Rinderpest neutralizing antibody was found to be transferred from the immune dam to the calf via the colostrum. No antibodies were detected in the sera of calves before suckling. The colostrum of immune cows contained rinderpest antibodies to a higher titre than that of the serum; 30–48 hr. after the ingestion of such colostra, newborn calves possessed high antibody levels in their sera, levels greater than those of their dams' sera but less than those of the colostrum ingested.

After the neonatal period the serum titres of calves declined linearly. The mean half-life of maternally derived rinderpest antibody in calves was 36.7 days and the extinction point 10.9 months.

Two young calves, from susceptible dams, which each ingested daily for 5 weeks 1 gallon of milk containing rinderpest antibodies failed to show evidence of their absorption from the intestinal tract.

Calves which were the progeny of rinderpest-susceptible dams were inoculated with lapinized rinderpest virus when 1 day to 2 months old. Their serological response, as measured by neutralizing antibody titre 21 days later, did not differ from that of adult susceptible cattle.

In calves born of rinderpest-immune cows, the serological response to caprinized rinderpest virus depended upon the level of maternally derived antibody. There were two critical levels, one below which all calves produced antibodies (serum titre of 0.7 or less) and another above which no antibody was formed (serum titre of 2.2 or more). Thus all animals aged 8 months or more at the time of inoculation were actively immunized but no calf aged 3 months or less reacted in this manner.

The response of calves with maternally derived antibody titres between 0.9 and 2.0 varied. There was a significant inverse relationship between the preinoculation titre and the amount of antibody formed during the following 3 weeks. A similar inverse relationship was shown between the pre-inoculation titre and the rate of production of antibody and its titre 1 year following inoculation.

Calves which possessed colostral antibody, and which were actively immunized by caprinized virus inoculation, did not necessarily show the usual clinical reaction. When such animals failed to become actively immunized there was no sensitization of the antibody-forming mechanism, a fact demonstrated by the lack of an anamnestic response to subsequent exposure to rinderpest virus antigen.

I owe thanks to many people: to Dr S. E. Piercy, Deputy Director, E.A.V.R.O., for advice and encouragement; to Mr G. R. Scott, Senior Virologist, E.A.V.R.O., for advice and encouragement and, with Mr G. J. Knight, for help in the statistical analysis of the data; to Dr M. H. French lately head of Division and Mr G. Lampkin, Joint Animal Industry Division of E.A.A.F.R.O. and E.A.V.R.O. for facilities for the inoculation of calves from rinderpest-immune dams with rinderpest vaccine; Mr J. M. Nightingale, Sasamua Estate, South Kinangop, and Mr J. Armstrong, Naivasha, for facilities for immunizing calves from rinderpest-susceptible dams; Mr C. S. Rampton, Mr N. Kerani and Mr F. Mwithiga for technical assistance.

This and the previous paper (see p. 427) are published by permission of the Director, East African Veterinary Research Organization.

A comparison has been made between the bacteriophage and serological methods for identifying types among coagulase-positive staphylococci. In only a few cases was one particular serotype clearly related to a particular phage-type, and in several cases single ‘types’ recognized by one method contained several different ‘types’ when tested by the second method. Nevertheless, when sets of strains isolated in the investigation of epidemics or of the nose and skin carrier state of particular individuals were tested by the two methods, consistent results were obtained: an individual combination of phage-type and serotype appeared to be stable.

The principal advantages of phage-typing are the facts that it is able to recognize more types than the serological method, and that the distinctions between the types are based on a greater number of different reactions. The advantages of the serological method are the smaller number of untypable strains and its greater technical simplicity.

Thanks are due to Miss Joan Rippon, Ph.D., for assistance in the analysis of the phage-typing results.

