Why did you choose psychiatry? a qualitative study of psychiatry trainees investigating the impact of psychiatry teaching at medical school on career choice.

BACKGROUND: There is no consensus regarding the optimal content of the undergraduate psychiatry curriculum as well as factors contributing to young doctors choosing a career in psychiatry. Our aim was to explore factors which had influenced psychiatry trainees' attitudes towards mental health and career choice. METHOD: Qualitative in-depth interviews with 21 purposively sampled London psychiatry trainees analysed using the Framework method. RESULTS: Early exposure and sufficient time in undergraduate psychiatry placements were important in influencing psychiatry as a career choice and positive role models were often very influential. Integration of psychiatry with teaching about physical health was viewed positively, although concerns were raised about the potential dilution of psychiatry teaching. Foundation posts in psychiatry were very valuable in positively impacting career choice. Other suggestions included raising awareness at secondary school level, challenging negative attitudes amongst all medical educators, and promoting integration within medical specialties. CONCLUSIONS: Improvements in teaching psychiatry could improve medical attitudes and promote recruitment into psychiatry.

Assessment of nonpenetrating captive bolt stunning followed by electrical induction of cardiac arrest in veal calves.

The purpose of this study was to evaluate the impact of nonpenetrating captive bolt stunning followed by electrical induction of cardiac arrest on veal calf welfare, veal quality, and blood yield. Ninety calves from the same farm were randomly assigned to 1 of 2 treatment groups in a balanced unpaired comparison design. The first treatment group (the "head-only" method-application of the pneumatic nonpenetrating stun to the frontal plate of the skull at the intersection of 2 imaginary lines extending from the lateral canthus to the opposite poll [CONTROL]) was stunned with a nonpenetrating captive bolt gun ( = 45). The second group ( = 45) was stunned with a nonpenetrating captive bolt gun followed by secondary electrical induction of cardiac arrest (the "head/heart" method-initial application of the pneumatic nonpenetrating captive bolt stun followed by 1 s application of an electrical stun to the ventral region of the ribcage directly caudal to the junction of the humerus and scapula while the stunned calf was in lateral recumbence [HEAD/HEART]). Stunning efficacy was the indicator of animal welfare used in this study. All calves were instantly rendered insensible by the initial stun and did not display common indicators of return to consciousness. For meat quality evaluation, all samples were collected from the 12th rib region of the longissimus thoracis. Meat samples were evaluated for color, drip loss, ultimate pH, cook loss, and Warner-Bratzler shear force. The L* values (measure of meat color lightness) were darker ( < 0.05) in the HEAD/HEART group (45.08 ± 0.72) than the CONTROL group (47.10 ± 0.72). There were no differences ( > 0.05) observed in a* (redness) and b* (yellowness) values between treatments. No differences ( > 0.05) were observed in drip loss, ultimate pH, cook loss, and Warner-Bratzler shear force. The blood yield from the CONTROL group (7,217.9 ± 143.5 g) was greater ( < 0.05) than that from the HEAD/HEART group (6,656.4 ± 143.5 g). Overall, the data indicated no difference between the CONTROL and HEAD/HEART groups with regard to animal welfare because the initial stun was effective in all calves. However, longissimus thoracis L* and blood yield were negatively impacted by the HEAD/HEART method. The data in this study suggest that secondary induction of cardiac arrest is not necessary with effective nonpenetrating captive bolt stunning in veal calves.

Catastrophic circulatory collapse following re-expansion pulmonary oedema.

Re-expansion pulmonary oedema is a recognised but rare complication following the rapid drainage of a large pleural effusion or pneumothorax [1,2], usually occurring on the side of re-inflation. The pathogenesis of the pulmonary oedema is poorly understood but is thought to be due to micro-vascular shearing resulting in neutrophil activation and adhesion to the vascular endothelium resulting in increased micro-vascular permeability [3-7]. Few reports appear in the literature of invasive haemodynamic monitoring following this catastrophe. We describe a patient who sustained fatal pulmonary oedema arising in the contralateral lung, with pulmonary flow catheter data documenting the initial circulatory collapse following the aspiration of a massive pulmonary effusion.

Disseminated BCG infection in severe combined immunodeficiency presenting with severe anaemia and associated with gross hypersplenism after bone marrow transplantation.

