10: Immunity and infection

Chapter 10 Immunity and infection

Bacterial, viral, parasitic and fungal infections are major causes of morbidity and mortality worldwide, especially in poorer societies with less access to medicines and vaccines, greater exposure to infectious agents and poorer nutrition. Infectious and parasitic diseases were responsible for 29.6% of the world’s disease burden in 1999, according to the World Health Organization (Table 10.1).

Table 10.1 Leading causes of infectious diseases worldwide

Infectious disease Cause Annual deaths
Acute respiratory infections (mostly pneumonia) Bacterial or viral 4 300 000
Diarrhoeal diseases Bacterial or viral 3 200 000
Tuberculosis Bacterial 3 000 000
Hepatitis B Viral 1 000 000–2 000 000
Malaria Protozoan 1 000 000
AIDS Viral 1 000 000
Measles Viral 900 000
Neonatal tetanus Bacterial 600 000
Pertussis (whooping cough) Bacterial 360 000

AIDS, acquired immune deficiency syndrome.

From The World Health Report (1999). WHO, Geneva.

All of the immunological mechanisms described in the previous two chapters are called upon to limit and eliminate infectious agents. However, pathogens have developed a remarkable variety of strategies to evade the host’s immune defences, and the immune response itself may damage host tissues.

Immunity to bacteria

Summary of defence mechanisms

Damage caused by immune responses to bacteria

Group A β-haemolytic streptococci cause sore throat and scarlet fever, which resolve on induction of specific antibody. Certain components of some strains of streptococci contain epitopes that are cross-reactive with epitopes present on heart tissue. Antibodies that eliminate the infecting bacteria can bind to heart tissue and cause complement-mediated lysis and antibody-dependent cellular cytotoxicity (rheumatic heart disease). Furthermore, circulating immune complexes can deposit in synovia and glomeruli, causing complement-mediated joint pain and glomerulonephritis, respectively. Induction of cross-reacting anti-heart antibody by group A streptococci is illustrated in Fig. 10.1 (see also Fig. 23.2).

Persistent infection of macrophages, e.g. with Mycobacterium tuberculosis or Mycobacterium leprae, provokes a chronic, local, cell-mediated immune reaction due to continuous release of antigen. Lymphokine production causes large numbers of macrophages to accumulate, many of which give rise to epithelioid cells or fuse to form giant cells (syncytia). These giant cells release high concentrations of lytic enzymes, which destroy the surrounding tissue. Incorporation of fibroblasts also occurs, and the persisting pathogen becomes walled off inside a fibrotic, necrotic granuloma. Because the macrophages in a granuloma are activated, this mechanism also enhances the activation of T-helper cells. Granulomas may replace extensive areas of normal tissue, e.g. in the lungs of tuberculosis patients.

Immunity to viruses

Viruses cannot proliferate outside a host cell. The infectious virion must attach to a suitable cell via a specific membrane receptor and enter the cell cytoplasm. Viral replication may or may not destroy the host cell. Viral genes may become incorporated within the host cell genome and remain in a state of latency for long periods. In some cases, integrated viral genes activate cellular oncogenes and induce malignant transformation.

Summary of defence mechanisms


At the end of the year 2008, approximately 40 million people worldwide had become infected with HIV and approximately 25 million had died of the acquired immune deficiency syndrome (AIDS) (see also Chapter 30). The virus causes depletion of CD4+ T-helper lymphocytes over many years. Patients eventually succumb to opportunistic infections (Pneumocystis carinii, M. tuberculosis, atypical mycobacteria, Histoplasma, Coccidioides, Cryptococcus, Cryptosporidium and Toxoplasma spp., herpes simplex, cytomegalovirus) and may develop Kaposi’s sarcoma, B cell lymphomas and other malignancies. Infection of the brain by HIV can cause dementia and encephalitis.

The major route of transmission of HIV is by sexual intercourse: male to female, female to male and male to male. It can also be transmitted from mother to foetus across the placenta, during delivery or by breast-feeding. Direct injection into the blood stream, e.g. by multiple use of needles and syringes for injection of drugs, also transmits HIV.

The life cycle of HIV is shown in Figure 10.2. The virus gains entry into target cells by binding its surface gp120 molecule (glycoprotein of 120 kDa) to CD4 on T-helper cells and a subset of macrophages. The latter can also take up opsonized HIV via Fc or complement receptors. A coreceptor is also required for infection of target cells: CXCR4, also known as fusin or LESTR, is the receptor for the chemokine SDF-1 and is the coreceptor for infection of T cells by HIV; CCR5, the receptor for chemokines RANTES, MIP-1α and MIP-1p, is the coreceptor for infection of macrophages. Viral gp41 cau/>

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Jan 4, 2015 | Posted by in General Dentistry | Comments Off on 10: Immunity and infection
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