Food poisoning

Food Poisoning
Dr. Suprakash Das
Assist. Prof.

Introduction
Food poisoning means illness resulting from ingestion of food with microbial
or non-microbial contamination.
The condition is characterized by
(a) History of ingestion of a common food
(b) Attack of many persons at the same time, and
(c) Similarity of signs and symptoms in the majority of cases.
 The World Health Organization estimates that there are more than 1000 million
cases of acute diarrhea annually in developing countries, with 3-4 million deaths.
 According to the Food Standards Agency (FSA) there are nearly 900000 cases of
food poisoning each year.
 Foodborne diseases result from ingestion of a wide variety of foods contaminated
with pathogenic microorganisms, microbial toxins, and chemicals.

Introduction
 Although most foodborne illnesses are sporadic, investigation of
outbreaks is an important way to identify the types of foods and
contaminants associated with foodborne illness.
 Our lifestyles have changed over the last few years which include an
increasing reliance on ready prepared meals, eating out rather
than cooking and taking more holidays abroad.
 People often cook several meals in advance and freeze them for a
long period of time or buy convenience food which only has to be put
in a microwave oven.
 This is the reason for increasing food poisoning cases in present
scenario.

Causes Of Food Poisoning
Bacteria Viruses
Bacillus cereus Rotavirus
Staphylococcus aureus Adenovirus
Salmonella group (except S. typhi) Norovirus
Shigella Sapovirus
Vibrio parahaemolyticus/vulnificus Astrovirus
Escherichia coli (STEC/ETEC/EAEC) Fungal
Campylobacter jejuni Aspergillus flavus
Yersinia enterocolitis Fusarium roseum
Clostridium perfringens Parasitic
Listeria monocytogenes Giardia lamblia
Aeromonas hydrophila Cryptosporidium
Enterococcus faecalis Cyclospora

Factors Leading To Food Poisoning
Inoculum size
 The number of microorganisms that must be ingested to cause disease varies
considerably from species to species.
 For Shigella, enterohemorrhagic Escherichia coli, Giardia lamblia, or
Entamoeba, as few as 10-100 bacteria or cysts can produce infection, while
 105-108 Vibrio cholerae organisms must be ingested orally to cause disease.
Adherence
 Many organisms must adhere to the gastrointestinal mucosa as an initial step in the
pathogenic process.
 Organisms that can compete with the normal bowel flora and colonize the mucosa
have an important advantage in causing disease.

Toxin Production
 The production of one or more exotoxins is important in the
pathogenesis of numerous enteric organisms.
Enterotoxins Cause watery diarrhea by acting directly on secretory
mechanisms in the intestinal mucosa;
Cytotoxins Cause destruction of mucosal cells and associated
inflammatory diarrhea; and
Neurotoxins Act directly on the central or peripheral nervous
system.

Invasion
 Dysentery may result not only from the production of cytotoxins but also
from bacterial invasion and destruction of intestinal mucosal cell.
 Shigella and enteroinvasive E. coli
Invasion of mucosal epithelial cells,
Intraepithelial multiplication, and
Subsequent spread to adjacent cells.
Host Defenses
 Normal host can protect itself against disease.
 Food poisoning depends upon host defense mechanisms e.g. Normal flora,
Gastric acid, Intestinal motility, Immunity and Genetic determinants.

Foodborne Syndromes Caused by Microbial Agents or Their Toxins
Nausea and Vomiting Lasting Less Than 24 Hours
 The major etiologic considerations are Staphylococcus aureus and Bacillus
cereus.
 These diseases are caused by preformed enterotoxins and have a short
incubation period of 1 to 8 hours.
 Another clue to the cause of staphylococcal and emetic B. cereus illnesses is
that their duration is typically less than 24 hours and often less than 12
hours.
 Staphylococcal food poisoning is characterized by
 vomiting (87% of cases),
 diarrhea (89%), and
 abdominal cramps (72%);
 fever is uncommon (9%).

