Page 932 - Veterinary Immunology, 10th Edition

eventually reach the intestine or lungs where they develop into
VetBooks.ir adults. Clearly, the mechanisms that destroy these migrating larvae

in the tissues must be very different from those that expel large
adult worms from the intestine or airways.

In general, larvae and adult worms within tissues trigger type 2
immune responses and as a result are attacked by eosinophils and
basophils. Adult worms attached to mucosal surfaces are expelled
by IgE and cytokine-mediated mechanisms. Type1, cell-mediated

responses are relatively less important.
Because nematodes trigger type 2 immune responses, IgE levels
and eosinophil numbers are usually elevated in parasitized
animals. Additionally, many helminth infestations are associated

with the characteristic signs of type I hypersensitivity, including
eosinophilia, edema, asthma, and urticarial dermatitis. For example,
pigs infested with Ascaris suum show cutaneous allergic reactions to
injected parasite antigens, as well as degranulation of intestinal

mucosal mast cells. Mammals eventually develop limited immunity
to tissue helminths after several months. One parasite, Ostertagia
ostertagi, is an exception. Cattle remain susceptible to reinfection by
Ostertagia for many months, and immunity that can inhibit the

production of viable larvae is not seen until an animal is more than
2 years old. It is not surprising that this is the most economically
important bovine helminth parasite.

Immunity to Tissue Helminths
Larvae and some adult worms migrate through tissues where they

are attacked by inflammatory cells and molecules. Unlike bacteria
or protozoa, however, larval worms have a thick cuticle that
protects their vulnerable hypodermal plasma membrane. As larvae

develop and undergo periodic molts, damaged cuticles may be
shed to be replaced with new ones. These cuticles cannot be
penetrated by the terminal complement complex nor by T cell
perforins. Thus eosinophils and macrophages are the key to
destroying migrating larvae. Both possess FcεR (CD23) and can

therefore bind and kill IgE-coated parasites. Chitinases can degrade
helminth cuticles. Chitinases are produced by mast cells,
macrophages, and neutrophils. Some mammalian chitinases may

lack enzyme activity but can bind to helminth cuticles and serve as

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