Coccidiosis of Pigs
PIGLET COCCIDIOSIS
Published: July 10, 2009
By: Dr. Justin Tan Yu- Wen
Piglet coccidiosis is caused by a protozoan parasite called Isospora suis. Although Eimeria debliecki has been known to cause clinical disease in piglets, it seems that the only important pathogenic species known to cause clinical disease in piglets is Isospora suis. This disease is very hard to eradicate and is commonly found on pig farms.
The developmental stages of Isospora suis occur both inside the host animal and outside, in the external environment. During the exogenous phase of the coccidial life cycle, the oocysts are spheroid to spherical in shape, measuring approximately 20 μ in diameter, with a smooth, single-layer capsule that is 1.5 μ thick. An oocyst contains two disporic sporocysts with four tetrazoic sporozoites each.
The target organ of this parasite is the small intestine, where it undergoes development within the mucosal tissue. The developmental stages produce a microscopic egg, called an oocyst. The oocysts of Isospora suis are excreted with the faeces. With the appropriate temperature, moisture level and oxygen content, the oocyst will then develop to form a sporulated oocyst within 1-3 days. Oocysts are highly resistant and are almost impossible to eradicate. In current swine production, where supplemental heat between 32°C and 35°C is provided to newborn piglets, oocyst sporulation may occur within 12 to 16 hours.
The developmental stages of Isospora suis occur both inside the host animal and outside, in the external environment. During the exogenous phase of the coccidial life cycle, the oocysts are spheroid to spherical in shape, measuring approximately 20 μ in diameter, with a smooth, single-layer capsule that is 1.5 μ thick. An oocyst contains two disporic sporocysts with four tetrazoic sporozoites each.
The target organ of this parasite is the small intestine, where it undergoes development within the mucosal tissue. The developmental stages produce a microscopic egg, called an oocyst. The oocysts of Isospora suis are excreted with the faeces. With the appropriate temperature, moisture level and oxygen content, the oocyst will then develop to form a sporulated oocyst within 1-3 days. Oocysts are highly resistant and are almost impossible to eradicate. In current swine production, where supplemental heat between 32°C and 35°C is provided to newborn piglets, oocyst sporulation may occur within 12 to 16 hours.
Epidemiology
Isospora suis can infect pigs of any age, but only causes clinical signs in piglets, usually those between the ages of 7 and 14 days. Older pigs act as carriers. Other Eimeria spp. can affect pigs as well, but they do not have as devastating an effect on the pigs.
Coccidia are present worldwide. Reports on the presence, prevalence and epidemiology of Isospora suis have come from virtually every country in the world. Studies conducted in most countries have shown a high prevalence of the disease on farms (45-85%) as well as a high incidence of litters affected by the disease (>30%).
It has been determined that the sow plays a minimal or no role in the transmission of Isospora suis. Lindsay et al. (1984) performed a study in the USA, where they examined the oocysts excreted by the sows on farms with and without a history of Isospora suis infections in piglets. The study reported a high infection rate to Eimeria spp. in the sows but less than 1% with Isospora suis.
The environment is the most important source of infection. Infected piglets excrete more than 100,000 oocysts per gram of faeces, but infection occurs even with a low dose of Isospora suis (as low as 100 oocysts). The oocysts are highly resistant to external influences and the environment in the farrowing houses is favourable to rapid sporulation and transmission of the disease. Once Isospora suis is established on a farm, it is most likely transmitted from one contaminated litter to another.
Isospora suis can infect pigs of any age, but only causes clinical signs in piglets, usually those between the ages of 7 and 14 days. Older pigs act as carriers. Other Eimeria spp. can affect pigs as well, but they do not have as devastating an effect on the pigs.
Coccidia are present worldwide. Reports on the presence, prevalence and epidemiology of Isospora suis have come from virtually every country in the world. Studies conducted in most countries have shown a high prevalence of the disease on farms (45-85%) as well as a high incidence of litters affected by the disease (>30%).
It has been determined that the sow plays a minimal or no role in the transmission of Isospora suis. Lindsay et al. (1984) performed a study in the USA, where they examined the oocysts excreted by the sows on farms with and without a history of Isospora suis infections in piglets. The study reported a high infection rate to Eimeria spp. in the sows but less than 1% with Isospora suis.
The environment is the most important source of infection. Infected piglets excrete more than 100,000 oocysts per gram of faeces, but infection occurs even with a low dose of Isospora suis (as low as 100 oocysts). The oocysts are highly resistant to external influences and the environment in the farrowing houses is favourable to rapid sporulation and transmission of the disease. Once Isospora suis is established on a farm, it is most likely transmitted from one contaminated litter to another.