 Staphylococci responsible for food poisoning produce one or more
serologically distinct enterotoxins (SEA through SEV, excluding SEF), but
not all cause vomiting.
 All of these toxins are highly heat resistant and withstand ordinary cooking.
 They are very resistant to proteolytic enzymes and therefore pass through
the stomach intact.
 Strains producing SEA alone account for most reported outbreaks of
staphylococcal food poisoning in the United States.
 The mechanisms by which enterotoxins lead to emesis may involve vagus
nerve stimulation.

B. cereus strains can cause two types of food poisoning syndromes
One with an incubation period of 0.5 to 6 hours (short-incubation EMETIC syndrome)
Second with an incubation period of 8 to 16 hours (long-incubation DIARRHEAL
syndrome).
The emetic syndrome is characterized by
 Vomiting (100% of cases),
 Abdominal cramps (100%)
 Less frequently, diarrhea (33%).
 The emetic toxin is Cereulide stimulates the vagus afferent nerve by binding to the 5-
hydroxytryptamine-3 receptor.
 Rarely, fulminant liver failure may develop via impairment of fatty acid oxidation caused
by the toxicity of cereulide to mitochondria.

Norovirus illness
Acute onset of vomiting,
Nonbloody diarrhea, or both,
Accompanied by nausea and abdominal pain.
Fever (40%) usually low grade, and lasts for less than 24 hours.
Symptoms usually resolve in 2 to 3 days.
 Noroviruses are among the most common foodborne pathogens.
 Even more cases of acute gastroenteritis are caused by nonfoodborne transmission
of noroviruses, directly from one person to another or by fomite contamination.
 Incubation period ≂33 hours.
 A group of related viruses in the Caliciviridae family, most notably the sapoviruses
can cause similar illness.

Watery Diarrhea Without Fever Lasting 1 to 2 Days
 The major pathogens involved Clostridium perfringens type A and B.
cereus.
 In C. perfringens type A food poisoning the most common symptoms are
Diarrhea (91%) and
Abdominal cramps (73%);
Vomiting (14%)
Fever (5%).
 C. perfringens food poisoning toxins produced in vivo, accounting for a
longer incubation period of 9 to 12 hours.
 Toxinotype A strains α toxin & C. perfringens enterotoxin (CPE).

Watery Diarrhea Without Fever Lasting 1 to 2 Days
 The toxin binds to the apical membrane of epithelial tight junctions in the small
intestines, triggering
 formation of pores influx and efflux of water, ions, and other small molecules
diarrhea and cytotoxicity.
 B. cereus strains [elaborate two enterotoxins (hemolysin BL and nonhemolytic
enterotoxin) & enterotoxin (CytK)] (Long-incubation syndrome)
Diarrhea (96%),
Abdominal cramps (75%),
Vomiting (33%), and
Fever.
 A foodborne infection (Necrotizing Enterocolitis), fatal in about 20% of patients,
is caused by C. perfringens type C in people with low protein intake; the disease is
rare outside of Papua New Guinea, where it is sometimes called pigbel.

Watery Diarrhea and Abdominal Cramps Lasting More Than 2 Days
 The major pathogens enterotoxigenic strains of E. coli (ETEC) and Vibrio
parahaemolyticus.
Diarrhea caused by ETEC
 Lasts a median of 6 days, often accompanied by
 Abdominal cramping for the full duration of illness
 Uncommon symptoms included vomiting (13% of cases) and fever (19%).
V. parahaemolyticus
 Virulence Factors Secreted toxins and Effector proteins.
 The median duration of diarrhea caused by V. parahaemolyticus is 6 days;
 Abdominal cramping (89%),
 Vomiting or fever (50%)
 Bloody diarrhea (29%).

Diarrhea, Abdominal Cramps, and Fever
The major etiologic considerations are
Nontyphoidal Salmonella (Incubation period6-48 hrs),
Shigella,
V. parahaemolyticus
Campylobacter jejuni (Incubation period2-4 days),
STEC,
Yersinia enterocolitica
L. monocytogens (Incubation period20-31 hours)
Norovirus does not consistently cause fever but should be considered.
 Fever is less common with STEC.
 These pathogens (exception, Norovirus) Inflammatory diarrhea, (invading the intestinal
epithelium Or, damaging it via secreted cytotoxins) Bloody diarrhea and vomiting.
 These illnesses usually resolve within 2 to 7 days.

