- Email: [email protected]
Human sparganosis
Volume 15 Number 5, Part 2 November, 1986
taneous polyarteritis nodosa, nor should it be used as a marker for systemic involvement. Moreover, H B s A g and associated immune complexes m a y play an important role in the pathogenesis of cutaneous polyarteritis nodosa. Hepatitis serologic studies and immunofluorescence studies of lesional and nonlesional skin should be done systematically in all cases of cutaneous polyarteritis nodosa to elucidate further the role of H B s A g in this form o f polyarteritis nodosa. REFERENCES
1. Lindberg K. Ein beitrag zin der pericutaneous nodosa. Acta Med Scand 1931;76:183. 2. Borrie P. Cutaneous polyarteritis nodosa. Br J Dermatol 1972;87:87-95. 3. Diaz-Perez JL, Winkelmann RK. Cutaneous periarteritis nodosa. Arch Dennatol 1974;110:407-14.
Polyarteritis nodosa with hepatitis B surface antigen
4. Gocke DJ, Hsu K, Morgan C, et al. Association between polyarteritis and Australia antigen. Lancet 1970;2:114953, 5. Trepo CG, Zuckerman AJ, Biro RC, et al. The role of cimulating hepatitis B antigen immune complexes in the pathogenesis of vascular and hepatic manifestations in polyartefitis nodosa. J Clin Pathol 1974;27:863-8. 6. McElgunn PSJ. Dermatologic manifestations of hepatitis B virus infection. J AM ACAD DERMATOL1983;8:53948. 7. Cohen RD, Conn DL, llstrup DM. Clinical features, prognosis and response to treatment in potyarteritis. Mayo Clin Proc 1980;55:146-55. 8. Gocke DJ. Extrahepatic manifestations of viral hepatitis. Am J Med Sci 1975;270:49-52, 9. Michalak T. Immune complexes of hepatitis surface antigen in the pathogenesis of periarteritis nodosa: a study of seven necropsy cases. Am J Pathol. 1978;90:619-32. 10. Beylot J, Doutre MS, Beylot C, et al. L'immunofluorescencc cutan6e dans les affections a virus B: cent observations. Presse Med 1984; 13:2363-6.
B
Human sparganosis Deba P. Sarma, M . D . , and T h o m a s G. Weilbaecher, M.D. New Orleans, LA A case of human sparganosis is reported. Approximately sixty-eight such cases have been reported from the United States, most having been found in the southern states. Clinically sparganosis appears as a subcutaneous nodule. Diagnosis is established after the larval worm has been identified in the excised tissue. Excision of the lesion is curative. (J AM ACAD DERMATOL 15:l 145-1148, 1986.)
Sparganosis is an infection by sparganum, the generic term for the migrating plerocercoid larva of a t a p e w o r m o f the species Spirometra. The adult t a p e w o r m s live in the intestines o f dogs and cats. In the United States m o s t of the human cases are thought to be acquired by drinking water contaminated with the larval stage o f the tapeworm. A p p r o x i m a t e l y sixty-eight cases of human sparganosis have been reported f r o m the United From the Departmentof Pathologyand Dermatology,LouisianaState UniversityMedical School, and the VeteransAdministrationMedical Center. Reprint requests to: Dr. D. Sarma, 1601 Perdido St., New Orleans, LA 70146/504-568-081 I.
States.~25 The actual n u m b e r o f cases diagnosed is probably higher; there are thirty examples o f sparganosis on file at the A r m e d Forces Institute of Pathology, Washington, DC. 23 M o s t of the cases have been reported f r o m the southern United States. Sparganosis has b e e n reported worldwide but is m o s t c o m m o n in China, Japan, and Southeast Asia. Cases have also been reported f r o m the Caribbean islands, South A m e r i c a , Africa, and Australia. ~ Because of the population m o v e m e n t , it is expected that cases o f sparganosis will be observed anywhere in the United States, especially among the immigrants f r o m various countries. Typically, a patient with sparganosis presents with 1145
1146
Journal of the American Academyof Dermatology
Sarma and Weilbaecher
Fig. 1. Cross section of sparganum (left panel). (Hematoxylin-eosin stain; × 40.) Right panel: Higher magnification shows tegument (T), smooth muscle fibers (M), and thinwalled excretory ducts (E). (Hematoxylin-eosin stain; × 80.)
