1070
Correspondence
Thrombosis of the Mesenteric Vein as a Complication of Mediterranean Spotted Fever
Correspondence: Dr. Z. Landau. Department of Internal Medicine 'B'. Kaplan Hospital, 76100 Rehovot, Israel.
Clinical Infectious Diseases 1992;15:1070-1 © 1992 by The Universityof Chicago.All rightsreserved. 1058-4838/92/1506-0042$02.00
An enlarged lymph node from the mesenterium was also taken for pathological examination. The following day a "secondlook" operation revealed viable small intestine with petechiae and hemorrhage. On the third postoperative day, a maculopapular rash appeared on his hands and legs; this rash spread to the abdomen. Specific fluorescent antibodies (IgM and IgG) to R. coronii were not present on the day of the patient's admission; however, these antibodies were present on the 21st day after his admission at a dilution of I: 100, a finding that confirmed the diagnosis ofMSF. Antibiotic therapy with parenteral minocycline, ciprofloxacin, amikacin, and metronidazole was administered, but the patient died of septic shock. Pathological examination of the small intestine revealed dilated, edematous intestinal loops with areas of transmural hemorrhage. The mesenteric veins showed vasculitis and organizing thrombi. The pancreas and the liver showed vasculitic changes, and the lymph nodes showed only reactive changes. Gastrointestinal manifestations are less common in MSF than in Rocky Mountain spotted fever, in which up to two-thirds of patients may experience nausea, vomiting, diarrhea, or abdominal pain [3-6]. There have been reports of patients who have developed the rash typical of MSF and the serological findings diagnostic of MSF after undergoing laparotomy because of severe abdominal pain and tenderness. It appears that rickettsial vascular injury to abdominal viscera may be responsible for gastrointestinal symptoms [7]. Rickettsial vascular injury results from replication of rickettsiae in endothelial cells [8]; this process elicits vasculitis associated with a perivascular polymorphonuclear and mononuclear inflammatory response involving the CNS, gastrointestinal tract, pancreas, heart, lungs, and kidneys [9]. Infected endothelial cells have an increased capacity for binding platelets, which might explain the thrombocytopenia and associated disseminated intravascular coagulopathy seen in severe cases of the disease. Activation of the protein C pathway has recently been demonstrated during the acute phase of MSF [10]. Reduction in levels of protein C may explain the hypercoagulable state of patients with severe cases of severe MSF. In our case, rickettsial vasculitis probably led to the hypercoagulable state and to the patient's unusual presentation with mesenteric vein thrombosis. In this case, surgical specimens were not examined by fluorescent-labeled IgG and IgM conjugant to R. conorii. Nevertheless, the clinical picture, the typical rash, the positive serology, and the season of the year when this patient became sick (early summer, the time when spotted fever is common in Israel) were consistent with a diagnosis of MSF. The fact that this patient received 2 days oftherapy with tetracyclines and steadily worsened could be attributed to intestinal infarction that led to malabsorption of the antibiotic. Although autopsies have demonstrated rickettsial vascular lesions associated with vasculitis or thrombosis in the stomach, small and large intestine, and pancreas, it appears that ischemic necrosis of the gastrointestinal tract is an extremely rare event. This is the first report, to our knowledge, of occlusion of a mesenteric vein leading to small-bowel infarction as a complication of R. conorii infection.
