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Phase 3 > Week 7 > Flashcards

Week 7 Flashcards

1
Q

What are the two categories of bacterial GI infection?

A

infection and intoxication

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2
Q

Describe infection

A

bacterial pathogens develop in the gut after ingestion of contaminated food
e.g salmonella, campylobacter, pathogenic E.coli
incubation time at least 8-12 hours before symptoms develop

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3
Q

Describe contamination

A

bacterial pathogens grow in foods and produce toxins
examples - bacillus cereus, staph.aureas
relative short incubation time because of preformed toxin in food

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4
Q

What is diarrhoea?

A 
abnormal frequency and/or watery stool
usually indicates small bowel disease
causes fluid and electrolyte loss
severity varies widely from mild self-limiting to severe/fatal
virulence of organism
degree of compromise of the host
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5
Q

Describe gastroenteritis

A

nausea, vomiting, diarrhoea and abdominal discomfort

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6
Q

Describe dysentery

A

inflammatory disorder of the large bowel
blood and pus in faeces
pain, fever and abdominal cramps

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7
Q

Describe enterocolitis

A

inflammatory process affecting small and large bowel

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8
Q

What are the manifestations of GI infection within the GIT?

A 
toxin effects (cholera)
inflammation due to microbial invasion (shigellosis)
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9
Q

Describe the manifestations of GI infection out with the GIT

A

systemic effect of toxins (STEC)

invasive infection of GIT with wider dissemination (metastatic salmonella infection)

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10
Q

What is the barrier in the mouth to GI infection?

A

lysozyme

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11
Q

What is the barrier in the stomach to GI infection?

A

acid pH

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12
Q

What are the barriers in the small intestine to GI infection?

A 
mucous
bile
secretory IgA
lymphoid tissue (Peyer's patches)
epithelial turnover
normal flora
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13
Q

what are the barriers to GI infection in the large intestine?

A

epithelial turnover

normal flora

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14
Q

What are the main sources of GI infection?

A

zoonotic - symptomatic animals and asymptomatic shredders
human carriers (typhoid)
environmental sources

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15
Q

What is meant by the faecal-oral route?

A

any means by which infectious organisms from human / animal faeces can gain access to GIT of another susceptible host

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16
Q

What are the three Fs?

A

food
fluid
fingers

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17
Q

When is person to person transmission more likely?

A

small infectious dose

ability to contaminate and persist in the environment

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18
Q

What is important in the history of GI infection?

A

vomiting, abdominal pain, diarrhoea, frequency and nature of symptoms, travel history, food history, other affected individuals, speed of onset of illness, blood in stols

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19
Q

What should be examined for GI infection?

A

abdominal exam
temperature
features of dehydration

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20
Q

What are the laboratory diagnosis techniques for bacterial GI infection?

A

enrichment broth
selective media
differential media

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21
Q

Which species of bacteria are non-lactose fermenters?

A

salmonella and shigella

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22
Q

Why are antibiotics not generally used to treat GI infections?

A

may prolong symptoms duration
may exacerbate symptoms
promotes emergence of antibiotic resistance
may actually be harmful (STEC infection)

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23
Q

How can GI infections be controlled?

A

adequate public health measures
education in hygienic food preparation
pasteurisation of milk and dairy products
sensible travel food practises

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24
Q

What is the microbiology of campylobacter?

A

curved gram negative bacilli
microaerophilic and thermophilic
culture of campylobacter selective agar
C.jejuni most important species

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25
Q

What is the epidemiology of campylobacter?

A 
commonest bacterial food borne infection in UK
large animal recevoir
transmitted via contaminated food
peaks in May and september 
person to person spread rare 
large point outbreaks uncommon
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26
Q

Describe the pathogenesis of campylobacter

A

inflammation, ulceration and bleeding in small and large bowel due to bacterial invasion
bacteraemia can occur
rarely causes post-infectious demyelination syndrome (guillain-barre) ascending paralysis

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27
Q

What are the clinical features of campylobacter infection?

A 
incubation 2-5 days
bloody diarrhoea
cramping abdominal pain
vomiting not common
fever 2-10 day duration
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28
Q

What is the treatment of campylobacter infection?

A

fluid replacement
clarithromycin for severe/persistent disease
quinolone or amino glycoside for invasive disease

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29
Q

What are the specific control points for campylobacter infection?

A

reduction of contamination in raw, retail poultry meat

adequate cooking

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30
Q

What is the microbiology go salmonella?

A 
gram negative bacilli
member of enterobacteriacaeae
most human infection caused by salmonella enteric
non-lactose fermenters
XLD plates used in labs
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31
Q

Describe the epidemiology of salmonella infection

A

found in animals
acquired via contaminated food - especially pork, poultry and other meat and dairy products
large foodbrone outbreaks can occur (can multiply on food)
secondary spread from person to person can occur
seasonal peals in summer and autumn

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32
Q

What is the pathogenesis of salmonella infection?

A

diarrhoea due to invasion of epithelial cells in distal small intestine and subsequent inflammation
bacteraemia can occur
distant organs may become seeded to establish metastatic foci _osteomyelitis, septic arthritis , meningitis

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33
Q

What are the clinical features of salmonella infection?

A 
incubation 12-72 hours
watery diarrhoea
vomiting is common
fever can occur with more invasive disease
duration 2-7 days
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34
Q

What is the treatment of salmonella infection?

A

fluid replacement

beta lactams, quinolone or ahminoglycosides for severe infections

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35
Q

What are the specific control points for salmonella infection?

A

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

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36
Q

Describe the microbiology of shigella infection

A 
gram negative bacilli
member of enterobacteriaceae
4 species - sonnei, body and flexneri, dysenteriae
non-lactose fermenters 
XLD plates used
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37
Q

Describe the epidemiology of shigella infection

A

mainly associated with diarrhoea disease in children
S.dysenteriae in developing world
humans only resevoir
large outbreaks can occur
does not persist in environment
person to person spread via person to person route
recent outbreaks associated with MSM

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38
Q

Describe the pathogenies of shigella infection

A

organisms attach to and colonise mucosal epithelium of terminal ileum and colon
no systemic invasion
S.dysenteriae produces an exotoxin (shiga toxin) which not only damages intestinal epithelium but can lead to HUS

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39
Q

What are the clinical features of shigella infection?

A 
dysentery
incubation 1-3 days
duration 2-7 days
initially watery diarrhoea followed by bloody diarrhoea
marked cramping abdominal pain
vomiting is uncommon
fever is usually present
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40
Q

what is the treatment of shigella infection?

A

usually self-limting
fluid replacement
some will need treatment for renal failure

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41
Q

What are the specific control points for shigella infection?

