Surgical outcomes of preoperative steroid for rhegmatogenous retinal detachment with associated choroidal detachment.

PurposeTo investigate the effect of preoperative steroid on anatomical and functional outcomes of vitrectomy in patients with rhegmatogenous retinal detachment with associated choroidal detachment (RRD-CD), a rare but particular type of RRD.Patients and methodsThis retrospective cohort study included RRD-CD patients at Siriraj Hospital during January 2005 to December 2014. Patients with preexisting uveitis or RRD with giant retinal tears were excluded. Preoperative, intraoperative, and postoperative data were reviewed and analyzed.ResultsA total of 76 patients (76 eyes) with RRD-CD were included: 37 patients without preoperative steroid (Group A) and 39 patients with preoperative steroid for a median of 7 days (Group B: 34 patients with oral prednisolone (0.5-1 mg/kg/day) and 5 patients with 20 or 40 mg of subtenon triamcinolone). The total retinal reattachment rate at 3 months after one operation was not different between the two groups (59 vs 51%) with adjustment for confounders. The proportion of patients with visual acuity (VA) improvement at 3 months was also not different (57 vs 54%). Survival analysis revealed that 96% of redetachment cases occurred within the first 3 months and redetachment rate was not different between the two groups for up to 3 years. However, Group B showed a significant regression (partial or complete) of CD prior to operation compared to Group A (82 vs 30%, P<0.001).ConclusionPreoperative steroid significantly improved CD before vitrectomy, but seemed not to improve the single-operation retinal reattachment rate or VA at 3 months when compared to no steroid treatment in RRD-CD patients.

Characteristics of Pasteurella multocida isolated from humans, swine and poultry in Thailand.

Pasteurella multocida is a pathogen of animals and humans. Most of the patients have been associated with animals but many cases had not contacted them. The failure to diagnose P. multocida infections is mostly due to misidentification on gram stained smears and inadequate laboratory identification techniques. In order to compile detailed characteristics of the organism we studied the physical and biochemical properties of 70 isolates of P. multocida - 17 human, 23 swine and 30 poultry. All isolates produced catalase, oxydase, indol, nitrate reduction and ornithine decarboxylase. They failed to produce urease, gelatinase, methyl red, acetoin and could not grow on MacConkey agar, SS-agar, in nutrient broth with 0% or 6% NaCl. With respect to fermentable sugars, all isolates consistantly produced acid from glucose, mannitol and mannose. None of the cultures fermented lactose, maltose and dulcitol. Marked variations in the patterns of fermentation of arabinose and xylose were found. The characteristics tested are important to facilitate identification of P. multocida but could not be used to differentiate the host of the bacterium.

Immunoconglutinin and antibody against fibrinogen products in hemolytic anemia and nephritis resulting from infection with a Haemobartonella-like agent.

An agent morphologically similar to Haemobartonella muris was isolated from the blood of rats infected with a strain of Trypanosoma lewisi kept at this Department. It caused acute hemolytic anemia, splenomegaly, glomerulonephritis, and death within 5 to 8 days in mature Sprague-Dawley rats. The disease was less severe in weanling rats which usually recovered within 3 to 4 wk. The anemia was accompanied by phagocytosis of erythrocytes by monocytes of the spleen and bone marrow, by high titers of cold-active hemagglutinin, high titers of antibody to the third component of fixed complement (immunoconglutinin), and antibody to fibrinogen/fibrin related products. Filtrates of blood from anemic rats passing a 0.20-micron filter did not produce disease or signs of infections, but filtrate from a 0.45-micron filter was infective. Attempts to grow the agent on rat embryo fibroblast cultures and in embryonated chicken eggs were successful. Tests for bacteria, mycoplasma, and spirochetes gave negative results. Blood of infected rats did not produce signs of infections when inoculated into laboratory mice, and normal rats housed in cages with acutely infected rats did not develop signs of infection or disease. Morphological similarity did not allow differentiation of the agent from H. muris. However, its virulence for mature rats differs markedly from that usually seen in H. muris infection.

Antibody to fibrinogen/fibrin products (Anti-F) in malaria, babesiosis, and trypanosomiasis of rodents.

Antibody to fibrinogen/fibrin related products (Anti-F) was stimulated during the course of Plasmodium chabaudi, Babesia rodhaini, and Trypanosoma lewisi infections in rats. Titers of this autoantibody remained elevated in serum from rats that had recovered from each of the infections. Column chromatographic studies indicated that Anti-F was a 19S globulin, possibly IgM. During acute infections high titers of Anti-F were associated with elevated titers of cold-active hemagglutinin (CAH) and immunoconglutinin (IK) and all were associated with anemia and elevated parasitemia. Titers of Anti-F and IK, but not CAH, remained elevated in serum of recovered rats. The presence of Anti-F indicated that the coagulation system had been activated during each infection to release fibrinogen/fibrin-related products (FRP) to serve as antigen(s) for Anti-F. Since IK is antibody to the third component of fixed complement, it could be assumed that complement fixing antigen-antibody complexes were also present during the acute stage of each infection. The possibility that complexes of FRP and Anti-F could have contributed to anemia in each infection is discussed.

Immunoconglutinin associated with nonspecific acquired resistance in malaria, babesiosis, and other anemia-inducing infections.

Rats recovered from infectious anemias had an acquired nonspecific resistance. Recovery from trypanosomal and babesial infections enhanced the resistance to infections with filterable rat infectious anemia (RIA) agent, and recovery from RIA made rats more resistant to plasmodial, babesial and trypanosomal infections. The resistance was manifested after challenge by reduced parasitemia accompanied by significant anemia, which became evident 2 or 3 days earlier in recovered rats than in controls. Mortality of the recovered rats was less than that of the controls. Immunoconglutinin (IK) was detected with high titers in animals during the acute stage of each infection and remained present with lower titers after recovery. After the recovered rats were challenged with a heterologous agent, the existing IK titers became elevated earlier and usually were higher than those of the controls. However, the infections also stimulated production of cold-active hemagglutinin (CAH). It was therefore not clear that the resistance could be attributed to IK. The nature of antigen-antibody complexes that may have fixed complement and stimulate IK is discussed. However, a specific complex was not implicated.

Anemia, splenomegaly, and glomerulonephritis associated with autoantibody in Trypanosoma lewisi infections.

Anemia with splenomegaly and signs of glomerulonephritis were found associated with the acute and post-acute phase of Trypanosoma lewisi infections of laboratory rats. The onset of the anemia was associated with the peak of parasitemia and the development of cold-active hemagglutinin (HA) for trypsinized rat erythrocytes. It persisted with gradual recovery for as long as the trypanosomes and HA were detected in the blood. Signs of glomerulonephritis consisted of hypercellularity of the glomerular tuft, swelling of vascular endothelium and tubular epithelium, thickening of Bowman's membrane and tubular basement membrane, and abnormal numbers of hyaline casts in the distal convoluted tubules. Residual damage to the kidneys was not evaluated.