Patricia Aruj

Nosocomial Acinetobacter pneumonia

Abstract:  Acinetobacter spp. (A. baumannii is the prevalent genomic species, but others may cause infection) has become an increasingly important cause of nosocomial pneumonia, particularly in mechanically ventilated patients (VAP). This organism has intrinsic resistance to some antimicrobials but easily acquires resistance to many others; Acinetobacter spp. can survive for long periods of time in the environment. All of these characteristics have contributed to protracted outbreaks associated with significant morbidity and mortality. High rates of colonization are found in debilitated hospitalized patients. Infecting or colonizing organisms in nosocomial infections are more likely to be from cross‐transmission or from the hospital environment than from endogenous sources. VAP caused by Acinetobacter spp. is emerging as a prominent hospital complication. The incidence of this microorganism varies from site to site, but it is the second commonest aetiological agent among the gram‐negative bacteria. Longer periods of hospitalization, longer time on mechanical ventilation and prior use of antibiotics are the recognized factors increasing the risk of VAP due to Acinetobacter spp. Treatment needs to clearly differentiate infection from colonization, and the agents with the most antimicrobial activity are imipenem/cilastatin, amikacin, colistin, ampicillin/sulbactam and tigecycline. Monotherapy can be adequate if the patient does not have significant comorbidities. Infection control procedures have a major role to play in preventing transmission of this microorganism. Emphasis on initial control measures should, however, be on strict isolation of infected or colonized patients to limit dissemination of outbreak strains in the environment. The variety of potential sources of contamination with Acinetobacter spp. in the hospital environment makes control of these outbreaks one of the more difficult challenges. Persistence of Acinetobacter spp. in the environment provides ample opportunities for contamination of patients and staff and may explain continuing long‐term outbreaks.

Blunted Hypercapnic Respiratory Drive Response in Subjects With Late-Onset Pompe Disease

BACKGROUND: Patients with late-onset Pompe disease develop progressive hypercapnic respiratory failure that can be disproportionate to the respiratory muscle compromise and/or thoracic restriction. Although recent studies have reported the presence of a blunted hypercapnic respiratory response in some subjects with neuromuscular disorders and chronic hypercapnia, no study has evaluated the integrity of the respiratory drive in subjects with late-onset Pompe disease. Thus, we endeavor to determine the CO2 rebreathing response in subjects with late-onset Pompe disease. METHODS: Respiratory muscle strength was assessed by measuring the maximum inspiratory pressure, and the maximum expiratory pressure. The maximum inspiratory pressure reflects the strength of the diaphragm and other inspiratory muscles, whereas the maximum expiratory pressure reflects the strength of the abdominal muscles and other expiratory muscles. We studied the hypercapnic drive response (measured as the ratio of the change in airway-occlusion pressure 0.1 s after the start of inspiration and end-tidal PCO2 in 13 subjects with late-onset Pompe disease and 51 healthy controls. RESULTS: Overall inspiratory muscle strength was within normal limits or slightly diminished in the late-onset Pompe disease group. Five subjects (38.5%) were chronically hypercapnic, and 9 (69.2%) had an increased breath-holding time. Compared with controls, the change in airway-occlusion pressure 0.1 s/change in end-tidal CO2 pressure slope (hypercapnic respiratory drive) was lower in the late-onset Pompe disease group (median 0.050 [interquartile range 0.027–0.118] vs 0.183 [0.153–0.233], P < .001). Nine subjects (69.2%) had a blunted change in airway-occlusion pressure 0.1 s/change in end-tidal carbon dioxide pressure slope. CONCLUSIONS: Subjects with late-onset Pompe disease had an impaired hypercapnic respiratory drive response. The clinical impact of this phenomenon in this subject subset deserves further investigation.