Microbiology Flashcards
What is a commensal?
What is an opportunist pathogen? What is virulence/ pathogenicity? What is asymptomatic carriage?
An organism which colonises the host but causes no disease in normal circumstances.
Microbe that only causes disease if host defences are compromised.
The degree to which a given organism is pathogenic.
When a pathogen is carried harmlessly at a tissue site where it causes no disease.
How are bacteria named? Most of what surfaces are colonised by bacteria? Gram positive bacteria turn what colour? Gram negative bacteria turn what colour?
Staphylococcus= genus, aureus= species.
Mucosal surfaces
Purple
Pink with subsequent stain
What bacteria requires a special stain? Gram positive bacteria have what? This connected to what?
TB bacteria
Ziehl-Neelsen stain
Single phospholipid bilayer
Peptidoglycan- forms dense polymer around cell
What does gram negative bacteria have? Some form what when conditions are not good?
Two membranes- thin layer peptidoglycan, outer membrane and lipopolysaccharide (endotoxin)= body’s toxic shock reaction
Spores- resistant to harsh chemicals, stores DNA until conditions better again e.g. cause of anthrax
Why do gram-negative bacteria appear pink with gram stain? Why do gram positive bacteria appear purple?
Cells lose outer lipopolysaccharide membrane and crystal violet-iodide complexes, pink with counterstain.
Decoloriser dehydrates the cell wall and CV-I gets trapped in multi-layered peptidoglycan, purple with counterstain.
E.g. of gram positive+ cocci? Gram negative+ cocci?
Staphylococci, streptococci, entercocci, anaerobic= peptostreptococci
Neisseria, mortadella, anaerobic= villanella spp
E.g. of gram positive+ bacilli? Of gram negative + bacilli?
Bacillus e.g. B.anthrancis clostridia, corynebacteria e.g. C.diptheriae
E.coli, campylobacter, pseudomonas, salmonella, shigella, proteus
E.g. of staphylococcus? E.g. of Beta haemolytic strepto? Alpha-haemolytic strepto? Non-haemolytic?
S.aureus, s.epidermis
S.pyogenes, s.agalactiae
S.pneumoniae, s.oralis, s.milleri, s.sanguis
S.bovis
E.g. of anaerobic gram positive? Enterococcus? What gram + bacteria are chains? Clusters? Tests for both of these?
Peptostreptococcus
E.faecalis
Chains= strepto, clusters= staphylococcus, strep test= haemolysis on BA, coagulase or DNAase test
Types of haemolysis tests and results? Test for staphylococcus?
Beta= beta haemolytic strep- antigenic group A,B,C,G, alpha- optochin test, sensitive= s.pneumoniae, resistant= viridans strep.
Coagulase, += s.aureus, -= coagulase negative staphylococcus
Class of anaerobic gram negative rods? 2 classes of aerobic gram negative rods? Tests for gram negative bacilli?
Bacteroides, coliforms and vibrio
Appearance on MacConkey or CLED or XLD
Non lactose fermentation= e.g. shigella, salmonella, pseudomonas, proteus–> oxidase test
Lactose fermentation= enterobacteriaceae (coliforms) e.g. ecoli, Klebsiella–> biochemical identification e.g. API strip and sensitivity tests
E.g. of bacteria with capsule? Cell wall made up of what? What do gram positive have and not have? Gram negative?
Pneumonia
PPL membrane
Single cytoplasmic membrane, large amount of peptidoglycan on outer surface, not endotoxin (lipopolysaccharide)
Two membranes, smaller amount of peptidoglycan, endotoxin–> endotoxic shock
Mucosal surfaces are areas open to bacterial colonisation? 4 things needed to be kept sterile? Some can store themselves in what? Bacterial conditions?
Nasal cavity, larynx, stomach, colon
Lungs, gall bladder, kidneys, eyes
Spores- which are very hardy and need to be autoclaved in order for them to be destroyed, only certain types
Between -80 and +80 degrees, pH= between 4-9, 2 hours- 3 months= water/ desiccation
How would you measure bacterial growth? Divide by what? Growth lag is due to what? Then there is what growth?
By shining light on bacteria and measuring absorption
Bacteria are taking in nutrients needed to divide and grow, then exponential growth until nutrient runs out, viable= death phase
Endotoxin produced by what? Exotoxin?
