Week 7 Flashcards
(313 cards)
1
Q
What are the two categories of bacterial GI infection?
A
infection and intoxication
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
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
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
5
Q
Describe gastroenteritis
A
nausea, vomiting, diarrhoea and abdominal discomfort
6
Q
Describe dysentery
A
inflammatory disorder of the large bowel
blood and pus in faeces
pain, fever and abdominal cramps
7
Q
Describe enterocolitis
A
inflammatory process affecting small and large bowel
8
Q
What are the manifestations of GI infection within the GIT?
A
toxin effects (cholera) inflammation due to microbial invasion (shigellosis)
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)
10
Q
What is the barrier in the mouth to GI infection?
A
lysozyme
11
Q
What is the barrier in the stomach to GI infection?
A
acid pH
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
13
Q
what are the barriers to GI infection in the large intestine?
A
epithelial turnover
normal flora
14
Q
What are the main sources of GI infection?
A
zoonotic - symptomatic animals and asymptomatic shredders
human carriers (typhoid)
environmental sources
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
16
Q
What are the three Fs?
A
food
fluid
fingers
17
Q
When is person to person transmission more likely?
A
small infectious dose
ability to contaminate and persist in the environment
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
19
Q
What should be examined for GI infection?
A
abdominal exam
temperature
features of dehydration
20
Q
What are the laboratory diagnosis techniques for bacterial GI infection?
A
enrichment broth
selective media
differential media
21
Q
Which species of bacteria are non-lactose fermenters?
A
salmonella and shigella
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)
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
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
25
What is the epidemiology of campylobacter?
```
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
```
26
Describe the pathogenesis of campylobacter
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
27
What are the clinical features of campylobacter infection?
```
incubation 2-5 days
bloody diarrhoea
cramping abdominal pain
vomiting not common
fever 2-10 day duration
```
28
What is the treatment of campylobacter infection?
fluid replacement
clarithromycin for severe/persistent disease
quinolone or amino glycoside for invasive disease
29
What are the specific control points for campylobacter infection?
reduction of contamination in raw, retail poultry meat
| adequate cooking
30
What is the microbiology go salmonella?
```
gram negative bacilli
member of enterobacteriacaeae
most human infection caused by salmonella enteric
non-lactose fermenters
XLD plates used in labs
```
31
Describe the epidemiology of salmonella infection
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
32
What is the pathogenesis of salmonella infection?
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
33
What are the clinical features of salmonella infection?
```
incubation 12-72 hours
watery diarrhoea
vomiting is common
fever can occur with more invasive disease
duration 2-7 days
```
34
What is the treatment of salmonella infection?
fluid replacement
| beta lactams, quinolone or ahminoglycosides for severe infections
35
What are the specific control points for salmonella infection?
the introduction of immunisation of poultry flocks lead to a dramatic reduction in S.enteridid in the UK
36
Describe the microbiology of shigella infection
```
gram negative bacilli
member of enterobacteriaceae
4 species - sonnei, body and flexneri, dysenteriae
non-lactose fermenters
XLD plates used
```
37
Describe the epidemiology of shigella infection
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
38
Describe the pathogenies of shigella infection
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
39
What are the clinical features of shigella infection?
```
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
```
40
what is the treatment of shigella infection?
usually self-limting
fluid replacement
some will need treatment for renal failure
41
What are the specific control points for shigella infection?
only found in humans, good standards of sanitation and personal hygiene are key measures
42
Describe the microbiology of vibrio cholerae
comma shaped gram negative bacilli
serotype O1, _classical and El Tor and serotype O130
sucrose fermenter. Thiosulphate bile sucrose selective / differential medium
43
What is the epidemiology of vibrio cholerae?
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
44
What is the pathogenesis of vibrio cholera infection?
flagella and mucinase facilitate penetration of intestinal mucosa
attachment by specific receptors
diarrhoea due to production of potent protein exotoxin
45
What are the clinical features of vibrio choleae infection?
severe, profuse, watery diarrhoea
profound fluid loss and dehydration pecipitates hypokalaemia, metabolic acidosis, hypovolaemic shock, metabolic acidosis and cardiac failure
46
What is the treatment of cholera?
prompt oral or IV rehydration is life saving
| tetracycline antibiotics may shorten duration of shredding
47
What are the specific control points for cholera?
no animal reservoir
| clean drinking water supply and proper sanitation are key preventative measures
48
What are the 6 diarrhoeagenic groups of e.coli?
