Download - Klostridit 2011 Eng
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Clostridia
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Clostridia
Large Grampositive anaerobic rods
Form of spores resistant to oxygen, drought,
freezing and cooking temperatures
The soil and in the intestines of warmblooded
Cause the food, the environment and the points of
through drug poisoning and infectious
the toxininfections
Page 3 A. Clostridium botulinum
1. The classic botulism
2. The infant botulism
3. The wound botulism
B. Clostridium perfringens
1. The classic food poisoning
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2. enteritis necroticans
C. clostridium tetani
1. Tetanus
D. Clostridium difficile
1. Clostridium difficile assossioitunut diarrhea (CDAD)
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A. Clostridium botulinum
1. Classical botulism
Food poisoning, the risk of food products, especially meat, fish, vacuum packed
Products and preserved home products
Clostridium botulinum secretes proteiinieksotoksiinia, which is the strongest
known as toxic (lethal dose: 0.1 ng / kg)
Neurotoxins are synthesized as an inactive polypeptide, i.e.,
protoksiineina (size 150 kDa), which are activated when the protease cleaves
polypeptide chain
C. botulinum are classified into seven serotypes AG during growth
on the basis of the antigenic characteristics of their production of toxins types A,
B, E and F cause botulism people
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A few other klostridilajit (C. butyricum, C. Barati) to produce
the same toxins as C. Botulinum
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Functional form of botulinum toxin can bind
nerve muscle joints and prevents the neurotransmitter
release of vesicles containing acetylcholine. Since
the muscle may no longer be any kind of messages to the nerve cells, muscle
paralyzed.
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the toxin is absorbed in the stomach and small intestine, from where it
spreads throughout the body, can also be absorbed by inhalation
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Symptoms begin 1236 hours after ingestion of food
The first botulism symptoms include fatigue, weakness,
vomiting, then voice and difficulty in swallowing and visual disturbances
Respiratory depression can ultimately lead to death
Mortality of the disease is about 65%, in developed countries is 10%..
Risk group: dangerous for everyone
Even one person's illness botulism epidemic is interpreted
a serious disease Due to the nature of the
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2009
In early September, it was found in France in three at the same
the family of a person who is Clostridium botulinum
botulism caused by bacteria, the suspected source
Purchased from Finland to hotsmoked whitefish. Vacuumpacked fish
was purchased in Eastern Finland in retail trade in August
At the end, transported by plane to France
and by a private individual eaten two weeks
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later on the last day of use. Journey, the fish
had been stored in a cool box
unknown temperature for 14 hours and then
After the home refrigerator. Before eating fish is not
was heated.
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2006
Clostridium botulinum caused in July 2006 for one
epidemic, which contracted by two persons of the same
family. The vehicles were
likely to be hotsmoked whitefish, which was purchased
packed in a local supermarket. Fishfinal
date was weeks away syömisajankohdasta. Fish
the country of origin was Canada, it was delivered to Finland
frozen. Defrosting and smoking, as well as the finished product
packaging took place in a domestic establishment.
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Older epidemics
1981 two German tourists got sick after eating
säilykemaksapasteijaa
1999 one person ill with whitefish roe
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Botulism treatment:
ABE trivalent antitoxin (given before symptoms
the start)
Gastrointestinal tract is cleared
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Missed the gut bacteria are destroyed penicillin
Artificial respiration
Forecast the worse the sooner the symptoms appear
Recovery may take months
Waiting for new nervemuscle junctions formation
Small doses of purified botulinum toxin can be
use of CNS lihaston dysregulation,
in the treatment of diseases, the cosmetic use of biological
warfare
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2. The infant botulism
C. botulinum produces toxin in the baby's gastrointestinal tract (n. 80
spores / g)
Risk foods honey, vegetables and fruits
Less than half years more likely to get infant botulism;
immature intestinal flora, and a higher pH in the digestive tract
allow bacterial spore growth and yield of the toxin in the gut
Symptoms of constipation, muscle slackening, weeping sluggish
The symptoms are surprisingly mild, and mortality only a few percent,
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causing sudden infant death syndrome
Power of treatment is usually rescued
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3. The wound botulism
C. botulinum spore's wound, where they germinate
The disease resembles tetanus
The use of injecting drugs
Cases detected in the Americas, Europe, rare
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Clostridium botulinum
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• task analysis in mice
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Clostridium botulinum
PCR / PFGE / ELISA
M. Lindström Finland, studied the method:
käytettään primeriparia 4, which are
specific neurotoxins botulinum toxin A, B, E or
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F. Four serotype simultaneous detection
possible.
