CONDITIONS/DISEASES IN WEANERS AND GROWER/FINISHERS
CONDITIONS/DISEASES IN WEANERS AND GROWER/FINISHERS
Contributors
Munetsi Tagwireyi - Assistant Professor, Large Animal Medicine
Ailbhe King, MVB DACVIM (LAIM) - Assistant Professor in Livestock Medicine
LEARNING OBJECTIVES
Common diseases in piglets during weaning & grower/finisher stages:
Edema disease
Erysipelas
Porcine circovirus
Glasser’s disease
Greasy pig disease
Swine dysentery
PPE (Porcine Proliferative Enteropathy)
Salmonella
Gastric ulcers
Trichuris suis
Describe the presentation, clinical signs, diagnosis & treatment for the following diseases:
Ascaris suum
APP (Actinobacillus Pleuropneumonia)
EP (Enzootic Pneumonia)
Swine flu
Atrophic rhinitis
Pseudorabies
Mulberry heart disease
CONDITIONS AFFECTING WEANERS
Common Health Issues in Weaners
Aural hematoma
Meningitis
Middle ear issues
Oedema disease
Progressive atrophic rhinitis
Ascaris suum
APP
Glasser's disease
Mulberry heart disease
Mycoplasma hyopneumoniae
Pasteurella
PRRSV (Porcine Reproductive and Respiratory Syndrome Virus)
Swine fever
Swine influenza
Coccidiosis
Colitis
E. coli infections
Gastric ulcers
Ileitis
Swine dysentery
TGE (Transmissible Gastroenteritis)
Trichuris suis
Abrasions
Abscesses
Dermatosis vegetans
Ear biting
Erysipelas
Greasy pig disease
Hernia
Mange
Parakeratosis
PDNS (Porcine Dermatitis and Nephropathy Syndrome)
Swine pox
Trauma
Vices
PMWS (Post Weaning Multisystemic Wasting Syndrome) affecting lymphatics
Zearalenone toxicity
Arthritis
Carpal injuries
Foot and Mouth disease
Streptococcus arthritis
Common Health Issues in Growers/Finishers
APP
Aujeszky's disease
Endocarditis
Glasser's disease
Mycoplasma pneumonia
PRRSV
PMWS
Salmonellosis
Swine fever
Swine influenza
Ascaris suum
Clostridial infections
Colitis
Epidemic diarrhea
Gastric ulcers
Glasser's disease
PIA (Porcine Intestinal Adenomatosis)
Rectal stricture
Salmonella infections
Swine dysentery
TGE
Torsions
Zearalenone toxicity (particularly in females)
Arthritis
Bursitis
Bushfoot
Foot and Mouth disease
Fractures
Glasser's disease
Kinky back syndrome
Mycoplasma arthritis
OCD (Osteochondritis Dissecans)
PSS (Porcine Stress Syndrome)
Sores
Spinal abscesses
EDEMA DISEASE
Definition: Acute, often fatal enterotoxemia of recently weaned pigs.
Etiology: Toxins produced in the small intestine by E. coli (most commonly with pilus type F18 or F4 (K88)) along with an elaborate Shiga-like toxin.
Pathophysiology: Degenerative angiopathy, vascular permeability increases, leading to accumulation of edema at various sites, notably the colon, stomach, small intestine, eyelids, and brain.
Clinical Signs: - Anorexia
Ataxia
Stupor and recumbency often accompanied by paddling and running movements
Abnormal squeal when handled
Characterized by edema and sudden deaths, occasionally with neurological signs.
Epidemiology: Sporadic cases in the USA.
Risk Factors: - Chilling
Diet changes
Low-quality feed
Frequent medications in feed
Switching diets regularly
Diagnosis
Fecal culture and toxin identification are key to confirm diagnosis.
Treatment
Administration of antibiotics, supportive care for dehydration and acidosis, and switching to low protein diets.
Control Measures
Management factors should minimize environmental stressors.
