1. Group members:
Viruses and Some Other Proven and Suspected
Foodborne Biohazards
Groups 10B
Name Matrix numbers
NURSYAHIRAH BT MD SANI UK29035
NUR NATJWA FATIHAH BiNTI RAMLAN UK28984
SITI NORAIDA BINTI JASMANI UK30010
NURUL WAHIDATUL FATIMAH BINTI
AZEMI
UK24924

2. Viruses
4 types of incidence viruses in foods :
 Being obligate parasites
- Do not grow on culture media as bacteria and fungi
- Methods of its cultivation consists tissue culture and chick embryo
technique
 Viruses do not replicate in foods
- Their numbers may expected relatively low compared to bacteria
- Extraction and concentration methods necessary for their recovery.
 Laboratory virological techniques are not practiced in many
food microbiology laboratories
 Not all viruses of potential interest to food microbiologist can

3.  Development of reverse transcription-polymerase chain reaction (RT-
PCR) is a detection methodology.
 It has allowed direct detection of some foodborne viruses in oyster and
clam tissue.
 This efficacy of RT-PCR technique to detect viruses in foods has been
demonstrated by a number of researcher:
- In 1 study, 4 concentration and extraction methods were compared for
recovery of added astrovirus, hepatitis A and poliovirus from
mussels, the glycine solutions and borate buffer methods were found
to be best.

4. Process of RT-PCR

5.  As stated by Cliver et al. noted that virtually any food can serve as a vehicle
for virus transmission, and they have stressed the importance of anal-oral
mode transmission especially for viral hepatitis of food origin.
 Nonintestinal bacteria of human origin are sometimes found in foods, the
same may be true virus. But because of their tissue affinities , food would
serve as vehicles only for intestinal or enteroviruses.

6. Incidence in Foods and
Environment
 Common food source of gastroenteritis-causing viruses is shellfish.
 Crustaceans do not concentrate viruses, molluskan shellfish do
because they are filter feeders.
 Shucked oyster artificially contaminated with 10^4 pfu of a
poliovirus retained viruses during refrigeration for 30-90 days with a
survival rate 10-13%.

7. Molluskan Shucked oyster
Types of crustaceans species

8.  Coliform index is proven value as an indicator of
intestinal bacterial pathogens in waters
 It appears to be inadequate for enteroviruses, which
more resistant to adverse environmental conditions
than bacterial pathogens.
 In a study, enteroviruses were found 35% of time in
waters that met acceptable standards for shellfish
harvesting.
 Investigators concluded that coliform standard for
waters does not reflects the presence of virus.

9.  With capacity of certain viruses to persist in foods, it
shown that enteroviruses persisted in ground beef up to 8
days at 23°C or 24°C. They were not affected by the
growth of spoilage bacteria
 In study in 14 vegetables samples for existence naturally
occurring viruses, none were found.
 But when coxsackievirus B5 inoculated onto vegetables
it did survive at 4°C for 5 days.
 Latter investigators in US examined 60 samples of
market foods but were unable to detect any. They
concluded that viruses in the US food supply are very
low.

10. Coxsackievirus B5
Enteroviruses species and
pathogenesis

11. Distruction in Foods
 The survival of hog cholera (HCV) and African
swine fever viruses (ASFV) in processed meat
was studied by McKercher et al.
 From partly cooked canned ham were prepared,
virus was not recovered. They recovered after
brining but not heating.
 HCV were survived when the addition of curing
ingredients and retained viability even after 22
days.

