Common Swine Diseases: Symptoms, Diagnosis, and Control
Rhinitis, Atrophic
Infectious and chronic condition characterized by hypoplasia and destruction of nasal turbinates. It is progressive and chronic.
- Progressive: Stronger. Caused by two bacteria: Bordetella bronchiseptica, Pasteurella multocida type D.
- Non-progressive: Caused only by Bordetella bronchiseptica.
Etiology
Multifactorial. Bacteria: Bordetella bronchiseptica, Pasteurella multocida type D (dermonecrotic toxin-producing).
Predisposing factors: Excess ammonia gas, inadequate ventilation, overcrowding, mixing animals of various ages, and high dust levels.
Symptoms
- Appear in lactating piglets: Sneezing, runny nose, formation of dark circles (due to lacrimal duct obstruction).
- Later: Misuse of the muzzle to one side or shortening (animal termination).
- Growth retardation.
- Turbinate destruction (primary lesion).
Diagnosis
Clinical signs and examination of turbinates (cutting off the nose at the 2nd premolar tooth or ninth fold of the palate). Bacteriological tests are of relative value.
Monitoring: Examination of turbinates.
Veterinary Action
On-farm examinations, material gathering, bacteriological tests. Identify predisposing factors and monitor turbinate health.
Treatment: Sulfamethazine in feed (100 to 400g/ton); tetracycline (300 to 600 ppm) in feed, 7 days before and 15 days after delivery.
Vaccination: Sows at 60 and 100 days of pregnancy; piglets at 7 and 28 days old.
Enzootic Pneumonia
Etiology
Mycoplasma hyopneumoniae. Complications can occur secondary to Pasteurella multocida type A. Predisposing factors: Overcrowding and poor ventilation. Incubation period: 20 days.
Epidemiology
Transmission via direct contact with respiratory secretions and by aerosol. Sows transmit to piglets (major pathway).
Clinical Signs and Lesions
Occur in pigs after weaning and finishing. Mismatched lots with the same age. On the farm: Dry cough, high morbidity, and low mortality. Secondary infections can lead to severe pneumonia. In slaughtered pigs: Areas of pulmonary consolidation (purple and gray) in the apical, cardiac, intermediate, and anterior diaphragmatic lobes, clearly defined, with fleshy consistency.
Diagnosis
Observation of clinical signs in the herd and typical lesions in slaughtered pigs, considering the number of affected lungs. Laboratory tests: Direct immunofluorescence, immunoperoxidase, PCR, and ELISA (serological profile of the herd).
Control
Living with the disease: Reduce the effects through management measures, correction, and therapeutic environment. Use the all-in/all-out system, hygiene, disinfection of premises, and reduce the number of animals per pen. Drug use in the diet is only economically indicated in severe cases.
Vaccination: Two doses to piglets (maternity and nursery). Gilts at 60 and 90 days of gestation. Sows at 90 days of gestation.
Treatment
Strategic medication with tiamulin (200 ppm), chlortetracycline (600 ppm), or lincomycin (110 ppm) in the diet.
Veterinary Action
Correct risk factors, determine herd severity (serological monitoring and slaughtered pig examination), decide on drug use in water or feed, and strategic medication and vaccination.
Pleuropneumonia
Severe lesions in the lungs and pleura. High mortality in the acute form and poor pig development in the chronic form.
Etiology
Actinobacillus pleuropneumoniae. Serotype 5 is most common in the UK.
Epidemiology
Pigs reach 70 to 100 days of life, but can occur at any age. Transmitted from pig to pig by direct contact. Chronic carriers are responsible for the spread (bacteria located in lung abscesses or tonsils). Transmission occurs via airborne particles or direct contact. Contagion is possible through boots and utensils. Immunity is serotype-specific. Autogenous vaccines are used, with sows transmitting antibodies through colostrum.
Symptoms
- Super acute form: Sudden death, often with blood from the mouth and nostrils.
- Acute form: Anorexia, prostration, fever, difficulty breathing, dog-sitting position, bloody discharge from mouth and nostrils preceding death. Survivors develop the chronic form.
- Chronic form: Poor growth and sporadic coughing. Carcass condemnation due to pleural adhesions.
Lesions
Found in the thoracic cavity. Pigs killed by the disease: Hemorrhagic areas of pulmonary consolidation with fibrin, fibrin-bloody fluid in the pleural and pericardial cavities. Carrier pigs: Pulmonary nodules, pleurisy, pericarditis, and pleural adhesions. Slaughtered pigs: Lung abscesses and pleural adhesions leading to carcass condemnation.
Diagnosis
Culture of Actinobacillus pleuropneumoniae. Immunofluorescence for microorganism identification in tissues. Serology: Identification of infected animals or herds by ELISA and complement fixation.
Control
Correct overcrowding, avoid ventilation fluctuations, and use the all-in/all-out system.
Vaccination
Piglets at 30 and 50 days old. Sows at 90 days of gestation. Gilts at 70 and 90 days of gestation.
Treatment
Antibiotics: Chloramphenicol, trimethoprim + sulfa, penicillin, and tetracycline. Parenteral use, individually or in feed, based on antibiogram. Prevents mortality but not infection.
Veterinary Action
Verify appropriate management, address overcrowding and mixing of lots, perform serological and bacteriological diagnosis, and monitor lesions in slaughtered pigs.