ELISA ready for a day when the toxin in the sample
A viable cell growth and toxin
generating identification of genes by PCR
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B. Clostridium perfringens
1. The classic food poisoning
C. perfringens Type A enterotoxin secreted last
years, the most commonly reported cause of food poisoning
In Finland
The risk of foodmeat and fish, incompletely cooked,
slowly chilled, at too high a temperature, stored and
incompletely cooked foods
Causing disease dose of 10 ^ 6 to 10 ^ 8 cells
The incubation period of 824 h
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C. perfringens cells increase in food, some of the cells die of the stomach
acidity, but some cells remain alive in the small intestine, where
they begin to proliferate
When the bacterial cell itiöi, consists poisoning causing CPE
enterotoxin, if the position is cpe gene encoding it (only 5%
strains)
CPE toxin damage the surface of the epithelial cells of the small intestine
by making holes in the cell membranes to small molecules such as anions,
cations and organic acids leak out
Symptoms of abdominal pain, nausea and intense diarrhea that last for 1 to 2
days, the elderly C. perfingens can cause persistent diarrhea
Enterotoxin can be demonstrated in faeces
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2. Enteritis necroticans (pigbel)
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Clostridium perfingens Type C secreted by β
enterotoxin can cause severe enteritis
necroticansin (necrotizing inflammation of the bowel)
The bacteria secrete a toxin from the food, which
lead to paralysis, haematomas and regional
necrosis, especially in the small intestine
Symptoms: vomiting, diarrhea, abdominal pain Hard,
hemorrhage
Rare
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Clostridium perfringens
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Clostridium perfringens plating
TSC Agar (Tryptose Sulfite
Cycloserine Agar)
to produce black colonies
cycloserine to prevent other bacteria
growth
In addition to kanamycin and polymyxin
inhibition of bacterial flora
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TSC
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Clostridium perfringens PCR and microarray
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Microarray technology with antibodies
Identification of C. perfingens toxins
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C. Clostridium tetani
1. Tetanus, or lockjaw
C. tetani produces two poison, and tetanoslysiinia
tetanospasmiinia, of which the latter is said to
tetanus toxin
Tetanus neurotoxin, and the second strongest poison
After botulinum toxin
The bacteria can come into the wound, where it begins to increase
under anaerobic conditions
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Infection is local, but the toxin spreads
via the bloodstream and lymph circulation, as well as directly to the
the nerve fibers along the spinal cord and brain stem
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toxin affects the central nervous system
hermosynapseihin and motor
end plates, blocks the inhibitory
neurotransmitters (e.g. glycine)
release, wherein the muscle
is prevented and the relaxation of the
muscle spasms
The incubation period of days to months
At the beginning of muscle spasms of the wound
close, spreads to the muscles of the jaw and
all parts of the voluntary muscles
Tetanus leads
if untreated, is almost always
death, manicured mortality
1030%
Prevented through vaccination
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Clostridium tetani
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C. tetani penetration
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Clostridium tetani determination
Genetically IgG ELISA IgG class are determined
antibodies
Mouse Test
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Clostridium tetani, the Mouse test
The left hind leg of the mouse injected
Tetanus toxin
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Clostridium difficile (40006000 cases / yr)
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Insulation CDS (C. difficile
SELECTIVE) agar containing a Dcycloserinia and
Cefoksitinia
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Clostridium difficile
Clostridium difficile associated diarrhea
(CDAD)
Diagnostic tests for CDAD: in
the determination of the market. They
of toxin B (CytoTox assay)
or toxins A and B (immunoassay)
the genetic analysis.
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Page 33Quick Test: Clostridium difficile Toxin A detection
of C. difficile toxin A in faeces with
Rapydtest®
10 15 min.
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Sources:
Austin, JW and Dodds KL 1997. Clostridium botulinum. In: Food Microbiology. ASM Press. Pages288304.Hielm, S. clostridia, the quiet. In: M. Salkinoja Salonen (ed.). Microbiological criteria. Microbiologypublications 49/2000.Microbiology Department of Applied Chemistry and Microbiology, University of Helsinki. Pages 652655.
SagittariusSomer, H. and Ristola, M. 2003. Clostridium species. In: P. Huovinen (ed.).Microbiology andinfectious diseases. Book 1. Duodecim Medical Publications. Pages 228236.
Madigan, MT 2003. Brock Biology of Microorganism. Pearson Educational.
Guide microbiological food and drinking water hazards. Evidential EELAOpas 1/2003. Pages 3744.
McClane BA in 1997. Clostridium perfringens. In: Food Microbiology. ASM Press. Pages 305326.
SalkinojaSalonen, M. clostridial toxins. In: M. Salkinoja Salonen (ed.). Microbiological criteria.Microbiology publications 49/2000.Division of Microbiology, Department of Applied Chemistry and Microbiology, HelsinkiUniversity. Pages 548549.
Pictures:
http://www.agen.ufl.edu/chyn/age2062/lect/lect_25/FG19_012.GIFhttp://wwwuser.gwdg.de/hbruegg/ct/tetanus2.gifhttp://www.agen.ufl.edu/chyn/age2062/lect/lect_25/FG19_011.GIF
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Fountains
Lindström, Miia; Keto, Riikka; Markkula, Annukka; Nevas, Mari; Hielm,
Sebastian; Korkeala, Hannu. Multiplex PCR Assay for Detection and
Identification of Clostridium botulinum toxin Types A, B, E, and ... & Applied
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Environmental Microbiology, Dec 2001, Vol. 67 Issue 12, p5694, 6p, 4
charts, 1bw; (AN 6063605)
http://www.cfsan.fda.gov/ebam/bam 17.html
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