TOXICOLOGY ON FISHERIES
PROCESSING– 3 (2 – 1)
DISEASE CAUSED BY MICROORGANISMS (1
stmeeting)
EKO SUSANTO – DIPONEGORO UNIVERSITY
EKO SUSANTO
Study Program of Fisheries Processing Technology
Diponegoro University
REFERENCES:
Peck, M.W., 2010.
Clostridium botulinum
. Edited by: Juneja,
K.V., and Sofos, K.N. Pathogens and Toxin in Food: challenges
and intervention. ASM Press. Washinton DC.
Juneja, K.V., Novak, J.S., and Labbe, R.J, 2010.
Clostridium
perfringens
. Edited by: Juneja, K.V., and Sofos, K.N. Pathogens
and Toxin in Food: challenges and intervention. ASM Press.
Washinton DC.
Beauchamp, C.S. and Sofos, J.N. 2010. Diarahegenic Eschericia
coli. Edited by: Juneja, K.V., and Sofos, K.N. Pathogens and Toxin
in Food: challenges and intervention. ASM Press. Washinton
DC.
Seo, K.S. Bohach, G.H., 2010. Staphylococal Food Poisoning.
Edited by: Juneja, K.V., and Sofos, K.N. Pathogens and Toxin in
Food: challenges and intervention. ASM Press. Washinton DC.
Wright, A.C. and Sceneider, K.R. 2010. Pathogenic vibrios in
seafood. Edited by: Juneja, K.V., and Sofos, K.N. Pathogens and
Toxin in Food: challenges and intervention. ASM Press.
Washinton DC.
REFERENCES: CONTINUE
Amastrong, G.D. 2008.
Pathogenic Mechanisms of the
Enterohemorrhagic Escherichia coli—Some New Insights.
Edited
by: Wilson, C.L. Microbial Food Contamination 2
nded. CRC
Press. Boca Raton.
Nilsson, L. and Gram, L. . 2002. Improving the control of
pathogens in fish products. Edited by: Bremmer, A.H.
Safety and quality issues in fish processing.
CRC Press.
Boca Raton.
WHO-FAO. 2005.
Microbiological risk assessment series: Risk
assessment of
Vibrio vulnificus in raw
oysters interpretative
summary and technical report. WHO-FAO UN.
Garbutt, J. 1997. Essentials of food microbiology. Arnold.
London.
Pelczar, M.J. & Chan, E.C.S. 1976. Dasar-dasar mikrobiologi.
Diterjemhakan: Hadioetomo et al., 1988. UI press.
Huss, H.H. 1994. Assurance of seafood quality. FAO fisheries
LECTURE
RULES
The lecture will be taken place during 4 meetings
10 minutes after lecturer starting lecture. Students
are prohibited to get in class.
If the lecturer is late 10 minutes after the start of
lecture time without confirmation to students, the
students are permitted to leaving class.
Final score consist of 35 % tasks and 65 % of final
examination
The students have to attend lecture 75 % minimally.
The lecture consist of class lecture and self study.
The students are permit to get out class during
lecture if they don’t want to joining lecture.
Eko Susanto – Diponegoro University
4
MATERIALS
1
st
meeting : bacteria toxins in food.
2
nd
meeting :
Clostridium botulinum
toxin
toxin, Staphylococcus aureus toxin,
Eschericia coli toxin.
3
rd
meeting : Vibrio toxin, Pseudomonas
cocovenenans toxin, Fungal toxin
(Penicillium).
4
th
meeting : Presentation
5
QUESTIONS
How do we know if food is being
contaminated by bacteria?
Please mention bacteria which cause
food borne?
What are the differences between
endotoxin and exotoxin?
Please answer those questions for 10
minutes.
Kerjakan selama 10 menit
6
INTRODUCTION
Food-borne diseases are of major concern to consumers, producers
and authorities alike.
Despite an increased awareness, the number of cases and outbreaks
does not appear to be decreasing.
Many foods are implicated in food-borne disease outbreaks.
