Micro Exam 3 - Gram Negative Rods

Front 1

Explain the pathogenesis of Bordetella avium. What species does this infect?

Back 1

Ingestion of organism via water or litter

--> Attaches to ciliated epithelium in URT --> interferes w/ ciliary clearance --> secondary invaders

Infects TURKEYS

Front 2

Is B. avium hemolytic?

Back 2

NO!

Front 3

This disease causes catarrhal or suppurative rhinitis, sinusitis, bronchopneumonia, and airsacculitis in turkeys.

Back 3

B. avium

Front 4

This causes infectious bovine keratoconjunctivitis (IBK; pinkeye) in cattle

Back 4

Moraxella bovis

Front 5

Is Moraxella bovis aerobic or anaerobic?

Back 5

Strict aerobe

Front 6

How is the cornea broken down during a Moraxella bovis infection?

Back 6

RTX (pore forming) toxin lyses corneal epithelial cells and neutrophils --> Lysed neutrophils release hydrolytic enzymes on corneal surface --> damage

NO collagenase

Front 7

Explain the pathogenesis for Moraxella bovis

Back 7

damaged corneal epithelium --> Moraxella bovis attaches to corneal epithelium --> inflammatory response --> cornea becomes opaque and may ulcerate --> possible blindness

Front 8

What are the 3 subspecies of Pasteurella multocida?

Back 8

1. multocida (most common)
   
2. septica
3. gallicida

Front 9

What is the morphology of Pastuerella multocida?

Back 9

Small gram (-) rods and coccobacilli (pleomorphic)

Front 10

What is the oxygen requirement of Pasteurella multocida?

Back 10

Facultative anaerobes

Front 11

Which type of P. multocida is mucoid?

Back 11

Type A

Has a heavy capsule made of hyaluronic acid

Colonies tend to coalesce

Front 12

This organism is a secondary invader. It's involved with shipping fever pneumonia in cattle, pneumonia with lung lesions in swine, mastitis and pneumonia in sheep, snuffles in rabbits, and fowl cholera in poultry.

Back 12

Pasteurella multocida type A

Front 13

This organism is involved with atrophic rhinitis in swine. It releases a cytotoxin that causes turbinate atrophy. It's also associated with snuffles in rabbits and superficial abscesses in cats.

Back 13

Pastuerella multocida type D

Front 14

This organism is common in the oral cavity of cats and dogs and is the most common organism isolated from superficial abscesses in cats.

Back 14

Pasteurella multocida type D

Front 15

This organism is involved with hemorrhagic septicemia in tropical regions. This is a major disease of cattle and water buffalo, but has also been isolated from bison in Yellowstone/Canada. There is no disease associated with this organism in the US.

Back 15

Pasteurella multocida type B & E

Front 16

True or False:

Pasteurella multocida is common in the upper respiratory tract and oral cavity of mammals and birds.

Back 16

False

P. multocida is NOT normal flora of birds.

Front 17

This disease is caused by P. multocida type A & F and is found in chickens and turkeys. It causes acute septicemia leading to death or joint infections and arthritis in recovered birds.

Back 17

Fowl cholera

Front 18

This is the #1 cause of poultry loss in the US.

Back 18

Fowl cholera (Pasteurella multocida type A and F)

Front 19

True or False:

An infection with P. multocida is difficult to treat once it is in the pyogenic phase.

Back 19

True

Front 20

What are the two types of typing systems used to classify Pasteurella multocida?

Back 20

1. Capsular (Carter)
2. Somatic antigen (Heddleston)
   

Front 21

How does P. multocida type D cause atrophic rhinitis

Back 21

Cytotoxin acts intracellulary to activate a G protein --> ↑ osteoclastic activity & ↓ osteoblastic activity; multiple systemic effects (hepatotoxicity) and ↓ bone growth

Front 22

This organism causes abscessing pneumonia, conjunctivitis, subcutaneous abscesses, and mastitis in lab rodents, hamsters, and guinea pigs.

Back 22

Pasteurella pneumotropica

Front 23

This organism has been documented in skin ulcers and bite wounds in Danish pig farmers, and is normal flora of the mouth and intestinal tract of swine.

Back 23

Pasteurella aerogenes

Front 24

This can cause respiratory tract and other infections in horses.

Back 24

Pasteurella caballi

Front 25

This is the most important bacterial cause of respiratory disease in CATTLE and SHEEP.

Back 25

Mannheimia hemolytica

Front 26

What is the morphology of M. hemolytica?

Back 26

Small gram (-) coccobacillus

Front 27

This organism causes mastitis in sheep and occasionally cattle, septicemia in neonatal lambs, penumonia in adult sheep, and is involved in shipping fever pneumonia in cattle.

Back 27

Mannheimia hemolytica

Front 28

Serotype 1/2 (choose one) is the most common serotype of Mannheimia hemolytica causing acute fibrinous pleuropneumonia in cattle.

