Increased otitis media rendering acute mastoiditis and mastoid lesions severe or intractable appear to be related to dominant drug-resistant strains and the dissemination of nursery school attendance. Acute mastoiditis involves middle-ear inflammation spreading to the antrum mastoideum and accompanied by subcutaneous abscess. This emergency condition risks progression to subperiosteal abscess and meningitis. Mastoid cavity opacity in computed tomography (CT) scan often occurs with recurrent or intractable otitis media similar to that with mastoiditis. Four of the 8 cases of mastoiditis we treated were infant in whom upper respiratory tract pneumococcus and group A streptococcus were detected. Treatment involved antibiotics and myringotomy in all cases and surgery in two. Nine of the 10 cases of mastoid lesions with otitis media we saw were infant. All had pneumococcus detected, with accociated sinusitis.

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Acute upper urinary tract infection may cause sepsis, especially in neonates and infants, mandating the choice of appropriate, effective antibacterials minimizing increasing bacterial resistance. Frequently prescribing broad-spectrum cephalosporinin is one such example. Different antibacterial therapies are initiated clinically due to treatment protocol differences among institutions, disease severity, etc. We studied the efficacy of cefazolin (CEZ), a first-generation cephalosporin, as first-line parenteral treatment in acute upper urinary tract infection. We found that 88.9％ of microbial infections have indications for CEZ. CEZ efficacy is 91.3％, and 97.2％ of urine cultures show negative results. Escherichia coli sensitivity to antibacterial agents is 90.9％ of the minimal inhibitory concentration (MIC) ＜4 for CEZ, 93.9％ of MIC＜1 for ceftazidime (CAZ), 63.6％ of MIC＜4 for ampicillin, and 81.8％ of MIC＜2 for gentamicin. CEZ thus has the same efficacy as CAZ and is more effective than other antibacterial agents against E. coli. We concluded that CEZ is an effective antibacterial in initial antibacterial pediatric therapy in acute upper urinary tract infection.

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Using quantitative Bayesian analysis as a clinical epidemiological approach, we developed a diagnosis for lower respiratory tract infection (LRTI) due to Methicillin-resistant Staphylococcus aureus (MRSA). We retrospectively reviewed the charts of 181 subjects―a derivation cohort-with MRSA retrieved from lower respiratory specimens June 2006 to March 2008. Dividing them into infection or colonization (no infection) groups, we compared them for the presence or absence of clinical parameters, including fever ＞38℃,MRSA ＞10⁶ CFU (colony-forming units)/mL, phagocytosis on Gram staining, serum albumin ＜3.0g/dL, and peripheral WBC count ＞15,000/mL. We them determined positive and negative likelihood ratios (LR＋, LR－) for these parameters to quantify MRSA-LRTI diagnostic probability based on combined likelihood ratios (Bayesian analysis). We then determined Bayesian MRSA-LRTI diagnostic probabilities (BDPs) in 40 subjects with respiratory MRSA―a validation cohort-from May 2008 to October 2008 clinically judged with either infection (n＝14) or colonization (n＝26) by infection control personnel (ICP) blinded to the test (parameter LR＋and LR－). BDPs (mean ± SD) quantified by combining the four parameters-fever, MRSA CFU, phagocytosis,and serum albumin-were 62.3±25.4％ for 14 judged with infection, and 40.2％±20.4％ for 26 patients judged with colonization (p＝0.005). Using a diagnostic probability of 51％ as the cut off, we compared positive and negative predictive Bayesian diagnoses ICP judgment, i.c., 77％ vs. 85％. The Bayesian approach proved useful in quantitatively diagnosing infectious disease such as MRSA-LRTI that lack established diagnostic, and may aid physicians in deciding the need for specific antimicrobial therapy.

