Microbiology Flashcards
Which 3 fungi are most likely to pose a threat/be able to infect humans?
- Candida species
- Aspergillus
- Cryptococcus species
What patients are at particular risk to fungal infections?
o immunocompromised due to fungi mauinly being opportunistic pathogens
- HIV patients are more likely to suffer from cryptococcus infections due to a lack of CD4 cells -> fungal meningitis
- pneumocystis pneumonia (PCP) caused by Pneumocystis jirovecii is associated with AIDS
o high risk patients have prolonged and profound neutropenia after treatment with highly cytotoxic chemotherapy for haematological malignancies and recipients of haematopoietic stem cell transplantation (HSCT)
How are dendritic cells and fungal infections linked?
- dendritic cells have an instrumental role in linking innate and adaptive responses to a range of pathogenic fungi
- signals transmitted by dendritic cells activated by exposure to fungi vary depending on the encountered fungus and its morphotype, helping to shape the appropriate adaptive immune response
What is the predominate protective mechanism to fungal infection?
- Th1 type CD4+ T cells
What cytokine is important in the Th1 type CD4+ T cell response to fungi?
- interferon-γ
Summarise cellular immunity to fungal infection.
- opsonisation by pentraxin 3 and mannose-binding lectin
- phagocytes are a critical first line of defence -> NK cells provide early interferon-gamma
- failure of innate immunity leads to adaptive responses -> dendritic cells influence T cell differentiation (Th1 and Th17 play a role)
o INNATE IMMUNITY IS MORE IMPORTANT THAT ADAPTIVE in fungal infection rather than the adaptive immunity -> loss of neutrophils is a big risk factor for infection
Where are most fungal infections found?
o mucosal surfaces
- mould (contains multicellular filaments) = lungs -> candida and aspergillus
- yeasts (single cells) = gut -> cryptococcus -> forms a capsule to evade phagocytosis
What receptors are important in sensing fungal components?
- toll like receptors
Name some human susceptibilities to fungi.
- human dectin-1 deficiency
- human CARD9 deficiency
- TLR4 mutations/polymorphisms
- some plasminogen alleles
How does human dectin-1 deficiency increase the risk of fungal infection?
- human dectin-1 is important in the phagocytosis of candida -> HD1 is important for immunity to chronic mucocutaneous candidiasis -> very unpleasant disease that leads to massive hypertrophy of the mucosa and many problems with fungal drug resistance
- loss of function in HD1 -> Mendelian susceptibility to chronic mucocutaneous candidiasis -> patients with the homozygous mutation have a reduced inflammatory response via IL-6
How does human CARD9 deficiency increase the risk of fungal infections?
- human CARD9 deficiency causes chronic mucocutaneous candidiasis
- CARD9 is an adaptor molecule downstream of the C-type lectins
- suffers are susceptible to mucosal and invasive infection (including CNS fungal disease)
- functional CARD9 is required for TNF-alpha production in response to beta-glucan stimulation and T cell Th17 differentiation in humans -> if deficient they can’t respond to fungi
When are patients with TLR4 mutations/polymorphism particularly vunerable to fungal infection?
- stem cell transplant patients -> are at high risk of candida and aspergillosis due to reduce immune system
Which white blood cell is the most important in the defence against fungi?
- neutrophils
Describe neutrophil nets.
- neutrophils can form neutrophil nets -> are extracellular fibres mainly comprised of DNA from the neutrophils which can bind to extracellulr pathogens and prevent them from replicating -> reduces damage to host cells
- the net is sticky -> reason for sputum being sticky during chest infection
- deficiency to create these increases infection risk
What is chronic granulomatous disease?
- sufferers have a loss of gp91 function (mutation) due to a defects in the enzyme NADPH oxidase -> NADPH oxidase is important for the generation of reactive oxidative species -> their neutrophils are unable to kill ingested pathogens
- patients are susceptible to invasive fungal infections, particularly with Aspergillus species
- confirms the crucial role of neutrophils in defence against fungal infections
What treatments are available for ghronic granulomatous disease?
- gene therapy can allow some restoration of function of the gp91 (FOX91)
What do many fungal spores cause?
- allergic disease -> rhinitis, dermatitis, asthma and ABPA
- spores can easily disperse and enter teh lungs hence the reasoning for them causing lung problems
What is ABPA?
