It is suggested that “Corrected value of patients” is a useful method in comparing prefecturalsurveillance data. “Corrected value of patients”is calculated as follows: Ratio of the number ofreported patients for 5 years of each prefecture of each infectious deseases to number of the nationalscale is called “Corrected rate”. The number to be divided is called “Corrected value of patient”, individually reported number of patients of the surveillance divided by “Corrected rate”.Because the “Corrected value of patients” is based on the number of reported patients for 5 years, the unequality among epidemics which differ become similar.As the value of practical usage is well recognized, 3-dimensional graphs can be used for weeklyreports, not only for Exanthema subitum but also for Erythem infectiosum.

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Shigella flexneri was isolated from 11 of 95 Japanese monkeys (Macaca fuscata) purchased by the Animal Research Center, Tokyo Medical and Dental University, during the period from 1988 through1990. The serotypes of the isolates were 4a (5 isolates), 2a (4 isolates), 2b (1 isolate), and var Yisolate. Although some of the strains in the same serotypes were similar, others were different in theirantibiotic susceptibility patterns or the plasmid profiles.
Our results suggested that various types of Shigella flexneri had infected the Japanese monkeys. However, the source (s) and the routes of infection were unclear. Dysentery in the Japanese monkeyhas not yet been reported. So, to our knowledge, this may be the first report of dysentery among Japanse monkeys.

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Pseudomonas aeruginosa Nos. 1 and 5, each co-existing growth-inhibitor-producing and-nonproducingcells, were used in this study. An equal number of both cells (each 10⁸ CFU/mouse) waschallenged intraperitoneally to mice, and these cells in the heart blood and kidneys of mice weredetermined. Furthermore, the effect of piperacillin, ceftazidime and sisomicin on the cell distributionin mice was studied in the model infection due to P. aeruginosa Nos. 1 and 5. As a control experimentboth cells of P. aeruginosa No.1 were each challenged intraperitoneally at a dose of 10⁸ CFU/mouse tomice of two groups, but there were no marked differences between the two types in cell counts of theheart blood or kidneys 9 hours after challenge.
When a concomitant challenge of both cells (each 10⁸ CFU/mouse) was performed in mice, thenumber of growth-inhibitor-producing cells of the heart blood and kidneys was about 100 times greaterthan that of the non-producing cells. These in vivo results were well comparable to the previous invitro results and indicated that the inhibitor affected the invasion of the non-producing bacteria in thebody in the model infection due to P. aeruginosa isolates consisting of the two types of cells. Similarresults were obtained in mice with the model infection due to P. aeruginosa No.5.
Anti-pseudomonal drugs such as piperacillin (50 mg/mouse) and ceftazidime (50 mg/mouse) andsisomicin (1 mg/mouse) were given intramuscularly to mice infected concomitantly with both cells of P. aeruginosa No.1. Nine hours after challenge (8 hours after dosing), these cells in the blood andkidneys of mice were determined. The number of growth-inhibitor-producing cells (drug-susceptible) in the heart blood and kidneys of mice decreased markedly, as compared with that of the non-treatedmice. On the other hand, the number of the non-producing cells (multi-drug resistant) in the heartblood and kidneys of infected mice increased markedly, as compared with that of the non-treated mice.
These results also suggested that cells of P. aeruginosa isolates differed in production of growthinhibitor, invaded into the body through the interaction under given environmental conditionsincluding antibacterial action of the administered drug.

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Polypeptide profiles were compared among Chlamydia pneumoniae strain of AC-43, which wasisolated from a Japanese child, and other strains of C. pneumoniae.
There was no distinctive differences among these strains. All strains showed marked band on 39.5KDa area, which is equivalent with the major outer membrane protein (MOMP).
Patients infected with C. pneumoniae were analyzed by Western blot using AC-43. Reaction for 98, 68, 60 KDa proteins were recognized among sera which showed positive results for anti-C. pneumoniaeIg G antibody. There were two family members from whom C. pneumoniae was not isolated and anti-C.pneumoniae Ig G antibody was negative. Sera obtained from them also showed weak reaction on 98KDa protein area. Strong reaction on MOMP area was demonstrated in one patient from whom C.pneumoniae was isolated. Monoclonal antibody produced from AC-43 strain showed no reactionagainst homologous antigen.
Reaction to 98 KDa protein was detected in all of the patients infected with C. pneumoniae.However, recognition to MOMP of C. pneumoniae seems to be different among patients. This resultmight suggest the presence of subtype among C. pneumoniae strains.

