Fish & Invertebrate Husbandry, WQ, & Enrichment Flashcards

Question

Describe the effects of improper hardness on fish. What is the difference between hardness and alkalinity? How is low hardness resolved? What about high hardness?

Answer 1

**Improper hardness.** * Hardness too low – add calcium. * Harness too high (aquaria) – do water change with deionized water or other low hardness water, filter water through peat. * Comments: * **Hardness vs alkalinity:** * **Hardness – measure of divalent metal cation i.e. calcium, iron, zn, mg in water.** * **Most waters entirely Ca and Mg.** * Total hardness usually similar to alkalinity because alk of most waters primarily from carbonate salts Ca and Mg. * Temporary hardness = hardness from carbonate salts. * Precipitated by boiling. * Permanent hardness – noncorbonate metal salts i.e. sulfate, nitrate, Cl, silicate. * Very hard but low alk waters. * Waters with alk due to Na or KCO3 may be low hardness with high alk. * Total water of SW very high. * Hardness requirements: * Spp dependent. * Salmonids – at least 100 mg/l optimal. * But can tolerate wide range once acclimated. * FW aquarium fish do poorly in moderately soft water and should be kept with high Ca content water. * Ca levels in tropical marine aq should be ~400 mg/l. * Often easier for fish to adapt to hard water vs soft. * Ca, Mg needed for osmoregulation. * Ca reduces permeability of gills to water, reduces electrolyte flux. * Dx: * Expressed as mg/l equivalents of CaCO3 or German hardness scale degrees of hardness dH. * Commercial kits measure both. * dH 3-10 most aq fish, \> 10 most Af rift lake cichlids. * Tx improper hardness: * Limit other Ca salts supplemental Ca for pond fish. * To reduce hardness, add distilled water. * Filter water over peat. * Sedimentary rocks may increase hardness. * Release Ca and Mg salts. * Metamorphic or volcanic rocks ie. Basalt, granite and quartz do not release divalent cations.

