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MBChB Year 3 > Week 7 - Clinical Microbiology 2 > Flashcards

Week 7 - Clinical Microbiology 2 Flashcards

1
Q

What are the 2 types of bacterial GI infections?

A
  1. Infection

2. Intoxication (poisoning)

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2
Q

Describe the Bacterial GI infection category?

A
  • Bacterial pathogens develop in the gut after ingestion of contaminated food
  • Examples: Salmonella, Campylobacter, pathogenic E. coli
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3
Q

What is the incubation period of the Bacterial GI infection category?

A

At least 8-12hr before symptoms develop

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4
Q

Describe the Bacterial GI intoxication category?

A
  • Bacterial pathogens grow in foods & produce toxins

- Examples: Bacillus cereus, Staphylococcus aureus

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5
Q

What is the incubation period of the Bacterial GI intoxication category?

A

Relative short incubation time (few hrs) because of preformed toxin in food

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6
Q

What is Diarrhoea?

A
  • Abnormal frequency &/or fluid stool
  • Causes fluid & electrolyte loss
  • Severity varies widely from mild self-limiting to severe/fatal
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7
Q

What does diarrhoea indicate?

A

Usually small bowel disease

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8
Q

Describe Gastroenteritis?

A

Nausea, vomiting, diarrhoea & abdominal discomfort

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9
Q

Describe Dysentery?

A
  • Inflammatory disorder of the large bowel
  • Blood & pus in faeces
  • Pain, fever & abdo cramps
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10
Q

Describe Enterocolitis?

A

Inflammatory process affecting small & large bowel

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11
Q

What toxins can cause manifestations of GI infections within the GI tract (GIT)?

A
  1. Toxin effects e.g. cholera

2. Inflammation due to microbial invasion e.g. shigellosis

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12
Q

What toxins can cause manifestations of GI infections outwith the GI tract (GIT)?

A
  1. Systemic effect of toxins e.g. STEC

2. Invasive infection of GIT with wider dissemination e.g. metastatic salmonella infection

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13
Q

What is the barrier to GI infections in the mouth?

A

Lysozyme

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14
Q

What is the barrier to GI infections in the stomach?

A

Acid pH

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15
Q

What are the 6 barriers to GI infections in the Small intestine?

A
  1. Mucous
  2. Bile
  3. Secretory IgA
  4. Lymphoid tissue (Peyer’s patches)
  5. Epithelial turnover
  6. Normal flora
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16
Q

What are the 2 barriers to GI infections in the Large intestine?

A
  1. Epithelial turnover

2. Normal flora

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17
Q

Describe the normal GIT flora?

A
  • 99% anaerobes
  • Still many important facultative organisms particularly Enterobacteriaceae e.g. E.coli, Proteus spp
  • Protective & metabolic function
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18
Q

What does each gram of faeces contain?

A

100,000,000,000 (10*10) microbes

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19
Q

What part of the GIT is very rich in microbial flora?

A

Lower GIT

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20
Q

What weight of bacteria are in the gut?

A

1kg of bacteria

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21
Q

What are the 3 types of sources of GI infections?

A
  1. Zoonotic
  2. Human carriers ie. Typhoid
  3. Environment sources
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22
Q

What are the 2 types of Zoonotic sources of GI infections?

A
  1. Symptomatic animals- Economic cost e.g. Salmonella Dublin

2. Asymptomatic shedders- E.g. reptiles & salmonella carriage, E.coli O157 in cattle

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23
Q

Describe the environmental sources of GI infections?

A

Contamination of soil & produce E.g. Listeria, E.coli O157

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24
Q

What are the 3 types of transmission of GI infections?

A
  1. Faecal-oral
  2. 3 F’s= food, fluids, fingers
  3. Person-to-person
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25
Q

Describe the 3F’s transmission of GI infections?

A
  1. Food- contamination (farm to fork), cross-contamination (distribution chain or domestic kitchen)
  2. Fluids- water, contaminated juices etc
  3. Fingers- importance of washing hands (after toileting, before & after preparing or consuming food and drinks)
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26
Q

Describe Person-to-person transmission of GI infection?

A
  • Infectious dose

- Ability to contaminate & persist in the environment

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27
Q

Even though aetiological diagnosis of GI infection cannot be made from a history, what are the useful clues you can get?

A

Vomiting, abdominal pain, diarrhoea, frequency & nature of symptoms, travel history, food history, other affected individuals, speed of onset of illness, blood in stools

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28
Q

Describe the Enrichment broth used in the lab to diagnose GI infection?

A

Contains nutrients that promote preferential growth of the pathogen

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29
Q

Describe the Selective media used in the lab to diagnose GI infection?

A

Suppress growth of background flora while allowing growth of the pathogen

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30
Q

When would you use antibiotics for GI infections?

A

Antibiotic treatment reserved for severe/prolonged symptoms

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31
Q

List the 4 negative effects of antibiotics on GI infections?

A
  1. May prolong symptom duration
  2. May exacerbate symptoms
  3. Promotes emergence of antibiotic resistance
  4. May actually be harmful e.g. STEC infection
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32
Q

What are the 4 general means of controlling GI infections?

A
  1. Adequate public health measures
  2. Education in hygienic food preparation
  3. Pasteurisation of milk & dairy products
  4. Sensible travel food practices
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33
Q

Describe the microbiology of Campylobacter?

A
  • Microaerophilic and thermophilic (42oC)

- Culture on Campylobacter selective agar

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34
Q

What type of bacteria is Campylobacter?

A

Curved Gram-negative bacilli

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35
Q

What is the most important species of Campylobacter?

A

C. jejuni

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36
Q

What is the commonest bacterial food borne infection in the UK?

A

Campylobacter 1

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37
Q

Describe the epidemiology of Campylobacter?

A
  • Large animal reservoir (poultry, cattle, sheep, rodents & wild birds)
  • Marked seasonal peaks of infection in May & September
  • Large point source outbreaks uncommon (doesn’t multiply in food)
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38
Q

How is Campylobacter infection transmitted?

A
  • Via contaminated food (esp. poultry), milk or water

- Person-to person spread rare

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39
Q

What % of raw retail fresh chicken is contaminated with Campylobacter?

A

~70%

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40
Q

Describe the pathogenesis of Campylobacter?

A
  • Inflammation, ulceration & bleeding in small & large bowel
  • Bacteraemia can occur (extremes of age, immunocompromised)
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41
Q

What can Campylobacter rarely cause?

A

Post-infectious demyelination syndrome (Guillain-Barre),

characterised by ascending paralysis

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42
Q

List the 4 clinical signs & symptoms of Campylobacter?

A
  1. Bloody diarrhoea
  2. Cramping abdominal pain
  3. Vomiting is not usually a feature
  4. Fever
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43
Q

Describe the treatment of Campylobacter infection?

A
  • Fluid replacement
  • Clarithromycin for severe/persistent disease
  • Quinolone (e.g. ciprofloxacin) or aminoglycoside (e.g. gentamicin) for invasive disease
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44
Q

What are the 2 specific control point for Campylobacter infection?

A
  1. Reduction of contamination in raw, retail poultry meat

2. Adequate cooking

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45
Q

What type of bacteria is Salmonella?

A

Gram-negative bacilli

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46
Q

Describe the microbiology of Salmonella?

A
  • Member of the Enterobacteriaceae
  • Non-lactose fermenters
  • XLD plates most commonly used in clinical labs
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47
Q

Describe the epidemiology of Salmonella?

A
  • Found in a wide range of warm & cold blooded animals
  • Secondary spread via person-to-person transmission may be a feature
  • Seasonal peaks in summer and autumn
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48
Q

What are the 2 causal organisms of enteric fever?

A

Salmonella Typhi & Salmonella Paratyphi

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49
Q

How is Salmonella acquired?

A
  • Via contaminated food, especially pork, poultry & other meat & milk/dairy products
  • Waterborne infection less common
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50
Q

Describe the pathogenesis of Salmonella?

A
  • Diarrhoea
  • Bacteraemia can occur (extremes of age, immunocompromised)
  • Distant organs may become seeded to establish metastatic infection e.g. osteomyelitis, septic arthritis, meningitis etc.
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51
Q

Why is there diarrhoea in Salmonella?

A

Due to invasion of epithelial cells in the distal small intestine, & subsequent inflammation

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52
Q

What is the incubation period of Salmonella?

A

12-72 hrs

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53
Q

List the clinical signs & symptoms of Salmonella?

A
  1. Watery diarrhoea
  2. Vomiting is common
  3. Fever can occur, & is usually associated with more invasive disease
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54
Q

What is the duration of Salmonella infection?

A

2-7 days

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55
Q

Describe the treatment of Salmonella infection?

A
  • Fluid replacement
  • Antibiotics reserved for severe infections & bacteraemia
  • Antibiotics & antimotility agents prolong excretion of salmonellae in the faeces
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56
Q

What are the 3 types of antibiotics that you can use for severe Salmonella infections?

A
  1. Beta-lactams
  2. Quinolones
  3. Aminoglycoside
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57
Q

What is the specific control point for Salmonella infections?

A

The introduction of immunisation of poultry flocks lead to a dramatic reduction in S.Enteritidis in the UK

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58
Q

What type of bacteria is Shigella?

A

Gram-negative bacilli

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59
Q

Describe the microbiology of Shigella?

A
  • Member of the Enterobacteriaceae
  • 4 species
  • Non-lactose fermenters (useful in differential media)
  • XLD plates most commonly used in clinical labs
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60
Q

What are the 4 species of Shigella & what are the associated with?

A
  1. Shigella sonnei associated with milder infections
  2. Shigella boydii & S. flexneri associated with more severe disease
  3. Shigella dysenteriae associated with most severe disease
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61
Q

Describe the epidemiology of Shigella?

A
  • S.dysenteriae in developing world
  • Large outbreaks can occur
  • Does not persist in the environment (unlike V. cholerae)
  • Contaminated food and water less important
  • Recent outbreaks associated with MSM
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62
Q

What is Shigella mainly associated with

A

Diarrhoeal disease in children

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63
Q

What is the transmission of Shigella?

A

Person-to-person spread via faecal-oral route is most important- associated with low infectious dose

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64
Q

What is the only reservoir for Shigella?

A

Humans

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65
Q

Describe the pathogenesis of Shigella?

A
  • Organisms attach to & colonise mucosal epithelium of terminal ileum & colon
  • Systemic invasion is not a feature
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66
Q

What describe the pathogenesis of S.dysenteriae species of Shigella?

A

Produces a potent protein exotoxin (Shiga toxin) which not only damages intestinal epithelium, but in some patients targets glomerular endothelium causing renal failure as part of haemolytic-uraemic syndrome (HUS)

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67
Q

What is the incubation period for Shigella?

A

1-3 days

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68
Q

What is the duration of Shigella infection?

A

2-7 days

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69
Q

List the 5 clinical signs & symptoms of Shigella?

A
  1. Dysentery
  2. Initially watery diarrhoea followed by bloody diarhoea
  3. Marked, cramping abdominal pain
  4. Vomiting is uncommon
  5. Fever is usually present
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70
Q

Describe the treatment of Shigella?

A
  • Usually self-limiting

- Fluid replacement is usually sufficient

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71
Q

What will some cases of S.dysenteriae infection require?

A

Treatment of renal failure

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72
Q

What is the specific control point for Shigella?

A

Only found in humans, so good standards of sanitation & personal hygiene are key measures

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73
Q

What type of bacteria is Vibrio cholerae?

A

Comma-shaped Gram-negative bacilli

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74
Q

Describe the microbiology of Vibrio cholerae?

