Staphylococcus  Grows at 7°C to 48°C; optimum 20–

37°C.
1. Introduction
 Tolerates low pH (4.8), Aw (0.86),
 Staphylococcus aureus causes and high salt/sugar.
foodborne intoxication via heat-
6. Toxin Production
stable enterotoxins.
 Seven enterotoxins (SEA to SEE),
 Five main enterotoxins: SEA, SEB,
heat-stable (26–30 kDa).
SEC, SED, SEE.
 Produced at >10^6–7 cells/g at
 S. aureus strains may produce one
~37°C in ~4 hours.
or more of these toxins in food.
 Can be produced at pH 5.0, Aw
2. Morphology
0.86, 10°C.
 Spherical cocci (~1 µm), grape-like
 SEA causes most outbreaks due to
clusters.
high potency.
 Non-motile, non-sporing, some
7. Disease and Symptoms
have capsules.
 Ingesting 100–200 ng toxin (from 30g
3. Classification
food) causes illness in 2–4 hours.
 Based on Coagulase:
 Lasts ~1–2 days, rarely fatal.
o Positive: S. aureus
 Symptoms: salivation, nausea,
o Negative: S. epidermidis, S. vomiting, cramps, diarrhea, chills.
saprophyticus
8. Food Association
 Based on Pathogenicity:
 Protein-rich, extensively handled,
o Common: S. aureus temperature-abused foods.

o Opportunistic: S.  High-risk: ham, beef, cream

epidermidis, S. pastries, salads, cheeses.
saprophyticus
 Major outbreak factors: poor
o Non-pathogenic: S. homonis hygiene, improper holding temp,
early prep.
4. Habitat & Distribution
9. Prevention
 Common on human/animal skin,
nose, wounds.  Maintain <4.4°C or >60°C (Danger
Zone: 4.4–60°C).
 Present in dairy herds, meats, goat
milk, dolphin skin, etc.  Good hygiene, cooking,
refrigeration.
5. Characteristics of S. aureus
 Avoid recontamination after heat
 Gram-positive, facultative
treatment.
anaerobe, non-motile.
 Chill food to ≤5°C within 1 hour.
 Ferments mannitol, produces
coagulase, hemolysin, 10. Identification Methods
thermonuclease.
  Food/vomit analysis for ≥10^6  Genus Salmonella includes one
CFU/g of S. aureus. species: Salmonella enterica.

 Biochemical tests: coagulase,  Six subspecies (e.g., S. enterica

hemolysis, thermonuclease. subsp. enterica, arizonae, etc.).

 Toxin detection:  Two most common serotypes in

humans: Typhimurium and
o Biological: Animals
Enteritidis.
(vomiting = positive result)
 Serotype naming: Salmonella
o Serological: ELISA, latex
enterica subsp. enterica ser.
agglutination (type-specific)
Typhimurium.
o Molecular: PCR, gene
3. Epidemiological Grouping
probing
 Group 1: Infect humans only (e.g.,
Salmonellae S. Typhi, S. Paratyphi A, C)

1. Introduction  Group 2: Host-adapted serovars

(e.g., S. gallinarum - poultry, S.
 Salmonella typhi and Salmonella
dublin - cattle)
paratyphi were historically major
causes of foodborne and  Group 3: Unadapted serovars — no
waterborne illness. specific host, includes most
foodborne strains
 Due to milk pasteurization and
water chlorination, their spread 4. Morphology and Characteristics
decreased in developed countries.
 Small, Gram-negative, non-sporing,
 Since the 1950s, non-typhoidal facultative anaerobic rods
Salmonella serovars have become a
 Motile, produce gas from glucose,
leading cause of foodborne illness.
ferment dulcitol (not lactose),
 Factors contributing to the rise: citrate +, H2S +

1. Antimicrobial-resistant  Do not produce indole or urease

strains
 Optimal growth: 35–37°C, range: 5–
2. More immunocompromised 46°C
individuals
 Killed by pasteurization, inhibited at
3. Egg-associated Salmonella pH ≤4.5 and Aw ≤0.94 (especially
Enteritidis (infected ovaries with pH 5.5)
in hens)
 Survive in frozen and dried states;
4. Centralized food production multiply without a ecting food
and wide distribution appearance