```
enteropathogenic (EPEC)
enterotoxigenic (ETEC)
enterohaemorrhagic (EHEC)
enteroinvasive (EIEC)
enters-aggregative (EAEC)
diffuse aggregative (DAEC)
```
49
Describe the microbiology of EPEC
no differential media available
test selection of colonies using polyvalent antisera for common EPEC serum types
not routinely done
50
Descrive the epidemiology of EPEC
sporadic cases and some outbreaks or diarrhoea in infants and children
cause of some cases of traveller's diarrhoea
51
Describe the pathogenesis of EPEC
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
52
Describe the clinical features of EPEC
incubation 1-2 days
duration 1-several weeks
watery diarrhoea with abdominal pain and vomiting
often accompanied by fever
53
Describe the microbiology of ETEC
no differential media available
test liquid cultures for production of toxins by immunoassays
not routinely done
54
describe the epidemiology of ETEC
major bacterial cause of diarrhoea in infants and children in developing world
major cause of travellers diarrhoea
55
Describe the pathogenesis of EHEC
diarrhoea due to action of 1 or 2 plasmid encoded toxins
heat labile (function analogue of cholera toxin)
heat stabile
56
Describe the clinical feats of ETEC
incubation 1-7 days
duration 2-6 days
watery diarrhoea, abdominal pain and vomiting
no associated fever
57
Describe the microbiology for EHEC
more than 100 serotypes
best known O157:H7
non-sorbitol fementer. Sorbitol MacConkey agar (SMAC)
58
Describe the epidemiology of EHEC
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)
59
Describe the pathogenesis of EHEC
attaching and effacing lesion
| production of shiga like toxins. structural and functional analogue of shigella dystenteriae toxin (STEC)
60
What are the clinical features of EHEC?
```
incubation 1-7 days
duration 5-10 days
bloody diarrhoea with abdominal pain and vomiting
no associated fever
haemolytic uraemic syndrome
```
61
Describe HUS
microangionpathic haemolytic anaemia
thrombocytopenia
acute renal failure
62
Describe the microbiology for staph. aureas
gram positive cocci
grow well in routine media
testing for enterotoxins not routinely performed
63
Describe the epidemiology and pathogenesis of staph.aureas
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
64
What are the clinical features of staph.aureas GIT infection?
incubation 30 minutes to 6 hours
duration 12-24 hours
profuse vomiting and abdominal cramps
no fever and no diarrhoea
65
What is the control of GIT staph.aureas infection?
hygienic food preparation to minimise contamination
| refrigerated storage
66
describe the microbiology of bacillus cereus
aerobic, spore forming gram positive bacilli
| not routinely tested for
67
Describe the epidemiology and pathogenesis of bacillus cereus infection
spores and vegetative cells contaminate wide range of foodstuffs
2 types of disease - emetic and diarrhoeal
68
Describe emetic bacillus cereus
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
69
Describe diarrhoea bacillus cereus
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
70
Describe the clinical features of emetic bacillus cereus
incubation 30 minutes to 6 hours
duration 12-24 hours
profuse vomiting with abdominal cramps and watery diarrhoea
71
Describe the clinical features of diarrhoeal bacillus cereus
incubation 8-12 ours
duration 12-24 hours
watery diarrhoea with cramping abdominal pain, but no vomiting
no fever
72
Describe the microbiology of clostridium perfringes
anaerobic, spore forming gram postive bacilli
| not routinely tested for
73
Describe the epidemiology and pathogenies of clostridium perfringes
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
74
Describe the clinical features of clostridium perfringens
incubation 6-12 hours
duration 12-24 hours
watery diarrhoea and abdominal cramps
no fever or vomiting
75
Describe the control of clostridium perfringens
rapid chilling/freezing of bulk-cooked foods
| thorough re-haeting before consumption
76
Describe the microbiology of clostridium botulinum
anaerobic, spore forming gram postive bacilli
| lab diagnosis bases upon toxin detection
77
Describe the epidemiology and pathogenesis of clostridium botulinum
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
78
Describe the clinical features of clostridium botulinum
neuromuscular blockade results in flaccid paralysis and progressive muscle weakness
involvement of muscles of chest/ diaphragm cause respiratory failure
high mortality if untreated
79
What is the treatment of botulism/
urgent intensive supportive care due to difficulties breathing and swallowing
antitoxin
80
What is the control for botulism?
proper manufacturing controls in canning industry
hygienic food preparation
proper cooking
refrigerated storage
81
describe the microbiology of C.dif
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
82
Describe the epidemiology and pathogenesis or c.dif
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
83
What are the clinical features of C.dif infection?
