738
Correspondence
from the respiratory tract in the diagnosis of invasive pulmonary aspergillosis. Am J Med 1986;81 :249-54. 4. Wiest PM, Flanigan T, Salata RA, Shlaes OM, Katzman M, Lederman MM. Serious infectious complications ofcorticosteroid treatment for chronic obstructive pulmonary disease. Chest 1989;95: 1180-4. 5. Bennet JE. Aspergillus species. In: Mandell GL, Douglas RG Jr, Bennet JE, eds. Principles and practice of infectious diseases. 3rd ed. New York: Churchill Livingstone, 1990: 1958-62. 6. Piotrowski WP, Pilz P, Chuang IH. Subarachnoid hemorrhage caused by a fungal aneurysm of the vertebral artery as a complication of intracranial aneurysm clipping. Case report. J Neurosurg 1990; 73:962-4.
Vibrio parahaemolyticus Septicemia in a Patient with Neutropenic Leukemia
Grant Support: This work was supported by the National Institute of Allergy and Infectious Diseases (AI-07183). Correspondence: Dr. Herbert B. Tanowitz, Department of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461. Clinical Infectious Diseases 1992;15:738-9 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1504-0031$02.00
7. Iihara K, Makita Y, Nabeshima S, Tei T, Keyaki A, Nioka H. Aspergillosis of the central nervous system causing subarachnoid hemorrhage from a mycotic aneurysm of the basilar artery-case report. Neurol Med Chir (Tokyo) 1990;30:618-23. 8. Peacock JE, McGinnis MR, Cohen MS. Persistent neutrophilic meningitis. Report of 4 cases and literature review. Medicine (Baltimore) 1984;63:379-95. 9. Gordon MA, Holzman RS, Senter H, Lapa EW, Kupersmith MJ. Aspergillus oryzae meningitis. JAMA 1976;235:2122-3. 10. Green M, Wald ER, Tzakis A, Todo S, Starzl TE. Aspergillosis of the CNS in a pediatric liver transplant recipient: case report and review. Rev Infect Dis 1991;13:653-7.
dime, and amphotericin B was added. V. parahaemolyticus grew in culture of the blood (API20E biochemical test panel, Analytab Products, Plainview, NY). The organism was sensitive to trimethoprim-sulfamethoxazole (TMP-SMZ), mezlocillin, ciprofloxacin, aztreonam, chloramphenicol, imipenem, tetracycline, and ceftazidime. Therapy with amphotericin B and vancomycin was discontinued. On the third hospital day, the hematocrit dropped from 25% to 19% in association with a rise in the level of LDH to 206.5 UIL. Intravascular hemolysis was suspected. Gradually, the patient's condition improved and he was discharged and received oral TMP-SMZ after completing a 14-day course of ceftazidime and gentamicin. V. parahaemolyticus, first recognized as a human pathogen in 1950 during an outbreak of acute seafood poisoning in Osaka, Japan [l], has since been implicated in numerous outbreaks along the Pacific, Atlantic, and Gulf Coasts and occasionally in sporadic cases of diarrheal illness following the ingestion of raw or improperly cooked seafood [2, 3]. Gastrointestinal illness caused by V. parahaemolyticus tends to be mild and self-limited, rarely lasting longer than 3 days. The organism is not generally enteroinvasive. Although V. parahaemolyticus is susceptible in vitro to many antibiotics, including TMP-SMZ, tetracycline, chloramphenicol, third-generation cephalosporins, ciprofloxacin, and the aminoglycosides, treatment is not indicated for most cases of gastroenteritis [4, 5]. Isolation of V. parahaemolyticus from sites other than the stool is rare but has been reported [6, 7]. In a lO-year survey of non-cholerae vibrio infections in the Gulf Coast, three cases of extraintestinal V. parahaemolyticus infections, including one of bacteremia [8], were reported. This last case occurred in a neutropenic patient similar to ours who had acute myelogenous leukemia and developed fulminant V. parahaemolyticus sepsis after sustaining lacerations on his hands while peeling shrimp. A notable feature in our patient's course was the drop in hematocrit associated with a rise in LDH. Intravascular hemolysis was reported in one previous case of V. parahaemolyticus sepsis [7] and may have occurred in our patient as well. Human pathogenicity of V. parahaemolyticus isolates is closely associated with in vitro hemolysis, the so-called Kanagawa phenomenon [9]. Unfortunately, we did not test our patient's isolate for this property. Despite his initial septic presentation, our patient recovered with antibiotic therapy. This case as well as that of the previously reported patient with leukemia suggest that patients with malignancy and neutropenia may be at increased risk ofatypical fulminant and invasive V. parahaemolyticus infections follow-
