Bronchopneumonia

Brains were retrieved from a total of 56 stroke survivors who came to autopsy. Six of these were demented at baseline (Fig. 1) but were included in the assessment for comparative purposes. Table 4 provides demographic details and the highest and last CAMCOG scores. In the majority of cases bronchopneumonia was recorded as the cause of death.
Macroscopic and microscopic pathology was assessed with standardized protocols as described (Kalaria et al., 2004 (link); Ihara et al., 2010 (link)). Briefly, macroscopic infarcts were detected by visual inspection while dissecting the brain, and their presence was subsequently confirmed by microscopy. Haematoxylin and eosin was used as standard stain for general neuropathological assessment of the structure of the brain, and for confirmation/detection of the infarcts. In this study, any infarct <5 mm in diameter was defined as a microinfarct. Gallyas and Bielschowsky's silver impregnation and tau immunohistochemistry were applied to assess neuritic plaques and neurofibrillary tangles for the ‘CERAD’ plaque score and ‘Braak and Braak’ neurofibrillary tangle staging. Additional staining included α-synuclein, ubiquitin and TDP-43 immunohistochemistry.
A clinical diagnosis of whether the dementia syndrome was present was made independently of neuropathological data prior to monthly clinicopathological consensus meetings where clinicians met with the pathologists to designate a final diagnosis for autopsied subjects. In all cases, additional pathologies such as Alzheimer's disease and dementia with Lewy bodies were noted. The pathological diagnosis of vascular dementia was then assigned if there was clinical evidence of dementia (DSM IV) and the presence of multiple or cystic infarcts involving cortical and subcortical structures, border-zone infarcts, lacunae, microinfarcts and small vessel disease in the general absence of a high burden of neurofibrillary pathology i.e. Braak staging et al., 2004 (link)) or obvious other primary neurodegenerative disease, and consistent with the clinical diagnostic criteria proposed by others (Chui et al., 1992 (link), 2000 (link); Roman et al., 1993 (link); Gold et al., 2002 (link)). After breakdown by diagnostic subgroups, the number of autopsies did not permit generation of sensitivity and specificity rates. Subjects were designated as mixed when there was pathological evidence of cerebrovascular disease with Alzheimer's disease-type pathology, Lewy bodies or tauopathy (frontotemporal lobar degeneration or progressive supranuclear palsy). The cases with mixed cerebrovascular disease and Alzheimer's disease had a Braak stage of V or VI and moderate to severe CERAD scores.

Pneumonia was diagnosed with chest radiography, and interpretation was accepted as written in the medical charts of patients, reporting either lobar pneumonia or bronchopneumonia, and empyema with or without pneumothorax. These reports are aligned to the WHO Standard for reporting chest radiographs in which there is presence of a dense or fluffy opacity that occupies a portion or whole of a lobe or of the entire lung, presence of fluid in the lateral pleural space between the lung and chest wall, or both.^{10 ,11 (link)}The endpoints were number of pneumonia hospitalizations and deaths among children 3–24-month-old. The proportion of pneumonia hospitalizations was calculated before and after vaccination periods. The case-fatality rates were calculated from the deaths among the pneumonia admissions.