Association between maternal antibodies to the external envelope glycoprotein and vertical transmission of human T-lymphotropic virus type I. Maternal anti-env antibodies correlate with protection in non-breast-fed children.

Vertical transmission of human T-lymphotropic virus type I (HTLV-I) depends primarily on breast-feeding; substitution of bottle-feeding has reduced the transmission rate from 20% in breast-fed children to 3% among bottle-fed. To determine the correlates of transmission for long breast-feeding (> or = 6 mo), short breast-feeding (< 6 mo), and bottle-feeding mothers, the antibody titers of transmitter (T) mothers and non-transmitter (nT) mothers were analyzed by using synthetic and recombinant epitopes representing the immunodominant epitopes of gag (Gag1a, r24), env (Env1/5, MTA1, RE3), and tax (Tax8/22-24) proteins. Seroreactivity to gag and tax epitopes was not significantly different except for anti-r24 antibody titer, which was significantly higher among T-mothers (geometric mean 134) when compared with nT-mothers (62) in the long-feeding group (P < 0.001). Profiles of antibody titers against env epitopes were different. Within the long-feeding group, Env1/5, MTA1, and RE3 titers were significantly higher among T-mothers (258, 1,476, and 738, respectively) when compared with nT-mothers (106, 279, and 320, respectively) (P < 0.01 for all three epitopes). In contrast, within the bottle-feeding group, antibody titers to Env1/5 (269) and RE3 (418) among nT-mothers were significantly higher than those among T-mothers (80 and 113, respectively) (P < 0.01). These data confirm that high-titered anti-HTLV-I antibodies in the long-feeding group correlate with milk-borne transmission of HTLV-I and, more importantly, imply that maternal anti-env antibodies may reduce the risk of non-milkborne infection.

Plasma fibronectin synthesis in normal and injured humans as determined by stable isotope incorporation.

In humans, plasma fibronectin decreases early after operative injury, burn, or trauma, followed by a rapid restoration with a secondary decline typically observed if such patients become septic. We determined the rate of plasma fibronectin and plasma fibrinogen synthesis in normal subjects and injured patients using a stable isotope incorporation technique with [15N]glycine. During a constant 14-h infusion of [15N]glycine, the enrichment of [15N]glycine in both the free plasma glycine precursor pool as well as the urinary hippurate pool was determined; the latter used as an estimate of intracellular hepatic precursor enrichment. [15N]Glycine enrichment in both plasma fibronectin and fibrinogen was also quantified. The synthesis rate (Js/V) expressed in micrograms per milliliter of plasma per hour and the fractional synthesis rate (FSR) expressed as percentage of the plasma pool produced per day were determined. In normal subjects, the FSR for plasma fibronectin using 15N enrichment into urinary hippurate was 35.35 +/- 1.46%/d, whereas the Js/V was 4.45 +/- 0.19 micrograms/ml plasma per h. In normal subjects, the FSR for plasma fibronectin using 15N enrichment into free plasma glycine was 14.73 +/- 0.63%/d, whereas the Js/V was 1.98 +/- 0.09 micrograms/ml plasma per h. Early (2-3 d) after burn injury, fibronectin synthesis was increased (Js/V = 5.74 +/- 0.36; P less than 0.05), whereas later after injury, fibronectin synthesis began to decline (Js/V = 3.52 +/- 0.24; P less than 0.05) based on 15N enrichment of urinary hippurate. In contrast, the Js/V and FSR of plasma fibrinogen, a well-documented acute-phase plasma protein, revealed a sustained elevation (P less than 0.05) after injury in both the trauma and burn patients. Thus, plasma fibronectin synthesis is elevated early postinjury, which may contribute to the rapid restoration of its blood level. However, once fibronectin levels have normalized, the synthesis of plasma fibronectin appears to decline.

Antibody response to human immunodeficiency virus in homosexual men. Relation of antibody specificity, titer, and isotype to clinical status, severity of immunodeficiency, and disease progression.

