases cholera like toxins to block absorption of NaCl, EPEC pathogenic adheres to brush border to cause damage and non-specific gastritis, EHEC acid stable and haemorrhagic releases shiga like toxin causing bloody diarrhoea, EIEC invasive cuasing dysentery with some blood
Four major types of diarrhogenic E. Coli?
Salmonella typhy causing typhoid fever and campylobacteria, no unless bloody, really ill or suspecited outbreak
What two bacteria often invade beyond submucpsa in GI tract? DO we usually find this out though?
Selenite broth containing lots of sodium, campylobacteria in low ox environment, MAC to select for gram -ve as has bile salts and want LNF, XLD selecting for shigella/salmonella with black indicator for salmonella producing hydrogen sulfide
What is a special thing we do to diarrhoea samples before we culture? A specialised culture? Two mainstay cultures we use?
Two, Enterica which has many subtypes, Typhi which has an incubation period of 12-48 hours, non-lactose fermenting and will often appear Black on XLD
How many species of salmonella are there? one we care about? Which subtype of this is often involved in GI infections? Features of it?
Giarda, entabmoeba and cyrptosporidium, rotavirus particularly in kids as well as adenovirus and norovirus
Three protozoa in GI tract infections? Viral?
Severe cholera/shigella, Systemic typhoid infections, Protozoa, Pseudomembranous colitis as can cause toxic megacolon
What severe cases do we treat GI infect with antibiotics? Systemic? Other type of pathogens? Specific disease and why?
Enters mucosa and binds Gb3 receptors on endothelia, blocks protein synthesis causing cell death and thus microthrombi and bleeding, will travel to damage kidneys and sue up platelets resulting in haemolytic uraemic syndrome
What does shiga toxin do? What systemic effects does it have and what this manifests as?
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