Anaerobes

Question 1

Key characteristics of anaerobes

Answer 1

present in the GIT of mammals, can be gram + or -
require anaerobic environment or devitalized tissue for growth. use anaerobic transport conditions for submitting specimens.
cause abscesses, wound infections, aspiration pneumonia, intra-abdominal infections, bacteremia, enteric infections, toxaemia
usually localized, often involve oral and GIT, spread by direction extension from mucosal surfaces.
Polymicrobial infections and synergistic relationships. Anaerobic infections are mostly of endogenous origin

Question 2

Clostridium key characteristics

Answer 2

gram + rods. motile by flagella. rapid multiplication, produce endospores.
Widespread in soil, GIT and feces. powerful toxin producers - epsilon toxin from c. perfringens is one of the most lethal toxins and considered a bioterrorism agent

Question 3

Tetanus

Answer 3

acute, potentially fatal intoxication with neurotoxic clostridia causing spastic paralysis. Widespread in soil and feces, grows in contaminated wounds. Produces terminal endospores and infection occurs upon entry of spores into traumatized tissue from soil or feces. Produce tetanospasmin - a neurotoxin and tetanolysin

Question 4

Ascending vs descending tetanus

Answer 4

ascending - toxin travels from regional motor nerve to then spreads to other areas
Descending - toxin in the blood stream affects motor nerve centres in the head and neck and then spreads to the limb

Question 5

Diagnosis of tetanus

Answer 5

5-10 day incubation.
CS: stiffness, localized spasms, altered HR and BR, dysphagia.
Can’t use culture or toxin in serum - difficult tests
animals that recover not necessarily immune - toxin levels may have been below threshold to produce antibodies

Question 6

Tetanus treatment

Answer 6

antitoxin - administered quickly to neutralize unbound toxin (IV or subarachnoid space). quick but short term protection
anti-tetanus equine serum (IM or IV)
toxoid - inactive vaccine to promote active immune response (SubQ or IM)
Penicillin - kill c. tetani cells in the lesion
surgical debridemnet of wound and flush with hydrogen to produce aerobic conditions
supportive care

Question 7

Tetanus control

Answer 7

toxoid immunization, post-exposure prophylaxis via toxoid booster, prompt wound management and rational antimicrobial therapy, aseptic techniques in surgery, proper sterilization of surgical instruments

Question 8

Botulism

Answer 8

intoxication by ingestion of pre-formed neurotoxin (food intoxication). diverse group of neurotoxic clostridia + toxin type determines species affinity. found in rotting carcasses, decaying vegetation, contaminated foods. toxin absorbed in GIT and distributed in blood stream
occasionally spread through wounds

Question 9

Botulism pathogenesis

Answer 9

inhibits neurotransmitters causing flaccid muscle paralysis. death results from paralysis of respiratory muscles

Question 10

Botulism in humans

Answer 10

foodborne, wound (via needles), infant botulism (spore-contaminated honey), inhalation botulism

Question 11

Botulism diagnosis

Answer 11

CS develop 3-17 days after ingestion of toxin.
CS = dilated pupils, dry mucus membranes, decreased saliva, flaccid tongue, dysphagia, abdominal breathing
demonstration of toxin in serum, or toxin in food and stomach contents
*select agent = potential threat to public health and safety

Question 12

Botulism control

Answer 12

toxoid vaccination of cattle in endemic regions (south africa, australia). routine vaccination of farmed mink and foxes, suspect foodstuffs should not be fed to domestic animals, avoid feeding and eating suspect foods. Proper preparation and preservation of feed and food!

Question 13

Blackleg in cattle and sheep

Answer 13

exogenous infection with necrotizing myositis caused by histotoxic clostridia C. chauvoei. Sheep = any age, cattle = young animals.
death in 24 hours (100% fatality), affects large muscle mass areas (limbs, back, neck)
acute, febrile, highly fatal disease with emphysematous swelling and necrotizing myositis
CS: lameness, edematous swelling with crepitation

Question 14

Blackleg pathogenesi

Answer 14

exogenous infection through wound –> anaerobic environment –> deposition of endospores, multiplication –> toxin causes tissue destruction.
Causes distinctive smell due to metabolic end products

Question 15

Malignant edema/gas gangrene

Answer 15

exogenous, necrotizing, soft tissue (wound) infections caused by histotoxic clostridia C. novyi type A and B and C. hemolyticum.
Deep, anaerobic, traumatic wounds. Characterized by rapid gas formation and toxemia. Clinically detectable as subcutaneous crepitation.

