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Microbiology > Lecture 17 and 18: Clostridium 2 and 3 > Flashcards

Lecture 17 and 18: Clostridium 2 and 3 Flashcards

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1
Q

What is the causative agent of botulism

A

Clostridium botulinum

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2
Q

Where is C. Botulinum found

A

Endospores distributed in soils and aquatic environments

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3
Q

What type of hemolysis does C. Botulinum have

A

B-hemolysis

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4
Q

What are the 7 types of toxins for C. Botulinum

A

A, B, C, D, E, F, G

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5
Q

T or F: the antitoxin for C. Botulinum must match the toxin type to be effective

A

True

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6
Q

What disease does C. Botulinum cause

A

Flaccid paralysis

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7
Q

What type of C. Botulinum is in most animal species

A

C1

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8
Q

What is the most common C. Botulinum toxin in cattle

A

Type D

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9
Q

How do cattle get type D C. Botulinum

A

Pica (starvation or phosphorus deficiency) leads to eating carcasses or bones that contain BoNT

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10
Q

85% of cases in horses with C. Botulinum are caused by what toxin type

A

B

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11
Q

What is shaker foal syndrome

A

Less than 4 week old foals are found dead or with progressive symmetric motor paralysis- stilted gait, muscular tremors, or unable to stand for >4-5 minutes to due ingestion of Type B C. Botulinum spores

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12
Q

Describe the action of Botulinum neurotoxin and how it results in flaccid paralysis

A
  1. Binds receptor and is endocytosed at NMJ
  2. Enters cytosine of host cell and cleaves SNARE proteins required for membrane fusion of synaptic vesicle and cell membrane
  3. Blocks release of ACh
  4. Muscles can’t contract—> flaccid paralysis
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13
Q

What are the main clinical manifestations of C. Botulinum

A
  1. Tongue, jaw, and tail flaccidity
  2. In coordination and knuckling at fetlocks
  3. Flaccid paralysis
  4. Paralysis of respiratory muscles ultimately leads to death
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14
Q

Based on these photos what are you worried about

A

c. Botulinum

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15
Q

How can you dx C. Botulinum

A
  1. Culture
  2. Detect BoNT or C. Botulinum in food
  3. Inoculate in mice- wasp waist
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16
Q

T or F: C. Botulinum toxin from dead animal proves that being cause of death

A

No not significant can inoculate after death

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17
Q

How can you dx C. Botulinum

A
  1. PCR- toxin genes
  2. ELISA
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18
Q

How do you tx C. Botulinum

A
  1. Evacuation of stomach and purging for recent ingestion
  2. Polyvalent antiserum- binds unbound toxin, is serotype specific
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19
Q

Is there a vaccine available for C. Botulinum

A

Yes, for foals and horses: Botvac- type B toxoid

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20
Q

What 3 diseases can Clostridium Chauvoei cause

A
  1. Blackleg
  2. Clostridial myositis
  3. Black quarter
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21
Q

What type of hemolysis is observed with C. Chauvoei

A

Beta

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22
Q

Where is C. Chauvoei that causes blackleg found

A

Naturally in intestinal tract of animals

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23
Q

Once C. Chauvoei that causes blackleg is in intestinal tract of animals where does it go

A

Organism crosses epithelial layer of GI tract and enters tissues (liver, skeletal muscle, cardiac muscle)

Phagocytized by macrophages and endospores remain dormant

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24
Q

Blackleg causes by C. Chauvoei is considered a ___ disease

A

Endogenous

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25
Q

What is the virulence factor for C. Chauvoei causing blackleg and what does it do

A

CctA: Clostridium Chauvoei toxin A: pore forming toxin that perforates cell membrane

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26
Q

Who is most commonly infected with C. Chauvoei that causes blackleg

A

Young well fed cattle 6 months to 2 years

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27
Q

What does C. Chauvoei cause in sheep

A

Gas gangrene

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28
Q

How does C. Chauvoei get into sheep

A

Wound infections following injury from shearing, docking, castration, crutching

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29
Q

T or F: C. Chauvoei that causes gas gangrene in sheep is nearly 100% fatal

A

True

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30
Q

What is the pathogenesis of blackleg caused by C. Chauvoei

A
  1. Germination of spores in anoxic tissues
  2. CctA generates lesions (dark, dry, emphysematous, hemorrhagic)
  3. Metabolism- gas
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31
Q