A
  • Serotypes defined on basis of “O” antigens
  • Sucrose-fermenter
  • Thiosulphate-bile sucrose selective/differential medium
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75
Q

Give to examples of Vibrio cholerae serotypes?

A
  1. SerotypeO1- Classical, El Tor (less severe disease, more carriage, better persistence in environment)
  2. SerotypeO139
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76
Q

What is the transmission of Vibrio cholerae?

A
  • Spreads via contaminated food or water

- Direct person-to-person transmission uncommon

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77
Q

Describe the pathogenesis of Vibrio cholerae?

A
  • Flagellae & mucinase facilitate penetration of intestinal mucous
  • Attachment to mucosa by specific receptors
  • Diarrhoea due to production of a potent protein exotoxin
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78
Q

What is the main clinical symptom of Vibrio cholerae?

A

Severe, profuse, non-bloody, watery diarrhoea (rice water stool)

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79
Q

What 4 things does the profound fluid loss & dehydration in Vibrio cholerae precipitate?

A
  1. Hypokalaemia
  2. Metabolic acidosis
  3. Hypovolaemic shock
  4. Cardiac failure
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80
Q

Describe the treatment of Vibrio cholerae?

A
  • Prompt oral or IV rehydration is lifesaving (mortality reduced to <1%)
  • Tetracycline antibiotics may shorten duration of shedding
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81
Q

What are the 2 specific control point for Vibrio cholerae?

A
  1. No animal reservoir

2. Clean drinking water supply & proper sanitation are key preventative measures

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82
Q

What type of bacteria is Escherichia coli?

A

Gram-negative bacilli

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83
Q

Escherichia coli is a member of _________?

A

Enterobacteriaceae

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84
Q

What is Escherichia coli an important component of?

A

Gut flora of man & animals

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85
Q

List the 6 different diarrhoeagenic groups of E.coli?

A
  1. Enteropathogenic E. coli (EPEC)
  2. Enterotoxigenic E. coli (ETEC)
  3. Enterohaemorrhagic E. coli (EHEC)
  4. Enteroinvasive E.coli (EIEC)
  5. Entero-aggregative E.coli (EAEC)
  6. Diffuse aggregative E.coli (DAEC)
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86
Q

What do some strains of normal gut Escherichia coli posses?

A

Virulence factors which enable them to cause infections

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87
Q

Describe the microbiology of Enteropathogenic E. coli (EPEC)?

A
  • No differential media available
  • Test selection of colonies using polyvalent antisera for common EPEC 􏱠”O􏰅” types
  • Not routinely done
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88
Q

Describe the epidemiology of Enteropathogenic E. coli (EPEC)?

A
  • Sporadic cases & outbreaks of diarrhoea in infants & children
  • Cause of some cases of 􏱠traveller􏰎s􏰅 diarrhoea
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89
Q

Describe the pathogenesis of Enteropathogenic E. coli (EPEC)?

A

Initial adherence via pili, followed by formation of characteristic 􏱠attatching & effacing􏰅 lesion mediated by intimin protein and Tir (translocated intimin receptor) with disruption of intestinal microvilli

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90
Q

List the 4 clinical signs & symptoms of Enteropathogenic E. coli (EPEC)?

A
  1. Watery diarrhoea
  2. Abdominal pain
  3. Vomiting
  4. Often accompanied by fever
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91
Q

Describe the 2 plasmid-encoded toxins that cause diarrhoea in Enterotoxigenic E. coli (ETEC)?

A
  1. Heat-labile (LT)- Structural & functional analogue of cholera toxin
  2. Heat-stable (ST)- Produced in addition to or instead of LT, similar mode of action
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92
Q

Describe the microbiology of Enterotoxigenic E. coli (ETEC) infection?

A
  • No differential media available
  • Test liquid cultures for production of toxins by immunoassays
  • Not routinely done
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93
Q

List the 4 clinical signs & symptoms of Enterotoxigenic E. coli (ETEC) infection?

A
  1. Watery diarrhoea
  2. Abdominal pain
  3. Vomiting
  4. No associated fever
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94
Q

Describe the microbiology of Enterohaemorrhagic E. coli (EHEC)?

A
  • More than 100 serotypes
  • Best known is E.coli O157:H7
  • O157 is a non-sorbitol fermenter. Sorbitol MacConkey agar (SMAC)
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95
Q

Describe the epidemiology of Enterohaemorrhagic E. coli (EHEC)?

A
  • Outbreaks & sporadic cases worldwide (~250 cases/year in Scotland)
  • Large animal reservoirs (esp. cattle & sheep)
  • Persistent in environment
  • Secondary person-to-person spread important (associated with low infectious dose)
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96
Q

How is Enterohaemorrhagic E. coli (EHEC) transmitted?

A
  • Consumption of contaminated food, water & dairy products
  • Direct environmental contact with animal faeces e.g. petting zoos
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97
Q

Describe the pathogenesis of Enterohaemorrhagic E. coli (EHEC)?

A
  • Attaching & effacing lesion (similar to EPEC)

- Production of Shiga-like toxins

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98
Q

Describe the shiga-like toxins produced by Enterohaemorrhagic E. coli (EHEC)?

A

Structural & functional analogue of Shigella dysenteriae toxin, sometimes strains called STEC (shiga-toxin producing EC) or VTEC (verotoxin- producing EC) because toxins are toxic for cultured vero cells

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99
Q

List the 4 clinical signs & symptoms of Enterohaemorrhagic E. coli (EHEC)?

A
  1. Bloody diarrhoea
  2. Abdominal pain
  3. Vomiting
  4. No associated fever
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100
Q

What can occur clinically in 5-10% of Enterohaemorrhagic E. coli (EHEC) cases?

A

Haemolytic uraemic syndrome (5-10% of cases)

  • Microangiopathic haemolytic anaemia
  • Thrombocytopaenia
  • Acute renal failure
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101
Q

What is the commonest cause of acute renal failure in children in the UK?

A

Enterohaemorrhagic E. coli (EHEC)

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102
Q

What are the 2 key causes of diarrhoea in children in the developing world?

A
  1. EPEC

2. ETEC

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103
Q

What may ETEC mimic clinically?

A

Cholera

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104
Q

What is the treatment of E.coli infections?

A
  • Adequate rehydration
  • Antibiotics not indicated, & in the case of EHEC may increase risk of HUS
  • Antimotility agents also increase HUS risk
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105
Q

What type of bacteria is Staphylococcus aureus?

A

Gram-positive cocci

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106
Q

What do 50% of Staphylococcus aureus produce?

A

Enterotoxins (types A-E)

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107
Q

Describe the pathogenesis of Staphylococcus aureus produce?

A
  • Food is contaminated by human carriers
  • Especially cooked meats, cakes and pastries
  • Bacteria multiply at room temperature & produce toxins
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108
Q

Describe the enterotoxins produced by Staphylococcus aureus?

A

Heat stable & acid-resistant protein toxins

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109
Q

What is the incubation period of Staphylococcus aureus?

A

30 mins- 6hrs

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110
Q

What is the duration of Staphylococcus aureus infection?

A

12-24 hrs

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111
Q

List the 3 clinical signs & symptoms of Staphylococcus aureus?

A
  1. Profuse vomiting
  2. Abdominal cramps
  3. No fever & no diarrhoea
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112
Q

What is the treatment for Staphylococcus aureus?

A

Self-limiting disease

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113
Q

List the 2 specific controls for Staphylococcus aureus?

A
  1. Hygienic food preparation to minimise contamination

2. Refrigerated storage

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114
Q

What type of bacteria is Bacillus cereus?

A

Aerobic, spore-forming Gram-positive bacilli

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115
Q

Would you test for Bacillus cereus?

A

NO

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116
Q

Describe the pathogenesis of Bacillus cereus?

A

Spores & vegetative cells contaminate wide range of foodstuffs

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117
Q

What are the 2 types of Bacillus cereus diseases?

A
  1. Emetic disease

2. Diarrhoeal disease

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118
Q

Describe the pathogenesis of Bacillus cereus Emetic disease?

A
  • Typically associated with fried rice
  • Spores survive initial boiling
  • If rice is bulk cooled & stored prior to frying, the spores germinate, multiply and re-sporulate
  • Protein enterotoxin produced during sporulation
  • Heat stable toxin survives further frying
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119
Q

Describe the pathogenesis of Bacillus cereus Diarrhoeal disease?

A
  • Spores in food survive cooking, germinate & organisms multiply in food
  • Ingested organisms produce a heat-labile toxin in the gut with similar mode of action to cholera toxin
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120
Q

List the 4 clinical signs & symptoms of Bacillus cereus Emetic disease?

A
  1. Profuse vomiting
  2. Abdominal cramps
  3. Watery diarrhoea
  4. No fever
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121
Q

List the 4 clinical signs & symptoms of Bacillus cereus Diarrhoeal disease?

A
  1. Watery diarrhoea
  2. Cramping abdominal pain
  3. No vomiting
  4. No fever
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122
Q

What is the treatment for Bacillus cereus?

A

Self-limiting disease

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123
Q

What type of bacteria is Clostridium perfringens?

A

Anaerobic, spore-forming Gram-positive bacilli

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124
Q

Would you test for Clostridium perfringens?

A

NO

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125
Q

Describe the epidemiology of Clostridium perfringens?

A
  • Spores & vegetative cells ubiquitous in soil & animal gut
  • Contaminated foodstuff (usually meat products)
  • Often involves bulk-cooking of stews, meat pies
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126
Q

Describe the pathogenesis of Clostridium perfringens?

A
  • Spores survive cooking, germinate & organisms multiply in cooling food
  • Food inadequately re-heated to kill organisms
  • Organisms ingested & sporulate in large intestine with production of enterotoxin
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127
Q

List the 3 clinical signs & symptoms of Clostridium perfringens?

A
  1. Watery diarrhoea
  2. Abdominal cramps
  3. No fever & no vomiting
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128
Q

What is the treatment for Clostridium perfringens?

A

Self-limiting disease

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129
Q

What are the 2 specific controls of Clostridium perfringens?

A
  1. Rapid chilling/freezing of bulk-cooked foods

2. Thorough re-heating before consumption

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130
Q

What type of bacteria is Clostridium botulinum?

A

Anaerobic, spore-forming Gram-positive bacilli

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131
Q

Describe the microbiology of Clostridium botulinum?

A

Laboratory diagnosis based upon toxin detection

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132
Q

Describe the pathogenesis of Clostridium botulinum?

A
  • Spores & vegetative cells ubiquitous in soil & animal GIT
  • Produces powerful heat-labile protein neurotoxin (types A, B & E cause human disease)
  • Absorbed toxins spread via bloodstream & enter peripheral nerves where they cause neuromuscular blockade at the synapses
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133
Q

What are the 3 types of Clostridium botulinum spread?

A
  1. Foodborne botulism- pre-formed toxin in food. Commonly associated with improperly processed canned foods
  2. Infant botulism- organisms germinate in gut of babies fed honey containing spores, & toxins are produced in gut
  3. Wound botulism- organisms implanted in wound produce toxin
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134
Q

List the 3 clinical signs & symptoms of Clostridium botulinum spread?

A
  • Neuromuscular blockade results in flaccid paralysis & progressive muscle weakness
  • Involvement of muscles of chest/diaphragm causes respiratory failure
  • High mortality if untreated
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135
Q

Describe the treatment of Clostridium botulinum?

A
  • Urgent intensive supportive care due to difficulties breathing and swallowing
  • Antitoxin
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136
Q

List the 4 specific controls of Clostridium botulinum?

A
  1. Proper manufacturing controls in canning industry
  2. Hygienic food preparation
  3. Proper cooking
  4. Refrigerated storage
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137
Q

What type of bacteria is Clostridium difficile?