12.  The boiling of crabs was found sufficient to kill 99.9%
of poliovirus 1 and rotavirus and echovirus were
destroyed within 8 minutes.
African swine fever viruses Hog cholera (HCV)

13. Hepatitis A Virus
 Prior to 1990s, there were more documented
outbreaks of hepatitis A traced to foods than any
other viral infections.
 The virus belongs to family Picomaviridae as do
polio, echo and coxsackie viruses and all have
single-stranded RNA.
 Fecal-oral route is the mode of transmission.
 Raw or partially cooked shellfish from polluted water

14.  Largest foodborne outbreak of hepatitis A recorded
in US occurred in November 2003.
 Vehicle foods that caused this foodborne was
imported green onions (scallions) served by fast food
restaurant chain.
 In 2001, an outbreak of >46 cases occurred in
Massachusetts.
 It associated with the consumptions of sandwiches.
3 death600 victims

15. Noroviruses
 Former Norwalk, Norwalk-like and small-round-
structured viruses (SRSV) have been placed in
this group as genus Norovirus of human
caliciviruses (HuCV).
 Norovirus in 2 genogroups:
- I
- II

16. Genogroups I Genogroups II
•Former Norwalk •Former Snow Mounain viruses
Similarities
• They are unenveloped
• ssRNA with a diameter of 27-40 nm
• Their genome consists of 7300 to 8300 base pairs

17.  Norwalk virus was first recognized in a school
outbreak in Norwalk, Ohio in 1968.
 Water was suspected but not proven as the
source.
 It is the most prevalent of the noroviruses in
foods.
 The virus is more resistant to destruction by
chlorine than other enteric viruses.
 About 3.75 ppm chlorine in drinking water failed
to inactivate the virus. Whereas poliovirus type 1

18. Noroviruses Poliovirus

19.  Norovirus are now the leading cause of
gastroenteritis in US with an estimated 23
millions cases per year
 During fall 2001, a rare waterborne outbreak of
norovirus gastroenteritis occurred in state of
Wyoming. There were around 84 victims.
 Ground water was contaminated with sewage. It
was the source of human HuCV

20. Rotaviruses
 First demonstration of the virus in 1973 in
Australia. First propagated in laboratory in 1981.
 6 groups been identified. 3 known to be
infectious for human.
 Group A:
- Among infants
- Young children throughout the world.

21.  Group B:
- Diarrhea in adults (been seen only in China)
 Rotaviruses belong to family Reoviridae.
 Characteristics:
- 70nm in diameter
- Nonenveloped
- Contain double stranded RNA(dsRNA)
 Fecal oral route is the primary mode of transmission

22. Noroviruses Vs. Rotaviruses
Noroviruses Rotaviruses
 They are
unenveloped
 ssRNA with a
diameter of 27-40 nm
 Their genome
consists of 7300 to
8300 base pairs
- Nonenveloped
- 70nm in diameter
- Contain double
stranded
RNA(dsRNA)

23.  Peak season for infection occurs during winter
months.
 Most susceptible are children between ages of 6
months and 2 years.
 Incubation period for rotavirus gastroenteritis is 2
days.

24.  Symptoms:
- Vomiting for 3 days accompanied by water
diarrhea for 3-8 days
- Often abdominal pain
- Fever
 The host cell receptor protein for rotavirus serves
as β-adrenergic receptor. Once inside cells, they
transported to lysosomes where uncoating
occurs.

25. Rotaviruses

27.  Yellow pigmented Enterobacter cloceae – cause of
neonatal necrotizing enterocolitis,neonetal meningtis and
sepsis
 Although it considered to be an opportunistic pathogen-
some strains produce enterotoxin-lethal to suckling mice
 Vehicles – milk formulas
- infant formulas – contain Citrobacter freundii cause
neonatal infection
 From 18 studies, 4 of them stated that E. sakazakii
strains produce enterotoxin
 All 18 isolates were lethal to suckling mice at 10^8
cfu/mouse and 2 were lethal by peroral route
 Suckling mice- potential virulence is manifested by
monolayers of CHO, Vero and Y-1 adrenal cells.
 Infant mortality rates – 40%-60%
 In belgium 2 infants died- from unused prepared formula &

28.  Studies of enteric bacteria
 From 141 powdered milk
formulas
 25% Pantoea agglomerans
 21% E.cloaceae
 14% E.sakazakii
• studies of 120 dried infant
formulas in Canada
- 6.7% contain E.sakazakii
 ISOLATED Test
 minimum growh T : 5.5- 8 ˚C
 Max growth T : 41 -45˚C
 No growth at 4 ˚C
• THERMAL RESISTANCE of
E.sakazakii >most Gram
negative bacteria
 Stationary phase of E.sakazakii is more
resistant to osmotic and dry stress than
E.coli and some other bacteria.