- allergic broncho-pulmonary aspergillosis
- is a condition associated with asthma
- involves an allergy to aspergillus and destruction of the airways -> bronchiectasis -> airway gets wider -> more prone to infections
What is the criteria for ABPA?
o patient has a predisposing condition -> asthma or cystic fibrosis
o obligatory criteria -> total baseline serum IgE > 1000 IU/ml and a positive immediate hypersensitivity skin test or Aspergillus-specific IgE
o 2 or more of the supportive criteria:
- eosinophilia > 500 cells/ul
- serum precipitating or IgG antibodies to aspergillus fumigatus
- consistent radiographic abnormalities -> dilated bronchi with thick walls, ring or linear opacities, upper or central region predilection, proximal bronchiectasis, lobar collapse due to mucous impaction, fibrotic scarring
How is ABPA managed?
- corticosteroids and itraconazole for steroid sparing effect
What is hypersensitivity pneumonitis?
- an allergic response requiring long-term allergen exposure (as a consequence, often occupational)
- cell-mediated delayed sensitivity reaction and allergen-specific precipitins usually present
What is the role of the IRF-7 gene?
o a key player in the interferon induction pathway
- can inherit two copies of a faulty IRF-7 gene -> gene product doesn’t work very well -> people therefore cannot produce interferon alpha in response to infection
What is the role of IFNAR2 gene?
o an interferon alpha receptor
- if you inherit 2 recessive defective/mutated IFNAR2 genes -> often due to deletion out of frame leading to a premature stop codon
- can’t respond to interferons produced in an infection
What should not be given to patients with autonomal recessive IFNAR2 gene mutated patients?
- live attenuated vaccines -> virus can manifest in the body and can kill these patients
What is the role of the IRF-3 gene?
- part of the interferon signalling pathway
- patients suffering from heterozygous mutations in this gene don’t respond well to viruses as they cannot produce interferon responses
What are interferons?
- a soluble protein factor that binds to receptors adn signals the activation of de novo transcritption of 100s of interferon stimulated genes (ISGs) that produce an anti-vrial state in cells -> cells can’t be infected by a virus
Why are interferons not used as a anti-viral, especially for illness such as the common cold?
- have many side effects -> all the aches, pain and fever that you have when ill with a virus
- taking interferons for most viral infections would make you feel more ill than you originally did
What are the 3 major functions of type I interferons?
- induce an anti-microbial state in both the infected and neighbouring cells
- modulate the innate response to promote Ag presentation and NK but inhibit pro-inflammation
- activate the adaptive immune response
What cell types produce type I interferons and what are their consequences?
- IFN-alpha = plasmacytoid dendritic cells -> recruits APCs and adaptive immune cells
- IFN-beta = all cells -> diffuse and interacts with neighbouring cells -> leads to switching on of ISGs in those cells too
Describe type II IFN.
- type II IFN is IFN-gamma which is a highly specialised immune signalling molecule produced by immune cells activated by T and NK cells
- signals through the IFN-gamma receptor
Describe type III IFN.
- type III INF is IFN-lambda
- thought to protect barriers of your body from viral infection -> present mainly on epithelial surfaces as a consequence -> especially found on the respiratory tract and liver
- signal through IL28 and IL10-beta receptors
How do we differentiate between self and non-self in the case of viruses?
- a virus cannot hide its nuclei acid
o PAMPS (pathogen associated molecular patterns) are unique to pathogens -> often foreign nucleic acid
o PAMPS are recognised by PRPs (pattern recognition receptors)
- PRPS can be RLRs (cytoplasmic RIG-I like receptors) or TLRs (endosomal Toll like receptors)
o cytoplasmic nucleotide oligomerisation domain receptors (NLRs) also exist
Describe interferon induction.
- PRRs (e.g. RIG-I like receptors) detect PAMPs such as single stranded RNA in the cytoplasm of the cell
- RIG-I will then signal through Mavs (located on the mitochondrion)
- this triggers signalling through various different pathways that result in the translocation of molecules from the cytoplasm to the nucleus
- transcription factors will become phosphorylated, they will bind to the promoter regions of target genes (in this case IFN beta). It will generate IFN beta transcripts
- IFN beta is then released from these cells and travels to neighbouring cells to induce an anti-viral state -> way we/the host controls the amount of virus in the body
How do TLRs and cytoplasmic sensors detect viral infection?
- TLRs can sense the nucleic acids in the endosome and it will signal to a molecule outside the endosome (MyD88) -> sends various transcription factors to the nucleus of the cell -> results in the switching on of expression of IFN-alpha
How are DNA viruses detected?