Mostly gram negative, action= non-specific, stable on exposure to heat, cannot be converted to a toxoid
Gram +ve and -ve= proteins, action is specific: can inhibit NS–> botulism, stimulate–> tetanus
Unstable on exposure to heat , mostly gram +ve, can be converted to a toxoid
2 stages of bacterial genetics? 3 forms of genetic variation? Plasmids initially known as what?
Transcription- RNA polymerase on bacterial chromosome–>mRNA, translation- occurs at 30S/ 50S ribosome to produce proteins
Base substitution, deletion, insertion
R (resistance) factor
3 ways of gene transfer?
Transformation- genetic alteration of a bacterial cell via uptake of exogenous substance e.g. via plasmid
Transduction- process by which foreign DNA is introduced into a bacteria via a vector or virus e.g. a bacteriophage (virus)
Conjugation- transfer of genetic material between bacterial cells by direct cell-cell contact e.g. via sex plus
3 features of staphylococcus? Reason for coagulase clumping/ no clumping? Common clinical presentation of staph aureus?
Normal habitat= nose and skin, at least 40 species and can be coagulase positive/ negative
Coagulase converts fibrinogen–> fibrin i.e. clot- some produce it to protect against WBCs e.g. staph. aureus
Pain in shoulder, elevated temp, MRI scan- disc injection and osteomyelitis C6 and C7
Treat staph. aureus? Coagulase positive or negative? Spread by what? MRSA resistant to what? Virulence factors?
Flucloxacillin for 3 months, responsible for 90% osteomyelitis
Coagulase positive, spread by aerosol and touch
B-lactams, gentamicin, erythromycin, tetracycline
Pore-forming toxins- e.g. PVL which causes haemorrhage pneumonia
Alpha-haemolysin- induce apoptosis at low levels or widespread necrosis at high levels
Proteases–> scalded ski syndrome
Toxic shock syndrome toxin- stimulates cytokine release
Protein A- surface protein binds immunoglobulins in wrong orientation
E.g. of coagulase negative staphylococci? Main virulence factor?
Staphylococcus epidermis- opportunistic infections in prosthetic limbs and catheters, persistent biofilms
Staph saprophyticus- acute cystitis
Streptococci can be classified in what 3 ways? What 3 colours with haemolysis?
Haemolysis, Lancefield typing, biochemical properties
Alpha= green- brown, Beta= clear/ colourless, gamma= no lysis
What is Lancefield typing? 2 most important groups?
Method of grouping coagulase negative bacteria based on bacterial carb cell surface antigens
20 groups= A-H and K-V
A- strep. pyogenes, and B- strep agalactiae; neonatal infections
Infections caused by strepto pyogenes? Complications? Assessment of risk estimated with what? Virulence factors?
Wound infections e.g. cellulitis, tonsillitis and pharyngitis, otitis media, Scarlet fever (by erythrogenic toxin)
Rheumatic fever, glomerulonephritis, needs prompt treatment
Anti-streptolysin O titre
Enzymes or toxins
Common presentation of strepto pneumo? Infections? Pre-disposing factors? Virulence factors?
Heavy smoker with nasal congestion and fever, 2 days later= cough, severe chest pain, rust-coloured sputum, CXR= fluid filled
Pneumonia, otitis media, sinusitis, meningitis
Impaired mucus trapping, hypogammaglobulinaemia, asplenia- no tuftsin–> impaired phagocytosis, diabetes, renal disease, sickle cell disease, young age
Polysaccharide capsule, teichoic acid- binds to choline receptors, peptidoglycan- protects bacteria, pneumolysin cytotoxin
Viridans strep also known as? Some cause what? Important in what? Most pathogenic are what group? Causes what?
Oral strepto, alpha or non-haemolytic
Dental caries and abscesses
Infective endocarditis: s.sanguinis, s.oralis
Milleri group- s.intermedius, s.anginosis, s.constellatus
Deep organ abscesses e.g. in brain and liver
Common presentation of corynebacterium diphtheria? Treatment? Spread by? Toxin does what? Toxin recognition using what? Prevention?
Child with severe sore throat, fever and malarse for 2 days, lymphadenopathy in neck, rapid breathing, thick greyish membrane on tonsils
Anti-toxin and erythromycin
Droplet spread
Inhibits protein synthesis, Elek plate, toxoid vaccination
3 parts of lipopolysaccharide endotoxin? Bacteria has not H antigen since no flagellum? Does have H antigen since does have flagellum?
Lipid A- toxin portion anchored in outer leaflet of outer membrane
Core R antigen- short chain of sugars, some unique to LPS
Somatic O antigen- highly antigenic repeating chain of oligosaccharides
Shigella
Salmonella- does have flagellum
Features of enterobacteria (coliforms)?
