Foodborne Infections and Intoxications

Foodborne Infections and Intoxications
Dr. Ravi Kant Agrawal (MVSc, PhD)
Senior Scientist (Veterinary Microbiology)
In-Charge, Food Microbiology Laboratory
Division of Livestock Products Technology
ICAR-Indian Veterinary Research Institute
Izatnagar 243 122 (Bareilly) UP

Food Safety
 Food safety has emerged as an important global issue due to international
trade and public health implications.
 Despite advances in hygiene, consumer knowledge, food treatment and
processing, foodborne diseases still represent a significant threat to public
health, worldwide.
 The term Food-borne diseases (also frequently referred to as food
poisoning), covers illnesses acquired through consumption of contaminated
food and includes foodborne intoxications and food-borne infections.
 Globally, the WHO has estimated that approximately 3-5 billion episodes
of diarrhea and more than 1.8 million deaths occur in children under
5 years of age, and a significant proportion of these results from
consumption of food mainly food of animal origin contaminated with
microbial pathogens or toxins.
 In response to the increasing number of food borne illnesses,
governments all over the world are intensifying their efforts to improve
food safety.

International Scenario: Developed Countries
 According to the CDC, an estimated 76 million cases of food-borne disease
are reported annually in the United States of America with approximately
5000 deaths.
 In USA, diseases caused by the major pathogens alone are estimated to cost
up to US $35 billion annually (1997) while in UK nearly £1.5 billion (2010), in
medical costs and lost productivity.
 Approximately $9.3 billion to $12.9 billion cost paid on human disease
treatment caused by six major pathogens including Salmonella,
Campylobacter jejuni, Escherichia coli O157:H7, Listeria monocytogenes,
Staphylococcus aureus, and Clostridium perfringens (USDA, 2011) and all
these are foodborne.

Indian Scenario: Developing Countries
 Developing countries bear the brunt of the problem due to the presence of a wide
range of food-borne pathogens, favorable conditions due to un-hygienic practices.
The burden of infectious diseases continues to be a major constraint in sustained
agricultural development and food security.
 In India, an estimated 5,00,000 children below five years age die each year due to
diarrhea (UNICEF estimate 1000/day).
 These figures jeopardize international and India’s own development efforts
including the achievement of the Millennium Development Goals (MDGs).
 Due to widespread poverty and malnutrition in developing countries, programs
directed towards the promotion of adequate access to food that satisfy calorie needs
and minimize hunger have precedence over programs designed to ensure
wholesomeness and quality of food. In short, the emphasis so far has been more on
food adequacy rather than on food quality.
 Therefore, the World Health Assembly adopted a resolution (WHA 53.15) in which,
the World Health Organization (WHO) was asked “to give greater emphasis on food
safety.

Indian Scenario….
 At present, the reporting and surveillance of food-borne diseases in
developing countries is grossly neglected.
 Therefore, the exact extent of the problem of food-borne diseases in
developing countries including India has not been fully understood.
 Most cases go unreported as scientific investigations are rarely feasible.
 Studies revealed that food-borne diseases are a serious health hazard and
important cause of morbidity and mortality in developing countries.
 Although, most of the studies showed the incidence of food-borne diseases,
they either lacked data on the organisms involved or the food implicated.
 The actual scenario of food-borne diseases can emerge only with proper
emphasis on foodborne disease surveillance including identification of
foodborne pathogens involved - ESTABLISHMENT OF A NATIONAL FOOD-
BORNE DISEASE SURVEILLANCE SYSTEM.

Foodborne Diseases
 Food borne diseases may be caused by bacteria and bacterial toxins, viruses,
fungi and fungal toxins, zoonotic parasites/protozoans, pesticide residues, drug
residues, heavy metals, food adulterants and food additives.
 Among these, microbiological contaminants are most important in the
context of developing countries.
 To date, 250 different foodborne diseases have been described and bacteria
are the causative agents of 2/3rd
of them.
 Among the predominant bacteria reported include, E. coli, Salmonella spp.,
Shigella spp., Bacillus cereus, Clostridium spp., Staphylococcus aureus, Vibrio
spp., Listeria monocytogenes, Campylobacter spp., Yersenia spp. Brucella spp.,
Mycobacterium spp. etc.
 Among viruses, rotavirus, norovirus (Norwalk lije viruses) and hepatitis (A&E)
virus etc are reported to be predominant.

Need for the foodborne pathogen surveillance
 Growing international trade, migration and travel has tremendously increased the
spread of dangerous pathogens and contaminants in food.
 Through the globalization of food marketing and distribution, both accidentally or
deliberately contaminated food products can affect the health of people in numerous
countries at the same time.
 In today’s interconnected and interdependent world, local foodborne disease
outbreaks may become a potential threat to the entire globe.
 In 1991, cholera which was thought to have originated from contaminated seafood
harvested off the coast of Peru, rapidly spread across Latin America resulting in
approximately 400,000 reported cases and more than 4000 deaths in several
countries.
 In early 2008, an outbreak of avian influenza in Bangalore, India, led to an import
ban of Indian poultry products in the Middle East, resulting in losses totaling hundreds
of thousands of US Dollars to the Indian economy.
 The identification of one single contaminated food ingredient can lead to the recall
of tonnes of food products leading to considerable economic losses in production and
from trade embargoes, as well as damage to the tourist industry.

Foodborne Diseases
 Caused by agents that enter the body through the ingestion of food. Occurs when a
pathogen or its toxin is consumed
 Commonly referred to as food poisoning
Foodborne diseases can be of three types
1) Foodborne infection- ingestion of viable pathogens along with food e.g.
typhoid
2) Foodborne intoxication (poisoning)- ingestion of foods containing
preformed toxins e.g. botulism, stapylococcal poisoning
3) Toxico-infection- organisms produce toxins insitu when ingested along with
food e.g. B. cereus poisoning
Foodborne
Pathogen
In
to
x
ic
a
tio
n
Toxins
Invasion and
Toxins
Toxico-Infection
Invasion
In
fe
c
tio
n

Food borne infections vs intoxication
Infections
• Bacterial / Viral / parasite /protozoa
• Invade and /or multiply in lining of
intestine
• Incubation period- hours to days
• S/s – Diarrhoea , nausea, vomitting ,
abdominal cramps, fever
• Communicable-spreads from person to
person
• Factors-inadequate cooking, cross
contamination , poor personal hygiene ,
bare hand contact
Intoxications
• toxins (natural / preformed bacterial /
chemical)
• No invasion or multiplication
• Incubation period- minutes to hours
• S/s – Vomitting, nausea, diarrhea ,
weakness, resp. failure , numbness,
sensory/motor dysfunction
• Not communicable
• Factors-inadequate cooking , improper
handling temperaturescan

Foodborne infections
• Food borne infections are caused by the entrance of pathogenic
microorganisms contaminating food into the body, and the reaction
of the body tissues to their presence.
• These can either be fungal, bacterial, viral, parasitic or protozoal
• Food borne infections tend to have long incubation periods and are
usually characterized by fever
Bacterial foodborne infections include Cholera, Vibrio parahemolyticus,
salmonellosis, typhoid fever, shigellosis, Yersiniosis Escherichia coli infection,
Campylobacteriosis, and Listeriosis
Mycotic foodborne infections include Candida spp., Sporothrix spp., Wangiella spp.
etc),
Viral foodborne infections include hepatitis A & E, Norwalk virus and poliomyelitis
virus
Parasitic foodborne infections include hydatidosis, Taeniasis, Anisakiasis,
Trichinosis
Protozoal foodborne infections include Cryptosporidiosis, toxoplasmosis,
Sarcocystosis and cyclosporiasis

Salmonellosis
 The salmonellae constitute a group of organisms with over 2500 different
serotypes
 These organisms are capable of causing disease in animals and man when
taken into the body in sufficient numbers
 Many salmonella species have a wide host range. These are the organisms
which commonly cause food poisoning. However, some are restricted to a
single host species e.g. Salmonella Abortusovis causing abortion in ewes, and
Salmonella Gallinarum the cause of fowl typhoid.
 Conversely, some salmonella serotypes are associated with human disease
and are not known to affect animals e.g. S. Typhi and Salmonella Paratyphi.
 Salmonellae are ubiquitous in the gut of human and animals and act as
sources of food contamination.