- in a normal, healthy cell, ALL the DNA should be in the nucleus
- DNa in the cytoplasma is detected by cGAS (an enzyme) whichs binds the DNA, and synthesises another small molecule (cGAMP), which binds to a STING molecule
- STING uses the same pathway as IRF-3 -> moves into the nucleus to transcribe some new IFN molecules
How do IFN contain viruses to a small area?
- IFN binds to the IFN receptor on neighbouring cell (present on every cell in the body) -> this activates the Jak and Tyk pathway
- then goes on to phosphorylate the STAT molecules -> STAT molecules dimerise and combine with IRF9 -> then goes to the nucleus and binds to a promoter region that is responsive to that TF -> cell becomes a very hostile place for a virus so it can’t move
Name some interferon stimulated genes.
- PKR Protein Kinase R -> inhibits translation
- 2’5’OAS -> activates RNAse L that destroys single stranded RNA including mRNA
- Mx -> inhibits incoming viral genomes -> wraps around viruses to prevent cell entry
- ADAR -> induces errors during viral replication (attacks the virus as it’s replicating)
- IFITM3 -> restricts virus entry through endosomes
- serpine -> activates proteases which digest viral proteins
- viperin -> inhibits viral budding
WHat viruses are prevented from replicating by Mx genes?
- Mx1 = influenza, rabdoviruses -> traps the viral DNA as they release their nucleic acid
- Mx2 = HIV -> upregulation of Mx2 prevents HIV from injecting its RNA genome into cell nucleus
How long do an anti-viral state triggered by interferons last in cells?
- IFN response may only be maintained for several hours (maybe a day) -> subsequently the ability to response to IFN is lost due to negative regulation
- negative feedback controls to turn off the IFN response as well as SOCS (suppressor of cytokine signalling) genes that turn off the response
How have viruses evolved to evade IFN responses?
- avoid detection by hiding the PAMP -> some create a membrane which they replicate within
- interfere globally with host cell gene expression and/or protein synthesis
- block IFN induction cascades by destroying or binding
- inhibit IFN signalling
- block the action of individual IFN induced antiviral enzymes
- activate SOCS
- replication strategy that is insensitive to IFN
How does hepatitis C virus prevent IFN control?
- produces NS3/4 protease which acts as an antagonist to interferon induction by cleaving MAVS
How does influenza virus prevent IFN control?
- produces NS1 protein which acts as antagonist to interferon induction by binding to RIG-I /TRIM25/RNA complex and preventing activation of signalling pathway and also prevents nuclear processing of newly induced genes
How do Pox viruses prevent IFN signals?
- pox viruses (and herpes) viruses are large DNA viruses -> over half the pox virus genome is comprised of accessory genes that modify immune response
- pox viruses encode soluble cytokine receptors (vaccinia virus B18), which mop up IFN -> IFN cannot interact with receptor
What is the potential clinical use for viruse endoced soluble cytokine receptors such as vaccinia virus B18?
- being developed as possible immune therapies for autoimmune and inflammatory conditions in which IFN and other cytokines are produced in abundance and contribute to the pathology of the condition
- e.g. rheumatoid arthritis
How does ebola virus evade the immune mechanisms?
- RIG-I and Mda-5 sense the ebola virus
- VP35 is a protein produced by ebola that BLOCKS the signalling cascade
- VP24 is another protein produced by ebola that blocks the signal from the IFN receptor into the nucleus -> no ISGs can be transcribed
How can viruses produce cytokine storms?
- virus replicates and induces high levels of IFN accompanied by massive release of TNF alpha and other cytokines -> differences in outcome may reflect vigour of the innate immune system, which varies with age
- typical of dengue haemorrhagic fever, severe influenza infections and ebola
What are the consequences of cytokine storms?
- cytokine storm will lead to pulmonary fibrosis, which is caused by the accumulation of immune cells in the lung spaces
- eventually the patient will succumb to the immune pathology rather than from damage from the virus
- young, healthy people infected by these viruses have a worse prognosis because they have vigorous immune system which will produce a strong response
What kind of viruses could be used as a new generation of live attenuated vaccines?
- viruses deficient in control of IFN are attenuated in IFN competent cells -> means that they induce high levels of interferon when they enter these cells
- high IFN levels they induce can also recruit useful immune cells, IFN acting as an ‘adjuvant’ -> IFN levels strongly switch on the antiviral response
How could viruses be used as a cancer treatment?
