Sphingobacterium multivorum septicemia: a case report.

A 47-year-old man presented with a history of fever, chills and weight loss for 3 months. He had been treated for diabetes mellitus during the past 3 years. He developed high fever with abnormal liver function tests. Both Widal and Weil-Felix reactions were negative with normal roentgenogram of the chest. His anti-HIV tests were positive. The cultures from the blood and sputum yielded pure Sphingobacterium multivorum sensitive to sulfamethoxazole-trimethoprim, chloramphenicol, tetracycline, cefotaxime, ceftazidine and ceftriaxone. On the next day, the patient developed signs and symptoms of meningitis with the CSF containing chronic and acute inflammatory cells but revealed no growth on culture. The patient was treated with a combination of ceftriazone and trimethoprim-sulfamethoxazole but he died on the 6th day after admission. This patient was the fifth reported case infected with S.multivorum. It illustrates that this potentially pathogenic organism can cause septicemia in an immunodeficient patient.

Serum transcobalamin II level in glucose-6-phosphate dehydrogenase deficient subjects with typhoid fever.

Transcobalamin II (TCII) is the vitamin B12 binding protein which is responsible for delivery of this vitamin to the tissues. High values for serum TCII have been reported in many clinical conditions. This paper describes the elevated serum TCII levels in three G-6-PD deficient patients with typhoid fever. They had severe hemolysis with hemoglobinuria associated with slight liver dysfunctions but without obvious increased serum creatinine and BUN concentrations. A remarkable increase in serum TCII level was observed during active hemolysis and decreased to the normal level within 2-3 days after hemolysis ceased. The mechanism of increased serum TCII during hemolysis is probably due to hemoglobinuria secondary to excessive hemolysis. As Hb is known to be efficiently reabsorbed by the proximal tubule cells and can competitively inhibit the tubular uptake of TCII-B12. It is possible that excess Hb interferes with TCII uptake and degradation at renal tubular cells. Therefore, the circulating TCII survival is prolonged resulting in the elevated TCII level. Furthermore, lysosomal degradation of newly synthesized TCII is a normal process that regulates the TCII secretion. Therefore, a reduced lysosome-mediated uptake of TCII-B12 by renal tubular cell may stimulate the TCII secretion as has been shown experimentally in vitro.

Serum transcobalamin II levels in patients with acute and chronic renal failure.

Serum TCII levels were determined in 57 patients with acute and chronic renal failure. They were divided into 3 groups, group I was malarial patients with acute renal failure, group II and III were patients with acute renal failure and chronic renal failure from other underlying causes, respectively. All patients in group I had serum TCII over 2000 pg/ml while these values were within the normal limits in the other 2 groups. These findings indicated that elevated serum TCII occurred only in malarial patients with acute renal failure. The clearance and urinary excretion of TCII in malarial patients were found to be lower and increased to the normal levels after recovery from azotemia, indicating that the failure of excretion of TCII by the kidneys may be responsible for elevated serum TCII levels. The pathophysiological changes in the kidneys in malarial patients may reduce the amount of filtered TCII-B12 through the glomeruli and decrease TCII-B12 uptake by the renal tubules resulting in the decreased TCII degradation by tubular cells. Therefore, the intravascular TCII survival is prolonged with elevated serum TCII levels in these patients.

Serum transcobalamin II levels in patients with malaria infection.

Serum transcobalamin II (TCII) levels were determined in 56 patients with P. falciparum malaria infection. They were divided into 3 groups: severe (malarial parasite > 5% or patients with cerebral malaria or renal insufficiency), moderate (1-5% infection without complications) and mild (1% infection). Elevated serum TCII values were found only in patients with severe malaria infection. These values correlated directly with parasitemia, blood urea nitrogen and creatinine, but were not correlated with alkaline phosphatase. As 17 patients with azotemia had elevated serum TCII levels while other 3 patients with normal BUN and creatinine concentrations had serum TCII levels within the normal limits. These findings indicated that malarial patients with renal insufficiency had increased serum TCII. A possible mechanism is the reduced TCII-B12 that filtered through the glomeruli due to the reduced renal blood flow with the decreased its uptake by proximal tubular cells resulting in the decreased degradation of TCII by the tubular lysosomal enzymes. Determination of serum TCII level may be used as an indicator of renal function in malarial patients with renal insufficiency.

