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Y2 MCD - Haem, Labs, Microbio, Cancer, Immunology > MICROBIOLOGY; Lecture 1, 2, 3, 4, 5 - Interferon, Skin infections, Viral evasion of host immunity, Community acquired bacterial infections, Hospital acquired bacterial infections > Flashcards

MICROBIOLOGY; Lecture 1, 2, 3, 4, 5 - Interferon, Skin infections, Viral evasion of host immunity, Community acquired bacterial infections, Hospital acquired bacterial infections Flashcards

1
Q

Microbio

What is Herpes Simplex encephalitis?

A

Most common cause of sporadic encephalitis in western world, commonly in childhood, affecting previously healthy individuals on primary infection with HSV-1

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2
Q

Microbio

Who can catch HSV-1 and why?

A

Due to the mutation in genes it can impair the interferon response, so can cause problems such as the encephalitis

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3
Q

Microbio

What are interferons?

A

Protein which is made by every cell in body -> transferable factor produced when cells are exposed to virus It binds to specific receptors and signals the activation of de novo transcription of hundreds of interferon stimulated genes (ISG) - these put the cells into an anti-viral state

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4
Q

Microbio

What are type 1 interferons and their 3 major functions?

A

Polypeptides secreted from infected cells -> Induce antimicrobial state in infected and neighbouring cells. Modulate innate response to promote antigen presentation and NK cells but inhibit proinflammation. Activate the adaptive immune response

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5
Q

Microbio

Summarise what is occurring in this picture.

A
  • Cells will sense a viral infection and make an interferon response that will result in the synthesis of new copies of IFN-beta (the first interferon to be made)
  • The IFN beta is secreted from these cells, from where it can diffuse and interact with receptors on neighbouring cells
  • This will lead to the switching on of genes in neighbouring cells to switch them into an anti-viral state
  • Plasmacytoid dendritic cells (PDCs) are specialised cells that are very good at making interferon (in particular IFN-alpha)
  • The secretion of type I interferon will recruit APCs and adaptive immune cells such that you amount an adaptive immune response.
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6
Q

Microbio

What are the 3 types of INF?

A

Polymorphisms in IFNL associated with improved outcome from HCV and HBV both spontaneous clearance and response to antiviral therapy

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7
Q

Microbio

How do we differentiate self from non self?

A

x

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8
Q

Microbio

How do the different pathogen sensors work?

A

TLRs are membrane proteins - they are found on the plasma membrane and on endosomal membranes

RLRs sense viruses in the cytoplasm and they signal through a mitochondrial located pathway

Out of the DNA sensors, the most famous is cGAS - this signals to a molecule called STING found on the endoplasmic reticulum

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9
Q

Microbio

How are INF induced?

A
  • The PRRs (e.g. RIG-I like receptors) will detect PAMPs such as single stranded RNA in the cytoplasm of the cell
  • RIG-I will then signal through Mavs (located on the mitochondrion), which will then trigger signalling through various different pathways that result in the translocation of molecules from the cytoplasm to the nucleus
  • These transcription factors will become phosphorylated, they will bind to the promoter regions of target genes (in this case IFN beta) and it will generate IFN beta transcripts
  • The IFN beta will then be released from these cells and it will travel to neighbouring cells to induce an anti-viral state
  • This is a way of the host controlling the amount of virus in the body
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10
Q

Microbio

What is the function of the toll-like receptors?

A
  • The virus enters the cells and at some point in their life cycle they will find themselves inside an endosome and their nucleic acids will be exposed inside the endosome
  • In a normal healthy cell, there shouldn’t be any nucleic acids inside the endosomes
  • The TLRs can sense the nucleic acids in the endosome and it will signal to a molecule outside the endosome (MyD88) that will then send various transcription factors to the nucleus of the cell
  • It will result in the switching on of expression of IFNa
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11
Q

Microbio

What is the cGAS system?

A
  • Carries out DNA sensing -> dsDNA in cytoplasm activates cGAS enzyme
  • which synthesises a second messenger cGAMP (small dinucleotide),
  • which through STING (found on ER) triggers phosphorylation of same sets of signalling molecules and TF that RNA viruses were triggering
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12
Q

Microbio

How does IFN type I signalling work?

