Diarrhea can occur in pigs of all ages, but diarrhea occurs mainly in these three age groups: piglets of 1 to 3 mouths after birth, piglets of 7 to 14 age, and piglets of post-weaning age. The incidence of diarrhoea in newborn piglets may increase, especially in pig farms where littering is intensively managed. The advent and widespread use of the fungal hair antigen vaccine has significantly reduced diarrhea in newborn piglets. Individual farms use oral homologous milk vaccines, but generally require two immunizations to achieve satisfactory preventive effects. However, the fungal hair vaccine is not necessarily effective for diarrhea in newborn piglets, and it is often difficult to control diarrheal diseases at this age.
Although the pathogens of piglet diarrhea are relatively numerous and complex, the most susceptible pathogen is the pathogen that is infected at the same time as the maternal antibody to a certain pathogen is resolved. Diarrhea occurs when there is a large number of pathogenic infections that exceed the immune control of colostrum or antibodies in the milk. These environmental factors, such as temperature, humidity, ventilation and hygiene in the delivery room, have a significant impact on the severity of diarrhoea and the survival rate and prevention of piglets.
The most common infectious agents of piglet diarrhea are E. coli, rotavirus, infectious gastroenteritis (TGE), and Coccidiosis such as piglets (Isospora suis). Nematodes such as Sarongyloides ransomi also often cause diarrhea in pigs in the southeastern United States. There is also a reported increase in many states in the central and eastern United States. According to survey statistics from the Illinois Diagnostic Office in Galeburg, the pathogens prevalent in mammalian pigs are: coccidiosis 32%, E. coli 21%, TGE virus 20%, rotavirus 10%, Clostridium gas-producing podella 11%, undiagnosed 6%. Isolation from the same pig often isolates and identifies more than one pathogen. Observations in recent years have shown an increasing trend in the prevalence of coccidiosis and Clostridium aeronasces.
E. coli disease: E. coli as a primary pathogen is less common in piglets than in juvenile piglets. The Illinois Diagnostic Laboratory surveyed 144 pigs that developed diarrhea, and the proportion of pathogenic E. coli isolated from 6 years of age to weaning was small (14 percent) and the proportion of piglets aged 1 to 5 years was higher (53 percent). E. coli isolated from newborn piglet diarrhea may often be a secondary pathogen. These E. coli may not necessarily be hemolytic or enterotoxic. Moxley reported endotoxemia in E. coli K88 strains infected with mammalian and weaned pigs. He believes that seeing small intestinal congestion indicates that the intestine is infected with p-hemolytic E. coli strains, which express the K88 bacterium hair antigen. Immunization of sows with a commercial fungal hair vaccine is not very effective in preventing Escherichia coli in newborn piglets.
Infectious gastroenteritis (TGE): Endemic DingGE is often the cause of diarrhea in newborn piglets if the pig producer's production plan continues to produce sows every week or month without an intermittent interval. Endemic TGE is most common when newborn piglets are kept together with 3- to 4-week-old piglets in a large delivery ward (50 to 100 birthing boxes). Older infected pigs will excrete a large number of pathogenic viruses, these large numbers of invasive viruses can break through the protective power of the mother antibodies of susceptible pigs, about one week of piglet age in the colostrum IgG antibody level has dropped to a certain extent, when a large number of viruses exceed the number of IgG antibodies in sow milk. Sows are partially immune, so clinical symptoms are rare. Due to the different degrees of immunity of sows, the severity of diarrhea is also different in the same littering room. Diarrhea is evident in one litter of piglets, while another litter of piglets adjacent to the birth box may be healthy. Piglets are protected during lactation due to immunity from sow milk, and diarrhea occurs after weaning. Piglets that eat front breast milk may not have diarrhea due to more milk, and piglets that eat back breast milk may have diarrhea because they have less milk and less protection. Therefore, the morbidity and mortality of piglets vary greatly, depending on the amount of intralactic immunity provided by each sow from the milk and the age of infection in the piglets. The incidence can reach 50 to 100%, and the mortality rate can be 10 to 30%, depending on the level of immunity of the pig population and environmental factors.
