1 Introduction

Goats should consume feeds with energy and essential nutrients to cover basic functions (maintenance and normal activity) plus productive functions (growth , pregnancy and lactation), particularly in those breeds selected for milk or meat. To achieve both energy and nutritional requirements, this species adapted its feeding behavior and metabolism to harsh environments. Goats are very selective browsers/grazers, flexible, broad-scale and opportunistic feeding behavior animals (Mellado 2016), but previous personal dietary experiences, i.e., the personal information should also be taken into account (Morand-Fehr 2003). The feeding behavior also is affected by goats’ social hierarchy. Barroso et al. (2000) reported that the most aggressive goats, apparently the large sized up and horned animals, are socially in the top; and this hierarchy affect the animal production. Additionally, the usual selection of forages when they are found abundantly decreases when their availability is scarce. Even if goats use social information, observing the feeding behavior of other individuals, the personal information seems to be prioritized when both information types are in conflict (Baciadonna et al. 2013).

Essential nutrients would be water , carbohydrates, proteins (amino acids), lipids, fat-soluble vitamins (A, D, E and K) and water -soluble vitamins (B complex and vitamin C) and minerals such as macrominerals (calcium, phosphorus, magnesium, potassium, and sodium) and microminerals (e.g., cobalt, copper, iodine, iron or selenium ). Goats, as most mammals, can synthesize the needed vitamin C and thanks to ruminal and intestinal microorganisms can also synthesize vitamins K and B vitamin complex. However, when ingestion of essential nutrients is significantly lower than daily requirements for a long enough period of time, then deficiencies would occur. Nutritional and metabolic deficiencies are more commonly seen in high milk producing goats, but in kids with increased daily weight gain are also commonly at risk.

A great variety of diseases are related with energy and nutritional imbalance at digestive and other body systems exchanging animal’s homeostasis, affecting several biological and biochemical systems and presenting lesional alterations in tissues and organs. Lactational ketosis , pregnancy toxemia (PT) , fatty liver in adult’s goats and hypoglycemia/hypothermia in kids (perinatal period) are common worldwide disorders of energy metabolism . Other diseases are caused by deficiencies or excess of vitamins and minerals (e.g., hypocalcemia and hipovitaminosis B1 or hypervitaminosis A and D), some others are (also) multifactorial and are provoked, or at least related, with nutrition , e.g., urolitiasis, and ruminal acidosis . However, it is necessary to empathizes that related nutritional disorders are not limited to these previous one. Several other nutrient-related disorders can also affect goats, such as, but not exclusively, caused by poisoning plants, fertilizers, poor feed storage (e.g., Listeria monocytogenes in silages, mycotoxins and botulism) and altered gut microbiome (enterotoxemia due Clostridium perfringens toxins production).

The present chapter supposes a review of the apparently more significant nutritional and metabolic diseases encountered in raising and managing goats around the world.

2 Lactational Ketosis and Pregnancy Toxemia

Lactational ketosis and PT (also named gestational ketosis) are manifestations of hyperketonemia in goats. In fact, both diseases are related with blood β-hydroxybutyrate (BHBA) levels usually greater than 0.4 mmol/L (Albay et al. 2014; Doré et al. 2015). These metabolic disorders are provoked by energy imbalance, i.e., negative energy balance (NEB) originated when outputs (to pregnancy or lactation) overpasses intakes (inputs) with detrimental energy flux. Lactational ketosis takes place in early post-partum and is normally related with high milk producing goats and more rarely with low-producing goats. In cows , it is considered a “production disease” with high prevalence in the first month of lactation. However, prevalence data are scarcely reported in goats, but probably a similar pattern to cows occurs (Zobel et al. 2015). PT, or the “twinning disease”, develops ante-partum, in the last 2–6 weeks of pregnancy due to enormous energy demands of fetuses (Edmondson et al. 2012). The prevalence of PT varies, according to farms and regions, from 1–4% to 40–60%, reaching a mortality  >80%, in both does and fetuses, even when a cesarean section is made as treatment (Andrews 1997; Rook 2000; Bousquet 2005; Ismail et al. 2008; Lima et al. 2012).