 Over 2000 serovars exist, 5. Habitat and Distribution

transmitted via fecal-oral route
 Found in GI tract of wild and
(food, water, direct contact).
domestic animals, birds, pets (e.g.,
2. Nomenclature and Classification turtles, frogs), insects
  Also present in soil, water, and  Shell eggs a major source of S.
sewage contaminated with fecal Enteritidis since the 1980s
matter
 S. Typhimurium also remains a
 Transmission: animal/human feces major causative agent
→ contaminated water/food →
9. Notable Outbreaks (U.S.)
humans → feces
 1994: >224,000 cases, ice cream
6. Toxins
(milk tankers previously carried
 Invade intestinal mucosa → multiply eggs) – S. Enteritidis
in epithelial cells → inflammation
 1985: ~200,000 cases, 2% milk from
and fluid buildup
a dairy – S. Typhimurium
 Produce thermostable cytotoxin
 1974: 3,400 cases, potato salad
(damages cells)
held at unsafe temps – S. Newport
 Produce thermolabile enterotoxin
10. Prevention and Control
(induces fluid/electrolyte secretion)
 Regulatory standard: no Salmonella
 Toxin production linked to pathogen
in ready-to-eat foods
growth rate
 Industry uses pathogen surveillance
7. Disease and Symptoms
and testing
 Foodborne salmonellosis is distinct
 Consumer education focuses on:
from typhoid/paratyphoid fevers
o Proper cooking (e.g., 71.7°C
 Infectious dose: ~10^5–10^6 cells
for 15 s)
(lower for acid-resistant strains)
o Rapid cooling (≤4°C within 2
 Incubation: 8–42 hours (typically
h)
24–36 hours)
o Preventing cross-
 Duration: 2–3 days, but can last
contamination
longer; carriers can shed for months
o Good hygiene and sanitation
 Symptoms: cramps, diarrhea,
nausea, vomiting, fever, chills, o Exclusion of sick food
prostration handlers
 Severe cases in infants, elderly, and o Proper reheating of stored
immunocompromised foods
8. Food Association 11. Detection Methods
 Commonly contaminated: beef,  Steps:
chicken, turkey, pork, eggs, milk,
dairy 1. Pre-enrichment in nutrient
broth
 Also found in: salads, vegetables,
seafood (from polluted water) 2. Selective enrichment

 Cross-contamination is a major 3. Streaking on selective-

cause (especially post-cooking) di erential agar
 4. Biochemical and serological  Five virulence groups:
confirmation
1. Enteroaggregative (EAggEC)
 Rapid methods: Immunological and
2. Enterohemorrhagic (EHEC)
molecular (e.g., PCR)
3. Enteroinvasive (EIEC)
Escherichia coli
4. Enteropathogenic (EPEC)
Introduction
5. Enterotoxigenic (ETEC)
 Identified as a foodborne pathogen
in 1971; caused illness in nearly 400  Each group has unique O:H
individuals. serotypes and virulence factors.

 Recognized as a cause of infant  EPEC and ETEC relate strongly to

diarrhea since the early 1700s. toxicoinfections.

 Used as an indicator of fecal Similarities and Di erences: EHEC vs

contamination. EPEC

 First description of E. coli O157:H7 Similarities Di erences

in 1982: linked to undercooked
Both possess eaeA EHEC produces
hamburgers; now a major concern
gene Shiga-like toxins
for physicians, public health, and
the food industry. Both create EHEC a ects large
Geographic Distribution attachment- intestine (shown in
e acement lesions piglets)
 E. coli O157:H7: Found worldwide,
except Antarctica. Morphology

 Other EHEC strains: Widely  Gram-negative rod, family

distributed with region-specific Enterobacteriaceae.
prominent serotypes.
 Normal GI tract commensals.
Morbidity and Mortality in Humans
 Dimensions: ~1.5 µm × 0.5 µm.
 Seasonal variation (summer and
 Motile (flagella), non-spore forming.
autumn peaks in North America).
Characteristics
 U.S. incidence (1996–2010): 0.9
cases per 100,000 people.  Gram-negative, small, curved rods;
facultative anaerobes.
 Mortality rates:
 Grow in various media and foods
o HUS: 3–10% in children, up
(10–50°C, optimal 30–37°C).
to 50% in elderly.
 Sensitive to:
Classification
o Low pH (<5.0)
 Serotyped like Enterobacteriaceae:
~200 "O" serotypes. o Low Aw (<0.93)
 Flagellar proteins (H-antigens) are o Low-heat treatments
less variable than O-antigens. (pasteurization).
Habitat  Severe cases: dehydration, shock.

 Asymptomatically colonize human  EHEC: hemorrhagic colitis, HUS

intestines. (acute kidney failure).

