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THE ETIOLOGY OF PORAL CLOSURE

IV. THE EFFECT OF LIP0ID SOLVENTS ON THE PORES OF THE SKIN.FINAL DISCUSSION OF PORAL CLOSURE

J. P. O'BRIEN, M.D.

Pathologist, The Prince Henry Hospital, Sydney, Australia

It is the purpose here to enlarge upon earlier experiments (2) wherein it wasnoted that lipoid solvents are apt to produce poral plugging whenever they arerepeatedly applied to the skin.

Private B. had been in the tropics for two months. He had neither a his-tory nor sign of skin disease. Cotton wool pads moistened in kerosene wereapplied to a test area of skin on one side of the abdomen for 15 minutes eachday. The other or control side of the abdomen was treated simultaneouslyin the same way except that the kerosene used there had been pre-satu-rated with anhydrous lanolin. After 3 days of treatment the test area showedthe first elements of a rash composed of small clear superficial vesicles on ared base. After 5 more days, during which only one further treatment wasgiven, the rash had become more florid, more infiltrated and more like mil-iaria. Biopsies were taken from both the test and control areas after a fur-ther 10 days during which another 3 intermittent applications had beenmade.Thirty separate experiments of this general type were carried out in the tropics

in 1945. Kerosene was chosen as the solvent partly because of its low volatilityand partly because of ease of supply.

In order to avoid severe reactions such as blistering, the applications werenever made more than once daily, and the routine was varied for each subjectaccording to the intensity of response. The experiments were discontinued ifno response was obtained within 2 weeks.

In half of the experiments a crystalline or a miliaria-like rash was producedwith varying ease on the test side. In the remainder the response was negativeor doubtful.

In only one instance was any rash produced on the control side; it was ofmacular type.

HISTOPATHOLOGIC CHANGES

This analysis is made from a study of 600 serial sections made from 5 biopsies.Three of the biopsies were from test areas and 2 from control areas.

Plate 43 gives a general view of the severity and extent of the changes in theskin exposed to the kerosene. For comparison, Plate 44 is from the control sideof the same subject and illustrates how pre-saturation with lanolin abolished theirritant effect.

In addition to these diffuse changes lipoid solvents have a special proclivityto enter and set up inflammation within the sweat pores and the pilosebaceousfollicles.

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142 THE JOURNAL OF INVESTIGATIVE DERMATOLOGY

PLATE 43. A general view showing the gross changes produced in the skin by applicationsof kerosene. (Haematoxylin and Biebrich Scarlet. X 200.)

PLATE 44. A section of the control area from the same subject as Plate 43. The area wastreated with lanolin-saturated kerosene; there are no pathologic changes. Note normal porewith its keratin ring on the left. (H. and B. S. >< 200.)

(i) The Sweat Pores: Both vesicular and parakeratotic lesions occur. Plate 45shows a vesicular lesion and suggests that the solvent penetrated by way of the

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ETIOLOGY OF PORAL CLOSURE 143

pore. In Plate 46 the inflammatory reaction is intense and the sweat pore isobscured by an infiltrate composed of neutrophils, monocytes and lymphocytes.Poral plugging is illustrated in Plates 47, 48, 49 and 50.

(ii) The Filosebaceous Follicles: These structures demonstrate analogouschanges of great severity. In Plate 51 there is an extreme degree of internal and

PLATE 45. Kerosene treated skin; the solvent has apparently entered by way of the pore.The vesiele is paraduetal and contains numerous neutrophils. (H. and B. S. X 400.)

external infiltration of a follicle. Distension and infiltration of the neck of a fol-licle is very striking in Plate 52. A commencing parakeratotic reaction is thefeature of Plate 53.

DI5CU55ION

Although these experiments with a lipoid solvent were originally undertakenwith the object of throwing light on lipoid depletion in natural miliaria (2), theonly valid conclusion to be drawn from them is that kerosene produces poralvesieulation and plugging in its own right.

The property of solvents to cause these changes does not appear to run paral-


Id to their capacity to dissolve lipoid. Thus, although both amyl acetate andacetone are potent lipoid solvents, they did not produce any rash in several ex-periments wherein I applied them to the skin. Such differences amongst solventscall for detailed study.

PLATE 46. Very dense cellular infiltration in relation to a sweat pore (indicated by ar-row). The appearances suggest poral penetration by the kerosene. The identity of thepore was confirmed with the aid of adjacent serial sections. (H. and B. S. X 400.)

Certain oils and greases are known to penetrate the piloscbaccous follicles andto cause acne. Moreover Ellcr and Wolff (46) have shown in experiments on rab-bits that lanolin and other natural lipoids have a special tendency to penetratethe follicles. It therefore seems to be a general rule for fat-like and oil-like sub-stances and their solvents to permeate the skin by way of its orifices; whetherirritation results depends on the particular agent used.