A

only found in humans, good standards of sanitation and personal hygiene are key measures

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42
Q

Describe the microbiology of vibrio cholerae

A

comma shaped gram negative bacilli
serotype O1, _classical and El Tor and serotype O130
sucrose fermenter. Thiosulphate bile sucrose selective / differential medium

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43
Q

What is the epidemiology of vibrio cholerae?

A

cause of epidemic and pandemic cholera
endemic in parts of SE asia, africa and south america
only infects humans, asymptomatic human resevoir
can only live in fresh water
spreads via contaminated food or water
direct person to person is uncommon

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44
Q

What is the pathogenesis of vibrio cholera infection?

A

flagella and mucinase facilitate penetration of intestinal mucosa
attachment by specific receptors
diarrhoea due to production of potent protein exotoxin

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45
Q

What are the clinical features of vibrio choleae infection?

A

severe, profuse, watery diarrhoea
profound fluid loss and dehydration pecipitates hypokalaemia, metabolic acidosis, hypovolaemic shock, metabolic acidosis and cardiac failure

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46
Q

What is the treatment of cholera?

A

prompt oral or IV rehydration is life saving

tetracycline antibiotics may shorten duration of shredding

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47
Q

What are the specific control points for cholera?

A

no animal reservoir

clean drinking water supply and proper sanitation are key preventative measures

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48
Q

What are the 6 diarrhoeagenic groups of e.coli?

A 
enteropathogenic (EPEC)
enterotoxigenic (ETEC)
enterohaemorrhagic (EHEC)
enteroinvasive (EIEC)
enters-aggregative (EAEC)
diffuse aggregative (DAEC)
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49
Q

Describe the microbiology of EPEC

A

no differential media available
test selection of colonies using polyvalent antisera for common EPEC serum types
not routinely done

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50
Q

Descrive the epidemiology of EPEC

A

sporadic cases and some outbreaks or diarrhoea in infants and children
cause of some cases of traveller’s diarrhoea

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51
Q

Describe the pathogenesis of EPEC

A

initial adherence via pilli followed by formation of characteristic attaching and effacing lesion mediated bt intimin protein and Tir (translocated intimin receptor) and disruption of intestinal microvilli

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52
Q

Describe the clinical features of EPEC

A

incubation 1-2 days
duration 1-several weeks
watery diarrhoea with abdominal pain and vomiting
often accompanied by fever

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53
Q

Describe the microbiology of ETEC

A

no differential media available
test liquid cultures for production of toxins by immunoassays
not routinely done

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54
Q

describe the epidemiology of ETEC

A

major bacterial cause of diarrhoea in infants and children in developing world
major cause of travellers diarrhoea

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55
Q

Describe the pathogenesis of EHEC

A

diarrhoea due to action of 1 or 2 plasmid encoded toxins
heat labile (function analogue of cholera toxin)
heat stabile

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56
Q

Describe the clinical feats of ETEC

A

incubation 1-7 days
duration 2-6 days
watery diarrhoea, abdominal pain and vomiting
no associated fever

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57
Q

Describe the microbiology for EHEC

A

more than 100 serotypes
best known O157:H7
non-sorbitol fementer. Sorbitol MacConkey agar (SMAC)

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58
Q

Describe the epidemiology of EHEC

A

outbreaks and sporadic
large animal resevoirs
persistent in environment
consumption of contaminated food, water and dairy products and direct environment l contact with animal faeces
secondary person to person spread important (low infectious dose)

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59
Q

Describe the pathogenesis of EHEC

A

attaching and effacing lesion

production of shiga like toxins. structural and functional analogue of shigella dystenteriae toxin (STEC)

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60
Q

What are the clinical features of EHEC?

A 
incubation 1-7 days
duration 5-10 days
bloody diarrhoea with abdominal pain and vomiting
no associated fever
haemolytic uraemic syndrome
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61
Q

Describe HUS

A

microangionpathic haemolytic anaemia
thrombocytopenia
acute renal failure

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62
Q

Describe the microbiology for staph. aureas

A

gram positive cocci
grow well in routine media
testing for enterotoxins not routinely performed

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63
Q

Describe the epidemiology and pathogenesis of staph.aureas

A

50% produce enterotoxins
heat stable and acid-resistant toxins
food is contaminated by human carriers
esepcilly cooked meats, cakes and pastries
bacteria multiply at room temperature and produce toxins

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64
Q

What are the clinical features of staph.aureas GIT infection?

A

incubation 30 minutes to 6 hours
duration 12-24 hours
profuse vomiting and abdominal cramps
no fever and no diarrhoea

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65
Q

What is the control of GIT staph.aureas infection?

A

hygienic food preparation to minimise contamination

refrigerated storage

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66
Q

describe the microbiology of bacillus cereus

A

aerobic, spore forming gram positive bacilli

not routinely tested for

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67
Q

Describe the epidemiology and pathogenesis of bacillus cereus infection

A

spores and vegetative cells contaminate wide range of foodstuffs
2 types of disease - emetic and diarrhoeal

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68
Q

Describe emetic bacillus cereus

A

typically associated with fried rice
spores survice initial boiling
if rice is bulk cooled and stored prior to frying, the spores germinate, multiply and re-sporulate
protein enterotxoni produced during sporulation
heat stable toxin survives further frying

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69
Q

Describe diarrhoea bacillus cereus

A

spores in food service cooking, germinate and organisms multiply in food
ingensted organisms produce and heat labile toxin in the gut with similar mode of action to cholera toxin

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70
Q

Describe the clinical features of emetic bacillus cereus

A

incubation 30 minutes to 6 hours
duration 12-24 hours
profuse vomiting with abdominal cramps and watery diarrhoea

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71
Q

Describe the clinical features of diarrhoeal bacillus cereus

A

incubation 8-12 ours
duration 12-24 hours
watery diarrhoea with cramping abdominal pain, but no vomiting
no fever

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72
Q

Describe the microbiology of clostridium perfringes

A

anaerobic, spore forming gram postive bacilli

not routinely tested for

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73
Q

Describe the epidemiology and pathogenies of clostridium perfringes

A

spores and vegetative cells ubiquitive in soil and animal gut
contaminated food stuff
often involves but-cooking of stews, meat pies
spores survice cooking, germinate and organisms multiply in cooling food
food inadequately reheated to kill organism
organisms ingested and sporulate in large intestine with production of enterotoxin

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74
Q

Describe the clinical features of clostridium perfringens

A

incubation 6-12 hours
duration 12-24 hours
watery diarrhoea and abdominal cramps
no fever or vomiting

