**4. Some immunological information**

Before discussing this point some general knowledge concerning immunology is required. We do not refer to immunology as a whole (as the matter covers very wide aspects), but only to infection resistance.

The host defence to bacterial infections happens through two classical mechanisms, i.e.:

a.natural **non-specific** immunoresistance (humoral and cellular factors mainly related to phagocyte reactions) [7].

b.acquired **specific** immunity (specific antibodies production and Ag-Ab reaction).

We shall mainly focus on the **former** mechanism, as its deficiency is considered as the major cause of chronic septical forms; it is the fastest and it arises through humoral and cellular factors (in order to summarise we shall treat the matter in very schematic terms).

Humoral factors may be divided principally in three species.

• **The complement (C)** (a biological entity showing itself through the concomitant action of several constituents, some of which are thermolabile) comprehends a group of known substances, that are present in fresh serum and able to interact, in clearly defined sequence, with all possible kind of Ag-Ab combination.

The **C** does not show any antibody activity and there is no evidence that its blood levels increase as a consequence of immunisation processes. It has been however evidenced (Lopow, Beker) that at least some C components have enzymatic activity against the bacterial cellular walls, that therefore are opsonised and become weaker to the phagocyte action.


Metchnikoff considers that cells with the capability to phagocitate are essentially:

**Figure 1.** *Genesis of the immunolgical cells.*

*Specific Bacterial Immunotherapy in Treating Chronic Osteomyelitis DOI: http://dx.doi.org/10.5772/intechopen.98751*


With reference to **specific activity** brought about by the production of most often Permanent Ab, it does not seem that staphylococci infections have such characteristics. A study by Ring shows indeed that only 26 cases on 112 have an increased antistaphylolysinic level.

It has been observed that the staphylococci pathogenicity appears on one side as an increased resistance to the defensive powers of the patient and on the other side as a capacity to establish a kind of allergy that further reduces body defences. The production of toxins might have only a minor role in the pathogenicity (Zironi) [2]; as a matter of fact there is no parallelism between germ virulence and the seriousness of the illness. It has been observed that the two factors provoking allergy (hypersensitivity against the germ or its products and increased reaction capacity) do not always evolve in parallel but may show different evolution.

Sensitivity to the micro-organism and its antigens, without variation of the host reactivity may beobserved and such a mechanism induces a very dangerous condition, called by immunologists "specific hyperreceptivity". Such a mechanism could account as an explication how this state may grow by inappropriate use of antibiotics.

Insufficient immunitary system predisposition to the entrance of the germ inadequate microbial sterilisation (inappropriate antibiotics – dosage – choice) bacterial persistence, even only latent stimulation repeated in the time hyper-receptivity (**Figure 2**).

**Figure 2.** *The cascade for arrive to the hyper-receptivity.*

**Figure 3.** *Summary opsonization-phagocytosis of the "macrophages".*

**Figure 4.** *Phagocytosis of the staphylococci from "macrophagis".*

We have many actions in the aspecific immunological activity but one of the most important action is the activity of the Macrofages to fight staphylococcus and the action is the opsonization (**Figures 3** and **4**) [10].