Rotavirus: Almost all piglets can be infected with rotavirus during the first few weeks of newborn piglets, but most cases present subclinical symptoms. Clinical symptoms of infection occur when the virus in the continuous littering room exceeds the passive immune protection of the piglets. Benfield reports that sows immune to rotavirus can excrete the virus in feces 3 days before and within 2 weeks after littering. Newborn piglets develop lemon yellow or cheese-like diarrhea after infection with rotavirus. Older piglets have milder diarrhea and shorter duration. If the piglet lacks passive immunity, the virus proliferates enough to infect the piglets aged 6 to 7 mouths, and its clinical symptoms are more serious. Morbidity is usually 80 to 100% and mortality is 5 to 20%. Mortality from secondary bacterial infection increases significantly if the virus is infected at the same time.
Coccidiosis: Piglets aged 6 to 10 years have increased oral benefits diagnosed with coccidiosis. Larger-scale intensive pig production may have increased the prevalence of coccidiosis. The incidence of coccidiosis in porcine coccidiosis may increase in July to August. Infected pigs begin to pull pasty yellow-brown to gray stool, which turns into watery diarrhea after a day or two. Diarrhea lasts for 4 to 8 days until severe dehydration. In a littering room with concrete floors or slats, the incidence of coccidiosis can reach 100%. In the birth room with a plank floor, the incidence can also be relatively high. Mortality rates range from 0 to 20 percent, depending on the presence of secondary infections and environmental stressors.
Although several coccidioides species have been identified in pigs, the only species known to be pathogenic to young piglets are Isosporn suis. After the egg sacs that form the broop are eaten by piglets, the broopia are released, most of which penetrate into the epithelial cells of the jejunum and ileum for asexual reproduction. After about 5 days (at the ingestion), the sexual reproduction phase is entered, and the egg sac is excreted through the feces. Arleman and Meyer reported extraintestinal history of coccidiosis such as pigs, which can cause a second peak in 10-14 days after ingestion. On popular pig farms, it is possible to know in advance which day piglets will have diarrhea. Pigs are usually inactive at first, lying near heat sources most of the time, and diarrhea can occur the next day.
Clostridium perfringens: Although Clostridium perfringens type C can usually cause acute diarrhea in piglets aged 3 to 5, Clostridium perfringens can also cause chronic infection with Clostridium aerocystis type C in piglets. These piglets develop diarrhea and dehydration 2 to 3 days after the onset of clinical disease. The disease is often sporadic, with only 3 or 4 piglets infected in the same litter, while the rest of the piglets may be healthy.
Strongyloidesransomi: Although intestinal nematodes are a problem primarily in the southeastern United States, veterinary personnel in Midwest states also value these parasites. The larvae can be passed from the colostrum of infected sows to nursing piglets. Ingested larvae can cause shedding of jejunal epithelial cells and cause diarrhea in 6-mouth piglets. Piglets may be seen with anorexia, diarrhea, dehydration and depression.
diagnosis
Regrettably, autopsies of diarrhea piglets are difficult to make a correct diagnosis. Lesions of viral infection may be thinning of the intestinal wall and translucent, thin chyle in the lymphatic vessels of the mesenteric tract, and stool usually < 7.0. However, these results are not as pronounced in piglets as in newborn piglets. Similar results can be seen in piglets suffering from coccidiosis. Necrotizing enteritis is often seen, which can occur with coccidiosis or subacute Clostridium infection. Fecal ph>7.0 may be E. coli disease, but it is also not specific. If the sows have no milk, the piglets do not have milk to digest, and the feces of these pigs are not necessarily alkaline p-day. Because autopsy results are not conclusive, laboratory methods are necessary to determine the pathogen of diarrhoea. For the best diagnosis, several untreated live pigs should be sent to the laboratory for diagnosis at the beginning of the diarrhea. If it is not possible to send the pigs, the sick pigs are dissected and some tissue samples are collected for testing. Samples of dead or dying pigs should not be used for laboratory diagnosis. Parts of the duodenum, jejunum, ileum and spiral colon can be collected and fixed with formalin and sent to the laboratory for histopathological examination. Fresh, refrigerated jejunum and ileum fragments are sent for viral fluorescent antibody testing and bacteriological culture (e.g., E. coli and Clostridium aeropherol). 5 to 6 pressure smears were made of the ileum for microscopic coccidiosis identification and fluorescent antibody testing for E. coli disease. Collect a few milliliters of fecal material for diarrhea and send them for electron microscopy for virion examination. Because the conditions of each laboratory are different, you should contact the laboratory staff when sending the material for testing, what kind of materials they need and how to transport them. Effective treatment and control measures can only be developed and applied on the basis of correct diagnosis.