29. POISONING
 What is scombroid poisoning?
 Foodborne illness/allergic resulting from a
contaminated fish that contain high amount of
histamine (eg: tuna, mackerel etc..etc..etc)
• How histamine produced?? Does anyone here know?
- Bacterial decarboxylation of generally large amount of histidine in
musle (reported caused by sailfish – non-scombroid)
- May also from product which is organoleptically unacceptable –
contracted from both fresh and organoleptically spoiled fish.

30. ETHIOLOGICAL OF HISTAMINE-ASSOCIATED
(SCOMBROID)
POISONING
 Bacteria associated :
1. Morganella spp.
- M. organii – all starins
produce histame
>5000ppm
- Isolate from
temperature-abused
albacore produced
5253ppm in tuna fish (
25˚C) and 2769 ppm
(15 ˚C)
- 4˚C – no growth or
production of histamine
2. P. phosphoreum –produces
histamine at <10 ˚C
Others that lead to histidine
decarboxylation
i. Raoulella planticola and R.
ornithinolytica
ii. Hafnia alvei
iii.Citrobacter freundii,
iv.Clostrodium perfringe
v. Enterobacter aerogenes
vi. Vibrio alginolyicus
vii. Proteus spp
SKIPJACK TUNA which spoiled at….
ROOM T
 31% of bacteria isolates
produced from 100-400mg/dl of
histamine in broth
Strong histamine formers –
M.morganii, Proteus spp and
Raoutella sp.,
Weak – H. alvei & Proteus spp.
SEAWATER (38 ˚C )

31. ETHIOLOGICAL OF HISTAMINE-ASSOCIATED
(SCOMBROID)
POISONING
 Anchovies (ikan bilis)
 A strain isolated- M.morganii
produce 2377 ± 350 ppm
histamine in a culture
medium at 37 ˚C for 24Hrs
 that Strain produce
putrescine and cadaverine
• Tuna sashimi
- K.Pneumoniae recovered
– produce 442 mg/dl
histamine in tuna fish
infusion broth
 Syndrome associated with
other than scombroid fish
- cheeses including swiss
cheese- 187 mg-dl
hitamine
• Syndrome outbreak : 30 mins –
 OUTBREAK REPORT to CDC
1972 – 1986  178 with 1096
cases  no death
Hawaii  51
California  29
New York  24
• OUTBREAK FROM FOOD
Mahi-mahi  66
Tuna  42
Bluefish  19
• Normally fresh fish contain 1mg/dl
histidine
BUT some may contain until 20
mg/dl (can cause symptom in some
individual)
• FDA hazardous for tuna 50 mg/dl 
toxic fish  product is unsafe

32. ETHIOLOGICAL OF HISTAMINE-ASSOCIATED (SCOMBROID)
POISONING
 Nomograph constructed
over the tenperature
range 70 – 100 F –
underscoring low T to
control histamine-
producing bacteria
 Histamine content can be
estimated in skipjack tuna
if incubation time and
storage T is known
Incubatio
n
Time
Storage
Temperatu
re
Histamine
content
46hours 70 F 100mg/dl
23 hours 90 F 100mg/dl
17 hours 100 F 100mg/dl

