Alpaki - złe żywienie

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//-->Small Ruminant Research 61 (2006) 153–164Nutritional diseases of South American camelidsRobert J. Van Saun∗Department of Veterinary Science, College of Agricultural Sciences, Pennsylvania State University,115 Henning Building, University Park, PA 16802-3500, USAAvailable online 24 August 2005AbstractLiterature describing nutritional or nutrition-related diseases of llamas and alpacas was reviewed. Case reports of coppertoxicity, polioencephalomalacia, plant poisonings and urolithiasis accounted for the greatest number of literature citationsrelative to llamas and alpaca nutritional diseases. However, the overall number of published studies detailing nutritional diseaseof llamas and alpacas is very limited. Metabolic bone disease, associated with Vitamin D deficiency, and hepatic lipidosis weremetabolic diseases for which controlled research studies were completed to address underlying mechanisms. Circumstantialevidence would suggest llamas and alpacas are similar to other ruminants relative to most nutrient deficiency or toxicity diseaseproblems. Llamas and alpacas are unique compared to other ruminant animals in their susceptibility to zinc and Vitamin Ddeficiency diseases. A zinc-responsive dermatosis has been described, but the true role of zinc deficiency is debated. Llamas andalpacas show a seasonal deficiency in Vitamin D resulting in a hypophosphatemic rickets syndrome. Camelids may have a lowercapacity to endogenously synthesize Vitamin D or higher requirement compared to other species. Although mechanisms are notfully understood, llamas and alpacas are somewhat different in metabolic responses to negative energy balance and subsequenthepatic lipidosis. Further research is necessary to better define llama and alpaca nutrient requirements and metabolism as theydirectly impact potential for nutritional disease.© 2005 Elsevier B.V. All rights reserved.Keywords:Llama; Alpaca; Nutritional disease; Rickets; Hepatic lipidosis1. IntroductionNutrition can play a number of roles in mediatingpotential for a disease state. Nearly all nutrients are pri-mary regulatory factors in controlling the immune sys-tem (Cunningham-Rundles,2002,pp. 21–39). Thus,This paper is part of special issue entitled Special Issue onCamelids, Guest Edited by Dr. Ahmed Tibary and Dr. Steve Parish.∗Tel.: +1 814 865 6995; fax: +1 814 863 6140.E-mail address:rjv10@psu.edu.0921-4488/$ – see front matter © 2005 Elsevier B.V. All rights reserved.doi:10.1016/j.smallrumres.2005.07.007one or more nutrient deficiencies or toxicities can resultin altered immune response and greater susceptibility todisease, primarily infectious. Altered nutritional statuscan adversely influence metabolic function resultingin a variety of metabolic diseases depending upon thenature of the aberrant nutrient or nutrients. Metabolicdiseases can also negatively influence immune functionand increase infectious disease susceptibility (Wentinket al., 1998; Lacetera et al., 2001).Consumption ofdeficient or toxic amounts of any essential nutrientcan directly result in disease state characterized by154R.J. Van Saun / Small Ruminant Research 61 (2006) 153–164nutrient-specific pathologic lesions. Clinical vitaminand mineral deficiency and toxicity diseases have beendescribed (NRC,1980, 1987; Underwood and Suttle,1999; McDowell, 2000).Subclinical nutritional dis-ease is present when nutrient intake is either aboveor below requirements, but not insufficient or exces-sive enough to induce classic signs of nutrient-specificdeficiency or toxicity disease, respectively. Subclini-cal nutritional disease is associated with immune dys-function, reduced reproductive capacity and productiveinefficiency.Although llamas and alpacas are considered to besusceptible to all nutrient deficiency and toxicity dis-eases described, very few published studies are avail-able. Nutrient related deficiency and toxicity diseasesare well recognized and appropriately treated, result-ing in an under reporting of these conditions. Basedon published reports, nutritional diseases of concernoutside of South America include hepatic lipidosis,rickets, obesity, urolithiasis and copper toxicity. Thispaper will review nutritional diseases in llamas andalpacas, focusing primarily on those diseases