حمى الوادي المتصدع "Rift Valley Fever" كيف ينتشر الفيروس وكيف تتم الوقاية؟

Quote: يتسبب المرض بموت 1% تقريبا من المصابين . تكون نسبة الموت كبيرة جدا بين الحيوانات المصابة. ويلاحظ أن 100% من المواشي الحبلى المصابة تجهض أجنتها

(عدل بواسطة Frankly on 11-29-2007, 10:25 AM)

Quote: أرجو أن تتحرى ذلك وتفدنا به

Quote: العزيز فرانكلي لك الود كتبت Quote: أرجو أن تتحرى ذلك وتفدنا به في الحقيقة انا اكتب لك من موقع خبرة والمام واطلاع وتخصص ولكن لا باس الرابط ادناه يحوي معلومات عن كل انواع الحمي النزفية ويوضح معلومات كثيرة بما فيها ال mortality rate اي نسبة الوفيات المتوقعة من اي نوع وهو خلاصة دراسات كثيرة (المراجع ايضا موضحة) في الحمي النزفية من موقع emedecine وهو من المواقع الجيدة للبرفيشنالس http://www.emedicine.com/ped/TOPIC2406.HTM وهذه الفقرة تتحدث عن نسبة الوفاة في كل نوع وهي 50 % في حمي الوادي المتصدع RVF Quote: Mortality/Morbidity Ebola and Marburg are considered the most severe VHFs, with 25-100% mortality rates. The infection rate is high, particularly for the Zaire subtype of Ebola virus. During pregnancy, Ebola infection has been universally fatal. The South American HF has a case-infection ratio of more than 50% of those exposed. The mortality rate is 15-30%. Lassa fever is a milder infection, with a fatality rate of 2-15%, and is probably much more common than is recognized. Approximately 1% of individuals exposed to RVF virus become infected, but the mortality rate of persons infected is 50%. CCHF has an infection rate of 20-100% and a fatality rate of 15-30%. لاحظ للجملة التي تتحدث عن حمي الوادي المتصدع Quote: Approximately 1% of individuals exposed to RVF virus become infected, but the mortality rate of persons infected is 50% . وترجمة الفقرة الاخيرة كالاتي (تقريبا واحد في المائة من الذين يتعرضون لفيروس حمي الوادي المتصدع يصابون بالمرض, الا ان نسبة الوفاة في الاشخاص المصابين هي 50 %) ولك خالص الود

Quote: شكراً فرانكلي على المعلومات الجيدة عن هذا الوباء اللعين. آمل أن تتعامل حكومة الخرطوم بجدية مع المرض وألا تدفن رأسها في الرمال كالعادة وتخفي الحقائق وتصدر بيانات النفي والتطمين. ونسأل الله أن يرفع البلاء عن أهلنا في كل مكان الشايقي

Quote: يتسبب المرض بموت 1% تقريبا من المصابين

Quote: Quote: يتسبب المرض بموت 1% تقريبا من المصابين هذه المقولة صحيحة حسب التقارير الواردة من مركز مكافحة المراض بالولايات المتحدة Center of Diseases Control Quote: Is the disease ever fatal? Approximately 1% of humans that become infected with RVF die of the disease. Case-fatality proportions are significantly higher for infected animals. The most severe impact is observed in pregnant livestock infected with RVF, which results in abortion of virtually 100% of fetuses. WWW.CDC.GOV وأعتقد انو دى فرصة مناسبة للأطباء فى السودان(ومنهم شخصى الضعيف) لعمل أبحاث تتعلق بالمرض مستندين بالاحصائيات الدقيقةوووووووو.........

Quote: يتسبب المرض بموت 1% تقريبا من المصابين هذه المقولة صحيحة حسب التقارير الواردة من مركز مكافحة المراض بالولايات المتحدة Center of Diseases Control Quote: Is the disease ever fatal? Approximately 1% of humans that become infected with RVF die of the disease. Case-fatality proportions are significantly higher for infected animals. The most severe impact is observed in pregnant livestock infected with RVF, which results in abortion of virtually 100% of fetuses. WWW.CDC.GOV

(عدل بواسطة Frankly on 12-01-2007, 07:34 PM)

Quote: فقط اتحفظ على كلماتك بأنّه يقتل 50% من المصابين لأني بصراحة أراه غير صحيح ومبالغ فيه جداً .

Quote: اتحفظ.... واميل... واتمني وما الي ذلك

Quote: وكما قلت لك أميل للمعلومة التي تقول أنّه يقتل 1% من المصابين كما ذكر في المقال أعلاه وكما ذكر الأخ أم بدة في مداخلته وقد ترتفع هذه النسبة إلى حد كبير عند المصابين بالمراحل النزفية منه وهم ال 1% من جميع المصابين دعنا نتخطّى هذه النقطة ونردف البوست بمعلومات تقلل من الإصابة بهذا المرض خاصّة مع قدوم العيد الكبير عيد الأضحى بعد أكثر من أسبوعبن إثنين تحياتي كمال

Quote: عموما كنت ايضا اود ان اصحح معلومات هي حقائق علمية وقد رجعت الي ال CDC ولم اجد اي مراجع للمعلومة التي وردت بشان ال 1 %

Quote: The largest reported human outbreak occurred in Kenya during 1997--1998, in which an estimated 89,000 persons (based on a systematic serosurvey) were infected and 478 died;

Quote: علي عجب تحية واحترام وشكراً على مرورك تابع معنا فرانكلي جداً

Quote: أخيرا عزيزى الوالى فقط من ناحية أمانة علمية أرجو أن تأتى وتعترف بخطأ المعلومة التى أوردتها ولا داعى للمكابرة

Quote: ويصل معدل الإماتة في الحالات بين المرضى المصابين بالشكل النـزفي للمرض إلى حوالي 50%. وتحدث الوفاة عادةً بعد ثلاثة أيام إلى ستة أيام من بداية ظهور الأعراض. ويمكن اكتشاف الفيروس في الدم لمدة تصل إلى 10 أيام في حالة المرضى المصابين بالشكل اليرقاني النـزفي لحمى الوادي المتصدِّع

(عدل بواسطة Frankly on 12-04-2007, 02:57 PM)

Quote: انا هنا انتقد ال CDC ولا انتقدك انت لانك ناقل للمعلومة

Quote: كنت اتمنى لو انك اعتمدت في مصادرك على الدراسات المنشورة في الدوريات العلمية المحكمة اما موقع emedecine فهو مصدر لا يليق بمن هو في مثل قامتك تشير الدراسات التي اجريت في الدول القريبة من السودان مثل اليمن و المملكة العربية السعودية في الفترة من اغسطس 2000 الى سبتمبر 2001 الى أن نسبة الوفيات هي 11,1% و 13,9% بالترتيب.