The titers and isotypes of antibodies to specific proteins of the human immunodeficiency virus were determined by Western blot analysis of sera from 107 homosexual men. Antibody titers were generally lower in sera from patients with the acquired immunodeficiency syndrome (AIDS) and in sera from men whose condition subsequently progressed to AIDS than in sera from men who had not progressed to AIDS. We found no evidence of isotypic prominence or restriction of the antibody response. In multivariate analysis, lower levels of CD4 helper cells were most highly associated with progression to AIDS. Lower antibody titers to the envelope protein gp110, the core protein p24, and the reverse transcriptase enzyme p51/65 were also predictive of progression to AIDS independent of their association with CD4 cell levels. These data suggest that differences in antibody levels are not simply a consequence of severe immunodeficiency but may be markers for control of infection.

A role for a 70-kDa amino-terminal fibronectin fragment in supporting soluble gelatin interactions with rat peritoneal macrophages.

Seventy-kilodalton amino-terminal and 180-kDa cell-binding fibronectin fragments were used to determine which fibronectin domains support soluble gelatin interactions with macrophages. At each time measured, intact and 180-kDa fibronectin supported significantly larger quantities of cell-associated gelatin than control levels (P < 0.05). Throughout the time course fibronectin supported more binding than 180 kDa. Seventy kilodalton did not augment gelatin binding until 2 h, but by 6 h 70 kDa supported more binding than intact fibronectin (P < 0.01). This appeared to result from a cellular response initiated by 70-kDa-gelatin interactions with the macrophages. Within 4 h the majority of gelatin associated with cells under control conditions, and in the presence of fibronectin or 180 kDa, was internalized. Seventy-kilodalton-mediated binding remained localized primarily to the cell surfaces at all times. The macrophages partially degraded the internalized and external gelatin fractions. These results demonstrate that intact fibronectin and specific fibronectin fragments support soluble gelatin interactions with macrophages.

Influence of prostaglandin I2 on fibronectin-mediated phagocytosis in vivo and in vitro.

This study evaluated the effect of prostaglandin I2 (PGI2) on fibronectin-mediated macrophage phagocytosis in vivo and in vitro. Phagocytosis measured in vivo in rats by the vascular clearance rate and hepatic localization gelatinized sheep erythrocytes was inhibited in a dose-dependent manner after intravenous administration of PGI2. Phagocytosis was assessed in vitro in terms of uptake of fibronectin-dependent gelatinized sheep erythrocytes by monolayers of casein-elicited rat peritoneal macrophages. Concentrations of 1 ng/ml PGI2 or greater resulted in inhibition of particle internalization but not attachment to macrophages. This inhibitory effect was enhanced by aminophylline, a phosphodiesterase inhibitor. PGI2 increased cAMP levels and these were further increased in the presence of aminophylline. These data indicate that PGI2 inhibits macrophage uptake of gelatinized particles and support the idea that this is mediated by increased intracellular levels of cyclic AMP. PGI2 should thus be considered a potential etiologic factor in the phagocytic depression observed in association with thrombosis.

A 70-kDa amino-terminal fibronectin fragment supports gelatin binding to macrophages and decreases gelatinase activity.

We previously reported that a macrophage response that increased binding to 125I-radiolabeled soluble denatured collagen (gelatin) was induced by preincubation of macrophage with a 70-kDa amino-terminal fibronectin fragment and soluble nonlabeled gelatin [S. F. Penc, F. A. Blumenstock, J. E. Kaplan (1995) J. Leukoc. Biol. 58, 501-509]. We now report that neither protein synthesis nor recycling of receptors between the cell surface and interior were required for this response. However, removal of cell surface components with trypsin demonstrated that induced gelatin binding required native cell surface constituents. It was found that in the presence of the 70-kDa fibronectin fragment and gelatin, matrix metalloprotease-2 (MMP-2) and matrix metalloprotease-9 (MMP-9) activity in the cell layers was significantly decreased or undetectable, respectively. Similar levels of increased gelatin binding could be reproduced after inhibition of matrix-degrading metalloprotease activity with 1'10-phenanthroline. These results demonstrate that a macrophage specific response that decreased gelatinase activity and increased gelatin binding was initiated by interaction with a 70-kDa fibronectin fragment and gelatin.

Reticuloendothelial-depressing substance: studies on the mechanism of action.

