Pasteurellaceae Flashcards
General characteristics of Pateurella and Bibersteinia spp.
gram neg
facultative anaerobes
oxidase pos
non motile
bipolar staining - Giemsa
What is the basis of serological typing for Pasteuerlla multocida
typing is based on the capsular composition of the different strains and somatic antigens
What is the habitat of Pasteurella spp?
commensals of mucous membranes of the upper respiratory tract, oral cavity and intestinal tract
How can Pasteurella spp cause infection?
endogenous opportunistic infections
exogenous infections via direct contact, inhalation a/o ingestion
Does P. multocida grow on MAC?
NO
How to diagnose P. multocida?
direct microscopy - bipolar staining with Giemsa, look like saftey pins
growth on BA
non-hemolytic
sweet odor on BA
What culture conditions improve primary isolation of P. multocida?
5-10% CO2 conditions
What can be done to differentiate Pasteruella, Bibersteinia and Mannheimia
sugar fermentation tests
biochemical testing and colony features
Which species show hemolysis on BA?
(m. hemolytica, p. multocida, b. trehalosi)
m. hemolytica
b. terhalosi
Which species show growth on MAC?
(m. hemolytica, p. multocida, b. trehalosi)
m. hemolytica
b. trehalosi
Which species have a distictive odor?
(m. hemolytica, p. multocida, b. trehalosi)
p. multocida
Which species are capable of indole production?
(m. hemolytica, p. multocida, b. trehalosi)
p. multocida
Which species are catalase positive?
(m. hemolytica, p. multocida, b. trehalosi)
m. hemolytica
p. multocida
Which species have ornithine decarboxylase activity?
(m. hemolytica, p. multocida, b. trehalosi)
p. multocida
Which species are urease pos?
(m. hemolytica, p. multocida, b. trehalosi)
NONE
What is a limitation to using biochemical strips when diagnosing pasteurellosis?
rapid but results may not be accurate
lack of differentiation from other Pasteurellaceae
When can serological diagnosis be used to diagnose P. multocida?
only possible in recovered animals
difficult in acute and fatal disease
Virulence factors of P. multocida
adhesins, capsule (hyaluronic acid capsule in types A and B), LPS endotoxin, iron acquisition mechanisms, proteases, lipases
Pasteuerlla mutocida toxin
What does Pasteurella multocida toxin cause?
induces osteoclast activity in the nasal bones causing atrophic rhinitis
Which strains of P. multocida is osteolytic toxin a major virulence factor in?
type D - atrophic rhinitis in pigs
type A - pneumonia in pigs and snuffles in rabbits
What is the causative agent of Hemorrhagic Septicemia?
P. multicodia B:2
P. multicodia E:2
What is another name for Hemorrhagic Septicemia?
Barbone
What are the predisposing factors for Barbone?
overwork
poor bcs
monsoon rains
high temp and high humidity
calving season
co-infections
How is Barbone transmitted?
direct contact with nasal a/o oral secretions
ingestion
inhalation
Describe the pathogenesis of Barbine
causes severe endotoxemia
disseminated intravascular coagulation
Describe the epidemiology of Barbone disease
all ages can be effected but most common in animals 6-24 months
latent carriers - organism in the tonsillar crypts - shed organism via nasal secretions
Clinical signs of Barbone Disease
sudden death
high fever, lethargy, salivation, lacrimation
respiratory distress
laryngeal edema
hemorrhaging
recumbancy
What is the incubation period for Barbone disease?
2-4 days
disease course lasts for 2-5 days
(very acute)
What is the mortality rate of Barbone disease?