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PLATES 47 to 49. A variety of poral plugs produced by kerosene. (H. and B. S. X 400.)

PLATE 48

SUMMARY OF PART IV

The frequent application of kerosene Icads to inflammation and parakeratosisof the sweat pores and pilosebaceous follicles.

Irritant lipoid solvents such as kerosene form a special category of substancesproducing poral closure.

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FINAL DISCUSSION OF PORAL CLOSURE

The present series of papers has given evidence showing that the causes ofclosure of sweat pores are manifold. Direct evidence has been given in relation

PLATE 49

PLATE 50. A very large poral plug produced by kerosene. (H. and B. S. )< 270.)

to staphylococcal infection, to the effect of overusing soap and to the action oflipoid solvents, all of which may seemingly give rise to a miliarial rash in theirown right. It also appears possible that edema of the stratum corneum maylike\vise lead to poral closure but in this case the effect is probably temporary

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ETIOLOGY OF POEAL CLOSURE 147

PLATE 51. This picture indicates deep penetration of a pilosebaceous follicle by kero-sene. The intra-follieular infiltration is composed chiefly of neutrophils and amounts to asmall abscess. The infiltrate around the follicle is composed chiefly of lymphocytes. (H.and B. S. X 200.)

and feeble and when uncomplicated is manifested clinically as crystallina (su-damen). Sebaceous deficiency of the stratum corneum is a further probable causeof closure. It was discussed herein and at greater length in an earlier paper (2).

The actual chain of causation of closure probably varies from case to case and

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from one clinical entity to another. In many instances it appears likely that thedifferent factors augment each other to the same end. Thus, since cutaneous

PLATE 52. A dense collection of neutrophils distending the neck of a follicle. From kero-sene-treated skin. (H. and B. S. X 400.)

lipoids are antibacterial, their depletion may indirectly promote infection. Sim-ilarly lipoid depletion may be expected to favor the production of edema. Edemamay promote infection.

However, apart from these generalities, it now seems justifiable to be morespecific in regard to some of the clinical entities :—

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(1) Staphylococcal poral infection appears to be the predominant cause ofacute tropical miliaria rubra. Despite an earlier view to the contrary (2),lipoid depletion of the stratum corneum probably plays at best a contrib-utory role.

(2) Bullous impetigo is also a form of staphylococcal poral infection.

PLATE 53. A parakeratotie plug in the mouth of a follicle. From kerosene-treated skin.(H. and B. S. )< 400.)

(3) On the basis of the lipoid response (2), the poral closure associated withchronic ichthyoid states of the skin, including post-miliarial anhidrosis, isprobably due simply and directly to lipoid depletion. Large keratin orparakeratotic plugs may or may not be present in the pores (2).

Increased temperature and edema of the stratum eorneum can be identifiedas contributory factors in both miliaria rubra and bullous impetigo.

The preceding conclusions largely derive from the use of a new technic wherebythe common staphyloeoccal infections of the skin can be experimentally producedunder controlled conditions.


I wish to thank the volunteers who cooperated in this study.The whole of the technical work, including the preparation of the sections and

photographs, was carried out by the author.Some plates (6, 29, 30, 42, 43, and 44) have been considerably reduced from

the magnifications stated in the legends.

REFERENCES

1. SULZBEEOER, MARION B., HEEEMANN, F., AND ZAK, F. C.: Studies of sweating: 1. Pre-liminary report with particular emphasis on a sweat retention syndrome, J. Invest.Dermat. 9: 221 (Nov.) 1947.

2. O'BEIEN, J. P.: A study of miliaria rubra, tropical anhidrosis and anhidrotic asthenia,Brit. J. Dermat. 59: 125 (Apr.—May) 1947.

3. KNOWLEs, R. B.: Factors influencing dermatitis in coal-miners, Brit. M.J. 2:430 (Sept.30) 1944.

4. SHELLEY, W. B., HoavATH, P. N., WEIDMAN, F. P., AND PILLsBURY, D. M.: Experi-mental miliaria in man: 1. Production of sweat retention anhidrosis and vesicles bymeans of iontophoresis, J. Invest. Dermat. 11: 275 (Oct.) 1948.

5. (a) ROBERTsON, A. M.: Prickly heat and tropical pemphigus, J. Roy. Nay. M. Serv.31: 25ft (Oct.) 1945. (b) D'AYANZO, C. S.: Impetigo Bullosa in the Tropics, Arch.Dermat. & Syph. 52: 28 (July) 1945. (c) SULZBEEGEE, MARION B., AND BAEE, R. L.:Year Book of Dermatology & Syphilology, Chicago, The Year Book Publishers,1945, p. 318. (d) Pn. SIMON5, R. D. C.: Studies on pyosis mansoni or impetigo bullosatropica, Dermatologica, 93: 189, 1946.