a subcutaneous nodule; the dermatologist, on biopsy of the lesion, may notice the larva in the excised specimen. We have seen two cases of human sparganosis since i982, one of which has been reported previously. ~Because of the rarity of such cases in the dermatologic practice, we are reporting a new c/tse, with an update of the literature on the entity of sparganosis in the United States. CASE REPORT A 47-year-old black man was evaluated for a lump that had been present in the abdominal wall for 6 weeks. There was no history of pain, fever, chills, weight loss, or trauma. Physical examination revealed a 1-cm nontender firm mobile mass in the subcutaneous tissue of the left upper quadrant of the abdomen. No other skin lesions were present. The clinical impression indicated a lipoma or fat necrosis. Results of the remainder of the physical examination and of routine laboratory tests, as well as the past medical history, were unremarkable. The excised lesion was submitted in multiple fragments of fibroadipose tissue together measuring 1 cm in diameter. Microscopically, fragments of a larval cestode with morphologic features of sparganum were noted (Figs. t and 2) in the midst of chronically inflamed fibroadipose tissue. The patient was born and raised in Louisiana. Additional questioning did not indicate the possible mode of acquisition of the infection. The patient had no additional lesions. He remains free of disease 3 years later.
DISCUSSION Sparganosis is an infection by sparganum, a larva of a tapeworm that lives in the intestines of cats and dogs. The eggs are passed in the feces and hatch in fresh water, releasing the first laryae, coracidia. These larvae are consumed by Cyclops (the first intermediate host), where the coracidia develop into second larvae. When the Cyclops organisms in the water are consumed by a second intermediate host, such as fish, shakes, frogs, mice, or raccoons, the larvae perpetrate the bowel wall of the new host, migrate through the capillaries to various organs and tissues, and develop into spargana. When a dog or cat eats the second intermediate host, the spargana develop into adult tapeworms in the intestine. A detailed life cycle of the parasite has been well documented, jJ'-'4 Man is an accidental intermediate host. He becomes infected in three ways: (i) by drinking water containing infected Cyclops organisms, (2) by ingesting the flesh of an intermediate host eonthining spargana, usually in the form of raw or inadequately cooked meat, and (3) by applying the flesh of an infected intermediate host as a poultice to an open wound, whereby the sparganum can directly invade human tissues. In the United States the usual mode of infection is through the drinking of contaminated water. The first case of human sparganosis in the
Volume 15 Number 5, Part 2 November, 1986
Hmnan sparganosis
1147
Fig. 2. Photomicrograph showing tegument (T), smooth muscle fibers (M), excretory ducts (E), and calcareous bodies (C). (Hematoxylin-eosin stain; × 200.) United States was reported by Stiles 2 in 1908. Most of the reported cases have been found in the southern United States: Louisiana, Texas, Florida, Mississippi, Arkansas, Georgia, North Carolina, South Carolina, Virginia, Kentucky, Tennessee, Alabama, Oklahoma, and Missouri. Isolated cases have been reported from California, New York, and Wisconsin. Clinically the patient usually presents with a slow-growing, occasionally migratory, tender or nontender subcutaneous mass. The overlying skin may be pruritic. Eosinophilia may or may not be present. Spargana may localize in other tissues, such as the eye, brain, lung, epididymis, urethra, bowel, and skeletal muscle. The diagnosis is rarely made until the lesion is excised and the presence of sparganum is identified on gross or microscopic examination. In the excised tissue the larval worm may be grossly recognized as a white, threadlike, flat worm of varying length (a few centimeters to 50 cm) and measuring about 1 mm in width. However, only the fragments of the larve are usually recognized microscopically in the cystic spaces within fibroadipose tissue showing marked granulomatous inflammation. The sparganum shows a dense eosinophilic cuticle, 5 to 15 b~m thick, with microvilli, two layers o f smooth muscle, and a row o f tegumental cells. The loose parenchyma contains fluid-filled spaces, smooth muscles, thinwalled excretory ducts, mesenchymal fibers, and basophilic calcareous bodies.
