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Bacterial community structure associated with white band disease in the elkhorn coral Acropora palmata determined using culture-independent 16S rRNA techniques

Culture-independent molecular (16S ribosomal RNA) techniques showed distinct differences in bacterial communities associated with white band disease (WBD) Type I and healthy elkhorn coral Acropora palmata. Differences were apparent at all levels, with a greater diversity present in tissues of diseased colonies. The bacterial community associated with remote, non-diseased coral was distinct from the apparently healthy tissues of infected corals several cm from the disease lesion. This demonstrates a whole-organism effect from what appears to be a localised disease lesion, an effect that has also been recently demonstrated in white plague-like disease in star coral Montastraea annularis. The pattern of bacterial community structure changes was similar to that recently demonstrated for white plague-like disease and black band disease. Some of the changes are likely to be explained by the colonisation of dead and degrading tissues by a micro-heterotroph community adapted to the decomposition of coral tissues. However, specific ribosomal types that are absent from healthy tissues appear consistently in all samples of each of the diseases. These ribotypes are closely related members of a group of alpha-proteobacteria that cause disease, notably juvenile oyster disease, in other marine organisms. It is clearly important that members of this group are isolated for challenge experiments to determine their role in the diseases.

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KARAKTERISTIK PENYAKIT WHITE BAND DISEASE DAN WHITE SYNDROME SECARA VISUAL DAN HISTOLOGI PADA KARANG Acropora sp. DARI PULAU GILI LABAK SUMENEP MADURA

ABSTRAKPenyakit white band disease dan white syndrome yang menyerang karang Acropora sp. di Pulau Gili Labak merupakan salah satu masalah yang perlu diperhatikan, sebab terjadinya kematian terumbu karang yang disebabkan oleh penyakit karang bukan hanya akan berpengaruh pada fungsi ekologis terumbu karang namun juga akan mempengaruhi fungsi ekonomis. Tujuan penelitian ini adalah untuk mendeteksi penyakit karang dengan metode histologi dengan studi kasus di Pulau Gili Labak, Poteran, Sumenep-Madura. Pengambilan sampel penelitian ini dilaksanakan pada bulan April 2017 di perairan Pulau Gili Labak Kabupaten Sumenep. Penelitian deteksi penyakit pada jaringan karang dengan metode histologi dilakukan pada Laboratorium Histologi Fakultas Kedokteran Universitas Brawijaya Malang. Analisa data dilakukan dengan metode analisa deskriptif. Ditemukan jaringan karang Acropora sp. yang terserang penyakit white band disease dan white syndrome yang terjadi banyak perbedaan antara jaringan karang yang sehat dengan yang sakit. Umumnya pada jaringan karang yang sehat terlihat susunan sel pada jaringan karang terlihat masih baik dan utuh, sedangkan pada jaringan karang yang sakit menunjukan bahwa jaringan mengalami degradasi disebabkan oleh jaringan yang lisis dan nekrosis, jaringan sakit terlihat hilang dan mulai hancur. Penyakit white band disease dicirikan dengan adanya jaringan yang mengelupas dari skeleton karang, sedangkan penyakit white syndrome hilangnya jaringan dimulai pada epidermis terlebih dahulu lalu merambat kedalam skeletonnya. ABSTRACTWhite band disease and white syndrome attacking Acropora sp. on the island of Gili Labak is one of the issues that need to be considered, because the loss of coral caused by disease will not only affect the ecological function of coral reefs but will also affect the economic function. The sampling of this research was conducted in April 2017 in the waters of Gili Labak Island of Sumenep Regency. Research on detection of coral tissue disease by histology method was done at Histology Laboratory Faculty of Medicine Universitas Brawijaya Malang. Data analysis was done by descriptive analysis method. Acropora sp. who are affected by white band disease and white syndrome showed the difference between healthy and affected coral tissues. Generally, on healthy coral tissue, the structure of the cells in coral tissue looks good and intact, whereas in diseased coral tissue show tissue degradation caused by lysis tissue and necrosis, tissue is lost and starts to disintegrate. The white band disease is characterized by the presence of peeling tissue from coral skeleton. While white syndrome disease loss of tissue begins in the epidermis first then propagate into their skeleton.

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Plague-Positive Mouse Fleas on Mice Before Plague Induced Die-Offs in Black-Tailed and White-Tailed Prairie Dogs.

