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ESA Revision > Infection > Flashcards

Infection Flashcards

1
Q

Examples of DNA enveloped viruses

A

Hepatitis B-inflamed liver, Herpes, Smallpox-vesicular rash

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2
Q

Examples of DNA non-enveloped viruses

A

HPV- warts and cervical cancer

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3
Q

Examples of RNA enveloped viruses

A

Rubella- rash, congenital rubella syndrome, most common cause of PDA= maternal rubella in 1st trimester of pregnancy, HIV (AIDS), rotavirus- most common cause of gastroenteritis in children, diarrohea, Coronaviruses(colds, SARS), Ortho and Paramyxo-viruses(Influenza, Measles, Mumps.)

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4
Q

Examples of RNA non-enveloped viruses

A

Picornaviruses(Polio-inflammation of SC), Hepatitis A- liver disease, Rhinoviruses- colds.

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5
Q

What is the group name for the antimicrobials penicillin, amoxicillin, flucoxacillin and cephalexin and what do they target?

A

Beta-lactams, cell wall

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6
Q

What is the group name for vancomycin and what does it target?

A

Glycopeptide, cell wall

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7
Q

What is the group name for gentamicin and what does it target?

A

Aminoglycoside, protein synthesis

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8
Q

What is the group name for erythromycin and what does it target?

A

Macrolide,protein synthesis

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9
Q

What is the group name for tetracycline and what does it target?

A

Polyketide, protein synthesis

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10
Q

What is the group name for ciprofloxacin and what does it target?

A

Chemotherapeutic, DNA

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11
Q

What does rifampicin target and why is it specific as an antimicrobial?

A

RNA polymerase, enzyme sufficiently different in bacteria than in humans

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12
Q

What do trimethoprim and metronidazole target?

A

Folate metabolism

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13
Q

Disease assoc with staphylococcus aureus?

A

Abscesses, TSS, food poisoning. Most common cause of septic arthritis. May cause endocarditis if enters bloodstream.

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14
Q

Disease assoc with streptococcus pyogenes?

A

Necrotising fasciitis, strep throat, scarlet fever, impetigo

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15
Q

Disease assoc with Group B steptococci?

A

Neonatal sepsis and meningitis.

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16
Q

Disease assoc with Streptococcus pneumoniae?

A

Pneumonia

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17
Q

Disease assoc with Clostridium perfringens?

A

Gas gangrene, food poisoning

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18
Q

Disease assoc with Clostridium difficile?

A

Antibiotic assoc diarrohea (can lead to pseudomembranous colitis), fever, intestinal diseases.

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19
Q

Disease assoc with Neisseria meningitidis

A

Meningitis and septicaemia. Mening ococcemia.

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20
Q

Disease assoc with Neisseria gonorrhoeae?

A

Gonorrhoea, which can lead to pelvic inflammatory disease in women and epididymitis in men.

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21
Q

Disease assoc with Escherichia coli?

A

Watery diarrhoea, acute renal failure, UTI, food poisoning

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22
Q

Disease assoc with Salmonella spp.?

A

Gastroenteritis- infection of stomach and bowel (infectious diarrohea), typhoid fever, septicaemeia

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23
Q

Disease assoc with Shigella?

A

Bloody diarrhoea, dysentery

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24
Q

Disease assoc with Pseudomonas aeruginosa?

A

Generalised inflammation, sepsis, necrotising enterocolitis, pneumonia if enters lungs of CF patient.

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25
Q

Disease assoc with Legionella spp.?

A

Legionnaire’s disease, pontiac fever

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26
Q

Disease assoc with Helicobacter pylori?

A

Peptic ulcers, espec. duodenal, stomach cancer, gastric ulcers, chronic gastritis.

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27
Q

Disease assoc with Bacteroides spp.?

A

Abscesses, lesions, diarrhoea

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28
Q

Disease assoc with Chlamydia spp.?

A

Chlamydia

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29
Q

Disease assoc with Mycobacterium tuberculosis?

A

TB

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30
Q

Disease assoc with Mycobacterium leprae?

A

Leprosy

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31
Q

What do we use instead of the gram reaction for mycobacteria?

A

Acid fast

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32
Q

Define pathogen

A

microorganisms capable of producing disease

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33
Q

Define non-pathogen

A

microorganisms which don’t cause disease and may perform essential ecological roles

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34
Q

Why do we use the Gram stain

A

to allow us to detect and begin to classify bacteria in order to predict their pathogenicity and likely response to treatment.

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35
Q

What is the difference in cell walls between gram +ve and gram -ve bacteria?

A

Gram +ve= thick peptidoglycan layer and a cell membrane.

Gram -ve= inner and outer membranes, and a thinner peptidoglycan layer.

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36
Q

Examples of eucaryotes and procarytoes.

A

Eucaryotes :fungi, protozoa Procaryotes: bacteria, archaea.

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37
Q

Compare eucaryotes, bacteria and viruses.

A

Eucaryotes: no cell wall, stable mRNA, 40S+60S=80S, introns present, many chromosomes, compartmentalised reactions, never flagellum/pilli/capsule, nucleus, membrane-bound organelles, no reverse transcriptase, DNA and RNA, no capsid or envelope.
Bacteria: peptidoglycan cell wall, labile mRNA, 30S+50S=70S, coupled transcription and translation, no introns, 1 chromosome, no nucleus, plasmids + circular DNA loops, no membrane bound organelles, may have flagellum/pilli/capsule, no reverse transcriptase, DNA and RNA, no capsid.
Viruses: can be enveloped, no organelles, proteins capsids, no pilli/flagella, can have reverse transcriptase e.g. HIV, DNA or RNA but NOT both.

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38
Q

Why are different individuals subject to different infections?

A

Due to:

  • weakened immune systems
  • no access to healthcare e.g. immunisations
  • poor living conditions
  • poor nutrition
  • genetic predisposition
  • lifestyle e.g. STDs
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39
Q

Describe the gram staining process

A
  • +vly charged crystal violet binds to -vly charged cell components
  • iodine forms large molecular complexes with crystal violet
  • acetone/methanol used to extract complexes through gram -ve cell wall, not gram +ve.
  • red dye used to stain now unstained gram -ve cells.

Gram -ve=stained red
Gram +ve=stained blue

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40
Q

How does penicillin target bacteria?

A

It targets the cell wall, inhibiting the transpeptidase enzyme which is responsible for forming peptidoglycan cross-links in the cell wall.

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41
Q

How does tetracycline target bacteria?

A

It binds reversibly to the 30S subunit on the ribosome, preventing binding of amino acyl-tRNAs to A site. Translation prevented as tRNA can’t bind, so mRNA cannot be used as template for protein synthesis.

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42
Q

Why does Rifampicin only target bacterial RNA polymerase?

A

Enzyme sufficiently different in bacteria to mammalian cells.

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43
Q

Why do bacteria become resistant to penicillin?

A

Overuse. Mutations in active site of transpeptidase enzyme, so many variants, which need use of newer antibiotics. Primary resistance by random mutation. Staph bacteria developed ability to cut beta-lactam ring of penicillin by producing beta-lactamase enzyme.

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44
Q

Describe mechanisms of resistance to the antifolate Pemetrexed.

