Gastrointestinal tract diseases interfering with the nutrients absorption and reducing feed conversion in pigs

Taking into account the growing competition for feed resources connected among others with the decline in arable land in many traditionally important agricultural regions, and rapid expanding of other groups of feed consumers: human food complex, poultry sector, biofuels sector, etc., it is necessary to make swine industry more efficient and competitive in the global protein production sector.

Improvement of feed conversion rate (FCR) in farm animals covers a broad range of scientific disciplines including: nutrition, genetics, veterinary medicine, physiology, feed processing, technology of animal production, welfare, management and many others.

It is well accepted that the health of animal has a significant influence on feed efficiency and FCR, however, in reality is not easy to quantify.

Considering continuously increasing costs of pork production, the feed conversion rate has a major impact on the economic efficiency in production of fatteners. This parameter is related with a significant number of different factors.

Two important processes are: proper digestion of nutrients and optimal absorption of them. These two processes are the results of different biochemical events and physiological status of the gut.

Variety of diseases, most of all infectious ones, may affect digestion and significantly disrupt absorption of nutrients. Several pathogens (E.coli, Lawsonia (L). intracellularis, Clostridium (C) perfringens, Brachyspira (B). hyodysenteriae, swine salmonellosis, rotaviruses, coccidia, etc.), influence not only the average daily feed intake (ADFI), and the average daily gain (ADG) but first of all the FCR.

Infections of the gastrointestinal tract by bacteria, viruses or parasites may modify conditions in the intestinal lumen that favor growth of some enteric bacteria. Excessive amount of undigested carbohydrates and proteins in the intestine leads to weaker absorption of these compounds. Parasitic infections can also cause damage to the intestinal mucosa, and lead to an increase for example on C. perfringens load concentration of their toxin in intestine. For example coccidia multiplying in the cryptic glands lead to inhibition of epithelial regeneration and cause damage to villi. In addition, increased mucus production stimulated by coccidia also promotes the growth of enteric bacteria (Collier et al., 2008).

Caused by pathogenic bacteria, viruses and parasites disturbances are connected with destroying of villi and microvilli. Finger like villi covered mucosal surface of the small intestine increase the intestinal surface area by 10-14 fold compared with a flat surface of equal size (Cunningham and Klein, 2007). The villi themselves are covered with a brush-like surface membrane known as the brush border. These are composed of sub microscopic microvilli that additionally enlarge the surface area. The epithelial cells covering the villi are called enterocytes. Playing an important role, crypts of Lieberkuehn are tubular depressions found between the villi. Crypts are the source of new cells that migrate to the villi. A significant portion of the digestive and all of the absorptive capacity of the small intestine occurs near and around of the villi and crypts. The marked changes that may occur in the gut structure, after colonization of small intestine by enteric bacteria, such as villus atrophy and crypt hyperplasia, are generally associated with the poor performance observed as they are thought to cause a temporary decrease in digestive and absorptive capacity of the small intestines (Pluske et al., 1996a, Pluske et al., 1996b). It should be underlined that the aetiology of these changes is multifactorial and their relationships to production parameters are not fully clear.

The aim of the paper is to present most often diseases of swine which may influence both the morphological structure and the digestive and absorptive capabilities of the gastrointestinal tract. Due to the fact that the role of E.coli is most prevalent and most often discusses enteric bacteria having profound influence on presented changes in small intestines and decrease FCR during weaning period, this will not be part of this paper. Other diseases affecting the gastro-intestinal tract and affecting negatively the FCR are: coccidiosis, proliferative enteropathies, swine dysentery, intestinal spirochetossis, swine salmonellosis, rotaviral infections, etc.

Important diseases of gastro-intestinal tract influencing significantly the FCR

Coccidiosis

Coccidia (Isospora suis and Eimeria spp.) are obligatory intracellular protozoan parasites. The number of species of intestinal coccidian that infect pigs is unknown because most of them are known only from the sporulated oocyst stage (Aliaga-Leyton et al., 2011, Lindsay and Dubey, 2006). Clinical signs of coccidiosis occur in nursing piglets between 7 and 11 days of age. Yellowish to grayish diarrhea is the major clinical sign of the disease. The feces are initially loose or pasty and become more watery as the disease progresses. The sick piglets usually continue to nurse, developed a rough hair coat, become dehydrated and have reduced weight gain. Not all piglets in the litter are equally affected (Aliaga-Leyton et al., 2011, Lindsay and Dubey, 2006). Morbidity is high but mortalities are usually moderate in uncomplicated cases. Destructive action of Coccidia on intestinal epithelium results in shortened intestinal villi and atrophy of epithelium. Diarrhea in suckling piglets 7-14 days of age that do not respond to antibiotic treatment are suggestive of Coccidia infection. Other pathogens like enteropathogenic E.coli, TGE, RV, C. perfringens type C should be considered in differential diagnosis (Aliaga-Leyton et al., 2011, Lindsay and Dubey, 2006). Diagnosis is best achieved by finding coccidian oocysts in the feces of clinically affected piglets. Individual dosing of anticoccidials (i.e. Baycox) is the best way to ensure that each piglet gets a proper dose of the drug.