Answer 2

* **Ammonia Toxicity (CGFM)** * Unionized form is more toxic, highest in warm freshwater * Nitrogenous waste product of most fish, can buld up if not oxidized by nitrifying bacteria ro removed via water changes * Etiology * Sources of ammonia: protein waste products, bacterial fermentation, organic decomposition; municipal or groundwater; leaching of fertilizers, industrial emissions * Ammonia builds up rapidly in closed systems or static (ie transport bags) * Ammonia-oxidizing (nitrifying) bacteria convert ammonia to nitrite using DO and bicarbonate ions, grow on every surface * Causes of inadequate nitrifying bacteria - immature systems, High stocking densities, high organic load (ie food), reduced H20 changes, acute envtal changes, low DO/alkalinity, high pH (\>8)/temp, recent algal bloom die off, some abx (enro/erythromycin), some antiparasitics (formalin, chloroquine, levamisole) * NH4+ (ammonium-ionized) and NH3 (ammonia - uniionized) are the two major forms, the latter is more toxic. Closed transport containers are a big risk, once opened, CO2 rushes in → pH incr converts NH4+ to NH3 → rapid ammonia incr * Signalment * Tetras and salmonids esp sensitive; air breathing spp more resistant * Clinical Findings * Acute - lethargy, inappetence, dyspnea/tachypena, erythema, incr mucus, dark coloration, neuro signs (erratic swimming) * Chronic - wt loss, reduced feeding, poor growth rates, some acute signs may be seen * Secondary infx common, incr in nitrite common * DDX: other envtal failure (low DO, contaminated water), ectoparasitic or bacterial dz * DX: * Testing the water (ammonia colorless, odorless. Most kits test total ammonia nitrogen, the NH3 should be calculated based on pH and temp (see table) * NH3 (unionized ammonia; UIA) should be \<0.02 mg/L, toxic if 0.5-1 mg/L * Husbandry * Incr aeration (target 95-100%) * Change 30-50% of water daily, remove excess organic material, reduce or stop feeding temporarily, check life support system, consider new source of organic carbon (i.e. chopped hay) as carbon can be a limiting nutrient for nutrifying bacteria * Consider adding substrate from another system with nitrifying bacteria * FW: consider adding zeolite to adsorb ammonia * Consider moving all of the fish * Ammonia is NOT removed by activated carbon * Medical tx * Commercial products that bind ammonia are available (i.e AmQuel); ammonia tests will remain high b/c they do not remove it * 1-3 g/L of salt in FW can reduce physiologic stress * Prevention * Test 1-2x/week in most systems, any ammonia should prompt response * Maintain DO and alkalinity within appropriate ranges * Mature biofilters in new systems with ammonium chloride or urea for 3-8 wks * If no cycling is possible prior to adding fish, the stocking density must be very low with fish relatively tolerant of ammonia * Maintain biofilters without fish and feed NH3Cl or urea as ‘biofarms’ as a source of nitrifying bacteria * Fast fish prior to shipping * Ammonia poisoning (Noga): * Lethal poisoning \> 1.00 UIA/L * Sublethal poisoning \> 0.05 mg UIA/L * Hx – Overcrowding, recent meds or chemicals, newly established tank, aquarium gravel or filters recently cleaned or changed, failure of bio filters, recent algal crash in pond, reduced water flow in raceway, hyperexcitability, other neuro signs if acute \> 0.2 mg/L; acute to chronic stress. * **Tx – 25-50% water change in aquarium; add zeolite; add buffer to FW to reduce pH; add nitrifying bacteria; add bio filtration; decrease density; temp reduce or stop feeding.** * Ponds or flow-through systems – Stop or reduce feeding, decrease density, add water or increase flow. * Ammonia is the primary nitrogenous waste product of fish, also from decay of proteins. * Aquaria – Inadequate number of bacteria oxidizing ammonia to nitrite. * Nitrosomonas europaea – predominant ammonia oxidizer. * Aka AOB – scarce in new aquaria, ammonia rises rapidly when fish added. * Aka new tank syndrome. * Can also occur in long-established tanks. * Overfeeding or adding too many fish to tank. * Overwhelms biofilter. * Bio filter and ammonia removal will be greatest where there is a high water flow over a large surface area. * Cleaning filters will also result in ammonia spike when bacteria are removed. * Ponds – Most likely near sunset, when pH, temp, and unionized ammonia are highest. * Algae and nitrosomonas bacteria major consumers of ammonia in ponds. * Increases in fall and winter, possibly because of decrease in algal and bacterial metabolism at low temps. * Ammonia may rise after algae crash. * CS – anorexia, hyperexcitability, hyperplasia and hypertrophy of gills (not specific). * **Two forms: unionized (NH3) and ionized (NH4+).** * **UIA toxic to fish.** * **High pH and temp and low salinity favors UIA.** * Concentration determined from chart. * False positives when measuring ammonia via Nessler method if formalin is present. Salicylate method fails to measure ammonia (false negative) if formalin. Use an ion probe to measure if during formalin treatment. * **Tx – Water changes, zeolite (efficacy decreases with inc salinity), reducing pH will reduce percentage of NH3 (for each 1 unit pH decreases there is 10x decreases in UIA), ammonia-neutralizing products. Ultimately need to fix the biofiltration situation.** * **Ammonia toxicosis aka New Tank Syndrome (ZP).** * Common scenarios – adding new fish prior to appropriate development of filter bacteria; changing filters, biomedia removed in excess; high stocking densities, marginal filter microorganism capacity; overfeeding, protein breakdown and generation of ammonia. * Risk factors – small water volumes, high animal densities, lack of appropriate microorganisms. * Assessment of water ammonia levels diagnostic. * Affected by pH, temperature. * Unionized ammonia \> 0.05 mg/L considered elevated, should be treated. \> 1 mg /L rapidly fatal. * CS – Range from no change to excess mucus production. * Lesions – Edema, epithelial degeneration, fusion of gill lamellae. * Severe cases – Alzheimer’s Type 2 gliosis.

