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Flashcards in Clostridia and Bacillus Deck (42)
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1

General characteristics of Bacillus species

gram positive large rods (largest bacteria morphologically)
produce resistant spores-spore is infectious form
aerobes or facultative anaerobes
grow very fast- large colonies at 24 hours
biochemically active
majority are non-pathogenic environmental organisms

2

Species of bacillus of veterinary importance

B. anthracis- ANTHRAX
B. cereus- food poisoning (rice borne outbreaks- spores survive heating) , eye and soft tissue infection (man), mastitis in cattle (rare)
B. licheniformis- sporadic abortion in cattle and sheep (also food poisoning-like symptoms in man)

3

General characteristics of anthrax (who it effects)

serious disease affects virtually all mammalian species. worldwide, endemic or in defined regions. ruminants are highly susceptible- develop rapidly fatal septicemia
Pigs, horses moderately susceptible
Carnivores moderately resistant
Birds almost totally resistant to infection
NB: the more spores you get, the more severe the dz.

4

Epidemiology of Anthrax

endospore formation is the most important factor regarding persistence in the environment and spread. endospores can survive for decades in the soil. outbreaks occur in herbivores when pasture contaminated by spores. infection acquired by ingestion of spores (inhalation, skin abrasion more common in man)

5

Epidemiology of anthrax continued

Spores ingested--> germination and multiplication in lymphatics and spleen, vegetative forms release in massive numbers into the blood in final hours of life-->veg. forms shed at death in hemorrhagic exudate--> sporulate on exposure to O2. Man can inhale spores, eat infected meat or contaminated vegetables, or can acquire cutaneously via lesion from handling infected meat/vegetables/contaminated materials.

6

Anthrax pathogenesis- virulence factors

Poly-D-glutamic acid capsule and a complex toxin. both virulence factors encoded on plasmids. Expression is regulated by host temp. and CO2.
Capsule- inhibits phagocytosis- upregulated in presence of CO2.
Toxin- consists of 3 antigenic components 1)protective antigen 2) oedema factor 3) lethal factor

7

Virulence factors of anthrax continued

Oedema factor: calmodulin dependent adenylate cyclase- increases cAMP--> oedema in tissue and inhibits neutrophil function
Protective antigen: binds to host cell surface receptor, and an enzyme cleaves the antigen, allowing OF and LF to enter the cell
Lethal factor: zinc-metalloprotease which stimulates macs to release IL-1 and TNF alpha and cleaves MAP kinase. MAP kinase is responsible for the host inflammatory response. Cytokine release--> shock.

8

Local effects of anthrax

Swelling and oedema, darkening of tissue, necrosis
Septicemia, leads to increased vascular permeability, hemorrhage, shock and death.

9

Clinical presentation of anthrax

Incubation: hours-days
Cattle and sheep show rapidly fatal septicemia- NO rigor mortis seen
Anthrax bacilli can occlude the lumen of blood capillaries, resulting in a massive bacteremia in the last hours of life.

10

Diagnosis of Anthrax (B. anthracis)

Carcasses are bloated, putrified and don't exhibit rigor mortis. Bleeding from nose, mouth and anus.
Blood of animal stained with polychrome methylene blue- blue bacteria with pink capsules- McFadyean's capsule stain
Characteristic colonial morphology
Any holes seen on the stain are spores, which don't gram stain.
B. anthracis culture is very characteristic: medusa-head colonies- serpentine cords of b. anthracis. Colonies are large and gray
Non-hemolytic.

11

Human anthrax (3 forms)

1) cutaneous- malignant pustule- endospores enter abraded skin- septicemia if untreated
2)pulmonary-"wool-sorters disease"- inhalation of spores- 80% mortality if no tx
3) intestinal- ingestion of infected material

12

Control of anthrax

Don't open carcass!--> this facilitates spore formation and environmental contamination
Report to regulatory authority
Annual vaccine (live spore vax, capsule minus toxin)
Chemoprophylaxis in outbreaks
Carcasses should be incinerated or buried away from water courses.
Contaminated material disinfected in 10% formalin or if appropriate, incinerated.

13

Clostridium Species- major characteristics

Gram positive large rods
STRICT anaerobes
resistant spores
Grow very fast
Biochemically active
produce VFAs
enzymes including proteases and saccharases
Produce toxins: tetanus toxin on plasmid, botulism toxin on lysogenic phage
Antimicrobial sensitive but resistance my occur

14

Clostridia- where it's found and what types of disease does it cause

Clostridia is ubiquitous: found in soil, alimentary tract of animals and in feces (normal flora). There are many species and not all of them are pathogens.
Pathogens are grouped according to the mode and sites of action of their potent toxins
1) neurotoxic 2) histotoxic- severe soft tissue infxn
3)enteropathogenic and enterotoxemia producing clostridia- produce diarrheal disease but also produces toxins.

