Prise en charge ortho-chirurgicale de l'inclusion d'incisive centrale maxillaire : à propos d'un cas

L'inclusion des incisives centrales maxillaires pose un problème esthétique et fonctionnel. La prise en charge ortho-chirurgicale est la thérapeutique la plus pratiquée et celle qui donne le meilleur rendu esthétique et fonctionnel. Elle nécessite cependant un bon diagnostic clinique et radiologique afin que la théra-peutique se déroule dans des conditions optimales. La désinclusion ortho-chirurgicale se fait en différentes étapes comme l'illustre le cas clinique présenté ici

Survey and genetic characterization of Vibrio cholerae in Apalachicola Bay, Florida (2012-2014).

AIMS: A small outbreak of gastroenteritis in 2011 in Apalachicola Bay, FL was attributed to consumption of raw oysters carrying Vibrio cholerae serotype O75. To better understand possible health risks, V. cholerae was surveyed in oysters, fish and seawater, and results were compared to data for Vibrio vulnificus and Vibrio parahaemolyticus. METHODS AND RESULTS: Enrichment protocols were used to compare prevalence of V. cholerae (0, 48, 50%), V. vulnificus (89, 97, 100%) and V. parahaemolyticus (83, 83, 100%) in fish, seawater and oysters respectively. Compared to other species, Most probable number results indicated significantly (P < 0·001) lower abundance of V. cholerae, which was also detected more frequently at lower salinity, near-shore sites; other species were more widely distributed throughout the bay. Genes for expression (ctxA, ctxB) and acquisition (tcpA) of cholera toxin were absent in all strains by PCR, which was confirmed by whole genome sequencing; however, other putative virulence genes (toxR, rtxA, hlyA, opmU) were common. Multi-locus sequence typing revealed 78% of isolates were genetically closer to V. cholerae O75 lineage or other non-O1 serogroups than to O1 or O139 serogroups. Resistance to amoxicillin, kanamycin, streptomycin, amikacin, tetracycline and cephalothin, as well as multidrug resistance, was noted. CONCLUSIONS: Results indicated minimal human health risk posed by V. cholerae, as all isolates recovered from Apalachicola Bay did not have the genetic capacity to produce cholera toxin. Vibrio cholerae was less prevalent and abundant relative to other pathogenic Vibrio species. SIGNIFICANCE AND IMPACT OF THE STUDY: These studies provide important baseline observations for V. cholerae virulence potential regarding: (i) genetic relatedness to V. cholerae O75, (ii) antibiotic resistance and (iii) prevalence of multiple virulence genes. These data will serve as a biomonitoring tool to better understand ecosystem status and management if bacterial densities and virulence potential are altered by environmental and climatic changes over time.

Exposure of fish to high-intensity sonar does not induce acute pathology.

This study investigated immediate effects of intense sound exposure associated with low-frequency (170-320 Hz) or with mid-frequency (2.8-3.8 kHz) sonars on caged rainbow trout Oncorhynchus mykiss, channel catfish Ictalurus punctatus and hybrid sunfish Lepomis sp. in Seneca Lake, New York, U.S.A. This study focused on potential effects on inner ear tissues using scanning electron microscopy and on non-auditory tissues using gross and histopathology. Fishes were exposed to low-frequency sounds for 324 or 628 s with a received peak signal level of 193 dB re 1 microPa (root mean square, rms) or to mid-frequency sounds for 15 s with a received peak signal level of 210 dB re 1 microPa (rms). Although a variety of clinical observations from various tissues and organ systems were described, no exposure-related pathologies were observed. This study represents the first investigation of the effects of high-intensity sonar on fish tissues in vivo. Data from this study indicate that exposure to low and midfrequency sonars, as described in this report, might not have acute effects on fish tissues.

Mycobacteria isolated from Chesapeake Bay fish.

