Swine Infectious Diseases: Respiratory and diarrheal diseases

Organisms that cause atrophic rhinitis in pigs?

P. multocida, B. bronchiseptica, and H. parasuis

How do the organisms that cause atrophic rhinitis and cytomegalovirus differ in pathogenesis?

Porcine cytomegalovirus (CMV), which is the cause of inclusion

body rhinitis, does not cause nasal turbinate atrophy. However, it may damage the nasal mucosa, predisposing it to colonization with one of these bacterial agents.

What are predisposing factors that cause Atrophic Rhinits?

high ammonia levels (50–100 ppm) and dust (Hamilton et al., 1999), and genetics as well as infection by cytomegalovirus.

What toxins are produced by pasteurella and bordatella that lead to atrophic rhinitis?

P. multocida strains A and D produce Pasteurella multocida toxin (PMT), which causes progressive nasal turbinate atrophy, which disrupts G-protein and rho-dependent pathways and stimulates mitogenesis resulting in degenerative and hyperplastic changes, especially within the bony turbinates of the nasal cavity. B. bronchiseptica produces a heat-labile dermonecrotic toxin (DNT) which alone will produce a moderate self-limiting form of the disease in which damaged tissues may regenerate in time.

These toxins include DNT, which

impairs bone formation; adenylate cyclase toxin (ACT),

which is responsible for disruption of innate immune

function; tracheal cytotoxin (TCT), which interacts with

LPS and is responsible for impaired ciliary function

Which cause more severe atrophic rhinitis (or progressive atrophic rhinitis)?

-Bordatella alone

-Bordatella and pasteurella together

-Bordatella and hemophilus parasuis together

-Pasteurella and Hemophilus parasuis together?

Bordatella and Pasteurella

Which cause more severe atrophic rhinitis (or non-progressive atrophic rhinitis)?

-Bordatella alone

-Bordatella and pasteurella together

-Bordatella and hemophilus parasuis together

-Pasteurella and Hemophilus parasuis together?

Recently, the term ‘nonprogressive atrophic rhinitis’

(NPAR) has been applied to the form caused by B. bronchiseptica alone, and the term ‘progressive atrophic rhinitis’

(PAR) to P. multocida alone and combined infections and B. bronchiseptica

Transmission of bordatella

B. bronchiseptica is spread from pig to pig by aerosol

droplets, which probably first occurs with snout-to-snout

contact between a sow and a newborn piglet,. Often from carrier pigs in a new herd. B. bronchiseptica colonizes the ciliated epithelial cells in the nasal epithelium.

Which immunoglobulins are required to clear bordatella from the immune system?

IgG and IgA are both required for complete clearance of the respiratory tract of B. bronchiseptica.

What conditions are required for P. multocida to colonize?

In order for P. multocida to colonize, decreased ciliary

function or increased mucous is typically required.

Clinical signs of bordatella bronchiseptica based on age?

The clinical signs of pure B. bronchiseptica infection (NPAR) generally appear in nursery pigs less than 4 weeks of age and consist of sneezing, snuffling, and a mucopurulent nasal discharge. In older pigs, these signs are mild or nonexistent.

Clinical signs of P. multocida based on age?

The clinical signs of P. multocida (PAR) typically

begin at 1–3 months of age and consist of sneezing and

snuffling, which progresses to more violent sneezing

with mucopurulent nasal discharge.

Most characteristic clinical signs of P. multocida?

The most characteristic clinical sign is the dorsal and/or

lateral deviation of the snout as the pig grows. This is

caused by abnormal bone growth due to unequal nasal

turbinate atrophy. Brachygnathia superior is the most

common form seen and is due to slower bone growth in

the upper jaw which gives it an upturned appearance.

What condition is this photo showing?

Atrophic rhinitis

Can atrophic rhinitis be cured?

Once lesions are present, there is no

cure. AR is a disease best prevented.

What is the treatment and prevention plan for NPAR and PAR?

A treatment plan for NPAR and PAR should include a combination of environmental and husbandry improvements followed by a vaccination and antibiotic program tailored to the facility.