Downloaded from http://cid.oxfordjournals.org/ by guest on August 17, 2015
SIR- Vibrio parahaemolyticus, usually associated with gastrointestinal infections following ingestion ofseafood, is occasionally isolated from extraintestinal sites, but bacteremia is rare. We report a case offulminant V. parahaemolyticus sepsis in a patient with neutropenic lymphoma. A 48-year-old man with lymphocytic lymphoma presented with fever and a painful right fifth finger. He had previously undergone splenectomy and had received chemotherapy for stage IlIA Hodgkin's disease in 1983; further chemotherapy was administered for a relapse in 1986. In November 1989, he developed T cell lymphoblastic lymphoma for which he received multiple chemotherapeutic regimens. The last dose of therapy had been administered 2 weeks before this admission. Two days before admission, while preparing fresh squid, the patient noticed a laceration on the fifth digit of his right hand. The next day he developed fever, pain, and swelling of that finger. He denied vomiting, diarrhea, or abdominal pain. On physical examination, he was an ill-appearing man with a blood pressure of90/60 mm Hg, a respiratory rate of24, a temperature of 38.6°C, and a pulse rate of 100. Paronychia was present on the right fifth finger. The oral mucosae were dry and coated with thrush, and petechiae were present on the lower extremities. The white blood cell count was 700/mm 3 ; hemoglobin, 10.0 mg/dL; and platelet count, 10,000/mm 3• The level of urea nitrogen was 37 mg/dL; creatinine, 1.4 mg/dL; glucose, 387 mg/ dL; and lactate dehydrogenase (LDH), 388 U/L. Blood samples for cultures were drawn, and therapy with cefoperazone, vancomycin, and gentamicin was started. A gram-stained preparation of purulent material from the paronychia showed numerous polymorphonuclear leukocytes with no organisms. Several hours after admission, the patient's condition deteriorated further, and he was transferred to the intensive care unit. Therapy with cefoperazone was changed to that with ceftazi-
CID 1992; 15 (October)
CIO 1992; 15 (October)
ing the handling of raw seafood, particularly in the presence ofa break in the skin barrier. Joanna Dobroszycki, Nancy T. Sklarin, George Szilagy, and Herbert B. Tanowitz Departments of Medicine. Pathology. Oncology. and Laboratory Medicine. Albert Einstein College ofMedicine. and Montefiore Medical Center. Bronx. New York
References I. Fujine T. Okuno T. Nakada D. et at. On the bacteriologic examination of shirasu food poisoning. Journal of the Japanese Association of Infectious Diseases 1951;25: 11-2. 2. Baress J. Liston J. Isolation of Vibrio parahaemolyticus from the northwest Pacific. Nature 1968;217: 1263-4.
SIR-Atmar's recent excellent review on complications of measles during pregnancy suggests that prenatal screening for immunity may be prudent in areas where outbreaks of measles are occurring [1]. Women infected with human immunodeficiency virus (HIV) deserve particular attention since measles is known to cause significant morbidity and mortality in both adults [2] and children [3]. Immunity to rubella is also of concern in pregnant women. Even though the number of cases of rubella has declined, infants with congenital rubella syndrome continue to be born [4]. Previous studies of seroprevalence among women not infected with HIV have shown protective immunity to measles in 97% [5] and that to rubella in 89%94% [6]. To determine the immunity to both measles and rubella in our HIV-infected female population, we screened all females born between 1957 and 1975 admitted to our outpatient HIV program at the Medical Center of Louisiana (previously known as Charity Hospital) between October 1991 and April 1992. Females born after 1975 were not screened but were routinely vaccinated with the measles-mumps-rubella (MMR) vaccine. Both measles and rubella IgG antibodies were tested by enzyme immunoassay (EIA) (rubella, Abbott Laboratory, Abbott Park, IL; measles, BioWhittaker Laboratory, Walkersville, MD). A total of 34 women were tested for both measles and rubella immunity. Seven (21 %) had no immunity to measles and four (12%) had no immunity to rubella. Therefore, II (32%) had no immunity to either measles or rubella. All women were considered to be of lower socioeconomic status. Other demographic features of the II women lacking immunity were as follows:
Correspondence: Dr. Rebecca Clark. Infectious Diseases Section. Tulane University Medical Center. 1430 Tulane Avenue. New Orleans. Louisiana 70112.
