Gastrointestinal infections Flashcards
Intoxication
microbial intoxication does not require ingestion microbes: just their biologically active toxins. These are usually protein exotoxins
Infection
disease due to ingestion of live microbes
Diarrhoea definition
- Abnormal frequency and/or fluid stool
- Usually indicates small bowel disease
- Causes fluid and electrolyte loss
- Severity varies widely from mild self-limiting to severe/fatal
a. Virulence of organism
b. Degree of compromise of the host
Gastroenteritis definition
Nausea, vomiting, diarrhoea and abdominal discomfort
Dysentery definition
inflammatory disorder of the large bowel
blood and pus in faeces
Pain, fever, and abdominal cramps
Enterocolitis
inflammatory process affecting small and large bowel
Where can GI infections arise
Within GI tract (GIT)
- Toxin effects e.g. cholera
- Inflammation due to microbial invasion e.g. shigellosis
Outwith GIT
- Systemic effect of toxins e.g. STEC
- Invasive infection of GIT with wider dissemination e.g. metastatic salmonella infection
Transmission of GI infection
3 F’s
- Food (contaimination farm to fork, cross contaimination: domestic kitchen)
- Fluids (water, juice)
- Fingers (importance of washing hands, after toileting)
Person-person transmission (infectious dose, ability to contaminate and persist in the environment)
Faecal-oral (any means by which infectious organisms from human/animal faecces can gain access to GIT of another susceptible host)
Diagnosis of GI infection
History
- Aetiological diagnosis cannot be made from history alone
- However may get useful clues
a. Vomiting, abdominal pain, diarrhoea, frequency and nature of symptoms, travel history, food history, other affected individuals, speed of onset of illness, blood in stools
Examination
-Abdominal, fever, features of dehydration
Laboratory diagnosis of GI infection
Enrichment media
-Liquid culture media containing nutrients that promote preferential growth of the pathogen
Selective media
-Liquid or solid media that suppress growth of background flora while allowing growth of the pathogen being sought
Differential media
-Solid media which distinguishes mixed microorganisms on the same plate. Uses biochemical characteristics of microorganisms growing in presence of specific nutrients combined with an indicator that changes colour. Best known examples are Salmonella and Shigella species which are non-lactose fermenters (NLF).
Campylobacter microbiology
Gram negative bacilli
Campylobacter transmission
Contaiminated food (poultry), milk or water
Campylobacter epidiemiology
Commonest bacerial foodbourne infection in UK
Peak in may and september
Pathogenesis of Campylobacter
- inflammation and ulceration and bleeding of large and small bowel
- bactermeia can occur - spread into bloodstream
- post infectious demyelination syndrome e.g Guillian barre syndrome, characterised by ascending paralysis
Clinical features of campylobacter
Bloody diarrhoea
Cramping abdominal pain
Vomiting is not usually a feature
Fever
Incubation period and duration of campylobacter
2-11 days
duration 3 days - 3 weeks
Treatment of campylobacter
Symptomatic
-adequate fluid replacmeent
Severe/persistent
-clarithromycin
Invasive
-quinolone (ciprofloxaine) or aminoglycoside (gentamicin) or invasive
Salmonella microbiology
Gram negative bacilii (member f enterobacteriacae)
Transmission of salmonella
Contaiminated food, pork, poultry and other meat
Secondary - via person-person
Pathogenesis of salmonella
- Diarrhoea due to invasion of epithelial cells in the distal small intestine, and subsequent inflammation
- Bacteraemia -spread into the bloodstream (extremes of age, immunocompromised)
- Bacteraemia causes -. osteomyelitis, septic arthritis, meningitis etc.