to whichliterature reports have documented. The term camelidswill be used in this paper to generically refer to llamasand alpacas and not inclusive of other members of thecamelid family.2. Nutrient deficiency diseases2.1. Protein-energy malnutritionStarvation is defined as a prolonged complete depri-vation of feed intake. True starvation cases are theexception rather than the rule, but is most likely underreported. More typically encountered is a situation ofprotein-energy malnutrition (PEM) where energy, pro-tein or both are deficient in the diet over a period oftime. Body weight loss and a decline in body condi-tion score are the most common clinical signs (Oetzel,1988; Carmalt, 2000).Growing animals will also showa slowing or near complete cessation in gain. Preg-nant and lactating females experiencing PEM may beprone to hepatic lipidosis (Tornquistet al., 1999).Dueto higher requirements, young growing animals, latepregnant females and lactating females are the firstto show signs (Oetzel,1988).Time frame and sever-ity of body weight and condition loss will be depen-dent upon the degree of dietary energy and proteindeficiency.Beyond physiologic state and its impact on increas-ing requirements, environmental conditions, especiallyextreme cold, will increase energy needs. Camelidsraised in northern regions of North America areexposed to environmental temperatures much lowerthan their native habitat. In these cold conditions,camelids will expend additional energy to maintainbody temperature. Data for other species suggest main-tenance energy is increased 1% for every 1◦C belowan animal’s lower critical temperature (NRC,1981).Based on data from sheep and assuming a full fleece,lower critical temperature for llamas and alpacas wouldbe approximately 0–10◦C (NRC,1981).If animals arewet, mud covered or exposed to wind chill, then main-tenance energy may be increased as much as 75%.Clearly, PEM is a potential risk for llamas and alpacasraised in extreme northern climates (Carmalt,2000).Routine body condition scoring or body weight esti-mates can be used to diagnose potential problems. Athick fleece can readily hide body weight and con-dition changes from view, thus requiring a hands-oncondition score or body weight measure. A body con-dition scoring system for llamas and alpacas rankingfrom 1 (emaciated) to 10 (obese) has been described(Johnson,1994; Hilton et al., 1998).Once unexplainedbody weight or condition score loss has been identi-fied, one needs to determine a cause. Chronic infec-tious, parasitic and dental diseases can induce bodyweight and condition losses similar to PEM (Oetzel,1988; Carmalt, 2000).However, most animals afflictedwith an infectious or parasitic disease have reducedappetites, in spite of their energy deficit. In contrast,PEM animals maintain a healthy appetite until near ter-minal stages. Protein-energy malnutrition is often a sec-ondary sequella to chronic disease conditions. Animalsidentified early in the disease process can be recov-ered with appropriate feeding therapy and supportivecare; however, those becoming weak and recumbenthave a very poor prognosis even with aggressive ther-apy (Oetzel,1988).The most common reason for PEM is poor qualityforages coupled with the animal’s inability to consumesufficient amounts or increased requirement (Oetzel,1988; Carmalt, 2000).In South America, growth andquality of forage is determined by seasonally intermit-tent precipitation pattern. During the wet season plantR.J. Van Saun / Small Ruminant Research 61 (2006) 153–164155growth is rapid and of high quality but, of short duration(3–4 mo). Dry season forage availability is extremelylimited, very mature and of low quality (Reineret al.,1987; San Martin and Bryant, 1989; Genin et al., 1994).Body weight and condition score changes will mimicseasonal forage growth patterns. Camelids will gainsignificant body weight and condition and will givebirth during the wet season in concert with high qual-ity forage availability. During the dry season, animalswill lose considerable weight and condition and be invarious stages of malnutrition (Lopezet al., 1998).Ani-mals giving birth during the dry season are much moreprone to PEM and secondary infectious and parasiticdisease problems, often leading to their demise.North American llamas and alpacas can potentiallyreceive