33. ETHIOLOGICAL OF HISTAMINE-ASSOCIATED
(SCOMBROID)
POISONING
FACTORS OF GROWTH
SYNDROME ( minutes  3
Hours)
 Low pH – but occurs if
below the T of fridge
 Lowest T for
production of
significant
levels30˚C
H.alvei, C.freundii,
E.coli
 15 ˚C – two strains
M.morganii
 Flushing of face and neck
 Feeling of intense heat
 General discomfort
 Diarrhea
 Flushthrobbing headache
 Dizziness
 Itching
 Faintnes burning of mouth and
throat
 Inability to swallow
 Min cause symptom: 100 mg/dl
 Cause by M.morganii : 50
mg/dl

34. ETHIOLOGICAL OF HISTAMINE-
ASSOCIATED (SCOMBROID)
POISONING
 50 incident in Great
Britain (1976-1979) 
19 incidents in 1979
 Vehicles : canned
&smoke mackerel with
bonita,sprats and
pilchards – one
outbreak each
 Common symptom:
dirrhea
 Hudson and Brown
believes the evidence
doesn’t favor histamine
per se as the agent
responsible for the
syndrome  suggest
synergistic relationship
histamine & other– yet
unidentified agent
 Based on inability of
large oral doses og
histamine and
histamine-spiked fish to
produce symptoms in

35. Aeromonas
 Several sp. Often found in
gastrointestinal specimen
i. A. caviae – entrotoxin
identified
ii. A. hydrophilia – entrotoxin
identified
iii. A. eucrenophila
iv. A. schubertti
v. A.sobrian
vi. A. veronii
• Aeromonas basically aquatoc forms-
but precise role in etiology in
gastrointestinal specimens is not
clear
 A. hydrophilia
 Found salt water > fresh water
 Common member of the biota
of pigs
 Significant pathogen
 Aligator
 Fish
 Turtles
 Frogs
 Snails
 Human
 Effect :
i. diarrhea
ii. Endocarditis
iii. Meningtis
iv. Soft tisue infection
v. bacteremia
Associated
with
diarrhea

36. Aeromonas
 Virulent strains of A.hydrophila
produce 52 kDa  single
polypeptide possesses
enterotoxic, cytotoxic and
hemolytic activities
 Multifunctional molecules
displays immunological cross
reactivity with cholera toxin
 InvestigatorsIt is actually
resembles aerolysin
 Aerolysin – pore/ channel 
forming toxin  kill cells by
formring discrete
 Channel created by
oligomerization of toxin molecule
 Cytotonic activity associated with
A.hydrophila toxin
 induced rounding and
steroidgenesis in Y-1 adernal
cells
 Positive respons in the rabbit
ileal loop, suckling mouse and
CHO assays

37. A.hydrophila
 Was isolated from various sources
 69% from 96 produce cytotoxins
 Isolated from diarrheal disease victims- 80% from 40 toxigenic
 Only 41% non-diarrheal positive for cytotoxin production
 Most enterotoxigenic starins are VP (Voges-Proskeur test) & haemolyisn
positive and arbinose negative  produce postive responses in suckling
mouse, Y-1 aderenal cells assay and rabbit ileal loop assays
• FROM 147 isolates from patient of diarrhea,
 91% were enterotoxigenic
 70% of 94 enviromental strains produced hemolysis of rabbit red blood
cells
 From 116 isolates Chesapeake Bay
 71% were toxic by the Y-1 adrenal cell assay,
 Toxicity correlated with lysine decarboxylase and VP reactions
• Another study- 48 of 51 cultures from humans, animals, water and sewage
 produce positive responses in rabbot ileal loop assays with or more
cells, and cell-free extracts from all were loop positive

38. A.hydrophila
 Isolation from meat and meat
products
 Shown to possess biochem markers that are generaly
associated with toxic strains of other species
 Mouse median lethal dose being log 8-9 cfu for
most strains tested.
 Latter investigation suggested – the possibility
immunosuppressive states are important factors in
food-associated infections by this organism-explain the
difficulty of establishing this organism as the sole
etiological agent of foodborne gastroenteritis

