The skin

The skin provides a major barrier to the invasion of pathogenic bacteria. Many of the immune responses are initiated within the epithelial and dermal layers of the skin where the mast cells, macrophages and dendritic cells are situated. At birth the skin is sterile but rapidly becomes colonised by micro‐organisms. The majority of these are harmless and are called commensal; they have a role in protecting the skin from being colonised by potentially pathogenic organisms. However, it is acknowledged that transmission of hospital‐acquired infection from the skin of healthcare workers can occur with transfer of organisms to patients and equipment. Good hand hygiene is considered to be the most effective factor in the control of infection (Weston, 2013). Chapter 19 in Peate and Gormley‐Fleming (2015) provides further detail on the anatomy and physiology of the skin.

The mucosal surfaces of the body

The epithelial membranes that line the respiratory, gastrointestinal and urogenital tracts contain goblet cells that produce mucus, which provides lubrication of those surfaces and can trap invading pathogens. In the respiratory tract, the cilia that line the tract move the mucus towards the mouth and nose so that inhaled pathogens can be removed by sneezing and coughing. Children with cystic fibrosis have recurrent respiratory tract infections because they are unable to expel the invading microbes. They require nebulised mucolytic drugs to reduce the viscosity of the mucus and daily physiotherapy to assist with its removal.

Apart from providing a physical barrier, the mucosal surfaces also produce chemical substances that are antimicrobial. Lysozyme is an antibacterial enzyme that is present in tears, perspiration and saliva, which can break down some bacterial cell walls. These secretions provide an acidic environment within which most bacteria are unable to survive. In the stomach, hydrochloric acid is secreted and the low pH in conjunction with the bile salts and digestive enzymes helps to destroy ingested pathogens. An individual who is unable to secrete gastric acid may be more susceptible to gastrointestinal infections such as Salmonella (Macpherson & Austyn, 2012; Helbert, 2017).

Another barrier to infection is the presence of commensal bacteria that are found on mucosal surfaces in the gastrointestinal tract, respiratory tract and the vagina and epithelial surfaces of the skin. These are micro‐organisms that are found normally on these surfaces; they are sometimes referred to as ‘friendly’ bacteria as they form a barrier and prevent colonisation of pathogenic bacteria. This barrier can be disrupted by antibiotic treatment, which removes the commensal bacteria and the resulting invasion of the pathogenic organisms causes disease.

Phagocytosis

Phagocytosis is the process by which an invading organism is destroyed by phagocytic blood cells – the neutrophils and macrophages. These cells provide the body’s first line of cellular defence and engulf, ingest and destroy the organism intracellularly. They are effective in removing small extracellular organisms, such as bacteria, small parasites (protozoa), fungi, and damaged and dead cells (Helbert, 2017). This is a crucial mechanism in the host defence against infection as it ensures that many infectious organisms do not become pathogenic to the individual as they are eliminated very quickly (see Fig. 5.4).

The two types of blood cells that are mainly involved in phagocytosis are neutrophils, and macrophages, which are derived from monocytes. Neutrophils and monocytes are both produced from the same stem cell in the bone marrow, more neutrophils than monocytes are produced on a daily basis. The neutrophils have a short life span (1–2 days) and are not normally present in tissues but, they respond very quickly when an infection occurs. They migrate quickly to the site of infection by a process of chemotaxis, where chemicals released by the invading bacteria and proteins at the site of infection stimulate this response.

The neutrophils have receptors that recognise bacteria and other pathogens (Helbert, 2017). They are essential for the defence against pyogenic (pus‐forming) bacteria such as Staphylococcus and Streptococcus. During an infection the number of neutrophils will increase rapidly and the blood levels of neutrophils will be increased. The rapid production of neutrophils by the bone marrow is further stimulated by colony‐stimulating factors released by the tissue macrophages. Neutrophils are highly phagocytic and once they have engulfed the invading microbe, antibactericidal enzymes such as lysozyme contained within the cytoplasmic granules are released to destroy it.