Metastrongylosis
Caused by nematodes of the genus Metastrongylus, leading to disordered breathing and pneumonia.
Etiology
M. elongatus, M. salmi, M. pudendotectus. Earthworm presence is essential to complete the cycle.
Symptoms
Usually asymptomatic. Coughing bouts occur when bronchioles are blocked with parasites.
Lesions
Restricted to the caudal ends of the diaphragm and lung edges. Parasites are observed when cutting the parenchyma.
Porcine Reproductive and Respiratory Syndrome (PRRS)
Etiology
Arterivirus. Affects nursery, growing, and finishing pigs.
Epidemiology
Some pigs present with bluish (cyanotic) ears, vulva, and abdomen. Transmission: Inhalation, ingestion, or through semen, secretions, feces, and urine.
Clinical Signs
- Acute form: Lasts 4 to 6 weeks. Abortion, stillbirth, mummification, weak piglets, sneezing, coughing, and dyspnea.
- Chronic form: Starts after the acute phase. Normal litters mixed with mummified and weak piglets of varying sizes.
Diagnosis
Virus cultivation from bone marrow, thymus, spleen, heart, brain, liver, kidneys, tonsils, and lymph nodes from adult pigs or aborted fetuses. Serum samples and chest fluid can also be used. PCR detects the virus in semen and other tissues. Serology: Indirect immunofluorescence, neutralization, and ELISA. Histologically, interstitial pneumonia and absence of alveolar macrophages can be observed. The virus causes persistent infections, sometimes without detectable antibodies.
Control
The disease does not exist in the UK; avoid introducing the virus.
Diseases with Nervous Symptoms
Edema Disease
Frequent in piglets 4-15 days after weaning. Sudden death and edema formation with signs of nervous incoordination.
Etiopathogenesis
Presence of pathogenic E. coli in the intestines, which under certain circumstances produce Verotoxin 2e (VT2e). When absorbed, it causes lesions in blood vessel walls. Exaggerated E. coli multiplication is associated with management and environmental factors at weaning:
- Change of feed to a ration difficult for piglets to digest.
- Sow separation and removal. Low temperature (ideal is 28°C).
- Mixing litters and overcrowding (>4/m²), continuous nursery use.
- Neutering and vaccination at weaning. Lack of cleanliness between batches.
Symptoms
Appear 1-14 days after weaning. Dead piglets, some with nervous disorders (incoordination, staggering gait, blindness), dyspnea, and elevated rectal temperature. In the final phase, piglets lie down, exhibit paddling motions, and die within 36 hours. Survivors recover slowly and experience wasting.
Lesions
Cutaneous edema of the eyelids, nose, face, and groin. Piglets with good nutritional status. Important autopsy findings: Edema in the stomach curvature and mesentery of the large intestine, sometimes in the larynx, lungs, and lymph nodes. Edema is observed in freshly killed pigs; it may be absent in piglets found dead.
Diagnosis
History, autopsy findings, and nervous symptoms. Histopathological examination of the brain. Bacteriological examination of the intestines (culture of pathogenic E. coli). Do not confuse with streptococcal meningitis and salt poisoning.
Control (Veterinary Action)
Food restriction as soon as symptoms appear or preventively in the first 10 days after weaning. Remove the sow, leaving piglets in the same environment for 15 days at 28°C. Avoid weaning stress. Fallowing of up to 5 days. Pre-starter feed for piglets. Vaccine use (still experimental). Antibiotics in feed.
E. coli vaccines for diarrhea exist; vaccines for this type are still experimental.
Streptococcal Meningitis
Affects piglets in maternity, nursery, and rearing. Sudden death due to sepsis.
Etiology
Streptococcus suis.
Epidemiology
Overcrowded stalls, introduction of carriers, and primiparous carriers infecting their piglets via the airway.
Pathogenesis
Streptococcus suis travels from the tonsils to the mandibular lymph nodes (without clinical signs), leading to sepsis and death.
Symptoms
- Maternity: Fever, swollen and painful joints, muscle tremors, hypersensitivity to touch, and shivering bristles.
- Weaned: Fever, incoordination, lateral recumbency, paddling, and death within 4 hours.
Hyperacute cases: Death without symptoms.
Lesions
Opacity and congestion of the meninges, focal myocarditis, vegetative endocarditis, creamy fluid in the joints, and lymph congestion.
- Septicemic form: Hyperemic carcass, congested and enlarged lymph nodes, pneumonia, fibrinous exudation in the peritoneum, pericardium, pleura, meninges, and rarely vegetative endocarditis.
- Nervous form: Fibrino-purulent exudate in the meninges and turbid cerebrospinal fluid.
Histopathology: Infiltration of neurons in the meninges.
Diagnosis
Bacteriological tests (swab of meninges and cerebrospinal fluid) and histopathology (brain and meninges). Differentiate from other nervous system diseases (Aujeszky’s disease, edema disease, salt poisoning). In asymptomatic pigs, isolate S. suis from tonsil swabs using molecular techniques.
Control (Veterinary Action)
Prevent risk factors. Use clean instruments, avoid overcrowding, adopt the all-in/all-out system with 7-day fallowing, aseptic care of piglet navels, teeth clipping, and tail docking. Use autogenous vaccines: Piglets at 25 and 45 days old and pregnant sows. Treat water for piglets. Antibiotics: Ampicillin, penicillin, sulfa-trimethoprim, and tetracycline.