50-100% mortality
Diagnosis of Barbone disease
history
gross pathological changes
petechial hemorrhages
enlarged hemorrhagic lymph nodes
blood tinged fluid
bipolar Giemsa stained blood smears
isolation, serotyping
indirect hemagglutination test
PCR
How to treat Barbone disease
antibiotic therapy with penicillin and tetracycline - early febrile stage in endogenous regions
regions where disease is exotic: slaughter infected and exposed
Prevention and control of Barbone disease
vaccines - bacterin, live heterotypic, or modified lice deletion mutation
Describe Enzootic Pneumonia of Calves
infectious respiratory disease of calves less than 6months old
peak occurtence from 2-10 weeks
can infect calves up to 1 year of age
more common in dairy than beef calves
more common in housed calves
What are the morbidity and mortality rates of Enzootic Pneumonia of Calves
morbidity 100%
mortality 20%
Enzootic Pneumonia of Calves aka
dairy calf pneumonia
summer pneumonia of beef calves
Describe Bovine Respiratory Disease Complex
most common and costliest problem encountered in feedlot cattle
severe bronchopneumonia, pleurisy
occurs within 4 weeks of weaning and is triggered by stressful events
Bovine Respiratory Disease Complex aka
Shipping Fever Complex
What causes Bovine Respiratory Disease Complex
combination of viruses, bacteria (P. multocida, M. haemolytica, M. bovis), endogenic factos, and exogenic factprs causing disease
Clinical Signs of Bovine Respiratory Disease Complex
sudden onset of fever, depression, anorexia, tachypnea, serious nasal discharge
mixed infections - cough and ocular discharge
Morbity and mortality rates of Bovine Respiratory Disease Complex
morbidity 50%
mortality 1-10%
Diagnosis of Bovine Respiratory Disease Complex
history, clinical signs
gross pathology: cranial lobes of lungs are red, swollen and consolidated. fibrinous pleurisy
cytospin preparations from bonchioalveolar lavage reveal large numbers of neutrophils
isolation of organism from trantracheal wash or affected lung tissue
Treatment of Bovine Respiratory Disease Complex
isolate affected animals
antibiotics but increasing resistance of M. haemolytica has been reported
Prevention and control of Bovine Respiratory Disease Complex
monitor new animals
minimize stress factors
vaccination
metaphylaxis
Causative agent of Atrophic Rhinitis in Pigs
toxigenic strains of P. multocida types A or D
What are the strains of P. multocida that cause atrophic rhinitis in pigs designated as?
AR+
At what age are pigs most vulnerable to atrophic rhinitis?
at 3-8 weeks old
What is the source of infection for atrophic rhinitis?
carrier pigs
Predisposing Factors of Atrophic Rhinitis in Pigs
infection with Bordetella bronchiseptica
overstocking
poor ventilation
mixing pigs
Describe the non-progressive form of atrophic rhinitis
caused by B. bronchioseptica
mild turbinate atrophy
predisposes to progressive atrophic rhinitis
Describe the progressive for of atrophic rhinitis
caused by toxogenix P. multocida AR+
What is the main virulence factor of progressive atrophic rhinitis
Pasteurella multocida toxin
causing cytoskeletal rearrangements and fibroblast growth
Clinical Signs of ATrophic Rhinitis
excessive lactrimation, sneezing, epistaxis
snout gradually becomes wrinkled
lateral deviation of the snout
pigs are underweight
Diagnosis of atrophic rhinitis
facial deformities
visual assessment of the extent of turinate atrophy (postmortem)
isolation and identification to demonstrate toxigenic strains
PCR
Prevention and Control of Atrophic Rhinitis
chemoprophylaxis - increasing antimicrobial resistance
improve husbandry and management
vaccination
Causative agent of Pasteurellosis in sheep
M. haemolytica
B. trehalosi
P. multocida causes sporatic cases
Clinical signs of Pasteurellosis in sheep
sudden deaths
acute respiratory disease
Describe Septicemic Pateurellosis
lambs less than 3 months of age - M. haemolytica
older animals 5-12 months of age - B. trehalosi
Diagnosis of Pasteurellosis
isolation of organism from lung lesions
ventral consolidation of the cranial lobes of the lungs and fibrinous pleural and pericardial effuses are observed post-mortem
Treatment of pateurellosis in sheep
long acting oxytetracycline
Control of pasteurellosis in sheep
multivalent bacterins
Causitive agent of Fowl Cholera
P. multocida types A and F
Fowl choldera aka
avian pasteurellosis
Describe Fowl Cholera
common avian disease
acute sepricemia that is often fatal
Which species of bird are more susceptible to fowl cholera?
