Eczemas due to mites and microorganisms ROBERT JACKSON,* MD, FRCP[C]
Eczema is a specific clinical, morphologic and microscopic reaction pattern of the skin. It has many causes, including external and internal chemicals and the action of various microorganisms - bacteria, fungi, yeasts, viruses and mites - and their products. Peripheral vesicles with undermined borders are a feature of all eczemas caused by fungi, yeasts and bacteria and are thus a useful diagnostic finding. L'eczema represente un sch6ma r6actionnel cutane cliniquement, morphologiquement et microscopiquement specifique. II y a plusieurs causes, y compris certains agents chimiques externes et internes et l'action de divers microorganismes bact6ries, fongus, levures, virus et acares - et de leurs sousproduits. Des v6sicules peripheriques aux contours profonds sont caracteristiques de tous les eczemas causes par les fongus, les levures et les bact6ries et constituent donc un element diagnostique utile.
products) may cause eczema (Table II) and to discuss what is known about the mechanisms involved. The term eczema, derived from the Greek word meaning to boil over or erupt, describes a reaction in the skin and certain adjacent mucosae. It is characterized by a series of gross lesions and histologic changes, as summarized in Table III. In some eczematous eruptions one or more of these findings may be present at any one time, to the apparent exclusion of some of the others. The fundamental lesion of eczema is the vesicle (Fig. 1) or the spongiotic intercellular edema (Fig. 2) that produces the vesicle; unless this is present at some stage or in some area the eruption cannot be called eczema.
Under the microscope it may be more difficult to find spongiosis or vesiculation because biopsy material allows one to examine only a small area at one stage of the eruption. Physicians trained in observation can construct a retrospective or prospective picture so that they can say of a nonvesicular eruption that it may have had at one time, or it may develop, vesicles. At times one cannot be certain. Bacterial eczema
Many patients with eczema have a
Eczema is a common multiform reaction pattern in the skin caused by numerous and varied external and internal stimuli (Table I). The purpose of this paper is to point out that different types of microorganisms (or their
FIG. 1-Eczema on dorsum of hand: large number of small crusted vesicles.
,;4.
*Dermatologist, Ottawa Civic Hospital; assistant professor of medicine (dermatology), University of Ottawa To be presented to the Ottawa Bacteriological Club Feb. 10, 1977
Reprint requests to: Dr. R. Jackson, Ste. 508, 1081 Carling Ave., Ottawa, Ont. K1Y 4G2
156 CMA JOURNAL/JANUARY 22, 1977/VOL. 116
*
,,
FIG. 2.-Acute eczema: intercellular edema of epidermis (spongiosis) and extensive intraepidermal vesiculation (hematoxylin-eosin; x250, reduced 50%).
large number of bacteria growing in the eczematous area and in the normal adjacent skin, although the contents of the initial intact vesicle may be sterile. Patch tests with autogenous broth cultures or filtrates of Staphylococcus aureus (or with mixed bacterial cultures) show a strongly positive reaction, as manifested by areas of eczema beneath the patch. Exacerbation of the primary focus of eczema may be seen after intracutaneous or subcutaneous injection of an autogenous or mixed vaccine. Some widespread eczemas, such as exudative "seborrheic" bacterial eczema, respond promptly to the administration of systemic antimicrobial agents. Storck1 reported that the eczematogenic agent in bacteria is a protein that can act as an antigen without acquiring a protein linkage with the epidermis. Loewenthal,2 however, considered that it was also possible (and perhaps more likely) for the spread of eczema to be due to autosensitization of a patient to his skin, which is not uncommon when large numbers of bacteria are present; in this case the bacteria would join with some epidermal protein (the protigen of Epstein.) and cause the release of antigenic epidermal protein into the blood stream, with subsequent development of eczema in distant areas. The long-claimed relation between foci of infection in such areas as the teeth, tonsils, sinuses, gallbladder and prostate has never been proven and is still based primarily on anecdotal reports. How do these findings relate to clinical disease? The most obvious and clear-cut* bacterial eczemas are those that appear in areas of skin bathed continuously in pus discharging from, for example, the middle ear, an osteomyelitis sinus or a leg ulcer. When the source of the pus is cleared up the eczema disappears (Fig. 3). All forms of true bacterial eczema are now rare, owing presumably to the widespread availability and use of antibacterial drugs to treat the underlying chronic purulent infection. Another type is the sharply marginated eczema with vesicles and pustules and a peripheral undermined border without any obvious underlying source of discharging pus. These were more common on the hands and fingers and had such names as dermatitis repens and acrodermatitis continua (Fig. 4). A third group consists of eczemas that present as discrete, coin-shaped erythematous plaques studded with small vesicles, usually on the legs, arms or forearms (nummular eczema) (Fig. 5). Clinical experience indicates that severe dryness (as produced by overzealous washing with soap) is probably an important causative factor.