Surgical removal of the worm is the treatment of choice. Ocular sparganosis may pose a difficult surgical problem. Intracerebral sparganum has been successfully removed, -'5 A good response to injections of neoarsphenamine has b e e n reported in some cases of sparganosis occurring in other countries. ~' A rare form of proliferative sparganosis 2 has been treated with anthelmintic drugs, such as mebendazole and praziquantel5 6 REFERENCES
1, Sarma DP, Tanjucto E, Human sparganosis. J La State Med Soc 1983;135:16-7. 2. Stiles CW. The occurrence of a proliferating eestode hnva (Spargmmmproliferum) in man in Florida. J Cutan Dis 1908;26:345-58. 3. Moore JT: SpargatJum mansoJti: first reported American case. Am I Trop Dis Prev Mcd t914-1915;2:518-29. 4. Read CP. Human sparganosis in south Texas. J Parasitol 1952;38:29-3 I. 5. Gleason NN. Human sparganosis in Alabama. J Parasitol 1960;46:230. 6. Brooks TJ, Hutchison WF, Safley TJ, et al. Haman sparganosis in Mississippi: report of two cases. Am J Trop Med 1960;9:192-4. 7. Wirth WA, Farrow CC. Human sparganosis: case report and review of the subject. JAMA 1961;177:6-9. 8. Cross JH. Sparganosis in two members of an Arkansas family. J Parasitol 1963;49:154. 9. Mueller JF, Hart EP, Walsh WP. Human sparganosis in the United States. J Parasitol 1963;49:294-6. 10. Swartzwelder JC, Beaver PC, Hood MW. Sparganosis in southern United States. Am J Trop Med Hyg 1964;13:43-7. 11. Strauss WG, Manwaring JH. Sparganosis: a new ease in
Journal of the American Academy of Dermatology
Sarma and W~eilbaecher
12. 13. 14. 15. 16. 17. 18. 19.
the United States and review of the literature. Dermatol Trop 1964;3:73-8. MarkelI EK, Haber SL: A case of human sparganosis from California. Am J Med 1964;37:491-4. Dudley JB, Pool RS. Sparganosis in North Carolina: report of two cases. NC Med J 1965;26:95-7. McQuay RM, Veiga S, Frumovitz WA. Sparganosis in a Chicago resident originally from Arkansas: report of a case. Am J Clin Pathol 1966;46:645-8. Cox EC. Sparganosis in South Carolina. J SC Med Assoc 1968;64:233-5. Rywlin AM, Beck JW, Snyder GB. Sparganosis in Florida. Arch Dermatol 1968;97:425-7. Sanson JG, Bode MJ. Human sparganosis: report of a case in Wisconsin. Wis Med J 1972;71:164-6. Daly JJ, Baker GF, Johnson BR. Human sparganosis in Arkansas. J Arkansas Med Soc 1975;71:397-402. Taylor RL. Sparganosis in the United States: report of a case. Am J Clin Pathol 1976;66:560-4.
20. Campbell EW, Beals C. Striking eosinophilia in sparganosis. Postgrad Med 1977;62:138-40. 21. Fischman NH, Blalock JB, Carrera GM. Human sparganosis in Louisiana: a case report. J La State Med Soc 1977;129:215-8. 22. Cho C, Patel SP. Human sparganosis in northern United States. NY State J Med 1978;78:1456-8. 23, Gardiner CH, Rutland ED, Watkins RW. Case for diagnosis. Milit Med 1979;144:600-2. 24. Norman SH, Kreutner A. Sparganosis: clinical and pathologic observations in ten cases. South Med J 1980;73:297-300. 25. Anders K, Foley K, Stern WE, et al. Intraeranial sparganosis: an uncommon infection: case report. J Neurosurg 1984;60:1282-6. 26. Moulinier R, Martinez E, Torres J, et al. Human proliferative sparganosis in Venezuela: report of a case. Am J Trop Med Hyg 1982;31:358-63.
