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Diseases caused by viruses

African Swine Fever (ASF)

ASF is a highly contagious viral disease of domestic pigs manifested by fever, blotching of skin, haemorrhage of the lymph nodes, internal organs and haemorrhage of the gastrointestinal tract. It is observed in acute and occasionally subacute and chronic forms.

Transmission : There is a natural cycle of the ASF virus between bush pigs, warthogs and giant forest hogs and some tick species (Ornithodorus) in which the virus replicates. The spread of the virus is by contact with affected pigs and infected fomites, ingestion of contaminated uncooked pork garbage, tick bites and contact with domestic and wild carrier pigs.

The virus is quite resistant to cleaning and disinfection. It survives for 2 – 4 months in an infected premises and 5 – 6 months in infected meats. The virus can survive in smoked or partly cooked sausages and other pork products. Humans are not susceptible to this disease.

Antemortem findings :

  1. Incubation: 3 – 15 days
  2. Fever (up to 42°C)
  3. Laboured breathing, coughing
  4. Nasal and ocular discharge
  5. Loss of appetite and diarrhoea
  6. Vomiting
  7. Incoordination
  8. Cyanosis of the extremities and haemorrhages of skin
  9. In chronic stage, emaciation and edematous swelling under the mandible and over leg joints
  10. Recumbency

Postmortem findings :

  1. Blotchy skin cyanosis and haemorrhage (Fig. 113)
  2. Enlarged spleen (splenomegaly, Fig 114)
  3. Petechial haemorrhage on the kidneys (Fig. 115)
  4. Enlarged and haemorrhagic gastrohepatic and renal lymph nodes
  5. Haemorrhage in the heart
  6. Hydrothorax, hydropericardium and ascites
  7. Haemorrhage of the serous membranes
  8. In chronic ASF pericarditis, and emaciated carcass

Judgement : Carcass of an animal affected with African Swine Fever is condemned. The animal is prohibited from entering the abattoir.

Differential diagnosis : Hog cholera, salmonellosis, erysipelas, Glasser's disease (Haemophilus suis) infection

fig 113

Fig. 113: African swine fever. Blotchy skin, cyanosis and haemorrhage.

fig 114

Fig. 114: African swine fever. Enlarged spleen (splenomegaly).

fig 115

Fig. 115: African swine fever. Petechial and ecchymotic haemorrhage in the kidneys. Note haemorrhagic areas in the renal pelvis and papillae.

Foot and Mouth Disease (FMD, Aphthous fever)

FMD is a contagious, viral disease of swine, cattle, sheep, goats and pigs and other cloven footed animals. The disease in pigs is mild and is important as being a potential danger for transmission to cattle.

Transmission : Direct and indirect contact with infected animals. The virus can also be spread by aerosol, saliva, nasal discharge, blood, urine, faeces, semen, infected animal by-products, swill containing scraps of meat or bones and by biological products, particularly vaccines. Pigs can transmit the disease to cattle and other animals.

Antemortem findings :

  1. Incubation 3 – 15 days. Pigs that are fed food wastes contaminated with FMDV may show signs of infection in 1 – 3 days.
  2. Snout (Fig. 116) and tongue lesions very common in pigs
  3. Dullness and lack of appetite
  4. Salivation and drooling
  5. Detachment of the skin on a pig's foot (Fig. 117)
  6. Shaking of feet and lameness due to leg lesions

Some strains of FMD in swine do not show vesicles but show erosions.

Judgement : Feverish animals with associated secondary bacterial infections call for total condemnation of the carcass. The meat of suspect animals may be conditionally approved after deboning, and condemnation of the head, feet, viscera and lymph nodes of the carcass. Such meat must be thoroughly cooked and could be used as canned meat.

Differential diagnosis : Swine vesicular disease, vesicular stomatitis and vesicular exanthema in pigs can be differentiated from FMD only by laboratory testing.

fig 116

Fig. 116: FMD. Vesicle on the snout in a pig.

fig 117

Fig. 117: FMD Detachment of epithelium on the pig's foot.

Hog cholera

Hog cholera is a highly infectious viral disease of swine manifested by septicemia and generalized haemorrhage. It is noted in acute, subacute and chronic forms.

Transmission : Direct contact with infected pigs and ingestion of uncooked contaminated food wastes containing infected pork scraps.

Antemortem findings :

  1. Incubation 5 – 10 days
  2. Morbidity 40 – 100 %
  3. Mortality 0 – 100 %. Mortality varies with herd susceptibility, virus strain and age of animals.
  4. Fever (40.6°C - 41.7°C)
  5. Reddened areas of skin
  6. Depression
  7. Vomiting and constipation
  8. Huddling and piling on top of each other
  9. Incoordination with staggering gait
  10. Tendency to sit like a dog
  11. Goose stepping (Fig. 118)
  12. Paddling
  13. Infection of pregnant cows result in abortion

Postmortem findings:

  1. Tonsillar necrosis (Fig.119)
  2. Splenic infarcts (Fig. 120)
  3. Button ulcers in the large intestine and intestinal necrosis
  4. Haemorrhage of the lymph nodes
  5. Pneumonia in chronic infection
  6. Petechial haemorrhage in the gall bladder, urinary bladder and kidneys (Fig.121); the latter is not present in acute hog cholera.

Judgement : Carcass of an animal affected with hog cholera is condemned if kidney lesions are associated with lesions in the lymph nodes and other organs. If the meat appears normal after the organoleptic examination (appearance, taste and consistency), the carcass may be conditionally approved pending heat treatment or sterilization. Emergency slaughter of animals affected with hog cholera would require bacteriological examination of the meat in order to eliminate secondary pathogens, mainly Salmonellae. The animals in contact with hog cholera can be conditionally approved if heat treatment is carried out.

Differential diagnosis : Erysipelas, septicemic conditions, pneumonia, streptococcosis and salt poisoning

fig 118

Fig. 118: Hog cholera. Goose stepping.

fig 119

Fig. 119: Hog cholera. Tonsillar necrosis.

fig 120

Fig. 120: Hog cholera. Splenic infarcts.

fig 121

Fig. 121: Hog cholera. Petechial haemorrhage in the kidneys (turkey egg kidney).