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75
Q

Describe the control of clostridium perfringens

A

rapid chilling/freezing of bulk-cooked foods

thorough re-haeting before consumption

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76
Q

Describe the microbiology of clostridium botulinum

A

anaerobic, spore forming gram postive bacilli

lab diagnosis bases upon toxin detection

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77
Q

Describe the epidemiology and pathogenesis of clostridium botulinum

A

very uncommon in UK
spores and vegetative cells ubiquitive in soil and animal GIT
produces powerful heat labile protein neurotoxin
foodborn botulism - pre-formed toxin in good. commonly associated with canned foods
infant botulism - organisms germinate in gut of babies fed honey containing spores and toxins are produced in gut
wound botulism - organisms implanted in wound produce toxin
absorbed toxins spread via blood an enter peripheral nerves were to cause neuromuscular blockade at synapses

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78
Q

Describe the clinical features of clostridium botulinum

A

neuromuscular blockade results in flaccid paralysis and progressive muscle weakness
involvement of muscles of chest/ diaphragm cause respiratory failure
high mortality if untreated

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79
Q

What is the treatment of botulism/

A

urgent intensive supportive care due to difficulties breathing and swallowing
antitoxin

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80
Q

What is the control for botulism?

A

proper manufacturing controls in canning industry
hygienic food preparation
proper cooking
refrigerated storage

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81
Q

describe the microbiology of C.dif

A

anaerobic, spore forming gram postive bacili
spores resistant to heat, drying, disinfection, alcohol
clinical featrures due to production of potent toxin
lab diagnosis based on two step algorithm

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82
Q

Describe the epidemiology and pathogenesis or c.dif

A

spores and vegetative cells ubiquitous in environment
carriage 3-5 % adults in community
30% of hospitalised patients
asymptomatic carriage rates may be very high in infants
infection requires the disruption of normal gut flora
predominantly affects the elderly
major cause of healthcare associated infections

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83
Q

What are the clinical features of C.dif infection?

A

mild to severe with abdominal pain
severe cases may develop pseudomembranous colitis
fulminant cases may progress to colonic dilatation and perforation
severe cases may be fatal
relapses are common and may be mutiple

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84
Q

What is the treatment of C.dif?

A

stop precipitating antibiotics
oral metronidazole or oral vancomycin is severe or not improving
refractory recurrent disease may require faecal transplant

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85
Q

Describe how C.dif can be controlled?

A

antimicrobial stewardship
infection and prevention control measures
cleaning/disinfection with hypochlorite disinfectants

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86
Q

Describe the microbiology listeria monocytogenes

A

gram postive coccobacilli
selective culture media available for culture from suspect foods
standard lab for blood and CSF samples

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87
Q

Describe the epidemiology and pathogenesis of listeria monocytogenes

A

widespread among animals and the environment
pregnant women, elderly and immunocompromised
contaminated foods - unpasteurised milk and soft cheese, pate, cooked meats, smoked fish and coleslaw
ready to eat food and produce
can multiply at 4 degrees
invasive infection from GIT results in systemic spread via bloodstream

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88
Q

Describe the clinical features of listeria

A

median incubation period 3 weeks
duration of illness 1-2 weeks
initial flu-like illness with or without diarrhoea
majority of cases present its severe systemic infection - septicaemia, mengingitis

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89
Q

What is the treatment of listeria?

A

IV antibiotics (ampicillin and synergistic gentamicin )

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90
Q

What is the control of listeria?

A

susceptible groups should avoid high risk foods
observe use by dates
wash raw fruit and vegetables and avoid cross contamination

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91
Q

Describe the microbiology of H.pylori

A

gram negative spiral shaped bacilli
microaerophilic. urease postive
diagnosis by detection of faecal antigen or urea breath test. serum antibody tests

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92
Q

Describe the epidemiology and pathogenesis of H.pylori

A

one of the most coon bacterial infections in the world
faecal oral or oral-oral
humans the only reservoir
infection acquired in childhood and persists life long unless treated
pathogenesis is complex involving cytotoxin production, and a range of factors to promote adhesion and coloniation

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93
Q

What are the clinical features of H.pylor?

A

infection is asymptomatic unless ulcer develops

gastric cancer risk

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94
Q

What is the treatment of H.pylori?

A

combined treatment with a PPI and combinations of antibiotics such as clarithromycin and metronidazole eradicates carriage and facilitates ulcer healing

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95
Q

Who are at higher risk of viral gastroenteritis?

A

children under 5
old age people especially in nursing home
immunocomprimised

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96
Q

What are the important viruses that cause gastroenteritis?

A 
norovirus
sappovirus
rotavirus 
adenovirus 40&41
astrovirus
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97
Q

What are the calciviridae viruses?

A

norovirus and sappovirus

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98
Q

Who is affected by norovirus?

A

all ages but often most serious in young and elderly

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99
Q

Who is affected by rotavirus/adenovirus/astrovirus?

A

mainly children under 2, elderly, immunocomprimised

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100
Q

What are the structural features of norovirus?

A

non enveloped, single stranded RNA virus
six gene groups, only 3 affect humans
genogroups divided into atleast 32 geneotypes
most common in UK if the GIi-4 strain

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101
Q

What is the transmission of norovirus?

A

person to person (faecal-oral, aerosolised)
food -borne
water
infectious dose very small
all ages
very stable and remain viable in the environment
24-48 hour incubation period
can shed for up to 3 weeks after infection

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102
Q

what are the clinical features of norovirus?

A 
may be asymptomatic 
vomiting
diarrhoea
nausea
abdominal cramps
headache
fever
dehydration in young and elderly 
usually lasts 12-60 hours
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103
Q

What are the complications of norovirus

A

significant proportion of childhood hospitalisation
illness in hospital last longer
post infection complications in elderly
chronic diarrhoea and virus shredding in transplant patients

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104
Q

What is the treatment of norovirus?

A 
symptomatic therapy 
oral and IV fluids
antispasmodics
analgesics
antipyretics
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105
Q

Describe the immunity to norovirus

A

immunity lasts only 6-14 weeks

can’t be cultured- no vaccine

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106
Q

Describe infection control in norovirus

A 
isolation or cohorting
exclude symptomatc staff until well for 48 hours
do not move patients
do no admit new patients 
thorough cleaning of wards
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107
Q

Describe roatvirus

A

reoviridae
double stranded, non enveloped RNA virus
5 stains G1-4 , G9
11 strands of RNA so potential for much antigenic variation
stable in environment and fairly resistant to hand washing

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108
Q

Describe transmission of rotavirus

A

low infectious dose
mainly person to person via faecal oral or fomites
food and water spread is possible spread via respiratory droplets is speculated

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109
Q

Describe the clinical featrures of rotavirus

A

incubation 1-3days
clinical manifestations depend of 1st infection or reinfection
watery diarrhoea
abdominal pain
vomiting
loss of electrolytes
lasts 3-7 days
1st infection after age of 3 months is most severe
hospital outbreaks in paediatric wards common

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110
Q

What are the complications of rotavirus?

