1165 chin and crowded teeth reflect hard food in infancy.
not
heredity
but lack of
really
A correspondent in New Zealand writes that an old Maori told him that hot food was the cause of the degeneration of his people’s teeth; and that William Colenso, the missionary, in his diary of the 1840s wrote that in Rotorua he noticed considerable tooth decay, which he had never seen in Maoris elsewhere, and which he attributed to a harmful element in the boiling pools in which they cook their food. The " harmful element", my correspondent adds, may have been the heat. A physician from New York writes that in her family she was the only one totally free of dental caries and she also differed from the others in that from childhood she had a pronounced aversion to eating or drinking anything hot. Mr. Dendy last week (p. 1104) mentions the " documented evidence pointing to bacteria and carbohydrates as the cause of dental caries, but review (e.g., the study in Vipeholm Hospital, Sweden, 1945-51) shows that: (1) it bears not on the cause but on the way the rate of caries differs under different dietary regimens, for under their best diets new caries continues to appear; (2) the carefully controlled experiments neglect to take into consideration the way this very control alters the heat in the food. A diet with plenty of milk, apples, and raw carrots which leads to less caries is also a less hot diet. An argument cannot very well be based on less caries in root-filled (dead) teeth or on how we might expect caries to begin or advance. Strychnine-killed pulp-filled teeth become grey and brittle, and crumble within a year or two. Appeal must now be to the court of experiment and practice. S. W. S. W. TAYLOR. TAYLOR. New Zealand. "
GRADING BACTERIAL AIRWAY INFECTIONS
SIR,-There is evidence that irreparable centrilobular emphysema occurs as a complication not in any case of chronic bronchitis, but chiefly as a consequence of relapsing bacterial infections.! The very common problem of infected bronchitis is therefore important. However, it is not easy to judge the significance of bacteria demonstrated in bronchial secretions. Large series of comparative bacteriological investigations on transtracheal-puncture specimens, bronchoscopic aspirates, upper-airway secretions, and washed sputahave shown that presence of recent infection cannot be inferred merely from bacteriological examination. For diagnosing this, the clinical laboratory has no choice but to compare at least four of the cytological and bacteriological results of such sputum examination : degree of purulence, eosinophil-count, gram-smear (for visible bacterial flora), and cultures (for detecting multiplying microorganism). In order to decide whether chemotherapy is necessary, these four laboratory tests can be used to give a simple and reliable scale by scoring each from 0 to 2 points as
infection is proved. Grades 4-6 are found either in the course of antibacterial treatment, or in consequence of technical differences. Such a scale not only allows easy assessment in follow-up studies, but also may be of value, within certain limits, in controlled therapeutic trials. Department of Chest Diseases, University Medical School, Diosárok 1/c, Budapest, Hungary.
METHOTREXATE IN PSORIASIS SIR,-Methotrexate has become a standard treatment for severe and resistant cases of psoriasis.! The side-effects are said to be temporary and reversible,2and, among the several hundred recorded cases so treated, there have been only two deaths.3 ’We should like to draw attention to a rapid and fatal reaction in two of our patients following administration of methotrexate. The first patient presented with generalised psoriatic erythroderma, and the second with generalised psoriasis and severe psoriatic arthropathy. Both patients had been on longterm corticosteroid therapy, from which they could not be weaned. Methotrexate was administered by mouth-in the first patient 5 mg. daily for five days, and in the second 5 mg. daily for seven days. The treatment was stopped in both cases because of pyrexia, which was assumed to be due to sepsis, though there was no laboratory confirmation for this assumption. Both patients had normal blood-counts and liver and renal function tests before treatment and on the day the treatment was discontinued. A few days later both became comatose and died-the first seven days and the second five days after the treatment was stopped. The white-blood-cell count on the day of death was 2600 per c.mm. (2"o lymphocytes) in the first case and 800 per c.mm. in the second case. The hemoglobin and the platelet-count were normal. Postmortem examination revealed nothing significant in either case apart from severe hypoplasia of the bone-marrow. In the first case a pure culture of klebsiella was obtained from the spleen, whereas in the second the culture was sterile. Three days before death the psoriatic lesions disappeared in both patients and were replaced by freely bleeding areas. We cannot explain the bone-marrow depression in these cases in terms of the known toxicity of the drug. Indeed we cannot exclude, in the first case, the possibility of chloramphenicol toxicity, since this drug was given together with the methotrexate; but in the second patient the reaction followed the methotrexate alone. Unlike the two other reported fatal cases,34 our patients received a low dose of the drug and only for a short time. It is noteworthy that both patients had been on long-term corticosteroid therapy.
follows : Purulence (three-minute microscopic examination of washed sputum deposit): less than 10% leucocytes 0, 10-50% leucocytes 1, more than 50°o leucocytes 2. Eosinophil-count (wet staining method 3) : more than 1 eosinophil per field, or groups of eosinophils 0, occasional eosinophil 1, no
eosinophils
2.
Gram-smear:
homogeneous bacterial flora 2, inhomogeneous
bacterial flora I,
no visible bacteria 0. Cultures (on different, partly selective, agar plates): homogeneous culture identical with that seen by staining 2, inhomogeneous culture 1, no growing bacteria, or culture not identical with gram-smear 0.
These examinations must be carried out by reliable and standard techniques. The sum of the four scores result in a scale of 0-8 which may be called the bronchial-infection grading ". Laboratory evidence of active bronchial infection is given by grades 7 and 8. Grades 0-3 mean that no bacterial "
1. Ciba
Symposium. Thorax, 1959, 14, 286; Bates, D. V., Christie, R. V. Respiratory Function in Disease. Philadelphia, 1964. 2. Miskovits, G., Lányi, M., Dubay, M. Orv. Hétil. 1967, 108, 9; Lányi, M. International Congress of Diseases of the Chest, Copenhagen, August, 1966; Z. Tuberk. 1967, 126, 156; Orv. Hétil. 1967, 108, 303. 3. Mulder, J. in Bronchitis (edited by Orie-Sluiter); p. 15. Assen, Netherlands, 1961.
MIKLÓS LÁNYI.
Departments of Dermatology and Internal Medicine B, Rambam Government Hospital, Haifa, Israel.
S. HAIM G. ALROY.
ALLERGIC DERMATITIS PRODUCED BY ORAL CLIOQUINOL SiR,łThis is a report on a 32-year-old man with periods of pustular psoriasis during the past ten years. After topical treatment of the left side of his body with an ointment containing 1°,,clioquinol (’Vioform’) he developed a contact dermatitis clearly localised on the treated side. The treatment was discontinued and the reaction disappeared within a week. During the past three months he has taken 200 mg. allopurinol (’ Zyloric ’) daily and has shown no signs of psoriasis. To treat a slight enteritis he recently took two tablets of Entero-Vioform ’, each containing 0-25 g. clioquinol. A few 1. 2.
Rees, B. R., Benett, J. H., Maiback, H. J. Archs Derm. 1967, 95, 2. Borrie, P. F., Robinson, T. M. E., Mackay, I. B. Br. J. Derm. 1967,
79. 7. 3. Black, R. L., O’Brien, W. M., Van Scot, E. J., Auerbach, A. Z., Bunin, J. J. J. Am. med. Ass. 1964, 189, 743. 4. Shrunk, A. B., Blondis, L. M. Br. med. J. 1965, ii, 156.
R., Eisen,