- Email: [email protected]
Hemophagocytic Syndrome Associated With Visceral Leishmaniasis in an Immunocompetent Patient
Ophthahnol. 112:1601-1609. 15. Yamamoto, S., et al. 1994. Detection of herpes simplex virus DNA in human tear film by the polymerase chain reaction. Am. J. Ophthahnol. 117:160-163. 16. Garweg, J., et al. 1993. An improved technique for the diagnosis of viral retinitis from samples of aqueous humor and vitreous. Graefes Arch. Clin. Exp. Ophthahnol. 231508-513. 17. Fox, G.M., et al. 1991. Detection of herpewirus DNA in vitreous and aqueous specimens by the polymerase chain reaction. Arch. Ophthalmol. 109:266271. 18. Nishi, M., et al. 1992. Polymerase chain reaction for the detection of the
varicella-zoster genome in ocular samples from patients with acute retinal necrosis. Am J. Ophthahnol. 114603-609. 19. Wiedbrauk, D.L., J.C. Warner, and A.M. Drevon. 1995. Inhibition of PCR by aqueous and vitrous fluids. J. Clin. Microbial. 33:2643-2646. 20. DeVincenxo J.P., and G. Thorpe. 1994. Mild herpes simplex encephalitis diagnosed by polymerase chain reaction: a case report and review. Pediatr. Infect. Dis. J. 13:662-664. 21. Schlesinger, Y.. et al. 1995. Herpes simplex virus type 2 meningitis in the absence of genital lesions: improved recognition with use of the polymemse chain reaction.
Clin. Infect. Dis. 20~842-848. 22. Aurelius, E., et al. 1991. Rapid diagnosis of herpes simplex encephalitis by nested polymerase chain reaction assay of CSF. Lancet 337:189-192. 23. Lakeman, F.D.. et al. 1995. Diagnosis of herpes simplex virus encephalitis: application of polymerase chain reaction to CSF from brain-biopsied patients and correlation with disease. J. Infect. Dis. 171:857-863. 24. Marcon, M. J., et al. Unpublished data. 25. Landry, M.L. 1995. False-positive polymerase chain reaction in the diagnosis of herpes simplex encephalitis. J. Infect. Dis. 172:1641-1643.
Case Report
Hemophagocytic Syndrome Associated With Visceral Leishmaniasis in an Immunocompetent Patient Pilar Cort&, MSc. Neus Cardefiosa,Ph.D. CarmenMuftoz, Ph.D. Servei de Microbiologia Hospital de la Santa Creu i Sant Pau Barcekwaa, Spain Ignaci Dur&n, M.D.
Ruben Leta, M.D. Alex Rota-Cusachs,M.D. Servei de Medic& interna HoJpital de la Santa Creu i Sant Pau BarceloM. Spain
Montserrat Gallego, Ph.D. Departament de Microbiologia Parasitologia Sanitciries Facultat de Farmcicia hiversitat de Barcelona Barcelona, Spain.
i
Hemophagocytosiswas describedas a characteristicfeature in histiocytic marrow reticulosis by Scott and RobbSmith in 1939 (1). In 1966,Rappaport (2) reported similar casesand introducedthe term malignant histiocytosis to describea diseasecharacterizedby a systemicinvasive proliferation of morphologically atypical histiocytes. More recently, somecaseswith clini-
14
0196-4399/97/$0.00
+ 17.00
cal and anatomopathologicalfeatures similar to malignant histiocytosis have been described,secondarynot only to neoplasmsbut also to reactive proliferations (3). Theseare related to a broad spectrumof infections that include several viruses, bacteria,rickettsiae, fungi, and parasites(4). We describea caseof reactive hemophagocytosisassociatedwith an infcction by Leishmania infantum belonging to a common zymodemein our geographical area,MON- 1. Although severalcasesof hematophagichistiocytosis, in which leishmania infections are involved, havebeenreported (5-13), to our knowledge this is the first casewith a fatal outcomein an immunocompetent patient.