A 
severe chronic diarrhoea
dehydration
electrolyte imbalance
metabolic acidosis 
immunodeficiency children may have more severe or persistent disease
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111
Q

Describe the immunity to rotavirus

A

antibodies and VP8 and VP4
IgA
1 st infection usually severe
doesn’t lead to permanent immunity - subsequent infections less severe
re-infection can occur at any age
young children may suffer up to 5 reinfections by age 2

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112
Q

Describe adenovirus

A

double stranded DNA virus
40 &41 cause gastroenteritis
fever and watery diarrhoea
supportive treatment

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113
Q

Describe astrovirus

A

single stranded, non enveloped RNA virus
astrovridae family
cause less severe infection than other enteric pathogens
mainly sporadic but can be outbreaks in young childern

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114
Q

How are gastroenteritis viruses diagnosed?

A

PCR
testing done in virology lab
vomit or stool samples

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115
Q

What is the common stain used to detect TB?

A

Ziehl Neelson

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116
Q

What can lead to the reactivation of TB?

A

immunosuppression, HIV infectionm smoking

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117
Q

What is a Goon complex?

A

a TB nodule found in the lung and a regional lymph node - central mediastinum and cervical chain

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118
Q

What is seen on chest X ray in primary TB?

A

consolidation

lymphadenopathy -

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119
Q

What are the two directions that primary TB infection can take?

A

90% healing, calcificaition, dormant organisms
which can lead to reactivation or reinfection later
or 10% lead to progressive primary tuberculosis
greater susceptibility in certain racial groups, children and immunocompromised

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120
Q

Describe the appearance on chest X-ray of secondary TB

A

attack and destruction of apices of lung
dramatic on CT scan
forms cavities
apex has highest PO2 - greatest oxygenation - attractive the the mycobacteriumTB

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121
Q

What does a lung infected with TB appear grossly?

A

caseous necrosis
breakdown of tissue
gas exchange impaired

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122
Q

What is milliary TB?

A

very widely disseminated
more common in children and immunosuppressed
also in CNS and other areas of the body
classically primary

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123
Q

Describe CNS TB

A

not too uncommon

can get TB meningitis if it is in the CSF - indolent course over weeks - clouding of conciousness

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124
Q

Describe renal TB

A

ascends from bladder

can invade reproduction tracts as well

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125
Q

Where else can TB infect?

A

bone and joint
axial skeleton -
back pain - spread from IV disc to invade adjacent vertebrae
can encroach spinal cord - infarction leading to paraplegia
psoas muscles through sheath - leading to psoas abscess

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126
Q

Describe a granuloma in TB

A

central necrosis
epitheloid cells (activated macrophages)
giant cells
lymphocytes

127
Q

Describe the immunity to MTB

A

cell mediated immunity crucial
macrophages key controlling cell
T cell production of interferon gamma
cytokines involved in this process are key

128
Q

Why does cell mediated immunity fail to clear the TB microbe?

A

TB can remain viable within macrophages - they can no longer divide, but are not killed either

129
Q

What test can be used to see if someone has been exposed to TB?

A

Mantoux reaction

130
Q

Describe the treatment of TB

A

long duration - 6 months
combination of drugs to reduce risk of resistance
at least 2 drugs to which the bacilli are sensitive must be present; drug resistance increasingly common
some drugs only effective when bacilli dividing rapidly and lack effect against slower growing forms - pyrazinamide

131
Q

Describe the drug therapy of TB

A

rifampicin, isonizid, pyrazinamide and ethambutol
drop ethambutol if sensitive to rif and iso
stop pyrazinamide after 2 months
continue rif and iso for further 6 months

132
Q

What is given with TB treatment as prophylaxis and why?

A

pyridoxine to prevent neuropathy caused by isoniazid

133
Q

What is latent TB treatment?

A

recent migrants , new workers.
Isoniazid and rifampicin for 3 months
or isoniazid for 6 months

134
Q

What are the important considerations with drug treatment of TB?

A

rifampicin induces cytochrome P450 and this alters metaobolims of many drugs - steroids
rifampicin, isoniazid and pyrazinamide metabolised in liver - potential for toxicity
ethambutol can affect vision
rifampicin turns urine reddish

135
Q

Describe the pathogenesis of pneumonia

A

lungs should be sterile below the carina

infection can occur if there is a host defence defect, large innocuous, or increased pathogen virulence

136
Q

What are the typical pathogens that cause pneumonia?

A

step. pneumoniae
haemophilus influenza
mortadella catharralis

137
Q

What is the most common cause of pneumonia?

A

strep. pneumonae

138
Q

What are the atypical pathogens that cause pneumonia?

A

mycoplasma pneumoniae
legionella pneumoniae
chlamoydophila pneumoniae
chlamydophilia psittaci

139
Q

What are the risk factors for strep pneumonia?

A 
alcohol 
HIV
smoking 
chronic lung disease
flu
140
Q

Describe the clinical features of strep pneumoniae

A 
abrupt onset
cough 
fever
pleuritic chest pain
dull percussion
coarse crepitations 
increased vocal resonance
141
Q

What is the treatment of Strep.P pneumonia?

A

penicillin

allergy then macrocodes or tetracyclines

142
Q

Where is penicillin resistant pneumonia common?

A

south europe, asia, north america

143
Q

In what patients in haemophilia influenzae pneumonia more common

A

older people

underlying disease

144
Q

What other infections can H.I lead to

A

otitis media
conjungtivitis
sinusitis
CNS infections

145
Q

Describe the clinical features of H.influenzae pneumonia

A 
abrupt onset
cough
fever
pleuritic chest pain
dull precision
coarse crepitations 
increased vocal resonance
146
Q

What is the treatment of H.influenzae?

A

amoxicillin
or if risk of beta lactamase - co amoxiclave
macrolides
tetracyclines

147
Q

Describe mycoplasma pneumoniae

A

smallest free living bacterium

lack of cell wall very difficult to grow

148
Q

When does M.pneumoniae peak?

A

autumn and winter

149
Q

Describe the clinical features of M.pneumoniae pneumonia

A

atypical
flu lik eillness
other symptoms dominate over cough

150
Q

What can M.pneumoniae lead to?

