Soilborne & Insect Transmitted Pathogens

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