A
  • Mutation of reduced folate carrier, so decreased accumulation of drug.
  • Decreased activity of folypolyglutamate synthase- decreased polyglutamation required for inhibiting enzymes in folate metabolism-required for cell division.
  • Increased activity of glutamylhydrolase-cleaves polyglutamate derivatives which the drug forms.
  • Increased activity of thymidylate synthase-Pemetrexed overwhelmed.
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45
Q

Describe resistance to rifampicin.

A

Mutations in gene encoding RNA polymerase.

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46
Q

Describe resistance to Tetracycline.

A

Increased efflux of drug, ribosomal protection and enzymatic inactivation of drug.

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47
Q

Give 2 bacterial causes of meningitis.

A

Neisseria meningitidis, Group B steptococci

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48
Q

Name common causes of hospital acquired infections

A

Staphylococcus aureus, pseudomonas aeruginosa

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49
Q

Classify streptococcus viridans

A

Gram +ve coccus

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50
Q

What infections does streptococcus viridans cause?

A

Dental caries (tooth decay), can cause endocarditis if patient has valve problems.

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51
Q

Classify proteus mirabilis and state infections it may cause

A

Gram -ve rod

Septicaemia, pneumonia, UTIs

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52
Q

Classify haemophilus influenzae and state infections it can cause.

A

Gram -ve rod

Bacterial meningitis, espec. in infants, otitis media, pneumonia.

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53
Q

Classify candida albicans and state infections assoc.

A

Yeast

Candidiasis (thrush- oral and vaginal)

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54
Q

Which bacterial organism is most common the skin?

A

Staphylococcus epidermidis

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55
Q

Describe mechanism of adenovirus infection

A

RME to enter cell, leaves cell via slow disintergration of dying cell, causes epithelial cell damage.

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56
Q

Where in the body is the adenovirus found?

A

Respiratory and intestinal tracts

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57
Q

Name some diseases the adenovirus is associated with

A

Gastroenteritis, conjuntivitis, RTIs

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58
Q

How is the adenovirus transmitted?

A

Inhalation- droplets and aerosols, and faecal-oral contamination.

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59
Q

Describe adenovirus composition

A

DNA virus, non-enveloped

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60
Q

Which immune cell is most important in controlling viral infections?

A

Lymphocytes

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61
Q

Which immune cell is most important in controlling bacterial infections?

A

Neutrophil

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62
Q

Name the 2 classes of fungi and state what the classes are based on.
Give an example of a fungus.

A

Yeast and mould
Unicellular or multicellular
Candida albicans- yeast, can cause oral and vaginal thrush.

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63
Q

Describe the features of systemic inflammatory response syndrome.

A 
a response to a non-specific insult e.g. infection, trauma, ischaemia.
2 or more of:
-temp >38C or 20/min (or PACO2 90/min
-WBC < 4x10^9, or >12x10^9 /L.
-HR >90/min
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64
Q

Describe differences between bacteraemia, sepsis and septicaemia.

A

Bacteraemia- presence of bacteria in blood, with or without clinical features, can’t be said simply by looking at a patient.
Sepsis- systemic response to infection, includes systemic inflammatory response syndrome and documented or presumed infection.
Septicaemia- clinical term for generalised sepsis, blood poisioning.

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65
Q

What is severe sepsis?

A

SIRS and organ dysfunction or organ hypoperfusion. so hypotension, decreased urine output as poor perfusion to kidney, resulting in failure.

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66
Q

What is septic shock?

A

severe sepsis and persistently low BP despite administration of IV fluids.

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67
Q

How do bacteria cause septic shock?

A

Endotoxins e.g. lipopolysaccharide-N.meningitidis, released, cause profound vasodilation, chemical and cytokine release? e.g. histamine and prostaglandins, so dramatic decease in TPR, fall in arterial pressure, so reduced perfusion to vital organs. Capillaries also become leaky with time, so reduced blood vol., decreasing arterial BP.
Decreased arterial pressure detected by baroreceptors-aortic arch and carotid sinus, stimualte increased sympathetic output, so HR and SV increased, so tachcardia and strong pulse. Vasoconstrictor effect via SNS overidden by toxins causing vasodilation but in later stages, vasoconstriction occurs via SNS, resulting in less blood flow to extremities, so pale and cold. Initially warm and red as vasodilation.
Cytokines can increase vascular permeability- IL-1 and TNF causes cytoskeletal reorganisation.

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68
Q

What antibiotic treatment is the empiric choice for meningitis caused by N.meningitidis?

A

Ceftriaxone- good against agent and can pass through inflamed blood-brain barrier into CSF.

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69
Q

What examples are they for multi-resistant infections?

A

TB, gonorrhoea

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70
Q

What enzyme do some bacteria produce e.g. staph aureus, to stop penicillin from functioning?

A

Beta-lactamase

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71
Q

What shape is neisseria meningitidis?

A

diplococcus- kidney-shaped

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72
Q

Why should most URT infections not be treated with antibiotics?

A

Most caused by viruses so antibiotics would have no benefit, but would kill certain bacteria of our normal flora which may alter the balance of bacteria in the body, may result in genital thrush if lactobacilli affected, and diarrhoea if the numbers of clostridium difficile bacteria increased in the large bowel.

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73
Q

What can we do to manage antibiotic resistance without stopping using them altogether?

A
  • selective with administering antibiotics

- combination therapy

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74
Q

Why would a patient with HIV, who is suffering a bacterial infection in hospital, need to be given antibiotics immediately without doing tests e.g. blood culture?

A

They are immunocompromised so the bacterium could very quickly result in septicaemia and death.
Lack CD4+T cells necessary to recognise bacterial peptides presented by MHC II molecules on antigen-presenting cells, and stimulate maturation of B cells into plasma cells to produce Igs, so adaptive immune response deficient.

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75
Q

What is New Delhi Metallo-beta-lactamase 1 and name a bacterium which produces it?

A 
an enzyme that makes bacteria resistant to a broad range of beta-lactam antibiotics e.g. penicillin, amoxicillin, flucoxacillin. These include the antibiotics of the carbapenem family, which are a mainstay for the treatment of antibiotic-resistant bacterial infections.
E-coli and klebsiella pneumoniae. Bacteria produce the enzyme which is part of a class of enzymes= carbapenemases - making carbepenem antibiotics ineffective (as well as virtually all other antibiotics).
If NDM-1 gene carried, bacterium resistant to nearly all antibiotics.
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76
Q

Give general examples of how bacteria can become resistant to antibiotics.

A
  • increased synthesis of target enzyme
  • increased efflux of drug
  • reduced influx of drug
  • prod. of different drug target which have lower affinity for drug
  • alterations to target of drug
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77
Q

Give examples of bacteria responsible for producing pneumonia.

A

Streptococcus pneumoniae
Neisseria meningitidis
Pseudomonas areuginosa
Proteus mirabilis

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78
Q

Describe C difficile

A

Gram +ve rod shaped bacterium
Spore-forming
Obligate anaerobe
Produces toxins- A and B

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79
Q

Describe pathogenecity of C.difficile

A

Toxins:
A- enterotoxin- increases fluid secretion and causes inflammation of lining of bowel wall. Gives pseudomembranous appearance
B- cytotoxin- disrupts protein synthesis within cells.

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80
Q

What antibiotics are given for C.difficle?

A

If no markers for severe disease, start metronidazole for 10 days. If markers present e.g. high wcc, low albumin, increases creatinince, clinical markers of sepsis or temp >38.3 degrees C, than start vancomycin, with or without metronidazole.

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81
Q

What global problems does antibiotic resistance create?

