The evidence presented supports the hypothesis that the experimental form of anthrax induced by depositing a cloud of single spores on lung epithelium is initiated in the lymphatic regions and not in lung tissue.Proportionately few of the deposited spores reach the lymph glands. The majority remain inactive in so far as induction of disease is concerned. Slowly, however, they seem to go through the first stages of germination but do not multiply and therefore die. This is probably the major factor operative in their disappearance from the lung.Effective prophylactic measures are suggested for dealing with an unimmunized host exposed to anthrax infection by the pulmonary route.

Experiments to determine the role of particle size in the infectivity of anthrax spores are described. Clouds of homogeneous particles were produced. The mortality-dosage curves for guinea-pigs and monkeys are given for clouds of various particle sizes. Data are given on the effect of time in the concentration-time relationship. The results are compared with those recorded by other workers on the relationship of particle size to respiratory retention.Infectivity was highest with single-spore clouds, falling off as particle size increased. Reasons are given for attributing this effect to difference in site of deposition of different-sized particles.

The infectivity of Brucella suis for the guinea-pig by the respiratory route has been studied. Br. Suis was dispersed in airborne particles of various sizes from single organisms to 12μ in diameter, and it was found that the infectivity decreased 600-fold with increasing particle size within this range. It is suggested that this is due to the ability of Br. Suis to multiply rapidly on the surface of the lower reaches of the respiratory tract.

The attachment organelle of Mycoplasma pneumoniae is a polar, tapered cell extension containing an intracytoplasmic, electron-dense core. This terminal structure is the leading end in gliding motility, and its duplication is thought to precede cell division, raising the possibility that mutations affecting cytadherence also confer a defect in motility or cell development. Mycoplasma surface protein P30 is associated with the attachment organelle, and P30 mutants II-3 and II-7 do not cytadhere. In this study, the recombinant wild-type but not the mutant II-3 p30 allele restored cytadherence when transformed into P30 mutants by recombinant transposon delivery. The mutations associated with loss of P30 in mutant II-3 and reacquisition of P30 in cytadhering revertants thereof were identified by nucleotide sequencing of the p30 gene. Morphological abnormalities that included ovoid or multilobed cells having a poorly defined tip structure were associated with loss of P30. Digital image analysis confirmed quantitatively the morphological differences noted visually. Transformation of the P30 mutants with the wild-type p30 allele restored a normal morphology, as determined both visually and by digital image analysis, suggesting that P30 plays a role in mycoplasma cell development. Finally, the P30 mutants localized the adhesin protein P1 to the terminal organelle, indicating that P30 is not involved in P1 trafficking but may be required for its receptor-binding function.

The LD50 dose of Past. pestis is much greater when tested by the respiratory route than by subcutaneous challenge. This is probably due to trauma inflicted on the airborne particles.Two forms of plague, both originating in the respiratory tract of the guinea-pig, can develop according to the size of the particle containing Past. pestis presented to the host. Small particles initiate a broncho-pneumonia which leads to septicaemia and death. Large particles establish a septicaemia, and death results more quickly without the development of a pneumonia.Cross-infection to normal animals occurs irregularly when they are exposed to others developing plague by the respiratory route. Such incident is rare when the initially infected animals are exposed to large particles. Cross-infected animals suffer from the disease characteristic of exposure to large particles. Attempts to establish an epizootic by cross-respiratory infection were abortive, probably due, in some measure, to the type of disease developing in first cross-infections.