Contd……
• People who are carriers of the salmonellae contaminate the food.
• A heavy dose up to 10,000 -1,000,000 organisms per gram of food is required
to cause infection
• Salmonellae grow well on food and can exist for a considerable period in feces,
and on pastures.
Common food poisoning serotypes
• Some of the salmonella species involved in food poisoning include; Salmonella
Typhimurium, Salmonella Enteritidis, Salmonella Dublin, Salmonella
Senftenburg, Salmonella Virchow, Salmonella Montevideo, Salmonella
Infantis, and Salmonella Newport.
• These species are also involved in causing diarrhoea in animals

Heat resistance
 The salmonellae are killed by temperatures attained in
commercial pasteurization.
 They can remain alive in moist earth for one year and in dry
earth for 16 months.
 They are not destroyed in carcasses or offal maintained at
chilling or freezing temperatures, or in the usual pickling
solutions.
Salmonella food poisoning outbreaks
Outbreaks occur in different forms:
1. Sporadic cases involving only one or two persons in a
household
2. Family outbreaks in which several members of the family are
affected
3. Institutional outbreaks which may be caused by a contaminated
single food item.
4. Large outbreaks caused by a widely distributed infective food
item

Factors associated with Salmonella food
poisoning outbreaks
• Consumption of inadequately cooked or thawed meat or
poultry,
• Cross-contamination of food from infected food handlers.
• Presence of flies, cockroaches, rats, in the food environment
that act as vectors of the disease.

Transmission
• Salmonellae reach food in many different ways;
a) Directly from slaughter animals to food
b) From human excreta, and transferred to food through
hands, utensils, equipments, flies etc.
• Food poisoning is more likely to occur if the total number of
microorganisms present is high. A smaller number may have no
ill effect.

Foods involved
• Any food contaminated with salmonellae may be involved.
• However, foods commonly involved are animal derived foods
such as:
a. meat and meat products,
b. milk and milk products,
c. egg and egg products

Clinical symptoms
 The ordinary symptoms include abdominal pain, headache,
diarrhea, fever, vomiting, prostration and malaise.
 In severe cases there is septicaemia with leucopenia,
endocarditis, pericarditis.
 Severe cases are encountered in babies, young children, the
sick and in elderly persons.
 The mortality is up to 13 %.

Control measures
 Efficient refrigeration and hygienic handling of food.
 Consumption of properly cooked meat,
 Complete thawing of frozen meats and adequate cooking.
 Heat processing of meat, milk, fish and poultry to destroy
salmonella organisms in food

Typhoid and Paratyphoid fever
(Enteric fevers)
 Enteric fevers include typhoid and paratyphoid fevers caused
by Salmonella Typhi and Salmonella Paratyphi A, B and C,
respectively.
 The serotypes are similar to other salmonella bacteria, but
unlike them, they are essentially parasites of man.
 S. Typhi possesses capsular (vi) antigen in addition to the usual
O and H antigens found in other serotypes.

Disease symptoms
 The incubation period is usually 2 weeks, but might vary
between 3 and 28 days for typhoid fever and between 1 and 15
days for the paratyphoid fevers.
 The enteric fevers are generalized septicaemic infections with a
frequent, if not constant bacteraemia during the first two
weeks of the disease.
 The abdominal symptoms are severe, while fever and illness
may continue for 4-6 weeks.

Transmission
 The typhoid and paratyphoid bacilli are essentially human
parasites and are acquired mostly from human sources, namely,
patients and carriers.
 The bacteria can be transmitted by the contamination of water,
milk or food by flies.
 Only a few organisms are needed to cause disease.

Control measures
• Hygienic control of food and water supplies
• Detection and treatment of chronic carriers
• Vaccination using TAB-vaccine. The vaccine contains a mixed
culture of S. Typhi, and S. Paratyphi. The vaccine protects for 5-7
yrs.

Diagnosis
•Done by culture, biochemical testing and serotyping.
•Culture: Pre-enrichment->Selective enrichment->
Selective Plating->Biochemical Testing-> Serotyping
•Pre-enrichment broth: Buffered peptone water
•Selective enrichment broth: Rappaport Vassiliadis
medium, Tetrathionate broth, Selenite broth
•Selective Media: Hektoen enteric agar, Brilliant Green
agar, Bismuth sulphite agar, SS agar, XLD agar (Xylose
Lysine Deoxycholate agar)
•IMViC: - + - + TSI: K/A + H2S Catalase +ve
Oxidase -
•Serotypig: O and H antigen
•Vi antigen also present in Typhi.
•Kauffmann & White scheme followed.
•Gallinarum-Pullorum- Only non-flagellate Salmonella
9,12: -: -
•Flagellar antigen occur in 2 phases: Phase 1 and 2
•S. Typhimurium: 1,4,5 12 : i : 1, 2
•Widal Test: S. Typhi, Paratyphi A and Paratyphi B
Salmonella on XLD
Salmonella species: red
colonies, some with black
centers. The agar itself
will turn red due to the
presence of Salmonella
type colonies.
Shigella species: red
colonies.
Coliforms: yellow to
orange colonies.

Campylobacteriosis
Campylo=curved/twisted
 Campylobacter are a group of tiny strictly micro-aerophilic, curved or spiral
(cork screw shaped), non-spore forming, Gram negative rods
 Organism is Oxidase POSITIVE.
 Motile by either unipolar or bipolar flagella.
 About 12 species of Campylobacter are known (C. jejuni, coli, lari,
hyointenstenalis, upsaliensis).
 Campylobacter jejuni and Campylobacter coli cause food poisoning and are
associated with acute enterocolitis in man.
 Campylobacter jejuni occur in large numbers in cattle feces, and poultry as
normal flora, where it remains as harmless commensal.
 C. jejuni is an EMERGING FOODBORNE PATHOGEN.
 Mishandling of raw poultry and consumption of undercooked poultry are the
major risk factors for human campylobacteriosis.
 Campylobacter coli are commonly associated with human diarrhoea, and
enteritis in pigs mostly in association with Treponema hyodysenteriae.
 C. fetus causes spontaneous abortions in cattle and sheep. May cause
infection in human.

Mode of infection
• The common routes of transmission are fecal-oral, ingestion of contaminated
food or water, and the eating of raw/contaminated meat.
• Foods involved includes meat from infected animals, un-pasteurized milk and
possibly cross-contamination from these sources to foods eaten uncooked or
un-refrigerated.
• Among the meats, poultry constitutes the greatest potential source of
infection to humans.
• Microorganisms are present in poultry gut and feces up to 1,000,000
organisms/g of feces.
• Carelessness in the kitchen e.g. cutting chickens with the same knife used to
cut other foods without proper cleaning prior to use.
• Pork is a major source of Campylobacter coli.
• Contamination of pork occurs during slaughter.