Clinicall features of salmonella
Watery diarrhoea
Vomiting is common
Fever can occur, and is usually associated with more invasive disease
Incubation period and duration of salmonella
incubation - 6hrs-2 days
duration 2-7 days
Treatment of salmonella
Symptomatic
-fluid replacement
Severe infections and bacteraemia
-beta lactams, quinolones or aminoglycosides
Shigella micro
Gram negative bacilli (memmber of the enterobacteriacae
4 species
mild- s . sonnei
moderate-severe - S boydii, S flexneri
most severe - S. dysenteriae
NO animal reservoir
Transmission of shigella
person to person via faecal-oral route
Epidemiology of shigella
Diarrhoeal disease in children
Humans only reservoir
Large outbreaks
Control of shigella
humans, so good standards of sanitation and personal hygiene
Pathogenesis of shigella
- organisms attach to and colonise mucosal epithelium of terminal ileum and colon
- systemic invasion not a feature
3, S dysenteriae - produces a potent exotoxin (Shiga toxin) which not only damages intestinal epithelium but in some patients targets glomerular endothelium causing renal failure as part of haemolytic-uraemic syndrom (HUS)
Clinical features of shigella
Inital watery diarrhoea followed by bloody diarrhoea
Marked, cramping abdominal pain
Vomitting is uncommon
Fever is usually present
Incubation period and duration of shigella
Incubation 1-4 days
Duration 2-3 days
Treatment of shigella
usually self-limiting
Symptomatic treatment with fluid replacement
Some cases of S dysenteriae infection with require treament of renal failure
Vibrio cholera microbiology
Comma-shaped gram ngative bacilli
Serotypes defned on basis of O-antigens
Transmssion of vibrio cholera
food and water
lives in freshwater
only infects humans
Epidiemiology of vibrio cholera
Eoedemic and pandemic cholera
Pathogeneiss of vibrio cholera
- polar flagellae and mucinance penterate intestinal mucous
- attachment to mucosa by specific receptors
- diarrhoea due to production of a potent protein exotoxin
Clinical features of virio cholera
Severe, profuse, non-bloody, watery diarrhoea (rice water stool)
Profound fluid loss & dehydration precipitates hypokalaemia, metabolic acidosis, hypovolaemic shock and cardiac failure
Untreated mortality 30-40%
Treatment of vibrio cholera
oral or intravenous rehydration is lifesaving
Tetracycline antibiotics may have a role in shortening duration f shedding only
Specific control point of vibrio cholera
Clean drinking water supply and proper sanitation key preventative measures
Escherichia coli microbiology
Gram-negative bacilli
members of the enterobacteiaea
Six different diarrhoeagenic groups of E.coli have been described
Different serogroups and serotypes are described on the basis of “O” and “H” antigens
Epidemiology of EPEC
Sporadic cases & outbreaks of diarrhoea in infants & children
Cause of some cases of “traveller’s” diarrhoea
Pathogeneis of EPEC
Initial adherence via pili, followed by formation of characteristic
“attatching & effacing” lesion mediated by intimin protein and Tir (translocated intimin receptor) with disruption of intestinal microvilli
Clinical features of EPEC
Watery diarrhoea with abdominal pain and vomiting
Often accompanied by fever
Incubation period and duration of EPEC
incubation 1-2 days
duration several weekes
Microbiology of Enterotoxigenic E coli (ETEC)
Differential routine media unavailable
Test liquid cultures for production of toxins by immunoassays
Epidiemiology of ETEC
The major bacterial cause of diarrhoea in infants & children in developing world
The major cause of “travellers” diarrhoea
Pathogeneis of ETEC
Diarrhoea due to action of 1 or 2 plasmid-encoded toxins
Heat-labile (LT). Structural and functional analogue of cholera toxin
Heat-stable (ST). Produced in addition to or instead of LT. Similar mode of action
Clinical features of ETEC
Watery diarrhoea with abdominal pain and vomiting
No associated fever
Incubation period and duration of ETEC
Incubation 1-7 days
Duration 2-6 days
Microbiology of EHEC (enterohaemorrhagic Ecoli)
More than 100 serotypes
Best known is E.coli O157:H7
O157 is a non-sorbitol fermenter. Sorbitol MacConkey agar (SMAC)
Epidiemiology of EHEC
Outbreaks & sporadic cases worldwide (~250 cases/year in Scotland)
Large animal reservoirs (esp. cattle & sheep)
Persistent in environment
Transmission of EHEC
Consumption of contaminated food, water and dairy products & direct environmental contact with animal faeces e.g. petting zoos
Secondary person-to-person spread important (associated with low infectious dose)
Pathogenesis of EHEC
- Attaching and effacing lesion (similar to EPEC)