L. monocytogens
Frequent watery diarrhea,
Fever,
Abdominal cramps,
Headache, and
Myalgias.
 Y. enterocolitica infection in older children and adults the illness may
manifest as
 Either a diarrheal illness or,

Pseudoappendicular syndrome; as ileocecitis, consisting of
Abdominal pain (resembling that of appendicitis);
Fever;
Leukocytosis; and, in some patients,
Nausea and vomiting.
 Joint pain beginning about 1 week after onset of diarrhea, is more common in
adults.
 Sore throat and rash can affect patients of all ages.
 The median duration of diarrhea is 2 weeks, but other symptoms may last longer.
 Campylobacter and Salmonella can also cause an ileocecitis that mimics
appendicitis.

Bloody Diarrhea with Minimal Fever
 Hemorrhagic colitis has been linked to STEC, most often serogroup O157.
 These strains produce one or both types of Shiga toxins (Shiga toxin 1 or 2).
 Shiga toxins a.k.a verotoxins, are cytotoxins that damage vascular
endothelial cells in target organs such as the gut and kidney.
 Strains that produce Shiga toxin 2 are more virulent than strains that
produce both Shiga toxin 1 and 2.
The illness is characterized by
 Severe abdominal cramping and
 Diarrhea, which is initially watery but may quickly become grossly bloody.

Bloody Diarrhea with Minimal Fever
 About one-third of patients report a short-lived low-grade fever that typically
resolves before seeking medical attention.
 Most patients fully recover within 7 days.
 However, overall 6% (15% in children <5 years of age) of patients develop
hemolytic-uremic syndrome (HUS), which is typically diagnosed about 1 week
after the beginning of the diarrheal illness, when the diarrhea is resolving.
 The fatality rate for HUS is 33% in adults 60 years of age or older.
 2% of adults 60 years old or older with only hemorrhagic colitis die.
 Non-O157 STEC are diverse in their virulence properties, causing illness ranging
from uncomplicated watery diarrhea to hemorrhagic colitis and HUS.
 Outbreaks reported have involved serogroups O26, O103, O111, O121, O145, and
O104.

Persistent Diarrhea Lasting 2 or More Weeks
 Parasites including Cryptosporidium, Giardia, and Cyclospora are the most common
causes of persistent (lasting ≥14 days) foodborne diarrhea.
 The incubation period averages about 1 week (range, about 2 days to 2 or more weeks)
 The most common symptoms are watery diarrhea, anorexia, weight loss, abdominal
cramps, nausea, and body aches, Vomiting and low-grade fever may occur.
 Untreated illness can last for weeks or months, with a remitting-relapsing course and
prolonged fatigue.
 A distinctive chronic watery diarrhea, known as Brainerd diarrhea, was first described
in people who had consumed raw milk.
 After a mean incubation period of 15 days, affected individuals developed acute watery
diarrhea with marked urgency and abdominal cramping.
 Diarrhea persisted for more than a year in 75% of patients Agent has not been
identified.

Cranial Nerve Palsies and Descending Paralysis
 Botulism should be strongly suspected in anyone with acute onset of
symmetrical cranial nerve palsies.
 In some patients, illness progresses to symmetrical descending flaccid
paralysis that may result in respiratory arrest.
 Among patients with botulism, 98% report at least one of the following
symptoms:
Dysphagia,
Blurred vision,
Slurred speech,
Double vision, and
Change in the sound of the voice.