Question 16

Malignant edema/gas gangrene prevention

Answer 16

surgical treatment of wounds to remove necrotizing muscle tissue and contaminating materials. Promote drainage of these wounds. Provide prophylaxis with penicillin if necessary

Question 17

C. novyi type A disease

Answer 17

exogenous, gas gangrene, big head in rams

Question 18

C. novyi type B disease

Answer 18

endogenous, black disease (infectious necrotic hepatitis), predisposed by fluke damage

Question 19

C. hemolyticum disease

Answer 19

endogenous, liver damage, bacillary hemoglobinuria, mainly in cattle and sheep

Question 20

Malignant edema, Braxy

Answer 20

Braxy = abomasitis of sheep caused by C. septicum
Malignant edema = exogenous infection through wounds or endogenous through dormant spores present in muscle tissues
Risk factors = IM injections, shearing, docking, lambing, traumatic parturition/castration
Local exotoxins cause excessive inflamation and myositis –> edema, necrosis, gangrene

Question 21

Diagnosis/treatment/control of histotoxic clostridia

Answer 21

D: fluorescent antibody staining tests. Anaerobic cultures are time consuming and not easy or rewarding
T: penicillin
C: routine vaccination with multicomponent toxoids

Question 22

Clostridium perfringens general characteristics

Answer 22

classified in biotype A-E based on toxins (alpha, beta, iota, epsilon). Alpha toxin is in all strains.
Found in soil, feces, GIT
Predisposing factors: inappropriate husbandry, sudden diet changes, local environment factors

Question 23

Lamb dysentery

Answer 23

caused by c. perfringens type B (alpha, beta and epsilon toxins)
Abdominal distension, pain, blood-stained feces, sudden death
Predisposing factors: low proteolytic activity in the neonatal intestine (presence of trypsin inhibitors in colostrum, low pancreatic secretion levels), immature intestinal microbiome, dietary influences of older animals

Question 24

Pulpy kidney disease/over-eating disease

Answer 24

C. perfringens type D in lambs 3-10 weeks
Predisposing factors: gorging on a high grain diet or succulent pasture. High starch content in intestine = good clostridium breeding grounds
epsilon toxin = activated by proteolytic enzymes, causes toxemia
CS: focal symmetrical encephalomalacia, hyperglycemia, glycosuria, rapid kidney autolysis, fluid-distended intestine (PM), petechial hemorrhage on serosal surfaces

Question 25

C. perfringens diagnosis

Answer 25

CS: sudden deaths in unvaccinated animals, PM findings, staining and microscopic exam, anaerobic culture to determine biotype, toxin detection in intestinal contents

Question 26

C. perfringens treatment and control

Answer 26

T: hyperimmune serum (give early)
C: routine immunization of farm animals with toxoid, avoid predisposing factors

Question 27

C. difficile enterocolitis

Answer 27

Affects the colon and cecum
Risk factors = antibiotic use, old age, hospitalization.
Neonates are resistant but may be carriers.
Endospores are widespread but low numbers in normal intestine
Disease results from dysbiosis, proliferation of C. difficile and toxin production
Tox A = enterotoxin
Tox B = cytotoxin
Nosocomial transmission may occur

Question 28

C. difficile diagnosis

Answer 28

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

Question 29

C. difficile treatment

Answer 29

supportive electrolytes and fluids, stop antibiotics if possible, administration of probiotics, avoid anti-diarrheals
Horses: clindamycin is a significant risk factor
FMT - fecal microbial transportation

Question 30

Enterotoxemia and explosive diarrheal disease in rabbits

Answer 30

4-8 weeks old
Commensal bacterium C. spiroforme produces Iota toxin
fluid-distended intestine with hemorrhage and the serosal surface
Lincomycin, clindamycin, erythromycin induce clostridium-related enterotoxemia due to their selective effects on gram + bacteria. dont use these in rabbits!

Question 31

Tyzzer’s disease

Answer 31

gram - 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

Question 32

Non-spore forming anaerobes general characteristics

Answer 32

involved in bacterial infections with breaks in mucosal or epithelial barriers. any chronic infection may contain these bacteria

Question 33

Foot rot/necrotic laryngitis/liver abscess

Answer 33

gram - anaerobic Fusobacterium necrophorum. Commensal in resp., intestinal and genital tract. Synergistic with trueperella pyogenes and dichelobactor nodosus

Question 34

Foot rot diagnosis

Answer 34

CS, anaerobic culture, PCR

Question 35

Foot rot treatment

Answer 35

remove necrotic tissue, dip in antiseptic foot baths, antimicrobials (metronidazole), aminoglycosides and sulfonamides are not effective

Question 36

Foot rot control

Answer 36

keep feet dry, avoid mechanical injury, vaccination