Disease in man-Clinical signs
• Campylobacter jejuni and C. coli cause illness characterized by diarrhoea,
abdominal pain, nausea, vomiting, abdominal cramps, and fever.
• Incubation period ranges between 2-11 days with an average of 3-5 days.
• The jejunum, ileum and colon are primarily affected (sites of tissue injury)
resulting in acute inflammation and occasionally, abscess formation.
• The organism produces diffuse, bloody, edematous, and exudative enteritis
leading to an inflammatory, sometimes bloody diarrhea (foul smelling and
watery diarrhea, which runs for 3-4 days) or dysentery syndrome.
• The diarrhea may sometimes contain blood and mucus in feces.
• Symptoms typically last for five to seven days.
• The infection is usually self-limiting (may last for up to 10 days).
• In most cases, symptomatic treatment by liquid and electrolyte replacement is
enough in human infections.
• THE USE OF ANTIBIOTICS, ON THE OTHER HAND, IS CONTROVERSIAL.
• Most strains of C. jejuni produce a toxin (cytolethal distending toxin) that
hinders the cells from dividing and activating the immune system. This helps
the bacteria to evade the immune system and survive for a limited time in the
cells.
• The condition is self-limiting but Campylobacter infection is considered to be
the underlying cause of Guillain–Barré syndrome.

Diagnosis
• Done by culture, biochemical testing and serotyping.
• Culture: Pre-enrichment->Selective enrichment-> Selective
Plating->Biochemical Testing-> Serotyping
• Pre-enrichment broth: Bolton Broth
• Selective enrichment broth: Antibiotics Added
• Selective Media: Blood containing: Butzlar selective medium,
Blaser-Wang medium, Skirrow blood agar, Preston
campylobacter selective medium
• Charcoal containing: Karmali agar or CSM (Charcoal selective
medium), CCDA (Charcoal cefoperazone deoxycholate agar)
• Serotypig: O and H antigen

Preventive measures
• Recognition, control and prevention of Campylobacter
infections in animals, and
• Thorough cooking of all foodstuffs derived from animal
sources.
• Prevention of re-contamination after cooking.
• Proper refrigeration of foods.
• Maintenance of high standard of hygiene.

Escherichia coli
 Escherichia coli is a Gram-negative, facultatively anaerobic, non-spore
forming rod-shaped bacterium (2.0x 0.25–1.0 μm ) of the genus
Escherichia that is commonly found in the lower intestine of
warm-blooded organisms.
 Organisms are catalase positive and oxidase negative.
 Mostly strains possess flagella and are motile (peritrichous
arrangement).
 Escherichia coli are potential food poisoning pathogens which are
widely distributed in low numbers in food environments.
 Each group is composed of unique O:H serotypes
 Each group posses virulence factors characteristic of that group.
 The serotypes are characterized by using O-somatic and H-flagellar
antigens.
 E. coli strains involved in food borne infection fall into the following
groups:
1. Enteropathogenic E. coli (EPEC),
2. Enterotoxigenic E. Coli (ETEC),
3. Enteroinvasive E. coli (EIEC) and
4. Enterohemorrhagic E. coli (EHEC) or VTEC.
5. Enterroaggregatice E. Coli (EAggEC)
• Diffusely adherent E. coli (DAEC) /Extraintestinal E. coli (ExPEC)

Enteroinvasive E. coli
• EIEC strains cause illness that is characterized by watery diarrhea
in most patients.
• In addition, there is fever, nausea, and abdominal cramps.
• Bloody diarrhea may occur in fewer than 10 % of patients.
• THE PRESENCE OF MUCUS AND POLYMORPHONUCLEAR
LEUCOCYTES IN STOOL IS TYPICAL OF THESE STRAINS.
• Illness is usually self-limiting, lasting for 2 to 3 days.
• A relatively high dose (108
cells) is necessary to produce disease in
volunteers.
• The median incubation period is 18 hours (range 2-48 hrs).
• Foodborne spread is the usual mode of transmission.
• Person-to-person spread has also been reported.

Enteroinvasive E. coli (EIEC)
Biochemically, genetically, and pathogenically closely related to
Shigella spp. - Shigella-like E. coli strains
Does not produce Shiga-toxin
Invasive (penetrate and multiply within epithelial cells)
Named EIEC as they have the capacity to invade interstitial
epithelial cells in vivo and penetrate HeLa cells in tissue culture.
EIEC cells invade intestinal epithelial cells, lyse the phagosomal
vacuole, spread through the cytoplasm and infect adjacent cell
-Shigella does the same thing
Clinically EIEC infection resembles shigellosis, ranging from mild
diarrhea to frank dysentery, severe inflammation, fever
Non-fimbrial adhesins, possibly outer membrane protein
Plasmid encoding a gene for a K surface antigen
Many are nonmotile, do not ferment lactose or ferment it late
with only acid production, and do not form lysine decarboxylase.
Many of these show O antigen cross reactivity with Shigella.
Earlier names given – Shigella alkalescens, Shigella dispar – and
were grouped under Alkalescens-Dispar group.

Cellular pathogenesis of invasive E coli

Sereny test:
Instillation of a suspension of freshly isolated EIEC or
Shigella into the eyes of guinea pigs leads to
mucopurulent conjunctivitis and severe keratitis.
Mice can also be used.
Virulent Sereny test-positive isolates carry a large (usually
140-megadalton) plasmid responsible for this property.
Cell Penetration in HeLa or HEP-2 cells.
Plasmid detection:
VMA ELISA: The plasmid codes for outer membrane
antigens called the virulence marker antigens (VMA)
which can be detected by the ELISA (VMA ELISA) test.

Enterotoxigenic E. coli (ETEC)
Adhere to intestinal mucosa by fimbriae
Produce enterotoxins
Plasmids contain genes for enterotoxins
Cause leakage of intestinal epithelial cells - Loss of
electrolytes and water
Cause diarrhea in children & adults
Traveler’s diarrhea
Weanling diarrhea
Persons from developed countries visiting endemic areas
often suffer from ETEC diarrhea – TRAVELER’S DIARRHEA.
Endemic in developing countries in tropics, all age groups.
Mild watery diarrhea to fatal disease indistinguishable
from cholera.

Enterotoxigenic E. coli (ETEC)
Pathogenesis of ETEC involves two
steps:
1. Intestinal colonization: fimbrial (K88,
K99) or colonization factor antigens
(CFA I, II, III, IV, etc) - non invasive
2. Diarrheagenic enterotoxin(s) -- LT
and/or ST toxin
Produce LT or ST or both. Cause
diarrhea in infants and travelers.
 Both traits are plasmid-encoded
Fimbriae:
K88 (F4): Pigs
K99 (F5): Calves and lambs
987P (F6):
F41: Calves

Resembles cholera toxin in its
structure, antigenic properties
and mode of action.
AB type toxin
It is a complex of polypeptide
subunits.
Each unit of toxin has 1 subunit
A and 5 subunits B.
CT is about 100 times more
potent than LT.
LT is a powerful antigen and
can be detected by serological
and biological tests.
LT = HEAT LABILE TOXIN
.

LT = HEAT LABILE TOXIN
MOA:
• The B (binding) subunit binds the toxin
to the target cells via a specific receptor
that has been identified as GM1
GANGLIOSIDE.
• The A (Active) subunit is then activated
by cleavage of a peptide bond and
internalized
• The activated subunit A then catalyzes
the ADP-ribosylation (transfer of ADP-
ribose from nicotinamide adenine
dinucleotide [NAD]) of a regulatory
subunit of membrane-bound adenylate
cyclase, the enzyme that converts ATP
to cAMP.
• This activates the adenylate cyclase,
which produces excess intracellular
cAMP, which leads to hypersecretion of
water and electrolytes into the bowel
lumen.
• Diagnosis done by demonstration of the
toxin. .