Swine dysentery

Swine Dysentery (SD) is a mucohemorrhagic colitis affecting pigs mainly during grow-finish period. SD has been reported worldwide and it may cause significant economic loss. The etiologic agent of SD is Brachyspira hyodysenteriae. Virulence attributes of B. hyodysenteriae are likely to consist of a set of virulence factors involved in initial colonization of large intestine and factors that are required to produce lesions. It has been proposed that chemotaxis, NADH oxidase activity and motility in porcine mucus is important in efficient colonization. The haemolytic activity of this pathogen is associated with its virulence, and the hemolysin is probably the most important virulence factor (Hampson et al., 2006).

SD is known to have a worldwide distribution, although the occurrence of disease varies in different parts of the world and changes with time. In economically developed agricultural countries it occurs sporadically (change of rearing system, multi-stage production, early weaning) but in some countries SD is responsible for economic losses reaching 25% mainly due to retarded weight gains (Hampson et al., 2006).

SD is most commonly observed in grower and finisher pigs. The infection can be also observed in weaners and adult pigs (i.e. sows) and occasionally in suckling piglets. On endemically infected farms clinical signs of SD may be observed in a cyclic manner. The symptoms of the disease may reappear at 3-4 weeks interval. During outbreaks of SD, morbidity in weaners may approach 90% and mortality may be around 30% (depending on treatment). In chronically infected herds the severity may be mild and disease may not be clinically evident (Hampson et al., 2006).

The pathogenesis of SD is quite complex and not completely explained to date. Pigs become infected with SD following ingestion of feces containing B. hyodysenteriae. Under experimental conditions 105 colony-forming units (cfu) are sufficient to produce clinical infection. Although the mechanism of tissue damage during SD has not been fully clarified, the hemolysin(s) and lipooligosaccharides (LOS) may play a main role. B. hyodysenteriae does not invade beyond the lamina propria of the large intestine. The entire pathogenesis of SD is directly connected with large intestine lesions. The systemic signs of SD are the results of fluid and electrolyte imbalance induced by enteritis. The diarrhea observed in sick pigs is a result of colonic malabsorption as a consequence of the failure of the epithelial transport mechanisms to actively transport sodium and chloride ions from lumen to blood. The first clinical sign of SD is usually soft, yellow to grey feces. Next the large amounts of mucus and often flecks of blood are observed in feces. Most of the pigs recover over a period of several weeks; however their growth rate remains reduced. The main pathological lesions observed in pigs with SD catarrhal are haemorrhagic inflammation of large intestines mucosa and presence of blood (streaks) within intestinal lumen (Hampson et al., 2006).

The control of the disease includes metaphylaxis, therapy (tiamulin) and depopulation. The role of immunoprophylaxis is questionable (Hampson et al., 2006).

Proliferative enteropathies (pe, adenomatosis ileitis)

Proliferative enteropathies are a group of acute and chronic conditions of widely differing clinical signs but with similar lesions observed at necropsy: a thickening of the mucosa of the small intestine and colon. The affected tissues show proliferation of immature epithelial cells of the crypts, forming a hyperplastic to adenoma-like mucosa. The chronic, subclinical and acute hemorrhagic forms of PE are now important enteric diseases in regions with modern pig industry (Collins 2013, McOrist and Gebhart, 1999).

Aetiological factor of PE is Lawsonia intracellularis, Gram-negative microorganisms that multiply intracellularly in cytoplasm of intestinal epithelial cells. The growth of L. intracellularis is always accompanied by localized proliferation of infected immature crypt epithelial cells. Lesions in the small intestines block absorption of vital feed nutrients. In vitro culture of L. intracellularis requires co-culture on transformed cell line such as intestinal epithelial cells, in micro-aerobic atmosphere (Collins 2013, McOrist and Gebhart, 1999).