Cranial Nerve Palsies and Descending Paralysis
 Paralysis may coincide with or be preceded by nausea in 42%, vomiting in
33%, and diarrhea in 16%.
 Botulism is usually caused by one of four immunologically distinct, heat-
labile protein neurotoxins—botulinum toxins A, B, E, and rarely F.
 The toxins irreversibly block acetylcholine release at the neuromuscular
junction.
 Nerve endings regenerate slowly, so recovery typically takes weeks to
months.
 Foodborne botulism Preformed toxin.
 Infant botulism Ingestion of spores Toxin production in vivo.

Systemic Illness
 Some foodborne diseases manifest mainly as invasive infections in immunocompromised
patients.
 Invasive listeriosis typically affects pregnant women, fetuses, and individuals with
compromised cellular immunity.
 In pregnant women, infection may be asymptomatic or manifest as a mild flulike illness
 20% of pregnancies Miscarriage.
 Neonatal listeriosis manifests Early-onset sepsis during the first several days of life or
Late-onset meningitis during the first several weeks after birth
 Neonatal fatality rate is approximately 20% to 30%.
 In elderly and immunocompromised persons, listeriosis causes meningitis, sepsis, and
focal infections.
 The median incubation period is 11 days.

Systemic Illness
 Vibrio vulnificus can cause septicemia after ingestion of contaminated food,
typically raw oysters.
 This severe syndrome, often accompanied by bullous skin lesions, is seen almost
exclusively in patients with impaired immunity, especially patients with chronic
liver disease including cirrhosis, alcoholic liver disease, and hepatitis.
 The association with liver disease may be related to portal hypertension, resulting
in reduced hepatic phagocytic function, elevated serum iron levels that promote
growth of V. vulnificus, or achlorhydria.
 The overall mortality rate is 15% to 30%.
 Nontyphoidal Salmonella can cause bacteremia and focal infections, often in
patients at the extremes of age or in patients with sickle cell anemia, inflammatory
bowel disease, or an immunocompromising condition.
 Campylobacter fetus, may cause systemic infection, especially in patients with
immunocompromising conditions.

Postinfection Syndromes
 The term reactive arthritis should be applied only to infections caused by Salmonella, Yersinia,
Campylobacter, or Shigella.
 Reiter’s Syndrome Triad of 1. aseptic inflammatory polyarthritis 2. urethritis 3. conjunctivitis.
 Associations between HLA-B27 positivity and reactive arthritis patients with more severe joint
or extraarticular involvement.
 Approximately 20% to 40% of Guillain-Barré syndrome cases have been attributed to recent C.
jejuni infection.
 Occurs 1-3 weeks after the diarrheal disease Manifested by
Ascending paralysis accompanied by
Sensory findings
Abnormal nerve conduction velocity.
 Campylobacter, STEC, Salmonella, Shigella, Giardia, and norovirus Postinfectious irritable
bowel syndrome.

Clinical algorithm for the approach to patients with community acquired
infectious diarrhea or bacterial food poisoning
1. Diarrhea lasting >2 weeks is generally defined as chronic; in such cases, many of the causes of
acute diarrhea are much less likely, and a new spectrum of causes needs to be considered.
2. Fever often implies invasive disease, although fever and diarrhea may also result from infection
outside the gastrointestinal tract, as in malaria.
3. Stools that contain blood or mucus indicate ulceration of the large bowel. Bloody stools without
fecal leukocytes should alert the laboratory to the possibility of infection with Shiga toxin–
producing enterohemorrhagic Escherichia coli. Bulky white stools suggest a small-intestinal process
that is causing malabsorption. Profuse “rice-water” stools suggest cholera or a similar toxigenic
process.
4. Frequent stools over a given period can provide the first warning of impending dehydration.
5. Abdominal pain may be most severe in inflammatory processes like those due to Shigella,
Campylobacter, and necrotizing toxins. Painful abdominal muscle cramps, caused by electrolyte
loss, can develop in severe cases of cholera. Bloating is common in giardiasis. An appendicitis-like
syndrome should prompt a culture for Yersinia enterocolitica with cold enrichment.