Downloaded from http://cid.oxfordjournals.org/ at University of Bath Library & Learning Centre on July 17, 2015
SIR-Mediterranean spotted fever (MSF) is an endemic disease in Israel for which the reported annual incidence is about 10 per 100,000 population [I]. Most cases occur between late spring and early winter and are acquired in the Sharon Plain, Western Galilee, and in the vicinity of Beer Sheva and Ashdod. MSF is usually a moderately severe self-limited illness caused by Rickettsia conorii. Gastrointestinal manifestations are uncommon in mild cases of MSF but are more frequently associated with severe disease [2]. We describe a patient with abdominal pain due to mesenteric vein thrombosis, a complication of MSF that, to our knowledge, was previously unreported. A previously healthy 70-year-old man complained of the sudden onset of high fever (temperature to 39.5°C), chills, and severe headache. Findings of physical examination were unremarkable. Laboratory tests revealed neutropenia (leukocytes, 3,000jmm3 ) and thrombocytopenia (platelets, 80,000jmm3 ) . Therapy with tetracycline (500 mg four times daily) was begun. Two days later the patient was hospitalized because of severe abdominal pain and bloody diarrhea. Physical examination revealed an acutely ill man who was alert but agitated and who had a temperature of 37.8°C, a pulse of 11Ojmin, and a blood pressure of 130j90 mm Hg. The abdomen was diffusely tender to palpation without rebound tenderness. A localized maculopapular rash was noted in the left inguinal area. Results of laboratory tests were as follows: hemoglobin, 15 g/dL; white blood cell count, 1O,000jmm 3 (the differential included 55% polymorphonuclear leukocytes, 33% band forms, and 12% lymphocytes); platelet count, 80,000jmm3 ; erythrocyte sedimentation rate (Westergren method), 30 mmjh; and prothrombin time, 100% of control value. Levels of serum glucose, sodium, potassium, creatinine, aspartate aminotransferase, alanine aminotransferase, and amylase were within the normal range. The result of the Weil-Felix test, for which Proteusstrains OX-19 and OX-2 are used, was negative. Findings of a chest roentgenogram were normal. Ultrasonography of the abdomen demonstrated ascites as well as a suspected mass in the head of the pancreas. Computed tomography did not confirm the presence of an intraabdominal mass, although ascites was again noted. Paracentesis revealed bloody ascitic fluid, and the patient underwent exploratory laparotomy. The peritoneal cavity contained 1.5 L of bloody fluid. The small intestine was dilated and edematous, with many petechiae and small hemorrhages scattered on it. The pancreas was enlarged and edematous, but no mass was found. Because of mesenteric vein occlusion, 1.5 m of necrotic ileum was resected and an end-to-end anastomosis was performed. Biopsies of the pancreas and liver were performed.
CID 1992; 15 (December)
CID 1992; 15 (December)
Correspondence
Z. Landau, S. Feld, S. Kunichezky, M. Grinspan, and M. Gorbacz Departments of Internal Medicine 'B', Surgery 'A', and Pathology, and Pulmonary Intensive Care Unit, Kaplan Hospital,* Rehovot, Israel
References
* Affiliated with the Medical Schools of the Hebrew University and Hadassah, Jerusalem.
Use of Tetracycline for Treatment of Vibrio vulnificus Infections SIR-In their recent review of infections due to Vibrio vulnificus [I], Chuang et aI. recommend that "third-generation cephalosporins should be the drugs of choice for early antimicrobial therapy" on the basis ofin vitro susceptibility testing, despite the fact that four of the five patients in this series who received third-generation cephalosporins died. The usual recommended antimicrobial agent ofchoice for treatment of V. vulnificus infections is tetracycline [2-5]; the single patient described by Chuang et aI. who received a tetracycline derivative survived his infection. Bowdre et al. [6] reported that cefotaxime was ineffective in a murine model of V. vulnificus sepsis, despite good in vitro activity. In their experiments, 12 of 12 animals who received tetracycline (3 mg/kg every 12 hours) survived; in dramatic contrast, one of the 10 animals who received cefotaxime (20 mg/kg every 6 hours) survived. Anecdotal clinical evidence also suggests that tetracycline is superior to other antibiotics in the treatment of serious V. vulnificus infections [6, 7]. One possible reason for the superiority of tetracycline in the treatment of V. vulnificus infections is its ability to inhibit protein synthesis. V. vulnificus elaborates a number of extracellular enzymes that are believed to contribute to its virulence, including hemolysin, proteases, lipase, hyaluronidase, rnucinase, DNase, and sulfatase [8, 9]. The use ofan antibiotic that inhibits enzyme synthesis rather than a cell-waIl-damaging antibiotic that might even increase the release of toxic microbial proteins would conceivably be advantageous in this setting. Notably, antibiotics that inhibit microbial protein synthesis have also been observed to be superior to ,B-Iactam antibiotics in experimental
Correspondence: Dr. Ferric C. Fang, University Hospital Clinical Microbiology Laboratory, University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Denver, Colorado 80262. Clinical Infectious Diseases 1992;15:1071 © 1992 by The Universityof Chicago. All rights reserved. 1058-4838/92/1506-0043$02.00
3. Kaplowitz LG. Fischer JJ. Sparling PF. Rocky Mountain spotted fever: a clinical dilemma. Curr Clin Top Infect Dis 1981;2:89-108. 4. Middleton DB. Rocky Mountain spotted fever: gastrointestinal and laboratory manifestations. South Med J 1978;71 :629-31. 5. Devriendt J, Staroukine M. Abdominal involvement in rickettsial disease [letter]. Arch Intern Med 1986;146:1447. 6. Randall MB, Walker DH. Rocky Mountain spotted fever: gastrointestinal and pancreatic lesions and rickettsial infection. Arch Pathol Lab Med 1984;108:963-7. 7. Walker DH. Gear JHS. Correlation of the distribution of Rickettsia conorii microscopic lesions and clinical features in South African tick bite fever. Am J Trop Med Hyg 1985;34:361-71. 8. Silverman DJ. Bond SB. Infection of human vascular endothelial cells by Ricksettsia rickettsii. J Infect Dis 1984; 149:20 1-6. 9. Walker D. The pathology of fatal Mediterranean spotted fever. Am J Clin Pathol 1987;87:669-72. 10. Vincente V. Espama F. Tabereno D, et al. Evidence ofactivation ofthe protein C pathway during acute vascular damage induced by Mediterranean spotted fever. Blood 1991;78:416-22.
