MicrobiologyBytes

The UK commercial poultry industry is an important industry to the British government, the consumer and farmers alike. Worth an estimated £3.4 billion at retail value, producing over 174 million birds for consumption per year, poultry diseases are of widespread interest, both from the point-of-view of understanding different poultry farming methods, and in terms of studying the potential impact of different diseases on poultry. However, our knowledge of how poultry farms in the UK are connected to each other by the movement of people and equipment is more limited. This is essential for effective prevention and control for potential outbreaks of diseases transmitted by the movement of people and equipment between farms within the commercial poultry industry. Diseases spread in such a way include avian influenza viruses (AIV), Newcastle disease virus, Salmonella and Campylobacter species.

An epidemic of any poultry disease with high mortality or which is zoonotic, such as AIV, would result in the culling of significant numbers of birds, as seen in the Netherlands in 2003 and Italy in 2000. Such an epidemic would cost the UK government millions of pounds in compensation costs, with further economic losses through reduction of international and UK consumption of British poultry. In order to better inform policy advisers and makers on the potential for a large epidemic in the UK, we investigate the role that interactions amongst premises within the British commercial poultry industry could play in promoting an AIV epidemic, given an introduction of the virus in a specific part of poultry industry in the UK.

Poultry premises using multiple slaughterhouses lead to a large number of premises being potentially connected, with the resultant potential for large and sometimes widespread epidemics. Catching companies can also potentially link a large proportion of the poultry population. Critical to this is the maximum distance traveled by catching companies between premises and whether or not between-species transmission could occur within individual premises. Premises closely linked by proximity may result in connections being formed between different species and or sectors within the industry.

Even quite well-contained epidemics have the potential for geographically widespread dissemination, potentially resulting in severe logistical problems for epidemic control, and with economic impact on a large part of the country. Premises sending birds to multiple slaughterhouses or housing multiple species may act as a bridge between otherwise separate sectors of the industry, resulting in the potential for large epidemics. Investment into further data collection and analyses on the importance of industry structure as a determinant for spread of AIV would enable us to use the results from this study to contribute to policy on disease control.

Contact structures in the poultry industry in Great Britain: Exploring transmission routes for a potential avian influenza virus epidemic. BMC Vet Res. 2008 4: 27

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• H5N1 influenza is no longer bird flu
• Negative sense RNA viruses
• Human Infections with Avian Influenza H5N1 Viruses
• Media coverage affects how people perceive the threat of disease

Listeria monocytogenes is a pathogen transmitted through contaminated food and is responsible for severe infections, including meningitis and abortion in animals and humans. It is known that many distinct strains of this pathogen exist, and that they differ in their virulence and epidemic potential. Unfortunately, there is currently no standard definition of strains and no comprehensive overview of their evolution. To tackle these serious limitations to the control of listeriosis and to improve knowledge of how virulence evolves, a new paper characterizes a large collection of isolates with sequence-based genotyping methods. The authors were able to identify precisely the most prevalent clones of L. monocytogenes, i.e., groups of isolates that descend from a single ancestral bacterium, which can now be characterized further for diagnostic purposes and determination of their precise ecology and virulence potential. They also determined how these clones evolved from their common ancestor and the evolutionary history by which they acquired their phenotypic characteristics, such as antigenic structures. Finally, they show that some particular strains tend to lose a virulence factor that plays a crucial role in infection in humans. This is a rare example of evolution towards reduced virulence of pathogens, and the discovery of the selective forces behind this phenomenon may have important epidemiological and biological implications.

