 |
|
||||
|
|||||
| About | Latest Articles | Back-Issues | Articles
|
Search | Instructions | Online Submission | Subscribe | Etcetera | Contact |
| |||||||||||||||||||||
|
Chronic bronchitis : Part I. A bacteriological study of acute exacerbation.
Chronic bronchitis is a disease fairly prevalent in the industrialized metropolitan cities of India. It causes a big drain on economy due to loss of man hours of work in industries. It also results in considerable morbidity and mortality due to its chronicity and tendency to repeated exacerbations, both infective and noninfective. Chronic bronchitis is defined as a disease in which there is chronic or recurrent increase in the volume of mucoid secretion sufficient to cause expectoration. The disease causes expectoration on most days during three consecutive months for more than two successive years.[7] These episodes of increased expectoration are termed exacerbations of the disease and are usually associated with marked increase in patient's clinical symptoms, signs and functional disability. Many organisms have been implicated in these exacerbations especially Haemophilus influenzae and Diplococci pneumoniae. However, the studies are inconclusive about the associations of these organisms with pathogenesis of exacerbations.[11] Efforts to quantitate the total contribution of all infections to episodes of exacerbation have shown that about 45% of such episodes can be accounted for by an infectious cause. Since many of the exacerbations are non-infective, the unnecessary use of antibiotics in these causes a lot of waste notwithstanding the inherent dangers of such therapy. However, these exacerbations are mainly responsible for the irreversible progression of the disease. The relentless progress of this disease can be halted and mortality and morbidity significantly reduced if these exacerbations could be controlled and prevented. This study was undertaken (1) to detect the common organisms responsible for the infective exacerbations of chronic bronchitis over a period of 2 years and (2) to detect the role of these infections in the progress of the disease.
The clinical material consisted of chronic bronchitis patients admitted to medical ward during exacerbations at the K.E.M Hospital. patients were subject to a thorough clinical examination with emphasis on their cardiorespiratory disability. A complete haemogram, X-ray chest, ECG, blood gases and all other routine bio-chemical investigations were done. Sputum was collected by peroral aseptic technique in the following way [Fig. 1] The patient, in the sitting position, was told to rinse the mouth with sterile normal saline. A bite block was kept to prevent closure of mouth till the procedure was over. A sterile endotracheal tube was introduced upto the opening of the pharynx. The patient was made to hold the tube in position. Then a plain suction catheter, with a 10 ml syringe attached, was introduced, in the pharynx through the endotracheal tube. The patient was asked to cough vigorously and the expectorate was aspirated through the suction catheter and transferred to a sterile petri dish. Alternatively, the routine method of sputum collection (i.e. rinsing the mouth with sterile saline followed by collecting the patient's expectorated sputum) was also carried out in a few patients. These methods did not show difference in the results by the criteria followed and hence both the methods were followed for collection of sputum depending upon the feasibility and patient's co-operation. The sputum was homogenised by using a mixture of pancreatin and trypsin (1:5). Equal quantity of sputum and the mixture (pancreatin-trypsin) were put in a sterile test tube and incubated at 37°C for 20 minutes. The smear was then made. The homogenised sputum was further diluted serially to the final dilution 10[10]. One ml each of these. dilutions was plated out on MacConkey, blood agar, Muller-Hinton agar and chocolate agar and incubated at 37°C for 18 hours. Colony counts were done. Antibiotic sensitivity was done with ampicillin, penicillin, sulfonamide, chloramphenicol, tetracycline, erythromycin, sterptomycin, kanamycin and gentamicin. Inhibition around the discs was measured and the sensitivity pattern was noted. Positive results obtained from sputum microscopy for estimation of etiological agents of respiratory tract infection are not helpful in incriminating the true aetiological agents, as the pathogens are irregularly distributed in the sputum. Therefore, quantitative microbiological analysis was attempted in this study.