Seafoods rank third on the list of products which have caused
food-borne disease.
Seafoodborne disease may be caused by a variety of agents, including
aquatic toxins, biogenic amines, bacteria, virus and parasites.
Bacteria are mostly found in low numbers in live fish with the exclude
of marine vibrios.
Marine vibrios, such as
V. parahaemolyticus and V. vulnificus, may be
found in high numbers in shellfish and in shellfish-eating
fish from
tropical waters and during the summer months in temperate zones
DEFINITION
Disease any harmful change in the tissues
and/or metabolism of a plant, animal &
human that produces the symptoms of
illness.
Pathogens MO that cause disease.
Toxin chemical substances produced by MO
that are harmful to human tissues and
physiology.
Food poisoning an acute (arising suddenly
and of short duration) gastroenteritis caused
by the ingestion of food
THE NATURE OF FOOD SPOILAGE
Major reasons 4 food being rejected:
Organoleptic changes growth MO
Chemical changes in food
Physical damage
Freezer burn
‘staling’ changes Aw
Ripening
Presence of foreign materials
FACTORS THAT CAUSE BACTERIA
GROWTH
Internal factor (
Aw, pH, redox potential,
nutrition, natural antibacteria, biology structure
)
Processing factors (
hot treatment, irradiation,
pasteurization, grinding
)
External factors (
environment, temperature
)
Implicit factor (
compt become dominant)
Factors of food
INTERACTIONS INVOLVED IN THE SELECTION OF
SPOILAGE MICROFLORA
Extrinsic factor
Extrinsic factor
Contaminating
microflora
Contaminating
microflora
Implicit factors
Implicit factors
Intrinsic factors
Intrinsic factors
Growth of specific
spoilage microflora
Growth of specific
spoilage microflora
Spoilage symptoms
Spoilage symptoms
Interaction
Source: Garbutt, 1997
MO CHANGES ON STORED FOOD
0 1 2 3 4 5 6 7 8 9 10
0 20 40 60 80 100
Bakteri gram (-) Bakteri gram (+)
MO CHANGES ON STORED FOOD ON COLD TEMPERATURE
0 1 2 3 4 5 6 7 8
0 20 40 60 80 100
Bakteri gram (-) Bakteri gram (+)
SOURCES OF CONTAMINATION OF
FOOD
Raw material with
natural micro flora
Raw material with
natural micro flora
Air
Diseased plants &
animals
Diseased plants &
animals
Packaging
materials
Packaging
materials
Pests
Pests
Humans
Humans
Sewage
Source: Garbutt, 1997
Natural surface & gut flora of fish
Water & possibly sediment from natural habitat
Fishing nets
Surfaces on board the fishing vessels
Fish boxes
Ice / refrigerated sea water
Human resources
Pests
Soil
COMPOSITION OF CONTAMINATING
MO
Gram-negative rods & coccobacilli.
Acinetobacter, aeromonas, Alcaligenes, Citrobacter,
Enterobacter, Escherichia, Flavobacterium,
Moraxella, Proteus, Pseudomonas, Salmonella,
Shewanella, & Yersinia
Gram positive rods
Bacillus, Brochothrix, Clostridium, Corynebacterium,
Lactobacillus, & Listeria
Gram negative cocci
PATHOGENESIS OF FOODBORNE &
RELATED ORGANISM
Skeletal muscle :
Trichinella spiralis
Stomach
:
Helicobacter pylori
Liver
:
Clonorchis
Small intestine :
Astroviruses
,
Bacillus cereus
,
Campylobacter jejuni
,
Clostridium
perfringens
,
E. coli
,
Salmonellae
,
S.typhi
,
Vibrio cholerae
,
V.parahaemolyticus
Large intestine/colon :
Campylobacter
(small intestine),
E.coli
,
Entamoeba histoytica
,
Salmonella
eneritidis
,
Shigellae
, especially
S.
dysenteridae.