Answer 3

* **Nitrite Toxicity** * By product of ammonia oxidation, can build up in closed systems * Less toxic than ammonia * Toxicity in FW mainly (Cl- ions in SW inhibit nitrite uptake by gills) * Nitrite exposure → MetHbemia * MC tx - water changes, aeration, sodium chloride additions * Etiology * Ammonia → nitrite (ammonia oxidizing bacteria) → nitrate (nitrite oxidizing bacteria) * Signalment: * FW fish in recirculating systems most susceptible * Salmonids, channel catfish and related spp are susceptible * Marine fish resistant * Clinical Findings * Gills may be red, pink, brown; dyspnea/tachypnea, poor growth rates with chronic exposure * DDX: * Brown gills - nitrite, nitrate, or chloramine toxicity, autolysis * Dx: * Commercial tests are usually measured as nitrite-nitrogen; convert to nitrite by multiplying by 3.3, i.e. 1 mg/L No2-N = 3.3 mg/L NO2 * Nitrite in water should be \<1 mg/L, signs at 0.5-1 mg/L * Husbandry * Similar to tx for ammonia toxicity, increased aeration, 30-50% water changes daily * Nitrite is not removed by activated carbon * Medical tx * Sodium chloride at 3-10 mg/L of chloride for each 1 mg/L of NO2-N, usually with aquarium salt * Ca carbonate can be more effective than sodium chloride * Nitrite (Noga): * **Nitrite poisoning – Brown blood dz aka new tank syndrome** * Method of dx: * Chemical measurement of high nitrite in water * Measurement of high methemoglobin in blood * Hx: * Overcrowding, recent meds or chemicals added, new aquarium, recent washing of filter or gravel, failure of biofilter, fall season in pond, **low Cl:NO2 ratio**, stress. * PE: * Dyspnea. * Light tan to brown gills and brown blood. * Tx: * Aquaria – 25-50% water change daily to weekly. * Add nitrifying bacteria, chloride. * Enhance biofilter. * Decrease density. * Reduce temp. * Reduce feeding. * Ponds. * Add chloride. * Maintain high DO. * Comments: * Nitrite builds after ammonia has peaked during cycle. * NOB that convert nitrite to nitrate require time to activate. * Nitrobacter, nitrospira spp. * NOB inhibited by high ammonia, high ammonium concentrations toxic to NOB. Also inhibited by strong light. * Spike in ammonia inhibits nitrite oxidizing bacteria leading to spike in nitrite. * Ponds, nitrite poisoning common in fall. * Can rise quickly \< 24h in catfish ponds. * Clinical signs: * **Nitrite transported across gill, enters blood, oxidizes Hb to MetHb.** * **MetHb cannot transport O2, tissues deprived.** * **MetHb conc around 40% results in brown blood coloration.** * **Dyspnea despite adequate O2.** * Dx: * Definitive – blood measurement of MetHb. \> 25% abnormal. * Measuring nitrite levels in water more common. * Kit measures nitrite-nitrogen (NO2-N), which is converted to total nitrite via multiplying by conversion factor (3.3). * Susceptibility is species dependent. * **Channel catfish in FW, nitrite should be undetectable (\< 0.1 mg/l).** * Sunfish tolerate high levels \> 50 mg/l. * Salmonids: \< 0.5 mg/l recommended. * **Extremely high levels required for toxicity in marine fish i.e. 900 mg/l.** * **Chloride prevents nitrite toxicity in these spp.** * Not always the case, some saltwater spp susceptible i.e. red drum. * If water contains high chloride or Cl has been added, dx also requires measurement of Cl-. * Nitrite toxicity also influenced by pH, fish size, prev exposure, nutritional status, DO level. * Fish may not always have brown gills and blood, can die from nitrite-induced hemolytic anemia rather than toxicity. * May have accumulation of high nitrite conc in spleen or foci of iron-containing MP caused by increased erythrocyte destruction. * Tx: * **Cl competitively inhibits nitrite uptake across gill.** * Channel catfish – nitrite toxicity can be prevented when at least 3 mg Cll to 1 mg nitrite present in water. * Does not prevent chronic erythrocyte damage that may cause anemia. * Ratios of 6 RBT to 16 channel catfish inhibit nitrite toxicity. * Sodium chloride or calcium chloride are effective. * Low level needed of salt for tx usually \< 50 mg/l is nontoxic to FW fish. * Hb should return to normal within 12-24h after initiation of tx. * Prevention: * Channel catfish – at least 20 mg/l Cl always present. * 1 ppt SW contains over 500 mg/l chloride. * Clinically encountered nitrite levels have never been shown to be toxic to fish in SW. * Bicarbonate and high dietary vit C may also protect against nitrite-induced MetHb formation. * Nitrite toxicity - ZP. * FW fish. * Primary effect of elevated nitrite is oxidation of hemoglobin, limiting O2 carrying capacity of blood. * Gills and blood may be grossly brown. * Anemia, methemoglobinemia, low chloride, and acidosis. * Dx – documentation of methemoglobinemia coupled with elevated nitrite in water. * Variable susceptibility by spp – FW nitrite levels \> 0.10 mg/L considered elevated for warm water spp. * Even with treatment, may have weeks of elevated sensitivity to other stressors/infectious dz.

