Infection prevention and control - Royal Marsden Manual of Clinical ...

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84 Infection prevention and control Cell wall Cytoplasmic membrane Lipoteichoic acid Sugar subunit Peptide side chain (a) Gram-positive Protein Phospholipid (b) Gram-negative the stain in 1884. Put simply, the structure of the cell wall determines whether or not the bacteria are able to retain a particular stain in the presence of an organic solvent such as acetone. The structure of the cell wall determines other characteristics of the bacteria, including their susceptibility to particular antibiotics, so knowing whether the cause of a bacterial infection is Gram positive or negative can help to determine appropriate treatment ( Goering et al. 2007 ). The structure of the two different types of cell wall is shown in Figure 3.1 . Other structures visible outside the cell wall may include pili, which are rigid tubes that help the bacteria attach to host cells (or, in some cases, other bacteria for the exchange of genetic material), fl agellae, which are longer, mobile projections that can help bacteria to move around, and capsules, that can provide protection or help the bacteria to adhere to surfaces. These are illustrated in Figure 3.2 . The presence or absence of different structures will play a part in determining an organism’s pathogenicity – its ability to cause an infection and the severity of that infection ( Goering et al. 2007 ). A fi nal bacterial structure to consider is the spore. Bacteria normally reproduce by a process called binary fi ssion – they create a copy of their genetic material and split themselves in two, with each ‘daughter’ cell being an almost-exact copy of the parent (there are mechanisms by which bacteria can transfer genetic material between cells and so acquire characteristics such as antibiotic resistance, but they are beyond the scope of this chapter). However, some bacteria, notably Clostridium diffi cile , have the capacity, in adverse conditions, to surround a copy of their genetic material with a tough coat. Because this structure is created within the bacterial cell, it is sometimes referred to as an endospore, but is more often simply called a spore . The parent cell then dies and disintegrates, leaving the spore to survive until conditions are suitable for it to germinate into a normal, ‘vegetative’ bacterial cell that can then reproduce ( Goering Peptidoglycan Cell wall Cytoplasmic membrane Protein Lipopolysaccharide Figure 3.1 Gram-positive (a) and Gram-negative (b) bacterial cell walls. Used with permission from Elliot (2007). Outer membrane Lipoprotein Peptidoglycan Inner membrane Phospholipid et al. 2007 ). Spores are extremely tough and durable. They are not destroyed by boiling (hence the need for hightemperature steam under pressure in sterilizing autoclaves) or by the alcohol handrubs widely used for hand hygiene – hence the need to physically remove them from the hands by washing with soap and water when caring for a patient with Clostridium diffi cile infection ( DH/HPA 2008 ). Some medically signifi cant bacteria are listed in Table 3.2 . A few bacteria do not easily fi t into the Gram-positive/ negative dichotomy. The most medically signifi cant of these are the Mycobacteria , which are responsible for diseases including tuberculosis and leprosy ( Goering et al. 2007 ). Capsule Cell Wall Cytoplasmic Membrane Ribosomes Pili Cytoplasm Nucleoid Figure 3.2 Bacterial structures. Flagella
Table 3.2 Medically signifi cant bacteria Gram positive Gram negative Viruses Spherical Rod-shaped Staphylococcus aureus Streptococcus spp Neisseria meningitides Neisseria gonorrhoeae Clostridium diffi cile Clostridium tetanii Bacillus spp Pseudomonas aeruginosa Escherichia coli Legionella pneumophila Acinetobacter baumanii Salmonella Viruses are much smaller, and even simpler, than bacteria. They are often little more than a protein capsule containing some genetic material. They do not have cells, and some people do not even consider them to be alive. They have genes and will evolve through natural selection, but have no metabolism of their own. The most signifi cant characteristic of viruses is that they can only reproduce within a host cell, by using the cell’s own mechanisms to reproduce the viral genetic material and to manufacture the other elements required to produce more virus particles. This often causes the death of the cell concerned ( Goering et al. 2007 ). The