The Complete Life Cycle of Coccidia
When a sporulated oocyst is ingested (a) by the piglet, the sporozoites leave the confines of the sporocyst and oocyst via the process of excystation. Mechanical processes of the upper gastrointestinal tract of the host make the sporocyst and oocyst walls more permeable. This occurs via both muscular contractions and enzymatic digestive processes involving trypsin and bile salts. Eventually, certain parts of each may be digested, or they may collapse or be broken. This releases their sporozoites (b). Once free within the milieu of the intestine, the sporozoites then penetrate the host epithelial cells (c).
Invasion of the host cell is complicated, involving a sequential series of steps including recognition of a host cell, attachment to surface components, formation of a tight junction, entry into the cell, and formation of a parasitophorous vacuole around the sporozoite. Once safely inside its parasitophorous vacuole, the sporozoite initiates asexual multiple fission, or also known as merogony.
During merogony (c-e), the mature merozoites rupture and kill the host cell (f), each seeking to penetrate a new epithelial cell to begin merogony again (g-i) for a number of generations, which result in a tremendous biological magnification of the parasite from these developmental stages.
When the last generation of merozoites (j) enters host epithelial cells, they develop not into additional meronts, but gamonts. The vast majority develop into macrogametocytes, which are also called macrogamonts. These form uninucleate macrogametes (k-n), while the remaining merozoites develop into microgametocytes, each of which undergoes multiple fission to produce thousands of motile, biflagellated microgametes (o-r). When they are mature, microgametes leave their host cell (s) to seek out and penetrate cells that have a mature macrogamete within (n), and fertilization occurs, restoring the diploid (2N) condition. Soon after fertilization, a delicate membrane forms around the zygote and two types of wall-forming bodies develop in the cytoplasm. These migrate toward the surface membrane and then fuse with the surface membranes to form the resistant oocyst wall. When the oocyst wall is fully formed, the oocyst ruptures from the host cell and leaves the host (t) via the faeces.
The prepatent period is termed as the time between when a suitable host first ingests a sporulated oocyst and when unsporulated oocysts leave the host in its faeces. During this interval, which is about 6 to 9 days, no oocysts are found in the feces because only merogony and the beginning of gamogony are occurring in the host. The patent period is the time interval during which oocysts are discharged from an infected host and lasts only until all the fertilized and unfertilized macrogametes have been released from their host cells, and this is usually 3 to 10 days.
Once outside the host, the oocyst must sporulate before it is infective to another piglet (u-x). The oocyst will then develop to form a sporulated oocyst within 1 to 3 days. The presence of oxygen, moisture, shade (direct exposure to UV radiation and sunlight will kill oocysts quickly) and generally, a temperature less than the body temperature of the host, are necessary for oocyst survival. Oocysts are highly resistant and are almost impossible to eradicate.
Invasion of the host cell is complicated, involving a sequential series of steps including recognition of a host cell, attachment to surface components, formation of a tight junction, entry into the cell, and formation of a parasitophorous vacuole around the sporozoite. Once safely inside its parasitophorous vacuole, the sporozoite initiates asexual multiple fission, or also known as merogony.
During merogony (c-e), the mature merozoites rupture and kill the host cell (f), each seeking to penetrate a new epithelial cell to begin merogony again (g-i) for a number of generations, which result in a tremendous biological magnification of the parasite from these developmental stages.
When the last generation of merozoites (j) enters host epithelial cells, they develop not into additional meronts, but gamonts. The vast majority develop into macrogametocytes, which are also called macrogamonts. These form uninucleate macrogametes (k-n), while the remaining merozoites develop into microgametocytes, each of which undergoes multiple fission to produce thousands of motile, biflagellated microgametes (o-r). When they are mature, microgametes leave their host cell (s) to seek out and penetrate cells that have a mature macrogamete within (n), and fertilization occurs, restoring the diploid (2N) condition. Soon after fertilization, a delicate membrane forms around the zygote and two types of wall-forming bodies develop in the cytoplasm. These migrate toward the surface membrane and then fuse with the surface membranes to form the resistant oocyst wall. When the oocyst wall is fully formed, the oocyst ruptures from the host cell and leaves the host (t) via the faeces.
The prepatent period is termed as the time between when a suitable host first ingests a sporulated oocyst and when unsporulated oocysts leave the host in its faeces. During this interval, which is about 6 to 9 days, no oocysts are found in the feces because only merogony and the beginning of gamogony are occurring in the host. The patent period is the time interval during which oocysts are discharged from an infected host and lasts only until all the fertilized and unfertilized macrogametes have been released from their host cells, and this is usually 3 to 10 days.