What is the likely cause and disease

A

C. Chauvoei, causing blackleg disease

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32
Q

What are the clinical manifestations of C. Chauvoei causing blackleg disease

A
  1. Gangrenous cellulitis and crepitant myositis- large muscles in back, limbs and neck
  2. Acute development of lameness, edema, crepitation
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33
Q

How can you dx blackleg caused by C. Chauvoei

A
  1. Muscles are dark red to black, dry, spongy, sweet odor, infiltrated with small bubbles, neutrophils
  2. Smear infected tissues gram + rods
  3. Fluorescent antibodies
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34
Q

What is treatment for blackleg in outbreak setting

A
  1. Vaccinate susceptible animals and tx prophylactically with penicillin up to 14 days (multivalent vax)
  2. Move cattle from affected grazing grounds
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35
Q

How can you control blackleg

A

Vaccinate with multivalent bacterin vaccine

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36
Q

What is the cause of infectious necrotic hepatitis aka black disease

A

C. Novyi

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37
Q

Where is C. Novyi found

A

Soil, often present in intestine and liver of herbivores

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38
Q

Black disease often coincides with presence of ___

A

Liver fluke: F. Hepatica

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39
Q

What are the virulence factors associated with C. Novyi type B and what do they do

A
  1. TcnA- Clostridium Novyi toxin A (alpha toxin)- lethal necrotizing, activates GTP binding proteins leading to edema
  2. B-toxin- potent phospholipase
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40
Q

What is the pathogenesis of black disease

A
  1. C. Novyi type B (in sheep and cattle)
  2. Endospores ingested and migrate to Kupffer cells in liver where they remain dormant
  3. Liver cell injury (flukes)—> tissue becomes anoxic so endospores germinate and produce toxins
  4. Sudden death ~2 days
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41
Q

Darkening of SQ tissues and blackening of carcass after death is a hallmark of what disease, caused by what

A

Black disease, caused by C. Novyi type B

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42
Q

How can you dx. black disease

A
  1. Liver lesions- grayish yellow gross lesions, fluke tracts
  2. Large gram + rods
  3. Fluorescent antibodies
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43
Q

Cow liver, what likely caused these lesions

A

C. Novyi causing black disease, also flukes

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44
Q

Black disease in pigs is due to infection with what intestinal roundworm

A

Ascaris

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45
Q

What is the most distinguishing sign of black disease in pigs

A

Spongy liver

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46
Q

Liver from pig, what is disease and cause

A

black disease caused by C. Novyi and infection with Ascaris

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47
Q

What is tx for C. Novyi type B

A

No treatment available, typically animals found dead to rapid deterioration

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48
Q

How can you control C. Novyi type B

A
  1. Vaccination with multivalent bacterin-toxoid (longterm immunity)
  2. Control flukes
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49
Q

What is the causative agent of bacillary hemoglobinuria (red water disease)

A

C. Haemolyticum

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50
Q

What species is commonly affected by C. Haemolyticum and where

A

Ruminants in Rocky Mountains, pacific coast, Gulf of Mexico

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51
Q

How do ruminants get C. Haemolyticum

A

Grazing in pastures infested with liver flukes encysted on vegetation which decrease O2 leading to sporulation of C. Haemolyticum endospores

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52
Q

What is the virulence factor on C. Haemolyticum and what does it do

A

B-toxin- hemolytic necrotizing phospholipase C

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53
Q

What is the pathogenesis of C. Haemolyticum

A
  1. Ingestion of endospores which are absorbed by intestine
  2. Spores transported to liver and remain dormant with high O2
  3. Grazing leads to ingestion of cysts for liver fluke
  4. Young liver flukes ex cyst in duodenum, burrow in intestinal wall and migrate to liver
  5. Burrow and feed on parenchyma of liver
  6. Create anaerobic tissue causing germination of C. Haemolyticum and toxic produced
  7. Leading to hepatocyte necrosis and endovascular thrombosis
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54
Q