II
I
Intrauterine herpes simplex infection resembling mechanobullous disease in a newborn infant H o l l y H a k e Harris, M . D . , * Elliott Foucar, M . D . , * * R i c h a r d D. A n d e r s e n , M . D . ,*** and T h o m a s L. Ray, M . D . *
Iowa City, IA We present a case of transplacentally acquired intrauterine herpes simplex virus infection in a newborn delivered at 36 weeks' gestation by cesarean section because of intrauterine growth retardation and maternal preeclampsia. The mother experienced a single episode of serotype 2 herpes progenitalis at 14 weeks' gestation. At birth the infant manifested clinical findings of herpes simplex virus infection, which resembled epidermolysis bullosa and aplasia cutis congenita. Preexisting cutaneous lesions and intact fetal membranes at delivery strongly support a transplacentally acquired intrauterine herpes simplex virus infection. Repeated Tzanck smears, viral cultures, and immunohistochemical studies of the skin were required to confirm the diagnosis. Intrauterine herpes simplex virus infection is associated with significant morbidity and mortality but responds to antiviral therapy. Therefore this diagnosis must be considered in the neonate born with bullous or eroded skin lesions. (J AM ACAD DERMATOL 15:1148-I 155, 1986.)
From the Departments of Dermatology,* Pathology,** and Pediatrics,*** University of Iowa College of Medicine, Reprint requests to: Dr. ThomasL. Ray, Departmentof Dermatology, College of Medicine, University of Iowa, Iowa City, IA 52242. 1148
Neonatal herpes simplex virus infections acquired at birth are a serious and frequent c o n s e quence of the current venereal herpes simplex e p idemic. By c o m p a r i s o n , reports o f intrauterine
taneous polyarteritis nodosa, nor should it be used as a marker for systemic involvement. Moreover, H B s A g and associated immune complexes m a y play an important role in the pathogenesis of cutaneous polyarteritis nodosa. Hepatitis serologic studies and immunofluorescence studies of lesional and nonlesional skin should be done systematically in all cases of cutaneous polyarteritis nodosa to elucidate further the role of H B s A g in this form o f polyarteritis nodosa. REFERENCES
1. Lindberg K. Ein beitrag zin der pericutaneous nodosa. Acta Med Scand 1931;76:183. 2. Borrie P. Cutaneous polyarteritis nodosa. Br J Dermatol 1972;87:87-95. 3. Diaz-Perez JL, Winkelmann RK. Cutaneous periarteritis nodosa. Arch Dennatol 1974;110:407-14.
Polyarteritis nodosa with hepatitis B surface antigen
4. Gocke DJ, Hsu K, Morgan C, et al. Association between polyarteritis and Australia antigen. Lancet 1970;2:114953, 5. Trepo CG, Zuckerman AJ, Biro RC, et al. The role of cimulating hepatitis B antigen immune complexes in the pathogenesis of vascular and hepatic manifestations in polyartefitis nodosa. J Clin Pathol 1974;27:863-8. 6. McElgunn PSJ. Dermatologic manifestations of hepatitis B virus infection. J AM ACAD DERMATOL1983;8:53948. 7. Cohen RD, Conn DL, llstrup DM. Clinical features, prognosis and response to treatment in potyarteritis. Mayo Clin Proc 1980;55:146-55. 8. Gocke DJ. Extrahepatic manifestations of viral hepatitis. Am J Med Sci 1975;270:49-52, 9. Michalak T. Immune complexes of hepatitis surface antigen in the pathogenesis of periarteritis nodosa: a study of seven necropsy cases. Am J Pathol. 1978;90:619-32. 10. Beylot J, Doutre MS, Beylot C, et al. L'immunofluorescencc cutan6e dans les affections a virus B: cent observations. Presse Med 1984; 13:2363-6.