Back 28

Serotype 1

Front 29

True or False:

Serotype 2 of M. hemolytica is common in cattle but rarely causes disease, so it is not considered a pathogen in cattle.

Back 29

True

Front 30

True or False:

Mannheimia hemolytica can also affect horses, swine, and poultry in addition to cattle and sheep/goats.

Back 30

True

Occasional infection

Front 31

M. hemolytica is involved in the shipping fever complex with which other organisms in cattle?

Back 31

1. P. multodica
2. H. somni

Front 32

_________ __________ is the most common cause of loss in the feeder cattle industry.

Back 32

Shipping fever

Front 33

What is the natural habitat of M. hemolytica?

Back 33

URT of cattle, sheep, and goats.

Found in tonsils of 95% of sheep.

Transmission is through inhalation.

Front 34

True or False:

antibody against cell surface components of M. hemolytica is better to have than antibody against the leukotoxin.

Back 34

True

Front 35

What toxin(s) are produced by M. hemolytica and what do they do?

Back 35

Leukotoxin - toxic for leukocytes and platelets of ruminants. Alters leukocyte function at LOW levels and lyses leukocytes at HIGH levels.

Front 36

What virulence factors are produced by M. hemolytica?

Back 36

• Lipopolysaccharide
• capsular polysaccharide
• fimbriae
• glycoprotease
• neuramidase
• outer membrane proteins

Front 37

____________ ____________ in the lungs of ruminants can handle a low dose of M. hemolytica, but are less likely to handle a high dose or handle the organism with stress or when a concurrent viral infection is present.

Back 37

Alveolar macrophges

Front 38

_____________ release enzymes on lung tissue when lysed by leukotoxin produced by M. hemolytica. This causes inflammation and pneumonia.

Back 38

Neutrophils

Front 39

This organism causes severe respiratory disease in dairy cows, feedlot pneumonias in cattle, and septicemia/pneumonia in feeder lambs and goats.

Back 39

Bibersteinia trehalosi

Front 40

This organism produces a leukotoxin identical to M. hemolytica.

Back 40

B. trehalosi

Front 41

What is the morphology of Actinobacillus lignieresii?

Back 41

Small gram (-) pleomorphic coccobacilli

Front 42

This organism produces glycocalyx capsule that cements organisms together to form small, cheese-like granules (microcolonies).

Back 42

Actinobacillus lignieresii

Front 43

This causes hard granulomatous masses in the tongue, head, and neck areas in cattle and sheep. Rarely found in bite wounds in humans.

Back 43

Actinobacillus lignieresii

"Wooden tongue"

Front 44

What is the natural habitat of A. lignieresii?

Back 44

Commensal of the buccal mucous membrane of cattle and sheep

Front 45

How do you treat an animal affected with A. lignieresii?

Back 45

Iodine

• sodium iodide IV
  
• organic iodide in the feed
  
• localized injections of aqueous iodine (Lugol's solution)
  

Also debride wounds or use antibiotics (Tet, sulfas, streptomycin)

Front 46

Describe the pathogenesis of A. lignieresii?

Back 46

Traumatic introduction (wounds) in the buccal epithelium most commonly caused by foreign material (stemmy roughage) or trauma

Front 47

True or False:

A. lignieresii infection may spread to internal organs ( lungs, lymphoid tissues, lesions in the walls of the stomach).

Back 47

True

Front 48

True or False:

Only a CMI response is important for immunity against A. lignieresii.

Back 48

False

Both CMI and humoral are important

Front 49

True or False:

Infection with A. lignieresii is very common, and routine vaccination with formalinized bacterins is used prophylactically.

Back 49

False

Infection is sporadic and many normal cattle have antibody to A. lignieresii, so usually don't immunize except in disease outbreaks.

Front 50

What is the morphology of Actinobacillus equuli?

Back 50

Small, gram (-) pleomorphic coccobacilli

Front 51

This organism causes shigellosis/equulosis ("Sleepy foal disease") and becomes septicemic in foals. Enteritis and acute death (24 hrs after birth) in 1/3 of foals. Severe purulent nephritis w/ multiple small abscesses in the kidney cortex and lameness in 2/3 of foals (death 4 days after birth).

Back 51

Actinobacillus equuli

Front 52

This organism is associated with verminous aneurysms due to Strongylus vulgaris in adult horses. S. vulgaris carries the organism from the GI tract. Also can cause peritonitis w/o verminous aneurysms.

Back 52

Actinobacillus equuli

Front 53

What is the natural habitat of A. equuli?

Back 53

Oralcavity and intestinal tract of normal horses

Front 54

True or False:

It's important to use caution when treating patients with A. equuli infection with bactericidal antibiotics because it can cause fatal endotoxemia if the patient is septic.

Back 54

True

Front 55

True or False:

Actinobacillus equuli is an opportunist and only causes disease sporadically in debilitated or stressed animals.

Back 55

True

Front 56

Foals can pick up what organism on passage through the birth canal or in-utero?