A
  • Increased mortality
  • People being ill for loner
  • Increased healthcare costs
  • Damaged trade
  • Jeopardises other HC gains
  • Possibility of returning to a pre-antibiotic era.
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82
Q

Name 2 bacterial organisms which commonly cause infection when the host’s normal flora is disrupted.

A

Clostridium difficile

Candida albicans

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83
Q

When might you want to use broad-spectrum antibiotics?

A

In an emergency situation where a patient has a life-threatening condition e.g. sepsis, and there isn’t sufficient time to work out the causative microbe before administering the antibiotic, so you need an antibiotic which will target a large range of bacteria.

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84
Q

What are the negatives of using broad-spectrum antibiotics?

A

They can result in antibiotic resistance, and target normal bacterial flora which can predispose the patient to infection as their innate immune system is compromised.

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85
Q

When might antimicrobials be used in prophylactic treatment?

A

When a patient who is immunocompromised is undergoing some type of hospital treatment, e.g. if they have diabetes, HIV, splenectomy, BM malignancy.

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86
Q

What does norovirus cause?

A

Gastroenteritis, projectile vomiting

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87
Q

Why would gram staining a stools culture be unuseful when trying to determine the bacterial cause of diarrhoea?

A

There would be many bacteria in the stools which would normally be there even if an infection wasn’t present, and so the gram stain will pick up on all of these bacteria.

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88
Q

Describe shape of H.pylori

A

Motile gram -ve spiral bacillus (rod)

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89
Q

What is a patient with infection by E coli 0157:H7 at risk of if given antibiotics- potentiate toxin production?

A

Haemolytic uremic syndrome- acute renal failure, haemolytic anaemia and thrombocytopenia.

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90
Q

Describe treatment of malaria.

A 
plasmodium falciparum (malignant) - quinine, artemisinin or doxycycline.
P.ovale, vivax or malariae (benign)- chloroquine, followed by 2 wk course of primaquine- for exo-erythrocytic stage.
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91
Q

Usual treatment for Enteric fever?

A

Ceftriaxone or azithromycin 7-14 days

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92
Q

How does Legionella pneumophila use innate IS to aid its replication?

A

Phagocytosed by macrophages but prevents resulting phagosome from fusing with a lysosome, so bacterium evades destruction by macrophage, can replicate with protected environment and then when cell ruptures, a new crop of bacteria is released.

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93
Q

Name opportunistic infections associated with HIV when CD4 cell count above 200 cells per microlitre.

A

Herpes zoster
TB
Oral candidiasis (thrush)

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94
Q

Name opportunistic infections assoc. with AIDS.

A

Eosophageal candidiasis
Mucocutaneous herpes
Pneumocystis caricii pneumonia
Cryptosporidiosis

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95
Q

Why do patients infected with HIV develop drug resistance quickly?

A

HIV is an RNA virus, which lacks efficient mechanisms for genetic proof-reading, so mutations arise rapidly.

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96
Q

Prevention measures for HIV

A

Absolute: -no Sex
-condoms
-knowing who you’ve had sex with and who they have had sex with.
-no IVDU
-clean needles
-screened negative blood products
-health education and free needle-exchange programmes for IV drug users.
Reducing risk:- mother to child transmission- mother antiretrovirals, caesarrean section
-circumcision
-pre exposure- drugs to a partner to stop HIV infection
-post exposure- antiretroviral prophylaxis should be given for infected needle-stick injuries.
-vaccination

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97
Q

Describe the stages of viral replication

A
  • adsorption- specific interaction, enveloped viruses have glycoproteins for attachment, may be unique folding of capsid protein forming attachment site
  • penetration-RME or membrane fusion-e.g. HIV
  • uncoating- so viral genes can be expressed for transcription
  • transcription
  • virion synthesis
  • assembly
  • release
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98
Q

How does HIV infect cells?

A

RNA retrovirus which gains entry to helper CD4+ T cells by binding to CD4 molecules- specific glycoproteins on surface. Genetic info. injected into cell cytoplasm, RNA converted to DNA via reverse transcriptase, and transcribe DNA then incorporated into host DNA. T cell them makes copies of virus, which are extruded from cell through exocytosis. IS responds by generating CD8+ cytotoxic T cells which kill infected HIV helper CD4+T cells, reducing no. of T helper cells, so infected individuals eventually become unable to generate an IR.***
Cytopathic effect of virus- production of viral particles within cell kills infected T cells.
Many opportunistic infections caused by viruses e.g. CMV. With AIDS, patients have defective CD8+ T cell responses despite these cells not being infected, as CD4+ helper T cells are required for full CD8+ cytotoxic T cell responses against many viral antigens.

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99
Q

How can risk of infection from central venous line be reduced?

A

Silver coating the central venous line

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100
Q

What is the difference between colonisation of a patient with normal flora and the carrier state?

A

Colonisation- normal flora present in body of a patient, potentially harmful as could become pathogenic, but not a pathogen currently.
Carrier state- patient carries a true pathogen which can be passed to others where it results in disease, but the patient carrying the pathogen is asymptomatic.

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101
Q

How do we get surface infections?

A

Invasion
Innoculation
Haematogenous
Migration

Prosthetic may also result from contamination

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102
Q

Organisms causing native valve endocarditis and prosthetic valve endocarditis >1 yr post-op

A

viridans Streptococci
Staph. aureus
candida

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103
Q

Organisms causing prosthetic valve endocarditis <1yr post-op

A

Coagulase -ve staphylococci- introd. from skin of patient or operator

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104
Q

Organisms causing prosthetic joint infections

A

coagulase -ve staphylococci

staph.aureus

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105
Q

Type of giant cell (macrophage) present when prosthetic joint infection

A

Foreign body cells

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106
Q

Cardiac pacing wire endocarditis organisms?

A

coagulase -ve staphylococci

staph.aureus

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107
Q

Why might an outbreak of infection occur with pathogen changes?

A

New antigens, so people no longer immune e.g. influenza-H and N antigens
New virulence factors causing disease e.g. C difficile toxins
Antibacterial resistance, so people remain infectious to others for longer as disease takes longer to find a cure e.g.MRSA

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108
Q

Why might infections e.g. from N.Meningitidis, come about after the age of 3 mnths?

A

Before this time, the baby has passive immunity via maternal Igs, but after 3 mnths, these disappear.

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109
Q

How can we reduce/ eradicate pathogens to prevent infection transmission?

A

Antibacterials-disinfectants
Decontamination
Sterilisation

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110
Q

How can patients be stopped from acquiring infections?

A

Improved health- nutrition and medical treatment

Immunity- passive and active-vaccination

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111
Q

How can practice prevent infection transmission?

A

Avoid pathogen or vector- don’t visit place with pathigen, protection- long sleeves and trousers, equipment- gloves, aprons, masks, behavioural- safe sex, safe disposal of sharps, food and drink prep.- boiling water

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112
Q

How can place prevent infection transmission?

A

Environmental engineering- safe water, safe air- prevent prosthetic joint contamination, good quality housing, well designed h.care facilities.

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113
Q

Humoral components of innate IS?

A
  • complement sytem- cascade of serum proteins- involved in recruitment, opsonisation
  • cytokines- can act as chemoattractants for recruitment of other inflammatory cells, activate phagocytes, and initiate inflammatory process for protection.
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114
Q

What organisms classically cause impetigo?

