Acinetobater infection Updated Medical Microbiological View

 Acinetobacter was found in soil and discovered in 1911 by M.W
Beijerinch German Microbiologist ,is a Gram negative bacteria
belonging to the wider class ofGammaproteobacteria
 The name of acinteobacter is coming from Greek words [α +
κίνητο + βακτηρ(ία)] which meaning (non motile rod )
 It naturally inhabits water and soil, and has also been isolated
from foods and arthropods .
 It has allots of species and causing allots of diseases for human
and Animals .
 commonly found on the skin of healthy humans as normal
floraa , also AC infections is broad and includes infection
associated with tropical environments, wars and natural
disasters, and hospital outbreaks in temperate climates .
Dr.Hythum Salah H.Mohamed
KAMC-IM-ID-Riyadh-December 2013.

 Acinetobacter baumanni , Since it was isolated and discovered in
1970s, the spread of multidrug-resistant (MDR) Acinetobacter strains
among critically ill, hospitalized patients, and subsequent epidemics,
have become an increasing cause of concern world wide . Reports of
community-acquired Acinetobacter infections have also increased over
the past decade in some parts of the world like south Asia and Australia
.

Microbiology
• Grame negative
Coccobacilli
• Strictely aerobic
• non motile (my exhibit
twitching motility ).
• Nitrate and Oxidase
• negative
• Catalase positive and
non fermenting

Description and Morphology
Rod shaped
Encapsulated (generally).
Frequently arranged in pairs
.

Epidemiological view :-
Global pockets of Acinetobacter baumannii infections

Acinetobacter in Wars

 Since Operation of Iraqi War began in 2003, more
than 700 US soldiers have been infected or
colonized with Acinetobacter baumannii. A
significant number of additional cases have been
found in the Canadian and British armed forces,
and among wounded Iraqi people it was called
Iragi Bacter , also it was the most common gram
negative bacillus contaminated wounds during the
Vietnam war as well .

Mode of Transmission

PATHOGENESIS Factors contribute to acinetobacter
virulence
1- organism can survive under dry and neutral condition for long period can survive
for months, making Nosocomial transmission extremely difficult to control.
2-one third of strains produce polysaccharide capsule that works with cell wall
liposccharide to prevent complement activation also delay phagocytosis .
3-colonization in the lung is facilitated by ability to adhere to bronchial epithelial
surface by fimbriae and also subsequent formation of biofilms .

Major infections due to Acinetobacter
 Hospital acquired Pneumonia
 Ventilator-associated pneumonia
 Urinary tract Infection
 Bloodstream infection
 meningitis
 Skin/wound / Bone infections
 Endocarditis
 Peritonitis in Peritoneal Dialysis Pt s .
 Ventriculitis
 Endophthamitis and Periorbital Cellulitis.

Hospital Acquired Pneumonia
 occurs predominantly in
intensive care unit (ICU)
patients who require
mechanical ventilation.
 occur in previously colonized
patients .
 associated with mortality rates
of 35 to 70 % .
 Patients are usually elderly
and immuncompromised
patients .

Community Acquired pneumonia
 It is uncommon form of AC infection ,most commonly occur in
southeast Asia and Australia .
 It sever , rapid fulminant infection , characterized by Bacteremia ,
ARDS , DIC , Respiratory failure and death .

Bloodstream infection
 AC infection accounts for 1.5 to 2.4 % of nosocomial bloodstream
infections .
 The most frequent sources of Acinetobacter bacteremia are vascular
catheters and the respiratory tract .
 Less common primary sites include wounds and the urinary tract
 Risk factors for Ac infection include ICU , mechanical ventilation, prior
surgery, prior use of broad-spectrum antibiotics, immunosuppression,
trauma, burns, malignancy, central venous catheters, invasive
procedures, and prolonged hospital stay
 Septic shock develops in up to one-third of patients with AC bacteremia
.
 mortality ranges from 20 to 60 % .

Acinetobacter Meningitis
 Most cases are hospital-acquired
 Often associated with neurosurgical procedures like
Craniotomy
 Risk factors:
• Heavy use of antibiotics in the neurosurgical ICUs .
• CSF leak
• Intracranial Hemorrhage
• Mortality ranges from 20 to 30 % .

Skin and Wounds Infections
 Acinetobacter may contaminate surgical and traumatic wounds,
leading to severe soft tissue infection that can also progress to
osteomyelitis.
 surgical wound infections with Acinetobacter are frequently related to
the presence of prosthetic material and usually require extensive
debridement.