Congenital Myoclonus
Birth of piglets with muscle tremors and difficulty walking. Death due to difficulty sucking and crushing by the sow.
Etiology
Various causes:
- Type A1 – Porcine circovirus type 2 (PCV2): Many litters affected, high morbidity and mortality, both sexes, cerebellar hypoplasia.
- Type A2 – Unclassified virus: Many litters affected, high morbidity, low mortality, both sexes.
- Type A3 – Landrace genetics: Few litters affected, low morbidity, high mortality, males; relapses in litters of the same sow.
- Type A4 – Wessex genetics: Few litters affected, low morbidity, high mortality, both sexes; relapses in litters of the same sow.
- Type A5 – Trichlorfon: Many litters affected, high morbidity and mortality, both sexes; relapses in litters of the same sow, cerebellar hypoplasia.
- Type A6 – Mycotoxins: Litters affected, low morbidity, high mortality, males; relapses in litters of the same sow.
In PCV2, the problem occurs due to infection of the pregnant female with a low pathogenic virus, usually after a disease outbreak. There are forms of unregulated myoclonus with unknown etiology.
Symptoms and Lesions
Asymptomatic in sows. Piglets are born with generalized muscle tremors. Death by crushing or hypoglycemia. Arthritis, skin lesions on legs and hooves, and diarrhea. Tremors disappear in the 3rd week of life in type A2 infections. Lesions: Cerebellar hypoplasia in types A1 and A5.
Control
First, obtain a negative diagnosis for PCV2. Prevent occurrences for different etiologies. For type A2, usually in primiparous gilts, immunize through ingestion of placentas from affected mothers. Mix in feed and provide before reproduction.
Veterinary Action
Research the causes. Laboratory tests for Aujeszky’s disease and PCV2. Check for occurrence in primiparous gilts, purebreds exposed to bathing or trichlorfon, and mycotoxins.
Salt Poisoning
Piglets walk aimlessly, experience epileptiform attacks, and high mortality occurs. Due to excessive salt intake and lack of water.
Etiology
Errors in diet composition, faulty drinkers, and lack of water supply.
Diagnosis
Based on history and symptoms. Confirmation by histopathology showing eosinophilic meningoencephalitis. Differentiate from edema disease, arsenic poisoning, bacterial meningitis, and Aujeszky’s disease.
Control
Animals with nervous symptoms usually die; there is no specific treatment. Provide water to piglets without symptoms. Ensure proper ration formulation. Antibiotics are unnecessary and ineffective.
Pathogenesis
Increased sodium concentration in blood and brain tissue leads to brain swelling and decreased intracranial pressure, reducing blood flow to brain tissue and causing nervous symptom degeneration.
Symptoms
- Hyperacute form: Prostration, paddling, coma, and rapid death.
- Acute form: 1-5 days. Aimless walking, head pressing, apathy, epileptiform seizures (lasting 1 minute and repeating every 7 minutes), and quietness between seizures.
Encephalomyocarditis
Viral disease primarily affecting young piglets, causing nervous symptoms or increased mortality.
Etiology
Picornaviridae, genus Cardiovirus.
Epidemiology
Rats are natural hosts and reservoirs, excreting the virus in feces. Outbreaks occur when rat populations are high. Infection occurs by ingesting contaminated food or rats. Pig-to-pig transmission is not significant. Lactating sows transmit to piglets. High mortality in piglets up to 3 weeks old. Pregnant sows may experience abortions, mummified fetuses, and stillbirths.
Pathogenesis
The virus multiplies in lymphoid tissues and intestines, affecting the heart muscle or CNS, causing encephalitis.
Symptoms
Sudden death, often when piglets move or become excited. Nervous form: Depression, anorexia, poor appetite, tremors, paralysis, vomiting, diarrhea, and cyanosis of the extremities.
Lesions
Excess fluid in chest and peritoneal cavities, pulmonary edema, and whitish areas of necrosis in the epicardium.
Diagnosis
Cardiac lesions, piglet deaths, and large numbers of rats in the barn. Definitive diagnosis: Virus isolation in cell culture or mouse inoculation (heart and spleen of dead piglets). Virus-neutralization tests, hemagglutination inhibition, and ELISA. For reproductive symptoms, differentiate from other reproductive diseases.
Control
No treatment or vaccine. Control rat populations as a preventive measure and disinfect with chlorine- or iodine-based products.
Veterinary Action
Perform autopsies and order laboratory tests on the heart, spleen, head, and aborted fetuses.
Septicemic Diseases
Septicemia is characterized by toxemia, fever, and circulating organisms (viruses, bacteria, and protozoa). Pathogenic action: Toxins and damage to vascular endothelium, leading to bleeding.
Classical Swine Fever (CSF)
Affects pigs of all ages. Acute form presents with widespread bleeding, high morbidity, and mortality. Reproductive symptoms are indistinguishable.
Etiology
Genus Pestivirus, family Flaviviridae. Only one serotype, containing RNA. Sensitive to 3% sodium hydroxide.
Epidemiology
The virus is eliminated in all secretions of infected or carrier animals. Infection modes: Direct contact, ingestion of contaminated food and water, transport, mechanical transmission (boots, clothing, hands), birds, insects, tools, surgical equipment, and syringes.