Vesicular exanthema of swine (VES)

An acute, contagious, viral disease of swine manifested by the formation of vesicles. Vesicular exanthema is indistinguishable from the other swine diseases such as FMD, VS and SVD.

Transmission: Direct contact with infected animals and ingestion of contaminated uncooked garbage containing infected pork scraps.

Antemortem findings:

  1. Incubation: 2–4 days
  2. Large number of hogs are affected.
  3. Heavy mortality in suckling pigs
  4. Blotchy rash in unpigmented skin (exanthema)
  5. Vesicles on the snout and in the mouth. Ruptured vesicles result in erosions
  6. Loss of weight
  7. Walking on their knees (Fig. 122) and lameness
  8. Squealing when forced to move

Postmortem findings : Vesicles on mucous membranes and skin

Judgement : Carcass of an animal affected with vesicular exanthema is condemned, if a feverish animal has generalized lesions throughout the body. In uncomplicated cases when an animal is recovering the carcass is conditionally approved pending heat treatment. Laboratory examination should be performed if secondary pathogenic bacteria and/or antibiotic residues are suspected.

Differential diagnosis: Foot and mouth disease, vesicular stomatitis, swine vesicular stomatitis, lameness and leg injuries.

The lesions in the heart and skeletal muscles present in FMD are not found in vesicular exanthema.

fig 122

Fig. 122: Vesicular exanthema. Pig walking on knees due to pain from the vesicular lesion on the feet.

Swine vesicular disease (SWD)

A contagious viral disease of swine clinically indistinguishable from vesicular stomatitis, foot and mouth disease and vesicular exanthema of swine.

Transmission : Infected swine, excretions, ingestion of contaminated uncooked pork wastes, minor skin wounds. The shedding of the virus begins before the appearance of clinical signs and may continue for up to 3 months. This virus is more resistant to disinfectants and environmental conditions than the FMD virus. The SVD virus is acid stable and was isolated from certain type of sausage prepared from infected pork meat 400 days after its manufacture. An effective disinfectant for SVD virus is a combination of acid and iodophor disinfectant mixed with detergent.

Antemortem findings :

  1. Incubation 2 – 4 days
  2. Fever 40 – 41°C
  3. Snout (Fig. 123), oral and feet vesicular lesions
  4. Lameness

Postmortem findings :

  1. Skin lesions
  2. Diffuse inflammation of brain on histopathology

Differential diagnosis : Vesicular stomatitis, vesicular exanthema, foot and mouth disease, foot rot, swine pox and chemical and traumatic injuries.

Judgement : Carcass of an animal affected with swine vesicular disease is disposed according to national animal health regulations. In countries with an eradication programme, the carcass is condemned. It is also condemned in a country free or nearly free of this disease. The animal should not enter the abattoir.

fig 123

Fig. 123 : Swine vesicular disease. Snout vesicular lesion.

Vesicular stomatitis

Viral disease of swine, cattle, horses and occasionally man. The disease is caused by two antigenically distinct types of virus namely Indiana and New Jersey types. Vesicular stomatitis in swine is most commonly manifested by snout and foot lesions.

Transmission : The mode of transmission is not completely known. Biting flies and mosquitoes, direct contact between the animals and droplet infection are possible ways of transmission.

Antemortem findings :

  1. Incubation 2 – 4 days
  2. Fever
  3. Lesion on the tongue (Fig. 124) and snout
  4. Lesion in the interdigital space or coronary band
  5. Refusal of food but acceptance of water
  6. Weight loss
  7. Lameness and exungulation

Judgement : Carcass of an animal affected with vesicular stomatitis is approved. Affected parts of the carcass and organs are condemned. If the disease is not confirmed upon differential diagnosis, the judgement is the same as for swine vesicular disease.

Differential diagnosis : Food and Mouth Disease, vesicular exanthema and swine vesicular disease.

Public health significance : The Indiana and New Jersey viruses are infective for humans. Human infection is characterized with chills, fever, malaise and muscle soreness. A mild vesicular stomatitis and tonsillitis may also be present. The recovery of most patients is within a week.

fig 124

Fig. 124: Vesicular stomatitis. Detachment of epithelium of the pig tongue.

Transmissible gastroenteritis (TGE)

TGE is a highly infectious viral disease of pigs characterized with vomiting, dehydration, diarrhoea and high mortality in pigs up to 3 weeks old.

Transmission : The virus can be spread via aerosol. The virus replicates in the respiratory tract and is excreted in nasal secretion, milk and faeces. Carrier pigs are a major source of infection and transmission of disease. In the herd, the disease spreads from the older pigs to newborn pigs and sows. Suckling piglets get infected by sucking an udder of an infected sow. Uncooked and infected pork scraps may also be the source of infection. Visitors and farm vehicles may transfer the infection to new locations. The virus persists in the infected premises for a few weeks. It can be destroyed with phenol and formalin solution, boiling and drying. Freezing will not destroy the virus.

Antemortem findings :

  1. Incubation 24 – 48 hours
  2. Transitory fever, but mostly normal temperature
  3. Depression
  4. Vomiting, pronounced dehydration and profuse diarrhoea
  5. Yellow green faeces
  6. Death 2nd – 5th day of disease
  7. Older pigs may show no clinical signs.
  8. Cessation of milk secretion in sows

Postmortem findings :

  1. Distended intestine with fluid ingesta (Fig. 125), thin translucent intestinal wall
  2. Degeneration of heart muscle and rarely skeletal muscles
  3. Microscopical villous atrophy of intestine (Fig. 126)
fig 125

Fig. 125: TGE. Distended intestine showing translucent intestinal wall and fluid ingesta.

fig 126

Fig. 126: TGE. Villous atrophy of intestinal mucosa.

Judgement : A slightly affected carcass of an older pig is approved if in good condition. The carcass and viscera of an animal showing signs of clinical disease and degeneration of muscle on postmortem inspection are condemned.

Differential diagnosis : Hog cholera in early stages of the disease and E. coli enteritis in young pigs. In enteritis, there is no vomiting and it is an enzootic disease.