Vaccines are generally given to the sow prefarrowing, as improved colostral immunity is considered more important than piglet vaccination

Which scroll is most commonly affected by atrophic rhinitis?

atrophy of the turbinates (most severe in the ventral scroll of the ventral turbinate)

What anatomical location is used by pathologists to cut to diagnose atrophic rhinitis?

turbinate atrophy is subjectively measured

at necropsy by visual scoring of a section at the

level of the second premolar

What other organ systems can be affected by Bordatella or P. multocida?

The toxin produced by severe infections of toxigenic strains of P. multocida will induce liver and kidney lesions as well as damage nasal turbinates.

What capsular serotypes are found in swine with P. multocida, which are most likely to cause lung disease and which are most likely to cause the most severe disease?

Capsular serotypes A, B, and D have been reported in swine, A being the most common in pneumonic lungs and B causing the most severe disease (septicemic)

Is P. multocida naturally found in the nasal cavity or always pathogenic when found?

P. multocida is a common inhabitant of the upper respiratory tract of swine.

Which infectious diseases cause thumping in pigs?

Dzs that cause thumping:

1. P. multocida

2. A. pleuropneumonia

3. M. hyopneumonia

4. Metastrongylus

What diseases are the acute and chronic form of P. multocida similar to?

The acute form is clinically similar to pleuropneumonia

(APP) without the frequency of sudden death; the

chronic form is similar to mycoplasmal pneumonia of

swine (MPS)

Is P. multocida usually a secondary or a primary pathogen?

secondary

What are common histopathologic findings of P. multocida?

Gross findings in the lungs are usually

confined to the cranioventral aspects of the lobes and

include red to gray areas of consolidation, frothy exudate

in the trachea, suppurative pleuritis and pericarditis,

pleural adhesions, and pulmonary abscesses

What is the etiology of Actinobacillus pleuropneumonia and what protein is required for its growth?

This bacterium is a gram-negative encapsulated

coccobacillary rod, which requires nicotinamide adenine

dinucleotide (NAD or factor V) for growth.

What are the three most important virulence factors of Actinobacillus pleuropneumonia?

Extracellular hemolytic toxins ApxI, ApxII, and ApxIII

are some of the more important virulence factors

Transmission of actinobacillus

Transmission is primarily by snout to snout and by aerosol

How quickly does death occur after innoculation?

Inoculation of pigs may result in death in as little as 3 h

Where does APP bind in the body?

APP binds squamous cells of the tonsil

followed by type I pneumocytes of the lower respiratory

tract

What is the pathogenesis of APP?

Tissue damage is primarily caused by the host immune response and from lytic Factors released from these cells when they are killed by Apx toxins released from APP, whereas death is primarily due to endotoxic shock from APP LPS

Common clinical presentation of APP

1. The peracute form is characterized by

   rapid development of fever to 41.7°C, anorexia, and

   depression.

2. the skin becomes cyanotic beginning at the extremities

3. Animals may be found dead with no prior signs

4. (pleuritis, abortion, endocarditis, arthritis, abscesses).

5. Dyspnea

Control of APP

treatment not rewards, maintaining APP herds essential

APP histopath findings?

Necropsy The gross findings in pigs with APP

are dependent upon time course and include fibrinous

pleuritis, pulmonary edema, and the presence of bloody

froth or clotted fibrin plugs in the trachea and bronchi.

The lungs contain bilateral lesions that are dark red and

firm with a predominance of lesions in the dorsal aspects

of the caudal lobes, and there may be a bloody nasal

discharge

What is the etiology of actinobacillus suis?

Actinobacillus suis is a gram-negative

bacterium in the Pasteurellaceae family.

Where does Actinobacillus suis colonize and is it common in pig herds?

A. suis colonizes the

upper respiratory tract with many herds infected, all of

which do not always show clinical signs.De

Describe the three forms of Actinobacillus suis based on age?

1. The first form is a septicemia

affecting suckling and recently weaned piglets

where the only signs may be that animals are found dead.

2. The second form is respiratory disease seen in growers

and finishers with clinical signs including cough and

fever, but they may also be found dead.

3. The third form

is an acute septicemia that affects adults with lethargy,

anorexia, fever, rhomboid skin lesions, and abortion in

pregnant sows.

Which other disease in pigs are findings similar for A. suis on necropsy?

Lesions include erysipelas-like lesions,

What is the agent that causes Mycoplasmal Pneumonia: Enzootic Pneumonia, Mycoplasmal Pneumonia of Swine?

