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clostridium Flashcards

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1
Q

characteristics of clostridium spp

A

gram positive rods
strict anaerobic organisms
spore forming
-show bulge
-location of spore can help ID

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2
Q

what is the causative agent of tetanus

A

clostridium tetani
-terminal spherical endospore (tennis racket shape)

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3
Q

what things can cause tetanus

A

-horses and humans highly susceptible
-carnivores are resistant

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4
Q

what are the the conditions for clostridium tetani to infect susceptible host

A

-spores introduced into the wound, needs to be anaerobic conditions
-anaerobisis caused by deep wound penetration and necrotic tissue
-facultative anaerobes in polymicrobic infection consume oxygen to allow that spores to germinate creating an environment for obligate anaerobes

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5
Q

what types of potent toxins are the vegetative cells in clostridium tetani producing

A

-tetanolysin: hemolytic spore forming toxin that lyses RBC
-tetanospasmin (tetanus neuron toxin): most potent toxin

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6
Q

what is the pathogenesis of tetanospasmin in clostridium tetani

A

AB subunit bind to presynaptic terminal of LMN > gets internalize > released A in motor neruon > gets up to the inhibitory neuron > blocks the release of gamma aminobutyric acid (GABA) and glycogen inhibitory neurotransmitter

-leading to spastic paralysis

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7
Q

diseases of clostridium tetani

A

rigid paraylsis
-ascending (for not susceptible animals) and descending (for highly susceptible animals)
-lockjaw (no feeding) - truisms
-raise eyebrows ad grinning
-sawhorse (stance)

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8
Q

diagnosis for clostridium tetani

A

-gram stain
-PCR for tetanus toxin genes from wound
-differentiate from strychnine poisoning dogs

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9
Q

treatment for clostridium tetani

A

-horses given antitoxin q12 along w muscle relaxants and barbiturates
-dogs and cats can give horse one but can cause anaphylaxis
-surgical debridment of wound
-supportive care bc toxins bind irreversibly so that synapse can regenerate

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10
Q

how to prevent clostridium tetani

A

-vaccination of farm animals yearly
-mares vax during last 6 weeks of pregnancy
-foals vax 5-8 weeks

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11
Q

why do you need to vaccinate regularly an animal that survived tetanus?

A

because antibiotic don’t kill endospores, and the endospores can persist and can germinate later on

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12
Q

what is the causative agent of botulism

A

clostridium botulinum

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13
Q

characteristics of clostridium botulinum

A

-gram + rods
-obligate anaerobes
-endospore subterminal endospores, bulge like mother cell

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14
Q

where are the endospores of botulism found?

A

endospores distributed in soils and aquatic environment

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15
Q

what are the 7 types of toxins for botulism?

A

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

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16
Q

when choosing an antitoxin for botulism what is the most important for it be an effective treatment?

A

antitoxin must match toxin

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17
Q

what is the most common toxin in cattle and what part if the cow contains the toxin?

A

bones and meat contain BoNT

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18
Q

what type pf paralysis is seen with C. botulinum?

A

flaccid paralysis

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19
Q

what is shaker foal syndrome

A

in horses from type B toxin (C. botulinum)
-foal found dead or progressive symmetric motor paralysis

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20
Q

how does botulinum neurotoxin cause disease?

A

eters the cytosol of host cell and cleaves SNARE proteins required for membrane fusion of synaptic vesicle and cell membrane > blocks release of AcH

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21
Q

what are the clinical manifestations of C. botulinum

A

-tongue, jaw, and tail flaccidity
-incordination and knuckling fetlocks
-flaccid paralysis

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22
Q

how do you diagnose clostridium botulinum?

A

eliminated other possible causes
-history, clinical signs, and ID of BoNT in serum/tissue before death

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23
Q

why are you likely unable to culture C. botulinum from non-toxicoinfections cases?

A

C. botulinum does grow well in the gut
-toxin is what is important for the disease not the bacteria

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24
Q

why is the toxin not useful in dead carcasses C. botulinum?

A

environmental organisms used to deregulate dead carcasses > false positive

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25
Q

what does PCR detect for botulism?

A

-toxic genes
-requires bacteria from culture or patient

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26
Q

how is C. botulinum treated and controlled?

A

-evacuation of stomach and purging for recent ingestion
-polyvaletn antiserum: binds unbound toxin, serotype specific

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27
Q

what diseases does C. chauvoei cause?