A
  • The IFN receptors are heterodimers of IFNAR1 and IFNAR2
  • On binding to the cell surface receptor, the interferon signals to the nucleus to switch on the transcription of a whole set of interferon stimulated signals..
  • There is a heterodimeric receptor - composed of IFNAR1 and IFNAR2
  • This IFN receptor is present on the surface of ALL cells in the body
  • It is capable of sensing IFNa and IFNb
  • If the IFN binds to the IFN receptor, it will activate Jak and Tyk which then goes on to phosphorylate the STAT molecules (STAT1 and STAT2)
  • The STAT molecules dimerise and combine with IRF9 - it then goes to the nucleus and binds to a promoter region that is responsive to that transcription factor.
  • IFN induces transcription of >300 via the tetradimer of STAT
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13
Q

Microbio

What are some of the genes that IFN stimulates to become activated?

A

x

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14
Q

Microbio

What is the function of IFITM3?

A
  • IFITM3 = interferon induced transmembrane protein 3
  • These proteins sit on the membrane of endosomes, in cells that have been previously stimulated with interferon
  • If a flu virus or dengue virus tries to enter cells it will normally pass through the endosomal pathway and fuse its membrane with the endosomal membrane and release its contents into the cytoplasm
  • If IFITM3 is being expressed then the virus cannot do that
  • The virus gets trapped in the endosome because the IFITM3 modifies the membrane of the endosome and prevents the virus from being able to fuse with the endosomal membrane and release its genome into the cell Mice and people lacking IFITM3 get more severe influenza
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15
Q

Microbio

What are Mx1/2?

A

GTPase with a homology to dynamin Mx can form multimers that wrap around the nucleocapsids of incoming viruses Mx1 = inhibits influenza Mx2 = inhibits HIV

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16
Q

Microbio

How long does the antiviral state last?

A

IFN response may only be maintained for several hours Subsequently the ability to respond to IFN is lost due to negative regulation SOCS genes suppress the cytokine signalling and turn off the response - if SOCS genes are switched on, even if the IFN is bound to the receptor the signals wont get through and no new PKR will be made

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17
Q

Microbio

How do viruses evade IFN response?

A

x

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18
Q

Microbio

Give 2 examples of viruses which control IFN production

A

x

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19
Q

Microbio

How do pox viruses evade IFN?

A

Pox and herpes viruses are large DNA viruses; More than half of the pox virus genome is comprised of accessory genes that modify the immune response Pox viruses encode soluble cytokine receptors (vaccinia virus B18) which mops up IFN and prevents it from ever reaching its receptor This could be useful because in some autoimmune and inflammatory conditions, IFN and other cytokines are produced in abundance and contribute to the pathology of the condition So these naturally evolved virus modifiers are thought of as potential therapies for things like autoimmunity

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20
Q

Microbio

How does Ebola evade the immune system?

A
  • Ebola is very good at counteracting our immune response
  • It encodes TWO proteins that are particularly important:
    • VP35 - inhibits the RIG-I pathway
    • VP24 - stops the signal from getting through from the IFN beta receptor to the nucleus (it stops the STAT1 molecules from getting to the nucleus)
  • The production of these virus proteins means that the virus can continue to replicate unchecked and accumulate to incredibly high titres because the patient is unable to amount a proper immune response
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21
Q

Microbio

How is the viral load and outcome of the infection decided?

A

A combination of damage of infected cells by the virus and damage of infected and bystander cells by the immune response The host senses the presence of the virus and switches on sets of genes to try and stop the virus At the same time the virus coevolves with the host to have a set of its own genes, which counteract what the host is trying to do

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22
Q

Microbio

What can IFN increase cause?

A

Many viruses modulate the immune response, presumably to increase their own replication and transmission This can result in inadvertent pathology The effect of interferon can vary from protective to immunopathologic (e.g. if you start making too much of it) This may depend on how much interferon is made - 100 times more IFN is required for IL-6 induction than for Mx

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23
Q

Microbio

What is the cytokine storm?

