Week 7 Flashcards
What are the two categories of bacterial GI infection?
infection and intoxication
Describe infection
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
Describe contamination
bacterial pathogens grow in foods and produce toxins
examples - bacillus cereus, staph.aureas
relative short incubation time because of preformed toxin in food
What is diarrhoea?
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
Describe gastroenteritis
nausea, vomiting, diarrhoea and abdominal discomfort
Describe dysentery
inflammatory disorder of the large bowel
blood and pus in faeces
pain, fever and abdominal cramps
Describe enterocolitis
inflammatory process affecting small and large bowel
What are the manifestations of GI infection within the GIT?
toxin effects (cholera) inflammation due to microbial invasion (shigellosis)
Describe the manifestations of GI infection out with the GIT
systemic effect of toxins (STEC)
invasive infection of GIT with wider dissemination (metastatic salmonella infection)
What is the barrier in the mouth to GI infection?
lysozyme
What is the barrier in the stomach to GI infection?
acid pH
What are the barriers in the small intestine to GI infection?
mucous bile secretory IgA lymphoid tissue (Peyer's patches) epithelial turnover normal flora
what are the barriers to GI infection in the large intestine?
epithelial turnover
normal flora
What are the main sources of GI infection?
zoonotic - symptomatic animals and asymptomatic shredders
human carriers (typhoid)
environmental sources
What is meant by the faecal-oral route?
any means by which infectious organisms from human / animal faeces can gain access to GIT of another susceptible host
What are the three Fs?
food
fluid
fingers
When is person to person transmission more likely?
small infectious dose
ability to contaminate and persist in the environment
What is important in the history of GI infection?
vomiting, abdominal pain, diarrhoea, frequency and nature of symptoms, travel history, food history, other affected individuals, speed of onset of illness, blood in stols
What should be examined for GI infection?
abdominal exam
temperature
features of dehydration
What are the laboratory diagnosis techniques for bacterial GI infection?
enrichment broth
selective media
differential media
Which species of bacteria are non-lactose fermenters?
salmonella and shigella
Why are antibiotics not generally used to treat GI infections?
may prolong symptoms duration
may exacerbate symptoms
promotes emergence of antibiotic resistance
may actually be harmful (STEC infection)
How can GI infections be controlled?
adequate public health measures
education in hygienic food preparation
pasteurisation of milk and dairy products
sensible travel food practises
What is the microbiology of campylobacter?
curved gram negative bacilli
microaerophilic and thermophilic
culture of campylobacter selective agar
C.jejuni most important species
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
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
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
What is the treatment of campylobacter infection?
fluid replacement
clarithromycin for severe/persistent disease
quinolone or amino glycoside for invasive disease
What are the specific control points for campylobacter infection?
reduction of contamination in raw, retail poultry meat
adequate cooking
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
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
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
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
What is the treatment of salmonella infection?
fluid replacement
beta lactams, quinolone or ahminoglycosides for severe infections
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
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
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
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
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
what is the treatment of shigella infection?
usually self-limting
fluid replacement
some will need treatment for renal failure
What are the specific control points for shigella infection?
only found in humans, good standards of sanitation and personal hygiene are key measures
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
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
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
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
What is the treatment of cholera?
prompt oral or IV rehydration is life saving
tetracycline antibiotics may shorten duration of shredding
What are the specific control points for cholera?
no animal reservoir
clean drinking water supply and proper sanitation are key preventative measures
What are the 6 diarrhoeagenic groups of e.coli?
