"this book addresses important themes in the molecular epidemiology of bacterial pathogens ... Another consistent strength of this book is the detailed coverage of antibiotic resistance across the entire spectrum of food and waterborne pathogens ... for clinicians, food or environmental scientists, or public health officials interested in gaining a foundation in the molecular microbiology of this important group of pathogens, this book would provide an excellent foundation. Alternatively, for those with expertise in specific organisms, this book provides an interesting look across the spectrum of food and waterborne bacterial pathogens." from Jason B. Harris (Harvard Medical School, Boston, USA) writing in Clin. Inf. Dis. (2013) read more ...

Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology Edited by: Shah M. Faruque ISBN: 978-1-908230-06-5 Publisher: Caister Academic Press Publication Date: July 2012 Cover: hardback "an excellent foundation" (Clin. Inf. Dis.)

"there is a wealth of detailed, up-to-date information on the epidemiology, pathogenesis and molecular biology of these pathogens written by experts in the field. This book would very useful to those studying gastrointestinal bacterial pathogens or food and water microbiology at postgraduate level and as a reference for specialists working in this area." from Kathie Grant (Health Protection Agency, UK) writing in Microbiology Today (2013) read more ...

Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology Edited by: Shah M. Faruque ISBN: 978-1-908230-06-5 Publisher: Caister Academic Press Publication Date: July 2012 Cover: hardback "a wealth of detailed, up-to-date information" (Microbiol. Today)

from Riikka Laukkanen-Ninios and Maria Fredriksson-Ahomaa writing in Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology:

Enteropathogenic yersiniosis is caused due to foodborne infection with Yersinia enterocolitica and Y. pseudotuberculosis. Several virulence factors have been identified that are common to these two pathogens even though Y. pseudotuberculosis is genetically more related to Y. pestis, which is typically transmitted by fleas and not through foods. Diarrhoea and abdominal pain are the most dominant symptoms for Y. enterocolitica and Y. pseudotuberculosis infections. Occasionally, complications such as joint pain and skin rash may occur, typically among adults. Most human cases are caused by Y. enterocolitica. The reported cases are mainly sporadic and outbreaks are uncommon. However, outbreaks of Y. pseudotuberculosis infection, often in school children, have occurred in Finland, Russia and Japan. The most important transmission route is proposed to be via contaminated foods even though these pathogens have seldom been isolated from foods. The low isolation rates are probably due to the low sensitivity of the culture methods. Y. enterocolitica infections have been linked to raw or under-cooked pork and pork products while Y. pseudotuberculosis infections have been linked to raw fresh produce and surface water. Pigs are so far the most important reservoir for human pathogenic Y. enterocolitica. The principal reservoir of Y. pseudotuberculosis is believed to be wild animals, especially rodents and birds. Transmission routes of these pathogens from animals to humans are mostly unknown.

Further reading: Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology

from Sangmi Lee, Robin M. Siletzky and Sophia Kathariou writing in Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology:

Listeria monocytogenes is a Gram-positive foodborne pathogen that causes a severe, potentially fatal illness (listeriosis) in animals and humans. The only human pathogen within the genus Listeria, this bacterium is equipped with sophisticated mechanisms to invade mammalian cells and proliferate inracellularly. Population genetics data indicate that some groups of L. monocytogenes are more frequently associated with human listeriosis. However, the ecology and potentially unique characteristics of such groups remain to be elucidated. This review discusses recent advances in the epidemiology of listeriosis and epidemic-associated clonal groups; the characterization of pathogenicity of L. monocytogenes; the evolution of Listeria species and L. monocytogenes; and the increasingly recognized importance of Listeria phages in the ecology of L. monocytogenes in food processing facilities.

Further reading: Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology

from T. Ramamurthy and M. John Albert writing in Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology:

There are five categories of diarrhoeagenic Escherichia coli (DEC) namely enterotoxigenic, enteropathogenic, enterohaemorrhagic, enteroinvasive and enteroaggregative. They have evolved from nonpathogenic commensal strains by acquisition of specific virulence genes through mobile genetic elements. Their pathogenesis differs and they produce distinct clinical syndromes and pathological lesions and have different epidemiological characteristics. The virulence genes are carried on plasmids, bacteriophages, transposons or pathogenicity islands. DEC produce an array of virulence factors which include colonization factors, enterotoxins, cytotoxins, haemolysins, invasins etc. The diseases they produce range from acute watery diarrhea to dysentery to bloody diarrhoea with haemolytic uraemic syndrome. Even though the major burden of the disease is in the developing world, no part of the world is free from them, and EHEC infections are predominant in developed countries. A variety of molecular tools have been developed to study the diversity and transmission of these pathogens. Even though attempts are being made, no ideal vaccine exists against any category of DEC, therefore maintaining appropriate food and water hygiene are the only ways to keep the infections under control. We must also be on guard against the emergence of new pathogenic strains. The recent emergence of a hybrid enteroaggregative-haemorrhagic E. coli with the rare serotype of O104:H4 in Germany that caused high mortality rates is a case in point.

