Lecture 2 - pigs and poultry

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41 Terms

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Cystoisospora suis

Trichuris suis

Oesophagostomum spp

Stephanurus dentatus

Metastrongylus spp

Pig coccidiosis

Trichurosis

Oesophagostomosis

Stephanurosis

Metastrongylosis

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Pig coccidiosis: Cystoisospora/Isospora suis

Location: small intestine

Cystoisospora (Isospora) suis: proven pathogenic;

Infected animals shed in the environment unsporulated oocysts;

Sporulation/sporogony: the oocysts require

• Humidity;

• Proper temperature:

Sporulated oocysts contain two sporocysts each with four sporozoites;

Infection of the host: ingestion of sporulated oocysts;

<p>Location: small intestine</p><p>Cystoisospora (Isospora) suis: proven pathogenic;</p><p>Infected animals shed in the environment unsporulated oocysts;</p><p>Sporulation/sporogony: the oocysts require</p><p>• Humidity;</p><p>• Proper temperature:</p><p>Sporulated oocysts contain two sporocysts each with four sporozoites; </p><p>Infection of the host: ingestion of sporulated oocysts;</p>
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Cystoisospora/Isospora suis

Morphology/life cycle

• Oocysts excyst in the small intestine  sporozoites are released and invade the epithelial cells;

• Asexual (merogony) and sexual (gamogony) development occurs in the enterocytes of the

small intestine

• Oocysts are shed in the faeces 4-5 days post infection in several peaks (each phase lasts for 2-3 days) for up to 2 weeks

Short PPT (4-5 days) and short sporulation time (12 h - 2 days);

<p>• Oocysts excyst in the small intestine  sporozoites are released and invade the epithelial cells;</p><p>• Asexual (merogony) and sexual (gamogony) development occurs in the enterocytes of the</p><p>small intestine</p><p>• Oocysts are shed in the faeces 4-5 days post infection in several peaks (each phase lasts for 2-3 days) for up to 2 weeks</p><p>Short PPT (4-5 days) and short sporulation time (12 h - 2 days);</p>
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Cystoisospora/Isospora suis

EPIDEMIOLOGY

 Infections occur all over the world in both indoor and outdoor systems (does not seem to be associated with a particular season);

 Pigs younger than 2 - 3 weeks more susceptible (most susceptible in the first 3 days of life)  age resistance develops

Infections of piglets older than 3 weeks are asymptomatic

Pigs that recover from infection are resistant to challenge infections;

Sows are not the source of infection for piglets

 Oocysts shed by previous piglets in the farrowing pen and that survived on floor and walls seem to be the source of infection --> management/cleaning of the farrowing pen is essential in prevention;

 Sporulated oocysts can survive for months in the environment and are resistant to most disinfectants

<p> Infections occur all over the world in both indoor and outdoor systems (does not seem to be associated with a particular season);</p><p> Pigs younger than 2 - 3 weeks more susceptible (most susceptible in the first 3 days of life)  age resistance develops</p><p>Infections of piglets older than 3 weeks are asymptomatic</p><p>Pigs that recover from infection are resistant to challenge infections;</p><p>Sows are not the source of infection for piglets</p><p> Oocysts shed by previous piglets in the farrowing pen and that survived on floor and walls seem to be the source of infection --&gt; management/cleaning of the farrowing pen is essential in prevention;</p><p> Sporulated oocysts can survive for months in the environment and are resistant to most disinfectants</p>
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Cystoisospora/Isospora suis

Pathogenesis/Pathology

Depends on the age of the pigs and infective dose:

Pathogenesis is caused by both asexual (meronts) and sexual (gamonts) stages

<p>Depends on the age of the pigs and infective dose:</p><p>Pathogenesis is caused by both asexual (meronts) and sexual (gamonts) stages</p>
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Cystoisospora suis

Clinical signs

 Commonly occur in pigs of 1-2 weeks of age;

 Appear 3-5 days after infection (associated with the asexual stages) and last 3-7 days;

 Yellowish/grayish diarrhoea, (non-haemorrhagic), liquid to pasty, foul smelling, that stains the perineum;