LT
1 SUBUNIT A
5 SUBUNITS B
bind to GM1 ganglioside
Receptors on intestinal
epithelial cells
activation of A subunit into A1 and A2
A1 activates adenyl cyclase in the enterocyte to form
cAMP, leading to increased outflow of water and electrolytes
into the gut lumen, with consequent diarrhoea.
.
MOA of LT (Labile Toxin)

Heat-stable toxin (ST)
LMW polypeptide, poorly antigenic.
Two types known – STA/ST1 and STB/ST2.
ST genes are carried on plasmids which may also carry other
genes, such as for LT and drug resistance.
MOA:
STa stimulate intestinal guanylate cyclase, the enzyme that
converts guanosine 5'-triphosphate (GTP) to cyclic guanosine 5'-
monophosphate (cGMP).
Increased intracellular cGMP inhibits intestinal fluid uptake.
Those termed STb do not seem to cause diarrhea by the same
mechanism.
STA STB
STA acts by activation of cGMP in the
intestine.
M/A not known.
Infant mouse test – STA acts very rapidly
and induces fluid accumulation in the
intestines of infant mice within four
hours of intragastric administration.
STB causes fluid accumulation in
young piglets but not in infant
mice.
Methanol soluble Not methanol soluble.

Enteropathogenic E. coli (EPEC)
Non-fimbrial adhesin (intimin)
Moderately invasive (not as
invasive as Shigella or EIEC)
“Attaching & effacing”
Effacement of microvilli
Adherence between
bacterium and epithelial cells
Unique histopathology
Locus of enterocyte
effacement
Does not produce LT or ST;
some reports of shiga-like
toxin
Usually infantile diarrhea;
watery diarrhea similar to
ETEC, some inflammation, no
fever; symptoms probably
result mainly from invasion
rather than toxigenesis
Clinical Microbiology Reviews 1998 11:142-201

Associated with diarrhea in infants and children.
Institutional outbreaks, sporadic diarrhea.
Do not produce enterotoxins.
Not much/ moderately invasive.
M/A: Attach to mucosa of upper small intestine, cause
disruption of brush border microvilli.
Enteroadherent E. coli is another name given to them because
they can adhere to HEp-2 cells.

Enteroaggregative E. coli (EAggEC)
• Appear aggregated in a stacked brick
formation on Hep-2 cells or glass.
• They have been associated with
persistent diarrhea in young children
without inflammation, no fever,
especially in developing countries.
• They form a LMW heat stable
enterotoxin called EAST1 (entero
aggregative heat stable enterotoxin-1)
and a hemolysin .
Adhere to HEp-2 and Human laryngeal
carcinoma cells
Adhesins not characterized
Non-invasive
Do not secrete enterotoxins
Bacterial cells autoagglutinate

Enterohemorrhagic E. coli
 EHEC infection is caused by Escherichia coli serotype O157:H7 (O26, O45,
O91, O103, O111, O121, O145, and O157)
 It causes hemorrhagic colitis in humans that is characterized by diarrhea,
abdominal pain which may be severe and vomiting.
 Patients with complications have bloody diarrhea, acute ulcerative or
ischemic colitis and sub-mucosal edema with severe colonic inflammation.
 Few patients develop fever.
 Illness lasts for 4 to 8 days, although it may extend to 13 days for severe
cases.
• Deaths occur in patients who develop hemolytic uremic syndrome (HUS).
• HUS can be recognized by acute renal failure, micro-angiopathic hemolytic
anemia and thrombocytopenia.

EHEC = ENTEROHAEMORRHAGIC E.COLI
• Produce VT
• Mild diarrhea to fatal hemorrhagic colitis and hemorrhagic
uremic syndrome (HUS) particularly in young children and
elderly.
• Primary target of VT = vascular endothelial cells.
• O157:H7, (O26:H1 , O45, O91, O103, O111, O121 and O145 etc)
• The disease may occur sporadically or as outbreaks of food
poisoning.
• Changing lifestyle and eating habits.
• Salad vegetables such as radish and alfalfa sprouts, in which
bacteria were found beneath the skin and in the deeper
tissues.
• Diagnosis: demonstration of VT.
. 44

Enterohemorrhagic E. coli (EHEC)
Severe gastrointestinal distress
Hemorrhagic colitis
Crampy abdominal pain
Watery diarrhea
Bloody diarrhea
Little or no fever
New serotype O157:H7 in 1983 - Undercooked hamburgers
157th
somatic O antigen/ 7th
flagellar H antigen
Hemorrhagic colitis: Abdominal cramps, blood stools, with minor
or no fever
Post diarrheal hemolytic ureamic syndrome
Acute renal injury
Thrombocytopenia: An abnormal decrease in the number of
platelets in circulatory blood.
Microangiopathic hemolytic anemia: The fragmentation of red
blood cells because of narrowing or obstruction of small blood
vessels.
Enterohemorrhagic E. coli (EHEC): Among the most dangerous
enteric pathogens

Enterohemorrhagic E. coli (EHEC)
Represented by a single strain
(serotype O157:H7)
Adhesins not characterized,
probably fimbriae
Moderately invasive
Produces shiga toxin but not
LT or ST
Copious bloody discharge
(hemorrhagic colitis), intense
inflammatory response, may
be complicated by hemolytic
uremia
Pediatric diarrhea caused by
this strain can be fatal due to
acute kidney failure
(hemolytic uremic syndrome
[HUS]).
The Lancet 1998 352:1207-1212

VT = VEROTOXIN = VEROCYTOTOXIN
A B type exotoxin - Has A and B subunits.
VT genes appear to be phage encoded.
VT1, VT2 identified.
Named so because it was first detected by its cytotoxic effect
on Vero cells, a cell line derived from African green monkey
kidney cells.
It is also known as SLT = shiga like toxin because it is similar to
the Shigella dysenteriae type 1 toxin in its physical, antigenic
and biological properties.
MOA: Very similar to toxin produced by Shigella dysenteriae
 Inhibits protein synthesis in host cell
 A subunit inactivates the 60S ribosomal subunit
• Most O157 strains produce Shiga toxin 2
– 25% produce Shiga toxin 1
.

Combinations of the O & H antigens identify the serotype

Diagnosis
• Pre-enrichment broth: Buffered peptone water
• Selective enrichment broth: MacConkey broth (Neutral Red
Indicator)
• Selective Media: MacConkey agar, EMB agar
• IMVic: ++-- TSI: A/A Oxidase: -
• EMB: Metallic Sheen
• Sorbitol MacConkey agar (In sorbitol MacConkey agar, lactose
is replaced by sorbitol) - E coli O157:H7 produces colourless
colonies while other bacteria will produce red/pink.
• Serotyping: O and H antigen

IMViC + + - - (Indole, methyl red, VP, Citrate
• Isolation and Identification of Causative Agent
DIAGNOSIS

Laboratory methods for isolation and identification of ETEC
ETEC

Identification: O157:H7
• MacConkey agar (SMAC)
– Does not ferment sorbitol rapidly
– Forms colorless colonies on sorbitol containing
MacConkey agar
• Serology
– Colorless colonies on SMAC are screened for the
0157 antigen

Confirmation: By serotyping (O and H antisera)
In septicemia: Blood culture
Enterotoxins: by ELISA or other immunological methods
Verotoxins/ necrotoxins: by Vero cell assay

Control measures
• Good personal hygiene.
– WASH YOUR HANDS thoroughly after using the bathroom, before
preparing or eating food, after contact with animals or their
environments.
– COOK MEAT THOROUGHLY. Ground beef and meat should be cooked to a
temperature of at least 160°F/70˚C.
– WASH FRUITS AND VEGETABLES thoroughly before cooking or eating raw
– PREVENT CROSS CONTAMINATION in food preparation areas by
thoroughly washing hands, counters, cutting boards, and utensils after
they touch raw meat.
– AVOID RAW MILK, UNPASTEURIZED DAIRY PRODUCTS, AND
UNPASTEURIZED JUICES (like fresh apple cider).
– AVOID swallowing water when swimming or playing in lakes, ponds,
streams, swimming pools, and backyard “kiddie” pools.

