Acinetobacter can cause suppurative infections in all organs of the human body and is more common in long-term hospitalized patients.
Acinetobacter is an obligate aerobic, nonfermentative, catalase-positive, peroxidase-negative, Gram-negative, nonmotile coccobacillus that can grow in the ordinary culture medium. The base content of guanine (G) and cytosine (C) is 39% - 47%. At present, according to DNA-DNA hybridization, the Acinetobacter family has more than 40 genomic species, of which only some species are named.
Genomic species 1 also known as A. calcoaceticus, genomic species 2 also known as A. baumannii, genomic species 3 also known as A. pittii, and genomic species 13TU also known as A. nosocomialis have very close genes and phenotypes, and it is difficult for clinical laboratories to distinguish these bacteria by biochemical phenotypes, so this group of bacteria is also called A. calcoaceticus - A. baumannii complex. Genomic species 1 is mainly distributed in soil and water, and has no pathogenicity to humans. Genomic species 2, genomic species 3, and genomic species 13TU are the main pathogens of nosocomial infections, and are also known as Acinetobacter baumannii group. Acinetobacter baumannii usually refers to Acinetobacter baumannii group in clinical practices. However, the epidemiology, clinical features, and bacterial drug resistance of the nosocomial infection caused by Acinetobacter baumannii, genomic species 3, and genomic species 13TU are not consistent. Researches have shown that Acinetobacter bloodstream infection is caused by Acinetobacter baumannii accounting for 63%, genomic species 13TU accounting for 21%, and genomic species 3 accounting for 8%, and the mortality rate is 36.9%, 16.4 %, and 13.0%, respectively, suggesting that the risk of death from Acinetobacter baumannii infection is higher compared to the other two Acinetobacter genomic species. Although it is generally believed that nosocomial infections in most areas are caused by Acinetobacter baumannii in the Acinetobacter baumannii group, some regions, such as Ireland and Germany, are mainly caused by genomic species 3, and mainly 13TU in Norway. In addition, due to the limitations of species identification techniques, the nosocomial epidemic caused by non-Acinetobacter baumannii spp. such as A. lwoffii, A. hemolyticus, and A. junii may be underestimated.
The knowledge of the natural distribution of Acinetobacter is not abundant. It is generally believed that most of them are environmental parasites and do not cause human infection. Common human Acinetobacter species are A. lwoffii, A. johnsonii, A. junii, A. radioresistens, genomic species 3, genomic species 15BJ, and A. baumannii. Some Acinetobacter species pathogenic to the human body are even normal flora on the surface of the human skin, respiratory tract, or digestive tract, so it is difficult to distinguish between colonization and infection.
Community acquired infections are more common in patients with underlying diseases, during wartime or after disasters. Risk factors for nosocomial infections usually include mechanical ventilation, admission to the intensive care unit (ICU), admission to the burn ward, long-term hospitalization, precious antibiotic treatment, increased exposure to infected patients, patients adjacent to the colonizer, medical staff, persons with low immunity, patients with chronic wasting diseases, and patients with diabetics. Common infections secondary to invasive procedures include ventilator-associated pneumonia, secondary meningitis, bloodstream infections, urinary tract infections, surgical site infections, and catheter-related bloodstream infections. Most cases are caused by contamination. Risk factors for postoperative complications include trauma or injury of skin, soft tissue, bone, or central nervous system. Since Acinetobacter baumannii is susceptible to acquired drug resistance, the prevalence of infection is more likely to occur under the pressure of antibiotic selection. Epidemiological investigations have shown that the risk of infection is significantly increased in patients with ICU due to weakness and the presence of Acinetobacter baumannii in the surrounding environment. Although there are reports of airborne transmission and medical staff infection due to exposure, direct contact transmission is the main route.
Acinetobacter baumannii infections occur mostly in hospitalized patients. Community-acquired infections occur mostly in the tropics. The mortality rate of Acinetobacter baumannii infection can reach 19% - 54%.
The respiratory system is the most common site of infection. Acinetobacter is easy to colonize in the tracheal incision, can lead to community-acquired bronchitis and tracheobronchitis in healthy children, and can cause tracheobronchitis after infection in adults with immunodeficiency. Hospital-acquired pneumonia usually manifests as involvement of multiple lung lobes. Secondary bacteremia and septic shock suggest a poor prognosis.
Acinetobacter can also cause suppurative infections in various organs of the body, such as the lungs, urinary system, skin, and soft tissues. In addition, in a few cases, Acinetobacter can also cause bacteremia, intracranial infection due to surgical intervention in neurosurgery, cellulitis or phlebitis due to indwelling venous catheter, ophthalmic infection, natural or prosthetic valve endocarditis, osteomyelitis, joint abscess, pelvic inflammatory disease, or liver abscess.
Bacterial isolation and culture from clinical specimens is often of little significance for diagnosis, because the bacteria can normally colonize in the human body.
Local cellulitis or phlebitis caused by foreign matter such as venous catheter or suture can be treated locally after removing the foreign matter. Tracheal and bronchial infection caused by tracheal intubation can be treated with pulmonary lavage alone. Patients with severe infections need antibiotics and debridement if necessary.
Acinetobacter baumannii has developed primary resistance to many antibacterial drugs very early. Multidrug-resistant Acinetobacter baumannii refers to the primary resistance of the strain≥3 antibiotics, and even some strains can be resistant to all present antibiotics. If the drug susceptibility results are unknown, carbapenems such as meropenem, imipenem, and doripenem, and polymyxin may be used for the treatment, fluoroquinolone may be combined with aminoglycosides or rifampicin, or a combination of these medications can be administered. Sulbactam has antibacterial activity against a variety of multi-drug resistant Acinetobacter baumannii strains. Glycylcyclines such as tigecycline are also effective. However, there have been reports of borderline activity and drug resistance during treatment.
Mild to moderate Acinetobacter infection can be treated with an antibiotic. The infection caused by trauma can be treated with minocycline alone. Severe infections usually require a combination of antimicrobial medications, such as imipenem or ampicillin/sulbactam in combination with aminoglycosides.