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Bacteriology Exam 2 > Bacteria (Caitlin's Half) > Flashcards

Bacteria (Caitlin's Half) Flashcards

1
Q

Trueperella pyogenes affects what species?

A

Cattle and swine

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2
Q

Is Trueperella pyogenes part of the normal flora? If so, where does it reside?

A

It is normal flora of skin and mucous membranes of upper respiratory, urogenital, and GI tract of cattle and swine

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3
Q

What is the gram stain and morphology of Trueperella pyogenes?

A

Gram-positive rod

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4
Q

How is Trueperella pyogenes primarily transmitted?

A

Endogenous infections primarily
Can be spread cow to cow by flies (exogenous)

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5
Q

Clinical presentation of Trueperella pyogenes?

A
  1. Purulent infection of the lung, jointa, uterus, and SQ tissue of ruminants and swine
  2. Mastitis in cattle
  3. Septic arthritis in sow after farrowing
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6
Q

How is Trueperella pyogenes treated?

A
  1. Incision of drainage in abscess if accessible
  2. Abx therapy should be initiated but often poor response due to poor penetration in presence of pus/bacteria encapsulation
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7
Q

When clinical presentation of Mycobacterium avium-mycobacterium intracellularae complex (MAC) infection is seen, it is usually due to one of two factors:

A
  1. Immunocompromised host
  2. High infectious dose
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8
Q

What species are affected by Mycobacterium bovis?

A

Cattle are the natural host
However, can also affect several other species
(humans, swine, primates, cats, dogs, sheep, goats, horse, deer, elk, other wildlife, etc.)

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9
Q

Is Mycobacterium zoonotic?

A

YES

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10
Q

What are the virulence factors of Mycobacterium?

A
  1. Lipid rich cell envelope
  2. Faculative intracellular pathogen of macrophages
  3. SLOW growing species - more virulent
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11
Q

What is the gram-stain/morphology of Mycobacterium?

A

Acid Fast. stain required
Rod Shaped

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12
Q

Where does Mycobacterium reside?

A

Within host (can survive for years - latent)
Can survive (NOT REPLICATE) in environment 4 days in summer and 28 in winter

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13
Q

How is Mycobacterium bovis transmitted?

A

Infected animals are the source
Spread through exhaled respiratory droplets
Inhaled/ingested by macrophages in new host

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14
Q

How are most cases of Mycobacterium bovis found?

A

At slaughter during routine inspections

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15
Q

Clinical signs of Mycobacterium bovis?

A

Granuloma/tubercles on infected organs
If signs present, depend on organs involved (respiratory signs, weight loss, enlarged nodes)
There may be no clinical signs

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16
Q

How is Mycobacterium bovis diagnoses?

A
  1. Caudal Fold Test
  2. Lesions and enlarged nodes (tuburcles) found at necropsy
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17
Q

What is a caudal fold test?

A

Skin test measuring immune response to tuburculin of Mycobacterium bovis. Look for swelling at 72hrs. Positive test must then be confirmed by cervical test

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18
Q

How is Mycobacterium bovis controlled?

A

Is a REPORTABLE disease
National TB Eradication Program
Quarantine herds
Positives slaughtered
Keep Closed herds or test before purchase and isolate after purchase

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19
Q

Is Mycobacterium bovis zoonotic?

A

YES

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20
Q

Mycobacterium bovis in deer (presentation and importance)

A

Susceptible
Pulmonary or disseminated dz
Put cattle in MI at risk

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21
Q

Mycobacterium bovis in humans (presentation and transmission)

A

Very susceptible
Pulmonary or disseminated dz
Serious zoonotic problem where unpasteurized milk is consumed

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22
Q

Is Mycobacterium bovis reportable?

A

YES

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23
Q

Mycobacterium tuberculosis usually effects what species?

A

Humans are the natural host
(Other species also susceptible, lap animals like cats and dogs especially)

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24
Q

1/3 of the world’s population is infected with this bacteria:

A

Mycobacterium tuberculosis

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25
Q

How is Mycobacterium tuberculosis transmitted?

A

Inhalation

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26
Q

How is Mycobacterium tuberculosis diagnosed?

A

PPD skin test

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27
Q

What is the treatment for Mycobacterium bovis?

A

There is no treatment

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28
Q

Describe the Mycobacterium tuberculosis vaccine:

A

BCG M. bovis based vaccine used for TB in people only

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29
Q

What is the treatment for Mycobacterium tuberculosis?

A

Dogs - long term anti-TB drugs
Humans - Abx
Cattle - would not treat

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30
Q

Mycobacterium leprae affects what species?

