Tropical fish medicine. Taking the history.
When treating fish, one needs to rely heavily on the history to collect the information needed to make a differential diagnosis, because physical examination will usually be quite limited.
Biomedical subjects
Publications and source records attributed to M K Stoskopf.
When treating fish, one needs to rely heavily on the history to collect the information needed to make a differential diagnosis, because physical examination will usually be quite limited.
The author considers the pros and cons of various routes of delivery of medication in fish as well as the drugs and doses used for treatment of bacterial infections and various parasitic infections. Also discussed are emergency and metabolic drugs.
Avian malaria (Plasmodium relictum) caused significant mortality in wild-caught Magellanic penguins (Spheniscus magellanicus) in 1986 at the Blank Park Zoo in Des Moines, Iowa (USA). In early winter, wild birds were captured off the southern coast of Chile and flown to Detroit, Michigan for a 38 day quarantine. After quarantine, 18 birds were dispersed to Lansing, Michigan, six to a facility in Maine, and 46 to Des Moines, Iowa. Upon arrival in Des Moines, several penguins became weak and inactive, had to be force-fed, and died after 2 days. Gross lesions at postmortem included splenomegaly, hepatomegaly, and pulmonary edema. Histopathological examination revealed numerous intraendothelial schizonts in spleen, lung, liver, heart and kidney. Schizonts were generally 16 to 28 micron by 11 to 16 micron and contained merozoites of two distinct sized (macromerozoites, nuclei 1.0 micron; micromerozoites, nuclei 0.5 micron). Based on the morphology of the abundant exoerythrocytic forms, a tentative diagnosis of avian malaria (Plasmodium sp.) was made. Subsequent transmission electron microscopic examination of schizonts in formalized tissue revealed merozoites with tear-shaped rhoptries. Antimalarial therapy was initiated early but deaths continued for 5 mo. Mortality, which eventually totaled 83%, occurred in three distinct waves, each separated by a hiatus of approximately 1 mo. Despite examinations of repeated blood smears, intraerythrocytic Plasmodium relictum was not detected until late in the outbreak. Diagnosis was based on morphologic characteristics including schizonts with eight to 12 merozoites/segmenter and round gametocytes that displaced and turned the infected erythrocyte nucleus. In addition to malaria, penguins showed evidence of aspergillosis, bacterial enteritis (Escherichia coli; Proteus sp.; and Edwardsiella sp.), and helminthiasis (Contracaecum sp. and Tetrabothrius sp.). Based on gross and histological lesions, disease prevalence in this group of penguins was malaria 58%, aspergillosis 61%, enteritis 60%, helminthiasis 26%. Epidemiologic investigation including group transport history, disease prevalence in co-quarantined birds not sent to Des Moines and climatological data implicated Des Moines as the likely site for initial exposure, although information is not conclusive. Stress and concurrent disease certainly contributed to the severe mortality in this group of penguins infected with P. relictum.
The effects of dietary administration of equimolar doses (5 mmol/kg body wt per day) of trimethylene oxide, trimethylene sulfide, coumaran, benzofuran, indole, and indole-3-carbinol on the activities of microsomal epoxide hydrolase and several other xenobiotic metabolizing enzymes were measured in the liver of female CD-1 mouse. Every compound, with the exception of indole, caused a significant increase (P less than 0.01) of the styrene oxide epoxide hydrolase activity over controls in hepatic microsomes. These results indicate that the enzyme activity is elevated in vivo by several heterocyclic compounds with strained bond angles to a nucleophilic hetero-atom. In addition, the ability of sulfur-containing trimethylene sulfide and nitrogen-containing indole-3-carbinol to elevate the enzyme activity indicates that the heterocyclic oxygen atom is not an absolute requirement for this effect. Data from the other xenobiotic metabolizing enzymes indicate that trimethylene oxide and trimethylene sulfide enhance the epoxide hydrolase activity rather specifically, while not affecting the activities of the other enzymes measured. While the oxygen-containing coumaran and benzofuran both increased the NADH: quinone reductase activity in hepatic cytosol, the nitrogen-containing indole and indole-3-carbinol did not. This indicated a specific requirement for the oxygen atom in elevating the quinone reductase activity, which was not the case for the elevation of microsomal epoxide hydrolase activity.