A

Staphylococcus aureus

Group A streptococci e.g. streptococcus pyogenes

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115
Q

Give 3 examples of encapsulated bactera an asplenic patient is at increased susceptibility to

A

Haemophilus influenzae
Streptococcus pneumoniae
Neisseria meningitidis

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116
Q

Why is the spleen so important to immune function?

A

Protection against blood-borne pathogens, e.g. encapsulated bacteria- most invasive
Antibody production- IgM acute, IgG long term
Splenic macrophages- removal of opsonised microbes and removal of immune complexes- antibody-antigen complexes

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117
Q

What is an immunocompromised host?

A

State in which IS unable to respond appropriately and effectively to infectious microbes

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118
Q

How can we recognise infections suggesting underlying immune deficieny?

A

SPUR- severe, persistent. unusual, recurrent

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119
Q

Give examples of latent infections which may be reactivated in immunocompromised host when IS can no longer keep infection under check

A

Cytomegalovirus
Mycobacterium TB
Varicella-Zoster virus
Epstein-Barr virus

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120
Q

Cytomegalovirus family?

A

Herpes (betaherpesvirinae) (enveloped DNA virus)

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121
Q

Difference between primary and secondary immunodeficiencies

A

Primary- intrinsic defect
Can be single gene disorder, polygenic, or polymorphisms. Congenital, but may present later in life
Secondary- acquired
Underlying disease or condition affecting immune components so decrease production or increase loss or catabolism

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122
Q

Which cells does HIV mainly infect?

A

CD4+ T cells, causing progressive destruction of these T lymphocytes. HIV particle= lipid envelope derived from infected host cells but containing viral proteins.

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123
Q

What is CD4?

A

A glycoprotein expressed on surface of T cells and some macrophages, which binds to class II MHC molecules on antigen-presenting cells, resulting in T cell activation

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124
Q

Describe chronic granulomatous disease, and example of a primary immunodeficiency of the phagocyte type, and describe how patient may present

A

group of disorders resulting from failure to produce bactericidal oxygen radicals during the ‘respiratory burst’ which accompanies activation of phagocytes. Defects in NADPH oxidase enzyme complex which normally generates increased oxygen consumption (the ‘respiratory burst’), essential for the clearance of phagocytosed micro-organisms via O2 dependent killing mechanism. Classic type inherited as an X-linked recessive disorder. Typically presents in 1st 3 months of life as severe skin sepsis caused by staphylococcous aureus or fungal infections. Complications include regional lymphadenopathy- disease of lymph nodes, hepatosplenomegaly, hepatic abscesses, septicaemia and osteomyelitis (infection of bone). Affected organs show multiple abscesses and non-caseating giant-cell granulomas where cells have large vesicular nuclei, plentiful eosinophilic cytoplasm and are often rather elongated.
May also present with pulmonary aspergillosis- fungal pulmonary infection with ground-glass opacification on CXR.

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125
Q

Give an example of a complement component deficiency and describe it

A

Hereditary angioedema- lack of inhibitor of 1st component of complement (C1 inhibitor) resulting in episodes of angio-oedema which involves recurrent attacks of cutaneous, intestinal or laryngeal oedema in patient which can be fatal if airway occluded. The oedema is triggered by increased permeability of the blood vessels; probably bradykinin is the main mediator involved. Bradykinin is generated from plasma kinins by kallikrein or kallidin. (In angio-oedema, the swelling is subcutaneous or submucosal rather than epidermal, so urticaria is absent.) The affected organs are the skin and mucosa, including the upper airway and gastrointestinal (GI) tract. Prophylaxis involves reducing triggers to the attacks e.g. drugs, trauma and infections. Symptoms and signs of laryngeal oedema: Throat - sore, tight, itchy, lump, ‘something stuck’, or dysphagia

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126
Q

Management of aspleinc/splenectomised patient?

A

Penicillin prophylaxis life-long
Immunisation against encapsulated bacteria at least 2 wks prior to splenectomy
Patient info., medical alert bracelet

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127
Q

Classify norovirus

A

ss +ve strand (1 that can serve as mRNA in infected cell) RNA non-enveloped virus

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128
Q

What factors can cause neutropenia (low neutrophil count), with management necessary when count < 1.0X10^9- suspected neutropenic sepsis- give empiric antibitotics?

A 
Drugs e.g. phenytoin*
AI
Infections e.g. hep B
BM infiltration with malignancy
Vit B12 or folate deficiency
Chemotherapy- targets rapidly proliferating cells- cytotoxics and immunosuppressants
Radiotherapy
129
Q

Most appropriate diagnostic test for meningitis?

A

Lumbar puncture- small amount of CSF removed by inserting a needle in to the lumbar spine

130
Q

describe enterohaemorrhagic E coli and where it is found

A

Gram -ve rod that binds to LI cells and produces 1 of 2 shiga-like toxins which cause a severe form of copious, bloody diarrhoea in absence of mucosal invasion or inflammation. 0157:H7 is most common strain to produce these toxins, and is assoc. with HUS- fever, acute renal failure.
Cattle- should thoroughly cook ground beef and pasteurise milk

131
Q

what are MHC molecules

A

membrane proteins found on the surface of antigen presenting cells that display peptide antigens for recognition by T lymphocytes

132
Q

3 functions of complement system

A

Opsonisation of microbes via C3b
Chemoattraction- C5a and C3a
Formation of a polymeric protein complex that inserts into microbial cell membranes, disrupting the permeability barrier and causing osmotic lysis or apoptosis of microbe.

133
Q

CD4+ T cells are T helper cells. What do T helper 1 cells release, what hypersensitivity reaction is this?

A

Interferon-gamma- type 4 hypersensitivity

134
Q

In what cause of infections are eosinophils most important?

A

Parasitic infections

135
Q

Examples of notifiable diseases?

A

Meningitis, TB

Must notify the health protection unit of PHE

136
Q

Where would you look for information on travel related infections?

A

Centres for disease control (CDC)
WHO
DOH

137
Q

Would you ever vaccinate neonates against TB?

A

Yes if high risk individuals

138
Q

Why so many drugs to treat TB?

A

To target multi-drug resistant TB?

139
Q

Which Ig is trasferrred across the placenta from the mother to the foetus?

A

IgG

140
Q

Which Ig is found in breast milk?

A

IgA

141
Q

Which Ig prevents adherence of bacteria to the mucosa?

A

IgA

142
Q

Which Ig is produced by plasma cells in atopic conditions?

A

IgE

143
Q

Which Ig is released immediately as part of the adaptive immune response on 1st exposure to antigen?

A

IgM

144
Q

Describe the difference between Bruton’s disease and Common variable immunodeficieny

A

Bruton’s disease is a primary immunodeficiency also known as X-linked agammaglobulinaemia, as B cell development is impaired, so no Igs are produced whatsoever, whereas Common variable immunodeficiency is a primary immunodeficiency where B cells fail to mature into plasma cells, and this results in a hypogammaglobulinaemia *

145
Q

Major causes for organ transplant rejection*

A

HLA mismatches

ABO antigen mismatches- blood group antigens

146
Q

What types of Igs are produced by plasma cells?

A

MADGE

Ig M,A,D,G and E

147
Q

Treatment for candida infection?

A

fluconazole

148
Q

infection risk in giving patient with menigococcal meningtiis ceftriaxone- a cephalosporin- type of beta lactam?

A

antibiotic associated diarrhoea- C difficile infection

149
Q

Which cells express MHC class II molecules?

