High tolerance of symbiotic larvae of Pocillopora damicornis to thermal stress.

BACKGROUND: When coral planulae, which use a horizontal mode of symbiont transmission, are inoculated with Symbiodinium, they suffer greater oxidative stress under strong light or high-temperature stress than non-symbiotic counterparts. Thus, dinoflagellate symbionts may become a source of reactive oxygen species (ROS) under stress. However, it remains unknown whether vertically transmitted symbionts negatively affect coral larvae under stress. We investigated the thermal tolerance of symbiotic planulae of a vertical transmitter coral, Pocillopora damicornis. RESULTS: P. damicornis larvae, which have a large number of symbionts, survived the high-temperature treatment (32 °C) for 2 weeks. Significant reductions in Symbiodinium cell density were observed, but these did not lead to increased mortality of planulae during the 2-week experimental period. Although no significant difference was detected in the percentage of apoptotic cells between temperature treatment groups, pre-bleaching larvae exposed to 31 °C tended to exhibit higher percentages of apoptotic (TUNEL-positive) cells in the gastrodermis than 32 °C-treated larvae, which contained reduced numbers of Symbiodiniumcells. CONCLUSIONS: Symbiotic larvae of P. damicornis survived well under high-temperature conditions, although their Symbiodinium cell density decreased. This suggests that P. damicornis larvae have the capacity to reduce the symbiont cell density without a harmful effect on their survivorship under thermal stress. Further studies on antioxidant systems and possible suppression of apoptotic pathways are necessary to elucidate the mechanism underlying the high thermal tolerance of symbiotic larvae of P.damicornis.

Cellular kinetics in growth anomalies of the scleractinian corals Porites australiensis and Montipora informis .

Growth anomalies (GAs) in corals are characterized by morphological abnormalities of the skeleton as well as polyps and coenosarcs. GAs commonly appear as protuberances with fewer polyps and are paler in color due to decreased zooxanthellae density. To test the hypothesis that morphological anomalies in GAs may be caused by unregulated cellular kinetics, the relative abundances of apoptotic cells and proliferating cells were compared between GAs and apparently healthy regions in 2 corals, Porites australiensis and Montipora informis. Apoptotic cells and proliferating cells were detected using TUNEL assays and BrdU incorporation assays, respectively. The labeling indices for apoptotic nuclei and BrdU-labeled nuclei were measured in the epidermis, oral gastrodermis, aboral gastrodermis, and calicodermis. The labeling index for apoptotic nuclei in the oral gastrodermis and the calicodermis was significantly lower in GAs than in healthy regions in both coral species. The index for BrdU-labeled cells in the calicodermis was significantly higher in GAs than in healthy regions in both coral species. When GA regions partially died, the GA tissues directly adjacent to the dead areas exhibited signs of necrosis, although some apoptotic cells were also present. Healthy oral gastrodermis adjacent to the border between the healthy and GA regions exhibited higher frequencies of apoptotic cells. These results suggest that apoptotic pathways were suppressed and cell proliferation was promoted in GA regions, although cells in GAs may die through both necrosis and apoptosis.

Skeletal structure and progression of growth anomalies in Porites australiensis in Okinawa, Japan.

Growth anomalies (GAs), one of the diseases recently reported for scleractinian corals, are characterized by an abnormal skeletal structure and reduced zooxanthella density. The pathological characteristics of GAs were studied in colonies of Porites australiensis on a reef in Kayo, Okinawa, Japan. Corallites in the GA region lost the skeletal architecture characteristic of P. australiensis, and polyp density had decreased in the GAs due to enlargement of both calices and the coenosteum. The gross productivity of isolated GA samples was lower than in healthy samples and decreased to almost 0 within 11 d after isolation. However, when GA samples were brought into contact with healthy-looking samples from the same colony, they fused and both the GA and healthy regions grew. Healthy samples fused with GA samples grew more slowly than those fused with healthy samples. For in situ GAs surrounded by healthy tissue, tissue death usually started at the center of the GA, probably due to a deficiency in the translocated energy supply from the surrounding tissue. The total area of the GA region and the dead area increased at a rate of 5.3 ± 2.9 cm2 yr-1. These results suggest that GA regions are maintained by energy supplies from surrounding healthy tissues and that GAs may have a negative impact on host corals.

Community-acquired Acinetobacter baumannii meningitis in a previously healthy 14-month-old boy.

