We report a familial case of visceral larva migrans (VLM) caused by Toxocara canis larvae. Patient 1 was a 45-year-old man who presented to our university hospital complaining of mild fever, general fatigue, and headache. Patient 2 was a 71-year-old man and was the father of Patient 1; he presented complaining of cough and hyper-viscous white sputum. Laboratory data from both patients showed extensive eosinophilia, their chest X-ray findings revealed multiple pulmonary infiltrates, and their bronchoalveolar lavage fluid (BALF) showed an elevated eosinophil count. The diagnosis of VLM was made based on a positive result in a serological test using T. canis larval excretory-secretory both in the serum and BALF. T. canis larvae were identified in meat that was prepared from chicken taken from the same source as that ingested. This is the first report to identify antibodies in BALF in patients with VLM.

To investigate the dynamic interplay between human immunodeficiency virus type I (HIV-1) replication and the extent of immune destruction in HIV-1-infected children, virus burden in lymphoid tissues (LN) and peripheral blood was compared with changes in LN architecture and cytokine levels constitutively expressed in LN. In agreement with results of a preliminary study, the plasma HIV-1 RNA level correlated with the amount of provirus in LN. However, the level was also associated with a degree of destruction of lymphoid follicular architecture and an alteration of immune cytokine expression. Expression of interleukin (IL)-4 was higher in LN with higher virus replication. Reduction of plasma viremia was associated with an increase in IL-2 mRNA levels in LN. These findings suggest that measurable virus burden in the peripheral blood is not a simple reflection of viral replication in LN but is also influenced by the extent of progressive immune destruction.

We attempted the simultaneous detection of cytomegalovirus DNA (CMV-DNA) and Pneumocystis carinii (carinii-DNA) in sputum samples obtained from 20 patients with haematological neoplasm with pneumonia, using rapid cycle DNA amplification (capillary PCR). We used a thermal cycler for capillary PCR which featured recirculation of hot air for rapid temperature control of 10 microliters reaction samples in thin glass capillary tubes. We extracted DNA from patients' sputa using a simple method. A comparison of the results obtained using the phenol extraction-ethanol precipitation method and those obtained using our simple method was made, and demonstrated complete agreement between the two. For detection of CMV-DNA and P. carinii-DNA with capillary PCR it was not necessary to vary temperature setting based on the primers used. Therefore, capillary PCR was used for the simultaneous detection of CMV and P. carinii. After amplification, the total time required for which was 20 min, amplified products were electrophoresed on agarose gels and visualized with ethidium bromide. Product sensitivity was higher with capillary PCR than with conventional PCR. We conclude that capillary PCR amplification is a valuable tool for rapid and simple diagnosis of CMV and P. carinii pneumonias.

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We examined biological properties of strains of methicillin-resistant Staphylococcus aureus (MRSA) which were isolated in our ward in 1991 and 1992. A total of 47 MRSA strains were isolated in 1991 and 64 in 1992. The majority of these strains of MRSA were highly resistant to DMPPC, CEZ and IPM, and were intermediately resistant to MINO. All these strains were, however, sensitive to VCM. The number of coagulase type II strains increased from 22 (46.8%) to 51 (79.7%), and that of enterotoxin type A strains from 27 (57.4%) in 1991 to 47 (73.4%) in 1992. The number of strains which produce Toxic Shock Syndrome Toxin-1 (TSST-1) also increased from 19 (40.4%) to 45 (70.3%), and those strains that produce beta-lactamase decreased from 24 (51.1%) to 21 (32.8%). From the above results, we confirmed the recent change in types of the epidemic strains of MRSA. Namely, there was a marked increase in number of strains which produce type II coagulase type A enterotoxin and TSST-1. For the prevention of a patient to patient-, room to room- and ward to ward-spread, strict isolation was indicated both the infection patients, immunocompromised patients who were at high risk for the infection and the proved carriers. Treatment with VCM was started immediately if MRSA infection was thought plausible. These countermeasures seemed to succeed in reducing the incidence of the infection in our ward.