A

APCs: macrophages, B cells, and especially dendritic cells

150
Q

treatment of influenza?

A

oseltamivir (tamiflu)

151
Q

treatment of varicella-zoster virus?

A

aciclovir

152
Q

are bacteria typically uni or multicellular?

A

unicellular

153
Q

meningitis classic triad of symptoms?

A

fever
headache
neck stiffness

154
Q

mechanism behind antibiotics increasing susceptibility to C difficile infections

A

antibiotics kill normal gut flora, reducing competition and allowing C difficile to proliferate and overgrow

155
Q

describe clostridium botulinum infection

A

causes muscle paralysis as botulinum toxin produced which inhibits release of ACh at NMJ

can be used for tment of urge urinary incontinence as causes flaccid paralysis of bladder, but then problem of urinary retention

156
Q

disease assoc with clostridium tetani

A

tetanus- involunatry muscle contractions

157
Q

complications of norovirus infection?

A

very young an elderly patients- problems of dehydration compliations as gastroenteririts and vomiting
providing hcare services- can result in loss of staff to sick leave and clinical areas closed

158
Q

describe ELISA, which can be used to look for C difficile toxins in stools culture

A

primary antibody specific to protein (toxin) immobilised on solid support, and solution to be assayed (containing toxin) is applied to antibody-coated surface, and antibody binds protein of interest. Secondary antibody specific to protein applied which binds to AA complex is added, and this antibody is conjugated to an enzyme so binding is measured by assaying for activity of enzyme.

159
Q

how does C.tetani cause involuntary muscle contractions?

A

produces an exotoxin which prevents the release of inhibitory neurotransmitters e.g. glycine*
tetany also may be result of hypocalcaemia as can occur with resp. alkalosis when patient is hyperventilating

160
Q

name some antibiotics with specific use in penicillin allergy

A

tetracycline and doxycycline- target protein synthesis

161
Q

why should tetracyclines not be given to children <12 yrs?

A

cause yellow teeth and bones

162
Q

how do macrolides inhibit protein synthesis?

A

bind to bacterial 50S ribosomal subunit

163
Q

groups of antibiotics causing C difficile infection?

A

quinolones e.g. ciprofloxacin
amoxicillin
cephalosporins e.g. ceftriaxone

164
Q

unwanted effects of antibiotics?

A

GI upsets e.g. nausea, vomiting, diarrhoea
haematological disturbances- BM
organ toxicity e.g. liver-rifampicin, ear, kidney- gentamicin
allergies- skin rashes
super-infections- C difficile, fungal infections, multi-resistant bacteria

165
Q

basis of choosing right antibiotic?

A
  • spectrum of activity e.g. gram+ve/-ve, anaerobes- metronidazole
  • site of infection- meninges- ceftriaxone
  • patient factors- age, interactions with other drugs, route of administration e.g. can’t give oral if unconscious, severity of infection, organ function, pregnancy, allergies
  • guidance- national/local, based on resistance patterns and epidemiology, epidemiology of HCAIs, costs
  • hosp/primary care guidance- BNF, antimicrobial website for your institution
166
Q

when is combined therapy indicated?

A

prevent emergence of resistance- TB
BS when pathogen unknown, or multiple pathogens possible e.g. peritonitis- may be septic-emergency
enhanced activity e.g. infective endocarditis

167
Q

define the incubation period

A

time between exposure and infection

168
Q

where to look for info regarding infection outbreaks abroad?

A 
WHO
DOH
CDC- centers for disease control
health protection agency
nathnac- national travel health network and centre
169
Q

initial investigations for patient presenting with diarrhoea?

A 
FBC
CRP
Us and Es
LFTs
Stools sample and culture, microscopy- 3 samples taken at different times can increase sensitivity, can do antigen tests on stools- EIA=enzyme immunoassay test
blood culture if fever
170
Q

what is the worry with giving a patient antibitoics for diarrhoea without knowing the pathogenic cause of the diarrhoea?

A

may precipitate HUS if enterohaemorrhagic E coli, serotype o157:h7

171
Q

oseltamivir can be given for influenza. what does it do?

A

neuraminidase inhibitor

172
Q

what investigations can be done when sample sent to microbiology?

A 
microscopy
ELISA
PCR
culture
antibody detection
use known antiserum to detect antigen
173
Q

how is legionella pneumophila spread?

A

inhalation, but NOT human to human transmission, so no need for isolation

174
Q

what does the local health protection unit fo?

A

collects info. on possible source, establishes whether other travellers at risk and coordinates action to reduce risk

175
Q

what must be done if legionella pneumophila pneumonia diagnosed?

A

give specific antibiotics- quinolones e.g. levofloxacin

notify local HPU of PHE

176
Q

How can patient factors be modified when concerning infection?

A

cure pathological condition, maximise physiological state e.g. good nutrition and hydration, modify social factors e.g. good sanitation and living conditions, education about STIs

177
Q

how is adenovirus transmitted?

A

inhalation
faecal-oral
inocculation and indirect contact

178
Q

how might adenovirus infect a person in a swimming pool?

A

inocculation by virus-contaminated hands from swimming pool, causing conjunctivitis
prevented by adequate chlorination

179
Q

how can adenovirus be detected in stools samples?

A

ELISA

180
Q

how does adenovirus kill cells?

A

productive cycle of virus within cells

181
Q

how is adenovirus detected?

A

Adenovirus infections can be identified using antigen detection (ELISA?), polymerase chain reaction assay, virus isolation, and serology.

182
Q

how can people be protected from adenovirus infection?

A
  • washing your hands often with soap and water
  • covering your mouth and nose when coughing or sneezing
  • not touching your eyes, nose, or mouth
  • avoiding close contact with people who are sick
  • staying home when you are sick
183
Q

Which pathogens are eucaryotes?

A

fungi and parasites

184
Q

how can viruses be used to target antimicrobial resistance?

A

some viruses can act as bacteriophages- infect bacteria, so could be used to treat bacterial infections rather than antibiotics to try and minimise emergence of resistance

185
Q

How can C difficle survive outside of body is obligate anaerobe?

A

it produces spores

186
Q

opportunistic infections with HIV?

A

herpes-zoster virus
TB
oral candidiasis

187
Q

problem with fungal chemotherapy?

A

fungi and host’s normal cells= eucaryotes, so therapy results in severe SEs as targeting of normal cells

188
Q

importance of pathological state in patient factor associated with infection?

A

diabetes
immunosuppression for diseases e.g. RA, so opportunisitc infection susceptibility
CVS disease
undergoing surgery for disease in hospital-HAIs

189
Q

How can infection be spread?

A 
direct spread
haematogenous
inocculation
vertical transmission
vextor
inhalation
faecal-oral (ingestion- e.g. eating a spore)
direct or indirect contact
190
Q

How do pathogens cause disease?

A

Virulence factors:
Toxins- exo-cytolytic- cell membranes broken down, enzymes, AB toxins- protein complexes and superantigens- cause non-specific activation of T cells with resultant massive release of inflammatory cytokines or endotoxins- LPS- gram -ve bacteria, integral part of cell wall that triggers inflammation
Direct host damage e.g. malaria- excessive haemolysis and haemolytic anaemia
Interaction with host defences
Inflammation

191
Q

What does specific t.ment involve?

A

Antimicrobials and surgery- e.g. abscess drainage and debridement, TB- infected lung used to be removed, heart valve removal

192
Q

What does supportive t.ment involve?