 Dehydration, pigs are less active and depressed;

 Reduced weight gains, weight loss  not all the piglets in the litter are equally affected  uneven weight gain and stunted growth;

<p> Commonly occur in pigs of 1-2 weeks of age;</p><p> Appear 3-5 days after infection (associated with the asexual stages) and last 3-7 days;</p><p> Yellowish/grayish diarrhoea, (non-haemorrhagic), liquid to pasty, foul smelling, that stains the perineum;</p><p> Dehydration, pigs are less active and depressed;</p><p> Reduced weight gains, weight loss  not all the piglets in the litter are equally affected  uneven weight gain and stunted growth;</p>
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Cystoisospora/Isospora suis

Diagnosis - LIVE ANIMALS

Live animals

 History & clinical signs: diarrhoea in 1-2 week pigs that does not respond to antibiotics is suggestive;

 Identification of oocysts in the faeces: faecal flotations or direct smears;

High fat content of the faeces  detection of oocysts is sometimes difficult  epifluorescence might help visualization of oocysts (oocysts show autofluorescence);

 PCR seems to be the most sensitive method

<p>Live animals</p><p> History &amp; clinical signs: diarrhoea in 1-2 week pigs that does not respond to antibiotics is suggestive;</p><p> Identification of oocysts in the faeces: faecal flotations or direct smears;</p><p>High fat content of the faeces  detection of oocysts is sometimes difficult  epifluorescence might help visualization of oocysts (oocysts show autofluorescence);</p><p> PCR seems to be the most sensitive method</p>
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Cystoisospora/Isospora suis

Diagnosis - DEAD ANIMALS

Dead animals

 Gut scrapings  endogenous stages (the amount of endogenous stages might be low relative to the pathological effects);

 Histopathology:

Differential diagnosis

 Enteropathogenic E. coli, Clostridium perfringens type 3, Strongyloides ransomi, rotivirus etc.

<p>Dead animals</p><p> Gut scrapings  endogenous stages (the amount of endogenous stages might be low relative to the pathological effects);</p><p> Histopathology:</p><p>Differential diagnosis</p><p> Enteropathogenic E. coli, Clostridium perfringens type 3, Strongyloides ransomi, rotivirus etc.</p>
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Cystoisospora/Isospora suis TREATMENT

Toltrazuril (Baycox) (oral and injectable formulations)

Treat all the piglets in a litter, all infected and ‘at risk’ litters in the farrowing house.

• In stocks at risk treat metaphylactically when pigs are 3-5 days of age (this treatment prevent deaths and reduce losses);

Chemoresistance has developed

<p>Toltrazuril (Baycox) (oral and injectable formulations)</p><p>Treat all the piglets in a litter, all infected and ‘at risk’ litters in the farrowing house.</p><p>• In stocks at risk treat metaphylactically when pigs are 3-5 days of age (this treatment prevent deaths and reduce losses);</p><p>Chemoresistance has developed</p>
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Cystoisospora/Isospora suis

Management and hygiene

 All-in all-out, optimum stocking density;

 Clean and disinfect the entire farrowing room after all the litters are weaned (use steam, burners etc);

 Keep the farrowing rooms/pens dry and clean;

 Disinfection with:

 Bleach (at least 50%) or ammonia compounds for several hours or overnight;  Neopredisan 135-1: associated with good results (availability in Australia?).

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Trichuris suis

Location: caecum and colon:

may infect humans

<p>Location: caecum and colon:</p><p>may infect humans</p>
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Trichuris morphology

Adult worms

Length: 6-8 cm female worms;

Body made up of two parts, slender, anterior one (2/3 of the body length) and a thick, posterior part;

Posterior end of the male: coiled, with one spicule;

Posterior end of the female: curved;

<p>Adult worms</p><p>Length: 6-8 cm female worms;</p><p>Body made up of two parts, slender, anterior one (2/3 of the body length) and a thick, posterior part;</p><p>Posterior end of the male: coiled, with one spicule;</p><p>Posterior end of the female: curved;</p>
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Trichuris eggs

Eggs

• 50-70 μm;• Lemon shaped;• Thick & smooth shell, yellow-brown; • Plugs at poles,• One cell inside;

<p>Eggs</p><p>• 50-70 μm;• Lemon shaped;• Thick &amp; smooth shell, yellow-brown; • Plugs at poles,• One cell inside;</p>
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Trichuris suis

Life cycle

Eggs are passed in the faeces

 infective larva develops slowly inside the eggs in 3-4 weeks (up to 6 months);

Infection: ingestion of embrionated eggs;

PPT: 6-8 weeks, life span: 4-5 months.

