12. anthrax (bacillus)

bacillus anthracis morphology

• gram positive rods

• spore-forming

how is sporulation triggered?

can be triggered by low oxygen, oxidative stress response, nutrient limitation, etc.

predisposing environmental conditions to anthrax

• alkaline soils; outbreaks associated with flooding

  • dry warm seasons followed by moderate to heavy rain events

  • post-flood organic detritus and/or short, dry grazing grasses

• topological lows (waterholes or riverbanks)

• loose, unconsolidated soils rich in calcium and nutrient content

how is anthrax transmitted?

ingestion of spores in environment

peracute clinical signs

• sudden death and rapid decomposition

• incomplete rigor mortis

**ruminants most susceptible, but can happen in horses

acute clinical signs

• edema, bleeding from body orifices, poor clotting

• fever, staggering, trembling, convulsions, excitation/depression

• difficult/increased respiration

• horses: swelling neck — colic signs

subacute/chronic clinical signs

• localization in pharyngeal tissues

• anorexia, vomiting, and diarrhea

**pigs, dogs, cats

anthrax transmission cycle

animal grazing in infested field ingests anthrax spores → anthrax infection in animal → animal death & bleeding from orifices contaminates environment → b. anthracis bacteria convert into spores and infest agricultural fields

**spores can survive for decades

anthrax pathogenesis

ingested spores invade epithelium directly or are phagocytosed → cross epithelium by transcytosis through epithelial cell or within phagocyte → travel to lymph nodes → germinate into vegetative bacteria → produce capsule and exotoxins → cause edema and clotting disorders to rapid death

**neutrophils are not involved in the pathogenesis of anthrax

what plasmids are essential for B. anthracis to be virulent?

• pXO2 — capsule gene (antiphagocytic)

• pXO1 — contains protective antigen, lethal factor, and edema factor → expresses lethal toxins

what 3 genes in pXO1 contribute to toxin production?

• protective antigen (PA): binds to host cells & helps introduce toxins into host cell

• lethal factor (LF): toxin that inhibits host cell signaling → cell death

• edema factor (EF): edema toxin also disrupts host cell signaling

  • in vivo, responsible for hemorrhagic lesions in multiple organs

major anthrax clinical signs (from summary slide)

• sudden death

• bleeding from orifices

diagnosing anthrax

• necropsy NOT recommended!!! (contaminate environment)

• gram stain & capsule stain of blood and organ smears

• culture

• PCR assays to detect plasmid genes

• REPORTABLE DISEASE

anthrax treatment/prevention

• treatment: penicillin & vaccination

• prevention: annual vaccination recommended — Sterne’s modified live vaccine

what is sterne’s spore vaccine?

• live, avirulent strain of anthrax

  • produces exotoxin (pXO1) but NOT capsule (missing pXO2)

• delivered as spore suspension (immunogenic)

• germinates, releasing exotoxin → immune response to toxin and surface antigens

• not suitable for human use

why doesn’t the sterne’s spore vaccine cause severe disease/death?

infection is controlled and eliminated by the animal because the agent is missing a key virulence factor, the capsule that resists phagocytosis (pXO2)

bacillus cereus source

environment; causes opportunistic infections

bacillus cereus virulence factors

produces enterotoxin (hemolysin) & emetic toxin (cereulide)

what kinds of diseases can bacillus cereus cause?

• acutely gangrenous mastitis in cows

  • predisposing factors = surgery or intramammary infusions that introduce bacteria into gland

• food poisoning