Ante- and post-partum hyperketonemia can represent a major nutritional and metabolic problem in goat production relating subclinical and clinical forms of the disease with milk production (Zobel et al. 2015) and animal losses, even in low-producing does. Commun clinical signs of lactational and gestational ketosis are reduced activity levels, ataxia, teeth grinding and anorexia (Brozos et al. 2011; Lima et al. 2016). In PT, anorexia with absence of ruminal motility and recumbency was even suggested as poor prognostic indicators in goats (Lima et al. 2016). Moreover, hyperketonemia also provokes immunity and inflammatory alterations with decreasing immunoglobulins serum levels of IgG, IgM and IgA (Hefnawy et al. 2010) and lymphocytes (Hefnawy et al. 2011), and increasing haptoglobins (González et al. 2011). Consequently, hyperketonemia can have a significant adverse influence in the general health and welfare of does.

2.1 Energy Metabolism and Hyperketonemia in Does

It is know that goats are well adapted to arid and semiarid environments, and show an appreciable feeding selectivity, choosing the best available forages when grazing (Mellado 2016) and consuming feed until approximately 5–6% (DM/daily) of BW. The daily DM intake increases progressively until the 2nd month of lactation, always after the lactation peak, and progressively decreases until the next kidding mainly due to the compression of the gravid uterus to the rumen. Consequently, during the first two months of lactation, energy requirements due to milk production are higher than the energy input, and lipolysis (glucagon-mediated) occurs trying to compensate this disbalance. The loss of body condition score (BCS) is a natural consequence of this process. In a subsequent lactation phase, when the input surpasses the lactational output of energy, lipogenesis (insulin-mediated) takes place with BCS improvement. Normally, this process stop at the last month of gestation, in this last case due to fetus energy requirements. At this time a new NEB occurs and will be prolonged during early lactation phase.

Briefly, during NEB, an intense adipose tissue (triacylglycerols storage) mobilization provides high plasmatic levels of nonesterified fatty acids (NEFA) from triacylglycerol hydroxylation and are transported into liver. In the hepatocyte mitochondrial apparatus, NEFA are metabolized (ketogenesis) into three types of ketones: acetone, acetoacetate and BHBA. These ketones are a source of energy, as acetyl-Coenzyme A precursor (after Acyl group combination with the limiting factor: coenzyme A), mainly in mitochondria of skeletal muscles, mammary gland (including ketone transformation to fatty acids ), heart and kidneys (Heitmann et al. 1987) with acid lactic production (causing metabolic acidosis). In normal conditions, and in pregnant and non-pregnant ruminants, all ketones are also significantly produced and absorbed from rumen to body. So, hyperketonemia occurs when the NEFA mobilization and their hepatic metabolism reach significant high levels, normally accomplished some degree of hepatic steatosis also denominated hepatic lipidosis or fatty liver disease (Fig. 11.1).

Fig. 11.1
figure 1

Fatty liver with enlargement of the organ (hepatomegalia) and signs of rib’s compression. Typical finding at post-mortem examination in a goat died from pregnancy toxemia (provided by the authors)

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Hepatic lipidosis is due to slow exportation of lipoproteins from hepatocyte membrane to blood in ruminants (Kleppe et al. 1988), although can also be caused by cobalt or vitamins E and B12 (cyanocobalamin) deficiencies (Johnson et al. 2004; Radostits et al. 2007). In consequence, a diffuse accumulation of lipids in hepatocytes occurs. This assumes special importance during a great lipid mobilization, when lipoprotein export limitation is more obvious. This lipidosis was associated with a decrease of hepatic metabolic functions (Bobe et al. 2004). When hepatic fat concentrations reach >35% of liver weight, a poor prognosis can be established, at least in dairy cows (Herdt 1988).