A
  • The virus replicates and induces high levels of IFN accompanied by massive release of TNF alpha and other cytokines
  • The differences in clinical outcome may reflect vigour of the innate immune system, which may vary with age
  • This is typical of dengue haemorrhagic fever, severe influenza infections and ebola
  • So in other words, there is a lot of virus and a lot of cytokines (which is very damaging)
  • The 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 direct damage from the virus
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24
Q

Microbio

How are attenuated vaccines formed?

A

Viruses deficient in the control of IFN are attenuated in IFN competent cells This will mean that they induce high levels of interferon when they enter these cells and strongly switch on the antiviral response This is what you would like in a vaccine - a live virus that can be injected into the host and wont replicate enough to cause disease but will replicate sufficiently such that other parts of the immune system (e.g. aquired immune response) can recognise it as being foreign and mount an immune response that can generate immunological memory There is a downside to engineering the virus so that it can’t control the host’s interferon system - it is no longer a fit virus so it’ll be difficult to propagate the virus sufficiently to produce enough virus for loads of vaccines As the virus has been debilitated in its ability to control the IFN response, it will NOT grow very well in healthy cells Solution - culture cells are genetically engineered to be deficient in the IFN response This means that the deficient virus can replicate in the deficient cells

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25
Q

Microbio

Which antiviral treatments are used in the clinic?

A

It was originally thought that interferon could become the first broad spectrum antiviral but then it was found to have several unpleasant side effects It stimulated the production of several cytokines (e.g. TNF-alpha and IL-6) which make patients feel pretty awful Interferon was used to treat Hepatitic C Virus - a combination of pegylated IFN was often used with ribavirin

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26
Q

Microbio

Can IFN lambda be used as an influenza therapeutic option?

A
  • Type 3 inteferons (IFN-lambda) is the type that is active on receptors present on EPITHELIAL SURFACES e.g. respiratory epithelium and liver cells
  • Good thing about type 3 interferon - it CANNOT signal through receptors present on immune cells
  • Type 1 interferon (IFN alpha or beta) can signal immune cells and induce some form of immunopathology - makes the patient feel sick
  • If you give IFN-lambda, on the other hand, this only signals epithelial cells so you can induce an antiviral state in these target cells (epithelial cells) without the knock on side-effects of immunopathology and inflammation
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27
Q

Microbio

How do oncolytic viruses take advantage of the IFN deficient state of cancer cells?

A

Engineer a virus that can replicate uniquely within cancer cells and kill them -> generally cancer cells can’t mount a proper IFN response, so virus that is unable to overcome IFN response can replicate in cancer cells, but not in surrounding cells because healthy cells mount powerful innate response against virus

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28
Q

Microbio

What is the epidemiology of skin disease, skin infections?

A

In hot humid countries, you have more skin infections, but in UK and non hot and humid countries it is mainly skin diseases

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29
Q

Microbio

What are the types of skin diseases in GP vs in hospitals?

A

x

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30
Q

Microbio

What is Staph aureus and what diseases can it cause?

A

x

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31
Q

Microbio

What are the different manifestations of Staph aureus in skin infections?

A

x

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32
Q

Microbio

What is impetigo?

A

Crusted surface -> staph aureus forms a gold colour, which can be seen; usually occurs around the nose/mouth; but can occur around the ear and on the scalp (doesn’t infect children below 5 usually on scalp)

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33
Q

Microbio

What is bullous impetigo?

A

Cleavage of corneocyte layer, forming a layer of pus

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34
Q

Microbio

What are viruses and how do they live?

A

Viruses are intracellular pathogens and so their proteins are easy targets for processing and presentation by MHC.

Cellular immunity clears viral infection but is short lived. Internal viral proteins can be targets of cellular immunity.

They tend to vary less than surface antigens.

Viruses that persist must evade cellular immunity.

The family of herpes viruses are the classic examples.

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35
Q

Microbio

How does the cell regulate viral Ag presentation?