A

symptom relief and physiological restoration

193
Q

long term problems that may result from prior meningits infection?

A

deafness
neurological damage
learning difficulties

194
Q

examples of disease determinants?

A

Pathogen- resistance to antimicrobials, inoculum size, virulence factors
Patient- infection site, and co-morbidities e.g. age, and other diseases- diabetes- immunocompromised?

195
Q

What is the most important virulence factor of N.meningitidis?

A

polysaccharide capsule

196
Q

symptoms of N.meningitis meningitis?

A 
fever
nausea
severe headache
weakness
general muscle aches
abdominal pain
eye pain on exposure to light- photophobia
197
Q

signs of N.meningitis meningits?

A

Neck stiffness- resistance to head being pulled forward
rash- non-blanching, pupuric
high temp, pale and cool extremities- SNS vasoconstriction
high pulse
low BP
high resp. rate
alertness- glasgow coma scale

198
Q

why is an increase in respiratory rate seen in septic shock?

A

mass vasodilation with huge decrease in TPR and arterial pressure, so reduced perfusion to vital organs- also due to cytokines stimulating clotting cascade, tissues which don’t receive sufficient blood supply don’t receive sufficinet O2, so revert to anaerobic metabolism with lactate production, so metabolis acidosis with pH decrease of blood, this is then compensated for by the lungs with an increase in resp. rate to expel more CO2

199
Q

what is a purpuric rash?

A

microvasculature problms cause bleeding under skin

200
Q

number of features needed e.g. HR and temp, for SIRS to be diagnosed?

A

2 or more

201
Q

how is meningitis spread?

A

direct contact with respiratory secretions e.g. coughing, sneezing, using an infected person’s cigarette or eating utensils or drink
and aerosols- inhalation

202
Q

composition of N.meningitidis>

A

LPS endotoxin which triggers inflammation
Polysaccharide capsule- promotes adherence and prevents phagocytosis
Pilus- enhance attachment to mucosa

203
Q

describe the inflammatory cascade in response to N.meningitis

A

endotoxin(LPS) binds to macropahges resulting in the release of cytokines e.g. TNF alpha and IL-1= locally, to promote wound repair and recruit RE system as want to get rid of insult, e.g. will lead to rearrangement of cytoskeleton- increase vessel permeability- protein movement- exudate, cytokines then released into circulation- systemic, stimulating GF macrophages and platelets, with the goal of homeostasis, but when homeostasis not restored, SIRS occurs, as cytokines lead to activation of humoral cascades and RE system, so circulatory insult
LPS also activates complement system- humoral component on innate IS

204
Q

how do cytokines affect coagulation?

A

they initiate thrombin prod, and inhibit fibrinolysis. so microvascular thrombosis occurs with organ ischameia, dysfunction and failure, microvascular injury is major cause of shock and multiorgan failure

can get DIC

205
Q

why might here be wet gangrene visible on feet of a patient with sepsis?

A

so liquefactive necrosis as a result of ischaemia as cytokines stimulate thrombus prod. with subsequent blocking of microvasculature, mass vasodilation means blood flow diverted away from less vital organs so feet become ischaemic

206
Q

Urgent investigations in sepsis?

A 
FBC
U and Es- assess kidney function- failure can result with ischaemia
EDTA bottle for PCR
blood sugar
LFTs
CRP
clotting studies
blood gases
207
Q

What are the sepsis 6?

A

Treatment: must be given withing 1 hr

  • high flow O2
  • take blood culture and other cultures, consider source control
  • give empirical IV antibiotics
  • measure serum lactate
  • start IV fluid resucitation
  • commence accurate urine output measurement- catheterise, so can quantitate in and out balance
208
Q

Life-threatening complications of meningitis?

A 
irreversible hypotension
acute kidney injury
respiratory failure
raised intracranial pressure
ischamic necrosis of digits/hands/feet
209
Q

confirming diagnosis of meningitis?

A

blood culture before antibiotics
PCR of blood
Lumbar puncture if safe- culture of CSF, and PCR

210
Q

What do we look for in a CSF sample?

A 
Biochemical: glucose-<60% of that in serum and protein- increased
Micriobiology: microscopy and culture
appearance- turbidity and colour
microscpy- WCs, RBCs
gram stain- red
referral for PCR
211
Q

What 3 things may happen when N.meningitidis is acquired?

A

clearance
colonisation- become a carrier- so not symptomatic but can be a source of infection to others
invasion
which occurs depends on your IS- are antibodies already present?

212
Q

Which group of meningococcal disease is found mainly in england?

A

Group B

213
Q

Prevention of menigococcal disease?

A

meningococcal C conjugate vaccine
other serogroup vaccines for immunocompromised and travel protection
prophylactic rifampicin

214
Q

management of meningits?

A

resucitation and supportive care, plus specific-antibiotics

consider others- notifiable disease- LHPU of PHE, who else is at risk of the disease

215
Q

problem with serogroup B vaccine for meningits?

A

b capsule poorly immunogenic- so not many antibodies produce against it, and similar to neural tissue so difficult to produce a vaccine that won’t damage normal host cells

216
Q

what are the virulence factors of salmonella typhi?

A

gram -ve endotoxin, VI antigen
invasin- allows intracellular growth- can evade host’s IS as taken up by macrohahges and carried to RE system where bacteria multiply IC, causing lymphoid hyperplasia and hypertrophy, then reenter bowel via liver or GB
fimbriae- adhere to epithelium over ileal lymphoid tissue- Peyer’s patches, then go to RE sytem

217
Q

treatment for enteric fever

A

used to be cloramphenicol, then ampicillin or co-trimoxazole, resistance led to ciprofloxacin use, but now resitance to that, so use ceftriaxone- also used in meningococcal meningitis, or azithromycin

218
Q

incubation period for typhoid fever?

A

7-14 days

219
Q

symptoms of typhoid fever?

A 
fever
abdominal discomfort
headache
constipation
dry cough
220
Q

examination of typhoid fever?

A

fever
hepatosplenomegaly
relative bradycardia
rash on trunk

221
Q

investigations of typhoid fever?

A

FBC- moderate anaemia, relative lymphopenia
serology- antibody detection
LFTs- increased AST and ALT
blood and faeces culture

222
Q

prevention of typhoid fever?

A

food and water hygiene precautions
typhoid vaccine- high-risk travel and larboratory personnel, Vi capsular polysaccharide antigen- parenteral, or live attenuated vaccine- oral

223
Q

what may act as a common source of infection?

A 
food
water
air
surfaces
animal
224
Q

compare antigenic drift and shift*

A

drift- antigen change, can cause an epidemic

shift- virus undergoes major genetic change e.g. gene reassortment, which can cause a pandemic

225
Q

which infections tend not to be transmitted from person to person?

A

food poisoning e.g. camplyobacter jejuni- unlikely that another person will contract infection from stools
legionella pneumophila infection
avian flu- influenza- H5N1
rabies

226
Q

What will determine the control mechanisms needed for infection?

A

how far the infection can spread

227
Q

how could environmental contamination be reduced for C difficile infection spread by faecal oral rounte?

A

use chloride containing agents for disinfection

228
Q

how should a patient with multi-drug resistant (rifampicin, isoniazid, pyrazinamide, ethambutol) TB be isolated in a hospital environ?

A

-ve pressure facilities in room so air can flow in but cannot leave the room

229
Q

control measures for infections spread by inhalation route in a hosptial?

