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47 Cards in this Set

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Bacteria cause disease by 2 major mechanisms:
1. Toxin Mediated Disease (i.e. clostridial toxin such as botulism toxin, no organisms req. in ingestion. Also, staphylococcus aureus enterotoxin (most common food born diarrheal disease in US)
2. Invasion and Inflammation - occur via direct tissue invation and then tissue damage from immune response of the host.
Pathogenic steps in establishing bacterial infections by ingesting toxins
1. toxins preformed in food (clostridium botulism is preformed in food. s. aureus enterotoxin is preformed in food. disease can occur in absense of orgnaism)
2. ingestion of microorganisms with adherance, colonization and TOXIN FORMATION IN THE GUT.(i.e. infant botulism (honey) and vibrio cholerae (ingestion and then secretion of cholera toxin))
Clostridium general features
2. G+ rods, Spore forming (location of spre may aid in species identification)
3. catalase NEGATIVE
4. oxidase NEGATIVE
5. found in soidl
Clostridia tetani
-generally noninvasive (very limited invasion potential
-causative agent of TETANUS
Clostridia botulinum
-noninvasive causing BOTULISM (could be an agent of bioterrorism)
Clostridia difficile
-noninvasive, secreted toxin causing pseudomembranous enterocolitis (antibiotic-associated diarrhea)
Clostridia perfringens

*other clostridial species can also cause gas gangrene and/or bacteremic
Pathogenisis of Clostridia
-ability of the organisms to make a variety of extracellular toxins.
1. botulism toxin - flaccid paralysis
2. tetanus toxin - tetanus (lock jaw)
4. Alpah toxin - lecithinase which is lysed in host cell membrane - (in combo. w/ other degradative enzymes is cause for GAS GANGRENE due to clostridium perfringens.)
botulism toxin
- flaccid paralysis
tetanus toxin
- tetanus (lock jaw)
exotosins A and B -
Alpah toxin
- lecithinase which is lysed in host cell membrane - (in combo. w/ other degradative enzymes is cause for GAS GANGRENE due to clostridium perfringens.)
Botulism Organisms
Clostridia botulinum - Anaerobic Gram + rod with oval subterminal spores
(spore locatinon is NOT diagnostic for this species)
Botulism Ecology
Soil organism, spores are very resistant to physical and chemical agents.

Contrary to known bacteria spores, BOTULISM TOXIN IS VERY HEAT LABILE....cook canned food!!!!
Botulism Incidence
very low (123 cases from 1976 to 1984)
Botulism Epidemiology
C. botulinum spores found in contaminated food under anaerobic conditions (i.e canned food) germinate, grow and make botulism toxin in 2-3 days. (a neurotoxin, causes flaccid paralysis)
Types of Botulism
-Food botulism (preformed toxin in canned food, ingestion of bacteria not required)
- Infant botulism (toxin from germinating spores inside the infant gut – from contaminated honey)
- Wound botulism (requires spore germination in the wound)
Botulism toxin
-Extremely potent toxin
-Two component toxin (subunits A and B)
-7 serotypes (A-G), with A, B and E most common

-HEAT LABILE (inactivated by 100°C for 10 min)
-Not destroyed by stomach acid
Botulism toxin action
-Absorbed in intestinte and travels via blood to peripheral nerve synapses of motor neurons, acting as a neurotoxin to cause flaccid paralysis
-toxin blocks the release of Ach by interfering with proteolytic processing (toxin is a protease)
Clinical manifestations of Food Botulism
-Short incubation period (18-36 hrs)
-weakness or flaccid but descending paralysis
-Affecting neurons of cranial and peripheral nerves (Symmetrical in distribution)
-May involve respiratory or cardiac muscles
No fever
Normal mental status
Botulism Diagnosis
-usually a clinical diagnosis
-culturing microorganisms is worthless b/c its the toxin doing damage
-detect toxin in serum, vomitus, or feces
-detect toxin in food
-EMG -diminished action potential of peripheral nerves (suggestive not diagnostic)
Differential Diagnosis of Botulism
Myasthenia gravis
Gullain Barre syndrome
Therapy for Botulism
Therapy for removal or neutralization of toxin
- Stomach lavage (if oral ingestion of toxin)
- horse anti-toxin serum, toxin-specific(Types A, B and E most common) (antixoin is toxin type SPECIFIC)
-Supportive care - resp. supprt
-12% fatality rate
Prevention - cook canned food for 100 deg. for 10min)
Infant Botulism
-Infants 1-8 months of age
Contaminated honey
Spores germinating in the gut → toxin (before the establishment of normal intestinal flora)
Serotypes A, B and F more common
Symptoms subtle in infants: poor head control, constipation, cranial nerve deficit
Diagnosis by detecting toxin or organism in the stool (or in honey)
Supportive therapy (may try anti-toxin)
Wound Botulism
C. botulinum - soil organism
-Spores from soil germinating in contaminated wounds → toxin
Diagnosis by wound culture and demonstration of toxin in the serum
Treatment: horse or human anti-toxin serum and supportive therapy
Tetanus (C. tetani)
-Gram+ rod with TERMINAL SPORE (tennis racket -highly diagnositc)
Tetanus Epidemiology
– Soil organism -rose bush
- Rare disease in the US, occurs primarily in non-immunized immigrants -resistant to heat and chemical agents -germinating under anaerobic conditions (e.g. deep puncture wound - dirty deep wound)
Tetanus Pathogenisis
-ONE SEROLOGICAL TYPE(not like botulism that has lots of serotypes)
-disease caused by tetanus toxin which is a NEUROTOXIN
-toxin transported from site of infection to perpheral and CNS nerves to affect anterior horns cells of spinal cord and and on brain stem)
Tetanus Toxin
-2 subunits (A and B)
-One binds to neuronal ganglioside other has neurotoxin activity
-inhibit the release of glycine and GABA (for muscle relaxatin) resulting in spastic paralysis and CONVULSIVE CONTRACTIONS (locked jaw)
Tetanus Clinical syndrome
-Incubation period (4 days to weeks-vague)
-Severe muscle SPASM, flexor muscle predominant – lockjaw (trismus), bent elbows, arch back to generalized spasm
-May involve pharyngeal or respiratory muscles
"NO SENSORY DEFICIT" conscious with intense pain due to muscle spasm
Tetanus: Diagnosis
-Clinical diagnosis
(organisms difficult to recover)
-culture positive only in 39% of the cases
Tetanus Treatment
Treatment – human anti-tetanus immunoglobulin (if early in the disease)
- penicillin (to kill remaining bugs)
- wound debridement (improve tissue oxygenation)
- respiratory support
immunization with tetanus toxoid

