The IgG and IgM titers to Bartonella henselae were determined by an enzyme immunoassay (EIA). The EIA test for detection of IgG and IgM antibodies to B. henselae concerning CSD showed that 8 (40%) of 20 patients with CSD had a serum IgG antibody titer of 12 EIA unit or more and that 5 (25%) patients had a serum IgM titer of 12 EIA unit or more. Totally 12 (60%) of the 20 patients with CSD were seropositive for B. henselae. The mean age of IgG positive patients were higher than IgM positive patients. The IgM antibodies to B. henselae disappeared within 4 to 12 weeks after onset of disease. The IgG antibodies to B. henselae disappeared within 3 to 8 weeks after onset of the symptoms in 2 cases of CSD. Another 2 cases CSD produced high levels of IgG antibodies in the acute phase of the disease. Different course of IgG and IgM antibody titers were found in sera from patients.
The reverse transcription-polymerase chain reaction (RT-PCR) gene assay, as well as electron microscopic examination, is commonly used to detect Norwalk-like viruses (NLVs). Types and number of primer pairs used are considered to be of critical importance for efficiency of the RT-PCR detection. This study was performed to determine primer pairs useful for the detection of NLVs. NLVs genes were detected by RT-PCR in 48 cases in Yamanashi Prefecture between December 1997 and March 2000. The probe type of the gene was G2P-C in 21, G2P-B in 10, G2P-A in 6, G1P-A in 3, G1P-B in 2, and a mixture of G2P-A and G2P-B in 6. The NLVs genes of G2P-C and G2P-B were estimated to have undergone mutation in the polymerase region and poorly specific to the primer pair 35/36, a combination that has been used most commonly for the RT-PCR assay in Japan. The primer pair G2R1/F1 that amplifies the capsid (CAP) region of NLVs genes can detect all NLVs genes of the Genogroup 2. The combination of this primer pair with another primer pair G1R1/Fl, which like G2R1/F1, amplifies the CAP region, makes discrimination between NLVs of different groups possible. Consequently, this combination, may be the most useful for the NLVs detection by RT-PCR.
Neonatal exanthematous diseases induced by toxic shock syndrome toxin-1 (TSST-1)-producing methicillin-resistant Staphyloccocus aureus (MRSA) is one of emerging infectious diseases in Japan, We experiened 36 patients with this disease in National Kagawa Children's Hospital and in 13 patients of them, investigated the role of both the toxin and cytokines in pathogenesis of it. The results are summarized as follows: 1. The TSST-1 level was high in the umbilical inflammatory exudate of cases induced by umbilical infection and in the gastric fluid of cases induced by respiratory infection. The blood TSST-1 level was below the detection limit in most of the exathematous cases examined, but it was detected in one of the nine cases induced by respiratory infection and a case secondary to severe MRSA infection (phlegmonous abscess in buttock). 2. Local cytokine levels were examined in the abscess pus obtained from a case of severe MRSA infection and in the gastric fluid from cases induced by respiratory infection. The local levels of TNF [α], IL-1 [β], IL-6 and IL-8 were markedly high, but the local levels of IL-2 and IFN-[γ] were simi-lar to their blood levels. 3. The severity of hypercytokinemia (IL-1[β], IL-2, IL-6, IFN-[γ]) was proportionate to the severity of exanthematous disease. Accompanied by increased levels of inhibitory factors sTNF-R, IL-1 ra, sIL-2R and IL-10, this hypercytokinemia normalized soon within four or five days. 4. As compared to cases induced by umbilical infection, cases induced by respiratory infection often had higher blood cytokine levels and some of them had cardiorespiratory disorders. Based on the results of this study, we consider that this disease is generally induced by toxemia with a small number of toxins without tissue destructive lesions by MRSA infection and that this is closely related to the course of the disease that shows a tendency to a spontaneous recovery.
Coccidioides immitis is a causative agent of coccidioidomycosis, which is one of the most dreadful mycosis because of its infectious and pathogenic nature. The endemic areas are in the southwestern parts of the United States and other semi-arid regions throughout the Western Hemisphere. During the early 1990s, the incidence of coccidioidomycosis in California increased dramatically, resulting in recognition for this mycosis as a reemerging infectious disease in the United States. The patients included a large number of non-informed visitors from non-endemic countries. Our report is on an imported case of primary pulmonary coccidioidomycosis. A 35-year-old Japanese male, after living in the United States for nine months, suffered from a combination of headache and fever. He was given a serological examination, and a chest radiograph in Phoenix, Arizona in the United States and was diagnosed as coccidioidomycosis. A daily dosage of 400mg of fluconazole was administered and he returned to Japan. His headache and skin rash persisted and he was admitted to our hospital to evaluate the severity of his disease. There were no fungi cultured from neither bronchoalveolar nor cerebrospinal fluid and he was discharged. The patient had been treated with fluconazole and his symptoms, high-resolution CT and serological antibody titer were monitored. After 18months, his clinical and radiological evolution was favorable and his serological IgM titer was below its sensitivity medication was stopped and there were no relapses.
A 49-year-old male who had been diagnosed as having amebic liver abscess when he was 32-year-old was admitted to our hospital with fever and watery diarrhea. Ultrasonography and CT examination demonstrated a solitary abscess in the right lobe of the liver. Cysts of Entamoeba histolytica were detected in the stool and an aspiration of the liver abscess looked like anchovy paste. Serum amebic antibody by the IFA method was positive and the case was diagnosed as amebic liver abscess. The patient was treated with metronidazole, and percutaneous transhepatic abscess drainage was performed. The liver abscess decreased remarkably in size and serum amebic antibody was negative after the treatment. Recurrence of amebic liver abscess is rare and we report this case with some literature.
The diagnosis of tuberculous peritonitis is quite difficult because the symptoms are not specific for the disease and the incidence of occurrence are relatively rare. We report a case of tuberculous peritonitis diagnosed by ultrasonography-guided peritoneal biopsy. A 64-year-old male was admitted to our hospital because of fever, dyspnea and abdominal pain. Laboratory findings revealed an elevated ESR (53mm/1hr.) and positive CRP. The tuberculin skin test was negative. The chest radiograph revealed bilateral pleural effusion. Abdominal ultrasonographic examination and computed tomography showed ascitic fluid, thickening of the mesentery and peritoneum, and inflammatory pseudotumor of the omentum. Ascitic fluid was exudate with a high lymphocyte count and elevated ADA (184IU/1). Microbiological studies with the fluid were negative. Peritoneal biopsy guided by ultrasonography was performed, and the specimens showed central caseous necrosis surounded by epitheloid cells and acid-fast bacilli were demonstrated. The size of the pseudotumor, pleural effusion and ascites decreased after antituberculous chemotheraphy with corticosteroid was given. Diagnosis of tuberculous peritonitis has often been made by laparotomy or laparoscopy. In a case of this kind, percutaneous peritoneal biopsy guided by ultrasonography is safe and useful.
A 48-year-old male was admitted to our hospital because of fever, cough and of loss appetite. Chest X-P revealed an abnormal shadow in the left upper lobe. Bronchoscopy was performed and Capnocytophaga gingivalis was cultured from the bronchial lavage and bronchial curreting fluid. Ceftizoxime sodium and Clindamycin phosphate was administerd intravenously. He was discharged after 30 days. He did not have any immunosuppressive underlying disease including HIV infection and diabetes mellitus which cause these lesions.