Anaerobic Bacteria Flashcards by Trenni Jefferson

Anaerobic gram + bacteria

Clostridium species (spore-forming)

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Anaerobic gram - genera

Dichelobacter (foot rot in cattle and sheep)
Fusobacterium (“… “)
Bacteroides (diarrhea, abortion, mastitis, abscess)

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Clostridia characteristics

Rod, spore-forming
Production of potent extracellular toxins (tetanus and botulism)
Neurotoxic, histotoxic, enterotoxic

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Which organisms are neurotoxins?

C. Botulinum and C. Tetani

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C. Tetani

Obligate anaerobe, spore have a drumstick shaped bacillus
Agent of Tetanus or Lockjaw
High mortality in all animals

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Where is C. Tetani found?

Soil and digestive tracts of all animals

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Tetanus

Horses, ruminants and swine most susceptible
Neuropathic intoxication due to neurotoxin and tetanospasm
Tonic- clonic convulsions and spastic paralysis

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Portal of entry to C. Tetani

Penetrating wounds or abrasions, surgical incisions, docking, injection site, postpartum lesions, etc.
Deep wounds and necrosis provide the reduced O2 microenvironment

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C. Botulinum

Obligate anaerobes, sub-terminal oval spores
1 ug can kill a person
Causes botulism

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Where is C. Botulism found?

Soil, plants growing on contaminated soil
Animals carcasses and rotting vegetation

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Botulism

Neuropathic intoxication with flaccid paralysis
Seen in ruminants, horses, waterfowl’s, mink

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Intoxication botulism

When toxins ingested:
Animals with pica (phosphorus-deficient lame) ingest animals bones
Invertebrate larvae ingests BoNT from animals carcasses then consumed by birds
Birds consume toxin bearing fish
Poultry litter fed to cows

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Toxicoinfecfion botulism

Produced inside gut of infected animals
Organism multiples in the body and produces BoNT

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C. Tetani and C. Botulinum pathogenesis

Neurotoxins inhibit NT release in the CNS and peripheral NS (respectively) by cleaving vesicle fusion proteins

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Tetanus pathogenesis

Toxin produced at wound site
Ascending: toxin travels along motor nerves to CNS where it acts on spinal inhibitory inter neurons
Descending: toxin disseminated through circulation

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Botulism pathogenesis

Toxin absorbed from stomach and and distributed via blood —> receptor- mediated endocytosis @ myoneural junction —> hydrolysis of docking proteins —> flaccid paralysis

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Common names of botulism

Horses: equine grass sickness, forage poisoning
Birds: limberneck
Babies: floppy baby syndrome

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Tetanus diagnosis

Gram stain smear
Culture from wound exudate in BA + antitoxin
PCR for TeNT gene

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Tetanus treatment

Injection for antitoxin (passive)
Toxoid for active immunization. (TeNT + formalin/ heat)

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Botulism diagnosis

Organism isolation from feed or tissue and culture on BA
PCR to amplify BoNT genes
ELISA for toxins/ ABs detection

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Botulism treatment

Supportive
Injection of antitoxin
Prevention by toxoid vx

Histotoxic clostridia

C. Septicum, chauvoei, novyi

Histotoxic clostridia general features

From soil or endogenous source
Entry gained through trauma
Bacteria multiple locally, produce toxins, cause tissue damage and rapid death

Commons features of all histotoxic clostridia species

Gas grangene and malignant edema

__________ can occur after C. hemilyticum and C. Perfringens infections

Hemolysis

C. Septicum

Obligate short rod anaerobe, motile Leading cause of wound infections in farm animals Malignant edema, gas gangrene and enteric infections

Malignant edema/ gas gangrene of C. Septicum

Initially painful, warm lesions, crepitant and necrosis

Enteric infection in sheep and cattle infected with C. Septicum

Causes braxy/ bradspot: hemorrhagic necrotic abomasitis from feeding on cold/ frozen feed Dies in 36 hrs

C. Chauvoei

Obligate rod, motile Intestine of cattle, sheep, goats and in soil Causative agent of Blackleg

C. Chauvoei pathogenesis

Dormant muscle-resident spore activated by tissue damage (local anoxia by overexercise)

C. Chauvoei CS

Lameness, crepitating emphysematous myositis, sudden death)

C. novyi

Obligate rod, motile, large oval spore Bacillary Hburia (red water) produced by bacteria colonizing the liver

C. novyi disease

Gas gangrene: big head of young rams from fighting → edema and death (2 days Black disease: infectious necrotic hepatitis of sheep and cattle (liver fluke migration)

Enterotoxic clostridia

C. perfinigens and C. difficile

C. perfinigens characteristics

Encapsulated, boxcar shaped, non motile, rod, spore forming anaerobe, CAMP + Most abundant cause of clostridial disease in domestic animals (intestinal tract)

C. perfringens lesions?

Gas gangrene or enterotoxemia in ruminants and diarrhea in other species

What disease does C. perfringens cause?

Gastritis, hemolytic disease in ruminants Hemorrhagic abomastitis in calves Enterotoxemic jaundice (yellow lamb disease) Jejunal hemorrhage syndrome in cattle Chicken necrotic enteritis

Enterotoxemia

Overeating disease / Pulpy kidney In sheep 3-10 weeks and up and in feedlots From rapid autolysis in toxin- damaged tissue

C. perfringens pathogenesis

Sudden change/ high concentrate diet (starchy) → upset GI flora balance/ indigestion —> rapid multiplication → epsilon toxin → toxemia with enteritis and CNS signs and sudden death

C. difficile

Motile, encapsulated, spore forming In intestinal tracts of normal humans and animals

What does C. difficile cause?

Fatal diarrheal disease in humans and horses → pseudomembranous colitis Enterocolitis and diarrhea

C. difficile human illness

Older adults in hospitals or long-term care facilities after use of abx medications Causes diarrhea linked to 14,000 US deaths/ year

Non-spore forming gram - anaerobes

Dichelobacter nodosus and Fusobacterium necrophorum

D. nodosus

Non-motile seen with swollen ends (dumbell)

F. necrophorum

Fusifrom shape with some beading Causes calf and avian diptheria, liver abscess, bullnose in swine, equine thrush, necrobacillosis

D. nodosus and F. necrophorum together

Cause footrot (interdigital dermatitis) of sheep and goats F. is primary pathogen + D. = lesions → synergistic interaction

Clinical footrot

Opportunistic pathogens (normal flora) Causes lameness

Clinical footrot pathogenesis

Non-sporulating anaerobes in GIT and environment → Extension of normal flora to compromised site —> inoculation with contaminated tool —> trauma, vasc. breakdown, bacterial infection

Bacteroides

Non-spore forming, gram - anaerobes Abscess, diarrhea and periodontal disease Bacterial pleuropneumonia/ pleuritis in horses

Obligate anaerobes diagnosis

Culture: time consuming, expensive Sites with suppurative and necrotic process No molecular O2 and refrigeration