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
84
What is the treatment of C.dif?
stop precipitating antibiotics
oral metronidazole or oral vancomycin is severe or not improving
refractory recurrent disease may require faecal transplant
85
Describe how C.dif can be controlled?
antimicrobial stewardship
infection and prevention control measures
cleaning/disinfection with hypochlorite disinfectants
86
Describe the microbiology listeria monocytogenes
gram postive coccobacilli
selective culture media available for culture from suspect foods
standard lab for blood and CSF samples
87
Describe the epidemiology and pathogenesis of listeria monocytogenes
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
88
Describe the clinical features of listeria
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
89
What is the treatment of listeria?
IV antibiotics (ampicillin and synergistic gentamicin )
90
What is the control of listeria?
susceptible groups should avoid high risk foods
observe use by dates
wash raw fruit and vegetables and avoid cross contamination
91
Describe the microbiology of H.pylori
gram negative spiral shaped bacilli
microaerophilic. urease postive
diagnosis by detection of faecal antigen or urea breath test. serum antibody tests
92
Describe the epidemiology and pathogenesis of H.pylori
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
93
What are the clinical features of H.pylor?
infection is asymptomatic unless ulcer develops
| gastric cancer risk
94
What is the treatment of H.pylori?
combined treatment with a PPI and combinations of antibiotics such as clarithromycin and metronidazole eradicates carriage and facilitates ulcer healing
95
Who are at higher risk of viral gastroenteritis?
children under 5
old age people especially in nursing home
immunocomprimised
96
What are the important viruses that cause gastroenteritis?
```
norovirus
sappovirus
rotavirus
adenovirus 40&41
astrovirus
```
97
What are the calciviridae viruses?
norovirus and sappovirus
98
Who is affected by norovirus?
all ages but often most serious in young and elderly
99
Who is affected by rotavirus/adenovirus/astrovirus?
mainly children under 2, elderly, immunocomprimised
100
What are the structural features of norovirus?
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
101
What is the transmission of norovirus?
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
102
what are the clinical features of norovirus?
```
may be asymptomatic
vomiting
diarrhoea
nausea
abdominal cramps
headache
fever
dehydration in young and elderly
usually lasts 12-60 hours
```
103
What are the complications of norovirus
significant proportion of childhood hospitalisation
illness in hospital last longer
post infection complications in elderly
chronic diarrhoea and virus shredding in transplant patients
104
What is the treatment of norovirus?
```
symptomatic therapy
oral and IV fluids
antispasmodics
analgesics
antipyretics
```
105
Describe the immunity to norovirus
immunity lasts only 6-14 weeks
| can't be cultured- no vaccine
106
Describe infection control in norovirus
```
isolation or cohorting
exclude symptomatc staff until well for 48 hours
do not move patients
do no admit new patients
thorough cleaning of wards
```
107
Describe roatvirus
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
108
Describe transmission of rotavirus
low infectious dose
mainly person to person via faecal oral or fomites
food and water spread is possible spread via respiratory droplets is speculated
109
Describe the clinical featrures of rotavirus
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
110
What are the complications of rotavirus?
```
severe chronic diarrhoea
dehydration
electrolyte imbalance
metabolic acidosis
immunodeficiency children may have more severe or persistent disease
```
111
Describe the immunity to rotavirus
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
112
Describe adenovirus
double stranded DNA virus
40 &41 cause gastroenteritis
fever and watery diarrhoea
supportive treatment
113
Describe astrovirus
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
114
How are gastroenteritis viruses diagnosed?
PCR
testing done in virology lab
vomit or stool samples
115
What is the common stain used to detect TB?
Ziehl Neelson
116
What can lead to the reactivation of TB?
immunosuppression, HIV infectionm smoking
117
What is a Goon complex?
a TB nodule found in the lung and a regional lymph node - central mediastinum and cervical chain
118
What is seen on chest X ray in primary TB?
consolidation
| lymphadenopathy -
119
What are the two directions that primary TB infection can take?
