Introduction
The genus Acinetobacter (from the Greek akinetos [akinetos], immotile)1 belongs to the family Moraxellaceae2, a group of Gram-negative, non-fermenting, strictly aerobic, catalase-positive, oxidase-negative coccobacilli3. This species has gained significant importance in recent years due to its high virulence and rapid resistance to broad-spectrum antibiotics, which places it as a growing cause of morbidity and mortality from outbreaks of healthcare-associated infections (HAIs), especially in Latin America4. In contrast, Acinetobacter spp. genospecies have been described in community-acquired infections, including natural disasters and wars, which has attracted interest from different researchers5.
More than 40 genospecies are currently known and have been identified by molecular techniques since their isolation is difficult by biochemical tests6. Of these species, Acinetobacter baumannii (genomic species 2) has been the most isolated and with the most significant clinical impact, and therefore the subject of more studies. Additionally, using DNA-DNA hybridization processes, other species have been defined, including Acinetobacter johnsonii (genomic species 7)3. This genospecies was first described by Bouvet and Grimont in 1986 and named after the American bacteriologist John L. Johnson7. This microorganism has an isolation incidence of 1.7-2.0% in adult and pediatric patients, with a marked difference compared to A. baumannii, which reaches 78-90%8,9.
A. johnsonii is characterized by optimal growth at 15-30°C and no growth at 37°C, an incubation period of 1-2 days, catalase-positive, cytochrome oxidase negative, and producing gamma hemolysis10. It inhabits humid climates, specifically soil, pure and wastewater, and animal reservoirs such as pets and arthropods. In humans, some studies have described the isolation of A. johnsonii in the gastrointestinal tract, skin wounds, chronic rhinosinusitis, endocarditis2,6, catheter-related bloodstream infections, and peritoneal dialysis-associated peritonitis6. A. johnsonii was the predominant Acinetobacter species in fecal samples from healthy individuals in the Netherlands (17.5%)1.
The most frequent clinical manifestations of infection by this genus are bacteremia and pneumonia associated with mechanical ventilation11 and soft tissue infection, urinary tract infection, endocarditis, and meningitis. The latter is significant since it has a high incidence in the pediatric population12. In this report, we describe the clinical case of a pediatric patient who developed bacterial meningitis with isolation of A. johnsonii in cerebrospinal fluid culture.
Clinical case
We present the case of a 15-year-old female patient who consulted for global headache and fever of 11 days, for which she received antipyretic treatment at home. She first went to a primary care institution, where migraine was suspected; the patient was later discharged with analgesic treatment. However, due to the persistence of symptoms and appearance of emesis, blurred vision, and diplopia, she was hospitalized for a specialized examination. As background, the patient was the product of a full-term pregnancy with adequate control and had a complete vaccination schedule. She presented with dengue hemorrhagic fever at 14 years of age. On admission, the patient presented with Glasgow 15/15 with generalized weakness, although with selective bilateral motor control of the neck in a standing position, good symmetrical reflexes, no Babinski's sign or clonus. The patient could stand upright with head instability, head bobbing, gait instability, horizontal nystagmus on extreme gaze, and 3/5 strength in the lower limbs. A simple cerebral axial computed tomography and nuclear magnetic resonance contrasted with cerebral venography were performed, showing the left transverse sinus hypoplasia as a normal anatomical variant. Blood count, liver function, amylase, urinalysis, and human chorionic gonadotropin hormone beta fraction (b-hCG) studies were normal, and polymerase chain reaction (PCR) test for SARS-CoV-2 was negative. Given the high suspicion of neuroinfection and infectious cerebellitis, a lumbar puncture was performed, reporting 100% pleocytosis, with increased neutrophils, hypoglycorrhachia, and hyperproteinorrhachia. Antibiotic treatment ceftriaxone and vancomycin was started. Chinese ink staining, Filmarray® meningitis/encephalitis panel, and VDRL (Venereal Disease Research Laboratory) serum and cerebrospinal fluid cytochemistry were negative. After the first 24 hours of cerebrospinal fluid incubation, growth of Gram-negative germs was documented, and vancomycin was discontinued. On the sixth day, cerebrospinal fluid culture was obtained, reporting isolation of multi sensitive A. johnsonii (Table 1), leading to a change in antibiotic treatment to ampicillin sulbactam. The final diagnosis of A. johnsonii meningoencephalitis was concluded. On the eighth day of antibiotic treatment, the patient presented two febrile peaks associated with bilateral retro-ocular pain and mild frontal headache. Therefore, in search of an additional focus, a complete blood count, chest X-ray, and blood cultures were performed again, with negative results for new findings. Subsequently, the dysthermia resolved spontaneously after 2 days, with febrile symptoms considered within the clinical framework of the current pathology. On day 14, the patient could not walk, with paresthesia and sensory alteration to temperature sensation in the right palmar region, without compromise of strength in the extremities, so peripheral neuropathy was suspected. A nerve conduction test was indicated, finding the right ulnar nerve entrapment at the elbow. The clinical picture of paresthesias, together with the results found in the nerve conduction test, were related to the entrapment, so it was considered an incidental finding that could not be related to the current meningoencephalitis. The control simple and contrasted brain magnetic resonance imaging study was reported within normal limits. On day 18 of treatment, a control lumbar puncture was performed. The cerebrospinal fluid cytochemical study showed the expected results for resolution of meningitis, no pleocytosis, scarce and fresh red blood cells secondary to puncture, ascending hypoglycorrhachia, normal protein concentration, and Gram without microorganisms. After completing 21 days of antibiotic treatment, the patient was discharged, followed by a physical rehabilitation program, improving her gait pattern without antibiotic prophylaxis and multidisciplinary follow-up.
