Acinetobacter

Jun 27, 2015Download as PPT, PDF37 likes18,972 views

Acinetobacter is a genus of gram-negative bacteria that includes opportunistic pathogens. The most clinically important species are A. baumannii and A. lwoffii. A. baumannii is commonly found in hospitals and can cause infections in immunocompromised patients. It is able to survive on surfaces and in the environment. Treatment is challenging due to high levels of antibiotic resistance, though carbapenems and polymyxins may be used. Proper hygiene and cleaning can reduce transmission in clinical settings.

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.
2

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
3

Acinetobacter
Gram-Negative
Coccobacilli
Strictly aerobic
Nonmotile
Catalase positive
Oxidase negative
4

Epidemiology
Environmental reservoirs
•Soil
•Fresh water
•Vegetables
•Animals
•Body lice, fleas, ticks
5

Epidemiology
In the hospital…
• Environmental surface
• Ventilators, dialysis machines, air ventilation
systems, water sources
• Hands
• Contaminated suction equipment
• Respiratory, urinary, GI tracts & wounds of
patients
6

Growth Requirment
Aerobic
Grow at 44° C
Differential Media
– MacConky Agar
Selective Media
– CHROM Agar
– Leeds Acinetobacter Agar
7

8
MacConky Agar
CHROM Agar
Leeds Acinetobacter Agar

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.
10

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.
11

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)
12

Transmission
• Acinetobacter can
be spread from
person to person
(infected or
colonized patients),
contact with
contaminated
surfaces of exposure
to the environment.
13

Antibiotic Resistance
• Acinetobacter species
are capable of
accumulating multiple
antibiotic resistance
genes, leading to the
development of
multidrug-resistant or
even panresistant
strains.
14

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)
15

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.
16

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
17

Summary
• Opportunistic pathogen
• Nosocomial infection
• Grow best at aerobic conditions
• Can be transmitted by contact
• Possessing antibiotic resistant
18

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Acinetobacter

1. ACINETOBACTER By Shahbaz Raza

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. 2

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 3

4. Acinetobacter Gram-Negative Coccobacilli Strictly aerobic Nonmotile Catalase positive Oxidase negative 4

5. Epidemiology Environmental reservoirs •Soil •Fresh water •Vegetables •Animals •Body lice, fleas, ticks 5

6. Epidemiology In the hospital… • Environmental surface • Ventilators, dialysis machines, air ventilation systems, water sources • Hands • Contaminated suction equipment • Respiratory, urinary, GI tracts & wounds of patients 6

7. Growth Requirment Aerobic Grow at 44° C Differential Media – MacConky Agar Selective Media – CHROM Agar – Leeds Acinetobacter Agar 7

8. 8 MacConky Agar CHROM Agar Leeds Acinetobacter Agar

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. 9

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. 10

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. 11

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) 12

13. Transmission • Acinetobacter can be spread from person to person (infected or colonized patients), contact with contaminated surfaces of exposure to the environment. 13

14. Antibiotic Resistance • Acinetobacter species are capable of accumulating multiple antibiotic resistance genes, leading to the development of multidrug-resistant or even panresistant strains. 14

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) 15

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. 16

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 17

18. Summary • Opportunistic pathogen • Nosocomial infection • Grow best at aerobic conditions • Can be transmitted by contact • Possessing antibiotic resistant 18

19. Acinetobacter pakistanensis 19

20. 20 Wash your hands and shut them off.

Editor's Notes

#3: A. Hemolyticum A. Junnii A. Johnsonii
#5: Short, broad rod during rapid growth Coccobacillary shape in stationary phase
#9: Colonies are 1 to 2 mm, nonpigmented, domed, and muciod, with smooth to pitted surfaces.
#10: Oxidase negative (opposite to Neisseria spp. or Moraxella spp.) Haemolytic Indole negative. Catalase positive.
#16: 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
#17: Polymyxin- Disruption of cell membrane Penicilline, cephalosporine and beta-lactam - inhibition of cell wall synthesis Sulfonamide and trimethoporine- inhibition of folic acid synthesis

Acinetobacter

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Editor's Notes