Further reading: Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology

from Marie Yeung and Kathryn J. Boor writing in Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology:

As a natural inhabitant of the marine environment, Vibrio parahaemolyticus is frequently present in seafood, and particularly in oysters. V. parahaemolyticus can multiply rapidly under favorable conditions, but also may exist in a viable but non-culturable state under unfavorable conditions. A small subset of this species can cause human disease, with acute gastroenteritis as the predominant clinical manifestation. Two pore-forming hemolysins, thermostable direct hemolysin (TDH) and TDH-related hemolysin (TRH), are recognized as contributors to V. parahaemolyticus pathogenesis. Therefore, many detection methods for pathogenic strains focus on determining the presence of the genes encoding these hemolysins or on detection of beta-hemolysis on Wagatsuma agar (i.e. the Kanagawa Phenomenon). Serotyping and molecular fingerprinting techniques are also used to subtype Vibrio parahaemolyticus isolates. One of the most effective strategies for preventing Vibrio parahaemolyticus infection from consumption of raw or uncooked seafood is to reduce seafood post-harvest storage temperatures to prevent the growth of this species.

Further reading: Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology

from Iddya Karunasagar and Anusha Rohit writing in Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology:

Vibrio vulnificus is a normal inhabitant of warm estuarine environments all over the world and may be associated with a wide variety of seafood. In susceptible individuals with underlying liver disease, diabetes or other immunocompromised condition and consuming raw seafood, the organism can cause primary septicaemia with a mortality rate of over 50%. A number of putative virulence factors such as capsule, cytotoxic factors, iron acquisition factors and factors responsible for evading the immune system of the host have been described and multiple factors seem to be involved in causing disease symptoms. The organism can be isolated, identified and enumerated by traditional microbiological methods as well as molecular methods such as polymerase chain reaction (PCR) and real time PCR. Clinical strains can be generally distinguished from most environmental strains by genetic fingerprinting techniques. The organism does not grow at temperatures below 13°C and therefore an important control measure is to cool the seafood to temperatures below this within a few hours of harvest. The organism is sensitive to mild heat, which can be used as a postharvest treatment method to minimise the risk of infection. Relaying shellfish to waters with salinity of >30 ppt has also been found to be an important control measure.

Further reading: Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology

from Shah M. Faruque and John J. Mekalanos writing in Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology:

Vibrio cholerae belonging to O1 and O139 seropgroups cause cholera, a life-threatening diarrhoeal disease, which spreads through consumption of water and food contaminated with the pathogen. Other serogroups of V. cholerae are also occasionally associated with mild to moderate enteric infections. Although V. cholerae is a human pathogen, the bacteria are part of the normal aquatic flora in estuarine and brackish waters, and thus are able to persist in the environment outside the human host. The ability of V. cholerae strains to cause disease in humans depends on their virulence gene content, which varies between pathogenic and nonpathogenic strains. Horizontal transfer of critical virulence genes among different V. cholerae strains, as well as microevolution of bacterial genes contribute significantly to the emergence of V. cholerae strains with altered antigenic and pathobiological properties. Seasonal cholera epidemics may selectively enrich genetic variants with unique properties that promote transmission or environmental persistence. The ecosystem comprising V. cholerae, the aquatic environment and the human host offers an understanding of the complex relationship between pathogenesis and the evolution of a typical waterborne bacterial pathogen.

Further reading: Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology

from Indrani Karunasagar, Krishna Kumar and G. Balakrish Nair writing in Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology:

Members of the Vibrionaceae family occurring in marine environment are responsible for many of the reported cases of infection worldwide. Among these, Vibrio parahaemolyticus is an important food-borne pathogen transmitted through contaminated seafood. Historically, food poisoning due to V. parahaemolyticus occurred as sporadic cases caused by different serotypes without the clustering of one particular serotype. With the emergence of the pandemic clone belonging to O3:K6 serotype in Kolkata, India, in 1996, the epidemiology of this organism changed abruptly causing large outbreaks and rapid hospitalizations. This new highly virulent strain is now globally disseminated. This review traces the epidemiology of the pandemic strain of V. parahaemolyticus, its emergence, molecular characteristics and clonal dissemination.