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
120
Describe the appearance on chest X-ray of secondary TB
attack and destruction of apices of lung
dramatic on CT scan
forms cavities
apex has highest PO2 - greatest oxygenation - attractive the the mycobacteriumTB
121
What does a lung infected with TB appear grossly?
caseous necrosis
breakdown of tissue
gas exchange impaired
122
What is milliary TB?
very widely disseminated
more common in children and immunosuppressed
also in CNS and other areas of the body
classically primary
123
Describe CNS TB
not too uncommon
| can get TB meningitis if it is in the CSF - indolent course over weeks - clouding of conciousness
124
Describe renal TB
ascends from bladder
| can invade reproduction tracts as well
125
Where else can TB infect?
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
126
Describe a granuloma in TB
central necrosis
epitheloid cells (activated macrophages)
giant cells
lymphocytes
127
Describe the immunity to MTB
cell mediated immunity crucial
macrophages key controlling cell
T cell production of interferon gamma
cytokines involved in this process are key
128
Why does cell mediated immunity fail to clear the TB microbe?
TB can remain viable within macrophages - they can no longer divide, but are not killed either
129
What test can be used to see if someone has been exposed to TB?
Mantoux reaction
130
Describe the treatment of TB
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
Describe the drug therapy of TB
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
What is given with TB treatment as prophylaxis and why?
pyridoxine to prevent neuropathy caused by isoniazid
133
What is latent TB treatment?
recent migrants , new workers.
Isoniazid and rifampicin for 3 months
or isoniazid for 6 months
134
What are the important considerations with drug treatment of TB?
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
Describe the pathogenesis of pneumonia
lungs should be sterile below the carina
| infection can occur if there is a host defence defect, large innocuous, or increased pathogen virulence
136
What are the typical pathogens that cause pneumonia?
step. pneumoniae
haemophilus influenza
mortadella catharralis
137
What is the most common cause of pneumonia?
strep. pneumonae
138
What are the atypical pathogens that cause pneumonia?
mycoplasma pneumoniae
legionella pneumoniae
chlamoydophila pneumoniae
chlamydophilia psittaci
139
What are the risk factors for strep pneumonia?
```
alcohol
HIV
smoking
chronic lung disease
flu
```
140
Describe the clinical features of strep pneumoniae
```
abrupt onset
cough
fever
pleuritic chest pain
dull percussion
coarse crepitations
increased vocal resonance
```
141
What is the treatment of Strep.P pneumonia?
penicillin
| allergy then macrocodes or tetracyclines
142
Where is penicillin resistant pneumonia common?
south europe, asia, north america
143
In what patients in haemophilia influenzae pneumonia more common
older people
| underlying disease
144
What other infections can H.I lead to
otitis media
conjungtivitis
sinusitis
CNS infections
145
Describe the clinical features of H.influenzae pneumonia
```
abrupt onset
cough
fever
pleuritic chest pain
dull precision
coarse crepitations
increased vocal resonance
```
146
What is the treatment of H.influenzae?
amoxicillin
or if risk of beta lactamase - co amoxiclave
macrolides
tetracyclines
147
Describe mycoplasma pneumoniae
smallest free living bacterium
| lack of cell wall very difficult to grow
148
When does M.pneumoniae peak?
autumn and winter
149
Describe the clinical features of M.pneumoniae pneumonia
atypical
flu lik eillness
other symptoms dominate over cough
150
What can M.pneumoniae lead to?
```
cold haemolysis
guillain-barre
erythema multiforme - target lesion
cardiac - conduction problems
arthrits- reactive arthritis
```
151
How is M.pneumoniae diagnosed?
serology
PCR
Cant culture
152
How is P.pneumoniae treated?
macrolides
tetracyclines
quinolones
153
Describe how legionella pneumophila infects people
lives in amoeba in the environment - hot tubs, showers
| hospitals, hotels , aircon outlets
154
Describe the symptoms of legionaires disease
headache, myalgia, fatigue, fever, maybe cough
155
how is legionella. pneumoniae diagnosed/
culture - difficult
serolgoy
urinary antigen test - most used
156
What is the treatment of L.pneumoniae
macrolides
quinolones
tetracyclines
157
What history is important in a patient with pneumonia?
```
fever
cough / sputum
chest pain
insidious/abrupt onset
non respiratory symptoms
underlying lung disease
immunosuppression
ill contacts
travel
water exposure
```
158
What is the CURB65 score?
```
confusion
urea >7
RR >30
B - BP, diastolic <60, or systolic <90
65 - aged over 65
```
159
What else has to be considered with the CURB65 score?