39. A.hydrophila
GROWTH TEMPERATURE HABITAT
 7 of 13 growth at 0-5˚C
 4 of 13 growth at 10 ˚C
 1 at minimum 15 ˚C
 Psychrotrophs had optimum
growth between 15 ˚C and 20 ˚C
 growth T for some strains
• Optimum (35 ˚C )
• Max( 40-45 ˚C)
 Was found in all
 12 of 147 lotic and lentic habitats
 Hypersaline lakes and geothermal spring
did not yield the organism
 Water- may contain until 9000/ml
 Ecological study in Chesapeake Bay
 Water column - < 0.3/1-5 x /ml
 Sediment – about 4.6 x /ml
• Presence of A.hydrophila supported by
 Total bacterial counts
 Aerobic bacterial counts
 Viable bacterial counts
 Heterotrophic bacterial
counts
 Inversely related
• Dissolved in Oxygen and
salinity

40. Plesiomonas
 P. shigelloides found in
 water surface
 Soil
 Aquatic animals
(fish,shellfish,etc…)
 Terrestrial meat animals
• Content of G+C DNA
differs from
A.hydrophila
 51% (Plesiomonas)
 58-62% (A.hydrophila)
 Isolated from diarrhea patient
 Associated with general
infection
 Produce heat –stable
enterotoxin
 Produce serogroup 0:17 strains
react with Shigella group D
Study of 16 strains of
P.shigelloides from human
with intestinal illness
 Did not always bind Congo red
 Non-invasive in Hep-2 cells
 Did not produce Shiga-like toxin
on Vero cells
 Low-level cytolysin was produce
consistently-mean for
outbread Swiss mice was 3.5 x
cfu
 No production of heat –stable
enterotoxin for 16 strains
 Conclusion : organism possess
low pathogenic potential

41. P. shigelloides
 Recovered from stools of 6
diarrheal patients  believe to be
the etiological agent althought
salmonella also recovered from 2
patients.
 Two outbreaks of acute diarrheal
disease occurred in Osaka THE
ONLY bacterial pathogen recovered
was P. shigelloides .
 1973 outbreaks
: 978 from 2141 persons became
ill  symptoms lasted 2-3 days
 88% diarrhea
 82% abdominal pain
 22% fever
 13 % headache
: from 124 stools
examined 21 yields P.
shigelloides 017:H2 same
serovar was recovered from tap
water
- 1974 outbreaks
: 24 from 35 persons  Ill with similar
symptom to those noted before
: P. shigelloides 024:H5 recovered
from 3 of 8 stools “virtually in pure
culture” recovered from 39% of
342 water and mud sample, aquatic
and newts
• A patient contracted gastroenteritis
take 1 tablet of trimethoprim-
sulfadiazine P.shigelloides recovered
from blood
 She passed up to 10 water stools daily
 39 ˚C
• Noted that some previous patiens
were immunocompromised or
presented with similar conditions
• Isolated strains reacts with
S.dysenteriae serotype 7 antiserum,
placing it in O group 22 of
P.shigelloides

42. Growth P. shigelloides
 Obserbed at 10 ˚C
 In 59% of 59 fish from Zaire water
 Organism content in River fish > lake fish
 Appear not to produce enterotoxin  only 4 from 29
isolates produced +ve response in rabit ileal loops
 No record of foodborne cases but resulting in two
outbreaks.

43. Bacteroides fragilis
 Obligately aerobic
 Gram –ve  produces an ileal loop-
positive enterotoxin potential
significance of foodborne disease
associated with diarhhea
 1984  enterotoxin first
demonstrated
 1987  enterotoxin strains of B.
fragilis were first associated with
human diarhhea.
 B. fragilis  estimated to constitute
between 1% - 2 % of human
intestinal biota
 non-pore former, more sensitive to
aerated environment than clostridia ,
yet has been recovered from
municipal sewage
 can grow in the presence of 20% bile
 Produced as single chain  MW
20KDa
 Differs from the classical bacterial
enterotoxin  belonging to class of
zinc-binding metalloprotease,
designated metzitcins
 Enterotoxins has wide range of
protein substrates undergoes
autodigestion
 Intestinal damage beliced to be due
to its proteolytic action
 Elicits a positive response in ileal
loops of lambs and others
 Etiological agents – only 50%
identified as foodborne outbreaks in
US  previously recognize agents
need to be included
 B.fragilis, Klebsilla pneumoniae and
Enterobacter clocae warrant more
attention  2 organisms produce
heat-stable enterotoxins that similar
with E.coli
 Their potential in food noted

