N. Paul Hudson

Relation of Olfactory Tracts to Intravenous Route of Infection in Experimental Poliomyelitis

Summary Section of the olfactory tracts of 5 monkeys prevented infection with poliomyelitis virus when administered intranasally. Later, these animals could not be infected by the intravenous route. We believe this is explicable on the basis that the virus, which has been detected in the nasopharynx by ourselves and others, did not reach the central nervous system after excretion onto the nasal mucosa, because of the break in the olfactory pathway.

A Note on the Interrelationship of Deficiency Diseases and Resistance to Infection.

Summary and Conclusions 1. Our observations in 150 patients from a region of Alabama in which deficiency diseases are endemic show a relationship between these diseases and the resistance to, and presence of, infections with Staphylococcus aureus and Streptococcus hemolyticus. 2. The lesions at the corners of the mouth, characteristic of riboflavin deficiency, contained pure or nearly pure cultures of hemolytic strains of Staphylococcus aureus in 80% of the cases, and in the remaining 20%, Streptococcus hemolyticus predominated. Following the oral or intravenous administration of riboflavin or substances rich in it, the fissures healed rapidly and the organisms were no longer demonstrable. 3. When the bacterial flora of the conjunctival sacs were studied in cases of dietary deficiency disease and associated conjunctivitis, hemolytic strains of Staphylococcus aureus were found to predominate in 14 of the 30 cases. Smears and cultures demonstrated the presence of Corynebacterium xerosis in a pure state in all of the spots of Bitot which occurred in 5 cases. 4. In addition to masses of Vincents organisms, 64% of the ulcerations of the tongue, gums, or buccal mucosa yielded Streptococcus hemolyticus, and the remaining 36% contained hemolytic strains of Staphylococcus aureus. Following specific therapy with anti-pellagric substances, the bacterial flora of these ulcerations, including the Vincents organisms, promptly disappeared. 5. A low complement titre exists in acutely deficient patients, and in the subclinical and mild cases the titre is slightly subnormal or normal. Following clinical improvement the complement titre increases. 6. In the whole blood of acutely deficient patients there is a distinct depression in the bactericidal power for Staphylococcus aureus, whereas, only a slight diminution in staphylococcidal power was observed in the blood of subclinical and mild cases of vitamin deficiency.

Protective and Complement-binding Bodies in the Serum of Human Yellow Fever Convalescents.

We have had the opportunity to make a serological study of 5 cases of yellow fever due to laboratory infections. The sera of 4 of these were examined for protective and complement-fixing bodies throughout convalescence so far as was practicable, while the serum of the other case was examined for the first property from the seventh week and for the second property from the eighth month after the onset of illness. Protective antibodies: The technic of testing for the protective property was that usually employed, namely, the intraperitoneal inoculation of monkeys with serum, followed after 6 hours by the subcutaneous injection of fresh monkey blood containing virus. The table giving the results of these tests indicates that antibodies protecting monkeys against massive doses of virus appeared about the fifth day of illness in 4 cases. In the one instance in which serum was examined for the first time 7 weeks after illness, this protective property was present and repeatedly demonstrated thereafter. Complement-binding bodies: The technic we employed in the complement-fixation tests was as described in a recent publication, 1 where the literature is briefly reviewed. It consisted essentially in the use as antigen of pooled infectious monkey serum preserved in a dry state, in the employment of a series of antigen dilutions against a constant dilution of serum, and in overnight fixation at 5°C. The usual controls were always included and in the experiments reported here were satisfactory. A positive reaction appeared in one case in the eighth week after the onset of illness, and in another in the ninth week. The sera of 2 individuals gave positive tests at their first examination, 4 and 8 months after onset, while the reaction with the serum of one person has been consistently negative during the 8 months of observation after the acute attack.