B
Human sparganosis Deba P. Sarma, M . D . , and T h o m a s G. Weilbaecher, M.D. New Orleans, LA A case of human sparganosis is reported. Approximately sixty-eight such cases have been reported from the United States, most having been found in the southern states. Clinically sparganosis appears as a subcutaneous nodule. Diagnosis is established after the larval worm has been identified in the excised tissue. Excision of the lesion is curative. (J AM ACAD DERMATOL 15:l 145-1148, 1986.)
Sparganosis is an infection by sparganum, the generic term for the migrating plerocercoid larva of a t a p e w o r m o f the species Spirometra. The adult t a p e w o r m s live in the intestines o f dogs and cats. In the United States m o s t of the human cases are thought to be acquired by drinking water contaminated with the larval stage o f the tapeworm. A p p r o x i m a t e l y sixty-eight cases of human sparganosis have been reported f r o m the United From the Departmentof Pathologyand Dermatology,LouisianaState UniversityMedical School, and the VeteransAdministrationMedical Center. Reprint requests to: Dr. D. Sarma, 1601 Perdido St., New Orleans, LA 70146/504-568-081 I.
States.~25 The actual n u m b e r o f cases diagnosed is probably higher; there are thirty examples o f sparganosis on file at the A r m e d Forces Institute of Pathology, Washington, DC. 23 M o s t of the cases have been reported f r o m the southern United States. Sparganosis has b e e n reported worldwide but is m o s t c o m m o n in China, Japan, and Southeast Asia. Cases have also been reported f r o m the Caribbean islands, South A m e r i c a , Africa, and Australia. ~ Because of the population m o v e m e n t , it is expected that cases o f sparganosis will be observed anywhere in the United States, especially among the immigrants f r o m various countries. Typically, a patient with sparganosis presents with 1145
1146
Journal of the American Academyof Dermatology
Sarma and Weilbaecher
Fig. 1. Cross section of sparganum (left panel). (Hematoxylin-eosin stain; × 40.) Right panel: Higher magnification shows tegument (T), smooth muscle fibers (M), and thinwalled excretory ducts (E). (Hematoxylin-eosin stain; × 80.)
a subcutaneous nodule; the dermatologist, on biopsy of the lesion, may notice the larva in the excised specimen. We have seen two cases of human sparganosis since i982, one of which has been reported previously. ~Because of the rarity of such cases in the dermatologic practice, we are reporting a new c/tse, with an update of the literature on the entity of sparganosis in the United States. CASE REPORT A 47-year-old black man was evaluated for a lump that had been present in the abdominal wall for 6 weeks. There was no history of pain, fever, chills, weight loss, or trauma. Physical examination revealed a 1-cm nontender firm mobile mass in the subcutaneous tissue of the left upper quadrant of the abdomen. No other skin lesions were present. The clinical impression indicated a lipoma or fat necrosis. Results of the remainder of the physical examination and of routine laboratory tests, as well as the past medical history, were unremarkable. The excised lesion was submitted in multiple fragments of fibroadipose tissue together measuring 1 cm in diameter. Microscopically, fragments of a larval cestode with morphologic features of sparganum were noted (Figs. t and 2) in the midst of chronically inflamed fibroadipose tissue. The patient was born and raised in Louisiana. Additional questioning did not indicate the possible mode of acquisition of the infection. The patient had no additional lesions. He remains free of disease 3 years later.