CHANGES IN FOODS CAUSED BY SPOILAGE MO
General appearance
moldy (F) & slimy (B)
Color
F (red/black) & B (colored); chemical
changes --> greening of meat (H
2
S)
Texture
Pseudomonas fluorescens
at fish -->
prod proteinase caused tissues to soften
Odor / flavor
MO prod chem. associated with
metab. act.
A mixture of the above
HOW DO MO CAUSE DISEASE?
1. The permanent Mo is essential in combating
invasion of the body by potential pathogens
by competing 4 space & nutrients, stms
producing antibiotics. Ex: E.coli prevent
salmonellae in the colon
2. Bacteria in the colon synthesize vit. K &
contribute significantly to our req. of protein
DISEASE PRODUCTION BY MO
Exotoxin:
toxin is secreted
by MO into the cell
environment
Endotoxin:
toxin is produced
by MO & secreted
if the MO cell
being damaged.
Sifat
Exotoxin
Endotoxin
MO
gram (+) & gram
(-)
gram (-)
Source
protein
lipopolisakarida
ketahanan panas
Inactive at 60 - 80
oC, exclude sev
exotoxin
stabile at
sterilization
temp
Lethal dose
rendah, sangat
toksik
> tinggi
eksotoksin
cara kerja
Spesifik untuk
sel/tenunan sel
< spesifik
EXOTOXIN
Characteristic:
1.
Generally proteins
synthesized by
metabolic activity.
2.
Produced by
positive &
gram-negative organism.
3.
No structural
components of the
cell
4.
Secreted into the
cell environment.
Exotoxin
Exotoxin – soluble protein
released into environment
by active cell
Enterotoxin
Enterotoxin
Neurotoxin
Neurotoxin
Affects the gut Affects the nervous system
ENDOTOXIN
Characteristic:
1.
Lypopolysacharid
es.
2.
Toxic components
of the cell wall
released when
the cell dies &
Fever Toxic
shock Rash Inflammation of organ
Endotoxin
Lipopolysaccharide in outer wall layer
FOOD POISONING
Food poisoning an acute (arising suddenly and of
short duration) gastroenteritis caused by the
ingestion of food (Garbutt, 2007).
Gastroenteritis is characterized by:
Abdominal pain;
Diarrhoea
With / without vomiting
With / without fever
Bacteria caused food poisoning:
S. aureus, C.
perfringens, C.botulinum,
&
Bacillus cereus
.
INTOXICATION &
INFECTION
INTOXICATION
Intoxications involve
food poisoning in
which the organism
grows in the food &
releases a toxin from
cells.
Toxin is ingested
along with the food,
toxin gives rise to the
food poisoning
syndrome.
Bacteria toxins that
produce intoxication
are
exotoxins. S
aureus & C
botulinum
Active organism secretes exotoxin (enterotoxin ) into food
Active organism secretes exotoxin (enterotoxin ) into food
Food eaten
Food eaten
Enterotoxin affect gut giving gastroenteritis
Enterotoxin affect gut giving gastroenteritis
Enterotoxin affect gut giving gastroenteritis
Enterotoxin affect gut giving gastroenteritis
INFECTIONS
Infection involve
food poisoning
caused by ingestion
of live organism when
the organisms grow
in the gastrointestinal
tract to produce the
disease.
Most food poisoning
caused by infection.
Ex.
Salmonella
spp &
C. perfringens
Organism ingested along with food
Organism ingested along with food
Dose sufficient to overcome host
defenses
Dose sufficient to overcome host
defenses
Organism grows in the host gut
Organism grows in the host gut
Organism affects gut giving
gastroenteritis
Organism affects gut giving
gastroenteritis
Organism appears in faeces in large
number
Organism appears in faeces in large
number
PHYSIOLOGICAL MECHANISM ASSOCIATED WITH FOOD
POISONING (GARBUTT, 1997)
NORMAL GUT PHYSIOLOGY
ENTEROTOXIN INGESTED WITH
FOOD
Vomit
Enterotoxin affects vomit receptors
H2O out Na+ out