enteropathogenic (EPEC) enterotoxigenic (ETEC) enterohaemorrhagic (EHEC) enteroinvasive (EIEC) enters-aggregative (EAEC) diffuse aggregative (DAEC)
Describe the microbiology of EPEC
no differential media available
test selection of colonies using polyvalent antisera for common EPEC serum types
not routinely done
Descrive the epidemiology of EPEC
sporadic cases and some outbreaks or diarrhoea in infants and children
cause of some cases of traveller’s diarrhoea
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
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
Describe the microbiology of ETEC
no differential media available
test liquid cultures for production of toxins by immunoassays
not routinely done
describe the epidemiology of ETEC
major bacterial cause of diarrhoea in infants and children in developing world
major cause of travellers diarrhoea
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
Describe the clinical feats of ETEC
incubation 1-7 days
duration 2-6 days
watery diarrhoea, abdominal pain and vomiting
no associated fever
Describe the microbiology for EHEC
more than 100 serotypes
best known O157:H7
non-sorbitol fementer. Sorbitol MacConkey agar (SMAC)
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)
Describe the pathogenesis of EHEC
attaching and effacing lesion
production of shiga like toxins. structural and functional analogue of shigella dystenteriae toxin (STEC)
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
Describe HUS
microangionpathic haemolytic anaemia
thrombocytopenia
acute renal failure
Describe the microbiology for staph. aureas
gram positive cocci
grow well in routine media
testing for enterotoxins not routinely performed
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
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
What is the control of GIT staph.aureas infection?
hygienic food preparation to minimise contamination
refrigerated storage
describe the microbiology of bacillus cereus
aerobic, spore forming gram positive bacilli
not routinely tested for
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
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
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
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
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
Describe the microbiology of clostridium perfringes
anaerobic, spore forming gram postive bacilli
not routinely tested for
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
Describe the clinical features of clostridium perfringens
incubation 6-12 hours
duration 12-24 hours
watery diarrhoea and abdominal cramps
no fever or vomiting
Describe the control of clostridium perfringens
rapid chilling/freezing of bulk-cooked foods
thorough re-haeting before consumption
Describe the microbiology of clostridium botulinum
anaerobic, spore forming gram postive bacilli
lab diagnosis bases upon toxin detection
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
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
What is the treatment of botulism/
urgent intensive supportive care due to difficulties breathing and swallowing
antitoxin
What is the control for botulism?
proper manufacturing controls in canning industry
hygienic food preparation
proper cooking
refrigerated storage
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
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
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
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
Describe how C.dif can be controlled?
antimicrobial stewardship
infection and prevention control measures
cleaning/disinfection with hypochlorite disinfectants
Describe the microbiology listeria monocytogenes
gram postive coccobacilli
selective culture media available for culture from suspect foods
standard lab for blood and CSF samples
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
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
What is the treatment of listeria?
IV antibiotics (ampicillin and synergistic gentamicin )
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
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
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
What are the clinical features of H.pylor?
infection is asymptomatic unless ulcer develops
gastric cancer risk
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
Who are at higher risk of viral gastroenteritis?
children under 5
old age people especially in nursing home
immunocomprimised
What are the important viruses that cause gastroenteritis?
norovirus sappovirus rotavirus adenovirus 40&41 astrovirus
What are the calciviridae viruses?
norovirus and sappovirus
Who is affected by norovirus?
all ages but often most serious in young and elderly
Who is affected by rotavirus/adenovirus/astrovirus?
mainly children under 2, elderly, immunocomprimised
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
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
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
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
What is the treatment of norovirus?
symptomatic therapy oral and IV fluids antispasmodics analgesics antipyretics
Describe the immunity to norovirus
immunity lasts only 6-14 weeks
can’t be cultured- no vaccine
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
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
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
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
What are the complications of rotavirus?
severe chronic diarrhoea dehydration electrolyte imbalance metabolic acidosis immunodeficiency children may have more severe or persistent disease
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
Describe adenovirus
double stranded DNA virus
40 &41 cause gastroenteritis
fever and watery diarrhoea
supportive treatment
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
How are gastroenteritis viruses diagnosed?
PCR
testing done in virology lab
vomit or stool samples
What is the common stain used to detect TB?