A

Anaerobic, spore-forming Gram-positive bacilli

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138
Q

Describe the microbiology of Clostridium difficile?

A
  • Spores resistant to heat, drying, disinfection, alcohol

- Clinical features due to production of potent toxins (A+B)

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139
Q

Describe the pathogenesis of Clostridium difficile?

A
  • Spores & vegetative cells ubiquitous in environment
  • Infection requires disruption of the normal “protective” gut flora
  • Major cause of healthcare associated infections
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140
Q

Who does Clostridium difficile predominantly affect?

A

Elderly

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141
Q

Describe Clostridium difficile clinically?

A
  • Mild to severe with abdominal pain

- Relapses are common & may be multiple

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142
Q

What can severe cases of Clostridium difficile develop into?

A

Pseudomembranous colitis (may be fatal)

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143
Q

What can fulminant cases of Clostridium difficile develop into?

A

Colonic dilatation & perforation

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144
Q

What is the treatment for Clostridium difficile?

A
  • Stop precipitating antibiotics
  • Oral metronidazole (mild [0 severity markers])
  • Oral vancomycin (severe [≥ 1 severity markers or no improvement after 5 days metronidazole])
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145
Q

What may refractory recurrent Clostridium difficile disease require?

A

Faecal transplant

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146
Q

What are the 3 specific controls for Clostridium difficile?

A
  1. Antimicrobial stewardship
  2. Infection Prevention & Control measures (source isolation, hand hygiene, PPE)
  3. Cleaning/disinfection with hypochlorite disinfectants
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147
Q

What type of bacteria is Listeria monocytogenes?

A

Gram-positive coccobacilli

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148
Q

Describe the microbiology of Listeria monocytogenes?

A
  • Selective culture media available for culture from suspect foods
  • Standard laboratory for blood & CSF samples
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149
Q

Describe the pathogenesis of Listeria monocytogenes?

A
  • Widespread among animals & environment
  • Pregnant women, elderly & immunocompromised
  • Mortality high
  • Can multiply at 4oC
  • Invasive infection from GIT results in systemic spread via bloodstream
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150
Q

What is Listeria monocytogenes infection associated with?

A

Contaminated foods, especially unpasteurised milk and soft cheeses, pate, cooked meats, smoked fish & coleslaw

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151
Q

Describe the clinical signs & symptoms of Listeria monocytogenes?

A

Initial flu-like illness, with or without diarrhoea

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152
Q

What do majority of Listeria monocytogenes cases present with?

A

Severe systemic infection ie. septicaemia, meningitis

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153
Q

What is the treatment for Listeria monocytogenes?

A

IV antibiotics (usually Ampicillin & synergistic gentamicin)

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154
Q

List the 3 specific controls for Listeria monocytogenes?

A
  1. Susceptible groups should avoid high risk foods
  2. Observe use by dates
  3. Wash raw fruit & vegetables & avoid cross contamination
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155
Q

What type of bacteria is Helicobacter pylori?

A

Gram-negative spiral shaped bacilli

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156
Q

Describe the microbiology of Helicobacter pylori?

A
  • Microaerophilic

- Urease-positive

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157
Q

How do you diagnose Helicobacter pylori?

A
  • Detection of faecal antigen or urea “breath test”

- Serum antibody tests mainly of use in epidemiological surveys of past or current infection

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158
Q

Describe the epidemiology of Helicobacter pylori?

A
  • Faecal-oral or oral-oral
  • Humans are the only reservoir
  • Infection acquired in childhood & persists life long unless treated
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159
Q

What is the pathogenesis of Helicobacter pylori?

A

Complex & involving cytotoxin production, & a range of factors to promote adhesion and colonisation

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160
Q

Describe the clinical signs & symptoms of Helicobacter pylori?

A
  • Infection is asymptomatic unless peptic ulceration develops
  • Now established as cause of >90% of duodenal ulcers & 70-80% of gastric ulcers
  • Gastric cancer risk
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161
Q

What is the treatment for Helicobacter pylori?

A

Combined treatment with a proton pump inhibitor & combinations of antibiotics (clarithromycin & metronidazole) eradicates carriage & facilitates ulcer healing

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162
Q

Pathogenicity determinants are often on what 3 mobile genetic elements?

A
  1. Bacteriophages
  2. Plasmids
  3. Transposons
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163
Q

Describe the effectiveness of current GI infection diagnostics?

A
  • Even if a stool sample is sent diagnostic yield is <50%
  • Reliant on differential/selective media
  • Lack sensitivity
  • Not available for may organisms/pathotypes
  • Expensive, demanding & slow
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164
Q

Describe the future of GI infection diagnostics?

A
  • Rapid expansion of molecular diagnostics
  • Target 􏰎generic􏱠 pathogen groups & pathogenicity genes
  • Rapidly screen for range of pathogens simultaneously (Bacteria, Viruses, Protozoa)
  • Transform ability to understand & control GI infections
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165
Q

What is viral gastroenteritis?

A

Inflammation of the stomach & intestines cases by virus(es)

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166
Q

What are 3 people at higher risk of viral gastroenteritis?

A
  1. Children under age 5
  2. Old age people especially in nursing home
  3. Immunocompromised
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167
Q

What are 5 important viruses that cause gastroenteritis?

A
  1. Norovirus (Norwalk virus)
  2. Sapovirus
  3. Rotavirus
  4. Adenovirus 40 & 41
  5. Astrovirus
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168
Q

Who is usually affected by Norovirus/Sapovirus?

A

Can affect all ages & healthy individuals but often most serious in young & elderly

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169
Q

Who is usually affected by Rotavirus/Adenovirus/Astrovirus?

A

Affects mainly children under 2 years, elderly & immunocompromised

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170
Q

Describe the structure of Norovirus?

A
  • Non enveloped, single stranded RNA virus

- 5 genotypes, only 3 affect humans (GI, GII and GIV)

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171
Q

What is the most common genotype of Norovirus in the UK?

A

GII-4 strain

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172
Q

What are the 3 routes of transmission of Norovirus?

A
  1. Person to Person (faecal-oral, aerosolised e.g. by toilet flush, fomites)
  2. Food-borne
  3. Water
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173
Q

Describe the transmission of Norovirus?

A
  • Infectious dose very small (10-100 virions)
  • Can affect all ages
  • Very stable & may remain viable for long periods of time in the environment
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174
Q

What is the incubation period of Norovirus?

A

24-48 hour

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175
Q

How long can Norovirus shed for?

A

Up to 3 weeks after infection

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176
Q

List the 8 clinical features of Norovirus?

A
  1. Can be asymptomatic
  2. Vomiting
  3. Diarrhoea
  4. Nausea
  5. Abdominal cramps
  6. Headache, muscle aches
  7. Fever (minority)
  8. Dehydration in young & elderly
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177
Q

What is the duration of Norovirus?

A

Usually lasts 12-60 hours

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178
Q

Describe the 4 complications associated with Norovirus?

A
  1. Significant proportion of childhood hospitalisation
  2. Hospital outbreaks lasts longer with an increased risk of mortality
  3. In elderly increased post infection complications
  4. Chronic diarrhoea & virus shedding in both solid organ transplant patients & bone marrow transplant patients
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179
Q

What is the symptomatic treatment for Norovirus?

A
  1. Oral &/or IV fluids
  2. Antispasmodics
  3. Analgesics
  4. Antipyretics
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180
Q

How long does Norovirus immunity last?

A

6-14 weeks

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181
Q

Why has there been issues creating a Norovirus vaccine?

A

Incomplete understanding of immunity & the fact norovirus can’t be cultured

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182
Q

What have reports shown a link to with Norovirus susceptibility?

A

Expression of human histo-blood group antigens (HBGAs) & the susceptibility to norovirus infection

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183
Q

Describe the infection control protocols for Norovirus?

A
  • Isolation or cohorting
  • Exclude symptomatic staff until symptom free for 48 hours
  • Do not move patients
  • Do not admit new patients
  • Thorough cleaning of ward/hotel/cruise ship/bus 48hrs after last case symptomatic
  • Patient/visitor/passenger/guest awareness
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184
Q

What are probably the single most common vector for spread of Norovirus?

A

Contaminated hands

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185
Q

Describe the structure of Rotavirus?

A
  • Double stranded, non enveloped RNA virus
  • 5 predominant strains G1-4, G9
  • 11 strands of RNA so potential for much antigenic variation
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186
Q

What does the GI strain of Rotavirus account for?

A

> 70% infections

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187
Q

Describe the transmission of Rotavirus?

A
  • Low infectious dose (10-100 virus particles)
  • Mainly person to person via feaco-oral or fomites
  • Food & water borne spread is possible
  • Spread via respiratory droplets is speculated
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188
Q

What do clinical manifestations of Rotavirus depend on?

A

If it is the 1st infection or reinfection

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189
Q

What are the 4 symptoms of Rotavirus?

A
  1. Watery diarrhoea
  2. Abdominal pain
  3. Vomiting
  4. Loss of electrolytes leading to dehydration
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190
Q

How long do symptoms of Rotavirus usually last?

A

3-7 days

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191
Q

Describe Rotavirus infections?

A
  • 1st infection after age 3 months is usually the most severe
  • Re-infection can occur at any age
  • Hospital outbreaks in paediatric wards common
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192
Q

List the 5 complications of Rotavirus?

A
  1. Severe chronic diarrhoea
  2. Dehydration
  3. Electrolyte imbalance
  4. Metabolic acidosis
  5. Immunodeficient children may have more severe or persistent disease
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193
Q

Describe immunity associated with Rotavirus?

A
  • 1st Infection doesn’t lead to permanent immunity
  • By age 3, 90% of children have serum antibodies to 1 or more types
  • Young children may suffer up to 5 re-infections by age 2 years of age
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194
Q

What is the vaccine called for Rotavirus?

A

Rotarix® (came out in July 2013)

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195
Q

How effective is Rotarix® vaccine overall?

A

Over 85% effective at protecting against severe rotavirus gastroenteritis in the first 2 years of life

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196
Q

Describe the structure of Adenovirus?

A
  • Double stranded DNA virus

- >50 serotypes causing range of illnesses

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197
Q

What 2 serotypes of Adenovirus cause gastroenteritis?

A

Adenovirus 40 & 41

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198
Q

List the 2 symptoms of Adenovirus gastroenteritis?

A
  1. Fever

2. Watery diarrhoea

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199
Q

What is the treatment for Adenovirus gastroenteritis?

A

Supportive

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200
Q

What is the vaccine for Adenovirus 40 & 41?

A

No vaccine

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201
Q

Describe the structure of Astrovirus?

A

Single stranded, non enveloped RNA virus

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202
Q

What does Astrovirus cause?

A
  • Less severe gastroenteritis than other enteric pathogens

- Infection usually as sporadic cases but can be outbreaks, usually in young children

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203
Q

How can all the viral gastroenteritis be detected by?

A

Polymerase chain reaction (PCR) which detects the DNA or RNA, Testing done at Virology lab, GRI

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204
Q

What 2 samples can be given for viral gastroenteritis diagnosis?

A

Vomit or stool

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205
Q

What are 3 viruses which can replicate in the gut and NOT cause diarrhoea & vomiting?

A
  1. Poliovirus (& all other enteroviruses)
  2. Adenoviruses OTHER THAN types 40 & 41
  3. Hepatitis A/E
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206
Q

What 2 things can an untreated joint infection lead to?

A
  1. Loss of cartilage –> Osteoarthritis in later life

2. Severe sepsis –> Septic shock

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207
Q

Describe the signs & symptoms of Septic Arthritis?