An infant with severe combined immunodeficiency (SCID) is described, who presented with severe anaemia and hepatosplenomegaly due to disseminated Bacillus Calmette-Guérin (BCG) infection involving the bone marrow, liver and spleen. After BMT, huge splenic enlargement occurred, presumably due to proliferation of engrafted donor lymphocytes, leading to severe hypersplenism. Peripheral blood cell consumption was resolved by splenectomy, but gradual loss of the marrow graft followed.

Human herpes virus-6 infection in marrow graft recipients: role in pathogenesis of graft-versus-host disease. Newcastle upon Tyne Bone Marrow Transport Group.

To investigate the hypothesis that target organ infection with human herpes virus-6 (HHV-6) exacerbates the clinical severity of GVHD, skin and rectal biopsies from 34 allogeneic bone marrow transplant (BMT) recipients and 23 comparative autologous recipients were studied. Biopsies and heparinised blood samples were obtained from all patients prior to and at regular intervals after BMT, and whenever GVHD was suspected. HHV-6 antigen was detected in cryostat sections by immunohistochemistry, and HHV-6 DNA in peripheral blood leucocytes (PBL) and biopsies by nested PCR. Twenty-eight (90%) of the 31 patients who engrafted developed clinical GVHD, which was mild in five, moderately severe in nine and severe in 14. Overall, HHV-6 DNA was detected in PBl in 74% of autologous recipients and 76% of allogeneic recipients, and in biopsy tissue in 48% of autos and 71% of allos. However, HHV-6 DNA was detected in skin and/or rectal biopsies more frequently in allogeneic recipients with severe GVHD (92%) than in those with either moderate (55%) or mild GVHD (22%), suggesting an association (P = 0.004) between HHV-6 DNA in biopsy tissue and GVHD severity. A significant linear trend (P = 0.03) was identified between detection of HHV-6 DNA in biopsy tissue obtained prior to or concomitant with the onset of GVHD and increased GVHD severity, suggesting that HHV-6 was causally linked to GVHD rather than reactivated as a consequence of GVHD therapy. Thus this study supports a role for HHV-6 in the initiation and/or exacerbation of GVHD, and suggests that the presence of HHV-6 DNA in the skin or rectum may be a factor in determining GVHD severity. If confirmed, these findings may have implications for the management of allogeneic BMT recipients.

Role of target organ infection with cytomegalovirus in the pathogenesis of graft-versus-host disease.

Skin and rectal biopsy tissue from 34 allogeneic and 23 autologous BMT recipients was prospectively analysed for CMV using immunohistochemistry and PCR to investigate the hypothesis that target organ infection with CMV initiates and/or exacerbates GVHD. Biopsies were obtained prior to and at 3, 8 and 26 weeks after BMT and whenever GVHD was suspected. Surveillance specimens of peripheral blood leucocytes (PBL), urine and throat swabs were obtained every 2 weeks until 12 weeks after BMT, and whenever CMV was suspected. Cryostat sections were analysed immunohistochemically for CMV antigens and PBL and biopsies for CMV DNA by PCR. Of the 31 patients who engrafted, 28 (90%) developed GVHD clinically, confirmed histologically in 56 biopsies. GVHD proved clinically severe in 14 patients, 4 of whom had treatment-resistant GVHD. CMV was detected in PBL more frequently in patients with severe GVHD than in those with mild/moderate GVHD (29% vs. 7%). However, in all but one patient the onset of GVHD preceded detection of CMV. In biopsy specimens, CMV was detected in only 2 patients, 1 of whom had an exacerbation of GVHD temporally associated with CMV. Thus, despite a high incidence of GVHD in this series, with 56 episodes of GVHD in 28 patients, only 1 patient had CMV in biopsy tissue temporally associated with GVHD. This suggests that biopsy infection with CMV is not a major factor in initiating or exacerbating GVHD in this cohort. This study thus does not support a role for target organ infection with CMV in the pathogenesis of GVHD.

Transfusion-associated graft-versus-host disease in fludarabine-treated B-chronic lymphocytic leukaemia.