3. Barker WH Jr. Vibrio parahaemolyticus outbreaks in the United States. Lancet 1974;1:551-4. 4. Bolon JL. Zawiska SA, Greenough WB III. Clinical features ofenteritis due to Vibrio parahaemolyticus. Am J Med 1974;57:638-41. 5. Blake PA. Weaver RE. Hollis DG. Diseases of humans (other than cholera) caused by Vibrios. Ann Rev MicrobioI1980;34:341-67. 6. Armstrong CWo Lake JL. Miller GB. Extraintestinal infectious due to halophilic Vibrios. South Med J 1983;76:571-4. 7. Roland FP. Leg gangrene and endotoxin shock due to Vibrio parahaemolyticus-an infection acquired in New England coastal waters. N Engl J Med 1970;282: 1306. 8. Bonner JR. Coker AS. Berryman CR. Pollock HM. Spectrum of Vibrio infections in a Gulf Coast community. Ann Intern Med 1983;99:464-9. 9. Miyamoto Y. Kato T. Obara Y. Akiyama S, Takizawa K. Yamai S. In vitro hemolytic characteristic of Vibrio parahaemolyticus: its close correlation with human pathogenicity. J Bacteriol 1969; 100: 1147-9.
nine (82%) were African American; the median age was 25 years (range, 18-35 years); and the median CD4 lymphocyte count was 636/mm 3 (range, 317-1 ,040/mm 3). Only three women had
Correspondence
from the respiratory tract in the diagnosis of invasive pulmonary aspergillosis. Am J Med 1986;81 :249-54. 4. Wiest PM, Flanigan T, Salata RA, Shlaes OM, Katzman M, Lederman MM. Serious infectious complications ofcorticosteroid treatment for chronic obstructive pulmonary disease. Chest 1989;95: 1180-4. 5. Bennet JE. Aspergillus species. In: Mandell GL, Douglas RG Jr, Bennet JE, eds. Principles and practice of infectious diseases. 3rd ed. New York: Churchill Livingstone, 1990: 1958-62. 6. Piotrowski WP, Pilz P, Chuang IH. Subarachnoid hemorrhage caused by a fungal aneurysm of the vertebral artery as a complication of intracranial aneurysm clipping. Case report. J Neurosurg 1990; 73:962-4.
Vibrio parahaemolyticus Septicemia in a Patient with Neutropenic Leukemia
Grant Support: This work was supported by the National Institute of Allergy and Infectious Diseases (AI-07183). Correspondence: Dr. Herbert B. Tanowitz, Department of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461. Clinical Infectious Diseases 1992;15:738-9 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1504-0031$02.00
7. Iihara K, Makita Y, Nabeshima S, Tei T, Keyaki A, Nioka H. Aspergillosis of the central nervous system causing subarachnoid hemorrhage from a mycotic aneurysm of the basilar artery-case report. Neurol Med Chir (Tokyo) 1990;30:618-23. 8. Peacock JE, McGinnis MR, Cohen MS. Persistent neutrophilic meningitis. Report of 4 cases and literature review. Medicine (Baltimore) 1984;63:379-95. 9. Gordon MA, Holzman RS, Senter H, Lapa EW, Kupersmith MJ. Aspergillus oryzae meningitis. JAMA 1976;235:2122-3. 10. Green M, Wald ER, Tzakis A, Todo S, Starzl TE. Aspergillosis of the CNS in a pediatric liver transplant recipient: case report and review. Rev Infect Dis 1991;13:653-7.