The 3 forms of ileitis infection have been proposed: acute (sudden deaths and acute bleeding disease – vaccine improving this problem), Chronic ileitis –PE-(diarrhea and weight loss) and subclinical ileitis (loss of production due to gut damage, but without obvious diarrhea or weight loss). PE develops initially as a progressive proliferation of immature epithelial cells occupied by numerous intracellular bacteria. The mechanism whereby L. intracellularis cause infected cells to fail mature is not yet clear. Loss of body protein and amino acids into the intestinal lumen and the reduced nutrient absorption by the intestinal mucosa lacking mature enterocytes are the likely causes of the reduction in weight gain and feed conversion efficiency seen in animals affected with chronic form of PE (Collins 2013, McOrist and Gebhart, 1999). Macrolides, lincosamides and pleuromutilins are the most effective antibiotics for PE treatment. The preferred antibiotics would be tiamulin or tylosin for 14 days in adequate dose to affected and contact pigs. Controlled field trials suggest that in controlling of PE the best results are observed when antibiotics are given just prior to the peak period of infection (strategic medication). It has been also proven that immunoprophylaxis with an attenuated live vaccine is an effective tool in reducing the economic loss due to infection (McOrist and Gebhart, 1999).

Intestinal spirochetosis

Intestinal spirochetosis (IS) also known as porcine colonic spirochetosis is a colitis that occurs mainly in weaner and grower pigs. The etiological agent of IS is a weak haemolytic anaerobic spirochete Brachyspira pilosicoli (Hampson and Duhamel, 2006). An analysis of risk factors revealed that reduced prevalences can result from using non-pelleted diets with reduced energy and protein content. Infection with this pathogen usually causes a mild to moderate typhlocolitis accompanied with watery diarrhea and stools with the consistency of “wet cement”. Based on the severity of the infection and the extent of the colonic damage, affected pigs display variable loss of condition and reduced growth rate (diversity of weights among fatteners) (Hampson and Duhamel, 2006). Diarrhea is usually self-limiting and lasts between 2 and 14 days, although some animals may relapse and again develop clinical signs after convalescence or treatment. Pathological lesions are limited to the large intestines (colon and caecum), colonal mucosa is thickened and covered with mucus. Blood is not present in faeces. The clinical signs of IS are difficult to differentiate from those associated with the proliferative enteropathy caused by Lawsonia intracellularis. In differential diagnosis of IS the following infections should also be considered: salmonellosis, postweaning colibacillosis, swine dysentery, yersiniosis and trichuriasis (Hampson and Duhamel, 2006).

Non effective vaccines have been developed to date. Implementation of antibiotic therapy can reduce B. pilosicoli infection and maximize productivity. Chemotherapeutics useful for the treatment of ileitis and dysentery are also effective against IS, however the potential for an emergence of resistant strains has become an international concern (Hampson and Duhamel, 2006).

Swine salmonellosis

The most common cause of salmonellosis in swine is host-adapted S. choleresuis and it is usually manifested as septicaemia. S. typhimurium is responsible for most of the remaining cases of salmonellosis in pigs which are usually manifested as enterocolitis. This serotype is not host-specific. Most salmonellosis outbreaks occur in intensively reared weaned pigs. The disease occurs worldwide but varies in prevalence, morbidity and mortality (Anderson et al., 2000, Boyen et al., 2006, Griffith et al., 2006).

In general, the source of salmonellae virulent for pigs is most likely to the other swine or environments contaminated by infected pigs. A vertical transmission also occurs. Because of dynamic relationship between salmonellae, environment and the host, and because infection is not always connected with the disease, ultimate statements regarding transmission, shedding and carrier states are apt to be misinterpreted (Anderson et al., 2000, Boyen et al., 2006, Griffith et al., 2006). The most frequent clinical signs of swine salmonellosis are due to septicaemia or to enterocolitis. Pigs surviving acute septicaemia may develop clinical signs of pneumonia, hepatitis, enterocolitis, meningoencephalitis. Pigs initially suffering from enterocolitis may develop chronic wasting disease or rectal stricture (Anderson et al., 2000, Brumme et al., 2007, Griffith et al., 2006).

Salmonella manifested as enterocolitis is most frequent in pigs from weaning to about 4-5 months of age. The most frequent serotypes diagnosed in the cases of enterocolitis are S. typhimurium and S. choleraesuis. The first clinical sign is watery yellow diarrhea without mucus and blood. Sick pigs are febrile, dehydrated and have reduced feed intake. Mortality usually is low, presumably as the result of hypokalemia and dehydration. Shedding of the pathogen may persist for months. The major lesion observed in intestine is focal or diffuse necrotic enteritis, colitis or typhlitis. The considerably enlarged mesenteric lymph nodes are also observed. Colon and cecal contents are bile stained and scant. The gross lesions may be present also in the descending colon and rectum (Brumme et al., 2007, Griffith et al., 2006). Salmonellosis may be differentiated from dysentery based on the localization of lesions and bacteriological examination.