high or low quality forages throughout theyear, with availability only constrained by sporadicregional drought conditions. As a result, feed-relatedproblems range from potential malnutrition to obesity,with a tendency toward greater incidence of obesity(Johnson,1989; Fowler, 1998).Llamas and alpacasraised in North America are exposed to a greater diver-sity of environmental conditions ranging from extremehot and humid environments (Southern United States)to extremely cold winter conditions (Northern UnitedStates, Canada and Alaska). Average winter daily tem-perature in northern North America falls below−15◦Cand may decline to−35◦C (Carmalt,2000).These areenvironmental extremes llamas and alpacas never expe-rience in their native environment. Hot and humid envi-ronments bring challenges of preventing heat stress,a significant health risk for llamas and alpacas. Cold,wet conditions also have challenges associated withproviding effective protective shelter and increasedenergy intake to compensate for additional mainte-nance requirements. Either environmental extreme canresult in a situation of potential PEM with poor qualityforage.Prevention of PEM is based on appropriate feedingregimes where forage quality is matched to nutrientneeds of the animal. Where forage quality is insuffi-cient, feeding of supplemental feeds is necessary. Toachieve such feeding programs, forage quality willneed to be evaluated by chemical analysis. Routineassessment of animal’s energy status by body weightor condition scoring is a recommended practice, espe-cially for those individuals with higher energy require-ments and prior to and during the cold weather season.Important times to assess body condition score wouldbe during early to mid pregnancy; early to mid lacta-tion and periodically (four to six times per year) to otheranimals of the herd to assess energy status (Hiltonetal., 1998).2.2. Mineral deficienciesAlthough there are limited published studiesdocumenting classic mineral deficiency diseases incamelids, circumstantial evidence based on veterinaryteaching hospital cases in the United States would sug-gest camelids are susceptible to all potential mineraldeficiency diseases. Based on clinician experiences,it is assumed the disease process in camelids is sim-ilar to other ruminant species.Smith (1989)reportedon a clinical case of hypocalcemia and hypomagne-semia in a recently parturient female llama. Clinicalsigns of extreme nervousness and muscle fasciculationswere recognized. Serum calcium and magnesium con-centrations were 1.6 and 0.4 mol/l, respectively, andthe llama responded to calcium and magnesium ther-apy.Belknap (1994)also reported a case of hypocal-cemia with serum ionized calcium concentration of0.6 mol/l (normal≥1.0mol/l) that responded to cal-cium therapy. Hypocalcemia, hypokalemia, hypophos-phatemia and hypomagnesemia are all consideredpotential metabolic causes of recumbency in camelids(Belknap,1994).Due to the recognized problem ofselenium deficiency in North America, selenium defi-ciency disease in camelids is of concern (Smith,1989;Pugh, 1993a; Belknap, 1994).Selenium deficiency hasbeen reported in dromedary camels (Hamliriet al.,1990),but no published reports were found for llamasand alpacas. Specific published cases of mineral defi-ciency disease in camelids have only been reported foriron and copper.2.2.1. Iron (Fe)Two published reports characterized clinical casesand experimentally induced Fe deficiency resultingin anemia and poor growth in llamas. Clinical casesin three llamas (14–29 mo of age) were identifiedby characteristic microcytic, hypochromic anemia andresponsiveness to parenteral Fe (iron dextran) supple-mentation (Morinet al., 1992).These clinical signsare consistent with Fe-deficiency anemia seen in otherspecies. Serum Fe concentrations in these cases were156R.J. Van Saun / Small Ruminant Research 61 (2006) 153–164between 3.6 and 10.7 mol/l, below established refer-ence range (11–29 mol/l) for adult llamas (Smithetal., 1998).Cause of Fe deficiency in these cases wasnot determined. Iron deficiency potentially results fromeither inadequate Fe intake, typical of growing animalson milk-based diets, or due to chronic blood loss.Morinet al. (1993)induced an Fe-deficient state with clini-cal signs consistent with naturally occurring conditionusing repeated