A 
cold haemolysis 
guillain-barre
erythema multiforme - target lesion
cardiac - conduction problems 
arthrits- reactive arthritis
151
Q

How is M.pneumoniae diagnosed?

A

serology
PCR
Cant culture

152
Q

How is P.pneumoniae treated?

A

macrolides
tetracyclines
quinolones

153
Q

Describe how legionella pneumophila infects people

A

lives in amoeba in the environment - hot tubs, showers

hospitals, hotels , aircon outlets

154
Q

Describe the symptoms of legionaires disease

A

headache, myalgia, fatigue, fever, maybe cough

155
Q

how is legionella. pneumoniae diagnosed/

A

culture - difficult
serolgoy
urinary antigen test - most used

156
Q

What is the treatment of L.pneumoniae

A

macrolides
quinolones
tetracyclines

157
Q

What history is important in a patient with pneumonia?

A 
fever
cough / sputum
chest pain
insidious/abrupt onset
non respiratory symptoms 
underlying lung disease
immunosuppression
ill contacts
travel 
water exposure
158
Q

What is the CURB65 score?

A 
confusion
urea >7
RR >30
B - BP, diastolic <60, or systolic <90
65 - aged over 65
159
Q

What else has to be considered with the CURB65 score?

A

SIRS

multilobar consolidation on CXR and /or hypoxia on room air

160
Q

What investigations should be done in a patient with pneumonia?

A 
FBCs, U&amp;E, ABGs/O2 sats
blood culutres
sputum cultures
throat swab
urine legionella antigen
chest x ray
ECG
161
Q

What is the management of patient with pneumonia?

A 
ABC
antibiotics - IV or oral?
Admission to hospital?
CURB65 >2
SIRS >2
hypoxia
162
Q

How can viral respiratory infections be prevented?

A

only flu has vaccine

basic hygiene is the most important

163
Q

How can viral respiratory infections spread?

A

direct contact
indirect contact
water droplets

164
Q

What causes the common cold?

A

rhinovirus and coronavirus

165
Q

Describe pharyngits

A

mostly viral
headache, cold, cough, aches and pain
most common cause is adenovirus
outbreaks of respiratory illness - preceding diarrhoea, conjunctivitis renal disease

166
Q

Describe croup

A

childhood infectious syndrome
distinctive barking cough
mostly mild but responsible for significant A&E visits (rapid onset, breathing difficulties )
parainfluenza virus supportive treatment - steroids and nebulisers if severe)

167
Q

When does parainfluenza 3 virus peak?

A

spring and summer

168
Q

What is bronchiolitis?

A 
affects children under 2
infection of brochioles
severe
URT symptoms 
wheeze, tachypnoea , poor feeding
need admission if increased O2 requirements 
supplemental feeding 
ventilation and nebulisers if severe
169
Q

Describe respiratory syncytial virus

A

(RSV)
paramyxovirus ssRNA
main cause of bronchiolitis worldwide
most children infected by age 2
major nosocomial hazard to at risk patients - cohering, PPE< hand washing
adults with chronic lung disease and the elderly

170
Q

How is RSV treated?

A

Ribivirin (oral, IV, aerosolised)
numerous side effects
prophylactic monoclonal antibody given to high risk children IM monthly

171
Q

Describe influenza virus

A 
ability to cause annual epidemics and occasional pandemics 
3 types A-4
A - most significant illness
B - endemics only 
C - not major infection
172
Q

What are the symptoms of the flu?

A 
headache
fever
muscle pain
joint pain
runny nose
sore throat
cough
vomiting
173
Q

What are the common complications of flu?

A 
acute otitis media
sinusitis 
pneumonia
exacerbation of underlying disease
dehydration (infants)
174
Q

What are the uncommon complications of flu?

A 
encephalopathy
Reye syndrome (children)
myositis
myocarditis
febrile seizures
175
Q

What type of drug is tyamiflu?

A

neuroadminidase inhibitor - prevents virus exiting cells

176
Q

What is a flu pandemic?

A

worldwide epidemics of a newly emerged strain of influenza

177
Q

What type of virus is SARS?

A

coronavirus

178
Q

What are the benefits of molecular testing for respiratory viruses?

A

highly sensitive
rapidly developed to detect new/emerging pathogens
can by multiplexed to detect multiple pathogens from a single sample
semi quantitative
rapid turn around time

179
Q

What is bacteriuria

A

bacteria in the urine

180
Q

What is urosepsis?

A

temp >38
HR >90
RR >20
WBC >15 or <4

181
Q

Who are at risk of bacteriuria?

A 
hospitalised
catheterised
diabetics 
anatomical abnormalities 
pregnant patients
182
Q

When should asymptomatic bacteriuria be treated?

A

only in preschool children
pregnancy
(renal transpant
immunocompromised)

183
Q

When is infection with multiple organisms more likely in UTI?

A

long term catheters
recurrent infection
structural / neurological abnormalities

184
Q

When are multi drug resistant organisms more likely to be present in UTIs?

A

anatomical/neurological abnormaliites
frequent infections
multiple antibiotic courses
prophylactic antibiotic use

185
Q

What are the clinical features of UTIs?

A 
suprapubic discomfort 
dysuria
urgency
frequency
cloudy, blood stained, smelly urine
low-grade fever
sepsis
failure to thrive, jaundice in neonates
abdominal pain and vomiting in children
nocturne, incontinence, confusion in the elderly
186
Q

What organisms are commonly involved in UTis?

A 
E.coli
Klebsiella sp
Proteus sp
pseudomonas sp
streptococcus so 
staph 
anaerobes (bladder cancer)
candida
187
Q

What investigations should be carried out in LUTIS in non-pregnant women?

A

1st presentation, culture not mandatory
dipstick - high false positive rate, check previous culture results
antibiotics for 3-7 days
urine culture and change antibiotic if no response to treatment

188
Q

What should the management be for a man with a LUTI?

A

send urine for each and every presentation

treat appropriately

189
Q

Describe management of UTI in pregnancy

A 
common
send urine at each presentaition
treat for 7-10 days 
amoxicillin and cefalexin quite safe
avoid trimethoprim 1st trimester avoid nifrofurantoin near term
hospital  for IV if severe 
can develop pyelonephritis (30%)
190
Q

Describe recurrent UTI

A

> 2 episodes in 6 months or >3 episodes in a year

mostly women

191
Q

How should recurrent UTIs be managed?

A

send sample with each episode
encourage hydration
encourage urge initiated and post coital voiding
cranberry productsintravaginal / oral oestrogen
urology investigation

192
Q

What is meant by CAUTI?

A

catheter associated UTI

193
Q

Why is infection more likely with catheters?

