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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
what does PCR detect for botulism?
-toxic genes -requires bacteria from culture or patient
26
how is C. botulinum treated and controlled?
-evacuation of stomach and purging for recent ingestion -polyvaletn antiserum: binds unbound toxin, serotype specific
27
what diseases does C. chauvoei cause?
blackleg clostridial myositis black quarter
28
what hemolysis does C. chauveoi have?
B hemolysis
29
30
where is C. chauveio found?
naturally in the intestinal tract of animals
31
how does C. chauveio enter the tissues?
likely ingested, organism crosses the epithelial layer in the GI tract, enters tissues
32
is C. chauveio an endogenous or exogenous disease?
endogenous disease- disease may occur without a wound
33
what is the virulence factor for C. chauveio? what does it do?
CctA: clostridium chauvoei toxin A > perforated host cell membrane
34
what age of cattle is blackleg most commonly found?
well-fed 6m-2yr most commonly
35
how is blackleg cause in sheep
C. chauvoei-associated gas gangrene wound infections> follows injury
36
what generated lesion in blackleg? describe lesions
CctA dry, dark, emphysematous
37
what are the clinical manifestations of blackleg?
-gangrenous cellulitis and crepitant myositis -acute development laxness, edema, crepitation
38
how is blackleg diagnosed?
39
how is blackleg treated?
vaccine susceptible animals and treat prophylactically with penicillin for up tp 14 days
40
how is blackleg controlled?
vaccination- Bacterin (killed bacteria) vaccine produced with local, previously indemnified clostridial strains of C. chauvoei in cases where toxoid vaccine is ineffective
41
what is the causative agent of infectious necrotic hepatitis (black disease)?
C. novyi
42
where is C. novyi found?
worldwide soil borne organism often present intention and liver of herbivores
43
what is the key virulence factor for C. novyi
TcnA- toxin A lethal, necrotizing activates GTP binding proteins leading to edema
44
what species is C. novyi type B found?
sheep and cattle
45
how are sheep and cattle infected with C. novyi Type B?
endospores ingested and migrate to Kupffer cells in liver where they remain dormant
46
how is liver injured with C. novyi type b?
fluke migration- tissues is anoxic so endospores germinate
47
what clinic signs are seen with black disease?
rarely observed and cattle are simply found dead
48
how is black disease diagnosed?
liver lesion- grayish yellow gross lesions- fluke tracts contain large gram + rods in liver
49
postmortem how does C. novyi contaminant liver?
from the GI tract
50
how is C. novyi type B controlled?
prophylactic vaccination with bacterin- toxoid combos control fluke and other hepatopathic agents
51
how often do animals have to be vaccinated for C. novyi type B?
long term immunity - 1 vaccination
52
what is the causative agent of bacillary hemoglobinuria (red water disease)?
C. haemolyticum
53
what type of disease is red water disease?
acute, infectious toxemic disease
54
what species does red water disease infect? where?
ruminants- Rocky Mountain, Pacific coast, gulf of Mexico
55
how are ruminants infected with C. haemolyticum
grazing in pastures infested with liver flukes encysted on vegetation
56
what is the virulence factor of C. haemolyticum
B-toxin- hemolytic and necrotizing phospholipase C
57
how do liver flukes contribute to C. haemolyticum infections?
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
what leads to hepatocyte necrosis and end-vascular thrombosis with C. haemolyticum?
toxin production by vegetative growth
59
what are the clinical manifestations with a subacute infection of C. haaemolyticum?
fever, jaundice, anorexia, abdominal pain, rapid deep breathing, decrease milk production, blood in feces
60
how is red water disease diagnosed?
clinical history necropsy- lesions (infarcts) in liver
61
how is C. haemolyticum confirmed?
C. haemolyticum in liver infarction
62
how is red water disease treated?
antibiotic treatment likely ineffective antitoxin
63
how is C. haemolyticum controlled
vaccination seasonal- 1 dose prior to dry season constant protection- semiannual vaccination
64
what is the primary cause of malignant edema- gas gangrene?
clostridium septicum
65
what species has the highest incidence of malignant edema and gas ganrene
cattle and horses
66
where does clostridium septicum occur?