Diseases caused by bacteria


Pneumonia is an inflammation of the lungs caused by bacteria, viruses, fungi, parasites or physical or chemical agents. It is frequently accompanied with inflammation of the bronchi, bronchioli and the pleura. Consequently, the terms “bronchopneumonia” is commonly used. In pigs, enzootic pneumonia caused by Mycoplasma hyopneumoniae and pleuropneumonia caused by Haemophilus pleuropneumoniae are most often seen.

Transmission : In infected herds, the infection spreads from the sow to the suckling pigs, and in adult pigs, by common contact and via air. Mycoplasma hyopneumoniae is not isolated from the respiratory tract of healthy animals. It persists in chronic lung lesions of recovered animals and is a source of infection particularly for the new animals in the herd.

Actinobacillus (Haemophilus) pleuropneumoniae is found in the nostrils and lungs of healthy animals. An outbreak of the disease may be triggered by environmental stresses.

Antemortem findings :

Enzootic pneumonia:

  1. Mortality may occur, but is very low.
  2. Fever is usually absent.
  3. Acute respiratory distress and a characteristic dry cough when excited

Chronic form:

  1. Dry hacking cough
  2. Retardation in growth


  1. Fever ( 41°C)
  2. Respiratory distress
  3. Bluish appearance of mucous membranes of the eye and mouth
  4. Bloody frothy discharge from nostrils
  5. Death

Chronic form

  1. Poor feed utilization and emaciation in “carrier” animals

Postmortem findings :

Enzootic pneumonia

  1. Plum coloured, greyish consolidation in apical, cardiac and diaphragmatic lung lobes (Fig. 127); lung lobes directed toward the front and bottom are mainly affected.
  2. Enlarged edematous bronchial lymph nodes
  3. Purulent pneumonia with abscessation usually seen with secondary infection (Fig. 128)
  4. Pleurisy and pericarditis may be seen with secondary infection


  1. Bloody froth in wind pipe
  2. Generalized consolidation and firmness in the entire lung (Fig. 129)
  3. Blood tinged fluid in the chest cavity and abdomen
  4. Pus-filled abscesses scattered throughout the lungs.
  5. Lesions commonly found in the upper part of lungs and often in diaphragmatic lobe.
  6. Whitish clot like adhesions on the lung surface and pleura

Judgement : A carcass affected with pleuropneumonia showing healing lesions is approved. The affected parts of the carcass and affected organs are condemned. Pneumonia associated with dry adhesions on the pleura and pericardium and without other lesions may be conditionally approved, pending heat treatment. The carcass must be carefully examined for injection sites. If bacteraemia is suspected, bacteriological examination must be performed. Carcass is condemned if pneumonia is accompanied with fever and septicemia or emaciation. Pulmonary necrosis with secondary toxic changes in the body also require carcass condemnation.

Differential diagnosis : African swine fever, swine influenza, rhinitis, Ascaris suum infestation, laryngitis, tracheitis, pulmonary edema and congestion, injuries and tuberculosis

fig 127

Fig. 127: Pneumonia. Enzootic pneumonia. Lung lesions affecting anterior and bottom portions of the lungs.

fig 128

Fig. 128: Chronic pneumonia with abscessation. This pneumonia was caused by Mycoplasma spp. and later infected with secondary bacteria. A beta-haemolytic Streptococcus was isolated. The animal may also have received antibiotic therapy.

fig 129

Fig. 129: Porcine pleuropneumonia. Pneumonic lesions throughout the lung tissue. Interstitial emphysema and edema are also noted.


Pleuritis is the inflammation of the pleura. It is usually associated with pneumonia. An infectious agent may reach the pleura by the blood stream, lymphatic system, penetrate from outside the chest cavity, oesophagus or extend from a mediastinal abscess.

Antemortem findings :

  1. Fever may or may not be present
  2. Shallow, rapid respiration
  3. Abducted elbows and unwillingness to move
  4. Loss of appetite and weight loss
  5. If associated with pneumonia as in pleuropneumonia, a cough may be present

Postmortem findings :

  1. Thickening of the pleura and presence of fibrin tags
  2. Purulent or fibrinous exudate in the pleural cavity
  3. Chronic pleuritis and lung abscessation (Fig. 130)

Judgement : Carcass affected with diffuse fibrinous or serofibrinous inflammation of the pleura is condemned. In a case of negative bacteriological and microbial findings, the carcass may be conditionally approved with heat treatment. Purulent or gangrenous pleuritis or acute pleuritis associated with inflammation in other organ systems would also require carcass condemnation. In localized or chronic pleuritis with no systemic changes, the carcass may be approved.

Differential diagnosis : Pneumonia, pulmonary congestion and edema, hydrothorax and haemothorax

Fig. 130: Pleuritis Chronic pleuritis and lung abscessation.

fig 130

Valvular endocarditis in pigs

Endocarditis is the inflammation of the endocardium of the heart. Bacterial endocarditis is one of the significant bacterial infections in pigs and other domestic animals.

The etiological agents in swine are Erysipelothrix rhusiopathiae, Actinomyces pyogenes, Streptococci spp. and Escherichia coli. Bacteraemia caused by infection in some remote organs, muscle or bones may be associated with a lesion in the endocardium. The valves are the most frequently affected. Emboli may detach from friable vegetation on the valves and pass through the blood stream to organs and cause infarcts. Emboli from the right heart are a frequent cause of pulmonary abscessation or pulmonary thrombosis.

Antemortem findings:

  1. Moderate fluctuating fever
  2. Loss of condition
  3. Pallor of mucosae
  4. Arthritis or tenosynovitis

Postmortem findings:

  1. Yellow-grey to yellow red valvular lesion (Fig. 131)
  2. Embolic lesions in lungs, spleen, kidneys etc.
  3. Inflammation of the heart muscle

Judgement: Carcass of an animal affected with endocarditis which had shown fever and loss of condition on antemortem examination and embolic lesions in organs on postmortem examination is condemned. Ulcerative or verrucose endocarditis with no signs of systemic changes may be conditionally approved, pending heat treatment. The affected organs are condemned.