44. Erysipelothrix rhusiopathiae
Phylogenetically closely related to
Listeria  cause disease in :
 Human erysipeloid
 Localized disease of hand and arms of
handlers of fresh meat and fish-
systematic involvements unknown
 Animal ( swine )  erysipelas
 Characterised by diamond-skin lesions
 similarities make it to be logic as
foodborne pathogen
• It is facultative anaerobes 
 catalase –ve
 Oxidase -ve
 Produce Hydrogen Sulphide gas
At least 23 serovars are known the
only other species is E.tonsillarum
(separated by habitat of porcine tounges
and different serovars)
STUDY
 1982 135 sample consists
of equal number of chicken,
beef and pork.
Found E.rhusiopathiae in:
- 36% pork
- 13% chicken
- None in beef
• In a plant, 54% of pork loins
+ve, many isolates possess
mouse virulance
• 112 sample retail pork in japan
- 34% contained this bacterium
- 14 from 38 isolates represents
serovars

45. Erysipelothrix rhusiopathiae
STUDY
 MEAT SAMPLE in Japan
Contain this organism:
 44 % of 93 wild boar
 50 % of deer
 Representing 13 serovars
• Chicken Sample in Japan
(750 samples)
- 15.7 % of skin samples
- 59.2 % of 179 feather samples
 E.rhusiopathiae 
represents 273 of 297
isolates
 RemainderE.tonsillarum
 Other study of 153 chicken
in Japan:
 30% contain Erysipelothrix
spp. with 65 of 67 is E.
rhusiopathiae

46. Klebsilla pneumoniae Streptococcus iniae
 Symptoms felt 6 hours
after consuming burger
by a patient
 Organisms along with
generic E.coli was
isolated from leftover
burger and patient blood
 Burger and blood match
in cultural methods
• Strain of K. pneumoniae
was LT+ and ST-
• Coliform in leftover
hamburger was 3.0 x
/g and 1.9 x /g in bun
6 human infections-traced to a fish product
1972- cause disease in Amazon dolphins
1986 – cause disease in tilapia and trout at
Israel
- Taiwan & US was next
1991 – first human case in Texas
1994 – second in Otawwa
1995-1996 -4 human cases (Ontario,
Canada)
 Organisms isolated from fish( tilapia
from US fish farms) and patients
• Appears to be fish pathogen- cause disease in
human
-Ontario case  organisms entered
body through hand lesions
•Beta-hemolytic in sheep blood
•Produce fulminant soft tissue infections in
human

47. Prion disease

48. Prion
 Are unique proteins that can convert other
proteins into damaging ones by causing them to
alter their shape.
 Normal cell prion protein (PrP) exists in the brain
cell membrane.
 It carries out some vital functions and is then
degraded by proteases.
 This normal PrP cell is protease sensitive so it does
not accumulate.