Symptoms
- Hyperacute form: Sudden death, hyperthermia, and skin bleeding.
- Acute form: Fever (≥15 days), staggering gait, constipation, diarrhea, edema of the eyelids, and nasal discharge. Skin redness, purple discoloration of ears, nose, and legs, and pneumonia.
- Subclinical form: Low pathogenic virus.
- Chronic form: Affects pigs that survived the acute phase; survival time varies.
- Atypical forms: Protracted course, observed after outbreaks, due to bacterial infection. Respiratory symptoms, diarrhea, gastric ulcers, or nervous symptoms.
Lesions
Lymph nodes with peripheral or extensive hemorrhage. Splenomegaly with areas of infarction and hemorrhage. Bleeding in the brain. Petechial hemorrhage in the epiglottis, larynx, pleura, epicardium, and endocardium. Hepatized lungs with dark red lobes. Necrotic purulent tonsillitis. Bleeding in the stomach. Sub-serosal bleeding in the small intestine and catarrhal enteritis. Small rounded ulcers with protruding lips near the ileocecal junction (secondary infection with Salmonella sp.). Petechiae in the renal cortex and medulla, and in the bladder.
Diagnosis
Clinical presentation and autopsy findings. Differentiate from erysipelas, salmonellosis, and African swine fever. Examine lymph nodes, spleen fragments, tonsils, and serum samples. Direct immunofluorescence. Histopathology reveals purulent meningoencephalitis, not allowing differentiation from bacterial septicemia.
Veterinary Action
Send material for laboratory examination. Notify animal health authorities in case of an outbreak.
Action of Animal Health Protection Bodies
Define a protection and surveillance zone, quarantine the farm, cull all pigs, and disinfect. Introduce sentinel pigs ≤60 days old from CSF-free farms around the affected premises. Test sentinel pigs for CSF antibodies using ELISA and neutralization tests. Repopulate the farm after 42 days if sentinel pigs remain antibody-negative.
African Swine Fever (ASF)
Lethal and highly contagious viral disease affecting pigs of all ages, similar to CSF. Brazil has been considered ASF-free since December 1984.
Etiology
Asfarviridae family. Low immunogenicity and high environmental resistance.
Epidemiology
- Sylvatic cycle (Africa): Subclinical infections in wild pigs and Ornithodoros moubata ticks (transovarial transmission).
- Domestic cycle: O. moubata ticks infect pigs through bites or pig-to-pig transmission.
Secretions and excretions from infected or carrier pigs introduce the virus to the respiratory and digestive mucosa of susceptible pigs. The virus multiplies, destroying monocytes, lymphocytes, and neutrophils, reducing platelet counts and causing bleeding.
Symptoms
Similar to CSF.
Lesions
Similar to CSF, but with more bleeding.
Diagnosis
Laboratory tests are essential for differentiating ASF from CSF.
Control
No vaccines available. Strict hygiene and sanitary measures are crucial to contain the spread.
Swine Erysipelas
Hemorrhagic disease with cutaneous, joint, heart lesions, and septicemia. Carrier pigs are asymptomatic. Present in all species, environmentally resistant. Can cause arthritis and abortion. Vaccine is associated with parvovirus, but erysipelas cases still occur.
Etiology
Erysipelothrix rhusiopathiae, serovars 13 and 18. E. tonsillarum is non-pathogenic.
Epidemiology
Carrier pigs (tonsils), feces (pigs ingest feces leading to acute infection), urine, saliva, and nasal secretions.
Pathogenesis
Carrier pig infects other pigs (orally or through injury), leading to sepsis (heart, spleen, kidneys, joints), skin lesions, abortions in sows, and changes in spermatogenesis.
Symptoms
Septicemia in gestating or lactating sows.
- Hyperacute form: Sudden death.
- Acute form: Fever, conjunctivitis, staggering, skin lesions, erythema. Gestating sows abort; boars experience infertility.
- Chronic form: Arthritis and heart failure (thickened limb joints with cloudy fluid inside the joint capsule) – economically important.
Lesions
Hemostasis in the ear, enlarged lymph nodes, congested and enlarged spleen and kidneys, petechiae, and vegetative endocarditis affecting valves. Diamond-shaped skin lesions appear in 2-3 days.
Diagnosis
Laboratory: Culture from the spleen and classification of the etiologic agent from tonsils, skin lesions, synovial fluid (arthritis cases), and spleen (septicemia). Use tonsils cautiously, as the animal may be a carrier. Differentiate from CSF, Salmonella choleraesuis septicemia, and Streptococcus suis infection.
Veterinary Action
Monitor arthritis cases in slaughtered pigs, send samples to the laboratory.
Vaccination
Gilts and sows before breeding. Boars every six months. Piglets in the nursery.
Treatment
Penicillin, amoxicillin, ceftiofur, clindamycin. Oxytetracycline in feed for 10 days.
Septicemic Salmonellosis
Etiology
Salmonella enterica serovars Enteritidis and Choleraesuis (spread from Peyer’s patches to mesenteric lymph nodes). Does not cause food poisoning if meat is thoroughly cooked.
