Histamine

Gram + bacteria: 2 cocci and 4 rods (2 spore forming, 2 not)
Gram+/Spore forming rods
Bacillus- aerobic
Clostridium- anaerobic

Bacillus
Bac. Anthracis (anthrax) , Bac. Cerus (food poisoning)

Bac. Anthracis
-Only bacteria with a protein capsule, poly-D glutamic acid, preventing phagocytosis
- Affects herbivores: cows, sheep.
- Humans exposed to infected animals (products- goat hair) or soil.
- Can enter through: skin abrasion, inspiration or ingested (GI)
- Skin: Release of an exotoxin causing local tissue necrosis (black w/rim of edema) “Malignant pustule”
- Lung: “Woolsorter’s disease”  fever, myalgia resp distress death
- GI: Intestinal necrosis
- The endotoxin effects of anthrax only occurs when the 3 enxotoxins act together, separately the cause no harm.
1. Edema Factor- cAMP, which is phaocytosed by neutrophils and macrophages preventing phagocytosis.
2. Protective antigen- Allows entry of the EF into phagocytic cells
3. Lethal Factor- May destroy macrophages.
- Vaccine of PA for animals only.

Bac. Cerus
Motile/No capsule/Penicillin resistant
Causes food poisoning from spores left in food
2 Main toxins
Heat Labile toxin- Nausea, abdominal pain, diahrrea 12-24 hrs
Heat stable toxin- Similar to Staph. aureus food poisoning
Antibiotics don’t alter symptoms because the toxin released is still effective.

Clostridium- Anaerobic (JAR)
Clostridium Botulinum- Botulism
- Lethal neurotoxin that prevents Ach release from the presynaptic terminal  Muscle paralysis
- In adults: Canned vegetables and smoked fish, bc they are anerobic they grow in the JAR
- Symptoms: Diplopia (x2 vision), dysphagia (difficulty swallowing), respiratory paralysis
MUST BE TREATED WITH ANTITOXIN and antibiotics
Infant Botulism
- ingestion of spores (infant-honey, adult-canned)
- 2-3 day constipation
- Dysphagia
- Muscle weakness
Clostridium Tetani
- Wound (rusty nail) introduces spore
- Thrive at the site of injury since necrotic tissue is anaerobic
TOXIN: Tetanospasmin, prevents the release of GABA and glycine (inhibitory interneurons)
Inhibition of the inhibitor
- Presentation: Trismus-lockjaw, risus sardonicus-ridiculous smile
Clinical 3 patients w/ skin wounds
1- immunized more than 10 yrs ago, booster
2- never immunized, booster and preformed antibodies
3- already presented w/ tetanus: neutralize toxin, booster, clean wound, antibiotics, supportive therapy.

Clostridium Perfringes (Gas Gangrene)
- Bacteria (from soil) enters wound, matures anaerobically and produces gas
- Release of exotoxin causes necrosis, more anaerobic conditions more exotoxin
-Cellulitis wound infection, when dead skin is exposed to Clos Per.  Moist skin and CREPITUS (gas pockets)
- Clostridium myonecrosis, traumaenters musclecauses necrosis black fluid exits skin

Clostridium difficile (Pseudomembranous Enterocolitis)
- responsible for diarrhea
- Part of GI flora
- Usually grows after administration of bradspectrum antibiotics
- Toxin A diarrhea
- Toxin B cytotoxic to colon cells
Symptoms- Diarrhea, cramping and fever
-Colonoscopy shows WHITE pseudomembranes (necrosis is underneath)
- Treatment: metronidazole and vancomycin PO don’t enter the blood stream but kill Clos. Diff