[11], two other infections caused by toxin-elaborating microorganisms. Although definitive studies of optimal antimicrobial therapy have not been performed, the existing experimental and clinical evidence supports the continued use of tetracycline as the agent of choice in the treatment of V. vulnificus infections.
Ferric C. Fang University Hospital Clinical Microbiology Laboratory, University of Colorado Health Sciences Center, Denver, Colorado
References I. Chuang Y-C, Yuan CoY, Liu C-Y, Lan C-K, Huang AH-M. Vibrio vulnificus infection in Taiwan: report of 28 cases and review of clinical manifestations and treatment. Clin Infect Dis 1992; 15:271-6. 2. CarpenterCCJ. Other pathogenic vibrios. In: Mandell GL, Douglas RG Jr. Bennett JE. eds. Principles and practice ofinfectious diseases. 3rd ed. New York: Churchill Livingstone. 1990: 1646-9. 3. Holmberg SO. Cholera and related illnesses caused by Vibrio species and Aeromonas. In: Gorbach SL. Bartlett JG, Blacklow NR, eds. Infectious diseases. Philadelphia: WB Saunders, 1992:605-12. 4. Hill MK, Sanders CV. Localized and systemic infection due to Vibrio species. Infect Dis C1in North Am 1987; I:687-707. 5. Koenig KL, Mueller J, Rose T. Vibrio vulnificus-hazard on the half shell. West J Med 1991;155:400-3. 6. Bowdre JH. Hull JH, Cocchetto OM. Antibiotic efficacy against Vibrio vulnificus in the mouse: superiority of tetracycline. J Pharmacol Exp Ther 1983;225: 595-8. 7. Klontz KC. Lieb S, Schreiber M, et al. Syndromes of Vibrio vulnificus infections-clinical and epidemiologic features in Florida cases, 198/-1987. Ann Intern Med 1988;109:318-23. 8. Kreger A. Lockwood D. Detection ofextracellular toxin(s) produced by Vibrio vu/nificus. Infect Immun 1981;33:583-90. 9. Holmberg SD. Vibrios. In: Gorbach SL. Bartlett JG. Blacklow NR, eds. Infectious diseases. Philadelphia: WB Saunders. 1992: 1493-6. 10. Stevens DL. Gibbons AE. Bergstrom R. Winn V. The Eagle effect revisited: efficacy ofclindamycin, erythromycin, and penicillin in the treatment of streptococcal myositis. J Infect Dis 1988; 158:23-8. II. Stevens DL, Maier KA, Laine BM, Mitten JE. Comparison of c1indamycin, rifampin, tetracycline, metronidazole, and penicillin for efficacy in prevention of experimental gas gangrene due to Clostridium perfringens. J Infect Dis 1987;155:220-8.
Downloaded from http://cid.oxfordjournals.org/ at University of Bath Library & Learning Centre on July 17, 2015
I. Shaked Y, Samra Y, Maeir MK, Rubinstein E. Murine typhus and spotted fever in Israel in the eighties: retrospective analysis. Infection 1988;16:283-9. 2. Devrient J. Staroukine M. Amson A, et al. Malignant Mediterranean spotted fever. Arch Intern Med 1985;145:1319-21.
