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Bacteriology > Clostridium Clostridioides > Flashcards

Clostridium Clostridioides Flashcards

1
Q

Characteristics

A

-biocontainment level 2 (except C. botulinum is level 3 where lab work can generate aerosols)
-gram positive, spore forming rods (not all species stain well)
-anaerobes (variably tolerant of O2)
-produce toxins!

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2
Q

Strict anaerobes

A

Clostridium haemolyticum and Clostridium novyi

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3
Q

Less fussy anaerobes

A

Clostridioides difficile, Clostridium perfringens

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4
Q

Clostrodium perfingens appearance

A

-gram positive, boxcar morphology

-2 zones of hemolysis on blood agar

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5
Q

Clostridium tetani appearance

A

-Presence of terminal spores= drumstick

-long flagella under special staining

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6
Q

Natural host or habitat of Clostridium and Clostridioides

A

-wide distribution
-found in environment (water and soil)
-many species part of normal microbiota such as in feces

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7
Q

Taxonomy of C. tetani

A

Differentiated from other species because of the presence of terminal spores

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8
Q

Virulence factors

A

TOXINS

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9
Q

Neurotoxic species

A
  1. Clostridium tetani= tetanus
  2. Clostridium botulinum= botulism (flaccid paralysis)
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10
Q

Histotoxic species

A
  1. Clostridium chauvoei= cattle- blackleg
  2. Clostridium septicum= large animals- malignant edema
  3. Clostridium novyi= sheep/cattle- necrotic hepatitis
  4. Clostridium perfringens= gangrene
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11
Q

Enterotoxin species

A
  1. Clostridium perfringens
    -Bloody diarrhea in lambs, pigs, chickens, humans
    -pulpy kidney disease in sheep
    -Acute hemorrhagic diarrhea syndrome in dogs and horses
  2. Clostridium piliforme- Tyzzer’s disease in horses
  3. Clostridium spiroforme in rabbits= antibiotic induced typhlocolitis
  4. C. difficile
    -pigs= scours, mesocolonic diarrhea
    -humans- natibiotis associated diarrhea
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12
Q

Clostridium tetani

A

Natural habitat: soil contaminated with feces

-Organisms enter through breaks in skin (stepping on rusty nail, fecal contamination of umbilicus, tail docking) Then organism will multiply in necrotic tissues

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13
Q

C. tetani presentation

A
  1. Production of toxins which disseminate from focus of infection
    -Tetanolysin enhances tissue invasion
    -Tetanospasmin causes spasms of both flexor and extensor muscles
  2. Results in spasmodic paralysis. Toxin causes extreme muscle stiffness
    -ex. Lockjaw; risus sardonicus (sardonic smile)
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14
Q

Treatment for tetanus

A

High dose penicillin and tetanus anti-toxin

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15
Q

Clostridium botulinum in environment

A

-widely present in soils and aquatic environment
-Botulism toxin is produced when spores germinate in anaerobic environments
-Toxin prevents the release of Ach at neuromuscular junction= flaccid paralysis

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16
Q

Clostridium botulinum spores

A

Extremely resistant
-survive boiling
-recommended to use pressure canner (autoclave) for home canning

Exposure: ingestion

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17
Q

Steps of C. botulinum in birds

A
  1. Spores on lake bottom
  2. Birds eat detritus or invertebrates from lake bottom
  3. Become intoxicated
  4. Results in droopy necks= drowning or respiratory failure
  5. Carcasses eaten by maggots
  6. Toxin laden maggots eaten by birds
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18
Q

Five forms of botulism

A
  1. Foodborne- eat foods with toxin (home canned food)
  2. Wound botulism-infection; occurs in IV drug users
  3. Infant botulism-replication of toxin in intestines and release of toxin (no honey for babies)
  4. Adult intestinal toxemia- colonization of gut similar to infant
  5. Latrogenic botulism- used in medical procedures and accidentally goes elsewhere
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19
Q

Treatment of C. botulinum

A
  1. Antibiotics used when animals have infection , not when they are intoxicated
  2. Can give antitoxin
  3. Supportive therapy
    - Respiratory ventilation
    -stool softeners, soft bedding to prevent bed sores
  4. Vaccination possible (horses)
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20
Q

Clostridium chauvoei

A

-causes blackleg
-organism is common in the environment and feces
-cattle or sheep ingest endospores which pass through body without incident but sometimes get stuck into hindquarters and cardiac muscle
-Disease occurs when spores germinate due to low O2 levels

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21
Q

Why does sporulation occur in C. chauvoei?

