Skeletal structure and progression of growth anomalies in Porites australiensis in Okinawa, Japan

Abstract

Growth anomalies (GAs), one of the diseases recently reported for scleractinian corals, are characterized by an abnormal skeletal structure and reduced zooxanthella density. The pathological characteristics of GAs were studied in colonies of Porites australiensis on a reef in Kayo, Okinawa, Japan. Corallites in the GA region lost the skeletal architecture characteristic of P. australiensis, and polyp density had decreased in the GAs due to enlargement of both calices and the coenosteum. The gross productivity of isolated GA samples was lower than in healthy samples and decreased to almost 0 within 11 d after isolation. However, when GA samples were brought into contact with healthy-looking samples from the same colony, they fused and both the GA and healthy regions grew. Healthy samples fused with GA samples grew more slowly than those fused with healthy samples. For in situ GAs surrounded by healthy tissue, tissue death usually started at the center of the GA, probably due to a deficiency in the translocated energy supply from the surrounding tissue. The total area of the GA region and the dead area increased at a rate of 5.3 ± 2.9 cm 2 yr −1. These results suggest that GA regions are maintained by energy supplies from surrounding healthy tissues and that GAs may have a negative impact on host corals. KEY WORDS: Coral · Disease · Growth anomaly · Porites australiensisResale or republication not permitted without written consent of the publisher

Cellular kinetics in growth anomalies of the scleractinian corals Porites australiensis and Montipora informis

“…However, previous field investigations demonstrated that GAs progressively spread toward healthy tissue on the host colonies (Cheney 1975, Bak 1983, Irikawa et al 2011, Yasuda et al 2012. Healthy fragments grafted to GA regions or fused with GA fragments exhibited reduced growth rates compared with non-grafted healthy fragments (Stimson 2010, Yasuda et al 2012. These findings suggest that GAs grow utilizing nutrient supplies from surrounding healthy regions (Yamashiro 2001et al, Domart-Coulon et al 2006, Yasuda et al 2012.…”

“…(Hunter & Field 1997, Domart-Coulon et al 2006, Yasuda et al 2012, low lipid storage in M. informis (Yamashiro et al 2001), and low photosynthetic productivity in A. cytherea and P. australiensis due to reduced numbers of zooxanthellae in the gastrodermis (Irikawa et al 2011, Yasuda et al 2012. However, previous field investigations demonstrated that GAs progressively spread toward healthy tissue on the host colonies (Cheney 1975, Bak 1983, Irikawa et al 2011, Yasuda et al 2012. Healthy fragments grafted to GA regions or fused with GA fragments exhibited reduced growth rates compared with non-grafted healthy fragments (Stimson 2010, Yasuda et al 2012.…”

“…Yamashiro et al 2000, Yasuda et al 2012. We compared the relative abundances of apoptotic cells and proliferating cells between healthy and GA tissues using the terminal deoxynucleotidyl transferase dUTP-biotin nickend labeling (TUNEL) and 5-bromo-2-deoxyuridine (BrdU) incorporation assays, respectively.…”

“…However, the processes leading to GA progression, i.e. how GA tissues invade surrounding healthy regions, have never been investigated.The partial death of GAs on coral colonies has been reported at gross and microscopic levels (Work et al 2008, Irikawa et al 2011, Yasuda et al 2012. The microscopic studies revealed that tissue necrosis of GAs are often, though not always, associated with infiltrating microorganisms such as algae and fungi (Work & Rameyer 2005, Work et al 2008.…”

“…(Work et al 2008). Initiation of necrosis has been reported to start at the region far from the GA progression area (Kaczmarsky 2006, Irikawa et al 2011, Yasuda et al 2012). Even though GAs are supported by nutritional supplies from surrounding healthy tissues, the compromised gastrovascular canals of GAs and the increased distance from healthy tissues may cause malnutrition in a GA (Domart-Coulon et al 2006, Work et al 2008, Yasuda et al 2012.…”