Endocarditis showing infiltration of fibrous tissue is approved. The heart is condemned.

Differential diagnosis : Pneumonia, pericarditis, pulmonary edema, emphysema, pleuritis, lymphoma, congenital heart disease, congenital valvular heart cysts and deformities

Fig. 131: Valvular endocarditis in a sow heart caused by Streptococcus suis.

fig 131

Porcine chronic pericarditis

Pericarditis is the inflammation of the pericardium. It is one of the frequent conditions found in swine at slaughter. The agents causing pericarditis include viruses, mycoplasma, bacteria, fungi and other microorganisms. It is a common complication of enzootic pneumonia due to secondary invasion with E. coli.

Pericarditis can occur secondary to heart infections, systemic infections, or result from metastases of neoplasms arising in remote sites. In swine, fibrinous pericarditis is associated with hog cholera, erysipelas and Glasser's disease. Inflammation of pericardium is also observed in pasteurellosis, porcine enzootic pneumonia and streptococcal infection in suckling pigs. Primary pericarditis occurs rarely and is of viral origin.

The purulent form of pericarditis is most commonly seen in animals as a result of bacterial, parasitic and mycotic invasions of the pericardium. Direct extension from a surrounding inflammatory area is noted in pneumonia, pleuritis, mediastinal infections, injury to the chest caused by trauma etc..

Antemortem findings:

  1. Reluctance to move
  2. Shallow respiration
  3. Signs of pleurisy and/or pneumonia
  4. Signs of heart disorder

Postmortem findings :

  1. Deposits of fibrin on the pericardium
  2. Pericardium adherent to the epicardium (heart surface) (Fig. 132)
  3. Adhesions of pericardium with lungs and/or pleura
  4. Purulent inflammation of pericardium
fig 132

Fig. 132: Porcine chronic pericarditis. Pericardial sac adhered to the heart by thickened fibrous tissue.

Judgement : Carcasses affected with pericarditis should be condemned if the inflammation is acute, diffuse or purulent, and associated with fever and systemic changes in other body systems. The rational for condemnation: the pathogenic bacteria are likely to be present in organs and musculature which would present some risk to consumers. A carcass in good condition without systemic changes can be passed even though the heart showed evidence of chronic infectious pericarditis. The organs and viscera are condemned.

Differential diagnosis : Abscess, Lymphomatosis


Tuberculosis is a chronic disease of pigs, manifested by development of tubercles in most organs and is caused by Mycobacterium bovis and Mycobacterium avium.

The infection occurs primarily by ingestion. The primary complex is incomplete if it develops in the pharyngeal lymph nodes of the head. In such case, the agent entry site is in tonsils. When the bacteria enter through the wall of the intestine, frequently at Peyer's patches, the primary complex includes the mesenteric lymph node. Tuberculosis lesions caused by the bovine type are similar in appearance to those seen in cattle. Avian type lesions in pigs differ from the bovine type.

Antemortem findings : Antemortem findings are similar to bovine tuberculosis. They include:

  1. Low grade fever
  2. Loss of appetite and emaciation
  3. Difficult breathing if lymph nodes of the head, neck, and lungs are affected.

Postmortem findings :

  1. Miliary lesions in the liver (Fig. 133), spleen (Fig. 134) and other organs
  2. Lesions in the tonsils, submaxillary, cervical, bronchial, mediastinal and mesenteric lymph nodes.
  3. Lesions in the joints and meninges are more common than those in cattle.

M. avium lesions of the lymph nodes are characterized by yellow caseous foci, which range in size from a pinhead to a small pea. Infection from the mesenteric lymph nodes in pigs spreads frequently to the liver by the portal system. Liver infection is common in pigs and is considered localized TB. In infection with M. bovis, tuberculosis liver lesions are part of a generalized infection via the hepatic artery.

Judgement : Carcasses with tuberculosis lesions in the head only are passed, after head condemnation. If the carcass contains lesions, it is condemned.

Differential diagnosis : Tumours, abscesses and parasitic lesions. The latter are often greenish. Corynebacterium equi infection of the submaxillary lymph node: This lesion can be easily enucleated from its capsule, contrary to tuberculosis lesion which is difficult to enucleate. Lesions caused by Mycobacterium intracellulare and M. scrofulaceum and other acid food organisms are also easily enucleated.

fig 133

Fig. 133: Tuberculosis. Miliary lesions in the liver tissue.

fig 134

Fig. 134: Tuberculosis lesions in a pig spleen.

Porcine brucellosis

Brucellosis in pigs is manifested by abortion and sterility in sows, heavy piglet mortality and orchitis in boars. It is caused by Brucella suis, although there are also outbreaks of this disease caused by Br. abortus. Brucella suis is found more often in adult pigs. It may also affect cattle and horses and is pathogenic for humans. Meat inspection should carefully examine suspicious livestock and carcasses in order to avoid that cases of brucellosis pass unrecognized in abattoirs.

Antemortem findings :

  1. Clinical signs may not be noted.
  2. Inflammation and necrosis of testicles in boars
  3. Lameness and inco-ordination; may be associated with arthritis and osteomyelitis.
  4. Posterior paralysis
  5. Abortion and infertility in sows
  6. Weak offspring

Postmortem findings :

  1. Abscess in the spleen, liver, kidneys, lymph nodes, joint capsule or tendon sheaths
  2. Abscess in the testicles or seminal vesicles of boars
  3. Catarrhal metritis in sows
  4. Arthritis and osteomyelitis of lumbar and sacral vertebral bodies

Judgement : Carcass affected with brucellosis is condemned. In some areas heat treatment of the carcass may be recommended because of economical reasons. In such cases, the mammary glands, genital organs and related lymph nodes must be condemned.

Differential diagnosis : Leptospirosis, erysipelas (if abortion present). Fractures of the lumbar vertebrae with osteomalacia. In posterior paralysis: Avitaminosis A, deficiency of vitamin B complex factors, and poisoning with rotenone, mercury, organic arsenicals etc.