Rods/ bacilli, most are motile, some are intestinal parasites, able to grow in anaerobic conditions, MacConkey used to differentiate lactose and non-lactose fermenting
Most facultative anaerobe in gut? Has what? Infections caused? There are many what? They share a common what?
E.coli Flagella Wound infections, UTIs, gastroenteritis, travellers' diarrhoea, bacteraemia, meningitis in infants Serotypes (pathovars) Common core genome
Pathogenic e.coli contains what not in commensal e.coli? Many have acquired pathogenicity how? How is travellers diarrhoea caused?
Blocks of genes
By mating and acquiring pathogenic blocks of genes
By ETEC strain, pilli= adhere to tissue of SI, labile toxin released–> alters role of Gs protein on GI cell surface–> adenyl cyclase not stimulated–> more Cl- released into GI lumen
4 species of shigella? Symptoms? Enter gut via what? Cross epithelial cell layer where what happens? Eventually destroyed by what? Some release what which doe what? Also from some what?
S.dysenteriae, s.felxneri, s.boydii, s.sonnei (commonest)
Low infective dose
Severe blood diarrhoea, frequent passage of stools, small volume pus and blood, prostrating cramps
M cells, engulfed by macrophages–> apoptosis and released of damaging free radicals, inflammatory response and cell damage
Neutrophils
Shiga toxin- disrupts protein synthesis–> necrosis
E.coli e.g. EHEC
2 species of salmonella? Infections x3?
S.enterica–> salmonellosis and s.bongori- reptile contact
Gastroenteritis- milk and poultry, 6-36 hour incubation, resolves in week, localised infection
Enteric fever- typhoid, systemic disease, by type and paratyphi, faecal-oral spread, fever, headache, dry cough
Bacteraemia- bacteria in the blood- uncommon
Pathogenesis of salmonella?
Ingestion of contaminated food/ water, high infective dose
Mediates endocytosis across gut lumen
Salmonella causing gastroenteritis?
Bacteria presence results in chemokine release and neutrophil recruitment, neutrophil-induced tissue injury
Fluid and electrolyte loss due to cell damage resulting in diarrhoea
Inflammation/ necrosis of gut mucosa
Salmonella causing enteric fever?
To basolateral membrane of cells in intestinal lumen- inflammation and ulceration
Initially= little damage to gut mucosa
Bacteria engulfed and survives, then spreads to lymph nodes
Enters bloodstream via thoracic duct, then multiples in macrophages of liver, spleen and bone marrow–> septicaemia, massive fever
Spreads to gall bladder from liver where person can be in carrier state from 1 year to rest of life
What does Klebsiella pneumoniae cause?
Opportunistic, nosocomial infections, pneumonia, bloodstream infections, wound/ surgical infections, meningitis
Features of vibrio cholera? There is no what and why? Treatment? Virulence determinants?
Facultative, curved rods/ bacilli with single polar flagellum
Faecal-oral route, high infective dose- sensitive to acid, incubation= 5 hours, results in rice-water stools
60% mortality- can lose 20 litre/ day plus electrolytes
Blood or fever- no invasion/ damage of mucosa
80% with oral rehydration
Pilli- for colonisation, cholera toxin- uncontrolled cyclic AMP production, protein kinases, loss of Cl- and Na+–> H2O loss
Features of pseudomonas aeruginosa?
Motile- single polar flagellum, opportunistic, multiple antibiotic resistance
Acute infections: localised- burn surgical wounds, UTIs, keratitis, systemic- neutropenic, ICU patients- nosocomial pneumonia
Chronic infection: cystic fibrosis suffers- dehydrated lung mucus–> bacteria grow
Features of haemophilia influenzae? Causes what? Only grow on what?
Exclusively human parasite, nasopharyngeal carriage in 25-80% population, infections mainly young children and adult smokers, non-motile
Meningitis crosses BBB, epiglottitis, sinusitis, otitis media, bacteraemia, cystic fibrosis and COPD lung infections
Chocolate agar- blood agar heated to 80 degrees to allow release of haem by RBCs
Virulence determinants of haemophilus influenzae?
Pilli- adherence to epithelial cells and mucin, commensals and resp tract pathogens= non capsulate, invasive strains (penetrate nasopharyngeal epithelium)= capsulate
Lipopolysaccharide endotoxin–> inflammation
Features of bordetella pertussis (Beta- Proteobacteria)?
