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Chapter 1: Introduction to Medical Microbiology

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Chapter 1: Introduction to Medical Microbiology Chapter 1: Introduction to Medical Microbiology Medical microbiology is the study of parasites, fungi, bacteria, and viruses that are the agents of infectious disease in humans. Modern medicine relies on the control of microorganisms to maintain human health and quality of life. The divisions of medical microbiology include bacteriology, the study of bacteria that inhabit and/or colonize the human body and cause disease; mycology, the study of fungi as causative agents of human disease; parasitology, the formal study of the human parasitic organisms (protozoans, helminths, nematodes, trematodes and arthropods); and virology, the study of viruses that cause infectious syndromes in humans. Sizes for the pathogens considered include the smallest, viruses (50-100nm), bacteria that range from 0.1 µm (Chlamydiae) to 10µm (Bacillus rods), fungi ranging from ~8µm (yeasts) up to 10mm in size (filamentous fungi) and metazoan parasites that are visible to the naked eye. Medical microbiology as a discipline requires a working knowledge of human anatomy and histology, and a comprehension of the pathologies associated with the infectious disease process. The human immune response to pathogens is key to the consideration of infectious disease. Understanding the relationship between pathogens and antimicrobial pharmacology is essential as well. Microbiology places information about pathogenic organisms and their specific characteristics within the context of host disease. Developing connections between microbiology and immunology will make learning more effective in both disciplines. Special patient populations are important to consider and should be appreciated for the distinctive infectious disease presentations they reflect. Age-related immuno-compromised status makes the elderly and the very young, especially newborn infants, particularly at-risk for respiratory infections. Health-related immunosuppression can predispose organ transplant recipients, and patients with immunodeficiency disorders, cancer, and diabetes to difficult infections. And, unique exposures due to occupation or travel can be a problem for some patient populations. An immunocompromised person is lacking in some aspect of innate or adaptive immunity due to either a primary or secondary immune deficiency. Whatever the route, the net result is that the immunocompromised individual becomes susceptible to infection with a range of opportunistic pathogens from the commensal microflora and conventional infectious agents that cause a more severe form of disease than in a 'normal' host. This depends on how the patient's condition affects each limb of the immune system, which in turn controls the most likely pathogens. Immunity to infection and sensitivity to normal commensal microbes as pathogens varies throughout life and not just in 'disease' states. Host-Parasite Relationships A parasite is an organism that makes its living at the expense of another organism, so in a broad sense, all human pathogens fall under the blanket term “parasite”. A parasite derives its nutrients and ecosystem from the host and is able to grow and reproduce in this environment. Medical microbiology presents concepts relating host-parasite relationships and the human immune system’s response to infectious disease. Microbial ecology and system imbalance are keys to the understanding of many common diseases. The development of an infection and its eradication frequently involves issues that are defined as much by the host as by the microbial parasite, a balance between host immunity and the virulence of the infectious agent. NORMAL FLORA The normal microbial flora of the human body is located mainly in the superficial layers and gastrointestinal tract. Gastrointestinal pathogens have some resistance to gastric acid and bile and agents of skin infections are resistant to drying. Lower respiratory and upper urogenital tracts are sterile normally, but they are susceptible to microbial “invasion” from adjacent sites. Contamination occurs when microbes come into contact with host surfaces. Colonization. The skin of a newborn infant is populated initially by the organisms carried in the urogenital tract of the mother and acquired by the baby at birth. The mother’s skin and breath are additional sources of normal bacteria that become the infant’s commensal population, especially the mucosal normal flora. The Oral Cavity. Many of the “normal” flora can be disease-causing organisms under the right conditions. Viridans streptococci are largely responsible for dental caries and pitting of tooth enamel by Streptococcus mutans acidic metabolic by-products is well documented. Beneficial Effects. Vitamin synthesis and bile pigment