The favourable response to systemic antibacterial therapy reported (anecdotally) for some cases in the last two groups has implicated bacteria as being important in the cause of these types of eczema. This response, however, is by no means always assured.
One form that infections of the skin due to Candida a)bicans can take is that of numerous small vesiculopustules that coalesce to form a red, glistening,
eroded surface with a peripherally undermined border (Fig. 6). This form characteristically occurs in warm, moist, body folds (for example, penanal, genitocrural and inframammary areas and fingerwebs), especially in persons with a deficient immune system. Often there are satellite vesiculopustules decreasing in number and size the farther they are from the primary intertriginous eruption. The earliest histopathologic changes are localized spongiotic areas in the upper epidermis, usually just below the stratum corneum,
FIG. 3-Pustular eczema with peripheral undermining on amputated thumb with underlying osteomyelitis.
FIG. 4-Coccal eczema in lower portion of retroanricular crease.
Yeast eczema
'1
H(.. 5-Nummular eczema on leg; bright red lesions.
FIG. 6.-Interdigital candidiasis with undermined border.
CMA JOURNAL/JANUARY 22, 1977/VOL. 116 157
which rapidly fill with polymorphonuclear leukocytes and serum.4 A filtered, sterile, phenol-treated extract of disintegrated Candida cells (oidiomycm) reproduces typical cutaneous candidiasis when applied to the skin as a patch test. This reaction is mediated by an endotoxin-like substance released by organisms on the surface of the skin. Opinion varies as to whether the spongiotic pustules are produced by the direct action of this substance or by an antigen-antibody reaction. Intradermal injection of oidiomycin gives a positive tuberculin response in most patients because most adults have been exposed either to these fungi or to microorganisms with similar antigenic or allergenic structures (hence, crossreaction occurs). Fungal eczema
There are several types of superficial fungal infections of the skin that are blistering and closely mimic the gross morphologic and the histologic features of nonparasitic eczemas5 (Fig. 7). One type is tinea cruris (eczema marginatum), which has an arcuate vesicular border with undermining of the epidermis at the periphery. The central portion has a tendency to heal, with slight scaling and browning and sometimes lichenification. The genitocrural, intergluteal and perianal areas are the sites of predilection. Epidermophyton floccosum is one of the fungi causing this condition. Blistering tinea also can produce eczematous changes in the interdigital and intertriginous areas (for example, tinea pedis due to Trichophyton mentagrophytes). The blistering causes the outer epidermal layer to lift and peripheral undermining can easily be seen. The moisture in the area makes the elevated epidermal layer appear white and macerated. Another type is the eczematous eruption due to a specific sensitivity of the skin to allergenic products of the fungi disseminated by the blood stream from a focus of infection (dermatophytid). A common form is the blistering eruption on the sides of the fingers and on the palms from an active blistering interdigital tinea pedis. Briefly, Sulzberger and colleagues6 gave the following criteria for the diagnosis of dermatophytid: 1. A site of primary infection due to a pathogenic fungus (proved by laboratory methods). 2. Evidence of allergic sensitivity from a positive trichophytin test. 3. A secondary eruption with clinical characteristics compatible with those of dermatophytid at a site removed from that of the primary lesion.