Further reading: Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology

from Shah M. Faruque writing in Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology:

Recent studies have provided remarkable insights to our general understanding of the epidemiology, genetics, and ecology of foodborne and waterborne bacterial pathogens. Some of these bacteria have recently been reclassified with updated nomenclature; identification methods have also improved substantially with more extensive use of molecular approaches. The bulk of information generated in different areas of research in these pathogenic organisms have been summarized to provide an over all impression of the progress made. Future directions for research into these organisms have also been discussed with a view to understanding general themes of bacterial pathogens, that cause foodborne and waterborne diseases. In addition, available preventive measures to reduce incidences of disease due to these organisms have been discussed.

Further reading: Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology

from Lieneke I. Bouwman and Jos P.M. van Putten writing in Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology:

Campylobacter species are one of the leading causes of bacterial foodborne disease. Campylobacter survives and flourishes in a variety of environmental niches but causes pathology mainly in humans. The pathogenesis of the disease is still poorly understood, and currently only a few Campylobacter virulence determinants have been proposed. Recent studies indicate that Campylobacter displays extensive genome plasticity and a range of environmental adaptation, that likely contribute to the success of the pathogen. In this review, we will discuss the state-of-the-art of the epidemiology, molecular biology, and pathogenesis of Campylobacter infection.

Further reading: Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology

from E. Fidelma Boyd writing in Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology:

The acquisition of new phenotypes by bacteria is largely driven by horizontal gene transfer (HGT), a process that is ubiquitous among bacteria and universally present among enteric pathogens. The common vectors of HGT in enteric pathogens include phages, pathogenicity islands and plasmids, all genetic elements that can encode virulence factors essential for host colonization and infection. In this review, Salmonella enterica, Escherichia coli, Vibrio cholerae and V. parahaemolyticus are discussed in terms of their virulence genes encoded within mobile and integrative genetic elements and their role in the mechanism of pathogenesis.

Further reading: Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology

from Lyudmila Boyanova writing in Helicobacter pylori:

Discovery of Helicobacter pylori by Marshall and Warren in 1982 was the start of a real revolution in the gastroenterology with a strong impact on medicine as a whole. In the 1870s, despite some reports on spiral bacteria in gastric tissues, stress and diet were thought to be the only causes of peptic ulcers. In 1979, Warren evaluated Campylobacter-like organisms (CLOs) in inflamed gastric tissues and in 1982, his co-worker, Marshall, isolated the bacteria. However, the discovery was initially met with much disagreement. For this reason, in 1985, Marshall performed self-inoculation by CLOs and proved their ability to cause gastritis. Originally called Campylobacter pyloridis and then corrected to Campylobacter pylori, the bacteria were renamed again due to taxonomic data as Helicobacter pylori in a new genus, Helicobacter. In 2005, Warren and Marshall were jointly awarded the Nobel Prize in Physiology or Medicine. Since the year of H. pylori discovery, various invasive and non-invasive diagnostic tests, susceptibility testing methods and treatment regimens for the infection have been developed and then improved. Participation of H. pylori in the pathogenesis of gastric cancer and MALT lymphoma has been proven. Moreover, H. pylori has been associated with several extragastric diseases. The enormous genetic diversity of the bacteria and their numerous virulence factors have been revealed and genomes of many strains have been sequenced. Presently, chronic gastritis and peptic ulcers are treated as bacterial infections by antibiotics combined with acid inhibitors. Improvement in eradication has been obtained by triple, quadruple, rescue, sequential or other regimens. The gift that Marshall and Warren's discovery has given to human medicine has been the consequent detection of the link between chronic bacterial infections and malignancy and, fascinatingly, the option to heal a tumour (as MALT lymphoma) by treating the associated microorganisms. However, at present, the treatment of H. pylori infection is not easy and still no vaccines are available for prophylaxis. Although the global rate of H. pylori infection is gradually decreasing, the antibiotic resistance of the bacteria is growing sharply in many countries. Regrettably, despite the fact that infection is often asymptomatic, H. pylori still infects half of the global human population and every fifth infected subject can develop severe disease. Therefore, it is important to stress that in the field of pathogenesis, epidemiology, diagnosis, prophylaxis and treatment of the infection, there are still approaches to be optimised and many questions to be answered.

