10 Bacterial infections
Although most bacteria are saprophytes which grow on organic matter in the environment, a small number, referred to as bacterial pathogens, produce infection and disease in animals and humans. The development and severity of infections with many pathogenic bacteria are influenced by host-related determinants such as physiological status and immune competence.
Animals may be exposed to infection from exogenous or endogenous sources. Exogenous infections occur after direct or indirect transmission from an infected animal or from the environment. Endogenous infections can be caused by commensal bacteria when an animal is subjected to stressful environmental factors. Infections can be acquired by a number of routes. In exogenous infections, pathogens may enter the host through the skin, the conjunctiva or the mucous membranes of the respiratory, gastrointestinal or urogenital tracts or be vector-borne. Other possible routes of entry include the teat canal and the umbilicus.
The virulence of a bacterium relates to its ability to invade and produce disease in a normal animal. Highly virulent organisms produce serious disease or death in many affected animals whereas bacteria of low virulence rarely produce serious illness. Factors which influence the outcome of interactions between host and pathogen are illustrated.
Avoidance of defence mechanisms is essential for successful invasion of the host by pathogens. Some of the mechanisms which assist bacterial survival in animals are presented in Table 10.1. Certain bacteria remain at the site of primary infection with local extension only. This localized invasion may be facilitated through breakdown of host tissues by collagenases, lipases, hyaluronidases and fibrinolysin produced by bacterial pathogens. Bacteria can be carried throughout the body in the bloodstream. In bacteraemia, bacteria are present transiently in the bloodstream without replication, whereas in septicaemia pathogenic organisms multiply and persist in the bloodstream, producing systemic disease.
Table 10.1 Mechanisms which assist bacterial survival in the host.
| Mechanism | Comments |
| O antigen polysaccharide chain | Length of polysaccharide chain hinders binding of the membrane attack complex of complement to the outer membrane of many Gram-negative bacteria |
| Capsule production | Antiphagocytic role in many bacteria |
| M protein production | Antiphagocytic activity in Streptococcus equi |
| Production of Fc-binding proteins | Staphylococci and streptococci produce proteins which bind to the Fc region of IgG and prevent interaction with the Fc receptor on membranes of phagocytes |
| Production of leukotoxins | Cytolysis of phagocytes by toxins produced by Mannheimia haemolytica, Actinobacillus species and other pathogenic bacteria |
| Interference with phagosome–lysosome fusion | Allows the survival of pathogenic mycobacteria within phagocytes |
| Escape from phagosomes | Survival mechanism used by Listeria monocytogenes and rickettsiae |
| Resistance to oxidative damage | Allows survival of salmonellae and brucellae within phagocytes |
| Antigenic mimicry of host antigens | Adaptation of surface antigens by Mycoplasma species to avoid recognition by the immune system |
| Antigenic variation of surface antigens | Mycoplasma species and borrelliae can partially evade detection by the host's immune response |
| Coagulase production | Conversion of fibrinogen to fibrin by Staphylococcus aureus can isolate site of infection from effective immune responses |
Bacteria can damage host tissues directly through the effect of exotoxins and endotoxins. Bacterial exotoxins and endotoxins differ in their structures and modes of action (Table 10.2). Exotoxins are produced by Gram-positive and Gram-negative bacteria. The effects of exotoxins, which include cell membrane damage or interference with protein synthesis, are summarized in Box 10.1. Endotoxins of Gram-negative bacteria contain a hydrophobic glycolipid (lipid A) and a hydrophilic polysaccharide composed of a core oligosaccharide and an O-polysaccharide (O antigen). The toxicity of this complex lipopolysaccharide molecule resides in the lipid A portion. The effects of endotoxins are summarized in Box 10.2.
Table 10.2 Comparison of exotoxins and endotoxins.
| Exotoxins | Endotoxins |
| Produced by live bacteria, both Gram-positive and Gram-negative | Component of the cell wall of Gram-negative bacteria released following cell death |
| Proteins, usually of high molecular weight | Lipopolysaccharide complex containing lipid A, the toxic component |
| Heat labile | Heat stable |
| Potent toxins, usually with specific activity; not pyrogenic. Highly antigenic; readily converted into toxoids which induce neutralizing antibodies | Toxins with moderate, non-specific generalized activity; potent pyrogens, weakly antigenic; not amenable to toxoid production. Neutralizing antibodies not associated with natural exposure |
| Synthesis determined extrachromosomally | Encoded in chromosome |
Some individual pathogens tend to produce a predictable clinical picture following infection of a susceptible animal. Anthrax in ruminants is invariably peracute and fatal. In contrast, infections with bacteria such as Salmonella Dublin in cattle may produce many different forms of disease. Bacterial infections can be conveniently categorized as acute, subacute, chronic or persistent. Acute infections usually have a short clinical course and the invading bacteria are often cleared from the body by the host's immune response. Chronic infections tend to occur when the host fails to eliminate the pathogen. Persistent infections may occur in certain sites such as the uriniferous tubules and the central nervous system in which cell-mediated and humoral immunity are unable to exert their full effect.