A
  • Foreign peptides inside the cell (e.g. viral peptides) will be chopped up into smaller peptides inside the proteasome
  • They then get fed in through the TAP protein into the endoplasmic reticulum where it gets loaded onto an MHC class I molecule
  • This loaded MHC then moves to the cell membrane where the viral peptide can be recognised by T cell receptors on the surface of cytotoxic T cells
  • The T cell can then kill the virus infected cell
  • Viruses that persist must be able to suppress this system
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36
Q

Microbio

How does the evasion of antigen loading to TAP mechanism in viruses work?

A

Proteosome chops up the viral peptides and loads them into the ER through TAP.

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37
Q

Microbio

How does the modulation of tapasin function and prevention of MHC transport affect virus evasion?

A

Kaposi’s sarcoma

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38
Q

Microbio

How do viruses avoid NK killing using the missing self mechanism?

A

Explains why Herpes can stay for years and years in the body

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39
Q

Microbio

How can we use the knowledge about how viruses manipulate infected cells to improve medical outcomes?

A

x

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40
Q

Microbio

What is influenza antigenic drift?

A
  • Continued rapid evolution driven by antigenic pressure from host;
  • e.g. HIV quasispecies;
  • rhinovirus causes common cold;
  • has more than 120 antigenically distinct serotypes that cocirculate
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41
Q

Microbio

What is influenza antigenic shift?

A

Introduction of new subtypes from animal source

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42
Q

Microbio

How does antigenic variation affect the virus?

A

Means viruses exist as diffrent genetically stable serotypes that cocirculate in humans -> polio 3 serotypes (trivalent vaccine), dengue 4 serotypes, rhinovirus 100s of serotypes; all due to consequence of vaccination; driven by evolutionary pressure

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43
Q

Microbio

What is the influenza vaccine?

A

New one every year, with usually 65% efficacy, but if wrongly predicted then could seriously reduce efficacy, in 2015/16 it was 27%

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44
Q

Microbio

How does HIV resist neutralising Ab?

A

BNab controls viral load but escape mutants do appear

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45
Q

Microbio

What is the antigenic variation of human rhinovirus?

A

x

46
Q

Microbio

What is the poliovirus vaccine?

A

Three serotypes of poliovirus required a trivalent poliovirus vaccine. For the live attenuated Sabin vaccine, administration of all 3 at once resulted in virus interference and poor response to one component. One serotype has been eradicated from the world..

47
Q

Microbio

What is the consequence of antigenic variation of Dengue virus?

A

x

48
Q

Microbio

How does Ab dependent enhancement of Dengue work?

A

x

49
Q

Microbio

How does ebola evade the Ab response and what is the role of sGP?

A

Soluble GP is the default coding for the GP gene.

Full length GP is made by polymerase stuttering.

sGP is an antibody decoy sGP is immunosuppressive, inhibits neutrophils.

Reston virus version only suppressive in macaques.

50
Q

Microbio

What is the virus cycle and immune evasion mechanisms of Ebola?

A

x

51
Q

Microbio

How does measles infection affect immune response in childhood?

A

x

52
Q

Microbio

What are the components of the bacterial cell wall?

A

x

53
Q

Microbio

What are common virulence factors?

A

Exotoxins and endotoxins also exist

54
Q

Microbio

What are the types of exotoxins?

A
  • Neurotoxins are exotoxins that act on the nerves or motor endplates to cause paralysis – Tetanus toxin and botulinum toxin are examples
  • Enterotoxins act on the GI tract to cause Diarrhea – Enterotoxins inhibit NaCl resorption, activate NaCl secretion or kill intestinal epithelial cells – commune end result is the osmotic pull of fluid into the intestine, which causes diarrhea
    • Infectious diarrhea: Baceria colonize and bind to the GI tract, continuously releasing their enterotoxin locally.
    • The diarrhea will continue until the bacteria are destroyed by the immune system or antibiotics (or the patient dies secondary to dehydration)
    • Examples are Vibrio cholera, Escherichia coli Campylobacter jejuni and Shigella dysenteriae
  • Food poisoning - bacteria grow in food and release enterotoxin into the food. The enterotoxin is ingested resulting in diarrhea and vomiting for less than 24 hours and examples are Staphylococcus aureus and Bacillus cereus.
  • Pyrogenic exotoxins stimulate the release of cytokines and can cause rash, fever and toxic shock syndrome
55
Q

Microbio

What are the common endotoxins?

