Draft Genome Sequence of Vibrio parahaemolyticus Strain M0605, Which Causes Severe Mortalities of Shrimps in Mexico

Gómez‐Gil, Bruno; Soto-Rodríguez, Sonia A.; Lozano, Rodolfo; Betancourt‐Lozano, Miguel

doi:10.1128/genomea.00055-14

Cited by 87 publications

(81 citation statements)

References 2 publications

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“…1B). None of the V. parahaemolyticus strains that we analyzed, except for RIMD2210633, contains T3SS2, consistent with previous reports that this system is associated with clinical isolates of V. parahaemolyticus only (4). Therefore, it is unlikely that the AHPND V. parahaemolyticus strains identified so far could infect human beings and cause gastroenteritis.…”

Section: Resultssupporting

confidence: 71%

“…V. alginolyticus strain 12G01 was used in bacterial competition assays (see below). All V. parahaemolyticus and V. alginolyticus strains were routinely cultured in marine Luria-Bertani (MLB) broth (Luria-Bertani broth containing 3% NaCl) or on marine minimal medium (MMM) agar (1.5% [wt/vol] 4 Cl) at 30°C. V. cholerae strain El Tor N16961 was used as prey in bacterial competition assays (see below) and was grown in LB at 37°C.…”

Section: Methodsmentioning

confidence: 99%

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Acute Hepatopancreatic Necrosis Disease-Causing Vibrio parahaemolyticus Strains Maintain an Antibacterial Type VI Secretion System with Versatile Effector Repertoires

Kinch

Ray

Dalia

et al. 2017

Appl Environ Microbiol

104

116

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Acute hepatopancreatic necrosis disease (AHPND) is a newly emerging shrimp disease that has severely damaged the global shrimp industry. AHPND is caused by toxic strains of Vibrio parahaemolyticus that have acquired a "selfish plasmid" encoding the deadly binary toxins PirA vp /PirB vp . To better understand the repertoire of virulence factors in AHPND-causing V. parahaemolyticus, we conducted a comparative analysis using the genome sequences of the clinical strain RIMD2210633 and of environmental non-AHPND and toxic AHPND isolates of V. parahaemolyticus. Interestingly, we found that all of the AHPND strains, but none of the non-AHPND strains, harbor the antibacterial type VI secretion system 1 (T6SS1), which we previously identified and characterized in the clinical isolate RIMD2210633. This finding suggests that the acquisition of this T6SS might confer to AHPND-causing V. parahaemolyticus a fitness advantage over competing bacteria and facilitate shrimp infection. Additionally, we found highly dynamic effector loci in the T6SS1 of AHPND-causing strains, leading to diverse effector repertoires. Our discovery provides novel insights into AHPND-causing pathogens and reveals a potential target for disease control.IMPORTANCE Acute hepatopancreatic necrosis disease (AHPND) is a serious disease that has caused severe damage and significant financial losses to the global shrimp industry. To better understand and prevent this shrimp disease, it is essential to thoroughly characterize its causative agent, Vibrio parahaemolyticus. Although the plasmidencoded binary toxins PirA vp /PirB vp have been shown to be the primary cause of AHPND, it remains unknown whether other virulent factors are commonly present in V. parahaemolyticus and might play important roles during shrimp infection. Here, we analyzed the genome sequences of clinical, non-AHPND, and AHPND strains to characterize their repertoires of key virulence determinants. Our studies reveal that an antibacterial type VI secretion system is associated with the AHPND strains and differentiates them from non-AHPND strains, similar to what was seen with the PirA/ PirB toxins. We propose that T6SS1 provides a selective advantage during shrimp infections.

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Section: Resultssupporting

confidence: 71%

Section: Methodsmentioning

confidence: 99%

Acute Hepatopancreatic Necrosis Disease-Causing Vibrio parahaemolyticus Strains Maintain an Antibacterial Type VI Secretion System with Versatile Effector Repertoires

Kinch

Ray

Dalia

et al. 2017

Appl Environ Microbiol

104

116

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“…shrimp | AHPND | Vibrio parahaemolyticus | Pir toxin | virulence plasmid S ince its first outbreak in China in 2009 (1), the newly emergent shrimp disease acute hepatopancreatic necrosis disease (AHPND) (2), originally known as early mortality syndrome, has spread through Southeast Asia to Vietnam, Malaysia, and Thailand to reach as far as Mexico in early 2013 (3,4). Shrimp production within the AHPND-affected region dropped to ∼60% compared with 2012, and the disease has caused global losses to the shrimp farming industry estimated at more than $1 billion per year (5).…”

mentioning

confidence: 99%

“…Previous studies on AHPND have focused on isolate variations (7), appropriate farming practices (8), or comparisons of draft genome sequences of AHPND-causing strains vs. non-AHPND strains (3,(9)(10)(11)(12). In our previous study (9), we used a next-generation sequencing (NGS) platform to sequence and compare three virulent strain and one nonvirulent strain, and found that a large (∼69-kbp) extrachromosomal plasmid was present in all AHPND V. parahaemolyticus strains but not in the non-AHPND strains.…”

mentioning

confidence: 99%

The opportunistic marine pathogen Vibrio parahaemolyticus becomes virulent by acquiring a plasmid that expresses a deadly toxin