 Shed in feces; spread via Food Association

contaminated food/water.
 Commonly implicated foods:
 Animals also carry and spread
o Meat, dairy, fish, vegetables,
serotypes.
baked goods, water.
Toxins and Toxin Production
o Undercooked meats (esp.
 ETEC strains produce: ground beef), unpasteurized
dairy.
o LT (heat-labile toxin): similar
to cholera toxin. o Contaminated produce
(fruits, vegetables).
o ST (heat-stable toxin): non-
antigenic. Foodborne Outbreaks

 EPEC strains: now known to  2012: Clover sprouts

produce LT-like or unique toxins.
 2011: Lettuce, bologna, hazelnuts
 Additional virulence factors aid
 2010: Cheese, romaine, steak
colonization.
 2009: Ground beef, cookie dough
 Toxin genes are plasmid-borne
(transferable).  Vehicles: milk, yogurt, pastries,
eggs, cereals, salads, meats.
 Optimal production in rich media,
pH 8.5, aerated broth at 35°C (range Contributing Factors
25–40°C).
 Holding food at warm temperatures.
Disease and Symptoms
 Inadequate refrigeration.
 Incubation: 1–16 days; shedding: 7–
9 days (may persist).  Preparing food too early.

 Infection progression (E. coli  Infected food handlers.

O157:H7):  Inadequate cooking.
o Day 0: Ingestion Common Prevention
o Day 3–4: Non-bloody  Good hygiene (handwashing,
diarrhea sanitation).
o Day 5: Bloody diarrhea  Prevent cross-contamination.
o Day 6–7: 94% resolve, 6%  Cook meats thoroughly.
develop HUS
 Avoid unpasteurized products.
 EPEC: infant diarrhea; ETEC:
traveler’s diarrhea.  Wash produce; protect water from
animals.
 High infectious dose (10⁶–10⁹ cells);
symptoms last 24–30 h.
Disease Prevention  Found in nature; 1–10% of healthy
humans may excrete it in feces.
 Prevent fecal contamination via
sanitation and sewage treatment.  Hardy organism: survives for years
in cold environments.
 Personal hygiene among food
handlers.  Human listeriosis known historically
but foodborne transmission
 Prevent temperature abuse
recognized recently.
(refrigerate, reheat properly).
 Opportunistic disease; healthy
Treatment
people may be asymptomatic or
 Supportive care. have mild enteric disease.

 Antibiotics usually avoided (risk of  High fatality rate (30–40%) in

HUS). fetuses, newborns, elderly, pregnant
women, and immunocompromised
 Antimotility drugs may worsen HUS. individuals.
Identification Methods  Can grow at refrigerated
 Enrichment and selective isolation. temperatures, reaching infectious
levels during storage of
 Biochemical and serological testing contaminated or post-heat-
(ELISA). contaminated foods.
 Toxin testing via animal models and  Increased risk from ready-to-eat
cell lines. and improperly reheated foods.
 Culture from fecal/rectoanal swabs;  Technology used in RTE foods may
selective media. allow contamination and
 Immunological and nucleic acid subsequent growth during cold
tests. storage.

Conclusion  Even short temperature abuse can

accelerate growth.
 Pathogenic E. coli includes Gram-
positive sporeformers and Gram-  Awareness has helped reduce
negative rods. incidence; U.S. cases dropped from
2000 (1986) to ~1000 (1991).
 Symptoms result from toxins; high
doses usually needed.  Pathogenic serogroups: 1/2a, 1/2b,
1/2c, 3a, 3b, 3c, 4b (1/2a, 1/2b in
 Prevent via sanitation and proper Europe; 4b in U.S. and Canada).
food handling.
Environment
Listeria monocytogenes  Found in decaying vegetation, soils,
Introduction animal feces, sewage, silage, and
water.
 Listeria monocytogenes is a Gram-
positive pathogen a ecting animals  Associated with lactic acid bacteria,
and humans. Brochothrix, and coryneform
bacteria.
Incidence  Ferments glucose without gas.

 Scotland: 25/160 milk tanks positive  Resistant to freezing, drying, high

(out of 260 farms). salt, and pH ≥ 5.0.

 Netherlands: 7.5% prevalence in  Killed by pasteurization (71.7°C for

fresh meat; lowest in ice cream 15s or 62.8°C for 30 min); higher
(0.2%). heat needed when intracellular.

 U.S.: 7.1% of 1,727 raw beef Habitat

samples positive.
 Found in soil, sewage, water, dead
Classification vegetation.

 Formerly "Listerella," renamed in  Isolated from intestines of animals

1940. and humans (carriers).

 Six recognized species; L. ivanovii  Found in raw meat, milk, eggs,

has two subspecies. seafood, fish, vegetables (especially
leafy and tubers).
 Di erentiated by fermentation of
ribose and not N-acetyl-β-D-  Present in heat-processed and RTE
mannosamine. meat/dairy foods.

