Overwhelming post-splenectomy infection (OPSI) is a serious complication of asplenia and is associated with encapsulated organisms, most commonly Streptococcus pneumoniae, but also Haemophilus influenzae and Neisseria meningitidis. We aimed to estimate the risk of infection in this patient group. We reviewed data collected by the Victorian Spleen Registry in Australia. On registration, all patients are asked about significant infections requiring admission to hospital for intravenous antibiotics; those requiring admission to ICU were defined as OPSI. In the 3274 asplenic patients registered 492 patients reported at least one episode of infection. There were 47 episodes of OPSI requiring intensive care (incidence rate 1·11/1000 patient-years). The risk of OPSI was highest in older patients, and there were no statistically significant differences in incidence by reason for splenectomy except for a higher rate in patients with medical hyposplenia. This study reinforces that post-splenectomy infection is a clinically significant but uncommon complication, and that fulminant infection requiring intensive care is a minority of all infections.

Purpura fulminans is a rare complication of septic shock, often associated with Streptococcus pneumoniae. Patients with anatomic or functional asplenia are at increased risk for infection because of impairment of their ability to defend against encapsulated pathogens. We report the case of a previously healthy, unimmunized 33-year-old female with functional asplenia who presented in septic shock and purpura fulminans and died in spite of maximal resuscitative measures. The clinical presentation, diagnosis, and management of purpura fulminans are reviewed. Purpura fulminans is a rare condition that requires early diagnosis and aggressive management by emergency physicians.

This study addresses the humoral and cellular basis of specific acquired immunity in the guinea-pig irradiated vaccine model of schistosomiasis mansoni. Rodents vaccinated with 500 gamma-irradiated cercariae and then splenectomized 4·5 weeks later showed a 33% reduction in resistance to challenge as compared to vaccinated animals or vaccinated/sham splenectomized controls. Serum harvested from once vaccinated individuals conferred modest levels of resistance upon naive recipients in some experiments, but transfer was not achieved consistently. Serum from vaccinated and thrice boosted rodents (Vbbb) routinely transferred around 45% immunity, however, provided it was given in 4 ml aliquots on day 9 post-challenge; Vbbb serum thus transferred 50% of donor immunity. Interestingly, multiple doses of this protective serum given on and either side of day 9 did not enhance the protection achieved with a single 4 ml aliquot. Neither peripheral lymph node cells nor splenocytes from the polyvaccinated serum donors were able to transfer resistance to recipient guinea-pigs and they failed to augment the protection achieved with Vbbb serum. Food-pad testing revealed no correlation between delayed hypersensitivity responses and immunity to challenge in vaccinated guinea-pigs. Although polyvaccine guinea-pig serum successfully protected homologous recipients, it failed to protect mice when administered either at the time of challenge (the optimal schedule for transfer of polyvaccine mouse serum), or around day 9 (the optimal schedule for guinea-pigs). Similarly, guinea-pigs could not be protected with polyvaccine rat serum that conferred 75% resistance upon naive recipient rats.

The treatment of visceral leishmaniasis (VL) in HIV-infected patients is characterized by having a protracted course and frequent relapses, despite the use of adequate anti-leishmanial drugs and effective anti-retroviral therapy. A small subset of patients with significant splenomegaly develops severe cytopaenias and chronic leishmania infection. The use of elective splenectomy is effective for restoring the haematological parameters and reduces the need for blood transfusions but it does not avoid relapsing visceral leishmaniasis.

The aim of this study was to examine the kinetics of neovascularisation of splenic autoimplants into the abdominal cavity after splenectomy in mice. Sixty-eight female Swiss mice were submitted to splenectomy. The spleen from each animal was sliced and the slices were implanted into the abdominal cavity. Groups of animals were killed after 1, 2, 3, 5, 7, 15, 21, 28, 42, 56, 70 and 84 d. Fluorescent polystyrene microspheres were injected via the orbital venous plexus before killing and the splenules were removed 5 min later for light and electron microscopy. Mesenteric blood vessels were injected with coloured latex to study the origin of the nutrient vessels. Three days after the implant the microspheres were observed at the periphery and then migrating to the internal parts of the implant in the subsequent days. The blood supply to the implants originated from branches of the splenic, short gastric, mesenteric and gastroepiploic arteries. It is concluded that revascularisation of splenic autografts proceeds centripetally, starting as early as 3 d after implantation.