- cancer cells don’t make a very good IFN response could lead us to the generation of rationally designed oncolytic viruses
- giving a cancer patients a virus defective to fight the IFN response throughout the body -> therefore only replicates in and kills the cancer cells. and all the healthy cells in a person’s body (have a perfectly good IFN) will not be killed
Name some common virulence factors associated with bacterial infections.
- diverse secretion systems -> allows them to get proteins from the cytoplasm of the cells into host cells
- flagella
- pili -> important adherence factors
- capsule -> protects against phagocytosis -> i.e. Streptococcus pneumoniae
- endospores -> metabolically dormant forms of bacteria -> I.e. Bacillus sp. and Clostridium sp.
- biofilms -> organized aggregates of bacteria embedded in polysaccharide matrix which can lead to antibiotic resistant -> i.e. Pseudomonas aeruginosa and Staphylococcus epidermidis
- exotoxins and endotoxins
Describe the different types of exotoxins.
- neurotoxins -> act on nerves or motor endplate -> i.e. Tetanus or Botulinum toxins
- enterotoxins -> act on the GI tract -> infectious diarrhea i.e. Vibrio cholera, Escherichia coli, Shigella dysenteriae and Campylobacter or food poisoning i.e. Bacillus cereus or Staphylcoccus aureus
- pyrogenic exotoxins -> stimulate release of cytokines -> i.e. Staphylcoccus aureus or Streptococcus pyogenes
- tissue invasive exotoxin -> allow bacteria to destroy and tunnel through tissue ->
i. e. Staphylococcus aureus, Streptococcus pyogenes, Clostridium perfringens - miscellaneous exotoxin -> specific to a certain bacterium and/or function not well understood -> i.e. Bacillus anthracis and Corynebacterium diphtheriae
Describe endotoxins.
- endotoxins are only produced by gram-negative bacteria
- are a lipid A moiety of the lipopolysaccharide layer -> are shed in steady amounts from living bacteria
- due to endotoxins treating a patient who has a gram-negative infection with antibiotics can sometimes worsen condition because when bacteria lyse they release large quantities of LPS/endotoxin -> septic shock
Define outbreak.
- a greater-than-normal or greater-than-expected number of individuals infected or diagnosed with a particular infection in a given period of time, or a particular place, or both
How can outbreaks be identified?
- surveillance -> provides an opportunity to identify outbreaks
- good and timely reporting systems are instrumental in idenitifcation
What is haemoltyic-uremic syndrome?
- characterised by a triad of acute renal failure, hemolytic anemia and thrombocytopenia
- usually found in children -> very rare in adults
- caused by the Shiga toxin producing E. coli strain O157:H7
- reservoir are normally ruminants – mostly cattle
- human infection occurs through the inadvertent ingestion of fecal matter and secondary through contact with infected humans
How does Shiga/vero toxin function?
- StxA (a subunit found in SHiga toxin family members) is an enzyme that cleaves the 28S ribosomal RNA in eukaryotic cells -> inhibition of protein synthesis -> decreased proliferation of susceptible bacteria -> can affect commensal gut microflora
- Shiga toxin does not only block protein synthesis in eukaryotic cells but also affects several other cellular processes
Can Shiga toxins move from bacteria to bacteria?
o yes
- Shiga toxins are encoded on a bacteriophage -> can be transferred from one strain to another via a phage
- phage particles enter the environment, and infect a closely related strain to produce the toxin
- highly mobile genetic elements and contributes to horizontal gene transfer
- toxins are highly expressed when the lytic cycle of the phage is activated
Where can E. coli strains colonize?
- EHEC = large bowel
- EAEC = both small and large bowel
What are the 6 categories of communicable disease in Europe?
- respiratory tract infections
- sexually transmitted infections, blood-borne viruses
- food and waterborne diseases and zoonoses
- emerging and vector-borne diseases
- vaccine-preventable diseases
- anti-microbial resistance and healthcare-associated infections
What respiratory tract infections must be reported in Europe?
- influenza - viral
- animal influenzas -> including avian and swine - viral
- SARS (severe acute respiratory syndrome) - viral
- Legionnaires’ disease -> Legionella pneumophila - gram -ve bacteria
- tuberculosis -> Mycobacterium tuberculosis - gram +ve bacteria
Where is Leigonella pneumophila found?
- gram negative bacterium is found in amoeba in ponds, lakes and air conditioning units
What is Leigonella pneumophila route of infection to humans?