 PCR-based fingerprinting: L.  Found frequently in food processing

innocua, L. welshimeri, L. grayi and storage areas.
show di erent profiles.
Toxins and Toxin Production
 Often associated with genus
 Virulence linked to hemolysin:
Erysipelothrix.
Listeriolysin O.
 Typically catalase-positive; L.
 Produced during exponential
monocytogenes is catalase-
growth.
negative.
 Toxin allows intracellular growth and
 17 serovars; L. monocytogenes has
cell death.
13.
Disease and Symptoms
 L. innocua (2 serovars) considered
non-pathogenic variant.  Healthy individuals may not show
symptoms or only mild flu-like
Characteristics
symptoms.
 Gram-positive, psychrotrophic,
 Incubation: 1–7 days; symptoms
facultative anaerobic,
include fever, cramps, diarrhea.
nonsporulating, motile rod.
 Infected individuals shed bacteria in
 Catalase-positive, oxidase-negative,
feces.
beta hemolytic.
 Severe symptoms in high-risk
 Short chains in fresh culture;
groups (pregnant, elderly,
ferments rhamnose (not xylose).
immunocompromised):
 Grows between 1–44°C; optimum at
o Initial: nausea, vomiting,
35–37°C; grows at 7–10°C rapidly.
cramps, fever, headache.
 o Later: septicemia,  1929: First human case.
meningitis, encephalitis,
 1981 (UK): 60 human cases.
endocarditis.
 1985: 140 human and animal cases.
o In pregnant women:
transmission through  1986–1988: 150% increase in
placenta. England/Wales.
o High fatality in fetuses and  1983–1987: 775 cases, 219 deaths.
immunocompromised.
 1993 (U.S.): 1,092 cases, 248
o Infective dose: ~100–1000 deaths.
cells in sensitive individuals.
Prevention and Control
Food Association
 Complete elimination not feasible;
 Sporadic and outbreak cases linked widespread presence.
to:
 Regulatory measures in place since
o Cole slaw 1991 reduce cases.
o Pasteurized/raw milk, dairy  Recent rise in sporadic outbreaks
products and recalls (e.g., 1999: 24 recalls).
o Soft cheeses (Mexican, Brie,  U.S. policy: Presence in 25g of RTE
Liederkranz) meat/poultry = adulteration;
product discarded.
o Meat pâté, cold cuts, turkey
franks  HACCP and sanitation enforced in
contaminated plants.
o Improperly cooked chicken,
smoked mussels  Potential for relaxing zero-tolerance
in future.
 Heat-treated foods often re-
contaminated or improperly heated.  Consumer education essential:
 Growth during long refrigerated o Cook raw animal foods
storage and temperature abuse. thoroughly.
 Raw or re-contaminated foods o Wash vegetables before
cause listeriosis. consumption.
 A ected groups: sensitive o Separate raw meat from
populations. ready-to-eat/cooked foods.
High-Risk Foods o Avoid raw milk or raw-milk
products.
 Raw milk, soft cheeses, fresh/frozen
meat, poultry, seafood, fruits, o Clean hands, knives, boards
vegetables, ice cream, RTE foods. after handling raw foods.
 Other Listeria spp. found in some  High-risk groups advised to:
foods, including L. innocua, L.
welshimeri, L. grayi, L. seeligeri. o Avoid soft cheeses (e.g.,
Feta, Brie, Camembert,
Foodborne Outbreaks blue-veined, cream cheese).
 o Reheat leftovers and RTE  Predominant species in U.S.
foods until steaming. changed from S. dysenteriae to S.
sonnei.
o Avoid deli foods.
 Associated with poor hygiene in
Treatment
food establishments.
 Antibiotics used:
Characteristics
o Ampicillin
 Gram-negative, facultative
o Erythromycin anaerobic, nonsporulating,
nonmotile rods.
o IV Trimethoprim–
Sulfamethoxazole  Catalase-positive, oxidase-negative,
lactose-negative.
o Cephalosporins,
Fluoroquinolones  Ferment sugars (no gas).

o Gentamicin + Ampicillin  Grow at 7–46°C (optimum: 37°C).

(clinical basis)
 Resistant to refrigeration, freezing,
Detection Methods 5% NaCl, pH 4.5; killed by
pasteurization.
 Pre-enrichment and enrichment in
selective broths. Habitat

 Streaking on selective-di erential  Only habitat: human/primate

agar. intestines.