Case report A 59-yr-old man, who lived in Barcelona (Spain), wasadmitted to our hospital in January1994becauseof anemia, weight loss(2 kg), li-equentepistaxis, and a 20&y history of fever. The patient had a long history of high blood pressureand, 8 mo before admission, had sufferedarthritis of the ankle of unknown etiology for 3 wk. He had not
0 1997 Else&r
Science Inc.
traveled abroad.On admission, the patient was febrile (38 to 39°C) and reported left lower-back pain. Examination revealeda homogeneous firm liver edge 8 to 9 cm below the right costal margin without splenomegaly.Laboratory findings showed: hemoglobin 11 g/L; white blood cell count 3. lx 109/L;platelets 80x109/L; an altered prothrombin time (65%) and a mild cholestastispattern. Tumor markers including prostate-specific antigen, carcinoembryonic antigen and alpha-fetoprotein were normal. Blood cultures and/or serological studies for HIV, cytomegalovirus, IgM antibodies, Epstein-Barr virus, hepatitis C and hepatitis B viruses, herpessimplex virus, Toxoplasma, Brucella, Q-fever, and typhoid fever were all negative. The tuberculin test was positive. Chest X-ray was normal. Abdominal ultrasonographyand CT scandisclosed hepatosplenomegalywithout adenopathy. Bone marrow biopsy showed no hematological anomaly and microscopic examination using Giemsa staining revealedpoorly staining Leishmania amastigoteforms. Two weeks after ad-
Clinical Micmbiology
Newsletter 19:2,1997
mission the patient developeda purpuric rash in the right lumbar region and relapsing fever in the evening together with progressivedyspnea.ChestX-ray showeda right pleural effusion with underlying parenchymaldamage.Arterial blood gaseswere pO2 62 mm Hg; pCO2 33 mm Hg; and pH 7.5. Three weeks later, a new bone marrow study was performed that showeda low number of Leishmuniu amastigoteforms in addition to hemophagocytosiswithout cytologic atypia. The diagnosis of visceral leishmaniasiswas confirmed by culture of flagellated forms of the pathogenincubatedin Nicolle-Novy-McNeal (NNN) medium and by two serological techniques,an immunofluorescenceantibody test that waspositive with a titer of 1,280,and an immunoblot, which was also positive. Isoenzymeanalysis of the strain was carried out (Departamentde Parasitologia,Facultat de Farm&&, Barcelona) using the current panel of 15 enzymes(MDHl, ME, ICD, F’GD,G6PD, GLUD, DL41, NPl, Np2, GOTl, GOT2,PGM, FH, MDI, and GPI) proposedby the Laboratoire d’Ecologie Mt?dicale(Montpellier, France) (14); the strain was identified asLeishmania infantum MON-1 (MHOM/E+94/BCN-109). During this time, with no changein the white blood cell count, the platelet count decreased progressively to 7x 109/L2 wk after admission. Treatmentwith corticosteroids (1 mg/kgJd)was begun and maintained throughout the hospitalization without improvement in the white cell or platelet counts.Becauseof the severepancytopenia, treatmentof leishmaniasiswith intramuscular antimonials was ruled out. For this reasonintravenous pcntamidmeat a daily doseof 4 mg/kg and allopurinol500 mg every 8 h was started.Epigastric pain and an enlargement of the QT interval led us to replace this drug with intravenous Glucantime at a daily doseof 850 mg for 20 d. The patient’s condition continued to deteriorateand becauseof his extremely critical pancytopeniahe required multiple platelet transfusions, which, nevertheless,did not improve the platelet count. Therefore daily intravenous infusions of gamma-globulin were begun at recommendeddosesfor
Clinical Micmbiology
Ne~slctta
19:2,1997
5 d. Thirty days after admission,the patient suddenly developeddeeppain in the left upper abdominal quadrant.Ultrasonographyand CT scanof the abdomen showedsplenic rupture. An emergencysplenectomywas performed and the patient was transferredto the intensive care unit, where he developeda fatal coursepresentingwith septic shock by Escherichia coli and multi-organ failure. He died in the first postoperative week.
which hasbeenregardedasa therapeutic approachin reactive hemophagocytosis (11); and (iii) to ourknowledge, this is the first casein which the responsible strain causing a hemophagocytic visceral leishmaniasis infection has been characterized as Leishmania infantum belonging to a common zymodeme in the Mediterranean basin, MON-1. Unlike in our patient, infection with this strain usually has a favorable outcome.
