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Bacteriology > Anaerobes > Flashcards

Anaerobes Flashcards

1
Q

Anaerobes

A

Present in the GI tract of mammals
Gram positive and gram negative species
G+ are spore forming (clostridium)
G- are non spore forming
Require anaerobic environment or devitalized tissue for growth
When submitting specimens: use anaerobic transport conditions
Causing abscesses, wound infections, aspiration pneumonia, intra-abdominal infections, bacteremia, enteric infections, toxaemia
Usually localized, often oral and GI tract associated
Spread by direct extension from mucosal surfaces
-transient bacteremia and secondary localization, esp on damaged heart valves
Polymicrobial infections and synergistic relationships
Anerobic infections are mostly endogenous orign

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2
Q

Clostridium

A

Large gram+ rods
Anaerobic
Motile by flagella (except C perfringens)
Rapid multiplication
Endospore producing
Widespread in soil, GI tract of animals and humans and in feces
Powerful toxin producers
Epsilon toxin from perfringens is one of most lethal toxins and considered bioterrorism agent
Classification-mode and site of action of their potent exotoxins

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3
Q

Neurotoxic clostridia

A

Affect neuromuscular function without inducing observable tissue damage

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4
Q

Histotoxic clostridia

A

Localized lesions in muscle and liver, subsequently causing toxaemia

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5
Q

Enteropathogenic and enterotoxaemia-producing clostridia

A

Infers with protein synthesis in cells

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6
Q

Clostridium: virulence factors and pathogenesis

A

All pathogenic clostridia produce one or more protein toxin or extracellular enzymes
Growth of clostridia in the body required anaerobic conditions
Necrosis is common predisposing factor for and host response to clostridial infection
Necrosis provides an initial opportunity for C to grow
Necrosis is host response for clostridial toxins
Necrosis facilitates rapid spread of infection through body
Pathogenic strains may be present in the intestinal microbiota but only produce disease in defined circumstances
enteropathogenic and enterotoxaemia-producing clostridia

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7
Q

Tetanus

A

Acute, potentially fatal intoxication with neurotoxic clostridia causing spastic paralysis
Widespread in soil and feces
Grown in contaminated wounds
Produced terminal endospores and infection occurs upon entry of spores into traumatized tissue from soil or feces
Production of tetanospasmin, a potent neurotoxin and tetanolysin, a haemolysin destructing tissue

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8
Q

Ascending Tetanus

A

Toxin travels from regional motor nerve in the limb -> tetanus in limbs then spread to other parts [occurs in less susceptible animals]

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9
Q

Descending Tetanus

A

Toxin in the blood stream affects motor nerve centers in the head and neck and then spread to the limbs [occurs in susceptible species]

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10
Q

Tetanus: diagnosis

A

Incubation period between 5 and 10 days
Latent tetanus: when wound at the site of infection is healed
CS: stiffness, localized spasms, altered heart and respiratory rates, dysphagia
Culture unrewarding and toxin in serum or tissue difficult to find
Animals that recover are not necessarily immune bc toxin could have been below threshold required to stimulate production of neutralizing antibodies

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11
Q

Tetanus: Tx

A

Antitoxin: administered promptly to neutralize unbound toxin (intravenously or into subarachnoid space) -> provides quick but short term protection
Anti-tetanus equine serum (intramuscular/intravenously)
Toxoid: inactive vaccine to promote active immune response (subQ/intramuscular)
Large doses or penicillin: kill toxin-producing vegetative cells of C tetani in lesions
Surgical debridement of wounds and flush with hydrogen to produce aerobic conditions
Supportive care: reduce external stimuli, sedatives, muscle relaxants

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12
Q

Tetanus: control

A

Toxoid immunization (human, horses, small ruminants)
Post exposure prophylaxis via a toxoid booster (human, horses)
Prompt wound management and rational antimicrobial therapy
Aseptic techniques while surgery
Proper sterilization of surgical instruments
Disease associated with toxins -> immunization with toxoids (inactive toxins) because of great susceptibility and widespread presence of C. tetani in the intestine and manure of horses all must be immunized
People working with farm animals should also be vaccinated

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13
Q

Tetanus: vaccine preventable

A

Rapid case identification and prompt administration of tetanus toxoid
Importance of surveillance: tetanus is preventable, so the possibility of failure to vaccinate should be investigated in every case
Promote awareness, provide feedback, review case data

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14
Q

Botulism

A

Serious, potentially fatal intoxication by ingestion of pre-formed neurotoxin (food intoxication)
Diverse group of neurotoxic clostridia (toxin types A-G) and toxin type determines species affinity
Germination of endospores with growth of vegetative cells and toxin production in rotting carcasses, decaying vegetation and contaminated canned foods
Toxin absorbed from GI tract and distributed in bloodstream
Occasional toxico-infectious wounds (spored germinate in wounds, uncommon in animals)
Botulism toxin most powerful exotoxin (1ug kills a person) and inhibits neurotransmitter release causing flaccid paralysis
Toxins in variety of sources including decaying vegetable matter, meat fish, carcasses, invertebrates