-occurs in soils worldwide -found in both animal and human intestine
67
where can infection occur in clostridium septicum?
contamination of wounds containing devitalized tissue or soil
68
virulence factors of clostridium speticum
ATX- alpha toxin pore forming lethal toxin
69
what can the toxin of C. septicum cause?
local and systemic signs (hematogenous spread of toxin)
70
what are the risk factors of C. septicum
poor hygiene practices traumatic injury
71
what are the general signs of C. septicum
-develop 6-48 hours after predisposition injury of enodspore activation -anorexia, intoxication, high fever, local lesions and reluctance to move
72
what do local lesions look like in C. septicum?
-large amounts of exudate -progressed state: extensive local sloughing of skin -specific form: post mortem gas gangrene
73
how do you diagnose C. septicum
-similar to backleg requires lab conformation- cattle and sheep -caution: active postmortem invader -PCR- direct ID and differentiation of clostridia
74
before confirmation of anaerobic culture C. septicum what do you need to do?
gram stain of fine-needle aspirates may confirm G+ rods
75
diagnosis of C. septicum in horses
immune-mediated hemolytic anemia with clostridial infections
76
what is the treatment for C. septicum
high dose parenteral penicillin, tetracyclines, or broad spectrum antibiotics
77
how does C. novyi type A toxin enter the sheep
young rams butting -breaks in the skin offer an opportunity for endosperm entrance
78
what is the cause of Big Head or swollen head
C. novyi type A TcnA toxin
79
how does C. novyi type A (Big head, swollen head)begin to present in the sheep once infected
begins under the eyes and spreads to head, face, and neck
80
how do you treat big head disease
varies according to text if treatable
81
where is clostridium perfringes type A found?
soil, marine sediment, and GI tract
82
what does clostridium perfringens type A cause
gas gangrene
83
what is the key virulence factor for clostridium perfringens
CPA- alpha toxin -phospholipase; hemolytic; necrotizing
84
clinical manifestations for clostridium perfingens type A
-rapid progression, extensive invasion of damages skeletal muscle tissue -gas production (h2)- subQ crepitation
85
how do you diagnose clostridium perfringens type A
-florsecent antibodies of bacteria -anaerobic isolation and culture
86
treatment for clostridium perfringens type A
penicillin or other broad-spectrum antibiotic administration early in debase
87
how do you control clostridium perfeingens type A
-vaccination- for cattle toxoid A -desgined for cattle; another vaccine for swine -not part of multivalent vaccine
88
what species does paeniclostridium sordellii target and what does it cause
ruminants and horses associated with fatal myositis and hepatic disease
89
what is the toxin associated with paeniclostridium sordellii
TcsL- toxin clostridium sordellii lethal
90
what are clinical manifestations of paeniclostridium sordellii
associated with acute rhabdomyolysis >break down of muscle tissue, leads to release of myoglobin in blood, harmful to kidneys
91
talking specifically about C. perfringens what is specific about their different types of toxins
different toxins are associated with specific diseases in certain hosts
92
what is the mechanism of action for alpha toxin (aka CPA or PLC) toxin of C. perfringens?
zince dependent protease -hydrolyzes phopshaptidylcholine (PC) and sphingomyelin (SM) > leads to production and release of IL-8
93
what is the mechanism of action for C. perfringens beta toxin (CPB)?
pore forming toxin targeting an array of host cells
94
what is the mechanism of action for C. perfringens epsilon toxin (ETX)?
pore forming toxin that bonds lipid reacts in host cell membranes
95
note that CPE is not epsilon toxin
a fact :)
96
what is the mechanism of action for C. pefringens Iota toxin (ITX)?
disrupts host cell actin leading to death of the cell
97
what is the mechanism of action for C. perfirngens CPE (enterotoxin)?
causes pore formation in apical side of epithelial cells > loss of ion homeostasis and apoptosis
98
what is the mechanism of action of C. perfringens NetB (necrotic enteritis toxin B)?
recognizes cholesterol-free regions in cell membranes, forms pores that allow the entry of ions
99
what disease is caused by clostridium perfringens Type A- CPA toxi?
