Porcine medicine is a critical component of the BCSE examination, with Domain 4 (Medicine) representing 50-55 questions, making it the LARGEST domain on the exam.
Overview and Clinical Importance
Porcine medicine is a critical component of the BCSE examination, with Domain 4 (Medicine) representing 50-55 questions, making it the LARGEST domain on the exam. Swine diseases have significant economic impact on the global pork industry and include several reportable/foreign animal diseases. This guide covers the major viral, bacterial, and multifactorial diseases affecting swine, with emphasis on etiology, clinical presentation, diagnosis, treatment, and prevention.
High-YieldThe BCSE tests practical clinical knowledge. Focus on differentiating diseases with similar presentations, understanding pathophysiology, and knowing key diagnostic tests and treatments.
| Feature |
Details |
| Etiology |
PRRSV (Arterivirus family). Two species: PRRSV-1 (European) and PRRSV-2 (North American). High mutation rate. |
| Target Cells |
Pulmonary alveolar macrophages and intravascular macrophages. CD163 receptor is essential for infection. |
| Transmission |
Direct contact, aerosol (up to 9.1 km documented), contaminated semen (shed up to 93 days), fomites, and needles. |
| Reproductive Signs |
Late-term abortions (last trimester), premature farrowing, stillbirths, mummified fetuses, weak-born piglets, increased preweaning mortality. |
| Respiratory Signs |
Interstitial pneumonia in nursery/finishing pigs. Decreased daily weight gain by up to 85%. Mortality 10-80% when complicated by secondary infections. |
| Diagnosis |
ELISA (detects antibodies to nucleocapsid protein - cannot predict immunity or carrier status), PCR assay (detects viral RNA), virus isolation. |
| Treatment |
No specific antiviral. Supportive care and control of secondary bacterial infections. Antimicrobials for opportunistic pathogens. |
| Prevention |
Modified live virus (MLV) vaccines (do not prevent infection but reduce viremia, lesions, clinical signs). Herd closure. Gilt acclimatization. |
| Disease Form |
Clinical Features |
| PCV2-SD (Systemic Disease) |
Formerly PMWS. Wasting, poor growth, enlarged lymph nodes, pallor, jaundice, diarrhea. Affects post-weaning pigs (5-12 weeks). Mortality can reach 10-30%. |
| PCV2-SI (Subclinical Infection) |
Most common form. Decreased average daily weight gain without overt clinical signs. Major economic impact. |
| PCV2-RD (Reproductive Disease) |
Late-term abortions, stillbirths, mummified fetuses. Virus in fetal hearts is diagnostic. |
| PDNS (Porcine Dermatitis and Nephropathy Syndrome) |
Red-purple macules/papules on skin (ears, hindquarters, abdomen). Enlarged kidneys with petechial hemorrhages. Type III hypersensitivity. |
| PCV2-LD (Lung Disease)/PRDC |
Component of Porcine Respiratory Disease Complex. Interstitial pneumonia. Often co-infected with PRRSV, SIV, Mycoplasma. |
Major Viral Diseases of Swine
Porcine Reproductive and Respiratory Syndrome (PRRS)
PRRS is one of the most economically significant diseases in the global swine industry, costing an estimated $664 million annually in the United States alone. It causes both reproductive failure in breeding animals and respiratory disease in growing pigs.
MEMORY AID - PRRS Features: Think 'PRRS = Pregnancy Problems + Respiratory Ruin in Swine' - The two main manifestations are reproductive failure and respiratory disease.
High-YieldPRRSV-infected boars can shed virus in semen for up to 93 days. Adults can be carriers for 86+ days, weaned pigs for 157+ days. ELISA positivity does NOT indicate protective immunity.
[Include Image: Figure 1. Interstitial pneumonia in a pig with PRRS infection showing diffuse tan consolidation]
Source: https://commons.wikimedia.org/wiki/Category:Veterinary_pathology - Search 'interstitial pneumonia swine'
Porcine Circovirus Type 2 (PCV2) and Associated Diseases
PCV2 is a small, non-enveloped, single-stranded circular DNA virus that causes a spectrum of diseases collectively known as Porcine Circovirus-Associated Disease (PCVAD). It is ubiquitous in swine populations worldwide.
MEMORY AID - PCVAD Manifestations: Remember 'PCVAD SWIRL' - Systemic (wasting), Wasting syndrome, Interstitial pneumonia, Reproductive disease, Lymphoid depletion. The virus causes lymphoid depletion and immunosuppression.
High-YieldMore than 98% of PCVAD cases involve co-infections! PRRSV is the most significant co-pathogen (52% of cases). Vaccination against PCV2 is highly effective - over 90% of US pigs are vaccinated before weaning.