6. (a) ALLISON, V. P., AND HoBBs, H. C.: An inquiry into the epidemiology of pemphigusneonatorum, Brit. M. J. 2: 1, (July 5), 1947. (b) PEELSTEIN, M. A.: Evaluation ofcertain preparations for care of the skin of newborn infants, Am. J. Dis. Child. 75:385 (Mar.) 1948.

7. DAVIES, J. H. T., DIXON, K., AND STUART-HARRIs, C. H.: A therapeutic trial of peni-cillin in infective conditions of the skin, Quart. J. Med. 14: 183 (Oct.) 1945.

S. O'BRIEN, J. P.: Tropical Anhidrotic asthenia: Its definition and relationship to otherheat disorders, Arch. mt. Med. 81: 799 (June) 1948.

9. SULZBEEGEE, MARION B., AND ZIMMERMAN, H. M.: Studies on prickly heat: 11. Experi-mental and histologic findings, J. Invest. Dermat. 7: 61 (Feb.) 1946.

10. RoBINsoN, A. R.: J. Cutan. Dis. 2: 362, 1884.11. STELwAGON, H. W.: Treatise on Diseases of the Skin, ed. 6, Philadelphia and London,

W. B. Saunders Company, 1911, p. 1051.12. POLLITZEE, S.: Prickly heat, lichen tropicus, miliaria papulosa, miliaria rubra, etc.,

J. Cutan. Dis. 11: 50 (Feb.) 1893.13. IJNNA, P. G.: The Histopathology of Diseases of the Skin, Edinburgh, William F. Clay,

1896, p. 908.14. AcTON, H. W.: Prickly Heat, md. Med. Gaz. 61: 321 (July) 1926.15. ANDEEWs, C. C.: Diseases of the Skin, Philadelphia and London, W. B. Saunders Com-

pany, 1932, p. 258.16. SULEBEEGEE, MARIoN B. AND EMIK, L. 0.: Studies of prickly heat: 1. Clinical and sta-

tistical findings, J. Invest. Dermat. 7: 53 (Feb.) 1946.17. SMITH, E. C.: Prickly heat: Its aetiology and pathology, Tr. Roy. Soc. Trop. Med. &

Hyg. 20: 344 (Jan.) 1927.18. CONANT, N. F. MARTIN, D. S., SMITH, .D. T., BAKER, R. D., AND CALLAWAY, J. L.:

Manual of Clinical Mycology, Philadelphia and London, W. B. Saunders Company,1944, p. 142.

19. (a) COLEBEOOK, L.: The disinfection of the skin, Bull. War Med. 2: 73 (Nov.) 1941. (b)REBELL, C. C.: Staphylococci and haemolytic streptococci from normal skin andcutaneous infections, J. Invest. Dermat. 8: 13 (Jan.) 1947. (c) DEYENI5H, E. A., AND

ETIOLOGY OF POEAL CLOSUEE 151

MILES, A. A.: Control of Staphylococcus Aureus in the operating theatre, Laneet 1:1058 (May 13) 1939.

20. PEICE, P. B.: The bacteriology of normal skin: A new quantitative test applied to astudy of the bacterial flora and the disinfectant action of mechanical cleansing, J.Infect. Dis. 63: 301 (Nov—Dec.) 1938.

21. BULL, J. P., SQUTEE, J. R., AND TOPLEY, E.: Experinents with occlusive dressings of anew plastic, Lancet 2: 213 (Aug. 7) 1948.

22. WILLIAMs, R. E. 0.: Skin and nose carriage of bacteriophage types of Staph. aureus,J. Path. & Bact. 58: 259 (Apr.) 1946.

23. BENHAM, H. W.: The cultural characteristics of Pityrosporum Oeale—a lipophylicfungus, J. Invest. Dermat. 2: 187 (Aug.) 1939.

24. (a) EMMONS, C. W.: The isolation and pathogenicity of Pityrosporuni Oeale, Pub.Health Rep. 55: 1306 (July 19) 1940. (b) SULZBEEOEE, MAHION B. in discussion of KILE,H. L., AND ENCMAN, M. F.: Further studies of relationship of Pityrosporum Ovate toseborrhoeic eczema, Arch. Dermat. & Syph. 37: 616 (Apr.) 1938.

