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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.

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


Pneumonia

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

Pleuropneumonia:

  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

Pleuropneumonia

  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

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

Parasitic diseases

Diseases caused by helminths

Trichinosis

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

Ascariasis

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.


Foot and Mouth Disease (FMD, Aphthous fever)

Exotic, not found in Australia

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.


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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