Field trials were conducted in the San Francisco Bay region to test the effectiveness of 5 and 10% DDT powder in rodent bait-boxes against fleas on native wild rodents and in the rodent nests. The principal species concerned were known flea vectors of sylvatic plague, Malaraeus telchinum and Hystrichopsylla linsdalei, and the meadow vole, Microtus californicus, an important plague reservoir. Preliminary trials with the bait-boxes showed that Microtus and other small native rodents would enter them quite readily and feed upon rolled oats. About 90 g of either 5 or 10% DDT powder, placed on the floor boards of the bait-boxes, was picked up by the rodents and resulted in effective immediate control of all flea species. Residual control of all flea species on Microtus (with the possible exception of Hystrichopsylla linsdalei) was obtained over a period of several months. Analyses of Microtus nests showed considerable amounts of DDT which had been transported to them by the rodents. All flea species in nests were effectively controlled by 5% DDT for at least 132 days after the DDT was removed from the area.

The field work was performed by Alva R. Kinney and Robert L. Martin. The fleas were identified by Harold E. Stark. The DDT analyses of rodent nests were done by the personnel of the Technical Development Laboratories, CDC, Savannah, Georgia, under the direction of J. A. Jensen.

Following primary vaccination no antibody was detected up to the tenth day. After this time neutralizing antibody and antihaemagglutinin were present in the majority of individuals, while, with the technique used, complement-fixing antibody was found in less than half those examined. Neutralizing antibody may be found in the blood more that 20 years after primary vaccination; by this time very few show antihaemagglutinin and then only in low titre. Complement-fixing antibody was not found more than 6 months after primary vaccination.

In revaccinated individuals the antibody response tended to be higher than after primary vaccination and, when it occurred, often appeared within a week. This suggests that prompt revaccination of smallpox contacts may offer even greater protection than does primary vaccination.

The neutralization test is a better measure of immunological response than are either of the other two tests, for these may give a negative result even though there may be a well-marked rise in neutralizing antibody. The ‘early’ type of reaction to revaccination was associated with an antibody response in only about half the subjects examined. In the remainder, the skin reaction, although identical in appearance, must be regarded as allergic in nature and not accompanied by increase in immunity.

From 117 cases of smallpox 140 sera have been examind for antihaemagglutinin, for complement-fixing and for variola-neutralizng antibody.

In smallpox patients who had not been vaccinated prior to infection, variola-neutralizing antibody and vaccinial antihaemagglutinin were present in all sera examined after the sixth day of illness. Complement-fixing antibody was not found until the eighth day of illness but was present in all examined after the ninth day.

In previously revaccinated smallpox patients variola-neutralizing antibody was present in all sera examined after the third day of illness and antihaemagglutinins in all after the fourth day. Complement-fixing antibody was present by the seventh day and was found in all sera examined after the ninth day. Not only did antibody in general appear earlier in previously vaccinated smallpox patients but the titres were generally considerably higher. In ten fatal cases antibody titres were low except in two in whom the level of variola-neutralizing antibody was quite high—in one case on the second day and in the other on the fourth day of illness.

In six variola contacts, who suffered febrile attacks without rash, antibody studies indicated the variolous nature of their illnesses. In these and other atypical smallpox infections, when laboratory confirmation of clinical diagnosis is only requested at a late stage of the disease, a high titre of antibody, particularly complement-fixing antibody, may enable a firm diagnosis to be made.

We wish to acknowledge our indebtedness to Dr W. H. Bradley of the Ministry of Health; Dr E. C. Benn of Seacroft Hospital, Leeds; Dr D. C. Liddle of Monsall Fever Hospital, Manchester; Dr E. R. Peirce of Liverpool and other Medical Officers for information concerning smallpox patients. Our thanks are also due to Dr F. O. MacCallum of the Virus Reference Laboratory, Colindale, who kindly sent us sera from some of the cases in the 1950 smallpox outbreak in Brighton.

For a study of the process of formaldehyde disinfection, cotton threads were used as test objects. These were, in most experiments, impregnated with a heavy suspension of a coagulase-negative micrococcus in 1% gelatin solution or in 90% horse serum, and dried. In other experiments Mycobacterium tuberculosis, Bacillus subtilis or smallpox virus was used. After exposure to formaldehyde, quarter-inch lengths of the threads were cut off and cultivated on agar plates; individual threads were recorded as fertile or sterile and the mean number of organisms per thread was estimated statistically. Neutralization of the formaldehyde was found to be unnecessary except when strong concentrations were used.