4. Failure to demonstrate fungi in the secondary lesion. 5. Spontaneous clearing of the secondary eruption when the primary lesion subsides, whether spontaneously or following treatment. As with oidiomycin, skin testing with trichophytin (a filtered, sterile extract of phenol-treated fungus culture) is not much help in diagnosing fungal infections. Apparently most of us are at some time exposed to the allergenic components, so many persons will have a positive test result even though they do not have an active fungal infection. Patch testing with some trichophytin extracts may produce an eczematous reaction.7 The allergic constituents are polysaccharides.8 Jones, Reinhardt and Rinaldi9 recently did intradermal testing with a purified trichophytin preparation, recorded the number of patients showing delayed sensitivity, and correlated this with the number of patients showing clinical and cultural evidence of dermatophytosis. Their data suggested that patients showing positive delayed sensitivity to trichophytin were immune and those with a negative test result were susceptible to chronic fungal infections. Cruickshank, Trotter and Wood" passively transferred trichophytin sensitivity in guinea pigs by means of pentoneal cells and, in so doing, established that the cell-mediated immune system is responsible for these delayedtype reactions. Viral eczema
Molluscum contagiosum is a delled papular eruption occurring in clusters, mainly in children (Fig. 8). It is caused by the molluscum contagiosum virus, a poxvirus. The lesions are usually treated by curettage but if left alone will disappear spontaneously in
FIG. 8-Delled papules of molluscum contagiosum. months or years. A perilesional halo of eczema about 5 to 10 cm in diameter develops in about 10% of patients," though not all the lesions in a patient will show this eczema. The eczema may occur on adjacent touching body parts; for example, molluscum contagiosum with perilesional eczema on the inner aspect of the arm can produce eczema on the lateral chest wall where the affected area of the arm touches it. Presumably, because not all the lesions cause an eczema, the process is local; also, because the eczema is transferable by contact, the eczematogenic substance must be water-soluble. I know of no reports of the identification or isolation of this antigenic material. Scabies mite eczema
Mellanby'2 showed that in nearly 900 men with scabies the mean number of parasites detected was 11.3, and that half the patients had only 1 to 5 adult Sarcoptes scabiei (de Geer 1778 var. hominis Hering 1880) (Fig. 9). Clearly, then, the nonlinear clusters of vesicles on the hands and wrists, particularly in children, are not due to the burrowing action of the mite. One would not expect that anyway from a morphologic viewpoint because these blisters
/1\I
\
(1
2OOmicrons'-.
FIG. 7-Tinen corporis with peripheral blistering border.
158 CMA JOURNAL/JANUARY 22, 1977/VOL. 116
FIG. 9-Mite of Sarcoptes scabiei. Reproduced from "Scabies"12 by permission of E.W. Classey Ltd., Farlngdon, Oxon, England.
Atromid.S* (clofi brate) to lower blood lipids safely and effectively Indications ATROMID-S is indicated where reduction of blood lipids is desirable; e.g., patients with hypercholesterolemia and! or hypertriglyceridemia. Contralndicatlons While teratogenic studies have not demonstrated any effect attributable to ATROMID-S, its use in nonpregnant women of childbearing age should only be undertaken in patients using strict birth control measures. If these patients then plan to become pregnant, the drug should be withdrawn several months before conception. The drug should not be given to lactating women. ATROMID-S is not recommended in children since, to date, an insufficient number of cases have been treated. ATROMID-S is not recommended for patients with impaired renal or hepatic function. Warning Caution should be exercised when anticoagulants are given in conjunction with ATROMID-S. The dosage of the anticoagulant should be reduced by one-third to one-half (depending on the individual case) to maintain the prothrombin time at the desired level to prevent bleeding complications. Frequent prothrombin determinations are advisable until it has been definitely determined that the levels have been stabilized. For PRECAUTIONS and ADVERSE REACTIONS, see scientific brochure. Dosage and AdmInistratIon For adults only: One capsule (500 mg) four times daily. Availability No. 3243 Each capsule contains 500 mg clofibrate N.F. in bottles of 100 and 360. Further information, references, and scientific brochure available on request.
AYERST LABORATORIES, division of Ayerst, McKenna & Harrison Limited, Montreal, Canada Made in Canada by arrangement with IMPERIAL CHEMICAL INDUSTRIES LTD. Regd.