dime, and amphotericin B was added. V. parahaemolyticus grew in culture of the blood (API20E biochemical test panel, Analytab Products, Plainview, NY). The organism was sensitive to trimethoprim-sulfamethoxazole (TMP-SMZ), mezlocillin, ciprofloxacin, aztreonam, chloramphenicol, imipenem, tetracycline, and ceftazidime. Therapy with amphotericin B and vancomycin was discontinued. On the third hospital day, the hematocrit dropped from 25% to 19% in association with a rise in the level of LDH to 206.5 UIL. Intravascular hemolysis was suspected. Gradually, the patient's condition improved and he was discharged and received oral TMP-SMZ after completing a 14-day course of ceftazidime and gentamicin. V. parahaemolyticus, first recognized as a human pathogen in 1950 during an outbreak of acute seafood poisoning in Osaka, Japan [l], has since been implicated in numerous outbreaks along the Pacific, Atlantic, and Gulf Coasts and occasionally in sporadic cases of diarrheal illness following the ingestion of raw or improperly cooked seafood [2, 3]. Gastrointestinal illness caused by V. parahaemolyticus tends to be mild and self-limited, rarely lasting longer than 3 days. The organism is not generally enteroinvasive. Although V. parahaemolyticus is susceptible in vitro to many antibiotics, including TMP-SMZ, tetracycline, chloramphenicol, third-generation cephalosporins, ciprofloxacin, and the aminoglycosides, treatment is not indicated for most cases of gastroenteritis [4, 5]. Isolation of V. parahaemolyticus from sites other than the stool is rare but has been reported [6, 7]. In a lO-year survey of non-cholerae vibrio infections in the Gulf Coast, three cases of extraintestinal V. parahaemolyticus infections, including one of bacteremia [8], were reported. This last case occurred in a neutropenic patient similar to ours who had acute myelogenous leukemia and developed fulminant V. parahaemolyticus sepsis after sustaining lacerations on his hands while peeling shrimp. A notable feature in our patient's course was the drop in hematocrit associated with a rise in LDH. Intravascular hemolysis was reported in one previous case of V. parahaemolyticus sepsis [7] and may have occurred in our patient as well. Human pathogenicity of V. parahaemolyticus isolates is closely associated with in vitro hemolysis, the so-called Kanagawa phenomenon [9]. Unfortunately, we did not test our patient's isolate for this property. Despite his initial septic presentation, our patient recovered with antibiotic therapy. This case as well as that of the previously reported patient with leukemia suggest that patients with malignancy and neutropenia may be at increased risk ofatypical fulminant and invasive V. parahaemolyticus infections follow-
Downloaded from http://cid.oxfordjournals.org/ by guest on August 17, 2015
SIR- Vibrio parahaemolyticus, usually associated with gastrointestinal infections following ingestion ofseafood, is occasionally isolated from extraintestinal sites, but bacteremia is rare. We report a case offulminant V. parahaemolyticus sepsis in a patient with neutropenic lymphoma. A 48-year-old man with lymphocytic lymphoma presented with fever and a painful right fifth finger. He had previously undergone splenectomy and had received chemotherapy for stage IlIA Hodgkin's disease in 1983; further chemotherapy was administered for a relapse in 1986. In November 1989, he developed T cell lymphoblastic lymphoma for which he received multiple chemotherapeutic regimens. The last dose of therapy had been administered 2 weeks before this admission. Two days before admission, while preparing fresh squid, the patient noticed a laceration on the fifth digit of his right hand. The next day he developed fever, pain, and swelling of that finger. He denied vomiting, diarrhea, or abdominal pain. On physical examination, he was an ill-appearing man with a blood pressure of90/60 mm Hg, a respiratory rate of24, a temperature of 38.6°C, and a pulse rate of 100. Paronychia was present on the right fifth finger. The oral mucosae were dry and coated with thrush, and petechiae were present on the lower extremities. The white blood cell count was 700/mm 3 ; hemoglobin, 10.0 mg/dL; and platelet count, 10,000/mm 3• The level of urea nitrogen was 37 mg/dL; creatinine, 1.4 mg/dL; glucose, 387 mg/ dL; and lactate dehydrogenase (LDH), 388 U/L. Blood samples for cultures were drawn, and therapy with cefoperazone, vancomycin, and gentamicin was started. A gram-stained preparation of purulent material from the paronychia showed numerous polymorphonuclear leukocytes with no organisms. Several hours after admission, the patient's condition deteriorated further, and he was transferred to the intensive care unit. Therapy with cefoperazone was changed to that with ceftazi-
CID 1992; 15 (October)
CIO 1992; 15 (October)
ing the handling of raw seafood, particularly in the presence ofa break in the skin barrier. Joanna Dobroszycki, Nancy T. Sklarin, George Szilagy, and Herbert B. Tanowitz Departments of Medicine. Pathology. Oncology. and Laboratory Medicine. Albert Einstein College ofMedicine. and Montefiore Medical Center. Bronx. New York
References I. Fujine T. Okuno T. Nakada D. et at. On the bacteriologic examination of shirasu food poisoning. Journal of the Japanese Association of Infectious Diseases 1951;25: 11-2. 2. Baress J. Liston J. Isolation of Vibrio parahaemolyticus from the northwest Pacific. Nature 1968;217: 1263-4.
