Anaerobes

Question 1

Anaerobes

Answer 1

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

Question 2

Clostridium

Answer 2

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

Question 3

Neurotoxic clostridia

Answer 3

Affect neuromuscular function without inducing observable tissue damage

Question 4

Histotoxic clostridia

Answer 4

Localized lesions in muscle and liver, subsequently causing toxaemia

Question 5

Enteropathogenic and enterotoxaemia-producing clostridia

Answer 5

Infers with protein synthesis in cells

Question 6

Clostridium: virulence factors and pathogenesis

Answer 6

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

Question 7

Tetanus

Answer 7

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

Question 8

Ascending Tetanus

Answer 8

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

Question 9

Descending Tetanus

Answer 9

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

Question 10

Tetanus: diagnosis

Answer 10

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

Question 11

Tetanus: Tx

Answer 11

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

Question 12

Tetanus: control

Answer 12

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

Question 13

Tetanus: vaccine preventable

Answer 13

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

Question 14

Botulism

Answer 14

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

Question 15

Difference btwn tetanus and botulinum toxin:

Answer 15

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

Question 16

Botulism in aquatic bird

Answer 16

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

Question 17

Botulism in humans

Answer 17

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)

Question 18

Botulism: diagnosis

Answer 18

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

Question 19

Botulism: control

Answer 19

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

Question 20

Blackleg in cattle and sheep

Answer 20

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

Question 21

Blackleg in cattle and sheep: CS

Answer 21

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

Question 22

Malignant Oedema, Gas gangrene

Answer 22

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

Question 23

C. novyi type A

Answer 23

Exogenous
gas gangrene
Big head in rams

Question 24

C. novyi type B

Answer 24

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

Question 25

C hemolyticum

Answer 25

Endogenous Liver damge Bacillary hemoglobinuria Mainly in cattle and sheep

Question 26

Malignant oedema, braxy

Answer 26

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

Question 27

Histotoxic clostridia: Dx, Tx, Control

Answer 27

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

Question 28

Enteropathy

Answer 28

Pathology of the intestine

Question 29

Enterotoxaemia

Answer 29

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

Question 30

C. perfringens

Answer 30

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

Question 31

Necrotizing hemorrhagic enteritis

Answer 31

In multiple species of animals | Can suddenly die without signs

Question 32

Lamb dysentery

Answer 32

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)

Question 33

Pulpy kidney disease, over-eating disease

Answer 33

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

Question 34

Pulpy kidney disease, over-eating disease: CS

Answer 34

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

Question 35

C. perfringens infections: Dx

Answer 35

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)

Question 36

C. perfringens infections: Tx

Answer 36

hyperimmune serum (if available and given early)

Question 37

C. perfringens infections: control

Answer 37

routine immunization of farm animals with toxoid | Avoid predisposing factors (sudden dietary changed or stress that impacts intestinal microbiota)

Question 38

C. difficile enterocolitis

Answer 38

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

Question 39

C. difficile enterocolitis: diagnosis

Answer 39

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)

Question 40

C. difficile enterocolitis: treatment

Answer 40

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

Question 41

Enterotoxaemia and explosive diarrheal disease in rabbits

Answer 41

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

Question 42

Tyzzers disease

Answer 42

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

Question 43

Gram negative non-spore forming anaerobes

Answer 43

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

Question 44

Foot rot, Necrotic laryngitis, liver abscesses

Answer 44

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

Question 45

Foot rot: diagnosis

Answer 45

CS | Anaerobic culture, PCR

Question 46

Foot rot: Tx

Answer 46

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

Question 47

Foot rot: Control

Answer 47

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

Question 48

Mastitis in dairy cattle: contagious

Answer 48

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

Question 49

Mastitis in dairy cattle: environmental

Answer 49

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