RCSI GI Infections Past Paper PDF

Leading the world to better health Enteric (GI) infections Dr Rachel Grainger Clinical Lecturer, Dept. of Clinical Microbiology, RCSI  RCSI Royal College of Surgeons in Ireland Coláiste Ríoga na Máinleá in...

Leading the world to better health Enteric (GI) infections Dr Rachel Grainger Clinical Lecturer, Dept. of Clinical Microbiology, RCSI  RCSI Royal College of Surgeons in Ireland Coláiste Ríoga na Máinleá in Éirinn Enteric (GI) infections Class Year 2, Semester 2 Course Undergraduate Medicine Lecturer Dr Rachel Grainger Date 10th September 2024 LEARNING OUTCOMES Discuss the epidemiology of clinically important foodborne pathogens Name the main virulence factors of clinically important foodborne pathogens and explain the biological role of each in the pathogenesis of infection Describe the pathogenesis of food poisoning Recognise and describe the clinical features and complications of food poisoning Outline the laboratory diagnosis of food poisoning Choose the appropriate measures to manage patients with food poisoning Use the appropriate measures to prevent the acquisition & spread of foodborne illnesses  DEFINITIONS Gastroenteritis: – Acute inflammation of the lining of the stomach & the intestines – Caused by food poisoning, irritating food or drink, or psychological factors, such as stress Food Poisoning: – Group of illnesses caused by ingestion of: Contaminated food OR Food that contains microorganisms/toxins/poisons – Can result in: Gastroenteritis (most commonly) Also systemic illness (e.g., listeriosis, enteric fever), neurological syndromes (botulism) & toxic states (mercury, mushrooms) DEFINITIONS Diarrhoea – 3 or more episodes of loose or liquid stool in a 24 hour period FOOD POISONING: EPIDEMIOLOGY Common Many infectious causes Usually sporadic May occur as outbreak Notifiable to Public Health (full list available on HPSC website) Transmission: – Contaminated food/water – Faecal-oral route Food implicated in food poisoning e.g. shellfish, poultry, eggs (undercooked or raw) (Humphreys & Irving)  INFECTIOUS CAUSES Bacterial: Viral: – S. aureus, – See lecture on viral – Clostridium spp, gastroenteritis – B. cereus Parasitic: – Campylobacter spp – Cryptosporidium parvum, – E. coli – Giardia lamblia – Non-typhoidal Salmonella, (giardiasis), Shigella spp – Entamoeba histolytica – Vibrio spp (amoebiasis), travel- – Yersinia spp associated – Listeria spp – Intestinal tapeworms LECTURE FOCUS Food poisoning caused by: 1. Toxins: S. aureus, Clostridia spp and B. cereus 2. Campylobacter spp 3. E. coli 4. Listeria 5. Cryptosporidium See your other lectures in this module for Salmonella, Shigella and viral causes and for additional information on botulism PATHOGENESIS 1. Ingestion of pre-formed toxin – e.g., S. aureus, B. cereus 2. Ingestion of pathogen or spores – in contaminated food/water 1. Toxin production in vivo e.g., e.g., B. cereus, C. perfringens 2. Multiplication/tissue invasion  CLINICAL FEATURES History: Examination: Onset of symptoms May have fever, but Duration not always Recent travel Usually otherwise Food normal unless not – takeout, restaurant, buffet, food poisoning picnic – E.g. abdominal Were other people sick? pathology Medications as a cause of diarrhoea or a contributory factor – e.g. gastric acid suppressants  INVESTIGATIONS Faeces – PCR – Selective culture for bacteria – Light microscopy for protozoa Blood culture – Hospitalized patients with pyrexia Food – Outbreak – Not usually individual cases TREATMENT & PREVENTION Usually supportive treatment only: – NO role for antibiotics in the vast majority of cases – Fluid and electrolyte replacement – Avoid anti-diarrhoeals, if possible – If hospitalised: Isolate with contact precautions Prevention: – HACCP: Hazard Analysis Critical Control Points Mandatory for all food premises such as restaurants, hospitals, schools, etc – Early recognition of outbreaks Notification to Public Health to investigate outbreaks PREVENTION Clean: Wash all fruit /vegetables fully before eating Cook: Cook food right through and serve when still very hot. Follow manufacturer's instructions in the preparation of all foods. Chill: Keep your fridge at 50C or below. Put chilled food in the fridge straight away. Check: Throw out food that has passed the ‘use by’ date, and if the food packet has been opened, use within 2 days. Separate: Keep cooked food and raw food away from each