A New Perspective on Listeria monocytogenes Evolution. 2008 PLoS Pathogens, 4 (9)
Listeria monocytogenes is a model organism for cellular microbiology and host–pathogen interaction studies and an important food-borne pathogen widespread in the environment, thus representing an attractive model to study the evolution of virulence. The phylogenetic structure of L. monocytogenes was determined by sequencing internal portions of seven housekeeping genes (3,288 nucleotides) in 360 representative isolates. Fifty-eight of the 126 disclosed sequence types were grouped into seven well-demarcated clonal complexes (clones) that comprised almost 75% of clinical isolates. Each clone had a unique or dominant serotype (4b for clones 1, 2 and 4, 1/2b for clones 3 and 5, 1/2a for clone 7, and 1/2c for clone 9), with no association of clones with clinical forms of human listeriosis. Homologous recombination was extremely limited, implying long-term genetic stability of multilocus genotypes over time. Bayesian analysis based on 438 SNPs recovered the three previously defined lineages, plus one unclassified isolate of mixed ancestry. The phylogenetic distribution of serotypes indicated that serotype 4b evolved once from 1/2b, the likely ancestral serotype of lineage I. Serotype 1/2c derived once from 1/2a, with reference strain EGDe (1/2a) likely representing an intermediate evolutionary state. In contrast to housekeeping genes, the virulence factor internalin (InlA) evolved by localized recombination resulting in a mosaic pattern, with convergent evolution indicative of natural selection towards a truncation of InlA protein. This work provides a reference evolutionary framework for future studies on L. monocytogenes epidemiology, ecology, and virulence.

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• Listeriosis in the UK up 80%
• Listeria monocytogenes replication in macrophage vacuoles
• Joseph Lister
• Video/Animations of Intracellular Pathogens

Ale, fermented using the yeast Saccharomyces cerevisiae, has been brewed since ancient times, possibly as early as 6000 BC. In contrast, lager beer, with its hallmark low-temperature fermentation (5°C–14°C), is a more recently developed alcoholic beverage, arising in Bavaria near the end of the Middle Ages. Lager gained worldwide popularity from the late 1800s with the advent of refrigeration, which allowed the necessary cool fermentation temperatures year-round. The lager yeast, Saccharomyces pastorianus, is distinct from S. cerevisiae in both physiological and genetic characteristics and is thought to have arisen in response to selective pressures from cold brewing temperatures. This selection may have taken place during successive rounds of cold-temperature fermentations resulting from a 16th century Bavarian law that prohibited brewing during summer months because of the inferior quality of summer-brewed beers. S. pastorianus has been shown to be a hybrid organism, and it is likely that lager yeast arose by “instantaneous speciation” due to an interspecific hybridization event between Saccharomyces cerevisiae and Saccharomyces bayanus that occurred during these selective growth conditions.

By examining the genome of S. pastorianus, a recently-published paper shows that the hybridization between yeast species which gave rise to lager yeasts happened independently at least twice, not once as previously thought, giving rise to two broad families of lager beer, Group 1 yeasts used to brew “Saaz”-type beers such as Pilsner and Budweiser, and Group 2 yeasts used to brew “Frohberg” lagers such as Orangeboom and Heineken. Both groups contain multiple copies of genes beneficial to brewing, such as those that ferment maltose. Likewise, genes that adversely affect the process have been lost.

This work paves the way for characterization of specific genetic features of each strain that could aid in the brewing process, and could lead to new insights on how to directly control flavor and aroma in beer.

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Reconstruction of the genome origins and evolution of the hybrid lager yeast Saccharomyces pastorianus. Genome Research, September 11, 2008
Inter-specific hybridization leading to abrupt speciation is a well-known, common mechanism in angiosperm evolution; only recently, however, have similar hybridization and speciation mechanisms been documented to occur frequently among the closely related group of sensu stricto Saccharomyces yeasts. The economically important lager beer yeast Saccharomyces pastorianus is such a hybrid, formed by the union of Saccharomyces cerevisiae and Saccharomyces bayanus-related yeasts; efforts to understand its complex genome, searching for both biological and brewing-related insights, have been underway since its hybrid nature was first discovered. It had been generally thought that a single hybridization event resulted in a unique S. pastorianus species, but it has been recently postulated that there have been two or more hybridization events. Here, we show that there may have been two independent origins of S. pastorianus strains, and that each independent group – defined by characteristic genome rearrangements, copy number variations, ploidy differences, and DNA sequence polymorphisms – is correlated with specific breweries and/or geographic locations. Finally, by reconstructing common ancestral genomes via array-CGH data analysis and by comparing representative DNA sequences of the S. pastorianus strains with those of many different S. cerevisiae isolates, we have determined that the most likely S. cerevisiae ancestral parent for each of the independent S. pastorianus groups was an ale yeast, with different, but closely related ale strains contributing to each group’s parentage.

