Infection

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Chapter 4 Infection

Infection 62–67
Acute Bacterial Infection 68–71
Chronic Bacterial Infection (Granulomas) 72–76
Virus Infections 77–80
Host/Virus Interaction 81, 82
Opportunistic Infections 83
Infection – General Effects 84, 85

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.

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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.

Routes of Entry of Infecting Organisms

1. Through the skin or mucous membranes

(a) By direct close contact, e.g. venereal disease, HIV.
(b) By contamination of abrasions and wounds, e.g. wound infections, rabies.
(c) By inoculation, e.g. insect bite – yellow fever, syringe – hepatitis B and C, AIDS.

2. By ingestion

Contaminated food and water, e.g. enteric fever, hepatitis A, poliomyelitis, cholera.

3. By inhalation

Dust and droplets, e.g. influenza: tuberculosis.

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.

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Chemical Action

(a) Acid secretion in stomach and urinary tract.
(b) Lysozymes – enzymes capable of dissolving bacterial capsules, e.g. in tears and saliva.
(c) Immunoglobulin A (IgA) – a specialised immunoglobulin (see p.97), – tears, intestinal secretions.
(d) Non-specific inhibitory substances – urine, sweat, sebum.

Innate Immune Response

(a) NK cells and macrophages.
(b) Plasma proteins including the complement system.
2. In the MICRO-ORGANISM

Factors potentiating invasive capacity include:

(a) Quantity of dose – the larger the dose the more likely that the defences are penetrated.
(b) Virulence – describes the degree of pathogenicity, includes:

(i) Capacity to resist phagocytosis and enzyme attack,
(ii) Adhesive properties,
(iii) Production of exoenzymes which act on host tissues, e.g. hyaluronidase (streptococci), coagulase (staphylococci) and of toxins, e.g. leucocidins, enterotoxins.

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

2. Hypersensitivity reaction causing tissue injury

This is a form of the immune response in which reaction between the bacterial protein and sensitised lymphocytes initiates the inflammatory reaction (see p.101).

3. Tissue invasion: lymphatic spread and invasion of blood stream

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Sepsis Syndrome

Sepsis is a very serious condition in which there is a whole-body inflammatory state (systemic inflammatory response syndrome (SIRS)) in the presence of infection.

Mortality is still between 20 and 50% even with modern medical treatment. It commonly occurs in response to lipopolysaccharide (LPS) in the wall of Gram negative bacteria.

Mechanisms

LPS triggers innate immunity via TLR4. With infection disseminated via the bloodstream there is widespread activation of phagocytes.

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The initial stimulus triggers production of proinflammatory cytokines, and monocytes and neutrophils adhere to endothelium. Activated macrophages, neutrophils and endothelial cells release secondary inflammatory mediators. This release of proinflammatory cytokines is known as a cytokine storm. Procoagulants produced by endothelial cells may trigger microthrombosis and if widespread this is known as disseminated intravascular coagulation.

Bacteraemia

(a) Occurs commonly: usually of no serious significance
(b) An integral part of some infections, e.g. typhoid fever.

Important Special Cases

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Pyaemia

Pyaemia occurs when pathogenic organisms escape into the bloodstream in the form of small aggregates – micro-emboli. This results in either:

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Acute Bacterial Infection

Pyogenic Bacteria

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Note: Rheumatic fever and acute glomerulonephritis are complications of streptococcal infection in which the heart and kidneys are damaged. This is caused by disturbance in the immune mechanisms (type III hypersensitivity reaction) and is not due to the actual presence of streptococci in the heart and kidneys.

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