In laboratory tests there was a linear relation between the concentration of formaldehyde and the killing rate. Little effect was observed on the speed of disinfection from variation in temperature over the range 0–30°C. There was some suggestion of an optimum relative humidity for disinfection at about 80–90%, but no great increase in disinfection rate was obtained by increasing the relative humidity above 58%. Threads impregnated from a suspension of the cocci in 90% serum were disinfected much more slowly than those impregnated with cocci suspended in a solution of gelatin. Covering the threads with several layers of blanket also slowed the killing rate considerably.

Tests were made of the sterilization of the threads in full-size disinfectors. Mattresses and other bedding absorbed a large quantity of formaldehyde so that the amount supplied had to be greatly in excess of that estimated from laboratory tests to provide a lethal concentration. A disinfector working at ambient temperature was found to kill over 99.99% of the micrococci on threads exposed on the surface of mattresses. The destruction of micrococci on threads placed under pillows or blankets was less, as was that of tubercle bacilli on fully exposed threads.

A disinfector in which the air temperature could be raised to about 100°C. was found to be more effective, partly because the increased temperature allowed much greater penetration of fabrics by the formaldehyde vapour; but the relative contribution of the heat and the formaldehyde to the disinfection process could not be fully determined.

In both the laboratory and the field experiments it was found difficult to obtain completely reproducible results. This constitutes one of the most disconcerting features of disinfection by formaldehyde. The process is influenced by so many different factors that it is impossible to predict with real assurance the result under any given set of conditions.

It is concluded that disinfection by formaldehyde vapour should be used only when no other method is available. It certainly cannot be recommended for disinfection of fabric contaminated with smallpox virus or with anthrax spores, when complete destruction has to be ensured; and unless carried out with special care it is not really suitable for woollen garments and toys soiled with tubercle bacilli.

A numerical investigation of three contagious distributions characteristic of epidemic data has been made using an electronic computer.

All three show a modified threshold effect such that the proportion of a community affected tends to 100% as its size increases though there is no abrupt change of form.

We would like to thank Mr M. J. R. Healy for assistance with one of the programmes, and Miss Molly Fretton for her help with the computing.

It is shown that bits of allantois-on-shell cut from any one egg do not differ either in susceptibility to infection by influenza viruses or in yield of haemagglutinin. For this reason the dose-response curve within any egg is Poissonian.

Bits cut from different eggs vary both in susceptibility and in haemagglutinin yield. Unlike in whole eggs however, the scatter is so small that it can be demonstrated only by refined tests done on a large number of subjects. For practical purposes the dose-response curve may still be taken as Poissonian.

Susceptibility and yield vary independently of one another.

The data are used to define the accuracy of infectivity tests in bits of allantois-on-shell; the expected errors are given both for straight replication and for tests done with different reagents, by different operators, or at different times.

It is shown that the assay for infectivity in bits of allantois-on-shell, which has been standardized on the BEL strain, is optimal also for nine representative strains of influenza virus tested.

On the average, the sensitivity of the technique is the same as of orthodox allantoic infectivity tests; its precision is always higher. The relative sensitivity of the two tests varies from strain to strain, the log tray/egg differences being SW (+0.88), MEL (+0.51), CAM (+0.31), PR8 (0.28), WSE (+0.25), HUT (−0.02), BEL (−0.22), FMI (−0.35), LEE (−0.47), BON (−1.02). This gradient is the same for fully infective and incomplete forms of influenza virus.

The tray/egg gradient of susceptibility is negatively correlated with the variation in host resistance.

The differences in susceptibility are not due to any effect of the plastic trays, to thermal inactivation of the virus, to differences in adsorption or viropexis in the two test systems or to the effect of allantoic fluid on the virus particle. The critical step has been shown to occur during the intracellular stage of multiplication.