Monocytes enter the tissues where they develop into macrophages. The macrophages are present in most body tissues and form an important part of the innate immune system. They possess receptors that can distinguish between different types of infectious agents, such as viruses, bacteria and fungi. Some of these receptors enable the macrophage to phagocytose the invading organism and others stimulate the release of cytokines. These are small hormone‐like enzymes that attract neutrophils to the site of infection and also initiate the adaptive immune response. When an infection occurs, large numbers of monocytes migrate to the site of infection with neutrophils and develop into macrophages that have enhanced phagocytic properties in addition to those of the resident tissue macrophages. These are sometimes known as inflammatory macrophages. Once phagocytosis has occurred further enzyme pathways are activated. This is known as the oxidative burst and toxic molecules are produced to damage the pathogens. Children with a rare immune deficiency called chronic granulomatous disease are unable to initiate this oxidative process and although they present with normal levels of neutrophils that can migrate and initiate phagocytosis, they are unable to kill the invading bacteria. These children will present with an increased incidence of fungal and pyogenic (staphylococcal and streptococcal) infections such as abscesses, ear, nose and throat infections and pneumonia, and their inability to clear these infections can result in the formation of granuloma – a feature of chronic infection (Helbert, 2017).

When the phagocyte dies at the site of inflammation, lysis occurs and the cell releases its contents including the enzymes into the surrounding tissues. This can cause the tissue damage associated with inflammation.

Inflammation

If microbes succeed in getting across these barriers, the innate immune system responds rapidly in an attempt to eliminate them by the process of inflammation and and by antiviral mechanisms (Abbas et al., 2016).

Inflammation is the body’s non‐specific response to tissue damage or injury and forms an essential part of the innate immune system. The role of inflammation is to localise and minimise the tissue damage and to ensure that the specialised cells and molecules that are required to deal with the infectious agent are transported to the correct place to allow healing to take place (Macpherson & Austyn, 2012).

Causes of inflammation

Any type of tissue damage will stimulate the inflammatory response even if infection is not present. This could be:

• trauma (this includes a cut with a sterile scalpel)
  
• irritation with chemicals, including extremes of pH
  
• extreme heat
  
• infection by pathogens.

Recognition of infection in a peripheral site leads to local inflammation. The characteristic signs of inflammation are redness, heat, swelling and pain. If the infection is of a short duration and the infectious agent is rapidly removed, the response is known as acute inflammation, such as in the case of a skin abscess, an otitis media (ear infection), meningitis and pneumonia.

In cases where the infection is prolonged and the microbes are still present, the inflammatory process continues with much more extensive tissue damage and this is described as chronic inflammation, which can be seen in wound infections, bone infections and deep‐seated infections associated with internal organs such as a liver abscess, which can be life threatening. There are also situations where the body is unable to clear the infection such as in tuberculosis. In this case the infective organism is Mycobacterium tuberculosis, which may persist for many months or years and lead to the formation of granulomas, which are groups of specialised macrophages that surround the infective organism to wall it off from the rest of the body.

Inflammation at the site of infection can also affect more distant sites and this is known as the systemic effects of infection. This leads to the rise in temperature (pyrexia), loss of appetite and malaise associated with an infection.

The inflammatory process

When injury, either from trauma or infection occurs, mast cells that are present in the connective tissue release the inflammatory mediators histamine and serotonin. These substances act on the blood vessels causing vasodilatation (increase in the diameter), which increases the blood flow to the affected area providing oxygen and nutrients for the cellular activity that takes place. There also changes within the endothelial cells of the blood vessels where the adhesiveness is increased. This allows the increased number of leukocytes that have been recruited to the area as part of the inflammatory response to enter the inflamed area (Murphy & Weaver, 2016). The increased blood flow causes the heat and redness associated with the inflammatory response.

The inflammatory mediators also make the blood vessels more permeable and, in conjunction with the increased blood flow, allow fluid from the plasma in the blood to leak out of the capillaries into the surrounding tissues. The fluid contains plasma proteins including antibodies and clotting factors. This increases the osmotic pressure within tissues, drawing more fluid out of the blood vessels, which forms swelling within the tissue called oedema.

