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Mekanisme System

Immun Sal. Cerna

Oleh :

Efrida Warganegara
Introduction
Microoragnism (parasites or pathogens)
where their presence in the body is
often associated with pathological
changes and they are rarely found in
healthy individuals identification of
these m.o. is important indication of
actual or potential disease state
The other organisme (in this chapter)
may cause diasease under certain
circumstances :
a) Newborn; b) Stressed; c)
Traumatized, or
Introduction
Many of m.o. this form what is
termed the indigenous or
normal flora of the body, a
collection of spesies routinely in
the normal, healthy individual
Some of this species are
positively benefecial to the host
M.O. that benefit from this
association without harming the
host are referred to as
Introduction
Term flora is used because the majority
of the m.o. are bacteria.
Antibiotic therapi can eliminated normal
flora, but is not possible to eliminate the
normal flora of the skin or intestine
antibiotica can drastically reduce their
number to a minimum
The host may then be overun by
introduce patogens or by overgrowth of
m.o. normally present in small number
Commensalism
The normal flora (commensals) is aquired
rapidly during and shortly after birth and
changes continously throughout life.
It has been estimated that human have
approximately 1013 cells in the body and
something like 1014 bacteria associated
with them, the majority in the large
bowel.
Virus, fungi and protozoa can also be
found in healthy individuals, although
these form only a minor component of
the total population or resident organism
Commensalism
Before birth the fetus is
essentially in a steril
environment, but at delivery m.o.
come into contact with the infant
Some of these m.o. are derived
from the mother or others who
come into contact with the infant
Constituent organism present at
any given time reflect the age,
nutrition and environmet of the
Commensalism
Most m.o. are transient paserby that are
destroyed by conditions in the host, but others
establish themselves and produce
microcolonies colonized the host
microflora established
Not all area of the body are occupied by
commensal spesies
There are appreciable numbers of m.o. in the :
Upper Resp. Tract, lower intestinal tract, and
skin
Esophagus, urinary tract and stomach contain
few m.o.
The blood, spinal fluid, urine and endothelial
tissues are normally steril
Commensalism
Microfloraremain with the host for life, with
only minor changes resulting disease,
diatery alteration, or hormonal changes
Thefactors that influence the kind and
number of m.o. at any body site are :
1. The availabiliy or unavailability oxygen
2. The availability of appropriate receptor
sites for attachment
3. The pH of the host site
4. The availability of nutrient
5. The influence exerted by other m.o. at
the site, and
6. The immunological respone of the host to
Advantages of Flora
Normal
Many of the flora normal may be important in
maintaining the health of the host, for
example :
1) some m.o. in intestinal capable sinthesizing
vitamin (pathothenic acid, riboflavin, B12, vit.
k) certain vitamine deficiencies in human
diet can be remedied by bacterial vitamin
synthesis in the inteswtinal tract ;
2) some flora normal produce metabolic
product that are effective in preventing
invasion by parasites (flora normal in intestinal
tarct produce fatty acid that inhibit ingested
bacteria that attempt to colonize the host
Advantages of Flora
Normal
3) Gut bacteria release a number
of factors with antibacterial
activity (bacteriocin, colicin) and
metabolic waste product, which,
together with lack of available
oxygen, prevent the
establishment of other species
4) Vaginal lactobacilli maintain an
acid environment that
supresses growth of other
organism
Disadvantages of Flora normal
Disadvantages of Flora normal lie primarily
in the potential for spread into previously
streile parts of the body.
This may happen under a variety of
circumstance : when intestine perforated or
skin is broken, during extraction of teeth, E.
coli from the perianal skin ascend the urethra
Overgrowth by potentially pathogenic
members of the normal flora can occur
when the composition of the flora normal
changes (after antibiotics), when the local
environment chabges (increases in stomach
or vaginal pH) or when the immune system
becomes ineffective (AIDS)
Under these conditions, potential pathogens
A). Distibution of flora normal
Commensals in Intestinal
Tract
Many m.o. can enter the intestinal tract
by ingestion of food and drink
The density of m.o. increases as one
passes along the GIT from stomach to
the large intestine
Stomach contents harbour only
transient organism, the acidic pH
providing an unfavorable environment
and forming an effective barrier.
However, the gastric mucosa may be
colonized by acid tolerant lactobacilli
and streptococcus
Commensals in Intestinal
Tract
The upper intestine is only lightly
colonized (104 organism per gram) but
population increase markedly in the
ilium, where streptococci, lactobacilli,
enterobacteria and Bacteroides spp.
may all be present
In the large bowel bacterial number are
very high (estimated at 10 11 per gram)
and many different species can be
found. The vast majority (95-99%) are
anaerobes, Bacteroides being especially
common and a major component of
fecal material
B). Commensals in Intestinal
Tract
Helicobacter
pylori

Oleh :

