Bakgrund: Barnets upplevelse av den första vårdkontakten är av stor betydelse, eftersom smärtsamma ingrepp på barn kan medföra problem vid framtida sjukvårdsbesök och kan orsaka långvarig sjukvårdsrädsla. På BVC kan procedurrelaterad smärta förorsakas vid venprovtagning eller vaccination. Exempel på smärtlindringsmetoder vid procedurrelaterad smärta är amning, EMLA och distraktion. Syfte: Studiens syfte var att beskriva BVC-personalens upplevelser av små barns behov av smärtlindring vid vaccination och/eller venprovtagning samt de metoder som användes för smärtlindring. Metod: För att besvara vårt syfte gjorde vi bandinspelade, semistrukturerade intervjuer med 8 personer som arbetar inom BVC med små barn i åldern 3 månader, 1-2 år och 5-6 år. Analys: Intervjutexten analyserades med kvalitativ innehållsanalys (Graneheim & Lundman, 2004). Resultat: Vid analysen framkom följande fyra domäner: Upplevda behov av att smärtlindra barn vid vaccination och Metoder för smärtlindring av barn vid vaccination, Upplevda behov av att smärtlindra barn vid venprovtagning och Metoder för smärtlindring av barn vid venprovtagning. Det framkom vid analysen att det var få som upplevde behov av att smärtlindra små barn vid vaccination, däremot vid venprovtagning var upplevda behov att smärtlindra små barn större. Med barnets stigande ålder använder sig intervjupersonerna av flera olika metoder samtidigt, så som att distrahera eller att använda sig av leksaker. Diskussion: Resultatet jämförs med metoder för smärtlindring som har stöd i forskning. Redan använda metoders verkan bekräftas men förslag på ytterligare smärtlindringsmetoder ges. Med ökad spridning av redan befintlig kunskap, kan BVC- personal med sin lyhördhet bemöta och guida barnet på ett sätt som kan motverka och lindra procedurrelateradsmärta.

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Since the introduction of vaccines, many deaths due to various diseases including measles, have been drastically reduced. In Canada, there is a recommended vaccine schedule for all residents of the country; however, vaccine practises and immunisation schedules can vary from location to location as well as vary from country to country, leading to discrepancies in vaccine coverage and herd immunities. In addition, some anti-vaccination movements have been noted to persuade individuals into refusing vaccines, even in historically well immunised locations. In order to investigate the effect of varying vaccine coverage, a two patch metapopulation model for measles incorporating a single dose vaccine is formulated and studied. / October 2016

Syften med uppsatsen var att ta reda på hur folk som är en del av anti-vaccinationsrörelsen kommunicerar i sociala medier. Uppsatsen undersöker hur de kommunicerar i inlägg och kommentarer i en sluten grupp på Facebook. Med hjälp av ett kodschema så blev 97 inlägg analyserade och placerad i olika kategorier med olika variabler. Utifrån kodschemat blev flera tabeller skapade som visade den mest relevanta faktan. Utifrån den information, och med flera detaljerat beskriva exempel-inlägg, beskrivs den generella stämningen i gruppen och hur de talar med varandra. Resultatet blev att de kommunicerar med varandra på ett vänligt och stöttande sätt, bidrar med relevant information när det frågas efter, men med lite fientlighet visas mot de som kommer med motsatta åsikter. Gruppen var sluten, vilket innebär att bara individer som delar samma åsikter som dem är medverkande på plattformen, vilket också betyder att åsikter blir så gott som aldrig utmanade. / The purpose of this essay has been to figure out how people that are a part of the anti-vaccination movement communicate in social media. The essay explores how they communicate in posts and comments in a closed group on Facebook. With the help of a coding scheme, 97 posts became analysed and placed in different categories with different variables. A couple of tables were created from the code scheme that demonstrated the most relevant facts. From that information, and with several detailed descriptions of example posts, describes the general mode in the group and how they speak with each other. The result was that they communicate with each other in a nice and supporting way, contribute with relevant information when it was asked for, but with some hostility shown towards those who come with opposite views. The group was closed, which means that only individuals who share the same views as them are involved with the platform, which also means that opinions are almost never challenged.

