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PIGEONS
661 in which the nebuliser jar is emptied and refilled with 0-25% acetic acid; the acid is then nebulised for 5 minutes either outside the nebuliser enclosure or away from the patient. The acid is then discarded, and the nebuliser jar is refilled with water and returned to use. This procedure is repeated daily. With this regimen, in contrast to the results presented in the table, during 1965 670 samples showed 87% to be comparable to ambient air. Additional studies using chlorhexidine diacetate diluted 1/5000 (0-02%) in distilled water were performed. The chlorhexidine solution was placed in the nebuliser jar, nebulised for 10 minutes, and then discarded, and the nebuliser jar was refilled with water. Samples were obtained with an Andersen air-sampler 6-8 hours after decontamination. This procedure was effective in decontaminating 90% of the equipment (see table), and is presented in support of the important observations of Dr. Phillips and Dr. Spencer. These studies
were
performed
under United States Public Health
Service training grants TI-AI-30 and TI-HE-5396. Chlorhexidine was made available through the courtesy of Ayerst Laboratories, Inc. E. BUD EDMONDSON Department of Internal Medicine, University of Texas Southwestern ALAN K. PIERCE Medical School, JAY P. SANFORD. Dallas, Texas 75235.
PIGEONS
SiR,—Your annotationand the reply by Mr. Osman (Jan. 15) prompts me to report here an investigation I carried out
during the
summer
of 1962-63.
Because of the prevalence of human Cryptococcus neoformans infection in Australia (at least 58 cases have been reported) a small survey was undertaken to check the distribution of the organism in and around Adelaide. Nineteen specimens of leaves and nineteen of top-soil humus were collected from bushland in the hills surrounding the city, twenty-nine fresh specimens of pigeon excreta were obtained from lofts by courtesy of members of a racing-pigeon association together with the same number of samples of garden soil into which the loft cleanings were usually deposited, and twenty-two samples of garden soil not known to be contaminated with pigeon or fowl excreta and five samples of fresh fowl excreta from back-yard hen coops were also obtained. A stock strain of C. neoformans isolated from a patient was used to control the isolation and identification of any organisms grown from the specimens. Primary isolation and identification was made by the method of Littman and Zimmerman.2 All capsulated, starch-producing, asporogenous, non-myceliated yeasts growing at 37 °C were tested for pathogenicity by intracerebral mouse inoculation. Seven strains of pathogenic C. neoformans were isolated, and back-checking showed that all came from fresh specimens of pigeon excreta taken from lofts. No pathogenic isolates were made from any other material, and in particular none were isolated from the soil known to be heavily contaminated with loft cleanings. The association of C. neoformans with pigeons is too well documented for further comment. The implication of Mr. Osman that it is only street pigeons that are involved is not borne out by this study. His contention that it is rare for the spores (sic) to become apparent until the droppings have remained for some time, and that the weekly cleaning of lofts averts this, is diametrically opposed by my findings. The warm dry climate of Adelaide is a possible reason for the loss of organisms from contaminated soil, but this reasoning should also apply to the conditions in the lofts, unless the organisms are either in or on the pigeons, or grow so rapidly that fresh droppings can become infected before the conditions in the older droppings become unsuitable. Pathology Department, University of Adelaide, K. D. MURRAY. South Australia. 1. 2.
Lancet, 1965, ii, 1335. Littman, M. L., Zimmerman, L. E. Cryptococcosis-Torulosis. New
York, 1956.
RESPIRATORY ACIDOSIS IN BRONCHIAL ASTHMA like to reply to the letter of Dr. Jean should SIR,-We 1 in which she refers to our article2 cited in your Langlands annotation.33 In regard to our report of two patients with status asthmaticus and respiratory acidosis who were benefited by the correction ofacidasmiawith sodium bicarbonate she asserts : " If... the two patients described in detail by Mithoefer et al. had been given just enough oxygen by means of a Venturi or Edinburgh mask to maintain the arterial P02 at 50-60 mm. (their accustomed level) they would not have developed such severe respiratory acidosis and their response to bronchodilators might have been retained." We are well aware of the potential dangers of oxygen therapyand useVentimasks ’ in chronic pulmonary disease when ventilation is depressed by high inspired oxygen concentrations. There appears to be some confusion, however, about the indications for this form of oxygen therapy, as exemplified by Dr. Langlands’ letter. We should like to point out that there are two ways by which a high concentration of inspired oxygen can result in the development of extreme respiratory acidosis.
