Biological Sciences
Pathogenic Bacteria
Pathogenic bacteria are microorganisms that can cause disease in humans, animals, and plants. They have the ability to invade and multiply within the host, leading to infections and illness. Pathogenic bacteria can produce toxins or trigger immune responses that contribute to the development of various diseases.
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10 Key excerpts on "Pathogenic Bacteria"
eBook - PDF- Barbara H. Iglewski(Author)
- 1990(Publication Date)
- Academic Press(Publisher)
Part I Introduction This page intentionally left blank THE BACTERIA, VOL. XI CHAPTER 1 The Zen of Bacterial Pathogenicity STANLEY FALKOW Department of Microbiology and Immunology Stanford University Stanford, California 94305 I. Introduction 3 II. The Attributes of Microbial Pathogenicity 4 A. Entry 4 B. Finding a Niche 5 C. Avoiding Host Defense Mechanisms 5 III. Corollaries of Microbial Pathogenicity 6 A. The Clonal Nature of Bacterial Pathogens 6 B. Extrachromosomal Determinants of Pathogenicity 7 C. Regulation of Bacterial Virulence Factors 7 IV. Concluding Remarks 8 I. Introduction A pathogen is often defined as a microorganism that has the capacity to cause disease in a particular host. This definition reflects the past and present emphasis in medical microbiology and medicine with disease, the end product of the infectious process. Not unexpectedly, a good deal of research effort has been, and is, directed to the treatment and prevention of infectious diseases. However, over the past decade there has been an increasing emphasis to understand the funda-mental biology of microorganisms that cause human infection and disease. These studies of infectious bacterial agents have provided a slightly different view of microbial pathogenicity; they also give new insights into the control and preven-tion of infectious diseases. A microbial pathogen is now recognized as a highly adapted microorganism that may cause disease (overt damage to a host) because its survival strategy includes a requirement for infection (persistence, usually by multiplication on or within another living organism). This view, from the standpoint of the micro-organism so to speak, emphasizes the point that disease is an inadvertent and unfavorable outcome of a microbial infection.
eBook - PDFThe Bacteria
Molecular Basis of Bacterial Pathogenesis
- Bozzano G Luisa(Author)
- 2012(Publication Date)
- Academic Press(Publisher)
Part I I n t r o d u c t i o n This page intentionally left blank THE BACTERIA, VOL. XI CHAPTER 1 The Zen of Bacterial Pathogenicity STANLEY FALKOW Department of Microbiology and Immunology Stanford University Stanford, California 94305 I. Introduction II. The Attributes of Microbial Pathogenicity 3 4 4 B. Finding a Niche C. Avoiding Host Defense Mechanisms III. Corollaries of Microbial Pathogenicity A. The Clonal Nature of Bacterial Pathogens B. Extrachromosomal Determinants of Pathogenicity C. Regulation of Bacterial Virulence Factors IV. Concluding Remarks I. Introduction A pathogen is often defined as a microorganism that has the capacity to cause disease in a particular host. This definition reflects the past and present emphasis in medical microbiology and medicine with disease, the end product of the infectious process. Not unexpectedly, a good deal of research effort has been, and is, directed to the treatment and prevention of infectious diseases. However, over the past decade there has been an increasing emphasis to understand the funda-mental biology of microorganisms that cause human infection and disease. These studies of infectious bacterial agents have provided a slightly different view of microbial pathogenicity; they also give new insights into the control and preven-tion of infectious diseases. A microbial pathogen is now recognized as a highly adapted microorganism that may cause disease (overt damage to a host) because its survival strategy includes a requirement for infection (persistence, usually by multiplication on or within another living organism). This view, from the standpoint of the micro-organism so to speak, emphasizes the point that disease is an inadvertent and unfavorable outcome of a microbial infection.
eBook - PDF- Edward Bittar(Author)
- 1998(Publication Date)
- Elsevier Science(Publisher)
These diseases are caused by normal flora (e.g., urinary tract infections in women), or by microorganisms that reside in the environment (e.g., cholera). Zoonoses are dis- eases that primarily occur in animals but can be transmitted to humans (e.g., bubonic plague). The different routes of transmission of bacterial infection are shown in Table 2. PATHOGENIC MICROORGANISMS The development of disease after exposure to an infectious agent depends on properties of both the bacterium and the host. Microorganisms vary in their ability Principles of Bacterial Pathogenesis 89 to cause disease. Those that are successful are pathogens and the manner in which a disease originates is referred to as its pathogenesis. Bacterial characteristics that contribute to pathogenicity are virulence factors. A pathogens' ability to cause disease in a given host varies due to individual differences in the host's defense mechanisms (immune response), and due to strain differences (these are sometimes referred to as differences in virulence or differences in pathogenicity). If one could infect the same individual multiple times with different strains of the same species of bacteria (and the host did not develop an immune response to the infection), differences in the outcome of each infection would reflect differences in the pathogenic potential of each strain. The severity of the disease reflects the total of the expression of the virulence determinants of the infecting strain(s). These differences in the severity of the disease are due to differential expression of virulence determinants. Some commensal microorganisms are unable to cause disease when present alone in certain biological niches. However, when other strains are present, the two nonpathogens can interact and cause disease. This synergistic interaction is commonly seen in infections caused by anaerobic micro- organisms.
