Rapid Tissue Loss Research Articles

Artificial Intelligence in Stroke Imaging: A Comprehensive Review.

The aging population challenges the health-care system with chronic diseases. Cerebrovascular diseases are important components of these chronic conditions. Stroke is the acute cessation of blood in the brain, which can lead to rapid tissue loss. Therefore, fast, accurate, and reliable automatic methods are required to facilitate stroke management. The performance of artificial intelligence (AI) methods is increasing in all domains. Vision tasks, including natural images and medical images, are particularly benefiting from the skills of AI models. The AI methods that can be applied to stroke imaging have a broad range, including classical machine learning tools such as support vector machines, random forests, logistic regression, and linear discriminant analysis, as well as deep learning models, such as convolutional neural networks, recurrent neural networks, autoencoders, and U-Net. Both tools can be applied to various aspects of stroke management, including time-to-event onset determination, stroke confirmation, large vessel occlusion detection, difusion restriction, perfusion deficit, core and penumbra identification, afected region segmentation, and functional outcome prediction. While building these AI models, maximum care should be exercised in order to reduce bias and build generalizable models. One of the most important prerequisites for building unbiased models is collecting large, diverse, and quality data that reflects the underlying population well and splitting the training and testing parts in a way that both represent a similar distribution. Explainability and trustworthiness are other important properties of machine learning models that could be widely adopted in clinical practices.

Monitoring of coral-killing sponge (Terpios hoshinota) caused rapid coral tissue loss assessment through environmental parameters in the Palk Bay

Coral-killing cyanobacteria sponge T. hoshinota has been affecting the Palk Bay coral reef since 2009, causing rapid destruction to coral tissues. Monitoring studies provide essential information on the prevalence of T. hoshinota and an understanding of the environmental parameters contributing to coral tissue loss, further helping conservation policies to be made. The study conducted a benthic transect survey using the standard method in 2017 and 2020 in the Palk Bay region. Results revealed that T. hoshinota prevalence has increased by 46.68% from the 2017 survey; it was (Mean ±SE) 11.25 ± 1.01% in 2017 and 21.09 ± 1.53% in 2020. Coral mortality due to T. hoshinota impact was observed in the 2017 survey at 0.84 ± 0.06% and significantly increased (75.29%) in the 2020 survey, recorded at 3.42 ± 0.11%. The Pearson correlation plot showed that SST and PAR were strongly correlated during the survey periods, while turbidity has not been correlated with any other environmental parameter. The R-based hierarchical regression analysis revealed that environmental parameters NO3 (β=0.58; p = 0.004) and PAR (β=0.35; p = 0.02) were associated with T. hoshinota causing rapid tissue loss in the Palk Bay coral reef. The coral-killing sponge T. hoshinota and associated environmental parameters rapidly progressed over the study period in the Palk Bay coral reef, resulting in rapid tissue loss and coral mortality. Consequentially, the live coral cover in Palk Bay would decline. Hence, T. hoshinota based conservation management activities have to be made in Palk Bay.

Similarities and Differences Between Two Deadly Caribbean Coral Diseases: White Plague and Stony Coral Tissue Loss Disease