SIRS
| multilobar consolidation on CXR and /or hypoxia on room air
160
What investigations should be done in a patient with pneumonia?
```
FBCs, U&E, ABGs/O2 sats
blood culutres
sputum cultures
throat swab
urine legionella antigen
chest x ray
ECG
```
161
What is the management of patient with pneumonia?
```
ABC
antibiotics - IV or oral?
Admission to hospital?
CURB65 >2
SIRS >2
hypoxia
```
162
How can viral respiratory infections be prevented?
only flu has vaccine
| basic hygiene is the most important
163
How can viral respiratory infections spread?
direct contact
indirect contact
water droplets
164
What causes the common cold?
rhinovirus and coronavirus
165
Describe pharyngits
mostly viral
headache, cold, cough, aches and pain
most common cause is adenovirus
outbreaks of respiratory illness - preceding diarrhoea, conjunctivitis renal disease
166
Describe croup
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
When does parainfluenza 3 virus peak?
spring and summer
168
What is bronchiolitis?
```
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
Describe respiratory syncytial virus
(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
How is RSV treated?
Ribivirin (oral, IV, aerosolised)
numerous side effects
prophylactic monoclonal antibody given to high risk children IM monthly
171
Describe influenza virus
```
ability to cause annual epidemics and occasional pandemics
3 types A-4
A - most significant illness
B - endemics only
C - not major infection
```
172
What are the symptoms of the flu?
```
headache
fever
muscle pain
joint pain
runny nose
sore throat
cough
vomiting
```
173
What are the common complications of flu?
```
acute otitis media
sinusitis
pneumonia
exacerbation of underlying disease
dehydration (infants)
```
174
What are the uncommon complications of flu?
```
encephalopathy
Reye syndrome (children)
myositis
myocarditis
febrile seizures
```
175
What type of drug is tyamiflu?
neuroadminidase inhibitor - prevents virus exiting cells
176
What is a flu pandemic?
worldwide epidemics of a newly emerged strain of influenza
177
What type of virus is SARS?
coronavirus
178
What are the benefits of molecular testing for respiratory viruses?
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
What is bacteriuria
bacteria in the urine
180
What is urosepsis?
temp >38
HR >90
RR >20
WBC >15 or <4
181
Who are at risk of bacteriuria?
```
hospitalised
catheterised
diabetics
anatomical abnormalities
pregnant patients
```
182
When should asymptomatic bacteriuria be treated?
only in preschool children
pregnancy
(renal transpant
immunocompromised)
183
When is infection with multiple organisms more likely in UTI?
long term catheters
recurrent infection
structural / neurological abnormalities
184
When are multi drug resistant organisms more likely to be present in UTIs?
anatomical/neurological abnormaliites
frequent infections
multiple antibiotic courses
prophylactic antibiotic use
185
What are the clinical features of UTIs?
```
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
What organisms are commonly involved in UTis?
```
E.coli
Klebsiella sp
Proteus sp
pseudomonas sp
streptococcus so
staph
anaerobes (bladder cancer)
candida
```
187
What investigations should be carried out in LUTIS in non-pregnant women?
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
What should the management be for a man with a LUTI?
send urine for each and every presentation
| treat appropriately
189
Describe management of UTI in pregnancy
```
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
Describe recurrent UTI
>2 episodes in 6 months or >3 episodes in a year
| mostly women
191
How should recurrent UTIs be managed?
send sample with each episode
encourage hydration
encourage urge initiated and post coital voiding
cranberry productsintravaginal / oral oestrogen
urology investigation
192
What is meant by CAUTI?
catheter associated UTI
193
Why is infection more likely with catheters?
disturbance of flushing system
colonisation of urinary catheter
biofilm production by bacteria
194
What are the complications of catheters?
```
CAUTI
obstruction hydronephrosis
chronic renal inflammation
urinary tract stones
long term risk of bladder cancer
```
195
How can catheter infections be prevented?
```
catheterise only if necessary
remove when no longer needed
remove/replace id causing infection
catheter care (bundles)
hand hygeine
```
196
How is CAUTI treated?
check previous microbiology
start empirical antibiotics
remove catheter if not needed
replace catheter under antibiotic cover
197
What is acute pyelonephritis?
```
upper urinary tract infection
moderate to severe
ascending infection involving pelvis of kidney
enlarged kidney
raised abscesses on surface of kidney
```
198
How is acute pyelonephritis managed?