Urinary Tract Infection
 urinary tract can become colonized readily with AC , particularly in the
setting of indwelling urinary catheters
 the incidence of infection is low , In a review of 5000 urinary tract
infections in medical intensive care units in the United States, 1.6 %
was due to Acinetobacter, 95 % of these infections were associated with
urinary catheters .
 Community-acquired urinary tract infection can occur but is rare .
 In the absence of other signs or symptoms of infection, isolation of
Acinetobacter may be attributed to colonization.

Diagnosis
 It is very important to distinguish between colonization and infection .
 As an example, Acinetobacter isolated from sputum of a ventilated
patient is more likely to represent colonization than infection in the
absence of fever, leukocytosis, increased respiratory secretions or
oxygen consumption , need for additional respiratory support, or a
new abnormality on chest imaging.

Documented mechanisms of
resistance in Acinetobacter baumannii
β-Lactamase
 The most prevalent mechanism of β-lactam resistance in A.
baumannii is enzymatic degradation by β-lactamases
 AmpC B-lactamases it is chromosomally encoded enzyme produce by
AC b .
 Cephalosporinases enzymes produce by AC b , make it resistant to
broad spectrum Cephalosporin's
 Cefepime and carbapenems appear to be stable in response to these
enzymes .

Carbapenems
Carbapenemase
 is one of B-lactamses that can produce by AC, has ability to
hydroloza Cabapenems and other Penciilins and Cephalosporins .
 Carbapenemases are members of the molecular class A, B, and D
beta-lactamases. Class A and D enzymes have a serine-based
hydrolytic mechanism
 class D carbapenemases consist of OXA-type beta-lactamases
frequently detected in Acinetobacter baumannii The first identified
OXA-type enzyme with carbapenem-hydrolyzing activity was
isolated from A. baumannii strain in 1985 in Edinburgh, Scotland .

Others
Aminoglycosides
 There is a genes coding for aminoglycoside-modifying enzymes
within class 1 integrons is highly prevalent in multidrug-resistant AC.
 This emerging resistance mechanism impairs aminoglycoside
binding to its target site and confers high-level resistance to all
clinically useful aminoglycosides, including gentamicin, tobramycin,
and amikacin
 Also there is documented resistant to Quinolones , Tetracycline's .

Tratment of MDR Acinetobacter
There is view list of Antibiotics that can be use in treatment of
MDR AC infection
 Colistin
 Tigecycline
 Polymyxin B.
 Carbapenems
 Amikacin.
 Rifampin.
 Minocycline .

General approach for Antibiotics
use
 Empiric antibiotic therapy for Acinetobacter, before results of
antimicrobial susceptibility testing are available, should be selected
based on local susceptibility data .
 In general, it should consist of a broad spectrum cephalosporin, a
combinationbeta-lactam/beta-lactamase inhibitor , or a carbapenem.
 For empiric therapy of patients with Acinetobacter infection in a
location where resistance to the chosen antibiotic is high, suggest is
to adde second agent like An antipseudomonal fluoroquinolone,
an aminoglycoside, or colistin are second agent option .

 Once results of antimicrobial susceptibility testing are
available, a regimen can be chosen from among the active
agents.
 Agent with the narrowest spectrum of activity is strongly
recommended.
 For patients with infections due to extensively-drug resistant
Acinetobacter, therapeutic options are generally limited to
polymyxins (colistin, or polymyxin E, and polymyxin B) and
tigecycline. For such patients, suggest is to using a second
agent in addition to polymyxins or tigecycline.

Pneumonia
 Inhaled colistin may be used in selected patients. especially
patients with severe pneumonia with MDR Acinetobacter that , since
intravenous colistin yields low lung concentration.
Among three studies evaluating inhaled colistin as adjunctive therapy to i.v
Antibiotics for ventilator-associated pneumonia with drug-resistant gram-
negative bacilli, predominantly A. baumannii, the pooled response rate was 80
%. Although in one series of 17 patients with Acinetobacter pneumonia, clinical
improvement with inhaled colistin without active systemic antibiotics was
observed in 57 % of cases .

it is favor to use inhaled colistin in such patients only with
concomitant administration of i.v antibiotics.
* The main adverse effect of inhaled colistin is
bronchoconstriction. Inhaled polymyxin B is an alternative
agent; there are reports of successful treatment of multidrug-
resistant respiratory infections with inhaled and systemic
polymyxin B.