Shigellosis (Bacillary dysentery)
• Shigellosis is caused by members of the genus Shigella.
• Gram -, Rod shaped, Non-encapsulated, NON-MOTILE, Non-spore
forming, Facultative anaerobic, Facultative intracellular, Obligate
pathogen
• All ferment glucose, some ferments mannitol
• The species involved include Shigella dysenteriae, Shigella
flexneri, Shigella boydii and Shigella sonnei.
Serogroup A: S. dysenteriae (15 serotypes)
Serogroup B: S. flexneri (six serotypes)
Serogroup C: S. boydii (19 serotypes)
Serogroup D: S. sonnei (one serotype)
• All strains of Shigella posses potent exotoxins (Shiga Toxin which
is similar to verotoxins) which are carbohydrate-lipid protein
complexes.
• The infective dose is smaller than that of salmonellae, except S.
Typhi.

Clinical symptoms
• The illness begins 1 to 4 days after ingestion of bacteria and may
last 4 to 7 days.
• Symptoms include watery or bloody diarrhea, fever, stomach
cramps, nausea or vomiting, dehydration and prostration in
severe cases and convulsions in young children.
• The diarrhea which starts as a thin watery discharge quickly
looses its fecal character to be composed of nothing but pus,
mucus threads and blood.
• At this stage, there are agonizing pains and constant tenesmus. It
is also commonly known to cause large and painful bowel
movements.
• Death from bacillary dysentery is uncommon when efficient
treatment is provided.
• However, S. dysenteriae infections have been reported to have a
case fatality rate of 20 % and the mortality rate is higher in
children than adults.

Transmission
• Human cases and carriers are the only important sources of
infection.
• Spread is by fecal-oral route, and person-to-person transmission
is common.
• The bacteria leaves the body in stool of an infected person and
infects another person through contaminated hands, food,
water, or objects (toys, pens etc).
• Any type of food can transmit the Shigella pathogens to cause
disease in man.
• Flies can spread Shigella when they get into contact with infected
stool and then contaminate drinking water or food.
• Shigella organisms may remain viable in tap water for as long as
6 months, and in sea water for 2 to 5 months.

Diagnosis
• Selective enrichment broth: MacConkey broth (Neutral Red
Indicator)
• Selective Media: MacConkey agar, Salmonella-Shigella agar
• IMVic: -+-- OR v+-- TSI: K/A H2S – Gas - Oxidase: -

Preventive measures
• Practice good hygiene and sanitation.
• Wash hands well with water and soap each time you use the
ablution.
• The home and surroundings should be kept clean to prevent
contamination of food and water supply.
• Proper disposal of human waste or sewage.
• Keep kitchen work surfaces clean.
• Use boiled or chlorinated water
• Eat properly cooked food and drink properly pasteurized milk
and other liquid foods such as juices.
• Reconstitute juice with potable water

Vibrio sps.
• Cholera is caused by Vibrio cholerae bacterium.
• Vibrio is a genus of Gram-negative bacteria possessing a curved
rod shape (comma shape)
• Usually associated with eating under-cooked seafood.
• Typically found in salt water.
• Vibrio spp. are facultative anaerobes that test positive for
oxidase and do not form spores.
• All members of the genus are motile and have polar flagella with
sheaths

Vibrio cholerae
• Cholera vibrios are ingested in drink or food.
• In natural infection, the dosage is usually very small.
• The organism multiply in the small intestine to PRODUCE A
POTENT ENTEROTOXIN, which stimulates a persistent out
pouring of isotonic fluid by the gut mucosal cells.
• Man is the only natural host of the cholera vibrios
• Spread of infection is from person-to-person, through
contaminated water or foods.
• Shrimps and vegetables are the most frequent carriers.
• Cholera is an infection of crowded poor communities and it tends
to persist in such areas.
• Cholera outbreaks occur either as explosive epidemics usually in
non-endemic areas or as protracted epidemic waves in endemic
areas

Clinical symptoms
• Cholera is typically characterized by the sudden onset of effortless vomiting
and profuse watery diarrhea (Rice water appearance of stool).
• Vomiting is seen frequently, but very rapid dehydration and hypovolemic
shock.
• The frequent watery stools may be accompanied with small parts of the
mucosa being liberated from the intestines.
• Death may occur in 12 to 24 hrs due to rapid dehydration.
• Patients may produce up to 20-30 stools per day, losing many litres of water
and electrolytes,
• Patients therefore exhibits extreme dehydration, urine is suppressed, the skin
becomes wrinkled, the eyeballs are sunken and the voice becomes weak and
husky.
• Blood pressure falls, the heart sounds become barely audible and the pulse
become rapid and weak just before death.
• In the acute stage, vibrios are abundantly present in watery stool (upto 107
to
109
organisms per ml).

Diagnosis
• Bacteriological examination can be done in stool, suspect water and food.
• Selective Media: TCBS (Thiosulfate-citrate-bile salts-sucrose) agar
(Bromothymol blue/thymol blue indicator)
V. cholerae: Large yellow colonies (due to sucrose fermentation).
V. parahaemolyticus: Colonies with blue to green centers (sucrose non-
fermenter).
V. alginolyticus: Large yellow mucoidal colonies.
V. harveyi/V. fischeri: Greyish-green to bluish-green colonies which show
luminescence in dark.
• A VIBRIO IMMOBILIZATION TEST with dark field microscopy: a serological test
done by mixing stool specimen with specific antisera → under dark field
agglutination will appear, causing non-motile micro-organism.
• Precise identification of biotype and serotype done using serological (e.g. CFT)
and phage sensitivity tests.

Control measures
1. Provision of potable water
2. Proper sewage disposal
3. Proper cooking and hygienic handling of food
4. Observation of personal hygiene
5. Vaccination -The heat killed, phenol preserved vaccine has
protection that lasts for 3 to 6 months.

Vibrio parahemolyticus
• Vibrio parahemolyticus is a pathogenic bacterium, whose natural
habitat is the sea.
• Human infections occur solely from sea foods such as oysters,
shrimps, crabs, lobsters, clams and related shellfish.
• Cross-contamination may lead to other foods becoming vehicles.

Symptoms of the disease
• V. parahemolyticus causes gastroenteritis and extra-intestinal
infections in man.
• The mean incubation period is 16.7 hrs (range 3-76 hrs)
• Symptoms include: diarrhea (95 %), cramps (92 %), weakness (90
%), nausea (72 %), chills (55 %), headache (48 %) and vomiting (12
%).
• Symptoms last from 1 to 8 days with a mean of 4.6 days.

Vibrio vulnificus
• Vibrio vulnificus can cause a severe foodborne infection
• Vibrio vulnificus Primary Septicemia- Most common
• Vibrio vulnificus Gastroenteritis – Less common
• Diarrhea
• Abdominal cramps
• The case fatality rate for V. vulnificus septicaemia exceeds 50 %.
• At risk populations (liver disease) – 70 to 80% mortality
• Fever/Chills
• Nausea
• Skin Lesions
• Diarrhea and vomiting
• In immuno-compromised hosts, V. vulnificus infections can cause fever,
nausea, myalgia and abdominal cramps, 24-48 hours after eating
contaminated food.
• The organism can cross the intestinal mucosa rapidly leading to sepsis within
36 hours of the initial onset of symptoms.
• Cases are most commonly reported in warm-weather months and are often
associated with eating raw oysters.

