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S S Arnon

Publications and source records attributed to S S Arnon.

At least 19 recordsLinked to original sources
PubMed1992

Distribution of HIV type 1 infection in childbearing women in California.

The incidence of acquired immunodeficiency syndrome (AIDS) is increasing among California heterosexuals and children. To assess human immunodeficiency virus (HIV)-1 infection in childbearing women, we conducted a blinded serosurvey of newborns. Dried blood specimens taken from 99% of California births during the third quarter of 1988 (n = 135,808) and linked only to maternal demographic categories were tested for HIV-1 antibody by enzyme immunoassay and confirmed by Western blot. Period prevalence of HIV-1 infection was 7.4 per 10,000 childbearing women. Prevalence was highest for Black women and was also elevated for Hispanic and San Francisco Bay Area women. Findings suggest that California Hispanic women will make up an increasing proportion of new AIDS cases.

Adult↗
PubMed1987

Evaluation of the Minitek system for characterization of Bacillus species.

Minitek (BBL Microbiology Systems, Cockeysville, Md.) substrate disks were evaluated as alternatives to conventional tests for the characterization of Bacillus species. Results were compared for 10 reference isolates and 87 isolates from food sources. The overall agreement of results between the Minitek and conventional tests was 92% for reference strains and 86% for food isolates.

Animals↗
PubMed1985

Improved selective medium for the isolation of lipase-positive Clostridium botulinum from feces of human infants.

Isolation of lipase-positive Clostridium botulinum from fecal specimens establishes the diagnosis of infant botulism, contributes to the diagnosis of food-borne botulism, and is most easily accomplished by use of selective media. Modification of an available selective medium, C. botulinum inhibitory medium (CBI), enabled more rapid isolation of C. botulinum. The modified medium (botulinum selective medium [BSM] contained (per liter) 25 g of dehydrated heart infusion broth, 20 g of agar, 30 ml of egg yolk suspension, 250 mg of cycloserine, 76 mg of sulfamethoxazole, 4 mg of trimethoprim, and 100 IU of thymidine phosphorylase at pH 7.4. The two media were compared by using 15 fresh fecal specimens from infant botulism patients (10 type A and 5 type B) and a C. botulinum isolate that had been obtained from an infant botulism patient and that was mixed into a fresh stool specimen from a healthy human infant. In comparison to CBI, BSM always provided better suppression of the nonbotulinum fecal flora and earlier emergence of lipase-positive colonies. Diagnosis of infant botulism was accomplished sooner with BSM than with CBI because isolation of lipase-positive C. botulinum was easier.

Botulism↗
PubMed1984

Rapid death of infant rhesus monkeys injected with Clostridium difficile toxins A and B: physiologic and pathologic basis.

Clostridium botulinum can colonize and produce botulinal toxin in the human infant intestine, which the toxin then permeates to cause generalized flaccid paralysis, and occasionally, sudden death. This study was undertaken to test the hypothesis that toxins produced by other intestinal clostridia, e.g., C. difficile, might also cause systemic illness and sometimes death in infants (J Pediatr 100:568, 1982). Because this hypothesis could not be evaluated clinically until the systemic manifestations of C. difficile toxins in primates were known, infant rhesus monkeys were given 6 to 11 micrograms/kg of the recently purified C. difficile toxins A or B, either intravenously or intraperitoneally. The animals showed no abnormalities for several hours, but then developed lethargy, hypotonia, hypothermia, and, shortly before death, sudden elevation of serum concentrations of potassium, magnesium, and phosphorus and of enzymes that derived mainly from skeletal muscle, heart and brain. Five of six animals died quietly 3.5 to 8.0 hours after onset of symptoms. Death appeared to result from cessation of breathing, after which the sinus tachycardia then deteriorated to a flat ECG. Necropsy findings were insufficient to explain the cause of death. It appears that in infant monkeys microgram amounts of C. difficile toxins A and B can produce a rapid quiet death, the cause of which is undetectable at necropsy, a situation pathologically reminiscent of crib death in human infants, although the possible clinical identity of these two conditions has yet to be established.

Animals↗
PubMed1982

Protective role of human milk against sudden death from infant botulism.

We examined the possibility that human milk and formula milk might differentially affect the severity of the infant botulism because they differ in immunologic composition and in influence on the normal intestinal microflora against which Clostridium botulinum must compete. A beneficial effect of human milk was suggested by the different feeding experiences of the moderate, hospitalized patients and the sudden death cases. Of patients hospitalized in California, 66% (33/50) were still being nursed at onset of illness, a percentage significantly greater than that of matched controls (P less than 0.01). In contrast, all ten California cases of sudden infant death attributable to C. botulinum infection were being fed iron-supplemented formula milk at death) unlike their controls, P less than 0.02) and had received no human milk within ten weeks of death. A beneficial effect of human milk was also observed in differences in mean age at onset; hospitalized breast-fed patients were almost twice as old (13.8 +/- 6.7 weeks) as were hospitalized formula-fed patients (7.6 +/- 2.9 weeks) (P less than 0.01). Human milk (or possibly other factors associated with breast-feeding) appeared to have moderated the severity at onset of infant botulism, allowing time for hospital admission, whereas for some infants with this illness, formula milk (or possibly other factors associated with formula feeding) was linked to sudden unexpected death.

Botulism↗
PubMed1980

Quantitative evidence of intestinal colonization by Clostridium botulinum in four cases of infant botulism.

Infant botulism is an infectious form of a disease heretofore principally known as food-borne intoxication. Previous epidemiologic and laboratory studies have shown that infant botulism results from the ingestion of spores of Clostridium botulinum that subsequently germinate in the infant intestine and produce botulinal toxin. A quantitative study of the fecal microflora of four infants with infant botulism revealed the presence of C. botulinum in numbers as high as 6.0 x 10(8) colony-forming units (cfu)/g. At various times after the onset of illness, the numbers of C. botulinum that were recovered from feces ranged from 10(3) to 10(8) cfu/g and constituted from 0.01% to 3.3% of the total fecal flora. It was concluded that the large numbers of C. botulinum found in patients' feces could occur only as a consequence of in vivo spore germination and outgrowth.

Botulinum Toxins↗
PubMed1980

Infant botulism.

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Age Factors↗