Further reading: Helicobacter pylori

from Shah M. Faruque writing in Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology:

Foodborne and waterborne bacterial pathogens are a major cause of mortality in developing countries and cause significant morbidity in developed nations. Some countries carry a disproportionately heavy burden of these infectious diseases due to inadequate resources to provide sanitation and hygienic facilities, and safe water. The most important bacterial pathogens transmitted through contaminated water and food include species or strains of Salmonellae, Vibrio (e.g., V. cholerae, V. parahemolyticus, V. vulnificus); Shigella (S. dysnteriae, S. flexneri, S. sonnie, S. boydii); Escherichia coli, Yersinia, Staphylococcus and Campylobacter. The pathogenic mechanisms of these bacteria involve synergistic actions of multiple virulence factors produced by the pathogen after infecting the host. Besides carrying sets of virulence genes which are often horizontally transferred between strains, many of these bacteria may also carry precise genetic programs that allow them to adapt and survive in water leading to enhanced transmission or prolonged persistence in the aquatic environment. Understanding the epidemiology, pathogenesis and evolution of these pathogens can contribute significantly to control foodborne and waterborne diseases.

Further reading: Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology

from Indrani Karunasagar, Patit Paban Bhowmick and Deekshit Vijaya Kumar writing in Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology:

Foodborne and waterborne infections due to Salmonella species are a major concern worldwide. Several virulence genes have been identified in Salmonella and located in clusters called Salmonella Pathogenicity Island (SPI). There are 17 Pathogenicity Islands of Salmonella reported to date. Salmonella possess two distinct type three secretion system (T3SS) encoded by genes present in two different SPI viz. SPI-1 and SPI-2 that play an important role in adhesion, invasion and survival in the host cells. It has been also reported that a variety of Salmonella phenotypes associated with bioluminescence, biofilm formation, conjugation, motility, competence, and antibiotic production, are regulated in response to signaling molecules of quorum-sensing systems. The development of resistance to various antibiotics (particularly in Asian countries) including extended-spectrum cephalosporins worldwide is a cause of concern. Some variants of Salmonella have developed multidrug-resistance as an integral part of the genetic material of the organism, and are therefore likely to retain their drug-resistance genes even when antimicrobial drugs are no longer used. The role of plasmids, bacteriophages, transposons and integrons in the transfer of resistance genes is discussed.

Further reading: Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology

from G. P. Pazhani and T. Ramamurthy writing in Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology:

Shigella species are often associated with diarrhoea/dysentery among children in developing countries of Asia-African regions and also cause foodborne infections in developed countries. During infection, this pathogen secretes a number of effectors via the type III secretion system. Recently, Shigella-infected cases have increased considerably in Asia, but the death rate decreased substantially due to nutritional and clinical interventions. Antimicrobials reduce the episodes of shigellosis. However, multiple antibiotic resistance in shigellae have increased over the years due to improper use of antimicrobials in the treatment of diarrhoea. Several mechanisms such as plasmids and other mobile genetic elements are involved in the transmission of resistance in shigellae. Due to poor efficacy of many of the existing Shigella vaccines, none has been licensed for use in endemic areas. This chapter reviews our current understanding of mechanism involved in the pathogenesis of Shigella, antimicrobial resistance and also its epidemiological importance and clinical management of shigellosis.

Further reading: Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology

from Kaisar Ali Talukder and Ishrat Jahan Azmi writing in Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology:

Shigellosis, also known as acute bacillary dysentery, produces inflammatory reactions and ulceration on the intestinal epithelium followed by bloody or mucoid diarrhoea. Shigellosis is caused by any one of the four species or groups of Shigella, namely, S. dysenteriae, S. flexneri, S. boydii, and S. sonnei. At least 54 serotypes or subtypes of Shigella are currently recognized, of which S. dysenteriae has 16 serotypes, S. flexneri has 17 serotypes and subserotypes, S. boydii has 20 and S. sonnei has a single serotype. Shigellosis can occur in sporadic, epidemic and pandemic forms. To develop an effective vaccine it is important to monitor the prevalent serotypes and their changes around the world because immunity to Shigella is serotype specific. The genetic variability between serotypes and emergence of atypical strains accentuates the problems to the development of an effective vaccine. In view of the emergence of new strains with altered characteristics than the ones established globally for many years, there is also a need for revising the nomenclature for the three groups of Shigella: flexneri, boydii and dysenteriae. This chapter discusses the recent serotyping scheme of Shigella with special focus on the emergence of new variants and the necessity to make an updated scheme. Furthermore, the epidemiology, phenotypic and molecular characteristics, population genetics and clinical impact of these variants have been described.