Back 56

Actinobacillus equuli

Front 57

What toxin is associated with hemolysis and virulence caused by A. equuli?

Back 57

RTX leukotoxin

Front 58

True or False:

Actinobacillus pleuropneumoniae does not require a Staph nurse.

Back 58

False

Front 59

What species does Actinobacillus pleuropnuemoniae infect, and what does it cause?

Back 59

SWINE: contagious pleuropneumonia

• Acute respiratory disease
  
• Exudative and proliferative bronchopneumonia with fibrinous pleuritis
  
• Anorexia, emesis, fever, hemorrhaging from the mouth and nose
  
• Can become chronic
  
• Low grade infection in partially immune animals
  
• Peracute form with death occurring within 8 hours or less
  

Front 60

Where is A. pleuropneumoniae normally found?

Back 60

Upper respiratory tract of swine usually 5-20 weeks of age.

Older pigs shed it into the environment.

Front 61

True or False:

Recovered pigs are susceptible to reinfection with A. pleuropneumoniae.

Back 61

False

Recovered pigs are IMMUNE

Front 62

Clostridial antibody to A. pleuropneumoniae at what age?

Back 62

6-8 weeks

Front 63

True or False:

Serotypes of A. pleuropneumoniae are partially cross-protective.

Back 63

True

Front 64

Which serotypes of A. pleuropneumoniae are present in the US?

Back 64

Serotypes 1, 3, 5, 7

Front 65

What toxins are produced by A. pleuropneumoniae?

Back 65

RTX-type toxins (Apx I, II, III, IV)

• 1 and 2 are hemolysins
• 4 is in-vivo
  

Endotoxin

Bacterial surface components

Front 66

Describe the pathogenesis for A. pleuropneumoniae.

Back 66

Endemic herds

• Piglets are infected as colostral immunity wanes
  
• Mild disease results

In naïve swine or older, susceptible swine

• Severe acute disease
  
• Fibrino-hemorrhagic pneumonia
  
• RTX toxins & surface components are important contributors
  
• High health status swine may be more severely affected
  

Front 67

True or False:

Actinobacillus suis requires a Staph nurse.

Back 67

False

Front 68

What is the disease caused by Actinobacillus suis and in what species does it cause disease?

Back 68

SWINE:

• Fatal acute septicemia in 1-8 week old pigs
  
• Acute fibrino-hemorrhagic pneumonia similar to APP in older pigs
  
• Arthritis and subcutaneous abscesses in older pigs
  

**similar lesions to APP or E. rhusiopathiae

Front 69

What is the natural habitat of Actinobacillus suis?

Back 69

Tonsils and upper resp. tracts of normal swine

Vagina of sows

Front 70

True or False:

A. suis is susceptible to many antibiotics.

Back 70

True

Front 71

What toxins are produced by A. suis?

Back 71

RTX toxins: Apx1 and 2 (possibly others)

**Identical to those of APP

Front 72

What is the pathogenesis of A. suis?

Back 72

• Respiratory transmission most likely (skin lesions also possible)
  
• Septicemia with acute death in young pigs (organism spreads rapidly throughout body)
  
• Older than 3 months: arthritis, pneumonia, skin lesions (mimics E. rhusiopathiae)
  

Front 73

This organism causes salpingitis and peritonitis in laying hens.

Back 73

Actinobacillus salpigitidis

Front 74

This organism causes epididymitis and abortions in sheep and is mostly a problem with decreased lamb fertility.

Back 74

Actinobacillus seminis

Front 75

What is the natural habitat of A. seminis?

Back 75

• Normal flora of prepucial and penile mucosa
  
• Localizes in the epididymis and testes
  
• Spread venereally
  

Front 76

This organism causes endocarditis, osteomyelitis, meningitis, and periodontal disease in humans.

Back 76

Actinobacillus actinomycetemcomitans

Front 77

What is the natural habitat of Actinobacillus actinomycetemcomitans?

Back 77

Dental plaque, periodontal pockets, gingival sulci

Front 78

This causes peritonitis in chickens and may possibly work with E. coli to cause severe disease.

Back 78

Galibacterium anatis

Front 79

What is the morphology of Haemophilus and Histophilus?

Back 79

Small gram (-) rods

Front 80

True or False:

Organisms with "para" in their name require hemin and are therefore hemolytic.

Back 80

False

Organisms with "para" in their name do NOT require hemin and are NOT hemolytic.

Front 81

What organism is the cause of "Glasser's disease" and which species are affected?

Back 81

Haemophilus parasuis - SWINE

Front 82

True or False:

Haemophilus parasuis requires a Staph nurse, which supplies NAD.

Back 82

True

Front 83

What lesions are caused by Glasser's disease?

Back 83

Polyserositis, meningitis, and arthritis.

Nasal and tracheobronchial infections occur amongst litter mates.

Often subclinical.