A

blackleg
clostridial myositis
black quarter

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28
Q

what hemolysis does C. chauveoi have?

A

B hemolysis

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29
Q
A
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30
Q

where is C. chauveio found?

A

naturally in the intestinal tract of animals

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31
Q

how does C. chauveio enter the tissues?

A

likely ingested, organism crosses the epithelial layer in the GI tract, enters tissues

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32
Q

is C. chauveio an endogenous or exogenous disease?

A

endogenous disease- disease may occur without a wound

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33
Q

what is the virulence factor for C. chauveio? what does it do?

A

CctA: clostridium chauvoei toxin A > perforated host cell membrane

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34
Q

what age of cattle is blackleg most commonly found?

A

well-fed 6m-2yr most commonly

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35
Q

how is blackleg cause in sheep

A

C. chauvoei-associated gas gangrene
wound infections> follows injury

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36
Q

what generated lesion in blackleg? describe lesions

A

CctA
dry, dark, emphysematous

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37
Q

what are the clinical manifestations of blackleg?

A

-gangrenous cellulitis and crepitant myositis
-acute development laxness, edema, crepitation

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38
Q

how is blackleg diagnosed?

A
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39
Q

how is blackleg treated?

A

vaccine susceptible animals and treat prophylactically with penicillin for up tp 14 days

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40
Q

how is blackleg controlled?

A

vaccination- Bacterin (killed bacteria) vaccine produced with local, previously indemnified clostridial strains of C. chauvoei in cases where toxoid vaccine is ineffective

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41
Q

what is the causative agent of infectious necrotic hepatitis (black disease)?

A

C. novyi

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42
Q

where is C. novyi found?

A

worldwide soil borne organism
often present intention and liver of herbivores

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43
Q

what is the key virulence factor for C. novyi

A

TcnA- toxin A
lethal, necrotizing
activates GTP binding proteins leading to edema

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44
Q

what species is C. novyi type B found?

A

sheep and cattle

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45
Q

how are sheep and cattle infected with C. novyi Type B?

A

endospores ingested and migrate to Kupffer cells in liver where they remain dormant

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46
Q

how is liver injured with C. novyi type b?

A

fluke migration- tissues is anoxic so endospores germinate

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47
Q

what clinic signs are seen with black disease?

A

rarely observed and cattle are simply found dead

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48
Q

how is black disease diagnosed?

A

liver lesion- grayish yellow gross lesions- fluke tracts
contain large gram + rods in liver

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49
Q

postmortem how does C. novyi contaminant liver?

A

from the GI tract

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50
Q

how is C. novyi type B controlled?

A

prophylactic vaccination with bacterin- toxoid combos
control fluke and other hepatopathic agents

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51
Q

how often do animals have to be vaccinated for C. novyi type B?

A

long term immunity - 1 vaccination

52
Q

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

A

C. haemolyticum

53
Q

what type of disease is red water disease?

A

acute, infectious toxemic disease

54
Q

what species does red water disease infect? where?

A

ruminants- Rocky Mountain, Pacific coast, gulf of Mexico

55
Q

how are ruminants infected with C. haemolyticum

A

grazing in pastures infested with liver flukes encysted on vegetation

56
Q

what is the virulence factor of C. haemolyticum

A

B-toxin- hemolytic and necrotizing phospholipase C

57
Q

how do liver flukes contribute to C. haemolyticum infections?

A

young liver flukes excyst in duodenum > burros through intestinal wall then migrate to and enter liver > damage creates anaerobic tissue > C. haemolyticum can grow

58
Q

what leads to hepatocyte necrosis and end-vascular thrombosis with C. haemolyticum?

A

toxin production by vegetative growth

59
Q

what are the clinical manifestations with a subacute infection of C. haaemolyticum?

A

fever, jaundice, anorexia, abdominal pain, rapid deep breathing, decrease milk production, blood in feces

60
Q

how is red water disease diagnosed?

A

clinical history
necropsy- lesions (infarcts) in liver

61
Q

how is C. haemolyticum confirmed?

A

C. haemolyticum in liver infarction

62
Q

how is red water disease treated?

A

antibiotic treatment likely
ineffective
antitoxin

63
Q

how is C. haemolyticum controlled

A

vaccination
seasonal- 1 dose prior to dry season
constant protection- semiannual vaccination

64
Q

what is the primary cause of malignant edema- gas gangrene?