Other plasma proteins are activated during the inflammatory process; these include the kinins and the complement system as well as the antibodies and clotting factors. Kinins affect the dilation and permeability of the blood vessels and also form bradykinin which, with prostaglandins, stimulate pain nerve fibres. The complement system consists of soluble proteins circulating in blood, becoming activated when in contact with foreign cells such as bacteria and fungi. They also cause vasodilation and attract the phagocytic cells (neutrophils and macrophages) to the affected areas by chemotaxis (release of chemicals to attract them). Another function of the complement is to enhance the process of phagocytosis by opsonisation where the microbes are coated with complement, and are directed to specialised receptors on the phagocytes, which increases their uptake and elimination by the phagocytes. Complement seems to be particularly effective against pyogenic (pus‐forming) bacteria such as Streptococcus pyogenes and Staphylococcus aureus, and children who have a genetic defect in their ability to produce complement are very susceptible to these infections. Complement deficiency may also contribute to autoimmune disease such as systemic lupus erythematosus and other immune deficiencies (Abbas et al., 2016; Helbert, 2017).

The clotting factors are stimulated to arrive at the site of inflammation and migrate through the permeable cell walls of the blood vessels where they start to produce fibrin. This forms an insoluble mesh within the tissue space, which helps to localise the infected area and to trap the invading bacteria and prevent the spread of infection. See Figures 5.5 and 5.6.

Wound healing and abscess formation

Acute inflammation causes tissue damage; an important part of inflammation is to stimulate the process of repair and healing (Macpherson & Austyn, 2012). Where there has been minimal destruction of tissue (e.g., when there has been a cut in a surgical incision) healing takes place by primary healing (also called first intention). Wounds heal by tissue regeneration and repair. Generally, in children, wounds will heal quickly and require minimal intervention (Jonas et al., 2010).

Platelets adhere to the cut surfaces; a blood clot is formed and stabilised by the fibrin laid down with cell debris filling other spaces. Monocytes move into the area and differentiate into inflammatory macrophages and they begin to remove the cell debris by ingesting and digesting the damaged cells (Macpherson & Austyn, 2012). They also stimulate the production of fibroblasts, which form collagen and other connective tissue within the inflamed area bringing wound margins together.

If the inflammation is caused by infection, the tissue damage is more extensive with increased recruitment of neutrophils and macrophages. The healing of the affected area may be delayed with increased formation of collagen and scarring of the tissue, known as healing by second intention. As part of the inflammatory process there may be separation of necrotic (dead) tissue from healthy tissue due to the action of phagocytes within the inflammatory exudate, this is known as slough. Figure 5.7 demonstrates the stages of wound healing.

Acute inflammatory reactions to extracellular bacteria result in the formation of pus. These extracellular bacteria are known as pyogenic (pus‐forming) and exist and multiply in extracellular tissues and fluids. Some of these bacteria include: Staphylococcus aureus, which can cause skin abscesses; Streptococcus pyogenes, which causes throat infections; Haemophilus influenzae and Streptococcus pneumoniae, which cause respiratory infections.

A collection of pus within a cavity is called an abscess, superficial ones often occur under the skin – a boil is a collection of pus within an infected hair follicle. Superficial abscesses often rupture spontaneously on to skin surface discharging pus whereas deeper‐rooted abscesses may rupture and only discharge some of the pus to the surface leaving an open infected channel or sinus. Fig. 5.8 demonstrates a pilonidal sinus.

Abscesses can also rupture and discharge into an adjacent organ forming a channel open at both ends called a fistula. In some chronic infections, these abscesses can be surrounded by fibrous tissue forming granuloma but containing live infective organisms as seen in tuberculosis.

Wounds

Jonas et al. (2012) describe the types of wounds commonly seen in children:

• cuts from accidental and non‐accidental injuries
  
• animal bites
  
• burns and scalds
  
• surgical wounds
  
• pressure‐related, which can be from equipment (e.g., saturation probe) or in relation to a child’s immobility
  
• extravasation following intravenous fluid and drug administration
  
• congenital abnormalities, e.g., epidermis bullosa.

When assessing a child’s wound, the children’s nurse needs to consider the size and location of the wound and the underlying cause. Other factors to consider are the progression of the wound healing and any evidence of exudate, infected, sloughy or necrotic tissue. The child will need to be assessed for pain during wound dressing, and analgesia should be administered prior to the procedure as required.