1071
Correspondence
Thrombosis of the Mesenteric Vein as a Complication of Mediterranean Spotted Fever
Correspondence: Dr. Z. Landau. Department of Internal Medicine 'B'. Kaplan Hospital, 76100 Rehovot, Israel.
Clinical Infectious Diseases 1992;15:1070-1 © 1992 by The Universityof Chicago.All rightsreserved. 1058-4838/92/1506-0042$02.00
An enlarged lymph node from the mesenterium was also taken for pathological examination. The following day a "secondlook" operation revealed viable small intestine with petechiae and hemorrhage. On the third postoperative day, a maculopapular rash appeared on his hands and legs; this rash spread to the abdomen. Specific fluorescent antibodies (IgM and IgG) to R. coronii were not present on the day of the patient's admission; however, these antibodies were present on the 21st day after his admission at a dilution of I: 100, a finding that confirmed the diagnosis ofMSF. Antibiotic therapy with parenteral minocycline, ciprofloxacin, amikacin, and metronidazole was administered, but the patient died of septic shock. Pathological examination of the small intestine revealed dilated, edematous intestinal loops with areas of transmural hemorrhage. The mesenteric veins showed vasculitis and organizing thrombi. The pancreas and the liver showed vasculitic changes, and the lymph nodes showed only reactive changes. Gastrointestinal manifestations are less common in MSF than in Rocky Mountain spotted fever, in which up to two-thirds of patients may experience nausea, vomiting, diarrhea, or abdominal pain [3-6]. There have been reports of patients who have developed the rash typical of MSF and the serological findings diagnostic of MSF after undergoing laparotomy because of severe abdominal pain and tenderness. It appears that rickettsial vascular injury to abdominal viscera may be responsible for gastrointestinal symptoms [7]. Rickettsial vascular injury results from replication of rickettsiae in endothelial cells [8]; this process elicits vasculitis associated with a perivascular polymorphonuclear and mononuclear inflammatory response involving the CNS, gastrointestinal tract, pancreas, heart, lungs, and kidneys [9]. Infected endothelial cells have an increased capacity for binding platelets, which might explain the thrombocytopenia and associated disseminated intravascular coagulopathy seen in severe cases of the disease. Activation of the protein C pathway has recently been demonstrated during the acute phase of MSF [10]. Reduction in levels of protein C may explain the hypercoagulable state of patients with severe cases of severe MSF. In our case, rickettsial vasculitis probably led to the hypercoagulable state and to the patient's unusual presentation with mesenteric vein thrombosis. In this case, surgical specimens were not examined by fluorescent-labeled IgG and IgM conjugant to R. conorii. Nevertheless, the clinical picture, the typical rash, the positive serology, and the season of the year when this patient became sick (early summer, the time when spotted fever is common in Israel) were consistent with a diagnosis of MSF. The fact that this patient received 2 days oftherapy with tetracyclines and steadily worsened could be attributed to intestinal infarction that led to malabsorption of the antibiotic. Although autopsies have demonstrated rickettsial vascular lesions associated with vasculitis or thrombosis in the stomach, small and large intestine, and pancreas, it appears that ischemic necrosis of the gastrointestinal tract is an extremely rare event. This is the first report, to our knowledge, of occlusion of a mesenteric vein leading to small-bowel infarction as a complication of R. conorii infection.