Mycobacteriosis in fish can result in ulcers, emaciation, and in some cases death. Mycobacteria have been previously isolated from a variety of Chesapeake Bay fish species, and the current study was designed to identify potential host specificity and location fidelity of mycobacterial isolates. Mycobacteria were isolated from wild fish of the Chesapeake Bay collected from the Upper Bay, the Choptank River, Herring Bay, the Chicamacomico River, the Pocomoke River and the Potomac River in 2003-2006. Mycobacterial isolates were recovered from striped bass, Morone saxatilis, Atlantic menhaden, Brevoortia tyrannus, white perch, Morone americana, summer flounder, Paralichthys dentatus, spot, Leiostomus xanthurus, largemouth bass, Micropterus salmoides, channel catfish, Ictalurus punctatus, common carp, Cyprinus carpio carpio, spotted seatrout, Cynoscion nebulosus, killifish, Fundulus sp., blueback herring, Alosa aestivalis, American gizzard shad, Dorosoma cepedianum and American silver perch, Bairdiella chrysoura. Twenty-nine well-defined mycobacterial groups resulted from gas chromatography dendrogram clustering of isolates. The majority of groups included more than one host species and more than one site of collection. However, four groups contained only striped bass isolates, three of which were similar to M. shottsii. Therefore, multiple Chesapeake Bay fish species are colonized with multiple mycobacterial isolates, of which few appear to be host or location specific.

In vitro kinetics of hepatic albendazole sulfoxidation in channel catfish (Ictalurus punctatus), tilapia (Oreochromis sp.), rainbow trout (Oncorhynchus mykiss) and induction of EROD activity in ABZ-dosed channel catfish.

Liver microsomes from market-size (n = 6) rainbow trout, channel catfish and tilapia were used to investigate in vitro biotransformation kinetics of albendazole (ABZ). ABZ was transformed to a single metabolite, ABZ sulfoxide (ABZ-SO). Catfish displayed the highest maximal velocity (V(max) = 264.0 +/- 58.6 pmols ABZ-SO/min/mg protein) followed by tilapia (112.3 +/- 8.2) and rainbow trout (73.3 +/- 10.3). V(max) in catfish was significantly different (P < 0.05) from the other two species. Michaelis-Menten constant (K(m)) values (microm) varied significantly among the species: rainbow trout (3.9 +/- 0.5), tilapia (9.2 +/- 1.7) and catfish (22.0 +/- 3.2). However, V(max)/K(m) ratios showed no difference among the three species, making them equally efficient performing this phase I biotransformation reaction. In a second series of experiments, channel catfish (n = 6 per treatment) were dosed in vivo with gel-food containing ABZ (10 mg/kg, p.o.). Fish were killed at 24, 48, 72 and 120 h after dosage. Control fish were fed ABZ-free feed. Induction of ethoxyresorufin-o-deethylase activity was significant (P < 0.05) in all ABZ-dosed treatments as compared with controls.

Harmful algal bloom toxins alter c-Fos protein expression in the brain of killifish, Fundulus heteroclitus.

The immediate early gene c-fos, and its protein product c-Fos, are known to be induced in neurons of mammals and fish as a result of neuronal stimulation. The purpose of this study was to quantitatively examine CNS alterations in killifish, Fundulus heteroclitus, in relation to harmful algal bloom (HAB) toxin exposure. c-Fos expression was visualized using immunocytochemistry in the brains of killifish exposed to the excitatory neurotoxins domoic acid (DA) and brevetoxin (PbTx-2), and a paralytic neurotoxin, saxitoxin (STX), released from HABs. In addition, a simulated transport stress experiment was conducted to investigate effects of physical stress on c-Fos induction. Groups of fish were exposed to the different stress agents, brain sections were processed for c-Fos staining, and expression was quantified by brain region. Fish exposed to DA, STX, and transport stress displayed significant alterations in neuronal c-Fos expression when compared to control fish (p< or = 0.05). DA, PbTx-2, and transport stress increased c-Fos expression in the optic tecta regions of the brain, whereas STX significantly decreased expression. This is the first study to quantify c-Fos protein expression in fish exposed to HAB toxins. General alterations in brain activity, as well as knowledge of specific regions within the brain activated in association with HABs or other stressors, provides valuable insights into the neural control of fish behavior as well as sublethal effects of specific stressors in the CNS.

Parodontites et maladies respiratoires au centre hospitalier national universitaire de Fann (Sénégal)