Further reading: Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology

from Mahbubur Rahman writing in Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology:

The genus Salmonella has three species namely Salmonella enterica, Salmonella bongori and Salmonella subterranean. The type species S. enterica is further classified into six subspecies: enterica (subsp. I), arizonae (subsp. IIIa), diarizonae (subsp. IIIb), houtenae (subsp. IV), indica (subsp. VI), and salamae (subsp. II). Salmonella strains belong to over 50 serogroups based on the O antigen, and to over 2500 serovars (each having a unique combination of somatic O, flagellar H1 and H2 antigens). Most of these serovars (1,531) belong to Salmonella subsp., enterica, and cause more than 99% of the diseases in humans including gastroenteritis and enteric fever (typhoid). Genome sequencing and comparative genomic analysis of 28 S. enterica serovars identified similarity of core regions of the genomes, together with evidence of recombination and rearrangement, genomic degradation, pseudogenes and clonal diversity both within and among the serovars. Genomic comparisons of host-restricted (S. Typhi, S. Paratyphi and S. Gallinarum) and host-adapted (S. Typhimurium and S. Enteridis) S. enterica serovars indicate that genomic degradation is a common evolutionary mechanism for host adaptation and increased pathogenicity of Salmonella. Drug resistances in Salmonella is mainly due to Salmonella genomic island 1 (an integrative mobile element) carrying various antibiotic resistance gene clusters, and to conjugative R plasmids which confer resistance to many antibiotics including extended-spectrum cephalosporins. Continuous genetic re-assortment in Salmonella leading to increased virulence and the emergence of resistance to multiple drugs are of significant public health concern.

Further reading: Foodborne and Waterborne Bacterial Pathogens: Epidemiology, Evolution and Molecular Biology

from Lyudmila Boyanova writing in Helicobacter pylori:

The Helicobacter genus belongs to class Epsilonproteobacteria, orders Campylobacterales, family Helicobacteraceae and already involves >35 species. Recently, new gastric (Helicobacter suis and Helicobacter baculiformis) and enterohepatic (Helicobacter equorum) species have been reported. Helicobacter pylori is of primary importance for medicine, however, non-pylori Helicobacter species (NPHS), which naturally inhabit mammals (except humans) and birds, have been detected in human clinical specimens. NPHS encompass two (gastric and enterohepatic) groups, showing different organ specificity. Importantly, some species such as Helicobacter hepaticus, Helicobacter mustelae and, probably, Helicobacter bilis exhibit carcinogenic potential in animals. NPHS harbour many virulence genes and may cause diseases not only in animals but also in humans. Gastric NPHS such as H. suis (most often), Helicobacter felis, Helicobacter bizzozeronii and Helicobacter salomonis have been associated with chronic gastritis and peptic ulcers in humans and, importantly, with higher risk for MALT lymphoma compared to H. pylori. Enterohepatic species e.g., H. hepaticus, H. bilis and Helicobacter ganmani have been detected by PCR in, but still not isolated from, specimens of patients with hepatobiliary diseases. Moreover, NPHS may be associated with Crohn's disease, inflammatory bowel disease and ulcerative colitis. The significance of avian helicobacters (Helicobacter pullorum, Helicobacter anseris and Helicobacter brantae) also has been evaluated extensively. NPHS such as Helicobacter cinaedi and Helicobacter canis can cause severe infections, mostly in immunocompromised patients with animal exposure. Briefly, the role of NPHS in veterinary and human medicine is increasingly recognised. However, despite the growing interest in the possible association between NPHS and the chronic hepatobiliary or intestinal diseases in humans, more studies are still required to prove the suggested association. Several other topics such as isolation of still uncultured species, antibiotic resistance and treatment regimens for NPHS infections and, last but not least, NPHS pathogenesis and possible carcinogenesis in humans should be additionally evaluated.

Further reading: Helicobacter pylori

from Lyudmila Boyanova writing in Helicobacter pylori:

H. pylori causes the second most common chronic bacterial infection in humans. As a result of the childhood-acquired and usually life-long (unless eradicated) infection, about 12-24% of the H. pylori positive subjects develop severe diseases e.g. peptic ulcers or gastric malignancy. In developed countries, the infection usually spreads intrafamilially; however, in developing countries or underdeveloped rural areas, it can be acquired often extrafamilially or via environmental contamination, leading to higher infection prevalence and greater intrafamiliar diversity of the strains there. Infected mother and older siblings are important factors for H. pylori transmission to children. The transmission routes are oral-oral (by saliva), which prevails in the developed world, faecal-oral (person-to-person or by contaminated water, or maybe food), mainly in the developing countries or gastro-oral (by vomiting and regurgitation). Role of viable but not culturable coccoids forms and biofilms appears to be important. Oral H. pylori seems to be associated with combined oral and gastric infections, probably more often in the developing countries. However, PCR accuracy for detection of extra-gastric H. pylori needs improvement. As a whole, the infection prevalence is still high in countries/groups with poor socio-economic status. In many developing countries, ≥50% of children and ≥70% of adults have been H. pylori positive vs. only >15% of children and ≤20-40% of adults in most developed countries. Detection of anti-CagA antibodies has been used to spot infections by virulent strains and the importance of East Asian CagA testing has been stressed. Both reinfection and infection clearance also have been reported, mainly in children, although in high-prevalence countries, the infection clearance is unimportant. Many risk factors for the infection mirror poor socioeconomic status and a strong birth cohort effect. Both dietary and environmental factors are likely to modify the infection prevalence and should be further evaluated. In brief, improved hygiene and living conditions, urbanisation and growing antibiotic use for H. pylori and many other infections, all have led to a decrease in both infection and reinfection rates in the developed countries and, already, in some developing countries. However, the infection still affects every second person worldwide. Moreover, many important questions on the infection transmission routes and reservoirs still need elucidation.

Further reading: Helicobacter pylori

from Ivan Mitov writing in Helicobacter pylori:

Helicobacter pylori infection induces almost all mechanisms of innate and acquired immunity. Different bacterial, environmental and host factors may influence the balance between the protective role of the immune mechanisms and their role in gastric mucosal damage, respectively, the possibility of lifelong asymptomatic colonisation of gastric mucosa or clinical manifestation and H. pylori infection. Bacterial virulence factors stimulate Toll-like and Nod-like receptors to induce innate and adaptive cell mediated and humoral immune response. Balance of Th1/Th2 response is of great importance in host protection and in pathogenesis of H. pylori-mediated diseases. The polarised Th1 response is not sufficient to clear the bacteria. Moreover, a predominant activation of Th1 cells plays a key role in tissue damage. Th2 response appears to be protective against gastric inflammation. Cytotoxic activities of T cells are important for the outcome of H. pylori infection. Protection due to anti-H. pylori humoral local and systemic immune response is minimal. Furthermore, the antibodies may promote colonisation of gastric mucosa.

Further reading: Helicobacter pylori

from Lyudmila Boyanova writing in Helicobacter pylori:

H. pylori are Gram-negative spiral and microaerophilic bacteria that undergo coccoid transformation under hostile conditions. The coccoids and bacterial biofilms may participate in the transmission of infection. Specific H. pylori characteristics such as its enormous genomic diversity, helical morphology, acid acclimation, Krebs cycle and lipopolysaccharide indicate the extreme adaptation of the bacteria to the gastric mucosa. Modern methods such as comparative genomics, transcriptomics and proteomics provide a deep insight on H. pylori genomic diversity and its expression according to the severity of the disease. Methods to diagnose the infection are invasive e.g., rapid urease test (RUT), histology, culture and molecular methods or less invasive such as string test, or non-invasive such as serology, urea breath test (UBT), stool antigen test (SAT) and some molecular methods. Choice of the test depends on the test characteristics e.g., type, preparation, accuracy, protocol, cut-off, availability and price, and on many patient characteristics, which indicate the likelihood of the infection. Recently, non-invasive methods such as immunoproteomics, new SATs and improved UBT and SAT protocols have been reported. Significance of anti-CagA antibodies for the risk of severe diseases has been highlightened. For the same purpose, a new test for serum pepsinogens and anti-H. pylori antibodies has been introduced. Recent molecular methods have been implemented to detect H. pylori and its resistance to both macrolides and quinolones or to spot non-invasively clarithromycin resistance. Advances have been made also in the invasive methods. In vivo histology has been suggested and, importantly, an operating link for histological estimation of gastric cancer risk (OLGA staging) has been published. However, further studies are strongly required on important issues, among them are applications of the present, or development of new, non-invasive tests for detection of H. pylori resistance to antibiotics, improvement of test accuracy in specific patient groups, use of most reliable biomarkers for severe diseases and strategy for H. pylori screening and eradication.