For several decades, white plagues (WPDs: WPD-I, II and III) and more recently, stony coral tissue loss disease (SCTLD) have significantly impacted Caribbean corals. These diseases are often difficult to separate in the field as they produce similar gross signs. Here we aimed to compare what we know about WPD and SCTLD in terms of: (1) pathology, (2) etiology, and (3) epizootiology. We reviewed over 114 peer-reviewed publications from 1973 to 2021. Overall, WPD and SCTLD resemble each other macroscopically, mainly due to the rapid tissue loss they produce in their hosts, however, SCTLD has a more concise case definition. Multiple-coalescent lesions are often observed in colonies with SCTLD and rarely in WPD. A unique diagnostic sign of SCTLD is the presence of bleached circular areas when SCTLD lesions are first appearing in the colony. The paucity of histopathologic archives for WPDs for multiple species across geographies makes it impossible to tell if WPD is the same as SCTLD. Both diseases alter the coral microbiome. WPD is controversially regarded as a bacterial infection and more recently a viral infection, whereas for SCTLD the etiology has not been identified, but the putative pathogen, likely to be a virus, has not been confirmed yet. Most striking differences between WPD and SCTLD have been related to duration and phases of epizootic events and mortality rates. While both diseases may become highly prevalent on reefs, SCTLD seems to be more persistent even throughout years. Both transmit directly (contact) and horizontally (waterborne), but organism-mediated transmission is only proven for WPD-II. Given the differences and similarities between these diseases, more detailed information is needed for a better comparison. Specifically, it is important to focus on: (1) tagging colonies to look at disease progression and tissue mortality rates, (2) tracking the fate of the epizootic event by looking at initial coral species affected, the features of lesions and how they spread over colonies and to a wider range of hosts, (3) persistence across years, and (4) repetitive sampling to look at changes in the microbiome as the disease progresses. Our review shows that WPDs and SCTLD are the major causes of coral tissue loss recorded in the Caribbean.

Environmental and biological drivers of white plague disease on shallow and mesophotic coral reefs

Outbreaks of coral white plague (WP) disease have caused significant regional declines of reef‐building Caribbean corals. Due to a greater availability of epidemiological data, studies have primarily focused on shallow coral reefs (< 30 m). In the U.S. Virgin Islands, however, WP disease prevalence appears to be higher on upper mesophotic (30–40 m) coral reefs when compared with shallow reefs and may be inhibiting coral recovery after environmental disturbances. The aim of this study was to investigate the relationship of environmental drivers with spatio‐temporal patterns of WP prevalence across shallow and mesophotic coral reefs in the U.S. Virgin Islands. We recorded WP prevalence at 13 reef sites (five shallow, three mid‐depth and five upper‐mesophotic reefs) across the south shelf of St. Thomas approximately monthly between 2012 and 2015 using a drop camera method. The influence of environmental factors on disease prevalence was investigated using Bayesian inference with generalized linear mixed‐effect models. We found that WP tended to increase during the beginning of the rainy season (June), and when levels of water turbidity and temperature were higher, and levels of oxygen and salinity lower. The disease prevalence was higher on mesophotic than on shallow or mid‐depth reefs, probably due to higher availability of corals (host), and a possible temperature threshold for WP occurrence that allows long‐term persistence (year‐round) of the disease on upper‐mesophotic reefs. This is the first study to implement the drop camera method to survey a coral disease over several reef sites and depths. This method can be applied on surveys of other rapid tissue loss diseases, such as the newly emergent stony‐coral‐tissue‐loss‐disease (SCTLD).

Variable Species Responses to Experimental Stony Coral Tissue Loss Disease (SCTLD) Exposure

Stony coral tissue loss disease (SCTLD) was initially documented in Florida in 2014 and outbreaks with similar characteristics have since appeared in disparate areas throughout the northern Caribbean, causing significant declines in coral communities. SCTLD is characterized by focal or multifocal lesions of denuded skeleton caused by rapid tissue loss and affects at least 22 reef-building species of Caribbean corals. A tissue-loss disease consistent with the case definition of SCTLD was first observed in the U.S. Virgin Islands (USVI) in January of 2019 off the south shore of St. Thomas at Flat Cay. The objective of the present study was to characterize species susceptibility to the disease present in St. Thomas in a controlled laboratory transmission experiment. Fragments of six species of corals (Colpophyllia natans, Montastraea cavernosa, Orbicella annularis, Porites astreoides, Pseudodiploria strigosa, and Siderastrea siderea) were simultaneously incubated with (but did not physically contact) SCTLD-affected colonies of Diploria labyrinthiformis and monitored for lesion appearance over an 8 day experimental period. Paired fragments from each corresponding coral genotype were equivalently exposed to apparently healthy colonies of D. labyrinthiformis to serve as controls; none of these fragments developed lesions throughout the experiment. When tissue-loss lesions appeared and progressed in a disease treatment, the affected coral fragment, and its corresponding control genet, were removed and preserved for future analysis. Based on measures including disease prevalence and incidence, relative risk of lesion development, and lesion progression rates, O. annularis, C. natans, and S. siderea showed the greatest susceptibility to SCTLD in the USVI. These species exhibited earlier average development of lesions, higher relative risk of lesion development, greater lesion prevalence, and faster lesion progression rates compared with the other species, some of which are considered to be more susceptible based on field observations (e.g., P. strigosa). The average transmission rate in the present study was comparable to tank studies in Florida, even though disease donor species differed. Our findings suggest that the tissue loss disease affecting reefs of the USVI has a similar epizootiology to that observed in other regions, particularly Florida.