Front 84

What are clinical signs of Hamophilus parasuis infection?

Back 84

Swollen joints, lameness, bronchitis, pleuritis, peritonitis, fever. Occasionally fatal.

Front 85

What is the natural habitat of Haemophilus parasuis?

Back 85

Nasopharynx of normal swine.

Spreads rapidly by aerosol and contact (highly contagious).

Frequently recovered from pneumonias in baby pigs but it may not be the cause of the pneumonia

Front 86

Haemophilus parasuis has many/one (choose) serotype(s).

Back 86

Many serotypes (at least 15)

Front 87

What antibiotics can be used to treat Hamophilus parasuis infection?

Back 87

Penicillin, Tetracycline, Tiamulin

Front 88

What is the pathogenesis of Haemophilus parasuis?

Back 88

• Stresses (weaning, shipping, concurrent infections)
  
• Viral infections predispose to H. parasuis

--SIV, PRRSV
--Coughing, fever, lobular pneumonia, occasional death

• Organism infects serosal surfaces (polyserositis)
  
• Fibrinous inflammation of the pericardium, pleura, peritoneum, joints, meninges (in severe cases)
  
• May predispose to infection w/ Pasturella and Bordatella spp.
  

Front 89

True or False:

Haemophilus suis requires a Staph nurse.

Back 89

True

Front 90

What disease is caused by Haemophilus suis?

Back 90

Confusionas to whether this organism exists.

Front 91

True or False:

Histophilus somni requires a Staph nurse.

Back 91

False

Front 92

What does Histophilus somni require for primary isolation?

Back 92

5% CO2

Front 93

Hsitophilus somni is hemolytic/non-hemolytic (choose one) and turns BAP agar green around the colonies.

Back 93

Non-hemolytic

Front 94

What organism causes thrombolytic meningoencephalitis (TME) and in what species is this found?

Back 94

Histophilus somni - CATTLE

2-4 weeks after shipping in feedlot cattle

Follows shipping fever pneumonia

Front 95

Besides TME, what else does H. somni cause in cattle, and what are the clinical signs?

Back 95

Septicemia and respiratory disease.

Clinical signs: fever,anorexia, lameness (suppurative polyarthritis), neuro signs, weakness,somnolence

Can also cause abortion, infertility, and retained placenta in cows

Front 96

This organism causes septicemia, epididymitis, abortion, meningitis, vulvovaginitis, and mastitis in sheep and respiratory infections in goats.

It's also been isolated from the tonsils and pneumonia in bison.

Back 96

Histophilus somni

Front 97

What is the natural habitat of Histophilus somni?

Back 97

Upper respiratory tract of cattle

Repro tract isolates (male & female cattle) --> low pathogenicity for resp. disease

Front 98

True or False:

Immunity is good following recovery from Histophilus somni infection.

Back 98

True

Front 99

More/less (choose one) severe respiratory disease may develop in immunized cattle compared to non-immunized cattle.

Back 99

More

IgG production helps with TME, not respiratory disease.

Front 100

Histophilus somni is an important bacterial agent in bovine respiratory disease, second only to what?

Back 100

Mannheimia hemolytica

Front 101

What toxins are produced by Histophilus somni?

Back 101

Endotoxin

• major toxin involved in disease production

LOS (lipooligosaccharide)

• less complex O-Ag chains than LPS
• apoptosis of endothelial cells
• poor antigen --> antigenic shifting (helps organism evade the host immune system)

Front 102

What virulence factors are produced by Histophilus somni and what do they do?

Back 102

Adenine, guanine, GMP

• released by the organism into surrounding medium
• important for intracellular survival by mitigating oxidative burst (immunosuppressive)

Fc-receptor proteins

• associated with fibrillary network on surface of virulent strains
  

Front 103

What characteristic of H. somni allows it to disseminate throughout the host's body?

Back 103

Can survive in blood monocytes

Front 104

What is the pathogenesis of Histophilus somni infection?

Back 104

• Starts as resp. disease (young calves, feedlot cattle)
  
• Septicemia can follow
  
• Infection via resp. tract leading to fibrinous meningitis w/ arterial thrombosis and necrosis
  
• Spreads to brain (Thrombotic meningoencephalitis; Fibrinous meningitis, arterial thrombosis and necrosis) --> May see hemorrhagic areas a few cm wide
• Spreads to joints, heart, etc. --> Severe lameness --> Hemorrhages on serous surfaces and in muscles may be widespread

Front 105

This organism produces histamine that may enhance an adverse host pulmonary response.

Back 105

Histophilus somni

Front 106

What is the morphology of Histophilus influenzae?

Back 106

Gram (-) rod, pleomorphic

Front 107

This organism was formerly the second leading cause of bacterial meningitis in infants.

Back 107

Histophilus influenzae

Front 108

What lesions are caused by an infection with Histophilus influenzae and what species does it infect?