A
  • Single hot joint: Knee 50%, Hip 20%
  • Polyarticular involvement in 10-20% of patients
  • Loss of movement
  • Pain
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208
Q

List the 5 key investigations for septic arthritis?

A
  1. Blood cultures
  2. Joint Aspirate (Gram, microscopy for crystals and culture)
  3. FBC
  4. CRP
  5. Imaging
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209
Q

List 9 common pathogens for septic arthritis?

A
  1. MSSA/MRSA
  2. Streptococci (S. pyogenes, Group G Strep, pneumococcus)
  3. H. influenzae
  4. Kingella
  5. N. meningitidis
  6. N. gonorrhoeae
  7. E.coli
  8. P. aeruginosa
  9. Salmonella species
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210
Q

What is the treatment for Septic Arthritis?

A
  • At least 2 weeks IV antibiotics

- Often 3 weeks IV antibiotics followed by 3 weeks oral

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211
Q

How do you monitor treatment of Septic Arthritis?

A

CRP & clinical

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212
Q

What is Arthroplasty?

A

Putting in an artificial joint

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213
Q

What is Resection arthroplasty?

A

Taking the diseased

joint out & putting in an artificial one

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214
Q

What is Revision arthroplasty?

A

Re-operating on an artificial joint

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215
Q

What is Arthrodesis?

A

Fusing 2 bones together

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216
Q

What is Arthrosis?

A

A joint

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217
Q

What is Pseudo-arthrosis?

A

Allowing 2 bones to articulate against 1 another but without a joint e.g. Girdlestone

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218
Q

List the 7 risk factors for Primary Arthroplasty?

A
  1. Rheumatoid arthritis
  2. Diabetes mellitus
  3. Poor nutritional status
  4. Obesity
  5. Concurrent UTI
  6. Steroids
  7. Malignancy
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219
Q

List the 3 risk factors for Revision Arthroplasty?

A
  1. Prior joint surgery
  2. Prolonged operating room time
  3. Pre-op infection (teeth, skin, UTI)
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220
Q

List the 5 most common microbial etiology for prosthetic joint infections?

A
  1. S. aureus
  2. Coagulase-negative staphylococci
  3. Streptococci
  4. Gram-negative bacilli
  5. Anaerobic organisms
221
Q

What are the 2 different pathogenesis of prosthetic joint infections?

A
  1. Haematogenous Spread (20-40%)

2. Local Spread (60-80%)

222
Q

Describe Local Spread pathogenesis for prosthetic joint infections?

A
  • Mostly organisms from skin surface
  • Direct communication between skin surface & prosthesis while fascial planes heal
  • Usually manifests in immediate post-op period (acute <4 weeks)
223
Q

When do upto 50% of prosthetic joint infections present?

A

2 or more years after surgery (delayed/late >4 weeks)

224
Q

Describe Haematogenous Spread pathogenesis for prosthetic joint infections?

A
  • Presents later
  • Intact surrounding connective tissue often limits infection to bone/cement interface
  • Can be any organism
225
Q

What is an organisms virulence?

A

Ability to infect

226
Q

What do low virulence organisms result in?

A

Low grade indolent infections which are tenacious e.g. coagulase negative staphylococci

227
Q

What do high virulence organisms result in?

A

Fulminant infection or septic shock e.g. MSSA, MRSA, Group A or G Beta Haemolytic Streptococcus

228
Q

Describe the pathogenesis of prosthetic joint infections?

A

Avascular surface allow survival of bacteria as protects from circulating immunological defences & most antibiotics

229
Q

What can prosthetic joint cement do?

A

Inhibit phagocytosis & lymphocyte/ complement function

230
Q

List the 5 clinical presentations of prosthetic joint infections?

A
  1. Pain
  2. Effusion
  3. Warm joint
  4. Fever & systemic symptoms
  5. Prosthetic joint- Loosening on Xray, Discharging sinus, Mechanical dysfunction
231
Q

Describe the effectiveness of antibiotic prophylaxis in prosthetic joint infections?

A
  • Single pre-op dose cephalosporin reduces risk of deep wound infection by 1.8% (3% to 1.2%)
  • Single pre-op dose & 2 post op doses reduce risk of deep wound infection by 2.9% (4.3% to 1.4%)
  • Evidence supports use of cephalosporin (+ vancomycin/teicoplanin if MRSA) in prevention of PJI (but not C. difficile)
232
Q

What does DAIR stand for?

A

Debride, Antibiotics, Implant Retained

233
Q

When would it be appropriate to perform DAIR & Leave the Infected Joint In?

A

If prosthesis infection is acute (<30 days since insertion), then it is still mechanically functional & can be kept in but infected tissues should be debrided & the joint washed out to reduce the burden of infection then IV antibiotics started for 4-6 weeks

234
Q

When would it be appropriate to take the infected joint out?

A
  • If the infection occurs over 30 days since surgery then it may no longer be fully functional & may need removed
  • Removal involves taking out the prosthesis & all cement (can􏰎t heal if foreign body retained)
235
Q

What are the 3 different options for taking an infected joint out?

A
  1. Girdlestone procedure
  2. 1 stage revision (put a new one in during the same operation as removing the infected one)
  3. 2 stage revision (delay putting in a new 1 until treated the existing infection for 4-6 weeks)
236
Q

What happens each time a joint revision is performed & why?

A

Chances of success & cure of infection reduce dramatically due to anatomical distortion & infection becomes harder to suppress making amputation a possibility

237
Q

What prosthetic joint samples would help identify infection pathogens?

A

Tissue or pus or fluid is always preferable to a surface swab

238
Q

What 3 things does diagnosis of prothetic joint infection depend on?

A
  1. Macroscopic appearance
  2. Histopathology
  3. Microbiology
239
Q

What are 3 reasons as to why negative cultures do not necessarily exclude infection?

A
  1. Bacteria present in very small numbers & require longer time to grow
  2. Bacteria died in transit if there was delay reaching the lab/if it was a fastidious organism e.g.anaerobes
  3. Antibiotics given pre-op (rarely necessary before revision surgery & 2 days to 2 weeks antibiotic free pre-op is ideal)
240
Q

What do the antibiotics given for prothetic joint infection need to be able to do?

A

Needs to penetrate to bone (cephalosporins, tazocin, carbapenems, fusidic acid, doxycycline, rifampicin, linezolid, trimethoprim, ciprofloxacin,clindamycin)

241
Q

Describe the antibiotic treatment for prothetic joint infection?

A

Oral antibiotics are unlikely to suppress infection if a prolonged course of IV therapy has not already been given & the CRP hasn’􏰎t begun to normalise or treating a virulent organism

242
Q

What types of antibiotic treatment has greater success in chronic staphylococcal osteomyelitis?

A

Combination therapies which include rifampicin (rifampicin & ciprofloxacin)

243
Q

When is the only time you would start a prosthesis patient on antibiotics pre-operatively?

A

If they have a life threatening infection

244
Q

What specimens/tissues should you send in a prosthesis patient?

A
  • Multiple intra-operative specimens to microbiology from at least 5 different sites
  • Debrided tissue to a histopathologist
245
Q

What are the the top tips for treating prosthetic joint infections?

A
  1. Start antibiotics rationally based on antibiograms & using drugs that penetrate bone
  2. Do not stop IV antibiotics immediately post-operatively
  3. Measure CRP regularly
246
Q

What is osteomyelitis?

A

Progressive infection of bone characterised by death of bone & the formation of sequestra (piece of dead bone tissue formed within a diseased or injured bone)

247
Q

What are the 2 ways osteomyelitis can spread?

A
  1. Haematogenous spread

2. Contiguous spread- overlying infection (e.g. cellulitic ulcer), trauma (compound fracture), surgical inoculation

248
Q

Who is acute osteomyelitis commoner in?

A

Children than adults

249
Q

Describe Acute osteomyelitis?

A
  • Often undertreated with oral antibiotics & so may recur
  • Causative bacteria similar to septic arthritis but also include anaerobes
250
Q

Describe the 2 surgical treatments for Osteomyelitis?

A
  1. Debulk infection back to healthy bone & manage dead space that remains (e.g. with muscle flaps)
  2. Stabilise infected fractures (external fixation often used) & debride sinuses & close wounds
251
Q

Describe the antibiotic treatment for Osteomyelitis?

A
  • Antibiotic choice is determined by what grows from debrided bone
  • May require long term antibiotic treatment (4- 6 weeks IV)
252
Q

Describe Diabetic Foot infection?

A
  • More complex than septic arthritis

- Usually involves bone (osteomyelitis) but can also involve joints

253
Q

How should you treat Diabetic Foot infection?

A

Need to optimise diabetic control as well as treat infection so should involve a diabetologist

254
Q

What is Vertebral discitis?

A
  • Infection of a disc space & adjacent vertebral end plates
  • Similar organisms to septic arthritis & osteomyelitis
255
Q

Describe the effects of Vertebral discitis?

A

Can be very destructive with deformity, spinal instability risking cord compression, paraplegia & disability

256
Q

What should you remember regarding Vertebral discitis?

A

Tuberculosis

257
Q

Describe the pathogenesis of bacterial pneumonia?

A
  • Host defense defect
  • Large innoculum
  • Increased virulence
258
Q

List the 3 typical bacteria causing pneumonia?

A
  1. Streptococcus pneumoniae (most common)
  2. Haemophilus influenzae
  3. Moraxella catharralis
259
Q

List the 4 atypical bacteria causing pneumonia?

A
  1. Mycoplasma pneumoniae
  2. Legionella pneumoniae
  3. Chlamydophila pneumoniae
  4. Chlamydophila psittaci
260
Q

What is the number 1 cause of community acquired pneumonia?

A

S. pneumoniae

261
Q

List 6 risk factors for S. pneumoniae?

A
  1. Decreased immune function from disease or drugs (HIV, flu)
  2. Smoking
  3. Lung disease, asthma
  4. Alcohol
  5. Cancer
  6. Heart disease
262
Q

List 4 presentations of S. pneumoniae?

A
  1. Abrupt Onset
  2. Cough
  3. Fever
  4. Pleuritic chest pain
263
Q

List 3 examination findings of S. pneumoniae?

A
  1. Dull percussion
  2. Coarse crepitations
  3. Increased vocal resonance
264
Q

What 2 antibiotics would you prescribe for S. pneumoniae in a patient with penicillin allergy?

A
  1. Macrolides (clarithromycin)

2. Tetracyclines (doxycycline)

265
Q

What are 2 risk factors for Haemophilus influenzae?

A
  1. Older people

2. Underlying lung disease

266
Q

What type of Haemophilus influenzae can we vaccinate against?

A

Type B (does not cause pneumonia)

267
Q

Where do the non-typeable Haemophilus influenzae go?

A

Colonisation of upper respiratory tract

268
Q

List the 4 presentations of Haemophilus influenzae?

A
  1. Abrupt Onset
  2. Cough
  3. Fever
  4. Pleuritic chest pain
269
Q

List the 3 examination findings of Haemophilus influenzae?

A
  1. Dull percussion
  2. Coarse crepitations
  3. Increased vocal resonance
270
Q

What makes Amoxicillin less effective against Haemophilus influenzae?

A

Some Haemophilus influenzae produce β-Lactamase

271
Q

What 3 antibiotics would you give to treat Haemophilus influenzae producing β-Lactamase?

A
  1. Co-amoxiclav
  2. Macrolides (clarithromycin)
  3. Tetracyclines (doxycicline)
272
Q

Describe the structure of Mycoplasma pneumoniae?

A
  • Smallest free living bacterium
  • Lack of cell wall
  • Very difficult to grow
273
Q

Describe Mycoplasma pneumoniae infection spread?