We report a previously healthy 14-month-old boy who developed community-acquired Acinetobacter baumannii meningitis. He had no history of immunodeficiency, and was brought to Konan Kosei Hospital with a high fever and vomiting. His consciousness was clear, but neck stiffness was noted. Examination of the cerebrospinal fluid (CSF) revealed a cell count of 10 112/microl; protein, 216 mg/dl; and glucose, 9 mg/dl. A CSF test kit for bacterial capsular antigens (Pastorex Meningitis; Bio-Rad Laboratories) was positive for Haemophilus influenzae type b antigen. On day 3 of admission, the microorganism isolated by CSF culture was identified as A. baumannii. Therefore, his treatment was changed to meropenem hydrate from the initial therapy with panipenem/betamipron and ceftriaxone sodium hydrate. Because the CSF cell count remained elevated, meropenem hydrate was administered for a total of 19 days. The meningitis resolved with no sequelae.

T serotypes and antimicrobial susceptibilities of group A streptococcus isolates from pediatric pharyngotonsillitis.

Group A streptococcus (GAS) is a major cause of pediatric pharyngotonsillitis. In this study we determined the T serotype and antimicrobial susceptibility of GAS isolates from Japanese children. From January to December 2006, a total of 438 isolates of GAS were obtained from pharyngeal swabs of 438 children with pharyngotonsillitis. The commonest T serotype was type 1 (110 strains, 25.1%), followed by type 12 (107, 24.4%) and type 4 (77, 17.6%). All GAS isolated from pharyngeal swabs were susceptible to beta-lactams (benzylpenicillin, amoxicillin, cefotaxime, ceftriaxone, imipenem, panipenem, and cefditoren) and vancomycin, but 19.6, 19.6, 3.2, 11.6, and 27.6% were resistant to erythromycin, clarithromycin, clindamycin, minocycline, and norfloxacin, respectively. Resistance varied considerably with the T serotype. In particular, type 4 isolates had the highest resistance (67.5, 67.5, 26.0, and 53.2% were resistant to erythromycin, clarithromycin, minocycline, and norfloxacin, respectively).

DNA sequence analysis of varicella-zoster virus gene 62 from subclinical infections in healthy children immunized with the Oka varicella vaccine.

A live attenuated varicella vaccine, the Oka vaccine strain (vOka), is routinely administered to children in Japan and other countries, including the United States. vOka consists of a mixture of genotypically distinct variants, but little is known about the growth potential of each variants in vivo. We isolated varicella-zoster virus (VZV) DNA sequences from the peripheral blood mononuclear cells (PBMCs) of asymptomatic healthy children immunized with the Oka varicella vaccine. VZV gene 62 DNA fragments were detected in 5 of 166 (3.0%) PBMC samples by nested PCR within 5 weeks of the vaccination. Sequence analysis of VZV DNA from these five PBMC samples indicated that multiple viral clones in the vaccine could infect vaccinees and replicate in vivo. We also provide evidence that a nonsynonymous substitution at position 105356 may affect viral replication in vivo.

Five-day oral cefditoren pivoxil versus 10-day oral amoxicillin for pediatric group A streptococcal pharyngotonsillitis.

We prospectively compared the efficacy of oral cefditoren-pivoxil and conventional oral amoxicillin for pharyngotonsillitis caused by group A streptococcus in children. Either oral cefditoren-pivoxil (3 mg/kg t.i.d. for 5 days) or amoxicillin (10 mg/kg t.i.d. for 10 days) was administered to patients with group A streptococcal pharyngotonsillitis attending the pediatric outpatient clinic of Showa Hospital (Konan, Japan) between January and December 2006. Diagnosis was based on isolation of bacteria from a pharyngeal swab. Culture was always done to confirm eradication, and urinalysis and follow-up were performed at least once weekly for 4 weeks. Among 258 patients, 103 (aged 5.5 +/- 2.3 years) received cefditoren-pivoxil and 155 (aged 5.2 +/- 2.0 years) received amoxicillin. There were no significant between-group differences in age, sex, or symptoms. Eradication was confirmed in 99% (102/103) of the cefditoren-pivoxil group and 100% of the amoxicillin group. Recurrence within 4 weeks occurred in 8 and 15 patients in the cefditoren-pivoxil and amoxicillin groups, respectively, showing no significant difference in the recurrence rate, and all isolates had the same serotypes as before. There were no clinically significant adverse reactions or complications. The 50%/90% minimum inhibitory concentrations (microg/ml) of cefditoren-pivoxil and amoxicillin for the 258 isolates were < or =0.03/< or =0.03 and < or =0.03/0.06, respectively, so all isolates were susceptible to both agents. Because the efficacy for pediatric group A streptococcus pharyngotonsillitis was similar between oral cefditoren-pivoxil for 5 days and amoxicillin for 10 days, the shorter treatment period may make the former regimen preferable.