Most of the past studies have taken colony count of 107 per ml as significant in sputa[8], [12]. However, an extensive study[2] carried out on the bacteriology of the lower respiratory tract in 697 patients, over a period of 4 years has shown that significant bacterial count of the sputum differs in pathogens and commensal organisms. For pathogens it is > 104/ml and for commensal it is > 107/ml. Our analysis is based on these criteria. There were 49 patients. Out of these, 46 were males and 3 females with ages varying between 26 and 66 years. Out of 49 samples, significant bacterial colony count was seen in 28 samples. In 14 samples, the bacterial growth was non-significant. Three samples did not show any growth and 4 showed contaminants. Among the group of pathogenic organisms (colony count > 104 per ml), Klebsiella, Staphylococcus coagulase positive and Pseudomonas were isolated in 11, 8 and 3 samples respectively. Among the group of commensals (colony count 107 per ml), Streptococcus viridans,> Staphylococcus coagulase negative and Achromobacter were isolated in 5, 2 and 2 samples respectively. The pattern of antibiotic sensitivity is shown in [Table - 1]
Several authors have published data regarding the bacterial flora in the sputum of patients with chronic bronchitis. Inspite of the knowledge about the rarity of occurrence of pathogenic organisms in the lower respiratory tract[9], May[6] has indicated the relative frequency of pathogens like Haemophilus influenzae, Diplococci pneumoniae and Staphylococcus aureus. Some studies have concentrated on the comparison of various methods of specimen collection e.g. throat swab, expectorated sputum and bronchoscopy. All these methods encounter the problem of mixing the pathogen with the normal inhabitant flora of the upper respiratory tracts.[1], [4], [5]. The irregular distribution of pathogens in sputum makes a qualitative culture unreliable for incriminating any organism as a pathogen. Quantitative sputum culture helps in proving pathogenic role of isolated organisms. Hence we have taken help of quantitative culture and this has brought out certain interesting points. Twenty eight out of total 49 patients i.e. 57% grew organisms in significant counts. The most common organisms grown in significant counts were Klebsiella and Staphylococcus coagulase positive. Klebsiella was the pathogen in 11 patients and Staphylococcus coagulase positive in 8 patients. Diplococci pneumoniae and Haemophilus influenzae have been a prominent feature of most of the Western studies[6], [9]. However, their absence in our, and other Indian studies may be explained by the following facts[2], [10]: (a) Haemophilus influenzae is usually absent in mouth and oropharynx (b) Inspite of the use of media like chocolate agar and Muller-Hinton agar, H, influenzae was not grown. The inadvertent use of antibiotics in these chronic sufferers might have eradicated this organism from the sputa. Out of these 28 sputa, 22 grew single causative organisms and 6 had multiple (2 or more) pathogens making a total of 31. All the patients were started on broad-spectrum antibiotic (ampicillin) after sputum collection. The antibiotic sensitivity showed resistance to ampicillin in majority of the patients. However, all these patients showed clinical improvement at the end of therapy. Three of the patients grew Klebsiella in a significant count after therapy. One patient grew Staphylococcus coagulase negative in significant number at the end of therapy. These observations suggest that: (a) in some of these patients effects of antibiotics were not the cause of improvement in clinical status; (b) antibiotics may not only change the bacterial flora but may allow growth of new or same organisms in significant number which may be hazardous. Out of the total 49 sputa, remaining 21 were divided in 3 groups: (a) Group with non-significant count: There were 14 samples in this group, out of which 8 samples grew organisms which were resistant to ampicillin. One sample grew Klebsiella in significant count following treatment, which also was resistant to ampicillin. Another who had grown Staphylococcus coagulase negative in colony count of 105/ml before therapy showed a stepping up of colony count to 107/ml. (b) Group with no growth: Following treatment of the 3 samples in this group, 1. grew Proteus in significant count which was resistant to ampicillin. (c) Group with contaminants: Four sputa grew contaminants-out of which 2 grew Klebsiella and 1 grew E. coli in significant count after treatment. Both were resistant to ampicillin. These observations (on the remaining 21 patients) not only support the earlier observations on hazards of antibiotics but also emphasise the non-bacterial/noninfectious nature of the exacerbations. The above points, observed in the group which had bacteria in a significant count with resistance to ampicillin, and observations in groups who had non-significant bacterial counts, no growth or contaminant growth, lead us to an important conclusion that these exacerbations are due to non-bacterial organisms i.e. viruses or mycoplasma, or are non-infective (i.e. due to any other yet unidentified cause). These viruses, mycoplasma or other factors may serve to sensitise the mucosa of the respiratory tract. The high prevalence of various organisms in sputum during exacerbations may be explained by impaired local defence mechanisms, allowing upper respiratory tract flora to colonise the lower respiratory tract.[3] It is quite possible that these bacteria act as non-invasive infectants. The whole process of exacerbation may be an altered immunologic response invoked by the sensitisation of the respiratory epithelium either to bacterial or viral antigens. This may lead to hypersensitivity reactions liberating biochemically active substances, under stresses like smoking, pollutant exposure, etc. causing bronchospasm. This explains how the isolated organisms indirectly acting as non-invasive infectants lead to the exacerbations of chronic bronchitis.;
We thank the Dean, Seth G.S. Medical College and K.E.M. Hospital, Bombay, for permission to publish this paper.
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
|||||||
