Failure to detect Plasmodium vivax in West and Central Africa by PCR species typing

<p>Abstract</p> <p>Background</p> <p><it>Plasmodium vivax </it>is estimated to affect 75 million people annually. It is reportedly absent, however, from west and central Africa due to the high prevalence of the Duffy negative phenotype in the indigenous populations. Despite this, non-African travellers consistently return to their own countries with <it>P. vivax </it>malaria after visiting this region. An attempt was made, therefore, to detect the presence of <it>P. vivax </it>parasites in blood samples collected from the indigenous populations of west and central Africa.</p> <p>Methods</p> <p>Parasite species typing (for all four human malaria parasites) was carried out by PCR on 2,588 blood samples collected from individuals from nine African malaria-endemic countries.</p> <p>Results</p> <p>Most infections (98.5%) were <it>Plasmodium falciparum</it>, <it>Plasmodium malariae </it>was identified in 8.5% of all infections, and <it>Plasmodium ovale </it>in 3.9%. The prevalence of both parasites varied greatly by country. Only one case of <it>P. vivax </it>was detected from Sao Tome, an island off the west coast of Africa, confirming the scarcity of this parasite in Africa.</p> <p>Conclusion</p> <p>The prevalence of <it>P. vivax </it>in local populations in sub-Saharan Africa is very low, despite the frequent identification of this parasite in non-African travellers.</p

米国ルイジアナ州におけるHIV/AIDS感染者とクリプトスポリジウム症の相関関係についての流行調査

クリプトスポリジウム(Cryptosporidium parvum)の人体寄生例が初めて報告されたのは1976年であったが,病原体として本格的に認識されるに至ったのは後天性免疫不全症候群(AIDS)に伴う日和見感染症としてである.1982年にはAIDS下痢患者にクリプトスポリジウム症の重症例が多数みとめられ,種々の抗生剤および抗原虫剤を投与しても治癒しないことが報告された.また,衛生管理先進国である米国において水質環境汚染や水道水供給システムの不備などに起因するクリプトスポリジウム症の大規模な流行が多発している.このような状況の中で全米第9位のAIDS感染率と第12位のAIDS患者数を抱えるルイジアナ州ではクリプトスポリジウム症の疫学的調査とそのデータ公開が感染状況の把握および予防対策に必要不可欠であるとの見地に立ち,ルイジアナ州公衆衛生局と米国疾病管理予防センター(CDC)によるASDスタディを基にした水質・環境衛生管理システムが確立されている.CDCはルイジアナ州において1997年に新たに904人のAIDS患者,1,338人のHIV感染者が確定診断され,同州のHIV感染者およびAIDS患者の総計は9,830人,そのうち4,414人がAIDS患者と診断されたと報告している.さらにCD4値が200cell/μl以下のルイジアナ州AIDS患者にクリプトスポリジウム症との強い相関関係が米国他州同様にみとめられ,水質汚染が原因とされるクリプトスポリジウム症感染は1998年のルイジアナ州の疫学調査によるとニューオリンズ市のHIV感染者のうち14人にみとめられた.このような現況を踏まえて過去10年間(1989～1998)に渡るルイジアナ州HIV/AIDSサーベイランスを軸に年齢,人種,性別,抗AIDS治療の有無,CD4値などを考慮したHIV感染者とAIDS患者に対するクリプトスポリジウム症感染の疫学調査の概略を報告する.Cryptosporidiosis is the most common causes of diarrhea in acquired immunodeficiency syndrome (AIDS) patients in the United States. First human case was diagnosed in 1976. Cryptosporidiosis persisted for 4 weeks in human immunodeficiency virus (HIV)-positive person confers the Centers for Disease Control and Prevention (CDC) defined diagnosis of AIDS. Cryptosporidiosis is most particularly a danger for the immunocompromised, especially HIV-positive persons and AIDS patients. About 2.2% of all patients whose cases of AIDS are reported to CDC have cryptosporidiosis as their AIDS-defining illness. Hospital-based studies indicate that cryptosporidiosis is diagnosed in 10～20% of AIDS patients who have diarrhea. Because diarrhea occurs in about half of all AIDS patients each year, which is estimated that the annual rate of cryptosporidial infection among all AIDS patients may approach 5～10%. Cryptosporidium parvum causes self-limited disease in immunocompetent hosts. In immunocompromised persons including HIV disease, profuse chronic watery diarrhea develops and leads to malabsorption, malnutrition, dehydration and cachexia. In the recent CDC HIV/AIDS Surveillance Report (Vol.9, No.2), Louisiana ranked 9th highest in state AIDS case rates and 12th in number of AIDS cases reported in 1997. Statewide during 1997, 904 new AIDS cases were diagnosed, and 1,338 new HIV cases were detected and reported. There were 9,830 persons living with HIV/AIDS in Louisiana, of which 4,414 had been diagnosed with AIDS at the end of 1997. The analysis data come from Adult/Adolescent Spectrum of HIV Disease (ASD) study. Cryptosporidiosis can occur at any time in the course of HIV infection. Data reported here suggest that among HIV-positive patients, cryptosporidiosis occurred more frequently among those with depleted CD4^+ cell counts and among those who developed AIDS-related opportunistic infections (AIDS-OIs). A strong association between cryptosporidiosis and depleted CD4^+ cell counts (&le;200 cells/μl) has been established in previous report