DISCUSSION Sparganosis is an infection by sparganum, a larva of a tapeworm that lives in the intestines of cats and dogs. The eggs are passed in the feces and hatch in fresh water, releasing the first laryae, coracidia. These larvae are consumed by Cyclops (the first intermediate host), where the coracidia develop into second larvae. When the Cyclops organisms in the water are consumed by a second intermediate host, such as fish, shakes, frogs, mice, or raccoons, the larvae perpetrate the bowel wall of the new host, migrate through the capillaries to various organs and tissues, and develop into spargana. When a dog or cat eats the second intermediate host, the spargana develop into adult tapeworms in the intestine. A detailed life cycle of the parasite has been well documented, jJ'-'4 Man is an accidental intermediate host. He becomes infected in three ways: (i) by drinking water containing infected Cyclops organisms, (2) by ingesting the flesh of an intermediate host eonthining spargana, usually in the form of raw or inadequately cooked meat, and (3) by applying the flesh of an infected intermediate host as a poultice to an open wound, whereby the sparganum can directly invade human tissues. In the United States the usual mode of infection is through the drinking of contaminated water. The first case of human sparganosis in the
Volume 15 Number 5, Part 2 November, 1986
Hmnan sparganosis
1147
Fig. 2. Photomicrograph showing tegument (T), smooth muscle fibers (M), excretory ducts (E), and calcareous bodies (C). (Hematoxylin-eosin stain; × 200.) United States was reported by Stiles 2 in 1908. Most of the reported cases have been found in the southern United States: Louisiana, Texas, Florida, Mississippi, Arkansas, Georgia, North Carolina, South Carolina, Virginia, Kentucky, Tennessee, Alabama, Oklahoma, and Missouri. Isolated cases have been reported from California, New York, and Wisconsin. Clinically the patient usually presents with a slow-growing, occasionally migratory, tender or nontender subcutaneous mass. The overlying skin may be pruritic. Eosinophilia may or may not be present. Spargana may localize in other tissues, such as the eye, brain, lung, epididymis, urethra, bowel, and skeletal muscle. The diagnosis is rarely made until the lesion is excised and the presence of sparganum is identified on gross or microscopic examination. In the excised tissue the larval worm may be grossly recognized as a white, threadlike, flat worm of varying length (a few centimeters to 50 cm) and measuring about 1 mm in width. However, only the fragments of the larve are usually recognized microscopically in the cystic spaces within fibroadipose tissue showing marked granulomatous inflammation. The sparganum shows a dense eosinophilic cuticle, 5 to 15 b~m thick, with microvilli, two layers o f smooth muscle, and a row o f tegumental cells. The loose parenchyma contains fluid-filled spaces, smooth muscles, thinwalled excretory ducts, mesenchymal fibers, and basophilic calcareous bodies.
Surgical removal of the worm is the treatment of choice. Ocular sparganosis may pose a difficult surgical problem. Intracerebral sparganum has been successfully removed, -'5 A good response to injections of neoarsphenamine has b e e n reported in some cases of sparganosis occurring in other countries. ~' A rare form of proliferative sparganosis 2 has been treated with anthelmintic drugs, such as mebendazole and praziquantel5 6 REFERENCES
1, Sarma DP, Tanjucto E, Human sparganosis. J La State Med Soc 1983;135:16-7. 2. Stiles CW. The occurrence of a proliferating eestode hnva (Spargmmmproliferum) in man in Florida. J Cutan Dis 1908;26:345-58. 3. Moore JT: SpargatJum mansoJti: first reported American case. Am I Trop Dis Prev Mcd t914-1915;2:518-29. 4. Read CP. Human sparganosis in south Texas. J Parasitol 1952;38:29-3 I. 5. Gleason NN. Human sparganosis in Alabama. J Parasitol 1960;46:230. 6. Brooks TJ, Hutchison WF, Safley TJ, et al. Haman sparganosis in Mississippi: report of two cases. Am J Trop Med 1960;9:192-4. 7. Wirth WA, Farrow CC. Human sparganosis: case report and review of the subject. JAMA 1961;177:6-9. 8. Cross JH. Sparganosis in two members of an Arkansas family. J Parasitol 1963;49:154. 9. Mueller JF, Hart EP, Walsh WP. Human sparganosis in the United States. J Parasitol 1963;49:294-6. 10. Swartzwelder JC, Beaver PC, Hood MW. Sparganosis in southern United States. Am J Trop Med Hyg 1964;13:43-7. 11. Strauss WG, Manwaring JH. Sparganosis: a new ease in
Journal of the American Academy of Dermatology
Sarma and W~eilbaecher
12. 13. 14. 15. 16. 17. 18. 19.
