Beijerinck in 1911 described a germ isolated from the ground, Micrococcus calcoaceticus.
In 1939 De Bord publishes preliminary work on a group of coccobacilli Gram (-) close Neisseria he considers the tribe Mimae (Mima polyphorma).
In 1940 Audureau described a species of Moraxella close it without their nutritional requirements, under the name of Moraxella Iwoffi.
Many authors have tried to impose their vision of the kind that is how synonyms are:
– For species forming acid from glucose:
Herellea vaginicola. De Bord 1942
Bacterium anitratum, Schaub and Hauber 1948
Neisseria winogradskyi, Lemoigne et al. 1952
Acinetobacter anitratum, Brisou and Provost 1954
Moraxella glucidolytica, Piéchaud 1956
– For species non acid from glucose:
Alcaligenes haemolysans, Henriksen 1937
Moraxella Iwoffi, Audureau 1940
Acinetobacter I woffi, Brisou and Provost 1954
Achromobacter haemotyticus var. Alcaligenes 1962
Baumann, Doudoroff Stanier in 1968 and proposed to bring all these varieties in one
species and one genus Acinetobacter calcoaceticus.
I – CLASSIFICATION – NOMENCLATURE:
It is coccobacilli, short, often diplocobacilles motionless Gram negative. They are strictly aerobic, often encapsulated, does not reduce nitrates, catalase (+), oxidase (-). Prototrophic, they can grow on a mineral medium with a carbon source. GC 39-47 mol%.
The latest edition (1984) of Bergey’s Manual recognizes a single species, Acinetobacter calcoaceticus, with 7 phenotypes (Rev A2, A3, Bp B2, B2, 84).
However, it is not rare to find in some textbooks distinguish between varieties or biotypes….. A. calcoacticus anitratus var, var haemolyticus, alcaligenes var, var Iwoffi The latest edition of the Manual of Clinical Microbiology prefer retaining two subspecies.. A. calcoaceticus subsp anitratusand subsp Iwoffi that actually correspond to the realities of current medical bacteriology.
In 1986, Bouvet and Grimont based on DNA-DNA hybridization studies have described 12 genospecies. This number is now twenty. The phenotypic characteristics of the six most common of them are shown in Table I.
A. baumannii is the species most often isolated in hospital.
II – GENERAL CHARACTERISTICS, PHYSIOLOGICAL AND METABOLIC:
The colonies 1-2 mm in 24 hours, they are often mucosal smooth, yellowish-white and buttery appearance.
The nitrates are reduced to nitrites or very rarely and very slowly.
Some strains acidify without gas production glucose, galactose, mannose, xylose, arabinose, lactose. Glucose is oxidized to gluconic acid, carbohydrates are oxidized and pentoniques hexonic acids by non-specific aldose dehydrogenase.
Acinetobacter able to use glucose as a carbon and energy source degrade this compound only in the way of Entner-Doudoroff.
The possibility for some Acinetobacter (glucidolytica} of forming acid aerobically from glucose is linked to the presence in these strains of a glucose dehydrogenase that oxidizes in D.glucose D.gluconolactone and the possibility for certain strains to grow at the expense of glucose, is a function of their ability to degrade gluconic acid. Oxygen is the terminal electron acceptor for the particulate form of this enzyme which is absent in the non saccharolytic strains.
Acinetobacter resembles Pseudomonas by the fact that it can use a wide variety of organic compounds as a carbon and energy source. It does not require specific growth factors and can grow in a simple mineral medium with a single source of carbon and energy. The metabolic pathways used by this organism for the biosynthesis or degradation of aromatic compounds, hydrocarbons, 2-3 butanediol are similar to those of Pseudomonas (Joni 1978).
Many Acinetobacter are capable of degrading hydrocarbons of 8 to 20, using as a source of carbon and energy, eg, n-hexadecane is converted hexadecanoic acid.
All enzymes of the citric acid cycle and glyoxylate cycle are present. Some strains using citrate others not.Acinetobacter contains a functional respiratory chain of electron carriers (cytochromes a1a2o d and b, cytochrome c is absent).
Under the usual conditions of the bacteriological identification, Acinetobacter does not reduce nitrate to nitrite, but the ammonium, nitrate and nitrite can be used as nitrogen sources. Grown in the presence of Acinetobacterammonium salts produces NADP-linked glutamate dehydrogenase. Cultivated in the presence of nitrate or nitriteAcinetobacter synthesizes an assimilatory nitrate reductase Molybdenum 96 kDa.