Nutritional management strategies to consider: - Creep feeding
Restricted feeding with multiple small feedings post-weaning
Addition of oats (fiber), acidifiers to feed and water, decreased protein in rations, addition of zinc oxide, and plasma protein in ration.
Antibiotics can be added to water.
Immunoprophylaxis with plasma or vaccination.
In negative herds, prevent introduction of infected breeding stock—eradication may be possible through depopulation and disinfection.
Genetic resistance exists in pigs lacking receptors for F18 and/or F4 (K88) pili.
ERYSIPELAS (DIAMOND SKIN DISEASE)
Definition: Multisystemic disease caused by Erysipelothrix rhusiopathiae, an aerobic Gram-positive rod.
Pathogenesis: - The bacterium gains access to the bloodstream via invasion of tonsils/gut lymphoid tissue, leading to widespread vasculitis.
It secretes exotoxins that damage vascular endothelium, leading to thrombosis of small arterioles and venules throughout the body, resulting in characteristic well-demarcated cutaneous lesions.
Epidemiology: Zoonotic; asymptomatic carriers and clinically affected pigs can shed bacteria in feces/body fluids.
Potential sources of infection include contaminated feed and water, as well as infection from birds, pets, and other livestock such as lambs and turkeys.
Clinical Signs
Acute Stage: - Septicemia
Sudden death in grower-finishers and adults
High fever (104-106 F)
Characteristic diamond lesions on skin—well-demarcated, red patches that are not raised or pruritic.
Chronic Stage: - Endocarditis
Poor body condition and heart failure
Arthritis, characterized by reluctance to stand, joint distension, and squealing when moving.
Diagnosis
Necropsy Findings: - Skin lesions, petechiae on multiple organs, congested lungs, liver, and spleen, with splenic infarcts.
Signs of septic arthritis: cloudy joint fluid, articular cartilage erosion, and synovial proliferation.
Endocarditis: cauliflower growths on heart valves.
Treatment and Control
Antibiotic of Choice: Penicillin.
Vaccination: - Considered protective under most circumstances; a killed bacterin requiring 2 doses for initial high titers and annual or bi-annual boosters.
PORCINE CIRCOVIRUS (PCVD)
Also referred to as Postweaning Multisystemic Wasting Syndrome (PMWS).
Etiology: Caused by Porcine Circovirus type 2.
Typical Onset: Occurs 4-8 weeks after placing pigs in a grow-finish operation, particularly in weaned pigs.
Clinical Signs: - Progressive wasting, ill thrift, and failure to thrive observed in pigs aged 6-18 weeks.
Other signs include lymphadenopathy (LN), patchy dermatitis, dyspnea, and icterus.
Mortality Rates: Non-responsive to antibiotic therapy, high case-fatality (> 50%), and group mortality rates of 15% or higher.
Diagnosis
Necropsy Findings: - Kidney enlargement with multifocal hemorrhagic areas within the cortex.
Mixture of granulomatous inflammation and lymphocyte depletion in lymph nodes.
Hallmark lesion: lymphoid depletion associated with PCV2 antigens or nucleic acids in tissues, visible cutaneous vasculitis, leading to Porcine Dermatitis and Nephropathy Syndrome (PDNS).
Prevention
Good management practices including control of co-infections and vaccination are essential (e.g., Porcine Circovirus Vaccine, Type 2).
GLASSER’S DISEASE (POLYSEROSITIS)
Etiologic Agent: Haemophilus parasuis, a small Gram-negative rod that is part of the normal respiratory flora but can become opportunistic.
Pathogenesis: The bacterium penetrates the nasal/tracheal mucosa, reaches the bloodstream, and exhibits a preference for serosal surfaces, causing fibrinous and purulent inflammation across multiple serosal surfaces, including pericardium, pleura, peritoneum, synovia, and meninges.
Clinical Signs
Initial signs include fever and lethargy.
Synovitis presents as reluctance to move and lameness, particularly in carpal and tarsal joints.
Meningitis can lead to tremors, ataxia, lateral recumbency, and seizures.
Terminally, dyspnea and cyanosis may occur, with highly virulent strains resulting in acute death.
