It is not known why these two different forms occur, but the size of the inoculum and the host factors are probably important determinants. However, this postulate does not explain why CAP-AB is more fulminant than HAP-AB. Patients with HAP-AB (especially those with VAP) are also immunocompromised in many ways, but AB seems to have caused a milder disease in HAP-AB patients.
Alternatively, the possibility of a specific immunologic predisposition to AB infection has also been postulated. Anstey et al proposed that complement deficiency might predispose an individual to AB infection and that this might have contributed to the higher prevalence of the disease in the Aborigines in Northern Australia. However, the occurrence of a complement deficiency as a cause of fulminant CAP-AB has not yet been documented. Moreover, complement deficiency cannot explain why CAP-AB occurs in older age and why these patients had not experienced severe infections caused by other encapsulated organisms in the past. Reading here
Perhaps a more promising hypothesis is that the strains causing CAP-AB and HAP-AB are different. Using pulsed-field electrophoresis to analyze the restriction fragments, Zeana and colleagues showed that AB isolates from the community were characterized by a large variety of unrelated strains (83.3%), and that they were distinct from hospital isolates of which 58.3% were closely related. Furthermore, the AB strains from the hospital had a higher rate of multiple drug resistance (hospital isolates, 36.6%; community isolates, 0%; p < 0.005). But this study was limited by the fact that the community strains were from healthy individuals instead of from patients with infection. In future studies, it would be imperative to examine whether there are important differences between the CAP-AB strains (especially in bacteremic patients) and the HAP-AB strains on proteomic and genomic levels.