small size of viruses (poliovirus, for example, is only 30 nanometres (nm) across) means that most are smaller than the wavelengths of visible light. They can only be ‘seen’ with a specialist instrument such as an electron microscope, which will only be available in a very few hospital microbiology laboratories. Diagnosis of viral infections is normally by the patient’s symptoms, with confi rmation by laboratory tests designed to detect either the virus itself or antibodies produced by the patient’s immune system as a response to infection ( Wilson 2000 ). There are viruses that specifi cally infect humans, or other animals, or plants, or even bacteria. This is one characteristic that can be used in classifying them. However, the main basis for classifi cation is by the type of genetic material they contain. This can be DNA or RNA, and may be in a double strand, as seen in other organisms’ DNA, or in a single strand. Other characteristics include the shape of the viral particle and the sort of disease caused by infection. The life cycle of all viruses is similar and can be summarized as follows ( Goering et al. 2007 ). 1 Attachment : a virus particle attaches to the outside of a host cell. Viruses are generally very limited in the types of cell that they can attach to, and normally infect only a single species or a limited range of related host organisms. Even a wide-ranging virus such as rabies is restricted to infecting mammals. 2 Penetration : the virus particle enters the host cell. The exact mechanism of this depends on the virus and the type of host. By cytolysis no envelope Release Assembly Infection prevention and control 3 Uncoating : the virus particle breaks down and exposes the viral genetic material. 4 Replication : the instructions contained in the viral genes cause the host cell mechanisms to create more viral particles. 5 Release : the new viral particles are released from the cell. Some viruses may ‘bud’ from the surface of the cell, acquiring their enclosing membranes in the process, but often release occurs due to cell rupture and destruction. This process is illustrated in Figure 3.3 . A fi nal point to consider in relation to viral structure and infection prevention and control is the presence or absence of a lipid envelope enclosing the viral particle. Those viruses that have a lipid envelope, such as herpes zoster virus (responsible for chicken pox and shingles), are much more susceptible to destruction by alcohol than those without, for example norovirus, which is a common cause of viral gastroenteritis. Fungi Infecting virus By budding forming envelope Capsids form around nucleic acid nucleus Penetration Replication Synthesis of viral messenger RNA. Synthesis of viral protein for new capsids. Synthesis of viral nucleic acid Uncoating Attachment receptor Capsid shed Figure 3.3 The viral life cycle. Used with permission from Perry (2007 ). Like bacteria, fungi exist in many environments on Earth, including, in some cases, as commensal organisms on human beings. Unlike bacteria, they are eukaryotic, so their cells share some characteristics with other eukaryotes such as humans, but they are distinct from both animals and plants. Fungi are familiar to us as mushrooms and toadstools and the yeast that is used in brewing and baking. They also have many uses in the pharmaceutical industry, particularly in the production of antibiotics. Fungi produce spores, both for survival in adverse conditions, as bacteria do, and to provide a mechanism for dispersal in the same way as plants ( Goering et al. 2007 ). 85
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Page 3 and 4: Box 3.1 Terms used when discussing
Page 5: Bacteria Bacteria are probably the
Page 9 and 10: the appearance of a sponge, hence t
Page 11 and 12: many of these organisms may be less
Page 13 and 14: of regular visits to clinical areas
Page 15 and 16: Assessment and recording tools Asse
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Page 27 and 28: Action Figure 5a Slide the fi ngert
Page 29 and 30: Postprocedure 11 At the end of the
Page 31 and 32: Action Figure 8d Push your hand thr
Page 33 and 34: ■ Traceability system for any reu
Page 35 and 36: Source isolation Evidence-based app
Page 37 and 38: Linen Place infected linen in a red
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Page 47 and 48: Table 3.7 (Continued) Management of
Page 49 and 50: DH/HPA ( 2008 ) Clostridium diffi c

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