Quote: Clinical Infectious Diseases 2003;36:245–252 © 2003 by the Infectious Diseases Society of America. All rights reserved. 1058-4838/2003/3603-0001$15.00 DOI: 10.1086/345671 MAJOR ARTICLE Epidemic Rift Valley Fever in Saudi Arabia: A Clinical Study of Severe Illness in Humans Mohammed Al-Hazmi,1 Ephraim Ayobanji Ayoola,1 Mahmoud Abdurahman,1 Subodh Banzal,1 Jammal Ashraf,1 Adil El-Bushra,1 Ali Hazmi,2 Mohammed Abdullah,1 Hamid Abbo,1 Abdulhadi Elamin,1 El-Tayeb Al-Sammani,1 Mohammed Gadour,1 Chandra Menon,1 Mirghani Hamza,1 Inam Rahim,1 Magdy Hafez,1 Manish Jambavalikar,1 Haider Arishi,3 and Ali Aqeel3 Departments of 1Medicine, 2Ophthalmology, and 3Pediatrics, King Fahd Central Hospital, Gizan, Saudi Arabia Received 26 June 2002; accepted 8 October 2002; electronically published 17 January 2003. Reprints or correspondence: Prof. E. A. Ayoola, PO Box 235 Abu-Arish, Gizan Province, Saudi Arabia ([email protected] or [email protected]). We describe the clinical patterns and case-fatality rate associated with severe Rift Valley fever (RVF) in patients who were admitted to the Gizan regional referral hospital during an outbreak of RVF in Saudi Arabia from September through November 2000. A total of 165 consecutive patients (136 men and 29 women) were prospectively studied; all were identified according to a strict case definition, were confirmed to have RVF by serologic testing, and were treated according to a predetermined protocol. The major clinical characteristics of RVF included a high frequency of hepatocellular failure in 124 patients (75.2%), acute renal failure in 68 patients (41.2%), and hemorrhagic manifestations in 32 patients (19.4%). Sixteen patients had retinitis and 7 patients had meningoencephalitis as late complications in the course of the disease. A total of 56 patients (33.9%) died. Hepatorenal failure, shock, and severe anemia were major factors associated with patient death. The Rift Valley fever (RVF) virus of the family Bunyaviridae is a cause of zoonotic viral disease that predominantly causes abortion and death among domestic ruminants; it is characterized by necrotic hepatitis with or without a hemorrhagic state [1, 2]. Infection in humans is acquired through mosquito bites or through contact with tissues of infected animals, and it is usually associated with uncomplicated acute febrile illness. However, severe complications, such as hemorrhagic disease, meningoencephalitis, and retinitis, occur in a minority of clinical cases [1]. Since the 1930s, when the first isolation of the virus occurred and the first detailed description of the disease in animals in the Rift Valley of Kenya was reported, there have been several epizootics in South Africa (1975), West Africa (1987), Madagascar (1990), Egypt (1977 and 1993), and, most recently, in Kenya (1977–1998) [1–4]. Serologic evidence that the virus existed throughout sub-Saharan Africa and Madagascar led to the prediction that the infection might subsequently extend beyond continental Africa and spread to the Middle Eastern countries [5]. In September 2000, an outbreak that caused unexplained hemorrhagic fever in humans and that was associated with deaths and abortions among animals in the far western Saudi-Yemen border region was subsequently confirmed to be an outbreak of RVF; this outbreak represented the first cases of RVF reported on the Arabian Peninsula [4]. In subsequent months, 516 clinical cases of RVF were identified in Saudi Arabia [6]. We report the results of a prospective study designed to determine the clinical pattern of RVF, the frequency of its complications, and the associated case-fatality rates among patients in Saudi Arabia. Patients and Methods Gizan province is a relatively small area of the southwestern part of Saudi Arabia adjacent to the Yemen border. It consists of a coastal plain with a mountainous hinterland rising >300 m above sea level. The province is relatively dense in population and is noted for its extensive agriculture and traditional irrigation practices. King Fahd Central Hospital, located in Gizan, is a well-equipped 500-bed referral center for the 14 general hospitals and many primary health care centers that serve the estimated 1 million inhabitants of the Gizan province. Patients. Patients with RVF were identified through an elaborate preexisting system of primary health care centers that refer acutely ill persons to general hospitals for assessment of hepatitis and other criteria for admission as RVF case patients (table 1) [4]. Of the 516 case patients in Saudi Arabia who were described during the epidemic, the largest number of case patients () was reported from the southwestern province of Gizan, and 122 case patients from the contiguous Asir region were described [6]. From the general hospitals in the Gizan region, critically ill patients were referred to the regional hospital, King Fahd Central Hospital in Gizan, for specialized care. Table 1. Case definition of Rift Valley fever. The subjects of the study were 165 consecutively seen patients who were treated from September through November 2000. At the time of admission to the hospital, a questionnaire was completed that detailed, for each patient, history of possible exposure to sick animals, travel out of the region or country, duration of symptoms, and medical history. A comprehensive examination that included indirect ophthalmoscopy was performed by one of the investigators (A.H.). Laboratory evaluation. The following laboratory values were assessed at the time of admission and then daily or more frequently as needed: complete blood count; prothrombin time; partial thromboplastin time; and levels of serum electrolytes, urea, creatinine, calcium, phosphate, blood sugar, liver enzymes (i.e., bilirubin, alkaline phosphate, alanine aminotransferase [ALT], and aspartate aminotransferase [AST]), total serum protein and albumin, creatine phosphokinase, lactic dehydrogenase, amylase, and lipase. Other tests, which were performed where indicated, included analysis of arterial blood gases, peripheral blood smears for the detection of malaria parasites, and examination of stool and urine samples for blood and pathogens. Chest radiography, abdominal ultrasound, abdominal CT, MRI of the CNS, and echocardiography were performed as indicated. Virologic and serologic tests. Serum samples obtained from all patients were tested for RVF antigen (RVFAg) and for IgM and IgG antibody to RVF virus (IgM-RVFAb and IgG-RVFAb). During the initial stage of the epidemic, the first few patients were tested by PCR for RVF RNA and virologic typing, as reported elsewhere [4, 6]. Markers of viral hepatitis A–C comprising IgM antibody to hepatitis A virus (IgM anti-HAV), hepatitis B surface antigen (HBsAg), IgM antibody to hepatitis B core antigen (IgM anti-HBc), and antibody to hepatitis C virus (anti-HCV) were tested by ELISA with commercial kits. Treatment. All patients were treated in the special RVF unit, where strict barrier and isolation nursing care were provided and where intravenous transfusion of fresh frozen plasma, blood, and albumin was performed as necessary. None of the