Epidemiology
Piglets 5 weeks to 4 months old are most affected. Pigs are reservoirs. Stressed animals excrete the bacteria. Bacteria invade the bloodstream from the ileum (part of the large intestine) through the ileocecal valve, causing septicemia within 24-72 hours.
Symptoms
Sudden death, elevated body temperature, red skin areas, huddling, and death within a few days. Chronic form: Anorexia, diarrhea, and weight loss.
Lesions
Acute: Splenomegaly, petechiae in kidneys, bladder, and epiglottis, and purulent pneumonia outbreaks. Chronic: Necrosis of the cecal and colonic mucosa, and enlarged mesenteric lymph nodes.
Diagnosis
Laboratory tests are essential for confirmation.
Control
Therapeutic measures combined with hygiene, disinfection, and management practices. Avoid risk factors.
Vaccination
Controversial. Piglets at 21 and 60 days old. Replacement gilts at 70 and 90 days of gestation. Sows at 90 days of gestation. Boars annually.
Treatment
Antibiotics based on antibiogram.
Anthrax
Three clinical forms: Pharyngeal (most common), intestinal, and septicemic.
Etiology
Bacillus anthracis (forms spores in the presence of oxygen). 10% formaldehyde at 40°C kills spores in 15 minutes.
Epidemiology
Ingestion of feed containing contaminated animal products. Pigs are resistant, so soil contamination is rare.
Pathogenesis
After ingesting contaminated food or carcasses, B. anthracis invades the tonsils and pharynx, multiplying in regional lymph nodes. Inflammation affects lymph flow, causing pharyngeal edema. In the intestinal form, bacteria penetrate the intestinal mucosa and lymph nodes, causing hemorrhagic lesions. Septicemic form is rare in pigs.
Symptoms
- Pharyngeal: Edema, dyspnea, difficulty swallowing, or death within 24 hours. Survivors become carriers.
- Intestinal: Clinical signs are not evident.
- Septicemia: Death without clinical symptoms.
Lesions
- Pharyngeal: Gelatinous edema in the neck and splenomegaly.
- Intestinal: Ulcers in the intestinal mucosa and mesenteric lymph nodes.
- Septicemia: Generalized hemorrhagic lesions.
Diagnosis
Laboratory tests are essential for confirmation.
Control
Bury or burn carcasses. Test feed and animal substances.
Vaccination
For uninfected pigs.
Treatment
Penicillin injections in early stages may be effective.
Septicemia caused by Streptococcus sp.
Described in nervous diseases.
Infection by Actinobacillus suis
Affects maternity and nursery pigs.
Etiology
Actinobacillus suis. Sensitive to most disinfectants.
Epidemiology
More common in piglets than adults. Introduced by carriers. Stress is a predisposing factor. Acute form: Sepsis and death within 15 hours to a few days. Chronic form: Endocarditis and arthritis. Skin lesions may occur. Affects up to 1/3 of the litter.
Pathogenesis
Respiratory tract infection leads to septicemia and death in 15 hours to 3 days. Vegetative endocarditis and arthritis may occur.
Symptoms
Sudden death in young piglets, fever, skin reddening, petechiae (ears and abdomen), and joint swelling. Survivors experience wasting. Pneumonia, subcutaneous abscesses, anorexia, metritis, and meningitis in older pigs, especially after farrowing.
Lesions
Skin redness, petechiae in kidneys, lungs, and heart, fluid in body cavities, vegetative endocarditis, pneumonia, and abscesses in lungs, liver, kidneys, and joints.
Diagnosis
Clinical data are non-specific; bacteriological examination is required. Send lung, blood, heart, kidney, and cavity fluid samples.
Control
Eliminate severely affected pigs.
Treatment
Penicillin, tetracycline, sulfa-trimethoprim. Add oxytetracycline (600g/ton) to sow feed for 10 days before farrowing. Inject piglets with penicillin or amoxicillin-dihydrostreptomycin (15mg/piglet).
Glässer’s Disease
Serous inflammation causing pleurisy, pericarditis, peritonitis, arthritis, and meningitis.
Etiology
Haemophilus parasuis.
Symptoms
Sudden onset with anorexia, fever, and lethargy. Depending on the affected site: Cough, dyspnea, cyanosis, fever, and sudden death (acute form). Joint inflammation and pain, nervous symptoms (ataxia, tremors, lateral recumbency) in the polyserositis form. Arthritis and adhesions in the chronic serous form. Three clinical forms:
- Polyserositis: Fibrinous-purulent exudation in synovium, peritoneum, pleura, pericardium, and meninges. Associated with stress in young pigs.
- Septicemia: No polyserositis – sudden death and bleeding.
- Pneumonia
Survivors experience wasting.
Lesions
Pleurisy, pericarditis, peritonitis, polyarthritis, meningitis, and hemorrhagic pneumonia (rare), alone or in combination. Pinpoint kidney hemorrhages (septicemia). Adhesion of pleura, pericardium, and peritoneum (chronic cases seen in slaughtered pigs).
Epidemiology
Pigs 2 weeks to 4 months old, most frequently after weaning due to stress. Transport also triggers the disease.
Pathogenesis
Infection via aerosol, but bacteria can be isolated from healthy pigs. H. parasuis has tropism for serous membranes, synovial fluid, meninges, and lung parenchyma.
Diagnosis
Pure bacterial cultures can be obtained from serofibrinous lesions and pericardial fluid.