What is the clinical manifestation for Bacillary hemoglobinuira caused by C. Haemolyticum

A
  1. Acute- sudden death in 10-12hrs
  2. Subacute (3-4) days- fever jaundice, anorexia, abdominal pain, rapid deep breathing, decreased milk production, blood in feces and urine
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55
Q

Cow bladder with red “water” in urine, what is likely cause and disease

A

C. Haemolyticum causing bacillary hemoglobinuria

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56
Q

How can you dx C. Haemoglobinuria/ bacillary hemoglobinuira

A
  1. Hx
  2. Necropsy- lesions/ infarcts on liver
  3. Decreased blood cell and hemoglobin concentration
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57
Q

What is tx for Bacillary hemoglobinuira

A
  1. Antitoxin
  2. Blood transfusion and fluid therapy
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58
Q

T or F: antibiotics are an effective tx for bacillary hemoglobinuira

A

False- likely ineffective

59
Q

How do you control C. Haemolyticum/ bacillary hemoglobinuira

A

Vaccination- seasonal 1 dose prior to dry season

60
Q

What is the primary cause of malignant edema- gas gangrene leading to necrotizing Clostridial infection of soft tissue

A

C. Septicum

61
Q

C. Septicum has high incidence in what species

A

Horses and cattle

62
Q

Where is C. Septicum found

A

Soils, animal and human small intestine

63
Q

How do animals get infected with C. Septicum

A

Endospores or vegetative cells contaminate wounds

64
Q

What are the virulence factors associated with C. Septicum and what does it do

A
  1. ATX- alpha toxin- pore forming lethal toxin—> leads to cell oncosis/ swelling or ischemic death
65
Q

How does the C. Septicum toxin spread

A

Hematogenous spread

66
Q

What are the risk factors for C. Septicum

A

Poor hygiene practices

67
Q

What are the general signs of C. Septicum

A

Develop 6-49ers after injury or endospore activation leading to anorexia, intoxication, high fever, local lesions, reluctance to move

68
Q

What local lesions are associated with C. Septicum

A
  1. Large amounts of exudate infiltrate SQ or intramuscular CT, muscles are dark brown, black or red
  2. Progressed state- extensive sloughing of skin
69
Q

What lesion occurs in post patruient cows caused by C. Septicum

A

1-3 days after calving get necrotizing vulvovaginitis and metritis associated with lacerations at parturition, marked edema, severe toxemia, and death

70
Q

What is likely cause. You also noted skin sloughing off locally.

A

C. Septicum

71
Q

How do you dx C. Septicum

A
  1. Fluorescent antibodies
  2. PCR
  3. Gram stain- gram + rods
72
Q

What is a helpful way to dx C. Septicum in horses

A

Clostridial diseases cause IMHA so do blood smear, notice echinocytosis: toxin altered RBC membranes

73
Q

Blood smear from horse, you also note dark brown/black muscles and sloughing of skin. What is likely cause and how does histo support that

A

C. Septicum
Histo: echinocytosis: toxin altered RBC membranes

74
Q

What is tx for C. Septicum

A

High dose penicillin, tetracycline or broad spectrum antibiotics

75
Q

How do you control C. Septicum

A

Multivalent vaccine

76
Q

What is causative against of Big head or swollen head

A

C. Novyi type A- TcnA toxin

77
Q

What is common cause of Big head or swollen head

A

Young rams butting heads, breaks in skin, endospores enter, bruising provides good conditions for endospore germination

78
Q

What is tx for big head or swollen head

A

Broad spectrum antibiotic or penicillin

79
Q

How do you control big head or swollen head

A

Multivalent vaccine

80
Q

What is likely cause and disease

A

C. Novyi type A causing big head/ swollen head

81
Q

What clostridial causes gas gangrene

A

C. Perfringens type A

82
Q

Where is C. Perfringens type A found

A

Soil, marine sediment, GI tract

83
Q

How do animals get infected with C. Perfringens type A

A

Infection following trauma

84
Q

What is key virulence factor for C. Perfringens type A

A

CPA-alpha toxin-phospholipase, hemolytic, necrotizing

85
Q

What are clinical signs of C. Perfringens Type A

A

Rapid progression, extensive invasion of damaged skeletal muscle, gas production- SQ crepitation

