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Tryland M.,Section for Arctic Veterinary Medicine | Nesbakken T.,Section for Food Safety | Robertson L.,Section for Microbiology | Grahek-Ogden D.,Norwegian Scientific Committee for Food Safety | Lunestad B.T.,National Institute of Nutrition And Seafood Research
Zoonoses and Public Health | Year: 2014

Only a few countries worldwide hunt seals and whales commercially. In Norway, hooded and harp seals and minke whales are commercially harvested, and coastal seals (harbour and grey seals) are hunted as game. Marine mammal meat is sold to the public and thus included in general microbiological meat control regulations. Slaughtering and dressing of marine mammals are performed in the open air on deck, and many factors on board sealing or whaling vessels may affect meat quality, such as the ice used for cooling whale meat and the seawater used for cleaning, storage of whale meat in the open air until ambient temperature is reached, and the hygienic conditions of equipment, decks, and other surfaces. Based on existing reports, it appears that meat of seal and whale does not usually represent a microbiological hazard to consumers in Norway, because human disease has not been associated with consumption of such foods. However, as hygienic control on marine mammal meat is ad hoc, mainly based on spot-testing, and addresses very few human pathogens, this conclusion may be premature. Additionally, few data from surveys or systematic quality control screenings have been published. This review examines the occurrence of potential human pathogens in marine mammals, as well as critical points for contamination of meat during the slaughter, dressing, cooling, storage and processing of meat. Some zoonotic agents are of particular relevance as foodborne pathogens, such as Trichinella spp., Toxoplasma gondii, Salmonella and Leptospira spp. In addition, Mycoplasma spp. parapoxvirus and Mycobacterium spp. constitute occupational risks during handling of marine mammals and marine mammal products. Adequate training in hygienic procedures is necessary to minimize the risk of contamination on board, and acquiring further data is essential for obtaining a realistic assessment of the microbiological risk to humans from consuming marine mammal meat. © 2013 Blackwell Verlag GmbH.

Larsen A.K.,Section for Arctic Veterinary Medicine | Larsen A.K.,Member of the Fram Center | Nymo I.H.,Section for Arctic Veterinary Medicine | Nymo I.H.,Member of the Fram Center | And 5 more authors.
PLoS ONE | Year: 2013

A high prevalence of Brucella pinnipedialis serology and bacteriology positive animals has been found in the Northeast Atlantic stock of hooded seal (Cystophora cristata); however no associated gross pathological changes have been identified. Marine mammal brucellae have previously displayed different infection patterns in human and murine macrophages. To investigate if marine mammal Brucella spp. are able to invade and multiply in cells originating from a presumed host species, we infected alveolar macrophages from hooded seal with a B. pinnipedialis hooded seal isolate. Hooded seal alveolar macrophages were also challenged with B. pinnipedialis reference strain (NCTC 12890) from harbor seal (Phoca vitulina), B. ceti reference strain (NCTC 12891) from harbor porpoise (Phocoena phocoena) and a B. ceti Atlantic white-sided dolphin (Lagenorhynchus acutus) isolate (M83/07/1), to evaluate possible species-specific differences. Brucella suis 1330 was included as a positive control. Alveolar macrophages were obtained by post mortem bronchoalveolar lavage of euthanized hooded seals. Phenotyping of cells in the lavage fluid was executed by flow cytometry using the surface markers CD14 and CD18. Cultured lavage cells were identified as alveolar macrophages based on morphology, expression of surface markers and phagocytic ability. Alveolar macrophages were challenged with Brucella spp. in a gentamicin protection assay. Following infection, cell lysates from different time points were plated and evaluated quantitatively for colony forming units. Intracellular presence of B. pinnipedialis hooded seal isolate was verified by immunocytochemistry. Our results show that the marine mammal brucellae were able to enter hooded seal alveolar macrophages; however, they did not multiply intracellularly and were eliminated within 48 hours, to the contrary of B. suis that showed the classical pattern of a pathogenic strain. In conclusion, none of the four marine mammal strains tested were able to establish a persistent infection in primary alveolar macrophages from hooded seal. © 2013 Larsen et al.