Persistently elevated serum transcobalamin II in a patient with cerebral malaria and typhus infections.

A 25-year-old man presented with a history of fever, chills and vomiting for three days. The parasite count was 207 ring-forms of P. falciparum per 1000 red cells. He developed hemoglobinuria and excreted hemoglobin in the urine 0.20-0.30 g/dl for 14 days during admission. Many blood transfusions were administered for correcting anemia. Although the malarial parasites disappeared one week after anti-malarial therapy, however, the fever and hemoglobinuria persisted. The Weil-Felix reaction OXK was positive with a titre of 1:40 on admission and increased to 1:160 on the second week. Chloramphenical and prednisolone were given for treatment of typhus fever and all symptoms subsided. Serum TCII levels were found to be increased and persisted high during the hemoglobinuria. The clearance of TCII was lower and increased relatively slowly to the normal level on day 30. On the other hand, TCII excretion in the urine was found to be increased during hemoglobinuria. These findings indicate that the catabolism and clearance of TCII in this patients is impaired with increased TCII excretion in the urine in parallel to the hemoglobinuria. Serum TCII level is, therefore, increased and persistently high in a patient with malaria and typhus fever infections with hemoglobinuria.

Abnormally elevated serum transcobalamin II levels in patients with cerebral malaria.

Transcobalamin II (TCII) levels have been reported to be elevated in patients with many clinical conditions including proliferative reticuloendothelial system. As reactive macrophage hyperplasia frequently occurs in patients with malaria, the objective of the present study was to determine TCII in patients with Plasmodium falciparum with cerebral symptoms. The studies were performed on 14 cerebral malaria patients as well as 60 normal subjects. The mean values of serum vitamin B12 and TCII levels were significantly higher in the patient group and 6 and 7 patients had serum vitamin B12 and TCII levels higher than the normal values. There was direct relationship between serum TCII levels and BUN or creatinine levels. These findings indicated that raised serum TCII level occurred only in patients with renal insufficiency. A decreased glomerular fiLtration rate reduced the amount of vitamin B12 and TCII-B12 that filtered through the glomeruli resulting in the reduced proximal tubular cells uptake and its degradation of TCII. This reduced lysosomal enzyme activity, therefore, prolongs the intravascular TCII survival and increased secretion of TCII into the circulation. Therefore, serum TCII levels were elevated in these cerebral malaria patients.

Optic neuropathy in a patient with vitamin B12 deficiency: a case report.

A 19-year-old man presented with blurring of vision for 2 weeks. He also complained of anorexia with weight loss during the past 4 months. Eight years ago, his small bowel from midportion of the jejunum, ileum, ascending colon and transverse colon were resected because of gangrene. He gave no history of exposure to tobacco, alcohol or other toxins. The bone marrow aspiration showed hypocellular with panhypoplasia. Serum vitamin B12 level was low while serum and red cell folate were within normal limits. His visual acuity was 5/200 in both eyes with centrocecal scotomas in both eyes. Other neurologic and ophthalmic examinations were found to be normal. The patient was given intramuscular injections of 1,000 micrograms of cyanocobalamin. Four months later, his visual acuity improved, serum vitamin B12 level and the bone marrow returned to be normal. This is a frank case of optic neuropathy in a patient with vitamin B12 deficiency due to a massive small bowel resection.

Vitamin B12 deficiency: report of a childhood case.

An 11-year-old boy who presented with anemia, premature grey hair, hyperpigmented skin, paresthesia, recurrent aphthous ulcers and epistaxis was eventually proved to be a case of vitamin B12 deficiency. Due to the paucity of this deficiency, the diagnosis may easily be delayed and overlooked resulting in unfavorable consequences. Therapeutic response to vitamin B12 was dramatic in this reported case.

The source and content of vitamin B12 in the tempehs.

Vitamin B12 contents were determined on 10 commercial tempeh samples purchased from various markets in Jakarta, Indonesia. A relatively high vitamin B12 content was found, i.e., 19 ng/g (ranges from 1.8 to 41.4 ng/g). As soybeans contain no vitamin B12, the amount of vitamin in the tempeh must therefore be derived from the other sources during the fermentation process. The tempeh prepared in the laboratory by inoculation of the commercial starter into the sterile soybean contained a much higher amount of vitamin B12, 127 ng/g (ranges from 122 to 136 ng/g). Pure mold and a single species of bacteria were isolated from the starter and commercial tempehs. Pure mold did not produce vitamin B12 in the sterile broth, soybean and medium used for vitamin B12 production. Only the isolated bacteria, identified as K. pneumoniae, could produce vitamin B12 in those substrates. The presence of mold did not significantly enhance or inhibit the vitamin B12 production by K. pneumoniae. It was, therefore, concluded that K. pneumoniae, the bacteria contaminated during the process of tempeh production, was responsible for the vitamin B12 production.