This study was carried out to evaluate the mechanism of action of a reticuloendothelial (RE)-depressing substance. This RE-depressing substance was obtained from the plasma of dogs subjected to 3 hr of intestinal ischemia. RE-depressing substance was partially purified by dialysis and reverse-phase column chromatography. The assay of RE-depressing activity was based on the depression of the rate of clearance of colloidal carbon from the blood of rats or mice. The effect of RE-depressing substance on three other RE system (RES) test particles (gelatinized lipid emulsion, formalinized sheep erythrocytes, and IgM-coated erythrocytes) was determined. RE-depressing substance did not affect the clearance rate or the organ localization of these three test particles. Therefore, RE-depressing substance affected only the clearance of colloidal carbon. Since platelet aggregation has been shown to contribute to the clearance of colloidal carbon, the effect of RE-depressing substance on platelet aggregation was evaluated. RE-depressing substance depressed in vitro platelet aggregation induced by ADP or collagen. It was concluded that the effect of RE-depressing substance on the clearance of colloidal carbon was due to a depression of platelet aggregation rather than to a depression of hepatic macrophage phagocytic function.

Viral load as an independent risk factor for opportunistic infections in HIV-infected adults and adolescents.

OBJECTIVE: We investigated whether HIV plasma RNA (viral load; VL) predicts risk for opportunistic infections (OI) in HIV-infected persons, independent of CD4 lymphocyte count and other factors that might affect disease outcome. METHODS: Among persons who had initiated antiretroviral therapy (ART), we studied the risk for OI following a VL measurement in the Centers for Disease Control and Prevention Adult and Adolescent Spectrum of HIV Disease (ASD) Project, a medical record review study of HIV-infected persons in 11 US cities. Analysis was limited to persons who had initiated ART and who had VL data, primarily from the period 1996-1999. Persons were considered at risk for OI for 1 to 6 months after a given VL; risk for OI was assessed using a Poisson multiple regression model controlling for CD4 lymphocyte count, ART, and other variables potentially associated with development of OI: history of AIDS OI, age, sex, race, HIV risk category, OI prophylaxis, and calendar year. RESULTS: Although decreasing CD4 count was the strongest predictor of risk for OI [relative risk (RR), 13.3 for persons with CD4 lymphocyte count < 50 x 10(6)/l compared with persons with CD4 lymphocyte count > or = 500 x 10(6)/l], increasing VL was independently associated with increased risk [RR, 1.6, 1.9, 2.7, and 3.5 for VL of 7000-19 999, 20 000-54 999, 55 000-149 999, and > or = 150 000 copies/ml (by reverse transcription-PCR), respectively, compared with VL < 400]. Similar results were obtained when the risk period was reduced to 5, 4, 3, and 2 months after VL measurement. CONCLUSIONS: VL is an independent risk factor for OI and should be considered in special situations, such as in decisions to discontinue primary or secondary OI prophylaxis after CD4 lymphocyte counts have increased in response to ART.

Toxoplasmic encephalitis in HIV-infected persons: risk factors and trends. The Adult/Adolescent Spectrum of Disease Group.

OBJECTIVE: To evaluate the incidence of and risk factors for toxoplasmic encephalitis among HIV-infected persons. DESIGN: Medical facility-based prospective medical record reviews of consecutive patients. METHODS: We analysed data collected from January 1990 through August 1995 in more than 90 inpatient and outpatient medical facilities in nine US cities. Incidence was calculated as cases per 100 person-years and risk ratios (RR) for annual incidence were calculated using proportional hazards regression while controlling for city, sex, race, age, county of birth, HIV exposure mode, and prior prescription of trimethoprim-sulfamethoxazole (TMP-SMX). RESULTS: The incidence of TE was 4.0 cases per 100 person-years among persons with a CD4+ T-lymphocyte count of < 100 x 10(6)/l. In multivariate analysis, among the nine cities the annual incidence of toxoplasmosis was significantly lower only in Denver [RR, 0.3; 95% confidence interval (CI), 0.1-0.7; referent city, Seattle]. Persons prescribed TMP-SMX were half as likely to develop toxoplasmic encephalitis as those who were not (RR, 0.5; 95% CI, 0.4-0.7). Of the 4173 persons with AIDS (1987 Centers for Disease Control and Prevention definition) who died during the study period, 267 (6.4%) had toxoplasmic encephalitis in the course of HIV disease. CONCLUSIONS: Toxoplasmic encephalitis in HIV-infected persons varies by geographic area in the United States. TMP-SMX reduces the risk for toxoplasmic encephalitis.

HIV risk factors in three geographic strata of rural Rakai District, Uganda.