phlebotomies. A mild anemia respon-sive to Fe supplementation was attributed to severeblood loss in a 1-mo-old female llama (Smith,1989,p. 115). Anemia is a commonly reported disease inllamas and alpacas and these reports suggest the patho-genesis associated with Fe-deficiency is similar acrossspecies.2.2.2. Copper (Cu)Andrews and Cox (1997)described anemia in twollamas that was attributed to Cu deficiency. In otherruminants, Cu deficiency can induce a macrocytic,hypochromic anemia due to low ceruloplasmin activity,a Cu-dependent enzyme necessary for mobilizing andutilizing storage Fe (Underwoodand Suttle, 1999,pp.295–303). In the report ofAndrews and Cox (1997),a 14-mo-old female and 23-mo-old male llamas pre-sented with anemia and poor condition. The female wasrecumbent and the male ataxic on presentation, bothattributed to generalized weakness. Nutritional assess-ment found only plasma Cu to be abnormal. PlasmaCu concentration was 1.3 and 2.5 mol/l for the femaleand male llama, respectively. Plasma Cu concentrationsin other similarly affected llamas within this group ofanimals were 2.2 and 0.6 mol/l. These Cu concen-trations are consistent with recognized Cu deficiencyin other species and are below reported values (mean5.6, range 2.6–8.7 mol/l) for healthy llamas (Smithetal., 1998).Affected llamas were treated with a numberof therapies, including Cu supplementation. Followingtherapy, plasma Cu concentrations increased to 10.5and 13 mol/l for the female and male llamas, respec-tively, and both showed clinical improvement in theircondition.Copper deficiency is also associated with neurologicdegeneration in sheep as a result of abnormal myelinformation (Underwoodand Suttle, 1999). Palmer et al.(1980)andMorgan (1992)published reports of lla-mas showing various degrees of hind limb ataxia andparalysis and suggested Cu deficiency as a potentialcause. Two llamas reported byPalmer et al. (1980)hadserum Cu concentrations of 3.15 mol/l compared to9.44 mol/l for other unaffected animals in the group.There was no response to Cu therapy and no causewas defined. Serum Cu concentrations were differ-ent between affected and unaffected animals, but bothwere within normal range for llamas (Smithet al.,1998),questioning the potential role for Cu deficiencyin the disease process.Morgan (1992)reported on an18-mo-old alpaca with ataxia and head tremors withblood Cu concentration of 9.1 mol/l.Grace et al.(1994)reported a normal serum Cu concentration of4.2–5.9 mol/l for alpacas, suggesting this animal wasof adequate Cu status. The affected alpaca responded totreatment with Cu oxide, but other therapies were alsoadministered.Smith (1989)also reported two possiblecases of spinal cord degeneration with Cu deficiency. A5-year-old llama had hind limb ataxia that progressedto paraplegia. This llama had a blood Cu concentrationof 13.8 mol/l. A 6-mo-old llama developed ascend-ing paralysis and was found to have 5 and 0 mg/kg Cuin her liver and kidney, respectively. In comparing theCu status of these cases to current reference ranges,one would question the role of Cu in these describedneurologic conditions. Only the case of the 6-mo-oldllama would Cu status be considered deficient. Moreevidence is needed to determine if there is a role for Cudeficiency in neurologic disease of camelids, similar tothat described for sheep.2.2.3. Zinc (Zn)Potential zinc deficiency is another disease processof great concern with camelids. A non-pruritic, idio-pathic hyperkeratosis syndrome recognized in 1- to2-year-old male and female llamas and alpacas hasbeen described (Rosychuk,1994; Clauss et al., 2004).Lesions are mostly noted on hairless areas of the bodyand are characterized by a thickening of the skin withtightly adhering crusts. Histologic changes of epithelialand follicular orthokeratotic hyperkeratosis are char-acterized in the lesions (Rosychuk,1994).Althoughparakeratotic hyperkeratosis is typically associatedwith Zn deficiency (Underwoodand Suttle, 1999,pp.477–512), Zn-responsive orthokeratotic hyperkerato-sis has been recognized in other ruminants (Rosychuk,1994).Affected animals seem to respond to supple-mental Zn, in spite of receiving an adequate Zn diet,gradually over a 2- to 3-mo period.R.J. Van Saun / Small Ruminant Research 61 (2006) 153–164157Clauss et al. (2004)reported a 25% incidence ofskin lesions