Listeria monocytogenes
• Listeria monocytogenes is a Gram positive bacterium that is pathogenic to
both animals and human beings.
• The organism is a facultative anaerobe and is catalase-positive, oxidase-
negative and motile .
• TUMBLING MOTILITY at <300
C. No motility at 370
C.
• The genus Listeria includes six different species (L. monocytogenes, L.
ivanovii, L. innocua, L. welshimeri, L. seeligeri, and L. grayi).
• Both L. ivanovii and L. monocytogenes are pathogenic in mice, but only L.
monocytogenes is consistently associated with human illness .
• There are 13 serotypes of L. monocytogenes that can cause disease, but more
than 90 percent of human isolates belong to only three serotypes: 1/2a, 1/2b,
and 4b.
• L. monocytogenes serotype 4b strains are responsible for 33 to 50 percent of
sporadic human cases worldwide
• The organism is widespread in nature and is a transient constituent of the
intestinal flora, excreted by 1-10% of healthy humans.
• It is extremely hardy and can survive for many years in the cold in naturally
infected sources.

Vehicle foods
• Listeria monocytogenes infection occurs after consumption of
raw vegetables, salads, raw milk, soft cheese, ice cream, cheese,
sauerkraut, salads, meat and meat products, poultry, sea foods
contaminated by Listeria.
• Delicatessens and other ready-to-eat (RTE) foods are important
in causing Listeria food poisoning. (delicatessen - a shop selling
cooked meats, cheeses, and unusual or foreign prepared foods.)

Clinical symptoms
There are two main types of listeriosis: a non-invasive form and
an invasive form.
Noninvasive listeriosis (febrile listerial gastroenteritis) is a mild
form of the disease affecting mainly otherwise healthy people.
Symptoms include diarrhoea, fever, headache and myalgia (muscle
pain). The incubation period is short (a few days). Outbreaks of this
disease have generally involved the ingestion of foods containing
high doses of L. monocytogenes.
Invasive listeriosis is a more severe form of the disease and affects
certain high risk groups of the population. These include pregnant
women, patients undergoing treatment for cancer, AIDS and organ
transplants, elderly people and infants. This form of disease is
characterized by severe symptoms and a high mortality rate (20%–
30%). The symptoms include fever, myalgia (muscle pain),
septicemia, meningitis.
The incubation period is usually one to two weeks but can vary
between a few days and up to 90 days.

Clinical symptoms
• Pregnant women, infants and elderly people are particularly at
risk of infection with Listeria monocytogenes.
• Listeria monocytogenes causes abortion in pregnant women
and meningitis in newborn infants and immuno-compromised
adults.
• The infection is fatal in susceptible individuals with a mortality of
25-30%.
• Deaths have been reported in fetuses, neonates and other
individuals with compromised health status.

• Growth on Mullar Hinton agar with sheep blood as enrichment
• Aerobic and facultative anaerobe
• Grow on nutrient agar: a very light growth and give bluish coloration ,
reflects blue light
• Specimens are enriched if the tissues are kept at 40
C and plated on the
media
• Hemolytic activity on blood agar has been used as a marker to
distinguish L. monocytogenes from other Listeria species, but it is not
an absolutely definitive criterion.
Cultural and growth characteristics
Listeria colonies are typically black
with a black halo (esculin positive)

FDA, USDA, ISO methods
Enrichment: Cold enrichment,
UVM I & II (University of Vermont Modification
Medium (UVM) )
Fraser’s broth
Tryptose phosphate broth with polymixin
Selective media : McBride
PALCAM
Oxford agar,
DRIA,
LiCl-ceftazidime agar, modified
Trypaflavine Nalidixic acid-serum agar
L. monocytogenes hydrolyzes esculin to esculetin and dextrose.
Esculetin reacts with ferric ions and produces black zones
around the colonies.
Polymyxin- Acriflavin- Lithium chloride-Ceftazidime - Aesculin-
Mannitol (PALCAM) Agar was formulated by Van Netten et al (1)
and is recommended for the isolation of L. monocytogenes
from foods.
Media used for isolation

• Bacteria are faculative anaerobic micobes
• Catalase + / oxidase -
• Motile
• Flagella are produced at room temperature, but not at 37 °C.
• Listeria produce acid and not gas in various sugar fermentation
tests.
• CAMP-positive Listeria monocyogenes inoculated at right angles
to β-hemolytic Staphylococcus aureus - Note the arrow shaped
zone of weak enhancement hemolysis indicating a positive CAMP
test.
Biochemical Reactions
Catalase positive“umbrella motility” at 25°C

Diagnosis
• Culture: Pre-enrichment->Selective enrichment-> Selective Plating-
>Biochemical Testing-> Serotyping
• Selective enrichment broth: Buffered listeria enrichment broth/ Fraser
broth/ UVM-1/UVM-II
• Selective Media: Oxford Medium, PALCAM agar, BCM, ALOA, MOX agar
• Isolation can be enhanced if the tissue is kept at 4 °C for some days before
inoculation into bacteriologic media (COLD ENRICHMENT).
• Oxidase: Negative Catalase: Positive Motility: < 300
C
• Anton Test: A test used in the identification of Listeria monocytogenes;
instillation of a culture into the conjunctival sac of a rabbit or guinea pig
causes severe keratoconjunctivitis within 24 hours.
• The Christie-Atkins-Munch-Peterson (CAMP) test: To perform the test,
streak a β-hemolytic Staphylococcus aureus culture on a sheep blood agar
plate. Streak several test cultures parallel to one another, but at right
angles to the S. aureus streaks. After incubation at 35° C for 24-48 h,
examine the plates for hemolysis. L. monocytogenes and L. seeligeri
hemolytic reactions are enhanced in the zone influenced by the S. aureus
streak.

Yersinia enterocolitica
• This organism has been isolated from beef, lamb, pork, sea foods, vegetables
milk and milk products, vacuum-packed meat.
• Of all the sources, swine appears to be major source of strains pathogenic to
man.
• At present, the genus Yersinia includes 11 established species: Y. pestis, Y.
pseudotuberculosis, Y. enterocolitica, Y. frederiksenii, Y. intermedia, Y.
kristensenii, Y. bercovieri, Y. mollaretii, Y. rohdei, Y. aldovae and Y. ruckeri.
• Among them only Y. pestis, Y. pseudotuberculosis and certain strains of Y.
enterocolitica are of pathogenic importance for humans.
• Virulence appears to be as a result of tissue invasiveness of this organism
• Source-faecal contamination, unhygienic practices
• Disease in man- Acute syndrome with appendicitis

Symptoms
• Acute Y. enterocolitica infections usually lead to mild self-limiting entero-
colitis or terminal ileitis in humans.
• Symptoms-fever, abdominal pain, diarrhea, vomiting
• Symptoms may include watery or bloody diarrhea and fever.
• After oral uptake yersiniae replicate in the terminal ileum and invade
Peyer's patches.
• From here yersiniae can disseminate further to mesenteric lymph nodes
causing lymphadenopathy. This condition can be confused with appendicitis
and is therefore called PSEUDOAPPENDICITIS.
• In immunosuppressed individuals, yersiniae can disseminate from the gut to
liver and spleen and form abscesses.
• Because Yersinia is a siderophilic (iron-loving) bacteria, people with
hereditary hemochromatosis (a disease resulting in high body iron levels) are
more susceptible to infection with Yersinia (and other siderophilic bacteria).
• Y. enterocolitica infections are sometimes followed by chronic inflammatory
diseases such as arthritis.
• Y. enterocolitica seems to be associated with autoimmune Graves-Basedow
thyroiditis.

Yersinia gastroenteritis symptoms
• Symptoms develop several days following ingestion of
contaminated foods include abdominal pain, diarrhea, fever,
vomiting, headache and pharyngitis.
• Children appear to be more susceptible than adults
• The organism may be shed in stools for up to 40 days following
illness.
• A variety of systemic involvement may occur as a consequence
of the gastroenteritis syndrome. They include pseudo-
appendicitis, mesenteric lymphadenitis, peritonitis, terminal
ileitis, reactive arthritis, colon and neck abscess, cholecystitis,
intussusceptions and erythema nodosum.
• The organism can be recovered from urine, blood,
cerebrospinal fluid and eye discharges of infected individuals.

