ABSTRACT
Resistance of falciparum malaria to antimalarial agents is prevalent in many areas, whereas chloroquine-resistant vivax malaria has been reported mainly around New Guinea since 1989. Concomitant with the spread of chloroquine-resistant P. vivax and increase in number of international travelers, imported cases of chloroquine-resistant vivax malaria in travelers returning from these areas has been reported. We experienced a case of chloroquine resistance P. vivax infection imported from Mangole Island, Indonesia. Its origin is confirmed not to be indigenous by the gene encoding analysis for the polymorphic region of apical membrane antigen-1 in P. vivax. Gene sequencing of the P. vivax mdr1 gene revealed only one substitution located at the codon 1076 (F1076L). The case was managed with oral quinidine with successful outcomes.
Subject(s)
Antimalarials , Chloroquine , Codon , Indonesia , Malaria , Malaria, Vivax , Membranes , New Guinea , Plasmodium , Plasmodium vivax , QuinidineABSTRACT
Resistance of falciparum malaria to antimalarial agents is prevalent in many areas, whereas chloroquine-resistant vivax malaria has been reported mainly around New Guinea since 1989. Concomitant with the spread of chloroquine-resistant P. vivax and increase in number of international travelers, imported cases of chloroquine-resistant vivax malaria in travelers returning from these areas has been reported. We experienced a case of chloroquine resistance P. vivax infection imported from Mangole Island, Indonesia. Its origin is confirmed not to be indigenous by the gene encoding analysis for the polymorphic region of apical membrane antigen-1 in P. vivax. Gene sequencing of the P. vivax mdr1 gene revealed only one substitution located at the codon 1076 (F1076L). The case was managed with oral quinidine with successful outcomes.
Subject(s)
Antimalarials , Chloroquine , Codon , Indonesia , Malaria , Malaria, Vivax , Membranes , New Guinea , Plasmodium , Plasmodium vivax , QuinidineABSTRACT
Acute Human immunodeficiency virus (HIV) syndrome should be considered in any patient with possible HIV exposure who presents with acute febrile disease. The diagnosis of acute HIV syndrome is difficult because symptoms are those of common illness. A high index of suspicion and possibility of HIV exposure are important diagnostic clue. Early diagnosis during primary infection permit patient education and treatment that may delay disease progression and improve immune preservation and reconstitution. We report two cases of acute HIV syndrome presenting as an acute febrile disease. The first case had severe illness presenting as acute severe hepatitis and disseminated intravascular coagulation, and the second had relatively mild form of disease. Two cases started the treatment with highly active anti-retroviral therapy (HAART) and have been well now with no other complications.
Subject(s)
Humans , Acquired Immunodeficiency Syndrome , Diagnosis , Disease Progression , Disseminated Intravascular Coagulation , Early Diagnosis , Hepatitis , HIV Infections , HIV , Patient Education as TopicABSTRACT
Candida species are uncommon cause of infectious arthritis. The increasing use of potent antibiotics, immunosuppressives, artificial joints, and especially the injection of steroid into the joints predispose to the fungal arthritis. Candida arthritis occurs by hematogenous dissemination or by direct inoculation of fungus into the joint cavity. Fifty three-year-old diabetic patient, who received intra-articular steroid injection into right ankle joint several times, was hospitalized because of aggravating ankle pain and swelling. Candida parapsilosis was isolated from the joint aspiration fluid and MRI findings were compatible with septic arthritis with osteomyelitis of distal tibia, distal fibula, talus, and calcaneus. The patient was successfully treated with 3 weeks of amphotericin B and 7 months of oral fluconazole. We report this case with review of pertinent literatures, emphasizing a high index of suspicion for the fungal infection in patients with predisposing risk factors.
Subject(s)
Humans , Amphotericin B , Ankle Joint , Ankle , Anti-Bacterial Agents , Arthritis , Arthritis, Infectious , Calcaneus , Candida , Fibula , Fluconazole , Fungi , Joints , Magnetic Resonance Imaging , Osteomyelitis , Risk Factors , Talus , TibiaABSTRACT
Candida species are uncommon cause of infectious arthritis. The increasing use of potent antibiotics, immunosuppressives, artificial joints, and especially the injection of steroid into the joints predispose to the fungal arthritis. Candida arthritis occurs by hematogenous dissemination or by direct inoculation of fungus into the joint cavity. Fifty three-year-old diabetic patient, who received intra-articular steroid injection into right ankle joint several times, was hospitalized because of aggravating ankle pain and swelling. Candida parapsilosis was isolated from the joint aspiration fluid and MRI findings were compatible with septic arthritis with osteomyelitis of distal tibia, distal fibula, talus, and calcaneus. The patient was successfully treated with 3 weeks of amphotericin B and 7 months of oral fluconazole. We report this case with review of pertinent literatures, emphasizing a high index of suspicion for the fungal infection in patients with predisposing risk factors.
Subject(s)
Humans , Amphotericin B , Ankle Joint , Ankle , Anti-Bacterial Agents , Arthritis , Arthritis, Infectious , Calcaneus , Candida , Fibula , Fluconazole , Fungi , Joints , Magnetic Resonance Imaging , Osteomyelitis , Risk Factors , Talus , TibiaABSTRACT
A large outbreak of Shigella sonnei gastrointestinal infections occurred at Cheju Island in Korea from May to August 2000. We selected 54 strains which were isolated from the primary treatment failure cases in the outbreak, and characterized the resistance-determining region of the R-plasmid. The 54 strains showed same antimicrobial resistance patterns; resistance against ampicillin, streptomycin, tetracycline, and trimethoprim-sulfamethoxazole. The resistance to ampicillin, streptomycin, and tetracycline were mediated by a conjugable plasmid of about 80 kb size, but the trimethoprim- sulfamethoxazole resistance was not transferred by this plasmid. The R-determining region of the plasmid was cloned and characterized. The 8,384 bp sequences contained resistance genes in the following order:strA, strB, tetR, tetA, and sul1. Fifty four isolates harbored the same sized plasmid and showed same ribotyping patterns, which suggested the clonal spread of S. sonnei in the outbreak.
Subject(s)
Ampicillin , Clone Cells , Korea , Plasmids , Ribotyping , Shigella sonnei , Shigella , Streptomycin , Sulfamethoxazole , Tetracycline , Treatment Failure , Trimethoprim, Sulfamethoxazole Drug CombinationABSTRACT
A large outbreak of Shigella sonnei gastrointestinal infections occurred at Cheju Island in Korea from May to August 2000. We selected 54 strains which were isolated from the primary treatment failure cases in the outbreak, and characterized the resistance-determining region of the R-plasmid. The 54 strains showed same antimicrobial resistance patterns; resistance against ampicillin, streptomycin, tetracycline, and trimethoprim-sulfamethoxazole. The resistance to ampicillin, streptomycin, and tetracycline were mediated by a conjugable plasmid of about 80 kb size, but the trimethoprim- sulfamethoxazole resistance was not transferred by this plasmid. The R-determining region of the plasmid was cloned and characterized. The 8,384 bp sequences contained resistance genes in the following order:strA, strB, tetR, tetA, and sul1. Fifty four isolates harbored the same sized plasmid and showed same ribotyping patterns, which suggested the clonal spread of S. sonnei in the outbreak.