If some strains Acinetobacter produce exo-enzymes: lipase, gelatinase, hemolysin (phospholipase C).
Gutnick and Rosenberg suggested in 1977 to make them play a role in the solution of pollution problems caused by oil transpon and the decomposition of the engines of motor oil. Acinetobacter produces a polyanionic emulsifier and uses chlorinated biphenyl compounds, properties which could be used in the control of pollutants.
III – HABITAT AND EPIDEMIOLOGY:
Ubiquitous bacterium, Acinetobacter is mostly found in soil and water (gifted, marine) the sewage sometimes isolated in milk and dairy products in food. It is frequently isolated in humans: skin, saliva, urine, conjunctiva. It is among the bacteria of the normal resident flora of the skin covering.
The sources of nosocomial Acinetobacter are numerous hospital. This bacterium has the ability to colonize many hardware: respirators, humidifiers, sinks, soaps and antiseptics. It can be carried by the hands of health care workers and the majority of infections are acquired in hospital. The fact that Acinetobacter are frequently isolated from the skin of hospitalized patients, but also normal subjects does not say for sure if it is commensal bacteria or contaminants.
Antisera labeled with fluorescein directed against the capsular antigens can be used as epidemiological markers to search for the source of nosocomial infection. The determination of phage strains is also used in specialized laboratories.
JF Vieu uses two phage systems. The first scheme includes 21 specific bacteriophages and allows distinguishing currently 112 phage types, non-typeable between 25 to 35%. A second complementary pattern of the first possible to limit to 20% and the proportion of the non-typeable strains subdivided into 20 subtypes, and a group of insensitive strains. The use of phage typing has shown that there is in hospital epidemic outbreaks due to the same phage type, the reality of flora substitutions by Acinetobacter strains of different phage types and ubiquitous nature of certain phage types in various hospitals in France, while others have a limited geographical location.
A biotypie system was developed by PMJ Bouvet for A. bawnannii.
IV – PATHOGENICITY NATURAL:
Acinetobacter are sometimes considered only as contaminants of samples. However, they are in a number of cases (where it will discuss the origin of the infection) responsible for serious meningitis, septicemia, pleurisy, conjunctivitis, sinusitis, skin abscesses, urinary tract infections, to intestinal ulcerations, pericarditis.
When Acinetobacter is isolated in blood cultures, the initial focus is often a catheter or was formed after a digestive surgery. There may be a bacterial or a real sepsis, this often on fragile field. These patients weakened by major surgery, trauma, old age.
In urinary tract infections, a mechanical cause is often found (prostatic adenoma, pregnancy, survey).
Meningitis may be secondary to a surgical operation or trauma, or primitives. The rigorous differential diagnosis withNeisseria is required. In genuine cases of meningococcal Acinetobacter, the prognosis is poor.
Suppurations Acinetobacter may occur especially in bone surgery by superinfection of wounds from prosthetics (hip), pins, of nailing.
In respiratory infections Acinetobacter can be isolated in pleurisy, pneumonia, in the sputum of patients, resuscitation aspirations.
V – PATHOPHYSIOLOGY:
The pathogen Acinetobacter natural power is low and it is necessary to inject high doses to animals to observe pathological manifestations or lethal.
It is primarily the collapse of the immune system that promotes colonization and superinfection in patients in intensive care units. It is likely that the capsular polysaccharides oppose phagocytosis in deficient subjects opsonic antibodies and phagocytic cells. As with all gram-negative bacteria, endotoxin is responsible of septic shock.
VI – BACTERIOLOGICAL CHARACTERS:
A – Identification (Table I):
Identification of Acinetobacter is based primarily on morphological characters: diplobacilli Gram (-), often polymorphic with elongated filamentous forms. This morphology should not be confused with Neisseria.
Culture is easy on the usual media. Some strains have an unpleasant odor; few strains are hemolytic on blood agar.They are all negative and immobile oxidase.
The main characters to be studied are:
– Absence of nitrate reduction
– Acidification of glucose
– Growth in broth at different temperatures (44 ° C, 41 ° C and 37 ° C)
– Simmons citrate
– Research B-xylosidase and a YGT
The differential diagnosis is easily done with Neisseria, Moraxella and other aerobic gram-negative bacilli.