Ziehl Neelson
What can lead to the reactivation of TB?
immunosuppression, HIV infectionm smoking
What is a Goon complex?
a TB nodule found in the lung and a regional lymph node - central mediastinum and cervical chain
What is seen on chest X ray in primary TB?
consolidation
lymphadenopathy -
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
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
What does a lung infected with TB appear grossly?
caseous necrosis
breakdown of tissue
gas exchange impaired
What is milliary TB?
very widely disseminated
more common in children and immunosuppressed
also in CNS and other areas of the body
classically primary
Describe CNS TB
not too uncommon
can get TB meningitis if it is in the CSF - indolent course over weeks - clouding of conciousness
Describe renal TB
ascends from bladder
can invade reproduction tracts as well
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
Describe a granuloma in TB
central necrosis
epitheloid cells (activated macrophages)
giant cells
lymphocytes
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
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
What test can be used to see if someone has been exposed to TB?
Mantoux reaction
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
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
What is given with TB treatment as prophylaxis and why?
pyridoxine to prevent neuropathy caused by isoniazid
What is latent TB treatment?
recent migrants , new workers.
Isoniazid and rifampicin for 3 months
or isoniazid for 6 months
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
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
What are the typical pathogens that cause pneumonia?
step. pneumoniae
haemophilus influenza
mortadella catharralis
What is the most common cause of pneumonia?
strep. pneumonae
What are the atypical pathogens that cause pneumonia?
mycoplasma pneumoniae
legionella pneumoniae
chlamoydophila pneumoniae
chlamydophilia psittaci
What are the risk factors for strep pneumonia?
alcohol HIV smoking chronic lung disease flu
Describe the clinical features of strep pneumoniae
abrupt onset cough fever pleuritic chest pain dull percussion coarse crepitations increased vocal resonance
What is the treatment of Strep.P pneumonia?
penicillin
allergy then macrocodes or tetracyclines
Where is penicillin resistant pneumonia common?
south europe, asia, north america
In what patients in haemophilia influenzae pneumonia more common
older people
underlying disease
What other infections can H.I lead to
otitis media
conjungtivitis
sinusitis
CNS infections
Describe the clinical features of H.influenzae pneumonia
abrupt onset cough fever pleuritic chest pain dull precision coarse crepitations increased vocal resonance
What is the treatment of H.influenzae?
amoxicillin
or if risk of beta lactamase - co amoxiclave
macrolides
tetracyclines
Describe mycoplasma pneumoniae
smallest free living bacterium
lack of cell wall very difficult to grow
When does M.pneumoniae peak?
autumn and winter
Describe the clinical features of M.pneumoniae pneumonia
atypical
flu lik eillness
other symptoms dominate over cough
What can M.pneumoniae lead to?
cold haemolysis guillain-barre erythema multiforme - target lesion cardiac - conduction problems arthrits- reactive arthritis
How is M.pneumoniae diagnosed?
serology
PCR
Cant culture
How is P.pneumoniae treated?
macrolides
tetracyclines
quinolones
Describe how legionella pneumophila infects people
lives in amoeba in the environment - hot tubs, showers
hospitals, hotels , aircon outlets
Describe the symptoms of legionaires disease
headache, myalgia, fatigue, fever, maybe cough
how is legionella. pneumoniae diagnosed/
culture - difficult
serolgoy
urinary antigen test - most used
What is the treatment of L.pneumoniae
macrolides
quinolones
tetracyclines
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
What is the CURB65 score?
confusion urea >7 RR >30 B - BP, diastolic <60, or systolic <90 65 - aged over 65
What else has to be considered with the CURB65 score?
SIRS
multilobar consolidation on CXR and /or hypoxia on room air
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
What is the management of patient with pneumonia?
ABC antibiotics - IV or oral? Admission to hospital? CURB65 >2 SIRS >2 hypoxia
How can viral respiratory infections be prevented?
only flu has vaccine
basic hygiene is the most important
How can viral respiratory infections spread?
direct contact
indirect contact
water droplets
What causes the common cold?
rhinovirus and coronavirus
Describe pharyngits
mostly viral
headache, cold, cough, aches and pain
most common cause is adenovirus
outbreaks of respiratory illness - preceding diarrhoea, conjunctivitis renal disease
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)
When does parainfluenza 3 virus peak?
spring and summer
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
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
How is RSV treated?