other. https://www.cdc.gov/foodsafety/food-poisoning.html  TOXINS: S. AUREUS Heat-stable enterotoxin ingested in food – (dairy, produce, meats, eggs, salads) Food handler contaminates food left at room temperature  organisms multiply  produce toxin – Person ingests enterotoxin It works fast! (1-8 hours) – Vomiting predominates, occasionally diarrhoea – Lasts 8-24 hours Outbreaks especially in summer Diagnosis = history Treatment = supportive  TOXINS: BACILLUS CEREUS Type 1: Emetic Syndrome Type 2 - Diarrhoeal Syndrome Ingestion of preformed toxin Spores ingested in food Cooked rice: – Meats, salads, chicken soup – Allowed to cool slowly at room Toxin production after temperature / held for long spores germinate period Incubation 6-14 hours – Germination from spores with release of toxin Diarrhoea mainly – Rapid heating does not – Lasts 8-24h destroy the toxin It works fast! (1-6 hours) For both: – Predominantly vomiting, – Diagnosis = history abdominal cramps – Treatment = supportive – May have diarrhoea – Lasts 2-10 hours TOXINS: CLOSTRIDIUM PERFRINGENS Food contaminated with heat-resistant spores ingested – Incorrectly stored cooked meat dishes, gravy, dairy products Toxin production in vivo – Multiplication in the small intestine – Sporulation + enterotoxin production Incubation 8-24 hours Profuse diarrhoea, occasionally vomiting Lasts about 1-3 days TOXINS: CLOSTRIDIUM BOTULINUM Food contaminated with toxin (neurotoxin) ingested – Improperly canned products, home bottled products e.g. pickles, honey Incubation 12-36 hours Toxin absorbed from GIT into bloodstream – Binds irreversibly to presynaptic nerve endings (peripheral and cranial nerves) – Inhibits acetylcholine release Acute descending symmetrical weakness / bilateral cranial nerve palsies – Paralysis, mechanical ventilation required – High mortality - 20% Treat with anti-toxin WHAT’S THE MOST LIKELY CAUSE? CAMPYLOBACTER SPP Most common cause of bacterial food poisoning in developed countries 4 species associated with human disease: 1. C. jejuni = most common 2. C. coli (cattle, swine, birds) 3. C. fetus 4. C. lari (seabirds in particular)  EPIDEMIOLOGY Source: Normal flora: cattle, swine, birds Zoonosis - to humans from animals/animal products - Carcasses/meat contaminated from faeces during slaughtering Route of transmission: Mostly Foodborne - Undercooked meat and meat products (e.g., chicken) - Raw or contaminated milk - Contaminated water or ice Person-person via faecal oral route, less common Cases peak in summer months (barbecue season)  PATHOGENESIS Ingested Adheres to jejunum and ileum – Cytotoxin causes local damage (mucosal invasion) – Occasionally severe haemorrhagic necrosis of the small intestine – May also have large bowel involvement with crypt abscess formation in severe cases – Differential Diagnosis = Ulcerative colitis Bloodstream spread in some people CLINICAL FEATURES Incubation period: 2-4 days, can be up to 8-9 days Clinical features: Prodromal illness (fever, headache) Diarrhoea (may be bloody) Abdominal pain (can be severe) Resolves 5-7days Complications: Toxic megacolon Bacteraemia (extremes of age / immunosuppressed) Guillain-Barre syndrome (< 1 in 1000 cases)  LABORATORY DIAGNOSIS Typical curved-shaped Greyish colonies on Positive oxidase test Hydrolyses Gram negative bacilli selective charcoal- hippurate (giving on Gram stain containing media rise to blue colour (Humphreys and Irving, Oxford incubated in CO2 at in tube on the University Press) 42°C. left) PCR (Faeces) Culture (Faeces / Blood)  TREATMENT Treatment: Rehydration Antibiotics not routine for gastroenteritis – Only if bacteraemic or immunosuppressed – Azithromycin or Ciprofloxacin if susceptible Prevention: Good food hygiene practices – Cooking and storing of meat/poultry, – Hand hygiene after contact with animals, meat etc  E. COLI ASSOCIATED WITH GASTROENTERITIS Not the same E coli that cause UTI 1. Enterohaemorrhagic E. coli (EHEC) a) Shiga toxin–producing E. coli (STEC), also called verotoxigenic E. coli (VTEC) 2. Enterotoxigenic E. coli (ETEC) 3. Enteropathogenic E. coli (EPEC) 4. Enteroinvasive E. coli (EIEC) 5. Enteroaggregative E. coli (EAggEC) 1. ENTEROHAEMORRHAGIC E. COLI Main reservoir: cattle Outbreaks and other ruminants - Often linked to – Survive for long periods undercooked minced beef, in environment petting animals, water, Transmission unpasteurised milk - Creches, residential – Food Minced beef products institutions, contaminated (e.g., burgers) wells – Contaminated Serotype O + H antigens E. coli O157:H7 most environment common Direct or indirect contact Particularly serious in with animals or their infants (bloody diarrhoea faeces and renal failure) – Person to person  Site of the infection = colon Adherence + Invasion of intestinal epithelial cells Shigella-like Vero toxin (cytotoxin) – Cell death by disrupting protein synthesis – Acute inflammatory response and tissue destruction – Bloody diarrhoea 1. ENTEROHAEMORRHAGIC E.COLI Clinical presentation – Incubation period: ~3 days (range 1-10 days) – Bloody diarrhoea +/- vomiting – More severe in extremes of age – Lasts 3 days Complications – Haemolytic uremic syndrome 10% children < 10yrs Acute renal failure Thrombocytopaenia Microangiopathic haemolytic anaemia 1. ENTEROHAEMORRHAGIC E. COLI Diagnosis: Management: PCR (faeces) Rehydration Culture in reference Antibiotics not indicated lab to confirm – Increased toxin release  further cell death and worsening of symptoms Require isolation in hospital – Contact precautions 2. ENTEROTOXIGENIC E. COLI (TRAVELLERS’ DIARRHOEA) Underdeveloped countries/ regions of poor sanitation Short incubation period 1-3 days Symptoms: – Watery (non-bloody) diarrhoea, fever and nausea – Minor discomfort to severe cholera-like syndrome Self-limiting 1-5 days  2. ENTEROTOXIGENIC E. COLI (TRAVELLERS’ DIARRHOEA) Site of infection: small intestine Adherence Does not invade Enterotoxins = secretion of fluid and electrolytes resulting in diarrhoea 1. LT (heat-labile): similar to cholera toxin 2. ST (heat-stable) 3. ENTEROPATHOGENIC E.COLI: Major cause of Infantile gastroenteritis – < 6 moa – Developing countries High mortality rate (severe dehydration) Person-person spread May cause outbreaks Site of infection: small intestine – Attach to intestinal mucosa – Loss of villi – Invasion of host cells and interference with normal cellular signal transduction = symptoms Watery diarrhoea, vomiting, fever  LISTERIA MONOCYTOGENES Grows in a wide range of temperatures (2-370C) Infection peaks in warmer months Transmission: – Contaminated milk, certain soft cheeses, pate, etc. – Vertical transmission (mother  foetus) – Animal contact Pathogenesis: – Crosses mucosal barrier & disseminates – Survives within macrophages – Need a T-cell response to activate infected cells and produce intracellular killing LISTERIA MONOCYTOGENES Clinical features Healthy adults: – Mostly asymptomatic or mild influenza-like illness / diarrhoea Occupational risk: farmers / vets / butchers At-risk groups (ie opportunistic pathogen): – Pregnant women – Neonates – Immunosuppressed patients: Pneumonia Meningoencephalitis LISTERIA & Neonatal infection: Early onset (1st 2 days of life) PREGNANCY – Acquired in utero BSI +/- pneumonia or cardiopulm Perinatal listeriosis: distress “Influenza-like illness” Hepatosplenomegaly Abscesses Usually 3rd trimester CNS involvement Complications: – High mortality (40-50%) – Miscarriage Late onset (typically >5 days of – Intrauterine death life) – Acquired from maternal genital – Premature labour tract – Neonatal listeriosis – More common than early onset – Meningitis / meningo-encephalitis > BSI – Mortality ~ 12% LISTERIA MONOCYTOGENES Diagnosis: – Blood cultures / CSF Mother: high vaginal swab / placenta – Microscopy: gram-positive bacillus, tumbling motility at 250C Treatment: – High dose ampicillin / amoxicillin with an aminoglycoside (e.g. Gentamicin) – Resistant to cephalosporins Prevention: – People at high-risk should avoid raw / partially-cooked foods of animal origin  CRYPTOSPORIDIUM Clinical presentation: C. parvum & C. hominis – Incubation: 2-10 days Transmission: – Watery diarrhoea (most – Faecal-oral common) – Contaminated food or – Last 1-2 wks water-source (immunocompetent hosts) – Oocysts allow survival – Refractory diarrhoea with outside the body for long malabsorption periods (immunosuppressed) Makes it resistant to Diagnosis: chlorine-based disinfectants – Faeces Microscopy (modified acid- fast or auramine stain) PCR CASE SCENARIO A 20yo attends Emergency Department: 48hr history of abdominal pain and diarrhoea – Became bloody on day 2 of the illness Attended summer barbeque 2 days prior to the onset of symptoms Remembers eating barbequed chicken No medical history or significant family history 1. What is the most likely cause & source? 2. How would this diagnosis be confirmed? 3. What is the treatment? 4. What else should happen? Thank you