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Bacteriology > Gram positive anaerobes > Flashcards

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
Q

Modes of infection of botulism

A

-Ingest preformed toxin-> intoxication not infection
-Produce toxin in gut-> toxico infection

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26
Q

Botulism Toxigenic types that affect animals

A

C and D

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27
Q

C. botulinum morphology

A

Subterminal spores

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28
Q

Botulism toxin

A

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

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29
Q

Animals more susceptible to botulism

A

-Chickens
-Cattle
-Sheep
-Goats
-Horses

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30
Q

Botulism in birds

A

-Limberneck
-Western bird disease

31
Q

Botulism in horses

A

-Forage poisoning
-Wound botulism
-Shaker foal syndrome

32
Q

Shaker foal syndrome

A

affects 2-8wks
-tremors

33
Q

Botulism in cattle

A

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
Q

Visceral botulism

A

In cattle
-get growth in intestinal tract and make toxins
-Looks like a typicall infections

35
Q

Clinical signs of visceral botulism

A

-Indigestion
-Laminitis chronic
-Edema of ventral abdomen

36
Q

iagnosis of botulism

A

Clinical signs : flaccid paralysis
-Isolate and PCR
-ELISA to identify the toxins

37
Q

Prevention of botulism

A

-Cook foods
-Good husbandry
-Dispose of carcasses
-Avoid spoiled feeds
-Phosphorus supplementation
-Vaccination

38
Q

Botulism in humans

A

-Food borne botulism (most common)
-Infant botulism
-Wound infection

39
Q

Dysautonomia

A

Degenerative neuropathy affecting autonomic nervous system. Seen mostly in outdoor dogs. Suspect botulinum toxin

40
Q

Clinical signs of dystautonomia

A

Vomiting
-inappetance
-No lacrimation or PLR
Protuding nictitating membrane
-Loss of anal sphincter function

41
Q

Diagnosis of Dysautonomia

A

-Dilute pilocarpine

42
Q

C. Perfringens

A

Double zone hemolysis with Theta and alpha toxin

43
Q

Habitat of C. perfringens

A

-Soil
-GI tract
-Postmortem invader of tissues

44
Q

C. perfringens types

A

A-G
-All produce alpha toxin
F-foodborne gastroenteritis
G- problem in chickens
A,C, D, and G important for animals

45
Q

Which toxins cause necrosis

A

Beta and NetB

46
Q

Other toxins in C. perfringens

A

Perfringolysin-pore forming hemolysin involved in gas gangrene

47
Q

Enterotoxemia

A

Describe systemic spread of C. perfringens toxins. Prefer to call necrotic enteritis because most the time it is confined to the intestines alone

48
Q

Type A infections

A

Gas gangrene
-Necrotic enteritis
-abomasal bloat and ulcers
-hemorrhagic bowel syndrome
-Yellow lamb disease
-Gangrenous dermatitis in chickens

49
Q

Type C infections

A

-Necrotic enteritis in many animals
-Struck

50
Q

Type D infections

A

-Enterotoxemia
-Necrotic enteritis

51
Q

Type A infection virulence factors

A

-Alpha toxins: hemolysin

52
Q

Yellow lab disease

A

In nursing lambs in the spring
-Alpha toxin enters blood and causes hemolysis

53
Q

Clinical signs of yellow lamb disease

A

Acute onset anemia
-dyspnea
-hemoglobinuria
-icterus
-Enlarged spleen

54
Q

Abomasal bloat and ulcers

A

Neonatal calves, lambs, and goats
-Copper or selenium deficiencies predisposing factors

55
Q

Clinical signs of abomasal bloat and ulcers

A

Acute onset
-anorectic
-Abdominal bloat and discomfort
-Gas
-Hemorrhage
-Coffee ground lesions

56
Q

Treatment of abomasal bloat and ulcers

A

-Tetracyclines
-Monensin
-0.1% formalin in milk replacers
-Type A toxoid vaccine

57
Q

Sarcina ventriculi

A

Gram positive anaerobic cocci
-Produces gas
-Survive acidic pH of abomasum
-May have a role in abomasal bloat

58
Q

Hemorrhagic bowel syndrome

A

Primarily dairy cows
-Intraluminal hemorrhage or submucosal hematoma in jejunum

59
Q

Clinical signs of hemorrhagic bowel syndrime

A

-Abdominal pain
-Inappetance
-Weaness
-Drop in milk production
-Scant feces
-Abdominal distension
-Death

60
Q

Gangrenous dermatitis clinical signs

A

-Depression
-Incoordination
-Weakness
-Inappetence
-Ataxia
-Skin edematous with or without gas and necrotic

61
Q

Pathogenesis of Type C infections

A

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
Q

Clinical signs of Type C infection

A

-Depression
-Hemorrhagic
-Diarrhea
-Death
-In really young animals
-Hemorrhagic inflammation of jejunum and ileum
-Necrosis with gas of mucosa and submucosa

63
Q

Epsilon toxin

A

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
Q

Pulpy Kidney disease

A

Sheep and goats on high grain diets
-Overgrowth of C. perfringens-> epsilon toxin major virulence factor

65
Q

Clinical signs of pulpy kidney disease

A

-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
Q

Foodborne enteritis from C. Perfringens

A

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
Q

Necrotic enteritis in chickens and turkeys

A

Type G
Two forms:
-Acute-death
-Subacute- diarrhea and slow growth

68
Q

Necrotic enteritis lesions in chickens and turkeys

A

Jejunum and ileum
-Coagulative necrosis
-Yellow/green pseudomembrane
-Contents dark brown or yellow green
-Thickened intestinal wall

69
Q

Diagnosis and treatment of necrotic enteritis in chickens and turkeys

A

-PCR for netB
-Lincomycin
-bacitracin
-Oxytet
-No vaccine

70
Q

Vaccines for clostridium

A

-Either bacterins or toxiod

71
Q

Ulcerative enteritis

A

Qual disease Clostridium colinum

72
Q

Mode of infection of C. colinum

A

-Oral
-Infection of GI tract
-Get in blood to the liver
-Diffuse necrosis

73
Q

Tyzzer’s disease

A

Clostridium piliforme
(stains gram negative)
-Rods and heavily fimbriated

74
Q

Pathogenesis of C. piliforme

A

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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