Once outside the host, the oocyst must sporulate before it is infective to another piglet (u-x). The oocyst will then develop to form a sporulated oocyst within 1 to 3 days. The presence of oxygen, moisture, shade (direct exposure to UV radiation and sunlight will kill oocysts quickly) and generally, a temperature less than the body temperature of the host, are necessary for oocyst survival. Oocysts are highly resistant and are almost impossible to eradicate.
Clinical Signs, Lesions & Economic Significance
The predominant sign of coccidiosis is diarrhoea, which usually persists for 4 to 6 days. The faeces may vary from white to yellow in colour and from a fluid to a pasty consistency, usually without the presence of blood. Coccidiosis predisposes the piglet to the incidence of secondary bacterial infections and severely affected piglets may die.
Although the morbidity is usually high, mortality is variable, probably due to the difference in the number of oocysts ingested, differences in the environment and the presence of other co-existing disease problems. Although the disease has only a slight influence on mortality, it does influence the presence of concomitant infections and the amount of antibiotics needed to control them. The disease also drastically affects the development of piglets, where the daily weight gain of the infected animals decreases compared to uninfected animals, causing herds to have poor uniformity at weaning age. There is notable emaciation and stunting. Coccidiosis reduces growth by about 15% on average, that is, 500g at weaning age, and this contributes to weaning herds that are highly heterogenous.
Isospora suis causes severe lesions that are restricted to the jejunum and ileum in the small intestine, causing large areas of mucous to be destroyed and the intestinal villi to atrophy, becoming notably shorter and with less capacity for nutrient absorption. There may also be ulceration and necrosis of the villi tips. In severe infections, there is usually the presence of a characteristic yellow fibrinonecrotic pseudomembrane that is loosely attached to the hyperaemic intestinal mucosa.
Treatment & Control
Piglets infected with Isospora suis display a high degree of acquired immunity to subsequent reinfection. Nevertheless, this immunity develops too slowly to offer any meaningful protection against the initial clinical disease. It is essential to establish programs that combine good management and high-hygiene practices to reduce the oocyst burden of the parasite and minimize the effects of the disease on animals. It is important to note that anticoccidial therapies serve little purpose once the piglets show clinical signs of diarrhoea. Therefore, a high health status of piglets should be maintained during the first week of age to prevent damage caused by Isospora suis.
Coccidial oocysts are resistant to various types of disinfectants. Procedures such as exposing pens to direct sunlight, cleaning pens properly with high-pressure hot water (>70°C) and keeping them dry during the first weeks of farrowing will help reduce oocyst numbers.
Chemoprophylactic attempts have been tried with various compounds, but most of these regimes yielded disappointing results and were practically found to be too labour-intensive. The continuous use of anticoccidials and the many types of ionophores in commercial poultry-rearing has also led to development of resistance and has given rise to multiple drug resistant strains of coccidia in the field.
The predominant sign of coccidiosis is diarrhoea, which usually persists for 4 to 6 days. The faeces may vary from white to yellow in colour and from a fluid to a pasty consistency, usually without the presence of blood. Coccidiosis predisposes the piglet to the incidence of secondary bacterial infections and severely affected piglets may die.
Although the morbidity is usually high, mortality is variable, probably due to the difference in the number of oocysts ingested, differences in the environment and the presence of other co-existing disease problems. Although the disease has only a slight influence on mortality, it does influence the presence of concomitant infections and the amount of antibiotics needed to control them. The disease also drastically affects the development of piglets, where the daily weight gain of the infected animals decreases compared to uninfected animals, causing herds to have poor uniformity at weaning age. There is notable emaciation and stunting. Coccidiosis reduces growth by about 15% on average, that is, 500g at weaning age, and this contributes to weaning herds that are highly heterogenous.
Isospora suis causes severe lesions that are restricted to the jejunum and ileum in the small intestine, causing large areas of mucous to be destroyed and the intestinal villi to atrophy, becoming notably shorter and with less capacity for nutrient absorption. There may also be ulceration and necrosis of the villi tips. In severe infections, there is usually the presence of a characteristic yellow fibrinonecrotic pseudomembrane that is loosely attached to the hyperaemic intestinal mucosa.
Treatment & Control
Piglets infected with Isospora suis display a high degree of acquired immunity to subsequent reinfection. Nevertheless, this immunity develops too slowly to offer any meaningful protection against the initial clinical disease. It is essential to establish programs that combine good management and high-hygiene practices to reduce the oocyst burden of the parasite and minimize the effects of the disease on animals. It is important to note that anticoccidial therapies serve little purpose once the piglets show clinical signs of diarrhoea. Therefore, a high health status of piglets should be maintained during the first week of age to prevent damage caused by Isospora suis.