A

Humans
Armadillos

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31
Q

What is the main reservoir of Mycobacterium leprae?

A

Armadillos in southern US (TX;LA)

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32
Q

Mycobacterium avium Complex (MAC) usually affects what species?

A

Birds, swine, sheep, goats, dogs, and cats
RARE in horses

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33
Q

What is generally required for clinical disease associated with Mycobacterium avium Complex (MAC) to occur?

A

Host with immunocompromised state
High infectious dose

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34
Q

What are the usual symptoms of Mycobacterium avium Complex (MAC)?

A

Weight loss, LN enlargement, sometimes enteritis

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35
Q

Mycobacterium avium Complex (MAC) is commonly found in what group of humans?

A

AIDS patients

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36
Q

Mycobacterium avium Complex (MAC) is diagnosed using what tests?

A

Biopsy of lesions
PCR
Culture
Comparative cervical skin testing in cattle/swine

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37
Q

Describe the treatment for Mycobacterium avium Complex (MAC):

A

Abx in people and can be attempted in dogs
Other species treatment is not attempted

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38
Q

How is Mycobacterium avium Complex (MAC) controlled?

A

Routine disinfection and exclusion of wild bird from livestock buildings/feed areas

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39
Q

How is Mycobacterium avium Complex (MAC) transmitted?

A

Ingestion

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40
Q

What is a main reservoir of Mycobacterium avium Complex (MAC)?

A

Feces of many domestic and wild birds

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41
Q

What is a significant problem regarding Mycobacterium avium Complex (MAC) in livestock?

A

Interference with TB skin testing because can give a false positive for TB.

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42
Q

Do hosts infected by Mycobacterium avium Complex (MAC) usually show signs of diease?

A

No. Only hosts who are immunocompromised or exposed to very high infectious dose show signs

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43
Q

Mycobacterium avium ssp. paratuberculosis (MAP) is transmitted through what route?

A

Fecal-oral spread primarily
Often when animals exposed shortly after birth by ingestion of small amounts of manure, contaminated food/water, or organisms on udder or in milk

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44
Q

What species are primarily affected by Mycobacterium avium ssp. paratuberculosis (MAP)?

A

Ruminants

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45
Q

Mycobacterium avium ssp. paratuberculosis (MAP) is the causative agent of what major ruminant disease?

A

Johne’s disease

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46
Q

Mycobacterium avium ssp. paratuberculosis (MAP) is _____ growing in vivo and in vitro, increasing virulence

A

Slow growing

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47
Q

Describe the clinical presentation of animals infected with Mycobacterium avium ssp. paratuberculosis (MAP):

A

Contagious, chonic enteritis, weight loss (emaciation)

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48
Q

Where does Mycobacterium avium ssp. paratuberculosis (MAP) reside?

A

Intestines of infected animals
LN and ilem affected by Johne’s dz

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49
Q

Is Johne’s disease reportable?

A

Yes in Georgia

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50
Q

How can Mycobacterium avium ssp. paratuberculosis (MAP) be controlled?

A

Eliminate infected animals
Keep closed herd
Keep birthing environment clean
Avoid manure contamination in feed and water

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51
Q

How is Johne’s Disease diagnosed?

A

DNA based PCR

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52
Q

There is a ____ USDA Johne’s Disease Herd Statud program for cattle

A

Voluntary

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53
Q

Describe the gram-stain and morphology of Nocardia:

A

Gram positive, partially acid fast
Filamentous

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54
Q

Where is Nocardia widely distributed?

A

Soil and water

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55
Q

Is Nocardia part of normal flora?

A

NO

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56
Q

Nocardia asteroides complex

A

Includes many species but species is rarely determined

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57
Q

Nocardia is a _________ intraceullar pathogen of ______

A

Facultative; macrophages

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58
Q

Virulence factors of Nocardia:

A

Cell wall lipids
Faculative intraceullular pathogen of macrophages
Inhibits phagosome fusion

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59
Q

How is Nocardia transmitted?

A

Contamination of wounds
Or by inhalation/ingestion (leads to more serious dz)

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60
Q

Nocardia asteroides has 3 forms of disease. What are they?

A
  1. Localized skin form
  2. Thoracic form
  3. Septicemic form
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61
Q

Clinical disease in patients infected by Nocardia asteroides may reflect underlying _______?

A

Immunosuppression

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62
Q

Nocardia asteroides causes rare ____ respiratory and disseminated disease

A

respiratory

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63
Q

How is Nocardia asteroides diagnosed?

A

Cytologyical prep with gram stain of lesion - shows branching filaments
Culture/PCR confirmative

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64
Q

How is Nocardia asteroides treated?