Introduction : Les parodontites sont des pathologies infectieuses associées à différentes maladies générales dont les pathologies respiratoires. L'objectif de ce travail était d'évaluer la distribution des parodontites chez les sujets atteints d'affections respiratoires en milieu hospitalier. Matériels et méthodes : Il s'agissait d'une étude descriptive transversale basée sur un recrutement de patients hospitalisés ou venus en consultation au Service de Pneumologie de l'hôpital Fann. Les patients atteints de tuberculose n'ont pas été inclus. La distribution de l'atteinte parodontale a été évaluée par les mesures des profondeurs de poche (PP) au sondage et la perte d'attache clinique (PAC) à l'aide de la sonde parodontale de Williams. Résultats : Un échantillon de 70 patients dont 25 femmes et 45 hommes a été sélectionné pour cette étude. La moyenne d'âge était de 42 ans ± 4,2.La prévalence des pneumopathies bactériennes était de 54,3%, celle des Broncho Pneumopathies Chroniques Obstructives (BPCO) de 22,9%. Des profondeurs de poche ≥4mm ont été retrouvées chez 50% des sujets et 64,7% ont présenté une perte d'attache clinique ≥2mm.Les profondeurs de poche étaient plus importantes chez les patients atteints de pneumopathie bactérienne et de BPCO. Conclusion : La prévalence élevée des parodontites nécessite une collaboration entre pneumologue et parodontologiste afin de limiter les effets délétères d'une mauvaise condition orale sur la santé générale

Altered brain activity in brevetoxin-exposed bluegill, Lepomis macrochirus, visualized using in vivo 14C 2-deoxyglucose labeling.

This study investigated the neurological effects of sublethal brevetoxin (PbTx-2) exposure in bluegill (Lepomis macrochirus) by measuring alterations in 2-deoxyglucose (2-DG) uptake in the brains of exposed fish. Changes in regional brain activity were quantified using digitized autoradiographs from exposed and control fish. Brains of brevetoxin-exposed fish had significantly higher labeling of 2-DG than brains of control fish. Regional increases in labeling were observed in the optic lobes, telencephalon, and cerebrum of PbTx-2 exposed fish. From these observations, we conclude that sublethal brevetoxin exposure in vivo in bluegill increases neurological stimulation, measured through quantification of [14C]2-DG uptake in the brain. Increases in the uptake of [14C]2-DG from this study may be indicative of differences in neural activity in the PbTx-exposed fish and are likely associated with the action of PbTx-2 on voltage-gated sodium channels (VGSC), as well as neurological alterations in calcium and neurotransmitter release downstream resulting from VGSC activation. These techniques quantify physiological alterations in fish brain activity resulting from exposure to brevetoxin and possibly other harmful algal bloom toxins.

Myxosporean plasmodial infection associated with ulcerative lesions in young-of-the-year Atlantic menhaden in a tributary of the Chesapeake Bay, and possible links to Kudoa clupeidae.

Ulcers in Atlantic menhaden Brevoortia tyrannus (Latrobe) (Clupeidae), observed along the USA east coast, have been attributed to diverse etiologies including bacterial, fungal and, recently, harmful algal blooms. To understand the early pathogenesis of these lesions, we examined juvenile Atlantic menhaden collected during their seasonal presence in Chesapeake Bay tributaries from April to October 1999 and from March to August 2000. We conducted histopathological examinations of young-of-the-year fish from the Pocomoke River tributary, which has a history of fish mortalities and high lesion prevalence. Kudoa clupeidae (Myxozoa: Myxosporea) spores were present in the muscles of fish collected in both years. Of the fish assessed by histology in April, 5 to 14% were infected, while in May 90 to 96% were infected. Infection rates remained high during the summer. Mature spores were primarily located within myomeres and caused little or no observable pathological changes. Ultrastructure showed spores with capsulogenic cells bearing filamentous projections, and a basal crescentic nucleus with mottled nucleoplasm containing cleaved, condensed chromatin. Also, a highly invasive plasmodial stage of a myxozoan was found in the lesions of juvenile Atlantic menhaden. The plasmodia were observed in fish collected between May and July, with the maximum occurrence in late June 1999 and late May 2000. Plasmodia penetrated and surrounded muscle bundles, causing grossly observable raised lesions in 73% of all fish infected with this invasive stage. Plasmodia were also detected in the visceral organs, branchial arches, and interocular muscles of some fish. Some of the invasive extrasporogonic plasmodial lesions were associated with ulcers and chronic inflammatory infiltrates. The plasmodial stage appeared to slough out of the tissue with subsequent evidence of wound healing. Ultrastructure showed plasmodia with an elaborate irregular surface, divided into distinct ectoplasm and endoplasm; the latter contained numerous spherical vegetative nuclei, secondary generative cells, and occasional cell doublets. Our ultrastructural studies indicate that the plasmodial organisms, which are important in the etiology of the skin lesions, are myxozoans, and they may represent early stages of K. clupeidae.

Tissue slices revisited: evaluation and development of a short-term incubation for integrated drug metabolism.

