Principles and Basic Mechanisms


Some infectious agents are strictly species selective. Amoebiasis, for example, only naturally affects humans. Even within a species, relative resistance is apparent, such as the decreased susceptibility of Duffy blood group negative individuals to Plasmodium vivax malaria.

Microorganisms are also highly specific with respect to the organ or tissue that they infect. This predilection for specific sites in the body relates partly to the milieu exterieur, i.e. the immediate environment in which the organism finds itself; for example, anaerobic organisms colonize the highly anaerobic colon, whereas aerobic organisms are generally found in the mouth, pharynx and
proximal intestinal tract. Other organisms that clearly show selectivity are:

• Streptococcus pneumoniae (respiratory tract)
• Escherichia coli (urinary and alimentary tract)

Even within a species of bacterium such as E. coli; different strains will show selectivity towards a particular organ, e.g. the enterotoxigenic E. coli causes acute diarrhoeal disease, whereas the uropathogenic E. coli is responsible for urinary tract infection.

Even within an organ a pathogen may show selectivity for a particular cell type. In the intestine, for example, rotavirus predominantly invades and destroys intestinal epithelial cells on the upper portion of the villus, whereas reovirus selectively enters the body through the specialized epithelial cells, known as M cells, that cover the Peyer’s patches.

Epithelial attachment

Many bacteria attach to the epithelial substratum by specific organelles called pili (or fimbriae) that contain a surface lectin(s): a protein or glycoprotein that recognizes specific sugar residues on the host cell. Such is the specificity of this attachment mechanism that it limits enterotoxigenic E. coli infection, for example, to certain species.

Some viruses and protozoa (Plasmodium, Entamoeba histolytica) also interact with their target -cell surface membrane by a similar mechanism. Other parasites such as hookworm have specific attachment organelles (buccal plates) that firmly grip the intestinal epithelium.

Multiplication and colonization

These follow epithelial attachment. Pathogens may then either remain within the lumen of the organ that they have colonized or may invade the tissues.

Invasion may result in:

1 An intracellular location for the pathogen (e.g. viruses,

Principles and Basic Mechanisms
Principles and Basic Mechanisms

Toxoplasma, Leishmania, Plasmodium)
2 An extracellular location for the pathogen (e.g. mycobacteria,
staphylococci and Entamoeba histolytica)
3 Invasion directly into the blood or lymph circulation (e.g. schistosome larvae, trypanosomes, Leishmania and Plasmodium) Once the pathogen is firmly established in its target tissue, a series of events follow that usually culminates in damage
to the host.

Tissue dysfunction or damage

The mechanism by which microorganisms produce disease has been the subject of intensive investigation and a number of well-defined mechanisms have now been described.

EXOTOXINS AND ENDOTOXINS. Microorganisms may secrete exotoxins. These have many diverse activities, including inhibition of protein synthesis (diphtheriatoxin), neurotoxicity (Clostridium perfringens, C. tetaniand C. botulinum) and enterotoxicity, which results inintestinal secretion of water and electrolytes (E. coli, v. cbolerae).Endotoxin is a lipopolysaccharide (LPS) in the cell wall of Gram-negative bacteria. It is responsible for many of the features of shock, namely hypotension, fever, intravascular coagulation and, at high doses, death.

TUMOUR NECROSIS FACTOR (TN F). This is released from a variety of phagocytic cells (macrophages/ monocytes) and non-phagocytic cells (lymphocytes, natural killer cells) in response to infections and inflammatory stimuli (Table 1.2). TNF itself then stimulates the release of a cascade of other mediators involved in inflammation and tissue remodelling, e.g. interleukin (IL-l and IL-6), prostaglandins, leukotrienes, corticotrophin. TNF is therefore responsible for many of the effects of an infection

Bacterial endotoxin (LPS)
Toxic shock syndrome toxin-l (TSST-l)
Mycobacterial cord factor (see p. 36)
Complement component CSa
Interleukin-l (tt-t)
Fungal and protozoal antigens
LPS, lipopolysaccharide.

TISSUE INVASION. Staphylococcus aureus has tissueinvasive qualities, e.g. abscess formation and bacteraemia, as well as producing toxins causing diarrhoea and a toxin responsible for a widespread erythema (staphylococcal scalded skin syndrome). Similarly, some pathogenic E. coli can produce tissue invasion without production of a specific toxin.

SECONDARY IMMUNOLOGICAL PHENOMENA. All organisms can initiate secondary immunological mechanisms, e.g. complement activation, immune complex formation and antibody-mediated cytolysis of cells.

Many infections are self-limiting, and immune and non-immune host defence mechanisms will eventually clear the pathogens. This is generally followed by tissue repair, which may result in complete resolution or leave residual damage.

Medical Assignments


Blastomycosis is a systemic infection caused by the biphasic fungus Blastomyces dermatitidis. Although initially believed to be

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