A
  • Septic shock: Sepsis that results in dangerous drops in blood pressure and organ dysfunction is called septic shock.
  • It is also referred to as endotoxin shock because endotoxin often triggers the immune response that results in sepsis and shock.
  • But you should remember that also different effectors molecules in Gram-positive bacteria or even fungi can trigger this adverse immune response – so the term septic shock is inclusive
  • The most effective treatment – find the site of infection the microbe responsible and eradicate it.
  • Lung, abdomen and urinary tract are commune places
56
Q

Microbio

What was the E.coli outbreak in Germany?

A

x

57
Q

Microbio

What is haemolytic-uremic syndrome?

A

x

58
Q

Microbio

How did the EU define the case of diarrhoea and haemolytic uremic syndrome caused by strain shiga toxin 2 producing E coli?

A

x

59
Q

Microbio

What did information was gained from genome sequence of the outbreak strain in Germany?

A

x

60
Q

Microbio

How does the Shiga toxin work?

A

x

61
Q

Microbio

How does the Shiga toxins move?

A

x

62
Q

Microbio

Where does each type of E coli colonise in the body?

A

x

63
Q

Microbio

What is the virulence factor of EAEC?

A

x

64
Q

Microbio

What is an outbreak?

A

An outbreak is 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.

65
Q

Microbio

How can an outbreak be identified?

A

Surveillance provides an opportunity to identify outbreaks Good and timely reporting systems are instrumental to identify outbreaks

66
Q

Microbio

What are the different types of communicable diseases in europe?

A

1) Respiratory tract infections 2) Sexually transmitted infections, including HIV and blood-borne viruses 3) Food- and waterborne diseases and zoonoses 4) Emerging and vector-borne diseases 5) Vaccine-preventable diseases 6) Antimicrobial resistance and healthcare-associated infections

67
Q

Microbio

Give some examples of RTI?

A

Influenza Animal influenzas, including avian influenza SARS - Severe acute respiratory syndrome Legionnaires’ disease (legionellosis - Legionella pneumophilia (Gram -)) Tuberculosis (mycobacterium tb gram +)

68
Q

Microbio

What is Legionella pneumophila?

A

x

69
Q

Microbio

How does L. pneumophila infect and replicate in human macrophages?

A

x

70
Q

Microbio

What is Mycobacterium Tb?

A

Around 70,000 cases reported in EU in 2011

Treatment of infections: with antibiotics BUT TAKES at least 6 months 77% success rate of treatment of new cases

Treatment success rate for second infection is 54%

Multi drug resistant (MDR) treatment success rate in is 32%

71
Q

Microbio

What are the STIs?

A

All gram -ve.

Chlamydis trachomatis – obligate intrecellular bacterium – can only grow and divide within host cells

Neisseria gonorrhoea – is a gram negative cocculs

Treponema pallidum the causative agent of Syphilis is a Gram-negative bacterium and it is a spirochete/

72
Q

Microbio

What are antimicrobials?

A

Interferes with growth and reproduction of a microbe -> antibiotics are types of antimicrobials

73
Q

Microbio

What is an antibacterial?

A

Commonly used to describe agents to reduce/eliminate harmful bacteria

74
Q

Microbio

What are hospital acquired infections?

A

x

75
Q

Microbio

What is the effect of hospital acquired infection on stay length in hospital?

A

x

76
Q

Microbio

What in hospitals act as a source of infection?

A

Dissemination, concentration of people, interventions

77
Q

Microbio

What are the major ESKAPE pathogen problems?

A

Clostridium difficile and enterobacteriaceae

78
Q

Microbio

Why are the ESCAPE pathogens a major problem?

A

x

79
Q

Microbio

What is pathogenic E coli?

A

x

80
Q

Microbio

What are cephalosporins and what is their resistance mechanism?