Mass mortality hits gorgonian forests at Montecristo Island.

Mediterranean gorgonian forests are species-rich habitats, and like many other marine habitats they are threatened by anthropogenic disturbances and mass mortality events. These mortality events have often been linked to anomalies in the temperature profiles of the Mediterranean region. On 5 September 2017, colonies of the gorgonians Eunicella singularis and Eunicella cavolini exhibited rapid tissue loss, down to a depth of 30 m along the steep cliffs of Montecristo Island, Tuscan Archipelago National Park, Tyrrhenian Sea, Italy. Interestingly, Montecristo has previously been identified as a reference site for the ecological quality assessment of the western Mediterranean benthic assemblages on rocky bottoms. The observed mortality event occurred during a period of increased sea temperature. By utilising a combination of high-resolution oceanographic analysis, forecast models and citizen science initiatives, we propose that an early warning system for the concomitance of heat waves and mortality events can be put in place. A temperature-based coral disease surveillance tool could then be established for the entire Mediterranean Sea. Such a tool would allow for the timely study of mass mortality phenomena and the implementation of prompt mitigation and/or restoration initiatives. Finally, this specific mortality event, in a Marine Protected Area, offers a unique opportunity to monitor and assess the resilience of gorgonian populations and associated benthic assemblages in the absence of other, more directly, anthropogenic disturbances such as pollution and land runoff.

In situ hybridisation detects pro-apoptotic gene expression of a Bcl-2 family member in white syndrome-affected coral

White syndrome has been described as one of the most prolific diseases on the Great Barrier Reef. Previously, apoptotic cell death has been described as the mechanism driving the characteristic rapid tissue loss associated with this disease, but the molecular mechanisms controlling apoptotic cell death in coral disease have yet to be investigated. In situ methods were used to study the expression patterns of 2 distinct regulators of apoptosis in Acropora hyacinthus tissues undergoing white syndrome and apoptotic cell death. Apoptotic genes within the Bcl-2 family were not localized in apparently healthy coral tissues. However, a Bcl-2 family member (bax-like) was found to localize to cells and tissues affected by white syndrome and those with morphological evidence for apoptosis. A potential up-regulation of pro-apoptotic or bax-like gene expression in tissues with apoptotic cell death adjacent to disease lesions is consistent with apoptosis being the primary cause of rapid tissue loss in coral affected by white syndrome. Pro-apoptotic (bax-like) expression in desmocytes and the basal tissue layer, the calicodermis, distant from the disease lesion suggests that apoptosis may also underlie the sloughing of healthy tissues associated with the characteristic, rapid spread of tissue loss, evident of this disease. This study also shows that in situ hybridisation is an effective tool for studying gene expression in adult corals, and wider application of these methods should allow a better understanding of many aspects of coral biology and disease pathology.

Did borers make corals more susceptible to a catastrophic disease outbreak in Hong Kong?