Ribivirin (oral, IV, aerosolised)
numerous side effects
prophylactic monoclonal antibody given to high risk children IM monthly
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
What are the symptoms of the flu?
headache fever muscle pain joint pain runny nose sore throat cough vomiting
What are the common complications of flu?
acute otitis media sinusitis pneumonia exacerbation of underlying disease dehydration (infants)
What are the uncommon complications of flu?
encephalopathy Reye syndrome (children) myositis myocarditis febrile seizures
What type of drug is tyamiflu?
neuroadminidase inhibitor - prevents virus exiting cells
What is a flu pandemic?
worldwide epidemics of a newly emerged strain of influenza
What type of virus is SARS?
coronavirus
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
What is bacteriuria
bacteria in the urine
What is urosepsis?
temp >38
HR >90
RR >20
WBC >15 or <4
Who are at risk of bacteriuria?
hospitalised catheterised diabetics anatomical abnormalities pregnant patients
When should asymptomatic bacteriuria be treated?
only in preschool children
pregnancy
(renal transpant
immunocompromised)
When is infection with multiple organisms more likely in UTI?
long term catheters
recurrent infection
structural / neurological abnormalities
When are multi drug resistant organisms more likely to be present in UTIs?
anatomical/neurological abnormaliites
frequent infections
multiple antibiotic courses
prophylactic antibiotic use
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
What organisms are commonly involved in UTis?
E.coli Klebsiella sp Proteus sp pseudomonas sp streptococcus so staph anaerobes (bladder cancer) candida
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
What should the management be for a man with a LUTI?
send urine for each and every presentation
treat appropriately
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%)
Describe recurrent UTI
> 2 episodes in 6 months or >3 episodes in a year
mostly women
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
What is meant by CAUTI?
catheter associated UTI
Why is infection more likely with catheters?
disturbance of flushing system
colonisation of urinary catheter
biofilm production by bacteria
What are the complications of catheters?
CAUTI obstruction hydronephrosis chronic renal inflammation urinary tract stones long term risk of bladder cancer
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
How is CAUTI treated?
check previous microbiology
start empirical antibiotics
remove catheter if not needed
replace catheter under antibiotic cover
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
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
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
What are the risk factors for perinephric abscesses?
untreated LUTI, anatomical abnormalities
renal calculi
bacteraemia, haematogenous spread
What are the symptoms of perinephric abscess?
similar to pyelonephritis
localised signs/ symptoms
What is the treatment of perinephric abscess?
usually positive blood cultures pyuria treat empirically as complicated UTI poor response to antibiotic therapy surgical management
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
What antibiotics can be used in uncomplicated UTIs?
amoxicillin, trimethoprim, nitrofurantoin, pivmecillinam, fosfomycin
What antibiotics are used in complicated UTIS?
amoxicillin/vanc
gent/ aztreonam/ temocillin
Describe acute bacterial prostatitis
localised infection usually spontaenois may follow urethral instrumentation fever, perineal/back pain, UTI, urinary retention diffuse oedema, micro abscesses
What are the likely organisms in acute prostatitis?
gram negative bacilli
S.aureas (MSSA,MRSA)
N.gonorrhoea
What are the investigations for acute prostatitis?
urine culture blood culture Trans-rectal U/S CT/MRI obtaining prostatic secretions not advisable
What are the complications of acute bacterial prostatitis?
prostate abscess spontaneous rupture -urethra, rectum epididymiitis pyelonephritis systemic sepsis
What is antibiotic management of acute bacterial prostatitis?
check recent/ previous microbiology
ciprofloxacin / oflaxacin (no strep cover)
D/W microbiology in systemic infections
Describe chronic prostatitis
rarely associated with acute prostatitis may follow chlamydia urethritis recurrent UTIs diagnosis difficult relapse common most asymptomatic
What are the symptoms of epdidymitis?
pain, fever, selling, penile discharge
symtoms of UTI/urethritis
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
What is orchitis?
inflammation of one or both testicles testicular pain and swelling dysuria fever penile discharge
What are the complications of orchitis?
testicular infarction abscess fomration
What is fournier’s gangrene?
form of necrotising fasciitis
usually >50 years of age
rapid onset and spreading infection
systemic sepsis
What are the risk factors for fournier’s gangrene?