CPA toxin is known to be critical to gas gangrene and gangrenous mastitis -common inhabitants of mammalian microbiota (this complicates diagnosis)
100
what is the most widespread toxoxtype in the environment?
Type A CPA toxin
101
where are infections by C. perfringens TypeB been described (location)?
Middle East, Europe, and South Africa
102
what disease is caused by C. perfringens Type B- (CPA, CPB, ETX toxins)?
-in young lambs up to 14 days old > lamb dysentery -in older lambs may have chronic form of disease > Pine (in UK)
103
what occurs when infection with C. perfringens Type C toxin - (CPA, CPB, some CPE toxins)?
changes to microbiota that lead to overgrowth
104
how is Type C toxin transferred?
transferring to piglets shortly after birth
105
how does type C toxin present in calves?
acute diarrhea, abdominal pain, convulsions, and opisthotonos -death within few days, less server cases can survive
106
how does type toxin present in pigs?
acutely ill within a few days, though less severe can survive -high fatality rate
107
how does type c toxin present in foals
acute dysentary, toxemia, and rapid death
108
how is type C toxin diagnosed?
on necropsy -hemorrahgic enteritis with ulceration of mucosa -intestine has deep blue-purple appearance
109
how is type C toxin treated?
type C antitoxin or antibiotic or both used for piglets less than 2 hours of age
110
how do you control type c toxin?
-vaccination pregnant animals in last third trimester of pregnancy -antitoxin to the newborn if unvaccinated mother
111
what toxin type has most likely caused this?
C. perfringens type C
112
what disease is caused by C. perfringens type D- )CPA, ETX, some CPE toxins) ?
classic enterotoxemia of sheep most commonly
113
what species and age group does type D toxin effect?
-worldwide and any age -most common in lambs from 3-10 weeks or weaned in feed lots
114
what are the virulence factors and pathogenesis of C. perfringens type D- (CPA, ETX, some CPE toxins) ?
ETX is absorbed into blood stream and disseminates -edema and necrotic lesions in brain, lungs, and kidneys
115
what is the effect of colostrum against type D toxin
colostrum contains trypsin inhibitors, blocks the activation of the toxin that (requires trypsin)
116
how do you diagnose C. perfringens type D
-fecal smears with gram + rods -confirmation of ETX gene via PCR on fluid sample
117
how do you control C. perfringens type D toxin
-vaccination -for outbreaks can use antitoxin and revaccinate
118
C. perfingens type F-(CPA and CPE toxin) clinical manifestations and presentation?
-clincal manifestation in dogs and cats -dehydration, fever, and abdominal pain with to without signs of hypovolemic shock (hemorrhage)
119
how do you diagnose type F toxin
large gram + bacilli in feces ELISA for CPE
120
how do you treat type F toxin?
vet commiunity may use metronidazole for any potential susceptible anaerobic infection
121
where is clostridium difficile found?
-in large intestine of healthy and sick animals -resistant spores found wherever animals housed -linked to changes in the intestinal microbiota
122
how is C. difficile spread/where contaminated spores?
massive numbers in feces of antibiotic treated animals
123
what are the two major toxins of C. diff
TcdA and TcdB
124
what do C. difficile TcdA and TcdB cause?
glycosylating toxins indice cytoskeletal changes compromising epithelial barrier -all three toxins disrupt actin cytoskeleton and induce severe inflammatory response
125
how do you diagnose C. diff
fecal PCR for toxin genens -culture is slow and hampered by death of microbe in transport ELISA for toxins TcdA and TcdB
126
what is the treatment for C.diff
metronidazole -resistant strains are fairly common

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