Chapter 4 Infection

Infection

There are very many infections: the chapter will deal only with principles and a few examples.

Type of Infecting Agent	Example	Example of Disease
BACTERIA (a very wide range)	STAPHYLOCOCCUS	ABSCESS
VIRUSES (a wide range)	HERPES ZOSTER	CHICKENPOX and SHINGLES
FUNGI (a limited range)	CANDIDA	BUCCAL and VAGINAL THRUSH
PROTOZOA	PLASMODIUM	MALARIA
Infestation with PARASITES WORMS and FLUKES	ECHINOCOCCUS GRANULOSIS	HYDATID DISEASE

Colonisation and Commensal Growth

Vast number of bacteria normally colonise the external body surfaces (skin, alimentary and upper respiratory tracts). These commensal inhabitants usually do not harm the host. Organisms that injure the host are said to be pathogenic. If the host defences are damaged a commensal organism may cause an opportunistic infection.

Infection and Infectious Disease

infection occurs when microorganisms invade the sterile internal body tissues. (Multiplication usually follows invasion.)

An infectious disease occurs when infection is associated with clinically manifest tissue damage.

Factors Influencing the Establishment of Infection

1. In the HOST

In addition to a good state of general health and nutrition, the following mechanisms operate in preventing and limiting infection.

Factors Influencing the Course of Infection

Once infection has occurred, important defence mechanisms operate:

1. Inflammation in the acute local reaction (see p.33) tends to limit the spread of organisms. In some important diseases, there is no acute local inflammatory response at the site of entry, e.g. Brucellosis (undulant fever) and many virus infections. In the chronic inflammatory reaction (see p.41), the formation of fibrous tissue also helps to localise infection.

2. Phagocytosis (see p.36) Note: some organisms may survive or multiply within phagocytes – usually associated with chronic infection. Good examples are tuberculosis, brucellosis, leprosy.

3. The Immune Response

(a) Humoral antibody reactions, e.g. agglutination, opsonisation, lysis via complement – especially important in bacterial infections.

(b) Cellular immunity reactions, e.g. cytotoxic T cells, especially important in viral infections.

4. Cytokines – signalling molecules that regulate the immune response to pathogens.

Examples of Failure of Protective and Defence Mechanisms

1. In skin – direct breach by wounding and burns; softening of the surface by exposure to water and sweat or due to skin disorders.

2. In the respiratory tract – inhibition of ciliary movement by nicotine in smokers potentiates infection.

3. In the stomach – in achlorhydria (no hydrochloric acid) organisms flourish in the stomach.

4. When secretions are prevented from flowing freely by narrowing of natural passages, bacterial growth in the ‘stagnant’ fluid is potentiated (e.g. enlarged prostate urethral obstruction, urinary infection).

5. When commensal growth is impaired by antibiotic treatment, pathogenic bacteria may colonise the ‘vacant site’.

6. Deficiency of the immunological system:

(a) natural deficiency due to hereditary defect, e.g. X-linked agammaglobulinaemia

(b) acquired due to administration of drugs in treatment of disease, e.g. steroids, cytotoxic drugs; specific virus infection, e.g. Human Immunodeficiency Virus (HIV) causing Acquired Immune Deficiency Syndrome (AIDS).

7. Deficiency of phagocytosis – especially polymorphs (either low numbers or deficient function – see page 36).

8. In debilitating diseases such as diabetes, chronic failure and nutritional deficiency.

9. Genetic susceptibility – may be a factor in some infections.

Mechanisms by which Disease is Produced

The local reaction to infections is usually INFLAMMATORY and is evoked by cellular damage and death. The detailed mechanisms are different in bacteria and viruses.

Bacteria

1. Production of toxins (poisons)

Exotoxins	Endotoxins
Secreted by living bacteria	Integral part of bactrial cell wall Release on death of organism (usually Gram-negative)
Simple proteins	Lipid-polysaccharide complexes
Neutralised by specific antibody (antitoxin)	Do not stimulate antibody production
Many actions – Enzymes, e.g. S. aureus protease – Action on intracellular signalling, e.g. V. cholerae – Neurotoxins, e.g. C. botulinum – Superantigens, e.g. S. pyogenes	Beneficialeffects:Inlowdosestimulatesprotectiveimmunity Harmful effects: In high dose ENDOTOXIC SHOCK – due to massive release of cytokines with activation of coagulation,fibrinolytic and complement cascades LPS binds cell surface receptor CD14 and is delivered to TLR4 that starts intracellular signalling cascade