patients was treated with ribavirin or any other antiviral agent. Bacterial superinfection was treated with antibiotics as necessary. Patients who had severe acute renal failure underwent hemodialysis as indicated. Other intensive care and supportive measures, such as mechanical ventilation, were provided as indicated. Statistical analysis. Descriptive statistics were used to summarize the demographic data at baseline. Continuous variables were presented as mean ± SD. Discrete or categorical variables were expressed as percentages. Comparison of data in proportions was performed using analysis, Fisher's exact test, or analysis of variance. Groups of continuous data were compared using Student's t test for parametric data and nonparametric data. was statistically significant. Results Demographic characteristics of the patients. A total of 165 patients (136 men and 29 women) were treated during the study period and comprised 127 Saudis, 35 Yemenis, and 3 non-Saudis aged 15–95 years (mean age, 47.5 years; median age, 50 years) (table 2). A total of 99 patients (60%) reported having had direct contact either with infected and sick relatives or with sick, aborted, or dead animals. A total of 52 patients (31.5%) had slept in the open air most of the time, and 132 (80%) had frequently sustained mosquito bites. Only 15 patients (9.1%) had traveled out of the country during the 6 months before admission to the hospital; 21 patients (12.7%) had ingested raw milk frequently. Table 2. Demographic characteristics of and clinical outcome for 165 patients in Saudi Arabia with Rift Valley fever. Clinical features of RVF. The mean duration (±SD) from the onset of symptoms to hospitalization was days (range, 1–15 days; median, 4 days). There was little variation in the clinical findings for the patients. Major symptoms and signs of RVF are summarized in table 3. Nausea or vomiting (in 151 patients) and fever (in 122 patients) were the most common symptoms. A total of 31 of 122 patients with fever experienced associated chills or rigors. Abdominal pain was poorly localized. In addition to significant anemia (in 55 patients), the major physical signs were hepatomegaly (in 21 patients) and splenomegaly (in 20 patients). Other features at presentation included altered sensorium (confusion, drowsiness, and coma) in 29 patients and shock in 21 patients. Table 3. Major clinical features of moderate to severe Rift Valley fever in 165 patients in Saudi Arabia. Laboratory investigations. The most prominent abnormal findings of the laboratory investigations were marked elevations of serum levels of ALT (range, 17–16,662 IU/L) and AST (range, 12–40,560 IU/L). Elevation of the lactic dehydrogenase level was found in 71 (44%) of 163 patients, and elevation of the creatine phosphokinase level was found in 50 (32.3%) of 155 patients. Thrombocytopenia and anemia occurred frequently (table 4). Table 4. Laboratory findings for patients in Saudi Arabia with severe Rift Valley fever. Hepatitis and hepatic failure. Abnormal levels of serum AST or ALT indicative of liver damage were present in 152 (95%) of 160 patients. A total of 142 patients (88.8%) had an AST level that was >3 times the upper limit of the range of AST levels considered to be normal (median AST level, 984.5 IU/L; mean AST level, 2088 IU/L) (table 5). Hepatic failure was diagnosed in 124 (75.2%) of 165 patients and was associated with hepatic encephalopathy in 74 patients, a finding that indicated a fulminant course. In 18 patients (16 males and 2 females), ALT and AST levels were less than the cutoff values, and, in 10 of them, such levels were within the range considered to be normal. Comparison of this subgroup with the subgroup that had high aminotransferase levels () did not show any difference with regard to the frequencies of the presenting clinical features, such as fever (13 vs. 108), myalgia (11 vs. 55), diarrhea (12 vs. 59), or oliguria (4 vs. 31), and the occurrence of major nonhepatic complications. These complications included renal failure (in 6 patients), retinitis (in 1 patient), meningoencephalitis (in 1 patient), and both retinitis and meningoencephalitis (in 1 patient). Two of the 18 patients demonstrated hemorrhagic manifestations. One of them had concomitant renal failure, shock, and disseminated intravascular coagulopathy and was 1 of the 2 patients in this subgroup who died. The other was a 30-year-old patient who presented with vaginal bleeding. RVFAg and IgM antibody were detected in 4 and 14 patients, respectively. Among the patients with high aminotransferase levels, RVFAg and IgM antibody were detected in 36 and 104 patients, respectively. Seven patients in the latter subgroup had both the antigen and antibody. Table 5. Frequency of detection of abnormal levels, according to the case definition of Rift Valley fever, during laboratory testing. Renal failure. Impairment of renal function was demonstrated by 91 patients (55.2%) at the time of admission. The mean creatinine and urea levels were 361.9 μM and 18.2 mM, respectively, and 74 patients (44.8%) had serum creatinine levels >150 μM. The abnormality of renal function (prerenal azotemia) resulting from dehydration was reversible in 23 patients. Acute renal failure was established and severe (creatinine level, >600 μM) in 68 (41.2%) of 165 patients, and 32 of the 68 patients required hemodialysis. Hemorrhagic manifestations. A total of 32 patients (19.4%) presented with hemorrhagic manifestations at admission. These manifestations included hematemesis (in 8 patients), vaginal bleeding (in 2 patients), and severe hemoptysis (in 1 patient), in addition to bleeding from the gums and venipuncture sites, petechial rashes, and ecchymoses of the skin. For 3 patients, upper gastrointestinal endoscopy confirmed that the presence of erosive mucosal lesions was the cause of bleeding. Severe coagulopathy with marked prolongation of prothrombin time and partial thromboplastin time was found in 61 patients, 31 of whom had evidence of disseminated intravascular coagulopathy. Retinitis and encephalitis. Macular and paramacular retinitis were found in 16 patients during their hospitalization. These patients were 9 males and 7 females whose age range was 15–77 years. The lesions (figures 1 and 2) were bilateral in 11 patients. Three patients experienced permanent loss of vision, and 4 patients with concomitant meningoencephalitis died. Table 6 summarizes the clinical and laboratory findings for patients who had meningoencephalitis diagnosed 2–60 days after the onset of the infection. All the patients had fever. Diarrhea and myalgia occurred in 1 patient (patient 4). One patient (patient 6) experienced paralysis of the left sixth and seventh cranial nerves, concomitant hepatitis, retinitis, and ecchymosis. CT of the brain revealed no abnormal findings for 4 patients, but it demonstrated hypodense lesions in 2 patients (patients 6 and 7) and atrophic changes in 1 patient. RVFAg was detected in 1 patient (patient 6), and the remaining 6 patients were positive for IgM antibody to RVF. One of the 3 patients who survived (patient 1) remained in a