Acinetobacter infection is infrequently correlated with meningitis, endocarditis, peritonitis, urinary tract infections, community-acquired pneumonia, and cholangitis. Acinetobacter unusually colonizes the gastrointestinal tract and is linked with nosocomial pneumonia and wound infections.
Acinetobacter baumannii is a pleomorphic aerobic gram-negative bacillus (similar in the form to Haemophilus influenza on Gram stain) usually isolated from hospital conditions and hospitalized patients. A baumannii is a water organism and preferentially establishes aquatic environments. It is also a natural occupant of soil. This organism is usually cultured from hospitalized patients’ sputum or respiratory secretions, wounds, and urine. In a hospital setting, Acinetobacter usually colonizes irrigating solutions and intravenous solutions. The organism has several characteristics which contribute to its virulence. Acinetobacter comprises fimbriae that can assist in attaching to various surfaces in the environment. The development of a biofilm is critical in allowing the organism to survive in dry environmental conditions. Most Acinetobacter isolates grown from hospitalized patients, especially those recovering from respiratory secretions and urine, represent colonization rather than infection. Multiple factors tend to raise the risk of getting an Acinetobacter infection, including previous antibiotic exposure, intensive care unit admission, use of a central venous catheter, and mechanical ventilation or hemodialysis use. Acinetobacter species can be transferred to patients because of their persistence on environmental surfaces and because of colonization of the hands of healthcare workers.
When Acinetobacter infections happen, they normally involve organ systems that have high fluid content (eg, respiratory tract, CSF, peritoneal fluid, urinary tract). Infections may involve continuous ambulatory peritoneal dialysis (CAPD) or produce catheter-associated bacteriuria. The appearance of Acinetobacter isolates in respiratory secretions of intubated patients may represent colonization. Acinetobacter pneumonias happen in outbreaks and are normally associated with colonized respiratory-support equipment or fluids.
When Acinetobacter produces actual infection, the pathological changes that happen depend on the organ system affected. The pathological changes, as observed in patients with pneumonia, are interchangeable from those caused by other noncavitating aerobic gram-negative bacilli that produce nosocomial pneumonias. Furthermore, Acinetobacter urinary tract infections are clinically indistinguishable from catheter-associated bacteremias caused by other aerobic gram-negative bacilli. The principal predispositions to infection involve colonization pressure, appearance to broad-spectrum antibiotics, and disruption of anatomic boundaries.
Acinetobacter usually migrates patients in the intensive care setting. Acinetobacter colonization is principally common in patients who are intubated and in those who have multiple intravenous lines, and indwelling urinary catheters. Acinetobacter infections happen almost exclusively in hospitalized patients. Although Acinetobacter is essentially a colonizer in the hospital environment, it occasionally produces infection. Mortality and morbidity resulting from A baumannii infection link to the underlying cardiopulmonary immune status of the host rather than the inherent virulence of the organism. Mortality and morbidity rates in patients who are very ill with multisystem disease are grown because of their underlying disease.
The prognosis of Acinetobacter infection depends on the underlying health of the organism and the degree of organ involvement; it is the same as for other aerobic gram-negative bacillary infections.
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