UTI
complications of IBD
trauma
recent surgery
what is the management of fournier’s gangrene?
blood cultures urine tissue/pus surgical debridement D/W microbiology broad spectrum/ combination antibiotics initially
Why is sex good for us?
fitter
lower rates of depressive symptoms
better cardiovascular health
When is sex bad for us?
non-consensual exploitative sexual dysfunction unwanted conception infection
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
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
What is the appearance of gonorrhoea under the microscope?
gram negative diplicocci in white cells
What is the test for gonorrhoea?
NAAT test
males urine is acceptable (first flow)
vulvovaginal swab for women (self taken is fine)
What is the main drug the gonorrhoea is resistant to in the UK?
ciprofloxacin
What is the syndromic management of male urethral discharge?
ceftriaxone 500mg IM
azithromycin Ig stat
partner notification
Describe chlamydia trachomatis
frequently asymptomatic
infection can lead to tubal damage/infertility
What is the treatment of chlamydia?
azithromycin oral stat
or doxycycline 100mgBDX 7 days - compliance may be an issue
Describe lymphogranuloma venereum
LGV lymphotrophic chlamydia severe proctitis causing constipation, rectal bleeding looks like cancer or Crohn's inguinal "bubos"
For which STI is it important to look at the palms and soles for rash?
syphilis
What is the natural history of syphilis?
exposure primary lesion (chancre) secondary lesion (rash) latent syphilis (+ve serology only) tertiary syphilis -gumma, cardiovascular, neurological
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
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
Give examples of viral STIs
HPV herpes simplex virus molluscum contagiosa HIV Hep B and C
What is the treatment for genital warts?
cryotherapy
condyline - dropper solution or cream
aldara - immune mediator - increases local immune response of skin
What is the treatment for genital herpes?
400mg 3X per day for 5 days
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
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
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
What is the general structure of HIV?
2 strands of RNA
3 of its own enzymes - reverse transcriptase, protease and integrate enzymes
What are drug targets for HIV?
fusion inhibitor, R5 inhibitor
NRTI, NNRTI (reverse transcriptase)
integrase inhibitors
protease inhibitors
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
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
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
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
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
What is the differential diagnosis for primary HIV infection rash?
infectious mononucleosis
secondary syphilis
drug rash
viral infections - CMV, rubella, influenza, parvovirus
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
What is HAART?
highly active antiretroviral treatment triple therapy 2 nucleosides and 1 drug from another class suppress viral load to undetectable CD4 recovery
What are the challenges with ART?
good adherence (>95% essential) psychological impact short term side effects drug-drug interactions emerging longer term toxicites
Describe the short term toxicity of ART=
rash hypersenstivity CNS side effects - sleep disturbance, vivid dreams, mood changes GI side effects renal hepatic
Describe drug interactions in ART
usually class specific
mediated by CYP450
PPIs, statins antipsychotics - QTc
Describe the long term toxicity of ART
body shape changes renal hepatic lipid bone
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
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
What can an untreated joint infection lead to?
severe sepsis - septic shock
loss of cartilage
osteoarthritis in later life
How does septic arthritis normally present?
fever
single or multiple hot joints
loss of movement
pain
What are the key investigations for septic arthritis?
blood cultures
joint aspiratie (gram, microscopy for crystals and culture)
FBC
CRP imaging
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
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
What is an arthroplasty?
putting in an artificial joint
What is resection arthroplasty?