vegetative state, and 1 patient was discharged with residual neurologic deficit and was lost to follow-up. Figure 1. (60 KB)Figure 1. Macular retinitis with exudates and hemorrhage in the macular and paramacular areas of a patient with Rift Valley fever. Figure 2. (39 KB)Figure 2. Scarring in the macular area of a patient with Rift Valley fever. Table 6. Clinical characteristics of and laboratory results for 7 patients with meningoencephalitis associated with Rift Valley fever (RVF) in Saudi Arabia. Case fatality. As summarized in table 2, the in-hospital case-fatality rate was 33.9% (56 of 165 patients died), with there being no difference with regard to the sex of the patient (33.8% of 136 men and 34.4% of 29 women died). Overall, the mean age of the survivors was significantly less than that of the patients who died (). Complications associated with death are shown in table 7. A total of 39 (70.9%) of 55 patients who had both hepatic and renal failure died, compared with 2 (7.1%) of 28 patients with neither of the complications, 12 (17.4%) of 69 patients with hepatic failure only, and 3 (23.1%) of 13 patients with renal failure only. The difference was statistically significant (). For a few patients who died, histopathologic examination of the liver revealed massive hepatic necrosis and inflammatory changes. Table 7. Major complications of Rift Valley fever in 165 patients in Saudi Arabia. Discussion The outbreak of RVF in the Gizan region of Saudi Arabia confirms the extension of its geographic distribution outside the continent of Africa into the Middle Eastern area of the world. It is evident that the RVF virus can establish itself wherever potential permissive vectors and animal reservoirs are present. The Gizan region is a rural area where the main occupations of the population include animal husbandry. The climate favors breeding of mosquitoes, and, despite the control measures instituted by the government, malaria transmission and severe clinical malaria continue to affect a significant proportion of the population in this area of Saudi Arabia [7]. The precise number of humans infected in the outbreak in Gizan is unknown. It was estimated that 20,000 people in the region might have been infected, with the majority of the infections being subclinical or mild in persons who did not seek care. RVF virus is perhaps unique in that it causes several different disease syndromes in humans, none of which seems to predispose to the other [1, 2]. All the clinical syndromes in humans usually begin with mild, nonfatal influenza-like illness. In a minority of patients, severe hepatic disease with hemorrhagic manifestations, encephalitis, and ocular lesions may complicate RVF [5, 8–14]. Our results indicate that the hepatic form of the disease was the predominant organ manifestation of RVF in the Saudi epidemic, occurring in 88% of the patients who were admitted with severe illness requiring management in a special unit for RVF. Clinical characteristics of the patients included marked elevations of aminotransferase levels, a high frequency of fulminant hepatic failure, and a high case-fatality rate. However, clinical and serologic profiles, the frequency of nonhepatic complications, and the case-fatality rate were similar among patients with lower aminotransferase levels and among those with severe hepatic damage. Our findings are consistent with previous observations that (1) hepatic necrosis is the most striking microscopic lesion, and (2) increased liver enzymes are early markers for fatal RVF in humans and are usually elevated 7–8-fold during the first 48 h of illness in the majority of cases [15]. Histopathologic examinations of liver samples obtained from patients who have died of RVF usually show striking hepatic necrosis with changes in the hepatocytes that include focal cytoplasmic degradation, formation of eosinophilic or dark bodies, and bizarre nuclear profiles similar to those observed previously in animals [16–18]. The lesions in target organs associated with acute infection are presumed to be the results of a direct lytic effect of the virus, and, on the basis of the results of titration of infectivity in organ homogenates, the liver and spleen are the major sites of viral replication [1, 18]. Renal impairment was a frequent occurrence among the patients studied, and it appeared to be the result of hypovolemia and multiple-organ dysfunction in the majority of patients. However, it is also possible that the renal failure might be related to a direct virus-related injury in a proportion of the patients. Inference from immunofluorescence studies showed that the sites of RVF viral replication corresponded to the glomerular lesions, in addition to necrosis of the lymphoid, adrenal, lung, and hepatic tissues, in animals and humans [1, 15, 18]. Schrire [19] and Freed [20] were the first to report ocular abnormalities leading to a loss of central vision in patients with RVF. Since the publication of those reports, there have been many more reports of ocular complications, which have been estimated to occur in association with 1% of all RVF infections [5, 11, 12]. Ten percent of Saudi patients studied were found to have retinitis that affected both eyes. Although ocular lesions occasionally may appear during the phase of acute febrile illness, they usually develop 4 weeks after the onset of illness. Therefore, a survey of hospitalized patients might have underestimated the prevalence of RVF-related retinitis. Another survey performed by the ophthalmologist on our team (A.H.), which assessed outpatients during follow-up, indicated that the prevalence was higher than that noted for hospitalized patients (A.H., personal communication) The high prevalence of ocular complications may be a unique feature of the Saudi epidemic. The clinical presentations vary from blurred vision to macular exudate-like lesions, retinal detachment, and retinitis [5, 11, 12, 19, 20]. The pathogenesis of the lesions is not well understood, but fluorescein angiography suggests that the lesions are often the result of primary occlusion of the retinal circulation, probably as a result of proliferation of virus particles on the endothelial cells [21]. A contributory role of the inflammatory process is suggested by the occurrence of maculopathy, vascular narrowing, sheathing, and retinal hemorrhages in some patients [12, 21]. Encephalitis, which was found in only 7 of our patients, is an uncommon and unpredictable complication of RVF infection occurring 1–4 weeks after the onset of RVF. It usually presents with variable clinical manifestations, including severe headache, confusion, disorientation, meningism, and coma [5, 11, 22, 23]. Although complete recovery from this complication is reported to occur, only one of our patients survived, and this patient remained in a vegetative state. It was interesting to note that 5 of the 7 patients had concurrent retinitis. Histopathologic characteristics include focal necrosis with leukocyte infiltration and perivascular cuffing [1]. These features and the delayed appearance of the clinical course of the disease suggest a