A massive outbreak of coral disease was recently recorded in Tolo Harbour and Channel (22.46°N, 114.29°E), a semienclosed embayment in northeastern Hong Kong. Preliminary photo-quadrat surveys registered a 20.6-51.4 % loss in total coral cover in five communities within March 2015. Platygyra spp., the most dominant corals, were most susceptible and often suffered near-complete colony mortality (Fig. 1a). Such large scale and rapid disease outbreak in Hong Kong is now documented for the first time since periodic monitoring started here over 20 years ago. The disease was first noticed by abnormal extensive protrusion of mesenterial filaments or tentacles from the coral colony surfaces of Cyphastrea, Dipsastraea, Echinophyllia, and Platygyra (Fig. 1b). Colony surfaces immediately around holes of boring bivalves, mainly Lithophaga spp. (ValentichScott 2003; Bouchet and Gofas 2015), appeared to suffer most from the disease attack. Lesion areas initiated around the boreholes (Fig. 1c) and from there radiated to other parts of the colony (Fig. 1d-f). As borer infestations are most common among massive, submassive, and encrusting corals, disease origins from multiple boreholes may have contributed to the rapid spread over the colony surface. The reasons behind this apparent association between borers and the disease are unclear. The disease pattern of rapid tissue loss closely resembles that exhibited by the white syndrome that is often associated with ciliates (Sweet and Bythell 2012). In collected samples, a complex microbial community involving ciliates, dinoflagellates, and diatoms was observed under the microscope in tissues of diseased lesions but not in the seemingly healthy areas nearby. Ciliates, the apparent causative agent, may always be present in the coral tissue (Qiu et al. 2010) and could spread out when conditions become favourable. Coral tissues around boreholes may be inherently stressed through physical movement or chemicals secreted by the borers (Glynn 1997) and thus, may be more vulnerable to disease attack.

Disease dynamics and potential mitigation among restored and wild staghorn coral, Acropora cervicornis.

The threatened status (both ecologically and legally) of Caribbean staghorn coral, Acropora cervicornis, has prompted rapidly expanding efforts in culture and restocking, although tissue loss diseases continue to affect populations. In this study, disease surveillance and histopathological characterization were used to compare disease dynamics and conditions in both restored and extant wild populations. Disease had devastating effects on both wild and restored populations, but dynamics were highly variable and appeared to be site-specific with no significant differences in disease prevalence between wild versus restored sites. A subset of 20 haphazardly selected colonies at each site observed over a four-month period revealed widely varying disease incidence, although not between restored and wild sites, and a case fatality rate of 8%. A tropical storm was the only discernable environmental trigger associated with a consistent spike in incidence across all sites. Lastly, two field mitigation techniques, (1) excision of apparently healthy branch tips from a diseased colony, and (2) placement of a band of epoxy fully enclosing the diseased margin, gave equivocal results with no significant benefit detected for either treatment compared to controls. Tissue condition of associated samples was fair to very poor; unsuccessful mitigation treatment samples had severe degeneration of mesenterial filament cnidoglandular bands. Polyp mucocytes in all samples were infected with suspect rickettsia-like organisms; however, no bacterial aggregates were found. No histological differences were found between disease lesions with gross signs fitting literature descriptions of white-band disease (WBD) and rapid tissue loss (RTL). Overall, our results do not support differing disease quality, quantity, dynamics, nor health management strategies between restored and wild colonies of A. cervicornis in the Florida Keys.