A
  • Spreads person-person

- Autumn & winter have the highest rates

274
Q

Describe M. pneumoniae presentation?

A

Atypical, may have flu-like illness with a cough

275
Q

What are 5 types of complications associated with M. pneumoniae?

A
  1. Haemolysis (cold agglutinins)
  2. Guillain-Barre
  3. Erythema multiforme
  4. Cardiac
  5. Arthritis
276
Q

Describe how to diagnose M. pneumoniae?

A
  • Can’t culture
  • Serology
  • PCR (sputum/throat swab) most common
277
Q

Since M. pneumoniae doesn’t have a cell wall, what antibiotics won’t work?

A

Beta lactams (penicillins/cephalosporins)

278
Q

What 3 antibiotics can treat M. pneumoniae?

A
  1. Macrolides (clarithromycin)
  2. Tetracyclines (doxycycline)
  3. Quinolones (ciprofloxacin)
279
Q

Describe Legionella pneumophila infection spread?

A
  • Humans inhale it from sources & it infects macrophages which get into the lungs
  • Organisms exist in the environment as amoeba’s
  • Outbreaks in hotels through air-con & water systems (hot tubs)
280
Q

Describe the presentation of Legionella pneumophila?

A

Atypical (tired, fever etc)

281
Q

How can you diagnose Legionella pneumophila?

A
  • Culture (rare)
  • Serology
  • Urinary antigen test (most common)
282
Q

Since L. pneumophila is an intracellular infection, what antibiotics won’t work?

A

Beta lactams (penicillins/cephalosporins)

283
Q

What 3 antibiotics are effective in treating L. pneumophila?

A
  1. Macrolides (clarithromycin)
  2. Quinolones (ciprofloxacin)
  3. Tetracyclines (doxycicline)
284
Q

List the 5 symptoms a patient with pneumonia will probably have?

A
  1. Fever
  2. Cough/sputum
  3. Chest pain
  4. Insidious/abrupt onset
  5. Non respiratory symptoms
285
Q

List the 2 past medical histories a patient with pneumonia will probably have?

A
  1. Underlying lung disease

2. Immunosupression

286
Q

List 3 common epidemiologies that a patient with pneumonia will probably have?

A
  1. Ill contacts
  2. Travel
  3. Water exposure
287
Q

What are the 2 clinical assessments/scores for assessing the severity of pneumonia?

A
  1. CURB65 score

2. Sepsis - qSOFA

288
Q

What does the CURB65 score stand for?

A 
C - Confusion
U- Urea>7
R- Respiratory rate ≥ 30
B- BP, diastolic<60 or systolic <90 
65- Age over 65 years
289
Q

What is the Sepsis - qSOFA score?

A
  • Systolic BP< 100mmHg
  • Altered mental status
  • Respiratory rate > 22 breaths/min
290
Q

How many CURB65 scores need to be positive for a diagnosis of severe pneumonia?

A

> 2

291
Q

What 2 other clinical assessments would lead to a diagnosis of severe pneumonia?

A

Multilobar consolidation on CXR &/or Hypoxia on room air

292
Q

What 3 blood tests would you perform to investigate pneumonia?

A
  1. FBC
  2. U&Es
  3. ABGs/Oxygen sats
293
Q

What 4 microbiology tests would you perform to investigate pneumonia?

A
  1. Blood cultures
  2. Sputum culture
  3. Throat swab
  4. Urine Legionella antigen
294
Q

What 2 investigations/tests would you perform to a patient with pneumonia?

A
  1. Chest X-ray

2. ECG

295
Q

How would you manage a patient with pneumonia?

A

A- Airway (Conscious level?)
B- Breathing (Oxygen, ITU)
C- Circulation (shock-fluids)

296
Q

What 3 factors determine whether a pneumonia patient needs IV or oral antibiotics &/or admission to hospital?

A
  1. CURB65- mortality increase with score 2 or more
  2. Sepsis qSOFA score
  3. Hypoxia
297
Q

What is the most common cause of illness in otherwise health adults & children?

A

Acute respiratory viruses

298
Q

What are the 2 common viruses causing the common cold?

A
  1. Rhinovirus

2. Coronavirus

299
Q

What are the 4 common viruses causing Pharyngitis?

A
  1. Adenovirus (12-23%)
  2. Rhinovirus
  3. Influenza
  4. Parainfluenza
300
Q

What is the common virus causing Croup?

A

Parainfluenza virus (1-4)

301
Q

What is the common virus causing Acute bronchitis/Bronchiolitis?

A

RSV

302
Q

What are the 2 common viruses causing pneumonia?

A
  1. Influenza

2. RSV

303
Q

Describe the common cold presentation?

A
  • Usually self-diagnosed
  • Sore “scratchy” throat
  • Rhinorrhoea
  • Nasal obstruction
  • Persists ~ 1 week
304
Q

Describe the onset of the common cold?

A

1-3 days after viral infection

305
Q

What are the 2 complications of the common cold?

A
  1. Otitis media

2. Sinusitis

306
Q

What 5 susceptible groups of people are prone to severe common cold infections?

A
  1. Elderly
  2. Immunocompromised
  3. Asthma
  4. COPD
  5. CF
307
Q

Describe Rhinovirus?

A
  • ssRNA
  • 3 species RV-A, RV-B, RV-C
  • > 100 types
308
Q

Describe the structure of Coronavirus?

A
  • ssRNA
  • Largest RNA virus genome
  • Enveloped
309
Q

Describe Pharyngitis?

A
  • Sore throat & pharyngeal inflammation
  • Viral infections 25-45%
  • 82% occurrence in infectious
    mononucleosis ie. Epstein Barr Virus (EBV), Saliva spread
  • HIV seroconversion illness
  • Herpes simplex virus
310
Q

What does nasal symptoms in Pharyngitis suggest?

A

Viral cause (monitor at home, gargle with salt water)

311
Q

What does pharyngitis without nasal symptoms suggest?

A

Bacterial cause (come to health centre)

312
Q

What is Croup?

A
  • Commonly encountered childhood infectious syndrome
  • Distinctive cough
  • Mostly mild but responsible for significant emergency visits (rapid onset, difficult breathing)
313
Q

How do you treat Croup?

A

Supportive

314
Q

What is Bronchiolitis?

A
  • Lower respiratory tract infection of young children
  • Leading cause hospitalisation in infants
  • Most children infected by 2 yrs of age
  • Reinfections are common but less severe
315
Q

Describe the presentation of Bronchiolitis?

A
  • Wheezing, tachycardia

- Persistent cough for up to 3 weeks

316
Q

What is the duration of Bronchiolitis?

A

7-10 days

317
Q

What does increasing evidence suggest Bronchiolitis has an association with?

A

Development of asthma

318
Q

What 3 groups of people is respiratory syncytial virus (RSV) also a significant burden to?

A
  1. Immunocompromised
  2. Adults with chronic lung disease
  3. Elderly
319
Q

Describe the treatment of respiratory syncytial virus (RSV)?

A
  • Ribavirin (oral, IV, aerosolised) has been used but benefit unclear
  • It has numerous side-effects
320
Q

Describe how to prevent respiratory syncytial virus (RSV)?

A

A prophylatic monoclonal antibody is available (Palivizumab/Synagis) given IM monthly

321
Q

What does the influenza virus have the ability to cause?

A

Annual epidemics & occasional pandemics

322
Q

What are the different types of influenza virus?

A

3 types (A-C)

323
Q

List the 8 possible symptoms of Influenza virus?

A
  1. Headache
  2. Fever
  3. Tiredness
  4. Aches
  5. Vomiting
  6. Coughing
  7. Runny nose
  8. Sore throat
324
Q

What is the incubation period of influenza virus?

A

1-2 days

325
Q

How long do systemic symptoms persist for in influenza virus?

A

3-5 days

326
Q

What are the 5 common complications of Influenza virus?

A
  1. Acute otitis media (children)
  2. Sinusitis
  3. Pneumonia
  4. Exacerbation of underlying diseases
  5. Dehydration (infants)
327
Q

What are the 5 uncommon complications of influenza virus?

A
  1. Encephalopathy
  2. Reye syndrome (children)
  3. Myositis
  4. Myocarditis
  5. Febrile seizures
328
Q

List the 11 patient risk factors for complicated influenza virus?

A
  1. Neurological
  2. Hepatic
  3. Renal
  4. Pulmonary
  5. Chronic cardiac
  6. Diabetes mellitus
  7. Severe immunosuppression
  8. Age >65 years
  9. Children <6 months
  10. Pregnancy (inc. up to 2 weeks post partum)
  11. Morbid obesity (BMI≥40)
329
Q

What are the 4 types of inhibitor drugs that are used to treat Influenza virus?

A
  1. M2 Inhibitors
  2. IMP dehydrogenase inhibitors
  3. RNA polymerase inhibitors
  4. Neuraminidase inhibitors
330
Q

Give 2 examples of M2 Inhibitors used to treat Influenza virus?

A
  1. Amantadine

2. Rimantadine

331
Q

Give an example of a IMP dehydrogenase inhibitor used to treat Influenza virus?

A

Ribavirin

332
Q

Give 2 examples of RNA polymerase inhibitors used to treat Influenza virus?

A
  1. Favipiravir

2. Baloxavir

333
Q

Give 4 examples of Neuraminidase inhibitors used to treat Influenza virus?

A
  1. Oseltamivir
  2. Zanamivir
  3. Peramivir
  4. Laninamivir
334
Q

Who can be affected by type A influenza virus?

A

Humans, swine, birds

335
Q

Who can be affected by type B influenza virus?

A

Humans only

336
Q

What leads to epidemics?

A

Antigenic drift (point mutations of HA & NA genes)

337
Q

Describe the influenza vaccination?

A
  • Live & inactivated influenza vaccines
  • Offered to risk groups: healthcare workers & children
  • Manufactured annually
  • Reduces severity, hospitalisations & death
338
Q

What are the 3 types of inactivated influenza vaccination?

A
  1. Trivalent vaccine
  2. Adjuvanted trivalent vaccine (given to >65yrs)
  3. Quadrivalent vaccine
339
Q

What type of influenza vaccine is given to children?

A

Live attenuated intranasal influenza vaccine

340
Q

Describe the Live attenuated intranasal influenza vaccine given to children?

A
  • 2 influenza A types & 2 influenza B types
  • Manufactured annually
  • 83% effective
341
Q

What are influenza pandemics?

A
  • Worldwide epidemics of a newly emerged strain of influenza

- New virus spreads widely, easily, and causes more serious illness

342
Q

What leads to a pandemic?

A

Antigenic shift

343
Q

What is Influenza A virus subtype H5N1?

A

Avian Influenza outbreak in Asia & Middle East

344
Q

What can Influenza A virus subtype H5N1 induce?

A

Acute respiratory distress syndrome

345
Q

What does Influenza A virus subtype H5N1 have a high resistance to?

A

Oseltamivir

346
Q

What is the emerging respiratory infection?

A

Coronaviruses more than the common cold

347
Q

Describe the prevalence/occurrence of SARS-CoV?

A
  • Fatality rate 9.5%
  • Contained in 2003
  • 3 cases accidental release lab stored
    strain in May 2004
  • NO NEW CASES REPORTED SINCE 2004
348
Q

Describe MERS-COV prodrome?

A

Flu-like illness (transmission unlikely)

349
Q

List the 5 clinical signs & symptoms of MERS-COV acute illness?

A
  1. Dyspnoea
  2. Vomiting
  3. Diarrhoea
  4. Chest pain
  5. Cough
    (transmission)
350
Q

List the 3 effects of fulminant MERS-COV illness?

