Differentiating characteristics of deafblindness and autism in people with congenital deafblindness and profound intellectual disability.

BACKGROUND: In persons with deafblindness, it is hard to distinguish autism spectrum disorders from several deafblind specific behaviours caused by the dual sensory impairments, especially when these persons are also intellectually disabled. As a result, there is an over-diagnosis of autism in persons who are deafblind leading to unsuitable interventions. METHODS: Autism as specified by the DSM-IV was studied in 10 persons with congenital deafblindness with profound intellectual disabilities. Behaviours of people with deafblindness and autism (n = 5) and of people with deafblindness without autism (n = 5) were observed in a semi-standardised assessment. RESULTS: All people with deafblindness showed impairments in social interaction, communication and language. In contrast to persons without autism, people with deafblindness and autism showed significantly more impairments in reciprocity of social interaction, quality of initiatives to contact and the use of adequate communicative signals and functions. No differences between the groups were found for quantity and persistence of stereotyped behaviour, quality of play and exploration and adequate problem-solving strategies. CONCLUSIONS: This study indicates that there are some possibilities to differentiate autism from behaviours specific for deafblindness. It also confirms the large overlap in overt behaviours between people with deafblindness and persons with autism.

Development of a simple passive haemagglutination-inhibition assay for Listeria monocytogenes lipoteichoic acid.

A simple assay for listeria lipoteichoic acid was devised. It is based on the property of this substance to attach spontaneously to erythrocytes. Thus coated rabbit erythrocytes were agglutinated by a rabbit antiserum raised towards dead listeria. Inhibition of this passive agglutination was used as a measure of listeria lipoteichoic acid. Cross-reactivity of lipoteichoic acid from Lactobacillus fermenti in the assay and inhibition by simple sugars suggest that the assay is specific for terminal galactose.

Transfer of enhanced resistance against Listeria monocytogenes induced with ribosomal RNA and the adjuvant dimethyldioctadecylammonium bromide.

In this study we investigated the mechanism of enhanced resistance against Listeria monocytogenes induced with Listeria ribosomal RNA and the adjuvant dimethyldioctadecylammonium bromide (DDA). Mice immunized with DDA alone (which were not protected against Listeria-infection) were used as negative controls. Mice immunized with RNA plus DDA were found to have an increased capacity to mobilize polymorphonuclear leukocytes (PMNs) and macrophages to the inflamed peritoneal cavity compared to mice immunized with adjuvant alone. Intraperitoneal (i.p.) inflammation was induced by injection of the sterile irritant proteose peptone. The protective capacity of various cell-populations was investigated by i.p. transfer of cells to normal recipient mice and concomitant challenge of recipient animals with a lethal dose of viable Listeria. Inflammatory PMNs as well as inflammatory macrophages from mice immunized with RNA plus DDA protected recipient animals against listeriosis whereas cells from mice immunized with DDA alone failed to do so. Therefore, enhanced mobilization as well as activation of PMNs and macrophages may have contributed to the expression of protection against L. monocytogenes induced with RNA plus DNA.

Ribonuclease-sensitive ribosomal vaccines.

This paper presents an analysis of the protective properties of the components in ribonuclease (RNase)-sensitive ribosomal vaccines, in particular the ribonucleic acid (RNA). The protective activities in mice of purified ribosomes derived from Pseudomonas aeruginosa and from Listeria monocytogenes were compared. Both ribosomal vaccines had to be combined with the adjuvant dimethyldioctadecylammonium bromide (DDA) in order to be protective, and both lost their activity after RNase treatment. The ribosomal vaccines as well as RNA purified from the ribosomes induced non-specific protection. Intraperitoneal injection of RNA with DDA induced an influx of peritoneal cells. Furthermore, RNA with DDA activated macrophages as shown by, a.o., enhanced phagocytic activity and killing capacity for L. monocytogenes. The results suggest that the observed macrophage activation is probably T-cell-independent. With regard to the ribosomal vaccine of P. aeruginosa it is concluded that RNA also contributed to the protective activity by increasing the humoral response against suboptimal concentrations of contaminating cell surface antigens. In conclusion, it is proposed that ribosomal vaccines may be considered as a combination of a non-specific immunomodulator (RNA) with pathogen-specific cell surface antigens. This concept of ribosomal vaccines is discussed in relation to the literature concerning RNase-sensitive ribosomal vaccines.