Discussion
References
The clinical and biological features and the bone marrow findings, in the setting of an immunocompetenthost, supportedthe diagnosisof reactive hematophagocytosisassociatedwith visceral Ieishmaniasis.In the reviews dealing with the hematophagocyticsyndrome (4), a clinical and biochemical improvement of between46 and 70% of patients who received supportive treatment and/or specific antibiotics is reported. When the casesof reactive hemophagocytosisare analyzed,this percentageis higher, and all casesassociated with Leishmania spp. described in the literature (5-13) had a successful outcome. Our experiencewas, unfortunately, different. After treatmentwith antimonials and the administration of corticosteroids,the patient did not improve. Therefore,we tried additional therapeutic alternatives.We beganimmunoglobulin treatmentbasedon the positive experiencereportedby someauthors (15,16). We did not observeany clinical or biochemical improvement. The patient also presentedwith an unusual complication, spontaneousrupture of the spleen,which forced us to perform a splenectomy.Although splenectomy hasbeendescribedas a therapeuticoption in patients with hemophagocytosis (17-19) in our patient no improvement was achievedin the hematologic values. A week after the surgery the patient died of septic shock. Our case has three important features: (i) our patient was an immunocompetent host with leishmaniasis and a reactive hemophagocytic syndrome, with a fatal outcome; (ii) the absence of positive response to the treatments used, especially the splenectomy,
1.
Scott, R. and A. H. T. Robb-Smith. 1939. Histiocytic medullary reticulosis. Lancet. ii:19+198.
2.
Rappaport, H. 1966. Tumors of the hematopoietic system, p. 49-63. In Atlas of Tumor Pathology, Armed Forces Institute of Pathology, Washington, D. C.
3.
Risdall, R. J. et al. 1979. Virus associated hemophagocytic syndrome. A benign histiocytic proliferation distinct from malignant histiocytosis. Cancer 44:993-1002. Reiner, A. P. and J. L. Spivak. 1988. Hematophagic histiocytosis. Medicine 67:369-388.
0 1997 Elscvicr Science Inc.
4.
5.
Matzner, Y. et al. 1979. Systemic leishmaniasis mimicking malignant hystiocytosis. Cancer 43:398-402.
6.
Orta, C. et al. 1986. I-eishmaniasis visceral sugiriendo reticulosis medular histiocitica. Sangre 31:9&95.
7.
Navarro, D. M., M. C. P&z Barrachina. and M. Giralt. 1986. Leishmaniasis visceral y hemofagocitosis. Sangre 31:372-374.
8.
Lazanas, M. et al. 1990. Leishmaniose visckrale r&tlie par une histiocytose avec kythrophagocytose. Presse. Med. (France) 19:765.
9.
Castanet, J. et al. 1990. Syndrome d’hkmophagocytose au tours d’une leishmaniose visc&ale. Presse. Med. (France) 19: 1906.
10. Rodriguez, A. et al. 1991. Haemophagocytic visceral Kala-Azar. Infection 19:184. 11. Mascort, G. et al. 1991. Sindrome histiocito hemofagocitario ascciado a una infecci6n por Leishmaniu. An. Esp. Pediatr. 351273-275. 12. Bessis, D. et al. 1993. Photo Quiz. Clin. Infect. Dis. 17:829. 13. Granert, C. et al. 1993. Kala-azar in a one-year-old Swedish child. Diagnostic difficulties because of active hemo-
0196-4399/97/$0.00+
17.00
15
phagocytosis. Acta. Paediatr. 82:794796.
treatment of infection-associated hemophagocytic syndrome. J. Pediatr. 1233479-481
14. Rioux, J. A. et al. 1990. Taxonomy of Leishmanio. Use of isoenzymes. Suggestions for a new classification. Arm. Parasitol. Hum. Comp. 65:111-125.
16. Fort, D. W. and G. R. Buchanan. 1994. Treatment of infection-associated hemophagocytic syndrome with immune globulin. J. Pediak. 124:332.
15. Freeman, B. et al. 1993. Intravenously administered immune globulin for the
17. Boruchoff, S. E. 1990. Parvovirus B19associated hemophagocytic syndrome.
Wanted-Case
Arch. Intern. Med. 150:897-899. 18. Ross, C. W. et al. 1991. Chronic active Epstein-Barr virus infection and virusassociated
hemophagocytic
syndrome.
Arch. Pathol. Lab. Med. 115(5):470474. 19. Bourquelot, P. et al. 1993. Hemophagocytic syndrome in HIV patients. Presse. Med. (France) 22:1217-1220.