Mycoplasma hyopneumoniae

Where does mycoplasma hypneumonia colonize?

M. hyopneumoniae is a common pathogen that colonizes the ciliated epithelium of the porcine respiratory tract.

What is the etiology of mycoplasma?

Mycoplasmas are small (0.2–0.3 μm), lack

a cell wall, and are nonmotile, fastidious, gram-negative

facultative anaerobes.

Is M. hyopneumonia is more likely enzootic or epizootic in pigs?

Enzootic disease is what is most commonly seen.

What pathogen is the most common cause of chronic pneumonia

mycoplasma hyopneumonia

At what age is M. hyopneumonia generally clinically apparent in pigs?

generally clinical signs are not

obvious until pigs are 3–6 months of age.

What two pathogens does M. hyopneumonia predispose pigs to?

It plays an important role in PRDC when concurrent infection with PRRSV or PCV2 occurs

Are mycoplasma’s easy to culture? What diagnostic modalities are used to identify mycoplasma?

Culture is not usually feasible since mycoplasmas and

M. hyopneumoniae, in particular, are difficult to isolate

and grow. IFA or IHC and PCR have all been used in

diagnosis. ELISAs are also currently

in use to diagnose M. hyopneumoniae

How do you treat Mycoplasma Hyopneumonia?

Experimental evidence has shown

that doxycycline has greater in vitro activity than oxytetracycline

against M. hyopneumoniae, A. pleuropneumoniae,

and P. multocida

What is likely the pathogen causing these gross necropsy lesions?

Mycoplasma Hyopneumonia

Regarding control of mycoplasma in swine herds, are swine immune after having M. hyopneumonia? Is there a vaccine? Does it work?

Yes swine are immune after infection and there is a vaccine that appears to work well for alleviating disease but not prevention of infection.

What are the classic pathology findings for M. hyopneumonia?

In acute disease, the lungs fail to collapse

and there is edema of the lungs. The lungs contain pale

gray or dark-red foci of consolidation that are most

commonly found in the apical lobes and the cranioventral

aspects of the middle, accessory, and caudal lobes. Additionally, there may be catarrhal exudate.

Which mycoplasma species is the easiest to isolate that affects swine?

Mycoplasma hyorhinis is probably the easiest of the porcine mycoplasmas to isolate, is a common contaminant of cell culture lines, and is ubiquitous in the swine population.

What is the common name for Mycoplasma hyorhinis in pigs?

Mycoplasmal Polyserositis and Arthritis

Which mycoplasma species of swine is the most likely to infect via cell culture lines?

M. hyorhinis

Is it common for M. hyorhinis to be found in the respiratory tract of swine without any clinical signs?

This organism is harboured in the respiratory tract of carrier swine, often without clinical disease. The organism adheres to cilia similar

to M. hyopneumoniae and is considered normal flora of

the respiratory tract.

What age groups are most predominantly clinically affected by M. hyorhinis? What are the clinical signs?

It causes polyserositis and polyarthritis in pigs less than 8 weeks old. In older pigs (3–6 months old), only arthritis is caused. The age group most commonly affected is 3–10 weeks of age. agent. The acute signs are lethargy, anorexia, labored respirations, arched back with tucked-up abdomen, lameness, and slight fever and swollen joints. These signs abate in about 2 weeks except that the lameness with swollen joints may persist for several months. Experimental

Common necropsy findings for M. hyorhinis?

Acute lesions include serofibrinous or fibrinopurulent pleuritis, pericarditis, and peritonitis, as well as serofibrinous arthritis with increased synovial fluid and swollen reddish yellow synovial membranes.

Inclusion body rhinitis is caused by what type of virus? What are a hallmark cytology finding for Inclusion Body Rhinitis?

Inclusion body rhinitis (IBR) is caused by porcine cytomegalovirus (PCMV) and is found through out the world. The causative agent is a member of the subfamily Betaherpesvirinae, genus Proboscivirus that produces cytomegaly with hallmark basophilic intranuclear inclusions in cytomegalic cells of nasal mucosa.

DNA enveloped, family herpesviridae

How is inclusion body rhinitis spread?

The virus can also be transmitted transplacentally.

Dissemination of the agent most commonly occurs

via nasal secretions and urine.