A

clostridium septicum

65
Q

what species has the highest incidence of malignant edema and gas ganrene

A

cattle and horses

66
Q

where does clostridium septicum occur?

A

-occurs in soils worldwide
-found in both animal and human intestine

67
Q

where can infection occur in clostridium septicum?

A

contamination of wounds containing devitalized tissue or soil

68
Q

virulence factors of clostridium speticum

A

ATX- alpha toxin
pore forming lethal toxin

69
Q

what can the toxin of C. septicum cause?

A

local and systemic signs (hematogenous spread of toxin)

70
Q

what are the risk factors of C. septicum

A

poor hygiene practices
traumatic injury

71
Q

what are the general signs of C. septicum

A

-develop 6-48 hours after predisposition injury of enodspore activation
-anorexia, intoxication, high fever, local lesions and reluctance to move

72
Q

what do local lesions look like in C. septicum?

A

-large amounts of exudate
-progressed state: extensive local sloughing of skin
-specific form: post mortem gas gangrene

73
Q

how do you diagnose C. septicum

A

-similar to backleg requires lab conformation- cattle and sheep
-caution: active postmortem invader
-PCR- direct ID and differentiation of clostridia

74
Q

before confirmation of anaerobic culture C. septicum what do you need to do?

A

gram stain of fine-needle aspirates may confirm G+ rods

75
Q

diagnosis of C. septicum in horses

A

immune-mediated hemolytic anemia with clostridial infections

76
Q

what is the treatment for C. septicum

A

high dose parenteral penicillin, tetracyclines, or broad spectrum antibiotics

77
Q

how does C. novyi type A toxin enter the sheep

A

young rams butting
-breaks in the skin offer an opportunity for endosperm entrance

78
Q

what is the cause of Big Head or swollen head

A

C. novyi type A
TcnA toxin

79
Q

how does C. novyi type A (Big head, swollen head)begin to present in the sheep once infected

A

begins under the eyes and spreads to head, face, and neck

80
Q

how do you treat big head disease

A

varies according to text if treatable

81
Q

where is clostridium perfringes type A found?

A

soil, marine sediment, and GI tract

82
Q

what does clostridium perfringens type A cause

A

gas gangrene

83
Q

what is the key virulence factor for clostridium perfringens

A

CPA- alpha toxin -phospholipase; hemolytic; necrotizing

84
Q

clinical manifestations for clostridium perfingens type A

A

-rapid progression, extensive invasion of damages skeletal muscle tissue
-gas production (h2)- subQ crepitation

85
Q

how do you diagnose clostridium perfringens type A

A

-florsecent antibodies of bacteria
-anaerobic isolation and culture

86
Q

treatment for clostridium perfringens type A

A

penicillin or other broad-spectrum antibiotic administration early in debase

87
Q

how do you control clostridium perfeingens type A

A

-vaccination- for cattle toxoid A
-desgined for cattle; another vaccine for swine
-not part of multivalent vaccine

88
Q

what species does paeniclostridium sordellii target and what does it cause

A

ruminants and horses
associated with fatal myositis and hepatic disease

89
Q

what is the toxin associated with paeniclostridium sordellii

A

TcsL- toxin clostridium sordellii lethal

90
Q

what are clinical manifestations of paeniclostridium sordellii

A

associated with acute rhabdomyolysis
>break down of muscle tissue, leads to release of myoglobin in blood, harmful to kidneys

91
Q

talking specifically about C. perfringens what is specific about their different types of toxins

A

different toxins are associated with specific diseases in certain hosts

92
Q

what is the mechanism of action for alpha toxin (aka CPA or PLC) toxin of C. perfringens?

A

zince dependent protease
-hydrolyzes phopshaptidylcholine (PC) and sphingomyelin (SM) > leads to production and release of IL-8

93
Q

what is the mechanism of action for C. perfringens beta toxin (CPB)?

A

pore forming toxin targeting an array of host cells

94
Q

what is the mechanism of action for C. perfringens epsilon toxin (ETX)?

A

pore forming toxin that bonds lipid reacts in host cell membranes

95
Q

note that CPE is not epsilon toxin

A

a fact :)

96
Q

what is the mechanism of action for C. pefringens Iota toxin (ITX)?

A

disrupts host cell actin leading to death of the cell

97
Q

what is the mechanism of action for C. perfirngens CPE (enterotoxin)?