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• Brewing Beer
• In Praise of Yeast

Campylobacter jejuni is a bacterium commonly found in the guts of birds and mammals. In humans, it is responsible for causing more gastro-enteritis than any other identified bacterial species. Humans may contract campylobacter infections from a variety of sources. Eating raw or undercooked meat or poultry, and poor food hygiene that leads to cross-contamination of uncooked food, can cause human disease. However, humans may be exposed to the faeces of infected wild animals, and Campylobacter can survive in water. Contamination of drinking water can lead to outbreaks, and previous genetic studies have suggested that livestock are not the principal source of human infection.

A new study found that 97% of campylobacteriosis cases sampled in Lancashire were caused by bacteria typically found in chicken and livestock. The work is based on DNA-sequence comparison of thousands of bacteria collected from human patients and animal carriers. Campylobacter jejuni causes more cases of gastroenteritis in the developed world than any other bacterial pathogen, including E. coli, Salmonella, Clostridium and Listeria combined. Wild and domestic animals act as natural reservoirs for the disease, which can also survive in water and soil. However, the relative importance of these sources is unclear, and recent work has suggested that livestock are not the main reservoir for human disease. Researchers sequenced the DNA of bacteria collected from 1,231 patients and compared it to C. jejuni DNA sequences collected from wild and domestic animals, and the environment. They used evolutionary modeling to trace the ancestry of human C. jejuni back to one of seven source populations. In 57% of cases, the bacteria could be traced to chicken, and in 35 percent to cattle. Wild animal and environmental sources were accountable for just 3% of disease. These results imply that the primary transmission route is the food chain and also add new impetus to measures that reduce infection in livestock and prevent food-borne transmission.

Tracing the Source of Campylobacteriosis. 2008 PLoS Genet 4(9): e1000203
Campylobacter jejuni is the leading cause of bacterial gastro-enteritis in the developed world. It is thought to infect 2–3 million people a year in the US alone, at a cost to the economy in excess of US$4 billion. C. jejuni is a widespread zoonotic pathogen that is carried by animals farmed for meat and poultry. A connection with contaminated food is recognized, but C. jejuni is also commonly found in wild animals and water sources. Phylogenetic studies have suggested that genotypes pathogenic to humans bear greatest resemblance to non-livestock isolates. Moreover, seasonal variation in campylobacteriosis bears the hallmarks of water-borne disease, and certain outbreaks have been attributed to contamination of drinking water. As a result, the relative importance of these reservoirs to human disease is controversial. We use multilocus sequence typing to genotype 1,231 cases of C. jejuni isolated from patients in Lancashire, England. By modeling the DNA sequence evolution and zoonotic transmission of C. jejuni between host species and the environment, we assign human cases probabilistically to source populations. Our novel population genetics approach reveals that the vast majority (97%) of sporadic disease can be attributed to animals farmed for meat and poultry. Chicken and cattle are the principal sources of C. jejuni pathogenic to humans, whereas wild animal and environmental sources are responsible for just 3% of disease. Our results imply that the primary transmission route is through the food chain, and suggest that incidence could be dramatically reduced by enhanced on-farm biosecurity or preventing food-borne transmission.