25. NAPIEE, L. E.: The Principles and Practice of Tropical Medicine, New York, TheMacMillan Company, 1946, p. 571.

26. HORNE, C. 0., AND MOLE, H. H.: The effect of water and salt intake on prickly heat,Lancet, 2: 279 (Aug. 13) 1949.

27. SULzBEEOEE, MAEION B.: Unpublished observations, see (Sc); O'BEIEN, J. P.: Unpub-lished observations.

28. (a) WILsoN, C. J.: Prickly heat: A simple remedy, Brit. M. J. 1: 318 (Feb. 14) 1948.(b) WALTON, W. F.: Aetiology of prickly heat, Brit. M. J. 1: 228 (Jan. 31) 1948. (c)BEOWNE, M. P.: Prickly heat: A simple remedy, Brit. M. J. 1:228 (Jan. 31) 1948. (d)BARBEE, C. H.: Prickly heat: A simple remedy, Brit. M. J. 1: 318 (Feb. 14) 1948.

29. Quoted by MUTE, H., AND RITCHIE, J.: Manual of Bacteriology, ad. 10, London, OxfordUniversity Press, 1937, p. 119.

30. MINOE, V.: Em neues Verfahren zu der klinishen Untersuchung der Schweissabson-derung, Deutsche Ztschr. f. Nervenh., 101: 302, 1928; quoted by PALMER, A. J.: Hy-perhidrosis, Arch. Neurol. & Psychiat. 58: 582 (Nov.) 1947.

31. ROTEMAN, S.: The principles of percutaneous absorption, J. Lab. & Clin. Mcd. 28: 1305(Aug.) 1943.

32. ARNOLD, L.: Relationship between certain physico-chcmical changes in the cornificdlayer and the endoganous bacterial flora of the skin, J. Invest. Dermat. 5: 207 (Oct.)1942.

33. HisL, J. H., AND WHITE, E. C.: Sodium chloride media for separation of certain gram-positive cocci from gram-negative bacilli, J. Bact. 18: 43 (July) 1929.

34. KOCH, F. E.: Elektivnahrbodcn für Staphylokokkan, Zentralbl. f. Bakt. (Abt. 1) 149:122 (June 30) 1942.

35. CHAPMAN, P. H.: The significance of sodium chloride in studies of staphylococci, J.Bact. 50: 201 (Aug.) 1945.

36. MAITLAND, H. B., AND MAETYN, C.: A selective medium for isolating staphylococcusbased on the differential inhibiting effect of increased concentrations of sodium chlo-ride, J. Path. & Bact. 60: 553 (Oct.) 1948.

37. CADNESS-CEAYES, B., WILLIAMS, H., HAEPEE, C. J., AND MILES, A. A.: Slide test forcoagulase-positive staphylococci, Lancet 1: 736 (June 12) 1943.

38. Brnaa, J. W., AND HonosoN, C. A.: Impetigo contagiosa, its cause and treatment,Lancet 1: 544 (May 1)1943.

39. SHEEHAN, H.L., and FEEOUSON, A.C.: Impetigo, Lancct 1: 547, (May 1)1943.40. BUETENSHAw, J. M. L.: The Autogenous Disinfection of the Skin in MacKcnna, H.

M. B.: Modern Trends in Dermatology, London, Butterworth and Co. 1948, p. 158.41. Medical Uses of Soap, A Symposium edited by FISHBETN, M., Philadelphia, J. B. Lip-

pincott Conpany, 1915.42. (a) JoanoN, J. W., WALKER, H. L., AND OSDOENE, E. D.: Studies in the eczematizing


properties of soaps, New York State J. Med. 36: 791 (May 15) 1936. (h) GOLDMAN, L.:The skin reactions of infants and children to soaps, J. A. M. A. 103: 1317 (Apr. 17)1937. (c) BLANK, I. H.: Action of soap on skin, Arch. Dermat. & Syph. 39: 811 (May)1939. (d) KOOYMAN, D. J., ANn SNYDER, F. H.: Tests for mildness of soaps, Arch.Dermat. & Syph. 46: 846 (Dec.) 1942.

43. Kii, H. L.: Clinical evaluation of a superfatted soap, Arch. Dermat. & Syph. 45:377 (Feb.) 1942.

44. (a) SHARLTT, H.: Soap and the soap proplem, New York State J. Med. 43: 160 (Jan. 15)1943. (b) SHARLIT, H.: Soap and soap as a vehicle for medicaments, Arch. Dermat.& Syph. 59: 560 (May) 1949.

45. WALKER, J. B.: The germicidal properties of chemically pure soaps, J. Infect. Dis. 35:557 (Nov—Dec.) 1924.

46. ELLER, J. J., AND WOLFF, S.: Permeability and absorptivity of the skin, Arch. Dermat.& Syph. 40: 900 (Dee.) 1939.

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