This work details the development of a model for the rapid evaluation of drug metabolism in an integrated fashion using in situ architecture of the liver. A Krumdieck tissue slicer was used to generate slices from 10-mm cores of rat liver (approximately 250-microm thick). Initial unsuccessful efforts with 6-well plate-based incubation were overcome with the use of a dynamic (rotating) incubation in 23-ml liquid scintillation vials containing titanium mesh supports for the slice. Incubation of 1 slice/5 ml of a Krebs-Henseleit solution buffered with HEPES showed a <2% increase over the initial 25% release of lactate dehydrogenase over 2 h of incubation at 37 degrees C under ambient oxygen conditions. Coupled O-dealkylase and conjugative metabolism of alkoxycoumarin derivatives was shown to be linear for both 7-methoxy- and 7-ethoxycoumarin (100 microM) with a low amount of nonconjugated 7-hydroxycoumarin (7-HC) at all time points. Metabolic profiles for 7-methoxy- and 7-ethoxycoumarin were compared between slice and microsomal incubations generated from the same tissue. The use of 7-HC as a primary substrate not only provided an assessment of the capacity-based differences in oxidative versus conjugative metabolism but also capacity-based differences in glucuronidation and sulfation. These studies underscore the physiological fact that phase I metabolism has a lower capacity for substrate metabolism than phase II metabolism. Additionally, this technique provides a model for examination of pharmacodynamic and pharmacokinetic influences in the context of maintenance of the in situ architecture of the liver.

New nephron development in goldfish (Carassius auratus) kidneys following repeated gentamicin-induced nephrotoxicosis.

Renal development in mammalian kidneys can only be studied in embryonic animals. Hence, research in this area is hampered by the need to maintain pregnant animals and by the small size of the embryonic kidney. Here, we describe a goldfish (Carassius auratus) model for studying renal repair and nephron development in an adult animal. Previous studies have indicated that chemically induced nephrotoxicosis in goldfish is followed by new nephron development. We tested the hypothesis that new nephron development is not a one-time only event and, thus, will occur after repeated nephrotoxic events. We used repeated injections of gentamicin (50 mg/kg of body weight), a nephrotoxic antibiotic, which has been used as a model nephrotoxicant to study renal repair. Fish were allowed either a recovery period of 9 or 24 weeks between injections. In both experiments, new nephrons developed after each injection of gentamicin, supporting our hypothesis. Nephron development occurring after a 9-week recovery period was similar to development observed after a 24-week recovery period; therefore, the shorter experimental paradigm appears sufficient and can save time and money. Future research using this fish nephrogenesis model may identify the genes responsible for nephron neogenesis. Such information is a prerequisite for developing alternative renal replacement therapies based on the induction of de novo nephrogenesis in diseased kidneys.

Effects of waterborne nitrite on phase I-II biotransformation in channel catfish (Ictalurus punctatus).

The effects of waterborne nitrite (3 mg/l NO2) on channel catfish were studied to evaluate changes in hematological parameters and phase I-II biotransformation in liver slices. Nitrite-exposed fish had significantly higher methemoglobin, blood and liver nitrite, and significantly lower pO2 than control fish. Total phase I-mediated metabolism of 7-ethoxycoumarin (EC) was not altered in nitrite-exposed fish compared with control fish (291 +/- 43 and 312 +/- 20 pmol/mg/h, respectively). However, phase II glucuronosyltransferase-mediated metabolism of 7-hydroxycoumarin (HC), both as a phase I metabolite of EC and as a parent substrate, was elevated in nitrite-exposed fish (204 +/- 17 and 1007 +/- 103 pmol/mg/h, respectively) as compared to control fish (149 +/- 14 and 735 +/- 87 pmol/mg/h) (P < 0.05). Sulfotransferase-mediated metabolism of HC (as a metabolite of EC and as a parent substrate) was not notably altered in nitrite-exposed fish (95 +/- 16 and 617 +/- 33 pmol/mg protein/h, respectively) as compared with control fish (118 +/- 24 and 575 +/- 55 pmol/mg/h, respectively). These studies indicate that in vivo nitrite exposure and associated changes in hematological parameters do not appear to affect hepatic phase I EC biotransformation in channel catfish. However, subtle but significant changes in phase II glucuronidation, but not sulfation activity, were observed. The mechanism of these alterations is unclear. However, the data suggest that environmentally realistic concentrations of nitrite may affect the dynamics of conjugative metabolism in exposed fish.