2.2 Pregnancy Toxemia

PT occurs during last 4–6 weeks of pregnancy. Multiparous does with high (≥4) or low (≤2) BCS and multiples fetuses (twins, triplets, …) are considered more susceptives (Chartier 2009; Brozos et al. 2011).

A low DM/energy intake associated with a quickly fetuses growth , reaching 60–80% of total live BW during last weeks of gestation are the main etiological factor. In fact, 30–40% of glucose apported by the dam during this period is consumated by fetuses, and it is know that the fetuses have energy flux priority. At this time, pregnancies with two or more fetuses increase energy requirements until 180 and 240% of a single fetus, respectively (Ermilio and Smith 2011).

Several other risk factors are the environment, such as ventilation, thermal amplitude and poor litter box, as well as lack of exercise and stress (Chartier 2009). Additionally, during this period, hormonal alterations such as the decrease of insulin serum levels, due to an improvement of steroid hormones (gestation) and glucagon, also stimulates ketogenesis (Vernon et al. 1981; Sensenig et al. 1985).

Primary PT is related with poor quality of forages or poor nutritional management (e.g., abrupt feed changes) whereas any disease provoking a decrease of DM or energy intake causes a secondary PT (Radostits et al. 2007). High BCS seems to lead to intra-abdominal pressure due to physical presence of abdominal adipocytes reducing the rumen volume (Morand-Fehr 2005). In does with low BCS, the few body fat reserves are quickly mobilized entraining an extreme condition of subnutrition.

Blood levels of BHBA are used to improve the subclinical and clinical PT diagnosis and management . However, BHBA threshold to confirm PT is not well defined and values between 0.8 and 1.7 mmol/L have been reported (Trevisi et al. 2005; Ismail et al. 2008; Brozos et al. 2011; Sadjadian et al. 2013; Pichler et al. 2014; Zobel et al. 2015). In an attempt to minimize this problem, Doré et al. (2015) proposed a dynamic scale predicting the PT according to each one of last five weeks; in the 5th, 4th, 3rd, 2nd and 1st week ante-partum, the threshold value was 0.4, 0.4, 0.5, 0.6 and 0.9 mmol/L, respectively; but the values of sensitivity (61.8–73.7%) and specificity (58.4–89.7%) of this classifications were considered low. Zobel et al. (2015) suggested a cut-off of 1.7 mmol/L to define PT and lactational ketosis . Additionally, glucose tissue intolerance is well documented in some goats affected by PT (Lima et al. 2016), which present hyperglycemia but whose occurence remains poorly understood. Even blood glycose concentration can be used, together with BHBA level, at farm level for PT and lactational ketosis control, although theses levels represent a handicap for individual treatment of does. Further research is needed to refine this metabolic query.

2.3 Lactational and Gestational Ketosis Prevention

The prevention of both diseases are related with the minimization of risk factors reported above.

Special attention should be given to treatment and prevention of general diseases (e.g., footrot, parasitism , pneumonia, etc.) (Rook 2000). Stress minimization improving adequate facilities and welfare are two other significant aspects to take in account. However, the crucial steps are related with ante- and post-partum nutritional management (Zobel et al. 2015). Feed should apport adequate energy and nutrients, under a controlled intraruminal environment, supervising significant decrease of pH, i.e., minimizing ruminal acidosis by adequate carbohydrate/fiber ratio intake.

The BCS evaluation, which must be improved during the second half of lactation at adequate levels, between 3 and 4 score points. Finally, both PT and lactational ketosis can be dynamically monitored ante- and post-partum using serum levels of BHBA as a tool (Doré et al. 2015; Zobel et al. 2015).

3 Hypocalcemia

Hypocalcemia is a mineral disorder with particularities between domestic ruminants. It is assumed that hypocalcemia occurs due to Ca demands, higher that it can be replaced in blood and interstitial fluids (Goff et al. 2014). According Wilkens et al. (2012, 2014), goats show efficient adaptation to Ca dietary restriction.

