54
CARL J. SINDERMANN
Raja ocellata Mitchill, varied seasonally, with minimum titers a t times
of minimum environmental temperatures. Hildemann (1 957) noted
acceleration of rates of homograft rejection in fish coincident with
increasing environmental temperature. The immune response was
measured by survival time and inflammatory reactions. Duration and
intensity of inflammation were closely associated with rapidity of
donor-tissue destruction. Fine and Drilhon (1961) demonstrated the
formation of precipitins in eels in response to injections of human
serum. Wolf (1941, 1954), Snieszko (1957b) and Ehlinger (1964) found
differences among strains of brook trout, Salvelinus fontinalis, in
resistance to ulcer disease and furunculosis. Papermaster et al. (1964),
in studies of the evolution of immune responses, found a rising level
of reactivity and complexity as the phylogenetic scale from hagfish
to teleost was ascended.
Goncharov (1959a) reported high antibody titers in fish immunized
against Achromobacter punctatum (Pseudomonas punctata), and also
pointed out the prevalence of cross agglutinations in work with such
immune sera. Earlier, Mann (1939) had shown that carp affected by
ascites (Bauchwassersucht) developed high agglutination titers against
Pseudomonas punctata, but Roegner-Aust et al. (1950) and Goncharov
(1959b) presented arguments that a virus was the primary etiological
agent. Sorvachev et al. (1962) described prophylactic immunization of
carp with an attenuated virus vaccine. According to their report, the
1 - and 2-year-old progeny of hyperimmunized carp suffered little
mortality during a severe outbreak of ascites, whereas young of
unvaccinated fish died in great numbers. Such findings are unique,
and are more suggestive of maintenance of immunity by natural
infections. Despite some continuing disagreement about the causative
organism, summarized by Schaperclaus (1965) and others in a recent
symposium (Snieszko et al., 1965), a body of literature on the epizootiology of this very important disease of carp has accumulated.
Included are indications of acquired immunity after infection, a
possible role of bacteriophage, changes in virulence and adaptation t o
new hosts-all problems that may be pertinent to certain marine fish
diseases.
Fungus or myxosporidean invasion of fish often produces only
tissue destruction with little indication of host inflammatory response.
Intramuscular parasites may cause hyalinization and lysis of muscle
tissue until only granular debris and spores remain. I n some individuals, however, fungus invasion elicits extensive formation of fibrous
connective tissue by the host (Fig. 16).
Evidence of local immunity t o monogenetic trematode infestation
CARL J. SINDERMANN
Raja ocellata Mitchill, varied seasonally, with minimum titers a t times
of minimum environmental temperatures. Hildemann (1 957) noted
acceleration of rates of homograft rejection in fish coincident with
increasing environmental temperature. The immune response was
measured by survival time and inflammatory reactions. Duration and
intensity of inflammation were closely associated with rapidity of
donor-tissue destruction. Fine and Drilhon (1961) demonstrated the
formation of precipitins in eels in response to injections of human
serum. Wolf (1941, 1954), Snieszko (1957b) and Ehlinger (1964) found
differences among strains of brook trout, Salvelinus fontinalis, in
resistance to ulcer disease and furunculosis. Papermaster et al. (1964),
in studies of the evolution of immune responses, found a rising level
of reactivity and complexity as the phylogenetic scale from hagfish
to teleost was ascended.
Goncharov (1959a) reported high antibody titers in fish immunized
against Achromobacter punctatum (Pseudomonas punctata), and also
pointed out the prevalence of cross agglutinations in work with such
immune sera. Earlier, Mann (1939) had shown that carp affected by
ascites (Bauchwassersucht) developed high agglutination titers against
Pseudomonas punctata, but Roegner-Aust et al. (1950) and Goncharov
(1959b) presented arguments that a virus was the primary etiological
agent. Sorvachev et al. (1962) described prophylactic immunization of
carp with an attenuated virus vaccine. According to their report, the
1 - and 2-year-old progeny of hyperimmunized carp suffered little
mortality during a severe outbreak of ascites, whereas young of
unvaccinated fish died in great numbers. Such findings are unique,
and are more suggestive of maintenance of immunity by natural
infections. Despite some continuing disagreement about the causative
organism, summarized by Schaperclaus (1965) and others in a recent
symposium (Snieszko et al., 1965), a body of literature on the epizootiology of this very important disease of carp has accumulated.
Included are indications of acquired immunity after infection, a
possible role of bacteriophage, changes in virulence and adaptation t o
new hosts-all problems that may be pertinent to certain marine fish
diseases.
Fungus or myxosporidean invasion of fish often produces only
tissue destruction with little indication of host inflammatory response.
Intramuscular parasites may cause hyalinization and lysis of muscle
tissue until only granular debris and spores remain. I n some individuals, however, fungus invasion elicits extensive formation of fibrous
connective tissue by the host (Fig. 16).
Evidence of local immunity t o monogenetic trematode infestation