Related:

• Campylobacter jejuni
• Utilization of iron by Campylobacter jejuni
• How Campylobacter jejuni survives within cells
• Protein promotes antibiotic resistance in Campylobacter

BBC news

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It was widely reported in the media that three million people went down last winter with Norovirus infection – winter vomiting disease. In truth, health authorities don’t know how many had it. They don’t even know how many went to the doctor with it. All they know is the 2,000 cases in the peak months that were confirmed in by laboratory diagnosis (you can’t be sure that someone is infected with Norovirus by looking at them). It is generally assumed that for every lab-confirmed case there are about 1,500 in the community, a ratio of 1:1,500. (Hence: 2,000 lab cases x 1,500 = three million). But how do the authorities know that? They don’t. Lurking beneath many statistics is a factor that changes everything, but is seldom admitted: doubt. Good statisticians admit the extent of their doubt. Journalists almost never do.

Here’s a technical term, the confidence interval – how sure you can be about data. If an estimate is based on a relatively small sample, the true number could be higher or lower. How much higher or lower? That is the confidence interval, the range of possibilities within which the true answer might lie. (Try it for yourself here)

What are the confidence intervals around the 1:1,500 ratio for Norovirus infections? The low end of the confidence interval is a lot lower, 1:140. That is, each lab case could equal 140 in the community. The high end is an astonishing 1:17,000. This implies that there could have been between 280,000 cases of winter vomiting (2,000 confirmed lab cases x 140 = 280,000) or 34 million. Thirty-four million people in the UK vomiting? Don’t you think we might have noticed?

Why so much doubt? Because researchers arrived at this imprecise ratio by looking at what happened years ago in a small town. They tried to find everyone with gastro-intestinal problems, whether they had been to the doctor or not. Then they found out how many cases were laboratory-confirmed and did their sums to find the all important ratio. And in that small town, how many laboratory-confirmed cases were there? One. And you can imagine that whether a single lab case turns up from a particular town is pretty much a matter of luck. Does a GP there send samples for lab analysis every time? Or do they ever bother? The result can be hugely affected by chance. Hence the enormous confidence intervals: they couldn’t be sure if this – the benchmark town – was typical or odd. That’s why the authorities concede that when the 1:1,500 ratio was applied to last winter’s lab cases, the resulting total (three million) could have been about 11 times too high, or 11 times too low. They even warned journalists that it was unreliable.

Interestingly, a recent study suggests that noroviruses may be more infectious to humans than any other virus ever studied (Norwalk virus: how infectious is it? J Med Virol 2008 80: 1468-1476). This conclusion was drawn from a study involving 22 human volunteers – not the biggest ever clinical study, but better and more controlled than the epidemiological study on which the official estimates are based. The researchers found that infected subjects had a dose-dependent probability of becoming ill, ranging from 0.1 at a dose of 1000 Norwalk virus genomes, to 0.7 with 100 million virus genomes. Out of 22 infected subjects, 15 (68%) developed acute symptoms of gastroenteritis. Preventing and controlling Norovirus transmission is a major challenge – especially in institutional settings, such as healthcare facilities, nursing homes, schools, hotels, cruise ships, military facilities and summer camps. Careful handwashing is probably the most effective way to prevent most Norovirus infections.

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• Noroviruses
• UK Norovirus Outbreak
• Norovirus outbreak strain characterization
• How Noroviruses cause repeated outbreaks of gastroenteritis

Researchers from the United States Department of Agriculture have identified a novel mutation in the bovine prion protein gene in a cow confirmed with atypical Bovine Spongiform Encephalopathy (BSE). This is the first report of a confirmed case of BSE (aka mad cow disease) with a potential pathogenic mutation within the bovine Prnp gene. BSE, a transmissible spongiform encephalopathy (TSE) or prion disease of cattle, was first discovered in the United Kingdom in 1986. BSE is considered to be the cause of a human prion disease known as variant Creutzfeldt-Jakob Disease (vCJD). Veterinary scientists have now identified a novel mutation, E211K, in the bovine Prnp gene. This mutation is identical to the E200K pathogenic mutation in the human Prnp, which has been described as the most common cause of genetic CJD. The study supports the view that all three etiological forms of TSEs in humans are also present in cattle: infectious, sporadic, and genetic. It further supports the hypothesis that the BSE epidemic may have originated from a genetic case of cattle BSE. Cattle with similar mutations can be expected in cattle herds world-wide and could be the source of new BSE outbreaks. It is therefore critical to continue world-wide surveillance for typical and atypical BSE cases including sequencing of the Prnp gene. A newly developed assay system for detecting the E211K mutation has been developed for this purpose. Finally, in order to protect humans it is essential to continue to exclude Specified Risk Materials from the food chain and to maintain the ruminant feed ban.