High mortality rate (40-60%)- pulmonary complications
Prevention of Tetanus with immunization
Tetanus toxoid (formaldehyde-inactivated toxin)
– given as part of DPT in kids or as Td in adults
3 shots, booster at 1 year and prior to school
-Booster every 10 years
Look at tetnus prophylaxis flow chart Slide 46 of lecture
Look at tetnus prophylaxis flow chart Slide 46 of lecture
Clostridia difficile
-cause of Pseudomembranous colitis (diarrhea) from antibiotic usage
-G + anaerobic G+ rod
C. Difficile Epidemiology
-Found in GI tract in ~3% of individuals
-30% of the hospitalized patients colonized with C. difficile in the GI tract (due to spores found on surfaces in hospitals)
-Overgrowth of C. difficile with oral antibiotic usage
C. difficile secretes two distinct exotoxins, A and B
-Exotoxin A is an enterotoxin
-Exotoxin B is a cytotoxin, damaging colonic mucosa, leading to pseudomembrane formation in the colon.
Pseudomembranous colitis due to C. difficile: pathogenisis
-antibiotic induced suppresion of normal flora
-makes 2 distinct toxins (exotoxins A and B)
-Exotoxin A - enterotoxin binds to gut receptor
-Exotoxin B - cytotoxin; damages colonic mucosa (bloody diarrhea, by ADP ribosylating Rho and GTP binding protein)
-Damage by exotoxin B causes pseudomembrane formatin.
Pseudomembranous colitis due to C. difficile: diagnosis
-history of antibiotic use (ampicillin, cephalosporins, clindamysin)
-Exotoxin B in filtrate of stool (bioassay), ELISA
-Stool culture for C. difficile not that useful
-sigmoidoscopy with visualization of pseudomembranes
Pseudomembranous colitis due to C. difficile: Treatment and Prevention
Stop the offending antibiotics (e.g. cephalosporin and clindamycin)
Treatment with metronidazole or vancomycin
Prevention: PRUDENT/judicious USE OF ANTIBIOTICS
Use contact precaution in an outbreak (implement disinfection strategy)
Clostridia perfringens
-anaerobic, spore-forming Gram + rods, nonmotile (all other clostridia are motile)
-Invasive and rapidly progressive, primarly a surgical disease
-Byproducts of anaerobic growth are acids and gasese (H2 and CO2)
Clostridia perfringens
Two major diseases
- gas gangrene – defined as necrosis and gas in tissues due to release of toxins and enzymes by C. perfringens

- food poisoning (watery diarrhea)
Clostridia perfringens Epidemiology:
- soil organism
- also found in human GI tract and vagina
Clostridia perfringens Pathogenisis
-synthesis of many toxins which lyse host tissue/cells = necrosis
-Lecithinase: ALPHA TOXIN - damage to host cell membrane
-Can grow RAPIDLY in anaerobic environment and gas in tissues!!!!
Clostridia perfringens Clincal syndromes
1. cellulitis - superficial
2. necrotizing cellulits - invasion of dermis and into underlying capillaries
3. necrotizing fasciitis - invades fascia around muscle
4. myositis or myonecrosis (invasion into muscle)
-can occur in absence of open wound
-rarely w/ uterine infection (septic abortion) or GI lesion
Diagnosis of Gas Gangrene (Clostridia perfringens)
-Rapidly progressing skin or wounds infection (necrosis)
-Gas in tissues (CREPITUS upon pressing the skin)
-X-ray shows subcutaneous air
-SKIN DISCOLORATION, edema and/or dark exudate
-Extreme PAIN
-Gram+ rod upon Gram stain of wound fluid (might not see spores)*remeber to culture fluid anaerobically!
Clostridial Sepsis
Clostridial cellulitis, fasciitis or myositis leading to bacteremia

GI mucosa can be invaded during bacteremia, resulting in GI bleed
Treatment of C. perfringens Gas Gangrene
-“SURGICAL approach” or wound debridement is top priority
-Penicillin to kill remaining bacteremia
-Hyperbaric oxygen in selected medical center

Prognosis: Can be rapidly fatal if left untreated