complex interaction of immune-mediated and direct cytopathic effects of the virus as the underlying mechanism of this complication [1, 14, 24]. No brain tissue was obtained from any of our patients for histologic examination. Serologic analysis is a useful tool for the identification of RVF infection. However, some patients who have clinical features consistent with the infection may have negative results of serologic analysis. In the outbreak in Kenya, possible causes of the cases of fever with hemorrhagic syndromes in patients found to be negative for RVF included the use of extremely sensitive case definitions, improper sampling, the presence of other pathogens and toxins, and complications of malnutrition [25, 26]. In the Saudi epidemic, 95% of severely infected case patients were confirmed to have RVF by either viral antigen or IgM antibody testing, perhaps because of the application of a very strict case definition [6]. It is essential that RVF be distinguished from Crimean-Congo hemorrhagic fever (CCHF) and similar diseases [1]. CCHF is a tickborne viral zoonosis that occurs in Europe, Asia, and Africa [27]. Before the RVF epidemic, a study that used the reversed passive hemagglutination inhibition test detected antibodies in 3 (0.8%) of 354 humans tested in Saudi Arabia [28]. In the initial phase of the epidemic, serologic testing of the patients excluded CCHF as the cause of the illness. Generally, it was estimated that only approximately 1%–2% of infections result in fatal hemorrhagic fever or encephalitis [25]. The overall case-fatality rate in the Saudi outbreak was reported to be 17% (87 of 516 case patients died) [6]. The 33.3% case-fatality rate for our patients admitted to the special RVF unit was reflective of the severity of the illness, which necessitated specialized management. The lethality of RVF was first recognized when 7 deaths occurred during the epidemic in South Africa in 1974–1976 [10, 14]. Since then, many more deaths have been attributed to RVF. The outbreak in Egypt in 1977–1978 was associated with an estimated 18,000 infections and 598 deaths, for a case-fatality rate of 33.2 deaths per 1000 individuals [1, 11]. In contrast, only 5 human deaths were reported in Zimbabwe in 1978 [29]. In 1987, an estimated 224 deaths occurred in the Mauritanian epidemic. The case-fatality rate was estimated to be 1%, although higher estimates of 4.8%–13.9% were reported for 2 different populations surveyed [30]. It is difficult to compare these aforementioned rates because of the differences in the characteristics of these epidemics and, also, because some of the data on the number of deaths associated with these epidemics are estimates. Factors that contributed to a fatal outcome in these patients included hepatic failure, shock, and renal failure, findings that are in agreement with findings reported elsewhere [24]. Additional host-related factors might be contributory. For example, it was suggested that the unusually high mortality rate noted in the Egyptian epidemic could have been due to infection with a more virulent strain of RVF virus or to infections in a host population compromised by previous diseases, such as schistosomiasis or chronic hepatitis B or C [14]. The Gizan province of Saudi Arabia is similar to Egypt in terms of the high prevalence of subclinical liver diseases caused by schistosomiasis and viral hepatitis. Therefore, it is possible, although speculative, that these factors might have influenced the case-fatality rates among the Gizan patients. It was interesting to observe that 21% of our patients habitually consumed raw milk. It is unclear whether this was a contributing factor to the acquisition of infection by these patients, because the majority were exposed to infected animals or humans before they became ill. However, low concentrations of RVF virus were found in the milk and body fluids of domestic animals, and, in the Mauritania epidemic, it appeared that there might have been a connection between RVF infection in humans and the consumption of raw milk [1, 31–33]. Some authors have warned that the population of the entire Mediterranean littoral must be considered to be at risk for RVF disease [5, 34]. The present report on the occurrence of RVF in Saudi Arabia confirms the extension of the disease beyond the sub-Saharan area. A comprehensive preventive strategy must be adopted to avoid future recurrence of RVF in Saudi Arabia and other Middle Eastern countries. References 1. Swanepoel R, Coetzer JAW. Rift Valley fever. In: Coetzer JAW, Thomson GR, Tustin RC, eds. Infectious disease of livestock, vol 1. New York: Oxford University Press, 1994:688–717. First citation in article 2. Peters CJ. Emergence of Rift Valley fever. In: JF Saluzzo, Dodet B, eds. Factors in the emergence of Arbovirus disease. Paris: Elsevier, 1997:253–63. First citation in article 3. Daubney R, Hudson JR, Garnham PC. Enzootic hepatitis or Rift Valley fever: an undescribed virus of sheep, cattle and man from East Africa. J Pathol Bacteriol 1931; 34:545–9. First citation in article, CrossRef 4. US Centers for Disease Control and Prevention. Update: outbreak of Rift Valley fever—Saudi Arabia, August–November 2000. 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Rift Valley fever in man, complicated by retinal changes and loss of vision. S Afr Med J 1951; 25:930. First citation in article, PubMed 21. Deutman AF, Klomp HJ. Rift Valley fever retinitis. Am J Ophthalmol 1981; 92:38–42. First citation in article, PubMed 22. Maar SA, Swanepoel R, Gelfand M. Rift Valley fever encephalitis: a description of a case. Cent Afr J Med 1970; 5:8–11. First citation in article 23. Peters CJ, Meegan JM. Rift Valley fever. In: Berab G, ed. CRC handbook series in zoonosis. Section B1. Boca Raton, FL: CRC Press, 1981:403–19. First citation in article 24. Peters CJ, Anderson GW. Pathogenesis of Rift Valley fever. Contrib Epidemiol Biostat 1981; 3:21–41. First citation in article 25. World Health Organization. An outbreak of Rift Valley fever, Eastern Africa 1997–1998. Wkly Epidemiol Rec 1998; 73:105–12. First citation in article 26. Johnson BK, Chanas AC, El Tayeb E, Abdel Wahab KS, Sheheta FA, Mohamed A El-D. Rift Valley fever in Egypt. Lancet 1978; 2(8092):745. 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Analytical study of a Rift Valley fever epidemic. Res Virol 1989; 40:175–86. First citation in article 34. Meegan JM, Niklasson B, Bengtsson E. Spread of Rift Valley fever from continental Africa. Lancet 1979; 2(8153):1184–5. First citation in article, CrossRef, PubMed Cited by Samantha Soldan, Francisco González-Scarano. (2005) Emerging infectious diseases: The Bunyaviridae. Journal of NeuroVirology 11:5, 412 CrossRef Shamsudeen F. Fagbo. (2004) Rift Valley Fever Epidemic in Saudi Arabia: Disconcerting Epidemiological Defects and Lack of Differential Diagnoses and Concordance in Studies. Clinical Infectious Diseases 38:10, 1503-1503 Online publication date: 1-Jan-2004. Citation-Full Text Paul Krogstad, Mart??n G. Mart??n. (2003) Evaluation of acute liver failure. The Pediatric Infectious Disease Journal 22:9, 831 CrossRef