Clinical algorithm for the approach to patients with community acquired
infectious diarrhea or bacterial food poisoning
6. Tenesmus (painful rectal spasms with a strong urge to defecate but little passage
of stool) may be a feature of cases with proctitis, as in shigellosis or amebiasis.
7. Vomiting implies an acute infection (e.g., a toxin-mediated illness or food
poisoning) but can also be prominent in a variety of systemic illnesses (e.g., malaria)
and in intestinal obstruction.
8. Asking patients whether anyone else they know is sick is a more efficient means
of identifying a common source than is constructing a list of recently eaten foods. If
a common source seems likely, specific foods can be investigated. See text for a
discussion of bacterial food poisoning.
9. Current antibiotic therapy or a recent history of treatment suggests Clostridium
difficile diarrhea. Stop antibiotic treatment if possible and consider tests for C.
difficile toxins. Antibiotic use may increase the risk of other infections, such as
salmonellosis.

Laboratory Diagnosis
Specimen collection
Transfer at least 5 ml of diarrheal stool, 1 g of material or a walnut-
sized portion of stool, to one of the following:
(1) Clean, leakproof container with a tight-fitting lid or
(2) Buffered glycerol saline (preferred for Shigella spp. but inhibits
Campylobacter)
(3) Modified Cary-Blair medium (modified to contain 1.6 g of agar per liter
rather than 5 g/liter)
(4) Stool enrichment broths
NOTE: Generally, fecal specimens are not placed directly into these broths at
collection, but it can be done.
(5) Anaerobic transport tube for C. difficile culture, not toxin assay (culture
is only for epidemiological or nosocomial studies)

Specimen collection
Rectal swabs
a. Pass the tip of a sterile swab approximately 1 in. beyond the anal sphincter.
b. Carefully rotate the swab to sample the anal crypts, and withdraw the swab.
c. Send the swab in Cary-Blair medium or buffered glycerol saline.
Timing and transport
1. Submit specimen during the acute stage of infection (usually 5 to 7 days), because pathogens
decrease in number with time.
2. If fresh stool is submitted for culture that is not in transport medium, the specimen should be
transported to laboratory and processed within 2 h after collection.
3. If fresh stool is submitted for culture in transport medium, the specimen may be refrigerated at
4C and transported to the laboratory within 24 h for the best recovery of pathogens.
4. If the initial stool culture is negative, then additional fecal samples may be submitted for testing
provided the patient collects them from different defecations on successive days.

Stool Culture and Other Tests
 In situations in which cholera is a concern, stool should be cultured on thiosulfate–citrate–bile
salts–sucrose (TCBS) agar.
 A latex agglutination test has made the rapid detection of rotavirus in stool practical for many
laboratories,
 Reverse-transcriptase polymerase chain reaction and specific antigen enzyme immunoassays
have been developed for the identification of norovirus.
 At least three stool specimens should be examined for Giardia cysts or stained for
Cryptosporidium if the level of clinical suspicion regarding the involvement of these organisms is
high.
 All patients with fever and evidence of inflammatory disease acquired outside the hospital should
have stool cultured for Salmonella, Shigella, and Campylobacter.
 Salmonella and Shigella can be selected on MacConkey’s agar as non–lactose-fermenting
(colorless) colonies or can be grown on Salmonella-Shigella agar or in selenite enrichment
broth, both of which inhibit most organisms except these pathogens.

Stool Culture and Other Tests
 Evaluation of nosocomial diarrhea should initially focus on C. difficile.
 Toxins A and B produced by pathogenic strains of C. difficile can be detected by rapid
enzyme immunoassays and latex agglutination tests.
 Isolation of C. jejuni requires inoculation of fresh stool onto selective growth medium
and incubation at 42°C in a microaerophilic atmosphere.
 E. coli O157:H7 is among the most common pathogens isolated from visibly bloody
stools.
 Strains of this enterohemorrhagic serotype can be identified in specialized laboratories by
serotyping but also can be identified presumptively in hospital laboratories as
 Lactose-fermenting,
 Indole-positive colonies of sorbitol non-fermenters (white colonies) on sorbitol
MacConkey plates.
 Fresh stools should be examined for amoebic cysts and trophozoites.

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