 Biochemical and serological testing.  Carriers can shed without

symptoms for months post-
 Rapid methods: immunological and recovery.
nucleic acid-based tests.
Toxins
Other Bacterial Species
 Plasmid-encoded invasive traits.
2.6.1 Shigellosis
 Shiga toxin (ST): exotoxin with
Introduction enterotoxigenic properties.

 Genus Shigella: four species – S.  Toxin expression optimal at 37°C.

dysenteriae, S. flexneri, S. boydii, S.
Disease and Symptoms
sonnei.
 Infective dose: 10–1000 cells.
 Human and primates are the only
hosts.  Incubation: 12 h to 7 d (usually 1–3
d).
 Transmission: fecal–oral route;
contaminated food/water.  Duration: 5–6 d (mild), up to 3 weeks
(severe).
 Common in Asia, Mexico, South
America; linked to poor sanitation.  Symptoms: abdominal pain,
diarrhea with blood/mucus/pus,
 In the U.S.: more common among
fever, chills, headache.
migrant workers, on reservations,
and in day-care centers.
  Carriers may remain infectious after Characteristics
symptoms.
 Gram-negative, nonsporulating,
Food Association motile, curved rod.

 Fecal contamination: direct (poor  Microaerophilic (5% O2, 8% CO2).

hygiene) or indirect (contaminated
 Catalase and oxidase positive.
water).
 Optimum growth at 42°C (range: 32–
 Commonly implicated: potato, tuna,
45°C).
shrimp, macaroni, and chicken
salads.  Grows in amino acids >
carbohydrates.
 Shellfish from polluted waters.
 Sensitive to oxygen, salt >2.5%, pH
 Growth in food is not critical due to
<5.0, heat, drying.
low infective dose.
Habitat
Outbreaks
 Found in feces of animals and birds.
 1983–1987: 44 outbreaks, 9971
people, 2 deaths.  Water, sewage, vegetables, and food
of animal origin.
 1987: outbreak linked to
commercial meals. Toxins
 1995–1996: Spain – >200 victims (S.  Thermolabile enterotoxin (cross-
sonnei) from pasteurized cheese. reacts with cholera toxin).
 2000: U.S. – 30 victims from a 5-  Invasive factor for epithelial cell
layer dip. colonization.
Prevention and Control Disease and Symptoms
 Educate food handlers on hygiene.  Infective dose: ~500 cells.
 Restrict sick individuals from  Incubation: 2–5 d; duration: 2–3 d
handling RTE foods. (up to 2 weeks).
 Sanitation, refrigeration, chlorinated  Symptoms: abdominal cramps,
water to wash vegetables. diarrhea (sometimes bloody),
nausea, vomiting, fever, chills.

 Carriers may shed for long periods.

2.6.2 Campylobacteriosis
Food Association
Introduction
 Found in beef, lamb, pork, chicken,
 Campylobacter jejuni and C. coli
turkey, milk, eggs, vegetables,
cause human gastroenteritis.
mushrooms, clams.
 C. jejuni most common in
 Contamination via feces or cross-
foodborne outbreaks.
contamination.
 Common sources: raw milk,
 Poor growth in food, but cells
undercooked chicken.
survive and cause infection.
Outbreaks Disease and Symptoms

 1979–1987: 53 U.S. outbreaks, 1547  Young children most susceptible.

cases, 2 deaths.
 Infective dose: ~10⁷ cells.
Prevention and Control
 Symptoms: abdominal pain
 Sanitation during (appendicitis-like), diarrhea,
handling/processing. nausea, vomiting, fever.

 Heat treatment and avoidance of  Duration: 2–3 d; latent onset: 24–30

post-heat contamination. h.

 Avoid use of contaminated  Can cause pseudoappendicitis,

fertilizers/water. arthritis, lymphadenitis, abscesses,
peritonitis.
 Ensure personal hygiene among
food handlers. Food Association

 Found in raw milk, dairy, meat,

vegetables, improperly chlorinated
2.6.3 Yersiniosis
water.
Introduction
 Contamination through
 First confirmed U.S. outbreak: 1976 recontamination or carriers.
(chocolate milk).
 Growth at refrigeration temp
 Common in Denmark; emerging enables spread.
pathogen.
Outbreaks
Characteristics
 1982: tofu and milk outbreaks.
 Y. enterocolitica: Gram-negative,
 1988: single outbreak.
facultative anaerobic,
nonsporulating, motile rod.  Rare in U.S.

 Grows at 0–44°C; optimum: 25– Prevention and Control

29°C.
 Heat treatment essential.
 Grows in 5% NaCl and pH >4.6.
 Sanitation and avoidance of
 Sensitive to pasteurization. raw/undercooked milk and meat.