Downloaded from http://cid.oxfordjournals.org/ at University of Bath Library & Learning Centre on July 17, 2015
SIR-Mediterranean spotted fever (MSF) is an endemic disease in Israel for which the reported annual incidence is about 10 per 100,000 population [I]. Most cases occur between late spring and early winter and are acquired in the Sharon Plain, Western Galilee, and in the vicinity of Beer Sheva and Ashdod. MSF is usually a moderately severe self-limited illness caused by Rickettsia conorii. Gastrointestinal manifestations are uncommon in mild cases of MSF but are more frequently associated with severe disease [2]. We describe a patient with abdominal pain due to mesenteric vein thrombosis, a complication of MSF that, to our knowledge, was previously unreported. A previously healthy 70-year-old man complained of the sudden onset of high fever (temperature to 39.5°C), chills, and severe headache. Findings of physical examination were unremarkable. Laboratory tests revealed neutropenia (leukocytes, 3,000jmm3 ) and thrombocytopenia (platelets, 80,000jmm3 ) . Therapy with tetracycline (500 mg four times daily) was begun. Two days later the patient was hospitalized because of severe abdominal pain and bloody diarrhea. Physical examination revealed an acutely ill man who was alert but agitated and who had a temperature of 37.8°C, a pulse of 11Ojmin, and a blood pressure of 130j90 mm Hg. The abdomen was diffusely tender to palpation without rebound tenderness. A localized maculopapular rash was noted in the left inguinal area. Results of laboratory tests were as follows: hemoglobin, 15 g/dL; white blood cell count, 1O,000jmm 3 (the differential included 55% polymorphonuclear leukocytes, 33% band forms, and 12% lymphocytes); platelet count, 80,000jmm3 ; erythrocyte sedimentation rate (Westergren method), 30 mmjh; and prothrombin time, 100% of control value. Levels of serum glucose, sodium, potassium, creatinine, aspartate aminotransferase, alanine aminotransferase, and amylase were within the normal range. The result of the Weil-Felix test, for which Proteusstrains OX-19 and OX-2 are used, was negative. Findings of a chest roentgenogram were normal. Ultrasonography of the abdomen demonstrated ascites as well as a suspected mass in the head of the pancreas. Computed tomography did not confirm the presence of an intraabdominal mass, although ascites was again noted. Paracentesis revealed bloody ascitic fluid, and the patient underwent exploratory laparotomy. The peritoneal cavity contained 1.5 L of bloody fluid. The small intestine was dilated and edematous, with many petechiae and small hemorrhages scattered on it. The pancreas was enlarged and edematous, but no mass was found. Because of mesenteric vein occlusion, 1.5 m of necrotic ileum was resected and an end-to-end anastomosis was performed. Biopsies of the pancreas and liver were performed.
CID 1992; 15 (December)
CID 1992; 15 (December)
Correspondence
Z. Landau, S. Feld, S. Kunichezky, M. Grinspan, and M. Gorbacz Departments of Internal Medicine 'B', Surgery 'A', and Pathology, and Pulmonary Intensive Care Unit, Kaplan Hospital,* Rehovot, Israel
References
* Affiliated with the Medical Schools of the Hebrew University and Hadassah, Jerusalem.
Use of Tetracycline for Treatment of Vibrio vulnificus Infections SIR-In their recent review of infections due to Vibrio vulnificus [I], Chuang et aI. recommend that "third-generation cephalosporins should be the drugs of choice for early antimicrobial therapy" on the basis ofin vitro susceptibility testing, despite the fact that four of the five patients in this series who received third-generation cephalosporins died. The usual recommended antimicrobial agent ofchoice for treatment of V. vulnificus infections is tetracycline [2-5]; the single patient described by Chuang et aI. who received a tetracycline derivative survived his infection. Bowdre et al. [6] reported that cefotaxime was ineffective in a murine model of V. vulnificus sepsis, despite good in vitro activity. In their experiments, 12 of 12 animals who received tetracycline (3 mg/kg every 12 hours) survived; in dramatic contrast, one of the 10 animals who received cefotaxime (20 mg/kg every 6 hours) survived. Anecdotal clinical evidence also suggests that tetracycline is superior to other antibiotics in the treatment of serious V. vulnificus infections [6, 7]. One possible reason for the superiority of tetracycline in the treatment of V. vulnificus infections is its ability to inhibit protein synthesis. V. vulnificus elaborates a number of extracellular enzymes that are believed to contribute to its virulence, including hemolysin, proteases, lipase, hyaluronidase, rnucinase, DNase, and sulfatase [8, 9]. The use ofan antibiotic that inhibits enzyme synthesis rather than a cell-waIl-damaging antibiotic that might even increase the release of toxic microbial proteins would conceivably be advantageous in this setting. Notably, antibiotics that inhibit microbial protein synthesis have also been observed to be superior to ,B-Iactam antibiotics in experimental
Correspondence: Dr. Ferric C. Fang, University Hospital Clinical Microbiology Laboratory, University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Denver, Colorado 80262. Clinical Infectious Diseases 1992;15:1071 © 1992 by The Universityof Chicago. All rights reserved. 1058-4838/92/1506-0043$02.00
3. Kaplowitz LG. Fischer JJ. Sparling PF. Rocky Mountain spotted fever: a clinical dilemma. Curr Clin Top Infect Dis 1981;2:89-108. 4. Middleton DB. Rocky Mountain spotted fever: gastrointestinal and laboratory manifestations. South Med J 1978;71 :629-31. 5. Devriendt J, Staroukine M. Abdominal involvement in rickettsial disease [letter]. Arch Intern Med 1986;146:1447. 6. Randall MB, Walker DH. Rocky Mountain spotted fever: gastrointestinal and pancreatic lesions and rickettsial infection. Arch Pathol Lab Med 1984;108:963-7. 7. Walker DH. Gear JHS. Correlation of the distribution of Rickettsia conorii microscopic lesions and clinical features in South African tick bite fever. Am J Trop Med Hyg 1985;34:361-71. 8. Silverman DJ. Bond SB. Infection of human vascular endothelial cells by Ricksettsia rickettsii. J Infect Dis 1984; 149:20 1-6. 9. Walker D. The pathology of fatal Mediterranean spotted fever. Am J Clin Pathol 1987;87:669-72. 10. Vincente V. Espama F. Tabereno D, et al. Evidence ofactivation ofthe protein C pathway during acute vascular damage induced by Mediterranean spotted fever. Blood 1991;78:416-22.