the United States and review of the literature. Dermatol Trop 1964;3:73-8. MarkelI EK, Haber SL: A case of human sparganosis from California. Am J Med 1964;37:491-4. Dudley JB, Pool RS. Sparganosis in North Carolina: report of two cases. NC Med J 1965;26:95-7. McQuay RM, Veiga S, Frumovitz WA. Sparganosis in a Chicago resident originally from Arkansas: report of a case. Am J Clin Pathol 1966;46:645-8. Cox EC. Sparganosis in South Carolina. J SC Med Assoc 1968;64:233-5. Rywlin AM, Beck JW, Snyder GB. Sparganosis in Florida. Arch Dermatol 1968;97:425-7. Sanson JG, Bode MJ. Human sparganosis: report of a case in Wisconsin. Wis Med J 1972;71:164-6. Daly JJ, Baker GF, Johnson BR. Human sparganosis in Arkansas. J Arkansas Med Soc 1975;71:397-402. Taylor RL. Sparganosis in the United States: report of a case. Am J Clin Pathol 1976;66:560-4.
20. Campbell EW, Beals C. Striking eosinophilia in sparganosis. Postgrad Med 1977;62:138-40. 21. Fischman NH, Blalock JB, Carrera GM. Human sparganosis in Louisiana: a case report. J La State Med Soc 1977;129:215-8. 22. Cho C, Patel SP. Human sparganosis in northern United States. NY State J Med 1978;78:1456-8. 23, Gardiner CH, Rutland ED, Watkins RW. Case for diagnosis. Milit Med 1979;144:600-2. 24. Norman SH, Kreutner A. Sparganosis: clinical and pathologic observations in ten cases. South Med J 1980;73:297-300. 25. Anders K, Foley K, Stern WE, et al. Intraeranial sparganosis: an uncommon infection: case report. J Neurosurg 1984;60:1282-6. 26. Moulinier R, Martinez E, Torres J, et al. Human proliferative sparganosis in Venezuela: report of a case. Am J Trop Med Hyg 1982;31:358-63.
II
I
Intrauterine herpes simplex infection resembling mechanobullous disease in a newborn infant H o l l y H a k e Harris, M . D . , * Elliott Foucar, M . D . , * * R i c h a r d D. A n d e r s e n , M . D . ,*** and T h o m a s L. Ray, M . D . *
Iowa City, IA We present a case of transplacentally acquired intrauterine herpes simplex virus infection in a newborn delivered at 36 weeks' gestation by cesarean section because of intrauterine growth retardation and maternal preeclampsia. The mother experienced a single episode of serotype 2 herpes progenitalis at 14 weeks' gestation. At birth the infant manifested clinical findings of herpes simplex virus infection, which resembled epidermolysis bullosa and aplasia cutis congenita. Preexisting cutaneous lesions and intact fetal membranes at delivery strongly support a transplacentally acquired intrauterine herpes simplex virus infection. Repeated Tzanck smears, viral cultures, and immunohistochemical studies of the skin were required to confirm the diagnosis. Intrauterine herpes simplex virus infection is associated with significant morbidity and mortality but responds to antiviral therapy. Therefore this diagnosis must be considered in the neonate born with bullous or eroded skin lesions. (J AM ACAD DERMATOL 15:1148-I 155, 1986.)
From the Departments of Dermatology,* Pathology,** and Pediatrics,*** University of Iowa College of Medicine, Reprint requests to: Dr. ThomasL. Ray, Departmentof Dermatology, College of Medicine, University of Iowa, Iowa City, IA 52242. 1148
Neonatal herpes simplex virus infections acquired at birth are a serious and frequent c o n s e quence of the current venereal herpes simplex e p idemic. By c o m p a r i s o n , reports o f intrauterine