are not related to linear or sinuous tracts with a pinhead-sized vesicle at one end. In patients with scabies, eczema occurs at sites where there are neither burrows nor mites. There are three possible explanations: 1. Trauma itself, as from scratching, may cause eczematous changes. This may explain some of the lesions but not all. Heilesen" reported papulovesicles in paralyzed patients in areas they were unable to scratch. In experimental scabies, lesions without mites developed in areas away from the inoculation sites, and the number of lesions was always much higher than could be accounted for by even the most rapid breeding of the mite.13 2. Many of the agents used to treat scabies contain elemental sulfur, which causes eczema in some patients. Also, over-the-counter preparations used before medical advice is sought may cause eczema. However, many untreated patients with scabies have eczema. 3. The most likely explanation is that scabetic eczema is a sensitivity reaction to the Sarcoptes mite. Mellanby12 has shown that an appreciable amount of itching does not develop in inoculated volunteers until about 1 month or longer after inoculation. Excoriated follicular papules and eczema in areas where burrows or organisms cannot be demonstrated are evidence of this itching. Careful history taking, in my experience, confirms the likelihood of a period after exposure before severe itching developed and clinical lesions appeared. Another finding favouring a sensitivity state is an increased proportion of eosinophils in the blood; this has been reported in 20% of patients with scabies.13'14 The fact that there is no itching time-lag in second attacks of scabies in inoculated volunteers is further evidence of a sensitivity state. A final and perhaps clinching clue is that the eczema disappears with treatment of scabies, even though the scabetic therapy has no antieczematous action. Prakken and van Vloten15 carried out intracutaneous tests with extracts prepared from the crusts of patients with severe generalized (or Norwegian) scabies, a condition in which there are innumerable mites. The tests were done in persons with typical scabies, persons who had been treated successfully for scabies and persons who had never had scabies. In the first group 12 of 14 reacted positively, in the second group 4 of 16 reacted positively and in the third group all 18 failed to react. Passive antibody transfer (Prausnitz-Kiistner reaction) was carried out successfully in the third group after the patients had been sensitized with serum
from a patient with severe scabies. Heilesen,13 however, found only 3 of 38 patients with scabies to have a positive reaction to intracutaneous testing with ground-up, formalin-treated extract of mites. I know of no studies that have determined the nature of the antigenic material in the mite. Conunents The slin as an organ has a limited number of reaction patterns, so one should not be surprised that many different stimuli may cause eczema. Urticaria is another reaction pattern in the skin that can result from many diverse external and internal stimuli. One morphologic feature of all "microbial" eczemas (except scabies mite eczema) is the tendency for the vesicles to be peripheral and to lift the upper layers of the epidermis. Thus the peripheral undermining so common in yeast, fungal and bacterial eczemas is a useful diagnostic feature. Many of the observations I have mentioned were made years ago. It would be profitable to investigate and identify the possible antigenic materials by newer techniques such as immunoelectrophoresis, ultracentrifugation, the Ouchterlony immune diffusion-in-gel technique, and gas chromatographymass spectrometry. The photographs and photomicrographs were prepared by the audiovisual department of the Ottawa Civic Hospital. References 1. STORCK H: The role of bacteria in eczema,
in The Eczemas, LOEWENTHAL UA (ed), Edinburgh and London, Livingstone, 1954, pp 112-26 2. LOEWENTHAL UA: Disseminated and endogenous eczemas, in The Eczemas, op cit, pp 142-62 3. EPSTEIN S: Progress in allergy; antigenantibody reaction in contact dermatitis; hypothesis and review. Ann Allergy 10: 633, 1952 4. MAIBACH HI, KLIGMAN AM: The bioiogy of experimental human cutaneous moniliasis
(Candida albicans). Arch Dermatol 85: 233,
1962 5. HABER H: Histopathologv of eczema, in The Eczemas, op cit, pp 86-98 6. SULZBERGER MB, WOLF J. WrrrEN VH. Ct ai:
Dermatology; Diagnosis and Treatment, 2nd
ed, Chicago, Year Bk Med, 1961, p 329 7. SULZBERGER MB, LEWIS GM: Trichophytin hypersensitiveness demonstrated by contact
tests. Arch Dermatol Syphiligr 22: 410, 1930 8. SuLzsEaoEa MB (ed): Dermatologic Allergy, Springfield, IL, CC Thomas, 1940, p 260 9. JONES EH, REINHARDT JH, RINALDI MG: A clinical, mycological and immunologic survey for dermatophytosis. Arch Dermatol 108: 61,
1973 10. CRUICKSHANK CND, TROTrER MD, Wooo SR: Studies on trichophytin sensitivity. / Invest Dermatol 35: 219, 1960 ii. DE Oaao GA, JOHNSON HH, BINKLEY GW: An eczematous reaction associated with molluscum contagiosum. Arch Dermatol 74: 344, 1956 12. MELLANBY K (ed): Scabies, 2nd ed, Faringdon, England, Classey, 1972 13. HEILESEN B: Studies on Acarus scablel and scabies. Acta Derm Venereol (Stockh) 26 (suppi 14): 1, 1946 14. ORMsBY OS, MONTGOMERY H (eds): Diseases ol the skin 8th ed Philadelphia, Lea & Febiger, 1954, p 128. 15. PRARKEN JR, VAN VLOTEN TI: Allergy in scabies; positive intracutaneous tests with antigen from Scables norvegica; passive transfer of antibodies (Prausnitz-Kilstner). Dermatologlca 99: 124, 1949
CMA JOURNAL/JANUARY 22, 1977/VOL. 116 161
Eczema is a specific clinical, morphologic and microscopic reaction pattern of the skin. It has many causes, including external and internal chemicals and the action of various microorganisms - bacteria, fungi, yeasts, viruses and mites - and their products. Peripheral vesicles with undermined borders are a feature of all eczemas caused by fungi, yeasts and bacteria and are thus a useful diagnostic finding. L'eczema represente un sch6ma r6actionnel cutane cliniquement, morphologiquement et microscopiquement specifique. II y a plusieurs causes, y compris certains agents chimiques externes et internes et l'action de divers microorganismes bact6ries, fongus, levures, virus et acares - et de leurs sousproduits. Des v6sicules peripheriques aux contours profonds sont caracteristiques de tous les eczemas causes par les fongus, les levures et les bact6ries et constituent donc un element diagnostique utile.