OBJECTIVES: To examine risk factors for HIV-1 infection in three geographic strata (main road trading centers that service local and international traffic, small trading villages on secondary dirt roads that serve as foci for local communications, and agricultural villages off main and secondary roads) in Rakai District, Uganda. DESIGN AND METHODS: Serological, sociodemographic, knowledge/behaviors and health survey conducted in 21 randomly selected community clusters; complete data were collected for 1292 consenting adults. RESULTS: Fifteen per cent of the men and 24% of the women were HIV-1-positive. On univariate analysis, several sociodemographic and behavioral factors were significantly associated with risk of HIV infection, including age, place of residence, travel, occupation, marital status, number of sex partners, sex for money or gifts, history of sexually transmitted disease (STD), and history of injections. On multivariate analysis, age, residence and number of sex partners remained significantly associated with HIV infection in both sexes; a history of STD and not having been circumcised were significant in men. There was a significant interaction between place of residence and reported number of sex partners: for any given level of sexual activity, the risk of HIV infection was markedly increased if the background community prevalence was high. CONCLUSION: Sexual transmission appears to be the primary behavioral risk factor for infection, but the risks associated with this factor vary substantially between the three geographic strata. These data can be used to design targeted interventions.

Effect of clinical events on plasma HIV-1 RNA levels in persons with CD4+ T-lymphocyte counts of more than 500 x 10(6) cells/l.

OBJECTIVE: Immune stimulation of CD4 lymphocytes is thought to enhance HIV-1 replication in vivo. Therefore, we sought to define the impact of clinical events identified as putative immune activators on the variability of plasma HIV-1 RNA levels in persons with CD4 cell counts greater than 500 x 10(6) cells/l. DESIGN: We prospectively recorded clinical events and measured plasma HIV-1 RNA levels weekly for 24 weeks in 16 HIV-1-infected adults who were not receiving antiretroviral therapy and who had CD4 cell counts greater than 500 x 10(6) cells/l. METHODS: Standard weekly interviews were conducted to capture potential immune activators (e.g., infections, immunizations, and allergic reactions). All plasma HIV-1 RNA levels were measured using the Amplicor HIV-1 Monitor assay (Roche Diagnostics, Branchburg, New Jersey, USA) according to the manufacturer's instructions. RESULTS: Participants had remarkably stable viral loads during the 6 month study period. Infections were significantly more frequent during the 7 days prior to individual HIV-1 RNA measurements that exceeded the assay variation thresholds determined for this study (+/- 0.324 log) than during the comparable time periods preceding stable measurements (P = 0.023). As a group, the eight participants who had one to four HIV-1 RNA measurements that exceeded the thresholds experienced more infections and declining CD4 cell counts over the study course compared to the eight participants whose measurements all fell within the thresholds (P = 0.058 and 0.053 respectively). CONCLUSIONS: Our study suggests that in untreated HIV-1-infected persons with CD4 cell count greater than 500 x 10(6) cells/l, viral load is generally quite stable, although acute minor infections are associated with transient fluctuations generally lasting no more than 1 week.

Ten-year follow-up of HIV-infected homosexual men with lymphadenopathy syndrome: evidence for continuing risk of developing AIDS.

Seventy-five homosexual men with lymphadenopathy syndrome (LAS), subsequently shown to be seropositive for the human immunodeficiency virus (HIV), were enrolled in a prospective study in Atlanta in 1982 and 1983. Subjects have been followed up at 3- to 6-month intervals with clinical and immunologic evaluations, including analysis of T-cell subsets. As of February 28, 1991, AIDS had developed in 36 (48%) of the 75 men. The AIDS cases continued to occur through the 10th year after onset of LAS; the 10-year cumulative incidence of AIDS was 56.6% (Kaplan-Meier survival analysis). Six-year incidence rates following the first observation of a T-helper cell count greater than or equal to 500/mm3, 400-499/mm3, 300-399/mm3, 200-299/mm3, and less than 200/mm3 were 29, 35, 50, 58, and 88%, respectively. Among individual symptoms and signs, only thrush conferred a poorer prognosis (odds ratio = 5.80; 95% confidence interval, 2.93, 11.39, p less than 0.001, Mantel-Byar analysis). The risk of AIDS persists 10 years after the onset of LAS. The AIDS incidence is related directly to T-helper cell depletion; with the exception of thrush, the presence or absence of symptoms and signs appears to be of lesser prognostic significance.

