Food poisoning
Definition
Illness caused by ingestion of food or water contaminated with:
bacteria and/or their toxins
viruses
parasites
chemicals
Contamination usually arises from improper handling, preparation, or storage of food or drinks
Risk Factors
older people, children, and pregnant women
chronic disease
recent hx of travel
immunocompromised state
hx of contact food poisoning
improper food handling and storage
consumption of undercooked meat
Associated with Salmonella, Campylobacter, Shiga toxin-producing E coli, and Clostridium perfringens
consumption of raw seafood
Associated with Norwalk-like virus, Vibrio organism, or hepatitis A
consumption of homemade canned foods
Associated with Clostridium botulinum
consumption of unpasteurised soft cheeses
Associated with Listeria,Salmonella, Campylobacter, Shiga toxin-producing E coli, and Yersinia
consumption of deli meats
Associated with listeriosis
consumption of unpasteurised milk or juice
Associated with Salmonella, Campylobacter, Shiga toxin-producing E coli, and Yersinia
consumption of raw eggs
Associated with Salmonella
Differential diagnosis
Very difficult to differentiate
Lack of exposure to specific foods or absence of specific behaviours may help in differentiating
May present with fatigue, diarrhoea, abdominal pain, weight loss, fever, and rectal bleeding
Other signs may include:
presence of oral ulcers, perianal skin tags, fistulae, abscesses, and sinus tracts
abdominal exam may reveal a palpable mass in the ileocaecal area
no mass present on digital rectal examination
May present with:
bloody diarrhoea
hx of lower abdominal pain
faecal urgency
presence of extraintestinal manifestations (e.g., erythema nodosum, acute arthropathy)
hx of primary sclerosing cholangitis
No mass present on digital rectal examination
History of exposure to certain foods known to cause intolerance or allergies (milk, lactose, gluten)
Relapsing symptoms with challenge
Irritable bowel syndrome (IBS)
Total duration of symptoms should be more than 6 months
Specific criteria of combination of:
abdominal bloating or pain relieved by defection
association with change in stool frequency and/or consistency
without evidence of alarm signs or symptoms
Physical examination reveals a healthy non-toxic appearance without evidence of dehydration.
Microscopic colitis
Typically present in older persons, long duration symptoms, and lack of haematochezia or blood in stool
Localised right lower quadrant pain and peritoneal irritation are classic (guarding)
CT scan of the abdomen is diagnostic.
Localised pain in RUQ and a positive Murphy sign are classic symptoms
Epigastric pain radiating to the back
History of excessive alcohol consumption in alcohol induced pancreatitis
Jaundice is usually present
Risk factors for acute hepatitis B and C include unprotected sex and IV drug use
History of excessive alcohol consumption in alcoholic hepatitis
History of hepatotoxic medication use or overdose in drug induced hepatitis
Neurological signs and Kayser-Fleischer ring in Wilson's disease
Malabsorption syndromes
Chronic symptoms and significant malnourishment
History of intestinal surgery
Extraintestinal manifestations of malnourishment and malabsorption are usually present
Distention is the more common presenting symptom
Vomiting, including vomiting of fecal matter, occur later in the course of the illness
Presents with abdominal distension and vomiting earlier on in course of the illness
May be history of abdominal surgery
Radiation enteritis
Patients have a history of receiving radiation therapy
Sudden onset of diffuse abdominal pain
Chronic symptoms of vague, diffuse abdominal pain may also be indicative of chronic mesenteric ischaemia
In contrast, ishaemic colitis may cause focal or diffuse abdominal pain
Often has a more insidious onset, over several hours or days
Medication and drugs side-effects/toxicity
History of drugs ingestion/use
Leukocytosis and fever in an older patient.