A

disturbance of flushing system
colonisation of urinary catheter
biofilm production by bacteria

194
Q

What are the complications of catheters?

A 
CAUTI
obstruction hydronephrosis
chronic renal inflammation
urinary tract stones 
long term risk of bladder cancer
195
Q

How can catheter infections be prevented?

A 
catheterise only if necessary
remove when no longer needed
remove/replace id causing infection
catheter care (bundles)
hand hygeine
196
Q

How is CAUTI treated?

A

check previous microbiology
start empirical antibiotics
remove catheter if not needed
replace catheter under antibiotic cover

197
Q

What is acute pyelonephritis?

A 
upper urinary tract infection
moderate to severe
ascending infection involving pelvis of kidney 
enlarged kidney 
raised abscesses on surface of kidney
198
Q

How is acute pyelonephritis managed?

A 
check previous microbio
send urine /blood culture/imagine
community - trimethoprim/cipro/coamxiclav
hospital - often broad spec
may remain symptomatic for a few days
no response warrants further investigation
uncomplicated 7-14 days antibiotics 
complicated >14 days antibiotics
199
Q

Describe renal abscesses

A 
complication of pyelonephritis 
similar symptoms 
usually positive urine and blood culture
gram negative bacilli likely 
can become life threatening 
poor response to antibiotics
200
Q

What are the risk factors for perinephric abscesses?

A

untreated LUTI, anatomical abnormalities
renal calculi
bacteraemia, haematogenous spread

201
Q

What are the symptoms of perinephric abscess?

A

similar to pyelonephritis

localised signs/ symptoms

202
Q

What is the treatment of perinephric abscess?

A 
usually positive blood cultures
pyuria 
treat empirically as complicated UTI
poor response to antibiotic therapy 
surgical management
203
Q

How should complicated UTIs be managed?q

A 
FBC, U&amp;E, CRP
urine sample
blood culture
renal ultrasound
CT KUB
antibiotic therapy 14 days or more
204
Q

What antibiotics can be used in uncomplicated UTIs?

A

amoxicillin, trimethoprim, nitrofurantoin, pivmecillinam, fosfomycin

205
Q

What antibiotics are used in complicated UTIS?

A

amoxicillin/vanc

gent/ aztreonam/ temocillin

206
Q

Describe acute bacterial prostatitis

A 
localised infection
usually spontaenois
may follow urethral instrumentation
fever, perineal/back pain, UTI, urinary retention
diffuse oedema, micro abscesses
207
Q

What are the likely organisms in acute prostatitis?

A

gram negative bacilli
S.aureas (MSSA,MRSA)
N.gonorrhoea

208
Q

What are the investigations for acute prostatitis?

A 
urine culture
blood culture
Trans-rectal U/S
CT/MRI
obtaining prostatic secretions not advisable
209
Q

What are the complications of acute bacterial prostatitis?

A 
prostate abscess
spontaneous rupture -urethra, rectum
epididymiitis
pyelonephritis
systemic sepsis
210
Q

What is antibiotic management of acute bacterial prostatitis?

A

check recent/ previous microbiology
ciprofloxacin / oflaxacin (no strep cover)
D/W microbiology in systemic infections

211
Q

Describe chronic prostatitis

A 
rarely associated with acute prostatitis
may follow chlamydia urethritis
recurrent UTIs
diagnosis difficult
relapse common
most asymptomatic
212
Q

What are the symptoms of epdidymitis?

A

pain, fever, selling, penile discharge

symtoms of UTI/urethritis

213
Q

What are the common organisms in epididymitis?

A

GNB, enterococci, staph
TB in risk areas and individuals
in sexually active men rule out chlamydia and gonrrohea

214
Q

What is orchitis?

A 
inflammation of one or both testicles 
testicular pain and swelling
dysuria
fever
penile discharge
215
Q

What are the complications of orchitis?

A

testicular infarction abscess fomration

216
Q

What is fournier’s gangrene?

A

form of necrotising fasciitis
usually >50 years of age
rapid onset and spreading infection
systemic sepsis

217
Q

What are the risk factors for fournier’s gangrene?

A

UTI
complications of IBD
trauma
recent surgery

218
Q

what is the management of fournier’s gangrene?

A 
blood cultures
urine
tissue/pus
surgical debridement 
D/W microbiology
broad spectrum/ combination antibiotics initially
219
Q

Why is sex good for us?

A

fitter
lower rates of depressive symptoms
better cardiovascular health

220
Q

When is sex bad for us?

A 
non-consensual
exploitative 
sexual dysfunction
unwanted conception
infection
221
Q

What are the principles of STI management

A 
diagnosis before treatment 
screen for accompanying STIs
simple treatment regimens
follow-up after treatment
partner notification
non-judgemental patient support, counselling, education
222
Q

What is important to know if a patient reports with an STI?

A

last time any type of sex
who was it with - gender, location
type of sex - e.g receptive anal sex
condom use or not

223
Q

What is the appearance of gonorrhoea under the microscope?

A

gram negative diplicocci in white cells

224
Q

What is the test for gonorrhoea?

A

NAAT test
males urine is acceptable (first flow)
vulvovaginal swab for women (self taken is fine)

225
Q

What is the main drug the gonorrhoea is resistant to in the UK?

A

ciprofloxacin

226
Q

What is the syndromic management of male urethral discharge?

A

ceftriaxone 500mg IM
azithromycin Ig stat
partner notification

227
Q

Describe chlamydia trachomatis

A

frequently asymptomatic

infection can lead to tubal damage/infertility

228
Q

What is the treatment of chlamydia?

A

azithromycin oral stat

or doxycycline 100mgBDX 7 days - compliance may be an issue

229
Q

Describe lymphogranuloma venereum

A 
LGV
lymphotrophic chlamydia
severe proctitis causing constipation, rectal bleeding
looks like cancer or Crohn's
inguinal "bubos"
230
Q

For which STI is it important to look at the palms and soles for rash?

A

syphilis

231
Q

What is the natural history of syphilis?

A 
exposure 
primary lesion (chancre)
secondary lesion (rash)
latent syphilis (+ve serology only)
tertiary syphilis  -gumma, cardiovascular, neurological
232
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

233
Q

What is the treatment of syphilis?

A

benzathine penicillin
1 injection is primary or recent
3 injections in more than 2 years
14 infections is neurological symptoms

234
Q

Give examples of viral STIs

A 
HPV
herpes simplex virus
molluscum contagiosa
HIV
Hep B and C
235
Q

What is the treatment for genital warts?

A

cryotherapy
condyline - dropper solution or cream
aldara - immune mediator - increases local immune response of skin

236
Q

What is the treatment for genital herpes?

