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Assessing Respiratory Immune Responses to Haemophilus Influenzae

Assessing Respiratory Immune Responses to Haemophilus Influenzae

Published on: June 29, 2021

Ampicillin resistance in Haemophilus influenzae from COPD patients in the UK

Satyanarayana Maddi¹, Umme Kolsum¹, Sarah Jackson¹

¹Division of Infection, Immunity and Respiratory Medicine, Medicines Evaluation Unit, University Hospital of South Manchester Foundation Trust, University of Manchester.

International Journal of Chronic Obstructive Pulmonary Disease

|June 6, 2017

Abstract

Background:

Haemophilus influenzae is commonly isolated from the airways of COPD patients. Antibiotic treatment may cause the emergence of resistant H. influenzae strains, particularly ampicillin-resistant strains, including β-lactamase-negative ampicillin resistance (BLNAR) strains. Genetic identification using ftsI sequencing is the optimum method for identifying mutations within BLNAR strains. The prevalence of BLNAR in COPD patients during the stable state has not been reported. We investigated the antibiotic resistance patterns of H. influenzae present in the sputum of stable COPD patients, focusing on ampicillin resistance; the prevalence of enzyme and non-enzyme-mediated ampicillin resistance was determined. A subset of patients was followed up longitudinally to study H. influenzae strain switching and antibiotic sensitivity changes.

Patients And Methods:

Sputum sampling was performed in 61 COPD patients, with 42 samples obtained at baseline; H. influenzae was detected by polymerase chain reaction in 28 samples. In all, 45 patients completed the follow-up for 2 years; 24 H. influenzae isolates were obtained.

Results:

Disk diffusion showed the highest antibiotic resistance in the penicillin antibiotic group (eg, 67% for ampicillin) and macrolides (eg, 46% for erythromycin), whereas all isolates were susceptible to quinolones. Of the 16 isolates resistant to ampicillin, 9 (56%) were β-lactamase positive. The β-lactamase-negative isolates were further investigated; none of these fulfilled the phenotypic BLNAR classification criteria of ampicillin minimum inhibitory concentration >1 µg/mL, and only one demonstrated an ftsI mutation. Frequent H. influenzae strain switching was confirmed using multilocus sequence typing and was associated with changes in the antibiotic sensitivity pattern.

Conclusion:

We observed an overidentification of ampicillin resistance by disk diffusion. The majority of ampicillin resistance was due to enzyme production. H. influenzae strain changes during the stable state may be associated with a change in antibiotic sensitivity; this has implications for empirical antibiotic prescribing.

Insights

Ampicillin resistance in Haemophilus influenzae in COPD patients is often due to enzymes, not mutations. Frequent strain changes in stable COPD patients can alter antibiotic sensitivity, impacting treatment choices.

Area of Science:

Microbiology
Pulmonary Medicine
Infectious Diseases

Background:

*Haemophilus influenzae* is frequently found in the airways of patients with Chronic Obstructive Pulmonary Disease (COPD).
Antibiotic use can lead to the development of resistant *H. influenzae* strains, including ampicillin-resistant strains.
The prevalence of β-lactamase-negative ampicillin resistance (BLNAR) in stable COPD patients remains largely unreported.

Purpose of the Study:

To investigate antibiotic resistance patterns of *H. influenzae* in stable COPD patients, focusing on ampicillin resistance.
To determine the prevalence of enzyme-mediated and non-enzyme-mediated ampicillin resistance.
To longitudinally track *H. influenzae* strain dynamics and antibiotic sensitivity changes in a subset of patients.

Main Methods:

Sputum samples were collected from 61 COPD patients, with 42 at baseline.
*H. influenzae* was detected using polymerase chain reaction (PCR).
Longitudinal follow-up for 2 years in 45 patients, with 24 *H. influenzae* isolates obtained for analysis.

Main Results:

The highest antibiotic resistance was observed for penicillin (67% ampicillin resistance) and macrolides (46% erythromycin resistance).
All isolates were susceptible to quinolones.
Of 16 ampicillin-resistant isolates, 9 (56%) were β-lactamase positive; no β-lactamase-negative isolates met phenotypic BLNAR criteria, and only one had an *ftsI* mutation.
Frequent *H. influenzae* strain switching was observed, correlating with altered antibiotic sensitivity patterns.

Conclusions:

Disk diffusion methods may overidentify ampicillin resistance in *H. influenzae*.
The primary mechanism for ampicillin resistance in this cohort was enzyme production.
*H. influenzae* strain turnover during stable COPD can lead to shifts in antibiotic susceptibility, with implications for empirical therapy selection.

Read full analysis

Keywords:

BLNAR COPD MLST ampicillin resistance

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