Múlt és jelen : históriai és politikai erdélyi hetilap

Cluj, 1841-1848. - Din 1844: Erdélyi hirla

Effect of genetic background on Ea(d) transgene-mediated protection from murine lupus

The expression of a transgenic encoding the I-E alpha-chain, Ea(d), is highly effective in the protection from systemic lupus erythematosus (SLE) in BXSB and (MRL x BXSB)F1 male mice, in which a mutant gene, Yaa (Y-linked autoimmune acceleration), plays a critical role. To gain further insight into the protective role of the Ea(d) transgene, we compared the effect of the transgene in two additional lupus-prone (NZB x BXSB)F1 and (NZW x BXSB)F1 hybrid mice, in which both F1 female mice develop typical SLE in the absence of the Yaa gene and their F1 males bearing the Yaa gene develop a more accelerated form of SLE. Comparative analysis of the clinical development of SLE in these F1 hybrid mice showed that Ea(d) transgene expression was much more effective in the protection from SLE occurring in the F1 females than in their male counterparts. Our results indicate that the Ea(d) transgene is capable of preventing SLE by inhibiting autoimmune responses, independently of the Yaa gene-accelerating effect, and that its protective capacity is strongly influenced by the genetic susceptibility to SLE in individual strains of lupus-prone mice. In addition, this autoimmune inhibitory effect was shown to be selective for IgG, but not IgM, anti-DNA autoantibody production, and is more specific for anti-gp70 autoantibody than for anti-DNA autoantibody. These results favour the hypothesis that the transgene expression may lead to the modulation of self-peptide presentation, thereby preventing excessive T-cell-dependent activation of autoreactive B cells

マウライ国における熱帯熱マラリア感染に対する抗マラリア薬剤効果 : chloroquineよりsufladoxine/pyrimethamineへの変更7年後の経過

マラウイでは,熱帯熱マラリア患者のchloroquine治療失敗例の増加に伴い,1993年からsulfadoxine/pyrimethamine (SP)がchloroquineに代り導入された.この変更から7年後,我々はサリマ地区の無症候性熱帯熱マラリア感染学童においてin vitroおよびin vivo抗マラリア剤効果,またそれぞれpyrimethamineおよびsulfadoxine耐性と関連する原虫dihydrofolate reductase遺伝子(dhfr)およびdihydropteroate reductase遺伝子(dhps)変異について検討した.対象学童は無作為にchloroquine 3日間の標準投与群(n=50)ないしはSP一回投与群(n=40)に分けられ,治療後28日間にわたり経過が追跡された.In vivoにおけるchloroquineおよびSP感受性率はそれぞれ92%および83%であった.分離熱帯熱マラリア原虫株のin vitro薬剤感受性はSP(n=52),pyrimethamine(52),quinine(36),mefloquine(17)およびamodiaquine(14)に対して検討された.分離株の92%がpyrimethamine耐性を示したにも関わらず,85%はSP感受性であった.Quinineおよびmefloquineに対して検討したすべて,およびamodiaquineに対する93%の分離株はin vitro感受性であった.173例の熱帯熱マラリア感染において,3重変異Asn-108/Ile-51/Arg-59 dhfrおよび2重変異Gly-437/Glu-540 dhpsを持つ原虫が高頻度(78%)で認められた.これらの結果は治療薬剤変更に伴う薬剤圧の減少が原虫chloroquine感受性の回復をもたらしたことを示唆した.高度のpyrimethamineに対するin vitro耐性は高頻度にdhfr3重変異が見られたことと一致した.それにもかかわらず観察された高いSPの効果は,高度pyrimethamine耐性原虫におけるsulfadoxineおよびpyrimethamine間の相乗作用の重要性を示唆した.In Malawi chloroquine was replaced by sulfadoxine/pyrimethamine (SP) in 1993 because of increasing chloroquine treatment failures in Plasmodium falciparum (P.falciparum) patients. Seven years after this change, we studied in vitro and in vivo efficacies of different antimalarial drugs and mutations of dihydrofolate reductase (dhfr)/dihydropteroate synthase (dhps) genes in P. falciparum infections of asymptomatic school children in Salima. The included children were randomly allocated to either treatment group with a standard dose of 3-days chloroquine (n = 50) or a single dose of SP (40) and followed up for 28 days. The in vivo sensitivity rate of chloroquine and SP were 92% and 83% respectively. P.falciparum isolates were successfully evaluated for in vitro drug sensitivity to SP (n = 52), pyrimethamine (52), amodiaquine (14), quinine (36), and mefloquine (17). Although 92% of the isolates were resistant to pyrimethamine, 85% showed in vitro sensitivity to SP. All isolates assessed for quinine and mefloquine and 93% of the isolates for amodiaquine showed in vitro sensitivity. A high prevalence rate (78%) of parasites with triple Asn-108/Ile-51/Arg-59 dhfr and double Gly-437/ Glu-540 dhps mutations was found in 173 P. falciparum infections. Our results suggest that the reduced drug pressure accompanying the policy change consequently resulted in recovery of chloroquine sensitivity in parasites. The high in vitro pyrimethamine resistance was consistent with the high prevalence of the dhfr triple mutant. However, the high efficacy of SP confirmed the important role of synergism between pyrimethamine and sulfadoxine in the treatment of highly pyrimethamine-resistant parasites

