Microbiology Enteric Infections Flashcards
Common
- Campylobacter ep.,
- Salmonella sp. (food poisoning)
- Shigella sp,.
- E.Coli
Less common
- Paratyphi (enteric fevers)
- Virbio parahaemolyticus
- Vibrio cholera
- C.Diff
- C. perfringens
- Listeri
- Helicobacter pylori
- Aeromonas sp.,
- Plesiomonas sp.
Performed Toxins
- Staphylococcis aureus
- Bacillus cereus (rice)
- Clostridium botuinum
- Perfringens
Common Gastroenteritis Viruses:
- Rotavirus (most common)
- Calciciviruses (Norovirus, Sapovirus)
- Adenoviruses
- Astrovirusus
- (Hepatitis A and E)
- Many others found in GI tract as part of systemic infection
Parasites
Protoazoa:
• Giardia intestinals
• Cryptosporidium parvum
• Entamoeba histolytica
Helminths
• Ascaris lumbricoides
• Hookworms
• Tapeworms
Acute gastroenteritis in USA
> 30 million episodes/yr
1.5 million OPD visits/yr
200,000 hospitalisations/yr
Around 300 deaths/yr
Developing Countries diarrhoea
Is a common cause of death in under 5’s – 2 million deaths per year
Oral Rehydration Therapy
Diarrhoea secretory (Chloride or calcium mediated) +/- osmotic (damage to villous brush border) Success of ORS relies on coupled transport of sodium and glucose into enterocytes so that water follows the gradient.
Common Presenting Features
Diarrhoea (uncomplicated or collities) – D & V may be first stages of UTI, meningitis Vomiting Fever Recent contact environmental link Epidemiology
Types of enteric infection
Type 1: Non-inflammatory (Watery diarrhoea) e.g. toxin mediated (c. perfringens, B. cerues, S. aureus), Giardia, Cryptosporidium, Rotavirus, Norovirus, ETEC, EPEC
Type 2: Inflammtory (dysentery, faecal leukocytes, lactoferrin) e.g. Shigella, VTEC, C. difficile, C. jejuni, S.enteritidus, Entamoeba.
Type 3: Penetrating (Enteric Fever) e.g. S. Typhi, yersinia
Standard Management
Often uncomplicated an self-limiting Mainstay of treatment is supportive • Rehydration • Little role for anti-diarrhoeal agents Specific: therapy may be required • Some bacteria and some parasites require antimicrobial therapy
Assessment of Dehydration
Correct, early assessment essential
Infants more prone as higher body surface to volume ratio, smaller fluid reservoir, dependent on others for fluids
Signs
Signs of severe dehydration
Apathy, tachycardia (bradycardia if extreme), weak pulse, deep breathing, deep sunken eyes, no tears, parched mouth, skin recoil >2 secs, minimal urine output.
Basic Diagnosis
Rarely possible on clinical features alone
Epidemiology (e.g. par of outbreak)
Microbiological investigation
• Rarely necessary unless dehydration, febrile, blood or pus in stool, or part of outbreak
• Stoll +/- blood culture, selective, indicator growth media (diagnostic yield Stool culture – 5%)
• Microscopy of stool for ova, cysts, parasites
• Specific typing
Prevention
Avoidance of risk • Don’t travel? • Basic Hygiene, hand washing • Clean water, clean food, adequate cooking • Immunisation (Typhoid, rotavirus) • Hospital infection control
E.Coli
Description
- E.coli is a major part of normal gut flora.
* Until recently role uncertain as difficult to distinguish pathogens from commensals
Pathogenic forms of E.Coli
- Enterotoxigenic E. Coli (ETEC)
- Verocytotoxic (VTEC) or Enterohaemorrhagic (EHEC)
- Enterinasive (EIEC)
- Enteropathogenic (EPEC)
Pathogenicity of ETEC
Produce 2 main types of toxin
• Polypeptide, like cholera toxin
• Stimulates hypersecretion
Pathogenicity of VTEC
Or Haemmohagic
• Cytotoxin, Kills cells, like Shigella toxin
• Haemorrhagic colitis and HUS (Haemolytic uremic syndrome)
Spread ecoli
All Faecal-oral, direct, food or water
ETEC epidemiology
Commonest cause bacterial diarrhoea in children in areas of poor hygiene, uncommon W Europe, important cause traveller’s diarrhoea.
Reservoir-human GI tract
VTEC Epidemiology
Several types, commonest O157, now common cause of acute renal failure in Western countries.