A

Surgical debridement with systemic abx
Treatment of thoracic and systemic forms minimally effective

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65
Q

Disease associated with Nocardia asteroides in dogs and cats usually presents as _______ and generalized ______ forms.

A

thoracic; systemic

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66
Q

Cats showing signs of Nocardia asteroides infection may be immunosuppressed with what diseases?

A

FeLV and FIV

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67
Q

What is a main characteristic of M. leprae clinical disease?

A

Granulomatous skin infections

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68
Q

Describe the gram-stain/morphology of Actinomyces:

A

Gram positive
Pleomorphic, filamentous branching, rod

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69
Q

Is Actinomyces part of normal flora?

A

YES - oropharynx, GI, and urogenital tract

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70
Q

How is Actinomyces transmitted?

A

Endogenous infection - trauma to oral mucous membranees

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71
Q

Actinomyces bovis is part of the normal flora of the mouth in what species?

A

Cattle

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72
Q

Actinomyces bovis causes actinomycosis, otherwise knows as what disease?

A

Lumpy jaw

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73
Q

“Lumpy Jaw” (actinomycosis) in cattle is granulomatous osteomyletitis of ___ and ____

A

Face and Jaw

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74
Q

‘Lumpy Jaw” causes _____ to develop and drain

A

Fistulas

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75
Q

“Lumpy Jaw” (caused by Actinomyces bovis) can cause ______ problems and tooth loss

A

mastication (chewing)

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76
Q

How is Actinomycosis diagnosed?

A

Clinical signs
Cytology and culture of exudate

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77
Q

How is Actinomycosis treated?

A

Antibacterial therapy - primarily iodides +/- penicillin
Surgical Debridement

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78
Q

How can “Lumpy Jaw” be prevented?

A

Avoid feeding course, stemmy hay
Treat early

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79
Q

Actinomyces viscosus is present in the oral mucosa of what species?

A

Dog, cat, and humans

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80
Q

What bacterium is associated with periodontal disease?

A

Actinomyces viscosus

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81
Q

Describe the gram-stain/morphology of Dermatophilus congolensis?

A

Gramp-positive
Filamentous branching
Zoospores with railroad track appearance

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82
Q

Dermatophilus congolensis replicates only on _____?

A

animals

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83
Q

______ animals are the primary source of Dermatophilus congolensis infection

A

Carrier

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84
Q

Transmission of Dermatophilus congolensis ia favored by these three events:

A
  1. Prolonged rainfall
  2. Higher temperatures
    3 Trauma to the skin
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85
Q

Epidemics of Dermatophilus congolensis can be seen during _____ seasons

A

Rainy

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86
Q

What bacterium can survive up to 3 years in crusts in the environment?

A

Dermatophilus congolensis

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87
Q

Dermatophilus congolensis is maintained in populations by?

A

carriers

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88
Q

Dermatophilus congolensis is transmitted how?

A

Direct contact
Contaminated fomites
Mechanically by flies or ticks

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89
Q

Soaking or trauma to the skin favors motile coccoid ________ growth, forming hyphal-like branches in the epithelium and invasion of hair follicles (associated with infection of Dermatophilus congolensis)

A

Zoospores

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90
Q

Dermatophilus congolensis organisms are eliminated from host as epithelium and _____ are shed.

A

Crusts

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91
Q

Dermatophilosis is a clinical disease associated with the infection of what bacteria?

A

Dermatophilus congolensis

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92
Q

Dermatophilosis is refered to as rain scald in ______ and called lumpy wool in _____?

A

Horses; sheep

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93
Q

Dermatophilosis affects what species?

A

Cattle, horses, sheep, and goats
(Infection is rare in pigs, dogs, cats, and humans)

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94
Q

Dermatophilosis (caused by D. congolensis is associated with what on the infected animal?

A

Purulent crusts and matted hair
The crusts are easily removed to reveal a moist, gray to pink surface

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95
Q

Dermatophilosis is treated by doing what?

A

Removing crusts by grooming (do not discard in environment)
Use iodine shampoo

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96
Q

Dermatophilosis can be prevented (or controlled) how?

A

Minimize exposure to rain
Flea Control

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97
Q

How is Dermatophilosis diagnosed?

A

Clinical signs
Stained, cytological prep of crusts
Culture

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98
Q

Clostridium gram-stain/morphology:

A

Gram-positive rods

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99
Q

Is Clostridium aerobic or anaerobic?

A

Anaerobic

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100
Q

Clostridial diseases are _______-based

A

Toxin

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101
Q

Clostridium produce ____?

A

Spores

102
Q

Several species of Clostridium are found where?