マウライ国における熱帯熱マラリア感染に対する抗マラリア薬剤効果 : chloroquineよりsufladoxine/pyrimethamineへの変更7年後の経過

マラウイでは,熱帯熱マラリア患者のchloroquine治療失敗例の増加に伴い,1993年からsulfadoxine/pyrimethamine (SP)がchloroquineに代り導入された.この変更から7年後,我々はサリマ地区の無症候性熱帯熱マラリア感染学童においてin vitroおよびin vivo抗マラリア剤効果,またそれぞれpyrimethamineおよびsulfadoxine耐性と関連する原虫dihydrofolate reductase遺伝子(dhfr)およびdihydropteroate reductase遺伝子(dhps)変異について検討した.対象学童は無作為にchloroquine 3日間の標準投与群(n=50)ないしはSP一回投与群(n=40)に分けられ,治療後28日間にわたり経過が追跡された.In vivoにおけるchloroquineおよびSP感受性率はそれぞれ92%および83%であった.分離熱帯熱マラリア原虫株のin vitro薬剤感受性はSP(n=52),pyrimethamine(52),quinine(36),mefloquine(17)およびamodiaquine(14)に対して検討された.分離株の92%がpyrimethamine耐性を示したにも関わらず,85%はSP感受性であった.Quinineおよびmefloquineに対して検討したすべて,およびamodiaquineに対する93%の分離株はin vitro感受性であった.173例の熱帯熱マラリア感染において,3重変異Asn-108/Ile-51/Arg-59 dhfrおよび2重変異Gly-437/Glu-540 dhpsを持つ原虫が高頻度(78%)で認められた.これらの結果は治療薬剤変更に伴う薬剤圧の減少が原虫chloroquine感受性の回復をもたらしたことを示唆した.高度のpyrimethamineに対するin vitro耐性は高頻度にdhfr3重変異が見られたことと一致した.それにもかかわらず観察された高いSPの効果は,高度pyrimethamine耐性原虫におけるsulfadoxineおよびpyrimethamine間の相乗作用の重要性を示唆した.In Malawi chloroquine was replaced by sulfadoxine/pyrimethamine (SP) in 1993 because of increasing chloroquine treatment failures in Plasmodium falciparum (P.falciparum) patients. Seven years after this change, we studied in vitro and in vivo efficacies of different antimalarial drugs and mutations of dihydrofolate reductase (dhfr)/dihydropteroate synthase (dhps) genes in P. falciparum infections of asymptomatic school children in Salima. The included children were randomly allocated to either treatment group with a standard dose of 3-days chloroquine (n = 50) or a single dose of SP (40) and followed up for 28 days. The in vivo sensitivity rate of chloroquine and SP were 92% and 83% respectively. P.falciparum isolates were successfully evaluated for in vitro drug sensitivity to SP (n = 52), pyrimethamine (52), amodiaquine (14), quinine (36), and mefloquine (17). Although 92% of the isolates were resistant to pyrimethamine, 85% showed in vitro sensitivity to SP. All isolates assessed for quinine and mefloquine and 93% of the isolates for amodiaquine showed in vitro sensitivity. A high prevalence rate (78%) of parasites with triple Asn-108/Ile-51/Arg-59 dhfr and double Gly-437/ Glu-540 dhps mutations was found in 173 P. falciparum infections. Our results suggest that the reduced drug pressure accompanying the policy change consequently resulted in recovery of chloroquine sensitivity in parasites. The high in vitro pyrimethamine resistance was consistent with the high prevalence of the dhfr triple mutant. However, the high efficacy of SP confirmed the important role of synergism between pyrimethamine and sulfadoxine in the treatment of highly pyrimethamine-resistant parasites