Porcine salmonellosis

Salmonellosis is one of the most significant infectious diseases of pigs. It is clinically characterized by one of three major syndromes: a peracute septicemia, an acute enteritis or a chronic enteritis. One form of the disease is more prevalent in any particular outbreak. The septicemic syndrome is usually seen in young animals and is generally caused by Salmonella cholerae suis. The mortality rate may reach 100 %, with death frequently occurring within a few days. Intercurrent diseases, particularly hog cholera and the nutritional stress caused by a sudden change in diet may predispose to infection with Salmonella organisms such as Salmonella typhimurium.

Transmission: Introduction of an infected carrier pig into the herd. Possible infection spread by flies and through farm activities. Healthy pigs may be carriers of Salmonella organisms.

Antemortem findings :

Septicemic syndrome

  1. High fever
  2. Dark red to purple discoloration of skin especially on the ears and abdomen
  3. Nervous signs manifested by incoordination of gait, tremor, paralysis, convulsions, recumbency and death.

Enteric syndrome (mainly seen in adult pigs)

  1. Enteritis
  2. High fever lasting 12 – 24 hours
  3. Severe watery diarrhoea and dehydration
  4. Pneumonia
  5. Emaciation and death
  6. A sequel to enteric salmonellosis may be rectal stricture
  7. Abdominal dilatation and frothy to pasty faeces in cases of rectal stricture

Postmortem findings :

Septicemic syndrome

  1. Discoloration of the skin
  2. Enlarged and engorged lymph glands
  3. Haemorrhages, petechiae and ecchymosis of the epiglottis, stomach, intestine and bladder
  4. Enlarged and pulpy spleen

Acute enteric syndrome

  1. Necrotic enteritis in the ileum and large intestine with S. typhimurium infection
  2. Congestion and hepatization of lungs
  3. Marked skin haemorrhage
  4. Prominent petechial haemorrhage in the kidneys

Chronic enteritis

  1. Areas of necrosis in the wall of the caecum and colon
  2. Enlarged mesenteric lymph nodes
  3. Chronic pneumonia
  4. Abdominal dilatation and low grade peritonitis in cases of rectal stricture

Judgement : Viscera and carcass affected with salmonellosis are condemned. In some areas the heat treatment of the carcass is recommended because of economical reasons.

Differential diagnosis : Swine erysipelas, hog cholera, swine fever

Swine erysipelas

Swine erysipelas is an infection characterized by diamond shaped skin lesions and in the chronic form, by vegetative endocarditis and arthritis. It is caused by Erysipelothrix rhusiopathiae.

Transmission : Healthy carrier pigs shed the bacteria in manure, where they may survive for 5 months. The manure is a reservoir of infection from which bacteria are transferred to non infected piggeries via boots, cloths, birds, flies or other animals. A carrier animal can infect other animals in the same pen.

Antemortem findings:

  1. High morbidity
  2. Fever in acute stages
  3. Conjunctivitis and vomiting in some cases
  4. Bright and alert, squealing in pain on movement
  5. Pig is lethargic and stops eating
  6. Raised red and edematous rhomboid wheals (acute and chronic forms)
  7. Sloughing of skin in the area of the rhomboid lesion
  8. Swollen joints and lameness (chronic stage)
  9. Sudden death in excited animals

Postmortem findings :

  1. Arthritis
  2. Diamond shaped skin lesions (Fig. 135)
  3. Vegetative endocarditis
  4. Enlarged and reddened spleen and congestion of the other organs
  5. Inflamed and haemorrhagic mucosa of the stomach (paint brush effect) and intestine
  6. Cloudy swelling of the kidney and often ecchymotic haemorrhage
  7. Edematous and haemorrhagic lymph nodes

Judgement : An animal affected with an acute disease of erysipelas with erythema or diffuse cutaneous erysipelas with erythema is condemned on antemortem inspection because of occupational hazards. Carcass showing skin lesions or arthritis complicated by necrosis or signs of systemic effects is also condemned. A localized skin lesion requires only the removal of skin and the rest of the carcass is approved. Localized endocardial lesions of erysipelas without systemic changes or localized chronic inflammation of joints call for conditional approval of the carcass with heat treatment. The carcass may be totally approved, if results of a bacteriological examination show that generalized disease is not present, antimicrobial substances are not found and there is no health hazards to consumers and food handlers.

Differential diagnosis : Dermatitis, allergies, external parasites, septicemia, hog cholera, African swine fever, vesicular exanthema, salmonellosis, arthritis and superficial bruises

fig 135

Fig. 135: Swine erysipelas. Diamond shaped skin lesions.


Melioidosis is an infectious disease of pigs, goats and occasionally of other animals caused by Pseudomonas pseudomallei, present in several tropical and subtropical countries in the Asia-Pacific, Middle East and Caribbean regions. It causes fatal infections in a significant proportion of infected humans, especially those who are immuno-compromised or have intercurrent disease.

Transmission : Infection occurs by ingestion of the infective material containing Pseudomonas pseudomallei, contamination of wounds or abrasions of the skin or perhaps bites of insects. Important sources of infection are rodents, contaminated swamps or muddy water. The organism can live up to three months in shaded soil.

Antemortem findings :

  1. Incubation period is variable, longer in pigs than in other animals.
  2. Fever up to 41°C especially in sheep and goats
  3. Enlarged lymph nodes, particularly the sub-mandibular nodes in pigs.
  4. Loss of appetite
  5. Posterior paresis and evidence of nervous signs
  6. Abortion and still births
  7. Orchitis in boars
  8. Most cases in pigs are chronic and these may not show clinical signs.

In sheep the clinical signs include high fever (41°C), nasal and ocular discharge and gradual emaciation.

Postmortem findings :

  1. Multiple abscesses in most organs especially in the regional lymph nodes, spleen (Fig. 136) and liver
  2. The abscesses contain a thick, caseous greenish yellow or off white turgid pus. There is usually no calcification.

In acute cases

  1. Pneumonic changes in the lungs
  2. Suppurative polyarthritis, the joint capsules contain fluid and large masses of greenish yellow pus.
  3. Meningoencephalitis

In sheep the gross finding includes abscesses and suppuration in the nasal mucosae.