taking the diseased joint out and putting in an artificial one
What is a revision arthroplasty?
re-operating on an artificial joint
What are the risk factors for infection in primary arthroplasty?
rheumatoid arthrits diabetes poor nutritional status obesity concurrent UTI steroids malignancy
What are the risk factors for infection in revision arthroplasty?
prior joint surgery
prolonged operating room time
pre-op infection
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
Describe haematogenous spread in PJIs
presents later
intact surrounding connective tissue often limits infection to bone/cement interface
can be any organism
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
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
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)
Which antibiotics can penetrate bone?
cephalosporins, taxocin, carbapenems, fusidic acid, doxycycline, rifampicin, linezolid, trimethoprim, ciprofloxacin, clindamycin
What is osteomyelitis?
progressive infection of bone characterised by death of bone and the formation of sequestra
How can osteomyelitis be established?
haematogenous spread
contiguous spread - overlying infection, trauma, surgical inoculation
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
Describe diabetic foot infection
more complex than septic arthritis
usually involves bone but can also involve joints
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
what are the biggest killers of children under 5?
neonatal
diarrhoea
malaria
pneumonia
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
How can the mother transfer immune protection to the baby?
IgG is transferred in the third trimester
breast feeding
What are LRTIs most likely to be caused by in neonates?
Grp B strep
e.coli
respiratory viruses
enteroviruses
What are LRTIS most likely to be caused by in young infants?
respiratory viruses
enteroviruses
chlamydia
What are LRTIs most likely to be caused by in infants and young children?
strep pneumonia, respiratory virsues
What are LRTIs most likely to be caused by in older children?
mycoplasma pneumonia
strep.pneumoniae
respiratory viruses
What is meningitis most likely to be caused by in neonates?
Grp B strep e.coli haemophilia type B meningococcus strep pneumoniae listeria
What is meningitis most likely to be caused by in 1-3 months olds?
meningiococcus
strep pneumoniae
hib
listeria
What is meningitis most likely to be caused by in children aged 3months to 5 years?
meningococcus,
strep pneumoniae
Hib (rare)
What is meningitis most likely to be caused by in children over 6 years old?
meningiococcus
strep pneumoniae
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
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
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
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)
What do adjuvants in vaccines do?
enhance the antibody response
What type of vaccines are WCpertussis and IPV?
inactivated bacteria/virus
What type of vaccines are tet/diptheria?
inactivated toxins
What sort of vaccine is pneumococcal?
capsular polysaccharide
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
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
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
What vaccines to children get at 2 months?
DTaP/IPV / Hib/ Hep B
pneumococcal vaccine
rotavirus vaccine
men B vaccine
What vaccines do children get at 3 months?
men C
DTaP/IPV?Hib (2nd)
rotavirus vaccine (2nd)
What vaccines do children get at 4 months?
DTaP/IPV/HiB (3rd)
pneumococcal (2nd)
Men B (2nd)
What vaccines do children get at 12-13 months?
MMR
Hib/men C booster
pneumococcal vaccine (3rd)
Men B vaccine (3rd)
What vaccines do children get at 2, 3, and 4 plus primary school?
children annual flu vaccine
What vaccines do children get at 3 years and 4 months?
DTaP/IPV
MMR (2nd)
What vaccines do children get from 12-13 years?
HPV
what vaccines to children get from 13-18 years?
Td/IPV
MenACWY
Which childhood vaccinations are live attenuated?
rotavirus
MMR
intranasal influenza
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
What are the most common presentations of invasive Hib disease?
meningitis
frequently accompanied by - epiglossitis
bacteraemia
pneumonia, cellulitis
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?
Describe the clinical approach to the febrile child?
good histroy fever - duration and measurement assessment of severity localising symptoms causations
How do you assess the severity of an infection in an infant?
feeding/vomiting
crying
sleeping
smiling
How do you assess the severity of an infection in a child?
feeding
activity levels
drowsiness