BSE Case Associated with Prion Protein Gene Mutation. PLoS Pathog 4(9): e1000156
Bovine spongiform encephalopathy (BSE) is a transmissible spongiform encephalopathy (TSE) of cattle and was first detected in 1986 in the United Kingdom. It is the most likely cause of variant Creutzfeldt-Jakob disease (CJD) in humans. The origin of BSE remains an enigma. Here we report an H-type BSE case associated with the novel mutation E211K within the prion protein gene (Prnp). Sequence analysis revealed that the animal with H-type BSE was heterozygous at Prnp nucleotides 631 through 633. An identical pathogenic mutation at the homologous codon position (E200K) in the human Prnp has been described as the most common cause of genetic CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. A recent epidemiological study revealed that the K211 allele was not detected in 6062 cattle from commercial beef processing plants and 42 cattle breeds, indicating an extremely low prevalence of the E211K variant (less than 1 in 2000) in cattle. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in the approximately 10-year-old cow carrying the E221K mutation.

Related:

• A novel approach in the molecular differentiation of prion strains
• Genes contributing to prion pathogenesis
• What the heck are prions for?
• Drugs for treatment of prion infections

The origin of the transmissible agent involved in the foodborne epidemic of bovine spongiform encephalopathy (BSE) remains a mystery. It has recently been proposed that this could have been the result of the recycling of an atypical, more probably sporadic, form of BSE (called bovine amyloidotic spongiform encephalopathy, or L-type BSE) in an intermediate host, such as sheep. A team from the French Food Safety Agency has identified a prion protein characteristic that is unique to some natural but unusual sheep scrapie cases. This finding may provide a novel method by which to study prion diversity and their possible changes during cross-species transmission. Mystery still surrounds the origin of the transmissible agent involved in the food-borne epidemic of bovine spongiform encephalopathy (BSE). Classical BSE, more commonly known as mad cow disease, is a known cause of a variant form of the incurable, degenerative neurological disorder Creutzfeldt-Jakob disease in humans. It has recently been proposed that this could have been the result of the recycling of an atypical, more probably sporadic form of BSE (called bovine amyloidotic spongiform encephalopathy, or L-type BSE) in an intermediate host, such as sheep. The team analyzed the molecular features of the disease-associated protease-resistant prion protein (PrPres) to determine any differences which might discriminate between scrapie and BSE cases. The researchers sampled PrPres from the brains of transgenic mice overexpressing the ovine prion protein after experimental infection with prions from bovine classical BSE, L-type BSE, and ovine scrapie. Scrapie cases were found to include rare “CH1641-Like” isolates, which share some PrPres molecular features with classical BSE and L-type BSE. The molecular features of the prion protein in the “CH1641-like” sheep scrapie cases more closely resemble those found in L-type BSE compared to classical BSE. However, from a series of four “CH1641-like” scrapie cases, the researchers found a pathological C-terminal prion protein product that was undetectable from both L-type and classical BSE transmitted to such mice, clearly suggesting that such scrapie isolates are not linked to these BSE forms. Further studies to confirm this discriminating factor are needed in sheep, especially from sheep experimentally infected with L-type BSE, which were not available for this study. These findings add a novel approach for the discrimination of prions that may help to understand their possible changes during cross-species transmissions.