Judgement : Carcasses suspected to be infected with melioidosis should be isolated and retained, and the affected tissues, preferably an excised unopened lymph node and the spleen with abscesses should be sent to the appropriate laboratory for examination. Diagnosis is made on the basis of isolation, cultural examination and pathogenicity test. If there are no facilities for retention in isolation, the carcass suspected or tentatively diagnosed to have melioidosis should be condemned and properly disposed of. Persons handling the suspect carcass or material should disinfect their hands, forearms, knives and other contaminated equipment. If the laboratory report is negative the carcass has to be treated on the basis of the lesions present and the subsequent diagnosis.

Differential diagnosis : Tuberculosis, non-specific purulent conditions. Caseous lymphadenitis in sheep and goats and actinobacillosis in sheep.

fig 136

Fig. 136: Melioidosis. Multiple abscesses in the spleen of a pig.

Anthrax (see page 80)

Parasitic diseases

Diseases caused by helminths


Trichinosis has a significant role in food hygiene particularly in countries where meat inspection is poor or inadequate. However, the parasite has not been reported in domestic pigs in a number of countries in developing regions.

Life cycle (Fig. 137): Trichinella spiralis is a nematode which parasitizes pigs, dogs, cats, mice, wild boar and other carnivorous game, humans and other mammals. Larvae penetrate the epithelial lining of the small intestine, undergo four moults and become sexually mature adults. The adult worms are 1 – 4 mm long. The newborn larvae pass to the striated muscles by the lymphatics and the blood stream. In the muscle they grow, curl up in a spiral coil and are encysted (Fig. 138). When they reach the length of 1 mm by 0.5 mm, they appear as oval nodules and are visible to the naked eye. The predilection sites for these larvae are the tongue, diaphragm, eye, masticatory and intercostal muscles. In the muscles, larvae may persist for a long period of time or they may die and become mineralized. Swine, carnivores and humans become infected from eating infected pork, horse, seal or other meat. The digestive juices will cause liberation of larvae from their cysts. They will later develop into adult worms and the cycle will be repeated. Larvae are rarely found in the muscles of cattle, and sheep. Larvae may survive for a long time in decaying and putrefying muscle and carrion.

The most characteristic symptoms of human trichinosis are high fever, weakness, arthralgia, myalgia, abdominal pain with diarrhoea, edema of the face and eyelids, and hives. Neurological symptoms include dizziness and paresis.

Remarks : If the laboratory examination for trichina is not performed in endemic areas heating or cooking and freezing or curing of pork product must be enforced.

Trichinella examination can be carried out as follows:

  1. Trichinoscopic examination

    Samples are taken from the diaphragm pillar at the transition of the sinewy part. Small pieces the size of an oat kernel are cut. These pieces are then compressed between glass plates and examined by using a microscope or trichinoscope.

  2. Artificial digestion of collective samples

    Approximately 1 g is taken from each of a number of carcasses (up to 100), pooled, minced, digested by using a solution of pepsin and hydrochloric acid at 37 –39°C. The fluid in Petri dishes is examined under the microscope at 40 times magnification.

Judgement : Carcass affected with trichinosis is condemned.

Differential diagnosis : Sarcosporidiosis and Cysticercus cellulosae infection and tyrosine crystals in muscles

Fig. 137: Life cycle of Trichinella spiralis (Courtesy G.J. Jackson, Division of Microbiology, US FDA, Washington D.C., USA)

fig 137
fig 138

Fig. 138: Trichinella spiralis. Encysted larvae in striated muscles.

Cysticercosis (Cysticercus cellulosae infestation)

Cysticercus cellulosae found in pigs is the intermediate stage of the tapeworm Taenia solium, which occurs in the small intestine of humans. T. solium is longer than T. saginata which also occurs in the small intestine of humans.

Cysticerci in pigs are found in the brain, liver, heart and skeletal muscles. They cause an inflammatory response in the muscle and central nervous system. In humans, auto-infection can occur from the adult worm in the intestine. The most frequently affected site is the central nervous system.

Life cycle : (Fig. 139) After 2 – 3 months of cysticercus development in pigs, pearly white cysts with an invaginated scolex may be seen in the muscles. With ingestion of infected pork by humans, the larvae evaginate and attach to the proximal part of the live for many years in the environment. The ingestion of proglottides by scavenging pigs is the most frequent way of transmission of cysticerci to swine. Larvae hatch from eggs in the pig intestine and they further migrate to muscle tissue, brain, liver and other organs. The use of inadequately treated human excrements as fertilizer is the other cause of porcine cysticercosis. The auto-infection of the central nervous system with the larval form of cysticercus in humans is manifested with headache, dizziness, hydrocephalus, loss of vision and nausea.

Antemortem findings :

  1. Fever in acute stages
  2. Muscle stiffness

Postmortem findings :

  1. Cysts in the heart (Fig. 140) and skeletal muscles
  2. Cysts in liver (Fig. 141), brain (Fig. 142) and meninges

Judgement : Heavy infestation with Cysticercus cellulosae calls for carcass condemnation. In light or moderate infestation, the carcass may be conditionally approved pending heat or freezing treatment. Due to scavenging nature of pigs, infection is usually found only in free range animals and not sty raised ones. Carcasses are usually severely affected (“pearly pork”) and are condemned despite provision for freezing treatment.

Differential diagnosis : Myositis, abscess and granuloma caused by injection

Fig. 139: Life cycle of Taenia solium (Courtesy G.J. Jackson, Division of Microbiology, US FDA, Washington D.C., USA)

fig 139

Fig. 140: Numerous cysts of C. cellulosae in the heart muscles.

fig 140

Fig. 141: Cellulosae cysts in the liver.

fig 141

Fig. 142: C. cellulosae cysts in the brain.

fig 142


Ascaris suum is a pathogenic parasite of mostly young pigs. Ascariasis accounts for significant losses to the swine industry due to reduction in growth rate, stunting of young pigs and liver condemnations. The liver lesions are seen as “milk spots” and degeneration of the liver parenchyma may occur with subsequent cirrhosis. In the lungs, the larvae may cause haemorrhage and frequently verminous pneumonia. Young animals may show marked respiratory signs called “thumps”.

