Seismic Hazards Implications of Uplifted Pleistocene Coral Terraces in the Gulf of Aqaba.

The Gulf of Aqaba transform plate boundary is a source of destructive teleseismic earthquakes. Seismicity is concentrated in the central sub-basin and decreases to both the north and south. Although principally a strike-slip plate boundary, the faulted margins of the Gulf display largely dip-slip extensional movement and accompanying footwall uplift. We have constrained rates of this uplift by measurements of elevated Pleistocene coral terraces. In particular the terrace that formed during the last interglacial (~125 ka) is found discontinuously along the length of the Gulf at elevations of 3 to 26 m. Global sea level was ~7 m higher than today at 125 ka indicating net maximum tectonic uplift of ~19 m with an average rate of ~0.015 cm/yr. Uplift has been greatest adjacent to the central sub-basin and like the seismicity decreases to the north and south. We suggest that the present pattern of a seismically active central region linked to more aseismic areas in the north and south has therefore persisted for at least the past 125 kyr. Consequently the potential for future destructive earthquakes in the central Gulf is greater than in the sub-basins to the north and south.

Residential segregation and mortality in New York City.

The objective of this research was to determine the effect of residential racial segregation on all-cause and cardiovascular disease mortality in New York City. A cross-sectional study of residents in New York City was conducted linking mortality records from 1988 through 1994, to the 1990 United States Census data stratified by zipcode. All-cause and cardiovascular disease mortality rates for non-Hispanic blacks and whites were estimated by zipcode. Zipcodes were aggregated according to the degree of residential segregation (predominantly (> or = 75%) white and black areas) and mortality rates were compared. Multiple regression analysis was used to associate population characteristics with mortality. In New York City, although overall mortality rates of blacks exceed whites, these rates varied substantially by locality according to the pattern of racial segregation. Whites living in the higher (mainly white) socioeconomic areas had lower mortality rates than whites living in predominantly black areas (1473.7 vs 1934.1 for males, and 909.9 vs 1414.7 for females for all-cause mortality). This was true for all age groups. By contrast, elderly blacks living in black areas, despite their less favorable socioeconomic status, had lower mortality rates for all-cause, total cardiovascular disease, and coronary heart disease, than did those living in white areas, even after adjusting for available socioeconomic variables. Racial segregation in residence is independently associated with mortality. Within racially segregated areas, members of the dominant group, for all age, among whites and elderly blacks, enjoy outcomes superior both to members of the minority racial group of their community, and to members of the same race residing in other areas, where they are in the minority, independent of socio-economic status.

Differential mortality in New York City (1988-1992). Part Two: excess mortality in the south Bronx.

To display the extent of variations in mortality according to geographic regions in New York City, we have compared mortality in New York City as a whole with that of the South Bronx. Mortality records for 1988 to 1992 and 1990 US census data for New York City were linked. The 471,000 residents of the South Bronx were younger, less educated, and more likely to lack health insurance than other New Yorkers. Using age- and gender-stratified populations and mortality in New York City as standards, age-adjusted death rates and excess mortality in the South Bronx were determined. All-cause mortality in the South Bronx was 26% higher than the city as a whole. Mortality for AIDS, injury and poisoning, drug and alcohol abuse, and cardiovascular diseases were 50% to 100% higher in the South Bronx than in New York City; years of potential life lost before age 65 in the South Bronx were 41.6% and 44.2% higher for men and women, respectively, than in New York City; AIDS accounted for the largest single share of excess premature deaths (21.8%). In summary, inequalities in health status, reflected by higher mortality rates in the South Bronx, are consistent with, and perhaps caused by, lower socioeconomic status and deficient medical care among residents of this inner-city community.

Transmission of tuberculosis in New York City. An analysis by DNA fingerprinting and conventional epidemiologic methods.

BACKGROUND: The incidence of tuberculosis and drug resistance is increasing in the United States, but it is not clear how much of the increase is due to reactivation of latent infection and how much to recent transmission. METHODS: We performed DNA fingerprinting using restriction-fragment-length polymorphism (RFLP) analysis of at least one isolate from every patient with confirmed tuberculosis at a major hospital in the Bronx, New York, from December 1, 1989, through December 31, 1992. Medical records and census-tract data were reviewed for relevant clinical, social, and demographic data. RESULTS: Of 130 patients with tuberculosis, 104 adults (80 percent) had complete medical records and isolates whose DNA fingerprints could be evaluated. Isolates from 65 patients (62.5 percent) had unique RFLP patterns, whereas isolates from 39 patients (37.5 percent) had RFLP patterns that were identical to those of an isolate from at least 1 other study patient; the isolates in the latter group were classified into 12 clusters. Patients whose isolates were included in one of the clusters were inferred to have recently transmitted disease. Independent risk factors for having a clustered isolate included seropositivity for the human immunodeficiency virus (HIV) (odds ratio for Hispanic patients, 4.31; P = 0.02; for non-Hispanic patients, 3.12; P = 0.07), Hispanic ethnicity combined with HIV seronegativity (odds ratio, 5.13; P = 0.05), infection with drug-resistant tuberculosis (odds ratio, 4.52; P = 0.005), and younger age (odds ratio, 1.59; P = 0.02). Residence in sections of the Bronx with a median household income below $20,000 was also associated with having a clustered isolate (odds ratio, 3.22; P = 0.04). CONCLUSIONS: In the inner-city community we studied, recently transmitted tuberculosis accounts for approximately 40 percent of the incident cases and almost two thirds of drug-resistant cases. Recent transmission of tuberculosis, and not only reactivation of latent disease, contributes substantially to the increase in tuberculosis.