Control
Autogenous vaccines for piglets at 6-8 weeks old; sometimes for sows during outbreaks. Limitations exist due to multiple serotypes, some not included in vaccines. Parenteral drugs (penicillins, cephalosporins, quinolones, sulfa-trimethoprim). Preventive medication via water or feed.
Veterinary Action
Use vaccines containing serotypes 4 and 5 in nursery and growing pigs. Send material for bacteriological examination. Reduce stress factors. Treat patients with antibiotics. Vaccinate gestating sows during outbreaks.
Enteric Diseases
Diarrhea occurs due to destruction of intestinal villi cells, leading to malabsorption.
Neonatal Colibacillosis
Affects piglets in the farrowing house.
Diarrhea color: Yellowish liquid.
Etiology
Escherichia coli.
Pathogenesis
E. coli from sow feces adheres to the piglet’s intestinal mucosa, producing LT and STa toxins, increasing secretory activity (crypt cells), leading to diarrhea and dehydration.
Epidemiology
Poor farrowing crate disinfection, poor drainage of sow urine and feces, dirty hands during farrowing, ineffective cleaning of the perineum, vulva, and teats, cold floors without bedding, difficulty sucking colostrum, and sow immune deficiency.
Symptoms
One or more piglets affected soon after birth with rapid diarrhea, dehydration, and death within 4-24 hours. High mortality. Less severe if partial immunity is transmitted through colostrum.
Diagnosis
Diarrhea color and culture/classification of E. coli.
Location and Lesions
Small intestine. Autopsy: Yellow liquid in the intestine.
Control and Veterinary Action
Correct risk factors. Use the all-in/all-out system.
Vaccination
Sows at 90 days of gestation. Gilts at 60 and 90 days of gestation.
Treatment
Antibiotics based on antibiogram.
Colibacillosis of the Third Week
Mild diarrhea in piglets 5-25 days old.
Diarrhea color: Yellowish liquid.
Etiology
E. coli associated with other agents (Isospora suis, rotavirus, enterovirus).
Pathogenesis and Epidemiology
: similar to neonatal colibacillosis. However, there are influences of changes in digestive physiology resulting from ingestion of pre-starter feed, dirty or in Fermented food trough.
Enterotoxins:
MATERNITY. Diarrhea occurs by increased permeability.
COLOR OF DIARRHEA: liquid dark with blood. By inflammation, there is an increase of the pores and blood goes to the light.
ETIOLOGY: Clostridium perfringens C.
PATHOGENESIS: piglet with up to seven days of life to ingest C. perfringens present in the stool portion bacteria cling to the jejunum and produce toxin proteolíticaà villous necrosis, hemorrhage, bacteremia, toxemia, death.
EPIDEMIOLOGY: Occurs rarely. Those who become ill often die.
SYMPTOMS: Acute: death in 1 to 3 days after birth, with rapid dehydration and dysentery. Chronic, intermittent diarrhea for a week or two, dark stools with mucus and growth retardation.
DIAGNOSIS: culturing the bacteria, send to the laboratory or the small intestine in piglets own refrigeration.
LOCAL AND INJURIES: small intestine.
CONTROL AND ACTION OF MED. VET.:
TREATMENT: The use of antibiotics after the onset of symptoms does not offer good results.
VACCINATION: nuts 70 and 90 days of gestation. The vaccine is used on farms that have or have had the disease.
Rotaviruses:
AFTER WEANING (maternity). Rest of milk occurs in diarrhea malabsorption.
COLOR OF DIARRHEA: yellowish liquid with milk is not digested.
ETIOLOGY: Reoviridae. Resistant to disinfectants used and survives in faeces.
PATHOGENESIS: ID the virus, destroys the villi enterocytes (atrophy and fusion = decrease of absorption area) to the intestinal contents to the fermentation of poorly absorbed to osmosis to yellowish watery diarrhea with undigested milk clots.
EPIDEMIOLOGY: piglet mortality, growth retardation, drug costs. Concomitant infection by E. coli, coronavirus and Coccidia aggravate the case. Piglets in contact with the feces of sows may be contaminated, cause the virus is eliminated until 5 days before and two weeks after delivery.
Symptoms: vary from farm to farm due to management, concurrent infections, level of immunity. Flocks of good management: infection is mild and of short duration. Anorexia, vomiting and occasionally diarrhea after ranging from watery to creamy yellow to green – containing undigested milk. Death until the 7 days after onset of symptoms. Piglets recovering: normalization of stool consistency may take 1 or 2 weeks, piglets waste due to malabsorption syndrome.
DIAGNOSIS: faeces collection and laboratory examination (virology). Electron microscopy, immunofluorescence and PAGE.
LOCAL AND INJURIES: small intestine.
CONTROL AND ACTION OF MED. VET.: The existence of multiple serotypes hinders the achievement of effective vaccine. Treat secondary infections with antibiotics, rehydrate the piglets, to improve management. Exposing the virus primiparous pregnancy.
Transmissible gastro-enteritis (TGE):
MATERNITY, CRECHE, RECRIA, TERMINATION.
DIARRHEA COLOR: yellow liquid, with remnants of undigested food.
Etiology: Coronavirus suis.
PATHOGENESIS: Occurs commonly economies in winter months because the virus and heat-sensitive.