A

Soil and intestine

103
Q

Clostridium tetani is associated with what clinical disease?

A

Tetanus

104
Q

Tetanus is due to _______ which enters the blood streat/lymphatics and is absorbed by ____ nerves..

A

Neurotoxin; Motor

105
Q

The neurotoxin associated with tetanus is?

A

Tetanospasmin

106
Q

In tetanus, the neurotoxin binds _______ to inhibitory neurons in the CNS

A

Irreversibly

107
Q

The binding of tetanospasmin (neurotoxin associated with tetanus) in the CNS results in _________ of the CNS and causes ______ paralysis (tonic contractions of muscles)

A

Excitation; Spastic

108
Q

What species are most susceptable to Clostridium tetani?

A

Horses and humans

109
Q

Susceptability to Tetanus Toxin from most to least (and most common source for each):

A

Horses and Humans (foot injuries most common source in horses)
Pig
Sheep/Goats (tail docking, castration)
Cattle (food injuries)
Dogs and cats - rare
Poultry - resistant

110
Q

What species is resistant to tetanus toxin?

A

Poultry

111
Q

Tetanus is also known as?

A

Lockjaw

112
Q

Tetanus presents as:

A

Rigidity throughout body
Paralysis of breathing muscles
Stiff-legged gait
“Saw-horse” Stance
Still tail
Evental recumbancy

113
Q

Diagnosis of tetanus:

A

Generally based on clinical signs +/- history of wound

114
Q

Treatment of tetanus:

A

Admin. anti-toxin to neutralize any unbound, circulating toxin

115
Q

Anti-Toxin

A

Give toxin antibodies to patient to stimulate passive immunity

116
Q

Toxoid

A

Give inactivated/modified version of toxin to stimulate active immunity

117
Q

______ immunization against tetanus in horses by administering toxoid, then boost when horse receives a wound.

A

Active

118
Q

Clostridium botulinum causes what disease?

A

Botulism

119
Q

Clostridium botulinum is found where in the environment?

A

Soil and aquatic sediment

120
Q

What are the sources of intoxication of Clostridium botulinum contamination?

A

Animal and plant material contaminated with the toxin

121
Q

What species are susceptible to Clostridium botulinum?

A

Chickens and ducks - most
Horses and cattle
Dogs, cats, pigs
Turkey buzzard/Vulture - least

122
Q

Transmission of Clostridium botulinum is primarily through?

A

Ingestion of toxin
Wound contamination

123
Q

______ motor paralysis results from Clostridium botulinum intoxication.

A

Flaccid

124
Q

_______ of C. botulinum toxin affects speed and potency (more toxin = faster and increased lethality)

A

Quantity

125
Q

C. botulinum neurotoxin irreversibly binds to the presynaptic portion of the peripheral cholinergic synapses of motor nerves, blocking ________ release

A

acetylcholine

126
Q

What is the most potent neurotoxin known?

A

C. botulinum neurotoxin

127
Q

Death caused by Botulism is usually due to _______ failure

A

respiratory

128
Q

What is the most common form of Botulism Intoxication?

A

Ingestion of preformed toxin

129
Q

What are the three forms of Botulism Intoxication?

A
  1. Ingestion of preformed toxin
  2. Wound botulism
  3. Toxicoinfectious botulism
130
Q

Toxicoinfectious botulism involves the ingestion of spores which germinate and vegetative bacteria release toxin in the gut. This is an __________ phenomenon.

A

Age-related: Occurs in human infants < 6 months and maybe in foals < 8 weeks

131
Q

Botulism in birds and poultry can be characterized by what symptom?

A

“Limber neck” - flaccid neck of botulism

132
Q

How do birds and poultry usually ingest botulism toxin?

A

Ingestion of toxin in decomposed vegetation, invertebrates (fish), or contaminated feed

133
Q

Describe the clinical signs and outcome of botulism in birds:

A

Occurs 12-48 hrs after ingestion
Birds appear drowsy (droops head)
Eyelid, wing, and leg paralysis
Death by respiratory failure, predation, and drowning

134
Q

How does Botulism usually occur in horses and ruminants?

A

Feedstuffs may be contaminated with carrion.
pH >. 5, moisture, and anaerobic conditions allow growth of C. botulinum in hay
Preformed toxin in forage or feed is absorbed from small intestine
May results from wound contamination with spores

135
Q

Clinical signs of botulism in horses and ruminants?

A

Slowness to consume feed
Grain falling from between lips when eating
Decreased tongue and tail tone
Dysphagia (difficulty swallowing)
Drooling in cattle
Muscle weakness
Mydriasis (dilated pupil)
Bladder distention
Decreased gut motility (borborygmus)

136
Q

What is Shaker Foal Syndrome?

