gram+ rods

non-motile

nonfastidious

non-hemolytic

spore-forming (resistant to heat, UV, gamma-radiation, & disinfectants; may be dormant for decades; "medusa head" on agar surf)

commonly infects grazing herbivores

more serious w/o animal vaccination

human-->human transmission: RARE

human infection (US): RARE

2 large plasmids account for ALL virulence:

1. pXO1: toxin proteins (PA; LF; EF) combine to form binary exotoxins = lethal toxin/LeTx (PA+LF); edema toxin/EdTx (PA+EF)

*individually, toxin proteins harmless

2. pXO2: genes encode protein for capsule syn 

*unique capsule: polyglutamate (antiphag)

--> PA oligomerizes => EF/LF binding sites --> toxins endocytosed --> PA conform chg w/ pH chg --> toxins in cytosol

EF (adenylate cyclase): releases cAMP

LF (protease): degrades MAPKK

cutaneous anthrax

common affected areas: head, neck, & extrem

description: nondescript 1* lesion (painless papule, no pus)

progression: w/in 2-3d vesicles --> central necrosis & drying => eschar (usually surrounded by eroded areas/edema- may be self-limiting)

left untx: bacteremic/fatal

inhalational anthrax (woolsorter's disease)

initial symptoms: flu-like (fever, cough, myalgia, malaise)

characteristic: widened mediastinum (this is where the org is prolif & prod toxins)

progression: 1-3d fulminant course (dyspnea, strident cough, chills, usually fatal)

associated: gastrointestinal & leptomeningeal lesions <= hematogenous spread

cause: eating anthrax-infected meat

fatality: 25-60%

symptoms: severe GI difficulty, vomiting blood, diarrhea, acute inflamm

(Bacillus anthracis)

fatality: 100%

symptoms: lots of edema, blood CSF (w/ gram+)

"Cardinal's cap" appearance (lots of hemorrhage of leptomeninges)

spreads: to CNS from any kind of anthrax infection

vesicular stage: vesicular fluid

eschar stage: eschar material

id bacillus anthracis on sheep blood agar

non-motile

non-hemolytic

irregularly round

medusa head colony (comma shaped projection)

PLET for isolation

bicarbonate agar => capsule formation

beta hemolytic on sheep blood agar

string of pearls test-

motile

glutamyl-polypeptide capsule-

heat-labile (diarrheal): stim adenylate cyclase (=> cAMP); SLOW onset

heat-stable (emetic): RAPID onset

Clostridium

part of normal colonic flora

most abundant: C. ranosum, then C. perfringes

most pathogenic: C. perfringes

most predominant (spores/vegetative bacteria): serotype A in human fecal flora & in soil (most virulent)

growth time: very fast (3xs faster than E. coli)

infections endo/exogenous

growth requirements: ~14 AAs & 6 other factors (most body fluids are deficient of these materials EXCEPT necrotic tissues)

*produces ~12 toxins  (alpha toxin=gas gangrene)

1. soft tissue infections: cellulitis, suppurrative myositis, myonecrosis (gas gangrene)

2. gastroenteritis: food poisoning, necrotizing enteritis

clostridial cellulitis

doesn't involve muscle/deeper tissue

anaerobic

less aggressive than gas gangrene

after surgery/trauma (dmg to arteries reduces 02 supply)

gas gangrene=clostridial myonecrosis

what does the "gas" come from?

organism replication (there will be crepitus present)

extensive hemolysis

bacteria present

inflammatory cells absent

symptoms: shock, renal failure, death w/in 2d

Clostridium perfringes, usually type A

induces Ca++ dependent alteration in permeability

symptoms: epigastric pain, nausea, cramps, watery diarrhea

necrotizing enteritis (enteritis necroticans, pig-bel)

cause: strains prod beta toxin

occurs w/: high protein/trypsin inhibitor (sweet potato)

incr risk: decr intestinal proteases

symptoms: peritonitis, abdom px, vomiting, bloody diarrhea, shock

fatality: 50%

Clostridium perfringes

non-motile, box-car shaped gram+ rod

*rod presence w/o leukocytes in specimen

nagler rxn+ (anti-alpha-toxin added to egg yolk agar cultures (on upper half)- prevents visible opacity <= lecithinase action of alpha toxin)

motile, spore forming, gram+ rod, anaerobe

common in soil

most cases (developing countries): newborns

1. chromosomally encoded 02 labile hemolysin (tetanolysin): unclear role 

2. plasmid encoded 02 labile neurotoxin (tetanospasmin-tetanus toxin): stationary phase, blocks release of inhibitory neurotrans

common entry to body: implanting spores in wounds

under anaerobic conditions: spores germinate --> produce toxins --> retrograde mvmt w/in CNS

char sympt: convulsive muscle contraction (lockjaw, back muscles)

cause of death: cardiac/respiratory complic

C. tetani

most common

masseter muscles (trismus, lockjaw); risus sardonicans

early signs: drooling, irritability, back spasm (opisthotonus)

clostridium tetani

confined to musculature of 1* site of infection

Clostridium tetani

head is the 1* site of infection

poor prognosis

tetanus neonatorum

clostridium tetani

common 1* infection site: umbilical stump (dirty tools to sever cord)

symptoms: excessive crying, trismus, tetanic spasms, opisthotonus

fatality: >90% (survivors have developmental defects)

1. foodborne botulism 

2. infant botulism

3. wound botulism

4. inhalational botulism

C. botulinum

characteristic: symmetric descending paralysis

*flaccid paralysis

initially: blurred vision, constipation, abd px, no fever

spores high conc in hospitals & LTCF (high antibiotic use)

risk of infection correl. to length of stay

spores survive gastric acidity (germinate in LGT)

2 toxins: enterotoxin A & cytotoxin B (disrupt epithel cell barrier)

*pseudomembranes seen on colon endoscopy

1. exposure to antibiotics

2. exposure to C. difficile capable of producing toxins

3. inadequate immune response (antibodies to toxin A-protective)

1. Clostridium difficile

2. Staphylococcus aureus