A

causes pore formation in apical side of epithelial cells > loss of ion homeostasis and apoptosis

98
Q

what is the mechanism of action of C. perfringens NetB (necrotic enteritis toxin B)?

A

recognizes cholesterol-free regions in cell membranes, forms pores that allow the entry of ions

99
Q

what disease is caused by clostridium perfringens Type A- CPA toxi?

A

CPA toxin is known to be critical to gas gangrene and gangrenous mastitis
-common inhabitants of mammalian microbiota (this complicates diagnosis)

100
Q

what is the most widespread toxoxtype in the environment?

A

Type A CPA toxin

101
Q

where are infections by C. perfringens TypeB been described (location)?

A

Middle East, Europe, and South Africa

102
Q

what disease is caused by C. perfringens Type B- (CPA, CPB, ETX toxins)?

A

-in young lambs up to 14 days old > lamb dysentery
-in older lambs may have chronic form of disease > Pine (in UK)

103
Q

what occurs when infection with C. perfringens Type C toxin - (CPA, CPB, some CPE toxins)?

A

changes to microbiota that lead to overgrowth

104
Q

how is Type C toxin transferred?

A

transferring to piglets shortly after birth

105
Q

how does type C toxin present in calves?

A

acute diarrhea, abdominal pain, convulsions, and opisthotonos
-death within few days, less server cases can survive

106
Q

how does type toxin present in pigs?

A

acutely ill within a few days, though less severe can survive
-high fatality rate

107
Q

how does type c toxin present in foals

A

acute dysentary, toxemia, and rapid death

108
Q

how is type C toxin diagnosed?

A

on necropsy
-hemorrahgic enteritis with ulceration of mucosa
-intestine has deep blue-purple appearance

109
Q

how is type C toxin treated?

A

type C antitoxin or antibiotic or both used for piglets less than 2 hours of age

110
Q

how do you control type c toxin?

A

-vaccination pregnant animals in last third trimester of pregnancy
-antitoxin to the newborn if unvaccinated mother

111
Q

what toxin type has most likely caused this?

A

C. perfringens type C

112
Q

what disease is caused by C. perfringens type D- )CPA, ETX, some CPE toxins) ?

A

classic enterotoxemia of sheep most commonly

113
Q

what species and age group does type D toxin effect?

A

-worldwide and any age
-most common in lambs from 3-10 weeks or weaned in feed lots

114
Q

what are the virulence factors and pathogenesis of C. perfringens type D- (CPA, ETX, some CPE toxins) ?

A

ETX is absorbed into blood stream and disseminates
-edema and necrotic lesions in brain, lungs, and kidneys

115
Q

what is the effect of colostrum against type D toxin

A

colostrum contains trypsin inhibitors, blocks the activation of the toxin that (requires trypsin)

116
Q

how do you diagnose C. perfringens type D

A

-fecal smears with gram + rods
-confirmation of ETX gene via PCR on fluid sample

117
Q

how do you control C. perfringens type D toxin

A

-vaccination
-for outbreaks can use antitoxin and revaccinate

118
Q

C. perfingens type F-(CPA and CPE toxin) clinical manifestations and presentation?

A

-clincal manifestation in dogs and cats
-dehydration, fever, and abdominal pain with to without signs of hypovolemic shock (hemorrhage)

119
Q

how do you diagnose type F toxin

A

large gram + bacilli in feces
ELISA for CPE

120
Q

how do you treat type F toxin?

A

vet commiunity may use metronidazole for any potential susceptible anaerobic infection

121
Q

where is clostridium difficile found?

A

-in large intestine of healthy and sick animals
-resistant spores found wherever animals housed
-linked to changes in the intestinal microbiota

122
Q

how is C. difficile spread/where contaminated spores?

A

massive numbers in feces of antibiotic treated animals

123
Q

what are the two major toxins of C. diff

A

TcdA and TcdB

124
Q

what do C. difficile TcdA and TcdB cause?

A

glycosylating toxins indice cytoskeletal changes compromising epithelial barrier
-all three toxins disrupt actin cytoskeleton and induce severe inflammatory response

125
Q

how do you diagnose C. diff

A

fecal PCR for toxin genens
-culture is slow and hampered by death of microbe in transport

ELISA for toxins TcdA and TcdB

126
Q

what is the treatment for C.diff

A

metronidazole
-resistant strains are fairly common

microbiology (12 decks)

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