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• W2609357002 abstract "Case ReportsA Case of Pancytopenia in Acute Brucellosis: With Review of Hematological Abnormalities Mansour M. Al-NozhaFRCP(Lond), MRCPI, DTM&H Mansour M. Al-Nozha Assistant Professor, Department of Medicine, College of Medicine, King Saud University, P.O. Box 2925, Riyadh 11461, Saudi Arabia Search for more papers by this author Published Online:1 Apr 1987https://doi.org/10.5144/0256-4947.1987.149SectionsPDF ToolsAdd to favoritesDownload citationTrack citations ShareShare onFacebookTwitterLinked InRedditEmail AboutINTRODUCTIONBrucellosis is an infectious disease transmitted to humans from animals or animal products containing bacteria of the genus Brucella. A wide spectrum of clinical manifestations resulting from involvement of virtually all the major organ systems in the body have been reported. Several types of hematologic abnormalities have been reported in brucellosis. These include anemia, leucocytosis, leucopenia and splenomegaly. Pancytopenia also has been documented as a hematologic complication in brucellosis but is relatively uncommon, with only six cases reported in the literature.1,2,3 In our hospital over 200 cases of Brucella infection were seen during the last 2 years, but only one case had pancytopenia. This communication describes that patient and reviews the literature.CASE REPORTA 42-year-old Saudi male farmer presented with one month's history of fever which was continuous and became worse in the afternoon. Fever was associated with sweating and occasional rigors. In addition to the fever, he had general symptoms of anorexia, loss of weight, headache and backache, as well as nausea and vomiting.The patient admitted to drinking raw camel's milk three to four weeks before he developed this illness. He had not had raw milk from other sources or contact with other animals.On examination he was febrile with a temperature of 38°C. He looked ill and was sweating profusely. Lymph nodes were not palpable, but liver was palpable 3 cm below the costal margin, and the spleen was just palpable. There was mild tenderness over the lower back. The rest of the examination was unremarkable.He was admitted to the hospital with a provisional diagnosis of brucellosis. His blood count on admission was as follows: hemoglobin 11.2 gm/dl [normal range (NR) 14.0-18.0 gm/dl]; white blood cell (WBC) count 2,500/mm3 (NR 4,000-10,000/mm3) with a differential count of 51% polymorphs, 45% lymphocytes, and 4% monocytes. Blood smear showed atypical lymphocytes. Platelet count was 97,000/mm3 (NR 250,000-400,000/mm3). Urine examination showed traces of protein and ketones. Liver function tests were as follows: bilirubin 1.41 mg/dl (NR 0.2-1.0 mg/dl), alkaline phosphatase (AP) 216 u/L (NR 43-154 u/L), aspartate aminotransferase (AST) 123 u/L (NR 7-40 u/L). HBsAg was negative. Liver ultrasound was normal. Widal test for Brucella revealed Brucella abortus 1:10,240, and Brucella melitensis 1:5,120. Widal test for typhoid was negative. Tests for lupus erythematosus cell and antinuclear factor were negative.Examination of bone marrow revealed active hemopoiesis of all cell lines. Erythropoiesis was normoblastic; granulopoiesis was well represented but shifted left; megakaryocytes were present in adequate numbers and were of normal morphology. There was no hemophagocytosis and no abnormal infiltrate.Cotrimoxazole was given on the sixth hospital day after the results of serology was available. Five days later a blood culture indicated that the organism isolated was B. melitensis, which was reported as resistant to cotrimoxazole. Therefore, therapy was changed to a combination of streptomycin (1 gm intramuscularly daily) and tetracycline (500 mg every six hours).The patient started to improve clinically and became afebrile on the third day of combination therapy and his full count started to rise (Table 1). On the tenth day of therapy he was discharged home in good health. As an outpatient he continued to have streptomycin and tetracycline for three weeks, and then tetracycline 500 mg every six hours for another three weeks. His liver function tests were normal on discharge. Blood count reversed to normal after five weeks of combination therapy (Table 1).Table 1. Changes in blood test values during and after hospital stay.DISCUSSIONThe total white blood cell count is usually normal in human brucellosis.4 However, abnormal WBC count in the form of leucopenia or leucocytosis is well known to occur in brucellosis. In one study,4 leucopenia was seen in 17% while leucocytosis occurred in 9% and the WBC count was normal in 74%. Schirger, et al,5 reported similar figures (Table 2).Table 2. WBC in cases of brucellosis.Pancytopenia is an infrequent complication in brucellosis.1,2,3 To the best of my knowledge, a total of six cases have been reported in literature. Lynch, et al,1 in 1968 reported the first case of severe pancytopenia and splenomegaly in a young woman with brucellosis. Culture grew B. abortus The hematological abnormalities