- C. H. Collins, A. J. Beale(Authors)
- 2015(Publication Date)
- Butterworth-Heinemann(Publisher)
5 Pathogenicity testing J. Hacker and M. Ott 1. Features of microbial pathogenicity Microbial pathogenicity has been defined as 'the biochemical mechanisms whereby microorganisms cause disease' (Finlay and Falkow, 1989). Thus, pathogenicity enables bacteria of several species to cause different kinds of infections, e.g. in the urinary, respiratory and gastrointestinal tracts, and other sites (Mims, 1987). In contrast, virulence is referred to as the degree of the 'pathogenic potential' of special microbial strains which can be quantified by suitable animal tests like LD 50 measurements (see below). With the exception of a few cases of intoxication (e.g. diphtheria, tetanus) microbial pathogenicity is a process which involves several factors known as 'virulence or pathogenicity factors'. As indicated in Figure 5.1, microbial infections may start via a non-specific contact of the pathogen with the mucosa, through lesions of the skin or through the bite of an arthropod (Mims, 1987). These non-specific events that lead to an attachment of microorganisms include the occurrence of 'long distance attractive forces' or the action of non-specific adhesins such as the type I fimbriae produced by several enterobacterial species (Mirelman, 1986; Hacker, 1990). In recent years it became attractive to distinguish between extracellular and intracellular pathogens. The former organisms are able to colonize tissues and multiply outside the eukaryotic cells, e.g. Vibrio cholerae or Escherichia coli wild-type strains which cause diarrhoeal diseases (Finlay and Falkow, 1989). Extracellular pathogens mostly produce specific attachment factors which bind to distinct receptor molecules on the eukaryotic site. Such adhesins may consist of protein organelles termed fimbriae, which are produced by numerous Gram-negative bacteria, of exopolysac-charides found by Pseudomonas aeruginosa, as well as lipoteichoic acids or glucan polymers produced by streptococci (Mirelman, 1986).
- OECD(Author)
- 2016(Publication Date)
- OECD(Publisher)
4 The WHO Laboratory Biosafety Manual (WHO, 2004, Chapters 2 and 16) provides helpful considerations on the risk/safety assessment of (potentially) pathogenic organisms. These considerations apply primarily to laboratory settings, but they can be easily adapted and applied to environmental settings. For genetically engineered bacteria, the risk group of the species is a first approximation of the degree of bacterial pathogenicity in humans. But assessing the degree of pathogenicity of a bacterial strain calls for an unequivocal identification of the location of the strain in the spectrum from clear non-pathogen to clear pathogen. This should be done with caution. Truly non-Pathogenic Bacteria will lack the ability to survive in a human host (with the exception of commensal bacteria), or cause any adverse effects. Bacteria that are incompatible with the human environment e.g. bacteria that cannot survive at temperatures between 30-42°C, or that are exclusively phototrophic or lithotrophic would be expected to be non-pathogenic. Still, one should be careful drawing this conclusion. For instance, lithotrophic bacteria have been found in infections associated with surgical implants in the human body (Dempsey et al., 2007). Indeed, Casadevall (2006) has pointed out that bacterial strains that have lifestyles that do not link them to pathogenicity in humans can carry genes that code for gene products with a 58 – I.1. BACTERIA: PATHOGENICITY FACTORS SAFETY ASSESSMENT OF TRANSGENIC ORGANISMS: OECD CONSENSUS DOCUMENTS, VOLUME 5 © OECD 2016 potential role as virulence factors in bacteria that are or could develop into human pathogens. Falkow (2008) argues that it is difficult to separate the pathogenic from the commensal lifestyle. What is the difference between a pathogen and a commensal? Pathogens possess the inherent ability to cross anatomic barriers or breach other host defenses that limit the survival or replication of other microbes and commensals.