A

x

81
Q

Microbio

What are carbapenems and what is their resistance mechanism?

A

x

82
Q

Microbio

Which hospital acquired infections do Kelbsiella pneumoniae and Pseudomonas aeruginosa cause?

A

x

83
Q

Microbio

What are methicilin and what is their resistance mechanism?

A

x

84
Q

Microbio

What are vancomycin and what is their resistance mechanism?

What is Vancomycin resistant Enterococcus faecium?

A

x

85
Q

Microbio

What is MRSA?

A

Methicillin resistant S. aureus -> most important cause of antimicrobial resistant infection worldwide

86
Q

Microbio

What is chlamydia trachomatis?

A
87
Q

Microbio

What is Neisseria gonorrhoeae?

A

x

88
Q

Microbio

List some food- and waterborne diseases and zoonoses?

A

x

89
Q

Microbio

What is campylobacter sp (mostly C. jejuni)?

A

x

90
Q

Microbio

What is salmonella sp.?

A

x

91
Q

Microbio

What is vibrio cholerae?

A

x

92
Q

Microbio

What are the actions of the cholera toxin?

A

Cholera toxin released from bacteria in infected intestine, binds to enterocytes via GM1 ganglioside receptor on the intestinal cell, triggering endocytosis of the toxin.

Once inside of enterocyte, GTP is upregulated, AC producing cAMP is also upregulated.

Higher cAMP levels activate CFTR causing dramatic efflux of water and ions from infected enterocytes, leading to watery diarrhoea

93
Q

Microbio

What is Listeria monocytogenes?

A

x

94
Q

Microbio

What are emerging and vector-borne diseases?

A

x

95
Q

Microbio

Which diseases are vaccine preventable?

A

Mass vaccination reduced by more than 97% incidence of 9 infectious diseases and eradicated 2 (smallpox and poliomyelitis)

96
Q

Microbio

What is ecthyma?

A

Necrosis of the skin can occur

97
Q

Microbio

What is Staphylococcus aureus?

A

This is a Gram positive bacterium. It is a commensal in approximately 30% of humans, with colonisation in nose, axillae and groins. It is the most common bacterial cause of skin infections including impetigo, folliculitis, ecthyma, boils and carbuncles. Through the production of toxins it can cause Staphyloccocal Scalded skin Syndrome (Exfoliative toxin), Toxic shock Syndrome (Toxic Shock Syndrome Toxin 1), food poisoning (Enterotoxin) and necrotising soft tissue infections (Panton Valentine Leucocidin virulence factor). It can also cause bone, joint, lung infections and sepsis. The infection can be treated with antibiotics. There is no vaccine.

98
Q

Microbio

What is Teponema pallidum?

A

Gram negative spirochaete which causes Syphilis

99
Q

Microbio

What are the stages of Syphilis?

A

Primary : painless ulcer (chancre) at site of inoculation Secondary: disseminated infection with rash and lymphadenopathy - widespread, maculopapular rash and condyloma lata (warts full of organisms) Latent (asymptomatic) period Tertiary: skin, neurological and vascular manifestations - bone lesions, gummatous skin lesions, thoracic aneurysm. Syphilis can also be vertically transmitted and cause congenital syphilis with a broad spectrum of clinical manifestations. No vaccine is available, but the infection can be treated with antibiotics.

100
Q

Microbio

What is Herpes simplex virus and what are the 2 types?

A

Members of the human herpes family of viruses, which are DNA viruses. Type 1 – usually causes oral infections Type 2 – usually causes genital infections Transmission by direct contact (e.g. kissing and sex). Clinical infection results in a painful vesicular rash which heals over 2-4 weeks. Due to latency in sensory neurons, there can be reactivation with recurrences of infection. No vaccine is available. Outbreaks can be treated with anti-viral medication such as acyclovir.

101
Q

Microbio

What is the varicella Zoster virus and what are its stages of infection?