A

Ingestion of preformed and toxicoinfectious form of C. botulinum toxin occurring in foals
Weakness is predominant finding
Drooling milk, lying down a lot, sleepy/dull appearance, unsteady gait, toe scuffling, muscle tremor
Other clinical signs same as in adult

137
Q

Is botulism in dogs and cats common or rare? Details of intoxication?

A

Rare, but usually associated with carrion ingestion
Symptoms same as in other mammals

138
Q

Hos is botulism diagnosed?

A

Often diagnosis of exclusion after routine lab work is normal
Toxin ID by ELISA in lab can give definitive diagnosis

139
Q

Describe the treatment for botulism:

A

Administer antitoxin to ruminants and horses. The antitoxin ties up circulating toxin but has no effect on bound toxin.
Recovery is by growth of new presynaptic nerve endings.
Rest! Muscular activity consumes acetylcholine and worsens symptoms.

140
Q

Botulism can be prevented by:

A

Proper storage of feedstuffs
Prevent access to carrion
Preventative vaccine in horses
Heating foods to boiling to destroy toxin

141
Q

What is carrion (a common source of botulism)?

A

The decaying flesh of dead animals

142
Q

Infant botulism is caused by what form of botulism?

A

Toxicoinfectious - is seen in babies < 6 months
Toxin usually ingested in honey or corn syrup which vegetate and produce the toxin in the intestine

143
Q

Clostridium haemolyticum is found where?

A

Spores are found in soil
NOT part of normal flora

144
Q

Clostridium haemolyticum causes what disease?

A

Redwater Disease - characterized by red/coffee colored urine (hemoglobinuria) from lysis of RBCs

145
Q

C. haemolyticum is associated with the presence of _________.

A

Liver Flukes

146
Q

What must occur for C. haemolyticum to grow and cause disease?

A

The liver is damaged by liver flukes causing anaerobic conditions, allowing the spores to germninate and produce a hemolytic-necrotoxin toxin.

147
Q

Intoxication of Clostridium haemolyticum involves the toxin (phospholipase C) _____ RBCs and causing intravascular hemolysis and capillary damage.

A

Lysing

148
Q

Redwater disease caused by C. haemolyticum is primarily seen in what species?

A

Cattle and sheep

149
Q

Redwater disease increases during what seasons due to the increased presence of liver flukes?

A

Summer and Fall

150
Q

Clinical signs of C. haemolyticum intoxication (Redwater Dz) include:

A

Hemoglobinuria
Fever
Anemia
Death due to destruction of RBCs and associated anoxia

151
Q

C. haemolyticum intoxication (Redwater Dz) is treated how?

A

Treatment is often ineffective if animal severely affected.
Penicillin, anti-toxin, and supportive care can be tried.

152
Q

C. haemolyticum intoxication is diagnoses through what means?

A

Necropsy:
Demonstration of Fluorescent Antibody (FA) of organisms in the live
PCR of organisms from liver and blood

153
Q

C. haemolyticum intoxication (Redwater Dz) is diagnosed through what means?

A

Necropsy:
Demonstration of Fluorescent Antibody (FA) of organisms in the live
PCR of organisms from liver and blood

154
Q

Redwater disease can be prevented by giving what?

A

A multivalent (mult. strains/species) bacterin (whole killed/modified bacteria) for affected regions

155
Q

What is the gram-stain/morphology of Clostridium perfringens?

A

Gram-positive, toxin producing, anaerobic, gas-producing, spore-forming rod

156
Q

Clostridium perfringens is ubiquitous in ____ and _____.

A

Soil; Water

157
Q

The types of Clostridium perfringens (A, B, C, D) is based on what?

A

The type of toxin they make

158
Q

Are the types of Clostridium perfringens part of normal flora? If so, where do they reside?

A

Yes - found in normal flora of the intestines of many animals and people

159
Q

Clostridium perfringens causes serious _____ disease with toxemia, _____ infections, and mastitis

A

enteric; wound

160
Q

C. perfringens Type A possess an ____ toxin (phospholipase) which hydrolyzes host cell membranes, especially ____, ____, and____.

A

Alpha
RBCs, WBCs, and platelets

161
Q

C. perfringens Type A possesses an ______ which causes necrosis of the intestinal wall

A

enterotoxin

162
Q

How is C. perfringens Type A transmitted?

A

Ingestion
Wound Contamination

163
Q

Characteristics of clinical disease due to C. perfringens Type A include:

A

Necrotic, hemorrhagic enteritis in many species (ADULT horses, cows, foals, pigs, dogs, poultry)
Food poisoning in people
Wound infection in animals and humans leading to gas gangrene

164
Q

Diagnosis of C. perfringens Type A intoxication is done by?