Answer 4

* **Nitrate Toxicity (CGFM)** * Nitrates less toxic than ammonia or nitrite, can reach high levels in long established recirculating systems; chronic stressors and endocrine disruptors * Removed through water changes, plants, anaerobic bacteria * Etiology * Risk factors: limited water changes, no denitification, no or few live plants, contamination of ponds with fertilizer, long established, large recirculating systems. * Signalment * FW fish and marine elasmobranchs in recirculating systems most susceptible * Eggs, fry, small fish more susceptible * Clinical Findings * Chronic, lethargy, inappetence, reduced growth, dyspnea/tachypnea, pale or discolored gulls, muscle rigidity, feminization of male fish, mortality low but chronic mortalities may be seen * Goiter (ventral throat swelling in elasmos, bilateral or unilateral opercular distention in teleost) * Dx: * Water testing. Multiply NO3-N (nitrate-nitrogen) on a colormetric test by 4.4 to get result * \<50 mg/L for most fish ideal * \<15 mg/L for inverts * \<2 mg/L for sensitive FW spp * Husbandry * Water changes, reduce stocking density, remove organic material * Medical tx * Iodid supplementation for goiters * Prevention * Frequent water changes, denitrification filters in large recirculating systems * **Nitrate (Noga):** * Nitrate poisoning aka old tank syndrome: * Dx: * Chemical measurement of high nitrate in water * Measurement of metHb in blood * Hx: * Overcrowding, inadequate water changes. * PE: * Dyspnea. * Tan to brown gills, stress. * Tx: * Water changes. * Denitrification apparatus. * Decrease density. * Comments: * **End product of nitrite oxidation -\> nitrate.** * Builds up after nitrite peak. * **Must be actively removed by water change or denitrification.** * Dependent upon fish biomass and feeding rate. * Can also enter aquatic ecosystems from agricultural runoff, industrial wastes, and effluents. * Clinical signs: * **Forms metHb.** * But gill uptake is limited compared to ammonia or nitrite. * Relatively low toxicity. * FW fish may be more sensitive. * Exposure of RBT fry for several days caused increased ferrihemoglobin, alteration in peripheral blood and hematopoietic centers, and liver damage. * Dx: * Measuring nitrate in water. * Kits measure nitrate-nitrogen, can be converted to total nitrate by multiplying by 4.4. * Toxic level for most fish testes is much higher than drinking water limit (10 mg). * In general nitrate is less toxic than ammonia or nitrate. * Some fish are highly sensitive. * Eggs and fry of RBT can die after 30 days at levels 1-8 mg. * 50 mg/l typically considered safe. * Typically more of a chronic problem. * Recommended to keep as low as possible. * Reef corals are very sensitive – levels should be \< 20 mg/L. * Tx, prevention: * Clinically encountered nitrate never really seen as toxic to marine fish and is rare in FW fish except some species. * Elevated nitrate may present uptake of iodine which predisposes marine fish to goiter.

Answer 5

* **Chlorine/Chloramine Toxicity** * Usually caused by exposure to untreated municipal water * Usually at levels toxic to fish 0.5-3 mg/L * Bleach contamination is another source, ozone disinfection can create chlorines/chloramines (although bromines are more common) * Risk factors: high water temperature, low organic load, low hardness and pH (\<7.5) * Clinical Findings * Lethargy, abnormal swimming, hiding → jumping, tetany, erratic movements * Pallor, darkened skin, increased mucus * Gills may be pale or tan-colored due to hemolytic anemia or methemoglobin formation * DDX: nitrite, nitrate, chloramine toxicity * Dx: levels of free and total chlorines in the water → free chlorine Cl2, OCl-, HOCl * Total chlorine should be \<0.03 mg/L for most fish, \<0.01 mg/L in sensitive spp * Gill hyperplasia on cytology/histology * Husbandry: * Aggressive aeration, 30-50% water change daily * Vigorously aerate new water ~24 hrs prior to use to get rid of chlorine and some chloramines * Activated carbon filter can help adsorb chloramine and chlorines * Consider moving the fish * Medical tx * Some products bind chlorines and chloramines - AmQuel * Sodium thiosulfate immersion neutralizes chlorines and chloramines * Prevention * Always treat water prior to use with fish using sodium thiosulfate, activated carbon filtration, or aeration