Back 108

HUMANS

Resp. infections & spreads systemically: cellulitis, otitis media, bacteremia, sinusitis, chronic bronchitis, pyoarthritis

Front 109

What is the natural habitat of H. influenzae?

Back 109

Normal flora of resp. tract of humans

Front 110

How many serovars does H. influenzae have and which one is most associated with systemic disease in humans?

Back 110

6 serovars (a-f) based on capsular antigens. Capsule type b (Hib) causes systemic disease.

Front 111

At what age are humans most susceptible to infection with H. influenzae?

Back 111

1-2 years of age

Don't develop significant antibody response to b capsular type, even in the face of an infection.

Human infants can't respond til ~2 years of age.

Front 112

True or False:

H. influenzae is carried by a high number of individuals, but a majority are low virulence and not a major cause of disease.

Back 112

True

Front 113

The vaccine for H. influenzae is complexed polysaccharide with a mutant diptheria toxin or the group B polysaccharide of which other bacterial organism?

Back 113

Neisseria meningitidis

Front 114

True or False:

Avibacterium paragalinarum requires a Staph nurse and 5% CO2.

Back 114

True

Front 115

What disease causes fowl coryza in chickens?

Back 115

Avibacterium paragallinarum

Front 116

Describe the lesions and clinical signs associated with fowl coryza in chickens.

Back 116

• Inflammation of turbinates
  
• Acute air sacculitis
  
• Sneezing, conjunctivitis, swelling of head and wattles, anorexia
  
• Marked loss of egg production
  
• Disease of ADULT chickens
  
• Not fatal (high mortality can occur w/ concurrent viral infection)
  

Front 117

What is the natural habitat of Avibacterium paragalinarum?

Back 117

Upper resp. tract of chickens

Recovered birds are carriers

Front 118

True or False:

Avibacterium paragallinarum has multiple serotypes.

Back 118

True

3 immunotypes and 9 serovars

Immunity is type specific

Front 119

True or False:

Ornithobacterium rhinotracheale requires a Staph nurse and CO2.

Back 119

False

Requires 7.5-10% CO2 but does NOT require a Staph nurse.

Front 120

What is the morphology of Ornithrobacterium rhinotracheale?

Back 120

gram (-) rods; highly pleomorphic

Front 121

What species does Ornithobacterium rhinotracheale infect and what does it cause?

Back 121

CHICKENS and TURKEYS

Resp. and other diseases

• Pneumonia
  
• Pleuritis
  
• Sinusitis
  
• Tracheitis
  
• Airsacculitis
  
• Pericarditis
  
• Peritonitis
  
• Hepatomegaly
  
• Oophoritis
  
• Blood-stained mucous in turkey mouths
  
• Concurrent infections make disease worse
  

Front 122

What is the natural habitat of O. rhinotracheale?

Back 122

URT of chickens and turkeys

Respiratory and egg transmission

Front 123

True or False:

O. rhinotracheale has many serotypes.

Back 123

True

18 serotypes --> type A predominates

Front 124

Describe how infection with O. rhinotracheale differs between turkeys 2 weeks of age and 12-14 weeks of age.

Back 124

If infected at 2 weeks of age

• Respiratory signs
  
• Swelling of infraorbital sinuses, facial edema
  

If infected at 12-14 weeks of age

• Much more severe disease
  
• Sudden death
  
• Marked dyspnea (caseous plugs in resp. passages)
  
• Up to 50% mortality
  

Front 125

Describe how infection with O. rhinotracheale differs between broiler chickens 3-4 weeks of age and layers/breeders.

Back 125

Broilers

• Mild respiratory disease at 3-4 weeks
  
• Sneezing, nasal discharge, sinusitis, increased mortality, poor rate of gain
  
• Infection most common in broilers at 6 mo.
  

Layers and breeders

• Mild resp. disease
  
• Slightly increased mortality
  
• Decreased egg production and quality
  

Front 126

True or False:

Most turkeys in the US are M. gallisepticum free.

Back 126

True

Front 127

What is the morphology of Taylorella equigenitalis?

Back 127

Small gram (-) rods/coccobacillus

Front 128

True or False:

Taylorella equigenitalis requires a Staph nurse and CO2.

Back 128

False

Requires 5% CO2 for 2-5 days, but does NOT require Staph nurse.

Front 129

What disease is caused by Taylorella equigenitalis and which species does it infect?

Back 129

HORSES - contagious equine metritis (CEM)

Front 130

What are the lesions and clinical signs associated with contagious equine metritis?

Back 130

• Venereal disease
  
• Localized infection of repro tract
  
• Vaginitis, cervicitis, endometritis
  
• Copious vaginal discharge (mucopurulent)
  

Front 131

True or False:

Taylorella equigenitalis causes abortions in horses.

Back 131

False

Front 132

What is the natural habitat of Taylorella equigenitalis?

Back 132

Clitoral fossa of mares

Stallions: carry on penis, sheath, and urethra (don’t showclinical signs)

Front 133

True or False:

Immunity to Taylorella equigenitalis is poor and mares often relapse.