Culture of Acinetobacter johnsonii | ||
---|---|---|
Antibiotic | MIC | Interpretation |
Ampicillin/Sulbactam | ≤ 2 | Susceptible |
Cefepime | 8 susceptible | Susceptible |
Ceftazidime | 8 susceptible | Susceptible |
Ceftriaxone | 8 susceptible | Susceptible |
Ciprofloxacin | ≤ 1.0 | Susceptible |
Gentamicin | ≤ 4 | Susceptible |
Meropenem | ≤ 1.0 | Susceptible |
Piperacillin/tazobactam | ≤ 16 | Susceptible |
Tigecycline | ≤ 1.0 | Susceptible |
Trimethoprim/sulfamethoxazole | ≤ 1 | Susceptible |
MIC, minimum inhibitory concentration.
Discussion
Bacterial meningitis in pediatric patients is a disease of significant morbidity that can generate considerable complications and neurodevelopmental alterations. In terms of etiology, Gram-negative bacilli are responsible for one-fifth of the cases of meningitis in this population11. According to the systematic review by Hu et al., neuroinfection is one of the most common presentations of pediatric Acinetobacter infection12.
Most infections caused by this microorganism have been described as HAIs, with A. baumannii as the main microorganism and a higher prevalence in neonates and children under 10 years of age13,14. The most frequently reported risk factors include neurosurgical procedures13, head trauma, intracranial hemorrhage11, bacteremia13, cerebrospinal fluid leakage, foreign body implantation14, and recent antibiotic administration. However, isolation of Acinetobacter in community-acquired infections is rare, with very few reports in the literature, which have occurred more frequently in patients with no comorbidities and no risk factors. In addition, other genospecies such as A. johnsonii6, A. calcoaceticus, and A. rufi are mainly sensitive to antimicrobials in different clinical trials, unlike A. baumannii, which is usually highly resistant14.
The clinical manifestations of Acinetobacter neuroinfection are similar to those described for meningitis caused by other microorganisms. Most patients present with fever, seizures, signs of meningeal irritation, focal manifestations, emesis, and headache, as observed in the present case14. Given the clinical suspicion of an intracranial infectious process and the lack of specificity of blood test findings, lumbar puncture is of great importance in diagnosing this condition. Therefore, the cerebrospinal fluid analysis should include the determination of proteins, glucose, cell count, and Gram stain. Typical findings include the presence of pleocytosis with neutrophilic predominance, hyperproteinemia, and hypoglycorrhachia4,5. The gold standard is cerebrospinal fluid culture for isolation of the infecting microorganism.
The treatment of neuroinfection caused by the genus Acinetobacter represents a challenge for the clinician, given the increasing antimicrobial resistance reported and the fact that most antibiotics have a low permeability at the blood-brain barrier, thus reducing the possibilities of treatment15. The state of antibiotic multidrug resistance of A. baumannii due to the irrational use of antibiotics in patients carrying resistance genes has been widely described16. A marked sensitivity pattern has been evidenced in other genospecies such as A. johnsonii, which is consistent with the antibiogram of the present case, which allowed a de-escalation of the initial empirical management.
According to the above, the local resistance pattern of the microorganisms causing meningitis in pediatric patients should be considered when deciding on empirical antibiotic therapy, which should be intravenous and broad-spectrum, initially covering Gram-positive and Gram-negative microorganisms. As for the coverage of Gram-negative bacteria, a broad-spectrum cephalosporin, a beta-lactam with a beta-lactamase inhibitor, or a carbapenem should be selected, depending on the local resistance pattern, while awaiting the antibiogram susceptibility pattern17. Finally, it is worth mentioning the high mortality rates documented in neuro infections due to Acinetobacter spp., which reach more than 50% in pediatric patients9,13, with higher mortality in post-surgical patients17. Furthermore, neurological complications and sequelae are frequent (61%) in surviving patients18, as in our case, which occurred, albeit mildly.
Compared to A. baumannii, A. johnsonii has not been the subject of many clinical studies. Even so, its clinical importance has increased in recent years due to the increase in potentially severe infections in pediatric patients, most frequently associated with bacteremia and meningitis. Given the increasing variety of Acinetobacter species and their presence in the environment and the hospital setting, early recognition of their clinical spectrum is of great importance for a rapid and accurate diagnosis that allows timely and essential treatment considering the high morbimortality of the pathological processes that these microorganisms could generate. In addition, further research is needed to determine new Acinetobacter species in the region and local resistance patterns.