Gram Positive Bacillus And Clostridium Pathogens

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Bacillus anthracis
1) physiology
2) virulence
3) epidemiology
4) Tx and Prevention

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1) spore forming, central located spores, gram positive bacilli, facultative anaerobes, non-fastidious, polypeptide capsule

2) capsule protein present on virulent strains (made of glutamate aa, disrupts cell metabolic activity), exotoxin: anthracin, spores can live for years

3) animal disease, transmitted to humans by direct contact or by inhalation and ingestion

4) penicillin, or can use erythromycin, chloramphenicol, doxycycline (prophylactic)
Prevention: animal and human vaccination of lab workers and employees of mills or military

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3 Clinical manifestations of Anthrax

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1) Cutaneous Anthrax: produces ulcer: eschar, 95% human cases, slow healing painless ulcer covered with black eschar with edema, infection can spread to lymphatics with local adenopathy, septicemia can develop, 20% mortality if untreated

2) Inhalation Anthrax: rare in humans, 100% mortality rate, Woolsorters Disease, pneumonic, meningitis may complicate disease, pharyngeal anthrax: fever, pharyngitis, neck swelling

3) Gastrointestinal Anthrax: rare in humans, 100% mortality, abdominal pain, hemorrhagic ascities, paracentesis fluid wont be sterile, gram-postive rods, hemorrhage

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Other Bacillus Spp.

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Bacillus cerus: in soil, opportunistic pathogen, spreads through contaminated foods, ocular infection, gastroenteritis

Bacillus thuringinesis: BT corn (toxin insecticide), other GMO's

Bacillus stearothermophilus: spores used to test efficiency of killing in autoclaves

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Clostridium spp. General

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anaerobic, gram-positive, endospore forming bacilli, ubiquitous in soil, water, human and animal intestine,

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Clostridium spp. Groups

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Histotoxic groups: tissue infections, tissue necrosis
1) C. perfringens: myonecrosis or gas gangrene

Enterotoxingenic group: gastrointestinal disease
1) C. perfringens: necrotizing enteritis
2) C. difficile: antibiotic associated diarrhea, normal flora but turn into spores after antibiotic use, produce enterotoxin, Pseudomembraneous colitis: large # C. difficult

Tetanus
1) C. tetani: produce neurotoxin

Botulinism
1) C. botulinum

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C. perfringens virulence factors

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Major lethal toxins
1) Alpha/Lecithinase/Phospholipase C: lysis cell membranes of RBC, WBC, endothelial cells, etc. acts on lecithin: phospholipid on membrane
2) B, E, I: increased capillary permeability: edema and swelling

Minor Toxins
Delta, K, M, N, Gamma: hyaluronidase, DNAase: tissue destruction, necrosis, invasiveness, neuraminidase

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C. perfringens - Nagler Reactions

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Lecithinase hydrolyzes phospholipids in egg-yolk agar around streak, opaque streak seen

Antibody against lecithinase inhibits activity and no opaque streak seen

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Disease caused by C. perfringens

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1)Food poisoning
2) Anaerobic cellulitis: infection of CT, no muscle involvement
3) Myonecrosis: gas gangrene, extensive cell killing (histolytic), enzymes break down ground substace (hyaluronidase), fermentaiton of tissue sugars yields gas and tissues look swollen, systemic toxemis, renal shock, requires amputation: no antitoxin

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Treatment of C. perfingens infection

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High dose penicillin therapy, symptomatic treatment of food poisoning, proper wound care and exposure of wound to O2

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Clostridium tetani general

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obligate anaerobe, gram-positive rod, drum-stick appearance due to terminal spore, spores resist boiling for 20 minutes, motile by peritrichous flagella

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C. tetani Virulence Factors

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Spore formation, plasmid-mediated A-B neurotoxin:Tetanospasmin: exotoxin, poisonous substance, binds gangliosides in synaptic membranes, blocks release of inhibitory neurotransmitters (GABA, glycine), get continuous stimulation by excitatory transmitter, retrograde neurotoxin: travels from injury site to CNS to find inhibitory neuron --> irreversible, only supportive care. Incubation time depends on distance of injury from CNS. death: affects diaphragm. No relaxation, No CO2 released, no exhalation

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C. tetani Treatment and Prevention

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Prevention: by active immunization (DPT, TT)

Treatment: antibiotic treatment, passive vaccination with TIG (tetanus Ig)

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Clostridium botulinum General and Virulence Factors

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General: gram positive rod, anaerobic, most dangerous poison in world

Virulence: spore formation, botulisum toxin (A,B,E types), exotoxin prevents release of neurotransmitter Acetylcholine, acts at neuromuscular junction , paralysis of muscles, death: affects diaphragm, cannot constrict, cannot inhale, no O2, asphyxiation,

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Botulisum toxin general

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poisoning, intoxication, anaerobic found improper canned food, 3 Clinical manifestations
1) Foodborne botulism: result from asphyxiation
2) Infant botulism: ingestion of endospores found in viscous food, cause of SIDS,
3) Wound botulism: contamination of wound by endospores
** irreversible like tetanus

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C. botulinum Tx and Preventions

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Tx: administer neutralizing antibodies against botulism toxin, only prevents free toxin, not toxin bound to neuron already, administer antimicrobial drugs in infant botulism cases

Prevention: proper canning of food, infants under 1: no honey