Life cycle: Adult worms live in the small intestine of pigs where it lays a great number of eggs. These eggs have a thick wall, and are resistant to different environments. They may survive in cool, moist surroundings for up to 5 years. The eggs become infective within a few weeks and, if they are ingested by a host, larvae are released in the small intestine. The larvae migrate through the intestinal wall and portal vein to the liver within 24 hours of being swallowed. From the liver, larvae enter the blood stream and reach the lungs. The larvae, during this migration, damage the liver and lungs and sometimes the kidneys. Larvae reach the pharynx through the bronchi and trachea, After they are swallowed by the host, they mature in the intestine and lay eggs.

Antemortem findings:

  1. Poor growth
  2. Rarely cough
  3. In severe infections difficult breathing
  4. Rarely vomiting up the adult worms

Postmortem findings:

  1. Mild inflammation of the intestine and rarely obstruction of the bile ducts caused by adult worms
  2. Obstruction of intestine (Fig. 143) by adult worms
  3. Large congested liver in early stages
  4. Lung edema, haemorrhage or parasitic pneumonia
  5. “White spots or milk spots” (Fig. 144) in the liver. These lesions are confluent in chronic cases.
  6. Jaundiced carcass and in poor flesh

Judgement : Severely “white spotted” and cirrhotic livers are condemned. Mild isolated lesions will disappear if the liver is held overnight in the offal cooler and it can be released for human consumption.

Differential diagnosis : Enzootic pneumonia, chronic enteritis caused by Salmonella and Treponema spp.

fig 143

Fig. 143: Ascariasis. Numerous round worms in the intestine of a market pig.

fig 144

Fig. 144: Numerous “milk spots” lesions throughout the liver parenchyma.


Sparganosis in pigs is seen in the Asia-Pacific region and some other parts of the world and is caused by spargana, the larval (plerocercoid) stages of the tape worm Spirometra erinacei.

Life cycle: The adult tape worm Spirometra erinacei lives in the small intestine of the cat, fox and dog. The egg passed in the faeces develops into a ciliated coracidium in water, which when ingested by cyclops (the water flea), the first intermediate host, develops into a procercoid. If the cyclops with the procercoid is eaten by a frog, the second intermediate host, the procercoid develops into a plerocercoid which resembles the adult tape worm in miniature but without the genitalia. When these frogs are eaten by a cat, fox and dog the plerocercoid develops into mature tape worms - Spirometra erinacei. However, if a frog is eaten by a pig or other animals such as snakes the plerocercoid migrates to certain tissues, particularly the skeletal muscles where they appear as cysts up to 6 mm long or as ribbon like structures (Fig. 145) about 5 cm long with a miniature scolex. These are termed spargana. Humans can be infected with spargana.

Antemortem findings : No significant signs

Postmortem findings:

  1. Caseated cysts or cysts up to 6 mm long with spargana in the skeletal muscle or elsewhere
  2. Ribbon like structures resembling nerve fibres up to 5 cm long (Fig. 145) in the flank just below peritoneum

Judgement : Carcasses with heavy infestations are condemned. In moderate to light infestations the lesions and parasites are removed and the carcass frozen at - 12°C or less for 5 or more days before being passed for human consumption. Such carcasses may not be acceptable for export.

Differential diagnosis: Sarcocystosis, trichinellosis, cysticercosis, myositis, nerve fibres

fig 145

Fig. 145: Sparganum. The plerocercoid stage of Spirometra erinacei released from a pig muscle. Note the rudimentary scolex.

Diseases caused by protozoa

Porcine babesiosis (Piroplasmosis, Texas fever, Red water, Tick fever)

Babesiosis of swine, cattle, horses, sheep and swine is a protozoan disease caused by various species of protozoa in the genus Babesia. Babesiosis in swine is caused by B. trautmani and B. perroncitoi. The percentage of parasitized erythrocytes may be up to 60 % in swine. Pregnant sows may abort. Abortion is associated with febrile animals. It is believed that the source of infection for domestic swine are often feral pigs.

Transmission: Different species of ticks in the family Ixodidae serve as vectors in different locations. Rhipicephalus spp. and Boophilus spp. are vectors in pigs. The Babesia parasites can be transmitted within a tick species. Contaminated surgical instruments and needles may also transmit the infection.

Antemortem findings: Antemortem findings are similar to bovine babesiosis.

  1. Fever
  2. Anaemia or jaundice
  3. Dark reddish-brown urine

Postmortem findings:

  1. Fever
  2. Thickened bile and reddish-brown urine
  3. Congestion of organs
  4. Yellowish-orange coloration of the carcass
  5. Edematous and haemorrhagic lymph nodes

Judgement: Carcass of an animal showing generalized signs of infection, jaundice and inadequate bleeding is condemned. An emaciated carcass showing yellow gelatinous fat is also condemned. Recovered animals and those showing a mild form of the disease are approved. Satisfactory carcass setting in the chiller is prerequisite for this approval.

Differential diagnosis : Theileriosis, haemobartenellosis, leptospirosis, bacillary haemoglobinuria and eperythrozoonosis, anaplasmosis and trypanosomiasis

Sarcocystosis in pigs (Sarcosporidiosis)

Sarcocystosis of pigs is caused by three species of Sarcocystis. They are: S. miescheriana, S. suihominis, and S. porcifelis. The first two species are macroscopic and when fully developed are fusiform and measure up to 1.5 mm in length. The overall prevalence of sarcocysts in pigs appears to be relatively low and the incidence appears to be decreasing largely due to methods of husbandry where pigs are being reared indoors.

S. suihominis uses humans and non human primates as definitive hosts. It is important as a zoonotic agent. However, it is rarely identified in meat inspection. S. miescheriana uses the dog, racoon, wolf and the jackal as definitive hosts. These hosts acquire the infection when they eat the tissues of pigs containing viable cysts of Sarcocystis. S. miescheriana has a world-wide distribution and is pathogenic causing weight loss and purpura. In some countries up to 20 % of carcasses from free range pigs harbour this parasite. S. porcifelis has been reported from the former USSR and very little information is available on this species.