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15
Q

Difference btwn tetanus and botulinum toxin:

A

Tetanus toxin travels up the nerve axon to the ventral horn of spinal cord
Botulinum toxin remains at the neuromuscular junction

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16
Q

Botulism in aquatic bird

A 
Toxin production takes place in decaying animal carcasses
maggots concentrate toxins
toxic maggots ingested
death and additional toxin production
major die off bc cycle accelerates
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17
Q

Botulism in humans

A 
Foodborn botulism (rare but fatal; ingestion of toxins formed in contaminated foods)
Wound botulism (needles)
Infant botulism (spore-contaminated honey)
Inhalation botulism (rare and does not occur naturally)
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18
Q

Botulism: diagnosis

A

CS develop 3-17 d after ingestion of toxin
CS: dilated pupils
-dry mucus membranes and decreased salivation
-tongue flaccidity and dysphagia
-paralysis of respiratory muscles > abdominal breathing
Demonstration of toxin in serum of animal
Demonstration of toxin in food and stomach contents
C botulinum and toxins are select agents

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19
Q

Botulism: control

A

Toxoid vaccination of cattle in endemic regions in south africa and australis
Routine vaccination of farmed mink and foxes
Suspect foodstuffs should not be fed to domestic animals
Avoid feeding and eating suspect foodstuffs
Preparation and preservation of feed and food

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20
Q

Blackleg in cattle and sheep

A

Acute exogenous infections with necrotizing myositis caused by histotoxic clostridia C chauvoei
Cattle: mainly young animals (3m-2y) sheep of any age
Exogenous infections occur through wounds > anaerobic environments > deposition of endospores, germination and multiplication -> toxins cause tissue destruction
Fermentation of muscle glycogen -> gas accumulation (hydrogen/methane) > metabolic end products (organic acids, amines) with distinctive smell
Death with toxemia and bacteremia in 24h
Affects large muscle masses: limbs, back and neck
Acute, febrile, highly fatal disease with emphysematous swelling and necrotizing myositis
100% fatality

21
Q

Blackleg in cattle and sheep: CS

A

characteristic edematous swellings with crepitation due to gas accumulation
Lameness (affected muscles in hip shoulder, chest, back and neck)
Myocardium and diaphragm can also be affected

22
Q

Malignant Oedema, Gas gangrene

A

Exogenous, necrotizing, soft tissue (wound) infections caused by histotoxic clostridia C. novyi type A, B and C. hemolyticum
Deep “anaerobic” traumatic wounds
Characterized by rapid gas formation and toxemia
Clinically detectable as subcutaneous crepitation
Prevention of malignant oedema is by surgical tx of serious wounds to remove necrotizing muscle tissue and contaminating materials, and to promote drainage and if necessary provide prophylaxis with penicillin

23
Q

C. novyi type A

A

Exogenous
gas gangrene
Big head in rams

24
Q

C. novyi type B

A 
Endogenous 
black disease (infectious necrotic hepatitis)
Predisposed by fluke damage
25
Q

C hemolyticum

A

Endogenous
Liver damge
Bacillary hemoglobinuria
Mainly in cattle and sheep

26
Q

Malignant oedema, braxy

A

Braxy: abomasitis of sheep caused by exotoxins of C septicum
Malignant edema: exogenous infection through wounds or endogenous through dormant spores present in muscle tissue
Risk factors: IM injections, shearing, docking, lambing, traumatic parturition and castration
Local exotoxins -> excessive inflammation and myositis ->edema, necrosis, gangrene

27
Q

Histotoxic clostridia: Dx, Tx, Control

A

Direct fluorescent antibody stainign tests
Anaerobic cultures are time consuming, not easy nor rewarding
Tx: antimicrobial tx (penicillin)
Control: routine vaccination of farm animals with multicomponent toxoids

28
Q

Enteropathy

A

Pathology of the intestine

29
Q

Enterotoxaemia

A

Absorption of large number of toxins -> localized and generalized effects

30
Q

C. perfringens

A

Classified in biotypes A-E based on presence and combo of toxins
4 major toxins: Alpha, beta, iota, epsilon
Alpha produced by all strians
Enterotoxin present in all strains cytotoxic
Found in soil, feces and intestinal tract of animals and humans
types B, C, D survive in soil as spores
Predisposing factors to clostridial proliferation in intestinge(multifactorial disease)
Inappropriate husbandry
Sudden dietary changes
local environmental influences

31
Q

Necrotizing hemorrhagic enteritis

A

In multiple species of animals

Can suddenly die without signs

32
Q

Lamb dysentery

A

Caused by type B (toxins alpha, beta, epsilon)
Abdominal distension, pain, blood-stained feces, sudden death
Factors predisposing to enterotoxaemias in sheep
-low proteolytic activity in neonatal intestine: presence of trypsin inhibitors in colostrum (Beta toxins sensitive to trypsin digestion); low levels of pancreatic secretion
-Immature intestinal microbiota
-dietary influences in older animals: abrupt change to rich diet; gorging on energy-rich diet; intestinal hypomotility (overeating)