Epidemiological markers (serotypes, phage) Acinetobacter are not available at a current laboratory, it is necessary to address a
B – Antigenic Structure:
Acinetobacter, ubiquitous germ, is complex from the standpoint of its antigenic structure surface. Several series of works have shown the different serological groups. Marcus 1969 using antibodies labeled with fluorescein showed the existence of 28 serovars saccharolytic strains but also other serovars strains not producing glucose oxidation by acid. Adam with antisera prepared with heated or formalin bacteria distinguishes 41 K factors by slide agglutination and 40 groups 0 IHA. Some antigenic kindreds have been described between the capsular polysaccharide and some strains of Acinetobacter streptococci B, G, pneumococcal Type 23. Similarly cross-reactions were observed between anti-Chlamydia antibody and a soluble antigen nondialyzable and thermostable Acinetobacter.
C – Immunity:
Healthy subjects is resistant to colonization and infection by this bacterium.
Only immunocompromised patients are frequently colonized and occasionally infected. It is likely that there are natural defense mechanisms against Acinetobacter but the shares of natural immunity and acquired immunity are unknown. It is known that the capsular heteropolysaccharide and the lipo-polysaccharide are antigenic. It is possible that the natural resistance to infection is partly due to the existence of cross reactions between the capsular antigensof Acinetobacter and those of B and G streptococci and S. pneumoniae type 23.
VII – TREATMENT:
The treatment of secondary infections due to Acinetobacter is often difficult because of multidrug resistance of this germ. Over the years, the trend towards resistance to several antibiotics was done regularly. This is dependent chromosomal elements (production of beta-lactamases immediately giving high resistance to beta-lactams) and factor plasmid encoding the epidemic resistance to aminoglycosides.
In 1983, a beta-lactamase TEM-type 1 (pi = 5.4) was demonstrated in A. calcoaceticus and is inhibited by clavulanic acid and sulbactam. This may indicate a therapeutic approach and the need to seek the activities of associations with these beta-lactamase inhibitors. In 1982, an MDR Acinetobacter strain responsible for an outbreak in an intensive care unit and cephalosporinases produced a penicillinase type TEM 2 and was resistant to many aminoglycosides as a plasmid resistance phenotype frequently observed in this hospital in Gram-negative bacteria.The inheritance of resistance to aminoglycosides, chloramphenicol and sulfonamides was linked to a transposon 16 billion from a plasmid conjugative R of hospital flora. Resistance phenotypes to aminoglycosides, diverse, are explained by the existence of aminoglycoside modifying enzymes in particular 3′-phosphoiransférase (APH 3 ‘), 3 N-acetyltransferase type 1 (aac3) 6’N- acetyltransferase (AAC6 ‘), 3 “adenyltransferase (AAD3”). In 1983 a autotransferable plasmid of exogenous origin, for resistance to chloramphenicol, aminoglycosides, ampicillin, sulfonamides and trimethoprim was characterized.
Acinetobacter are highly resistant to most antibiotics. The new beta-lactam antibiotics do not bring across a substantial gain in activity. The MIC 50 of the meziocilline, aziocilline, cefoperazone, ceftriaxone are high and only piperacillin and ticarcillin are distinguished from molecules marketed about 60 and 20% of sensitive strains. Among the newer antibiotics there is significant activity of ceftazidime and especially imipenem which is sometimes the only active antibiotic.
The activity of aminoglycosides still varies on hospital strains of Acinetobacter. Gentamicin then showed a decrease in activity due to the increase of its use. Figures released MIC 50 does not reflect the current situation where there is a large number of strains resistant to one or more aminoglycosides: gentamicin, tobramycin, netilmicin, amikacin.
Amikacin and tobramycin are generally the most active.
The new quinolones certainly bring this species a new therapeutic option. Nalidixic acid was some activity, but the emergence of second-generation quinolones (pefloxacin, norfloxacin, ofloxacin, ciprofloxacin) increases the number of stem damage for relatively low MIC values. The use of some of these quinolones constitutes progress in the treatment of Acinetobacter infections.
Trimethoprim-sulfamethoxazole and rifampin can sometimes be effective. Acinetobacter is sensitive to polymyxin.