FOOD POISONING
& DIARRHEA
• Describe the terms diarrhea,
dysentery and food poisoning
• Discuss in detail about
microorganisms causing diarrhea
and dysentery
• Identify the common microbial
causes of food poisoning.
• Discuss the laboratory diagnosis
Definition
• Food poisoning
• Any illness resulting from the consumption of food
• There are two types of food poisoning: food
infection and food intoxication.
1) Food infection refers to the presence of bacteria or other
microbes which infect the body after consumption.
2) Food intoxication refers to the ingestion of toxins contained
within the food, including bacterially produced exotoxins,
which can happen even when the microbe that produced
the toxin is no longer present or able to cause infection
• Diarrhea
• Increase in water content, volume, or
frequency of stools
• Dysentery
• Dysentery is an inflammation of the intestine
causing diarrhea with blood
Microorganisms causing diarrhea
BACRTERIA
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Salmonella(GNR)
Vibrio(GNR)
Clostridium perfringens(GPR)
Clostridium difficile(GPR)
Campylobacter(GNR)
Enterotoxigenic E.coli(GNR)
Enterohemorrhagic E.coli
Enteropathogenic E.coli
Yersinia enterocolitica (GNR)
Bacillus (GPR)
Parasites
1.
2.
3.
4.
5.
Giardia lamblia(cysts and trophozoite)
Cryptosporidium(oocysts)
Ankylostoma duodenale(eggs)
Enterobius vermicularis
Taenia saginata
viruses
1. Rotavirus
2. Adenovirus
3. Norwalk virus
fungi
candida
Dysentery
• Ameabic dysentery
• Entameaba histolytica
• Bacillary dysentery
• Shigella
• Enteroinvasive E coli
Mechanism of diarrhea and dysentery
• Noninflammatory/secretory
• Clinical manifestation
• Diarrhea - watery to loose, ±
nausea/vomiting/abd pain
• Mechanism:
• Preformed toxin, enterotoxin
• Inflammation & invasion
• Clinical manifestation
• Diarrhea/dysentery – mucoid or bloody,
fever, tenesmus, ± abd pain
• Mechanism:
• Cytotoxin, cellular invasion
Salmonella
• Member of Enterobacteriacae
• Morphology :Gram negative bacilli, motile with peritrichous
flagella
• Non lactose fermenter, form acid and gas from sugar
fermentation
• Produce H2S
• Classification: into two species
1.
Salmonella enterica (5 subspecies)
2.
Salmonella bongori
• Human infections are caused by subspecies I strains(Salmonella
enterica subspecies enterica)
• Salmonella enterica subspecies enterica serotype Typhimurium
can be shortened as S typhimurium
• S typhi, S paratyphi A & B, S cholerasuis are primarily infective to
humans
Salmonella: laboratory diagnosis
• Specimen: blood, bone marrow, urine and stool
• Culture on
1. differential media: Mac conkey ,DCA, -non
lactose fermenter
2. Selective media: salmonella shigella agar (SS
agar), XLD agar
3. Enrichment media for stool: selenite F broth,
tetrathionate broth-after 1-2 days this is plated
on differential and selective media
4. Final identification: biochemical and slide
agglutination tests with specific sera
• Serology :
1. Agglutination with sera
2. Widal test(tube dilution agglutination test)
Non typhoidal salmonellae infections
• Salmonellae
• NTS can be acquired from multiple
animal reservoirs. Transmission is
most commonly associated with
animal food products, especially
eggs, poultry, undercooked ground
meat, and dairy products and
fresh produce contaminated with
animal waste.
Mechanism of NTS food poisoning
• NTS gastroenteritis is characterized by massive
neutrophil (PMN) infiltration into both the
large- and small-bowel mucosa. The
degranulation and release of toxic substances
by neutrophils may result in damage to the
intestinal mucosa, causing the inflammatory
diarrhea
• occur 6–48 h after the ingestion of
contaminated food or water.
• Fever, Nausea, vomiting, and diarrhea and
abdominal cramping
• Dysentery may occur.
• Usually self-limited and resolves within 3–7
days
Vibrio cholera
• The disease called cholera
• Once in the human small bowel, the
organism produces a powerful exotoxin
called cholera toxin
• Cholera toxin consists of two parts (A
subunit) and a (B subunit). The B subunit
binds to GM1 receptor on intestinal cells
and delivers the A subunit inside the
cell. The A subunit increases the
intracellular levels of cyclic AMP. The,
cAMP inhibits the sodium transport
system in villus cells and activates chloride
secretion, and thus causing accumulation
of sodium chloride in the intestinal lumen.
Water moves passively from the cell into
the lumen by osmosis. Watery diarrhea
results
Clinical features of cholera
• 24- to 48-h incubation period
• Sudden onset of painless watery
diarrhea that may quickly become
voluminous
• vomiting
• Fever is usually absent
• The stool has a characteristic
appearance: , slightly cloudy fluid with
flecks of mucus, no blood, and a
somewhat sweet, inoffensive odor. It
has been called "rice-water" stool
because of its resemblance to the
water in which rice has been washed
Complications of cholera
• Dehydration follows quickly due
to fluid and electrolyte loss
hypovolemic shock and death
ensues. Signs of dehydration
•
•
•
•
Intense thirst
Loss of skin turgor
Sunken eyes
Week pulse
• Renal failure due to acute
tubular necrosis
Shigella
• Gram negative bacilli
• Shigella as the etiologic agent of dysentery—a clinical
syndrome of fever, and bloody stools
• Shigella species are classified by four serogroups:
• S. dysenteriae
• S. flexneri
• S. boydii
• S. sonnei
• Bacteria are transmitted most efficiently by the fecaloral route.