MEMORY AID - PCV2 Co-infections: Think 'PRRS Makes Pigs Sick' - PRRSV (52%), Mycoplasma hyopneumoniae (36%), Porcine Parvovirus (15%), Swine Influenza (5.4%) are common co-pathogens.
[Include Image: Figure 2. Lymph node from a pig with PCV2 showing lymphoid depletion and histiocytic replacement]
Source: https://www.pig333.com/pathology-atlas/ - Filter by 'PCV2' for lymphoid tissue images
Porcine Enteric Coronaviruses (PED, TGE, PDCoV)
Three coronaviruses cause similar enteric disease in swine: Transmissible Gastroenteritis Virus (TGEV), Porcine Epidemic Diarrhea Virus (PEDV), and Porcine Deltacoronavirus (PDCoV). Clinical differentiation is difficult; laboratory confirmation is required.
MEMORY AID - Coronavirus Diarrhea: Remember 'Baby Pigs Die (from coronaviruses)' - All three cause severe watery diarrhea with highest mortality in neonatal piglets. TGE and PED are Alphacoronaviruses, PDCoV is Deltacoronavirus. NO cross-protection between them!
High-YieldThe 2013 PEDV outbreak in the USA killed over 8 million pigs. Villous atrophy in small intestine (jejunum/ileum) causes malabsorptive diarrhea, dehydration, and metabolic acidosis. Neonates are most susceptible due to slow epithelial regeneration.
Clinical Signs (All Three): Profuse watery diarrhea (often described as 'pea soup' or green-tinged), vomiting, severe dehydration, marked thirst, shivering, rapid weight loss. Pigs of all ages affected in naive herds, but mortality inversely related to age.
Diagnosis: PCR assays (can test feces, oral fluids, environmental samples). Immunohistochemistry on fixed tissues. Clinical signs alone cannot differentiate these viruses.
Treatment and Prevention: No specific treatment - supportive care (oral or IV fluids, warmth, electrolytes). Control secondary infections. Strict biosecurity is essential. Vaccines available in Asia; feedback (controlled exposure of sows to infectious material to stimulate lactogenic immunity) used in some outbreaks.
[Include Image: Figure 3. Small intestine from piglet with coronavirus infection showing thin, transparent walls and watery contents due to villous atrophy]
Source: https://www.pig333.com/pathology-atlas/ - Filter by 'PED' or 'TGE'
Swine Influenza Virus (SIV)
Swine influenza is a highly contagious respiratory disease caused by type A influenza viruses. Common subtypes in pigs include H1N1, H1N2, and H3N2. SIV is a component of PRDC and has zoonotic potential.
MEMORY AID - Swine Flu Features: Remember 'Flu Hits Fast and Fades' - Sudden onset (1-3 days incubation), high morbidity (up to 100%), LOW mortality (less than 1% uncomplicated), rapid recovery (5-7 days). Think 'barking cough.'
High-YieldSIV is a ZOONOSIS - farm workers can transmit influenza to pigs and vice versa. The 2009 H1N1 pandemic originated from reassortment involving swine, avian, and human influenza strains.
African Swine Fever (ASF) - REPORTABLE DISEASE
African Swine Fever is a HIGHLY LETHAL hemorrhagic disease with up to 100% mortality in domestic pigs and wild boar. There is NO approved vaccine and NO treatment. ASF is a REPORTABLE/NOTIFIABLE DISEASE requiring immediate notification to regulatory authorities.
MEMORY AID - ASF Recognition: Think 'ASF = A Serious Fatality' - Up to 100% case fatality rate. Key features: HIGH fever (up to 42 C), HEMORRHAGIC splenomegaly (enlarged dark spleen is pathognomonic), CYANOSIS of ears/snout/extremities. MUST differentiate from Classical Swine Fever (requires lab tests).
High-YieldASF is NOT present in the USA or Canada. If you suspect ASF, immediately contact your state/provincial veterinarian. The hemorrhagic, enlarged, dark spleen (almost black) occupying much of the abdominal cavity is the most characteristic lesion. ASFV only affects pigs - it is NOT zoonotic.