Quote: عملت نخبة من الأطباء السودانيين مع هذا المرض فى جنوب المملكه العربيه السعوديه فى 2003م عندما انتشر الوباء ولهم دور مميز فى إكتشافه منذ اللحظة الأولى منهم الأخ الدكتور محمود عبدالرحمن إستشارى الباطنيه بمستشفى الملك فهد المركزى بجيزان والدكتور معتمد خبير منظمة الصحه العالميه والدكتور مصطفى عكود خبير الطفيليات وتمكنوا بنجاح من السيطرة عليه عندما تم استنفارهم فى ذلك الوقت بعضهم عاد وربمالايزال يبحث عن عمل.....؟؟؟؟ولا أدرى إن وجد أم لم يجد؟؟؟

Quote: Research Genetic Analysis of Viruses Associated with Emergence of Rift Valley Fever in Saudi Arabia and Yemen, 2000-01 Trevor Shoemaker,*† Carla Boulianne,*† Martin J. Vincent,* Linda Pezzanite,* Mohammed M. Al-Qahtani,‡ Yagub Al-Mazrou,‡ Ali S. Khan,* Pierre E. Rollin,* Robert Swanepoel,§ Thomas G. Ksiazek,* and Stuart T. Nichol* *Centers for Disease Control and Prevention, Atlanta, Georgia, USA; †Emory University, Atlanta, Georgia, USA; ‡Ministry of Health, Riyadh, Saudi Arabia; and §National Institute of Virology, Johannesburg, South Africa Suggested citation for this article: Shoemaker T, Boulianne C, Vincent MJ, Pezzanite L, Al-Qahtani MM, Al-Mazrou Y, et al. Genetic analysis of viruses associated with emergence of Rift Valley fever in Saudi Arabia and Yemen, 2000-01. Emerg Infect Dis [serial online] 2002 Dec [date cited];8. Available from: URL: http://www.cdc.gov/ncidod/EID/vol8no12/02-0195.htm -------------------------------------------------------------------------------- The first confirmed Rift Valley fever outbreak outside Africa was reported in September 2000, in the Arabian Peninsula. As of February 2001, a total of 884 hospitalized patients were identified in Saudi Arabia, with 124 deaths. In Yemen, 1,087 cases were estimated to have occurred, with 121 deaths. Laboratory diagnosis of Rift Valley fever virus (RVFV) infections included virus genetic detection and characterization of clinical specimens by reverse transcription-polymerase chain reaction, in addition to serologic tests and virus isolation. Genetic analysis of selected regions of virus S, M, and L RNA genome segments indicated little genetic variation among the viruses associated with disease. The Saudi Arabia and Yemen viruses were almost identical to those associated with earlier RVF epidemics in East Africa. Analysis of S, M, and L RNA genome segment sequence differences showed similar phylogenetic relationships among these viruses, indicating that genetic reassortment did not play an important role in the emergence of this virus in the Arabian Peninsula. These results are consistent with the recent introduction of RVFV into the Arabian Peninsula from East Africa. Rift Valley fever (RVF) (caused by Rift Valley fever virus [RVFV], family Bunyaviridae) is an emerging epidemic disease of humans and livestock, as well as an important endemic problem in sub-Saharan Africa. The virus is transmitted to livestock and humans by the bite of infected mosquitoes or exposure to tissues or blood of infected animals. Massive epizootics are typically observed in livestock during times of unusually high and sustained rainfall because of the presence of breeding sites and overabundance of adult competent mosquito vectors (1). Infections caused by RVFV are characterized by severe disease and abortion in livestock, particularly sheep and cattle. Persons in the epidemic region are at high risk for RVFV infection, potentially leading to thousands of human cases. Humans infected with RVFV typically have self-limited febrile illness, but retinal degeneration (5–10%), hemorrhagic fever (<1%), or encephalitis (<1%) may also develop (2). We report the first confirmed outbreak of RVF outside Africa, in the Kingdom of Saudi Arabia and Yemen. On September 10, 2000, the Ministry of Health in Saudi Arabia began to receive reports of unexplained hemorrhagic fever in humans near the Saudi-Yemeni border, with associated animal deaths and abortions. Patient samples from the outbreak were sent to the Centers for Disease Control and Prevention (CDC), where laboratory analysis confirmed the cases as being caused by RVFV. Genetic analysis was performed on all three viral RNA segments from human clinical samples, and the sequences were compared with previously characterized RVFV isolates to determine their genetic relatedness and geographic distribution. Materials and Methods Clinical Specimens On September 15, 2000, acute-phase sera from four seriously ill, hospitalized patients with unexplained hemorrhagic fever were received by Special Pathogens Branch, CDC for diagnostic assessment (Table 1). The shipment also contained sera from nine close contacts, mainly household members. A second shipment, which arrived on September 20, 2000, contained acute-phase sera from an additional 15 hospitalized patients and 12 contacts. Subsequent specimens from Saudi Arabia and Yemen were submitted for confirmation and more detailed analysis. All work with potentially infectious material was performed in a biosafety level 4 maximum containment facility. Virus Antigen, IgM, and IgG Detection in Patient Sera Patient sera were tested for the presence of RVFV or Crimean-Congo hemorrhagic fever virus (C-CHFV) antigen, or immunoglobulin (Ig) M or IgG antibodies reactive with these viruses and Alkhurma virus, a member of the tick-borne encephalitis (TBE) complex that was recently discovered in Saudi Arabia (4). RVFV and C-CHFV antigen-capture assays were performed in an enzyme-linked immunosorbent assay (ELISA) format essentially as described (5). The RVFV assay used polyclonal hyperimmune ascitic fluid raised against RVFV strain Zagazig 501 as the capture antibody and rabbit hyperimmune serum raised against RVFV Zagazig 501 as the detector antibody. The C-CHFV assay used a sheep hyperimmune serum raised against a South African C-CHFV strain as the detector antibody, and a mouse hyperimmune ascitic fluid raised against C-CHFV strain IbAr10200 as the capture antibodies (6). IgM antibody titers were determined by IgM antibody–capture ELISA, with RVFV, C-CHFV, or Alkhurma virus–infected cell slurry prepared as described (5). IgG antibody titers were determined by using RVFV, C-CHFV, and Alkhurma virus–infected cell antigens in an ELISA format similar to that described previously (5). Virus Isolation and RNA Extraction Viral RNA was obtained directly from patient blood or serum collected during the outbreak or from virus isolated from patient serum that was passaged once in Vero E6 cells. A virus stock was prepared by placing 100 µL of patient serum (200010901) onto a confluent monolayer of Vero E6 cells in a T-25 flask. After the virus was allowed to absorb for 1 h at 37°C, 6–7 mL of Dulbecco, modified Eagle medium supplemented with 5% fetal calf serum (FCS) and antibiotics, was added to the T-25 flask and allowed to incubate at 37°C, 5% CO2. Cell cultures were checked daily for cytopathic effect (CPE), and after approximately 75% CPE was observed, remaining cells were scraped off and combined with the supernatant. A low-speed centrifugation removed most debris, and the resulting supernatant was stored at -80°C. Some cells were retained to perform immunofluorescence (IFA) directed at RVFV to check for positive cultures. Two hundred microliters of passage 1 cell/supernatant