A

400mg 3X per day for 5 days

237
Q

How is HIV transmitted?

A

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

238
Q

What are activities that allow HIV transmission?

A 
anal or vaginal intercourse
very low risk from oral sex
mother to child transmission 
healthcare settings
transmission via donated blood or clotting factors
239
Q

How does HIV cause illness?

A

infects cells in the immune system such as T helper cells, macrophages and T helper cells that all carry CD4 receptors
HIV infection causes depletion of CD4 helper cells by direct killing, apoptosis of uninfected “bystander” cells
CD8 cytotoxic killing of infected cells
abnormal B cell activation resulting in excess Immunoglobulin production

240
Q

What is the general structure of HIV?

A

2 strands of RNA

3 of its own enzymes - reverse transcriptase, protease and integrate enzymes

241
Q

What are drug targets for HIV?

A

fusion inhibitor, R5 inhibitor
NRTI, NNRTI (reverse transcriptase)
integrase inhibitors
protease inhibitors

242
Q

Describe HIV latency

A

viral latency is a state of reversible nonproductive infection of individuals cells
IN HIV, the term latency is generally used to describe the long asymptomatic period between initial infection and advanced HIV
HIV is actively replicating at this time even during the asymptomatic period

243
Q

Describe HIV resistance

A

As it multiplies in the body, it mutates and produces variations of itself, variations develop while a person is taking HIV medications can lead to drug resistant strains of HIV

244
Q

Describe the CD4 cell count

A

calculated from total lymphocyte count
HIV negative- 600-1200 per mm3
risk of opportunistic infection increases sharply below 200/mm3

245
Q

What is the HIV viral load?

A

“set point” the lower the better
measured using log 10 scale
below 10,000 low above 100000 is high
undetectable means below 40 copies / ml

246
Q

What are the main symptoms of acute HIV infection?

A 
fever
weight loss
mouth sores, thrush
oesophageal sores
myalgia
liver and spleen enlargement
malaise headache 
neuropathy 
lymphadenopathy 
rash
nausea
vomiting
247
Q

What is the differential diagnosis for primary HIV infection rash?

A

infectious mononucleosis
secondary syphilis
drug rash
viral infections - CMV, rubella, influenza, parvovirus

248
Q

What are the UK national HIV testing guidelines?

A

increase testing levels in primary care settings
increase testing levels among non-HIV specialists in secondary caer
to make HIV testing routine in secondary care settings where HIV indicator conditions are present

249
Q

What is HAART?

A 
highly active  antiretroviral treatment
triple therapy 
2  nucleosides and 1 drug from another class
suppress viral load to undetectable 
CD4 recovery
250
Q

What are the challenges with ART?

A 
good adherence (>95% essential)
psychological impact
short term side effects
drug-drug interactions 
emerging longer term toxicites
251
Q

Describe the short term toxicity of ART=

A 
rash
hypersenstivity
CNS side effects - sleep disturbance, vivid dreams, mood changes
GI side effects 
renal 
hepatic
252
Q

Describe drug interactions in ART

A

usually class specific
mediated by CYP450
PPIs, statins antipsychotics - QTc

253
Q

Describe the long term toxicity of ART

A 
body shape changes
renal
hepatic
lipid
bone
254
Q

How is mother to child HIV transmission prevented?

A 
treat mother during pregnancy 
minimise risk at delivery
treat baby early on
avoid breast feeding 
universal antenatal HIV screening
255
Q

What are the social dimensions of HIV?

A

vulnerable populations - further marginalisation
access to healthcare
provision od ARVs - life long, management of ARV complications
single parent families / orphaned children
disabilities
stigma

256
Q

What can an untreated joint infection lead to?

A

severe sepsis - septic shock
loss of cartilage
osteoarthritis in later life

257
Q

How does septic arthritis normally present?

A

fever
single or multiple hot joints
loss of movement
pain

258
Q

What are the key investigations for septic arthritis?

A

blood cultures
joint aspiratie (gram, microscopy for crystals and culture)
FBC
CRP imaging

259
Q

What are the common pathogens in septic arthritis?

A 
MSSA or MRSA
streptococci (s.pyrogenes, Group G s.pneumoccocus in children)
H.influenzae
king ella
N.meningitidis
N.gonorrhoea
E.coli
P.aeruginosa
salmonella species
260
Q

What is the treatment of septic arthritis?

A

At least 2 weeks of IV antibiotics
often three weeks IV followed by 3 weeks oral
monitor response by CRP and clinical

261
Q

What is an arthroplasty?

A

putting in an artificial joint

262
Q

What is resection arthroplasty?

A

taking the diseased joint out and putting in an artificial one

263
Q

What is a revision arthroplasty?

A

re-operating on an artificial joint

264
Q

What are the risk factors for infection in primary arthroplasty?

A 
rheumatoid arthrits
diabetes 
poor nutritional status
obesity
concurrent UTI
steroids 
malignancy
265
Q

What are the risk factors for infection in revision arthroplasty?

A

prior joint surgery
prolonged operating room time
pre-op infection

266
Q

Describe local spread in prosthetic joint infections

A

60-80% of PJIs
mostly organisms from skin surface
direct communication between skin surface and prosthesis while fascial planes heal
usually manifests in immediate post-op period

267
Q

Describe haematogenous spread in PJIs

A

presents later
intact surrounding connective tissue often limits infection to bone/cement interface
can be any organism

268
Q

Describe the pathogenesis of PJIs

A

prosthesis requires fewer bacteria to establish sepsis than does soft tissue
avascular surface allow survival of bacteria as protects from circulating immunological defences and most antibiotics
cement can inhibit phagocytosis and lymphocyte/complement function

269
Q

What is the clinical presentation of a septic arthritis?

A 
pain
effusion
warm joint
fever and systemic symptoms
prosthetic joint - loosening on Xray
discharging sinus
mechanical dysfunction
270
Q

What are the surgical options in an infected prosthetic joint/

A

debride, antibiotics, implant repair or take the infected joint out (put in replacement then or at a later date)

271
Q

Which antibiotics can penetrate bone?

A

cephalosporins, taxocin, carbapenems, fusidic acid, doxycycline, rifampicin, linezolid, trimethoprim, ciprofloxacin, clindamycin

272
Q

What is osteomyelitis?

A

progressive infection of bone characterised by death of bone and the formation of sequestra

273
Q

How can osteomyelitis be established?

A

haematogenous spread

contiguous spread - overlying infection, trauma, surgical inoculation

274
Q

How is osteomyelitis treated?

