Lecture 12 - Actinobacteria II Flashcards

1
Q

What are the general characteristics of arcanobacterium?

A

Pleomorphic, non-spore forming

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2
Q

What cell morphology can occur with acracnobacterium?

A

Coccobacillus + Rod + Club-shaped

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3
Q

What is the oxygen preference of arcanobacterium?

A

Facultative anaerobes + aerobes

Capnophiles

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4
Q

What is the living style of arcanobacterium?

A

Commensal - mucous membranes

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5
Q

What does A. pyogenes do on blood agar?

A

Beta-hemolysis

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6
Q

What is the cell morphology of A. pyogenes?

A

Coccobacillary to short rods

Club-shaped in young cultures

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7
Q

What is the oxygen preference of A. pyogenes?

A

Facultative anarobe

Capnophilic

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8
Q

Where does A. pyogenes normally occur?

A

Upper respiratory + Urogenital + GI tract

Of ruminant, swine, etc.

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9
Q

What is the common way in which A. pyogenes infections occur?

A

Traumatic inoculation + Secondary infection

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10
Q

How does host to host transmission of A. Pyogenes occur?

A

Mastitis in cows

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11
Q

What type of mastitis is A. pyogenes known for causing?

A

Summer mastitis

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12
Q

What are the virulence factors of A. pyogenes?

A

Pyolysin O + Neuraminidase

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13
Q

What does pyolysin O do?

A

Cytotoxic to macrophages + NEU + RBC’s

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14
Q

What does Neuraminidase do?

A

Bind to host cells and ECM

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15
Q

What does A. pyogenes act as a synergistic pathogen for?

A

F. necrophorum

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16
Q

What does A. pyogenes tend to do in the body?

A

Suppurative lesions in many organs

Abscesses + Empyemas + Pyogranulomas

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17
Q

What does the exudate from A. pyogenes tend to contain?

A

Bacteria + Live/Dead NEU + Host cell debris

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18
Q

What is the disease pattern seen in swine infected with A. pyogenes?

A

Septic arthritis (after farrowing )

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19
Q

What is the disease pattern seen in cattle infected with A. pyogenes?

A

Severe mastitis (heifers + dry cows)

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20
Q

How does transmission occur in cattle with A. pyogenes?

A

Flies + Teat contact w/ environment

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21
Q

What allows for there to be a contagious spread of A. pyogenes?

A

Profuse, purulent secretions

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22
Q

What is the basic treatment for A. Pyogenes?

A

Incision + drainage of abscesses

Susceptible to AB’s but poor response

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23
Q

Why does A. pyogenes have poor response to AB’s?

A

Encapsulated abscesses

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24
Q

What are cellular characteristics of Rhodococcus spp.?

A

Pleomorphic, gram positive to gram variable non spore forming

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25
Q

What cellular morphology can occur with Rhodococcus spp.?

A

Cocci + Rods + Filaments

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26
Q

What is the cellular preference with Rhodococcus?

A

Aerobes

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27
Q

What is the typical cell morphology found with R. Equi?

A

Cocci + Coccobacilli + Rods

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28
Q

What is the reservior for R. equi?

A

Soil + GI/Feces of healthy animals

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29
Q

What age is R. equi most commonly a oppurtunistic pathogen?

A

Young foals

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30
Q

What is the main route of infection in R. equi?

A

Inhalation or ingestion of virulent strains found in contaminated soil

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31
Q

What type of hemolysis is seen with R. equi?

A

None, aka gamma

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32
Q

What is seen with R. Equi infections?

A

Granulomas + Pyogranulomas + Abscesses

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33
Q

Where does R. Equi “set up camp” in the body?

A

Macrophages

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34
Q

What allows R. equi to grow in macrophages?

A

Vap proteins

35
Q

What do Vap proteins do?

A

Protect against phagocytic killing

36
Q

What is the disease pattern of R. Equi seen in foals?

A

Pyogranulmatous bronchopneumonia

37
Q

Why are young foals at risk of R. Equi infections?

A

Decreased protective Type I Response

38
Q

Where can lesions occur in foals infected with R. equi?

A

Pulmonary + Mesenteric LN’s

Intestines

39
Q

What is the disease pattern of R. Equi in adult horses?

A

Pneumonia + Extrapulmonary lesions

40
Q

When do you tend to see R. equi infections in adult horses?

A

Immunodeficent

41
Q

What is the disease pattern of R. Equi in swine?

A

Submandibular + Cervical lymphadenitis

42
Q

What is the basic treatment for R. Equi?