was placed into 1 mL of TriPure (Roche, Indianapolis, IN) for RNA purification. Saudi Arabia sample 2003043 and Yemen sample 2001373 were prepared by placing 200 µL of blood or serum, respectively, directly into 1 mL of TriPure. RNA was extracted onto glass beads by using a RNAid kit (Bio101, Carlsbad, CA) according to a modified protocol (7). Indirect Immunofluorescence Assay and RT-PCR Virus-infected cells were tested for RVFV antigens by indirect immunofluorescence assay essentially as described (5), except cells were incubated with anti-RVFV immune mouse ascitic fluid. The nucleic acid sequences of the partial S, M, and L segments of RVFVs were amplified by using a one-step reverse transcriptase polymerase chain reaction (RT-PCR) (Promega Access kit, Madison, WI), according to manufacturer’s protocol. The primers NSn (5'- TATCATGGATTACTTTCC-3') and NSc (5'- CCTTAACCTCTAATCAAC-3') were used to amplify a 661-Nt region (excluding primer sequences) of the virus S segment region encoding the NSs protein (8). The primers RVFFORI (5'-GTCTTGCTTGAAAAGGGAAAA-3') and RVFREVE (5'-CCTGACCCATTAGCATG-3') were used to amplify a 708-Nt region (excluding primers) of the virus M segment region encoding the G2 protein. Primers Wag (5'-ATTCTTATTCCCGAATAT-3') and Xg (5'-TTGTTTTGCCTATCCTAC-3') were used to amplify a 176-Nt (excluding primers) region of the L segment (9). The primers RVFREVE together with primer RVFFORA (5'-TGCTACCAGACTCATTTGTC-3') were used to amplify the initial diagnostic fragment of 186 Nt (excluding primers) of the virus M RNA genome segment region encoding the G2 protein. Electrophoresis of amplified DNA products was done on a 1.7% agarose gel in Tris-acetate-EDTA buffer. Following staining with ethidium bromide, specific DNA bands were located by UV translumination, sliced from the gel, and purified by using Qiaquick spin columns (Qiagen, Valencia, CA). Dye terminator cycle sequencing reactions were performed by using ABI PRISM Dye Terminator Cycle Sequencing Ready Reaction Kits with AmpliTaq DNA Polymerase FS (Applied Biosystems, Foster City, CA). Reaction products were purified by using Centri-sep spin columns (Princeton Separations, Adelphia, NJ) and sequences determined with an ABI 377 automated DNA sequencer (Applied Biosystems). Output chromatograms were analyzed with Sequencher 3.0 software (Gene Codes Corp., Ann Arbor, MI). RVFV sequences were aligned with those of previously characterized RVFVs (10) by using the PILEUP program of the Wisconsin Package Version 10.2 (Genetics Computer Group, Inc., Madison, WI). Maximum likelihood phylogenetic analysis was carried out by using PAUP4.0b10 (Sinauer Associates Inc., Sunderland, MA). Results Initial RVF Diagnosis In early September 2000, the Ministry of Health of Saudi Arabia received reports of unexplained hemorrhagic fever cases in the southern Tehama (coastal plain) region of southwestern Saudi Arabia. Subsequently, reports were also obtained by the Yemen Ministry of Health of a similar disease in the adjoining Tehama region of Western Yemen. Initial specimens included acute-phase sera from four hospitalized patients with suspected cases and sera from nine contacts (mostly family members). Based on the available clinical information, the differential diagnostic included Rift Valley fever, Crimean-Congo hemorrhagic fever, and Tick-borne encephalitis-like viruses. The four serum samples from the suspected case-patients were tested by antigen-capture ELISA with RVFV- or C-CHFV-reactive antibodies; IgM-capture ELISA with RVFV, C-CHFV, or Alkhurma virus–infected cell lysate antigens; IgG ELISA with RVFV, C-CHVF, or Alkhurma virus–infected cell slurry antigen; virus isolation with Vero E6 cells; and RT-PCR assays for detection of RVFV, C-CHFV, or TBE-complex virus RNA. Evidence of RVFV infection was found in all four patients with suspected cases (Table 1). No evidence of C-CHFV or Alkhurma virus infection was found. Three of four acute-phase sera were positive by RVFV antigen-capture ELISA, and the single negative serum was positive for RVFV IgM and IgG, suggesting a later stage of infection in this case. All four sera were positive by RVFV RT-PCR assay and subsequently yielded infectious RVFV by culture on Vero E6 cells. Of the nine sera from close contacts, two showed evidence of RVFV infection. One was RT-PCR positive and virus isolation positive, and the other was positive for RVFV IgM antibodies. A second shipment of specimens yielded similar results, again confirming that RVFV was responsible for the outbreak in Saudi Arabia. In this second shipment, 13 of 15 hospitalized suspected case-patients had evidence of RVFV infection. Four contacts of case-patients also showed evidence of RVFV infection. The rapid RVFV RT-PCR assay appeared to be a useful complement to the RVFV antigen and IgM-capture ELISA tests for diagnosis of acute illness, as it detected virus RNA in 15 of 16 serum samples that were subsequently found to be RVFV positive. Overall correlation between the various RVFV diagnostic assays was good. Nucleotide sequence analysis of the 186-Nt (excluding primer regions) PCR products amplified from these initial specimens confirmed the virus identity as RVFV and showed no nucleotide differences between the viruses detected in these Saudi Arabian patients. In addition, no nucleotide differences were detected in this 186-Nt region relative to viruses detected in an earlier outbreak in East Africa in 1997 (data not shown) (11). Detailed Genetic Analysis RNA extracted from three representative viruses was chosen for more detailed genetic analysis. These included RNA from RVFV isolate (strain 200010901) obtained from the first RVFV-infected case-patient to be laboratory confirmed and representing the early phase of the outbreak in Saudi Arabia. This isolate was obtained from a serum sample collected on September 13, 2000, from this case-patient (Table 1), who was infected in Jizan Province. RNA extracted from a serum sample collected late in the outbreak in Saudi Arabia was also included (Table 2). This serum sample was collected on November 22, 2000, from a case-patient infected in Asir Province. The third RNA sample was extracted from a blood sample obtained from a case-patient in Yemen. With these RNA samples, we hoped to detect any genetic variation in the RVFVs active during the early and late phases of the outbreak in Saudi Arabia and to evaluate whether the same virus strain was responsible for disease in Saudi Arabia and Yemen. A single nucleotide difference was observed between each of the Saudi Arabia and Yemen virus S RNA genome segment fragments analyzed (601 nt). Similarly, no nucleotide differences were found between the Saudi Arabia 200010901 and Yemen 2003043 virus M RNA genome segment fragments we analyzed (510 nt), and these differed from the Saudi Arabia 2001373 virus fragment by only 1 nt. All three viruses were identical for the L RNA genome segment fragment we analyzed (129 nt). These data demonstrate that the viruses in the early and late stages of the RVF outbreak in Saudi Arabia are virtually identical to one another and to the virus causing disease in Yemen. Figure Click to view enlarged image Figure. Phylogenetic relationship of the