degradation are two beneficial effects provided by bacteria to the host (Bacteroides species make vitamin K and degrade intestinal bile). Resident microflora inhibit the of growth of potential pathogens, as well as providing mechanical advantages such as suppression of competitor’s adherence, antigen priming of the immune system, maintenance of low redox potential, and bacteriocin secretion (inhibits the growth of bacterial competitors). NUMBER OF MICROORGANISMS IN COLLECTED SAMPLES Nasal Washings 106 microbes/ml fluid Saliva 108 microbes/ml Tooth Surfaces 108 microbes/ml Gingival crevices 1011-1012 microbes/ml PROKARYOTIC cells outnumber EUKARYOTIC cells in the human body, by a factor of 10 to 1! DISEASE PROGRESSION The period of total infection is from point of first contact until point of complete elimination of the pathogen. Overt disease is associated with the onset of symptoms. In a recurrent infection, the disease reappears over time with a characteristic rise and fall of agent shedding and symptomatic disease. The seropositive phase occurs where the patient has been exposed to a pathogen and has mounted an antibody response that is reflected in detectable levels of specific serum immunoglobulin. Incubation is defined as the period from the point of first contact until the point of appearance of symptoms of infection (when “disease is present”). Latent infections remain dormant, and then re-emerge after stress or a lapse in immune function. During the period of communicability the infectious agent is being continuously shed by the patient. To complete the cycle of infection, infectious agents are excreted, and the route of excretion dictates the mechanism of spread. Fecal-oral spread involves excretion within stool samples and may be aided by diarrhea. Pathogens are often aerosolized in respiratory secretions by sneezing and coughing. STD agents are transmitted by sexual contact with vaginal, cervical or urethral fluids. Zoonotic infections are diverse and cause diseases where humans are either a part of the normal infectious cycle or accidental hosts by contact with vectors or reservoir animals. Some of these agents are excreted in feces and urine, but also through parasitemia (widespread presence of the parasite). Examples include bloodstream parasitemia, to ensure uptake by blood-sucking insects (e.g. Anopheles mosquitos and malaria) and rabies virus budding from salivary gland cells to aid viral spread through animal bites. Pathogen Virulence Mechanisms. Host-parasite interactions can be described as pathogenic vs nonpathogenic (pathogenicity=ability to cause disease or multiply within a host), or invasive as opposed to a successful commensal avirulent status quo (the human as an ecological niche). Virulence is a concept of “degree of pathogenicity”. Some viruses and other pathogenic microbes characteristically cause disease and these may express highly specific adhesins or toxins. Virulent organisms cause a specific host injury that is removed when the gene encoding a specific toxin or trait is deleted. The genes controlling the synthesis of these factors are grouped together under the control of a single promoter in pathogenicity islands. Examples of virulence factors include the neurotoxin secreted by Clostridium tetani (tetanospasmin) and the capsule of Streptococcus pneumoniae that subverts phagocytosis by preventing ingestion. Toxin production is a common virulence factor and bacterial exotoxins can inhibit host cell protein synthesis, stimulate watery secretions, and cause violent symptoms of disease in the host. Attachment and adherence via specific epithelial and mucosal receptors (integrins) is another form of virulence because adhesion protects pathogens from the flushing of mucosal surfaces. Vibrio cholera binds to sites on the villi of the jejunum or ileum. Virulence is mediated by strength of attachment phenomena. Specifically pathogenic strains of Escherichia coli have capsular antigens (K1) that make the bacteria neurotrophic; most strains of E. coli are harmless commensal organisms that occupy space in the human gastrointestinal system. Inhibition of host immune mediators. Inhibiting host immune cell products to blunt the anti-microbial response is a strategy of many pathogens. Some organisms produce leukocidins that kill neutrophils and macrophages. Others have intracellular growth patterns that allow them to avoid detection by the host’s immune system (these will be discussed with the pathogen groups). Streptococcus pyogenes and Pseudomonas aeruginosa degrade human C5a using a peptidase enzyme. IgA protease is an immunoglobulin-destroying enzyme produced by Streptococcus pneumoniae, Neisseria meningitidis and Haemophilus influenzae. Complement compoenent C3b binding is inhibited by HSV envelope glycoprotein and vaccinia virus accelerates the decay of complement
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