Efrida Warganegara
Introduction -- Classification
Campylobacter spp. are curved
or S-shaped, Gram negatif
rods, oxidative-positive,
nonsporeforming, micro-
aerophilic, motile by lopotrichous
flagellum from 1950s until
1970s they not recoqnized as a
common human pathogen
Today, Genus Campylobacter is
recoqnized as one of the causes
Introduction -- Classification
One of species : Campylobacter
pylori, in the last 10 years then
transfferred to the new genus / now
reclassified as Helicobacter pylori
is an important cause of gastritis
and gastric/duodenal ulcers
Helicobacter pylori was first
isolated from human gastric
mucosa in 1983
The mechanism of pathogenicity
Pathogenesis
The organism appears to be spread
by close familial contact but the
route of transmission is nor known.
The incidence of infection
increases after the age of 7 years
The pathogenic mechanism of
helicobacter pylori are as yet
poorly defined
The organism colonized only
Pathogenesis
The organism produces urease and it
has been postulated that this
compound acts as a protective device.
Ammonia is a product of urease
activity and it could protect the m.o.
from stomach acidity
High concentration of ammonia
produced by large numbers of bacteria
could also be responsible for the
inflamatory condition in the stomach
Chronic inflammation often remains
Pathogenesis
Helicobacter pylori can colonize the
duodenum as well as the stomach and
may be responsible for peptic ulcer.
Several studies have pointed to an
association between Helicobacter pylori
and carcinoma of the stomach
When individuals with peptic ulcer are
treated with acid-reducing therapies,
there is temporary cure
Once the treatment is stopped, the ulcers
reappear in about 70 percent of patients
If these individuals are later treated with
Diagnosis
Diagnosis is usually ;
1. made on the basis of
stained, culture, histological
examination of the biopsi
spesimen for the presence
of bacteria, or
2. detection of urease
Specimen collection and
Processing
Collection by gastric biopsy transported
immediately to the laboratory in sterile
saline solution, processed by grinding, and
plated without delay.
Ifshort delayed are expected, the specimen
can be keep at 4oC without a significant loss
in viability of Helicobacter pylori.
Ifmore than 6 hours is required before
processing of the specimen, Stuart transport
medium has been shown to increase survival
of the organisms for up to 48 hours,
especially if storage temperatures are below
15o C
Growth Requirements
To isolate Helicobacter pylori,
biopsy specimen should be
inoculated onto choccolate
agar, incubated as for enteric
campylobacter at 37o C, and
examined daily for 5 days.
The ideal selective medium
not yet been develop.
Several laboratorium have had
success utilizing Skirrow
Growth Requirements
Regardless of the medium
utilized, Helicobacter pylori grows
best on fresh, moist media in a
humid environment
Cultures for Helicobacter pylori
should be placed in an
environment with increased
humidity
A wet paper towel added to the
jar or bag is helpful
Cultural Characteristic
Helicobacter spp. are Gram-negative
rods, which , in addition to appearing
like campylobacters, can be straight
cells
Their
size is also similar to the
campylobacters
Two of the spesies, H. cinaidi and
H.fennelliae, are motile by means of a
single polar flagellum, Helicobacter
pylori is usually lopotrichous
Coloniesare 1 to 2 mm in diameter,
smooth, convex, and transluscent
Biochemical Identification
Helicobacterpylori can be identified
presumptively by oxidase activity , and
the presence of strong urease activity,
and urea hydrolysis.
The organism produce large amounts of
urease, probably a useful strategy for
survival in the acid environment of the
gastric mucosa
InChristensen medium a color change is
usually observed in as little as10
minutes
Serologies
Serological diagnosis may in
future play a valuable part in
investigation of patients
thereby avoiding invasive
procedures
ELISA is the most common
serological test and can be
used to monitor eradication of
helicobacter pylori.
Treatment
Treatment with combination of
bismusth salts with metronidazole
or tinidazole with amoxicillin or
tetacyclin, is successful but relapse
is common
At present the epidemiology of
Helicobacter pylori is unknown and
it is impossible to distinguish
between relaps due to the failure of
treatment to eradicate all organism
Daftar kepustakaan
Mims
Boyd
Barbara J Howard
Microorganism causes of
Gastro-Intestinal Infection

Oleh :

Efrida Warganegara
Introduction
A wide range of microbial
pathogens is capable of
infecting the gastrointestinal
tract and the important
bacterial and viral ones are
listed (Fig. 1)
They are aquired by the fecal-
oral route, from faecally-
contaminated food, fluids or
Introduction
Bacteria or viral are aquired
by the fecal-oral route, from
faecally-contaminated food,
fluids or fingers.
Infection associated with
consumption of contaminated
food is often termed food
poisoning, but food-
Introduction
True Food poisoning occurs after
consumption of food containing
toxins; these may be chemical
(heavy metal); or bacterial in origin
(from Clostridium botulinum or
Staphylococcus aureus)
The bacteria multiply and produce
toxin within contaminated food
The organism may be destroyed
during food preparation but the
Introduction
In Food-association infection, the
food may simply act as a vehicle
for the pathogen (e.g.
Campylobacter) or provide
condition in which the pathogen
can multiply to produce numbers
large enough to causes disease
(e.g. salmonella)
For infection to occur, the
pathogen must be ingested in
adequate number and/or posses
Introduction
Here they remain localized and
causes disease as a result of
multiplication and / or toxin
production, or they may invade
through the intestinal mucosa
to reach the lymphatics or the
bloodstream - fig. 4
Thedamaging effects resulting
from infection of the GIT are
ea
I. Diarrhoeal Disease
Infection of the GIT range in their
effects,
from : - Mild diarrhoea
- Self-limited diarrhoea
- Sometimes fatal diarrhoea
There may be associated vomiting, fever,
and
malaise.
Diarrhoea is the result of an increase in
fluid and
electrolyt loss into the gut lumen,
I. Diarrhoeal Disease
Many cases of diarrhoea disease go
undiagnosed because : 1) mild and self-
limiting, and 2) patient does not seek medical
attention, because medical and lab. facilities
are unavailable, particularly in developing
country.
However, information on the patients recent
food and travel history and macroscopic and
microscopic examination of the faeces and
pus may provide helpful clues
Diagnosis laboratorium especially important
in outbreaks, because of the need to
appropriate epidemiological investigation and
control measures
GIT Infections
I. Diarrhoeal Disease
I. Bacterial causes of Diarrhoea
2. Antibiotic-associated Diarrhoea
3. Viral Diarrhoea
4. Food Poisoning

II. Systemik Infection Initiated in


the GIT
1. Enteric Fever (Typhoid and
Paratyphoid)
Terima
Kasih

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