Typescript (photocopy). / Digitized by Kansas Correctional Industries

Francisella tularensis is a Gram-negative pathogenic organism that causes the disease tularemia. This disease can be potentially fatal without treatment. Francisella tularensis virulent strains can cause disease in humans with an infectious dose as low as 10 organisms. As a result of this low infectious dose, high mortality, and ease to produce an aerosol inoculum, the Centers for Disease Control and Prevention has classified Francisella tularensis as a Tier I select agent, the highest threat level. Much research has been done to determine the cause for the extreme virulence. However, despite these efforts, little is known about the mechanisms by which Francisella goes undetected inside host cells until it is too late for the host to respond. Researchers in the Jones' laboratory utilized a transposon site hybridization (TraSH) screen with human monocyte derived macrophages (MDMs) as the host cell and an enzyme-linked immunosorbent assay (ELISA) screen of pools of transposon mutants searching for virulence determinants and genes responsible for Francisella capsule or LPS. Through the TraSH screen, our group identified a locus of genes, FTT1236, FTT1237, and FTT1238c as being important for survival within human MDMs. From the mutant library screen using ELISA, I identified the same genes, FTT1236 and FTT1238c. In addition, I also identified wzy, wbtA, FTT0846, and hemH as being involved in LPS and or capsule production. A similar ELISA screen was done by researchers in Apicella laboratory using a different monoclonal antibody that identified insertions in, dnaJ, manB and an intergenic region between FTT0673 and FTT0674c that potentially disrupted LPS and capsule biogenesis. Previously, FTT1236, FTT1237, and FTT1238c mutants were observed by our laboratory to be serum sensitive and activate MDMs by an unknown mechanism. I further characterized these mutant strains by analyzing the changes in the LPS core. I identified core truncations for the FTT1236 and FTT1237 mutants, but not FTT1238c. Combining this new data with previously published work and bioinformatical analysis of the FTT1236, FTT1237 and FTT1238c proteins, I hypothesized that these proteins have functions similar to Waa proteins of other organisms, which are involved in LPS core assembly and O-antigen ligation. With functional complementation and mass spectrometry of LPS preparations, I have designated FTT1236, FTT1237, and FTT1238c as WaaY, WaaZ, and WaaL respectively. In addition to this work characterizing the biochemical functions of these gene products, I examined the effect of mutations in these genes on the virulence of Francisella. In contrast to infection with wild type Schu S4, mice infected either intraperitoneally or intranasally displayed significant inflammatory responses to infection and the strains were significantly attenuated by either route of infection. I also observed that waaY and waaL mutant strains disseminated to the liver and spleen after an intranasal infection despite their lack of O-antigen and capsule. At an i.n. dose of 106 CFU these mutant strains still caused lethal murine infection, but death occurred around day 12 post infection; mice infected with <20 CFU of Schu S4 succumb at day 5 post infection. The cause of the death in mice infected with these mutant strains was pulmonary edema, rather than multiple organ failure induced by Schu S4. Of the additional seven mutant strains identified from the ELISA screens, I characterized their physical phenotypes, virulence defects, and their potential as an attenuated live vaccine. All of these strains were determined to be sensitive to human pooled serum to various degrees. Three of these strains, dnaJ::Tn5, hemH::Tn5, and FTT0673p/prsAp::Tn5 did not have identifiable defects in capsule or LPS biosynthesis, nor were they attenuated in mice. The remaining four strains, FTT0846::Tn5, manB::Tn5, wzy::Tn5, and wbtA::Tn5, were found to have LPS O-antigen and capsule defects, and two of these strains had LPS core defects (FTT0846::Tn5 and manB::Tn5). Each of these four strains was attenuated in mice, when compared to WT. I also tested the ability of mice infected with waaY::TrgTn, waaL::TrgTn, and wbt::Tn5 to be protected from lethal challenges of Schu S4. All three strains provided some level of protection against lethal Schu S4 challenges. In addition, I also tested Francisella LPS and capsule to provide protection against lethal challenges of LVS and Schu S4. I determined that LPS and capsule protected against high doses of LVS, but LPS did not provide any protection when immunized mice were challenged with Schu S4. Interestingly, we observed that mice immunized with capsule were partially protected from lethal Schu S4 challenges. In addition, I observed a novel difference between virulent Francisella strains and LVS, in that virulent strains have O-antigen glycosylated and LVS appears to be lacking this characteristic. Collectively, this work adds to the growing data of the importance of LPS and the role of capsule role in immune evasion as well as the significance of capsule and LPS mutant strains to provide protection against Schu S4.

Streptomycin resistance in both gram-positive and gram-negative bacteria is usually caused by a single mutation in the rpsL gene. The rpsL gene encodes the S12 protein of the ribosomal complex. The rpsL genes of various bacteria have consensus regions in their sequences. Primers were designed from these consensus pockets and a fragment of the rpsL gene was sequenced from S. gordonii using PCR based methodologies. Using the Multiplex Restriction Sequence PCR(mRS PCR), which used the known primer at one end and a restriction site primer on the other, a gene walk was conducted. In streptomycin resistant strains of S. gordonii, namely GP204, SP204 and SP635, the AAA coding for Lys56 was mutated to ACA, coding for Thr56. The lysine to threonine transition, causing resistance to streptomycin was identical to that expected from the literature. The streptomycin resistance gene of S. pyogenes was mapped using similar techniques. Streptomycin resistant strains S43 ATCC, 543/192/4 and S43/192/30R were studied. In streptomycin resistant S43 ATCC and S43/192/30R strains, the lysine 56 changed to isoleucine and threonine respectively. Surprisingly, the 192/4 had two mutations, in each of the two hotspots in the rpsL gene where mutations due to streptomycin resistance occur. It had the amino acid 56, lysine, mutated to arginine and lysine 101 changed to asparagine. To check if this mutation was stable in the host animal, S43/192/4 P8 (S43/192/4 passaged eight times in mice) was sequenced and the sequence was identical to the streptomycin resistant 192/4. Hence, the lys101 mutation was stable and unlike the ancillary mutations in E.coli and S. typhimurium, which are compensated by new mutations. The pathogenesis of S. pyogenes depends in part on the ability of the pathogen to adhere to the epithelial cells of the throat and the quantity of M protein. Pathogenesis studies done on mice revealed the avirulence of S43/192/4smR strain. To elucidate the reason for this avirulence, the adherence properties and the production of M protein of the two strains S43/192/4smR and S43/192/30R were tested. Qualitative immunoblot analysis of the M protein of 192/4 and 30R revealed no significant difference. Competition ELISA was conducted to quantitate the M protein, and this also did not show any significant difference in the M protein levels. The adherence of 30R and 192/4 was measured on human pharyngeal epithelial cell line. The adherence properties of S43/192/4 SmR, was no different from other strains in this experiment. Electron microscopy, using immunogold to highlight the M protein on the cell surface showed no differences. / Graduation date: 2000