In goats, the total Ca levels in blood serum varies from 8.9 to 11.7 mg/dL (2.2–2.9 mmol/L) (Kaneko et al. 1997), and the cation Ca2+ form is the diffusive portion to tissues (blood acid-base balance can affect Ca2+ levels). Hypocalcemia occurs below this normal range and can present both subclinical and clinical forms. The first symptoms occur at blood serum Ca levels reach 6 mg/dL, but can decrease until 2 mg/dL, or even less, before doe reach death (Yamagishi et al. 1999). Ataxia and recumbence are two major clinical signs of hypocalcemia , other than all consequences provoked by skeletal, cardiac and smooth muscle cells relaxation (Fig. 11.2).

Fig. 11.2
figure 2

Clinical form of hypocalcemia in a peri-parturient multiparous goat. Note the sagging udder in an old high milk producing goat (provided by the authors)

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Similar to cows , and inversely to ewes (Oetzel 1988), with milk yield increases in high-producing goats , hypocalcemia (milk fever) is developed during early lactation. In fact, during lactation a significant flux of Ca arises from blood to milk (DeGaris and Lean 2008) and milk contents high Ca concentration, approximately 130 mg/dL (32.5 mmol/L) (Bar1owska et al. 2011). However, hypocalcemia can also occurs ante-partum in goats, due to high fetuses Ca requirements (Härter et al. 2017), especially from 80 days of pregnancy onward when maternal body Ca reserves, mainly in bones, are transferred for fetal development and colostrum production (Härter et al. 2015). During pregnancy, Härter et al. (2017) estimated 60.4 mg/kg daily net requirements of Ca for maintenance in goats.

The Ca homeostasis is regulated by hormonal ambience (the serum Ca level is increased by parathormone and decreased by calcitonin) but calcitriol (11,25-(OH)2D3), the active form of vitamin D, assumes an important role. İn fact, dietary Ca restriction (0.22% Ca in DM) increases plasma concentrations of endogenous calcitriol, which, in turn, improves intestinal absorption of Ca in goats, but without renal excretion exchangement (Wilkens et al. 2012; Herm et al. 2015). Moreover, calcitriol also is related with Ca mobilization from bone in early lactation (Wilkens et al. 2014). Herm et al. (2015) suggested that the higher calcitriol production in goats than in ewes can justify the greater ability to regulate Ca homeostasis observed in goats. Calcitriol also improves milk excretion by mammary epithelium when sufficient intracellular glucose is available (Sun et al. 2016).

Goats can efficiency adapt to dietary anion–cation balance, namely in presence of anionic diets that causes metabolic acidosis, which increases the rate of intestinal Ca absorption and a greater bone resorption rate (Liesegang et al. 2006; Liesegang 2008), but without blood Ca levels improvement.

4 Obstructive Urolithiasis

Obstructive urolithiasis is a common disorder in goats (Amarpal Kinjavdekar et al. 2013), as well as in other ruminant species, originated by cristaloid calculi formation which develops from an initial organic matrix (e.g., proteins and cells) followed by mineral deposition in the urinary tract (Osborne et al. 1985). The most frequent uroliths in goats are composed by struvite (ammonium magnesium phosphate) and silicate, followed by apatite (calcium phosphate), calcium carbonate and calcium oxalate (Gutiérrez et al. 2000; George et al. 2007; Makhdoomi and Gazi 2013), and can be found in renal pelvis, bladder and uretra (Ewoldt et al. 2006) (Fig. 11.3).

Fig. 11.3
figure 3

Hidronefrosis (a) in a goat died from urinary obstruction (struvite calculi). Urianalysis (b) at microscope (×40) showing a cluster of struvite crystals in another goat with a disbalanced diet in favor of concentrate (provided by the authors)

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The urethral obstruction caused by calculi, which can be partial in small ruminants (Makhdoomi and Gazi 2013), is mainly observed in males due to the long and sinuous traject of urethra. The urethral obstruction mainly occurs in distal loop of penial sigmoid flexure, but also can be located in proximal loop and urethral process. Crystals can be observed in the prepuce hairs of some males in those farms with urolithiasis problems. Affected goats present anorexia, bloat, pain (false colic), dysuria/stranguria, restlessness and progressive ventral abdominal distention due to urine infiltration, and uremic odor when urethral rupture occurs. The rupture of urethra always needs a surgical correction which intents to open a new via for urine excretion (Van Metre and Fubini 2006).

