Black band disease of corals: Ecology and physiology of Phormidium corallyticum

Black band disease of corals consists of a microbial community dominated by the cyanobacteriurn Phormidium corallyticum. The disease primarily affects reef-framework coral species, Active black band disease continually opens up new substrate in reef environments by destroying coral tissue as the disease line advances across the surface of infected colonies. A field study was carried out to determine the abundance and distribution of black band disease on the reef building corals in the Florida Keys. During July of 1992 and 1993, up to 0.72% of coral colonies were infected with black band disease. Analysis of the distribution showed that the disease was clumped. Seasonal patters varied, with some coral colonies infected year round, others exhibiting reinfection from summer 1992 to summer 1993, and some colonies infected for one year only. Statistical analysis of black band disease incidence in relation to various environmental parameters revealed that black band disease was associated with relatively shallow water depths, higher temperatures, elevated nitrite levels, and decreased ortho-phosphate levels. Additional field studies determined recovery of scleractinian coral colonies damaged or killed through the activities of black band disease over a five-year period. These studies determined if the newly exposed substrate was recolonized through scleractinian recruitment, if there was overgrowth of the damaged areas by the formerly diseased colony, or if coral tissue destruction continued after the cessation of black band disease activity. Tissue loss continued on all coral colonies with only one colony exhibiting new tissue growth. The majority of recolonization was by non-reef-framework corals and octocorallians, limited recruitment by framework species was observed. Physiological studies of P. corallyticum were carried out to investigate the photosynthetic capacity of this cyanobacterium, and to determine if this species has the ability to fix dinitrogen. The results of this research demonstrated that P. corallyticum reaches maximum photosynthetic rates at very low light intensities (27.9 μE/m/sec), and that P. corallyticum is able to carry out oxygenic photosynthesis in the presence of sulfide, an ability that is uncommon in prokaryotic organisms. ^

The relationship of thymulin activity, immune parameters of HIV disease progression and substance use in a cohort of HIV seropositive alcohol and drug users

Zinc is essential for the activity of thymulin, a thymic hormone involved in T-lymphocyte differentiation and activation. Zinc deficiency is widespread in populations with HIV infection, and HIV+ drug users are particularly susceptible to zinc deficiency and immune suppression. This dissertation explored the relationship of zinc-bound active thymulin to plasma zinc, CD4+ and CD8+ cell count, the CD4+/CD8+ ratio, and drug use in HIV-infected drug users. Zinc-bound active thymulin was assessed in plasma of HIV+ drug users who were participating in a 30 month zinc supplementation trial. Plasma from 80 participants at the 12 month visit, and 40 of these same participants, randomly selected, at the baseline visit were assessed for zinc-bound active thymulin levels using a modification of the rosette inhibition assay. Thymulin activity was directly associated with CD4+ cell count (β = 0.127, p = 0.002) and inversely associated with cocaine use (β = −0.908, p = 0.026; R2 = 0.188, p = 0.019) independent of HIV viral load, age, gender and antiretroviral use. An increase in thymulin activity was 1.4 times more likely when CD4+ cell count increased (OR = 1.402, 95%CI: 1.006–1.956), independent of change in viral load, antiretroviral use, and age. Participants who used cocaine consistently, were 7.6 times less likely to have an increase in thymulin activity (OR = 0.133, 95%CI: 0.017–1.061). There was a direct correlation between change in plasma zinc and change in zinc-bound active thymulin (r = 0.243, p = 0.13). Analysis of CD4+ cell count decline in 222 participants in the zinc supplementation trial across the 30 months showed that both crack cocaine use and heavy alcohol use accelerated CD4+ cell count decline. Thymulin activity is directly associated with HIV disease progression, measured by CD4+ cell count, and is depressed with cocaine use independent of antiretroviral use and HIV viral load. Cocaine and heavy alcohol accelerate CD4+ cell count decline. The effect of cocaine on thymic output requires further evaluation as a mechanism for the association of cocaine use with faster HIV disease progression.