Rotaviral infections

Rotaviruses (RV) are important causes of diarrheal disease and a common cause of gastroenteritis in sucking and post-weaning pigs. Based on VP6 antigens RV are classified into seven groups (A-G). Groups A-C infect humans and other animals; group E has only been detected in pigs in UK, groups D, F, G have been found only in avian species. Rotaviruses are ubiquitous in the environment and in swine herds. Multiple RV serogroups (A-C, E) and multiple serotypes within serogroups A and C have been found in pigs.

Rotavirus pathogenesis is complex and diarrhea induction involves several mechanisms. Maladsorption caused by loss of intestinal absorptive cells resulting from villous atrophy is the most probable mechanism of RV-induced diarrhea in pigs as well as in humans. RV replicates mainly in the cytoplasm of small intestinal villous epithelial cells and in cecal or colonic epithelial cells, most intensively in the jejunum and ileum of small intestine. Rotavirus replication results in cell lysis and attendant villous blunting and atrophy.

Naturally occurring RV diarrhea is usually less severe than experimental disease due to impact of maternal immunity. Because RV infection is endemic in many herds gilts and sows have immunity to RV which is passed to their piglets. Diarrhea in piglets occurs when the oral dose of RV exceeds a protective level of lactogenic immunity. Uncomplicated RV diarrhea in suckling pigs resolves in 2- days. Feces are yellow or white, watery-to-creamy, variably flocculant. Morbidity does not exceed 20% and mortality is typically less than 15%. The importance of RV diarrhea in weaned pigs is less clear. Lesions caused by RV are localised only in small intestines and are due to RV replication and destruction of villous epithelial cells.

The clinical signs of RV infection in pigs is not unique, thus diagnosis requires detection of virus or RNA. General supportive therapy, management procedures and antibiotics are recommended to minimize mortality due to RV and secondary bacterial infections.

Pcv2-associated enteritis

Porcine circovirus-associated disease (PCVAD) is caused by a small pathogenic DNA virus, Porcine circovirus type 2 (PCV2). PCVAD has emerged to become one of the most economically important pig diseases globally. One of the less commonly recognized clinical manifestations of PCVAD is PCV2-associated enteritis in growing pigs which appears to be a distinct clinical manifestation of PCV2 (Kim et al., 2004, Jensen et al., 2006, Opriessnig et al., 2011). The disease is seen mostly in 8 to 16 weeks old pigs but it may occur any time in the grow-finish phase.

The lesions can be observed in the small or large intestine. In affected animals the yellow to dark diarrhea is observed. Morbidity is quite low (10-20%), however mortality could be high (50-60%). In sick pigs the reduced growth is observed. The most unique lesions were granulomatous inflammation affecting Peyer’s patches, characterized by infiltrates of epithelioid macrophages and giant multinucleated cells. Large, multiple, basophilic or amphophilic, grape-like intracytoplasmic inclusion bodies were often seen in the cytoplasm of histiocytic cells and giant multinucleated cells. Villus atrophy and fusion together with multinucleated giant cells within the lamina propria have also been reported. No microscopic lesions were observed in the lymphoid tissue, such as lymph node, spleen, and tonsil (Kim et al., 2004, Jensen et al., 2006, Opriessnig et al., 2011).

PCV-2 associated enteritis should be considered as a differential diagnosis for grow-finish pigs with antibiotic non-responsive diarrhea.

Table 1. Negative effects of immunological stress on feed conversion ratio.

Immunological stress (cytokines) as another factor of FCR decrease

It has been shown that pigs kept in environments where they are exposed to a high number of pathogens have reduced feed intake and growth, even without no obvious signs of acute disease (Johnson, 2012). This chronic drain on production efficacy is called immunological stress. Every infection stimulates macrophages to the synthesis and secretion of pro-inflammatory cytokines, important regulators of both innate and adaptive immune response. Cytokines rearrange the metabolism priorities, resulting in re-directing of nutrients away from productive process towards responses that support the immune system (e.g. inflammation, fever, etc.) and in this way influence the FCR. Thus, the immune system is the critical chain link connecting the environment to productivity (Grimble, 1992, Johnson, 2012).

Pigs can grow most efficiently when they exist in harmony with the environment. Chronic stress significantly impacts the dietary lysine requirements for growth. Stimulation of Toll-like receptors on macrophages or mast cells lead to the synthesis and secretion of cytokines, thereby initiating the inflammatory response. Pro- inflammatory cytokines set of a “systemic alarm” – the acute phase response – which is connected with the synthesis of huge amounts of new proteins, called acute phase proteins. In this stage the synthesis of muscle proteins is inhibited (Grimble, 1992, Johnson, 2012). Moreover, degradation of skeletal muscle probably provides substrate to fuel acute phase protein synthesis by the liver. A shift in balance between anabolic and catabolic processes forms the basis for impaired production of pigs subjected to pathogenic agents.