- production of Shiga-like toxins. Structural and functional analogue of Shigella dysenteriae toxin (sometimes strains called STEC [shiga-toxin producing EC] or VTEC [verotoxin-producing EC] because toxins are toxic for cultured vero cells
Clinical features of EHEC
Bloody diarrhoea with abdominal pain and vomiting
No associated fever
Haemolytic uraemic syndrome (5-10% of cases)
- Microangiopathic haemolytic anaemia
- Thrombocytopaenia
- Acute renal failure
E.coli O157 infection is the commonest cause of acute renal failure in children in the UK
Treatment of all ecoli infections
Adequate rehydration important
Antibiotics not indicated, and in the case of EHEC may increase risk of HUS
Antimotility agents also increase HUS risk with EHEC
Staph aureus Micro biology
gram-positive cocci
Grow well on routine media
Epidemiology & pathogeneiss of staph aureus
- 50% of S.aureus produce enterotoxins (types A-E)
- Heat stable and acid-resistant protein toxins
- Food is contaminated by human carriers
- Especially cooked meats, cakes and pastries
- Bacteria multiply at room temperature and produce toxins
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Clinical features of staph aureus
Profuse vomiting and abdominal cramps
No fever and no diarrhoea
Incubation period and duration of staph aureus
Incubation 15 minutes – 6 hours
Duration 12 hours - 1 day
Treatment of staph aureus
self-limiting
Bacillus cerus micro
Aerobic, spore-forming gram positive bacilli
Pathogeneis bacillus cereus
2 types of disease
Emetic disease
- “fried rice”- survive initial boiling, if rice is cooked and stored prior to frying, the spore germinate, multiply and re-sporulate
Diarrhoeal disease
- spores in food survive cooking, germinate and orgnisms multiply in food
- ingested organisms produce a heat-labile toxin in teh gut with similar mode of action to cholera
Clinical features of bacills cereus
Emetic disease
- Incubation 15 minutes - 4 hours
- Duration 12 hours-2 days
- Profuse vomiting with abdominal cramps and watery diarrhoea
- No fever
Diarrhoeal
- Incubation 8-12 hours
- Duration 12 hours-1 day
- Watery diarrhoea with cramping abdominal pain, but no vomiting
- No fever
Treatment of bacillus cerus
self-limiting
Clostridium perfringes micro
Anaerobic, spore-forming gram-positive bacilli
Epidiemiology and pathogenesis of clostriudium perfringes
- Spores & vegetative cells ubiquitous in soil and animal gut
- Contaminated foodstuff (usually meat products)
- Often involves bulk-cooking of stews, meat pies
- Spores survive cooking, germinate and organisms multiply in cooling food
- Food inadequately re-heated to kill organisms
- Organisms ingested & sporulate in large intestine with production of enterotoxin
Clinical features of clostridium perfringens
Watery diarrhoea and abdominal cramps
No fever and no vomiting
Incubation period and duration of clostridium perfringens
Incubation 8 hours -1 day
Duration 12 hours - 1 day
Treatment of clostrium perfringens
self-limiting
Clostridium botulinium micro
Anaerobic, spore-forming Gram-positive bacilli
Laboratory diagnosis based upon toxin detection
Pathogeneis of Colstridium botulinum
- spores and vegetative cells ubiquitos in soil and animal GIT
- Produces powerful heat-labile toxin protein neurotoxin
- Absorbe toxins spread via the blood stream and enter peripheral nerve
- Block Ach and causes descending paralysis
Clinical features of clostrium botulinum
Neuromuscular blockade results in flaccid paralysis & progressive muscle weakness
Involvement of muscles of chest/diaphragm causes respiratory failure
High mortality if untreated
Treatment of clostridium botulinum
urgent intensive supportive care due to difficulties breathing and swallowing
Listeria monocytogenes micro
Gram-positive coccobacilli
Selective culture media available for culture from suspect foods
Can be grown on standard laboratory media from blood and CSF samples
Pathogeneis of listeria monocytogenes
- Widespread among animals and the environment
- Pregnant women, elderly and immunocompromised
- Overall number of cases small, but mortality high
- Infection associated with contaminated foods, especially unpasteurised milk and soft cheeses, pate, cooked meats, smoked fish, and coleslaw
- Outbreaks occur associated with contaminated ready to eat foods and produce
- Can multiply at 4oC
- Invasive infection from GIT results in systemic spread via bloodstream
Clinical features of listeria monocytogenes
Initial flu-like illness, with or without diarrhoea
Majority of cases present with severe systemic infection
- Septicaemia
- Meningitis
Incubation period and duration of monocytogenes
Median incubation period 3 weeks
Duration of illness 1-2 weeks
Treatment of listeria
Intravenous antibiotics (usually Ampicillin and synergistic gentamicin) is required