• Most cases of shigellosis are caused by person-toperson transmission, although some outbreaks
reflect contamination of water or food.
• Shigella can also be transmitted by flies
• A very few organisms are required for infection [103
organisms].
Pathogenesis of shigellosis
• Invasion and inflammation:
• Shigella invade colonic epithelial
cells; followed by intracellular
multiplication, spread of bacteria
to adjacent cells, recruitment of
inflammatory cells, and in the
process destruction of colonic
mucosa
• Shiga toxin produced by S.
dysenteriae type 1
• Inhibit cell protein biosynthesis
and cell death
Bacillary dysentery(shigella)
• The incubation period usually
lasts 1–4 days
• Typical manifestations are
• Initial watery diarrhea
• vomiting
• dysentery—a clinical syndrome of
fever, abdominal cramps and
frequent passage of small bloody
stools
• tenesmus
Hemolytic uremic syndrome
• The shiga toxin enters the systemic
circulation where it is attached to (strong)
Gb3 receptors on vascular endothelium .
Toxins move into the cell,and shut down
protein synthesis, resulting in cell
death. Injury activates blood platelets and
clot formation (thrombocytopenia)
• The red blood cells are
damaged(hemolysis) as the cells attempt
to pass through partially obstructed
microvessels.
• Kidney failure occurs because of high
distribution of microvasculature and Gb3
receptors.
Pathogenic Escherichia coli
ETEC - Enterotoxigenic
• Enterotoxin (similar to cholera toxin), elaborated locally
• Non-inflammatory: watery diarrhea known as travellers
diarrhea
EPEC- Enteropathogenic
• EPEC causes diarrheal disease primarily in young children,
including neonates
• responsible for outbreaks of infantile diarrheas
• The actual mechanism of diarrhea production is not known
EHEC - Enterohemorrhagic / STEC
• Cytotoxin (Shiga toxin), can cause hemolytic-uremic syndrome
• Inflammatory: bloody diarrhea without fever
EIEC - Enteroinvasive
• Invasion
• Dysentery: fever, abdominal pain, tenesmus, bloody or mucoid
stool
Campylobacter
• Campylobacters are motile, curved, gramnegative rods
• Campylobacters are found in the
gastrointestinal tract of many animals
used for food (including poultry, cattle,
sheep, and swine) and many household
pets (including birds, dogs, and cats).
• These microorganisms usually do not
cause illness in their animal hosts
• The invasion of the intestinal cells is the
main pathogenic mechanism
• Clinical manifestations are acute onset of
crampy abdominal pain, profuse diarrhea
that may be grossly bloody, headache,
malaise, and fever
Amoeabic dysentery
• Entameaba histolytica
• Protozoa
• Feco-oral transmission
• PATHOGENICITY
• Exist in two forms
• Cyst is the infective form that is ingeted
• Inside gut cyst changes to Trophozoite
that are the active form that attach to the
large gutInvadeflask shape ulcers
• Acute-Extreme abd tenderness,
dysentery, dehydration, Diarrhoea, abd
cramps, vomiting, tenesmus
• Liver abcess
• Lab diagnosis
• Trophozoites with pseudopodal
movement in stool
• Cysts in stool
• Treatment
• Metronidazole
Staphylococcus food poisoning
• S. aureus may harbor up to 15
enterotoxins, (staphylococcal
enterotoxin A [SEA], B, Cn, D, E, G, H, I,
J, K, L, M, N, O)
• S. aureus food poisoning follows
ingestion of preformed toxins that
have been released into food or
beverages. The toxins are heat stable
and thus are not denatured by
cooking. The disease typically starts 2
to 6 hours after ingestion with general
malaise, nausea, vomiting, abdominal
pain, and diarrhea but no fever.
• Implicated foods are usually dairy,
meat, bakery products
Bacillus food poisoning
• Bacillus cereus
• Gram positive spore producing rod
• Bacillus foodborne illnesses occur due to
survival of the bacterial endospores when food
is improperly cooked at less than or equal to
100°C allow some spores to survive. The food is
then not refrigerated, allowing the spores to
germinate. Germination and growth generally
occur between 10°C and 50°C
• Bacteria produces 2 types of toxins
• The emetic toxin, called cereulide, which is highly
heat resistant. This causes nausea and vomiting 16 hours after consumption
• Diarrheal toxin causes diarrhea and abdominal
pain 8-16 hrs after consumption
Lab diagnosis
• Culture
• Stool
• Vomitus
• Left over food
• Staphlocoocus enterotoxin
detection
Treatment(diarrhea)
• Rehydration
• Very important to replace fluid
and electrolytes
• Monitor blood pressure
• Antibiotics
• Not all pts require antibiotic
therapy
• Indications for therapy include
high fever, bloody diarrhea, severe
diarrhea, persistence for >1 week,
and worsening of symptoms
MYCOTIC POISONING
• Many fungi form poisonous
substances
• It is of 2 types:
1. Mycetism in which a fungus which
is eaten for itself causes toxic
effects
2. Mycotoxicosis :in which fungal
toxins contaminate some article of
food
• The best known mycotoxin is Aflatoxin
produced by Aspergillus flavus present
in foods like groundnuts, corn, peas,
mushrooms