Pertussis= whooping cough, short rods, highly contagious with low infect dose, aerosol transmission
Adhere to ciliated epithelia of upper resp tract
Symptoms of bordetella pertussis and can lead to what?
Non-specific flu-like symptoms followed by paroxysmal coughing (cough–> inhalation resulting in whooping sound)
Sub-conjunctival haemorrhage
2 species of neisseria? Where found during infection? Prevalence, transmission and symptoms of n.meningitis?
Non-flagellated diplococci
N.meningitis, n.gonorrhoeae
Polymorphonuclear lymphocytes of CSF or urethral discharge
In nasopharynx of 5-10% population, aerosol transmission, crosses NP epithelium and enters bloodstream in small proportion of colonised individuals
Asymptomatic if low/ septicaemia if high
Virulence determinants of n.meningitis?
Capsulated in nasopharynx, capsule= anti-phagocytic
Pilli= cell invasion
Lipopolysaccharide= cytokine cascade–> sepsis
Transmission and symptoms of n.gonorrhoea?
Not a commensal but can be asymptomatic (30% of infected females), person to person only
STD–> urethritis with additional infection of female genitalia, can lead to infection of Fallopian tubes if infection ascends
Non-capsulated unlike n.meningitis
E.g. of e-Proteobacteria? Features and symptoms of campylobacter? Virulence factors?
Campylobacter- C.jejuni, C.coli
Spiral rods/ bacilli, most common cause of food poisoning in UK and US, undercooked poultry, low infective dose, mild-severe diarrhoea often with blood, shed in faeces for around 3 weeks
Invasins- invades ideal and colonic epithelial cells–> local acute inflammatory response i.e. tissue damage
Cytolethal distending toxin (CDT)- arrests cell cycle meaning target cells swell and lyse
Features of helicobacter pylori? Virulence factor?
Requires CO2, spiral shaped, present in 50% of global population but only fraction will develop disease
Major role in gastritis and peptic ulcer disease
Implicated in gastric adenocarcinoma
Urease- hydrolyses urea to generate ammonia to act as a buffer to gastric acid
Features of chlamydia and 2 developmental stages in growth cycle?
Very small, non-motile Elementary bodies (EBs)- dormant: infectious, enter cell through endocytosis, prevents phagosome fusion Reticulate bodies (RBs)- metabolically active and fragile
Features and symptoms of chlamydia trachoma’s?
Most common STD
Can spread to uterus and ovaries–> pelvic inflammatory disease, usually asymptomatic, can cause conjunctivitis, trachoma- blindness spread via flies
Most common sites/ modes of infection caused by gram negative pathogens?
Resp tract- bordetella pertussis, haemophilus influenzae
Urinary tract- some e.coli strains, Klebsiella pneumoniae
GI tract- vibrio cholera, shigella dysentriae, some e.coli strains, campylobacter jejune, helibacter pylori
Most common modes of infection by gram negative pathogens?
Meningitis: Neisseria meningitidis, haemophilus influenzae
STIs: Klebsiella pneumoniae, chlamydia trachoma’s
Wound infections: pseudomonas aeruginosa, some e.coli strains
Features of fungal cells? What are dimorphic fungi?
Eukaryotic, chitinous cell wall
Heterotropic- gets nutrients from what they are living on
Yeast- small single celled organisms divide by budding
Moulds= from multicellular hyphae and spores
Some fungi exist as both yeasts and moulds switching between the two when conditions suit e.g. coccidioides immitis- grows as mould at ambient temp–> yeast form at body temp after inhalation
Fungi have inability to grow at what temp? Cannot evade what also? Burden of fungal disease?
37 degrees
Adaptive/ innate immune response
Enormous- most will have had at least one in lifetime e.g. nappy rash, tinea pedis and fungal asthma
Life-threatening fungal infection is rare in healthy hosts
Invasive fungal disease in immunocompromised hosts, post surgical patients and healthy hosts?
Immunocompromised= Candida line infections, pneumocystis, invasive aspergillosis
Post-surgical patients- intra-abdominal infections
Healthy hosts- fungal asthma, travel associated fungal infections e.g. dimorphic fungi
Aim of antimicrobial drug therapy? Relies on what?
Achieve inhibitory levels of agent site of infection with host cell toxicity
Identifying molecules with selective toxicity for organisms targets:
Target does not exist in humans
Target is significantly different to human analogue
Drug is concentrated in organism cell with respect to humans
Organism has an increased permeability to the compound
Human cells are rescued from toxicity by alternative metabolic pathways
Why is selective toxicity harder to be achieved for fungi as opposed to bacteria? Drugs targeting DNA/ RNA synthesis and protein synthesis?