The search for human infection with simian type D retroviruses.

Evidence has recently been presented for an infection with a simian type D retrovirus in a patient with AIDS and lymphoma. We tested for simian type D infection in three groups of subjects: 375 patients with lymphoproliferative diseases (255 non-Hodgkin's, 88 Hodgkin's, and 32 chronic lymphoproliferative disease), of whom 75 were human immunodeficiency virus (HIV)-1 infected; seven persons with unexplained low CD4 lymphocyte counts with clinical conditions; and 45 blood donors, of whom 37 were human T-lymphocyte virus (HTLV)-I/II seroindeterminate and eight were HTLV-I/II and HIV-1 seronegative. Serum samples were screened for antibodies against simian type D retroviruses by an enzyme immunoassay, and reactive samples were analyzed by Western blotting. None of the samples were seropositive, but eight (five from non-Hodgkin's and three from Hodgkin's lymphoma patients) were seroindeterminate. Polymerase chain reaction analysis of genomic DNA from peripheral blood lymphocytes of all eight of these patients was carried out using simian type D gag generic primers with generic internal oligoprobing. All samples were negative. We conclude that simian type D infection is rare among HIV-infected and noninfected lymphoma patients, persons with unexplained low CD4 counts, and persons with HTLV-seroindeterminate test results.

The risk of development of HTLV-I-associated myelopathy/tropical spastic paraparesis among persons infected with HTLV-I.

Using data obtained in national surveys of human T-lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) conducted in Japan in 1987 and 1988, we estimated the yearly and lifetime risk that HAM/TSP will develop in an HTLV-I-infected person. "Definite" HAM/TSP was defined as slowly progressive myelopathy with antibodies to HTLV-I in both serum and cerebrospinal fluid. Estimates of HTLV-I infection rates in eight endemic prefectures, by age group and sex, were obtained from serologic studies of blood donors; population figures, by age group, sex, and prefecture, were obtained from the census. Of 589 definite cases of HAM/TSP reported nationally, 397 occurred in residents of the eight endemic prefectures; of these, 170 reported onset of illness during the years 1982-1988 (average incidence, 24.3 cases/year). Using the estimated HTLV-I infection rates and the 1985 census figures, we estimated the number of HTLV-I-infected persons in the eight prefectures in 1985 at 794,800. We therefore estimated the incidence of HAM/TSP among HTLV-I-infected persons at 3.1 x 10(-5) cases/year; assuming a lifetime of 75 years, the lifetime incidence is approximately one quarter of 1%. This estimate is important in counseling persons such as blood donors found to be infected with HTLV-I.

Guillain-Barré syndrome in the United States, 1978-1981: additional observations from the national surveillance system.

During the period January 1978-March 1981, 2,575 cases of Guillain-Barré syndrome (GBS) were reported by participating neurologists in the national GBS surveillance system. The incidence of GBS was highest in the 50- to 74-year-old age group, but a lesser peak was observed in persons aged 15 to 35. The frequencies of antecedent respiratory (43%) and gastrointestinal (21%) illness exceeded frequencies of such illnesses in the US population (10 and 0.8%, respectively), based on survey data compiled by the National Center for Health Statistics; the differences in these frequencies of illness were similar in all seasons of the year, in males and in females, and in persons less than 6, 6 to 16, 17 to 44, and greater than 44 years of age. Nineteen percent of adult patients for whom information was available (67% of the total) reported receiving an A/New Jersey influenza vaccine in 1976, a lower percentage than would be expected on the basis of a survey conducted in that year. The data suggest that persons who received this vaccine have not been at increased risk and may even have been at decreased risk of acquiring GBS during the period covered by this study.

HTLV-I-associated myelopathy/tropical spastic paraparesis in the United States.

HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is endemic in the Caribbean basin and Japan. Because of the close proximity of the United States to the Caribbean and the presence of HTLV-I-seropositive persons in the United States, we sought reports of patients who were HTLV-I seropositive and had a slowly progressive myelopathy. Over a 2-year period, there were 25 patients reported, 19 of whom were black and 12 of whom had been born in the United States. All patients except two had become symptomatic while living in the United States. Six patients had no apparent risk factor for acquiring HTLV-I. These data demonstrate that HAM/TSP is occurring in the United States and that the diagnosis of HAM/TSP should be considered in patients with a slowly progressive myelopathy regardless of risk factors for acquiring HTLV-I.