Lee

Chen

Yang

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

461

442

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Acute hepatopancreatic necrosis disease (AHPND) is a severe, newly emergent penaeid shrimp disease caused by Vibrio parahaemolyticus that has already led to tremendous losses in the cultured shrimp industry. Until now, its disease-causing mechanism has remained unclear. Here we show that an AHPND-causing strain of V. parahaemolyticus contains a 70-kbp plasmid (pVA1) with a postsegregational killing system, and that the ability to cause disease is abolished by the natural absence or experimental deletion of the plasmid-encoded homologs of the Photorhabdus insect-related (Pir) toxins PirA and PirB. We determined the crystal structure of the V. parahaemolyticus PirA and PirB (PirAvp and PirBvp) proteins and found that the overall structural topology of PirAvp/PirBvp is very similar to that of the Bacillus Cry insecticidal toxin-like proteins, despite the low sequence identity (<10%). This structural similarity suggests that the putative PirABvp heterodimer might emulate the functional domains of the Cry protein, and in particular its pore-forming activity. The gene organization of pVA1 further suggested that pirABvp may be lost or acquired by horizontal gene transfer via transposition or homologous recombination.

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“…Recently, Sirikharin et al (14) identified two proteins (58 and 12 kDa) from extracts without cells from pathogenic strains of V. parahaemolyticus from Asia; these proteins were homologous to bacterial toxins against insects (www.enaca.org) and are the basis upon which the first AP3 primers were developed (T. W. Flegel, personal communication). These proteins were also identified in the genome of isolated strains in the present study (15) and had significant homology to bacterial delta endotoxins PirA and PirB of Photorhabdus luminescens, which are highly active against insects (32).…”

Section: Discussionmentioning

confidence: 82%

Field and Experimental Evidence of Vibrio parahaemolyticus as the Causative Agent of Acute Hepatopancreatic Necrosis Disease of Cultured Shrimp (Litopenaeus vannamei) in Northwestern Mexico

Soto-Rodríguez

Gómez‐Gil

Lozano‐Olvera

et al. 2015

Appl Environ Microbiol

Self Cite

308

212

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Moribund shrimp affected by acute hepatopancreatic necrosis disease (AHPND) from farms in northwestern Mexico were sampled for bacteriological and histological analysis. Bacterial isolates were molecularly identified as Vibrio parahaemolyticus by the presence of the tlh gene. The tdh-negative, trh-negative, and tlh-positive V. parahaemolyticus strains were further characterized by repetitive extragenic palindromic element-PCR (rep-PCR), and primers AP1, AP2, AP3, and AP and an ems2 IQ2000 detection kit (GeneReach, Taiwan) were used in the diagnostic tests for AHPND. The V. parahaemolyticus strains were used in immersion challenges with shrimp, and farmed and challenged shrimp presented the same clinical and pathological symptoms: lethargy, empty gut, pale and aqueous hepatopancreas, and expanded chromatophores. Using histological analysis and bacterial density count, three stages of AHNPD (initial, acute, and terminal) were identified in the affected shrimp. The pathognomonic lesions indicating severe desquamation of tubular epithelial cells of the hepatopancreas were observed in both challenged and pond-infected shrimp. The results showed that different V. parahaemolyticus strains have different virulences; some of the less virulent strains do not induce 100% mortality, and mortality rates also rise more slowly than they do for the more virulent strains. The virulence of V. parahaemolyticus strains was dose dependent, where the threshold infective density was 10 4 CFU ml ؊1 ; below that density, no mortality was observed. The AP3 primer set had the best sensitivity and specificity. Field and experimental results showed that the V. parahaemolyticus strain that causes AHPND acts as a primary pathogen for shrimp in Mexico compared with the V. parahaemolyticus strains reported to date.

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Draft Genome Sequence of Vibrio parahaemolyticus Strain M0605, Which Causes Severe Mortalities of Shrimps in Mexico

Cited by 87 publications

References 2 publications

Acute Hepatopancreatic Necrosis Disease-Causing Vibrio parahaemolyticus Strains Maintain an Antibacterial Type VI Secretion System with Versatile Effector Repertoires

Acute Hepatopancreatic Necrosis Disease-Causing Vibrio parahaemolyticus Strains Maintain an Antibacterial Type VI Secretion System with Versatile Effector Repertoires

The opportunistic marine pathogen Vibrio parahaemolyticus becomes virulent by acquiring a plasmid that expresses a deadly toxin

Field and Experimental Evidence of Vibrio parahaemolyticus as the Causative Agent of Acute Hepatopancreatic Necrosis Disease of Cultured Shrimp (Litopenaeus vannamei) in Northwestern Mexico

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