Fungi= eukaryotic and so are human cells, thus they are more similar and harder to differentiate
Flucytosine
Fungal cell wall contains what? Drugs targeting these?
Plasma membrane contains what? Drugs targeting these?
Mannoproteins, B1,3 gluten, B1,6 gluten, chitin
Echinocandins
Ergosterol- cholesterol in humans
Amphotericin, azoles and Terbinafine
E.g. of a polyene? Polyenes cause what? What times lower affinity for cholesterol? Toxicities in humans?
Amphotericin B
Pore formation in ergosterol containing membranes i.e. its a fungicidal
x10 lower- more specific for fungi, can still cause toxicity to humans
Nephrotoxicity- dose dependent; usually reversible, distal renal tubular acidosis, can cause hyperkalaemia if infused rapidly–> cellular damage
Chills/ rigors/ hypotension and acute anaphylactoid reactions
E.g. allylamines? Causes what? Distributes extensively to where? Primarily used against what? Does result in what though?
Terbinafine
Reversible inhibition of squalene epoxidase (enzyme required for growth of fungi), its a fungicidal
Undergoes extensive first pass metabolism resulting in bioavailability of only 45%
Poorly perfused sites such as skin and nail beds
Candida and aspergillus
Well tolerated and only results in taste disturbance and deranged LFTs
CYP450 metabolism- by multiple enzymes and is minimally inhibitory
What are azaleas? E.g. and active against what x3?
Dose-dependent inhibitors of 14a-sterol demthylase- important in pathway cholesterol and ergosterol production
Clotrimazole and ketoconazole= candida
Fluconazole= cryptococcus
Itraconazole= aspergillus and dimorphic e.g. coccidiodes and sporothrix
Adverse events: all associated with? Rare to cause what? What with long term fluconazole? Itranazole symptoms?
Transaminitis and GI side effects Relatively safe Rare to cause severe hepatitis Alopecia GI symptoms more pronounced: nausea, abdominal pain and diarrhoea, rate life threatening liver failure
Fluconazole is what so does what? Less significant interactions with what?
Hydrophilic so excreted unchanged
Warfarin, calcineurin inhibitors, anxiolytics
Itraconazole is a potent what? Interactions with what? Azole resistance in what?
CYP3A4 inhibitor
Same as fluconazole, steroids, statins
Multiple mechanism in Candida, fluconazole and voriconazole most affected
Echinocandins inhibits what? What fungi generate that do not have large amounts of 1,3 B glucan in cell wall are intrinsically resistant to this drug class?
1,3B glucan synthase- interferes with fungal cell wall
Fungicidal to susceptible yeasts
Fungistatic to moulds
Crytococcus, zygomycetes, trichosporon, limited activity against Scedosporium
Echinocandins have activity against what? Has poor what and is only what? Has few what? What 3 limited drug toxicities?
Mould but not yeast forms of dimorphics
Poor oral bioavailability thus IV only
Poor penetration into CSF, eye and urine
Drug interactions
Rare type-1 hypersensitivity, hepatotoxicity, hypokalaemia
Blood cultures are half as sensitive for what? Better to pick-up from what? If what? Pretty much all what are sensitive to echinocandins? Also sensitive to what?
Fungi as for bacteria Tissue/ fluids If cultured properly, if these samples can be obtained Candida Amphotericin B
1,3 B-D glucan is cell wall component of many fungi including what? Released into serum what?
Ascomycetous pathogens and pneumocystis
Released into serum during invasive infection
Onychomycosis is what? Caused by what? Grow best at what temp? Most common cause? Most specific test?
Fungal infection of the nail Very common Dermatophyte moulds: grow best at about 30 degrees Trichophyton rubrum Microscopy- 30% culture negative
Different forms of fungal differential diagnosis? Limited treatment options?
Psoriasis, lichen planus, trauma, eczema, malignant melanoma, results of sampling can be confusing
Topical amorolfine, systemic itraconazole or terbinafine
Treatment takes ages, high failure rate with all therapies
Pneumocystis infection of healthy people is what? Disease develops only with what? Signs of this infection?
Frequent and occurs early in life
Moderate-severe immunocompromised especially in HIV, transplant and steroids
Hypoxia more severe than chest X-ray would suggest- especially with gradual onset or risk factors
Treatment of pneumocystis? Why can fungi be challenging to treat?
