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Gram positive anaerobes Flashcards

1
Q

Spore forming

A

Clostridium and clostridiodes

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2
Q

Non spore formers

A

Actinobaculum

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3
Q

Clostridium

A

Motile, ferment CHO and proteins and products have a putrid odor

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4
Q

Habitat of clostridium

A

Ubiquitous in soil and alimentary tract

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5
Q

Mode of infection of clostridium

A

-Ingestion with feed and water
-Wound contamination
-Not contagious
-Need Oxygenfree environment

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6
Q

Clostridiodes difficile

A

Major human pathogen but see in animals. Causes enterocolitis in animals. Based on 16S rRNA not clostridium

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7
Q

Group I Neurotoxigenic clostridia

A

-C. tetani
-C. botulinum

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8
Q

C. tetani toxins

A

Tetanolysin (hemolytic, causes tissue necrosis) and tetanospasmin (neurotoxin)

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9
Q

C. botulinum toxins

A

Botulinum (neurotoxin)

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10
Q

Group II enterotoxigenic clostridia

A

-Perfringens
-Colinum
-piliformis
-Spiroforme

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11
Q

Group III histotoxic clostridia

A

-Haemolyticum
-Noyvi
-Chauvoei
-Septicum
-Serdelli
-Villosum

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12
Q

C. tetani morphology and habitat

A

Gram positive rod with terminal spore. Like a match stick. In the soil and intestinal tract

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13
Q

Mode of infection of tetanus

A

-Wound contamination
-Nail wounds
-Castration and doxking tails
-Umbilicus
-Castration, dehorning, nose ringing etc

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14
Q

How soon do you see clinical signs after infection of tetanus

A

1-3weeks

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15
Q

Mechanism of action of tetanospasmin

A

BInds to ganglioside receptors on nerve cells and blocks the release of NT GABA and glycine in CNS resulting in spastic parallysis

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16
Q

Pathogenesis of tetanus ascending tetanus

A

-Enters wounds as spores or vegetative cells and start to grow.
-Start making toxins and those move along axon fibers to spinal cord (ascending tetanus)
-First see regional muscles affected

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17
Q

Animals most susceptible to tetanus

A

Horses and cattle for food animals

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18
Q

Clinical signs tetanus

A

-Stiff gait, difficulty walking
-Third eyelid prolase
-Lockjaw and drooling
-Stiffness of head, neck, ears, extremities and tail
-Dehydration

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19
Q

Generalized tetanus signs

A

-Regurgitation
-Drooling
-Exaggerated response to external stimuli
-Opisthotonous
-Risus sardonicus
-Convulsions

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20
Q

Descending or generalized tetanus

A

-THen enters lymphatic and blood
-Affects nerve centers of face and neck then limbs (descending tetanus, generalized)
-Die from respiratory failure

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21
Q

Diagnosis of tetanus

A

-Clinical signs and history see site of infection
-Smear from site of infection to see drum stick
-PCR fto confirm
-Toxin demonstration

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22
Q

Treatment of tetanus

A

-Wound debridement and topical antibiotics (penicillin)
-Tetanus antitoxin
-Sedation and muscle relaxation therapy
-Keep in dark quiet place

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23
Q

Prevention of tetanus

A

-Toxoid effective for a year
-Vaccinate horses before surgery
-Passive immunization with tetanus antitoxin
-Skin and instrument disinfection