49.  The pathogenic form(PrPSc )is
distorted
 is resistant to proteases
 it accumulates in brain tissue
and gives rise to diseases.
 It has been postulated >
Distorted prion molecule act as
template > Converts normal
protein to distorted form.
 Normal protein (α-helical form)
takes on protease-resistant β-
flat form when it become
pathogenic.
 Pathogenic forms tend to
aggregate into amyloid fibrils
where they cause nerve cell
degeneration, it leads to clinical

51. Transmissible Spongiform
Encephalopathies (TSEs)
 TSE’s are a family of rare
progressive
neurodegenerative
disorders that affect both
humans and animals
 They are distinguished by
long incubation periods,
characteristic spongiform
changes associated with
neuronal loss, and a
failure to induce
inflammatory response

52. Bovine spongiform
encephalopathy (BSE)
 BSE also known as “mad cow disease”.
 BSE is a progressive neurological disorder of cattle
that results from infection by an unusual transmissible
agent called a prion.
 First recognized in Great Britain in 1984.
 1986 - Specifically diagnosed in cattle
 1990 - 14,000 confirmed cases out of 10 million cattle
had been recognized.
 1993 - The epidemic seemed to peak around 1,000
new cases per week.
 February 1998 - Total of 172,324 cases were seen
cattle in the United Kingdom.
- Total of 600 cases were recorded in 8 countries
outside U.K with 256 in Switzerland.

53.  Since 1996 - 4.5 cows have been destroyed.
 Between 1986 and November 2003:
 183,634 cattle were diagnosed with BSE in U.K
 4,469 cattle were diagnosed in other 22 countries.
 Around 84 humans death were recorded in U.K in
the year 2000.
 The first case confirmed in:
Countries Year
Japan September,2001
North Africa (cow
in Alberta,
Canada)
May 20, 2003
United States (in
Holstein downer
cow in Mses
December,2003

54.  Around 35 million beef animals
up to age 24 months are
slaughtered annually in United
States. With an additional 6
million of older dairy cows.
 Testing for prion proteins
consists of:
 Immunohistochemistry method.
 Considered to be the gold
standard
 Conformation-dependent
immunoassay (CDI) ; develop in
2003.
 Screening test ; develop by the
Bio-Rad Corporation (TeSeE).
 Herdchek BSE Antigen Test;
develop by IDEXX Laboratories.
 5 to 6 other post mortem test for
central nervous system tissue of
cattle.
Normal cell
brain
Brain with
BSE cell

55. Creutzfeldt-Jakob Diseases
(CJD,vCJD)
 CJD is a degenerative
neurological disorder that is
incurable and invariably fatal.
 CJD is at times called a human
form of mad cow disease.
 CJD normally appears in persons
around age 60 or older.
 In March 1996, new variant of
CJD (nvCJD, vCJD) was reported
in the United Kingdom in a small
group of people, whom were
much younger than individuals
with CJD.
 vCJD was found to afflict
individuals in the late teens to the

56.  It can be concluded that vCJD is the human equivalent
BSE and the agents for BSE and vCJD appear to be the
same.
 Between February 1994 and October 1995
 10 persons in United Kingdom were found to
have new variant form of CJD.
 8 died.
 Most were under age 30.
 For the years 1995-1998 – there were 39 cases of vCJD.
 2003 around 150 vCJD cases were seen in humans
throughout Europe.
 about one-third in the United Kingdom.

57.  For 5 year period ; between 1991-1995 ; in the
United States:
 94 CJD deaths were recorded.
 9 were below age 55.
 None conformed to vCJD.
 Over 85% of CJD patients die within one year of onset.
 The average annual death rate from CJD was 1.2/1
million population.
 Using a mouse assay, prions could not be detected
in beef muscle and milk from infected cattle.

58.  The latter investigator suggested that the brain
tissue of a TSE infected cow can be expected to
contain about 1011 prions per gram.
 The nerve tissue is ground with muscle tissue = 108
prions per gram or 1010 prions in a 100g portion.
 To effect 12D reduction, 22D is required.

59.  Some of the times in minutes needed to achieve a 22D
were calculate as follows:=
 D160
0
C = 1.0
 D140
0
C = 11.0
 D120
0
C = 110.15
 It has been suggested that there is need for new
processing or packaging technologies such as:
 high temperature short time (HTST) treatments be
carried out in order to render products free of prions.