products) may cause eczema (Table II) and to discuss what is known about the mechanisms involved. The term eczema, derived from the Greek word meaning to boil over or erupt, describes a reaction in the skin and certain adjacent mucosae. It is characterized by a series of gross lesions and histologic changes, as summarized in Table III. In some eczematous eruptions one or more of these findings may be present at any one time, to the apparent exclusion of some of the others. The fundamental lesion of eczema is the vesicle (Fig. 1) or the spongiotic intercellular edema (Fig. 2) that produces the vesicle; unless this is present at some stage or in some area the eruption cannot be called eczema.
Under the microscope it may be more difficult to find spongiosis or vesiculation because biopsy material allows one to examine only a small area at one stage of the eruption. Physicians trained in observation can construct a retrospective or prospective picture so that they can say of a nonvesicular eruption that it may have had at one time, or it may develop, vesicles. At times one cannot be certain. Bacterial eczema
Many patients with eczema have a
Eczema is a common multiform reaction pattern in the skin caused by numerous and varied external and internal stimuli (Table I). The purpose of this paper is to point out that different types of microorganisms (or their
FIG. 1-Eczema on dorsum of hand: large number of small crusted vesicles.
,;4.
*Dermatologist, Ottawa Civic Hospital; assistant professor of medicine (dermatology), University of Ottawa To be presented to the Ottawa Bacteriological Club Feb. 10, 1977
Reprint requests to: Dr. R. Jackson, Ste. 508, 1081 Carling Ave., Ottawa, Ont. K1Y 4G2
156 CMA JOURNAL/JANUARY 22, 1977/VOL. 116
*
,,
FIG. 2.-Acute eczema: intercellular edema of epidermis (spongiosis) and extensive intraepidermal vesiculation (hematoxylin-eosin; x250, reduced 50%).
large number of bacteria growing in the eczematous area and in the normal adjacent skin, although the contents of the initial intact vesicle may be sterile. Patch tests with autogenous broth cultures or filtrates of Staphylococcus aureus (or with mixed bacterial cultures) show a strongly positive reaction, as manifested by areas of eczema beneath the patch. Exacerbation of the primary focus of eczema may be seen after intracutaneous or subcutaneous injection of an autogenous or mixed vaccine. Some widespread eczemas, such as exudative "seborrheic" bacterial eczema, respond promptly to the administration of systemic antimicrobial agents. Storck1 reported that the eczematogenic agent in bacteria is a protein that can act as an antigen without acquiring a protein linkage with the epidermis. Loewenthal,2 however, considered that it was also possible (and perhaps more likely) for the spread of eczema to be due to autosensitization of a patient to his skin, which is not uncommon when large numbers of bacteria are present; in this case the bacteria would join with some epidermal protein (the protigen of Epstein.) and cause the release of antigenic epidermal protein into the blood stream, with subsequent development of eczema in distant areas. The long-claimed relation between foci of infection in such areas as the teeth, tonsils, sinuses, gallbladder and prostate has never been proven and is still based primarily on anecdotal reports. How do these findings relate to clinical disease? The most obvious and clear-cut* bacterial eczemas are those that appear in areas of skin bathed continuously in pus discharging from, for example, the middle ear, an osteomyelitis sinus or a leg ulcer. When the source of the pus is cleared up the eczema disappears (Fig. 3). All forms of true bacterial eczema are now rare, owing presumably to the widespread availability and use of antibacterial drugs to treat the underlying chronic purulent infection. Another type is the sharply marginated eczema with vesicles and pustules and a peripheral undermined border without any obvious underlying source of discharging pus. These were more common on the hands and fingers and had such names as dermatitis repens and acrodermatitis continua (Fig. 4). A third group consists of eczemas that present as discrete, coin-shaped erythematous plaques studded with small vesicles, usually on the legs, arms or forearms (nummular eczema) (Fig. 5). Clinical experience indicates that severe dryness (as produced by overzealous washing with soap) is probably an important causative factor.
