Isospora-type oocysts were excreted by cats following the ingestion of Toxoplasma fromn infected mice. Oocysts appeared 3 to 5 days after cyst. were ingested and 8 to 10 days after trophozoites were ingested, and also 21 to 24 days after the administration of infective fecal suspensions from cats. A close quanititative and biologic correlation between oocysts and Toxoplasma infectivity of the feces was observed which could not be separated by density gradient centrifugation and filtration methods. Toxoplasma is an intestinal coccidian of cats which is fecally spread. It has evolved to multiply in brain and muscle and in other species, making it possible for carnivorism to become another means of transmission.

Toxoplasma infection is c o m m o n in m a n and animals, yet for 60 years the life cycle of Toxoplasma gondii remained unknown. R e c e n t l y a new form of Toxoplasma was found in the feces of cats that had eaten Toxoplasma-infected mice (for review of earlier work see [1]). This fecal form is biologically different from the known stages of Toxoplasma. While searching the feces of cats for a morphological equivalent of Toxoplasma, several candidate forms such as fungi, cysts of flagellates, and coccidian oocysts resembling those of Isospora fells, I. rivolta, and I. bigemina were found. Of these only oocysts resembling [. bigemina were constantly and q u a n t i t a t i v e l y associated with fecal Toxoplasma infectivity. W e will describe and characterize these oocysts and show b y a series of m u t u a l l y independent determinations that they should be regarded as oocysts of Toxoplasma got~dii. Some of these findings were briefly reported (2). DEFINITION O F TER3£STrophozoites refer to intracellular and free forms of Toxoplasma which are actively proliferating in the tissues of acutely infected animals (Fig. 1). Free trophozoites are quickly digested in solutions of pepsin at pH 1.3.Cyst refers to an accumulation of Toxoplasma (merozoites) characteristically occurring in the brain and muscle of chronically infected animals (Fig. 2). Cysts are surrounded by an elastic argyrophilic and periodic acid Schiff positive wall and contain much stored glycogen. The cyst wall is destroyed immediately on exposure to pepsin but the released merozoites survive in it for some time.

No abstract

To investigate the possibility that premature infants may be vulnerable to aluminum toxicity acquired through intravenous feeding, we prospectively studied plasma and urinary aluminum concentrations in 18 premature infants receiving intravenous therapy and in 8 term infants receiving no intravenous therapy. We also measured bone aluminum concentrations in autopsy specimens from 23 infants, including 6 who had received at least three weeks of intravenous therapy. Premature infants who received intravenous therapy had high plasma and urinary aluminum concentrations, as compared with normal controls: plasma aluminum, 36.78 +/- 45.30 vs. 5.17 +/- 3.1 micrograms per liter (mean +/- S.D., P less than 0.0001); urinary aluminum:creatinine ratio, 5.4 +/- 4.6 vs. 0.64 +/- 0.75 (P less than 0.01). The bone aluminum concentration was 10 times higher in infants who had received at least three weeks of intravenous therapy than in those who had received limited intravenous therapy: 20.16 +/- 13.4 vs. 1.98 +/- 1.44 mg per kilogram of dry weight (P less than 0.0001). Creatinine clearances corrected for weight did not reach expected adult values until 34 weeks of gestation. Many commonly used intravenous solutions are found to be highly contaminated with aluminum. We conclude that infants receiving intravenous therapy have aluminum loading, which is reflected in increased urinary excretion and elevated concentrations in plasma and bone. Such infants may be at high risk for aluminum intoxication secondary to increased parenteral exposure and poor renal clearance.