Further reading: Helicobacter pylori

from Lyudmila Boyanova writing in Helicobacter pylori:

As standard regimens for the eradication of H. pylori infection often fail owing to antibiotic resistance or low patient compliance, there is an increasing need for new drugs such as non-antibiotic agents (NAAs) or optimised treatment regimens. Anti-H. pylori activity has been detected in vitro by many NAAs such as lactobacilli, Saccharomyces boulardii, lactoferrin, green tea, garlic, propolis, broccoli, resveratrol, plant oils etc. Many NAAs have been active against both antibiotic susceptible and resistant H. pylori strains. So far, cell line, animal or clinical trials have shown H. pylori eradication, although often low, using NAAs alone e.g., black caraway, garlic, green tea, turmeric, broccoli and mastic gum. Combinations of standard regimens with NAAs such as lactobacilli, S. boulardii, turmeric, Korea red ginseng, N-acetylcysteine and vitamin C have improved the eradication often by >10% and most of them have reduced the side effects of the regimens. Advantages of some NAAs are their anti-adhesive, anti-urease, anti-inflammatory and anti-tumour effects and bactericidal activity on H. pylori. Moreover, anti-adhesive NAAs can prevent H. pylori colonisation or reinfection. In addition, aspirin, monoclonal antibodies, redox protein inhibitors and synthetic antimicrobial peptidomimetics have been evaluated as applicants for therapeutic intervention. Synergy between NAAs is a very attractive topic, which should be evaluated, however, with caution. To choose an agent, it is necessary to consider the source, safety or toxicity, dose-depending deleterious effects and allergenicity of some NAAs as well as their quality control and evidence-based trials. At present, we await further studies, especially clinical trials, to suggest the choice, dosage, start time and duration of administration aiming at the routine use of the NAAs. In conclusion, NAAs probably carry greater than the expected potential for prophylaxis or adjuvant therapy of H. pylori infection and can help to control the rising bacterial resistance to antibiotics.

Further reading: Helicobacter pylori

from Borislav Vladimirov writing in Helicobacter pylori:

Treatment of Helicobacter pylori infection remains a significant clinical problem despite the extensive research on the topic over the last 25 years. For H. pylori eradication, combined regimens of non-antibiotic (bismuth compounds and/or proton pump inhibitors) and usually two antibiotics are used. The antibiotic choice may involve amoxicillin, clarithromycin, metronidazole, tetracycline, levofloxacin, rifabutin and furazolidone. A number of factors such as duration of treatment, choice of antibiotics, new drug combinations, improved patient compliance and novel agents may help to improve the eradication rates. In this chapter, data on triple, quadruple, sequential and rescue therapeutic regimens are discussed. However, H. pylori resistance to antibiotics, poor patient compliance and host genetic polymorphism can strongly reduce the success of eradication. Recent data have shown that the rates of eradication have decreased worldwide. In the last years, many new drugs and combinations have been applied with aims to raise the eradication rates to more acceptable levels but more evidence is needed to support the routine use of the new antibiotics and modified treatment regimens for eradication of H. pylori.

Further reading: Helicobacter pylori

from Ivan Mitov writing in Helicobacter pylori:

An effective vaccine is needed to improve the success of anti-H. pylori therapy. Cooperative action of cell-mediated, humoral and molecular responses is necessary for effective protection against H. pylori. Vaccines against H. pylori can be used as prophylactic vaccines to prevent the infection or as therapeutic vaccines to cure the infection, to improve the eradication success of standard regimens or reduce the bacterial density in the gastric mucosa and the risk for emergence of antibiotic resistant strains. In recent years, many attempts, using various H. pylori antigens such as urease, CagA, HP-NAP, HspA or combinations, many adjuvants and different routes of immunisation have been made to create vaccines against H. pylori infection. Although some attempts are promising, no effective and safe vaccine against H. pylori is currently available for humans. New directions for immunisation with the use of DNA, living vectors, microspheres etc. are currently under evaluation. The vaccination plan and the groups who should receive vaccination are still to be determined but the vaccination will be useful, especially in developing countries.

Further reading: Helicobacter pylori

from Lyudmila Boyanova writing in Helicobacter pylori:

H. pylori infection outcomes strongly depend on the strain virulence. H. pylori displays enormous genetic diversity by frequent mutations, intra- or intergenomic recombinations and natural transformation, and additional phase variations by slipped-strand mispairing. H. pylori spiral shape, urease, motility, lipopolysaccharide (LPS) and outer membrane adhesins enable the establishment of the infection. H. pylori genetic diversity and induced immunomodulation contribute to the infection chronicity. Prevalence of virulence factors varies according to the patient disease, ethnicity, age and country. H. pylori VacA causes vacuolation, pore formation, disruption of endo-lysosomal activity, apoptosis in gastric cells and immunomodulation. CagA oncoprotein alters cell-signalling pathways and induces morphological changes, chromosomal instability, cell proliferation and apoptosis, interleukin (IL)-8 release and proto-oncogene activation. CagA type D EPIYA and increased number of C repeats has been linked to increased SHP-2 phosphatase activity and hence high risk for gastric cancer. In East Asia, nearly all strains have been highly virulent, carrying intact cagPAI, East Asian CagA and vacA s1/i1/m1 type, which can help to explain the high gastric cancer incidence there. Although the infection outcomes have shown strong association with cagA, cagPAI and vacA status of the strains, mainly in Western countries, the combined activity of all H. pylori virulence factors, involving also dupA, oipA, iceA, homB, babA, sabA, hopQ and other genes/gene status appears to be crucial for the infection pathogenesis. Tipα protein, HP-NAP, heat-shock-proteins, LPS mimicry and interaction with toll-like receptors influence the infection course as well. By the complex and well-coordinated interplay of its virulence factors, H. pylori adapts to the changing environment and can either increase or suppress the gastric inflammation. Moreover, microevolution of the virulence genes emerges in the individual patient over years. Briefly, the direct effects of H. pylori virulence factors and the chronic gastric inflammation can lead to the development of peptic ulcers or malignancy. Targeting the virulent strains in a country or region is important to explain better the clinical significance of some virulence factors and their interaction, to choose local diagnostic markers, to imply aggressive eradication strategies in the concerned patients and to provide new agents and improved regimens to control the infection.