Back 133

True

Front 134

True or False:

In severe cases of Taylorella equigenitalis, euthanasia is the only solution.

Back 134

False

Quarantine infected horses and do repeated uterine flushes in mares w/ chlorhex and antibiotics. Stallions are treated w/ daily cleansing w/ chlorhex and nitrofurazone.

Front 135

True or False:

Taylorella equigenitalis has been eradicated from the US.

Back 135

False (?)

Was previously erradicated but there was an outbreak in 2009.

Front 136

What is the morphology of Bordetella pertussis?

Back 136

small gram (-) rods

Front 137

What is the oxygen requirement (or lack thereof) of Bordetella pertussis?

Back 137

Obligate aerobe

Front 138

What species does Bordetella pertussis infect and what disease does it cause?

Back 138

HUMANS - whooping cough

• Kids < 1 year old
  
• Sporadic/spasmatic cough
  
• Deep breaths that sound like “whoops”
  
• Formerly infected 90% of humans --> tracheobronchitis & toxemia
  

Front 139

What vaccine is used for Bordetella pertussis?

Back 139

DPT vaccine

Front 140

How is Bordetella parapertussis different from B. pertussis?

Back 140

1 frameshift mutation in the tox gene

Virtually the same as B. pertussis

Front 141

What is the morphology of Bordetella bronchiseptica?

Back 141

small gram (-) rods

Front 142

What is the oxygen requirement (or lack thereof) of Bordetella bronchiseptica?

Back 142

Obligate aerobes

Front 143

What species is affected by Bordetella bronchiseptica and what disease does it cause?

Back 143

DOGS: kennel cough (infectious tracheobronchitis)

SWINE: atrophic rhinitis; severe fibrinous pneumonia in piglets

CATS/RABBITS: respiratory infections

Front 144

Kennel cough is a combination of what 3 organisms?

Back 144

Bordetella, canine adenovirus (CAV), parainfluenza virus (PI3)

Front 145

Describe the pathogenesis of Bordetella bronchiseptica in dogs.

Back 145

Transmitted via aerosol --> adheres to tracheal cilia --> damage (epithelium remains INTACT) --> dry hacking cough (non-productive)

Front 146

Describe the pathogenesis of Bordetella bronchiseptica in swine.

Back 146

w/P. multocida --> smooth phase attaches via fimbriae to cilia of nasal mucosa --> damage to cilia and epithelium --> colonization of P. multocida (D) --> dermonecrotic toxin from P. multocida causes most of damage

Front 147

True or False:

Cats should be vaccinated for B. bronchiseptica because it is very common.

Back 147

False

Not common in household cats, but can be transmitted from dogs --> cats in a household.

Front 148

What is the natural habitat of B. bronchiseptica?

Back 148

URTof dogs, swine, rabbits; can be found in many other species

Front 149

What toxins/virulence factors are produced by B. bronchiseptica?

Back 149

• adenylate cyclase, dermonecrotic toxin, histamine sensitizing factor, filamentous hemagglutinin, fimbrial adhesins
  
• dermonecrotic toxin causes cilial stasis
  
• histamine sensitizing factor --> chronic persistent coughing
  

Front 150

How are pigs immunized against B. bronchiseptica?

Back 150

Bacterins: 2 doses in young pigs (Bordetella + Pasteurella), booster in sows (pre-farrowing)

Most pigs have antibody at slaughter

Rhinocell: modified live intranasal (used for severe problems; can produce disease)

Front 151

How are dogs immunized against B. bronchiseptica?

Back 151

Attenuated live intranasal or intraoral

Immunity lasts up to 14 mo.

Front 152

True or False:

B. bronchiseptica should be given to all dogs, regardless of their exposure to other dogs.

Back 152

False

Pets not being shown or kenneled don't need the vaccine

Front 153

What can happen if an IN B. bronchiseptica vaccine is given SQ?

Back 153

Causes an abscess at the site of injection because it is a live bacterin that will grow)

Front 154

What is a characteric feature of B. bronchiseptica colony growth?

Back 154

Small colonies at 24 hours, larger at 48 hours.

Front 155

True or False:

Bordetella bronchiseptica requires a Staph nurse.

Back 155

False

Front 156

How many phases does B. bronchiseptica have and what is the purpose of these phases?

Back 156

4 different phases

• Phase shift - permanent
  
• Changes antigens and virulence factors
  
• Phase changes as colonies age
  

Front 157

What is the morphology of Bordetella avium?

Back 157

Small gram (-) rods

Front 158

What is the oxygen requirement (or lack thereof) of B. avium?

Back 158

obligate aerobe

Front 159

What species does B. avium affect and what disease does it cause?

Back 159

TURKEYS: bordatellosis/rhinotracheitis (coryza)

Front 160

What is the pathogenesis of B. avium?