60. Chronic Wasting Diseases
(CWD)
 This is a prion or TSE diseases first detected in
captive mule deer in 1967 in the state of
Colorado.
 Has been diagnosed in wild deer and elk at:
 Wyoming
 Colorado
 Nebraska
 Sasktchewan Province
of Canada

61.  This diseases appears to be
transmitted through saliva or
feces.
 It is estimated that 4-6 % of
mule deer and <1% of free
ranging elk are infected in the
endemic areas.
 Primary system in elk are
emaciation and drooling.
 In December 2003, the U.S
Department of Agriculture put
in place a herd certification
program along with
restrictions on the interstate
movement of captive deer

62. TOXIGENIC PHYTOPLANKTONS

63. Paralytic Shellfish Poisoning
(PSP
 contracted by eating toxic mussels, clams,
oyster, scallops, or cocklesis a saxitoxin .
 saxitoxin exerts through cardiovascular collapse
and respiratory failure
 it blocks the propagation of nerve impulses
without depolarization
 there is no known antidote

64.  heat stable
 water soluble
 generally not destroyed by cooking
 can be destroyed by boiling for 3-4 hours at pH
3.0
 D value at 250◦F (121.1◦C) of 71.4 minutes in
soft-shell clams has been reported
Characteristics of saxitoxin

65.  develop within 2 hours after ingestion of toxic
mollusks
 characterized by paresthesia
 which begins about the mouth, lips, tongue and
spread over the face, scalp, neck and to the
fingertips and toes
 mortality rate is variously reported to range from
1-22%
Symptoms of PSP

66. 1793-1958 o 792 cases were recorded
o 173 (22%) deaths
1973-1987 o 19 outbreaks ( mean=8 cases)
were reported by state health
departments to CDC
1990 o 2 outbreaks (19 cases) in the
states of Massachusetts & Alaska
alone
o 6 fishermen became ill after
eating boiled mussels that
contained 4280 µg/100g saxitoxin
o raw mussels contained 24,400
µg/100g
o max safe level of SPS toxin is 80
µg/100g

67.  occur between May and October on the US
West Coast
 August and October on the US East Coast
 mollusks may become toxic in the absence of
red tides
 detoxification of mollusks can be achieved by
transfer to clean water
Outbreaks of PSP

68.  contracted from ingestion of any 1 of over 300
fish species that feed on herbivorous or reef
fishes
 example: barracuda, sea bass
 which in turn feed on phytoplankton, especially
the dinoflagellates
 Dinoflagellate is Gambierdiscus toxicus
which produces ciguatoxin.This toxin
concentrated more in fish organs such as
liver than in muscle tissue
Ciguatera Poisoning

69.  symptoms occur within 3-6 hours
 consist of nausea and paresthesia about the
mouth, tongue and throat
 the symptoms are quite similar to those for
paralytic shellfish poisoning
Toxic fish

70.  consequence in the absence of appropriate
therapy
 the disease has been associated with farm-
raised salmon fish
Respiratory paralysis

71.  uncommon amino acid that antagonizes
glutamic acid in the central nervous system
 produce by a diatom, Psedonitzshia pungens
and its structure
 causes amnesic shellfish poisoning (ASP)
following the consumption of mussels or
scallops harvested from marine waters with a
bloom of the diatom noted
Domoic Acid

72. Outbreaks1988 o human cases occurred in eastern
Canada
o consumption of mussels from Prince
Edward Island
o 107 victims, 3 deaths
1996 o ASP episode affected scallops in
northwest Spain

73.  first recognized in the early 1990s
 as the cause of death of 1000 of fish in
tributaries of the Chesapeake Bay
 an animal-like organism that produces potent
toxins
 reproduces sexually after a fish kill
 can encyst one toxin stuns fish within a few
second for animal, die within a few minutes
 causes the fish epidermis to slough off
Pfiesteria piscicida

74.  unclear, as their effect on humans
 cause memory loss, confusion, acute skin
burning
 cause general symptoms such as headache,
skin rash, muscle cramps
Identity of toxins