After what age is inclusion body rhinitis subclinical?

This disease is usually subclinical in pigs more than 3 weeks of age.

What are the common clinical presentation of Inclusion body disease in young pigs, under 3 weeks of age?

The clinical sequelae typically associated with this disease include unexpected fetal and piglet death, runting, rhinitis, conjunctival discharge, pneumonia, sometimes neurological signs, and poor weight gain in young pigs

Common necropsy findings of inclusion body disease?

The clinical sequelae typically associated with this disease include

unexpected fetal and piglet death, runting, rhinitis, conjunctival

discharge, pneumonia, sometimes neurological

signs, and poor weight gain in young pigs

What letter type of influenza causes most common swine influenza?

Influenza A, Influenza A viruses belong to the family of RNA viruses, Orthomyxoviridae, Enveloped

Transmission of influenza in a swine herd?

Swine influenza typically appears as a result of new animals entering the herd. Outbreaks rapidly spread through all animals within a group.

The primary route of transmission is via direct contact.

The swine influenza viruses (SIVs) have a very wide

host range.

The virus enters via the respiratory

epithelium.

Clinical presentation of influenza in swine

Animals appear very ill with anorexia, labored open-mouthed breathing, and a strong reluctance to move.

Clinical signs of influenza in swine

Clinical Signs/Diagnosis: Animals appear very ill

with anorexia, labored open-mouthed breathing, and a

strong reluctance to move. The animals have fever, rhinitis,

and nasal discharge, and during recovery, will cough.

Despite the apparently severe clinical signs, the animals

typically recover rapidly within 5–7 days of developing

clinical signs. Morbidity is nearly 100% with less than 1% mortality

Treatment of influenza in swine

amantadine has been shown to reduce the febrile response and the shedding of virus in experimentally infected pigs.

Gross findings on necropsy for influenza in pigs?

There is fibrinous to mucopurulent exudate in nasal passages, trachea, bronchi, and bronchioles, and sharply demarcated dark-red to purple firm foci of consolidation in apical and cardiac lobes of the lung along with interlobular edema.

What are the common species that cause Verminous Pneumonia (Verminous Bronchitis)?

Metastrongylus spp. include one or more of M. salmi,

M. pudendotectus, or M. elongates apri, with the latter

being the most common.

Ascaris suum

Which parasites have a direct cycle vs. indirect cycle for verminous pneumonia?

Metastrongylus has indirect lifecycle (earthworm), Ascaris has a direct lifecycle (still risk of transmission in doors)

Prepatent periods for metastrongylus and ascaris?

Prepatent period 28 days for metastrongylus

40 - 53 days for Ascaris

Pathogensis of Metastrongylus elongatus?

M. elongatus larvae migrate through

the lung parenchyma, causing alveolar hemorrhage fol

lowed by inflammation and consolidation of the lungs. Eggs are coughed, swallowed and excreted in feces.

Pathogenesis of Ascaris suum?

Migrating A. suum create liver lesions (white spots), which are

seen grossly as white spots that peak at about 1 week

post infection. The pathogenesis of the lung lesions is similar to that of M. elongatus; however, the larvae are coughed up and

then swallowed and mature into adults in the small

intestine.

Clinical signs of verminous pneumonia?

clinical signs consist of dyspnea and decreased weight gain.

What is best for sanitation for verminous pneumonia?

Neopredisan (p-chloro-m-cresol)

disinfectant has been shown to be a very efficacious ovicide

and larvicide for A. suum

Risk factors for diarrhoea in young pigs

Young swine commonly develop diarrhea associated

with shipping stress, changes in diet, primary or mixed

infection with a variety of enteric pathogens, or the perioperative

use of antibiotics that may upset the balance

of normal gut microbiota.

Cause of swine dysentery?

Brachyspira hyodysenteriae, a gram-negative anaerobic spirochete

What is the hallmark clinical sign and what age is most affected by swine dysentary?

severe mucohemorrhagic diarrhea of pigs of postweaning age

What types of diets predispose and are protective against infection by B. hyodysentariae?

diets rich in rapidly fermentable carbohydrates may

exacerbate clinical signs whereas highly digestible diets,

or those high in inulin are protective against disease

Transmission of B. hyodysenteriae?