<p>Eggs are passed in the faeces </p><p> infective larva develops slowly inside the eggs in 3-4 weeks (up to 6 months);</p><p>Infection: ingestion of embrionated eggs;</p><p>PPT: 6-8 weeks, life span: 4-5 months.</p>
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Trichuris suis

Epidemiology

Prevalence higher in free range/organic farms;

Eggs develop/become infective very slowly and in the intensive systems they are eliminated by cleaning/disinfection before they get infective

Common in herds housed on dirt lots/inadequate drainage of stagnant water etc (less common in pigs housed on concrete);

Growers and finisher (2-6 months of age) pigs are generally the most (heavily) infected - sows and boars have the lowest levels of

infection

Infection: ingestion of embrionated eggs

Eggs are very resistant in the environment (up to 6-11 years)

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Trichuris suis

Pathogenesis/pathology

• Cause enterocyte destruction, ulcers --> secondary bacterial (Serpulina (Treponema) hyodysenteriae, Campylobacter and Pseudomonas aeruginosa) and Balantidium/Balantioides coli infections -> infections with T. suis might mimic swine dysentery

Erosion of the dilated blood vessels and mucosa -> hemorrhage, anemia and hypoalbuminaemia;

<p>• Cause enterocyte destruction, ulcers --&gt; secondary bacterial (Serpulina (Treponema) hyodysenteriae, Campylobacter and Pseudomonas aeruginosa) and Balantidium/Balantioides coli infections -&gt; infections with T. suis might mimic swine dysentery</p><p>Erosion of the dilated blood vessels and mucosa -&gt; hemorrhage, anemia and hypoalbuminaemia;</p>
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Trichuris suis

Clinical signs

• Light infections: no clinical signs;

• Massive infections (hundreds/thousands of parasites): anorexia, anemia, mucoid to bloody diarrhea, dehydration, retarded development and death;

<p>• Light infections: no clinical signs;</p><p>• Massive infections (hundreds/thousands of parasites): anorexia, anemia, mucoid to bloody diarrhea, dehydration, retarded development and death;</p>
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Trichuris suis

Diagnosis LIVE animals

Clinical signs and history are not specific;

Detection of eggs in the faeces:

Clinical signs caused by larval stages;

Intermitent egg layers;

Eggs do not float easily;

<p>Clinical signs and history are not specific;</p><p>Detection of eggs in the faeces:</p><p>Clinical signs caused by larval stages;</p><p>Intermitent egg layers;</p><p>Eggs do not float easily;</p>
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Trichuris Suis

Diagnosis DEAD animals

• Visualization of the worms is relatively easy; • Histopathology;

<p>• Visualization of the worms is relatively easy; • Histopathology;</p>
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Trichuris suis

Treatment

Benzimidazoles

- Fenbendazole (Safe-guard), flubendazole (Flubenol) and oxibendazole

Macrocyclic lactones

- Doramectin

Imidazothiazoles & tetrahydropyrimidines

- Levamisole

- Pyrantel: not active.

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Oesophagostomum spp. (nodular worms)

Oesophagostomum dentatuum

Adult worms

Stout, whitish body;

Anterior end: cephalic vesicle present;

Posterior end: bursa in males;

Eggs

• Ovoid;

• Thin shelled, morula stage;

<p>Adult worms</p><p>Stout, whitish body;</p><p>Anterior end: cephalic vesicle present;</p><p>Posterior end: bursa in males;</p><p>Eggs</p><p>• Ovoid;</p><p>• Thin shelled, morula stage;</p>
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Oesophagostomum dentatuum: Life cycle

• Eggs are shed in the environment;

