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Gram-Positive Rod

Bacillus anthracis, Listeria monocytogenes, and Streptococcus pyogenes

Highly lethal

Spore-forming

Intracellular and Environmental

Intracellular is triggered by recombination (unpredictability of activation)

Recurrent infections

Recombination that allows for cycling between harmless and lethal forms

Harmless form is very hard to treat

Causes pneumonia & skin infections

Both disease forms lead to immune system breakdown, and death if not treated

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Worldwide

Around 10,000 cases worldwide, annually

Cases more common in countries with undeveloped health care systems

50-60% of all cases are fatal if left untreated

100,000 people live with the harmless form today

At-Risk Populations:

Agricultural workers

Healthcare workers (in rural, more undeveloped hospitals)

Rural populations (with limited medical access)

Infections are more prevalent during warmer months

Intracellular spore form makes reinfection a common issue

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Present in the environment

Spreads through:

Contact with contaminated soil or water

Contact with infected animals (particularly through open wounds)

Inhalation of aerosolized spores

Direct contact with infected corpse (reinfections being more virulent)

Can live dormant or in environmental reservoirs

Soil and water with no nutrients

Farm animals (cattle, sheep, and goats)

Low levels of spread among wild mammal population facilitates increasing distribution

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Bacillus feroxis infects a host and replicates extracellularly, releasing toxins along the way.

Listeriolysin O

Lyses phagosomes and allows for the bacteria to live intracellularly

Protection from the complement system and antibodies

Cysteine Protease SpeB, irritation and necrosis factor

Anthrax Toxin

When the environment becomes overcrowded, or when the cell becomes stressed, Bacillus feroxis will change to a more dormant form.

Live host cells then become infected with Bacillus feroxis by receptor-mediated phagocytosis.

Internalins - InlA & InlB - These bind to E Cadherin and Met receptors respectively, initiating phagocytosis.

Remains dormant intracellularly in host cells, until a genetic switch occurs to switch to the active form again.

Edema factor, lethal factor, protective antigen

Immune system evasion and function disruption (cell signaling & migration)

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Anthrax Toxin (B. anthracis)

Edema factor, lethal factor, protective antigen

Immune system evasion and function disruption (cell signaling & migration)

Cysteine Protease SpeB (S. pyogenes)

Irritation and necrosis factor

Superantigens - SpeA, SpeC (S. pyogenes)

Massive immune response and disruption of adaptive immunity

M Protein (S. pyogenes)

Highly variable and destroys attacking C3 convertase

Prevents effective antibody treatment

Internalins - InlA & InlB (L. monocytogenes)

Entry into cells and internalization

Listeriolysin O (L. monocytogenes)

Lyses phagosomes and allows for the bacteria to live intracellularly

Protection from the complement system and antibodies

C3 convertase homolog

Acts as a separate pathway of complement activation that is non-specific, causing self targeting & using up available C3 preventing further complement activation.

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Initiates through spores of the skin or inhalation

Temperature raises from mammalian body as activation signal

Mixture of warmth and other environmental conditions from skin signal for activation (seasonal time i.e summer results in greater morbidity)

Nutrient rich environments (i.e more people outdoors and less moisture promotes dry soil)

upon successful entry to host anthrax normal toxins would be enough to breech epithelial in the sweat glands and lungs

Antimicrobial resistance:

Effectively none in regards to treating with ciprofloxacin and doxycycline

Anthrax

Colloidal suspension in air can cause Pneumonia

More lethal if aerosolized due to anthrax base functions being maintained(normal disease as skin but much more fast)

Skin:

Starts to form a rash leads to skin sores w/ keratinized skin degrade

Immune system activation begins upon bacteria entry through epithelial cell wall (hours of exposure), often the bacterium's own virulence factors kills it

Survival of some bacteria survive through dormancy or shear numbers

Severe infection occurs from large scale immune activation

Superantigen

Death is caused by the ensuring cytokine storm or secondary infections

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Antibiotics can be effective when clearing active infections

Dormant cells will remain due to not being easily treated in host

Intracellular form is metabolically inactive so it is largely unaffected and will resurface

Treatment is needed throughout the healing process to ensure no reactivation

If bacteria reactivates immunosuppressants are needed to reduce lethality(both initial and secondary infections)

Antimicrobials:

Microbe- specific treatment (antitoxins) can halt autoimmune response without suppressing the immune system if caught early

If not caught need to either suppress the immune system or watch said immune system kill the patient.

Can have serious side effects

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Highly weaponizable organism originating from anthrax, with very high mortality and low virulence

Superantigen and C3b convertase reduce self tolerance, causing overactivation and self targeting (necessitates immunosuppressants to treat)

Environmental spore form is highly resistant and easily aerosolized with soil kickup (anytime the pathogen is not in a warm environment like us)

Intracellular spore is untreatable and will reactivate to cause infection to flare back (low normal uptake but increases as pathogen becomes more stressed)

Requires a relatively long time to pierce the skin (6+hours) so washing often reduces chance of invasion, active form is treatable with most antibiotics

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Ryan, Kenneth J., and C. George Ray. Sherris Medical Microbiology. Vol. 6, McGraw-Hill Education/Medical, 2014.