The favourable response to systemic antibacterial therapy reported (anecdotally) for some cases in the last two groups has implicated bacteria as being important in the cause of these types of eczema. This response, however, is by no means always assured.
One form that infections of the skin due to Candida a)bicans can take is that of numerous small vesiculopustules that coalesce to form a red, glistening,
eroded surface with a peripherally undermined border (Fig. 6). This form characteristically occurs in warm, moist, body folds (for example, penanal, genitocrural and inframammary areas and fingerwebs), especially in persons with a deficient immune system. Often there are satellite vesiculopustules decreasing in number and size the farther they are from the primary intertriginous eruption. The earliest histopathologic changes are localized spongiotic areas in the upper epidermis, usually just below the stratum corneum,
FIG. 3-Pustular eczema with peripheral undermining on amputated thumb with underlying osteomyelitis.
FIG. 4-Coccal eczema in lower portion of retroanricular crease.
Yeast eczema
'1
H(.. 5-Nummular eczema on leg; bright red lesions.
FIG. 6.-Interdigital candidiasis with undermined border.
CMA JOURNAL/JANUARY 22, 1977/VOL. 116 157
which rapidly fill with polymorphonuclear leukocytes and serum.4 A filtered, sterile, phenol-treated extract of disintegrated Candida cells (oidiomycm) reproduces typical cutaneous candidiasis when applied to the skin as a patch test. This reaction is mediated by an endotoxin-like substance released by organisms on the surface of the skin. Opinion varies as to whether the spongiotic pustules are produced by the direct action of this substance or by an antigen-antibody reaction. Intradermal injection of oidiomycin gives a positive tuberculin response in most patients because most adults have been exposed either to these fungi or to microorganisms with similar antigenic or allergenic structures (hence, crossreaction occurs). Fungal eczema
There are several types of superficial fungal infections of the skin that are blistering and closely mimic the gross morphologic and the histologic features of nonparasitic eczemas5 (Fig. 7). One type is tinea cruris (eczema marginatum), which has an arcuate vesicular border with undermining of the epidermis at the periphery. The central portion has a tendency to heal, with slight scaling and browning and sometimes lichenification. The genitocrural, intergluteal and perianal areas are the sites of predilection. Epidermophyton floccosum is one of the fungi causing this condition. Blistering tinea also can produce eczematous changes in the interdigital and intertriginous areas (for example, tinea pedis due to Trichophyton mentagrophytes). The blistering causes the outer epidermal layer to lift and peripheral undermining can easily be seen. The moisture in the area makes the elevated epidermal layer appear white and macerated. Another type is the eczematous eruption due to a specific sensitivity of the skin to allergenic products of the fungi disseminated by the blood stream from a focus of infection (dermatophytid). A common form is the blistering eruption on the sides of the fingers and on the palms from an active blistering interdigital tinea pedis. Briefly, Sulzberger and colleagues6 gave the following criteria for the diagnosis of dermatophytid: 1. A site of primary infection due to a pathogenic fungus (proved by laboratory methods). 2. Evidence of allergic sensitivity from a positive trichophytin test. 3. A secondary eruption with clinical characteristics compatible with those of dermatophytid at a site removed from that of the primary lesion.