RNase-sensitive and RNase-insensitive protective components isolated from Listeria monocytogenes.

Crude ribosomes were isolated from Listeria monocytogenes serotype 4b and separated into two fractions by molecular sieve chromatography. Chemical analysis indicated that fraction I contained cell envelope components while fraction II contained the ribosomes. Both fractions protected mice against Listeria, but only in combination with the adjuvant dimethyldioctadecylammonium bromide (DDA). RNase-treatment, but not proteinase K-treatment destroyed the protective properties of fraction II, and RNA purified from fraction II also induced protection. Protection induced by fraction I was not affected by either RNase- or proteinase K-treatment. Both subcutaneous and intraperitoneal, but not intravenous administration of fraction I, fraction II, or purified RNA induced significant protection against intraperitoneal infection, the intraperitoneal route of administration being the most effective. All preparations induced high levels of protection 3 to 7 days after administration, but protection was already decreased after 14 days. Protection induced with RNA appeared to be biphasic, because it also protected mice 1 day, but not 2 days after administration. Protection induced with both fraction I and RNA was at least in part non-specific, because both preparations also protected mice against L. monocytogenes serotype 3, Streptococcus pneumoniae and Pseudomonas aeruginosa. Results are discussed in relation to previous work with analogous preparations from P. aeruginosa.

Interactions of killed Listeria monocytogenes with the mouse complement system.

Incubation of mouse serum with Listeria monocytogenes involved activation of the alternative complement pathway, resulting in depletion of both classical and alternative pathway activity. The activation process gave rise to reactive (calcium- and magnesium-independent) lysis of, specifically, rabbit erythrocytes, which become resistant to this form of hemolysis by sensitization with antibodies. The possible implications of these findings for L. monocytogenes as an intracellular parasite and for rabbit erythrocytes as target cells for mouse alternative complement pathway activity are discussed.

T-cell-independent macrophage activation in mice induced with rRNA from Listeria monocytogenes and dimethyldioctadecylammonium bromide.

Purified rRNA from Listeria monocytogenes or Pseudomonas aeruginosa injected in combination with dimethyldioctadecylammonium bromide (DDA), protects mice nonspecifically against a lethal challenge of various extra- and intracellular bacteria. In the present study vaccination of BALB/c as well as C57BL/Ka mice with listerial RNA-DDA resulted in activation of fixed-tissue macrophages, as measured by an enhanced in vivo L. monocytogenes killing in spleen and liver. Evidence was found that macrophage activation by vaccination with rRNA-DDA occurred by a T-cell-independent mechanism. Treatment of mice with cyclosporin A had no effect on the enhanced L. monocytogenes killing induced with RNA-DDA; in vitro exposure of RNA-DDA to spleen cell cultures did not give rise to any lymphocyte proliferation. No evidence could be found for a possible adjuvant activity for RNA-DDA in cellular responses; in fact, RNA-DDA had an inhibitory effect on lymphocyte proliferative responses to Listeria antigen and to concanavalin A.

Dissociation between enhanced resistance and delayed hypersensitivity induced with subcellular preparations from Listeria monocytogenes and the adjuvant dimethyl-dioctadecyl-ammonium bromide.

In this study we investigated the relation between enhanced resistance and delayed hypersensitivity (DH) induced with subcellular preparations from Listeria monocytogenes and the adjuvant dimethyldioctadecylammonium bromide (DDA). Ribosomal RNA as well as cell envelope fragments (fraction I) protected mice against lethal Listeria infection. However, only fraction I induced DH against killed Listeria. For the induction of protection with fraction I or RNA as well as for the induction of DH with fraction I, preparations had to be administered in combination with DDA. Fraction I elicited a DH response in mice immunized with viable Listeria, but RNA did not. These observations pointed to a dissociation between DH and enhanced resistance induced with RNA, and to a dissociation between fraction I and RNA with respect to their ability to induce or elicit DH. Also DH and enhanced resistance induced with fraction I could be dissociated. Intracutaneous administration of fraction I induced high levels of DH without concomitant induction of protection against lethal challenge with Listeria. On the other hand, intraperitoneal administration of fraction I fully protected mice against lethal infection, but only induced a moderate DH response. DH induced with fraction I was largely specific, whereas enhance resistance induced with this preparation was nonspecific. Finally, proteinase K-sensitive proteins were found to be essential for the induction of DH but not for the induction of protection with fraction I.