Comparing Bacterial Community Composition between Healthy and White Plague-Like Disease States in Orbicella annularis Using PhyloChip™ G3 Microarrays

Coral disease is a global problem. Diseases are typically named or described based on macroscopic changes, but broad signs of coral distress such as tissue loss or discoloration are unlikely to be specific to a particular pathogen. For example, there appear to be multiple diseases that manifest the rapid tissue loss that characterizes ‘white plague.’ PhyloChip™ G3 microarrays were used to compare the bacterial community composition of both healthy and white plague-like diseased corals. Samples of lobed star coral (Orbicella annularis, formerly of the genus Montastraea [1]) were collected from two geographically distinct areas, Dry Tortugas National Park and Virgin Islands National Park, to determine if there were biogeographic differences between the diseases. In fact, all diseased samples clustered together, however there was no consistent link to Aurantimonas coralicida, which has been described as the causative agent of white plague type II. The microarrays revealed a large amount of bacterial heterogeneity within the healthy corals and less diversity in the diseased corals. Gram-positive bacterial groups (Actinobacteria, Firmicutes) comprised a greater proportion of the operational taxonomic units (OTUs) unique to healthy samples. Diseased samples were enriched in OTUs from the families Corynebacteriaceae, Lachnospiraceae, Rhodobacteraceae, and Streptococcaceae. Much previous coral disease work has used clone libraries, which seem to be methodologically biased toward recovery of Gram-negative bacterial sequences and may therefore have missed the importance of Gram-positive groups. The PhyloChip™data presented here provide a broader characterization of the bacterial community changes that occur within Orbicella annularis during the shift from a healthy to diseased state.

Disturbance Driven Colony Fragmentation as a Driver of a Coral Disease Outbreak

In September of 2010, Brewer's Bay reef, located in St. Thomas (U.S. Virgin Islands), was simultaneously affected by abnormally high temperatures and the passage of a hurricane that resulted in the mass bleaching and fragmentation of its coral community. An outbreak of a rapid tissue loss disease among coral colonies was associated with these two disturbances. Gross lesion signs and lesion progression rates indicated that the disease was most similar to the Caribbean coral disease white plague type 1. Experiments indicated that the disease was transmissible through direct contact between colonies, and five-meter radial transects showed a clustered spatial distribution of disease, with diseased colonies being concentrated within the first meter of other diseased colonies. Disease prevalence and the extent to which colonies were bleached were both significantly higher on unattached colony fragments than on attached colonies, and disease occurred primarily on fragments found in direct contact with sediment. In contrast to other recent studies, disease presence was not related to the extent of bleaching on colonies. The results of this study suggest that colony fragmentation and contact with sediment played primary roles in the initial appearance of disease, but that the disease was capable of spreading among colonies, which suggests secondary transmission is possible through some other, unidentified mechanism.

Dynamics of an Acute Coral Disease Outbreak Associated with the Macroalgae Dictyota spp. in Dry Tortugas National Park, Florida, USA

Reports of coral disease outbreaks have increased in recent decades, but often few details are known about these outbreaks, such as environmental triggers, associated biological variables, or even the precise temporal span of the outbreak. Here we document an acute outbreak of a rapid tissue loss disease on the highest live coral cover (15%-30%) reefs within Dry Tortugas National Park, Florida, USA. This disease exhibited similar signs to white plague disease with the notable exception that a white film often was observed on the recently denuded skeleton. The temporal span of the disease was short (<2 mo). Partial mortality was recorded but there was no detectable impact to overall coral cover. A significant increase and then decrease in the cover of macroalgae, primarily of the genus Dictyota, occurred simultaneously with the increase and drop in disease lesion density (number of lesions per living tissue area), respectively. No other anomalous biological or physical factors (e.g., unusual temperature, turbidity, passage of storms) corresponded with the outbreak, although it is likely that some environmental anomaly that was undetectable with the methods employed favored both disease and Dictyota expansion. This is the first study to associate a rapid increase in a macroalgal population with a coral disease outbreak. We highlight the need for increased study of the initiation of such outbreaks in the caribbean.