The etiology of obstructive urolithiasis is multifactorial, even diet assumes a main role, and varies according to the system production, region and season (Nwaokorie et al. 2015), and physiologic/health status of animals. Struvite (pH: 7.2–8.8), calcium carbonate and calcium phosphate (pH: 6.6–7.8), are developed very well under alkaline urine ambience and mineral supersaturation (Jacobs et al. 2001; Straub et al. 2005; Jones et al. 2009). Table 11.1 reports the main factors involved in calculi formation.

Table 11.1 Main risk factors involved in urolitiasis occurrence in goats and sheeps
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The prevention includes the elimination or minimization of risk factors according to the respective calculi type (Ewoldt et al. 2006). The Ca:P ratio should be 2–2.5:1, and Mg should be limited to 0.2–0.6% of DM (phosphatic magnesium-based calculi). Water intake should be increased (3–5% of DM) to promote diuresis and consequently crystals elimination. Acidification of urine at pH 5.5–6.5 range can be achieved using anionic salts (e.g., sodium chloride, calcium chloride or ammonium chloride) provoking dissolution of alkaline uroliths. However, these salts can decrease the feed palatability and, thus, acidificants can present inconsistent efficacy. Jones et al. (2009) suggested a target DCAD of 0 mg/kg in DM. The ammonium chloride can be preventively added to diet at low levels (0.5–1% of DM) to prevent the feed unpalatably.

Both water intake improvement (sodium chloride) and urine acidification (ammonium chloride) procedures are also used at farm level to treat all animals when alkaline uroliths occur. In unsurveilled urine pH individuals, uretral rupture in fast grown males (high DM intake) are an indicator of urolitiasis problem in the herd. However, Freeman et al. (2010) suggested that urolithogenic crystals by microscopic observation is an easy test to predict uroliths formation.

5 Polioencephalomalacia

Polioencephalomalacia is a metabolic disorder associated with thiamine deficiency in both adults and young ruminants including goats (Thomas et al. 1987; Lima et al. 2005; Chigerwe and Aleman 2016). Thiamine or vitamin B1 is a cofactor in the metabolism of carbohydrates necessary for their supply to the neurons in the brain as exclusive source of energy (Kevelam et al. 2013). Consequently, alterations following the death of nerve cells occur promoting a cerebrocortical necrosis, the synonymous denomination of polioencephalomalacia (Gould 1998). However, the specific biochemical mechanisms of these degenerative lesions are not well understood. Interactions between sulfur based metabolism and reduced activity of thiamine pyrophosphate, the active form of thiamine, seem to play a major role (Olkowski 1997; Amat et al. 2013a, b).

Thiamine is synthesized by ruminal bacteria in normal conditions (Alves de Oliveira et al. 1996). Alterations in ruminal fauna reduce the production of thiamine, accelerate the thiamine degradation or inactivation leading to a lack of absorption of this vitamin. Thiamine degradation occurs by Thiaminase I enzymatic catabolism (Kraft et al. 2014). Thiaminase II seems not have a significant role, but it is under reappraisal by some researchers (Murata 1982; Amat et al. 2013b). Thiaminase I can be produced by bacteria (e.g., Bacillus spp. and C. sporogenes) (Brent and Bartley 1984; Cebra and Cebra 2004), whose population increases in rumen when goats ingest highly digestible carbohydrates and low roughage, provoking subclinical or clinical ruminal acidosis with dysbiosis in ruminal flora and fauna. Thiaminases I (and II) replace the thiazole moiety by organic nucleophiles (Costello et al. 1996; Toms et al. 2005). In dependence of a cofactor (cosubstrates present in ruminal fluid, e.g., proline, pyridoxine and imidazol), thiaminase I produces thiamine analogues which inhibe thiamine dependent reactions. Levamisole and promazines substances seem to act as cofactor under specific ruminal conditions (Cebra and Cebra 2004; Amat et al. 2013a, b). Treatment (Vitamin B1 and corticosteroids) can be effective in early phases and polioencephalomalacia prevention is related with elimination or control of main causes of non absorption of vitamin B1.