- inhalation of contaminated aerosols -> will infect and grow in alveolar macrophages
- human infection is “dead end” for the bacteria/bacteria can’t survive here on
Describe the importanr virullent factor of Legionella pneumophila.
o type IV secretion system
- allows L. pneumophila to infect and replicate in human macrophages by allowing the bacterium to secrete from inside to the outside
- macrophages take up these bacteria in humans and are able to replicate in macrophage vacuoles, because it can release special virulence factors (due to the type IV secretion system)
Describe mycobacterium tuberculosis.
- grouped as a gram-positive bacteria, but it has a very different cell wall -> has an extra lipid layer which makes treatment more difficult as drugs cannot access the bacteria
- is treated with antibiotics, but this takes AT LEAST 6 months and success rate of treatment for second infection is lower
- M. tuberculosis can enter a dormant state -> latent TB = evidence of infection by immunological tests but no clinical signs/symptoms of active disease
What sexually transmitted diseases must be reported in Europe if there is an outbreak?
- Chlamydia trachomatis infection - gram -ve
- gonorrhoea -> Neisseria gonorrhoeae - gram -ve
- syphilis -> Treponema pallidum - gram -ve
- Hepatitis B and C - viral
- HIV/AIDS - viral
Describe Chlamydia trachomatis.
- obligate intracellular pathogen -> cannot culture it outside host cell
- most frequent STI in Europe with around 350.000 cases/year (infection likely higher due to underreporting)
- can cause eye infections -> 84 million people infected and 8 million visually impaired -> responsible for more than 3% of the world’s blindness
How does Neisseria gonorrhoeae establish infection?
- establishes infection in the urogenital tract by interacting with non-ciliated epithelial cells
- important virulence factors and traits are pilli and antigenic variation as well as being able to escape detection and clearance by the immune system
Name the 3 most common food and waterborne bacterial disease in Europe and the most common globally.
o campylobacteriosis -> Campylobacter sp., mostly C. Jejunio
o salmonellosis -> Salmonella sp.
o cholera -> Vibrio cholerae
- listeriosis -> Listeria monocytogenes
Describe campylobacter sp..
- most commonly reported infectious GI disease in the EU -> you have to consume the live organism -> infection is most likely through undercooked poultry
- usually sporadic cases and not outbreaks
- small children of 0-4 years are the highest risk group
- virulence factor -> adhesion and invasion factors, flagella motility, type IV secretion system and toxins
Describe salmonella sp..
- one of the most common GI infections in the EU -> mainly due to undercooked poultry
- otbreaks are seen
- highest infection rate in small children (0-4 years)
What is the virulence of salmonella sp.?
o type III secretion systems encoded on pathogenicity islands (SPI)
o salmonella enterica has type III secretion system
- SPI1 -> required for invasion
- SPI2 -> intracellular accumulation
Describe vibrio cholerae.
- cholera is an acute, severe diarrheal disease -> without prompt rehydration, death can occur within hours of the onset of symptoms
- last outbreak was in Haiti, and has caused many deaths
What are the important virulence factors of vibrio cholerae?
- type IV fimbria
- cholera toxin carried on a phages -> makes eukaryotic cells produce high levels of cyclic AMP (cAMP) -> activates a transporter, resulting in chloride ions EFFLUX from the cell -> water and sodium leaves the cell -> DIARRHOEA -> people die from the dehydration
Describe Listeria monocytogenes.
- risk groups are the immunocompromised, elderly, pregnant women and their foetus
- listeria can enter non-phagocytic cells and cross three tight barriers due to its motility -> intestinal barrier, BBB and materno/foetal barrier
State some of the emerging and vector-borne diseases whihc must be reported in Europe.
- malaria - parasite
- plague -> Yersinia pestis - gram negative -> not a problem anymore really
- SARS - viral
- yellow fever - viral
- Q fever -> Coxiella burnetti - gram negative
What vaccine prevntable diseases outbreaks must be reported in Europe?
- diphtheria -> Clostridium diphtheria- gram positive
- invasive Haemophilus influenzae disease - gram negative
- invasive meningococcal disease -> Neisseria meningitidis - gram negative
- invasive pneumococcal disease (IPD) -> Streptococcus pneumoniae - gram positive
- pertussis -> Bordetella pertussis - gram negative
- Measles, Mumps and Rubella - viral
- polio - viral
- rabies - viral
- tetanus -> Clostridium tetani - gram positive
What bacteria are the major causes of hospital/healthcare acquired infections?
o Enterococcus faecium -> vancomycin resistance
o Staphylococcus aureus -> methicillin resistant (MRSA)
o Clostridium difficile -> can establish infection due to previous antibiotic treatment
o Acinetobacter baumanii -> highly drug resistant
o Pseudomonas aeruginosa -> multi drug resistant
o Enterobacteriaceae -> pathogenic E. coli (multi drug resistant), Klebsiella pneumoniae (multi drug resistant), Enterobacter species (multi drug resistant) etc
Describe pathogenic E. coli.