Bacterial communities associated with healthy and Acropora white syndrome-affected corals from American Samoa

Acropora white syndrome (AWS) is characterized by rapid tissue loss revealing the white underlying skeleton and affects corals worldwide; however, reports of causal agents are conflicting. Samples were collected from healthy and diseased corals and seawater around American Samoa and bacteria associated with AWS characterized using both culture-dependent and culture-independent methods, from coral mucus and tissue slurries, respectively. Bacterial 16S rRNA gene clone libraries derived from coral tissue were dominated by the Gammaproteobacteria, and Jaccard's distances calculated between the clone libraries showed that those from diseased corals were more similar to each other than to those from healthy corals. 16S rRNA genes from 78 culturable coral mucus isolates also revealed a distinct partitioning of bacterial genera into healthy and diseased corals. Isolates identified as Vibrionaceae were further characterized by multilocus sequence typing, revealing that whilst several Vibrio spp. were found to be associated with AWS lesions, a recently described species, Vibrio owensii, was prevalent amongst cultured Vibrio isolates. Unaffected tissues from corals with AWS had a different microbiota than normal Acropora as found by others. Determining whether a microbial shift occurs prior to disease outbreaks will be a useful avenue of pursuit and could be helpful in detecting prodromal signs of coral disease prior to manifestation of lesions.

The Ecology of ‘Acroporid White Syndrome', a Coral Disease from the Southern Great Barrier Reef

Outbreaks of coral disease have increased worldwide over the last few decades. Despite this, remarkably little is known about the ecology of disease in the Indo-Pacific Region. Here we report the spatiotemporal dynamics of a coral disease termed ‘Acroporid white syndrome’ observed to affect tabular corals of the genus Acropora on the southern Great Barrier Reef. The syndrome is characterised by rapid tissue loss initiating in the basal margins of colonies, and manifests as a distinct lesion boundary between apparently healthy tissue and exposed white skeleton. Surveys of eight sites around Heron Reef in 2004 revealed a mean prevalence of 8.1±0.9%, affecting the three common species (Acropora cytherea, A. hyacinthus, A. clathrata) and nine other tabular Acropora spp. While all sizes of colonies were affected, white syndrome disproportionately affected larger colonies of tabular Acroporids (>80 cm). The prevalence of white syndrome was strongly related to the abundance of tabular Acroporids within transects, yet the incidence of the syndrome appears unaffected by proximity to other colonies, suggesting that while white syndrome is density dependant, it does not exhibit a strongly aggregated spatial pattern consistent with previous coral disease outbreaks. Acroporid white syndrome was not transmitted by either direct contact in the field or by mucus in aquaria experiments. Monitoring of affected colonies revealed highly variable rates of tissue loss ranging from 0 to 1146 cm−2 week−1, amongst the highest documented for a coral disease. Contrary to previous links between temperature and coral disease, rates of tissue loss in affected colonies increased threefold during the winter months. Given the lack of spatial pattern and non-infectious nature of Acroporid white syndrome, further studies are needed to determine causal factors and longer-term implications of disease outbreaks on the Great Barrier Reef.

Successional changes in bacterial communities during the development of black band disease on the reef coral, Montipora hispida

Black band disease (BBD) consists of a mat-forming microbial consortium that migrates across coral colonies causing rapid tissue loss. Although BBD-associated microbial communities have been well characterized, little is known regarding how these complex bacterial consortia develop. This study analyzed successional changes in microbial communities leading to the development of BBD. Long-term monitoring of tagged corals throughout outbreaks of BBD in the central Great Barrier Reef documented cyanobacterium-infected lesions, herein termed cyanobacterial patch(es) (CP), which were macroscopically distinct from BBD and preceded the onset of BBD in 19% of the cases. Dominant cyanobacteria within CP lesions were morphologically distinct from ones dominating BBD lesions. Clone libraries and terminal restriction fragment length polymorphism analysis confirmed shifts within cyanobacterial assemblages, from Blennothrix sp.-affiliated sequences dominating CP lesions, to Oscillatoria sp.-affiliated sequences, similar to those retrieved from other BBD samples worldwide, dominating BBD lesions. Bacterial 16S ribosomal RNA clone libraries also showed shifts in bacterial ribotypes during transitions from CP to BBD, with Alphaproteobacteria-affiliated sequences dominant in CP libraries, whereas gammaproteobacterial and cyanobacterial ribotypes were more abundant in BBD clone libraries. Sequences affiliated with organisms identified in sulfur cycling were commonly retrieved from lesions showing characteristic field signs of BBD. As high sulfide concentrations have been implicated in BBD-mediated coral tissue degradation, proliferation of a microbial community actively involved in sulfur cycling potentially contributes to the higher progression rates found for BBD compared with CP lesions. Results show how microbial colonization of indistinct lesions may facilitate a common coral disease with proven ecological effects on coral populations.

