Clinical evaluation of brief cognitive assessment measures for patients with severe dementia.

BACKGROUND: Alzheimer's disease has become an important public health burden for older adults. Clinicians face a challenging task to efficiently evaluate cognition in dementia in clinical settings. We sought to assess the validity and inter-correlations of brief cognitive assessments in a cohort of severely demented patients. METHODS: In total, 49 individual patients (N = 49) ranging in age from 62 to 97 years old were included in this performance improvement project. Over the course of two-three sessions, five cognitive instruments were administered to each patient: Severe Impairment Battery (SIB), Severe Impairment Battery-8 (SIB-8), Mini Mental State Examination (MMSE), Severe Mini Mental State Examination (sMMSE) and Brief Interview of Mental Status (BIMS). We sought to assess patient factors that might have been barriers to optimal performance on cognitive/functional tests. Researchers assessed her impression of the participants' difficulty comprehending instructions, distractibility, apparent fatigue, and frustration, which were the four barriers rated. RESULTS: Data were analyzed for 49 patients from the inpatient dementia unit with a total of 51 samples. All of the inter-correlations between the five cognitive instruments had Spearman coefficients of (rs) > 0.7 and were statistically significant with p < 0.001. The SIB-8 and sMMSE were positively correlated with the SIB. The perceived barrier scores ranged from 0- no issue to 1-mild issue on all five cognitive instruments. CONCLUSION: Brief cognitive tests designed for severe dementia such as the SIB-8 and sMMSE have been evaluated in this project to be shorter in administration duration and highly correlated with gold standard instruments: the SIB and MMSE.

The majority of 9,729 group A streptococcus strains causing disease secrete SpeB cysteine protease: pathogenesis implications.

Group A streptococcus (GAS), the causative agent of pharyngitis and necrotizing fasciitis, secretes the potent cysteine protease SpeB. Several lines of evidence suggest that SpeB is an important virulence factor. SpeB is expressed in human infections, protects mice from lethal challenge when used as a vaccine, and contributes significantly to tissue destruction and dissemination in animal models. However, recent descriptions of mutations in genes implicated in SpeB production have led to the idea that GAS may be under selective pressure to decrease secreted SpeB protease activity during infection. Thus, two divergent hypotheses have been proposed. One postulates that SpeB is a key contributor to pathogenesis; the other, that GAS is under selection to decrease SpeB during infection. In order to distinguish between these alternative hypotheses, we performed casein hydrolysis assays to measure the SpeB protease activity secreted by 6,775 GAS strains recovered from infected humans. The results demonstrated that 84.3% of the strains have a wild-type SpeB protease phenotype. The availability of whole-genome sequence data allowed us to determine the relative frequencies of mutations in genes implicated in SpeB production. The most abundantly mutated genes were direct transcription regulators. We also sequenced the genomes of 2,954 GAS isolates recovered from nonhuman primates with experimental necrotizing fasciitis. No mutations that would result in a SpeB-deficient phenotype were identified. Taken together, these data unambiguously demonstrate that the great majority of GAS strains recovered from infected humans secrete wild-type levels of SpeB protease activity. Our data confirm the important role of SpeB in GAS pathogenesis and help end a long-standing controversy.