Back 160

Attaches to ciliated epithelium in URT --> interferes w/ ciliary clearance --> secondary invaders --> Catarrhal or suppurative rhinitis, sinusitis, bronchopneumonia, and airsacculitis

Front 161

What age of turkeys are susceptible to infection with Bordetella avium?

Back 161

Affects YOUNG POULTS

Hard to induce disease without other pathogens after 2 weeks of age

Front 162

What is the natural habitat of Bordetella avium and how is it transmitted?

Back 162

URT of turkeys and broiler chickens.

Transmission is via water, litter, or direct contact

Front 163

What is the morphology of Moraxella bovis?

Back 163

Short rods or cocci

Pair or chains with adjacent sides flattened

Front 164

What is the oxygen requirement (or lack thereof) of Moraxella bovis?

Back 164

Strict aerobe

Front 165

Moraxella bovis has ___________ motility, which allows it to bore into the agar.

Back 165

Twitching

Front 166

What species is affected by Moraxella bovis and what disease is caused by this organism?

Back 166

CATTLE - infectious bovine keratoconjunctivitis (IBK, pinkeye)

Front 167

What is the pathogenesis of Moraxella bovis infection in cattle?

Back 167

Initial trauma to cornea and conjunctiva --> Mycoplasma bovoculi --> Moraxella bovis attaches to damaged tissues

Front 168

What is the natural habitat of Moraxella bovis?

Back 168

Conjunctiva of cattle (normally non-invasive)

Front 169

True or False:

Antibody response in tears (IgA) is highly protective against Moraxella bovis.

Back 169

False

Not highly protective - immunity is not solid and infections can reoccur

Front 170

Why aren't vaccines for Moraxella bovis effective?

Back 170

Fimbrial bacterins are given SQ and produce IgG antibody which is not specific on mucosal surfaces like the conjunctiva and cornea.

Front 171

How many serotypes are there for Moraxella bovis and what are they based on?

Back 171

7 serotypes based on fimbrial antigens

Front 172

What toxins/virulence factors are produced by Moraxella bovis?

Back 172

Fimbriae

• attachment to corneal epithelium
• 21 antigenically different types
• only attach when corneal epithelium is damaged

Cytotoxin

• RTX (pore forming): lyses corneal epithelial cells and neutrophils
• lysed neutrophils release hydrolytic enzymes on corneal surface --> damage

Hemolysin

• similar to the cytotoxin
• loss of hemolysin = loss of virulence

Enzymes

• break down jxns between corneal epithelial cells and initiate an inflammatory response
• hyaluronidase, fibrinolysin, aminopeptidase, phosphodiesterase, phosphatase

Front 173

True or False:

Moraxella bovis produces collagenase which it uses to break down the corneal epithelium and cause damage.

Back 173

False

No collagenase --> can't break down collagen in the cornea (but lysed neutrophils can)

Front 174

What species is infected by Moraxella ovis and what disease does it cause?

Back 174

SHEEP - pinkeye (also cattle)

Low pathogenicity - role in IBK is uncertain

Front 175

What species is infected by Moraxella lacunata and what disease does it cause?

Back 175

HUMANS - pinkeye

Front 176

What species are affected by Alcaligenes spp. and what disease is caused?

Back 176

Contaminant

Occasionally associated with disease in animals

Isolated from blood, sputum, urine, ears, spinal fluid, wounds, IV solutions, catheters, etc.

Front 177

What is the morphology of Alcaligenes spp.?

Back 177

Gram (-) rods

Front 178

What is the oxygen requirement (or lack thereof) of Alcaligenes spp.?

Back 178

obligate aerobes

Front 179

What is the natural habitat of Alcaligenes spp.?

Back 179

Water, soil, GI tracts of vertebrates as a saprophyte

Front 180

What are the 3 species of Neisseria?

Back 180

N. meningitidis

N. gonorrhoeae

N. canis

Front 181

What is the morphology of Neisseria spp.?

Back 181

Gram (-) cocci with flattened sides

Paired

Front 182

What species is affected by Neisseria and what disease does it cause?

Back 182

HUMANS - 20% of meningitis cases, gonorrhea, bite wounds (N. canis)

Front 183

What is the natural habitat of Neisseria spp.?

Back 183

Nasopharynx of 5-90% of some groups of normal humans

Front 184

True or False:

IgA promotes invasion of Neisseria meningitidis through mucous membranes.

Back 184

False

IgA blocks invasion through mucous membranes

Front 185

How does septicemia result in an infection with Neisseria meningitidis?

Back 185

Once organism breaks through mucosa --> IgA in serum can block opsonization by IgG and IgM --> septicemia results since phagocytosis of Neisseria doesn't occur.

Front 186

How is Neisseria gonorrhoeae transmitted?

Back 186

Venereally (one of the most common venereal diseases of humans)

Front 187

True or False:

Many infections with Neisseria gonorrhoeae are asymptomatic so the rate of infection is probably much higher than what is reported.