eBook - PDF- Nina Parker, Mark Schneegurt, Anh-Hue Thi Tu, Brian M. Forster, Philip Lister(Authors)
- 2016(Publication Date)
- Openstax(Publisher)
Silver Spring, MD: US Food and Drug Administration; 2012. Chapter 15 | Microbial Mechanisms of Pathogenicity 669 Primary Pathogens versus Opportunistic Pathogens Pathogens can be classified as either primary pathogens or opportunistic pathogens. A primary pathogen can cause disease in a host regardless of the host’s resident microbiota or immune system. An opportunistic pathogen, by contrast, can only cause disease in situations that compromise the host’s defenses, such as the body’s protective barriers, immune system, or normal microbiota. Individuals susceptible to opportunistic infections include the very young, the elderly, women who are pregnant, patients undergoing chemotherapy, people with immunodeficiencies (such as acquired immunodeficiency syndrome [AIDS]), patients who are recovering from surgery, and those who have had a breach of protective barriers (such as a severe wound or burn). An example of a primary pathogen is enterohemorrhagic E. coli (EHEC), which produces a virulence factor known as Shiga toxin. This toxin inhibits protein synthesis, leading to severe and bloody diarrhea, inflammation, and renal failure, even in patients with healthy immune systems. Staphylococcus epidermidis, on the other hand, is an opportunistic pathogen that is among the most frequent causes of nosocomial disease. [5] S. epidermidis is a member of the normal microbiota of the skin, where it is generally avirulent. However, in hospitals, it can also grow in biofilms that form on catheters, implants, or other devices that are inserted into the body during surgical procedures. Once inside the body, S. epidermidis can cause serious infections such as endocarditis, and it produces virulence factors that promote the persistence of such infections. Other members of the normal microbiota can also cause opportunistic infections under certain conditions.
eBook - PDF- Rodney P. Anderson, Linda Young, Kim R. Finer(Authors)
- 2020(Publication Date)
- Wiley(Publisher)
Juergen Berger/Science Source Vibrio cholerae, the pathogen that causes cholera, growing in the digestive tract. If untreated, cholera kills about half of those affected. CHAPTER 16 Microbial Pathogenesis Infection and Disease CHAPTER OUTLINE 16.1 Transmission of Microbes 409 • Microbial Reservoirs • Modes of Transmission Case Study: The Cholera Epidemic in Goma, Zaire • Horizontal and Vertical Transmission 16.2 Entering and Adhering to the Host 413 • Portals of Entry and Exit • Adhering to Host Cells 16.3 Overcoming Host Defenses 415 • Evading Immune Attack • Altering Pathogen Antigens • Damaging the Host Immune System 16.4 Damaging Host Tissues 420 • Direct Damage • Enzymes • Endotoxins • Exotoxins Clinical Application: Toxoid-Based Vaccines • Immunopathy The Microbiologist’s Toolbox: Analysis of Hemolysis on Blood Agar 16.5 Factors Influencing Disease Outcomes 427 • Host Factors What a Microbiologist Sees: Stress and Infection • Microbial Factors Simple infection by a pathogen does not necessarily mean that disease will follow. Additional factors such as health sta- tus and environmental conditions are also involved. At times, several factors may combine with devastating consequences. For example, cholera can still cause large epidemics in areas where natural disasters or wars disrupt safe water supplies. After the devastating earthquake in Haiti in January 2010, the subsequent cholera outbreak spread to approximately 500,000 people, causing about 8000 deaths. The disease has still not been contained. This chapter presents the key features of pathogenesis that all microbes must follow to cause disease. 408 16.1 Transmission of Microbes 409 Microbial Reservoirs Microbial reservoirs vary depending on the specific pathogen. The three general categories of reservoirs are humans, other animals, and environmental sources. Generally, pathogens with human reservoirs attach only to human tissues and do not actively grow in the environment.