Plague is a lethal zoonotic disease associated with rodents worldwide. In the western United States, plague outbreaks can decimate prairie dog (Cynomys spp.) colonies. However, it is unclear where the causative agent, Yersinia pestis, of this flea-borne disease is maintained between outbreaks, and what triggers plague-induced prairie dog die-offs. Less susceptible rodent hosts, such as mice, could serve to maintain the bacterium, transport infectious fleas across a colony, or introduce the pathogen to other colonies, possibly facilitating an outbreak. Here, we assess the potential role of two short-lived rodent species, North American deer mice (Peromyscus maniculatus) and Northern grasshopper mice (Onychomys leucogaster) in plague dynamics on prairie dog colonies. We live-trapped short-lived rodents and collected their fleas on black-tailed (Cynomys ludovicianus, Montana and South Dakota), white-tailed (Cynomys leucurus, Utah and Wyoming), and Utah prairie dog colonies (Cynomys parvidens, Utah) annually, from 2013 to 2016. Plague outbreaks occurred on colonies of all three species. In all study areas, deer mouse abundance was high the year before plague-induced prairie dog die-offs, but mouse abundance per colony was not predictive of plague die-offs in prairie dogs. We did not detect Y. pestis DNA in mouse fleas during prairie dog die-offs, but in three cases we found it beforehand. On one white-tailed prairie dog colony, we detected Y. pestis positive fleas on one grasshopper mouse and several prairie dogs live-trapped 10 days later, months before visible declines and plague-confirmed mortality of prairie dogs. On one black-tailed prairie dog colony, we detected Y. pestis positive fleas on two deer mice 3 months before evidence of plague was detected in prairie dogs or their fleas and also well before a plague-induced die-off. These observations of plague positive fleas on mice could represent early spillover events of Y. pestis from prairie dogs or an unknown reservoir, or possible movement of infectious fleas by mice.

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Plague in a complex of white-tailed prairie dogs and associated small mammals in Wyoming.

Fleas were collected from white-tailed prairie dogs (Cynomys leucurus) and other small mammals trapped on six grids during a field study near Meeteetse (Wyoming, USA) in 1989 and 1990 to investigate the dynamics of plague in this rodent population. Fleas were identified and tested for Yersinia pestis by mouse inoculation. Yersinia pestis-positive fleas were found on prairie dogs and in their burrows. Flea species on prairie dogs changed from spring to late summer. White-tailed prairie dog numbers were significantly lower in the presence of Y. pestis-positive fleas; however, affected populations generally recovered 1 to 2 yr following absence of detectable plague. Grids where recovery occurred had a high proportion of juvenile male prairie dogs. Eighteen flea species were identified on small mammals, six of which were infected with Y. pestis. Some flea species were associated with a particular small mammal species, while others were found on a broad range of host species. Flea species most important in the potential interchange of Y. pestis between associated small mammals and white-tailed prairie dogs were Oropsylla tuberculata cynomuris, Oropsylla idahoensis, and Oropsylla labis. Plague cycled through the white-tailed prairie dog complex in an unpredictable manner. Each summer the complex was a mixture of colonies variously impacted by plague: some were declining, some were unaffected by plague, and others were recovering from plague population declines. These data provide insight into the dynamics of plague in white-tailed prairie dog complexes, but predicting movement of plague is not yet possible and the role of associated mammals in maintenance of plague is not understood.

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Prevalence and Bacteria Associated with White Band Disease on Acropora sp. from Gili Labak Island Sumenep District Indonesia

Coral reefs have many problems including coral diseases. One of the coral diseases that infect Acropora sp. from Gili Labak Island is the White Band Disease (WBD). Their prevalence and bacteria associated with the WBD on Acropora sp. is warranted further investigation. This study aims to determine the disease prevalence and bacteria associated with WBD on Acropora sp. from the Gili Labak Island. The samples were collected from coral infected. The laboratory analysis includes bacterial isolation, DNA extraction, DNA amplification, electrophoresis, sequencing, and phylogenetic analysis. The results showed that the disease prevalences of WBD on Acropora sp. were between 0 to 23%, in which the highest prevalence was found in the site where marine tourism activities and boat mooring occurred. Four bacterial isolates were identified based on morphological features. These four isolates were then analyzed using the Mega 5.2 program and resulted in a complete nucleotide sequence and had similarities to the bacteria present in the Gen Bank through BLAST analysis. The result of BLAST analysis showed that ACWB2A isolate had 99% similarity with Vibrio alginolyticus bacteria; ACWB 6 had 99% similarity with Vibrio owensii; and isolates 5 and 8 had 99% similarity with Pseudoalteromonas rubra bacteria. These are the first record that Pseudoalteromonas rubra bacterium is associated with White Band Disease.

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Bacterial communities associated with healthy and Acropora white syndrome-affected corals from American Samoa

Acropora white syndrome (AWS) is characterized by rapid tissue loss revealing the white underlying skeleton and affects corals worldwide; however, reports of causal agents are conflicting. Samples were collected from healthy and diseased corals and seawater around American Samoa and bacteria associated with AWS characterized using both culture-dependent and culture-independent methods, from coral mucus and tissue slurries, respectively. Bacterial 16S rRNA gene clone libraries derived from coral tissue were dominated by the Gammaproteobacteria, and Jaccard's distances calculated between the clone libraries showed that those from diseased corals were more similar to each other than to those from healthy corals. 16S rRNA genes from 78 culturable coral mucus isolates also revealed a distinct partitioning of bacterial genera into healthy and diseased corals. Isolates identified as Vibrionaceae were further characterized by multilocus sequence typing, revealing that whilst several Vibrio spp. were found to be associated with AWS lesions, a recently described species, Vibrio owensii, was prevalent amongst cultured Vibrio isolates. Unaffected tissues from corals with AWS had a different microbiota than normal Acropora as found by others. Determining whether a microbial shift occurs prior to disease outbreaks will be a useful avenue of pursuit and could be helpful in detecting prodromal signs of coral disease prior to manifestation of lesions.

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