Habitat

 Found in intestines of food animals, 2.6.4 Gastroenteritis by Vibrio spp.

birds, pets, and humans.
Introduction
Toxins
 Four Vibrio species involved:
 Pathogenic strains (esp. in pigs)
o V. cholerae (01 and non-01),
produce heat-stable toxin and
V. mimicus, V.
invasive factor.
parahaemolyticus, V.
 Heat-stable toxin acts post- vulnificus.
colonization.
  V. parahaemolyticus and V.  1971 U.S. outbreak from steamed
vulnificus discussed here. crabs.

Characteristics (V. parahaemolyticus)  Japan: accounts for 40–70% of

bacterial foodborne illnesses.
 Gram-negative, nonsporulating,
motile curved rods. Prevention and Control

 Catalase and oxidase positive.  Avoid raw seafood.

 Glucose fermenter (no gas), does  Ensure proper cooking and

not ferment lactose/sucrose. sanitation.

 Grows at 5–42°C (optimum: 30–  Avoid temperature abuse.

37°C).

 Salt tolerant (3–5% NaCl), heat and

Cholera (V. cholerae)
refrigeration sensitive.
Characteristics
 pH sensitive (<5.0).
 Gram-negative, motile, curved rods.
Habitat
 01 serotype (El Tor biotype) causes
 Halophilic; estuarine environments.
epidemics.
 High counts in summer; attach to
 Non-01 strains also cause
plankton in winter.
gastroenteritis.
Toxins
 Sensitive to cooking; rapid growth at
 Kanagawa-positive strains produce 30–35°C.
TDH (23-kDa hemolysin).
 Alkaline and cooked foods support
 Adhere to intestinal cells; toxin growth.
production depends on growth
Habitat
conditions.
 Human disease; transmission via
Disease and Symptoms
contaminated food/water.
 Infective dose: 10⁵–10⁷ cells.
 Marine environments are reservoirs.
 Incubation: 10–24 h; duration: 2–3
 Gulf Coast and U.S. coastal waters.
d.
Toxins
 Symptoms: diarrhea, nausea,
vomiting, abdominal cramps,  Heat-labile, 85-kDa cytotoxin (A+B
headache, fever, chills. subunits).
Food Association  A subunit activates adenyl cyclase →
water/electrolyte loss.
 Found in fish, shrimp, crabs,
oysters, lobster.  Non-01 produces cytotoxin +
hemolysin.
 Outbreaks due to improper cooking
and cross-contamination. Disease and Symptoms
Outbreaks  Infective dose: ~10⁶ cells.
  Incubation: 1–5 d (usually 2 d).  Categorized into: Protozoa,
Flatworms, Roundworms.
 Symptoms: profuse watery diarrhea,
vomiting, dehydration, cramps. Host Types:

 Non-01 may cause septicemia.  Definitive Host: Where the adult

parasite completes its sexual cycle
Food Association
(e.g., Cryptosporidiosis,
 Contaminated seafood (crabs, Diphyllobothriasis, Trichinosis).
oysters, finfish).
 Intermediate Host: Where
 Poor hygiene; contaminated larval/juvenile forms develop.
water/handlers.

Outbreaks
Protozoa:
 1963–1994: outbreaks in multiple
1. Giardiasis (Giardia lamblia)
countries.
o Water/foodborne; common
 1991–1992: major South American
in areas with poor
epidemic.
sanitation.
Prevention and Control
o Symptoms: Diarrhea,
 Water treatment, sanitation. cramps, nausea, vomiting,
fatigue.
 Avoid raw seafood.
o Diagnosis: Trophozoites in
 Adequate cooking. stool (wet mounts or stains).
 Isolate and treat infected persons. o Treatment: Quinacrine,
 Detection: enrichment → selective metronidazole, tinidazole.
agar → biochemical/serological o Found in raw vegetables,
confirmation → immunoassay/PCR. salads, sandwiches.
Animal Parasites 2. Amebiasis (Entamoeba
histolytica)

Introduction: o Fecal-oral route, food/water

contamination.
 Includes intestinal and tissue
helminths (roundworms, flatworms, o Anaerobic protozoa without
tapeworms) and protozoa. mitochondria.