Contamination estomagoà mouth to duodenum, jejunum and ileum destroys the cells of acute absorption syndrome in a bad absorption to increase osmolality to diarrhea.
Epidemiology: infection through feces, contaminated food, people and vehicles.
SYMPTOMS: vomiting, diarrhea, thin and watery, yellowish, with leftovers. Weight loss, and unquenchable thirst. Growing-finishing pigs: elevated body temperature, vomiting, lethargy, weight loss and diarrhea yellow watery foul smelling. Sows may agalactia.
DIAGNOSIS: consider the occurrence at all ages, no effect of antibiotic use, mortality of piglets until 10 days of life and quick recovery of other age groups. Laboratory tests: virus isolation, immunofluorescence, histopathology, detection of antibodies by neutralization.
LOCAL AND INJURIES: small intestine. Becomes strained, with content merged with pasty yellow. Villous atrophy occurs, visible by histopathology.
CONTROL AND ACTION OF MED. VET.: No specific treatment. Controlling for non-occurrence of secondary infection. Alternative is to immunize herds: collect feces and intestines of pigs infected patients and pregnant sows up to at least two weeks before delivery in order to produce antibodies in the colostrum.
COCCIDIOSE:
MATERNITY AND CRECHE.
COLOR OF DIARRHEA: pasty yellow, fetid and that persists for more than eight days.
ETIOLOGY: Isospora suis, can sometimes occur by Eimeria sp.
PATHOGENESIS: oocyst (eliminated in feces) to sporulate in the environment are eaten, releasing sporozoites in the gut to enter the cells of the jejunum and ileum: meronts with merozoites, rupture the cells to cause diarrhea or invade other – 2nd generation meronts the sexual stage (the cycle begins again).
Epidemiology: incidence is higher in piglets 5-25 days of life. Adult animals are carriers. Morbidity rate can reach 100%, but mortality is less than 5%. Piglets become infected by ingestion of oocysts remaining in the maternity floor (washing and disinfecting the disabled).
SYMPTOMS: diarrhea fetid yellow creamy, pasty, watery rarely. Persists for 5 to 12 days, does not respond to antibiotics. Dehydration, developmental delay, refuse.
LOCAL AND INJURIES: ID and IG. Microscopic: crypt hyperplasia, diarrhea malabsorption. Fusion of villi, necrosis at the top of the crypts. Merozoites and meronts appear. Decreased villus height.
DIAGNOSIS: demonstration of forms of the parasite in the epithelial cells of the jejunum and ileum via mucosal smears stained by Giemsa or Wright, or by histopathological examination.
CONTROL: medication in the diet of nuts, amprolium (500 ppm), 10 days before and two weeks after delivery. Oral medication for piglets on the third day of life, using toltrazurik (20mg/kg) five days after repeating.
ACTION OF MED. VET.:Preventive measures: medication for sows and piglets; elimination of oocysts of the environment, hygiene at the hospital.
SWINE DYSENTERY:
Growing and finishing. Infectious disease.
COLOR OF DIARRHEA: Diarrhea with mucus and dark blood.
ETIOLOGY: Brachyspira hyodysenteriae. Anaerobic spirochete.
PATHOGENESIS: growing or finishing pigs: ingestion of contaminated feces to B. hyodysenteriae to mucosal inflammation, edema, large intestine crypt to diarrhea with mucus and blood.
EPIDEMIOLOGY: occur at any age but is most common in animals from 15 to 70 kg Contamination by sick animals, contaminated food and water. Introduction of carriers in the herd. Rats can be considered vectors. Piglets born in infected herds may not have symptoms and transmit the disease to which they are sold. PI 4 to 14 days.
SYMPTOMS:
- Hyperacute form: death within 24 hours, more rare.
- Chronic, persistent diarrhea or alternating with normal stools and delayed development (sequelae of the acute phase).
- Acute diarrhea and mucus, blood and food particles in feces. Later the stools get chocolate-brown, mucus is bloody or foul smelling. Affected animals lose weight, have perinea dirty stool, ribs, sunken eyes.
LOCAL AND INJURIES: large intestine.
DIAGNOSIS: clinical data and necropsy, cultivation of microorganisms, the microscope, direct immunofluorescence stool or mucosa. Use of PCR and serological tests.
CONTROL AND ACTION OF MED. VET.: In case of outbreak: medicate all pigs on the farm for feed or water. Cleaning and disinfection of environmental and vector control: rodents, dogs and cats. Manure removal and disinfection.
COMPLEX proliferative enteropathy intestinal adenomatosis = = = necrotic enteritis regional ileitis and proliferative haemorrhagic enteropathy.
Growing and finishing. It is transferable.
COLOR OF DIARRHEA: liquid, yellowish tint may be bloody.
Etiology: Lawsonia intracellularis. Bacteria difficult to culture.
PATHOGENESIS: swine from the growing phase with oral infection, L. intracellularis multiplies in cells of the crypts of the ileum to the cells break down, bacteria penetrate into other cells to the inflammatory reaction, proliferation of immature epithelial cells of the crypts to adenomas OR epithelial necrosis or hemorrhage.
SYMPTOMS: chronic diarrhea with weight loss and poor performance in piglets àAfeta growth, but can reach adult and young animals. Brown diarrhea that affects pigs aged 20 to 40 kg. The diarrhea usually contains no blood or mucus. The pigs eat normally but do not gain weight.