Multisystem involvement (skin, joints, blood) and chronic presentation
Biopsy shows vasculitis pattern (leukocytoclastic, necrotising)
Epidemiology
In 1995, foodborne diseases caused in England and Wales an estimated:
2,366,000 illnesses
21,138 hospital admissions
718 deaths
By 2000, this had fallen to 1,338,772 cases, 20,759 hospital admissions, and 480 deaths
The most important pathogens identified were:
Campylobacter
Salmonella
Clostridium perfringens
Verocytotoxin-producing Escherichia coli
The annual incidence of foodborne disease in the US is estimated to be 1 case per 4 persons
Aetiology
Ingestion of food or water contaminated with bacteria and/or their toxins, viruses, parasites, or chemicals
Contamination usually arises from improper handling, preparation, or storage of food or drinks
Clinical features
Key common features:
Diarrhoea
Vomiting
Staphylococcus aureus, Bacillus cereus, or norovirus is suspected when vomiting is the major presenting symptom
Other features:
Abdominal pain (common)
Fever (common)
Blood or mucous in stool (common)
Dehydration (common)
Profuse rice-water stool (uncommon)
Suggests cholera or a similar process
Reactive arthritis (uncommon)
Can be seen with Salmonella, Shigella, Campylobacter, and Yersinia infections
Skin rash (uncommon)
Rose spot macules on the upper abdomen and hepatosplenomegaly may be seen in Salmonella typhi infection
Erythema nodosum and exudative pharyngitis are suggestive of Yersinia infection
Patients with Vibrio vulnificus or V alginolyticus may present with cellulitis and otitis media
Symptoms of botulism
Diplopia (uncommon)
Slurred speech (uncommon)
Poor muscle tone (uncommon)
Difficulty swallowing (uncommon)
Pathophysiology
Diarrhoea results from the action of enterotoxins on the secretory mechanisms of the mucosa of the small intestine
May be preformed before ingestion or produced after ingestion
May occur:
Without invasion (non-inflammatory)
In the large intestine, with invasion and destruction (inflammatory)
In some types of food poisoning vomiting is caused by a toxin acting on the CNS
Staphylococci, Bacillus cereus
The clinical syndrome of botulism results from the inhibition of acetylcholine release in nerve endings by the botulinum toxin
The pathophysiological mechanisms that result in acute GI symptoms from some of the non-infectious causes of food poisoning are not well known
e.g. naturally occurring substances such as mushrooms and toadstools and heavy metals such as arsenic, mercury, and lead
Investigations
Stool microscopy for WBC and RBC
Easy, inexpensive, and widely available.
Helps to differentiate invasive or inflammatory from non-invasive disease.
Stool microscopy for WBCs and RBCs should be done in cases of:
Patients presenting with blood in stool
Fever
Suspected invasive pathogens (such as Escherichia coli O157:H7)
When other diagnoses are considered (such as inflammatory bowel disease, ischaemic or infectious colitis)
With prolonged symptoms (3 days or more)
Dark-field microscopy can be done to identify Vibrio cholera
Stool culture
Bacterial culture for enteric pathogens such as Salmonella, Shigella, and Campylobacter organisms becomes mandatory:
In any patient with grossly bloody stools
If a stool sample shows positive results for WBCs or blood
If patient has fever or symptoms persisting for longer than 3 to 4 days
If symptoms persist and the pathogen is isolated, specific treatment should be initiated
Stool O+P
Microscopic examination of the stool for ova and parasites
FBC with differential
Helps to assess the inflammatory response and the degree of haemoconcentration
Additionally, may detect evidence of haemolytic uraemic syndrome (HUS) when Shiga toxin-producing E coli (e.g., O157:H7) is suspected
Results:
High WBC with most inflammatory/invasive pathogen associated diarrhoea
Low WBC are associated with typhoid fever and some viruses
Anaemia
High Hb and haematocrit could reflect haemoconcentration
Serum creatinine and electrolytes
Should be done to rule out electrolyte abnormalities and renal dysfunction:
In all patients with evidence of moderate or severe dehydration
In those with severe vomiting or diarrhoea or symptoms without improvement after 24 hours
Results:
HUS suspected when uraemia present
Hypokalaemic metabolic acidosis secondary to diarrhoea
Hyper- or hyponatraemia and elevated blood urea nitrogen secondary to dehydration
Stool/serum botulinum toxin detection test
If patient has symptoms/signs of botulism, stool or serum should be sent for toxin identification/confirmation
Blood culture
Blood culture is performed to exclude bacteraemia if the patient is notably febrile (e.g., temperature >101°F [38.5°C]) and there are signs of sepsis
Tachycardia, hypotension, poor capillary refill, tachypnea, acute mental confusion, decreased urine output
Signs of sepsis are difficult to differentiate from signs of severe dehydration
Amylase and lipase
Helps to distinguish food poisoning from acute pancreatitis
LFTs
Helps to distinguish food poisoning from acute cholecystitis or acute hepatitis
May be elevated in patients with wild mushroom toxicity or invasive pathogens associated with systemic illness
Particularly Salmonella and Campylobacter
May show hypoalbuminaemia secondary to malnourishment or as an acute-phase reactant
Hepatitis A IgM antibodies
Performed when history or occupation (daycare, nursing) suggestive of exposure to hepatitis A or if LFTs abnormal