A

Combination therapy - Rifampin + Macrolide

Supportive care

43
Q

What is the cellular morphology of Listeria?

A

Gram+, non-spore forming coccobacilli

44
Q

What is the oxygen preference of Listeria?

A

Facultative anaerobes

45
Q

Where is listeria commonly found?

A

Terrestrial + Aquatic

46
Q

What are the two important spp. of Listeria for us?

A

Ivanovii + Monocytogenes

47
Q

What is seen with L. ivanoii?

A

Abortion in ruminants

48
Q

What is seen with L. monocytogenes?

A

Septicemia + Abortion + CNS infections

49
Q

How is L. monocytogenes transmitted?

A

Vertical in utero

Ingestion of contaminated foods

50
Q

How does L. monocytogenes get into the body, basic methods?

A

Transcellular + Paracellular routes

51
Q

How does L. monocytogenes get into the CNS?

A

Breaks into oral or nasal mucosa
Gets to CN
Enters brains

52
Q

What are the characteristics of brain lesions caused by L. monocytogenes?

A

Microabscesses - primarily in brainstem

53
Q

Where does L. monocytogenes tend to grow and live in the body?

A

Phagocytic + Non-phagocytic cells

54
Q

What are the virulence factors in L. monocytogenes?

A

Adhesins + Listeriolysin O

55
Q

What is listerolysin O?

A

Allows the bacteria to move around without being detected by AB’s

56
Q

What is the pattern of disease seen in ruminants with a listeriosis infection?

A

Encephalitis
Abortion
Septicemia

57
Q

When is septicemia most commonly seen in cattles with listeria?

A

Neonates

58
Q

When do abortions normally occur with listeria?

A

3rd trimester

59
Q

What happens with direct inoculation of listeria in cattle?

A

Conjunctivitis + Opthalmitits

60
Q

What pattern of disease is seen with pigs + dogs + cats with listeria?

A

Septicemia form with focal hepatic necrosis

61
Q

What pattern of disease is seen with horses with listeria?

A

Neonatal septicemia and abortion

62
Q

What pattern of disease is seen with poultry with listeria?

A

Septicemic form with lesions on heart, liver, and abdominal visceria
Pericarditis
Splenomegaly

63
Q

What is the basic treatment for listeria?

A

Susceptible to many AB’s

64
Q

What are the general characteristics of Erysipelothrix?

A

Gram-positive

Non-spore forming

65
Q

What is the cell morphology of erysipelothrix?

A

Rods + Non-branching filaments

66
Q

What is the oxygen preference of Erysipelothrix?

A

Facultative anaerobes

67
Q

What is the most important Erysipelothrix to vet med?

A

E. rhusiopathiae

68
Q

What is a specific example of where E. rhusiopathiae can be found in nature?

A

Fish slime

69
Q

What is the main reservior for E. rhusiopathiae?

A

Swine

70
Q

Where is E. rhusiopathiae found in pigs?

A

Tonsil + GI tract

71
Q

How does E. rhusiopathiae invade the body?

A

Bloodstream - vascular damage and hemorrhagic lesions in diverse organs
Damage to synovial tissues

72
Q

What are the virulence factors found in E. rhusiopathiae?

A

Neuraminidase + Hyaluronidase + Capsule

73
Q

What does neuraminidase do?

A

Adherence to endothelial cells

74
Q

What does hyaluronidase do?

A

helps with invasion of tissue

75
Q

What does the capsule in E. rhusiopathiae allow for?

A

Survival and growth in phagocytes

76
Q

At what age are swine most susceptable to E. Rhusiopathiae?

A

3 to 18 months

77
Q

What is seen in swine with E. Rhusiopathiae?

A

Acute swine erysiplelas

Severe/mild septicemia

78
Q

What occurs in swine with chronic forms of E. Rhusiopathiae?

A

Arthritis + Endocarditis

79
Q

What is seen in young lambs with E. Rhusiopathiae?

A

Polyarthritis

80
Q

How does infection of E. rhusiopathiae occur in young lambs?

A

Umbilicus + Skin wounds

81
Q

What occurs in adult sheep with E. rhusiopathiae?

A

Post-dipping lameness

Pneumonia + Endocarditis

82
Q

What is seen with poultry that have an E. rhusiopathiae infection?

A

Actue septicemia w/ sudden death

Chronic arthritis with endocarditis may occur

83
Q

What is the basic treatment for E. rhusiopathiae?

A

Penicillin + Tetracyclines

None effective for chronic disease