Reservoir-GI tract of healthy cattle
Contaminated food/animal carcasses (hamburgers0, unpasteurised milk, farms, paddling pools person to person rare e.g. nurseries
E.Coli Clinical Features (general)
Incubation usually 1-5 days (up to 14)
Abrupt onset vomiting and diarrhoea – later profuse watery diarrhoea only
Mild fever, little pain
Similar to viral gastroenteritis/salmonellosis (early stage but complications)
E.Coli
Severe complications
Haemorrhagic Colitis
Haemolytic Uraemic Syndrome
E.Coli
Haemorrhagic Colitis
- May complicated O157 infection in children and adults 699 positive stool cultures in 2004
- Typical diarrhoea progressing to bloody with abdominal pain
- Fever usually low
- May be mistaken for acute inflammatory bowel disease (as the preceding infection not severe)
E.Coli
Haemolytic Uraemia Syndrome
- May accompany colitis as a complication – 10% children in outbreaks
- Rising urea and creatinine, haemolytic anaemia and thrombocytopaenia
- Raising BP, fitting
- More than half need haemodialysis, almost all caes recover (most deaths in elderly, fatal <5%)
- Preceding GI illness may be unrecognised
- Mucosal damage and microangiopathic haemolytic anaemia and renal vascular disease
E.Coli
Laboratory Diagnosis
- Difficult – pathogen and normal flora are same species
- O157 phage typing
- O157 doesn’t ferment sorbitol
- Immunological cytotoxin detection
- PCR detection of cytotoxin gene
E.Coli
Management
- Supportive
- Many E.coli resistant to broad spectrum penicillins, cephalosporins, trimethoprim
- Ciprofloxacin 500 mg BD, 3-5 days
- Avoid antibiotics in HUS
- Anti-motility drugs probably increase change of HUS through delayed clearance of toxin
Salmonella → Description
Food Poisoning
• Infect humans and other animals
• >2000 serotypes
Salmonella →Commonest serotypes
S. enteritidis
S. typimurism
S. Virchow
Typhoid and paratyphoid fevers
Exclusive human pathogens – more torpical causes
Salmonella → Source
Contaminated poultry/ dairy products common source – not usually from food handlers or person-to-person spread. Reservoire – GI tract of birds, reptiles, amphibians
Salmonella → Seasonally timing
Commoner in summer/hot weather – 11,415 positive stool isolates In 2004
Salmonella → Microbiology
Identified on specific media by biochemical features:
1. Non-lactose fermenter
2. Produces H2s
LPS is O antigen, flagellae H antigen, defines serotype
Salmonella Food poisoning
Infection of gut epithelium
• Does not extend beyond membrane
• Excessive fluid secretion from ileum/jejunum
• If transported through cells, leads to systemic infection
Survives in macrophages
Clinical Features salmonella
Incubation 12-72 hrs Malaise Nausea Vomiting Fever Watery brown diarrhoea follows rapidly Abdominal Pain common but not severe Often resolves in several days, some cases last several weeks Children and elderly at risk of hypovolaemia
Salmonella Complications
- Salmonella Collitis (Up to 10% colic and bloody stools)
- Bacteraemia – seeding to bones/ joints (sickle-cell), aneurysms
- Post-infectious reactive arthritis
- Prolonged excretion – diverticulosis, IBO, HIV
Salmonella Microbiology
Stool cultre, blood culture if high fever/very unwell
Selective agar to inhibit normal flora and indicator, often lactose red resulting in pink colonies due to fermentation of lactose and acid production
Salmonella Typing
Bacteriophage
Antiobiotic panels
Salmonella Management
Rehydration
Antibiotics if no recovery after 8 rs, shock, high risk (valve disease/prosthesis), bacteraemia
Ciprofloxacin first line (alternative is cefotaxime)
Shigellosis (Bacillary dysentery) → Epi
- Worldwide problem
- Western countries endemic Shigellae usually cause mild illness
- Tropical strains tend to be more severe and persistent
- Person to person spread and via contaminated food and water → Reservoir – human GI tract
- Fw thousand cases/yr in UK Commonest S. sonneir, others flexneri, boydii, dysenteriae
Shigellosis (Bacillary dysentery) → Invasion
- Invade gut by destroying submucosa, infecting enterocytes, spread from cell to cell
- S.dysenteriae type 1 produces exotosin (shiga toxin)
Shigellosis (Bacillary dysentery) → Clinical Features
Incubation 1-7 days
High fever, high WBC, fever resolves and diarrhoea and colic begin sonnei and boydii mild, rarely colitis
Flexneri and dysenteriae more severe, mucus and blood in stools, marked cells
Asymptomatic excretion
Shigellosis (Bacillary dysentery) → Microbiology
Like E.coli (difficult to differentiate)
-Non-lactose fermenters
Non-motile
Serotype on basis of I antigens
Shigellosis (Bacillary dysentery) → Management
Symptomatic, antispasmodics, rehydrate
Abx in severe cases, ciprofloxacin (trimethoprim may be active, ceftriaxone also alternative)
Campylobacter: Epi
Commonest causes of food poisoning >50,000 cases/yr UK
Mostly sporadic, undercooked poultry, bird pecked milk – large food/waterbourne outbreaks can occur
Campylobacter: Incidence
Higher in summer
Campylobacter: Spread
Person-person spread uncommon
Campylobacter: Pathogen type
Animal Pathogen; several species infect humans – C.jejuni, coli, fetus, lari
Campylobacter: C. Jejuni
Low infective dose
Cell-wall LPS (Lipopolysaccarides)
Enterotoxin and cytotoxin
Campylobacter: Clinical Features
- Incubation period 2-5 days (up to 9)
- 24 hr prodrome, fever, headache
- Watery diarrhoea, can be bloody, vomiting
- Pain significant, constant, not colicky
- Pain with little diarrhoea may occur – like acute abdomen
- Systemic infection rare
- Commonest antecedent infection identified in Guillain Barre Syndrome (a post-infectious peripheral neuropathy).