Co-trimoxazole, clindamycin, pentamidine, trimetrexate
Relatively few classes of agents effective against them
What is the single most effective method of preventing cross infection? What does infection require?
Hand hygiene
Harm to be done to the individual- invasion, toxin, host response
What does CPE stand for? Also known as what? Colonisers of what? Most common causes of what? In past vast majority of these were what?
Carbapenemase producing enterobacteriaceae
Coliforms- standard gut germs i.e. e.coli, Klebsiella, Serratia, enterobacter
Large bowel, skin below waist and moist sites
UTI and intra-abdominal infection
Occasional resp tract infection and skin and soft tissue infection
Susceptible to antibiotics that we use for gram negative infection
What are carbapenems? They have moved from what to what?
Broadest spectrum beta-lactam antibiotics that we have available
Being rarely used last resort antibiotics to frequently used second-line agents and even first-line therapy for patients with severe sepsis as resistance of gram negatives to other agent like cephalosporins and piperacillin-tazobactam has increased
Carbapenemases hydrolyse what? What is an endogenous infection?
Carbapenems but also other beta-lactams effectively conferring resistance to entire class of antibiotic Infection of a patient by their own flora- important in hospitalised patients, especially those with invasive devices or surgical patients
Size of viruses? Only visualised using what? What does obligate intracellular mean? They have what?
20-220nm diameter, by electron microscopy
Dependent on living cells for their replication and existence
Receptor binding protein to dock to cells and all contain genetic material
When diagnosing don’t need to come from where? Possess and don’t possess what? 3 shapes of viruses? Exist as what outside of infected cells?
Sterile sites- no commensal viruses to confuse with
One type of nucleic acid/ RNA/ DNA, no cell wall structure but outer protein coat surrounded in some viruses by lipid envelope
Helical/ icosahedral/ complex
Virions- genetic material, protein coat (capsid)
What are the 6 stages of virus replication?
Attachment, cell entry, interaction with host cells, replication, assembly, release
E.g. of attachment via viral and cell receptors? Only what of virus are freed into host cell cytoplasm? What doesn’t enter?
e.g. HIV= gp120, CD4 on T cell
Only viral ‘core’- nucleic acid and some associated proteins acting as enzymes for replication and negation of intracellular host defence factors are freed
Outer protein coat does not enter
Involved in interaction of viruses with host cells? What is produced during replication of viral material?
Virus uses cell materials for own replication, also needs to subvert host cell defences
Progeny viral nucleic acid and viral proteins in nucleus, cytoplasm or both
Where does assembly occur for herpes, polio and influenza virus? How does release of viral material occur for rhinovirus and HIV/ influenza?
Nucleus- herpes, cytoplasm- polio, cell membrane- influenza
Rhinovirus= lysis, ‘leaking’= HIV and influenza (2-3 days from upper resp tract)
5 ways in which viruses can cause disease?
Destruction of host cells e.g. polio
Modification of host cell e.g. rotavirus
Over-reactivity of immune system e.g. Hep B
Damage through cell proliferation e.g. HPV
Evasion of host defences e.g. i) cellular level e.g. herpes viridae
ii) molecular level e.g. influenza, HIV, rhinovirus
Types of polio and most severe? How does polio enter and cause disease?
3 types, type 1= most severe
Enters body orally then invades and replicates in gut then travels in bloodstream and targets brain, can destroy brain cells
Infection reaches brain in unimmunised person- difficult to deal with–> paralysis
2 forms of modification of host cell? Pathogenesis of how rotavirus causes disease by modifying host cell structure/ function?
Physical e.g. rotavirus/ HIV and functional e.g. rotavirus, RSV, HIV
1) Infects epithelial cells of small intestine- mainly jejunum
2) Atrophy of villi, flattening of cells, stripping of microvilli, decreased SA of SI
3) Limits synthesis of digestive enzymes
4) Nutrients not absorbed
5) Hyperosmotic effects–> profuse diarrhoea- need fluid replacement therapy, early treatment
Majority of HBV hep B infection is what? That and hep C spread by what? Following symptomatic HBV infection there are what? Results in what?
Asymptomatic
Blood/ sexual contact
Massive antibody and cell mediated immune (CMI) response, destroy many virally infected hepatocytes–> extensive liver damage–> jaundice
During acute hep B infection, large numbers of what are produced? If you recover (most do,) then you will be a what and what % asymptomatic?
Infectious HBV particles
Carrier and 80% will be asymptomatic