```
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
Describe renal abscesses
```
complication of pyelonephritis
similar symptoms
usually positive urine and blood culture
gram negative bacilli likely
can become life threatening
poor response to antibiotics
```
200
What are the risk factors for perinephric abscesses?
untreated LUTI, anatomical abnormalities
renal calculi
bacteraemia, haematogenous spread
201
What are the symptoms of perinephric abscess?
similar to pyelonephritis
| localised signs/ symptoms
202
What is the treatment of perinephric abscess?
```
usually positive blood cultures
pyuria
treat empirically as complicated UTI
poor response to antibiotic therapy
surgical management
```
203
How should complicated UTIs be managed?q
```
FBC, U&E, CRP
urine sample
blood culture
renal ultrasound
CT KUB
antibiotic therapy 14 days or more
```
204
What antibiotics can be used in uncomplicated UTIs?
amoxicillin, trimethoprim, nitrofurantoin, pivmecillinam, fosfomycin
205
What antibiotics are used in complicated UTIS?
amoxicillin/vanc
| gent/ aztreonam/ temocillin
206
Describe acute bacterial prostatitis
```
localised infection
usually spontaenois
may follow urethral instrumentation
fever, perineal/back pain, UTI, urinary retention
diffuse oedema, micro abscesses
```
207
What are the likely organisms in acute prostatitis?
gram negative bacilli
S.aureas (MSSA,MRSA)
N.gonorrhoea
208
What are the investigations for acute prostatitis?
```
urine culture
blood culture
Trans-rectal U/S
CT/MRI
obtaining prostatic secretions not advisable
```
209
What are the complications of acute bacterial prostatitis?
```
prostate abscess
spontaneous rupture -urethra, rectum
epididymiitis
pyelonephritis
systemic sepsis
```
210
What is antibiotic management of acute bacterial prostatitis?
check recent/ previous microbiology
ciprofloxacin / oflaxacin (no strep cover)
D/W microbiology in systemic infections
211
Describe chronic prostatitis
```
rarely associated with acute prostatitis
may follow chlamydia urethritis
recurrent UTIs
diagnosis difficult
relapse common
most asymptomatic
```
212
What are the symptoms of epdidymitis?
pain, fever, selling, penile discharge
| symtoms of UTI/urethritis
213
What are the common organisms in epididymitis?
GNB, enterococci, staph
TB in risk areas and individuals
in sexually active men rule out chlamydia and gonrrohea
214
What is orchitis?
```
inflammation of one or both testicles
testicular pain and swelling
dysuria
fever
penile discharge
```
215
What are the complications of orchitis?
testicular infarction abscess fomration
216
What is fournier's gangrene?
form of necrotising fasciitis
usually >50 years of age
rapid onset and spreading infection
systemic sepsis
217
What are the risk factors for fournier's gangrene?
UTI
complications of IBD
trauma
recent surgery
218
what is the management of fournier's gangrene?
```
blood cultures
urine
tissue/pus
surgical debridement
D/W microbiology
broad spectrum/ combination antibiotics initially
```
219
Why is sex good for us?
fitter
lower rates of depressive symptoms
better cardiovascular health
220
When is sex bad for us?
```
non-consensual
exploitative
sexual dysfunction
unwanted conception
infection
```
221
What are the principles of STI management
```
diagnosis before treatment
screen for accompanying STIs
simple treatment regimens
follow-up after treatment
partner notification
non-judgemental patient support, counselling, education
```
222
What is important to know if a patient reports with an STI?
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
What is the appearance of gonorrhoea under the microscope?
gram negative diplicocci in white cells
224
What is the test for gonorrhoea?
NAAT test
males urine is acceptable (first flow)
vulvovaginal swab for women (self taken is fine)
225
What is the main drug the gonorrhoea is resistant to in the UK?
ciprofloxacin
226
What is the syndromic management of male urethral discharge?
ceftriaxone 500mg IM
azithromycin Ig stat
partner notification
227
Describe chlamydia trachomatis
frequently asymptomatic
| infection can lead to tubal damage/infertility
228
What is the treatment of chlamydia?
azithromycin oral stat
| or doxycycline 100mgBDX 7 days - compliance may be an issue
229
Describe lymphogranuloma venereum
```
LGV
lymphotrophic chlamydia
severe proctitis causing constipation, rectal bleeding
looks like cancer or Crohn's
inguinal "bubos"
```
230
For which STI is it important to look at the palms and soles for rash?
syphilis
231
What is the natural history of syphilis?