Disease and cell death in white syndrome of Acroporid corals on the Great Barrier Reef

White syndromes (WS) are among the most prevalent coral diseases, and are responsible for reef demise on the Great Barrier Reef. The disease manifests as a clear differentiation between tissue and exposed skeleton and results in rapid tissue loss. Fluorescence in situ hybridisation (FISH) was used in conjunction with histology and transmission electron microscopy (TEM) to investigate bacterial communities and cell death associated with WS. No evidence of bacterial communities or microbial association (using six bacterial probes, TEM and histopathology) was evident within the lesion or adjacent tissues, despite the presence of dense possible secondary invaders in the exposed skeletal regions. Despite widespread reference to necrosis in coral disease literature, there was no evidence of necrosis in any WS lesion or the adjacent tissues in this study. However, in situ end labelling, light microscopy and TEM of WS and healthy coral tissue sections showed evidence of extensive programmed cell death (PCD) exclusively in WS. This study provides the first evidence of intrinsic or PCD as a primary mechanism of cell death in WS, and may provide some explanation for the failure to isolate pathogens from over 80% of identified coral diseases, many of which show similar lesion patterns and WS characteristics.

IgG subclass specific antibody response to periodontopathic organisms in HIV-positive patients.

We previously reported an increased rate of progression of periodontal disease over an 18-month period in human immunodeficiency virus (HIV)-positive subjects compared to controls. The mechanism for disease progression and rapid tissue loss was unknown. Data on the microbiological studies failed to show any significant difference in the microbial characteristics of the periodontal lesions in HIV-positive patients compared to HIV-negative controls. Immunological analysis had identified neutrophils as an important component of the host defense against periodontal infection, especially against rapid tissue loss. Serum IgG reactivities to periodontal pathogens in HIV-positive patients with periodontitis were reduced. Other data provided circumstantial evidence to suggest that IgG subclass (IgG2) specific antibody might assist bacterial clearing in periodontal infection. The aim of the current study was to examine the specific IgG subclass antibody response to a panel of periodontopathic organisms: Actinobacillus actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Prevotella Intermedia (Pi), Fusobacterium nucleatum (Fn), Campylobacter rectus (Cr), and Bacteroides forsythus (Bf) in HIV-positive patients compared to HIV-negative controls. Sera from 120 HIV-positive patients (40 periodontitis, 69 gingivitis, and 11 no oral diseases) were tested for IgG subclass specific antibody response to the above listed 6 organisms using enzyme-linked immunosorbent assay. Data were compared with those obtained from 40 HIV-negative control subjects (35 periodontitis, 2 gingivitis, and 3 no oral diseases). In the HIV-positive group, a consistently high response rate was found in IgG1 to all the bacteria tested. In addition, high levels of IgG3 and IgG4 to Pg and IgG1 and IgG2 to Pi were also present. However, no significant difference was detected among the periodontitis, gingivitis, and no oral disease subgroups. When the periodontitis patients from the HIV-positive group were compared to the HIV-negative group, no difference in the antibody levels and response rates was noted. We conclude that in HIV-positive patients, the specific IgG subclass antibody response to periodontopathic organisms was similar to that of HIV-negative subjects.