A

Culture
PCR toxin ID

165
Q

What is the treatment for C. perfringens Type A intoxication?

A

Antibiotics for wound infection
Supportive treatment for diarrhea

166
Q

How is C. perfringens Type A intoxication prevented?

A

Toxoid available for cows

167
Q

C. perfringens Type C most commonly associated with diarrhea in ______ animals.

A

Neonatal (foals, ruminants, and piglets)

168
Q

Pathogenic features of C. perfringens Type C:

A

Produces multiple toxins which cause hemorrhagic necrosis of intestine
Immaturity of GI tract may allow overgrowth of C. perfringens Type C (related to most common type in neonatal animals)

169
Q

Acute necrotic enteritis (bloody diarrhea) and abdominal pain in foals, piglets, lambs, kids, and calves is due to the overgrowth of what bacteria?

A

C. perfringens Type C

170
Q

C. perfringens Type C intoxication can be diagnosed using what means?

A

Culture
PCR for toxin ID

171
Q

C. perfringens Type C is treated how?

A

Antibiotics
Supportive care

172
Q

C. perfringens Type D in low numbers is part of the ___________ of __________.

A

Normal flora; ruminants

173
Q

High ____ diet and ______ results in proliferation of C. perfringens Type D in sm. intestine and release of many toxins

A

Grain; stress

174
Q

Toxins produce in the intestine by C. perfringens Type D results in increased cell _________. The toxin is absorbed and effects of toxin are _______.

A

Permeability; Systemic

175
Q

C. perfringens Type D leads to what two diseases?

A

“Over eating disease”
“Pulpy kidney disease”

176
Q

Clinical disease associated with C. perfringens Type D is characterized by what symptoms?

A

Rapid onset of ataxia
Convulsions
Coma
May see diarrhea and sudden death

177
Q

C. perfringens Type D can be diagnosed using what methods?

A

Culture to identify organism
Elisa/PCR to ID toxin type

178
Q

What is the treatment of C. perfringens Type D usually unsuccessful?

A

Clinical course too rapid

179
Q

How is C. perfringens Type D managed?

A

Vaccination with Type D toxoid or bacterin.
Adjust feeding practices (i.e. reduce concentrate in diet)

180
Q

Match types of C. perfringens (A, C, D) with common host:

A

C. perfringens Type A - ADULT horses, cows, pigs, dogs, and poultry (can be seen in foals) - A for Adult
C. perfringens Type C - Neonatal animals (foals, ruminants, piglets) - C for “crib” for babies
C. perfringens Type D - Ruminants

181
Q

Clostridium chauvoei spores are found where?

A

In soil and intestinal tract of normal ruminants (esp. cattle, but also seen in sheep)

182
Q

Clostridium chauvoei vegetative bacteria produce a group of toxins that increase capillary permeability and cause emphysematous necrotic _______ and systemic _______.

A

Myositis; toxemia

183
Q

Risk factors for Clostridium chauvoei are?

A

Rapidly growing animal on high plane of nutrition (well fed cattle)

184
Q

Clinical disease of Clostridium chauvoei is known as?

A

Blackleg

185
Q

Manifestation of Blackleg (clinical dz associated with Clostridium chauvoei) is characterized by the sudden onset of what symptoms?

A

Muscle inflammation with necrosis

186
Q

What are the steps of Blackleg transmission?

A
  1. Ingestion of spores in soil or endogenous in intestine
  2. Spores enter blood/lymph from intestinal tract
  3. Spores seed muscle
  4. Unknown stimulus triggers germination of spore
  5. Fever, lameness, or rapid/sudden death without signs
187
Q

Blackleg is associated with what clinical symptoms?

A

Acute lameness and stiff gait but skin is normal (no wound)
- or -
Necrotic muscle (gangrenous)
Often lesion confined to part of the limb, sometimes mult. lesions

188
Q

How is C. chauvoei diagnosed?

A

Sporulated gram-positive rods can be found in muscle
PCR of muscle tissue
FA test for organisms in tissue can provide definitive dx

189
Q

Is treatment of C. chauvoei successful?

A

No.

190
Q

How can Blackleg associated with C. chauvoei be prevented?

A

Vaccination with bacterin

191
Q

Clostridium septicum is found where?

A

In soil and the GI tract

192
Q

How does Clostridium septicum enter the body?

A

Enters muscle via wounds (shearing, tail docking, lambing, castrations, etc.)