```
exposure
primary lesion (chancre)
secondary lesion (rash)
latent syphilis (+ve serology only)
tertiary syphilis -gumma, cardiovascular, neurological
```
232
Describe secondary syphilis
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
What is the treatment of syphilis?
benzathine penicillin
1 injection is primary or recent
3 injections in more than 2 years
14 infections is neurological symptoms
234
Give examples of viral STIs
```
HPV
herpes simplex virus
molluscum contagiosa
HIV
Hep B and C
```
235
What is the treatment for genital warts?
cryotherapy
condyline - dropper solution or cream
aldara - immune mediator - increases local immune response of skin
236
What is the treatment for genital herpes?
400mg 3X per day for 5 days
237
How is HIV transmitted?
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
What are activities that allow HIV transmission?
```
anal or vaginal intercourse
very low risk from oral sex
mother to child transmission
healthcare settings
transmission via donated blood or clotting factors
```
239
How does HIV cause illness?
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
What is the general structure of HIV?
2 strands of RNA
| 3 of its own enzymes - reverse transcriptase, protease and integrate enzymes
241
What are drug targets for HIV?
fusion inhibitor, R5 inhibitor
NRTI, NNRTI (reverse transcriptase)
integrase inhibitors
protease inhibitors
242
Describe HIV latency
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
Describe HIV resistance
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
Describe the CD4 cell count
calculated from total lymphocyte count
HIV negative- 600-1200 per mm3
risk of opportunistic infection increases sharply below 200/mm3
245
What is the HIV viral load?
"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
What are the main symptoms of acute HIV infection?
```
fever
weight loss
mouth sores, thrush
oesophageal sores
myalgia
liver and spleen enlargement
malaise headache
neuropathy
lymphadenopathy
rash
nausea
vomiting
```
247
What is the differential diagnosis for primary HIV infection rash?
infectious mononucleosis
secondary syphilis
drug rash
viral infections - CMV, rubella, influenza, parvovirus
248
What are the UK national HIV testing guidelines?
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
What is HAART?
```
highly active antiretroviral treatment
triple therapy
2 nucleosides and 1 drug from another class
suppress viral load to undetectable
CD4 recovery
```
250
What are the challenges with ART?
```
good adherence (>95% essential)
psychological impact
short term side effects
drug-drug interactions
emerging longer term toxicites
```
251
Describe the short term toxicity of ART=
```
rash
hypersenstivity
CNS side effects - sleep disturbance, vivid dreams, mood changes
GI side effects
renal
hepatic
```
252
Describe drug interactions in ART
usually class specific
mediated by CYP450
PPIs, statins antipsychotics - QTc
253
Describe the long term toxicity of ART
```
body shape changes
renal
hepatic
lipid
bone
```
254
How is mother to child HIV transmission prevented?
```
treat mother during pregnancy
minimise risk at delivery
treat baby early on
avoid breast feeding
universal antenatal HIV screening
```
255
What are the social dimensions of HIV?
vulnerable populations - further marginalisation
access to healthcare
provision od ARVs - life long, management of ARV complications
single parent families / orphaned children
disabilities
stigma
256
What can an untreated joint infection lead to?
severe sepsis - septic shock
loss of cartilage
osteoarthritis in later life
257
How does septic arthritis normally present?
fever
single or multiple hot joints
loss of movement
pain
258
What are the key investigations for septic arthritis?
blood cultures
joint aspiratie (gram, microscopy for crystals and culture)
FBC
CRP imaging
259
What are the common pathogens in septic arthritis?
```
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
What is the treatment of septic arthritis?
At least 2 weeks of IV antibiotics
often three weeks IV followed by 3 weeks oral
monitor response by CRP and clinical
261
What is an arthroplasty?
putting in an artificial joint
262
What is resection arthroplasty?
taking the diseased joint out and putting in an artificial one
263
What is a revision arthroplasty?
re-operating on an artificial joint
264
What are the risk factors for infection in primary arthroplasty?
```
rheumatoid arthrits
diabetes
poor nutritional status
obesity
concurrent UTI
steroids
malignancy
```
265
What are the risk factors for infection in revision arthroplasty?
prior joint surgery
prolonged operating room time
pre-op infection
266
Describe local spread in prosthetic joint infections
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
Describe haematogenous spread in PJIs
presents later
intact surrounding connective tissue often limits infection to bone/cement interface
can be any organism
268
Describe the pathogenesis of PJIs
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
What is the clinical presentation of a septic arthritis?
