Summary auto-generated
Withering syndrome is a fatal disease affecting wild and cultured abalone (Haliotis spp.) along the west coast of North America, characterized by digestive gland degeneration and muscle atrophy leading to death. Researchers identified the causative agent as a previously unknown Gram-negative, obligate intracellular bacterium belonging to the family Rickettsiaceae, order Rickettsiales. The bacterium resides in membrane-bound vacuoles within gastrointestinal epithelial cells and cannot be cultured on synthetic media. Using morphological, serological, and 16S rDNA sequence analysis, the authors propose the provisional name 'Candidatus Xenohaliotis californiensis' for this pathogen. Phylogenetic analysis places it in the α-subclass of Proteobacteria, distinct from the four recognized α-Proteobacteria subtaxa. The bacterium is pleomorphic with multiple size variants and divides by binary fission. Importantly, the infection responds to tetracycline antibiotics (oxytetracycline and tetracycline) but not to chloramphenicol, clarithromycin, or sarafloxacin. Detection methods include tissue microscopy, PCR, and in situ hybridization using the organism's unique 16S rDNA sequence.
Key findings
- 'Candidatus Xenohaliotis californiensis' is a novel, unculturable, intracellular Gram-negative bacterium in family Rickettsiaceae that causes withering syndrome in abalone
- The bacterium is pleomorphic, divides by binary fission, lacks a visible peptidoglycan layer, and forms inclusions in gastrointestinal epithelial cell cytoplasm
- Phylogenetic analysis of 16S rDNA shows the organism belongs to α-Proteobacteria but represents a distinct lineage not belonging to recognized α-Proteobacteria subtaxa
- Oxytetracycline treatment effectively eliminates infection in both red and black abalone, while chloramphenicol, clarithromycin, and sarafloxacin are ineffective
- The unique 16S rDNA sequence enables reliable detection via PCR and in situ hybridization for diagnostic purposes
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Abstract
Withering syndrome is a fatal disease of wild and cultured abalone, Haliotis spp., that inhabit the west coast of North America. The aetiological agent of withering syndrome has recently been identified as a member of the family Rickettsiaceae in the order Rickettsiales. Using a combination of morphological, serological, life history and genomic (16S rDNA) characterization, we have identified this bacterium as a unique taxon and propose the provisional status of 'Candidatus Xenohaliotis californiensis`. The Gram-negative, obligate intracellular pleomorphic bacterium is found within membrane-bound vacuoles in the cytoplasm of abalone gastrointestinal epithelial cells. The bacterium is not cultivable on synthetic media or in fish cell lines (e.g. CHSE-214) and may be controlled by tetracyclines (oxytetracycline) but not by chloramphenicol, clarithromycin or sarafloxicin. Phylogenetic analysis based on the 16S rDNA of 'Candidatus Xenohaliotis californiensis' places it in the alpha-subclass of the class Proteobacteria but not to the four recognized subtaxa of the alpha-Proteobacteria (alpha-1, alpha-2, alpha-3 and alpha-4). The bacterium can be detected in tissue squashes stained with propidium iodide, microscopic examination of stained tissue sections, PCR or in situ hybridization. 'Candidatus Xenohaliotis californiensis' can be differentiated from other closely related alpha-Proteobacteria by its unique 16S rDNA sequence.