A

side room isolation
-ve pressure facilities
use of face masks by HCPs, visitors, and the patient if they are moved rooms

230
Q

what are endemic infections?

A

transmitted at a fairly constant rate in a particular area, so usual background rate

231
Q

what is an outbreak of infection?

A

2 or more cases linked in time and place, so more cases seen in a very specific setting, in a relatively short period of time

232
Q

what is an epidemic?

A

rate of infection greater than usual background rate

233
Q

Pandemic?

A

very high rate of infection, spreading across many regions, countries, continents

234
Q

what is the basic reproduction rate (R0) ?

A

average no. cases 1 case generates over course of its infectious period, in an otherwise uninfected, non-immune pop.

235
Q

How can pertussis toxin interfere with GPCRs?

A

causes ADP ribosylation of Gi type G proteins, stopping GDP/GTP exchange, so GTP doesn’t bind, hence signalling pathway shut off

236
Q

what are outbreaks,epidemics/pandemics result of?

A

result of changes in pathogen/patient/place

237
Q

how can pathogen changes cause an epidemic?

A

prod of new virulence factors e.g. C diffice- toxins A and B= protein complexes, A= enterotoxin, B= cytotoxin
new antigens people not immune to e.g. influenza- swine-H1N1
new antimicrobial resistance genes e.g. MRSA- new penicillin binding protein encoding different transpeptidase enzyme

238
Q

how can patient changes cause an epidemic?

A

new, non-immune hosts e.g. may enter environement where humans not been before, or short-lived immunity e.g. bordatella pertussis- more and more non-immune people come into contact as no.s previously kept down by vaccinating children
healthcare advances e.g. central lines- breach skin- allow coagulase -ve oragnisms to enter blood

239
Q

how can practice changes, allowing pathogen and patient to come together, cause outbreaks of infection?

A

lifestyle- sexual practices

engineering- air cond.- legionella pneumophila

240
Q

what is the infectious dose and why does it vary?

A

number of microbes required to cause infection
varies by microbe, presentation of microbe e.g. protein covering, and immunity of potential host e.g. limited sites for microbe binding will confer resistance

241
Q

where can interventions be implemented using infection model to prevent infection?

A

stop pathogen
stop patient
stop pathogen and patient from causing infection once come together
stop infection spread from person to person

242
Q

what is infection prevention based on in simple terms?

A

pathogen
patient
practice place

243
Q

how can we eradicate a vector to stop pathogen causing infection?

A

eliminate vector breeding sites

244
Q

how can we eradicate a pathogen

A

sterilisation- single use equipment, gamma rays in instrument prod., pressure cook instrument to be used again
decontamination- commodes, reduce faecal oral transmission and direct contact
disinfection- antibacterials- reduce bacteria carried on patients skin- clean inpatients, reduce risk of wound infection by disinfecting skin pre-op, reduce person to person transmission

245
Q

bad consequences of infection prevention mechansims?

A

reduce pathgoen exposure- reduce immune status- reduced antibody- increased suceptibility- outbreak
later average age of exposure- increased severity- e.g. polio, hepA, chicken pox, congenital rubelle syndrome- mother rubella in pregnancy, may cause PDA in child

246
Q

where does the thoracic duct drain into?

A

the left subclavian vein

247
Q

which white cells are important as first line of defence?

A

neutrophils

248
Q

where does the r lymphatic duct drain into?

A

R subclavian vein

249
Q

what is a hickman line?

A

An artificial plastic line inserted through the skin and directly into the vascular system. This is a source of direct entry for micro-organisms. In addition it provides an artificial surface within the body for organisms to attach to.

250
Q

what is CRP?

A

C reactive protein
an acute phase protein
produced by the liver
production stimulated by macrophages as microbial toxins – e.g. endotoxin – triggers the production of cytokines by monocytes and macrophages. These in turn circulate in the blood to the liver where they stimulate the production of the acute phase proteins.

251
Q

what is the role of CRP in the innate immune response?

A

acts as an opsonin- coats microbes promoting their phagocytosis with enhanced attachment of phagocytes and clearance of the microbe

252
Q

why can a fungal infection not be diagnosed just from a blood culture?

A

fungal infections often localised

253
Q

what is the cell wall of fungi composed of?

A

chitin

254
Q

why do standard antibiotics not target fungi?

A

different cell wall to bacteria targeted by antibiotics

255
Q

where does aspergillus- a mould- assoc. with pulmonary aspergillosis in CGD, commonly reside?

A

found in dust in buildings

256
Q

if a blood viral titre shows varicella-zoster IgG +ve in a 50 yr old man, what does this indicate?

A

this indicates the patient is immune to the virus as he has produced antibodies against it, and so probably had chickenpox as a child

257
Q

specific treatment of shingles if patient immunocompromised?

A

aciclovir

258
Q

confusing presentation of shingles?*GI

A

RIF pain as involvement of proximal part of somatic nerve referring pain to distal dermatome of that nerve

259
Q

what microbial structure is recognised by the innate IS?

A

pathogen associated molecular patterns (PAMPs)

260
Q

what cannot be achieved by passive immunisation?

A

immunological memory

261
Q

which cells control antibody synthesis and isotype switching?

A

B cells

262
Q

which surface molecules does HIV interact with?

A

CD4

chemokine receptors CXCR4 and CCR5

263
Q

3 benefits of early HAART in HIV?

A

decrease in HIV symptoms
reduction of disease progression
lower risk of drug resistance

264
Q

important antigens for successful renal grafting?

A

MHC

ABO red cell

265
Q

give examples of 2 live vaccines

A

BCG

oral polio

266
Q

what immunity is lacking if reduced response to previous vaccines?

A

adaptive: B cells and antibodies

267
Q

cytokine released in latent infection of TB?

A

Interferon gamma- produced by T helper 1 cells= delayed type IV hypersensitivity

268
Q

why is passive immunisation useful?

A

provides immediate protection

provides antibody more rapidly

269
Q

name given to disease in asplenic patient due to increased susceptibility to encapsulated bacteria?

A

overwhelming pneumococcal septicaemic illness (OPSI)

270
Q

function of APCs?

A

present antigen to T and B cells in order to mount an immune response as T cells unable to respond to antigen unless presented by an APC

271
Q

why are APCs located in strategic areas?

A

to maximise interaction between APCs and T cells and B cells

272
Q

why do B cells present antigens to T helper cells?

A

cells enable B cells to become plasma cells

273
Q

how has the adaptive immune response been used for medical achievements?

A

disease prevention-vaccination
immunoglobulin therapies e.g. for primary immunodeficiences e.g. CVID
immediate protection- passive immunisation- antibody transfer e.g. diptheria
diagnostic tests- infectious disease, AI disease and blood type and HLA types, all antibody-based

274
Q

roles of the IS?

A

pathgoen recognition
regulates itself
contain or eliminate infection
remember pathogens

275
Q

what TLR (pattern recognition receptor) recognises LPS endotoxin?

A

TLR4

276
Q

What TLR recognises peptidoglycan in gram +ve bacteria?

A

TLR2

277
Q

why does opsonisation allow an enhanced clearance of microbes?

A

phagocytosis is promoted as phagocytes have receptors for opsonins and so there is increased recognition by the phagocyte

278
Q

give 4 examples of opsonins

A

C3b, CRP, IgG, IgM

279
Q

in what type of bacteria are opsonins important?