A C-Terminal Protease-Resistant Prion Fragment Distinguishes Ovine “CH1641-Like” Scrapie from Bovine Classical and L-Type BSE in Ovine Transgenic Mice. 2008 PLoS Pathog 4(8): e1000137
The protease-resistant prion protein (PrPres) of a few natural scrapie isolates identified in sheep, reminiscent of the experimental isolate CH1641 derived from a British natural scrapie case, showed partial molecular similarities to ovine bovine spongiform encephalopathy (BSE). Recent discovery of an atypical form of BSE in cattle, L-type BSE or BASE, suggests that also this form of BSE might have been transmitted to sheep. We studied by Western blot the molecular features of PrPres in four “CH1641-like” natural scrapie isolates after transmission in an ovine transgenic model (TgOvPrP4), to see if “CH1641-like” isolates might be linked to L-type BSE. We found less diglycosylated PrPres than in classical BSE, but similar glycoform proportions and apparent molecular masses of the usual PrPres form (PrPres #1) to L-type BSE. However, the “CH1641-like” isolates differed from both L-type and classical BSE by an abundant, C-terminally cleaved PrPres product (PrPres #2) specifically recognised by a C-terminal antibody (SAF84). Differential immunoprecipitation of PrPres #1 and PrPres #2 resulted in enrichment in PrPres #2, and demonstrated the presence of mono- and diglycosylated PrPres products. PrPres #2 could not be obtained from several experimental scrapie sources (SSBP1, 79A, Chandler, C506M3) in TgOvPrP4 mice, but was identified in the 87V scrapie strain and, in lower and variable proportions, in 5 of 5 natural scrapie isolates with different molecular features to CH1641. PrPres #2 identification provides an additional method for the molecular discrimination of prion strains, and demonstrates differences between “CH1641-like” ovine scrapie and bovine L-type BSE transmitted in an ovine transgenic mouse model.

Related:

• New forms of bovine spongiform encephalopathy
• Four separate types of Creutzfeldt-Jakob disease?
• Genes contributing to prion pathogenesis
• What the heck are prions for?

Many Gram-negative bacteria use a population density-dependent regulatory mechanism called quorum sensing (QS) to control the production of virulence factors during infection. In the bacterial plant pathogen Pectobacterium atrosepticum (formerly Erwinia carotovora subsp. atroseptica), an important model for QS, this mechanism regulates production of enzymes that physically attack the host plant cell wall. A recent study used a whole genome microarray-based approach to investigate the entire QS regulon during plant infection. Results demonstrate that QS regulates a much wider set of essential virulence factors than was previously appreciated. These include virulence factors similar to those in other plant and animal pathogens that have not previously been associated with QS, e.g. a Type VI secretion system (and its potential substrates), shown for the first time to be required for virulence in a plant pathogen; and the plant toxin coronafacic acid, known in other pathogens to play a role in manipulating plant defences. This study provides the first evidence that Pectobacterium may target host defences simultaneously with a physical attack on the plant cell wall. Moreover, the study demonstrates that a wide range of previously known and unknown virulence regulators lie within the QS regulon, revealing it to be the master regulator of virulence.

Quorum sensing (QS) in vitro controls production of plant cell wall degrading enzymes (PCWDEs) and other virulence factors in the soft rotting enterobacterial plant pathogen Pectobacterium atrosepticum (Pba). 26% of the Pba genome exhibited differential transcription in a QS mutant, compared to the wild-type, suggesting that QS may make a greater contribution to pathogenesis than previously thought. novel components of the QS regulon were identified, including the Type I and II secretion systems, which are involved in the secretion of PCWDEs; a novel Type VI secretion system and its predicted substrates; more than 70 known or putative regulators, some of which have been demonstrated to control pathogenesis and, remarkably, the Type III secretion system and associated effector proteins, and coronafacoyl-amide conjugates, both of which play roles in the manipulation of plant defences. These findings indicate that QS is a master regulator of phytopathogenesis, controlling multiple other regulators that, in turn, co-ordinately regulate genes associated with manipulation of host defences in concert with the destructive arsenal of PCWDEs that manifest the soft rot disease phenotype.