[11], two other infections caused by toxin-elaborating microorganisms. Although definitive studies of optimal antimicrobial therapy have not been performed, the existing experimental and clinical evidence supports the continued use of tetracycline as the agent of choice in the treatment of V. vulnificus infections.
Ferric C. Fang University Hospital Clinical Microbiology Laboratory, University of Colorado Health Sciences Center, Denver, Colorado
References I. Chuang Y-C, Yuan CoY, Liu C-Y, Lan C-K, Huang AH-M. Vibrio vulnificus infection in Taiwan: report of 28 cases and review of clinical manifestations and treatment. Clin Infect Dis 1992; 15:271-6. 2. CarpenterCCJ. Other pathogenic vibrios. In: Mandell GL, Douglas RG Jr. Bennett JE. eds. Principles and practice ofinfectious diseases. 3rd ed. New York: Churchill Livingstone. 1990: 1646-9. 3. Holmberg SO. Cholera and related illnesses caused by Vibrio species and Aeromonas. In: Gorbach SL. Bartlett JG, Blacklow NR, eds. Infectious diseases. Philadelphia: WB Saunders, 1992:605-12. 4. Hill MK, Sanders CV. Localized and systemic infection due to Vibrio species. Infect Dis C1in North Am 1987; I:687-707. 5. Koenig KL, Mueller J, Rose T. Vibrio vulnificus-hazard on the half shell. West J Med 1991;155:400-3. 6. Bowdre JH. Hull JH, Cocchetto OM. Antibiotic efficacy against Vibrio vulnificus in the mouse: superiority of tetracycline. J Pharmacol Exp Ther 1983;225: 595-8. 7. Klontz KC. Lieb S, Schreiber M, et al. Syndromes of Vibrio vulnificus infections-clinical and epidemiologic features in Florida cases, 198/-1987. Ann Intern Med 1988;109:318-23. 8. Kreger A. Lockwood D. Detection ofextracellular toxin(s) produced by Vibrio vu/nificus. Infect Immun 1981;33:583-90. 9. Holmberg SD. Vibrios. In: Gorbach SL. Bartlett JG. Blacklow NR, eds. Infectious diseases. Philadelphia: WB Saunders. 1992: 1493-6. 10. Stevens DL. Gibbons AE. Bergstrom R. Winn V. The Eagle effect revisited: efficacy ofclindamycin, erythromycin, and penicillin in the treatment of streptococcal myositis. J Infect Dis 1988; 158:23-8. II. Stevens DL, Maier KA, Laine BM, Mitten JE. Comparison of c1indamycin, rifampin, tetracycline, metronidazole, and penicillin for efficacy in prevention of experimental gas gangrene due to Clostridium perfringens. J Infect Dis 1987;155:220-8.
Downloaded from http://cid.oxfordjournals.org/ at University of Bath Library & Learning Centre on July 17, 2015
I. Shaked Y, Samra Y, Maeir MK, Rubinstein E. Murine typhus and spotted fever in Israel in the eighties: retrospective analysis. Infection 1988;16:283-9. 2. Devrient J. Staroukine M. Amson A, et al. Malignant Mediterranean spotted fever. Arch Intern Med 1985;145:1319-21.
1071