A
  1. ARDS
  2. Renal failure
  3. Multi-organ failure (transmission)
351
Q

What are 2 ways to diagnose respiratory viral infections in the lab?

A
  1. Electron microscopy

2. Tissue culture

352
Q

What are the 8 benefits of Molecular testing?

A
  1. Improves the diagnosis of previously under diagnosed infections
  2. Rapid
  3. Rapidly developed to detect new pathogens
  4. Monitoring of the effectiveness of treatment
  5. Reduces unnecessary antibiotic treatment
  6. Informs public health
  7. Vaccine effectiveness
  8. New treatments
353
Q

What does POCT stand for?

A

Point of Care Testing

354
Q

What is POCT & what can it do?

A
  • Gargle
  • 20 min for positive test
  • Distinguish between Flu A, Flu B & RSV
355
Q

What are the 3 roles for the laboratory in respiratory viral infections?

A
  1. Resistance
  2. Epidemiology
  3. Outbreak investigation
356
Q

What is a bacterium that causes tuberculosis (TB) in humans?

A

Mycobacterium tuberculosis

357
Q

List 2 different types of media that tuberculosis (TB) can grow on?

A
  1. Ziehl Neelsen Stain

2. Auramine stain (not specific)

358
Q

List 7 different TB mycobacteria?

A
  1. M. tb
  2. M. bovis
  3. M. kansasii
  4. M. chelonae
  5. M. abscessus
  6. M. fortuitum
  7. M. leprae
359
Q

Describe the pathogenesis of TB?

A
  • M. Tuberculosis inhaled & goes into the lungs
  • Taken up by macrophages
  • Can form a TB lesion in lungs
  • Haematogenous spread in 90-95%
  • 5-10% progress to cavitary TB
360
Q

How is M. tuberculosis DNA detected in tissues?

A

In situ PCR

361
Q

What are 3 ways that TB can be reactivated?

A
  1. Immunosuppression
  2. HIV infection
  3. Smoking
362
Q

Describe Cavitary TB?

A

Cavities open into the bronchi, allowing spread of M. tuberculosis through coughing

363
Q

What is physically evidence of old TB in the lungs?

A

Ghon complex (calcified areas)

364
Q

What happens to >90% of primary TB?

A
  • Healing, Calcification & dormant organisms

- This can lead to reactivation or reinfection –> Secondary (cavitary) TB

365
Q

What happens to <10% of primary TB?

A

Goes on to be progressive primary TB

366
Q

What 3 types of people have a greater susceptibility to progressive primary TB?

A
  1. Certain racial groups
  2. Children
  3. Immunocompromised hosts
367
Q

What is commonly seen on a chest X-ray of Mycobacterium tuberculosis?

A

Apical destruction

368
Q

What can result in disseminated TB?

A

Miliary TB (potentially fatal)

369
Q

What 2 locations can TB spread to?

A
  1. CNS

2. Renal

370
Q

Describe the granuloma in mycobacterium TB?

A
  • Contains mostly blood-derived macrophages, epithelioid cells (differentiated macrophages) & multinucleated giant cells surrounded by T lymphocytes
  • Caseous granulomas are typical of TB
371
Q

Describe the immunity to M. TB?

A
  • Cell mediated immunity crucial
  • Macrophages key controlling cell
  • T cell production of interferon gamma
  • Cytokines involved in this process all key
372
Q

How can you assess if a patient has latent TB infection?

A

Mantoux Reaction

373
Q

How can you screen for TB?

A

T spot test- single-visit blood tests, also known as an interferon gamma release assay (IGRA).

374
Q

What is the duration for drug treatment of TB?

A

6 months

375
Q

List the 4 current drug treatments for TB?

A
  • Rifampicin
  • Isonizid
  • Pyrazinamide
  • Ethambutol
376
Q

When would you drop the Ethambutol in drug treatment of TB?

A

If senstive to Rifampicin & isoniazid

377
Q

When would you stop pyrazinamide in TB treatment?

A

After 2 months

378
Q

What prophylactic drug can you give TB patients to prevent neuropathy caused by isoniazid?

A

Pyridoxine

379
Q

What are the 3 disadvantages of Rifampicin drug treatment for TB?

A
  • Induces cytochrome P450 & alters metabolism of many drugs e.g. steroids
  • Metabolized in liver: potential for toxicity
  • Turns urine reddish
380
Q

What can Ethambutol affect?

A

Vision

381
Q

Give 3 reason why sex is good for us?

A
  1. Fitter
  2. Lower rates of depression
  3. Better cardiovascular health
382
Q

Give 5 reasons when sex is bad for us?

A
  1. Non-consensual sex
  2. Exploitative sex
  3. Sexual dysfunction
  4. Unwanted conception
  5. Infection
383
Q

List the 6 principles of STI management?

A
  1. Diagnosis before treatment (antibiotic use)
  2. Screen for accompanying STIs
  3. Simple treatment regimens
  4. Follow-up after treatment +/- TOC
  5. Partner notification
  6. Non-judgemental patient support, counselling, education
384
Q

What has a huge effect on the populations sexual behaviour?

A

Technology (apps ie. tinder)

385
Q

Where do STI’s cluster geographically?

A

Cities with higher populations

386
Q

What 4 things do you need to know in a sexual health history?

A
  1. Last time ANY type of sex
  2. Who that was with: Gender & Location
  3. Type of sex e.g. receptive anal sex
  4. Condom use or not
387
Q

What does unprotected anal sex in men tend to lead to?

A

Gonorrhoea

388
Q

What does unprotected female sex tend to lead to?

A

Mycoplasma genitalia/ Chlamydia

389
Q

Describe the microbiology of gonorrhoea?

A

Gram negative diplococci & white cells

390
Q

Describe the presentation of gonorrhoea?

A

Ulcers, skin changes, dysuria & urethral exudate discharge

391
Q

Describe the test for gonorrhoea?

A
  • NAAT test
  • Male urine sample acceptable +/- rectal/throat (MSM)
  • Vulvovaginal swab (self-taken is fine)
392
Q

What are the symptoms of disseminated gonorrhoea?

A
  1. Skin pustules

2. Joint infections

393
Q

What is the main issue with gonorrhoea?

A

Its turning drug resistant

394
Q

What are the 3 syndromic managements of male urethral discharge?

A
  1. Ceftriaxone 500 mg IM
  2. Azithromycin 1g stat
  3. Partner notification
395
Q

List the 5 drugs gonorrhoea is resistant to and their %?

A
  1. Penicillin- 9.9%
  2. Tetracycline- 29.4%
  3. Ciprofloxacin- 31.4%
  4. Cefixime- 0.1% (susceptible to ceftriaxone)
  5. Azithromycin- 3% had reduced susceptibility (46% of these had HL-AziR)
396
Q

Chlamydia trachomatis is frequently _______?

A

Asymptomatic

397
Q

What can Chlamydia trachomatis infection lead to?

A

Tubal damage / infertility:

  • About 16% of women infected will develop PID
  • No current evidence that screening programme has reduced prevalence or PID or infertility
398
Q

What are the 2 current areas of interest regarding Chlamydia trachomatis?

A
  1. Extra-genital testing in women

2. Is single-dose treatment adequate?

399
Q

How do you treat Chlamydia trachomatis?

A
  1. Doxycycline 100 mg BD x 1 week (3 weeks for LGV)

2. Azithromycin 1g oral stat, followed by 500mg od 2 days (recent change to BASHH guidance)

400
Q

Describe Lymphogranuloma venereum (LGV)?

A
  • Lymphotropic chlamydia
  • Severe proctitis causing constipation , rectal bleeding
  • Looks like cancer or Crohn’s
  • Inguinal ‘bubos’
401
Q

Describe the natural progression of syphilis?

A

Exposure –> 1° lesion (chancre) –> 2° lesion (rash) –> Latent syphilis (+ve serology only) –> 3° syphilis –> Gumma, Cardiovascular, Neurological

402
Q

Who is most commonly affected by infectious syphilis?

A

Men who have sex with men (MSM)

403
Q

Describe secondary syphilis?

A
  • Highly infectious
  • Can be confused with many other medical conditions or ignored by patient
  • Blood tests always strongly positive
  • Not universal: many patients have no secondary stage
404
Q

What 2 clinical signs can result from late syphilis?

A
  1. Aortic dilatation

2. Neurosyphilis- hearing loss, visual disturbances

405
Q

How do you treat syphilis?

A

Benzathine penicillin injection in butt cheeks

406
Q

List 6 examples of viral STI’s?

A
  1. Human Papilloma Virus
  2. Molluscum contagiosum
  3. Herpes Simplex Virus
  4. HIV
  5. Hepatitis B
  6. Hepatitis C
407
Q

What types of HPV cause genital warts?

A

HPV-6 & 11

408
Q

What types of HPV cause cervical & penile cancer?

A

HPV 16 & 18

409
Q

Describe the vaccination for HPV?

A
  • Gardasil: HPV strains 6/11/16/18
  • School aged girls
  • MSM attending sexual health/HIV clinics <45y
  • Soon to be school aged boys
410
Q

What are the 3 types of treatment for genital/anal warts?

A
  1. Cream form- direct toxin effect on skin cells
  2. Immunomodulation
  3. Cryotherapy- toxic effect to skin
411
Q

Describe Molluscum contagiosum?

A
  • Pox virus
  • Sexual transmission
  • Pubic area/groin
  • Extensive/Face may indicate immunosuppression in adults
  • Usually self limiting
412
Q

Describe the presentation of Herpes Simplex?

A
  • May be asymptomatic but may cause ulcers
  • Flu-like symptoms
  • Pain in genitalia
  • Dysuria
413
Q

Describe the rates of anogenital herpes (1st episode) in Scotland?

A

Diagnoses decreases with age & is more common in women

414
Q

What are the 3 types of treatment for Herpes Simplex?

A
  1. Aciclovir 400mg TDS 5 days- 1st episode
  2. Aciclovir 800mg TDS 2 days- recurrence
  3. Aciclovir 400mg BD 6-12 months- suppression
415
Q

List 4 other types of STIs?

A
  1. Trichomonas vaginalis- 2% prevalence in Glasgow. Vaginal discharge & pain in women but asymptomatic in men. Presents as bacterial vaginosis
  2. Mycoplasma genitalium- NO test, 1 week Doxycycline
  3. Donovanosis
  4. Chancroid- Rare in UK
416
Q

What detects viral shedding more- urine or seminal fluid?

A

Seminal fluid

417
Q

What may seminal fluid be an important vehicle for transmission of?

A

CMV

418
Q

What infection must be considered in a differentiation for previously healthy homosexual males with dyspnea & pneumonia?

A

Pneumocystis carinii infection

419
Q

What were the 4 possible causes of homosexual males having infections?

A
  1. Related to sexually activity
  2. CMV related
  3. Drug use
  4. Environmental- sauna related
420
Q

What is Haemophilia A?

A

Sex-linked, inherited disorder characterized by a deficiency in Factor VIII activity

421
Q

How can Factor VIII deficiency be treated?

A

IV administration of exogenous Factor VIII as either cryoprecipitate made from fresh frozen plasma or lyophilized Factor VIII concentrate manufactured from plasma pools collected from thousand+ donors

422
Q

How did the HIV virus jump species?

A
  • “Bush meat” theory: a hunter was bitten or cut while butchering an animal
  • How SIV transformed into HIV in the human & became capable of replicating in humans is not known
423
Q

What are the 3 factors which may have triggered an epidemic of HIV transmission?

A
  1. Social changes & urbanization
  2. Unsterile injections: vaccines, antibiotics, sleeping sickness
  3. Genital ulcer diseases & sexual promiscuity
424
Q

Describe HIV’s spread from Africa?