- most frequent cause of bacteraemia by a gram-negative bacterium
- most frequent cause of community and hospital acquired UTI
- increase in multi-drug resistant strains -> resistance to 3rd generation cephalosporsins as high as 20% in some countries and most isolates that are resistance to cephalosporin express the extended spectrum beta lactamase
- still sensitive to carbapenems
Describe cephalosporins.
- class of beta-lactam antibiotics -> e.g. penicillin
- target pathway = inhibition of peptidoglycan synthesis
- target protein = inhibit the activity of penicillin binding proteins (PBPs)
- resistance to cephalosporins arises from extended spectrum beta lactamases encoded on a plasmid -> cleave the cephalosporin antibiotic
Describe carbapenems.
- class of beta-lactam antibiotics
- target pathway = inhibit peptidoglycan synthesis
- target protein = inhibit the activity of penicillin binding proteins (PBPs)
- resistance to carbapenems arisse from the carbapenemase enzyme, blakpc encoded on a transposon -> enzyme cleaves the carbapenem antibiotic
Describe Klebsiella pneumoniae.
- important cause of UTI and respiratory tract infections
- risk group are immunocompromised patients
- high proportion of resistance to 3rd generation cephalosporins, fluroquinolones and aminoglycosides -> carbapenem-resistant Klebsiella pneumoniae (CRKP) is the species of CRE most commonly encountered in the US
Describe Pseudomonas aeruginosa.
- important cause of infection in immunocompromised patients
- high proportions of strains are resistant to several antimicrobials -> in ½ of EU countries resistance to carbapenems is above 10%
Describe MRSA.
- most important cause of antimicrobial resistance infection worldwide
- methicillin is a beta-lactam antibiotic -> target pathway is inhibition of peptidoglycan synthesis by inhibitingthe activity of penicillin binding proteins
- resistance mechanim = expression of additional penicillin binding protein -> PBP2A has low affinity for methicillin and can still function in the presence of the antibiotic
Describe Enterococcus faecium.
- third most frequently identified cause of nosocomial blood stream infections (BSI) identified in the US
- vancomycin resistance is around 60%
- resistance arises from multiple proteins (genes encoded on plasmid or transposon) resulting in the synthesis of a different PG precursor
Name three factors, which contribute the acquisition of hospital acquired infections.
- intervention -> catheter etc
- dissemination
- concentration
True or False. Cephalosporsin is a beta-lactam antibiotic and resistance is due to production of an extended spectrum beta lactamase.
- True
True or False. Methicillin and carbapenem are both beta-lactam antibiotics.
- True
True or False. Carbapenem resistence is frequently found in Klebsiella pneumoniae.
- True
Describe staphulococcus aureus.
- Staphylococcus aureus is a gram positive bacterium
- produces toxins including exfoliative toxin, toxic shock toxin, and enterotoxins
- is a commensal bacteria -> 30% of the population carry it, either in the nostrils or on the skin
- can causes skin, bone, joints and lung infections as well as sepsis
- some strains are resistant to standard antibiotics -> MRSA
What is the virulence factor of staphylococcus aureus?
- panton valentine leuocidin toxin -> produces a much more necrotising infection
What toxins are produced by staphylococcus aureus?
- panton valentine leuocidin toxin -> virulence factor -> Produces a much more necrotising infection
- exfoliative toxin -> causes cleavage of the epidermis -> blistering
TSST-1 toxin -> causes sickness, fever, malaise etc. -> organ failure -> 50% of infections with staphylococcus aureus that produce TSST-1 toxin are related to tampons
- enterotoxin -> a problem in food consumption
What are infections of the skin called?
o depends on the layer that they affect
- impetigo = infection of the top layer of the skin - stratum corneum
- ecthyma = full thickness involvement of the epidermis
- folliculitis = infection and inflammation of a hair follicle - can progress into a n abscess (then called a boli) -> carbuncle describes multiple abscesses next to each other
What are the common sites of burrows in scabies?