turkeys > chickens
waterfowl
mostly adult birds (worldwide)
Transmission of gowl cholera
asymptomatic carriers
chronically infected birds
contaiminated equipment
wild birds
rodents may act as reservoirs
direct and indirect contact with excretions and secretions
Clinical Signs of Fowl Cholera
septicemia
high mortality and morbidity
paracute/acute: sudden death, septicemic lesions
chronic: depression, inappetence, green diarrhea, weight loss, riffled feathers, oral and nasal discharge, swelling, discoloration and necrosis of wattles, sternal bursae and joints, torticollis
Diagnosis of acute septicemic fowl cholera
bipolar staining organisms in blood smears
P. multocida isolated from blood, bone marrow, liver and spleen
ELISA, agar diffusion tests, serum plate agglutination
Diagnosis of chronic fowl cholera
organism may be difficult to isolate
ELISA, agar diffusion tests, serum plate agglutination
Prevention and Control of fowl cholera
medication of feed a/o water early in an outbreak
confine sick birds
vaccines: polyvalent adjuvant bacterins, autogenous vaccines, modified live vaccines
improved management
Causative agent of Snuffles in rabbits
P. multocida type A
Bordetella bonchiseptica
Describe Snuffles in Rabbits
common, recurring disease resulting in purulent rhinitis
Predisposing Factors for Snuffles in rabbits
stress
overcrowding
poor ventilation
co-infections
Transmission of Snuffles
highly contagious
direct transmission
aerosolization
Clinical Signs of Snuffles
purulent nasal discharge
sneezing
coughing
conjunctivitis
otitis media
subcutaneous abscessation
bronchopneumonia (young rabbits)
Diagnosis of Snuffles
clinical signs
culture and serotyping
Treatment of Snuffles
antibiotics
supportive care
eliminate stress factors
Is there a vaccine for Snuffles?
NO
Where is Bibersteinia trehalosi found?
normal flora of the tonsils and nasopharynx of ruminants - mostly sheep
What disease conditions are associated with Bibersteinia trehalosi infections?
septicemia and respiratory disease
What are the predisposing factors associated with Bibersteinia trehalosi infections?
stress
bacterial and viral agents
Virulence factors of Bibersteinia trehalosi
endotoxin
leukotoxin
capsular polysaccharides
adhesins
Clinical Signs of Bibersteinia trehalosi
fever, listessness, loss of appetite, fever
sudden death in young sheep
fibro-necrotic oneumonia
infection may be localized in joints, uddder, meninges
Diagnosis of Bibersteinia trehalosi
sudden death
clinical signs
post moterm findings: enlargement of tonsils, oharynx, oesophagus and peracute, multifocal, embolic, necrotizing lesions in the lung and liver
Treatment of Bibersteinia trehalosi
antibiotic treatments are only successful if begun very early
strains vary in their susceptibility
Control and prevention of Bibersteinia trehalosi
vaccination
General characteristics of Mannheimia haemolytica
small gram-neg rods
facultative anaerobe
grows on MAC
oxidase pos
non-motile
hemolytic
Where is Mannheimia haemolytica commonly found?
commensal of the mucosa of the upper respiratory tract - cattle and sheep
resides in the tonsillar crypts
opportunistic
What is considered to be the main bacterial agent in bovine respiratory disease complex?
Mannheimia haemolytica
Common diseases caused by Mannheimia haemolytica
shipping fever in young cattle
enzootic pneumonia of calves - dairy cattle
occasionally mastitis in cattle
septicemia and enzootic pneumonia in young sheep
necrotizing ovine mastitis
Predisposing factors to Mannheimia haemolytica infection
stress
co-infection
castration, de-horning, weaning
transportation
mixing, overcrowding
nutritional changes
Transmission of Mannheimia haemolytica
endogenous transmission: opportunistic pathogen
exogenous transmission: from environment, direct contact, indirect transmission
Post-mortem findings of Mannheinmia haemolytica
marbling of the lungs, especially cranio-central lobes
hemmorhage/coagulation necrosis in lobules
onterlobular septae are distended with fibrin rich exudate
brochioles are obstructed with exudate
neutrophils, macrophages and fibrin accumulate in alveoli
Speciment collection - Mannheimia haemolytica
live animals: tracheobronchial aspirates, bronchioalveolar lavage, nasal swabs
necropsy: lung tissue
milk
blood
Mannheimia haemolytica virulence factors
capsule
adhesins: Omp A and Lipoprotein 1
endotoxin: lipid A
leukotoxin
iron regulated proteins
Diagnosis of Mannheimia haemolytica
history
PE
necropsy findings
leukotoxin neutralization assay
anti-leukotoxin ELISA
culture
fluorescent antibody tests
IHC
PCR
Treatment of Mannheimia haemolytica
antibiotic therapy early
Prevent and control of Mannheimia haemolytica
disease management
vaccines
What is the normal habitat of Haemophilus spp?
commensal of mucous membranes of URT and lower genital tracts
What are the growth requirement factors for Haemophilus spp?