in a group of llamas and alpacas. Ani-mals were fed a grass hay and commercial supplementfeed containing 15.8 and 51.3 mg/kg Zn, respectively.Intakes of each feed were not reported. Mean serumZn for llamas and alpacas were 3.4 and 2.6 mol/l,respectively (Clausset al., 2004).Species means weredifferent (P = 0.02), but without individual feed intakes,interpretation of a true species difference is limited.Both Zn concentrations would be considered deficientcompared to reported values for camelids (Smithetal., 1998).Affected animals responded to 4 g Zn sup-plementation within 3 wk. All of the affected animalswere female, in contrast to observations ofRosychuk(1994).Colored fleeced animals were more suscep-tible to the problem, consistent with observations ofRosychuk (1994)andFowler (1998).Whether or notthis condition is truly a Zn-deficiency is debated, butthese new data support the hypothesis that Zn is a pri-mary factor in the disease.2.3. Vitamin deficienciesOne published report has documented a VitaminE-related muscular disease in a llama, with muscu-loskeletal lesions similar to what is seen in other species(Chauvetet al., 1996). Dart et al. (1996)characterizedblood Vitamin A concentration in llamas fed an alfalfahay diet that was considered low in Vitamin A content(0.9 mg/kg). No signs associated with Vitamin A defi-ciency were observed and adequate serum Vitamin Aconcentration was maintained. Mobilization of reserveVitamin A or lower susceptibility to Vitamin A defi-ciency might account for the observed effects. Of allnutrients, it would seem there is a significant differentbetween llamas and alpacas compared to other rumi-nants relative to Vitamin D. Llamas and alpacas seemto be highly sensitive to Vitamin D deficiency resultingin a rickets syndrome (refer to Section4.2).high a quality forage relative to requirements as wellas overfeeding of additional supplements are the pri-mary causes of obesity. Many commercial supplementsavailable in North America are touted as low energyfeeds, but fiber can be readily fermented to availableenergy sources. Deleterious effects of obesity includegreater susceptibility to heat stress, metabolic derange-ments, infertility and associated locomotive problems.To prevent obesity one has two options, eitherincrease energy expenditure or reduce energy intake.An animal’s energy requirement is primarily a func-tion of lean body weight (3.0 condition score weight)and their physiologic state (maintenance, growth, preg-nancy, lactation). Packing and other activities willincrease energy expenditure, but this is not always aviable option. Reducing energy intake is the obviousapproach. Energy dense supplements should be limited.Forage intake, quality or both need to be reduced forobese animals. Feed lower quality forages exclusivelyor prior to grazing to minimize pasture intake. Segre-gate obese animals so they cannot “steal” food fromothers. Increase stocking density or grazing intensityto reduce intake. Graze obese animals only on maturepastures. There is much individual animal variation inpropensity for obesity. Body weight or condition scoremust be routinely assessed to achieve the appropriatenutritional balance to maintain optimum condition fora given animal.3.2. Mineral and vitamin toxicityWith the exception of Cu, no other mineral orvitamin toxicity disease in llamas and alpacas werefound in the literature. Sheep are well known to beextremely sensitive to excess dietary Cu (>10 mg/kg)(NRC,1985);however, camelids do not seem to beas keenly sensitive but, are prone to toxicity (Pugh,1993b).Four studies have reported cases of Cu tox-icity in llamas and alpacas (Jungeand Thornburg,1989; Mullaney et al., 1996; Weaver et al., 1999;Carmalt et al., 2001).Clinical Cu toxicity in sheepis characterized by severe hemolysis and subsequenthemoglobinuria and hemoglobinemia (UnderwoodandSuttle, 1999).Acute massive hepatic necrosis withouthemolysis was observed in Cu toxic llamas (JungeandThornburg, 1989)and alpaca (Carmaltet al., 2001).Elevated hepatic enzymes were recognized in llama,but not alpaca, cases. Affected llamas had serum and3. Nutrient toxicity diseases3.1. ObesityObesity is considered one of the more prevalentnutritional problems in North American llamas andalpacas (Johnson,1994; Fowler, 1998).Feeding too [ Pobierz całość w formacie PDF ]