and splenomegaly disappeared after treatment with tetracycline and streptomycin. He conduced that hypersplenism was the most likely cause of the pancytopenia. Zuazu, et al,2 reported a case of acute brucellosis in which the clinical picture and bone marrow finding mimicked malignant histiocytosis. Blood culture grew B. melitensis and bone marrow showed increased number of histiocytes with erythrophagocytosis. More recently Martin-Moren, et al,3 reported four cases of brucellosis with pancytopenia they attributed the pancytopenia to hemophagocytosis in the bone marrow and not due to hypersplenism.In an unpublished study from Peru consisting of 38 patients with B. melitensis, Crosby found a variety of hematologic abnormalities including anemia (74%), leucopenia (45%) and thrombocytopenia (39%).6 Pancytopenia was present in 8 (21%) of the cases, and 7 of these patients had splenomegaly. This would imply that pancytopenia is perhaps more common than the paucity of reported cases seems to indicate.From the above mentioned data, it is apparent that pancytopenia in patients with brucellosis is probably caused by two mechanisms, namely, hypersplenism and hemophagocytosis by the histiocytes of the reticuloendothelial system. In our case, examination of bone marrow revealed no evidence of hemophagocytosis. Furthermore, the presence of active hemopoiesis with a left shift strongly indicated the possibility of peripheral destruction as the case of pancytopenia. Thus, the possibility of hypersplenism in our case appears quite likely.Although the patient's serum showed a high titer against B. abortus antigen, his blood culture grew B. melitensis. This is not surprising as sometimes it is difficult to differentiate between B. abortus and B. melitensis infection by serological tests only.It seems that our patient acquired the infection through ingestion of camel's milk. No attempt was made to examine the milk for the organisms because of practical difficulties. Brucellosis in camels has been studied by Okoh,7 Waghela, al,8 Kulshrestha, et al,9 and Mathur and Bahargava.10 B. abortus has been isolated from aborted fetuses, genital discharge, and milk and urine of camels.11 In some parts of Saudi Arabia where drinking raw camel's milk is traditional, the health hazard of transmission of brucellosis to man could be great. Radwan, et al,12 have shown for the first time, by examining serum samples of 143 camels, that local camels in Saudi Arabia are infected (2.8%). Kambal, et al,13 reported that one of thirty patients they studied gave a history of drinking raw camel's milk. There is a great need for more studies to look into the prevalence of brucellosis in camels in Saudi Arabia. Once such a study is available, a plan to control the disease in camels could be implemented.ARTICLE REFERENCES:1. Lynch EC, McKechnie JC, Alfrey CP. Brucellosis with pancytopenia . Ann Intern Med. 1968; 19:319–22. Google Scholar2. Zuazu JP, Duran JW, Julia AF. Hemophagocytosis in acute brucellosis [letter] . N Engl J Med. 1979; 301(21):1185–6. Google Scholar3. Martin-More no S, Soto-Guzman O, Bernaldo-de-Quiros J, et al.. Pancytopenia due to hemophagocytosis in patients with brucellosis: a report of four cases . J Infect Dis. 1983; 147(3):445–9. Google Scholar4. Pfiscner WC, Ishak KG, Neptune EM, et al.. Brucellosis in Egypt. A review of experience with 228 patients . AMJ Med. 1957; 915–29. Google Scholar5. Schirger A, Nichols DR, Martin WJ, et al.. Brucellosis: experiences with 224 patients . Ann Intern Med. 1960; 52:827–37. Google Scholar6. Young EJ. Human brucellosis . Rev Infect Dis. 1985; 5(5):821–42. Google Scholar7. Okoh AE. A survey of brucellosis in camels in Kano, Nigeria . Trop Anim Hlth Prod. 1979; ll(4):213–4. Google Scholar8. Waghela S, Fazil MA, Gathuma JM, Kagunya DK. A serological survey of brucellosis in camels in Northeastern Province of Kenya . Trop Anim Hlth Prod. 1978; 10(l):28–9. Google Scholar9. Kulshrestha RC, Arora RG, Kalra DS. Brucellosis in camels and horses . Indian J Anim Sci. 1975; 45(9):673–5. Google Scholar10. Mathur KN, Bhargava SC. Seroprevalence of Q fever and brucellosis in camels of Jorbeer and Bikaner, Rajasthan State . Indian J Med Res. 1979; 70:391–3. Google Scholar11. World Health Organization. Brucellosis in camels. WHO technical report series, 1971:464–6. Google Scholar12. Radwan Al, Asmar JA, Frerichs WM, et al.. Incidence of brucellosis in domestic livestock in Saudi Arabia . Trop Anim Hlth Prod. 1983; 15(3): 139–43. Google Scholar13. Kambal AM, Mahgoub ES, Jamjoom GA, Chowdhury MN. Brucellosis in Riyadh, Saudi Arabia . A microbiological and clinical study. Trans R Soc Trop Med Hyg. 1983; 77(6):820–4. Google Scholar Previous article Next article FiguresReferencesRelatedDetails Volume 7, Issue 2April 1987 Metrics History Accepted8 July 1986Published online1 April 1987 ACKNOWLEDGEMENTI wish to thank Mr. Ehsan Chaudhry for typing the manuscript.InformationCopyright © 1987, Annals of Saudi MedicinePDF download" @default.
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