Egg -> L1 -> L2 -> L3: 7 days at 25-26C;

After ingestion L3s enter the submucosa of the large intestine and molt to L4 (cause nodules);

L4s return to the lumen and molt into adults;

Infection by ingestion of L3  L3 can survive one year outdoors

PPT: as short as 18-21 days

<p>• Eggs are shed in the environment;</p><p>Egg -&gt; L1 -&gt; L2 -&gt; L3: 7 days at 25-26C;</p><p>After ingestion L3s enter the submucosa of the large intestine and molt to L4 (cause nodules);</p><p>L4s return to the lumen and molt into adults;</p><p>Infection by ingestion of L3  L3 can survive one year outdoors</p><p>PPT: as short as 18-21 days</p>
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Oesophagostomum dentatuum: Epidemiology

Common in indoor and outdoor systems;

Low immunogenicity -> may accumulate in time -> infections are common in adult animals (breeding stock);

Pigs’ diet and age can have a significant influence on establishment and fecundity:

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Oesophagostomum dentatuum: Pathology

• Adult worms cause minimum damage to the mucosa

of the large intestine;

L3 enters the mucosa of the caecum and colon -> the host responds by forming a nodule (hypersensitivity reaction) up to 5 mm in diameter;

Pathology caused by:

• Inflammation and nodular reaction induced by

invasion of the mucosa by larvae;• Emergence of the larvae from mucosa;

Heavy infections =congestion of the mucosa

<p>• Adult worms cause minimum damage to the mucosa</p><p>of the large intestine;</p><p>L3 enters the mucosa of the caecum and colon -&gt; the host responds by forming a nodule (hypersensitivity reaction) up to 5 mm in diameter;</p><p>Pathology caused by:</p><p>• Inflammation and nodular reaction induced by</p><p>invasion of the mucosa by larvae;• Emergence of the larvae from mucosa;</p><p>Heavy infections =congestion of the mucosa</p>
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O. dentatuum: Clinical signs

In pigs Oesophagostomum spp. seem to be less pathogenic

than in ruminants;

Infections with up to 5000 parasites per sow -> usually subclinical, greater burdens -> inappetence, weight loss (thin sow syndrome), reduced litter size and weaning weight;

<p>In pigs Oesophagostomum spp. seem to be less pathogenic</p><p>than in ruminants;</p><p>Infections with up to 5000 parasites per sow -&gt; usually subclinical, greater burdens -&gt; inappetence, weight loss (thin sow syndrome), reduced litter size and weaning weight;</p>
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O. dentatuum: DIAGNOSIS

•Finding eggs in the faeces (patent infections);

Thin shell, morula stage;

<p>•Finding eggs in the faeces (patent infections);</p><p>Thin shell, morula stage;</p>
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Oesophagostomum dentatuum: Treatment

Tetrahydropyrimidines: Pyrantel

Imidazothiazoles: Levamisol

Benzimidazoles: Fenbendazole, Flubendazole

Macrocyclic lactones (MLs): Abamectin, Ivermectin, Doramectin

Anthelmintic resistance to Pyrantel and Levamisole mentioned in the past;

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Stephanurus dentatus (Kidney worm of the pig)

Adults worms

Perirenal fat in cysts that are connected to the pelvis of the kidney or to the ureters;

Pelvis of the kidney;

Walls of ureters;

Larvae

• Liver, peritoneal cavity and other organs.

<p>Adults worms</p><p>Perirenal fat in cysts that are connected to the pelvis of the kidney or to the ureters;</p><p>Pelvis of the kidney;</p><p>Walls of ureters;</p><p>Larvae</p><p>• Liver, peritoneal cavity and other organs. </p>
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Stephanurus dentatus (Kidney worm of the pig)

Morphology

Adult worms

Stout worms, males up to 3 cm and

females up to 4.5 cm;

The cuticle is rather transparent  internal organs are easily seen in fresh specimen;

The buccal capsule is cup shaped and thick walled, small leaf crown; triangular teeth at base of buccal capsule;

<p>Adult worms</p><p>Stout worms, males up to 3 cm and</p><p>females up to 4.5 cm;</p><p>The cuticle is rather transparent  internal organs are easily seen in fresh specimen;</p><p>The buccal capsule is cup shaped and thick walled, small leaf crown; triangular teeth at base of buccal capsule;</p>
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Stephanurus D EGGS

Thin shelled, morula stage (32-64 cells);

Passed in the urine.