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Erythrocyte C3b receptors (E-CR1) were assayed by ELISA in 16 patients with acute viral hepatitis. In13 patients with hepatitis type A, type B, or type non-A non-B, the E-CR1 level was significantly lower inthe acute phase than in healthy controls, and recovered in the convalescent phase. The E-CR1 levels in 3patients with non-A, non-B hepatitis remained below the mean level of the healthy controls. These findingssuggest that the E-CR1 level fluctuates in acute viral hepatitis, and that itcontinues to be reduced in somepatients with non-A non-B acute hepatitis.

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The intensity of reaction in the IDEIA CHLAMYDIA ^® test kit to lipopolysaccharide of seven strains of Chlamydia pneumoniae was examined by using highly purified elementary bodies (EBs).The strains were divided into two groups according to whether the EBs were pear-shape or round. The group with the pear-shaped EBs consisted of TW-183, AR-39 and AR-388 strains; the group with the round EBs consisted of I0L-207, Kajaani-6, YK-41 and KKpn-1 strains. The number of EBs at the cutoff level of the test kit were determined as follows: TW-183, 7.0×10³; AR-388, 8.4×10³;AR-39, 2.4×10⁴; I0L-207, 6.0×10³;Kajaani-6, 1.2×10⁴;KKpn-1 2.8×10⁴;and YK-41, 4.0×10⁴ per assay. The number of EBs of C. trachomatis L₂/434/Bu and C. psittaci Cal 10 were 1.0×10³ and 2.7×10⁴ per assay, respectively. The results demonstrated that the EBs of C. pneumoniae were detected with the test kit at different reaction intensities ranging from 6.0×10³ to 4.0×10⁴ per assay and that there was no correlation between EB number and morphology.

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The incidence of pulmonary tuberculosis in Japan has decreased remarkably. However, high frequency of tuberculosis can still be noticed in those subjects with underlying diseases, the so-called compromised host. This study aimed at to clarify the clinical characteristics of pulmonary tuberculosis in the compromised host. To achieve our objective we compare the clinical and radiological findings in patients with and without underlying diseases. This study comprised 44 pulmonary tuberculosis patients. Among these, 24 cases (55%) of tuberculosis occurred in those with a pre-existing disease. Most patients of the compromised host group were seen because of pulmonary symptomatology. There were 3 cases (15%) with cavitated pulmonary infiltration in the normal host group, whereas in the compromised host group 7 cases (29%) presented cavitary lesions. From these results, it was confirmed the high frequency of pulmonary tuberculosis in patients with an underlying disease. In addition, this work suggests that the presence of an atypical radiological findings should orient the clinician to start an early work-up for the diagnosis of pulmonary tuberculosis in those high risk group of patients.

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Herpes simplex virus type 1 (HSV1) and type 2 (HSV2) were differentiated on the basis of different plaque appearance on semicontinuous rabbit lens epithelial (RLE) cells. Plaques produced by HSV1 strains were small; the mean diameter was 1.29±0.37 mm 3 days after inoculation. HSV2 strains produced large and small plaques, with the ratio of large to small about 20: 1. The mean diameters of the large and the small plaques of HSV2 were 3.34±0.56 mm and 0.97±0.31 mm respectively 3 days after inoculation. The clones from the large plaques consistently produced large and small plaques and the small-plaque clones produced only small plaques. Round cells plus heterokaryotes were characteristic of the CPE of HSV1. Large plaques of HSV2 were produced by a large membranous syncytium that was liable to lyse. Small round cells were characteristic of the CPE of the small-plaque clones of HSV2. Glycoprotein C-negative (gC^-) strains produced intermediate-sized plaques and a few pin point ones that consisted of membranous syncytia and round cells, respectively. Except for the HF strain (a reference strain of HSV1 producing a membranous syncytium on RLE cells), the result of the differentiation of HSV1 (179 strains) and HSV2 (40 strains) with the RLE plaque assay system was consistent with that of Syva's monoclonal antibody assay system and the restriction endonuclease digestion method.