Diagnosis and Necropsy Findings
Diagnosis: - Culture requires specialized media from fluid, synovial tissue, meninges, or representative serosal lesions.
Histology is essential for confirmation.
Necropsy: Fibrinous, opaque fluid is found in pleural, pericardial, and peritoneal cavities, as well as in joints and meninges. Lesions may be similar to those of Streptococcus suis infections.
Treatment and Prevention
Primary treatment involves parenteral antibiotics, including Ceftiofur, Oxytetracycline, Ampicillin, and Tulathromycin.
Preventative measures include the use of commercial or herd-specific bacterins administered to sow herds and weaned piglets, along with reducing stressors that might weaken the immunity of weaned piglets.
Proper nutrition, ventilation, temperature, humidity control, sanitation, and avoiding overcrowding are also key.
EXUDATIVE EPIDERMATITIS (GREASY PIG DISEASE)
Etiologic Agent: Staphylococcus hyicus, characterized as the dominant cause in the nursery stage (4-8 weeks) but also occasionally seen in baby piglets and older pigs.
Pathogenesis: Normal flora can have pathogenic strains under certain conditions, leading to disease. Poor nursery hygiene, overcrowding, abrasions, and deficiencies in trace minerals have been implicated.
Clinical Signs
Lesions typically begin on the face and legs, leading to localized brown patches that merge into larger areas across the body, including the axillae, flanks, belly, and inguinal area.
Skin appears dark, thickened, and wrinkled with large scabs and crusts developing over necrotic epidermis.
Associated Signs: Pigs often appear lethargic with poor appetite, and in severe cases, mortality from toxemia can occur especially in younger pigs. Renal lesions may occur in fatal cases alongside pyelonephritis.
Treatment and Control
Severely affected pigs may require euthanasia. Localized infections might respond to improved sanitation and reduction in crowding, mite control, systemic antibiotics, and topical antiseptics.
One suggested treatment includes mixing mineral oil with Nolvasan and dish detergent for topical application alongside systemic penicillin and dexamethasone.
SWINE DYSENTERY AND SPIROCHETAL DIARRHEA
Definition: Infectious typhlocolitis characterized by mucoid, hemorrhagic diarrhea.
Etiology: Brachyspira hyodysenteriae, a Gram-negative, motile, anaerobic (yet oxygen-tolerant) spiral-shaped bacterium.
Transmission: Through asymptomatic carriers, rodents, mice, and dogs, which serve as reservoirs and can persist in environments for extended periods.
Clinical Signs
Symptoms start with soft yellow/gray feces, progressing to watery diarrhea with mucus, blood, and fibrin.
Chronic presentations may result in a rough haircoat, thin condition, and specifically colored feces.
Diagnosis
Methods: - Culture of feces or colonic mucosa and necessary PCR for definitive identification.
Necropsy Findings: Segmental lesions within the large intestine, swollen and edematous colonic mucosa with a pseudomembrane potentially forming.
Treatment and Control
Effective control typically involves depopulation or mass medication and strict biosecurity practices across the facility post-outbreak.
PORCINE PROLIFERATIVE ENTEROPATHY (PPE)
Etiologic Agent: Lawsonia intracellularis, a Gram-negative obligate intracellular bacterium.
Common forms include: - Porcine Intestinal Adenomatosis (PIA) characterized by chronic mild diarrhea, and Proliferative Hemorrhagic Enteropathy (PHE), an acute, potentially deadly form associated with severe gastrointestinal bleeding.
Clinical Signs
In PIA, signs may include chronic diarrhea, poor growth performance, and in severe cases, necrotic enteritis.
In PHE, rapid weight loss followed by death due to intraluminal hemorrhage is typical, with an elevated case fatality rate (up to 90%).
Diagnosis and Treatment
Diagnosis includes histopathology, serology, and supportive treatment with antibiotics.
SALMONELLA
Key Agents: Salmonella cholerasuis and Salmonella typhimurium, primarily affecting weaners and growers.