```
pain
effusion
warm joint
fever and systemic symptoms
prosthetic joint - loosening on Xray
discharging sinus
mechanical dysfunction
```
270
What are the surgical options in an infected prosthetic joint/
debride, antibiotics, implant repair or take the infected joint out (put in replacement then or at a later date)
271
Which antibiotics can penetrate bone?
cephalosporins, taxocin, carbapenems, fusidic acid, doxycycline, rifampicin, linezolid, trimethoprim, ciprofloxacin, clindamycin
272
What is osteomyelitis?
progressive infection of bone characterised by death of bone and the formation of sequestra
273
How can osteomyelitis be established?
haematogenous spread
| contiguous spread - overlying infection, trauma, surgical inoculation
274
How is osteomyelitis treated?
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
Describe diabetic foot infection
more complex than septic arthritis
| usually involves bone but can also involve joints
276
Describe vertebral discitis
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
what are the biggest killers of children under 5?
neonatal
diarrhoea
malaria
pneumonia
278
Describe pregnancy and immunity
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
How can the mother transfer immune protection to the baby?
IgG is transferred in the third trimester
| breast feeding
280
What are LRTIs most likely to be caused by in neonates?
Grp B strep
e.coli
respiratory viruses
enteroviruses
281
What are LRTIS most likely to be caused by in young infants?
respiratory viruses
enteroviruses
chlamydia
282
What are LRTIs most likely to be caused by in infants and young children?
strep pneumonia, respiratory virsues
283
What are LRTIs most likely to be caused by in older children?
mycoplasma pneumonia
strep.pneumoniae
respiratory viruses
284
What is meningitis most likely to be caused by in neonates?
```
Grp B strep
e.coli
haemophilia type B
meningococcus
strep pneumoniae
listeria
```
285
What is meningitis most likely to be caused by in 1-3 months olds?
meningiococcus
strep pneumoniae
hib
listeria
286
What is meningitis most likely to be caused by in children aged 3months to 5 years?
meningococcus,
strep pneumoniae
Hib (rare)
287
What is meningitis most likely to be caused by in children over 6 years old?
meningiococcus
| strep pneumoniae
288
Describe immunisation
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
Describe antibody mediated immunity
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
Describe cell mediated immunity
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
How do vaccines work?
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
What do adjuvants in vaccines do?
enhance the antibody response
293
What type of vaccines are WCpertussis and IPV?
inactivated bacteria/virus
294
What type of vaccines are tet/diptheria?
inactivated toxins
295
What sort of vaccine is pneumococcal?
capsular polysaccharide
296
Describe conjugate vaccines
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
Describe live attenuated viruses
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
Describe herd immunity
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
What vaccines to children get at 2 months?
DTaP/IPV / Hib/ Hep B
pneumococcal vaccine
rotavirus vaccine
men B vaccine
300
What vaccines do children get at 3 months?
men C
DTaP/IPV?Hib (2nd)
rotavirus vaccine (2nd)
301
What vaccines do children get at 4 months?
DTaP/IPV/HiB (3rd)
pneumococcal (2nd)
Men B (2nd)
302
What vaccines do children get at 12-13 months?
MMR
Hib/men C booster
pneumococcal vaccine (3rd)
Men B vaccine (3rd)
303
What vaccines do children get at 2, 3, and 4 plus primary school?
children annual flu vaccine
304
What vaccines do children get at 3 years and 4 months?
DTaP/IPV
| MMR (2nd)
305
What vaccines do children get from 12-13 years?
HPV
306
what vaccines to children get from 13-18 years?
Td/IPV
| MenACWY
307
Which childhood vaccinations are live attenuated?
rotavirus
MMR
intranasal influenza
308
Describe streptococcus pneumonia in children
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
What are the most common presentations of invasive Hib disease?
meningitis
frequently accompanied by - epiglossitis
bacteraemia
pneumonia, cellulitis
310
Describe the clinical assessment of a child with infection
```
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
Describe the clinical approach to the febrile child?
```
good histroy
fever - duration and measurement
assessment of severity
localising symptoms
causations
```
312
How do you assess the severity of an infection in an infant?
feeding/vomiting
crying
sleeping
smiling
313
How do you assess the severity of an infection in a child?
feeding
activity levels
drowsiness