Childhood tuberculosis in the Bronx, New York.

The resurgence of tuberculosis (TB) in New York City in the period 1978-92 has been closely linked to the AIDS epidemic but the increase of active TB in areas of urban poverty also implies increased community exposure. We have examined the ecological relation between community rates of AIDS and residential crowding and cases of active TB in Bronx children under age 5. Residential crowding was defined as the percent of households with more than 1 person per room. All childhood TB cases reported between 1986 and 1992 for the Bronx (n = 75) were included. Cumulative AIDS mortality rates for adult females through 1990 represented community HIV burden. All data were coded by the 64 health areas of the borough. We examined trends in these data and used Poisson regression to model the effect of HIV burden and residential crowding on TB risk. For the Bronx as a whole the two variables of TB and residential crowding showed a clear temporal correspondence for the period 1970-90. Residential crowding was associated with poverty and greater dependence on public assistance, large household size, Hispanic ethnicity, and a higher proportion of young children. The overall TB case rate increased with the proportion of crowded households, with a rise from 1.47 to over 8 cases per 10,000 children as the proportion of crowded households increased. At both the lowest and highest levels of AIDS mortality in these areas, the childhood TB risk increased as crowding increased. Children living in areas of the Bronx in which over 12 percent of homes are severely overcrowded were 5.6-fold more likely to develop active TB, even after holding constant the presumed HIV burden in each local community. While HIV infection, the newest risk factor for TB, appears to play a critical role in the resurgent epidemic, our findings show that the earliest known TB risk factors, poverty and household crowding, are still potent forces.

Antistreptolysin O titers of cats infected with Brugia malayi and with streptococci.

This study evaluated the usefulness of determining antistreptolysin O(ASO) titers in filariasis. The ASO titers were elevated in most convalescence sera, but did not reflect comparable pathology resulting from dual Brugia-streptococcal infections in cats.

Lymphatic patterns of cats infected with Brugia malayi and streptococcus.

Approximately 50% of the hind legs of cats infected with Brugia malayi and insulted with a beta haemolytic streptococcus became elephantoid in appearance after four to six weeks. This condition was found to be reversible. Collateral lymphatic vessels were seen by lymphography in most of the Brugia-streptococcus-infected legs. The popliteal draining systems in two of three cats, which harboured no worms, appeared normal by lymphography at 18 weeks.

Infective larvae of Brugia: escape from mosquitoes into water and subsequent oral infectivity in jirds.

Published work showed that third-stage larvae (L-3s) escape into water from dead or dying, Brugia pahangi-infected, Aedes aegypti. The present study revealed the same escape phenomenon among B. pahangi-infected Armigeres subalbatus, Anopheles quadrimaculatus, and Aedes togoi, and among Brugia malayi-infected Ae. aegypti and Ae. togoi. L-3s maintained in water or in Lum's solution for 3 hours retained infectivity when tested in orally or subcutaneously exposed jirds; furthermore, L-3s recovered from mosquitoes dead for 24 to 48 hours were also infective by either portal of entry in jirds. Since L-3s may escape and remain infective in the field, it is conceivable that natural filarial infections might thus be acquired orally by definitive hosts.

Oral transmission of Brugia pahangi to dogs.

Oral transmission of Brugia pahangi, already demonstrated in jirds, has now been accomplished in dogs. Beagle puppies, four anesthetized and two unanesthetized, were exposed to B. pahangi by instilling third-stage larvae (L-3s) into the mouth. Infections matured in all the dogs, and adult worms were recovered mainly from the mandibular, retropharyngeal, and axillary lymphatics. Worms were relatively numerous and peripheral microfilaremia developed in the dogs exposed under anesthetic, while worms were infrequent and microfilariae were found only intracardially in the dogs exposed without anesthetic. It appears that in orally exposed dogs, as in jirds studied earlier, the successful L-3s probably penetrated mucosa in or near the mouth.

Distribution and development of Brugia malayi in reinfected cats.

At various time periods after an initial exposure to 50 Brugia malayi larvae on one hind foot cats were reexposed to an additional 50 larvae in one of 3 ways: on the previously infected limb only, on the contralateral, uninfected limb only, or on both hind limbs simultaneously. At the time of reexposure uninfected controls were exposed to 50 larvae on one hind foot in a similar manner. From 2 to 4 weeks after reexposure to larvae, the cats were necropsied and the appropriate lymph nodes and vessels examined for adult or developing worms. An existing infection in one limb did not influence early migration or development of larvae introduced into the contralateral leg. Previous infection in the same limb did not consistently result in decreases in the number of developing larvae from the second exposure but did alter the distrubution of larvae. In repeat infections, larvae were consistently located in a moe distal area of the limb than were larvae from an initial infection at a comparable time.