Transmission: Fecal-oral route, contaminated feed, and stressful events can precipitate outbreaks.
Clinical Signs
Salmonellosis can manifest as acute death, severe septicemia, enterocolitis with watery diarrhea, and potentially high morbidity and mortality rates.
Diagnosis and Control
Diagnosed through culture and PCR from fecal specimens, with control measures emphasizing proper sanitation and biosecurity.
GASTRIC ULCERS
Affects predominantly grower-finishers around 3-6 months of age; risk factors include finely ground feed, lack of fiber, and fasting.
Clinical Signs
Signs include sudden deaths due to rapid blood loss and chronic anemia leading to lethargy, hypovolemia, and potential for gastric rupture.
Diagnosis and Treatment
Biosecurity measures along with dietary improvements (coarse feed) and specific medications are recommended to manage and treat this condition effectively.
TRICHURIS SUIS (WHIPWORMS)
Characteristic of colitis in outdoor pigs, often leading to diarrhea indistinguishable from other conditions.
Diagnosis primarily through fecal analysis for characteristic eggs and treated with specific anthelmintics.
ASCARIS SUUM
Most prevalent nematode infecting pigs, leading to gastrointestinal damage and respiratory implications. The lifecycle is characterized as hepato-tracheal.
Treatment with dewormers is essential to mitigate weight loss and economic losses due to infestations.
ACTINOBACILLUS SUIS (APP)
Causing pleuropneumonia in pigs, characterized by severe respiratory distress and high mortality rates during outbreaks.
Diagnosis and Treatment
Morbidity is typically high; already identified strains may respond effectively to specific antibiotic treatments, with preventive measures emphasizing herd health management and biosecurity.
ENZOOTIC PNEUMONIA (EP)
Definition: Chronic respiratory disease primarily caused by Mycoplasma hyopneumoniae.
Etiology: Mycoplasma hyopneumoniae, often complicated by secondary bacterial infections (e.g., Pasteurella multocida).
Clinical Signs: - Chronic dry cough, especially noticeable during feed-eating or exercise.
Reduced daily gain and feed efficiency.
Mild fever, dyspnea, and respiratory distress, particularly in severe cases or with secondary infections.
Pathology: Cranioventral lobar consolidation of the lungs, often plum-colored or grayish.
Diagnosis: - PCR from bronchial swabs or lung tissue.
Serology (ELISA) to detect antibodies.
Histopathology of lung lesions.
Treatment: - Antimicrobials (e.g., tetracyclines, tiamulin, tulathromycin) reduce clinical signs and shedding.
Symptomatic treatment for secondary infections.
Control Measures: - Vaccination is widely used and effective in reducing clinical signs and lung lesions.
All-in/all-out management.
Good ventilation and air quality.
Reduction of stressors.
SWINE INFLUENZA (SWINE FLU)
Definition: Acute, highly contagious respiratory disease caused by influenza A viruses.
Etiology: Influenza A viruses (H1N1, H3N2, H1N2 being common strains).
Clinical Signs: - Sudden onset of high fever (104-107 F).
Lethargy, anorexia, prostration.
Barking cough, sneezing, and mucopurulent nasal discharge.
Dyspnea and labored breathing.
Rapid spread through the herd, often affecting nearly all animals in a short period.
Epidemiology: Zoonotic potential. Spreads rapidly via aerosol and direct contact.
Diagnosis: - RT-PCR from nasal swabs or lung tissue (most common and rapid).
Virus isolation.
Serology to detect antibodies.
Treatment: - Supportive care (e.g., electrolytes in water, comfortable environment).
Antibiotics to control secondary bacterial infections.
Control Measures: - Vaccination significantly reduces clinical signs and viral shedding.
Biosecurity measures to prevent introduction.
Isolation of sick animals.
ATROPHIC RHINITIS
Definition: Progressive inflammatory disease of the nasal turbinates, leading to their atrophy and facial distortion.
Etiology: - Primarily caused by toxigenic strains of Pasteurella multocida (type D).