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We studied the relationship between features of β-hemolytic streptococci (n＝45) isolated from blood in adult invasive infection and the clinical background factors observed from January 2001 through August at a hospital for the elderly. The meanage of subjects having invasive streptococcal infection with 22 invasive Streptococcus dysgalactiae subspecies equisimilis (SDSE) strains, 2 S. pyogenes isolates, and 21 S. agalactiae (GBS) was 80 years, and 85.7％ and 86.4％ had underly diseases in the GBS and SDSE infections. SDSE-infected were mainly emergency woman outpatients and GBS infected were mainly man inpatients. The clinical syndrome involved pneumonia, urosepsis, and cellulitis. GBS mortality was 14.3％and SDSE mortality 27.3％. Compared to survivors, nonsurvivors had more thrombocytopenia and marked serum C-reactive protein elevation when blood culture were performed. No difference was seen in white blood cell count between bath groups. Our observations suggest that blood culture should be obtained before antimicrobials administration in elderly individuals with underlying illness who are seen at the emergency department and have laboratory blood data suggestive of infectious disease.

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We analyzed the clinical background of 63 patients with serologically confirmed cat scratch disease (CSD). Age range of the patients was 0 to 83 years old and mean age was 35.0 years old. Seasonal patterns of cases was observed. A number of patients with CSD was increased during the summer and fall. The peak incidence of CSD occurred in October. Infection followed direct cat or dog contact. Cat contact occurred in 61 cases (96.8％) and dog contact in 2 cases (3.2％). A specific contact with kittens occurred in3 9 cases (61.9％). About 49.2％of patients had a cat scratch, 3.2％had a cat bite, 3.2％had a cat flea bite, 41.2％had no history of animal bite. The papule of inoculation site were seen in 27 cases (42.9％) of CSD. The upper extremities were the most likely locations for scratches. Sixty cases (95.2％) of CSD developed lymphadenopathy, 51.7％ of the involved nodes were in the axillary, 31.7％ were in the inguinal, 21.7％ were in the cervical, 16.7％ were in the elbow. The mean incubation period of patients with CSD was 18.9 days. The mean duration of lymphadenopathy after the treatment of antibiotics was 44.2 days. The mean value of white blood cell counts was 8130/µL. The mean value of C-reactive protein level was 2.83mg/dL.

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Adult autoimmune hemolytic anemia (AIHA) caused by influenza virus infection is very rare. I report a case of AIHA induced by type A influenza infection in a patient with alcoholic liver cirrhosis. A 67-year-old man with alcoholic liver cirrhosis was hospitalized with jaundice and ascites. At 7 days after admission, type A influenza infection was diagnosed, and this progressed to hemolytic anemia. Direct and indirect Coombsʼtests were positive, and his anemia was diagnosed as warm-type AIHA. Prednisolone administration improved the anemia, but the patient died due to hepatorenal syndrome 14 weeks after admission.

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A 67-year-old man clinically diagnosed a year earlier with sarcoidosis based on low-grade fever, lymphadenopathy, trunk skin rash, and histopathological skin tests was admitted for newly developing subcutaneous nodules on the trunk and arms and fever of 38℃. Although initially suspected of recurrent sarcoidosis,he was diagnosed with Mycobacterium chromogenicum infection isolated from skinl esion culture.Combined clarithromycin of 800 mg/day, ethambutol of 750mg/day, and embiomycin of 0.5g/day was started, after which fever declined and WBC count and CRP decreased to normal in a week. One month later, skin lesions had disappeared. This case is interesting considering the association of nontuberculous mycobacterial infection with sarcoidosis.

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The incidence of Acinetobacter baumannii pneumonia in hospital-acquired pneumonia in Japan is rare. We report a case of ventilator-associated A. baumanii pneumonia. A 69-year-old man admitted for fever was diagnosed with Streptococcus pneumoniae pneumonia based on chest radiography, urine antigen, and sputum examination. Despite appropriate antibiotics, the pneumonia progressed, necessitating intensive respiratory management. Ten days there after, he suffered sudden septic shock and superimposed pneumonia despite both carbapenem and fluoroquinolone administration. A. baumanii was detected from blood and sputum. Piperacilline/tazobactam, amikacin, and intensive care saved his life.

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