Reports
If your laboratory has isolated an uncommonorganism from an unusual patient site, or an organism that presented a particular diagnostic challenge, why not share the information with your colleagues through the Clinical Microbiology Newsletter. The editors would like to receive interesting casereports from our readersfor possi-
ble publication in the Newsletter. Submitted casereports should contain (i) a brief clinical history summarizing the symptoms and course of illness; (ii) a description of how the organism(s) were cultured and differentiated from closely associatedorganisms; and (iii) the method of susceptibility testing for the isolate(s) and the results obtained.
Editors
General Information
Mary JaneFerraro Paul A. Granato JosephineA. Morel10 R.J. Zabransky Q 1997 Elsevier Science Inc. MN Ol%-4399 CMNEEJ 19(2) 9-16, 1997 Elsevier
Sendthe original typescript, four copies, and a diskette to: Tina Bonanno Clinical Microbiology Newsletter Elsevier ScienceInc. 660 White Plains Road Tarrytown, NY 10591-5153
Subscription information can be found inside the front cover. This newsletter has been registered with the Copyright Clearance Center, Inc. Consent is given for copying articles for personalor internal use,or for the personalor internal use of specific clients. This consent is given on the condition that the copier pay through the Center the per-copy fee stated in the code on the first page for copying beyond that permitted by the US Copyright Law. If no code appears on an article, the author has not given broad consent to copy and permission to copy must be obtained directly from the author. This consent does not extend to other kinds of copying, such as for general distribution, resale, advertising and promotional purposes, or for creating new collective works. Address orders, changes of address, and claims for missing issues to Journal Fulfillment Department, Elsevier Science Inc., 655 Avenue of the Americas, New Yolk, NY 10010. Claims for missing issues can be honored only up to three months for domestic addresses and six months for foreign addresses. Duplicate copies will not be sent to replace ones undelivered due to failure to notify Elsevier of change of address. Postmaster: Send address changes to Clinical Microbiology of the Americas, New York, NY 10010.
Newsletter, Elsevier Science inc., 655 Avenue
Editorials and letters printed in this newsletter are published for the interest of the readers and do not necessarily reflect the opinions of the editors.
lllIllIIIIllll~l~ll~ Illlllllllllllllllllllll 0196~4399~19970115)19:2:1-Q
16
0196-4399/97#0.00+ 17.00
Clinical Microbiology Newsletter is abstracted in Tropical Diseases Bulletin, Abstracts on Hygiene and Communicable Diseases and Current AIDS Literature. 0 1997Else&r ScienceInc.
Clinical Micmbiology Newsletter 19:2,1997
varicella-zoster genome in ocular samples from patients with acute retinal necrosis. Am J. Ophthahnol. 114603-609. 19. Wiedbrauk, D.L., J.C. Warner, and A.M. Drevon. 1995. Inhibition of PCR by aqueous and vitrous fluids. J. Clin. Microbial. 33:2643-2646. 20. DeVincenxo J.P., and G. Thorpe. 1994. Mild herpes simplex encephalitis diagnosed by polymerase chain reaction: a case report and review. Pediatr. Infect. Dis. J. 13:662-664. 21. Schlesinger, Y.. et al. 1995. Herpes simplex virus type 2 meningitis in the absence of genital lesions: improved recognition with use of the polymemse chain reaction.
Clin. Infect. Dis. 20~842-848. 22. Aurelius, E., et al. 1991. Rapid diagnosis of herpes simplex encephalitis by nested polymerase chain reaction assay of CSF. Lancet 337:189-192. 23. Lakeman, F.D.. et al. 1995. Diagnosis of herpes simplex virus encephalitis: application of polymerase chain reaction to CSF from brain-biopsied patients and correlation with disease. J. Infect. Dis. 171:857-863. 24. Marcon, M. J., et al. Unpublished data. 25. Landry, M.L. 1995. False-positive polymerase chain reaction in the diagnosis of herpes simplex encephalitis. J. Infect. Dis. 172:1641-1643.
Case Report
Hemophagocytic Syndrome Associated With Visceral Leishmaniasis in an Immunocompetent Patient Pilar Cort&, MSc. Neus Cardefiosa,Ph.D. CarmenMuftoz, Ph.D. Servei de Microbiologia Hospital de la Santa Creu i Sant Pau Barcekwaa, Spain Ignaci Dur&n, M.D.