A
  • Was introduced to Haiti by unknown individual/individuals who contracted it in the Democratic Republic of the Congo
  • Mini-epidemic followed, &≈1969, another individual brought HIV from Haiti to the United States
  • Vast majority of cases of AIDS outside sub-Saharan Africa can be traced back to that single unknown person
425
Q

Why was HIV not noticed for years?

A

Long incubation period before illness

426
Q

Who is Patient Zero?

A

One of the most demonised patients in history - Gaetan Dugas - has been convincingly cleared of claims he spread HIV to the US, say scientists

427
Q

Describe the HIV at risk groups in Scotland?

A
  • Almost always acquired sexually
  • Successful needle exchange programmes limiting the injecting drug use transmission seen in the early 80s
  • MSM most infections occur in Scotland
  • Infected heterosexually acquire HIV either overseas/ through sexual contact here with someone from high-prevalence country
428
Q

How is HIV transmitted?

A

Enters the body through open cuts, sores or breaks in the skin, through mucous membranes, such as those inside the anus or vagina, or through direct injection

429
Q

List 5 activities that allow HIV transmission?

A
  1. Anal or vaginal intercourse (oral sex not an efficient route)
  2. Injecting drugs + sharing equipment
  3. Mother-to-child (before / during birth, or through breast milk)
  4. Health care settings
  5. Via donated blood or blood clotting factors
430
Q

What 3 fluids have an extremely low concentration of HIV?

A
  1. Saliva
  2. Tears
  3. Urine
431
Q

What 6 day-to-day activities cannot lead to HIV transmission?

A
  1. Shaking hands
  2. Hugging
  3. Casual kissing
  4. Sharing food/ eating utensils
  5. Toilet seats
  6. Drinking fountain
432
Q

What 4 fluids have the potential to transmit HIV?

A
  1. Blood (including menstrual blood)
  2. Semen
  3. Vaginal secretions
  4. Breast milk
433
Q

What fluid has the highest concentration of HIV?

A

Blood followed by semen followed by vaginal fluids then followed by breast milk

434
Q

How does HIV cause illness?

A
  • Infects cells in the immune system such as T helper Cells, macrophages & dendritic cells
  • All these cells carry CD4 receptors which allow HIV entry
  • Causes depletion of CD4 T helper cells
  • Abnormal B cell activation resulting in excess / inappropriate immunoglobulin production
435
Q

What happens when HIV causes a persons CD4+ cells to fall below a critical level (≤ 200)?

A

The person is at risk of opportunistic infections & some cancers

436
Q

How does HIV cause depleting of CD4 T helper cells?

A
  1. Direct viral killing of cells
  2. Apoptosis of uninfected “bystander cells”
  3. CD8+ cytotoxic T cell killing of infected CD4+cells
437
Q

Describe the structure of HIV?

A
  • Spherical
  • Diameter of ~120nm
  • 2 copies of positive single-strandedRNA codes for the virus’s 9genesenclosed by conicalcapsidcomposed of copies of viral proteinp24
  • Single-stranded RNA is tightly bound to nucleocapsid proteins, p7, & enzymes needed for the development of the virion
  • Matrix composed of the viral protein p17 surrounds the capsid
  • Surrounded by theviral envelopeof 2 layers of phospholipids
438
Q

What are the 4 enzymes needed for the development of the virion?

A
  1. Reverse transcriptase
  2. Proteases
  3. Ribonuclease
  4. Integrase
439
Q

What is embedded in the HIV viral envelope?

A

Proteins from the host cell & about 70 copies of a complex HIV protein (Enz) that protrudes through the surface of the virus particle

440
Q

List the 4 types of drugs targeting HIV life cycle?

A
  1. Fusion inhibitor, R5 inhibitor
  2. Protease inhibitor
  3. NRTI, NNRTI
  4. Integrase inhibitor
441
Q

How long is the HIV life cycle?

A

6hrs

442
Q

What is the purpose of HIV Enz glycoprotein complex?

A

Enables the virus to attach to & fuse with target cells to initiate the infectious cycle

443
Q

What does the RNA genome of HIV consist of?

A
  • At least 7 structural landmarks (LTR,TAR,RRE, PE, SLIP, CRS, & INS)
  • 9 genes (gag, pol,env,tat,rev,nef,vif, vpr,vpu) encoding 19 proteins
444
Q

What 3 HIV genes contain information needed to make the structural proteins for new virus particles?

A

Gag,pol &env

445
Q

What do the remaining 6 HIV genes (tat,rev,nef,vif,vpr, &vpu) do?

A

Regulatory genes for proteins that control the ability of HIV to infect cells, produce new copies of virus (replicate), or cause disease

446
Q

What is viral latency?

A

A state of reversibly non-productive infection of individual cells

447
Q

What does the term latency mean in HIV?

A

Generally used to describe the long asymptomatic period between initial infection & advanced HIV (AIDS)

448
Q

What has PCR shown in HIV?

A

HIV replicates actively throughout the course of the infection even during the asymptomatic period

449
Q

What happens once HIV virus genetic material is incorporated into the host DNA?

A

There is no cure as no way to remove it

450
Q

What can lead to HIV drug-resistance?

A
  • HIV multiplies in the body, the virus sometimes mutates (changes form) & produces variations of itself
  • Variations of HIV can develop while a person is taking HIV medicines
451
Q

When can HIV resistance occur in a person?

A

A person can initially be infected with drug-resistant HIV or develop drug-resistant HIV after starting HIV medicines

452
Q

What does drug-resistance HIV testing identify?

A
  • Which, if any, HIV medicines won’t be effective against a person’s HIV
  • Drug-resistance testing results help determine which HIV medicines to include in an HIV treatment regimen
453
Q

What reduces the risk of HIV drug-resistance?

A

Medication adherence- taking HIV medicines every day & exactly as prescribed

454
Q

What are the 6 clinical markers of HIV?

A
  1. CD4 cell count (T-helper lymphocyte count)
  2. HIV-1 plasma RNA (Viral load test)
  3. HIV-1 subtypes (Clade typing)
  4. Genotypic & phenotypic resistance tests
  5. Tropism tests (CCR5 status)
  6. HLA-B*5701 to predict Abacavir reactions
455
Q

How is CD4 cell count calculated?

A

From total lymphocyte count

456
Q

Describe CD4 cell count?

A
  • HIV-negative: 600-1200 per mm3

- Risk of opportunistic infection increases sharply below 200/mm3

457
Q

How is HIV viral load calculated?

A

Using log 10 scale

458
Q

Describe HIV viral load?

A
  • “Set point” lower the better
  • Below 10,000 (104) low - Above 100,000 high
  • “Undetectable” means below 40 copies/ml
459
Q

Describe the natural history of HIV infection?

A
  • Primary infection
  • +/- acute HIV syndrome: wide dissemination of virus, seeding of lymphoid organs
  • Clinical latency
  • Constitutional symptoms
  • Opportunistic diseases
  • Death
460
Q

List 6 opportunistic diseases/infections which can occur years after onset of HIV infection once the persons CD4+ cells have decreased?

A
  1. Thrush
  2. TB
  3. Pneumocystis carinii pneumonia
  4. Cytomagalovirus disease (CMV)
  5. Mycobacterium avium complex disease
461
Q

What are the 10 main symptoms of acute HIV infection?

A
  1. Systemic- fever, weight loss
  2. Pharyngitis
  3. Mouth- sores, thrush
  4. Oesophageal- sores
  5. Muscles- myalgia
  6. Liver & spleen- enlargement
  7. Gastric- nausea, vomiting
  8. Skin- rash
  9. Lymphadenopathy
  10. Central- malaise, headache, neuropathy
462
Q

What type of rash is typical of HIV?

A

Maculopapular rash

463
Q

What are the 4 differential diagnoses for HIV primary infection?

A
  1. Infectious mononucleosis
  2. Secondary syphilis
  3. Drug rash
  4. Viral infections- CMV, Rubella, Influenza, Parvovirus
464
Q

What are the 3 UK national HIV testing guidelines?

A
  1. Increase testing levels in primary care settings
  2. Increase testing levels among non-HIV specialists in secondary care
  3. HIV testing routine in secondary care settings where HIV indicator conditions are present
465
Q

List the 5 HIV Indicator Conditions?

A
  1. These prompt HIV testing
  2. It’s the condition not the behaviour
  3. Just like any other medical investigation
  4. You get it done & give the result
  5. Diagnose HIV & you will save that person’s life
466
Q

What is 90-90-90?

A

An ambitious treatment target to help end the AIDS epidemic (90% diagnosed, 90% on treatment & 90% virally suppressed)

467
Q

Describe the threshold for HIV treatment?

A
  • Moved from CD4 count of 200 to 350
  • START (When to start)
  • SPARTAC (seroconversion)
  • NOW: Test & Treat (prevention)
468
Q

What is HIV treatment a balance between?

A

Improvement in mortality/morbidity & complications of HAART

469
Q

What does HAART stand for?

A

Highly Active AntiRetroviral Treatment

470
Q

Describe HAART HIV treatment?

A
  • ‘Triple therapy’ (cART)
  • 2 nucleosides + 1 drug from another class
  • Aim to suppress viral load to undetectable
  • CD4 recovery
  • Combination pills available
471
Q

What are the 5 challenges with HAART?

A
  1. Good adherence (>95%) essential
  2. Psychological impact
  3. Short term side-effects
  4. Drug-drug interactions
  5. Emerging longer term toxicities
472
Q

List the 6 short term toxicities with HAART?

A
  1. Rash
  2. Hypersensitivity (Abacavir & Nevirapine)
  3. CNS side effects (Efavirenz)- sleep disturbance, vivid dreams, mood changes
  4. GI side effects
  5. Renal
  6. Hepatic
473
Q

What are HAART drug interactions mediated by?

A

CYP450 (induction/inhibition)

474
Q

What are 3 drugs which interact with HAART?

A
  1. PPIs
  2. Statins
  3. Antipsychotics- QTc
475
Q

List the 5 long term toxicities with HAART?

A
  1. Body shape changes- lipoatrophy or lipodystrophy (particularly older drugs)
  2. Renal – Tenofovir disoproxil
  3. Hepatic
  4. Lipid
  5. Bone
476
Q

Describe the % change of mother-child HIV transmission?

A

Fallen from 20-25% to under 0.1%

477
Q

What are 5 ways to prevent mother-child HIV transmission?

A
  1. Treat mother during pregnancy
  2. Minimise risk at delivery
  3. Treat baby early on
  4. Avoid breast feeding
  5. Universal antenatal HIV screening
478
Q

Describe the benefits of long-term HIV treatment?

A
  • Highly cost-effective
  • Major impact on morbidity & mortality
  • Prevents HIV transmission
  • BUT can’t treat HIV if it is undiagnosed
479
Q

What are 4 reasons why you should always offer a HIV test?

A
  1. HIV is a treatable long-term condition
  2. Essential to test if the symptoms could be HIV
  3. Don’t let absence of a “risk group” put you off
  4. Can prevent transmission if HIV is diagnosed
480
Q

Describe the % NHSGGC HIV Prevalence Data?

A
  • 25 % remain undiagnosed (as UK wide)
  • 93% of diagnosed attending for monitoring
  • 97% of attenders on treatment
481
Q

What does NESI stand for?

A

Needle Exchange Surveillance Initiative

482
Q

Describe the ‘outbreak’ amongst homeless PWIDs in Glasgow?

A
  • Despite good IEP provision
  • Change of service model to adapt to need
  • Challenges of providing care to vulnerable group
  • Over 100 diagnoses in past 3 years
483
Q

What are 4 ways to reduce your risk of getting HIV?