<p>Thin shelled, morula stage (32-64 cells);</p><p>Passed in the urine.</p>
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Stephanurus dentatus: Life cycle

Eggs are passed in the urine;

L1 -> L2 -> L3 in the environment; Earthworms may serve as transport hosts;

Infection of the host:

Ingestion of L3

Ingestion of transport hosts

Transcutaneously

- Larvae develop in the liver and migrate through peritoneal cavity to the perirenal region but they can migrate anywhere in the body;

PPT 6-11 months.

<p>Eggs are passed in the urine;</p><p>L1 -&gt; L2 -&gt; L3 in the environment; Earthworms may serve as transport hosts;</p><p>Infection of the host:</p><p>Ingestion of L3</p><p>Ingestion of transport hosts</p><p>Transcutaneously </p><p>- Larvae develop in the liver and migrate through peritoneal cavity to the perirenal region but they can migrate anywhere in the body;</p><p>PPT 6-11 months.</p>
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Stephanurus dentatus EPIDEMIOLOGY

Common in feral pigs (N Qld)

Limited to warm, moist areas in Australia (L3 are highly susceptible to desiccation);

<p>Common in feral pigs (N Qld)</p><p>Limited to warm, moist areas in Australia (L3 are highly susceptible to desiccation);</p>
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Stephanurus dentatus - effect on host + DIAGNOSIS

Fibrosis in liver, abscesses in carcases -> organs condemned at slaughter;

Weight loss;

Diagnosis

• Detection of eggs in the urine sediment;

<p>Fibrosis in liver, abscesses in carcases -&gt; organs condemned at slaughter;</p><p>Weight loss;</p><p>Diagnosis</p><p>• Detection of eggs in the urine sediment;</p>
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Stephanurus dentatus - TREATMENT + PREVENTION

Treatment

MLs: Ivermectin and Doramectin;

Imidazothiazoles: Levamisol;

Benzimidazoles: Fenbendazole (yes), Flubendazole (?);

Prevention

-Avoid exposure to L3 in wet/muddy conditions;

-House on concrete or slats;

-Separate young pigs from those >9 mos. which shed eggs (long PP).

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Metastrongylus spp.

Location: bronchi, bronchioles

<p>Location: bronchi, bronchioles</p>
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Metastrongylus MORPHOLOGY

Adult worms

White, filiform body;

Mouth with 2 trilobed lips;

Bursal rays of specific shape (some end in swellings);

The spicules are long and transversally striated;

The posterior end of the female appears digitiform (prevulvar swelling);

<p>Adult worms</p><p>White, filiform body;</p><p>Mouth with 2 trilobed lips;</p><p>Bursal rays of specific shape (some end in swellings);</p><p>The spicules are long and transversally striated;</p><p>The posterior end of the female appears digitiform (prevulvar swelling);</p>
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Metastrongylus EGGS

Have a corrugated surface and are embryonated when

laid.

<p>Have a corrugated surface and are embryonated when</p><p>laid.</p>
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Metastrongylus spp. Life cycle

Intermediate hosts: earthworms -> outdoor systems;

Pigs become infected after ingestion of earthworms that have in their body infective larvae;

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Metastrongylus spp. Clinical signs

• Pigs 4 - 6 months old usually affected: coughing, dyspnoea, unthriftiness;

<p>• Pigs 4 - 6 months old usually affected: coughing, dyspnoea, unthriftiness;</p>
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Metastrongylus spp. Diagnosis

Clinical signs, outdoor systems, age;

Identification of the eggs in the faeces

<p>Clinical signs, outdoor systems, age; </p><p>Identification of the eggs in the faeces</p>
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Metastrongylus spp. Treatment

Benzimidazoles

Fenbendazole

Flubendazole

MLs

ivermectin

doramectin

Imidazothiazoles

levamisole