Bordetella bronchiseptica often acts as a predisposing agent, creating conditions for P. multocida to thrive.
Clinical Signs: - Sneezing, nasal discharge (serous to mucopurulent).
Epistaxis (nosebleeds).
Facial distortion (shortening or deviation of the snout) in severe, chronic cases.
Reduced growth rates due to impaired breathing and feed intake.
Tear staining below the eyes.
Pathology: Atrophy and distortion of the nasal turbinate bones, visible upon cross-sectioning the snout.
Diagnosis: - Clinical signs and history.
Necropsy findings (turbinate atrophy).
Bacterial culture to identify causative agents and toxin production.
Treatment: - Antimicrobials (e.g., sulfonamides, tetracyclines) may help reduce disease severity but often don't reverse turbinate damage.
Control Measures: - Vaccination of sows and piglets provides passive immunity and active protection.
Improved ventilation and reduction of stocking density.
Management of concurrent respiratory diseases.
Eradication (depopulation/repopulation) in severely affected herds.
PSEUDORABIES (AUJESZKY'S DISEASE)
Definition: Highly contagious viral disease affecting swine, caused by Suid herpesvirus 1 (SHV-1).
Etiology: Suid herpesvirus 1 (SHV-1), a DNA virus.
Clinical Signs: - Neonatal Piglets: High mortality (100%), neurological signs (tremors, ataxia, convulsions), fever.
Weaned/Grower Pigs: Respiratory signs (coughing, sneezing), fever, neurological signs (ataxia, posterior paralysis).
Finisher Pigs: Milder respiratory signs, anorexia, weight loss.
Adult Swine/Sows: Reproductive failure (abortions, stillbirths, mummified fetuses), mild respiratory signs, neurological signs during acute outbreaks.
Other Species (dead-end hosts): "Mad itch" (intense pruritus), neurological signs, always fatal.
Transmission: Direct contact with infected secretions (nasal, ocular, oral), venereal, transplacental, aerosol.
Diagnosis: - PCR from tissue (brain, tonsil, lung) or swabs.
Virus isolation.
Serology (ELISA) to detect antibodies.
Treatment: No specific antiviral treatment available for pigs.
Control Measures: - Vaccination (modified live or inactivated vaccines) reduces clinical signs and shedding.
Strict biosecurity to prevent introduction.
Eradication programs (successfully implemented in many countries, including the USA, via systematic testing and removal of infected animals).
MULBERRY HEART DISEASE
Definition: Acute cardiac muscle degeneration and necrosis, leading to sudden death in fast-growing pigs.
Etiology: Caused by a severe deficiency of Vitamin E and/or selenium, leading to oxidative damage to cell membranes, particularly in the heart.
Risk Factors: - Rapid growth in young, heavily muscled pigs.
Diets low in Vitamin E and selenium or containing rancid fats that deplete Vitamin E.
Concurrent stress or infections.
Clinical Signs: - Sudden death with no premonitory signs, often in apparently healthy, fast-growing pigs (2-4 months of age).
Occasional dyspnea, weakness, and reluctance to move prior to death.
Necropsy Findings: - Heart: Enlarged, pale, and often hemorrhagic, with areas of necrosis (giving it a "mulberry" appearance).
Excessive pericardial fluid, often with fibrin.
Pulmonary edema, ascites, and often liver degeneration.
Diagnosis: - Necropsy findings are highly suggestive.
Histopathology of the heart muscle confirms myocardial degeneration and necrosis.
Measurement of Vitamin E and selenium levels in feed or liver tissue.
Treatment: Limited due to the acute nature, but high doses of Vitamin E and selenium by injection may be attempted in affected groups.
Control Measures: - Ensure adequate supplementation of Vitamin E (100-200 IU/kg) and selenium (0.3 mg/kg) in all pig diets.
Avoid rancid fats in feed.
Provide good feed quality and storage.
A FINAL EMPHASIS ON PREVENTION
Critical management factors include reduction in stressors, nutritional support, early identification of disease signs, and consistent vaccination protocols to maintain herd health and productivity.