4. Failure to demonstrate fungi in the secondary lesion. 5. Spontaneous clearing of the secondary eruption when the primary lesion subsides, whether spontaneously or following treatment. As with oidiomycin, skin testing with trichophytin (a filtered, sterile extract of phenol-treated fungus culture) is not much help in diagnosing fungal infections. Apparently most of us are at some time exposed to the allergenic components, so many persons will have a positive test result even though they do not have an active fungal infection. Patch testing with some trichophytin extracts may produce an eczematous reaction.7 The allergic constituents are polysaccharides.8 Jones, Reinhardt and Rinaldi9 recently did intradermal testing with a purified trichophytin preparation, recorded the number of patients showing delayed sensitivity, and correlated this with the number of patients showing clinical and cultural evidence of dermatophytosis. Their data suggested that patients showing positive delayed sensitivity to trichophytin were immune and those with a negative test result were susceptible to chronic fungal infections. Cruickshank, Trotter and Wood" passively transferred trichophytin sensitivity in guinea pigs by means of pentoneal cells and, in so doing, established that the cell-mediated immune system is responsible for these delayedtype reactions. Viral eczema
Molluscum contagiosum is a delled papular eruption occurring in clusters, mainly in children (Fig. 8). It is caused by the molluscum contagiosum virus, a poxvirus. The lesions are usually treated by curettage but if left alone will disappear spontaneously in
FIG. 8-Delled papules of molluscum contagiosum. months or years. A perilesional halo of eczema about 5 to 10 cm in diameter develops in about 10% of patients," though not all the lesions in a patient will show this eczema. The eczema may occur on adjacent touching body parts; for example, molluscum contagiosum with perilesional eczema on the inner aspect of the arm can produce eczema on the lateral chest wall where the affected area of the arm touches it. Presumably, because not all the lesions cause an eczema, the process is local; also, because the eczema is transferable by contact, the eczematogenic substance must be water-soluble. I know of no reports of the identification or isolation of this antigenic material. Scabies mite eczema
Mellanby'2 showed that in nearly 900 men with scabies the mean number of parasites detected was 11.3, and that half the patients had only 1 to 5 adult Sarcoptes scabiei (de Geer 1778 var. hominis Hering 1880) (Fig. 9). Clearly, then, the nonlinear clusters of vesicles on the hands and wrists, particularly in children, are not due to the burrowing action of the mite. One would not expect that anyway from a morphologic viewpoint because these blisters
/1\I
\
(1
2OOmicrons'-.
FIG. 7-Tinen corporis with peripheral blistering border.
158 CMA JOURNAL/JANUARY 22, 1977/VOL. 116
FIG. 9-Mite of Sarcoptes scabiei. Reproduced from "Scabies"12 by permission of E.W. Classey Ltd., Farlngdon, Oxon, England.
Atromid.S* (clofi brate) to lower blood lipids safely and effectively Indications ATROMID-S is indicated where reduction of blood lipids is desirable; e.g., patients with hypercholesterolemia and! or hypertriglyceridemia. Contralndicatlons While teratogenic studies have not demonstrated any effect attributable to ATROMID-S, its use in nonpregnant women of childbearing age should only be undertaken in patients using strict birth control measures. If these patients then plan to become pregnant, the drug should be withdrawn several months before conception. The drug should not be given to lactating women. ATROMID-S is not recommended in children since, to date, an insufficient number of cases have been treated. ATROMID-S is not recommended for patients with impaired renal or hepatic function. Warning Caution should be exercised when anticoagulants are given in conjunction with ATROMID-S. The dosage of the anticoagulant should be reduced by one-third to one-half (depending on the individual case) to maintain the prothrombin time at the desired level to prevent bleeding complications. Frequent prothrombin determinations are advisable until it has been definitely determined that the levels have been stabilized. For PRECAUTIONS and ADVERSE REACTIONS, see scientific brochure. Dosage and AdmInistratIon For adults only: One capsule (500 mg) four times daily. Availability No. 3243 Each capsule contains 500 mg clofibrate N.F. in bottles of 100 and 360. Further information, references, and scientific brochure available on request.
AYERST LABORATORIES, division of Ayerst, McKenna & Harrison Limited, Montreal, Canada Made in Canada by arrangement with IMPERIAL CHEMICAL INDUSTRIES LTD. Regd.
