Diagnosis and molecular detection of Paenibacillus larvae, the causative agent of American foulbrood in honey bees in Saudi Arabia

2017 ◽  
Vol 37 (03) ◽  
pp. 137-148 ◽  
Author(s):  
Mohammad Javed Ansari ◽  
Ahmad Al-Ghamdi ◽  
Adgaba Nuru ◽  
Ashraf Mohamed Ahmed ◽  
Tahany H. Ayaad ◽  
...  

AbstractApis mellifera jemenitica, the only indigenous honey bee race of Saudi Arabia, is well adapted to the harsh local environmental conditions. A large-scale field survey was conducted to screen major Saudi Arabian beekeeping locations for infection byPaenibacillus larvae. Paenibacillus larvaeis one of the major bacterial pathogens of honey bee broods and is the causative agent of American foulbrood disease. Larvae from samples suspected of infection were collected from different apiaries and homogenized in phosphate-buffered saline. Bacteria were isolated on MYPGP agar medium. Two bacterial isolates, ksuPL3 and ksuPL5 (16S rRNA GenBank accession numbers, KR780760 and KR780761, respectively), were subjected to molecular identification usingP. larvae-specific primers. A BLAST sequence analysis revealed that the two isolates wereP. larvaewith more than 98% sequence identity. This detection ofP. larvaein the indigenous honey bee is the first recorded incidence of this pathogen in Saudi Arabia. This study emphasizes the need for the relevant authorities to take immediate steps towards treating and limiting the spread of this disease throughout the country.

2018 ◽  
Vol 7 (12) ◽  
Author(s):  
Diane G. Yost ◽  
Carolyn Chang ◽  
Lucy LeBlanc ◽  
Erin Cassin ◽  
Ceara Peterman ◽  
...  

We present the complete genome sequences of four phages that infect Paenibacillus larvae, the causative agent of American foulbrood disease in honeybees. The phages were isolated from beehives and beeswax products from Las Vegas, Nevada.


2019 ◽  
Vol 43 (25) ◽  
pp. 10109-10117 ◽  
Author(s):  
Diego Rodríguez-Hernández ◽  
Weilan G. P. Melo ◽  
Carla Menegatti ◽  
Vitor B. Lourenzon ◽  
Fábio S. do Nascimento ◽  
...  

Strong activity against the bacteria Paenibacillus larvae ATCC9545, the causative agent of the American Foulbrood disease of honey bees.


2015 ◽  
Vol 3 (5) ◽  
Author(s):  
Philippos K. Tsourkas ◽  
Diane G. Yost ◽  
Andrew Krohn ◽  
Lucy LeBlanc ◽  
Anna Zhang ◽  
...  

We present here the complete genome sequences of nine phages that infect Paenibacillus larvae , the causative agent of American foulbrood disease in honeybees. The phages were isolated from soil, propolis, and infected bees from three U.S. states. This is the largest number of P. larvae phage genomes sequenced in a single publication to date.


2021 ◽  
Author(s):  
◽  
Samantha Amy Montrose Graham

<p>Though the honey bee (Apis mellifera) is exposed to an extensive diversity of parasites and pathogens from multiple kingdoms, few are as devastating as American foulbrood. American foulbrood is a highly contagious bacterial disease, of which the causative agent (bacterium Paenibacillus larvae) infects honey bee brood through the ingestion of its spores, ultimately leading to the death of the infected larva and the collapse of the infected hive. Paenibacillus larvae’s genotypes (ERIC I-IV) exhibit differing ‘killing time’ of infected larvae, resulting in different larval and colony level virulence of the disease within hives.  American foulbrood is found in New Zealand’s registered hives, and poses a threat to the country’s apiculture industry. The first objective of this thesis was to perform a genetic analysis on New Zealand’s P. larvae field strains using the well-established methodology of rep-PCR with MBO REP1 primers. A total of 172 bacteria isolates were gathered from registered hives from 2011 to 2014 and examined. The MBO REP1 primer identifies the ‘beta’ genetic subgroups of P. larvae. By identifying beta subgroups, the ERIC genotypes that are present in New Zealand can also be concluded. The genetic analysis of P. larvae using rep-PCR is a first for New Zealand, and appears to be a first for Australasia. The second objective of this thesis was to conduct a temporal and geographical statistical analysis on American foulbrood infection rate trends in New Zealand’s national and regional, divided into seven regions, registered hives and apiaries from 1994 to 2013.  The genetic analysis of P. larvae detected three ‘beta’ genotypic subgroups: B, b, and Б. From these findings it was concluded that ERIC I and ERIC II are present in New Zealand. Previous to my findings, subgroup B and Б and ERIC II genotype had not been recorded outside of Europe. The statistical analysis reported that American foulbrood infection rates were significantly decreasing nationally. Results also reported that four of the seven regions’ infection rates were significantly decreasing, whilst three regions were significantly increasing.  Conclusions on the subgroups and genotypes present in New Zealand gives the first insight to the virulence and occurrence of P. larvae strains. Additionally, the use of rep-PCR for the genetic analysis of P. larvae enables this thesis to contribute to the increasing knowledge on American foulbrood. By examining the temporal and geographic dynamics of American foulbrood, the results allow for the evaluation of current management strategies and the most recent understanding on the national and regional infection rates of the disease.</p>


2017 ◽  
Vol 17 (5) ◽  
Author(s):  
Israel Alvarado ◽  
Joseph W Margotta ◽  
Mai M Aoki ◽  
Fernando Flores ◽  
Fresia Agudelo ◽  
...  