86
Q

How do you dx C. Perfringens type A

A
  1. Fluorescent antibodies of bacteria
  2. Anaerobic isolation and culture- double zone of hemolysis on blood agar (target shape)
87
Q

What is likely cause

A

C. Perfringens type A

88
Q

What is tx for C. Perfringens type A

A

Usually ineffective but Penicillin or other broad spectrum antibiotic

89
Q

How do you control C. Perfringens type A

A

Vaccination for cattle: toxoid A
NOT PART OF MULTIVALENT VACCINE

90
Q

What clostridium is associated with ruminants and horses and causes fatal myositis and hepatic disease

A

Paeniclostridium sordellii

91
Q

What is toxin for P. Sordellii and what does it do

A

TcsL- toxin clostridium sordellii- modifies Ras and Rac GTPases altering cell cytoskeleton leading to apoptosis

92
Q

Myonecrosis caused by __organism is fatal

A

P. Sordellii

93
Q

What are the clinical manifestations in horses with P. Sordellii

A
  1. Acute rhabdomyolysis- breakdown muscle tissue leading to release of myoglobin in blood
  2. Hepatic disease
  3. Fatal disease in perinatal foals
94
Q

What does P. Sordellii cause in sheep

A

Fatal uterine infections post labor

95
Q

What is tx for P. Sordellii

A

There is no tx

96
Q

How do you control P. Sordellii

A

Multivalent vaccine

97
Q

What does the alpha toxin associated with C. Perfringens do and what is it also known as

A

Aka CPA or PLC
Hydrolyzes phosphatidylcholine and sphingomyelin and leads to production and release of IL-8, neutrophil chemoattractant

98
Q

What does beta toxin of C. Perfringens do and what is it also known as

A

Aka CPB
Pore forming toxin targeting array of host cells

99
Q

What does epsilon toxin of C. Perfringens do and what is it also known as

A

Aka ETX
Pore forming toxin that binds lipid rafts in host cell membranes leading to ion exchange and apoptosis

100
Q

What does the iota toxin for C. Perfringens do and what is it also known as is

A

Aka ITX
Ia enters cell via Ib pore and disrupts host cell actin leading to cell death

101
Q

What does enterotoxin for C. Perfringens do and what is it also known as

A

Aka CPE
Causes pore formation in apical side of epithelial cells- loss of ion homeostasis and apoptosis

102
Q

What does NetB toxin of C. Perfringens do and what is it also known as

A

Aka necrotic enteritis toxin B
Recognizes cholesterol free regions in cell membranes, forms pores that allow entry of ions

103
Q

What is the most widespread toxotype for C. Perfringens in environment

A

Type A-CPA toxin

104
Q

What C. Perfringens toxin is a common inhabitant of mammalian microbiota

A

Type A- CPA toxin

105
Q

CPA toxin is known to be a critical toxin in what 2 diseases

A
  1. Gas gangrene
  2. Gangrenous mastitis
106
Q

Abomasum from cow, what C. Perfringens toxin likely caused this

A

type A- CPA toxin

107
Q

What toxins are included in type B C. Perfringens

A

CPA, CPB, ETX toxins

108
Q

What clostridium type causes lamb dysentery

A

Type B- CPA, CPB and ETX toxins

109
Q

Older lambs that have loss of condition, depression, reluctance to suckle and neurological signs likely have what perfringens type

A

Type B-CPA, CPB, ETX (ETX causes brain lesions)

110
Q

What toxins are associated with C. Perfringens type C

A

CPA, CPB and some CPE

111
Q

Changes to __lead to overgrowth of C. Perfringens type C

A

Microbiota

112
Q

C. Perfringens type C is often detected in feces of __that is transferred to ___ shortly after pig

A

Sows, piglets

113
Q

What happens in calves with C. Perfringens type C

A

Acute diarrhea, abdominal pain, convulsions, opsithotonos (necrotizing enteritis)

114
Q

What happens in pigs with infected with C. Perfringens type C

A

Acutely ill within few days of birth: diarrhea, dysentery, reddening of anus (necrotizing enteritis)