The second form of ileitis is the hemorrhagic form occurs in pigs with agudaà next age at slaughter and young breeders, because the antibiotics are removed from the diet in this phase. Anemic pigs are found dead suddenly.
LOCAL AND INJURIES: small intestine. Terminal ileum wall thickening occurs (garden hose), crypt hyperplasia, the bacteria multiply inside the cells and rupture.
DIAGNOSIS: there is no way to diagnose an animal alive. You can diagnose by histopathology and PCR (send ileum appear to be positive crypt hyperplasia). Differential for salmonellosis, swine dysentery, gastric ulcer and chronic TGE.
CONTROL AND ACTION OF MED. VET.: Avoid mixing pigs of different ages. Determine measures of hygiene in the premises. Necropsy pigs with diarrhea and send material for examination, examination of feces for PCR.
TREATMENT: in-feed tylosin 100g/ton. For 14 days to keep 40g/ton. Oxytetracycline: 400 ppm for 14 days to start and for another 14 days.
Salmonellosis:
CRECHE, growing and finishing. Symptoms occur when there is stress or other diseases.
COLOR OF DIARRHEA: liquid, dark, yellowish, greenish with necrotic material.
ETIOLOGY: Salmonella choleraesuis and Salmonella typhimurium. The bacterium resists months in the environment, but is sensitive to disinfectants (phenols, chlorinated or iodinated).
PATHOGENESIS: OR pigs with contaminated feed to other pigs: oral Salmonella multiplies in the intestine by bad diarrhea – absorption and increased permeability of the intestine (inflammation) OR symptoms of sepsis (endotoxemia).
Epidemiology: usually occur in pigs for 5 weeks to 4 months of life. Young piglets are protected by the colostrum. The bacterium enters the farm animals introduced by q carry stress and release the microorganisms or by contaminated feed.
Becomes the source of poisoning for humans: the spread of housing and derivatives and elimination in feces.
Most often occurs due to intercurrent disease (CRP, nutritional deficiencies, Ascari suum) or stress (wet, vaccination of animals debilitated, transportation). Mixing animals from different batches.
SYMPTOMS:
- ACUTE FORM: sudden death, elevated temperature (40.5 to 41.5), difficulty walking, weakness, piling up, occasionally diarrhea. Red areas on skin (ears, belly, groin). Death in 1-4 days after onset of symptoms.
- CHRONIC FORM: increased body temperature, decrease in appetite, diarrhea (liquid stools smelling, yellowish, greenish or bloody, with streaks of necrotic material). The diarrhea is intermittent, can last several weeks. They become scrap the survivors.
LOCAL AND INJURIES: large intestine.
ACUTE FORM: hemorrhagic gastroenteritis with bleeding in the stomach lining, enlarged spleen, petechiae hemorrhages in the epiglottis, bladder and kidneys, purulent pneumonic foci in the lung.
CHRONIC FORM: areas of necrotic tissue in the mucosa of the cecum and colon. Contents of the intestine is fetid liquid containing clumps of necrotic tissue. Mesenteric increased.
DIAGNOSIS: bacteriological examinations, isolation of salmonella. Live animal feces or rectal swab. Dead animals: spleen and intestine. Make differential diagnosis with PSC, necrotic enteritis and Swine Dysentery.
CONTROL: Avoid ingestion of contaminated food, eliminate or isolate sick animals, antibiotic therapy, cleaning, disinfection and proper management, avoiding overcrowding.
VACCINATION: nuts in the last month of pregnancy, females of replacement at 70 and 90 days of gestation and piglets 20 days old, revaccinated at 60 days.
ACTION OF MED. VET.: Isolate sick pigs, perform autopsies on some, send material for laboratory examination (stool and spleen). Recommend a good feed source. Cleaning, disinfection. Avoid mixing lots of different origins. Avoid stress. Recommend treatment based on antibiogram.
Spirochetal Colitis:
Growing and finishing. Self-limiting. Reduced weight gain and worsening daily and feed conversion.
COLOR OF DIARRHEA: pasty-colored cement.
ETIOLOGY: Brachypira pilosicoli.
PATHOGENESIS: pigs in the early stage of growth not medicated feed OR OR oral contamination (faecal bacteria) bacteria to adhere to mucus in the large intestine enterocytes to diarrhea because of poor – absorption.
EPIDEMIOLOGY: bacteria have also been detected in humans, primates, birds and dogs. In swine disease has been diagnosed in all countries with organized swine, occurring mainly when the feed contains no antibiotics.
SYMPTOMS: feces pasty, grayish color like cement, weight loss and culling of some pigs.
LOCAL AND INJURIES: large intestine. Mucosa congested, bright (excess mucus on the surface).
ACUTE FORM: enlarged spleen, petechiae hemorrhage, pneumothorax purulent foci.
CHRONIC FORM: necrotic tissue (cecum and colon), focuses tires.
DIAGNOSIS: bacteriological anaerobiosis may show weakly beta hemolytic colonies of B. pilosicoli. Molecular techniques such as PCR are used.
CONTROL: Control measures are similar to those used for swine dysentery. Avoid overcrowding and mixing lots of different origins.
VACCINATION: nut in the last month of pregnancy. Piglet 15 to 30 days old. Only once has the problem.