SIR-Atmar's recent excellent review on complications of measles during pregnancy suggests that prenatal screening for immunity may be prudent in areas where outbreaks of measles are occurring [1]. Women infected with human immunodeficiency virus (HIV) deserve particular attention since measles is known to cause significant morbidity and mortality in both adults [2] and children [3]. Immunity to rubella is also of concern in pregnant women. Even though the number of cases of rubella has declined, infants with congenital rubella syndrome continue to be born [4]. Previous studies of seroprevalence among women not infected with HIV have shown protective immunity to measles in 97% [5] and that to rubella in 89%94% [6]. To determine the immunity to both measles and rubella in our HIV-infected female population, we screened all females born between 1957 and 1975 admitted to our outpatient HIV program at the Medical Center of Louisiana (previously known as Charity Hospital) between October 1991 and April 1992. Females born after 1975 were not screened but were routinely vaccinated with the measles-mumps-rubella (MMR) vaccine. Both measles and rubella IgG antibodies were tested by enzyme immunoassay (EIA) (rubella, Abbott Laboratory, Abbott Park, IL; measles, BioWhittaker Laboratory, Walkersville, MD). A total of 34 women were tested for both measles and rubella immunity. Seven (21 %) had no immunity to measles and four (12%) had no immunity to rubella. Therefore, II (32%) had no immunity to either measles or rubella. All women were considered to be of lower socioeconomic status. Other demographic features of the II women lacking immunity were as follows:
Correspondence: Dr. Rebecca Clark. Infectious Diseases Section. Tulane University Medical Center. 1430 Tulane Avenue. New Orleans. Louisiana 70112.
3. Barker WH Jr. Vibrio parahaemolyticus outbreaks in the United States. Lancet 1974;1:551-4. 4. Bolon JL. Zawiska SA, Greenough WB III. Clinical features ofenteritis due to Vibrio parahaemolyticus. Am J Med 1974;57:638-41. 5. Blake PA. Weaver RE. Hollis DG. Diseases of humans (other than cholera) caused by Vibrios. Ann Rev MicrobioI1980;34:341-67. 6. Armstrong CWo Lake JL. Miller GB. Extraintestinal infectious due to halophilic Vibrios. South Med J 1983;76:571-4. 7. Roland FP. Leg gangrene and endotoxin shock due to Vibrio parahaemolyticus-an infection acquired in New England coastal waters. N Engl J Med 1970;282: 1306. 8. Bonner JR. Coker AS. Berryman CR. Pollock HM. Spectrum of Vibrio infections in a Gulf Coast community. Ann Intern Med 1983;99:464-9. 9. Miyamoto Y. Kato T. Obara Y. Akiyama S, Takizawa K. Yamai S. In vitro hemolytic characteristic of Vibrio parahaemolyticus: its close correlation with human pathogenicity. J Bacteriol 1969; 100: 1147-9.
nine (82%) were African American; the median age was 25 years (range, 18-35 years); and the median CD4 lymphocyte count was 636/mm 3 (range, 317-1 ,040/mm 3). Only three women had