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The opsonic activity of plasma fibronectin (FN) by rat alveolar macrophage (AM) was examined, and the in vivo effect of FN in Staphylococcus aureus (S. aureus) experimental rat pneumonia was evaluated.
The chemiluminescence response of AM was enhanced by the presence of FN (300μg/ml) in S. aureus and Streptococcus pneumoniae, but was not enhanced in gram-negative rods (Haemophilus influenzae, Branhamella catarrhalis, Pseudomonas aeruginosa). FN (300μg/ml) promoted the phagocytosis of S. aureus by AM, but did not promote the bactericidal activity of that by AM. In the experimental rat pneumonia with S. aureus inoculation, plasma FN concentration decreased with time, but increased by the administration of FN (1mg). The number of bacteria in the lung, peripheral white blood cell and BAL fluid cell also decreased by the administration of FN. Furthermore, FN was significantly improved on inflammatory findings of rat lung tissue 24 hours after inoculation with S. aureus.
These results suggest that FN plays an important role as an opsonic by alveolar macrophage, and that FN has utility for clinical trials in patients with pneumonia.

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We recently had three patients with pelvic dead space infection caused by methicillin-resistant Staphylococcus aureus (MRSA) after total cystectomy for urothelial cancer. All were male and aged from 67 to 74 years old. As for underlying diseases, two of them had bladder cancer and one of them had bladder cancer and right ureteral cancer. Total cystectomy and ileal conduit were performed for two patients with bladder cancer, and total cystectomy, nephroureterectomy and ureterocutaneoustomy were performed for a patient with bladder cancer and ureteral cancer. Pelvic dead space infections caused by MRSA appeared after 15-30 days postoperatively. All patients were cured after we locally administered 0.5 g of vancomycin twice a day for 10-11 days from the drains to the pelvic dead spaces. All patients had preoperative antitumor chemotherapy and the postopertive administrations of β-lactams in common.
From these results, we suggest that local administration of vancomycin is effective for the pelvic dead space infection caused by MRSA after total cystectomy.

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Chlamydia pneumoniae (C. pneumoniae) was isolated from respiratory tract of 4 girls.
Case 1 is 5-year-old, diagnosed as pneumonia, had had a prolonged productive cough. She was treated with RKM with improvement of symptoms, however, C. pneumoniae was isolated repeatedly and was not deleted. Neither anti-mycoplasmal nor viral antibodies were positive and no significant pathogens were cultured from nasophrayngeal swabs.
Case 2, the sister of case 1, is a 3-year-old girl with acute bronchitis treated with EM. C. pneumoniae was negative on the tenth day after treatment.
Case 3, a 5-year-old girl, had a fever and was diagnosed as bronchopneumonia with a mild attack of bronchial asthma. She was initially treated with CFIX followed by therapy including EM. Her symptoms had disappeared after treatment and anti-mycoplasmal antibody was 1: 320.
Case 4 was an asymptomatic carrier of C. pneumoniae. Specimen was obtained at regular health examinations of junior high school. C. pneumoniae was isolated from a 14-year-old girl without respiratory symptoms.
Clinical figures of C. pneumoniae infections varies from asymptomatic carrier to pneumonia. Pathogens other than C. pneumoniae could modify symptoms of infections. Precise examinations of these cases would establish a proper management of a C. pneumoniae infection.

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We experienced an adult patient with EDTA-dependent pseudothrombocytopenia due to rubella virus infection. A 23-year-old male complaining of eruption and fever was admitted to our hospital on June 21, 1992. Laboratory findings on admission showed the platelet count 1.5×10⁴/μl with EDTA, but 11.5×10⁴/μl with heparin. Platelet agglutination was absorbed in the peripheral blood smear samples with EDTA. The hemagglutination inhibition titer for rubella virus raised from 1: 32 to 1: 52 in paired sera. We diagnosed this patient as having EDTA-dependent pseudothrombocytopenia and mild true thrombocytopenia due to rubella virus infection.

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