During the inflammatory response the local activated macrophages release an endo-
genous pyrogen which acts on the part of the brain — the hypothalamus — that
controls the body temperature. The result is a slight increase in body temperature — a
fever, a symptom of inflammation. During inflammation the stimulated macrophages
secrete the cytokine interleukin-1 (IL-1) which has been shown to induce fever and
stimulate lymphocytes (T cells). Another cell secretion released into the blood serum
during inflammation is colony-stimulating factor (CSF) which induces the production of
leukocytes.
During the initial stages of inflammation the system generates products that firstly
enhance inflammation and then the same products serve as feedback to control the
inflammatory process. An example are the acute-phase reactants, a group of plasma pro-
teins synthesised by liver cells (hepatocytes) within 6–12 h of the commencement of the
immune response. These proteins serve mainly as protease inhibitors that try to limit the
damage to tissues.n 7. 3REACTION TO PARASITIC HELMINTHS
Once a helminth, whether an adult, juvenile or larval stage, enters the body proper (ie
it does not remain within the lumen of the alimentary canal), a host response is activated.
However most parasites have adapted to this situation (Fig. 1.2) and have evolved differ-
ent methods of avoiding the host’s immediate response. As long as the parasite remains
healthy and virile, the protective devices seem to be able to protect the parasite.
Host phagocytic cells try to adhere to the parasite but generally without any real
impact. If the parasite is damaged in any way, or becomes sluggish through age, many of
these host cells adhere and attempt to invade the parasite through its cuticle or tegument.
Neutrophils and tissue monocytes (histocytes) are usually the first cells on the scene
and, if they are activated, the parasite becomes sluggish and the neutrophils are replaced
by eosinophils. These cells and any other phagocytic cells that may become attached
release compounds that contain either reactive nitrogen and/or reactive oxygen inter-
mediates. These molecules damage the parasites and if their concentration increases they
can even become destructive to host tissue. Eosinophils adhere to the surface of parasites
and degranulate, releasing ingredients such as major basic protein (MBP), which is
destructive to parasite tissue. At this stage the parasite may be weakened by age or sim-
ply not properly adapted to the environment.
The number of adhering cells increases with new cells replacing the spent ones. These
cells gradually destroy the internal cells of the parasite and its tissues begin to degener-
ate. As destruction of the parasite increases the eosinophils on the outside are replaced
by epitheloid and fibrocyte (fibre-forming) cells.
With nematodes the cuticle often remains intact although the internal tissues degener-
ate, whereas in the tapeworm metacestode and the trematode adult and juvenile stages the
tegument also disintegrates. Eventually a fibrous capsule forms a round the dead worm.
Once the capsulation process is complete calcium is deposited in the capsule layers.
The system just described can be observed under experimental conditions. The filar-
ial nematode Dipetelonema viteaecan survive subcutaneously in a hamster — a permissive
host, but not in a mouse — a non-permissive host. If live adult worms are surgically trans-
planted just beneath the dermal layers of a mouse the process of inflammation and grad-
ual encapsulation of the parasite begins and, at about 20 days post-infection, the worms
are dead and completely encapsulated. If worms are killed by immersion in formalde-
hyde before transplantation, then the process of inflammation and encapsulation of the
worm begins after 1–2 days.PARASITOLOGY