Inflammatory markers of lower respiratory tract infection in elderly people

Age and Ageing, July, 1994 by M.K. Albazzaz, C. Pal, P. Berman, D.J. Shale

Summary

Bacterial infections of the respiratory tract are a major cause of morbidity and mortality in elderly people. The inflammatory response to such infection is an important protective process and has been suggested to be less effective in elderly patients. To investigate the inflammatory response in respiratory infections acquired in the community by elderly people we studied 52 consecutive patients who met the criteria for either a non-pneumonic chest infection or pneumonia. After exclusion, 41 patients were available for evaluation, with 25 fulfilling the criteria of pneumonia and 16 the criteria of chest infection. Pyrexia was a feature of the patients with pneumonia. Circulating levels of neutrophil elastase-alpha-l-antitrypsin complex and C-reactive protein were greater in the patients with pneumonia than in those with a chest infection and were reduced following antibiotic treatment. No changes occurred in the chest infection group for these markers of inflammation. In both groups, a further neutrophil granule protein, lactoferrin, was unaffected by antibiotic treatment. This study indicates that elderly patients with pneumonia can initiate an appropriate inflammatory response as demonstrated by clinical indicators and circulating mediators of the inflammatory response.

Introduction

Elderly patients are susceptible to bacterial infections of the respiratory and urinary tract, which are a major cause of death exceeded only by cancer and myocardial infarction(1). The inflammatory response to such infection is a host defence process which includes fever, increased circulating concentrations of acute-phase reactants, such as C-reactive protein(2), mobilization of neutrophils from the bone marrow with margination, migration and activation at the site of infection where phagocytosis and bacterial killing occurs. The last is dependent upon the production of reactive oxygen metabolites and the release of cytoplasmic granule products into phagosomes. External release of such products will cause local tissue injury. Neutrophil granule products and C-reactive protein have been used as indicators of the intensity of the inflammatory response in respiratory disorders, such as cystic fibrosis (3)(4)(5)(6)(7)(8)(9).

It has been proposed that reduction in immune function and attenuation of the inflammatory response may modify the clinical presentation of infection in old age. However, most of the investigation of this hypothesis has focused on lymphocyte function(10)(11)(12), with less attention being devoted to the polymorphonuclear leucocyte, despite its primary role in the defence against infection. We assessed the inflammatory response to lower respiratory tract infection in elderly subjects by measuring serum C-reactive protein and plasma neutrophil elastase-[[alpha].sub.1]-antiproteinase complex and lactoferrin in patients with pneumonia and chest infection.

Methods

Patients: All patients aged over 65 years with suspected acute lower respiratory tract infection admitted to health care of the elderly wards at the City Hospital Nottingham, England during a 4-month period were studied. Each patient was reviewed as soon as possible after admission by an investigator (M.K.A. or C.P.). History, including antibiotic treatment, and physical examination were noted. Patients with severe, chronic illness or disability in whom lower respiratory tract infection was an expected terminal event, those receiving immunosuppressive treatment and patients with diabetes mellitus were excluded from the study.

Patients were classified as having either pneumonia or a chest infection. Pneumonia was defined by new symptoms of cough, increased sputum production and dyspnoea with new shadowing on the chest radiograph. A chest infection was defined as new respiratory tract symptoms not associated with new shadowing on the chest radiograph.

Investigations: Blood was obtained for full and differential blood counts and for bacterial culture. Serum was obtained at admission and on day 14 or prior to discharge for complement fixation studies for Influenza virus A and B, Respiratory syncytial virus, Adenovirus, Coxiella burnetti, Chlamydia psittacii and Mycoplasma pneumoniae. Immunofluorescence for Legionnella pneumophila serotype I was performed. Capillary blood gases were estimated, and plasma (disodium EDTA) and serum were obtained at admission and 14 days later. After separation both were stored at -70[degrees]C until assayed. The concentrations of neutrophil elastase-[[alpha].sub.1]-antiproteinase complex (elastase complex), lactoferrin and C-reactive protein were determined by double antibody capture enzyme-linked immunosorbent assays (ELISA)(4)(5)(6). Assays were performed blind of clinical details in batches after all samples had been collected. A postero-anterior chest radiograph and a lateral view, whenever possible, were performed at the time of admission and prior to discharge. Patients were treated with the appropriate antibiotic as indicated by culture and sensitivity testing or the choice of the admitting physician and were reviewed regularly whilst in hospital.