HTLV-I-associated myelopathy associated with blood transfusion in the United States: epidemiologic and molecular evidence linking donor and recipient.

Six months after receiving 58 units of blood components, a 65-year-old white man from New York City, with no other risk factors for human T-lymphotropic virus type I (HTLV-I) infection, developed HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Investigation of blood donors identified a 25-year-old white Hispanic woman from Florida whose platelets had been given to the patient and who was seropositive for the virus on a serum specimen obtained 2 years after the donation. She was born in Cuba and had had 2 sexual relationships with men who either had been born in or had resided in the Caribbean. Polymerase chain reaction (PCR) studies of peripheral blood mononuclear cells indicated that both donor and recipient were infected with HTLV-I. Molecular studies of a 595-nucleotide sequence in the 5' envelope region of HTLV-I indicated that the viruses from donor and recipient were identical in each of 32 positions in which published HTLV-I sequences demonstrate molecular heterogeneity; the donor and recipient viruses were also identical in 2 additional positions in which they differed from all published sequences. Transfusion-associated HAM/TSP has occurred in the United States, but additional cases should be prevented by screening blood donations for HTLV-I. Molecular studies of HTLV-I may prove useful in defining the genetic heterogeneity of HTLV-I isolates in the United States and in studying transmission of this virus.

Guillain-Barré syndrome in Larimer County, Colorado: a high-incidence area.

During the period 1981-1983, 19 cases of Guillain-Barré syndrome (GBS) occurred in residents of Larimer County, Colorado, for an incidence of 4.0 cases per 100,000 population per year, compared with 1.2 cases per 100,000 per year in 1975-1980 (p less than 0.05). The higher incidence of GBS in 1981-1983 may represent an unusual chance occurrence, since no patient characteristics or predisposing events could be found to explain the increase. Nevertheless, the findings demonstrate that over a period of as long as 3 years, the crude average annual incidence of GBS in a large, well-defined population may exceed by twofold the upper limit of the previously reported range (0.6 to 1.9 cases per 100,000 per year).

Withdrawal of immunosuppresive agents in the treatment of disseminated coccidioidomycosis.

Disseminated coccidioidomycosis is a systemic fungal infection that causes high mortality in the renal transplatn patient. Cell-mediated immunity, which appears to be the relevant host defense mechanism, is impaired by the immunosupressive agents used to prevent allograft rejection. In the case presented, immunosuppressive therapy was stopped as an adjunct to treatment of this infection. The patient has shown evidence of improvement, and his allograft has continued to function nine months after the withdrawal of immunosuppressive therapy and 18 months after the diagnosis. In vitro lymphocyte function studies indicate that the impairment in cell-mediated immunity detected prior to withdrawal of immunosuppressive therapy has persisted, probably accounting for allograft survival. Withdrawal of immunosuppressive therapy may prolong survival in renal transplant patients with disseminated coccidioidomycosis. Additionally, depression in cell-mediated immunity associated with the fungal infection itself may be sufficient to prevent allograft rejection in these patients.

Teichoic acid antibody and circulating immune complexes in the management of Staphylococcus aureus bacteremia.

Optimal antibiotic therapy for patients with Staphylococcus aureus bacteremia remains controversial. The results of two serologic tests, teichoic acid antibody and circulating immune complexes, have shown promise in detecting patients who have serious bacteremia (sustained bacteremia with endocarditis or metastatic abscess) and require longer, more intensive treatment. These tests were performed on serial samples from 38 patients with staphylococcal bacteremia prospectively categorized by severity of infection and by risk factors associated with serious disease (sustained bacteremia, valvular heart disease, absence of focus of infection, metastatic abscess). A surprisingly large group of these patients (20, or 53 percent) could not be prospectively defined as having "serious" or "benign" bacteremia. Neither test differentiated patients with serious bacteremia from those with benign bacteremia. Although it is possible that additional significant associations with risk factors might have been obtained with the teichoic acid antibody test had more patients been included, positive tests were found more frequently only in patients in whom metastatic abscesses developed. The teichoic acid antibody test was found to be a sensitive, but not specific, indicator of serious staphylococcal disease and was of value in excluding serious infection only when a negative results was supported by clinical evidence for benign disease. Other than this use, neither assay was helpful in determining optimal therapy of staphylococcal bacteremia.