Iron excretion in thalassemia children treated with deferoxamin methansulfonat: intravenous drip compared to the subcutaneous routes.

The iron excretion in the three beta-Thal/Hb E patients were determined comparing the effect of DF given by subcutaneous push, subcutaneous drip and intravenous drip. The subcutaneous drip or intravenous drip increased urine iron excretion by 5.6-11.2 times whereas the subcutaneous push, 3.5-5.3 times only. It is recommended that for countries where the infusion machine is very expensive the DF should be given by intravenous drip or the modified, simple and inexpensive equipment for subcutaneous drip.

Superoxide dismutase and catalase activities of cultured erythrocytes infected with Plasmodium falciparum.

It has already shown that catalase activity is significantly decreased in red cells of patients with P. falciparum. The mechanism suggested was by this enzyme inactivation through increased H2O2 generated during malarial infection. The present study was performed to verify this hypothesis. Catalase activities of red cells with high or low parasitemia in patients with P. falciparum were found to be lower than those of normal red cells. However, P. falciparum-infected red cells cultured for one week showed similar SOD and catalase levels to normal red cells. There was also no significant difference in the catalase levels between the parasitized and non-parasitized red cells. The difference in catalase activity of infected red cells before and after culture could be explained in terms of the activation of mononuclear cells and macrophages in vivo. During the sojourn of the parasitized red cells in close proximity to the macrophages of the spleen, they might trigger oxidative bursts resulting in increased H2O2. In order to protect themselves from oxidant damage, the catalase in the infected red cells could be inactivated by H2O2 resulting in the reduction of this enzyme.

Renal plasma flow in rhesus monkeys infected with Plasmodium knowlesi.

Renal plasma flow was studied in six rhesus monkeys before and during infection with Plasmodium knowlesi using 125I-sodium orthoiodohippurate (125I-OIH) as a tracer. The mean renal plasma flow and the rate constant from the intravascular compartment to the kidneys were significantly reduced in the infected monkeys. As both intravascular and extravascular compartments were slightly but not significantly elevated, which resulted in the prolonged mean transit time of 125I-OIH in monkeys infected with P. knowlesi. The parasitemia showed a reverse relationship with the renal plasma flow and a direct relationship with the mean transit time. These findings indicated that the renal plasma flow in the infected monkeys was depressed in proportion to the number of P. knowlesi parasites. The mechanism of reduced renal plasma flow was probably due to renal vasoconstriction.

Renal clearance, tubular reabsorption and urinary excretion of albumin in monkeys infected with Plasmodium knowlesi.

The glomerular filtration rate (GFR) and the glomerular clearance rate of albumin were determined in 6 rhesus monkeys infected with P. knowlesi as well as in 6 control monkeys by using 51Cr-EDTA and 125I-HSA respectively. The excreted albumin in the urine was also determined and used for calculating the renal clearance value. The amount and rate of albumin filtered in the glomeruli and reabsorbed by the tubules were then calculated from these parameters. The present study showed that the rate and amount of albumin filtered through the glomeruli, reabsorbed by tubules and excreted in the urine of normal monkeys, which were similar to results reported earlier in normal human, dogs and rats. In the monkeys infected with P. knowlesi the glomerular filtration rate was reduced while the glomerular clearance rate of albumin increased which resulted in the significantly elevated filtered albumin in the glomeruli. The tubular reabsorptive capacity to plasma albumin was also found to be significantly increased in parallel to the elevated filtered load of albumin. However, as this capacity was limited, the excess albumin was therefore excreted into the urine in the infected monkeys. All these findings indicated that the albuminuria in P. knowlesi-infected monkeys was due to the increased glomerular capillary permeability to plasma albumin, although the tubular reabsorptive capacity increased but could not cope with a very high filtered load, therefore, excess albumin was detected in the urine.