 Cause illness through ingestion of o Symptoms: Diarrhea,

contaminated food. abdominal pain, vomiting,
heme-positive stools.
 Do not proliferate in food or grow in
culture media. o Diagnosis: Trophozoites and
cysts in stools/scrapings.
 Larger than bacteria; detected using
concentration and staining o Treatment: Metronidazole,
methods. chloroquine.
3. Toxoplasmosis (Toxoplasma o Symptoms: Prolonged
gondii) diarrhea, severe in HIV
patients.
o Transmitted via
undercooked meat, o Diagnosis: Wet mount, acid-
contaminated milk, cat fast staining.
feces.
o Treatment: Trimethoprim-
o Flu-like symptoms; sulfamethoxazole.
dangerous in
immunocompromised
individuals. Flatworms (Phylum Platyhelminthes):
o Treatment: Sulfonamides, 1. Fascioliasis (Fasciola hepatica)
pyrimethamine,
clindamycin, fluconazole. o Liver rot; found in areas with
cattle/sheep.
o Prevention: Cook meat
>70°C, freeze at −20°C, o Symptoms: Fever, fatigue,
avoid cat litter. liver pain.

4. Sarcocytosis (Sarcocystis o Diagnosis: Eggs in

hominis/suihominis) stool/fluids.

o Extraintestinal disease; o Treatment: Praziquantel.

definitive hosts are humans. 2. Fasciolopsiasis (Fasciolopsis
o From beef (S. hominis) or buski)
pork (S. suihominis). o Found in aquatic plants;
5. Cryptosporidiosis common in Asia.
(Cryptosporidium parvum) o Symptoms: Diarrhea, weight
o Waterborne; resistant loss, possible death.
oocysts. o Diagnosis: Eggs in stool.
o Symptoms: Diarrhea, o Treatment: Niclosamide,
abdominal pain, nausea. praziquantel.
o Diagnosis: Acid-fast stains, 3. Paragonimiasis (Paragonimus
sugar flotation. westermani)
o Treatment: Spiramycin, o Lung fluke; found in Asia,
paromomycin, geneticin. Americas.
o HTST pasteurization o Symptoms: Chronic cough,
e ective. chest pain.
6. Cyclosporiasis (Cyclospora o Diagnosis: Eggs in
cayetanensis) sputum/stool; ELISA.
o Related to cryptosporidia; o Treatment: Praziquantel.
acid-fast oocysts.
4. Clonorchiasis (Clonorchis
sinensis)
 o Liver fluke from raw fish. o Symptoms: Myalgia,
di iculty
o Symptoms: Liver damage,
breathing/swallowing, fever.
cirrhosis.
o Diagnosis: Muscle biopsies,
o Diagnosis: Eggs in
eosinophilia,
feces/duodenal fluid.
immunoassays.
o Treatment: Praziquantel.
o Treatment: Thiabendazole,
o Prevention: Cook fish mebendazole.
properly.
o Prevention: Cook meat
5. Diphyllobothriasis >60°C, freeze, proper
(Diphyllobothrium latum) hygiene.

o Broad fish tapeworm; from 2. Anisakiasis (Anisakis simplex,

raw/undercooked fish. Pseudoterranova decipiens)

o Symptoms: Abdominal o From raw fish; A. simplex

cramps, vomiting. more harmful.

o Diagnosis: Eggs in stool. o Symptoms: Epigastric pain,

nausea, eosinophilic
o Treatment: Niclosamide, granuloma.
praziquantel, surgery.
o Diagnosis: Endoscopy,
o Prevention: Cook fish. tissue resection,
6. Taeniasis/Cysticercosis (Taenia immunofluorescence.
saginata/solium) o Treatment: Thiabendazole,
o Humans definitive hosts; surgery.
from beef/pork. o Prevention: Freeze fish -
o Symptoms: Eosinophilia, 20°C/60h, cook to 60°C for 1
tissue cysts. min.

o Diagnosis: Eggs/proglottids
in stool, biopsies. Outbreak Highlights:
o Treatment: Niclosamide,  1985 (USA): Toxoplasmosis: 2.3
praziquantel, surgery. million; Giardiasis: 120,000;
o Prevention: Proper Amebiasis: 12,000;
sanitation, cook meat. Cryptosporidiosis: 50.

 Food vehicles: apple cider, chicken

salad, green onions, raspberries,
Roundworms (Phylum Nematoda): mesclun lettuce.
1. Trichinosis (Trichinella spiralis)

o Contracted via
raw/undercooked pork or
bear meat.
Viruses o NLVs: Cannot be cultivated;
detected by ELISA and
nucleic acid sequencing.
Enteric Viruses Overview:

 Enteric viruses are a major cause of

Habitat:
foodborne illness.
 Enteric origin, excreted in large
 Di icult to detect and recover from
numbers in feces.
contaminated food.
 Do not multiply outside the human
 Some lack suitable isolation
body.
methods.
 Killed by pasteurization.
 Detection techniques are still
developing.