Ruben Leta, M.D. Alex Rota-Cusachs,M.D. Servei de Medic& interna HoJpital de la Santa Creu i Sant Pau BarceloM. Spain
Montserrat Gallego, Ph.D. Departament de Microbiologia Parasitologia Sanitciries Facultat de Farmcicia hiversitat de Barcelona Barcelona, Spain.
i
Hemophagocytosiswas describedas a characteristicfeature in histiocytic marrow reticulosis by Scott and RobbSmith in 1939 (1). In 1966,Rappaport (2) reported similar casesand introducedthe term malignant histiocytosis to describea diseasecharacterizedby a systemicinvasive proliferation of morphologically atypical histiocytes. More recently, somecaseswith clini-
14
0196-4399/97/$0.00
+ 17.00
cal and anatomopathologicalfeatures similar to malignant histiocytosis have been described,secondarynot only to neoplasmsbut also to reactive proliferations (3). Theseare related to a broad spectrumof infections that include several viruses, bacteria,rickettsiae, fungi, and parasites(4). We describea caseof reactive hemophagocytosisassociatedwith an infcction by Leishmania infantum belonging to a common zymodemein our geographical area,MON- 1. Although severalcasesof hematophagichistiocytosis, in which leishmania infections are involved, havebeenreported (5-13), to our knowledge this is the first casewith a fatal outcomein an immunocompetent patient.
Case report A 59-yr-old man, who lived in Barcelona (Spain), wasadmitted to our hospital in January1994becauseof anemia, weight loss(2 kg), li-equentepistaxis, and a 20&y history of fever. The patient had a long history of high blood pressureand, 8 mo before admission, had sufferedarthritis of the ankle of unknown etiology for 3 wk. He had not
0 1997 Else&r
Science Inc.
traveled abroad.On admission, the patient was febrile (38 to 39°C) and reported left lower-back pain. Examination revealeda homogeneous firm liver edge 8 to 9 cm below the right costal margin without splenomegaly.Laboratory findings showed: hemoglobin 11 g/L; white blood cell count 3. lx 109/L;platelets 80x109/L; an altered prothrombin time (65%) and a mild cholestastispattern. Tumor markers including prostate-specific antigen, carcinoembryonic antigen and alpha-fetoprotein were normal. Blood cultures and/or serological studies for HIV, cytomegalovirus, IgM antibodies, Epstein-Barr virus, hepatitis C and hepatitis B viruses, herpessimplex virus, Toxoplasma, Brucella, Q-fever, and typhoid fever were all negative. The tuberculin test was positive. Chest X-ray was normal. Abdominal ultrasonographyand CT scandisclosed hepatosplenomegalywithout adenopathy. Bone marrow biopsy showed no hematological anomaly and microscopic examination using Giemsa staining revealedpoorly staining Leishmania amastigoteforms. Two weeks after ad-
Clinical Micmbiology
Newsletter 19:2,1997
mission the patient developeda purpuric rash in the right lumbar region and relapsing fever in the evening together with progressivedyspnea.ChestX-ray showeda right pleural effusion with underlying parenchymaldamage.Arterial blood gaseswere pO2 62 mm Hg; pCO2 33 mm Hg; and pH 7.5. Three weeks later, a new bone marrow study was performed that showeda low number of Leishmuniu amastigoteforms in addition to hemophagocytosiswithout cytologic atypia. The diagnosis of visceral leishmaniasiswas confirmed by culture of flagellated forms of the pathogenincubatedin Nicolle-Novy-McNeal (NNN) medium and by two serological techniques,an immunofluorescenceantibody test that waspositive with a titer of 1,280,and an immunoblot, which was also positive. Isoenzymeanalysis of the strain was carried out (Departamentde Parasitologia,Facultat de Farm&&, Barcelona) using the current panel of 15 enzymes(MDHl, ME, ICD, F’GD,G6PD, GLUD, DL41, NPl, Np2, GOTl, GOT2,PGM, FH, MDI, and GPI) proposedby the Laboratoire d’Ecologie Mt?dicale(Montpellier, France) (14); the strain was identified asLeishmania infantum MON-1 (MHOM/E+94/BCN-109). During this time, with no changein the white blood cell count, the platelet count decreased progressively to 7x 109/L2 wk after admission. Treatmentwith corticosteroids (1 mg/kgJd)was begun and maintained throughout the hospitalization without improvement in the white cell or platelet counts.Becauseof the severepancytopenia, treatmentof leishmaniasiswith intramuscular antimonials was ruled out. For this reasonintravenous pcntamidmeat a daily doseof 4 mg/kg and allopurinol500 mg every 8 h was started.Epigastric pain and an enlargement of the QT interval led us to replace this drug with intravenous Glucantime at a daily doseof 850 mg for 20 d. The patient’s condition continued to deteriorateand becauseof his extremely critical pancytopeniahe required multiple platelet transfusions, which, nevertheless,did not improve the platelet count. Therefore daily intravenous infusions of gamma-globulin were begun at recommendeddosesfor
Clinical Micmbiology
Ne~slctta
19:2,1997
5 d. Thirty days after admission,the patient suddenly developeddeeppain in the left upper abdominal quadrant.Ultrasonographyand CT scanof the abdomen showedsplenic rupture. An emergencysplenectomywas performed and the patient was transferredto the intensive care unit, where he developeda fatal coursepresentingwith septic shock by Escherichia coli and multi-organ failure. He died in the first postoperative week.