15

Neurotoxic clostridia

C. tetani and C. botulinum

16

C. tetani (tetanus)- general characteristics

Potentially fatal intoxication affecting many species. Horses and humans are highly susceptible. ruminants and pigs are moderately susceptible. carnivores comparatively resistant. poultry are resistant.
Results in spastic paralysis

17

C. tetani culture and gram stain

Culture: very easy to miss- a little bit of hemolysis but get growth that spreads across the entire plate. Flat colonies with irregular edges. C. tetani cells are differentiated from other common clostridia by the presence of a terminal spore. look like little drumsticks.

18

Tetanus (c. tetani) epidemiology/presentation

Neurotoxin= tetanospasmin (antigenically uniform which means that one vaccine can be used world-wide). toxin is encoded by a plasmid.
Infection occurs when endospores are introduced into tissue traumatized or from soil or feces. vegetative bacteria develops from spore in the wound. vegetative bacteria produce the toxin.
Common trauma resulting in tetanus:
-deep penetrating wounds in horse- presumably tetanus caused by spores from own GI tract
-castration and docking in sheep
-abrasions in cows and ewes
-umbilicus in all animals.

19

Tetanus pathogenesis/how toxins cause disease

-Tetanus toxin=2 chains (light and heavy) joined by disulphide bridge. Light chain is toxic, heavy is responsible for receptor binding and internalization.
-Binds irreversibly to ganglioside receptors on motor nerve terminals and transported to CNS by intra-axonal flow.
-toxin blocks pre-synaptic transmission of inhibitory signals
-hydrolyses synaptobrevins- proteins of vesicles containing NTs
-inhibits glycine and GABA release-->spastic paralysis
-cramps on opposing muscle groups
-bound toxin is NOT neutralized by antitoxins- meaning, get antibodies quickly!

20

Botulism- C. botulinum- general characteristics

Serious, potentially fatal intoxication by pre-formed neuro toxin (types A-G)
Different antigenic form of toxins for different species
Types C and D cause outbreak in domestic animals
Types A, B and E account for most human cases

21

Botulism epidemiology

Germination of endospores, growth of vegetative carcasses, decaying vegetation, contaminated canned food

22

Botulism in cattle

Marked increase in cattle in UK since 2003 due to deep litter containing poultry carcasses on pasture. Clinical signs of botulism- process of elimination, usually find animal dead.
Detection of toxin in serum is difficult

23

Botulism- pathogenesis

Neurotoxins are most potent bio toxin known. 0.1-1 microgram will kill a human (if ingested).
Toxin is synthesized as a single polypeptide chain, then nicked by a bacterial protease to form 2 chains.
Pre-formed toxin in food is absorbed from GIT and circulates in blood
Acts at neuromuscular junction of cholinergic nerves and peripheral autonomic synapses and remains at junction
Irreversible interference with acetylcholine resulting in FLACCID paralysis
Death from paralysis of respiratory muscles.
BT blocks ACh fusion and release

24

Comparison of Tetanus and Botulism toxins

Very similar in structure and function despite diametrically opposed clinical manifestation--> due to action at different sites!
Both toxins are zinc-dependent metalloproteases
Proteins clamp the vesicle to the presynaptic membrane
Clostridial neurotoxins inhibit vesicle release by cleaving peptide bonds in these proteins. Each toxin has a specific locus of activity.

25

Histotoxic clostridia- general characteristics

sever soft tissue infection. ingested endospores excreted but some may leave intestine and lie dormant in tissue. tissue injury leading to reduced O2 tension required for germination and vegetative replication. local necrosis produced by exotoxins of replicating bacteria allows further proliferation and tissue damage

26

Histotoxic clostridia- Endogenous infection

Spores are already in the tissues. ingested and then migrate. usually no clinical event, but if you get trauma, set up anaerobic condition spores will go to vegetative state.
Examples: blackleg, infectious necrotic hepatitis and bacillary hemoglobinuria result from activation of dormant spores in muscle or liver.

27

Histotoxic clostridia- Exogenous infection

infection from outside, when spores contaminate the wound. gas gangrene (myositis) result from introduction of clostridia into wounds. Anaerobic environment of necrotic tissue allows replication, local and systemic toxin production.

28

Species of histotoxic clostridia

C. chauvoei- blackleg in cattle
C. septicum- malignant oedema in cattle pigs and sheep, braxy in sheep
C. novyi type A- big head in rams, wound infxn
C. perfringens type A- necrotic enteritis in chickens, gas gangrene (myositis)
C. sordellii- myositis in cattle, sheep, horses; braxy in lambs
C. novyi type B- black disease in sheep (necrotic hepatitis)
C. hemolyticum- bacillary hemoglobinuria in cattle and occasionally sheep.

29

Endogenous infection- C. chauvoei (Blackleg in cattle) (gas gangrene)-- bacteria produce large amount of gas as a byproduct of metabolism. gas builds up in affected tissue.

Black leg--> commensal/ingestion--> relocalization to muscle from blood--> bruising of affected muscle group--> spore germination and toxinogenesis--> hemolysis, crepitation, necrosis

30

Endogenous infection- C. novyi Type B (Black's disease in sheep)

Black's disease--> commensal/ingestion--> relocalization to liver--> fluke migration--> spore germination and toxinogenesis--> oedema, shock, necrosis of liver