[Include Image: Figure 4. Hemorrhagic splenomegaly in acute African Swine Fever showing massively enlarged, dark spleen]
Source: https://pmc.ncbi.nlm.nih.gov/articles/PMC11232652/ - Open access images in Figure 3
| Feature |
TGE |
PED |
PDCoV |
| First Reported |
1946 (USA) |
1971 (UK), 2013 (USA) |
2012 (Hong Kong), 2014 (USA) |
| Incubation |
18 hours - 3 days |
3-4 days |
Similar to PED |
| Mortality (neonates) |
Nearly 100% in less than 1 week old |
50-100% in suckling pigs |
Lower than PED |
| Spread Rate |
Very rapid |
Slower than TGE |
Similar |
| Older Pig Mortality |
Low (rarely die after 1 month age) |
Low in growing pigs |
Low |
| Cross-Protection |
PRCV provides immunity to TGE |
None from TGE or PDCoV |
None |
| Feature |
Details |
| Etiology |
Type A Influenza virus (Orthomyxovirus). Subtypes H1N1, H1N2, H3N2 most common. Segmented RNA genome allows reassortment. |
| Transmission |
Aerosol transmission is primary. Direct contact with nasal secretions. Human-to-pig and pig-to-human transmission occurs. |
| Clinical Signs |
High fever (40-41.7 C), lethargy, anorexia, coughing (barking), sneezing, nasal discharge, labored breathing. Abortions possible. |
| Characteristic Course |
Explosive onset, high morbidity (near 100%), low mortality (less than 1% if uncomplicated), recovery in 5-7 days. |
| Diagnosis |
PCR (nasal swabs), virus isolation, serology (HI test). Necropsy shows cranioventral consolidation. |
| Treatment |
Supportive care. NSAIDs for fever. Antibiotics ONLY for secondary bacterial infections. |
| Prevention |
Inactivated vaccines available. All-in/all-out management. Reduce stress. Personnel biosecurity (bidirectional zoonotic risk). |
Major Bacterial Diseases of Swine
Swine Erysipelas
Swine erysipelas is one of the oldest recognized diseases of pigs, caused by Erysipelothrix rhusiopathiae. It occurs in acute, subacute, and chronic forms. It is also a ZOONOSIS causing erysipeloid skin infection in humans.
MEMORY AID - Diamond Skin Disease: Remember 'DIAMONDS are PENICILLIN's best friend' - Erysipelas causes characteristic DIAMOND-shaped raised skin lesions (rhomboid urticaria). PENICILLIN is the treatment of choice!
High-YieldErysipelothrix rhusiopathiae is gram-positive and commonly resides in pig tonsils - pigs are often healthy carriers. Diamond skin lesions are almost DIAGNOSTIC but can also occur with CSF, ASF, and Actinobacillus suis. Erysipelas is a ZOONOSIS - humans get localized skin infection (erysipeloid) from handling infected pigs/meat.
[Include Image: Figure 5. Diamond-shaped (rhomboid) urticarial skin lesions characteristic of swine erysipelas]
Source: https://www.pig333.com/pathology-atlas/ - Filter by 'Erysipelas'
Actinobacillus pleuropneumoniae (APP)
Actinobacillus pleuropneumoniae causes severe fibrinous pleuropneumonia in pigs. It is highly contagious and can cause peracute death within 6 hours of infection in naive herds. APP is host-specific to swine.
MEMORY AID - APP Features: Remember 'APP = Acute Pig Pleuropneumonia' - Peracute to acute respiratory disease with FIBRINOUS pleurisy. Key features: (1) Dark red lung INFARCTS, (2) FIBRIN covering lungs and in pleural cavity, (3) Bloody froth at nose. Time from infection to death can be only 6 HOURS!
High-YieldThe RTX toxins (ApxI, II, III) are the major virulence factors - they are cytotoxic and hemolytic, causing the characteristic hemorrhagic necrosis of lung tissue. Differentiate from Actinobacillus suis which can cause similar lesions but also septicemia with skin lesions resembling erysipelas.
[Include Image: Figure 6. Lung from pig with acute APP showing hemorrhagic necrosis and fibrinous pleurisy]
Source: https://www.pig333.com/pathology-atlas/pleuroneumonia_368/ - University of Murcia Veterinary Pathology images
Glasser's Disease (Glaesserella/Haemophilus parasuis)
Glasser's disease is a systemic infection caused by Glaesserella parasuis (formerly Haemophilus parasuis). It primarily affects young pigs and is characterized by fibrinous polyserositis, polyarthritis, and meningitis. It is an important component of PRDC.
MEMORY AID - Glasser's 3 Ps: Remember 'Glasser's = Polyserositis, Polyarthritis, Pleurisy' (and meningitis) - Fibrin deposits on ALL serous surfaces. Think of a 'fibrin-wrapped' pig. Penicillin works well but must be given EARLY!