A

Relatively unknown
-could be due to injury (vaccination, bumping into something) which causes damage and results in locally anaerobic environment

22
Q

Acute febrile disease

A

-lameness
-sudden death (necrotizing myositis and systemic toxemia)
>crepitation (due to gas production), dark red muscle (black, spongy, rancid)
-often find with affected leg up

23
Q

Treatment of C chauvoei

A

**typically not practical or possible

Can try penicillin and surgical debridement of affected tissues

24
Q

C. septicum

A

-typically from soil
-affects large animals of all ages and causes malignant edema

25
Q

C. septicum presentation

A
  1. Infection occurs following a deep puncture + trauma
    -outbreaks may occur after group procedures (ie. tail docking)

2.May result in acute fatal toxemia
-production of necrotoxins causing edema and gangrene

  1. Lesion at site of infection, edema at other body sites
26
Q

Treatment of C. septicum

A

-high dose penicillin systemically and injected around primary lesion

-Can also use antitoxin but very expensive

27
Q

Control of C. septicum

A
  1. Hygiene when performing invasive procedures (ex.docking)
  2. vaccination
28
Q

C. septicum in people

A

-Rare
-infections are fatal
-associated with colon carcinoma

29
Q

C. novyi type B

A

-occurs in sheep (well nourished), cattle, and rarely in pigs and horses
-acquired from environment, fecal contamination by carrier of pasture plays a role
-causes acute, necrotic hepatitis (animals are usually found dead)

30
Q

Mechanism of C. novyi type B

A

Spores reach liver hematogenously, germinate with necrotic insult and release alpha toxin
»disease associated with liver flukes (Fasciola hepatica) or liver trauma

31
Q

Treatment and control of C. novyi type B

A

Treatment: none

Control: Vaccination and control of inciting causes such as liver fluke

32
Q

TOXIN SLIDE??

A
33
Q

Type A C. perfringens

A

-most widespread toxinotype
-found in the guts of both healthy and diseased animals
-Causes enteric diseases, and gas gangrene, and emphysematous abomasitis

34
Q

Type B C. perfringens

A

Lamb dysentery
-high morbidity and mortality, sudden death
-predisposed by abrupt change in diet

-Seen in young because colostrum contains anti-trypsin substances which prevent toxin degradation

35
Q

Type C C. perfringens

A

-causes hemorrhagic enteritis in piglets, and sometimes in calves, foals, lambs
>outbreaks in entire litters
>acute onset, high mortality, death within 24 hrs

-trypsin susceptibility of toxin explains disease predilection for neonates

36
Q

Type G C. perfringens

A

Causes necrotic enteritis in chickens
-acute enterotoxemia
-anorexia, depression, dehydration, ruffled feathers
-sudden death, necrosis of small intestine

37
Q

Type D C. perfringens

A

Over eating disease- associated with gorging on grain or lush pasture
-high starch content stimulates overgrowth of C. perfringens, and the increase in toxin production leads to toxemia

-Results in acute disease in otherwise healthy lambs= pulpy kidney (autolysis resulting in soft renal cortex)

**control by managing diet

38
Q

Type A C. perfringens

A

-NetF producing
-occurs in dogs and horses

Dogs:
-Acute hemorrhagic diarrhea syndrome
-rapid onset
-may include necrotic lesions and frank blood in feces
-mortality rate unknown because diarrhea causes not often brought into vet

Horses:
-Enterocolitis in young foals under 3 days of age

39
Q

Type F C. perfringens

A

-food and water borne; 2nd most common cause of bacterial foodborne illness
-can cause necrotizing intestinal disease= Fire bowels
>associated with foods containing trypsin inhibitors (peanuts, sweet potatoes, casava)

40
Q

C. piliforme

A

-commonly seen in apparently thriving foals and in some rabbits
-animals often found dead or comatose
-disease classically described as multifocal hepatic necrosis, and can find lesions in heart and intestines

41
Q

C. difficile

A

-results in early onset scours, sudden death, mesocolonic edema in pigs

**important differential diagnosis for edema disease from E.coli

42
Q

Enterotoxins from C. difficile

A
  1. Toxin A-enterotoxin, causing fluid accumulation
  2. Toxin B- potent cytotoxin

Results in Colonic dysregulation and cellular death; not all strains are toxigenic (pathogenic)

43
Q

C. difficile in dogs and cats

A

Very little evidence of association with disease in small animals (found in healthy and diarrheic animals)

44
Q

C. difficile in humans

A

Debilitating disease
-antibiotic associated diarrhea

Treatment challenging
-Vancomycin, metronidazole
-Fecal transplants (oral or suppository)

45
Q

Sample collection and handling for C. tetani

A

-gram stained smears revealing drumstick organisms

-classically, serum from affected animal was injected into a mouse to ID circulating neurotoxin

46
Q

sample collection and handling for C. botulinum

A

-Toxicity studies, injecting mice with serum or filtrate of rumen contents

47
Q

Sample collection and handling for C. chauvoei, septicum, and novyi

A

-Culture possible (collect large chunk of tissue to maintain anaerobic center)

-fixed tissues for histology

-fluorescent antibody test for C. chauvoei

48
Q

Sample collection and handling of C. perfringens

A
  1. Culture feces (diarrhea), renal tissue (pulpy kidney disease)
  2. Gram stain= box car cells
  3. ID toxin by PCR
  4. Tissues for histopathology
49
Q

Sample collection and handling for C. difficile

A
  1. Culture feces
  2. ID of toxin by PCR (on fecal samples or on pure cultures)
50
Q

Lab ID

A

-Variety of ID diagnostic available

-Ask lab about how to interpret findings. Ex. Does positive culture indicate an infection or just colonization??

-C. piliforme is not cultureable

51
Q

Zoonosis of C. perfringens

A

-common cause of foodborne illness

52
Q

Zoonosis of C. difficile

A

-can be zoonotically acquired from pigs

Bacteriology (20 decks)

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