eBook - PDF- Anthony Pometto, Kalidas Shetty, Gopinadhan Paliyath, Robert E. Levin(Authors)
- 2005(Publication Date)
- CRC Press(Publisher)
These methods allow rapid strain “fingerprinting” for epidemiological studies to assist in disease management and control. If an outbreak of disease is caused by a specific strain of a pathogen, and foods containing that specific strain can be found, it will allow epidemiologists to very precisely identify the source of the outbreak. Molecular subtyping has been an important tool used Genetics and Physiology of Pathogenicity 1321 in tracking recent outbreaks of L. monocytogenes and E. coli O157:H7, as well as for a wide variety of other pathogens (26,62,112). Finally, researchers hope that understanding the molecular mechanisms of pathogen-esis will allow them to design new treatments or antibiotics which specifically attack those mechanisms. The better pathogens are understood at a molecular level, the better we are able to confront them at a clinical level. The continued emergence of new food borne pathogens and antibiotic resistant strains of known pathogens means that we will require innovative strategies to combat these bacteria and preserve the safety of the food supply. Studies of the genetic and molecular mechanisms of pathogenesis provide an important part of the information necessary to formulate these strategies. 2.6 RECOMMENDED READING The following review articles and books may be useful to those interested in more in depth treatments of the organisms and concepts discussed in this chapter: 1. Regulation of virulence: a. Salyers, A.A., D.D. Whitt. Bacterial Pathogenesis: A Molecular Approach , 2nd ed. Washington, D.C.: ASM Press, 2002. b. Cotter, P.A., V.J. DiRita. Bacterial virulence gene regulation: an evolutionary perspective. Ann . Rev. Microbiol. 54:519–565, 2000. 2. Clostridium botulinum : a. Smith, L.D.S, H. Sugiyama. Botulism: the organism, its toxins, the disease . American lecture series in clinical microbiology , 2 nd ed. Springfield, IL: Charles C. Thomas, 1988. b. Johnson, E.A., M.
- Kumar, Har Darshan(Authors)
- 2021(Publication Date)
- Daya Publishing House(Publisher)
In the former case, it is the immune system of the host, comprising the specific humoral or cellular responses and all the non-specific mechanisms contributing to removing the bacteria from host tissues or cells. In the case of antibiotic resistance, the selection pressure is exerted by the antibacterial drugs either administered by physicians or found naturally in foodstuffs and the environment. Because they can be essential to bacterial survival, genes that encode pathogenic factors or antibiotic resistance are easily spread among bacteria by such processes as conjugation, transformation, transduction or transposition. Selection pressure coupled with gene transfer leads to the emergence of micro-organisms with increased pathogenicity and/or antibiotic resistance. The evolution of bacteria is associated with continuous generation of novel genetic variants. The major driving forces in this process are point mutations, genetic rearrangements, and horizontal gene transfer. A large number of human and animal bacterial pathogens have evolved the capacity to produce virulence factors that are directly involved in infection and disease. Further, many bacteria express resistance traits against antibiotics. Both virulence factors and resistance determinants are subject to intrastrain genetic and phenotypic variation. They are often encoded on unstable DNA regions. Thus, they can be readily transferred to bacteria of the same species or even to non-related prokaryotes. Whereas microevolution leads to the emergence, in the short term, of new pathogenic or resistant variants, macroevolution over long periods of time, leads to the stable fixation in the pathogen genome of sequences encoding improved or new adaptive properties (Piffaretti and Frey, 1999). Different classes of repetitive DNA sequences are found in bacterial genomes and have a role in microbial pathogenesis and evolution.
eBook - PDF- Michele S. Swanson, Elizabeth A. Joyce, Rachel E. A. Horak(Authors)
- 2022(Publication Date)
- ASM Press(Publisher)
EVOLUTION • Mutations and horizontal gene transfer, with the immense variety of microenviron- ments, have selected for a huge diversity of microorganisms. CELL STRUCTURE AND FUNCTION • Bacteria have unique cell structures that can be targets for antibiotics, immunity, and phage infection. INFORMATION FLOW AND GENETICS • The synthesis of viral genetic material and proteins is dependent upon host cells. • Cell genomes can be manipulated to alter cell function. MICROBIAL SYSTEMS • Microorganisms, cellular and viral, can interact with both human and nonhuman hosts in beneficial, neutral, or detrimental ways. 648 | PART IV MICROBIAL PATHOGENESIS Introduction O ne way that microbes cause disease is by secreting toxins. If you’ve endured an acute episode of nausea and vomiting only hours after dining out, the culprit may well have been a heat- stable toxin deposited in your food by Staphylococcus aureus. In fact, microbes produce an impressive variety of toxins. Some are general- ists, such as the cytotoxins that kill host cells by either degrading or form- ing pores in their membranes. Others act with exquisite specificity, as the paralysis caused by Clostridium tetani’s neurotoxin dramatically illustrates. Certain toxins are encoded on mobile genetic elements acquired by some— but not all—strains of the species; the genes for other toxins are embedded in the species’ core genome. To illustrate the power of a toxin and horizontal gene transmission, here we will focus on one pathogen, Vibrio cholerae. By analyzing cholera epidemics, we’ll see how lysogenic and lytic phages can drive the evolution of their bacterial hosts. In addition, we’ll appreciate the impact of lipopolysaccharide (LPS) recognition by host antibodies and by predator phages.
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