Campylobacter: Microbiology
- Selective media with antibiotics
- 43oC may improve selection
- Gull wing morphology
Campylobacter: Management
- Mild cases self-limiting
- Severe/ prolonged, use 3-4 day course oral erythromycin
- Ciprofloxacin active/ erythromycin
Campylobacter: Clinical presentation
- Asymptomatic carriage
- Antibiotic – associated diarrhoea
- Antibiotic-associated colitis
Campylobacter: Complications
• Acute abdominal syndrome/ toxic megacolon, colonic perforation, pseudomembranous colitis, recurrence ( in 20%)
Clostridium difficile: Risk Groups
>65 years Antibiotic treamtnet (esp. clindamycin, cephalosporins, penicillins) GI surgery/manipulation Long stay in hospital/residential care Immunosuppression
Clostridium difficile: Management
Confirm diagnosis (C.Diff toxin testing) Stop or change antiobiotics if possible Fluid/electrolyte replacement Avoid antiperistaltics If above not possible or unsuccessful, treat with metronidazole (2nd line vancomycin) Infectino contorl
Viral Gastroenteritis: Epi
Commonest cause of symptomatic intestinal infection in Western World
Rarely severe or fatal in UK
Significant cause of infant mortality in resource poor countries
Viral Gastroenteritis: Management
|All self-limiting in the normal host Rehydration is the key Prevention of spread • Faecal-oral, person-person, food Antiviral therapy not used/available
Viral Gastroenteritis: Diagnosis
Rarely possible on clinical grounds
Epi
Stool electron microscopy, ‘catch all’
Stool enzyme imunoassays (e.g. rotavirus)
Molecular diagnosis – stool PCR
Outbreak typing and molecular epi
None of these viruses can be grown in cell culture
Rotavirus: Epi
Commonest cause of viral gastroenteritis in young children
• 1 mllion eaths/yr worldwide
• >10,000 cases/yr UK, under-reported
Rotavirus:Peak incidence
6-24 months, uncommon >5 yrs but adult infection occurs and can be symptomatic – may cause outbreaks in elderly care homes
Seasonal, late winter – march/april
Rotavirus:Virology
Reovirus:
• Segmented dsRNA genome
• No envelope
• Seven serogroups (A-G)
• Gp A human, others infect different animals e.g. pigs
• Genomes can reassert (like flu A), possibility of new human strains
Reservoir GI tract humans: 1 billion viruses/ml faeces, only 10 needed for infection
Rotavirus: Clinical
Incubation around 1 day
Abrupt onset D and V (D-V)
Mild fever, short-lived
Recovery in 48 hrs usual (D for up to a week)
Blood in stool can ovvur – investigate further
Gross dehydration and shock
Adults may have mild disease, transient vomiting
Persistent diarrhoea may occur in immunosuppressed
Rotavirus: Rotavirus Vaccine
Original tetravalent rhesus monkey/human reassortment vaccine 9Rotashield) withdrawn over concerns regarding intussusception
New live attenuated vaccines (Rotarix and Rota Teq) highly effective against severe disease
Protection severe disease not necessarily against infection
Rotarix added to UK Chidhood immunization programme in 2013-2 dosease given at 2 months and 3 months of age
Caliciviruses: Types
Norovirus
Sapovirus (SRSV)
IEM demonstrated Norwalk virus as vomiting agent (winter vomiting) +ssRNA, non-enveloped, does not grow in routine cell culture
Reservoir human GI tract – may be concentrated in bivalve molluscs (osyters)
Norovirus Gastroenteritis clinically
Incubation 10-50 hrs
Asymptomatic to explosive vomiting and diarrhoea
Headache and abdominal cramps
Lasts 24-48 hrs
Norovirus outbreaks
Common defined outbreak – Closed communities/hospitals/cruise ships
Breathe in aerolised vomit/faeces and swallow
Infectious dose low
Enteric Adenoviruses
Second most common cause of infantile diarhhoea in temperate climates
Adenovirus causing disease
Non-enveloped, dsDNA
Subgrou[s A-F, Gastroenteritis agents are gp F types 40,41
Poor growth in cell culture
Adenovirus Standard clinical picture
Incubation period up to 10 days, watery diarrhoea, mild fever, illness may last longer in general (3-11 days)
Astroviruses
Infants and elderly exhibit significance illness
• Severity lower than other agents
• Often co-infection with rotavirus/norovirus
Astrovirus epi
<5% hospitalised cases viral gastroenteritis
Winter time
+ssRNA, non-enveloped, 5-6 pointed star
Several Serotypes