(1) Oxygen administered in high concentration may accentuate respiratory acidosis by its well-known ventilatory depressant effect in patients with chronic pulmonary disease. When ventilation is depressed by high concentrations of inspired oxygen the use of a Venturi mask or some other form for administering a low concentration of oxygen is indicated. But there are potential dangers inherent in the use of ventimasks, because, although a fixed inspiredoxygen concentration may be adequate at one moment, under conditions of steady state, it may become seriously inadequate if the patient’s condition suddenly deteriorates owing to long-continued coughing or increased bronchospasm. This is because alveolar oxygen tension not only is determined directly by the inspired-oxygen tension and the alveolar carbon-dioxide tension but also is an inverse function of the exchange ratio, R. This is expressed by the alveolar gas equation:
accompanying figure Part is plotted against R, with three levels of PACO= in a person breathing representing isopleths In the
oxygen from
a
24%
ventimask at sea level. As shown by the arrow marked 1, PACOz is 60 mm., and the exchange ratio 0-8: a rise in PAC02 to 80 mm. will depress alveolar oxygen by only 25 mm. if R remains It is unconstant.
that R would remain constant during a sudden attack of increased
likely, however,
bronchospasm or long-continued cough (R falls from 0-8 to 0-3 within ten seconds after the onset of breath-holding in normal man 5). The arrow marked 2 indicates a fall in PA02 from 100 to 50 mm. in association with the same 20 mm. rise in Pay02 when R is slightly decreased from 0-8 to 0-6. This would represent a potentially fatal degree of hypoxia in a patient with respiratory failure and a large alveolar-arterial (A-a) oxygen gradient. The inverse relation between alveolar oxygen tension and exchange ratio is not taken into account in the calculations which form the basis for the recommendation of the use of ventimasks.6 Attacks of acute
Langlands, J. H. M. Lancet, 1965, ii, 854. Mithoefer, J. C., Runser, R. H., Karetzky, M. S. New Engl. J. Med. 1965, 272, 1200. 3. Lancet, 1965, ii, 632. 4. Mithoefer, J. C. J. Am. med. Ass. 1952, 149, 1116. 5. Mithoefer, J. C. Handbook of Physiology-Respiration; p. 1011. Washington, 1965. 6. Campbell, E. J. M. Lancet, 1960, ii, 10. 1. 2.
were
performed
under United States Public Health
Service training grants TI-AI-30 and TI-HE-5396. Chlorhexidine was made available through the courtesy of Ayerst Laboratories, Inc. E. BUD EDMONDSON Department of Internal Medicine, University of Texas Southwestern ALAN K. PIERCE Medical School, JAY P. SANFORD. Dallas, Texas 75235.
PIGEONS
SiR,—Your annotationand the reply by Mr. Osman (Jan. 15) prompts me to report here an investigation I carried out
during the
summer
of 1962-63.
Because of the prevalence of human Cryptococcus neoformans infection in Australia (at least 58 cases have been reported) a small survey was undertaken to check the distribution of the organism in and around Adelaide. Nineteen specimens of leaves and nineteen of top-soil humus were collected from bushland in the hills surrounding the city, twenty-nine fresh specimens of pigeon excreta were obtained from lofts by courtesy of members of a racing-pigeon association together with the same number of samples of garden soil into which the loft cleanings were usually deposited, and twenty-two samples of garden soil not known to be contaminated with pigeon or fowl excreta and five samples of fresh fowl excreta from back-yard hen coops were also obtained. A stock strain of C. neoformans isolated from a patient was used to control the isolation and identification of any organisms grown from the specimens. Primary isolation and identification was made by the method of Littman and Zimmerman.2 All capsulated, starch-producing, asporogenous, non-myceliated yeasts growing at 37 °C were tested for pathogenicity by intracerebral mouse inoculation. Seven strains of pathogenic C. neoformans were isolated, and back-checking showed that all came from fresh specimens of pigeon excreta taken from lofts. No pathogenic isolates were made from any other material, and in particular none were isolated from the soil known to be heavily contaminated with loft cleanings. The association of C. neoformans with pigeons is too well documented for further comment. The implication of Mr. Osman that it is only street pigeons that are involved is not borne out by this study. His contention that it is rare for the spores (sic) to become apparent until the droppings have remained for some time, and that the weekly cleaning of lofts averts this, is diametrically opposed by my findings. The warm dry climate of Adelaide is a possible reason for the loss of organisms from contaminated soil, but this reasoning should also apply to the conditions in the lofts, unless the organisms are either in or on the pigeons, or grow so rapidly that fresh droppings can become infected before the conditions in the older droppings become unsuitable. Pathology Department, University of Adelaide, K. D. MURRAY. South Australia. 1. 2.