Kashulin A.,University of Tromso | Sorum H.,Section for Microbiology
Aquaculture | Year: 2014

Cold-Water Vibriosis (CWV) is a well-known disease which significantly influences the aquaculture industry of the North Atlantic coasts (Egidius et al., 1981). Due to wide implementation of apparently effective vaccines in all farmed Atlantic salmon (Salmo salar) the phenomenon of CWV was not a research focus for nearly two decades (Lillehaug, 1990, 1991). Although prevented by vaccination since the 1980s, CWV was again reported in farmed, vaccinated Atlantic salmon in 2012 (Johansen, 2012). Since CWV emerged as a recognized infection in the early 1980s (Egidius et al., 1981; Sørum et al., 1990), several attempts have been undertaken to identify the initial steps of the pathogenesis of CWV. However, no final explanation to how Aliivibrio (Vibrio) salmonicida enters the host has been reported. In this study, we present a novel and simple model for analyzing the initial steps of CWV. Our results demonstrate that initiation of CWV is more complex than was previously thought. In particular, A. (V.) salmonicida enters the host much faster than was anticipated. To identify the initial pathogenic steps in CWV, Atlantic salmon fry were differentially immersed in a suspension of A. (V.) salmonicida and the number of bacteria entering the host was measured. The putative roles of the gills, skin, rectal and oral routes as well as the role of the fin blood vessels as portals of infection were investigated. Bacterial counts were obtained from freshly collected blood samples, thus representing immediate snapshots of the early stages of host invasion. The results clearly indicated that skin was a major route of infection. The experimental design reported in this study provides a new, rapid and cost-effective model for studying CWV. © 2013 Elsevier B.V.

Bjelland A.M.,Section for Microbiology | Johansen R.,Norwegian Veterinary Institute | Brudal E.,Section for Microbiology | Hansen H.,University of Tromso | And 2 more authors.
Microbial Pathogenesis | Year: 2012

Cold-water vibriosis (CV) is a bacterial septicemia of farmed salmonid fish and cod caused by the Gram-negative bacterium Vibrio (Aliivibrio) salmonicida. To study the pathogenesis of this marine pathogen, Atlantic salmon was experimentally infected by immersion challenge with wild type V. salmonicida and the bacterial distribution in different organs was investigated at different time points. V. salmonicida was identified in the blood as early as 2 h after challenge demonstrating a rapid establishment of bacteremia without an initial period of colonization of the host. Two days after immersion challenge, only a few V. salmonicida were identified in the intestines, but the amount increased with time. In prolonged CV cases, V. salmonicida was the dominating bacterium of the gut microbiota causing a release of the pathogen to the water. We hypothesize that V. salmonicida uses the blood volume for proliferation during the infection of the fish and the salmonid intestine as a reservoir that favors survival and transmission. In addition, a motility-deficient V. salmonicida strain led us to investigate the impact of motility in the CV pathogenesis by comparing the virulence properties of the mutant with the wild type LFI1238 strain in both i.p. and immersion challenge experiments. V. salmonicida was shown to be highly dependent on motility to gain access to the fish host. After invasion, motility was no longer required for virulence, but the absence of normal flagellation delayed the disease development. © 2011 Elsevier Ltd.

Bjelland A.M.,Section for Microbiology | Sorum H.,Section for Microbiology | Tegegne D.A.,University of Tromso | Winther-Larsen H.C.,Section for Microbiology | And 3 more authors.
Infection and Immunity | Year: 2012

Vibrio (Aliivibrio) salmonicida is the causal agent of cold-water vibriosis, a fatal bacterial septicemia primarily of farmed salmonid fish. The molecular mechanisms of invasion, colonization, and growth of V. salmonicida in the host are still largely unknown, and few virulence factors have been identified. Quorum sensing (QS) is a cell-to-cell communication system known to regulate virulence and other activities in several bacterial species. The genome of V. salmonicida LFI1238 encodes products presumably involved in several QS systems. In this study, the gene encoding LitR, a homolog of the master regulator of QS in V. fischeri, was deleted. Compared to the parental strain, the litR mutant showed increased motility, adhesion, cell-to-cell aggregation, and biofilm formation. Furthermore, the litR mutant produced less cryptic bioluminescence, whereas production of acylhomoserine lactones was unaffected. Our results also indicate a salinity-sensitive regulation of LitR. Finally, reduced mortality was observed in Atlantic salmon infected with the litR mutant, implying that the fish were more susceptible to infection with the wild type than with the mutant strain. We hypothesize that LitR inhibits biofilm formation and favors planktonic growth, with the latter being more adapted for pathogenesis in the fish host. © 2012, American Society for Microbiology.

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