A
  1. HIV testing
  2. HIV PEPSE
  3. TasP
  4. HIV PrEP?
484
Q

List the 6 social dimensions of HIV/AIDS?

A
  1. Vulnerable populations- further marginalisation
  2. Access to healthcare- HIV & associated infections/illnesses
  3. Provision of ARVs- Lifelong, Management of ARV complications
  4. Single parent families/orphaned children
  5. Disabilities
  6. STIGMA
485
Q

What are the 3 most common causes for childhood mortality?

A
  1. Pneumonia
  2. Malaria
  3. Diarrhoea
486
Q

What age group has the faster decreased rates of under 5s mortality?

A

Faster in children aged 1-59 months than they were in neonates (2.9% per year vs 2.1% per year)

487
Q

What country has the World’s highest child mortality rate?

A

Sub-Saharan Africa

488
Q

Describe the sustainable development goals for under 5s mortality rates?

A

U5MR of no more than 25 per 1000 live births in every country of the world by 2030

489
Q

What have Community randomised trials in Africa have shown for full coverage with insecticide-treated nets?

A

Can halve the number of episodes of clinical

malaria and reduce all-cause mortality in children younger than 5 years of age

490
Q

What can full coverage with insecticide-treated nets lead to when used by pregnant women?

A

Substantial reductions in low birthweight, placental parasitaemia, stillbirths & miscarriages

491
Q

By reducing the vector population, what does insecticide-treated nets provide?

A

Protection for all people in a community, including those who do not sleep under a net themselves

492
Q

What was the conclusion of the community case management of severe pneumonia with oral amoxicillin in children of rural Pakistan?

A

Lady health workers (LHWs) in Pakistan were able to satisfactorily diagnose & treat severe pneumonia at home

493
Q

What are the 5 interventions attributed to a % of lives saved in 2009 (Niger)?

A
  1. Insecticide-treated bednets (25%)
  2. Improvements in nutritional status (19%)
  3. Vitamin A supplementation (9%)
  4. Treatment of diarrhoea with oral rehydration salts and zinc & careseeking for fever, malaria, or childhood pneumonia (22%)
  5. Vaccinations (11%)
494
Q

Describe the immune system at birth?

A
  • Immunodeficient at birth

- Move from sterile environment to pathogenic

495
Q

Describe the woman’s immune system during pregnancy?

A
  • Mother needs to ignore foetal alloantigens (half of antigens being of paternal i.e. foreign origin)
  • ‘Immunosuppressive’ environment of womb moving to ‘dampened’ responsiveness to avoid inflammatory responses to benign/harmless antigens
496
Q

Describe the immune system during late gestation?

A

Balance of Th1 (cell-mediated immunity) & Th2 (humoral immunity) cytokines is characterized by an initial prevalence of Th2 cytokines, followed by a progressive shift toward Th1 predominance

497
Q

Describe the immune system in neonates?

A

Increased susceptibility to pathogens & reduced responses to vaccines

498
Q

Describe the transfer of protection during pregnancy?

A
  • Immunoglobulin (IgG) predom in third trimester

- Breast feeding

499
Q

List the 4 LRTI pathogens prevalent in neonates?

A
  1. Grp B Strep
  2. E coli
  3. Resp viruses
  4. Enteroviruses
500
Q

List the 3 LRTI pathogens prevalent in young infants?

A
  1. Resp viruses
  2. Enteroviruses
  3. Chylamydia
501
Q

List the 2 LRTI pathogens prevalent in infants & young children?

A
  1. Strep pneumonia

2. Resp viruses

502
Q

List the 3 LRTI pathogens prevalent in older children?

A
  1. Mycoplasma pneumonae
  2. Strep. Pneumonia
  3. Resp viruses
503
Q

List the 6 meningitis pathogens prevalent in neonates?

A
  1. Grp B Strep
  2. E coli
  3. Haemophilus Type B (Hib)
  4. Meningiococcus
  5. Strep Pneumonia
  6. Listeria
504
Q

List the 4 meningitis pathogens prevalent in 1-3 months?

A
  1. Meningiococcus
  2. Strep Pneumonia
  3. Hib
  4. Listeria
505
Q

List the 3 meningitis pathogens prevalent in 3 months-5 years?

A
  1. Meningiococcus
  2. Strep Pneumonia
  3. Hib (rare)
506
Q

List the 2 meningitis pathogens prevalent in >6yrs?

A
  1. Meningiococcus

2. Strep Pneumonia

507
Q

Describe acquiring active immunity?

A

Generally involves cellular responses, serum antibodies or a combination acting against one or more antigens on the infecting organism

508
Q

Describe immunity acquired by natural disease or vaccination?

A

Antibody mediated or cell mediated components

509
Q

Describe Antibody mediated immunity?

A
  • B cell encounters an antigen that it recognises, it’s stimulated to proliferate & produce large numbers of lymphocytes secreting an antibody to this antigen
  • Replication & differentiation of B cells into plasma cells is regulated by contact with the antigen & by interactions with T cells
510
Q

Describe Cell medicated immunity?

A
  • T cells mediate 3 principal functions: help, suppression & cytotoxicity
  • T-helper cells stimulate immune response of other cells (stimulate B cells to produce antibodies)
  • T-suppressor cells play an inhibitory role & control level & quality of the immune response
  • Cytotoxic T cells recognise & destroy infected cells & activate phagocytes to destroy pathogens they have taken up
511
Q

How do vaccines work?

A

Induce active immunity & immunological memory

512
Q

What can vaccines be made from?

A

Inactivated (killed) or attenuated live organisms, secreted products, recombinant components or the constituents of cell walls

513
Q

What type of vaccine is WCPertussis & IPV?

A

Inactivated bacteria/virus

514
Q

What type of vaccine is Tet/Diptheria?

A

Inactivated toxins

515
Q

What type of vaccine is Pneumococcal?

A

Capsular polysaccharide

516
Q

Describe the primary response to a vaccine?

A
  • IgM mediated followed by IgG
  • Commonly need 2 or more injections to elicit response in young infants (primary or priming course)
  • Further injections lead to accelerated response lead by IgG (secondary reponse)
517
Q

What do some inactivated vaccines contain?

A

Adjuvants which are substances that enhance the antibody response

518
Q

Describe the issue with vaccines with plain polysaccharide antigens?

A
  • They do not stimulate the immune system as broadly as protein antigens such as tetanus, diphtheria or influenza
  • Protection is not long-lasting & response in infants & young children is poor
519
Q

How have some polysaccharide vaccines been enhanced?

A

By conjugation- the polysaccharide antigen is attached to a protein carrier (e.g. Hib & MenC vaccines) giving better immunological memory

520
Q

What should happen for an immune response with live attenuated vaccines?

A

The live organism must replicate (grow) in the vaccinated individual over a period of time (days or weeks)

521
Q

Describe live attenuated vaccines?

A
  • Usually promote a full, long lasting immune response after 1-2 doses
  • Vaccine virus is weakened or ‘attenuated ‘ but a mild form of the disease may rarely occur
  • Not to be given to immunocompromised individuals
522
Q

List 3 live attenuated vaccines?

A
  1. MMR
  2. VZV (rotavirus)
  3. Intranasal influenza
523
Q

What is herd immunity?

A
  • Vaccinated individuals not only less likely to get disease but also less likely to be a source of infection to others
  • Unvaccinated individuals are therefore protected
  • Interrupts cycle of infection & reservoirs e.g. Small pox
524
Q

What is the recommendation for the MMR vaccine & why?

A

At least 95% of children to receive a first vaccination MMR vaccine before age 2 years & a booster before 5 years to achieve herd immunity & prevent outbreaks

525
Q

What are the 4 UK immunisations given at 2 months?

A
  1. DTaP/IPV/HiB/HepB
  2. Pneumococcal vaccine
  3. Rotavirus vaccine
  4. Men B vaccine
526
Q

What are the 2 UK immunisations given at 3 months?

A
  1. DTaP/IPV/HiB/HepB (2nd dose)

2. Rotavirus vaccine (2nd dose)

527
Q

What are the 3 UK immunisations given at 4 months?

A
  1. DTaP/IPV/HiB/HepB (3rd dose)
  2. Pneumococcal vaccine (2nd dose)
  3. Men B vaccine (2nd dose)
528
Q

What are the 4 UK immunisations given at 12-13months?

A
  1. MMR vaccine
  2. Hib/Men C booster vaccine
  3. Pneumococcal vaccine (3rd dose)
  4. Men B vaccine (3rd dose)
529
Q

What is the UK immunisation given at 2-8years?

A

Children’s annual flu vaccine

530
Q

What are the 2 UK immunisations given at 3 years- 4 months?

A
  1. DTaP/IPV

2. MMR vaccine (2nd dose)

531
Q

What is the UK immunisation given at 12-13 years (girls)?

A

HPV vaccine

532
Q

What are the 2 UK immunisations given at 13-18years?

A
  1. Td/IPV

2. Men ACWY vaccine

533
Q

What does DTa/IPV vaccine stand for?

A

Diptheria, tetanus, acellular pertussis & inactivated polio virus

534
Q

Describe Streptococcus Pneumonia?

A
  • Capsule: major virulence factor
  • Over 90 different capsular types have been characterised
  • Prior to PCV 80% of invasive infections in children were caused by 8-10 capsular types
535
Q

What type of infection can some serotypes of pneumococcus cause?

A

May be carried in the nasopharynx without symptoms, with disease occurring in a small proportion of infected individuals

536
Q

What 2 things does Streptococcus Pneumonia cause?

A

Bacteraemia (community acq) & meningitis (major cause of morbidity & mortality)

537
Q

What 3 individuals is Streptococcus Pneumonia particularly problematic?

A
  1. Under 2s
  2. Immunocompromised
  3. Asplenics
538
Q

What is the vaccine for Streptococcus Pneumonia ?

A

Prenevar13

539
Q

What is the most common presentation of Haemophilus influenza (Hib)?

A

Meningitis

540
Q

What is Haemophilus influenza (Hib) meningitis frequently accompanied by?

A
  1. Bacteraemia 60%
  2. Epiglottis 15%
  3. Pneumonia
  4. Cellulitis
541
Q

What individuals have the highest incidence of Haemophilus influenza (Hib)?

A

Under 5s

542
Q

What does Meningococcal infection (Neisseria meningitidis) most commonly present as?

A

Either meningitis or septicaemia, or a combination of both

543
Q

Describe the 4 clinical assessments of childhood infections?

A
  1. Poor responses to vaccines
  2. Unable to communicate/localise
  3. Unable to tolerate oral meds
  4. Correct dose of meds
    ‘the younger the age, the more cautious the approach’
544
Q

What are 2 infectious factors for people who are functionally immunocompromised?

A
  1. Wider range of pathogens

2. Infections disseminate more easily

545
Q

What is the clinical approach to the febrile child?

A
  • Take a good history
  • Fever duration & measurement
  • Assessment of severity
  • Localising systems
  • Causation (pathogen)
  • Is the patient well/unwell?
  • Should I be acting now or do I have time to observe?
546
Q

What are the 4 clinical signs for assessing infection severity in an infant?

A
  1. Feeding/vomiting
  2. Crying
  3. Sleeping
  4. Smiling
547
Q

What are the 3 clinical signs for assessing infection severity in a child?

A
  1. Feeding
  2. Activity levels
  3. Drowsiness
548
Q

What 2 factors are important in assessing infection of a child/infant?

A
  1. Localising symptoms- cough, coryza, vomiting, diarrhoea, rash, dysuria, headache, sore ears/throat
  2. Causation- nursery contacts etc.

MBChB Year 3 (15 decks)

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