Research Progress on Porcine Transmissible Gastroenteritis Virus
Introduction
Coronaviruses belong to the order Nidovirales and are RNA viruses. They have two subfamilies:
· Coronaviridae, composed of the genus Alphacoronavirus, the genus Betacoronavirus, and the genus Gammacoronavirus.
· Toroviridae, including the genus Torovirus and the genus Bafinivirus.
These viruses can cause five diseases in pigs, in chronological order:
1. Transmissible gastroenteritis (TGE-1946)
2. Hemagglutinating encephalomyelitis (HEV-1962)
3. Porcine epidemic diarrhea (PED-1977)
4. Porcine respiratory coronavirus (PRCV-1984)
5. Porcine deltacoronavirus (PRCV-1984)
Threetypes of swinecoronaviruses are associated with digestive system diseases (TGE, PED and PDCoV). Porcine respiratory coronavirus (PRCV) is associated with respiratory diseases, and hemagglutinating encephalomyelitis virus can cause two different sets of symptoms: vomiting and wasting, and encephalomyelitis.
There have been no reports of human infection with porcine coronaviruses.
1 Transmissible gastroenteritis virus
Transmissible gastroenteritis virus is a coronavirus that has rarely been detected since the late 20th century. It was first reported in 1946 and reached its highest prevalence in Europe and the United States in the 1970s, 1980s and 1990s; in the 1980s, more than 95% of European pig farms were positive. It is a highly contagious virus that can cause diarrhea, dehydration and occasionally vomiting, and can lead to high mortality in piglets. Porcine transmissible gastroenteritis virus has been completely sequenced, and only one serotype is known.
There is homology between porcine transmissible gastroenteritis virus and bovine and human coronaviruses as well as porcine respiratory coronavirus. From an epidemiological point of view, there are both epidemic cases and endemic cases. It is a relatively heat-resistant virus, resistant to low pH and many disinfectants. At 37°C, it is inactivated in less than two hours. It is very sensitive to light and extremely resistant to freezing. This virus can survive for a long time in frozen carcasses. This means that most disease outbreaks occur in the cold months (winter).
Pathogenesis
The route of transmission is fecal-oral. The virus mainly multiplies in gastrointestinal cells. After 4-5 hours, the virus is found in the cytoplasm of infected cells, mainly at the base of the small intestinal villi. It causes villous atrophy, which significantly reduces the absorption of nutrients and leads to osmotic diarrhea, while the reduction in sodium and glucose transport worsens the osmotic diarrhea, resulting in hypoglycemia in affected animals. At the same time, it proliferates in different extraintestinal organs such as the lungs (alveolar macrophages), mammary tissue and lymph nodes.
IgA in colostrum can protect piglets aged 6-12 weeks. Active antibodies appear one week after infection and can persist for 6 months in finishing pigs and for two years in sows. After clinical symptoms disappear, the virus can persist in pigs, and it can be shed in feces for up to 10 weeks, thereby becoming an asymptomatic carrier with the risk of spreading infection. Breeding sows can transmit the virus through milk. Other routes of transmission include trucks, boots, slurry, and even dogs and cats, because the virus stays in their digestive tract for two weeks and can be excreted. The incubation period is only 1-2 days, and the duration of clinical symptoms is 7-10 days.
Clinical symptoms
In pig farms free of transmissible gastroenteritis, the most typical infection is acute infection and the onset of acute cases, showing sudden and severe diarrhea, affecting various production stages within a few days. The diarrhea is severe, watery, pale yellow-green, and sometimes has a foul odor.
In suckling piglets, vomiting is common, accompanied by loss of appetite, with no fever or neurological symptoms. Dehydration occurs within 24-48 hours, with high mortality. Mortality in piglets less than 1 week old can be as high as 100%, up to 50% in the second week of lactation, and up to 25% in the third week. Piglets die after dehydration, with gastric dilation, mother's milk and hemorrhagic petechiae in the small intestine, hypertrophy of mesenteric nodules (characteristic lesion), atrophy of intestinal microvilli (duodenum, jejunum and ileum), thinning of the intestinal wall, necrosis of intestinal epithelial cells in the jejunum, and reduced enzyme activity.
In piglets, mixed infections with gastrointestinal bacteria such as Escherichia coli and Clostridium are common, thereby worsening and prolonging the clinical symptoms.In pigs over one month of age, the symptoms are similar, but the severity is much lower, with high morbidity and very low mortality.
In pig farms where the disease is endemic, pigs become infected later, until they enter the finishing stage.The main effects on finishing pigs are slow growth and low feed conversion rate.
In breeding sows, apart from diarrhea, the abortion rate and sow mortality only increase slightly within 1-3 weeks. Lactating sows show anorexia and occasional agalactia.
Diagnosis
The clinical symptoms and lesions are quite obvious, but we must carry out differential diagnosis against enterotoxigenic Escherichia coli, Clostridium, rotavirus, coccidia and Cryptosporidium strains. The age of the infected pigs and the clinical symptoms will also help us narrow the diagnosis down to coronaviruses.
Laboratory analysis confirmation depends on:
· ELISA with specific monoclonal antibodies in porcine serum to detect antigens in feces and intestinal contents.
· Electron microscopy to detect the virus in intestinal contents.
· Serum neutralization testing at 7-8 days after infection and for 18 months thereafter.
· Immunoperoxidase in fixed intestinal tissue to detect the virus in piglets.
· PCR to isolate the virus from intestine, tonsils, lymph nodes and feces.
Treatment
Only symptomatictreatmentis possible. No commercial vaccine is available. There used to be one in the United States, but it is no longer on the market. Hydration is the maintreatmentmeasure; controlling concurrent infections helps us reduce the impact, while strengthening biosecurity measures, extending downtime and strictly controlling environmental conditions are crucial for piglets. The main aim is to infect all animals on the farm as quickly as possible in order to obtain active immunity. The main control measures focus on prevention:
1. Biosecurity: clothing used only on the farm, visitor control, feed transport and animals.
2. Strictly implement all-in/all-out in different production areas. Clean and disinfect with hot water at 65ºC.
3. Prevent dogs and cats from entering the pig farm.
4. Effective disinfection, rodent control and pest control programs.
5. Negative replacement gilts and boars entering the breeding barn.
6. Replacement gilts undergo 8-9 weeks of isolation and acclimatization, with strict observation for gastrointestinal symptoms.
7. Drinking water disinfection program.
8. Piglets consume colostrum within 24 hours of birth.