Pathology of fathead minnows (Pimephales promelas) exposed to chlorine dioxide and chlorite.

Fathead minnows (Pimephales promelas) were exposed to the biocide chlorine dioxide (0.13 and 0.19 mg l-1) for up to 12 h and to its primary decomposition product, chlorite (177 and 304 mg l-1), for up to 96 h followed by recovery periods of up to 14 days. Chlorine dioxide exposure produced dose-dependent gill pathology including epithelial lifting, hypertrophy, hyperplasia, lamellar fusion, and necrosis. Complete recovery, even in fish with severe hypertrophy and lamellar fusion, was achieved within 4 days. Chlorite did not produce gill pathology even at a lethal exposure level (304 mg l-1 for 96 h) but did elicit a chronic inflammatory response with a marked increase in circulating and fixed phagocytes within hematopoietic and vascular tissues. This study indicates that chlorine dioxide is approximately 1000 times more toxic to fathead minnows than chlorite. Further, exposure of fathead minnows to these distinct but related compounds is consistently associated with very different pathologies.

Etiologies, observations and reporting of estuarine finfish lesions.

Lesions in estuarine finfish are associated with a variety of organisms including parasites and bacterial, viral, and fungal infectious agents. In addition, trauma, suboptimal water quality, and other abiotic stress factors may result in the loss of homeostasis. We have observed solitary ulcerative lesions on menhaden sampled from the Chesapeake Bay, Maryland, the Pimlico River, North Carolina, and the St. Johns River, Florida. Histologically, the lesions demonstrated a marked chronic inflammatory infiltrate and granulomas in response to fungal hyphae throughout large areas of exposed necrotic muscle. Gram-negative rod-shaped bacteria were also observed in the lesions, a common finding in ulcers of aquatic organisms. Similar observations in menhaden and other species have been described previously in the literature as ulcerative mycosis, mycotic granulomatosis, red spot disease, and epizootic ulcerative syndrome. Despite the many different known causes of fish lesions, the popular press and the scientific literature have recently emphasized Pfiesteria piscicida and other Pfiesteria-like dinoflagellates (and their bioactive compounds) as the primary causative agent for finfish lesions, particularly mycotic granulomatous ulcers in Atlantic menhaden. While some laboratory data suggest that Pfiesteria may play a role in field-observed lesions, much more cause-and-effect evidence is needed to determine the importance of other risk factors, both alone or and in combination with Pfiesteria. In order to better understand the etiology of lesion initiation and progression in estuarine finfish, accurate assessments of environmental conditions collected on appropriate temporal and spatial scales, and fish morphological indicators consistent with gross and histological pathologic terminology, should be used for reporting fish lesion observations and kills. Further, this outlook will help to avoid bias and may foster a broader perspective for examining the health of estuarine systems in general.

Superoxide production in phagocytes obtained from Mycobacterium marinum-stimulated goldfish (Carassius auratus) that were exposed to copper.

OBJECTIVE: To investigate the effects of copper exposure and recovery from copper toxicosis on the nonspecific immune response in Mycobacterium marinum-inoculated goldfish. ANIMALS: Goldfish (Carassius auratus) with a mean weight of 33.5 g. PROCEDURE: Superoxide (O2-) production was measured in fish 2 to 6 weeks after injection with phosphate-buffered saline (PBS) solution or M marinum (10(2) to 10(7) colony-forming units [CFU]/fish). Then, paired groups of fish were injected with PBS solution or 10(4) CFU of M marinum and exposed to copper (100 microg/L) for 7 days or for 4 days with 3 days of recovery. One paired group not exposed 14 days later to copper served as control fish. Phagocyte production of O2-was measured by use of the nitroblue tetrazolium reduction assay. Inflammation and bacterial colony counts were determined by use of routine histologic and microbiologic procedures. RESULTS: Superoxide production achieved a maximal response 2 to 4 weeks after M marinum inoculation. Compared with control fish, O2- production increased in the groups exposed to copper but then decreased in the exposed groups that were allowed to recover. Superoxide response and peritoneal inflammation were greater in M marinum-inoculated groups than in non-inoculated groups. CONCLUSIONS: Copper exposure and inoculation with M marinum increased O2- production, whereas recovery after exposure decreased O2- production, even in fish that were immunostimulated by M marinum. CLINICAL RELEVANCE: When the antimicrobial oxidative response is suppressed after copper exposure, steps should be taken to avoid imposing additional stress and minimize the possibility of resurgent or secondary pathogenic infections.