Diagnosis
• Selective enrichment broth: Peptone-sorbitol-bile broth
• Selective Media: CIN (cefsulodin-Irgasan-novobiocin) medium
• Oxidase: Negative Catalase: Positive

Arcobacter
 Arcobacter is a genus of Gram-negative, spiral-
shaped bacteria in the epsilonproteobacteria class.
 It shows an unusually wide range of habitats, and
some species can be human and animal pathogens.
 Species of the genus Arcobacter are found in both
animal and environmental sources, making it unique
among the epsilonproteobacteria.
 This genus currently consists of five species: A.
butzleri, A. cryaerophilus, A. skirrowii, A. nitrofigilis,
and A. sulfidicus, although several other potential novel
species have recently been described from varying
environments.
Three of these five known species are pathogenic.
 Members of this genus were first isolated in 1977
from aborted bovine fetuses.
 They are aerotolerant Campylobacter-like organisms,
previously classified as Campylobacter.
 The Arcobacter genus, in fact, was created as
recently as 1992.
 Although they are similar to Campylobacter,
Arcobacter species can grow at lower temperatures
than Campylobacter as well as in the air, which
Campylobacter cannot.

Agent: M. tuberculosis and M. bovis
2 types-
Pulmonary TB
Non pulmonary TB
Source- Milch animals, handlers, environment, feed
Symptoms- Cough, fever, fatigue, weight loss, pleurisy,
Diagnosis- Examination of sputum, faeces, serum for the presence
of bacilli using Ziehl Neelson’s staining
Food: Milk and milk products/ meat
Media: Dorset Egg medium, LJ, Middlebrook 7H9, 7H10
Tuberculosis

Brucellosis
Species: B. melitensis, B. abortus, B. suis, B. canis, B. ovis, B.
neotomae, B. microti, B. pinnipedialis, B. ceti
Source-environment, persons, diseased animals
Disease in man-Malta fever, undulent fever
Symptoms-headache, sweating, chills, joint and muscle pain
Diagnosis- blood culture, CFT, Agglutination, ELISA
Media: Potato dextrose agar, serum dextrose agar, Blood Agar

Caustive agent: Coxiella burnetti
The bacterium is an obligate intracellular pathogen
 can survive pasteurization and freezing temp
 Incubation period between 2-4 weeks.
Symptoms: include a sudden onset of high fever, headache,
malaise, severe sweating, pneumonia, weakness, dry cough and
chest pain due to a pneumonitis. Hepatic disorders which include
slight jaundice occur in severe cases.
Symptoms: mastitis in animals
 Mortality is low with complete recovery.
 Q-fever is mostly an occupational disease among people who
handle livestock and raw animal products (e.g. farm and
slaughterhouse workers etc).
 Infection occurs through consumption of raw milk,
contaminated butter and cheese
 Infection may also occur through contact with infected
placentas, contaminated straw beddings and animal carcasses or
slaughterhouse offals.
Rickettsial disease: Q fever

Diagnosis
• Diagnosis: Usually difficult
• Serology including CFT, micro-agglutination and FAT.
• Isolation facility not usually available in microbiology labs. Done
on cell lines/ embryonated eggs.
• Isolation of agent (in well equipped laboratory due to the high
risk of infection).
• Samples: Milk
Control
• Pasteurization of milk and milk products (heating at 63o
C for 30
min or 72o
C for 15 sec).
• Safe disposal of offal

Paratuberculosis
 Paratuberculosis is a contagious, chronic and
sometimes fatal infection that primarily affects the small
intestine of ruminants.
 It is caused by the bacterium Mycobacterium avium
subspecies paratuberculosis.
 Infections normally affect ruminants.
 Paratuberculosis is found worldwide, with some states
in Australia (where it is usually called Bovine Johne's
Disease or BJD) as the only areas proven to be free of the
disease.
There are clinical similarities between Johne's disease
in ruminants and inflammatory bowel disease in humans
and because of this, some researchers contend that the
organism is a cause of Crohn's disease.
Diagnosis done by milk/manure/diarrhoeic
faeces/biopsy (rectal pinch)
Diagnosis:
Difficult as very slow grower.
The cultivation of M. paratuberculosis is always
performed using special media supplemented with
mycobactin.
Media: Herrolds’s egg yolk medium (HEYM) LJ,
Middlebrook etc.

Pseudomonas infection
Species: Ps. putrifaciens, Ps. viscosa, Ps. fragi, Ps. aeruginosa
Sources- water, utensils, udder, teat, cowshed environment
Disease in humans- causes UT infections, eye and ear infections, abscesses,
meningitis, enteritis, septicemia, gastrointestinal disturbances
Diagnosis: Any nutrient rich media
Oxidase: positive Pigment producer

VIRAL FOODBORNE INFECTIONS
• Viruses are Non-living
– Protein coat with DNA/RNA
– Must have a host to reproduce (obligate intracellular)
– Do not consume nutrients
– Do not excrete waste products
– they cannot multiply in foods or water.
• Smallest microbial contaminant-
Submicroscopic/ultramicroscopic
• Low Infective Doses
– Fairly communicable through foods and direct contact
– Viruses are common pathogens transmitted through
food.
– These viruses are highly infectious and may lead to
widespread outbreaks
– High numbers of viral particles are further transmitted
via feces of infected persons (up to 1011
particles per gram
of feces).
 Food borne virus are relatively stable and resistant outside
host cells. Resistance varies greatly. Many virus resistant
to: Sanitizers, Freezing and Heat
• Hepatitis A, E, Roraviruses and Norwalk-like virus
(Novovirus) are the important viral food borne
pathogens.

Hepatitis A & E
• Infectious Hepatitis - Disease of the liver
• Multiple types of Hepatitis A,B,C,D,E,F
– A & E – only one relevant to food service
– A-Picorna virus E-Calcivirus/Hepevirus
Sources
– Human GI tract, RTE foods, Polluted H2O, Raw Shellfish, raw
fish / Crustaceans
The incubation period is long, being an average of 30 days
(range 15-50 days). The duration of the disease could be
from a few weeks to several months.
Systemic infection. Disease can vary greatly from mild to life
threatening
– Nausea -- Fever
– Diarrhea -- Fatigue
– Vomiting -- Abdominal Pain
– *Jaundice -- liver enlargement
• Can still be infectious weeks after symptoms gone
• Spread via fecal-oral route
Prevention
– Good Personal Hygeine
– Exclude all infected workers
– NO raw shellfish
– Purchase from reputable suppliers
– Steam shellfish for 90 sec (184-194° F)
• Deli meat
• Produce
• Salads

Norovirus (Norwalk Like viruses)
• Disease: Norovirus Gastroenteritis (Calciviridae family)
• 1st
outbreak – Norwolk, Ohio- Contaminated drinking water
• Non-life threatening
• Also k/a WINTER VOMITTING BUG (in UK)
 Symptoms
 Diarrhea, Vomiting, Cramps, Nausea, Headache, Anorexia
 Asymptomatic infection are common and may contribute to the spread of the
infection.
 EXTREAMLY Contagious
 Low Infectious dose
 Novovirus infection is relatively mild with an incubation period of 3 days.
 Contagious for 3 days after symptoms disappear
• Implicated Foods
– RTE
– Shellfish contaminated by sewage
k/a “Cruise Ship Poisoning”
• Resistant to Chlorine Sanitizers
• Prevention
– Good Personal Hygiene
– Exclude all infected workers
– NO raw shellfish
– Purchase from reputable suppliers

Parasites
• Living Organisms
– Require host to survive
• Larger than Bacteria
– Often still require microscope

Hydatidosis
Agent: A tapeworm- ingestion of
gravid segments of Echinococcus
granulosus of dog.
Cysts get localized in organs like
liver, heart muscle.
Taeniasis
T. saginata, T. solium
Source- consumption of raw and
undercooked meat, unhygienic
conditions
Symptoms- nervousness,
anorexia, weight loss, abdominal
pain, digestive disturbances