A

encapsulated

280
Q

give 4 different examples of areas in which cytokines can act?

A

liver- opsonin prod e.g. CRP
BM- increase neutrophil number
inflammation- vasodilation, increases vascular permeability and adhesion molecules for neutrophil attraction
hypothalamus- increase body temp

281
Q

give 4 different examples of areas in which cytokines can act?

A

liver- opsonin prod e.g. CRP
BM- increase neutrophil number
inflammation- vasodilation, increases vascular permeability and adhesion molecules for neutrophil attraction

282
Q

what is chediak higashi syndrome?

A

reduced function of neutrophils as no phagolysosome formation

neutrophil function also reduced in CGD

283
Q

symptoms of varicella-zoster virus infection when patient is contagious?

A

fever

rash

284
Q

where is varicella-zoster virus found in its latent state?

A

ganglia

285
Q

describe response of IS to varicella-zoster virus

A

Innate Immune system:
A number of the general features of barriers help prevent viral infections.
Viral infected cells can produce cytokines (Interferon) that are secreted and helps to protect surrounding cells.

Adaptive Immune response
Viral PAMPs :pathogen-associated molecular patterns
These are recognised by antigen-presenting cells which has pattern recognition receptors (PRRs).
The antigen-presenting cells process and present the viral PAMPS via MHC class I molecules.
They are presented to T cells
They activate CD4 T cells , which produce CD4 T helper 1 cells, which help activate CD8 cytotoxic T cells
They activate CD8 T cells
Results in cell-mediated immunity with:
• killing of infected cells by cytotoxic T cells and Natural Killer cells
• phagocytosis by macrophages
• antibody production by plasma cells in response to B cell activation by T helper cells

286
Q

how is a rash produced by VZ virus?

A

it escapes ganglia and invades the skin

287
Q

what are some of the virulence factors of Staph. aureus?

A

Cell wall virulence factors: The polysaccharide capsule and Protein A in the cell wall inhibit phagocytosis
Exotoxins: Staphylococci can produce exotoxins that attack red blood cells
Superantigen exotoxins: These toxins can activate T cells and may result in ‘toxic-shock syndrome’. Some toxins cause diarrhoea, some affect the skin with peeling of the skin (scalded skin syndrome)

288
Q

infections a SCID host is susceptible to?

A 
pneumocystis pneumonia
epstein-barr virus
cytomegalovirus
herpes
varicella-zoster
289
Q

what latent infections can become reactivated in IC host?

A

TB
VZ
cytomegalovirus
epstein-barr virus

290
Q

management of primary antibody deficiencies?

A

Ig replacement therapy
prompt/prophylactic antibiotics
resp function management e.g. postural drainage of mucus in bronchiectasis
avoid unecessary exposure to radiation e.g. CT scans

291
Q

managment of phagocyte deficiencies?

A

stem cell transplantation
prophlylactic antibiotics and anti-fungals- e.g. for aspergillosis
interferon G -CGD
steroids- CGD

292
Q

tment for CGD?

A

steroids

interferon G

293
Q

management of Digeorge syndrome?

A 
no live vaccines e.g. BCG and oral polio
use only X-irradiated and CMV (-) blood
BM transplantation
supplement to correct hypocalcaemia
if T cell count less than 4 cell per microlitre, then pneumocytstis prophylaxis with antibiotics
neonatal cardiac surgery
294
Q

tment of secondary immune deficinecies?

A

treat underlying cause

treat suspected neutropenic sepsis as acute ME and offer empiric antibiotic therapy immed

295
Q

FH of primary immunocompromised patient?

A

unexplained death

296
Q

IDs: types of organisms assoc with T and B cell deficiencies?

A

T cell: bacteria and viruses

B cell: bacteria and fungi

297
Q

laboratory investigation of immunodeficiency?

A

FBC and differential
exclusion of secondary immunodeficiency

tests of humoral immunity (antibody)- IgG, IgA, IgM, with or without IgE, IgG subclasses 1-4. IgG levels to previous vaccines e.g. pneumococcus, rubella, measure antibody in response to test immunisation

tests for cell mediated immunity- lymphocyte count- FBC, subset analysis- CD4, CD8, Nk and B cells, in vitro tests of T cell function

tests for phagocytic cells- neutrophil count- FBC, neutrophil function tests, adhesion molecule expression for LAD

complement tests- components and function

definitive tests: molecular testing and gene mutations

298
Q

4 STIs?

A

syphillis
gonorrhoea
HIV
chlamydia

299
Q

when might episodes of hereditary angioedema be triggered?

A

trauma
drugs
infection

300
Q

describe hepatitis B

A

dsDNA enveloped virus

301
Q

transmission of Hep B?

A

blood borne virus- transmitted by unprotected sex and IV drug use

302
Q

presenting symptoms and signs of patient with Hep B?

A 
jaundice
clubbing
ascites
fever
nausea
vomiting
malaise
dark urine- investigation
RUQ pain
leuconychia
303
Q

Hep B prevention?

A

vaccination- generalised and targeted- e.g. HCPs
safe sex
mother to child interventions e.g. Igs to child at birth and vaccination of baby immediately after birth, antivirals to mother
screening blood/products
post exposure prophylaxis- needlestick injury

304
Q

which Hep infection is there a greatly increased risk of hepatocellular carcinoma?

A

Hep B

305
Q

investigations of HepB

A 
LFTs
FBC
Us and Es
cancer screen
image liver- ultrasound, MRI
306
Q

tment of Hep B?

A

interferon

tenofovir

307
Q

which hep viruses do we have vaccinations for?

A

Hep A and B

308
Q

why do B cells present antigens to T cells?

A

so T cells can help with isotype switching- CD4+TH2 cells

309
Q

problem with detecting patient with blood borne viruses?

A

asymptomatic period where patient feels fine but is infectious and so can transmit infection to other people

310
Q

how does HIV work?

A

binds to host CD4 cells as can use its viral envelope to gain entry via CD4 glycoprotein. enters cell and uses reverse transcriptase to make DNA from RNA, DNA then incorporated into host cells nucleus, then reproduction of viral components, assembly of new HIV viruses, and then release.

311
Q

how might a patient with primary HIV (few wks after infection) present?

A 
fever
weight loss
rash
flu-like illness
pharyngitis
generalised lymphadenopathy
312
Q

how long is the latent period in HIV?

A

10 yrs- stable virus level, susceptible to opportunisitic infections

313
Q

taking history from a patient with HIV?

A

PMH: infections like shingles or oral thrush- SPUR
DH: interactions with anti-virals
SH: sex history, IV drugs, travel
FH: have family members dies unexpectedly

314
Q

how is HIV diagnosed?

A

blood test for antibodies and antigen

315
Q

investigations for HIV?

A

CXR- opportunistic
FBC
status of IS

316
Q

why treat HIV?

A 
prevent HIV related disease
reduce morbidity and mortality
improve life quality
prevent resistance
prevent transmission
317
Q

reduce risk of HIV transmission to child in pregancy?

A

mother given antiretrovirals and casarrean section

318
Q

problem with being HIV antibody +ve?

A

antibodies not effective in eliminating the infection

319
Q

why would you advise a Hep B patient to not drink alcohol?

A

as toxic, can cause further damage to liver, may promote development of liver cirrhosis- irreversible liver damage,- problem of PH, hepatocellular carcinoma and LF

ESA Revision (15 decks)

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