which hasbeenregardedasa therapeutic approachin reactive hemophagocytosis (11); and (iii) to ourknowledge, this is the first casein which the responsible strain causing a hemophagocytic visceral leishmaniasis infection has been characterized as Leishmania infantum belonging to a common zymodeme in the Mediterranean basin, MON-1. Unlike in our patient, infection with this strain usually has a favorable outcome.
Discussion
References
The clinical and biological features and the bone marrow findings, in the setting of an immunocompetenthost, supportedthe diagnosisof reactive hematophagocytosisassociatedwith visceral Ieishmaniasis.In the reviews dealing with the hematophagocyticsyndrome (4), a clinical and biochemical improvement of between46 and 70% of patients who received supportive treatment and/or specific antibiotics is reported. When the casesof reactive hemophagocytosisare analyzed,this percentageis higher, and all casesassociated with Leishmania spp. described in the literature (5-13) had a successful outcome. Our experiencewas, unfortunately, different. After treatmentwith antimonials and the administration of corticosteroids,the patient did not improve. Therefore,we tried additional therapeutic alternatives.We beganimmunoglobulin treatmentbasedon the positive experiencereportedby someauthors (15,16). We did not observeany clinical or biochemical improvement. The patient also presentedwith an unusual complication, spontaneousrupture of the spleen,which forced us to perform a splenectomy.Although splenectomy hasbeendescribedas a therapeuticoption in patients with hemophagocytosis (17-19) in our patient no improvement was achievedin the hematologic values. A week after the surgery the patient died of septic shock. Our case has three important features: (i) our patient was an immunocompetent host with leishmaniasis and a reactive hemophagocytic syndrome, with a fatal outcome; (ii) the absence of positive response to the treatments used, especially the splenectomy,
1.
Scott, R. and A. H. T. Robb-Smith. 1939. Histiocytic medullary reticulosis. Lancet. ii:19+198.
2.
Rappaport, H. 1966. Tumors of the hematopoietic system, p. 49-63. In Atlas of Tumor Pathology, Armed Forces Institute of Pathology, Washington, D. C.
3.
Risdall, R. J. et al. 1979. Virus associated hemophagocytic syndrome. A benign histiocytic proliferation distinct from malignant histiocytosis. Cancer 44:993-1002. Reiner, A. P. and J. L. Spivak. 1988. Hematophagic histiocytosis. Medicine 67:369-388.
0 1997 Elscvicr Science Inc.
4.
5.
Matzner, Y. et al. 1979. Systemic leishmaniasis mimicking malignant hystiocytosis. Cancer 43:398-402.
6.
Orta, C. et al. 1986. I-eishmaniasis visceral sugiriendo reticulosis medular histiocitica. Sangre 31:9&95.
7.
Navarro, D. M., M. C. P&z Barrachina. and M. Giralt. 1986. Leishmaniasis visceral y hemofagocitosis. Sangre 31:372-374.
8.
Lazanas, M. et al. 1990. Leishmaniose visckrale r&tlie par une histiocytose avec kythrophagocytose. Presse. Med. (France) 19:765.
9.
Castanet, J. et al. 1990. Syndrome d’hkmophagocytose au tours d’une leishmaniose visc&ale. Presse. Med. (France) 19: 1906.