S, M, and L RNA segments of Rift Valley fever viruses.... The results of phylogenetic analysis of the nucleotide sequence differences among the S, M, and L RNA genome fragments of the Saudi Arabia and Yemen viruses and previously described RVFVs are shown (Figure). Earlier maximum likelihood analyses had separated RVFVs into three broad groups, which predominantly contained viruses from North Africa, West Africa, and East/Central Africa (10). All three RNA segment trees obtained here have the Saudi Arabia and Yemen viruses grouped with the East/Central Africa viruses. Specifically, the S, M, and L RNA genome segments of the Saudi Arabia and Yemen viruses are closely related to those of viruses previously detected in outbreaks in East Africa, as represented by the Kenya 1997 and Madagascar 1991 virus isolates (Figure, A, B, and C). The nucleotide changes in the S, M, and L RNA genome segment fragments observed among the closely related Saudi Arabia/Yemen viruses and the Kenya 1997 and Madagascar 1991 viruses are synonymous changes, resulting in no amino acid differences among these viruses. Discussion Using a combination of RVFV IgM and antigen-capture ELISA tests, along with the RT-PCR assay, we quickly identified RVFV as the cause of a large outbreak in Saudi Arabia reported in September 2000. The RT-PCR assay proved to be an excellent complement to the antigen and antibody ELISA detection systems for the initial rapid diagnosis of RVF. Virus-specific antibodies were present in three of four specimens that were positive by both virus isolation and PCR but negative by antigen capture, suggesting that immune complex formation (antibody blocking of antigen) may be the basis for the lower sensitivity of the antigen-capture assay. Although the IgM assay failed to identify 9 of 17 laboratory-confirmed (by virus isolation or PCR) acute RVF cases, the assay did detect recent RVFV infections in five contacts (mostly close family members) and one acute case that would have been missed on the basis of virus isolation or PCR assay only. The data from this study and others (12) demonstrate the importance of combining assays for the detection of virus (antigen capture, RT-PCR, or virus isolation) and the detection of virus-specific IgM to ensure that no acutely ill RVFV patients are missed. This RVF outbreak, the first confirmed outside Africa, illustrates the potential for this disease to spread to other regions of the world. Virus activity on the Arabian Peninsula resulted in a considerable amount of disease activity from September 2000 to February 2001 (3,13). In Saudi Arabia, as of February 2001, 884 seriously ill, hospitalized RVF patients were identified, with 124 deaths. In Yemen, 1,087 cases were estimated to have occurred, with 121 deaths (14). The outbreak involved a broad geographic area, including Jizan and Asir Provinces in southwestern Saudi Arabia and much of the western coastal plain of Yemen. Because of the magnitude of this outbreak and the large geographic area it encompassed, the total number of human RVFV infections remains unknown. Data from previous outbreaks suggest that the number of hospitalized RVF patients identified during a large outbreak represents only a small percentage (<1%) of the total number of infections (2). Our finding of six laboratory-confirmed RVFV infections among household contacts is consistent with the view that hospitalized patients represent a small fraction of the number of infected persons. Based on these and earlier observations, the number of human infections during this epidemic must have been considerable. Large numbers of livestock were also affected, causing substantial losses and economic impact in the rural areas hardest hit by the disease. Further impact of the outbreak included trade and travel restrictions. Genetic analysis of S, M, and L segments of the viruses detected in Saudi Arabia and Yemen indicated that essentially the same virus caused both outbreaks. Few genetic differences were detected between viruses sampled early and late in the outbreak or from the distant geographic regions of Jizan and Asir Provinces in Saudi Arabia and areas of Western Yemen. The lack of substantial genetic variation in these viruses, together with the lack of earlier disease reports, suggests that RVFV has only recently been introduced onto the Arabian Peninsula. Phylogenetic comparison of the nucleotide sequence differences between the Arabian Peninsula RVFV S, M, and L segments and those of previously characterized RVFV isolates showed a close relationship between the Saudi Arabia/Yemen RVFVs and those circulating earlier in East Africa, particularly with the viruses responsible for the large RVF outbreak seen in the region in 1997–98 (11). These results are consistent with the introduction of RVFV into Saudi Arabia and Yemen from East Africa. While genetic reassortment has been observed in RVFVs associated with outbreaks in various geographic regions of Africa (10), the close phylogenetic relationship of the S, M, and L RNA segments of the 2000–01 Saudi Arabia and Yemen viruses and the earlier 1997 and 1991 Kenya and Madagascar viruses, respectively, provided no evidence of genetic reassortment among these viruses. The mechanism of introduction of the virus into the Saudi Arabia and Yemen remains unknown. However, commercial trade of livestock is active from East Africa to the Arabian Peninsula, and disease is known to be endemic in the East African region. While no hospitalized RVF patients have been reported in 2002, whether this RVF lineage has become established in the Arabian Peninsula remains unclear. Surveillance of humans, livestock, and vector populations will continue to address this question. Acknowledgments We thank Thomas Stevens, Patrick Stockton, Debi Cannon, and Kim Slaughter for performance of serologic tests and John O’Connor for editorial assistance. We are indebted to the Ministry of Health of the Kingdom of Saudi Arabia for their invitation to participate and for their kind hospitality and support during the outbreak investigation. We also thank the Ministry of Health of Yemen and the U.S. Navy Medical Research Unit 3 for their assistance in obtaining clinical materials. Mr. Shoemaker has an MPH degree from University of California, Berkeley, and completed this work while a regular fellow in the Special Pathogens Branch, Division of Viral and Rickettsial Diseases, National Center for Infections Diseases, Centers for Disease Control and Prevention. His current interests include the integration of epidemiologic and molecular approaches to investigate emerging diseases and potential bioterrorism events. References Linthicum KJ, Anyamba A, Tucker CJ, Kelley PW, Myers MF, Peters CJ. Climate and satellite indicators to forecast Rift Valley fever epidemics in Kenya. Science 1999;285:397–400. Meegan JM, Bailey CL. In: Monath TP, editor. The arboviruses: epidemiology and ecology. Boca Raton (FL): CRC Press; 1989. Centers for Disease Control and Prevention. Outbreak of Rift Valley fever—Saudi Arabia, August–October, 2000. MMWR Morb Mortal Wkly Rep 2000;49:905–8. Charrel RN, Zaki AM, Attoui H, Fakeeh M, Billoir F, Yousef AI, et al. 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