Bloodstream infection
 Because tigecycline rapidly enters tissues following administration,
resulting in low serum levels, it may not be an appropriate choice for
extensively drug-resistant Acinetobacter bacteremia.
 Additionally, bloodstream infections with drug-resistant isolates are
associated with particularly poor outcomes, regardless of therapy. In
one study, treatment with colistin did not reduce mortality in patients
with bacteremia due to multidrug-resistant Acinetobacter compared
to mortality rates prior to the availability of colistin in that institution .
 If the bacteremia is associated with an intravascular catheter, that
device should be removed .
The duration of therapy is typically 10 to 14 days.

Meningitis
 variable CSF penetration of antibiotic agents further limits the
therapeutic choices for Acinetobacter CNS infections. Additional
considerations include the possible use of intrathecal antibiotics for
drug-resistant isolates and the removal of CNS devices, if present.
 Of the first line agents, the carbapenems most reliably enter into the
CSF, particularly when inflammation of the meninges is minimal .
 Because of the association between high dose imipenem and
seizures and the limited clinical experience with doripenem,
meropenem is the most appropriate choice of the carbapenems.
.

 For carbapenem-resistant isolates, polymyxins have been
used with some success.
 Meropenem dose should be 2 g every eight hours. If
susceptible, ceftazidime or cefepime can also be used at
meningeal doses
 When colistin is administered intravenously, there is moderate
penetration of inflamed meninges and spinal fluid levels reach
approximately 25 % of serum levels , for this reason,
intrathecal or intraventricular colistin in the setting of central
nervous system infections with drug-resistant Acinetobacter
can be used .

 Colistin can be administered intraventricularly or intrathecally,
usually in conjunction with an active intravenous agent, if
possible .
 Complications of intraventricular and intrathecal colistin
include aseptic chemical meningitis .
 The treatment of Acinetobacter meningitis is usually at least
for three weeks. The response should be assessed clinically .

Skin, soft tissue, and bone infection
 The initial approach to empiric and directed antimicrobial therapy of
skin, soft tissue, and bone infections caused by Acinetobacter is the
same as that for Acinetobacter infections in generality .
 debridement of affected tissue, particularly in the case of osteomyelitis,
may be necessary for optimal control of the infection.
 The usual duration of therapy for skin and soft tissue infections is 10 to
14 days or until local signs of infection have resolved.
 Patients with osteomyelitis should be treated for 4 to 6 weeks following
surgical debridement.

Urinary tract infection
 Treatment for infection should only be initiated if a positive
culture is accompanied by pyuria and systemic signs or
symptoms in the absence of another source of infection.
 Tigecycline has poor excretion in the urinary tract. Given this,
along with the observed increased risk of mortality with
tigecycline use , this agent should only be used when no other
options are available.
 If present, any urinary catheter should be removed , duration
of therapy is typically 10 to 14 days.

Preventing Acinetobacter
Transmission
 Hand hygiene
• Use of alcohol-based hand
sanitizers
 Contact precautions
• Gowns/gloves
 Environmental decontamination
 Prudent use of antibiotics
 Alcohol-based products
containing chlorhexidine should
be considered the hand
hygiene agents of choice.

Message Take to Home
 Acinetobacter spp . can colonize almost any human body site either
transiently or as normal flora.
 A. baumannii is an emerging opportunistic pathogen in healthcare setting as
one of most important MDROs .
 MDR AC baumannii is associated with high mortality and being difficult to
treat , especially in an immunocompromised patient
 Control requires good hand hygiene, barrier precautions & environmental
decontamination and Staff Education .
 Rationale use of Antibiotics can decrease emerging of MDROs .
 Differentiate between colonization and infection is vital for safety of patient
form unwanted SE of Antibiotics and for proper use of antibiotics .
 For patients with infections due to extensively-drug resistant Acinetobacter,
therapeutic options are generally limited to polymyxins (colistin, or polymyxin
E, and polymyxin B) and tigecycline.

Resources
 Center for Disease Control and Prevention
http://www.cdc.gov .
 Infectious Diseases Society of America (IDSA)
www.idsociety.org
 Journal of Clinical Microbiology http://jcm.asm.org/
 Up to date .com www.uptodate.com
 www.google.com .

Thank You
for
Attending

Acinetobater infection Updated Medical Microbiological View

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