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SPOREFORMERS

Bacillus anthracis
Aerobic
Gram positive
Bacilli in chains
Causes anthrax
Humans are infected incidentally
Acquired thru entry of spores thru:
1. Injured skin: cutaneous anthrax (95%)
2. Mucous membrane: gastrointestinal anthrax
(rare)
3. Inhalation: inhalation anthrax/Wool Sorter's
Disease (5%)
Spores germinate at the site of entry
Formation of gelatinous edema and congestion
Spread via lymphatics
Virulence: poly-D-glutamic acid capsule (anti-
phagocytic)
Edema toxin
Lethal toxin: major virulence factor and cause death
to humans and animals
Organism remains localized
Cutaneous Anthrax
o Edema, lymphangitis, and lymphadenopathy
o Systemic signs and symptoms
o Eschar will dry and heal with granulation with a
scar
o 20% lead to sepsis
Gastrointestinal Anthrax
o Ulcers at the site of invasion: regional
lymphadenopathy, edema sepsis
Inhalation Anthrax (Wool Sorter's Disease)
o Rapid onset of sepsis with fever, edema, and
mediastinal lymphadenopathy
o Most patient will die unless immediate treatment
is initiated








Diagnostic Laboratory Tests
o Specimen: fluid/pus from lesion, blood, or
sputum
o Dry smear: immunofluorescence staining
o ELISA: detect edema and lethal toxins
o BAP: non-hemolytic gray to white colonies with a
rough texture and a ground-glass appearance
o Comma-shaped outgrowths (Medusa head) may
project from the colony
Treatment and Prevention
o Drug of choice: Ciprofloxacin
o Active vaccination: live attenuated bacilli

Bacillus cereus
Aerobic
Gram positive
Bacilli in chains
Causes food poisoning
Hemolysis on BAP
Motility by "swarming"
Eye Infections
o Severe keratitis
o Endomophthalmitis
o Panophptalmitis
Systemic Infection
o Medical devices and IV drugs
o Endocarditis
o Meningitis
o Osteomyelitis
o Pneumonia

Clostridium sp.
Anaerobic
Gram positive
Motile bacilli
Causes botulism, tetanus, gas gangrene, and
pseudomembranous colitis





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Clostridium botulinum
Causes botulism
Found in soil and animal feces
Different types based on antigenic type of toxin
produced
Types A, B, and E cause human illness
Disease is an intoxication
Most common source: vacuum packed or canned
alkaline foods
Infants: honey
Pathogenesis
o Toxin blocks release of acetylcholine
o Flaccid paralysis
Clinical Findings
o Symptoms appear 18-24 hours after toxin
ingestion
o Visual disturbances, inability to swallow, speech
difficulties, bulbar paralysis
o Death: respiratory paralysis or cardiac arrest
o Infants: poor feeding, weakness, "floppy baby"
o Cause of sudden infant death syndrome
Diagnostic Laboratory Tests
o Demonstration of toxin by passive
hemagglutination or radioimmunoassay
o Adults: serum and left over food
o Infant: stool
Treatment
o Trivalent anti-toxin (A, B, and E)
o Supportive

Clostridium tetani
Worldwide distribution in soil and animal feces
Causes tetanus
Neurotoxin: tetanospasmin
Tetanospasmin
o Blocks release of inhibitory glycine and GABA
o Motor neurons are not inhibited
o Spastic paralysis
Not an invasive organism
Infection remain localized in devitalized tissues
Disease in toxemia
Toxin produced by the vegetative cells reach the CNS


Clinical Findings
o Incubation: 4-5 days up to weeks
o Tonic contraction of voluntary muscles
o External stimuli may precipitate generalized
tetanic muscle spasm
o Patient remain conscious
o Death: interference with the mechanics of
respiration
Risus sardonicus
Opisthotonos
Prevention and Treatment
o Active immunization with toxoids
o Proper care of contaminated wounds
o Prophylactic use of anti-toxin (immunoglobulin)
o Drug of choice: Penicillin

Clostridium perfringens
Produce invasive infection including myonecrosis
and gas gangrene
An enterotoxin of C. perfringens is a common cause
of food poisoning
Invasive clostridia produce a large variety of toxins
and enzymes that result in a spreading infection
Many of these toxins have lethal, necrolizing, and
hemolytic properties
Some strains of C. perfringens produce a powerful
enterotoxin
Pathogenesis
o Distention of tissue and interference with blood
supply, together with the secretion of
necrotizing toxin and hyaluronidase, favor the
spread of infection
o Tissue necrosis extends, providing an
opportunity for increased bacterial growth,
hemolytic anemia, and, ultimately, sever toxemia
and death
Cellulitis
o Localized edema and erythema with gas
formation in soft tissue, generally not painful
Suppurative Myositis
o Accumulation of pus in muscle planes without
muscle necrosis or systemic symptoms


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Myonecrosis
o Infection spreads in 1-3 days to produce
crepitation in the subcutaneous tissue and
muscle
o Foul-smelling discharge, rapidly progressing
necrosis, fever
o Toxemia, shock, and death
Food Poisoning
o Food poisoning usually follows the ingestion of
large numbers of clostridia that have grown in
warmed meat dishes
o Diarrhea, usually without vomiting or fever
o Lasts only 1-2 days
Diagnostic Laboratory Tests
o Specimens consist of material from wounds, pus,
and tissue
o Gram stain: large gram-positive rods
o BAP: double zone of hemolysis around colonies
Treatment
o Most important aspect of treatment is prompt
and extensive surgical debridement of the
involved area and excision of all devitalized
tissue
o Penicillin

Clostridium difficile
Administration of antibiotics results in proliferation
of drug resistant C. difficile that produces two toxins
Toxin A: potent enterotoxin, cytotoxic activity, binds
to the brush border membranes of the gut at
receptor site
Toxin B is a potent cytotoxin
Pseudomembranous Colitis
o Detection of one or both C. difficile toxins in
stool
o Endoscopic observation of pseudomembranes or
microabscesses
o Patients who have diarrhea and have been given
antibiotics
o Diarrhea may be watery or bloody
o Abdominal cramps, leukocytosis, and fever
o Most common antibiotics associated:
clindamycin, fluoroquinolones, cephalosporins