Quorum Sensing Coordinates Brute Force and Stealth Modes of Infection in the Plant Pathogen Pectobacterium atrosepticum. 2008 PLoS Pathogens 4(6): e1000093

Related:

• Quorum Sensing in Bacteria: We Two Are One
• Communication, cooperation, competition and cheating – bacteria are just like us

Iron is a nutrient that bacteria need for many essential processes in the cell. As part of the response to infection by bacteria, animals restrict the amount of iron available. In mammals lactoferrin (in mucosal secretions) and transferrin (in serum) tightly bind free iron to restrict its availability. Unfortunately, successful disease-causing bacteria have found ways to grab iron back from the host. The bacterial mechanisms involved in acquiring iron in the host usually consist of a specific pore on the outer surface of the bacterial cell and an associated transport system that makes the iron available inside the cell.

The most important food-associated bacterium that infects humans is Campylobacter and as such is responsible for much misery and economic loss in the UK. Campylobacter normally lives in the intestine of many animals, notably chickens, where they do not always cause disease. However, when humans eat food contaminated with campylobacters, an highly unpleasant cramping diarrhoea can follow. Food producers strive to minimise the risks of food poisoning for consumers, but if Campylobacter could be eliminated from the intestines of farm animals, particularly chickens, it would have a significant impact on human health by preventing many thousands of cases of food borne disease each year.

If control is to be achieved it is important that we better understand how Campylobacter colonises the intestine. Several components of campylobacters that are essential for growth in the intestine are involved in acquiring iron within the host. In our preliminary work, we have identified a system in campylobacters that can grab iron directly from lactoferrin and transferrin to support bacterial growth. This work has identified candidates for the specific pore on the outer surface of the bacterial cell and the associated transport system that moves the iron to the inside of the cell. Work by my colleague Julian Ketley, Department of Genetics, University of Leicester, aims to verify the identify of the components of the system and determine the methods by which iron is removed from lactoferrin/transferrin to allow bacterial growth. With a better understanding of the iron acquisition system we will be able to determine if it would be an suitable target for intervention on the farm in order to block growth in the animal gut and reduce food contamination.

Utilization of lactoferrin-bound and transferrin-bound iron by Campylobacter jejuni. J Bacteriol. 2008 190:1900-11
Campylobacter jejuni NCTC 11168 was capable of growth to levels comparable with FeSO4 in defined iron-limited medium (minimal essential medium alpha [MEMalpha]) containing ferrilactoferrin, ferritransferrin, or ferri-ovotransferrin. Iron was internalized in a contact-dependent manner, with 94% of cell-associated radioactivity from either 55Fe-loaded transferrin or lactoferrin associated with the soluble cell fraction. Partitioning the iron source away from bacteria significantly decreased cellular growth. Excess cold transferrin or lactoferrin in cultures containing 55Fe-loaded transferrin or lactoferrin resulted in reduced levels of 55Fe uptake. Growth of C. jejuni in the presence of ferri- and an excess of apoprotein reduced overall levels of growth. Following incubation of cells in the presence of ferrilactoferrin, lactoferrin became associated with the cell surface; binding levels were higher after growth under iron limitation. A strain carrying a mutation in the cj0178 gene from the iron uptake system Cj0173c-Cj0178 demonstrated significantly reduced growth promotion in the presence of ferrilactoferrin in MEMalpha compared to wild type but was not affected in the presence of heme. Moreover, this mutant acquired less 55Fe than wild type when incubated with 55Fe-loaded protein and bound less lactoferrin. Complementation restored the wild-type phenotype when cells were grown with ferrilactoferrin. A mutant in the ABC transporter system permease gene (cj0174c) showed a small but significant growth reduction. The cj0176c-cj0177 intergenic region contains two separate Fur-regulated iron-repressible promoters. This is the first demonstration that C. jejuni is capable of acquiring iron from members of the transferrin protein family, and our data indicate a role for Cj0178 in this process.

Related:

• Campylobacter jejuni
• How Campylobacter jejuni survives within cells
• Protein promotes antibiotic resistance in Campylobacter