6 Hypomagnesemia

Adult’s goats, mainly when grazing growing pastures (less Mg contents), in final Winter/Spring, or when fertilized (high levels of potassium and nitrogen) or also in kids with fast growth fed with milk replacers can develop hypomagnesemia (blood Mg levels <1.1 mg/dL; <0.6 mmol/L). The lack of Mg exchanges neuromuscular transmission and, consequently, the muscle excitability. Goats show mainly periodic tetanic contractions and convulsions, especially when stimulated, leading to death during one of these episodes (Stelletta et al. 2008).

Mg is mainly absorbed in rumen and any cause decreasing persistently its absorption or the high milk production, increase hypomagnesemia incidence. So, this disorder was also called grass tetany, stall tetany, lactation tetany, milk tetany or transport tetany. Prevention is based in (unpalatable) Mg salts (e.g., magnesium oxide) dietary supplementation until 0.6% of DM, mainly during risk periods (Martens and Schweigel 2000; Stelletta et al. 2008).

7 Selenium and Vitamin E Deficiencies

Selenium and vitamin E deficiencies cause a nutritional/metabolic disease named white muscle disease or nutritional muscular dystrophy, which mainly affects to kids with fast growth in arid and semiarid regions, where soil/forage present low levels of the mineral/vitamin. In goats presenting this disorder, serum values of Se and Vitamin E are under 0.08 mg/L (0.9 mmol/L) and 1.0 mg/L, respectively (Bickhardt et al. 1999; McComb et al. 2010), and are due to low intact of both nutrients. Se and Vitamina E are responsive for antioxidant processes in tissues, limiting muscular skeletal and cardiac dystrophy (Fig. 11.4), and promoting integrity and production of muscle fibers. Kids appears to be more sensitive than lambs to vitamin E deficiency under low SE intake ambiance (Liesegang et al. 2008), and both nutrients improve immune status (Malá et al. 2009; Shokrollahi et al. 2013).

Fig. 11.4
figure 4

Mascrocopic aspect of a young male kid’s heart affected by nutritional muscular dystrophy showing typical pale and discolorated areas. The kid suffered sudden death after moderate exercise (provided by the authors)

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Se supplementation (combinated with iodine) can improve kids ’ growth and inclusive Se (Aghwan et al. 2016) and NEFA (Aghwan et al. 2014) meat concentration (source for human population), but selenosis risk should be avoided. A positive effect of Se and vitamin E on milk yield and composition in lactating goats has also been reported (Tufarelli and Laudadio 2011). Moreover, Se supplementation seems to improve the fetal development in pregnant goats (Sevcikova et al. 2011) and also affects spermatogens in young bucks (Ganabadi et al. 2010).

A major question regarding Se and Vit. E management in farms would be that the supplementation of these nutrients are more valuable in Se deficient areas, i.e., the response to dietary supplementation is more significant when goats are in effective Se homeostatic unbalancement; and can vitamin E interact with Se more deeply in Se deficiency environment. Some studies supporting this hypothesis has been reported (Sánchez et al. 2007; Liesegang et al. 2008).

Regarding all aspects reported above, these trace elements joint to l vitamin E play an important role in the normal metabolism of kids and goats, not only promote their welfare and resistance to disease, but also can contribute for an adequate production performance.