High fatality rate

115
Q

What happens in foals infected with C. Perfringens type C

A

Acute dysentery, toxemia, and rapid death (necrotizing enteritis)

116
Q

How do you dx C. Perfringens type C

A

Necropsy- hemorrhagic enteritis with ulceration of mucosa

Intestines have deep blue-purple appearance

117
Q

What is tx for C. Perfringens type C

A

Usually ineffective but type C antitoxin or antibiotic in piglets less than 2hrs of age

118
Q

How do you control C. Perfringens

A
  1. Vaccination of pregnant animals in last 3rd or pregnancy
  2. Antitoxin to newborn of unvaccinated mother
119
Q

Intestines of piglet, calve, or foal that had acute diarrhea, dysentery. What is likely cause

A

C. Perfringens type C

120
Q

What toxins are associated with Type D C. Perfringens

A

CPA, ETX, and some CPE

121
Q

What C. Perfringens type is also called overeating disease, pulpy kidney

A

Type D

122
Q

What species is likely infected with C. Perfringens type D and what is cause

A

Lambs from 3-10 weeks or weaned in feedlots due to high carbohydrate diets, lush green pastures

123
Q

What is the virulence factor and pathogenesis associated with C. Perfringens type D

A
  1. Overgrowth of type D with production of ETX
  2. ETX is absorbed into blood stream and disseminates
  3. Edema and necrotic lesions in brains, lungs, and kidneys
124
Q

Why would colostrum be effective at preventing C. Perfringens type D

A

Colostrum contains trypsin inhibitors which is what activates protoxin in GI tract

125
Q

How do you dx C. Perfringens type D

A
  1. Fecal smears with G+ rods
  2. Confirmation of ETX gene via PCR
126
Q

How do you control for C. Perfringens type D

A
  1. Vaccination
  2. For outbreaks use antitoxin and revaccinate
127
Q

What toxins are in C. Perfringens type F

A

CPA and CPE toxins

128
Q

What species are typically affected by C. Perfringens type F

A

Cats and dogs

129
Q

What are some clinical signs of C. Perfringens type F in dogs and cats

A

Diarrhea, dehydration, fever abdominal pain, with or without hypovolemic shock (hemorrhage)

130
Q

How do you dx C. Perfringens type F

A

Large gram + bacilli in feces or ELISA for CPE

131
Q

How do you tx C. Perfringens type F

A

IV fluids and metronidazole

132
Q

What is mechanism of action of metronidazole

A

Breaks DNA blocks replication and transcription

133
Q

What toxins are present in C. Perfringens type G

A

CPA and NetB toxins

134
Q

What does C. Perfringens type G cause in birds

A

Necrotic enteritis in poultry

135
Q

What are some signs of C. Perfringens type C in poultry

A

Sudden increase in morality, depression, ruffled feathers, diarrhea

136
Q

What does the necropsy look like of poultry infected with C. Perfringens type G

A

Dark, swollen, and firm liver, distended gall bladder, watery brown, blood tinged fluid, foul-smelling brown fluid in intestines

137
Q

Where is C. Difficicle found

A

Large intestine of healthy and sick animals, resistant spores found wherever animal is housed

138
Q

C. Difficle associated with diarrhea is linked to changes in ___ caused by ___

A

Intestinal microbiota caused by antibiotics, feed changes, stress, NSAIDS

139
Q

C. Difficle disease is worse in animals with expanded LI like __, ___, and ___

A

Horses, rabbits and swine

140
Q

How is C. Difficle spread

A

Massive number in feces of antibiotic treated animals

141
Q

What toxins are associated with C. Difficle and what do they do

A
  1. CDT- C. Difficle transferase
  2. TcnA and TcdB: glycosylating toxins induce cytoskeletal changes compromising epithelial cell barrier

All 3 toxins disrupt actin cytoskeleton and induce severe inflammatory response

142
Q

How do you dx C. Difficle

A
  1. Fecal PCR for toxin genes
  2. ELISA for TcdA and TcdB toxins
143
Q

How do you tx C, Difficle

A

Metronidazole, fecal transplants

144
Q

How do you control C. Difficle

A

Probiotics at time of antibiotics to reduce risk

Microbiology (31 decks)

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