High-YieldDifferentiate Glasser's disease from Streptococcus suis which also causes meningitis and polyserositis in young pigs. S. suis meningitis typically shows more pronounced paddling/convulsions, while Glasser's more commonly shows twitching. Both respond to penicillin.
Streptococcus suis
Streptococcus suis is another major cause of meningitis, septicemia, arthritis, and endocarditis in pigs. It is a gram-positive coccus with 35 serotypes (type 2 most common and important). S. suis is a ZOONOSIS - can cause severe disease in humans including meningitis, septicemia, and deafness.
MEMORY AID - Strep suis vs Glasser's: Both cause meningitis and polyserositis in young pigs. Remember: S. suis = Gram POSITIVE coccus = ZOONOTIC (can infect humans who handle infected pigs). G. parasuis = Gram NEGATIVE rod = NOT zoonotic. Both respond to PENICILLIN.
Porcine Respiratory Disease Complex (PRDC)
PRDC is a MULTIFACTORIAL syndrome affecting nursery, grower, and finisher pigs. It results from complex interactions between multiple viral and bacterial pathogens, host factors, and environmental conditions. Understanding PRDC is essential for the BCSE.
MEMORY AID - PRDC Pathogens: Think 'PRDC = Pigs Requiring Diagnostic Clarity' - Primary agents (PRRSV, SIV, PCV2, Mycoplasma hyopneumoniae) predispose to secondary bacterial infections (APP, Pasteurella multocida, Streptococcus suis, Glaesserella parasuis, Bordetella bronchiseptica).
High-YieldPRDC morbidity is typically 10-40% with 2-20% mortality. Control requires a comprehensive approach addressing multiple pathogens, optimizing environment (ventilation, temperature, stocking density), reducing stress, and implementing appropriate vaccination programs.
| Feature |
Details |
| Etiology |
African Swine Fever Virus (ASFV). Family Asfarviridae. Large, complex dsDNA virus. Only DNA arbovirus. 24 genotypes identified. |
| Transmission |
Direct contact, contaminated meat products (survives curing/freezing), fomites, Ornithodoros soft ticks (biological vector in Africa). Virus survives in environment. |
| Incubation |
3-15 days depending on route and viral strain. |
| Acute Signs |
High fever (40-42 C), anorexia, lethargy, prostration, cyanosis (ears, snout, tail, extremities), hemorrhages, vomiting, bloody diarrhea, dyspnea, epistaxis, abortions. Death in 7-10 days. |
| Key Lesions |
HEMORRHAGIC SPLENOMEGALY (pathognomonic - dark, friable, enlarged spleen), hemorrhagic lymphadenitis (marbled appearance), petechial hemorrhages (kidneys, heart, serosa), pulmonary edema. |
| Diagnosis |
MUST be laboratory confirmed. PCR (gold standard), virus isolation with hemadsorption test, ELISA for antigen/antibody, FAT on tissues. |
| Differential |
Classical Swine Fever (CSF/hog cholera), erysipelas, acute salmonellosis, PDNS - laboratory differentiation REQUIRED. |
| Control |
NO vaccine (some experimental in Vietnam). NO treatment. Depopulation, quarantine, strict biosecurity. Import restrictions on pork products. |
| Form |
Clinical Features |
| Acute/Septicemic |
Sudden death (may be first sign), high fever (40-42 C), depression, anorexia, reluctance to move. Skin: generalized erythema or DIAMOND-SHAPED raised red lesions. Mortality up to 50% untreated. |
| Subacute (Urticarial) |
Less severe. Classic diamond skin lesions most prominent. Lesions may become necrotic and slough ('tip necrosis' of ears/tail). |
| Chronic (Arthritis) |
Follows acute/subacute infection. Enlarged joints (especially hocks, stifles, carpus), lameness, stiffness. Hot, painful joints initially. |
| Chronic (Endocarditis) |
Vegetative valvular endocarditis (cauliflower-like growths on heart valves). May show sudden death with exertion, dyspnea, cyanosis. Major cause of carcass condemnation. |
| Diagnosis |
Clinical signs (diamond skin lesions almost pathognomonic), bacterial culture from blood or affected tissues, response to penicillin treatment. |
| Treatment |
PENICILLIN is drug of choice (highly effective for acute form). Also sensitive to cephalosporins, fluoroquinolones. Chronic form usually unresponsive. |
| Prevention |
Vaccination highly effective. Bacterins and live attenuated vaccines available. Vaccinate breeding stock and growing pigs in endemic herds. |