8 Production Diseases in High-Producing Dairy Goat

Under pastoralism , the ruminal pH fluid in low-producing dairy goats is usually higher than 6 due to low concentrate/fiber ratio in feed intake . So, subacute ruminal acidosis and low milk fat syndrome are not expected to occur in these goats. However, the increase in milk yield production is because of genetic selection programs that needs to be accomplished with nutrients and energy intakes, not only to maximize lactation potential, but also to minimize lactational ketosis and hepatic lipidosis. This can be achieved improving the density energy in terms of DM, i.e., increasing the concentrate/fiber ratio (1.5; 60% concentrate) in diet.

A major problem of this nutritional management is the decrease of ruminal pH for levels <5.8 for longer than 5–6 h per day, i.e., subacute ruminal acidosis (Jia et al. 2014; Huo et al. 2014), which alters local fauna (Liu et al. 2015), volatile fatty acid production (Huo et al. 2013; Liu et al. 2015), local bacterial digestion with toxic protein formation, e.g., histidine (Hollmann et al. 2013), as well as chemical (pH) inflammation of rumen wall (rumenitis). This process is very well know in dairy cows and is related with ruminal parakeratosis (ruminal papillae atrophy), laminitis, liver abscesses and pulmonary bacterial emboli (superior vena cava syndrome), as well as ketosis (in a more advanced phase) and low milk fat syndrome (Kleen et al. 2013; Abdela 2016).

On one hand, diets with high carbohydrates content (energy) are needed to cover lactational requirements, avoiding ketosis and its consequences. On the other hand, these high energetic density diets can provoke disorders previously reported. To achieve a balance of these two sides, several procedures should be taken into account also regarding feed management practices, e.g., grouping goats by production level, improving fresh diet accessibility, using total mixed ration (minimizing feed selectivity behavior ) or pelleted diets (due to goat selectivity for small particle size).

Low milk fat syndrome is classically related with ruminal acidosis and volatile fatty acid profile alteration, i.e., ↑propionate:↓acetate:↓butyrate ratio (Bauman and Griinari 2003; Urrutia and Harvatine 2017). In fact, ruminal acidosis decreases fat and protein milk contents at long-term in goats (Dong et al. 2013). Even, the etiopathophysiology of this syndrome remains poor understandable. Ruminal biohydroxigenation of polyunsaturated fatty acids to intermediate fatty acids , e.g., at least trans-10 and Cis-12 conjugated linoleic acids (Ventto et al. 2017), seems to play a significant role. In goats, this conjugated linoleic acids methyl esters seems to be dose-effect dependent in reduction of milk fat secretion (Fernandes et al. 2014) but improving energy balance (Baldin et al. 2014). However, probably the regulation of fat synthesis in mammary gland is also involved in the low milk fat syndrome occurence (Suárez-Vega et al. 2017; Ventto et al. 2017).

No effective prevention has been found until today to limit conjugated linoleic acids methyl esters produced in rumen, keeping the production levels. Best practices for nutritional, feed and health managements evaluating feed intakes, milk yield and contents, BCS, metabolic profiles, ruminal and urinary pH and the health status of individuals are strongly recommended.

9 Concluding Remarks

Nutritional and metabolic disorders are closely related modifying the homeostasis with negative impact in production, reproduction , health and welfare of goats. These animals are exceptional selective browsers/grazers, which allow the best use of biomass and nutrients intake in harsh environments. In these conditions, the plants diversity seems to be the best option to minimize the potential lack of energy, mineral and vitamins. As prevention of nutritional deficiencies, diet should be supplemented regarding epidemiology disorders in each region of the world.

Goat genetic improvement for milk yield and composition need to be complemented by nutritional and feed management programs. Similar to dairy cows , but with several particularities mainly related with feeding behavior, metabolism and diseases’ ethiophisiopathology, goats present several disorders called “production diseases ”. Even a major factor can be originally involved, the interrelationship of several body systems, which can be affected by several risk factors. Consequently, a holistic approach is needed to control or even prevent nutritional and metabolic disorders.