Coccidial oocysts are resistant to various types of disinfectants. Procedures such as exposing pens to direct sunlight, cleaning pens properly with high-pressure hot water (>70°C) and keeping them dry during the first weeks of farrowing will help reduce oocyst numbers.
Chemoprophylactic attempts have been tried with various compounds, but most of these regimes yielded disappointing results and were practically found to be too labour-intensive. The continuous use of anticoccidials and the many types of ionophores in commercial poultry-rearing has also led to development of resistance and has given rise to multiple drug resistant strains of coccidia in the field.
Orego Stim & Piglet Coccidiosis
Orego-Stim is active against all intracellular developmental stages of coccidia, including schizonts, micro and macrogamonts. To effectively control coccidiosis, the phenolic compounds speed up the process of the normal shedding of enterocytes from the intestinal mucosae, causing a disruption in the life cycle of Isospora suis and as a result, the protozoa are not able to complete its life cycle to cause either clinical or subclinical disease.
Orego-Stim is active against all intracellular developmental stages of coccidia, including schizonts, micro and macrogamonts. To effectively control coccidiosis, the phenolic compounds speed up the process of the normal shedding of enterocytes from the intestinal mucosae, causing a disruption in the life cycle of Isospora suis and as a result, the protozoa are not able to complete its life cycle to cause either clinical or subclinical disease.
How Should OS Be Administered To Piglets?
The drenching method is the most effective way to treat, control and prevent coccidiosis in piglets. Orego-Stim Liquid can be administered via oral drenching in suckling and weaning piglets as follows:
Dilute Orego-Stim Liquid with fresh drinking water at an equal ratio of 1:1. Shake well and the suspension is now ready for administration. Administer 1-4 ml of the suspension to each piglet for two to three times, 12 hours apart.
This scheme was originally developed by pig farmers to minimize stress and proved to be very successful for individual treatment of piglets with coccidiosis. It is very reliable, safe and helps the piglets to make an amazing recovery. Finally, it is recommended to prepare a fresh suspension each morning instead of using leftovers, just to ensure that the desired outcome is secured.
Orego-Stim not only controls coccidia infection, but also kills all intracellular developmental stages of the parasite without impairing the piglet’s ability to acquire lifelong immunity against coccidiosis, thus promoting resistance to reinfection.
The benefits of using Orego-Stim go way beyond coccidiosis control. Orego-Stim as an appetizer will help piglets to get quickly accustomed to solid feed consumption and also will help their digestive system to mature earlier. This ensures that piglets are heavier and more uniform at weaning, with fewer weak piglets, and achieve market weight as quickly as possible. Orego-Stim also helps to prevent piglet diarrhoea caused by other aetiological agents such as Salmonella, E. coli, Clostridium perfringens type C, Campylobacteriosis, coronavirus and rotavirus. This leads to a decrease in the incidence of clinical diarrhoea, a decrease in the use of antibiotics for secondary bacterial infections in piglets following coccidiosis, and satisfaction on the part of the vet and the pig farmer at finding a solution to early diarrhoea problems.
The drenching method is the most effective way to treat, control and prevent coccidiosis in piglets. Orego-Stim Liquid can be administered via oral drenching in suckling and weaning piglets as follows:
Dilute Orego-Stim Liquid with fresh drinking water at an equal ratio of 1:1. Shake well and the suspension is now ready for administration. Administer 1-4 ml of the suspension to each piglet for two to three times, 12 hours apart.
This scheme was originally developed by pig farmers to minimize stress and proved to be very successful for individual treatment of piglets with coccidiosis. It is very reliable, safe and helps the piglets to make an amazing recovery. Finally, it is recommended to prepare a fresh suspension each morning instead of using leftovers, just to ensure that the desired outcome is secured.
Orego-Stim not only controls coccidia infection, but also kills all intracellular developmental stages of the parasite without impairing the piglet’s ability to acquire lifelong immunity against coccidiosis, thus promoting resistance to reinfection.
The benefits of using Orego-Stim go way beyond coccidiosis control. Orego-Stim as an appetizer will help piglets to get quickly accustomed to solid feed consumption and also will help their digestive system to mature earlier. This ensures that piglets are heavier and more uniform at weaning, with fewer weak piglets, and achieve market weight as quickly as possible. Orego-Stim also helps to prevent piglet diarrhoea caused by other aetiological agents such as Salmonella, E. coli, Clostridium perfringens type C, Campylobacteriosis, coronavirus and rotavirus. This leads to a decrease in the incidence of clinical diarrhoea, a decrease in the use of antibiotics for secondary bacterial infections in piglets following coccidiosis, and satisfaction on the part of the vet and the pig farmer at finding a solution to early diarrhoea problems.
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Authors:
Meriden Animal Health Limited
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