Life cycle : The general pattern of life-cycle of Sarcocystis spp. in pigs is similar to that described for S. cruzi in cattle except that each species of Sarcocystis uses a different definitive host as indicated.

Antemortem findings :

  1. Weight loss
  2. Purpura of the skin especially of the legs and buttocks
  3. Dyspnea
  4. Muscle tremors
  5. Abortion

Postmortem findings : Elongated fusiform cysts 1.5 × 2 cm in various muscle (Fig. 146)

Judgement : In heavy infestation the carcass is condemned. In moderate to light infestations the lesions are removed and the carcass passed.

Differential diagnosis : Trichinosis, toxoplasmosis, myositis, C. cellulosae

fig 146

Fig. 146 : Sarcocystosis in pigs. Sarcocystis miescheriana in pig muscle.


Toxoplasmosis is contagious disease of swine, sheep and other species characterized with encephalitis, pneumonia and neonatal mortality. It is caused by protozoon Toxoplasma gondii in animals and humans. Toxoplasma is most frequently found in pigs and sheep. Young animals are infected to a lesser degree than old animals. Cattle are rarely affected with clinical toxoplasmosis. Young pigs may die from pneumonia caused by toxoplasmosis.

Humans can get infected with Toxoplasma cysts by ingestion of uncooked animal tissue. In humans clinical symptoms may vary from fever, malaise, skin rash, pneumonia, myocarditis, lymphadenopathy and encephalitis. Infected pregnant women may transfer the tachyzoites to the fetus.

Life cycle : (Fig. 147) Asexual, sexual and oocyst stages of this organism develop in the small intestine of wild and domestic cats. Cats get infected by eating mice or birds or animal tissue containing infective oocysts. In the intestine, the parasite develops through the typical coccidian life cycle. Unsporulated oocysts are shed in the faeces. After a few days the oocysts sporulate and become infective for over a year. The oocysts are further ingested by the intermediate host (pig, sheep, cattle and humans). From the intestine, oocysts move to various tissues including myocardium, lungs, placenta and most frequently to muscle, brain and liver where they encyst. In the host, they may remain viable for the life span of the host. By eating the infected tissue mice, birds, cats and humans may get infected. The life cycle is then completed.

Antemortem findings :

  1. Neonatal mortality
  2. Fever (40 – 42°C) and pneumonia in young pigs
  3. Difficult breathing and coughing
  4. Weakness and wasting
  5. Incoordination and trembling
  6. Diarrhoea
  7. Abortion in pregnant sows and stillbirths

Fig. 147: Life cycle of Toxoplasma (Coutesy G.J. Jackson, Division of Microbiology, US FDA, Washington D.C., USA)

fig 147

Postmortem findings :

  1. neumonia
  2. Hydrothorax
  3. Ascites
  4. Intestinal ulceration
  5. Necrosis in the liver, spleen and kidneys
  6. Inflammation of the lymph nodes
  7. Multiple granulomatous lesion in the brain

Judgement : Carcasses of animals showing clinical signs of acute disease are condemned. Recovered and reactor animals are approved.

Differential diagnosis : Abortion in pigs: Brucellosis, leptospirosis, porcine parvovirus infection, hog cholera and Aujeszky's disease. Encephalitis: Salt poisoning, chlorinated hydrocarbons, lead, mercury, Vitamin A deficiency, hypoglycaemia, encephalomalacia, meningitis, rabies and scrapie

Miscellaneous conditions

Porcine stress syndrome (PSS)

The susceptibility to PSS is inherited by a single recessive gene. This condition is more prevalent in the Pietrain, Poland China, Landrace and Landrace cross breeds of hogs. It is more frequent in short, well muscled meat type hogs. Pork stress syndrome has been commonly associated with the PSE (Pale Soft Exudative) condition of the meat. Normal hogs may sometimes produce PSE meat and PSS hogs may produce normal or dry, dark meat. The occurrence of PSE/DFD (Dry Firm Dark) meat in pork may be associated with stress particularly during transport, change of temperature, fighting and chilling. The prevalence of PSE pork is increased in hogs slaughtered in warm weather months as compared to hogs slaughtered in cold months. The pH of PSE pork is less than 6 approximately 1 hour after slaughter and the temperature is above 41°C immediately after slaughter and drops to 4.4 – 4.6 within 24 hours. In DFD pork the pH usually remains high at about 6 after slaughter or even higher after 24 hours. PSE pork has inferior taste, cooking and cooling qualities.

It is thought that the cause of PSE meat is related to excessive postmortem glycolysis, production of lactic acid, fall in pH with depigmentation and consequently reduced water binding.

Antemortem findings (PSS) :

  1. Signs of anxiety
  2. Muscle or tail tremor
  3. Skin blushing or paleness
  4. Mouth breathing
  5. Collapse or death

Postmortem findings :

  1. Extremely dark, firm, dry pork (Fig. 148)
  2. Extremely pale, soft exudative pork (Fig. 148)
  3. Visceral congestion and edema

Remarks : Criteria for sensory assessment of PSE/DFD pork include colour and structure.

The following colours are observed:

  1. Extremely pale
  2. Pale
  3. Normal
  4. Dark
  5. Extremely dark

Muscle may be:

  1. Extremely soft, wet
  2. Soft
  3. Normal
  4. Firm, dry
  5. Extremely firm, dry

The final assessment of pork muscle can be carried out after chilling of the carcass for 24 hours. The normal setting of meat requires a lowering of pH.

Judgement : Carcass affected with PSE or DFD is approved if slight lesions are present. Extensive involvement of the carcass may require down grading for manufacturing purposes, or condemnation.

Differential diagnosis : Hypocalcemia and pyridoxine deficiency. Both are restricted to home mixed diets. Porcine viral encephalomyelitis should also be considered in differential diagnosis.

fig 148

Fig. 148: Porcine stress syndrome (PSS). Dark, firm and dry pork (right); pale, soft and exudative pork (left); the normal pork is in the middle.

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