Acute abdominal series
Flat and upright abdominal radiographs should be obtained urgently if the patient experiences severe pain or obstructive symptoms, or if perforation is suspected
Sigmoidoscopy/colonoscopy
Sigmoidoscopy/colonoscopy is considered in cases where:
Bloody diarrhoea in whom no enteric pathogen has been identified
Bloody diarrhoea persists or increases in severity
Patients whose clinical picture and tests results are incompatible with a diagnosis of foodborne illness
Can be useful in diagnosing inflammatory bowel disease, antibiotic-associated diarrhoea, shigellosis, and amoebic dysentery
Colonoscopy is more expensive, requires full preparation and sedations, and should be performed in a special setting (endoscopy suite)
Careful colonoscopy is indicated in patients with persistent symptoms or not responding well to initial treatment
Other possible investigations
Oesophagogastroduodenoscopy
Immunocompromised patients
Patients receiving chemotherapy
Patients with persistent, severe symptoms lasting more than 5 days or not responding well to initial treatment
Biopsy
Considered when performing endoscopy
May distinguish inflammatory bowel disease from acute infectious enteritis or colitis
Presence of crypt architectural changes such as crypt branching or sparsity
However, these features take several weeks to develop and are not likely to be present in an infectious colitis
Duodenal aspirate
Considered in immunocompromised patients, patients receiving chemotherapy, and patients with persistent symptoms or not responding well to initial treatment
PCR of stool
PCR may be useful when available to detect Campylobacter,Salmonella, and Shiga toxin-producing E coli O157 but is not widely available
Management
a) conservative
Oral hydration
A simple oral rehydration solution (ORS) may be composed of 1 teaspoon of salt and 4 teaspoons of sugar added to 1 litre of water
ORS promotes co-transport of glucose, sodium, and water across the gut epithelium, a mechanism unaffected in cholera
The WHO recommends a solution containing 3.5 g of sodium chloride, 2.5 g of sodium bicarbonate, 1.5 g of potassium chloride and 20 g of glucose per litre of water
b) medical
Antiperistaltics
Can be offered to patients with uncomplicated watery diarrhoea whose diarrhoea interferes with their ability to work or those with traveller’s diarrhoea
Antiperistaltics (opiate derivatives) should not be used:
In patients with fever, systemic toxicity, or bloody diarrhoea
In patients whose condition either shows no improvement or deteriorates
Antidiarrhoeals
The value of non-prescription antiperistaltics or antidiarrhoeals (e.g., loperamide) in patients with mild-to-moderate diarrhoea is under discussion
They can be offered to patients whose diarrhoea interferes with their ability to work or those with traveller’s diarrhoea
Adsorbents (e.g., aluminium hydroxide) help patients have more control over the timing of defecation but do not alter the course of the disease or reduce fluid loss
Antisecretory agents (e.g., bismuth) may be useful
In mild cases, loperamide is safe and effective
When invasive pathogens are suspected, antidiarrhoeals that target motility should be generally avoided
Decrease in intestinal motility in patients taking diphenoxylate/atropine may be detrimental to those with diarrhoea resulting from Shigella or Salmonella organisms.
IV rehydration
Intravenous solutions are indicated in patients who are severely dehydrated or who have intractable vomiting
Rehydrate can generally be done rapidly without complication
For example, if there is 10% dehydration in a 75 KG adult, and the fluid deficit is 5 to 7 L, the volume can be administered over 2 to 4 hours (i.e., 2-4 L/hr)
Potassium may be added but not to exceed 10 mEq/hour with IV administration
Botulin antitoxin
Notifiable, discussion with local authority/CDC for provision of antitoxin
Antitoxin works to block the toxin produced by Clostridium botulinum
Antibiotics
Shigella species
fluoroquinolone or trimethoprim/sulfamethoxazole
Non-typhi species of Salmonella
fluoroquinolone or trimethoprim/sulfamethoxazole
Escherichia coli species (excluding enterohaemorrhagic [Shiga toxin-producing])
fluoroquinolone
Campylobacter species
erythromycin
Yersinia species
fluoroquinolone or doxycycline or aminoglycoside
Vibrio cholerae + Vibrio parahaemolyticus
fluoroquinolone or doxycycline or tetracycline or trimethoprim/sulfamethoxazole or azithromycin
Giardia species
antiparasitics
Cryptosporidium species
paromomycin or nitazoxanide
Cystoisospora belli
trimethoprim/sulfamethoxazole or pyrimethamine and folinic acid
Microsporidium species and immunocompromised
albendazole
Entamoeba histolytica
metronidazole + paramomycin or diiodohydroxyquinoline
Listeria monocytogenes
ampicillin or trimethoprim/sulfamethoxazole
c) surgical
n/a
Prognosis
Because most cases of food poisoning are self-limited, prolonged follow-up care is not required
Stool cultures should be monitored in individuals working in settings such as hospitals, food establishments, and daycare centres who are infected with:
Shiga toxin-producing Escherichia coli (e.g., O157:H7) or Salmonella or Shigella organisms
Continue until they become culture-negative without antibiotics
These people should not return to work until that time
Mortality is relatively rare (<0.1%) but more likely in very young, elderly or immunocompromised persons