Pathogenicity of Mycobacterium fortuitum and Mycobacterium smegmatis to goldfish, Carassius auratus.

Despite the ubiquitous presence of atypical mycobacteria in the environment and the potential risk of infection in humans and animals, the pathogenesis of diseases caused by infection with atypical mycobacteria has been poorly characterized. In this study, goldfish, Carassius auratus were infected either with the rapidly growing fish pathogen, Mycobacterium fortuitum or with another rapidly growing mycobacteria, Mycobacterium smegmatis. Bacterial persistence and pathological host response to mycobacterial infection in the goldfish are described. Mycobacteria were recovered from a high percentage of inoculated fish that developed a characteristic chronic granulomatous response similar to that associated with natural mycobacterial infection. Both M. fortuitum and M. smegmatis were pathogenic to fish. Fish infected with M. smegmatis ATCC 19420 showed the highest level of giant cell recruitment compared to fish inoculated with M. smegmatis mc(2)155 and M. fortuitum. Of the three strains of mycobacteria examined, M. smegmatis ATCC 19420 was the most virulent strain to goldfish followed by M. fortuitum and M. smegmatis mc(2)155, respectively.

Febrile-range temperature modifies early systemic tumor necrosis factor alpha expression in mice challenged with bacterial endotoxin.

Fever improves survival in acute infections, but the effects of increased core temperature on host defenses are poorly understood. Tumor necrosis factor alpha (TNF-alpha) is an early activator of host defenses and a major endogenous pyrogen. TNF-alpha expression is essential for survival in bacterial infections but, if disregulated, can cause tissue injury. In this study, we show that passively increasing core temperature in mice from the basal (36.5 to 37.5 degrees C) to the febrile (39.5 to 40 degrees C) range modifies systemic TNF-alpha expression in response to bacterial endotoxin (lipopolysaccharide). The early TNF-alpha secretion rate is enhanced, but the duration of maximal TNF-alpha production is shortened. We identified Kupffer cells as the predominant source of the excess TNF-alpha production in the warmer animals. The enhanced early TNF-alpha production observed at the higher temperature in vivo could not be demonstrated in isolated Kupffer cells or in precision-cut liver slices in vitro, indicating the participation of indirect pathways. Therefore, expression of the endogenous pyrogen TNF-alpha is regulated by increments in core temperature during fever, generating an enhanced early, self-limited TNF-alpha pulse.

Fish lesions in the Chesapeake Bay: Pfiesteria-like dinoflagellates and other etiologies.

Ulcerative lesions and mass mortalities of Atlantic estuarine fish, particularly menhaden (Brevoortia tyrannus), have been associated with exposure to Pfiesteria-like dinoflagellates and their toxins. We collected fish from the Chicamacomico River, Maryland, and observed solitary ulcerative lesions on the majority of menhaden sampled. One striped bass (Morone saxatilis) had an area of reddening around the base of the dorsal fin. Bluegill (Lepomis machrochirus), channel catfish (Ictalurus punctatus), yellow perch (Perca flavescens), and carp (Cyprinus carpio) were externally nonremarkable. Histologically ulcerative menhaden lesions demonstrated marked chronic inflammatory infiltrate in large areas of exposed necrotic muscle. The ulcers contained granulomata with fungal hyphae in the necrotic tissue. Gram negative rod-shaped bacteria were also observed in the lesions, a common finding in ulcers of aquatic organisms. Our data suggest that typical ulcerative lesions observed on fish from areas of Pfiesteria-like dinoflagellate blooms are reflective of dermatosis, which may be related to a variety of individual or combined environmental stressors. Exposure to dinoflagellate toxin)s) potentially represents one such stressor. The role of Pfiesteria-like dinoflagellate toxin in fish primary lesion development is currently under investigation.

Abdominal ascites in electric eels (Electrophorus electricus) associated with hepatic hemosiderosis and elevated water pH.

Six electric eels (Electrophorus electricus) from various centers that house aquatic organisms presented clinically with abdominal distension following prolonged exposure to elevated environmental pH. Postmortem examination revealed marked ascites. Culture of the abdominal fluid from three of the eels yielded either Aeromonas hydrophila or Citrobacter freundii, which were most likely secondary invaders. Histopathology showed marked iron accumulation in both hepatocytes and hepatic macrophage aggregates.