A non-oncogenic retrovirus was isolated from an explanted skin biopsy from a captive California sea lion (Zalophus californianus) with a history of recurring skin lesions. The morphology of the viral particles in electron photomicrographs was characteristic of a foamy virus, a retrovirus in the subfamily Spumavirinae. Viral cytopathic effects consistent with foamy virus infection were observed in subsequent explants of skin and lymph nodes and co-cultivated peripheral blood leukocytes. The sea lion with the persistent foamy virus infection later died from pericarditis caused by Pasteurella multocida. A herpesvirus was isolated from explants of lung.
Eyes of 1,716 wild northern fur seals (Callorhinus ursinus; 1,501 subadults and 215 adults) were examined for the prevalence of ocular anterior segment disease; 4.6% of the seals had clinically recognizable eye lesions. Six seals had bilateral eye lesions. Corneal scars were the most frequently observed lesion, followed by prominent lens sutures, cataracts, and iris depigmentations. Corneal edema, active corneal ulceration, or inflammation was not observed. Examination of normal corneas indicated an epithelial structure similar to that of the California sea lion, with 11 to 14 layers of nucleated superficial stratified squamous cells that lacked keratohyaline granules. The seal corneal endothelium had less hexagonality than do human corneal endothelial cells, with mean endothelial cell areas of 331 to 396 micron2, similar to that found in primates.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The necropsy files of the National Zoological Park and Baltimore Zoological Society were reviewed for cases of distal extremity necrosis (DEN) in birds. Nineteen cases of DEN occurred following either trauma or frostbite. Six birds developed an apparently primary type of DEN in which no predisposing factors were obvious clinically. The toes and feet were most commonly involved, and in several cases the beak was also affected. Some pathologic evidence is provided that certain cardiovascular lesions may predispose birds to DEN by compromising circulation of the extremities.
Two juvenile robins (Turdus migratorius) died shortly after being captured in Baltimore, Maryland. Both had high erythrocytic parasitemias of mixed Plasmodium infections. Postmortem examination revealed large numbers of exo-erythrocytic malarial schizonts in the liver, spleen, lungs and brain of both cases. Avian malaria was considered the primary cause of death.
Ten captive-reared African black-footed penguins (Spheniscus demersus) from a large outdoor colony were monitored for avian malaria, using several diagnostic tests. One treatment regimen was evaluated. Thin smear blood evaluation enabled detection of seven parasitemias involving Plasmodium relictum and Plasmodium elongatum in the penguins. Leukocytosis (relative lymphocytosis) was characteristic of infected birds. Parasitemia was detected as early as 21 days prior to onset of clinical signs (depression, anorexia, regurgitation, pale mucous membranes, and respiratory distress). The single bird that died had clinical signs only a few hours prior to its death. Treatment consisted of 0.03 mg of primaquine phosphate base/kg body weight, administered orally once daily for 3 days. Oral chloroquine phosphate therapy, given simultaneously, was administered in an initial loading dose of 10 mg of chloroquine phosphate base/kg body weight, followed by doses of 5 mg/kg at 6, 18 and 24 hours after the initial chloroquine dose. This treatment regimen prevented mortality and cleared parasites from the blood. Recurrences of malaria occurred in two birds that had received this treatment.
The identification of an actual or potential toxicity problem in an aquatic system immediately poses several questions of practical importance. Is the toxic agent still being added to the system? Where is the toxin coming from? Are the current filtration systems removing it? How soon will it be reduced to an acceptable level? How can it be removed faster? These questions in turn suggest an equally important question. What samples should be examined? Analysis of animal tissues from bioassays is the most common investigative technique in use, but alternatives do exist. Testing of water has not been utilized to its fullest potential. The need for an orderly approach to sampling and interpretation has been a major factor in this under utilization. Mathematical modeling through the use of toxicokinetics can be used to maximize the efficiency of analysis of a toxic accident by water sampling. Strategies of sampling and interpretation of results will be discussed using the tools of toxicokinetic modeling.