10. Rodriguez, A. et al. 1991. Haemophagocytic visceral Kala-Azar. Infection 19:184. 11. Mascort, G. et al. 1991. Sindrome histiocito hemofagocitario ascciado a una infecci6n por Leishmaniu. An. Esp. Pediatr. 351273-275. 12. Bessis, D. et al. 1993. Photo Quiz. Clin. Infect. Dis. 17:829. 13. Granert, C. et al. 1993. Kala-azar in a one-year-old Swedish child. Diagnostic difficulties because of active hemo-
0196-4399/97/$0.00+
17.00
15
phagocytosis. Acta. Paediatr. 82:794796.
treatment of infection-associated hemophagocytic syndrome. J. Pediatr. 1233479-481
14. Rioux, J. A. et al. 1990. Taxonomy of Leishmanio. Use of isoenzymes. Suggestions for a new classification. Arm. Parasitol. Hum. Comp. 65:111-125.
16. Fort, D. W. and G. R. Buchanan. 1994. Treatment of infection-associated hemophagocytic syndrome with immune globulin. J. Pediak. 124:332.
15. Freeman, B. et al. 1993. Intravenously administered immune globulin for the
17. Boruchoff, S. E. 1990. Parvovirus B19associated hemophagocytic syndrome.
Wanted-Case
Arch. Intern. Med. 150:897-899. 18. Ross, C. W. et al. 1991. Chronic active Epstein-Barr virus infection and virusassociated
hemophagocytic
syndrome.
Arch. Pathol. Lab. Med. 115(5):470474. 19. Bourquelot, P. et al. 1993. Hemophagocytic syndrome in HIV patients. Presse. Med. (France) 22:1217-1220.
Reports
If your laboratory has isolated an uncommonorganism from an unusual patient site, or an organism that presented a particular diagnostic challenge, why not share the information with your colleagues through the Clinical Microbiology Newsletter. The editors would like to receive interesting casereports from our readersfor possi-
ble publication in the Newsletter. Submitted casereports should contain (i) a brief clinical history summarizing the symptoms and course of illness; (ii) a description of how the organism(s) were cultured and differentiated from closely associatedorganisms; and (iii) the method of susceptibility testing for the isolate(s) and the results obtained.
Editors
General Information
Mary JaneFerraro Paul A. Granato JosephineA. Morel10 R.J. Zabransky Q 1997 Elsevier Science Inc. MN Ol%-4399 CMNEEJ 19(2) 9-16, 1997 Elsevier
Sendthe original typescript, four copies, and a diskette to: Tina Bonanno Clinical Microbiology Newsletter Elsevier ScienceInc. 660 White Plains Road Tarrytown, NY 10591-5153
Subscription information can be found inside the front cover. This newsletter has been registered with the Copyright Clearance Center, Inc. Consent is given for copying articles for personalor internal use,or for the personalor internal use of specific clients. This consent is given on the condition that the copier pay through the Center the per-copy fee stated in the code on the first page for copying beyond that permitted by the US Copyright Law. If no code appears on an article, the author has not given broad consent to copy and permission to copy must be obtained directly from the author. This consent does not extend to other kinds of copying, such as for general distribution, resale, advertising and promotional purposes, or for creating new collective works. Address orders, changes of address, and claims for missing issues to Journal Fulfillment Department, Elsevier Science Inc., 655 Avenue of the Americas, New Yolk, NY 10010. Claims for missing issues can be honored only up to three months for domestic addresses and six months for foreign addresses. Duplicate copies will not be sent to replace ones undelivered due to failure to notify Elsevier of change of address. Postmaster: Send address changes to Clinical Microbiology of the Americas, New York, NY 10010.
Newsletter, Elsevier Science inc., 655 Avenue
Editorials and letters printed in this newsletter are published for the interest of the readers and do not necessarily reflect the opinions of the editors.
lllIllIIIIllll~l~ll~ Illlllllllllllllllllllll 0196~4399~19970115)19:2:1-Q
16
0196-4399/97#0.00+ 17.00
Clinical Microbiology Newsletter is abstracted in Tropical Diseases Bulletin, Abstracts on Hygiene and Communicable Diseases and Current AIDS Literature. 0 1997Else&r ScienceInc.
Clinical Micmbiology Newsletter 19:2,1997