X factor (haemin)
V factor (nicotinamide adenine dinucleotide)
Glaesserella parasuis general characteristics
short gram neg rods
What disease is caused by Glaesserella parasuis?
Glasser’s disease in pigs
At what ages are pigs affected by Glaesserella parasuis?
from weaning up to about 12 weeks old
Virulence factors of Glaesserella parasuis
capsule
adhesins and fimbria
biofirms
lipo-oligosaccharide (LOS)
outer membrane proteins
iron acquisition mechanisms
What is LOS
lighter form of LPS
How is Glasser’s disease transmitted?
sows are reservoirs
piglets are colonized during suckling
Pathogenesis of Glaesserella parasuis
invade endothelial cells
avoid complement mediated killing
Clinical signs of Glasser’s disease
anorexia, pyrexia, lamnesess, recumbancy and convulsions
polyserositis
arthitis
pneumonia
mild memnigitis
sudden death
Differentials for Glasser’s Disease (Glaesserella parasuis)
Streptococcus suis
E. coli
Mycoplasama hyorhinis
Samonella enteria serotype Choleraesuis
Clinical Specimens taken to diagnose Glasser’s disease
joint fluid, heart blood, CSF, post-mortem tissues
NOTE: keep on dry ice
What agar is used to culture Glaesserella parasuis? Under what conditions?
Chocolate agar
5-10% CO2 at 37C for 2-3 days
Treatment of Glasser’s disease
parenteral antibiotic therapy ASAP given at high doses
Prevention of Glasser’s disease
proper management
vaccination (bacterins)
Histophilus somni general characteristics
gram neg
pleomorphic
facultative anaerobe
non-motile
Is Histophilus somni part of the Bovine Respiratory Disease Complex?
YES
What age of cattle are most affected by Histophilus somni?
young growing cattle aged 6-12 months
Clinical signs of Histophilus somni
acute, often fatal
depression, recumbency, fever, anorexia, blindness
pericarditis, myocarditis, pneumonia
brain lesions: multifocal, dark-red areas of hemorrhagic necorsis
herd infertility
Virulence factors of Histophilus somni
adhesins
induction of apoptosis
LOS
inhibit destruction by phagocytes
histamine and hemolysin production
iron uptake
Pathogenesis of Histophilus somni
thrombus formation - causing TME
occlusion of blood vessels
cellular death - formation of necrotic sequestrum
clinical signs associated with extent of organ involvement: TME, BRCD, myocarditis, polysynovitis, otitis media, mastitis and reproductive tract diseases
Specimens used for diagnosis of Histophilus somni
blood, CSF, joint and pleural fluids, brain, liver, and kidney (post-mortem)
Diagnosis of Histophilus somni
culture and iolation on BA, 10% CO2
variable hemolysis
NO Growth on MAC
serology
IHC
post-mortem histologic lesions
Treatment of Histophilus somni
isolation
antibiotics in early stages
Prevention of Histophilus somni
avoid stressful conditions
proper management
vaccination
Histopholus ovis host
sheep
Diseases caused by histophilus ovis
edididymitis in young rams
vulvitis, mastitis, reduced reproductive performance in ewes
septicemia, arthritis, meningitis and pneumonia in lambs
Avibacterium spp general characteristics
gram neg
facultatively anaerobic
rod shaped
What is the infectious agent of coryza in chickens?
Avibacterium paragallinarum
Describe infectious coryza
affects the upper respiratory tract and paranasal sinuses
chickens become susceptible about 4 weeks after hatching
How is Coryza in chickens transmitted?
carried by chronically ill or clinically normal carrier birds
transmitted via direct contact, aerosols, contaminated water
Clinical Signs of Coryza in chickens
mild: depression, serious nasal discharge, mild facial swelling
severe: swelling of the infraorbital sinuses, conjunctivitis, eye closure, swollen wattles, delayed or reduced egg production
What specimens are taken to diagnose Coryza in chickens?
nasal discharge
sinus aspirate
How is Coryza in chickens diagnosed?
culture and cofirmation with biochemical tests
requires V factor
PCR
Differentials for Avibacterium paragallinarum
Avibacterium gallinarum
P. multocida type A
Treatment for Coryza in chickens
medicate drinking water with sulphonamindes or oxytetracycline early in outbreak
Control of Coryza in chickens
all-in/all-out management policy
good management
vaccination