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24
Q

Causes of botulism

A

C. botulinum, C. butyricum, and C. barati

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25
Modes of infection of botulism
-Ingest preformed toxin-> intoxication not infection -Produce toxin in gut-> toxico infection
26
Botulism Toxigenic types that affect animals
C and D
27
C. botulinum morphology
Subterminal spores
28
Botulism toxin
A-B toxin -Enter blood, and binds to ganglioside receptors at neuromuscular junctions -Internalized in nerve cell and blocks Ach release and produces flaccid paralysis
29
Animals more susceptible to botulism
-Chickens -Cattle -Sheep -Goats -Horses
30
Botulism in birds
-Limberneck -Western bird disease
31
Botulism in horses
-Forage poisoning -Wound botulism -Shaker foal syndrome
32
Shaker foal syndrome
affects 2-8wks -tremors
33
Botulism in cattle
Lamziekte or loin disease -Chew on bones and flesh in P deficient areas and ingest toxin in the flesh -Silage -Main symptom is the tongue hangs out
34
Visceral botulism
In cattle -get growth in intestinal tract and make toxins -Looks like a typicall infections
35
Clinical signs of visceral botulism
-Indigestion -Laminitis chronic -Edema of ventral abdomen
36
iagnosis of botulism
Clinical signs : flaccid paralysis -Isolate and PCR -ELISA to identify the toxins
37
Prevention of botulism
-Cook foods -Good husbandry -Dispose of carcasses -Avoid spoiled feeds -Phosphorus supplementation -Vaccination
38
Botulism in humans
-Food borne botulism (most common) -Infant botulism -Wound infection
39
Dysautonomia
Degenerative neuropathy affecting autonomic nervous system. Seen mostly in outdoor dogs. Suspect botulinum toxin
40
Clinical signs of dystautonomia
Vomiting -inappetance -No lacrimation or PLR Protuding nictitating membrane -Loss of anal sphincter function
41
Diagnosis of Dysautonomia
-Dilute pilocarpine
42
C. Perfringens
Double zone hemolysis with Theta and alpha toxin
43
Habitat of C. perfringens
-Soil -GI tract -Postmortem invader of tissues
44
C. perfringens types
A-G -All produce alpha toxin F-foodborne gastroenteritis G- problem in chickens A,C, D, and G important for animals
45
Which toxins cause necrosis
Beta and NetB
46
Other toxins in C. perfringens
Perfringolysin-pore forming hemolysin involved in gas gangrene
47
Enterotoxemia
Describe systemic spread of C. perfringens toxins. Prefer to call necrotic enteritis because most the time it is confined to the intestines alone
48
Type A infections
Gas gangrene -Necrotic enteritis -abomasal bloat and ulcers -hemorrhagic bowel syndrome -Yellow lamb disease -Gangrenous dermatitis in chickens
49
Type C infections
-Necrotic enteritis in many animals -Struck
50
Type D infections
-Enterotoxemia -Necrotic enteritis
51
Type A infection virulence factors
-Alpha toxins: hemolysin
52
Yellow lab disease
In nursing lambs in the spring -Alpha toxin enters blood and causes hemolysis
53
Clinical signs of yellow lamb disease
Acute onset anemia -dyspnea -hemoglobinuria -icterus -Enlarged spleen
54
Abomasal bloat and ulcers
Neonatal calves, lambs, and goats -Copper or selenium deficiencies predisposing factors
55
Clinical signs of abomasal bloat and ulcers
Acute onset -anorectic -Abdominal bloat and discomfort -Gas -Hemorrhage -Coffee ground lesions
56
Treatment of abomasal bloat and ulcers
-Tetracyclines -Monensin -0.1% formalin in milk replacers -Type A toxoid vaccine
57
Sarcina ventriculi
Gram positive anaerobic cocci -Produces gas -Survive acidic pH of abomasum -May have a role in abomasal bloat
58
Hemorrhagic bowel syndrome
Primarily dairy cows -Intraluminal hemorrhage or submucosal hematoma in jejunum
59
Clinical signs of hemorrhagic bowel syndrime
-Abdominal pain -Inappetance -Weaness -Drop in milk production -Scant feces -Abdominal distension -Death
60
Gangrenous dermatitis clinical signs
-Depression -Incoordination -Weakness -Inappetence -Ataxia -Skin edematous with or without gas and necrotic
61
Pathogenesis of Type C infections
See in healthy animals -See increased feed intake -Gut stasis -Overgrowth of bacteria and production of toxins -Toxin may or may not be absorbed -Acute illness and death
62
Clinical signs of Type C infection
-Depression -Hemorrhagic -Diarrhea -Death -In really young animals -Hemorrhagic inflammation of jejunum and ileum -Necrosis with gas of mucosa and submucosa
63
Epsilon toxin
Third most potent clostridial toxin -Must be activated by trypsin -Enhances intestinal permeability -Rapid absorption of toxin -Affects CNS and other organs -Get perivascular edema, foci of necrosis, and hemorrhage in meninges
64
Pulpy Kidney disease
Sheep and goats on high grain diets -Overgrowth of C. perfringens-> epsilon toxin major virulence factor
65
Clinical signs of pulpy kidney disease
-Sudden death -Neurological signs precede -Dullness -Blindness -Ataxia -Convulsion -Hemorrhage and foci of necrosis on meninges and other serosal surfaces -Kidney: hyperemia and degenerative changes
66
Foodborne enteritis from C. Perfringens
Type F (third most common) Grows in food-> sporulates in stomach-> produces enterotoxin in SI-> signs 8-12hr after ingestion Diarrhea, cramps, self limiting infections
67
Necrotic enteritis in chickens and turkeys
Type G Two forms: -Acute-death -Subacute- diarrhea and slow growth
68
Necrotic enteritis lesions in chickens and turkeys
Jejunum and ileum -Coagulative necrosis -Yellow/green pseudomembrane -Contents dark brown or yellow green -Thickened intestinal wall
69
Diagnosis and treatment of necrotic enteritis in chickens and turkeys
-PCR for netB -Lincomycin -bacitracin -Oxytet -No vaccine
70
Vaccines for clostridium
-Either bacterins or toxiod
71
Ulcerative enteritis
Qual disease Clostridium colinum
72
Mode of infection of C. colinum
-Oral -Infection of GI tract -Get in blood to the liver -Diffuse necrosis
73
Tyzzer's disease
Clostridium piliforme (stains gram negative) -Rods and heavily fimbriated
74
Pathogenesis of C. piliforme
Invades intestinal epithelial cells -Enteritis -Colitis -Hepatitis -Necrosis -In horses (Lethargy, fever, seizures, death in 1-4wk old foals)

Bacteriology (29 decks)

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