Medical Microbiology and Infection at a Glance - Stephen H. Gillespie

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       Endospore: The presence, shape and position of the endospore within the bacterial cell are noted.

       Fastidiousness: Certain bacteria have specific O2/CO2 requirements, need special media or grow only intracellularly.

       Key enzymes: Presence or absence of certain enzymes, for example, lack of lactose fermentation helps distinguish salmonellae from E. coli.

       Serological reactions: Interaction of antibodies with surface structures may for example help to distinguish subtypes of salmonellae, Haemophilus and meningococcus.

       DNA sequences: DNA sequencing of key genes (e.g., 16S ribosomal RNA or DNA gyrase) can identify the organism precisely.

      Gram‐positive cocci are divided into two main groups: the staphylococci (catalase‐positive), the major pathogen being S. aureus; and the streptococci (catalase‐negative), the major pathogens being Streptococcus pyogenes, which causes sore throat and rheumatic fever, and S. agalactiae, which causes neonatal meningitis and pneumonia (see Chapters 18 and 19).

      Gram‐negative cocci include the pathogens N. meningitidis, an important cause of meningitis and septicaemia, and N. gonorrhoeae, the agent of urethritis (gonorrhoea).

      Gram‐negative coccobacilli include the respiratory pathogens Haemophilus and Bordetella and zoonotic agents, such as Brucella and Pasteurella (see Chapter 27).

      Gram‐positive bacilli are divided into sporing and non‐sporing. The sporing types are subdivided into those that are aerobic (Bacillus; see Chapter 16) and those that are anaerobic (Clostridium; see Chapter 24). Pathogens include Bacillus anthracis, which causes anthrax; and clostridia, which cause pseudomembranous colitis, tetanus and, more rarely, gas gangrene and botulism. The non‐sporing pathogens include Listeria and corynebacteria (see Chapter 20).

      Gram‐negative bacilli (including the family Enterobacteriaceae) can be part of the normal flora of humans and animals, and in the environment. They include many pathogenic genera: Salmonella, Shigella, Escherichia, Proteus and Yersinia (see Chapters 28 and 29). Pseudomonas and Burkholderia are environmental saprophytes that are naturally resistant to antibiotics and are important healthcare associated pathogens (see Chapter 31). Legionella lives in the environment in water but can cause human infection if conditions in the built environment allow it to gain a foothold (see Chapter 31).

      Spiral bacteria include the small gastrointestinal Helicobacter that colonizes the stomach, and may lead to gastric ulcers, duodenal ulcers and gastric cancer. Campylobacter spp. can cause acute diarrhoea (see Chapter 33). The Borrelia may cause a chronic disease of the skin joints and central nervous system, Lyme disease (Borrelia burgdorferi), or rarely relapsing fever (Borrelia duttoni and Borrelia recurrentis). The Leptospira are zoonotic agents that cause an acute meningitis syndrome that may be accompanied by renal failure and hepatitis. The Treponema include the causative agent of syphilis (Treponema pallidum) (Chapter 33).

      Mycoplasma and Chlamydia are responsible for common respiratory and sexually transmitted infections (Chapter 33).

      Rickettsia are the agents of typhus and rarer severe infections (see Chapter 32).

Schematic illustration of the anatomy of innate immune system.

      The innate immune system, which consists of the normal flora, physical barriers such as the skin, antibacterial proteins and phagocytic cells, is an important defence mechanism against infection. Many responses to ‘harm’ are detected by pattern recognition molecules such as the Toll‐like receptors (TLRs), which trigger cascades that activate phagocytes and the immune response. For example, TLR‐4 recognizes lipopolysaccharide and TLR‐9 recognizes unmethylated CpG dinucleotides. The main components of the system are listed in the Table in the next chapter. Variation in the expression/composition of each component affects an individual’s resistance to infection.

      Complement is a system of plasma proteins that collaborate to resist bacterial infection, which is activated by antigen–antibody binding (the classical pathway) or by direct interaction with bacterial cell wall components (the alternative pathway). The products of both processes attract phagocytes to the site of infection (chemotaxis), activate phagocytes, cause vasodilatation and stimulate phagocytosis of bacteria (opsonization). The final three components of the cascade form a ‘membrane attack complex’ that can lyse Gram‐negative bacteria. Complement deficiencies render patients susceptible to acute pyogenic infections, especially with Neisseria meningitidis, Neisseria gonorrhoeae and S. pneumoniae.

      Multiple plasma proteins work to protect against infection and some of these increase very significantly in response to inflammation; these are known as acute phase proteins. Some of these are antibacterial e.g., mannose‐binding protein and can activate complement. C‐reactive protein (CRP), activates complement when it binds to bacteria and, uniquely there are no fully deficient patients. Other proteins such as transferrin sequester iron that is vital for invading organisms, and limits the amount available them.

      The adaptive immune response is essential for defence against infection. This complex system provides immune responses to individual microorganisms. Organisms express a multiplicity of antigens that are displayed on the surface of the pathogen and detected by cells of the immune system. Antigens depend on the tertiary structure of the surface proteins or polysaccharides. Short peptide or carbohydrate sequences bound by immune responsive cells are called epitopes. These immunogenic epitopes are organism sub‐components such as surface proteins, parts of toxin molecules or virus proteins expressed

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