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Campylobacter
Helicobacter
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Vibrio cholerae
Morphology :
- coma-shaped rod
- aerob
- actively motile : single
flagellum polar
- pili
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Colony
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Positive
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Flagellar H antigen
Lipopolysaccharides : serologic specifity
139 O antigen groups :
- Strain O1 & O139 : cause classic cholera
- non O1 & non O139 : causing cholera like disease
Strain O1 : - serotype inaba & Ogawa
- biotype : classic & El Tor (hemolysin + &
resistant polymyxin B)
V. cholerae O139 V. cholerae O1 biotype El Tor
V. cholerae O139 makes polysaccharides capsule, V
cholerae O1 does not
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V. cholerae enterotoxin
V.
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PATHOGENESIS
Vibrio cholerae Ingestion
Adheres to and colonizes
Small-intestinal mucosa
Produces toxin
Cholera toxin acts on mucosal cells
Ekstensive fluid & ion loss from tissues
Leading to hypotention,
Electrolyte imbalance, and death
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Diarhea
CLINICAL FINDING
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V. parahaemolyticus
Halofilic
Acute
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CAMPYLOBACTERIACEAE
a.
. Optimum
temeperature 36-37C
. Culture on 42C (inhibit others feces bacteria)
. LPS (lipopolisaccharida) with endotoxin activity.
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Campylobacter jejuni
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Transmition
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d.Helycobacter pylori
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STAPHYLOCOCCUS
NEISSERIAE
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Cocci
Gram
Positive
Staphylococcus
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Negative
Streptococcus
Neiserriae
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Gram-positive Cocci
Staphylococcus
Streptococcus
Grapelike cluster
- Chain and pair
- Catalase +
- Catalase .
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STAPHYLOCOCCUS
CHARAKTERISTIC :
Cells : spherical
Arrangement : irregular cluster (grapelike)
Gram +
non motile
Lack of spores and flagel
May be encapsulated
aerob/ microaerofilic
Optimum temperature 370C
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Staphylococcus
aureus
Virulent factors :
1.
Capsular polysaccharides : promote the adherence to host cells
2.
Pentidoglycan and teichoic acid : adherence to mucosal surface
3.
Protein A : interfering opsonizations and ingestion by polymorphonuclear
cells
4.
Catalase : differentiated them from Streptococcus
2H2O2
2H2O
+
O2
5.
Coagulase : convert fibrinogen to fibrin which coat bacteria with fibrin
prevent opsonizations.
6.
Hyaluronidase : dygest connective tissue of the host
7.
Staphylokinase : dygest blood clot (beku
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8.
9.
10.
11.
12.
13.
14.
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Others Staphylococcal
S. Epidermidis : normal habitat skin and mucous
membranes
S. Homini : skin areas rich in apocrine glands (kel.
Keringat)
S. Capitis : scalp, face and external ear
Infections
barrier
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NEISSERIA
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NEISSERIAE
.
.
.
.
.
.
.
.
.
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Characteristics :
Gram negative
Cell : bean-shape and paired (diplococcus)
Non-motile
Capsule : pathogen Neisseria, pili
Koloni : konveks, shinny, mukoid
Aerobic or microerophilic
Oxsidase +
Ferment carbohydrates producing acid, no gas
Pathogen intracellular
Yulia Tanti Narwati (Departemen Mikrobiologi)
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Antigenic Structure :
Pilin : attachment to host cell, resistance to phagocytosis.
Por : occurs in trimers to form pore in the surface through
which nutrient enter the cell
Opa : adhesion cell within colony and
Rmp (reduction modifiable protein) : associated with Por to
form pore on cell surface
Lopooligosaccharide (LOS) : avoid immune recognition (
glicosphyngolipid on human membrane cell).
Others protein
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Pathogenesis :
Gonococcus attack mucous membrane or genitourinary
tract, eye, rectum and throat
Acute supuration (penanahan akut)
Tissue invation
Chronic inflammation and fibrosis
In males : urethritis with yellow creamy pus & painful
urination
In female : primary infection endocervix --- salpingitis
(radang sal. telur), fibrosis
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Neisseria meningitidis
(meningococcus)
Antigenic structure :
.
.
.
.
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Pathogenesis
Portal of entry : nasopharynx
Attach to epithelial cell (pili)
Enter the blood stream (bacteremia)
Spread: arthritis, meningitis etc
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Laboratory Diagnose :
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VIRUS
1.
2.
3.
4.
5.
6.
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ORTHOMYXOVIRIDAE
PARAMYXOVIRIDAE
RUBELLA
ADENOVIRIDAE
VIRUS RABIES (RHABDOVIRIDAE)
SLOW VIRUS INFECTION & PRION
DISEASES
Yulia Tanti Narwati (Departemen Mikrobiologi)
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