12 



INTRODUCTION TO PARASITOLOGY 



Resistance and Immunity to Para - 

 sites . This is such a tremendous sub- 

 ject that its facets can only be hinted at. 

 The general principles of immunology 

 apply to animal parasites as much as they 

 do to bacteria, viruses and other micro- 

 organisms. However, since the associ- 

 ation of many of the larger parasites with 

 their hosts is not as intimate as that of 

 microorganisms, the hosts' immune res- 

 ponses may not be as great. This is 

 especially true with regard to the forma- 

 tion of circulating antibodies. 



Immunity or resistance may be either 

 natural {innate) or acquired. Natural re- 

 sistance is the basis of host-parasite 

 specificity, but, as mentioned above, 

 little is known of its mechanism. Ac- 

 quired immunity may be either active or 

 passive. Active immunity results from 

 the body's own action. It follows expo- 

 sure to living or dead disease agents, and 

 can result from natural infection or arti- 

 ficial administration of virulent, attenu- 

 ated or killed organisms. 



One type of active immunity is pre- 

 munition. This is immunity due to the 

 continued presence of the disease agent. 

 It occurs in such diseases as babesiosis 

 and anaplasmosis. 



Passive immunity results from the 

 introduction of antibodies produced by 

 some other animal. It may be acquired 

 naturally, thru the colostrum or milk in 

 mammals or thru the egg yolk in birds, 

 or artificially by injection of antiserum. 

 Passive immunity is seldom as long- 

 lasting as active immunity. 



Immunity against parasites and dis- 

 ease agents generally increases with age. 

 There are exceptions, however. Young 

 cattle, for instance, are more resistant 

 to Babesia and Anaplasnia than are adults. 

 Age immunity may be either developed as 

 the result of previous exposure or it may 

 be natural. Not all the factors operating 

 in the latter case are known. An impor- 

 tant one is that very young animals can- 

 not mobilize their body defenses against 

 invasion as efficiently as adults. For in- 

 stance, they do not produce antibodies at 



first, depending on those acquired from 

 their mothers. Another factor, discov- 

 ered by Ackert and his co-workers (cf. 

 Ackert, Edgar and Frick, 1939) to explain 

 the relative resistance of older chickens 

 to Ascaridia galli, is that these birds have 

 more intestinal goblet cells than do young 

 birds. The goblet cells secrete mucus 

 which inhibits the development of the 

 worms. For further information on im- 

 munity in parasitic infections, see Talia- 

 ferro (1929), Culbertson (1941) and Soul- 

 sby (1960). 



Genetic constitution is also important 

 in determining resistance to parasites. 

 For instance, Ackert el al. (1935) showed 

 that Rhode Island Red and Plymouth Rock 

 chickens are more resistant to Ascaridia 

 galli than are Buff Orpingtons, Minorcas 

 and White Leghorns. Cameron (1935) 

 found that in a mixed flock of sheep. Chev- 

 iots were less heavily parasitized with 

 gastrointestinal nematodes than Shetlands 

 and Scottish Blackface, and that these in 

 turn were less heavily parasitized than 

 Border Leicesters. Stewart, Miller and 

 Douglas (1937) found that Romney sheep 

 were markedly resistant to infection with 

 Ostertagia circunicincta. while Rambouil- 

 lets were less so and Southdowns, Shrop- 

 shires and Hampshires were least resist- 

 ant. Certain individuals among the more 

 susceptible breeds, however, were just as 

 resistant as the Romneys. Whitlock(1958) 

 has studied genetic resistance to tricho- 

 strongylidosis in sheep in some detail. 



The nutritional status of the host may 

 affect its resistance. Poorly nourished 

 animals are usually more susceptible to 

 infection and suffer more severely from 

 its effects. Protein depletion or protein 

 starvation is particularly important. 

 Lack of specific vitamins and minerals 

 generally decreases resistance, but there 

 are cases in which lack of a certain vita- 

 min which the parasite requires may af- 

 fect the parasite adversely. Thus, Becker 

 and Smith (1942) found that when calcium 

 pantothenate was added to a ration con- 

 taining restricted vitamins B,, Bg and pan- 

 tothenate, the number of oocysts produced 

 hy Einteria nieschulzi infections in the rat 

 was increased. 