Treatment and control
The use of all-in, all-out production, or at least 3 months between births, can help control viral diarrhea. The key to treating endemic TGE or rotavirus is to prevent and control secondary infections of E. coli. Piglets should be fed fresh oral electrolyte solution through a low-nipple dispenser or slow-water tank, and antimicrobials (eg, spectinomycin, gentamicin, aramycin (Apra myci n, Nitrofurans, Quinoloes, and neomycin) should be used to reduce secondary bacterial infection. Even young piglets with diarrhea consume a considerable amount of water if they have access to water. During the addition of the drug, the intake of water is monitored to evaluate the edible and palatial nature of the drug.
If E. coli is considered to be the leading cause of diarrhea, antibiotic susceptibility testing should be done so that appropriate antibiotic therapy may indicate a possible concurrent infection if treatment is not apparent, and the diagnosis should be re-evaluated.
Local epidemic TGE is very difficult to control and prevent. At present, the effect of TGE commodity seedlings in the field is not very satisfactory. Some veterinary personnel have been reported to obtain better results by using homologous live viruses obtained from early-stage infection in pigs. The virus is taken from newborn piglets that were infected before eating colostrum. The small intestine is segregated and frozen and inoculated 3 weeks before the sow gives birth. Halterman and Harris reported, respectively, that once a live pathogenic virus was vaccinated against the entire herd's mouth, eliminating the ongoing epidemic of TGE within the herd. Yugoslavia also reported the same results of eliminating TGE. Some veterinarians report that injecting TGE commercial seedlings 3 to 5 days after sows give birth has had limited success.
Rotavirus vaccines are not yet fully satisfactory in preventing rotavirus diarrhea. Bohl and Saif have reported different antigenicity between rotavirus strains and no cross-protection between heterologous serotypes. There is little value in treating clinically symptomatic coccidiosis. Giving coccidiosis medication to piglets 3 to 4 days before diarrhea is expected to be effective is generally effective. Veterinarians have also reported a variety of results using coccidiosis drug blends,(including ampheramic pyridium, Decoquinate, and Sulfas)," which are not currently approved for use in pigs in the United States.
The center of coccidiosis control should revolve around the hygiene of pregnancy and littering facilities and the treatment of sows before littering. The basic premise is to prevent newborn piglets from eating insect eggs. The source of exposure to coccidiosis such as pigs has not been identified. Attempts to find the eggs from the debris cut from the floor of the littering room were unsuccessful. The researchers found that sows rarely excrete eggs such as pig coccidiosis, and if eggs are detected in pig manure, they are generally members of Emeral coccidiosis.
In order to reduce the production of eggs by sows and prevent possible infection of young pigs, coccidiosis drugs are added to the feed 2 weeks before sow spawning and 2 weeks after littering. After giving coccidiosis drugs to sows, the preventive effect on diarrhea in piglets is unpredictable. Amethyrin, decoxywa vinegar, or Monensin are some of the most commonly used drugs, but have not yet been approved. The appropriate relationship between veterinary personnel and sick animals after drug use needs to be understood. Giving sows chlortetracycline-sulfamethamine-penicillin bindings 4 to 6 weeks before calving has been shown to be helpful in the control of coccidiosis. If sulfamethamine is given to sows, the urine of the bred pigs should be examined for sulfadimethexim to avoid cross-contamination of the feed in the production and transport system.
For most pig farms, the fundamental way to control coccidiosis is to implement strict hygiene measures and control concomitant infections at the same time. For some pig farms, the use of metal mesh as the floor of the littering room may be the only way to effectively control coccidiosis. But if the sows that the pig producer put in the litter box are dirty, or if the producer wears contaminated boots when moving between the pig pens, then even if the metal mesh floor is used, it will not work. Some veterinarians sometimes regret violating hygiene measures.
Treatment of piglets with chronic infection with Clostridium aeratus is not useful, but immunization of sows with the C-type Clostridium aeratus vaccine prevents this infection. On some farms, vaccination of sows with bacillus or Virginiamycin prior to littering may also prevent this infection. Treatment of Lan's garden nematode infection can be done with thiazole thiazole twice at 5 and 10 mouth ages. All sows before littering are treated with benzthiazole or evromin. Raising all breeding herds and piglets in well-drained, dry-ground barns prevents the presence and spread of live larvae.
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