26. respiratory pathogens II (bacteriology)

pasteurella gram stain

gram negative rods

what is the source of pasteurella multocida? how is it transmitted?

1. normally colonizes mucous membranes of orophaynx; part of normal microflora of mouth and nasopharynx

   • colonizes a wide range of species (birds, reptiles, and mammals)

2. naive animals infected via contact (direct or by fomites)

pasteurella multocida virulence factors

• capsule (multiple types)

• adhesins: fimbriae, outer membrane proteins

• endotoxin (LPS)

• exotoxins:

  • p. multocida toxin [PMT] (rho activating toxin)

    • disrupts host cell signaling pathways

    • plays role in bone remodeling in atrophic rhinitis in swine

  • dermonecrotic toxin (DNT)

how does p. multocida toxin (PMT) affect bone tissue?

• kills osteoblasts

• promotes osteoclast differentiation and activation → nasal turbinate destruction

progressive atrophic rhinitis (PAR) in swine is caused by what bacteria?

pasteurella multocida (type A or D) + bordetella bronchiseptica (co-infection synergism)

• b. bronchiseptica by itself causes self-limiting form of disease

progressive atrophic rhinitis clinical signs

• sneezing piglets (3-8 weeks of age)

• mucopurulent nasal discharge

• epistaxis

• some of the older animals have distorted snouts

porcine pasteurella bronchopneumonia predisposing factors/pathogenesis

• predisposing factors

  • shipping

  • prior infection (viral)

  • poor air quality

• pathogenesis

  • disruption in innate immunity allows p. multocida to spread to lower airways → LPS triggers inflammation

  • p. multocida type D sticks to damaged epithelium (not healthy epithelium)

pasteurella multocida bronchopneumonia in cattle

• dairy calf pneumonia

• bacterial pneumonia typically secondary to primary insult that disrupts normal respiratory tract (e.g. viral respiratory infection)

pasteurella multocida lesions in rabbits

• otitis media

• pyometra

• pneumonia

• septicemia also possible

  • organism disseminates from oropharynx to multiple body sites; usually type A or D

how is pasteurella multocida treated in rabbits?

• antibiotics may be effective in early cases

  • usually give parenterally to avoid disrupting gut microbiota

• prebiotics often recommended to avoid clostridial diarrhea

• vaccination: bacterin may reduce morbidity, but will not prevent infection

general clinical signs of pasteurella multocida infection (summary slide)

• vary based on serotype and host innate immunity

  • can be subclinical in healthy animals

• respiratory tract disease:

  • URT = atrophic rhinitis in pigs; “snuffles” in rabbits

  • LRT = bovine and porcine pneumonia

• septicemia (ruminants & birds) → usually die within 24 hours

p. multocida diagnosis (summary slide)

based on clinical signs, necropsy findings, and culture (blood agar)

p. multocida treatment/prevention (summary slide)

treatment

• not realistic with septicemia

• rabbits with simple infections may respond to antibiotics

• pneumonia may respond to cephalosporins & tetracyclines

prevention

• in food animal production, focus is on management

• vaccines exist for swine, cattle, and rabbits

p. multocida zoonotic infections are caused by what?

in humans, most commonly occur through dog and cat bites

bordetella bronchiseptica gram stain

gram negative coccobacilli

bordetella bronchiseptica virulence factors

• adhesins

• capsule

• exotoxins

  • dermonecrotic toxin → alters host cytoskeleton → nasal turbinate destruction

  • adenyl cyclase toxin → pore-forming; kills leukocytes

  • osteotoxin → kills tracheal and bone cells

bordetella bronchiseptica transmission

aerosols from carrier animals → highly contagious

bordetella bronchiseptica contributes to what disease in dogs? what is its source/what are predisposing factors?

• “kennel cough” or infectious tracheobronchitis, or CIRDC (canine infectious respiratory disease complex)

• chronic carriers can serve as reservoirs of infection

• infection with canine distemper may predispose to secondary b. bronchiseptica pneumonia

• relapses can occur in stressed animals

canine kennel cough treatment/prevention

• uncomplicated cases — anti-inflammatories and antitussives to alleviate cough response triggered by tracheal inflammation

• antibiotics may be administered in severe cases (co-infections) or puppies that may be at risk of developing pneumonia

• vaccine available

is bordetella bronchiseptica a primary or secondary pathogen in cats? what environmental factors are associated with disease?

• considered a primary pathogen in cats

• associated with overcrowding and shelters

bordetella bronchiseptica clinical signs in cats

• clinical signs slightly different than dogs:

  • fever

  • sneezing

  • ocular discharge

  • lymphadenopathy

  • coughing is uncommon

• self-limiting disease in adults (similar to dogs)

• cats, especially kittens, are more susceptible to pneumonia than dogs

bordetella bronchiseptica treatment/prevention in cats

• antibiotics recommended because of potential susceptibility to developing bronchopneumonia

• intranasal vaccine recommended in cats that may be at risk (shelters or potential boarders)

bordetella bronchiseptica general clinical signs (summary slide)

vary by host

• URT → atrophic rhinitis in pigs

• tracheobronchitis (kennel cough in dogs and cats)

• bronchopneumonia (piglets and kittens)

bordetella bronchiseptica diagnosis

based on clinical signs, necropsy findings, and culture (blood and MacConkey agar)

bordetella bronchiseptica treatment/prevention (summary slide)

treatment

• mild disease not usually treated with antimicrobials

• antibiotics (macrolides, fluoroquinolones, trimethoprim-sulfamethoxazole, and aminoglycosides) are effective

prevention

• quarantine infected and recovering animals (highly contagious)

• vaccines (bacterins) and management practices

glaesserella parasuis gram stain

gram negative rods

glaesserella parasuis is the causative agent of what disease in pigs? what ages are most susceptible to infection?

• glasser’s disease

• primary agent of nursery mortality → mostly affects young pigs (2 weeks to 4 months old)

• sporadic disease in naive adults (specific pathogen-free colonies)

glaesserella parasuis source/transmission

• commensal of upper respiratory tract (oropharynx and tonsils)

• sows transfer to piglets during first 10 days of life

glaesserella parasuis virulence factors

• capsule-producing strains associated with disease

• LPS may exacerbate inflammation and vasculitis

glaesserella parasuis pathogenesis

• organism enters bloodstream → vasculitis and colonization of serosal surfaces → fibrinopurulent inflammation on serosal surfaces (neutrophils & macrophages)

• endotoxin → microthrombi in tissues and disseminated intravascular coagulation (DIC)

• older animals may develop acute pneumonia without polyserositis

clinical signs of glasser’s disease

depends on site of infection

• meningoencephalitis → tremors, incoordination, posterior weakness, lateral recumbency (CNS signs)

• polyarthritis/lameness

• vasculitis → cyanosis of extremities

• bronchopneumonia → respiratory distress/dyspnea

where should you collect samples for glaesserella parasuis PCR? why?

• sample from lesions, NOT nasal cavity (commensal)

  • fibrinous exudates on any serosal surfaces

  • serous fluid (preferably aseptic aspirate)

  • swabs of serosal joints, meninges

• current diagnostic methods do not differentiate virulent from avirulent isolates

  • avirulent strains typically colonize URT, whereas virulent strains are found in other tissue sites

  • sample only from systemic sites, such as pleura, pericardium, peritoneum, joints, and brain

glaesserella parasuis treatment/prevention

• vaccines available, but efficacy is serotype-dependent

• antimicrobials offer mixed responses because of peracute nature of disease

• minimize stress conditions on farm