A

Another human herpes virus. Primary infection causes Chicken Pox. This manifests with a prodrome of fever and malaise followed by the development of a widespread vesicular rash (with vesicles that look like in different stages -> highest conc in face > trunk > imbs ). The clinical infection usually lasts about 2 weeks. The virus remains latent in the sensory neurons and can reactivate years later to cause Herpes Zoster (Shingles). Herpes Zoster or shingles is where there is reactivation of the VZV and a painful vesicular rash appears only along the course of a dermatome (sensory nerve). This usually heals over about 2-4 weeks. There can be serious eye consequences if the distribution of the Ophthalmic Division of the Trigeminal nerve is involved. A vaccine is available. Anti-viral medication such as acyclovir is prescribed in certain circumstances (>70YO). Can also cause erosion of cornea and necrosis of retina if trigeminal affected; bilateral trigeminal infection can be blinding

102
Q

Microbio

What is trichophytum?

A

This is a common cause of superficial fungal infections. It is a dermatophyte, which is a type of fungus which particularly infects parts of the body which have keratin, ie skin, nails and hair. Trichophytum rubrum is an example of a common species. The names of clinical infections have the prefix ‘tinea’ then the Latin body part involved, eg tinea capitis (use systemic fungicide as topical isn’t effective; Kerion is a type of tinea capitis, similar to a staph infection), tinea manuum, tinea unguium, tinea pedis, tinea cruris, tinea facei The clinical manifestations are often of an erythematous scaly rash on skin or scalp or discoloured and crumbly nails. These infections can be treated with topical or systemic antifungal medication such as Terbinafine.

103
Q

Microbio

What is scabies?

A
  • This is a skin infestation with the mite Sarcoptes Scabei.
  • The mite burrows in the surface (within the epidermis) of the skin.
  • Exposure to mite faeces and eggs causes a delayed allergic reaction which results in a wide spread eczematous rash which usually occurs about 4 weeks after the original infestation, and this is usually very itchy.
  • The scabetic burrows can be found in certain regions of the body e.g. genital region, nipples, wrists, finger webs, instep of the feet, axillae.
  • Secondary bacterial infection is common.
  • Transmission is by skin to skin contact. Treatment is with topical of systemic insecticides
104
Q

Microbio

What is an abcess?

A

Pustule with hair growing out of it, with folliculitis. To treat: remove pus and then give antibiotics

105
Q

Microbio

What is staphylococcal scalded skin syndrome?

A

Infection affecting subcorneal level of skin -> treat: give flucloxacilln and emolients to grow back skin and antibiotics to kill S. aureus. NB: doesn’t occur above age 9 as the system becomes resistant

106
Q

Microbio

What is congenital syphillis?

A

Miscarriage Still birth Prematurity Rashes (like 2ry syphillis, and if survive then get brain and neurological problems) Brain and neurological problems Bone disease Saddle shaped, depressed nose -> will also be retarded

107
Q

Microbio

What are the different types of herpes virus in the human herpes virus family?

A

x

108
Q

Microbio

How do type 1 and 2 herpes simplex present?

A

Vesicular rash - 2 weeks Ulcers formed and the clears up but lives in nerves Eczema herpeticum Herpes encephalitis. If in mouth can be severe, involving entire oral cavity, being too painful to swallow/eat. If in genitals then also very painful, making urination and defecation difficult. Can appear anywhere on the body, as long as there is skin-to-skin contact with someone with active herpes

109
Q

Microbio

What is eczema herpeticum?

A

People with eczema have a less strong skin barrier, which leads to herpes penetrating through more easily

110
Q

Microbio

How would you treat a patient with all 3 eczema, impetigo and herpes?

A

IV acyclovir for HSV, oral/IV flucloxacillin to treat Staph. aureus (impetigo) and then mild steroid for eczema needed; all 3 need to be treated at once

111
Q

Microbio

What is latency in a disease?

A

HSV 1/2 and VZV have latency -> live in nerves and wait to flare up when immunocompromised

112
Q

Microbio

What is candidal intertrigo?

A

Skin to skin acquisition of candida fungus, in places with sweat and irritation, here bacteria and fungus collects

Y2 MCD - Haem, Labs, Microbio, Cancer, Immunology (12 decks)

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