193
Q

Clostridium septicum toxins produced at wound site cause _________ _________ which is gangrenous myonecrosis with edema and systemic toxemia

A

Malignant Edema

194
Q

What is systemic toxemia?

A

Rapid shock-like syndrome

195
Q

Can be seen in all domestic animals, but typically _______ cases affecting random, individual animals under the right circumstances

A

Sporadic

196
Q

T/F? Malignant Edema can also be caused by other clostridium species?

A

True.

197
Q

Malignant Edema caused by C. septicum is diagnosed how?

A

Clinical signs
Culture/PCR of muscle
FA on muscle for Clostridial organisms

198
Q

How is Malignant Edema treated?

A

Antibiotics
Drainage
Supportive care

199
Q

How can Malignant Edema caused by C. septicum be controlled/prevented?

A

Good hygiene!
Multivalent Clostridial bacterin or toxoid for ruminants for prevention

200
Q

T/F? An injection given IM can cause Malignant Edema given the right circumstances.

A

True.

201
Q

Where can Clostridium difficile be found?

A

Large intestine of normal and clinically affected animals

202
Q

Where are the spores of Clostridium difficile found?

A

In the environment where animals are housed

203
Q

Clostridium difficile can cause hemorrhagic _______.

A

enterocolitis

204
Q

What species are affected by Clostridium difficile?

A

Foals, horses, dogs, cats, and humans

205
Q

What bacterial infection is often associated with long-term antibiotic use due to changes in normal flora and resulting in increased numbers of this bacteria?

A

Clostridium difficile

206
Q

Clostridium difficile may respond to what drug commonly used to treat diarrhea?

A

Metronidazole

207
Q

All Clostridium species do these two things:

A

Produce toxins
Form spores

208
Q

What is the gram-stain/morphology of Bacillus?

A

Gram-positive, spore-forming, rod (often chains)

209
Q

What are the spore forming bacteria?

A

All Clostridium species
Bacillus

210
Q

What is the most important pathogen in Bacillus genus?

A

Bacillus anthracis (anthrax agent)

211
Q

B. anthracis spores are found worldwide in _____ and persist for _____.

A

Soil; years

212
Q

What form of Bacillus anthracis grows poorly in soil?

A

Vegetative form

213
Q

When do outbreaks of B. anthracis always occur?

A

In summer (temp. > 60F)

214
Q

What are the environmental risk factors for B. anthracis?

A
  1. Summer (temps >60F)
  2. Heavy rain following drought or dry summer
  3. Livestock usually infected by ingesting spores while grazing
215
Q

Where are the virulence determinants encoded for B. anthracis?

A

On two plasmids. Virulent bacteria carry both plasmids.

216
Q

What does each of the two virulent determining plasmids in B. anthracis carry?

A

One encodes a capsule - resists phagocytosis
One encodes toxins (A-B Toxin)

217
Q

What species are most commonly affected by B. anthracis?

A

Cattle, sheep, goats, horses, cats, dogs, swine, and humans

218
Q

Is B. anthracis part of the normal flora?

A

No.

219
Q

The toxin associated with B. anthracis is a 3 component toxin. What are the 3 components?

A
  1. EF - edema factor
  2. PA - protective antigen
  3. LF - lethal factor
    All encoded on a plasmid
220
Q

T/F. The toxin components associated with B. anthracis (EF, PA, LF) are harmful as individuals.

A

FALSE.
Individually, the components are harmless.

221
Q

In _____ combinations, edema toxin (PA and EF) and lethal toxin (PA and LF) are formed and called A-B toxins

A

binary

222
Q

Which toxin component is the cell binding component?

A

PA - protective antigen

223
Q

__________ is a protease which inhibits Mitogen Activated Protein Kinases (MAPK) perturbing host signaling (host cells die)

A

Lethal toxin

224
Q

How is B. anthracis transmitted?

A

Ingestion of spores (in soil, in contaminated foodstuffs, or water)
Cutaneous (spores enter through skin abrasions)
Inhalation of spores (minor route in animals but rapidly fatal)

225
Q

What is the most common route of transmission for B. anthracis?

A

Ingestion of spores (esp. grazing cattle)

226
Q

Forms of Clinical Disease: Anthrax

A

Peracute (found dead)
Acute
Intestinal Form
Chronic

227
Q

What are the characteristics of clinical disease, Anthrax, peracute form?

A

Sudden death in cattle, sheep, goats

228
Q

What are the characteristics of clinical disease, Anthrax, Acute form?

A

Fever, mucosal hemorrhages in cattle, sheep, goats, and horses.
Diarrhea, edema of the tongue and throat, bleeding from body openings because of clotting disruption

229
Q

What are the characteristics of clinical disease, Anthrax, intestinal form?