are not related to linear or sinuous tracts with a pinhead-sized vesicle at one end. In patients with scabies, eczema occurs at sites where there are neither burrows nor mites. There are three possible explanations: 1. Trauma itself, as from scratching, may cause eczematous changes. This may explain some of the lesions but not all. Heilesen" reported papulovesicles in paralyzed patients in areas they were unable to scratch. In experimental scabies, lesions without mites developed in areas away from the inoculation sites, and the number of lesions was always much higher than could be accounted for by even the most rapid breeding of the mite.13 2. Many of the agents used to treat scabies contain elemental sulfur, which causes eczema in some patients. Also, over-the-counter preparations used before medical advice is sought may cause eczema. However, many untreated patients with scabies have eczema. 3. The most likely explanation is that scabetic eczema is a sensitivity reaction to the Sarcoptes mite. Mellanby12 has shown that an appreciable amount of itching does not develop in inoculated volunteers until about 1 month or longer after inoculation. Excoriated follicular papules and eczema in areas where burrows or organisms cannot be demonstrated are evidence of this itching. Careful history taking, in my experience, confirms the likelihood of a period after exposure before severe itching developed and clinical lesions appeared. Another finding favouring a sensitivity state is an increased proportion of eosinophils in the blood; this has been reported in 20% of patients with scabies.13'14 The fact that there is no itching time-lag in second attacks of scabies in inoculated volunteers is further evidence of a sensitivity state. A final and perhaps clinching clue is that the eczema disappears with treatment of scabies, even though the scabetic therapy has no antieczematous action. Prakken and van Vloten15 carried out intracutaneous tests with extracts prepared from the crusts of patients with severe generalized (or Norwegian) scabies, a condition in which there are innumerable mites. The tests were done in persons with typical scabies, persons who had been treated successfully for scabies and persons who had never had scabies. In the first group 12 of 14 reacted positively, in the second group 4 of 16 reacted positively and in the third group all 18 failed to react. Passive antibody transfer (Prausnitz-Kiistner reaction) was carried out successfully in the third group after the patients had been sensitized with serum
from a patient with severe scabies. Heilesen,13 however, found only 3 of 38 patients with scabies to have a positive reaction to intracutaneous testing with ground-up, formalin-treated extract of mites. I know of no studies that have determined the nature of the antigenic material in the mite. Conunents The slin as an organ has a limited number of reaction patterns, so one should not be surprised that many different stimuli may cause eczema. Urticaria is another reaction pattern in the skin that can result from many diverse external and internal stimuli. One morphologic feature of all "microbial" eczemas (except scabies mite eczema) is the tendency for the vesicles to be peripheral and to lift the upper layers of the epidermis. Thus the peripheral undermining so common in yeast, fungal and bacterial eczemas is a useful diagnostic feature. Many of the observations I have mentioned were made years ago. It would be profitable to investigate and identify the possible antigenic materials by newer techniques such as immunoelectrophoresis, ultracentrifugation, the Ouchterlony immune diffusion-in-gel technique, and gas chromatographymass spectrometry. The photographs and photomicrographs were prepared by the audiovisual department of the Ottawa Civic Hospital. References 1. STORCK H: The role of bacteria in eczema,
in The Eczemas, LOEWENTHAL UA (ed), Edinburgh and London, Livingstone, 1954, pp 112-26 2. LOEWENTHAL UA: Disseminated and endogenous eczemas, in The Eczemas, op cit, pp 142-62 3. EPSTEIN S: Progress in allergy; antigenantibody reaction in contact dermatitis; hypothesis and review. Ann Allergy 10: 633, 1952 4. MAIBACH HI, KLIGMAN AM: The bioiogy of experimental human cutaneous moniliasis
(Candida albicans). Arch Dermatol 85: 233,
1962 5. HABER H: Histopathologv of eczema, in The Eczemas, op cit, pp 86-98 6. SULZBERGER MB, WOLF J. WrrrEN VH. Ct ai:
Dermatology; Diagnosis and Treatment, 2nd
ed, Chicago, Year Bk Med, 1961, p 329 7. SULZBERGER MB, LEWIS GM: Trichophytin hypersensitiveness demonstrated by contact
tests. Arch Dermatol Syphiligr 22: 410, 1930 8. SuLzsEaoEa MB (ed): Dermatologic Allergy, Springfield, IL, CC Thomas, 1940, p 260 9. JONES EH, REINHARDT JH, RINALDI MG: A clinical, mycological and immunologic survey for dermatophytosis. Arch Dermatol 108: 61,
1973 10. CRUICKSHANK CND, TROTrER MD, Wooo SR: Studies on trichophytin sensitivity. / Invest Dermatol 35: 219, 1960 ii. DE Oaao GA, JOHNSON HH, BINKLEY GW: An eczematous reaction associated with molluscum contagiosum. Arch Dermatol 74: 344, 1956 12. MELLANBY K (ed): Scabies, 2nd ed, Faringdon, England, Classey, 1972 13. HEILESEN B: Studies on Acarus scablel and scabies. Acta Derm Venereol (Stockh) 26 (suppi 14): 1, 1946 14. ORMsBY OS, MONTGOMERY H (eds): Diseases ol the skin 8th ed Philadelphia, Lea & Febiger, 1954, p 128. 15. PRARKEN JR, VAN VLOTEN TI: Allergy in scabies; positive intracutaneous tests with antigen from Scables norvegica; passive transfer of antibodies (Prausnitz-Kilstner). Dermatologlca 99: 124, 1949
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