Diagnostic Approach Summary
| Feature |
Details |
| Etiology |
Actinobacillus pleuropneumoniae. Gram-negative coccobacillus. 19 serovars (1, 3, 5, 7 most common in North America). Produces RTX toxins (ApxI, II, III, IV). |
| Transmission |
Aerosol, direct contact. Does NOT survive long in environment. Carrier pigs are main reservoir. |
| Age Affected |
Most common in 6-20 week old pigs in endemic herds. All ages susceptible in naive herds. |
| Peracute Signs |
Sudden death (may be first sign). Death within 6 hours possible. |
| Acute Signs |
High fever (41.5 C), severe respiratory distress, cyanosis, open-mouth breathing, bloody froth at nose and mouth, reluctance to move. |
| Chronic Signs |
Intermittent coughing, poor weight gain, reduced feed conversion. Sequestered lung nodules. |
| Lesions |
Dark red to black hemorrhagic INFARCTS (especially diaphragmatic lobes), fibrinous pleurisy (yellowish fibrin tags), blood-tinged fluid in thorax. Chronic: sequestra (encapsulated necrotic nodules). |
| Diagnosis |
Culture (requires NAD/V-factor for biotype I), PCR for RTX toxin genes, serology (complement fixation, ELISA). |
| Treatment |
Early antimicrobial therapy critical. Penicillins, cephalosporins, florfenicol, tiamulin, tilmicosin. Treatment ineffective once lung necrosis occurs. |
| Prevention |
Commercial and autogenous bacterins. Vaccination, medication, husbandry improvements. Depopulation may be cost-effective for endemic herds. |
| Feature |
Details |
| Etiology |
Glaesserella parasuis (formerly Haemophilus parasuis). Gram-negative pleomorphic rod. 15 serovars. Normal inhabitant of upper respiratory tract. |
| Predisposing Factors |
Stress (weaning, mixing, transport, overcrowding), viral infections (PRRSV, PCV2, SIV), early weaning, breakdown of maternal immunity. |
| Age Affected |
Most common 4-8 weeks (around weaning). Can occur 2 weeks to 4 months. |
| Acute Signs |
High fever (41+ C), depression, anorexia, joint swelling and lameness, respiratory distress, cyanosis (ears, abdomen), neurological signs (paddling, tremors). Sudden death possible. |
| Chronic Signs |
Poor growth, rough hair coat, swollen joints, lameness, chronic coughing. |
| Lesions |
Fibrinous polyserositis (pericarditis, peritonitis, pleuritis - 'bread and butter' appearance), fibrinopurulent meningitis, polyarthritis with fibrin/purulent exudate in joints. |
| Diagnosis |
Clinical signs and lesions suggestive. Culture from sterile sites (joint fluid, CSF, pericardial fluid). PCR available. |
| Treatment |
PENICILLIN-based antibiotics most effective (must treat early). Also cephalosporins, florfenicol, enrofloxacin. NSAIDs for fever and inflammation. |
| Prevention |
Commercial and autogenous vaccines. Reduce stress. Control concurrent viral infections (especially PRRS). Optimize environment. |
| Primary Pathogens (Viral) |
Role in PRDC |
| PRRSV |
Most important primary pathogen. Damages alveolar macrophages, causes immunosuppression, predisposes to secondary infections. |
| PCV2 |
Causes lymphoid depletion and immunosuppression. Potentiates effects of other pathogens. |
| Swine Influenza Virus |
Damages respiratory epithelium, impairs mucociliary clearance. |
| Primary Pathogens (Bacterial) |
|
| Mycoplasma hyopneumoniae |
Colonizes respiratory tract, damages cilia, predisposes to secondary infections. Causes enzootic pneumonia. |
| Secondary Pathogens |
|
| APP, P. multocida, S. suis, G. parasuis, B. bronchiseptica |
Opportunistic bacteria that cause more severe disease when primary infections compromise host defenses. |
| Disease |
Primary Diagnostic Tests |
Key Sample Types |
| PRRS |
PCR (RT-PCR), ELISA |
Serum, oral fluids, lung tissue |
| PCV2/PCVAD |
PCR, IHC on tissues |
Lymph nodes, spleen, lung, serum |
| PED/TGE/PDCoV |
PCR (multiplex available) |
Feces, oral fluids, small intestine |
| Swine Influenza |
PCR, virus isolation, HI serology |
Nasal swabs, lung tissue |
| ASF |
PCR, hemadsorption test, ELISA |
Spleen, lymph nodes, blood, tonsils |
| Erysipelas |
Bacterial culture, clinical signs |
Blood, affected tissues |
| APP |
Culture (NAD-dependent), PCR |
Lung tissue, pleural fluid |
| Glasser's Disease |
Culture from sterile sites, PCR |
Joint fluid, CSF, pericardial fluid |