33
Q

Pulpy kidney disease, over-eating disease

A

Type D enterotoxaemia in lambs (3-10 w of age)
Predisposing factors: gorging on a high grain diet or succulent pasture
Ingestion of excessive amounts -> carry-over of partially digested food from rumen into intestine -> high starch content = substrate for rapid clostridial proliferation
Production of epsilon toxin: activated by proteolytic enymes -> toxaemia

34
Q

Pulpy kidney disease, over-eating disease: CS

A

Focal symmetrical encephalomalacia -> dullness, convulsions, terminal coma
Hyperglycaemia and glucosuria
Post mortem: fluid distended intestine with petechial hemorrhage on serosal surfaces
Rapid kidney autolysis -> pulpy cortical softening

35
Q

C. perfringens infections: Dx

A

CS- sudden deaths in groups of unvaccinated animals; post mortem findings
Staining and microscopic examination
Anaerobic culture to determine biotype of isolates
Toxin detection in intestinal contents (biological mouse assays, serological tests)

36
Q

C. perfringens infections: Tx

A

hyperimmune serum (if available and given early)

37
Q

C. perfringens infections: control

A

routine immunization of farm animals with toxoid

Avoid predisposing factors (sudden dietary changed or stress that impacts intestinal microbiota)

38
Q

C. difficile enterocolitis

A

Affects colon and cecum of humans, horse, pig, dog, car, lab rodent etc
Risk factors: antibiotic use, old age, hospitalization
Neonates are resistant but may carry toxigenic strains
Endospores are widespread but low numbers in normal intestine
Disease results from dysbiosis, proliferation of C difficle and toxin production
Tox A enterotoxin: diarrhea and mucosal tissue damage
tox B cytotoxin
Most strains produce both toxins which act together
Nosocomial transmission may occur
Produces often fatal colitis in humans, hamsters, horses, swine given broad spectrum ABs which destroy normal microbial flora and allow c diff to proliferate
damages cells, triggering inflammation and fluid buildup
cells burst and die

39
Q

C. difficile enterocolitis: diagnosis

A

Culture
- obligate anaerobes
-vegetative cells sensitive to handling and tx
-selective media for germination of spores
Direct toxin detection
-tissue culture assay with specific antibody neutralization (toxin B): gold standard test
-Toxin antigen detection (ELISA, agglutination)

40
Q

C. difficile enterocolitis: treatment

A

Supportive electrolytes and fluids
Stop ABs if possible
Horses: clindamycin is a significant RISK factor for AB induced cdiff acute diarrhea and colitis
Administration of probiotics
Avoid antidiarrheals bc these may result in accumulation of toxins
Fecal microbial transplantation=transfer stool from healthy donor into GI

41
Q

Enterotoxaemia and explosive diarrheal disease in rabbits

A

in rabbits 4-8 wks old
Commensal bacterium C spiroforme which produces iota toxin
Fluid distended intestine with hemorrhage and serosal surface
Lincomycin, clindamycin and erythromycin induce clostridium-related enterotoxemia due to their selective effect on G+ bacteria as part of normal microbiots
These antimicrobials are contraindicated in rabbits

42
Q

Tyzzers disease

A

G- clostridium piliforme
Acute fatal diarrheal disease of lab animals with associated focal liver necrosis
CS: watery diarrhea, anorexia, dehydration, lethargy, death
Associated with poor sanitation and stress
Tx: oxytetracycline
Prevention: disinfection and decontamination

43
Q

Gram negative non-spore forming anaerobes

A

Characteristically, non-spore forming bact found in mixed bacterial infections involving breaks in mucosal or epithelial barriers
Any chronic infection, particularly where extensive purulence or necrosis is present, may contain anaerobic bacteria

44
Q

Foot rot, Necrotic laryngitis, liver abscesses

A

G- anaerobic Fusobacterium necrophorum
Commensal in respiratorym intestinal and genital tract of animals
Synergistic with Trueperella pyogenes and Dichelobacter nodosus

45
Q

Foot rot: diagnosis

A

CS

Anaerobic culture, PCR

46
Q

Foot rot: Tx

A

Remove necrotic tissue
Dip in antiseptic foot baths
Antimicrobials: penicillin, metronidazole, clindamycin, chloramphenicol
Aminoglycosides and sulfonamides are not effective

47
Q

Foot rot: Control

A

Keep feet dry
Avoid mechanical injury
Vaccination (sheep and cattle)

48
Q

Mastitis in dairy cattle: contagious

A

Pathogens that cause mastitis tend to live on/in the cows udder and teat skin and transfer from affected cow to unaffected cow during milking
They adhere easily to skin, colonize the teat and multiply in teat canal

49
Q

Mastitis in dairy cattle: environmental

A

Pathogens present in housing and bedding and can transfer during milking or between milking when cow is loafing, eating or lying down
These environmental pathogens do not generally possess the same ability as contagious pathogens to adhere to and colonize the teat

Bacteriology (12 decks)

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