A

Gastroenteritis
More common in swine, dogs, and cats

230
Q

What are the characteristics of clinical disease, Anthrax, chronic form?

A

Pharyngeal edema, tonsillar involvement, dysphagia
May see hemorrhaging of mouth and through
More common in swine, dogs, and cats

231
Q

T/F? Dogs and cats are highly susceptible to anthrax.

A

FALSE.
Dogs and cats are relatively resistant. If seen, usually associated with outbreaks in farm animals.

232
Q

What form of transmission of anthrax is seen in 95% of cases in people? What are the clinical symptoms?

A

Cutaneous - entry via skin wound.
Solitary, initially painless, necrotizing, hemorrhagic, ulcerous

233
Q

What form of anthrax transmission is NOT common in animals?

A

Cutaneous anthrax

234
Q

Clinical signs of inhaled anthrax in humans:

A

Pulmonary - due to inhalation of spores.
Severe lung edema.
Almost always fatal.
Very rare.

235
Q

What clinical symptom most commonly associated with ingested anthrax in humans?

A

Intestinal - gastroenteritis

236
Q

Diagnosis of Anthrax?

A

Hallmark signs:
Absence of rigor mortis
Dark, tarry blood at orifices which do not clot

237
Q

You find a group of cattle suddenly dead on your farm. You suspect they have died of anthrax. What do you do?

A
  1. Seek advice from regulatory vets (state and federal) regarding disposal and disinfection
  2. Infected carcasses and contaminated bedding and soil should be burned or possibly buried 6ft deep.
  3. Care must be taken to avoid human exposure during clean up. Wear proper PPE.
238
Q

A neighbor is concerned about your suspicion that your cattle died from anthrax and tells you to ask the local vet for a necropsy to determine whether or not it was actually anthrax.

What do you tell your friend?

A

If anthrax is suspected, NEVER perform a necropsy.
The vegetative B. anthracis will die in an unopened carcass. If exposed to air, the bacteria can sporulate and you risk personal exposure and further environmental contamination.

239
Q

Since you cannot perform a necropsy on the cows that died of suspected anthrax, how would the diagnosis be confirmed?

A

Blood can be collected aseptically from an ear vein, and a PCR can detect the presence of the organism in the blood and tissues.

240
Q

Describe anthrax treatment:

A

Isolate affected animals
Quarantine premises for 3-4 weeks from last case
Antibiotics (penicillin or oxytetracycline for sick animals in early stages)
Supportive care

241
Q

ESCutaneous form of anthrax in humans responds well to what?

A

Antibiotics

242
Q

Is anthrax a reportable disease?

A

YES!

243
Q

B. anthracis is a _______ _______. This is a bio-agent with potential to cause a severe threat to public health and safety.

A

Select agent

244
Q

How can anthrax be prevented?

A

Vaccination with a plasmid-cured (lacks plasmid) non-enacpsulated live-attenuated vaccine (Sterne-strain) to livestock provides good protection.

245
Q

For prevention of anthrax in humans, what could be done?

A

Administer a subunit vaccine (PA adsorbed to alum) to at risk personnel (military, researchers, etc.)

246
Q

Which bacteria are zoonotic?
(9)

A
  1. Staphylococcus aureus
  2. Streptococcus suis
  3. Streptococcus equi ssp. zooepidemicus
  4. Listeria monocytogenes
  5. Rhodococcus equi
  6. Erysipelothrix rhusiopathiae
  7. Mycobacterium bovis (humans - erysepeloid)
    Mycobacterium avium complex (humans w/ AIDS)
    Mycobacterium leprae (leprosy)
247
Q

Is every bacteria on test 2 Gram Positive?

A

All but one! Mycobacterium bovis is stained with Acid fast stain, so not declared pos/neg.

248
Q

Which bacteria are rod shaped? (8)
LECTMACB

A
  1. Listeria
  2. Erysipelothrix
  3. Corynebacterium
  4. Trueperella
  5. Mycobacterium
  6. Actinomyces
  7. Clostridium
  8. Bacillus
249
Q

Which bacteria are cocci? (Coccus in name)
SSER

A
  1. Staphylococcus
  2. Streptococcus
  3. Enterococcus
  4. Rhodococcus
250
Q

Which bacteria are filamentous? (3)
NAD

A
  1. Nocardia
  2. Actinomyces
  3. Dermatophilus
251
Q

What characteristics do streptococcus and staphylococcus share?

A
  1. Normal flora causes dz
  2. Common cause of mastitis in cattle
  3. Similar morphology
  4. Neutrophil infiltration typical of lesions

Bacteriology Exam 2 (2 decks)

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