Further reading: Helicobacter pylori

from Lyudmila Boyanova writing in Helicobacter pylori:

H. pylori resistance to antibiotics emerges most often from point mutations but also from efflux mechanisms, natural transformation, altered membrane permeability and, probably, β-lactamase. The resistance especially that to clarithromycin and quinolones often causes treatment failures. For this reason, if national or regional primary resistance rates are ≥15-20% for clarithromycin and ≥40% for metronidazole, the agents should be avoided for primary therapy of the infection unless susceptibility testing of the strains is carried out. Clarithromycin resistance-associated A2143G point mutation most often predicts eradication failures. Moreover, heteroresistance in H. pylori strains has been reported for metronidazole, clarithromycin, amoxicillin and quinolones. From <10% to >37% of the strains exhibit mixtures of genotypes. Importantly, both clarithromycin and quinolone resistance rates have grown sharply in many countries and multidrug resistance has been found in <5% in Europe and >14% in Brazil and South Korea. High primary resistance rates to clarithromycin (20->40%) and fluoroquinolones (20->33%) have been reported mostly in developed countries. Conversely, high primary resistance to metronidazole (≥76%), amoxicillin (6->30%) and tetracycline (≥15%) has been observed in some developing countries. Primary resistance and its evolution often depend on the country and national antibiotic consumption, patient characteristics such as age, sex, disease, prior antibiotic use and comorbidity, strain characteristics such as virulence as well as other factors. Post-treatment resistance rates have been usually much higher, often >3 times for clarithromycin and clarithromycin and metronidazole and ≥1.5 times for metronidazole and quinolones, compared with those of the primary resistance. In brief, a worrying evolution of antibiotic resistance in H. pylori and disturbing multidrug resistance hamper more and more the success of the eradication of the infection. Knowledge on current H. pylori resistance patterns and evolution at global and local levels is highly important to show the efficacy or need for changes in treatment regimens and to improve the overall eradication success that also means the cure of the individual patient.

Further reading: Helicobacter pylori

from Borislav Vladimirov writing in Helicobacter pylori:

Helicobacter pylori plays a main role in the development of gastritis all over the world. In addition, it is well known that H. pylori infection is associated with many nonmalignant and malignant gastrointestinal and extra-gastric diseases. H. pylori remains one of the most common causes of peptic gastro-duodenal ulcers, gastric mucosa associated lymphoid tissue (MALT) lymphoma and gastric cancer. In recent years, many clinical data have been collected about the relationship between H. pylori infection and gastro-oesophageal reflux disease (GORD), nonsteroidal anti-inflammatory drugs⁄acetylsalicylic acid-induced gastric injury and functional dyspepsia as well as about pathogenetic mechanisms of these correlations. There are also evidences confirming the role of genetic differences in host and bacterial factors and the role of environmental factors. Recent data have shown a decline in incidence and prevalence rate of peptic ulcer related to H. pylori. For patients with functional dyspepsia, eradication of H. pylori offers a modest but significant benefit. An inverse relationship between H. pylori infection and reflux oesophagitis, and Barrett oesophagus has been also confirmed. Despite of the controversial results, eradication of H. pylori infection has been recommended for nonsteroidal anti-inflammatory drugs and acetylsalicylic acid-induced gastric injury as well as for patients treated with antiplatelet therapy. The beneficial effects of H. pylori eradication on MALT lymphoma and on the prophylaxis of gastric cancer have been proven. On the other hand, an increasing amount of evidence for extra gastric manifestation of H. pylori infection has been shown.

Further reading: Helicobacter pylori