Toxins (ETEC vs EPEC):

Key Characteristics:  ETEC strains produce two

enterotoxins:
 Do not multiply in food systems.
o LT (Heat-labile, antigenic,
 May die o rapidly under certain
similar to cholera toxin).
food storage conditions.
o ST (Heat-stable, non-
 Viral foodborne infections rank third
antigenic, low molecular
behind salmonellosis and
weight).
shigellosis.
 EPEC strains do not produce these
 Incidence may increase with
enterotoxins.
improved detection.

 Only pathogenic human enteric

viruses cause foodborne infections. Disease and Symptoms:

Historical Perspective:  Low infectious dose required.

 Pre-1940s: Polio virus via raw milk.  HAV:

 Recent years: Hepatitis A (HAV), o Incubation: ~4 weeks (2–7

Norwalk-like viruses (NLV), week range).
Rotaviruses, non-A–non-B hepatitis.
o Symptoms: Fever, malaise,
Predominant Viruses: nausea, vomiting,
abdominal discomfort, liver
 HAV and NLVs:
inflammation, jaundice.
o Small RNA viruses (27–28
o Virus shed in feces during
nm).
incubation's second half.
o HAV can be cultured and
 NLVs:
used for vaccines.
o Gastroenteritis: vomiting,
diarrhea.
 o Incubation: 12–24 hrs; Detection Methods:
symptoms last 1–2 days.
 Viruses do not multiply in food and
are present in low amounts.

Food Association:  Initial concentration of virus is

needed.
 Main source: Food contaminated
with feces from infected individuals.  HAV: cell culture and immunological
methods.
 Raw vegetables/salads via polluted
water.  RT-PCR for HAV and NLVs:

 Shellfish (oysters, clams, mussels, o Amplifies RNA using virus-

cockles) from sewage-polluted specific primers.
water.
o Detects as few as 10²–10³
 Ready-to-eat foods contaminated viruses in samples (e.g.,
by food handlers. ham, turkey, roast beef).

 Poor hygiene and equipment

contamination are major factors.
Hepatitis A Virus (HAV):
 Common vehicles: Raw meat,
 Belongs to Picornaviridae
poultry, eggs, unpasteurized milk,
(alongside polio, echo, coxsackie
raw shellfish.
viruses).

 Contains single-stranded RNA.

Prevention:
 Incubation: 15–45 days; lifelong
 Main Strategies: immunity post-infection.

o Kill viruses in food.  Transmitted via fecal–oral route.

o Maintain hygiene and  Major vehicle: raw/partially cooked

sanitation. shellfish.

 Heat treatment (e.g., pasteurization)  Largest US outbreak: Nov 2003 (600

is e ective. victims, 3 deaths from green onions
in a fast-food chain).
 Steaming shellfish lightly is not
su icient.

 Hydrostatic pressure (>300 MPa) Noroviruses:

can destroy viruses.
 Formerly Norwalk, Norwalk-like,
 Sanitation using oxidizers like and SRSVs.
hypochlorite.
 Classified as Norovirus under
 Exclude infected individuals from human caliciviruses (HuCV).
food handling.
 Genogroups: I (e.g., Norwalk) and II
 HAV vaccination is available. (e.g., Snow Mountain).

 Properties:
 o Unenveloped, ssRNA, 27–40 Comparison: Noroviruses vs. Rotaviruses
nm, genome size: 7300–
Feature Noroviruse Rotaviruses
8300 bp.
s
o Includes Sapovirus genus.
Envelope Unenvelope Nonenvelope
 First identified in Norwalk, Ohio d d
(1968).
Genome ssRNA dsRNA
 Highly chlorine-resistant: 3.75 ppm (7300–8300
failed to inactivate (unlike bp)
poliovirus, rotavirus).
Size 27–40 nm 70 nm

Peak Winter Winter

Rotaviruses: Infection
 First identified in 1973 (Australia), Target General Children 6
cultured in 1981. Group population months – 2
 Groups Infecting Humans: years

o Group A: Most common in Incubatio 12–24 hrs ~2 days

infants and children. n

o Group B: Infects adults Symptom 1–2 days Vomiting (3

(reported in China). s Duration days),
Diarrhea (3–8
 Family: Reoviridae. d)
 Properties:

o 70 nm, nonenveloped,
double-stranded RNA
(dsRNA).

o Transmitted via fecal–oral

route.

 Causes ~1/3 of all hospitalizations

for diarrhea in children <5 years.

 Peak season: Winter; most children

infected by age 4.

 Symptoms:

o Vomiting (~3 days), watery

diarrhea (3–8 days),
abdominal pain, fever.

o Incubation ~2 days.

o Host cell receptor: β-

adrenergic receptor.