Lancet, 1965, ii, 1335. Littman, M. L., Zimmerman, L. E. Cryptococcosis-Torulosis. New
York, 1956.
RESPIRATORY ACIDOSIS IN BRONCHIAL ASTHMA like to reply to the letter of Dr. Jean should SIR,-We 1 in which she refers to our article2 cited in your Langlands annotation.33 In regard to our report of two patients with status asthmaticus and respiratory acidosis who were benefited by the correction ofacidasmiawith sodium bicarbonate she asserts : " If... the two patients described in detail by Mithoefer et al. had been given just enough oxygen by means of a Venturi or Edinburgh mask to maintain the arterial P02 at 50-60 mm. (their accustomed level) they would not have developed such severe respiratory acidosis and their response to bronchodilators might have been retained." We are well aware of the potential dangers of oxygen therapyand useVentimasks ’ in chronic pulmonary disease when ventilation is depressed by high inspired oxygen concentrations. There appears to be some confusion, however, about the indications for this form of oxygen therapy, as exemplified by Dr. Langlands’ letter. We should like to point out that there are two ways by which a high concentration of inspired oxygen can result in the development of extreme respiratory acidosis.
(1) Oxygen administered in high concentration may accentuate respiratory acidosis by its well-known ventilatory depressant effect in patients with chronic pulmonary disease. When ventilation is depressed by high concentrations of inspired oxygen the use of a Venturi mask or some other form for administering a low concentration of oxygen is indicated. But there are potential dangers inherent in the use of ventimasks, because, although a fixed inspiredoxygen concentration may be adequate at one moment, under conditions of steady state, it may become seriously inadequate if the patient’s condition suddenly deteriorates owing to long-continued coughing or increased bronchospasm. This is because alveolar oxygen tension not only is determined directly by the inspired-oxygen tension and the alveolar carbon-dioxide tension but also is an inverse function of the exchange ratio, R. This is expressed by the alveolar gas equation:
accompanying figure Part is plotted against R, with three levels of PACO= in a person breathing representing isopleths In the
oxygen from
a
24%
ventimask at sea level. As shown by the arrow marked 1, PACOz is 60 mm., and the exchange ratio 0-8: a rise in PAC02 to 80 mm. will depress alveolar oxygen by only 25 mm. if R remains It is unconstant.
that R would remain constant during a sudden attack of increased
likely, however,
bronchospasm or long-continued cough (R falls from 0-8 to 0-3 within ten seconds after the onset of breath-holding in normal man 5). The arrow marked 2 indicates a fall in PA02 from 100 to 50 mm. in association with the same 20 mm. rise in Pay02 when R is slightly decreased from 0-8 to 0-6. This would represent a potentially fatal degree of hypoxia in a patient with respiratory failure and a large alveolar-arterial (A-a) oxygen gradient. The inverse relation between alveolar oxygen tension and exchange ratio is not taken into account in the calculations which form the basis for the recommendation of the use of ventimasks.6 Attacks of acute
Langlands, J. H. M. Lancet, 1965, ii, 854. Mithoefer, J. C., Runser, R. H., Karetzky, M. S. New Engl. J. Med. 1965, 272, 1200. 3. Lancet, 1965, ii, 632. 4. Mithoefer, J. C. J. Am. med. Ass. 1952, 149, 1116. 5. Mithoefer, J. C. Handbook of Physiology-Respiration; p. 1011. Washington, 1965. 6. Campbell, E. J. M. Lancet, 1960, ii, 10. 1. 2.