Back 187

True

Front 188

True or False:

"Natural" antibodies are generated in response to cross-reactive antigens on other gram negative bacteria which provides protection against Neisseria spp.

Back 188

True

Front 189

What is the morphology of Acinetobacter spp.?

Back 189

Gram (-) rods

May pair or chain

Front 190

What are the subspecies of Acinetobacter?

Back 190

A. baumannii

A. calcoaceticus

A. lwoffii

Front 191

What species is affected by Acinetobacter baumannii and what disease does it cause?

Back 191

HUMANS - most human infections (~80%) - usually in imunosuppressed patients

Front 192

What species are affected by A. calcoaceticus and A. lwoffii and what disease do they cause?

Back 192

Sporadic (opportunist) disease in animals and humans

Nosocomial infections (more common in immunocompromised people)

Occasional UTIs in animals (dogs and cats)

Front 193

What is the natural habitat of Acinetobacter spp.?

Back 193

Water, soil, sewage, feces

Colonize in the skin

Front 194

True or False:

Acinetobacter can have an MDM1 gene that makes it resistant to all beta lactams and most other antimicrobials.

Back 194

True

The NDM1 gene is more commonly found in E. coli and K. pneumoniae but it can be spread between species.

Front 195

What is the morphology of Francisella tularensis?

Back 195

small, pleomorphic gram (-) rods

Front 196

What species are affected by Francisella tularensis and what disease does it cause?

Back 196

RABBITS - "rabbit fever" (small, necrotic, granulomatous foci in the liver, spleen, and lymph nodes)

HUMANS - granulomatous nodules that may ulcerate (regional lymph nodes, liver, spleen, bone marrow)

CATS - feline tularemia

Front 197

What is the natural habitat for Francisella tularensis biovar tularensis?

Back 197

Ticks, wild rodents, and rabbits

Found only in N. America

Front 198

What is the natural habitat for Francisella tularensis biovar palaearctica?

Back 198

Water rodents and beavers (or water itself)

More widespread than biovar tularensis; common in Scandanavian countries and Russia

Front 199

What are the two forms of tularemia infection in humans?

Back 199

Pneumonic form: organism is inhaled

Typhoidal form: organism is ingested

Front 200

What is the pathogenesis of F. tularensis?

Back 200

Very low infectious dose (1-10 organisms) --> commonly transmitted via contact with infectious rabbits or rodents or ticks (most common route of transmission) --> gains entry via skin abrasions, conjunctivae, ingestion, and aerosol

Front 201

What is the morphology of Coxiella burnetii?

Back 201

small, pleomorphic gram (-)

Front 202

What species are affected by Coxiella burnetii and what disease does it cause?

Back 202

HUMANS - Q-fever

• infection from contaminated animal products
• acute: fever followed by myalgia, headache, sweating
• chronic: may start 2-20 years after infection --> chronic vegetative valvular endocarditis

RUMINANTS - abortion and respiratory disease

Infects a wide variety of animal species - chronic hepatitis and glomerulonephritis may occur

Front 203

What is the natural habitat of Coxiella burnetii?

Back 203

Shed in large numbers in urine, milk, feces, and especially in the placenta.

Front 204

True or False:

Coxiella burnetii has multiple phases.

Back 204

True

Phase I: highly infectious and is the phaseisolated from diseased animals

Phase II: antigenically distinct and lessinfectious

• Antibody to it is first to arise in a hostinfected w/ Phase I organisms
  

Front 205

True or False:

Coxiella burnetii has a high infectious dose.

Back 205

False

ID50 = 1-10 organisms

Front 206

How is Coxiella burnetii transmitted?

Back 206

Maintained in domestic animals (mainly cattle, sheep, goats) --> most transmission is airborne, but can be transmitted via ticks

Front 207

What species is infected by Legionella spp. and what disease does it cause?

Back 207

HUMANS - respiratory disease (Legionaire's disease)

Pontiac fever is caused by several other Legionella species --> acute influenza-like disease

Front 208

True or False:

Gastric ulcers in pigs have been linked to infection with Legionella spp.

Back 208

False

Front 209

90% of cases are associated with which species of Legionella?

Back 209

Legionella pneumophila

46 species of Legionella

Front 210

What is the morphology of Helocobacter pylori?

Back 210

Gram (-)

Curved in tissues but U-shaped, rods, or rounded in lab

Front 211

What is the oxygen requirement (or lack thereof) of Helicobacter pylori?

Back 211

Microaerophilic

Front 212

What species is affected by Helicobacter pylori and what disease does it cause?

Back 212

HUMANS - acute gastritis, gastric and duodenal ulcers

Gastric disease in animals

One of the most common human pathogens

Front 213

True or False:

There are multiple species of H. pylori.

Back 213

True

At least 18 species

Front 214

Production of what enzyme contributes to the disease process of H. pylori?

Back 214

Urease enzyme --> cause of lesions (ammonia production)