A

surgery to debunk infection back to healthy bone and manage dead space that remains
stabilise infected fractures and to deride sinuses and close wounds
antibiotic choice is determined by what grows from debrideed bone
may require 4-6 weeks IV antibiotics

275
Q

Describe diabetic foot infection

A

more complex than septic arthritis

usually involves bone but can also involve joints

276
Q

Describe vertebral discitis

A

infection of a disc space and adjacent vertebral end plates
can be very destructive with deformity, spinal instability risking cord compression
remember TB
similar organisms to septic arthritis and osteomyelitis

277
Q

what are the biggest killers of children under 5?

A

neonatal
diarrhoea
malaria
pneumonia

278
Q

Describe pregnancy and immunity

A

immune system functionally immunodeficient at birth
move from sterile environment to pathogenic
mother needs to ignore foetal antigens
“immunosuppressive” environment of womb moving to dampened responsiveness to avoid inflammatory responses to benign antigens
balance between Th1(cell mediated) and Th2 (humeral) shifts towards Th1 predominance at the end of gestation
increased susceptibility to pathogen and reduced responses to vaccines in neonates

279
Q

How can the mother transfer immune protection to the baby?

A

IgG is transferred in the third trimester

breast feeding

280
Q

What are LRTIs most likely to be caused by in neonates?

A

Grp B strep
e.coli
respiratory viruses
enteroviruses

281
Q

What are LRTIS most likely to be caused by in young infants?

A

respiratory viruses
enteroviruses
chlamydia

282
Q

What are LRTIs most likely to be caused by in infants and young children?

A

strep pneumonia, respiratory virsues

283
Q

What are LRTIs most likely to be caused by in older children?

A

mycoplasma pneumonia
strep.pneumoniae
respiratory viruses

284
Q

What is meningitis most likely to be caused by in neonates?

A 
Grp B strep
e.coli
haemophilia type B
meningococcus
strep pneumoniae
listeria
285
Q

What is meningitis most likely to be caused by in 1-3 months olds?

A

meningiococcus
strep pneumoniae
hib
listeria

286
Q

What is meningitis most likely to be caused by in children aged 3months to 5 years?

A

meningococcus,
strep pneumoniae
Hib (rare)

287
Q

What is meningitis most likely to be caused by in children over 6 years old?

A

meningiococcus

strep pneumoniae

288
Q

Describe immunisation

A

acquiring active immunity - generally involves cellular responses, serum antibodies or a combination acting against one or more antigens of the infected organisms
acquired by natural disease or vaccination - antibody mediated or cell mediated components

289
Q

Describe antibody mediated immunity

A

when a B cell encounters an antigen that it recognises, the B cell is stimulated to proliferate and produce large numbers of lymphocytes secreting a antibody to this antigen. Replication and differentiation of B cells into plasma cells is regulated with the antigens and by interactions with T cells

290
Q

Describe cell mediated immunity

A

T cells mediate three principle functions - help, suppression and cytotoxicity. Helper cells stimulate the immune response of other cells. suppressor cells play an inhibitory role and control the level and quality of the immune response, Cytotoxic T cells recognise and destroy infected cells and activate phagocytes to destroy pathogens they have taken up

291
Q

How do vaccines work?

A

induce active immunity and immunological memory
primary response - IgM followed by IgG - commonly need 2 or more injections to elect response in young infants
further injections lead to accelerated response lead by IgG (secondary)

292
Q

What do adjuvants in vaccines do?

A

enhance the antibody response

293
Q

What type of vaccines are WCpertussis and IPV?

A

inactivated bacteria/virus

294
Q

What type of vaccines are tet/diptheria?

A

inactivated toxins

295
Q

What sort of vaccine is pneumococcal?

A

capsular polysaccharide

296
Q

Describe conjugate vaccines

A

plain polysaccharide antigens do not stimulate the immune system as partly as protein antigens such as tetanus diphtheria or influenza
protection from these vaccines is not long lasting and response in young children is poor
in conjugation polysaccharide antigens is attached to protein carrier (His, MenC) giving better immunological memory

297
Q

Describe live attenuated viruses

A

to produce an immune response, the live organism must replicate in the vaccinated individual over a period of time
usually promote a full, long lasting immune response in 1-2 doses
vaccine is weakened but a mild form of the disease may rarely occur
MMR, VZV, intranasal influenza
not to be given in immunocompromisedd individuals

298
Q

Describe herd immunity

A

vaccinated individuals not only less likely to get disease but also less lily to be a source of infection to others
unvaccinated individuals are therefore protected
interrupts cycle of infection and reservoirs

299
Q

What vaccines to children get at 2 months?

A

DTaP/IPV / Hib/ Hep B
pneumococcal vaccine
rotavirus vaccine
men B vaccine

300
Q

What vaccines do children get at 3 months?

A

men C
DTaP/IPV?Hib (2nd)
rotavirus vaccine (2nd)

301
Q

What vaccines do children get at 4 months?

A

DTaP/IPV/HiB (3rd)
pneumococcal (2nd)
Men B (2nd)

302
Q

What vaccines do children get at 12-13 months?

A

MMR
Hib/men C booster
pneumococcal vaccine (3rd)
Men B vaccine (3rd)

303
Q

What vaccines do children get at 2, 3, and 4 plus primary school?

A

children annual flu vaccine

304
Q

What vaccines do children get at 3 years and 4 months?

A

DTaP/IPV

MMR (2nd)

305
Q

What vaccines do children get from 12-13 years?

A

HPV

306
Q

what vaccines to children get from 13-18 years?

A

Td/IPV

MenACWY

307
Q

Which childhood vaccinations are live attenuated?

A

rotavirus
MMR
intranasal influenza

308
Q

Describe streptococcus pneumonia in children

A

capsule - major virulence factor
over 90 different capsular types
some serotypes may be carried in nasopharynx without symptoms
most frequent cause of bacteraemia and meningitis
particularly problematic in under 2s, immunocomromised and asplenics

309
Q

What are the most common presentations of invasive Hib disease?

A

meningitis
frequently accompanied by - epiglossitis
bacteraemia
pneumonia, cellulitis

310
Q

Describe the clinical assessment of a child with infection

A 
functionally immunocompromised - wider range of pathogens, infections disseminate more quickly
poor responses to vaccines
unable to communicate /localise
unable to tolerate oral meds
correct doe of meds?
311
Q

Describe the clinical approach to the febrile child?

A 
good histroy
fever - duration and measurement 
assessment of severity 
localising symptoms 
causations
312
Q

How do you assess the severity of an infection in an infant?

A

feeding/vomiting
crying
sleeping
smiling

313
Q

How do you assess the severity of an infection in a child?

A

feeding
activity levels
drowsiness

Phase 3 (15 decks)

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