Transfusion-associated graft-versus-host disease (TA-GVHD) is a rare but serious complication of blood component therapy in patients with haematological malignancies. B-chronic lymphocytic leukaemia (B-CLL), however, has rarely been associated with TA-GVHD. We report three patients with advanced B-CLL who developed TA-GVHD. All these had been treated with fludarabine. Suppression of T cells by fludarabine may have contributed to an increased susceptibility to TA-GVHD. The use of irradiated blood products to prevent this complication should be considered for patients with advanced B-CLL treated with fludarabine or other purine analogues.

Differentiation of materno-fetal GVHD from Omenn's syndrome in pre-BMT patients with severe combined immunodeficiency.

Materno-fetal GVHD is commonly a fatal condition occurring in patients with severe combined immunodeficiency (SCID). Definitive diagnosis is often difficult. We describe a patient with clinical features suggestive of materno-fetal GVHD but in whom histology was atypical. Y chromosome-specific PCR amplification analysis of DNA extracted from the skin biopsy was performed to detect chimeric evidence of infiltrating maternal T cells. This revealed strong positivity for the Y chromosome, indicating lack of maternal T cell engraftment and thus confirming a diagnosis of Omenn's syndrome, a variant of SCID in which atypical lymphocyte clones give rise to a similar picture. In contrast, Y chromosome-specific PCR analysis of skin biopsy DNA from a male patient with a rash clinically and histologically typical of materno-fetal GVHD revealed absence of the Y chromosome, indicating infiltration of maternal cells and thus confirming the diagnosis of materno-fetal GVHD. Y chromosome-specific PCR analysis is thus a useful investigation for the differentiation of materno-fetal GVHD from Omenn's syndrome in pre-BMT SCID patients presenting with unexplained rash.

Late development of graft-versus-host disease in an autologous BMT recipient.

Clinical and histological changes consistent with GVHD have been described in recipients of both syngeneic and autologous grafts. The mechanism of autologous GVHD is well documented. However, cases of autologous GVHD previously reported have all occurred within the first 2 months post-BMT. We report the case of an autologous BMT recipient in whom histological features consistent with GVHD emerged 7 months post-BMT, which may have implications for the long-term follow-up of autologous marrow graft recipients.

Diagnostic features of transfusion associated graft versus host disease.

AIMS: To define the immunopathological profile of transfusion associated graft versus host disease (TA-GvHD) to elucidate its pathophysiology and to determine if any features are of diagnostic value. METHODS: Nine patients (age range 14-61 years) who developed histologically confirmed TA-GvHD between 1989 and 1992 were studied. Immunohistochemical analysis of frozen and formalin fixed skin biopsy tissue was performed. Sections were stained with antibodies to CD3, CD8, CD4 and HLA-DR, using a routine streptavidin-biotin technique with standard diaminobenzidine development. RESULTS: All biopsy specimens showed aberrant positive expression of HLA-DR by epidermal keratinocytes. In four patients, all of whom died, HLA-DR was diffusely expressed throughout the epidermis; in the other five cases keratinocyte expression of HLA-DR was more focal. In all biopsy specimens T cells had infiltrated the dermis and epidermis. In all nine cases CD4+ T helper/inducer cells were the predominant T cells. DISCUSSION: Immunohistochemical studies are of value in the diagnosis of TA-GvHD. Aberrant keratinocyte expression of HLA-DR and dermal and epidermal infiltration of CD4+ T cells are immunopathological features of TA-GvHD. Immunohistochemical analysis of skin biopsy tissue using antibodies to these markers is thus a useful investigation in pancytopenic patients presenting with unexplained rashes.

Pathogenesis of GVHD: role of herpes viruses.

The pathogenesis of GVHD is not fully elucidated. Some groups of patients have a higher risk of developing GVHD post-BMT than others. Environmental factors may be important. Much attention has focused on the role of viruses, particularly herpes viruses, in GVHD. CMV in particular has been implicated as a pathogenic agent. Data from animal work and from observations of the frequent clinical association of CMV with GVHD have suggested a pathogenic link. Several large multi-centre seroepidemiological studies have been performed in an attempt to clarify this issue. This review discusses the data implicating herpes viruses in the pathogenesis of GVHD and considers the mechanisms by which viruses may exacerbate or initiate GVHD. Implications for the management of allogeneic BMT patients are discussed.