Trichinosis
• Illness: A nematode parasite
-Trichinella spiralis
• Food of concern – Pork
• Habitat – Swine, boar, wild
boar, marine mammals, fox
• Source- raw and undercooked
pork and pork products
• Symptoms- diarrhoea,
abdominal pain, influenza &
typhoid like fever
Prevention
– Cooking - 145°F
– Freezing 5°F for 30 days
– Curing/Salting/Smoking
– Irradiation
• Purchase Pork from approved
sources
• Avoid Cross-contamination
with other meats and grinders

Anisakiasis
• Agent: Anisakis simplex
• Fish Parasite
• Nematode – Round worm
• Fish and Squid – Bottom feeders
– Marine – Salt Water
• Implicated foods –
Raw/undercooked fish
– Sushi --Pacific salmon
– Ceviche --Cod
– Sashimi
– Pickled Herring

a) Cryptosporidiosis
Agent: a protozoan C. parvum
Source: raw or undercooked meat, offal
Symptoms- acute watery non-bloody diarrhoea,
nausea, vomitting abdominal pain
 Infection is caused by ingestion of sporulated oocysts
 Transmitted by the faecal-oral route.
 Obligate intracellular pathogen.
b) Sarcocystosis
Agent: a protozoan Sarcocystis
Sarcocyst occurs in skeletal and heart muscles of mammals
Source- Infection occurs when undercooked meat is
ingested.
 Consumption of food contaminated by carnivore excreta
containing sarcocyst ova
 Prevention: Infection can be prevented by cooking the
meat before eating.
c) Toxoplasmosis
Agent: a protozoan: Toxoplasma gondii
Source- meat and organs containing tissue cysts, infected
meat eaten raw or undercooked
Symptoms- transplacental transmission leading to
congenital nervous and ocular lesions
iii) Protozoan Diseasesiii) Protozoan Diseases

Cyclospora cayetanensis
 Cyclospora cayetanensis is a protozoan that causes disease in humans, and
perhaps primates.
 It has been linked in the United States to fecally contaminated imported
raspberries and was virtually unknown before about 1990, but has been on the
rise since.
 The health risk associated with the disease is usually confined to adult
foreigners visiting regions where the species is endemic and acquiring the
infection: this is why C. cayetanensis has been labeled as causing "traveler's
diarrhea.“
Syptoms: Gastroenteritis, with the extent of the illness varying based on age,
condition of the host, and size of the infectious dose.
Symptoms include "watery diarrhea, loss of appetite, weight loss, abdominal
bloating and cramping, increased flatulence, nausea, fatigue, and low-grade
fever“
Source: infection occurs via fecally contaminated food and water in endemic
environments

Foodborne intoxication
• Exotoxin – Toxin that is produced by a cell and is then expelled
outside of the cell
• Endotoxin – Toxin that is produced and remains inside the cell
until the ruptures (cell death) and is then released
• Types of toxins based on target organ
– Enterotoxin – of the intestines; GI tract
– Neurotoxin – Affects the CNS
– Hepatotoxin – Affects the liver
– Nephrotoxin – Affects the kidneys

Bacillus cereus
• Rod shaped, Gram +ve, Facultative Anaerobe
Spore Former (Endospore)
• Habitat: Soil
• Common Foods
– Cooked Corn
– Cooked Potatoes
– Cooked Vegetables
– Meat Products
– Cooked Rice dishes: Fried Rice, Rice Pudding
– Starchy Foods: Potatoes, Pastas
• Symptoms
– Watery diarrhea
– Abdominal cramps/Pain
– Nausea,
– Vomiting

B. Cereus – emetic type
Symptoms:
– Nausea
– Vomiting
– Diarrhea, occasionally
– Abdominal cramps, occasionally
• Onset: 15 min – 6 hrs
• Duration: less than 24 hr
Control Measures:
• Cook food to required minimum internal
temperature
• Prevent Bacterial Growth and Toxin Production
– Hold food at the proper temperature
– Cool food Properly

Staphylococcus aureus
 Gram +ve, Cocci in clusters
 Habitat: Hair, nose, throat, feathers and sores/boils/pimples
 Disease: Staphylococcal Gastroenteritis
 FB Intoxication – Exotoxin- Enterotoxin
• Symptoms:
– Nausea, Vomiting, Diarrhea
– Abdominal pain, Headache
– Sweating, with a decrease in body temp.
• Implicated Foods
– High protein foods which are cooked
– Meat, poultry, gravies, puddings, egg products
– Salads containing PHF (egg, tuna, chicken, macaroni)
• Common associations
– Temperature abuse
– Foods on hot holding lines not hot enough
– Refrigeration not cold enough
– Re-contamination from humans
• Prevention Measures
– Personal Hygiene
– Properly covered cuts on hands and arms
– Restrict infected food handlers from working with or around food or food
equipment
– Minimize the time food spends in the Temperature Danger Zone
• Cook, hold and cool food properly

Clostridium botulinum
• Rod shaped, Obligate anaerobe, Spore Former
• Habitat: Soil, Air, Water
• Food Intoxication: Exotoxins
– All neurotoxins
– Heat stable to a point (Boil for 10 min)
• Disease: Botulism
• Botulism toxin mechanism: Blocks the release of a neurotransmitter ACh
– Causes Paralysis
• Symptoms
– Nausea, Vomiting, Abdominal pain
– Diarrhea (constipation), Headache
– Diplopia, Speech impairment, In-coordination
– Paralysis, Cardiac Failure
– Respiratory Failure, Death

Botulism
Implicated Foods
• Improperly canned foods (often home-canned)
• FDA regulation – NO home-canned foods may be served
• Modified Atmosphere Packaging
• Controlled Atmosphere
• Other Foods
– Baked potatoes
– Garlic-in-oil
– Sautéed onions
– Processed meats
• Nitrates/Nitrites
Control
– Avoid temperature abuse of Potentially Hazardous Food
– Use only commercially prepared canned foods
Infant botulism – toxin mediated infection
– “Floppy Baby Syndrome”
– Underdeveloped gut flora
– Honey/Syrup – not under 1 yr of age

Clostridium perfringens
• Rod shaped, Obligate anaerobe, Spore Former
• Habitat: Ubiquitous - Soil, Air, Water, GI tract
• Toxin-mediated infection
• Double every 8 minutes in right environment
• 2-6% of humans are asymptomatic carriers
Disease:
Clostridium perfringens Gastroenteritis
• Symptoms:
– Violent cramps
– Explosive diarrhea – due to gas production
– Headache
– Nausea
– NO vomiting

Fungal intoxications
Aflatoxicosis: A. flavus, A. parasiticus
Animals fed with aflatoxin containing feed excrete toxins M1, M2 in milk
Recommended upper permissible limit – 90ppm
Sources-
environment, soil and contaminated food, poor storage conditions
Disease in humans- Acute aflatoxicosis
Symptoms-
liver hyperplasia, tissue hemorrhage, anorexia, hepatitis
organs like kidney, spleen, pancreas may also get affected

Thanks
Acknowledgement: All the material/presentations available online on the subject
are duly acknowledged.
Disclaimer: The author bear no responsibility with regard to the source and
authenticity of the content.
Questions???

Foodborne Infections and Intoxications

Recommandé

Recommandé

Contenu connexe

Tendances

Tendances (20)

Similaire à Foodborne Infections and Intoxications

Similaire à Foodborne Infections and Intoxications (20)

Plus de Ravi Kant Agrawal

Plus de Ravi Kant Agrawal (20)

Dernier

Dernier (20)

Foodborne Infections and Intoxications

Notes de l'éditeur