Abstract Paenibacillus larvae, a Gram-positive bacterium, causes American foulbrood (AFB) in honey bee larvae (Apis mellifera Linnaeus [Hymenoptera: Apidae]). P. larvae spores exit dormancy in the gut of bee larvae, the germinated cells proliferate, and ultimately bacteremia kills the host. Hence, spore germination is a required step for establishing AFB disease. We previously found that P. larvae spores germinate in response to l-tyrosine plus uric acid in vitro. Additionally, we determined that indole and phenol blocked spore germination. In this work, we evaluated the antagonistic effect of 35 indole and phenol analogs and identified strong inhibitors of P. larvae spore germination in vitro. We further tested the most promising candidate, 5-chloroindole, and found that it significantly reduced bacterial proliferation. Finally, feeding artificial worker jelly containing anti-germination compounds to AFB-exposed larvae significantly decreased AFB infection in laboratory-reared honey bee larvae. Together, these results suggest that inhibitors of P. larvae spore germination could provide another method to control AFB.


2015 ◽  
Vol 32 (6) ◽  
pp. 765-778 ◽  
Author(s):  
Sebastian Müller ◽  
Eva Garcia-Gonzalez ◽  
Elke Genersch ◽  
Roderich D. Süssmuth

The Gram-positive spore-forming bacterium Paenibacillus larvae is the causative agent of the fatal disease American Foulbrood of the western honey bee. This article highlights recent findings on secondary metabolites synthesized by P. larvae.


2021 ◽  
Author(s):  
◽  
Samantha Amy Montrose Graham

<p>Though the honey bee (Apis mellifera) is exposed to an extensive diversity of parasites and pathogens from multiple kingdoms, few are as devastating as American foulbrood. American foulbrood is a highly contagious bacterial disease, of which the causative agent (bacterium Paenibacillus larvae) infects honey bee brood through the ingestion of its spores, ultimately leading to the death of the infected larva and the collapse of the infected hive. Paenibacillus larvae’s genotypes (ERIC I-IV) exhibit differing ‘killing time’ of infected larvae, resulting in different larval and colony level virulence of the disease within hives.  American foulbrood is found in New Zealand’s registered hives, and poses a threat to the country’s apiculture industry. The first objective of this thesis was to perform a genetic analysis on New Zealand’s P. larvae field strains using the well-established methodology of rep-PCR with MBO REP1 primers. A total of 172 bacteria isolates were gathered from registered hives from 2011 to 2014 and examined. The MBO REP1 primer identifies the ‘beta’ genetic subgroups of P. larvae. By identifying beta subgroups, the ERIC genotypes that are present in New Zealand can also be concluded. The genetic analysis of P. larvae using rep-PCR is a first for New Zealand, and appears to be a first for Australasia. The second objective of this thesis was to conduct a temporal and geographical statistical analysis on American foulbrood infection rate trends in New Zealand’s national and regional, divided into seven regions, registered hives and apiaries from 1994 to 2013.  The genetic analysis of P. larvae detected three ‘beta’ genotypic subgroups: B, b, and Б. From these findings it was concluded that ERIC I and ERIC II are present in New Zealand. Previous to my findings, subgroup B and Б and ERIC II genotype had not been recorded outside of Europe. The statistical analysis reported that American foulbrood infection rates were significantly decreasing nationally. Results also reported that four of the seven regions’ infection rates were significantly decreasing, whilst three regions were significantly increasing.  Conclusions on the subgroups and genotypes present in New Zealand gives the first insight to the virulence and occurrence of P. larvae strains. Additionally, the use of rep-PCR for the genetic analysis of P. larvae enables this thesis to contribute to the increasing knowledge on American foulbrood. By examining the temporal and geographic dynamics of American foulbrood, the results allow for the evaluation of current management strategies and the most recent understanding on the national and regional infection rates of the disease.</p>


2005 ◽  
Vol 71 (11) ◽  
pp. 7551-7555 ◽  
Author(s):  
Elke Genersch ◽  
Ainura Ashiralieva ◽  
Ingemar Fries

ABSTRACT Virulence variations of Paenibacillus larvae subsp. larvae, the causative agent of American foulbrood disease of honeybees, were investigated by analysis of 16 field isolates of this pathogen, belonging to three previously characterized genotypes, as well as the type strain (ATCC 9545) of P. larvae subsp. larvae, with exposure bioassays. We demonstrated that the strain-specific 50% lethal concentrations varied within an order of magnitude and that differences in amount of time for the pathogen to kill 100% of the infected hosts (LT100) correlated with genotype. One genotype killed rather quickly, with a mean LT100 of 7.8 ± 1.7 days postinfection, while the other genotypes acted more slowly, with mean LT100s of 11.2 ± 0.8 and 11.6 ± 0.6 days postinfection.


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