1. Fecal oral

2. Can transmit after clinical signs stop.

Pathogenesis of B. hyodysenteriae

These organisms do not invade the gut wall below

the lamina propria. The organism produces a hemolysin

that is cytotoxic and an endotoxin. Diarrhea caused by

B. hyodysenteriae is the result of colonic malabsorption

from failure of colonic epithelial cells to transport sodium

and chloride from the lumen to the blood (Argenzio

et al., 1980; Schmall et al., 1983). The mechanism of diarrhea

is therefore very different from that of Salmonella,

Shigella, and E. coli

Clinical signs of Swine dysentery?

severe diarrhea and fever with

accompanying dehydration, weight loss, and weakness

develop over several days. Diarrhea of acute onset is

usually watery with large amounts of mucus

Diagnosis of swine dysentery?

Culture, Warthin–Starry positive spirochetes in colonic crypts, PCR

Control methods for Swine Dysentery?

Swine dysentery is usually

introduced to a facility by the purchase of an asymptomatic

carrier pig. Wild rodents are also reservoirs. Pigs

should be purchased from herds SPF for B. hyodysenteriae

Where are gross lesions confined to in the pig?

Large Bowel

What causes Porcine Intestinal/Colonic Spirochetosis?

Brachyspira pilosicoli

What ages does B. pilosicoli affect?

intestinal spirochete that causes porcine colonic spirochetosis, a nonfatal diarrheal disease that affects pigs during the growing and finishing stages

Transmission dynamics of B. pilosicoli? Is it zoonotic?

B. pilosicoli can be found in contaminated water and colonizes chickens, wild ducks, and immunocompromised humans. Transmission is fecal–oral

What type of diet increases the risk of B. pilosicoli?

pelleted diets increase the risk of colonization

Clinical signs of B. pilosicoli?

Signs include loose stool in

finishers, but younger animals often have watery green

to brown mucoid diarrhea with flecks of blood (Duhamel

et al., 1998). Concurrent diseases that may lead to exacerbation

include swine dysentery, salmonellosis, proliferative

enteropathy, or PCV2 infection

Where are gross lesions primarily in B. pilosicoli?

Gross lesions are limited to the cecum and

colon. Organisms may also be found

within goblet cells

Cause of Proliferative enteropathy?

Lawsonia intracellularis

Are Lawsonia itnracellularis difficult to culture?

Yes, only grow on tissue culture

Other names for Lawsonia intracellularis in pigs and what is the hallmark necropsy finding?

the excessively proliferative lesions found

at necropsy in the terminal ileum, proliferative enteropathy

(PE) of the pig has historically been referred to

as porcine intestinal adenomatosis, terminal or regional

ileitis, intestinal adenoma, and porcine proliferative

ileitis.

Transmission dynamics for Lawsonia Intracellularis in pigs?

Lawsonia is shed in feces, and transmission is by fecal–oral contact. In endemic areas, 15–30% of the herds are estimated to be affected with a 5–20% infection rate within a herd. There is risk of environmental contamination, as L. intracellulare can remain viable in feces for at least 2 weeks. L. intracellulare has also been reported in wild pigs which may also serve as a source of infection

Pathogenesis of lawsonia

The infected crypt cells fail to mature and are not shed, so the crypts become elongated and tortuous resulting in decreased nutrient absorption.

Clinical signs and what age groups are affected?

Clinical disease attributed to PE is most often observed in postweaned pigs between 6 and 20 weeks of age. Clinical signs range from none to marked dullness, anorexia, and diarrhea. Diarrhea is typically moderate with loose to watery stools of normal color. More chronic form associated with passage of black tarry feces.

Treatment of Proliferative enteritis?

Tylosin phosphate can be effective for prevention and for

treatment of PE. Often self-limiting requiring supportive care in severe cases.

What are the necropsy findings for proliferative enteritis?

The gross lesions of PE are found in the

ileum, cecum, and the most proximal one-third of the

spiral colon and consist of a markedly thickened gut

wall and mucosa containing multiple transverse or longitudinal fold

What is this?

Lawsonia intracellularis in the apical portion of the gut

10 week old pig presents with loose watery diarrhea?

Lawsonia

Pigs necropsied after dieing from dehydration associated diarrhea. Path photos show elongated villi.

Lawsonia