2. Introduction
• The name, Acinetobacter, comes from the
Latin word for "motionless," because
they lack cilia or flagella with which to
move.
• Have 32 species, A. baumanii and A.
lwoffii have greatest clinical importance.
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3. Introduction
• Most species are not significant sources of
infection. However, one opportunistic
species, Acinetobacter baumannii, is
found primarily in hospitals and poses a
risk to people who have supressed
immunity.
• >2/3 of Acinetobacter infections are due to
A. baumannii
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9. Biochemical Profile
• Both A.baumennii and
A.lwofii are Catalase
positive and Oxidase
Negative.
• A.baumennii ferment
glucose, xylose and
lactose but A.lwofii
cannot ferment.
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10. Rapid Detection
• Rapid detection of Acinetobacter can be
done by RapID ONE Panel (remel) and
Api 20 E strips. These can differentiate up
to species level.
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11. Molecular Detection
• A.baumennii and A.lwofii can be detected
by PCR.
• recA specific primers are used to detect
recA gene in A.baumennii, giving a 382 bp
fragment
• est specific primers are used to detect est
gene in A.lwofii, giving a 309 bp product.
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12. Pathogenesis
Opportunistic pathogen…
Survive under dry conditions
Virulence Factors
• Polysaccharide capsule, prevent complement
activation, delay phagocytosis
• Fimbriae (adhere to human bronchial epithelium)
• Pilli (colonization of environmental surface to form
biofilms)
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13. Transmission
• Acinetobacter can
be spread from
person to person
(infected or
colonized patients),
contact with
contaminated
surfaces of exposure
to the environment.
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14. Antibiotic Resistance
• Acinetobacter species
are capable of
accumulating multiple
antibiotic resistance
genes, leading to the
development of
multidrug-resistant or
even panresistant
strains.
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15. Antibiotic Resistance
Mechanisms
• Antibiotic-altering enzymes (beta-lactams,
carbapenems, aminoglycosides)
• Reduced outer membrane porin expression
(beta-lactams, carbapenems)
• Altered penicillin-binding proteins (beta-
lactams, carbapenems)
• DNA gyrase and topoisomerase IV
mutations (quinolones)
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16. Treatment
• Multidrug-resistant A. baumannii is a
common problem in many hospitals. First
line treatment is with a Carbapenems
antibiotic such as imipenem, but
carbapenem resistance is increasingly
common. Other treatment options include
Polymyxin, Tigecycline and
Aminoglycosides.
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17. Treating the Resistant Infections
• Colistin and Polymyxin B have been used
to treat highly resistant Acinetobacter
infections. The choice of appropriate
therapy is further complicated by the
toxicity of colistin which is mainly renal.
• Acinetobacter isolates resistant to colistin
and Polymyxin B have also been reported
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18. Summary
• Opportunistic pathogen
• Nosocomial infection
• Grow best at aerobic conditions
• Can be transmitted by contact
• Possessing antibiotic resistant
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Short, broad rod during rapid growth
Coccobacillary shape in stationary phase
Colonies are 1 to 2 mm, nonpigmented, domed, and muciod, with smooth to pitted surfaces.
Oxidase negative (opposite to Neisseria spp. or Moraxella spp.)
Haemolytic
Indole negative.
Catalase positive.
Quinoloine and nalidixic acid- inhibit DNA/RNA synthesis
Rifamycine- prevent DNA synthesis
Erythromycine, chloramphenicol- disruption of 50s subunit of ribosome
Tetracycline, gentamycine and streptomycine- 30s subunit disruption
Polymyxin- Disruption of cell membrane
Penicilline, cephalosporine and beta-lactam - inhibition of cell wall synthesis
Sulfonamide and trimethoporine- inhibition of folic acid synthesis