Anthrax
Association with history
5th & 6th plaques of exodus
Black Bane in 17th century Europe
Epidemics in Europe during 18th & 19th centuries
Bacillus anthracis
Sporulating
Disease due to toxin
Aerobic
3 forms
Cutaneous anthrax
Gastrointestinal anthrax
Inhaled anthrax
Zoonosis
Transmission in animals by ingestion of spores while grazing
Transmission to humans by contact with contaminated animal products or inhalation of spores
Anthrax — Virulence Factors
Capsule 2-binary toxins with common B-component
Types of Anthrax
Cutaneous anthrax
Eschar formation after endospores enter through abrasions
Pulmonary anthrax
Spores are picked up by aveolar macrophages which may transport them to lymph nodes
Spores resist phagocytosis and germinate in macrophages eventually lysing them
Symptoms: flu-like to pneumonia-like
Vaccines
Anthrax vaccines first produced by Louis Pasteur
Current vaccines are accellular
Clostridium perfringens
Gram positive rod
Spore form in soil
Germinates in animal intestine or in damaged tissue (anaerobic)
The only clostridia sp. to invade tissue
Major Toxin — α Toxin
Other major toxins present:
β toxin: loss of intestinal mucosa
ε toxin: increase permeability of GI wall
ι toxin: AB toxin with ADP ribosylating activity
C. perfringens Nagler Reaction
Lecithinase (α-toxin; phospholipase) hydrolyzes phospholipids in egg-yolk agar around streak on right
Antibody against α-toxin inhibits activity around left streak
Minor Toxins — C. perfringens type A
δ Hemolysin
ν DNase
μ Hyalurnidase
κ Collagenase
θ Hemolysin
λ Protease
Organic Acids — C. perfringens type A
H2
CO2
H2S
C2H4O2
C4H8O2
Clostridial myonecrosis
Treatment
Antibiotics
Surgical excision, debridement
Hyperbaric oxygen
Clostridium tetani
Tetanus toxin — A-B toxin (plasmid encoded)
Small polypeptide of tetanus toxin blocks release of inhibitory neurotransmitter
Both muscles fully contract. The arm flexes because biceps brachii is larger and stronger
Symptoms begin in head & neck region then progress through body
Treatment & prevention
Passive immunization with tetanus immunoglobulin to bind any circulating toxin
Antibiotics to destroy any tetanus bacteria
Vaccination with tetanus toxoid induces antibody against the heavy chain, preventing attachment of toxin to target cells
Borrelia hermsii
Hosts
Small rodents or humans
Vectors
Insects
Humans are often accidental hosts for most vector-borne diseases
Dead end host
Not a complete cycle
Antigenic variation — type C
Borrelia burgdorferi
Lyme disease transmitted by deer tick (Ixodes)
Borrelia changes outer surface protein (OSP) expression depending upon host
Borrelia Osp C binds a tick salivary protein (Salp15) on its way from the tick’s midgut to a new animal host
Once inside its new animal host, the OspC-Salp15 complex protects Bb from antibody-mediated killing
Has also been shown to inhibit the activation and proliferation of CD4+ helper T-cells
Borrelia binds to complement regulatory protein Factor H, a protein that prevents complement lysis of our own cells
Erythema migrans
Early symptoms
Malaise, fatigue, fever, chills, head & body aches
Long-term complications
Arthritis
Cardiac-conduction system
Secondary erythema migrans
Acrodermatitis chronica atrophicans
Brain damage
Human Monocytic Ehrlichiosis vs Human Granulocytic Anaplasmosis
These two illnesses are similar in terms of symptoms but are typically found in different areas of the U.S. Why might this be?
Which of the two may have something in common with Lyme disease? What is it that they share?
Yersinia pestis
Endemic foci
Flea is actually infected. The Hemin system of Yersinia causes a blockage between the esophagus and midgut
Transmission of Y. pestis occurs during the futile attempts of the flea to feed
Ingested blood dislodges bacteria lodged in the blocked area and is regurgitated back into the host circulatory system