Normal serum IgA and secretory IgA (sIgA) of subclass IgA 1 were isolated from pooled human serum and milk, respectively. They were tested for their susceptibility to bacterial IgA proteases from Haemophilus influenzae, Streptococcus pneumoniae, Neisseria gonorrhoeae, and Neisseria meningitidis that cleave IgA of only the IgA 1 subclass. They were also tested for susceptibility to a novel IgA-protease from Clostridium ramosum that cleaves IgA of the IgA 1 as well as the IgA2 subclass of the A2m(1) allotype. Both normal serum IgA 1 and sIgA 1 exhibited resistance to most IgA proteases. The one exception was the IgA protease from C. ramosum which readily cleaved both the serum IgAl and sIgAl into Fab and Fc fragments. Secretory component (SC) had nothing to do with the resistance of these IgAs. The resistance of these IgAs to most of the IgA proteases was found to be due to their enzymeneutralizing antibody activity, since the Fab but not the Fc fragment of sIgA I showed enzyme-inhibitory activity against these IgA proteases. Similar enzyme-neutralizing antibody activity was found in the pepsin-digested normal serum IgG-(Fab')2 fragment. These results indicate that the induction of the enzyme-neutralizing antibodies against the bacterial IgA proteases took place not only in mucosal sIgA but also in serum IgA and IgG. No enzyme-neutralizing antibody activity against the novel IgA-protease of C. ramosum was detected in any immunoglobulin preparations used in the present study or in the serum of a patient who carries the IgA protease-producing strain of C. ramosum in his feces.

A 7-year-old boy with sex-linked agammaglobulinaemia developed meningoencephalitis caused by echovirus type 11. He had convulsions, right hemiplegia, cortical motor aphasia, left abducens nerve paralysis, left hypoglossal nerve paralysis, and later became unconscious. Treatment by intravenous injection of conventional gammaglobulin and intrathecal alpha-interferon brought no clinical improvement, but intrathecal administration together with intravenous injection of gammaglobulin containing a high titre of anti-echovirus type 11 antibody was associated with a dramatic improvement in his clinical symptoms. After subsequent periodical (once or twice a week) administration of specific gammaglobulin for 8 months, the echovirus in his cerebrospinal fluid was no longer detected. These findings suggest that intrathecal injection combined with intravenous injection of high titre anti-echovirus type 11 antibody was effective in treating this case of echovirus meningoencephalitis in sex-linked agammaglobulinaemia.

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