Answer 6

* **Heavy Metal Toxicity** * Sources: contamination of water from plumbing, decor, therapeutic agents, runoff, groundwater, food contamination * Copper MC\*\*\*, zinc, lead * Activated carbon can adsorb heavy metals * Etiology * Copper * Immersion MC source, ie frm Cu sulfate txs * Zinc * Coins containing zinc, galvanized steel tanks or plumbing * Lead * Lead plumbing, lead-based paints, metal strips * Iron * Contaminated well water * Low pH, hardness and alkalinity can increase heavy metal dissolution and uptake in the gills * Signalment * Low tolerance for Cu ions * Most elasmos, inverts, teleosts in soft, acidic FW; larval and juvenile teleosts, syngnathids * Findings * Signs are variable, nonspecific; lethargy, erratic swimming * Gill pallor from nonregenerative anemia * Copper toxicity - gill hyperplasia, edema, curling of distal tips of primary lamellae * Coelomic distention from ileus * Acute or chronic mortalities * Dx: * Measure ionic form via commercial testing * Toxic levels vary by species, life stage, rate of change, water chemistry, water temperature * Zinc → 0.02-100 mg/L of Zn sulfate * Lead → 0.05 - 30 mg/L * Heavy metals in tissue \> serum * Husbandry * Remove the source, 30-50% water change, add activated carbon filters, consider zeolite or other ion exchange resin filters * Consider water conditioners that bind heavy metals * Vigorous aeration for iron toxicity * Medical tx * EDTA (IM) or DMSA (immersion), the latter has been reported to improve signs in rainbow trout, lower blood levels in an electric eel * Prevention * Only use Cu sulfate if CaCO3 is \>50 mg/L * Only aquarium safe products should be added to aquariums * Remove coins * Run ground FW high in heavy metals should be run through activated carbon, zeolite, or other ion exchange filter prior top use

Answer 7

* **Hydrogen Sulfide Toxicity** * Gas produced under anoxic conditions, acutely toxic in most fish, prognosis poor * Etiology * Toxic, soluble, flammable gas produced from sulfates or anaerobic bacteria * Can be high in groundwater or hot springs, wastewater from paper mills, chemical plants * Effects worse at low pH, high water temperature * The gas created sulfhemoglobin, which directly damages gills and blocks oxygen using a similar mechanism to metHb * Signalment * Toxicity is more likely in saltwater and brackish water, almost all fish susceptible * Clinical Findings * Most fish affected in the system, inappetence, dyspnea/tachypnea common, acute mortalities common, up to 100% * Dx: * \>0.3 ug/L there is a rotten egg smell * Black material on substrate in some cases due to metal sulfides * Commercial test kits to test in water * Clubbing, hyperplasia of lamellae on gill bx * Husbandry * Aerate aggressively, move fish asap to new system, if not possible, change 80-100% of the water rapidly, reduce water temp slightly, consider incr pH * Medical tx * Husbandry changes * Prevention * Degas and aerate groundwater prior to use * Avoid substrate \>10cm * Excess organic material removed * Take filters that have held stagnant water for \>2hrs off-line to run water through

Answer 8

* **Organophosphate and Carbamate Toxicity** * Common pesticides, exposure usually from runoff into ponds or tx of ectoparasites * Trichlorfon (Dylox) is the most common organophosphate used on fish, often to treat copepods or leeches * Can be adsorbed transdermally * Signalment * Many elasmos are sensitive * Ponds * Serrasalmidae (red hooks and pacus) * Clinical Findings * Neuro signs - erratic swimming, seizures, vertebral fractures * Pect fins may be held cranially, * Lethargy, paralysis may be seen * DDX: * Toxin, nutrition, inxfx * Dx: * History, concentrations can be measured at specialist labs * Husbandry * Wear PPE (toxic to humans too) * Consider moving fish or 50-80% water change daily * Add AC filters * Consider adding zeolite * Medical tx * Supportive * Atropine IM or IV used commonly due to affected Achesterase activity * Prevention * Avoidance * When using as an immersion tx, a bioassay is essential, use minimum effective dose. Pretreatment with intramuscular atropine may reduce risk of toxicity.

Answer 9

**Improper salinity.** * Marine \< 30 or \> 35 ppt (\< 1.020 or \> 1.026 spec grav). * Hx: * Improper housing of spp in FW or SW. * Incorrect calc of SW mix. * Replacing SW with FW during water changes. * Failure to replace evaporative loss of FW. * Tx: Add salt or FW. * Comments: * Salinity – amount of all ions in water. * Parts of ions per thousand parts water. * Full-strength SW 30-40 ppt. * Salinity requirement/tolerance: * Salinity can rapidly increase due to evaporation. About 2ppt per week. * Best to keep sal of tank at lower end of the optimal range. * Use balanced salt mixtures rather than pure sodium chloride. * NaCl lacks other valuable divalent cations. * **2ppt generally safe for FW fish.** * **Some spp i.e. tetras, catfishes, more sensitive.** * **Can still tolerate 1 ppt usually.** * Dx: * Measured by conductivity, chlorinity, refractive index, specific gravity. * Hand-held refractometer or electric meter. * Tx; * Do not change more than 1 ppt/hr. * Estuarine fish, sal should not be adjusted more than 10 ppt in a few hours. * Salt is useful prophylactic and can be added to reduce prevalence of infectious dz in FW aquaria.