Aerobic G+ Bacilli Flashcards
Three classifications of G+ rods & aerobic examples of each
Spore-forming: Bacillus sp.
Non spore-forming: Listeria & Erysipelothrix (uniform shape), Corynebacterium (irregular shape)
Acid-fast: no aerobic examples
B. anthracis: main targets of infection
Herbivores; humans are accidental hosts (no human-human transmission)
Cutaneous anthrax symptoms
Painless papule progresses to ulceration with surrounding vesicles, eschar; painful lymphadenopathy, edema; may dev systemic signs
GI antrax symptoms
Ulcers at site of invasion leading to regional lymphadenopathy, edema, sepsis
Inhalation anthrax symptoms
Initially nonspecific, then rapid sepsis with fever, edema, mediastinal lymphadenopathy, meningeal symptoms in ½ pts; will die unless imm tx
*Endospores can remain latent in nasal passages/ lower airways
Virulence factors of B. anthraces, functions, location of genes
All on plasmid pXO1 Protective Ag: binds cellular receptor on many cells Edema factor + PA = edema toxin Lethal factor + LF = lethal toxin Polypeptide capsule
How does protective Ag work in B. anthracis?
Binds cell surface receptor and acts as a carrier to move EF or LF into cell in acidic endosome
Lethal factor mechanism
Zn-dep metalloprotease, binds MAPKK, cleaving it and interrupting its signaling -> cell death
Edema factor mechanism
Calmodulin-activated AC exotoxin, binds calmodulin and this complex converts ATP to cAMP -> increased intracellular Ca2+ and cell death
Possible routes of exposure to anthrax
Zoonotic infection: exposure to infected cows, goats or animal products like hide, goat hair, wool
Bioterrorism agent
Prevention of B. anthracis
Vaccinate animals and humans in endemic areas, who work with animal products imported from those areas, and military personnel
B. cereus: where found, & why
Soil organism, spores ubiquitous throughout environment
Spores resist pasteurization and gamma radiation, so found in pasta, rice, milk products, grains, spices, vegetables, meat, chicken, sea food
B. cereus diseases
Gastroenteritis: emetic illness & diarrheal illness
Ocular infections secondary to trauma
IV line or CNS shunt infxns
Endocarditis
Features of B. cereus emetic vs. diarrheal illness
Emetic: 1-6 hr post ingestion; for 8-10 hours; fried rice, cream, milk products, pasta, reconstituted infant formula
Diarrheal: 8-16 hours post ingestion; profuse watery diarrhea for 20-36 hours; meat and veggies
Virulence factors of B. cereus
Heat stable enterotoxin causes emetic form of disease
Heat labile enterotoxin causes diarrheal form of disease (AC/cAMP system)
Listeria monocytogenes physical characteristics
G+ short rods, weak beta-hem, low temp growth, facultative intracellular growth, ubiquitous within env/soil, outbreaks assc. with contaminated food
Intracellular growth mechanism of L. monocytogenes
Phagolysosomal uptake and lysis, replication, actin-propelled protrusion into adjacent cell
L. monocytogenes in utero diseases & mechanism
Early-onset, invasion of placental endothelium
Stillborn, abortion, or granulomatosis infantiseptica (disseminated abscesses/ granulomas), septicemia, pneumonia
L. monocytogenes late-onset diseases
Benign colonization of skin, nasopharynx, umbilical stump
Meningitis
Epidemiology of L. monocytogenes
70% cases in immunosuppressed
Infxn from domestic animals/birds, soil/water/sewage, contaminated food (raw milk, veg, fish, poultry, meat, sea food, refrig. col cuts)
High risk populations for listeriosis
Neonates, pregnant women, elderly, immunocompromised
L. monocytogenes virulence factors & mechanisms
Internalin - adherence to cells (binds E-cadherin on enterocytes/M cells)
Listeriolysin O & phospholipases (act at low pH of phagolysosome to release bacteria into host)
ActA - catalyzes assembly of actin until bacterium expelled through cell membrane into adj cell
Erysipelothrix rhusiopathiae characteristics
Non spore-forming, slender G+ rod
Worldwide in swine, turkey, cattle, fish, and decomposing organic matter; occupational disease of butchers, farmers, vets, meat processors
E. rhusiopathiae diseases
Localized skin infxn: raised edge & central clearing, self-limited (2-4 w), more severe w/ hemorrhagic bullae & regional lymphadenopathy
Systemic infxn in immunocompromised: bacteremia, sepsis, endocarditis, myocardial abscesses, septic arthritis
E. rhusiopathiae virulence factors
Capsule to enhance replication in MF, protection from phago
Neuraminidase for attachment, cellular invasion
Hyaluronidase
Corynebacterium diphtheriae characteristics
Small, irregularly-sharped (club), G+ rods
Often attached after cell division = pleomorphic, like Chinese characters
C. diphtheriae: where found & how transmitted
Humans are the only reservoir: maintained in oropharynx or skin of carriers (immune or vaccinated)
Transmission by resp droplets or skin contact
Uncommon in U.S. bc vaccine (more common in poor/urban areas)
C. diphtheriae cutaneous disease
Chronic, nonhealing ulcer d/t colonization of skin and invasion of subcutaneous tissue via skin breaks
C. diphtheriae nasopharyngeal disease
Exotoxin destroys local tissue -> malaise, sore throat, exudative pharyngitis; *pseudomembrane of dead cells, bacteria, fibrin, lymphocytes can lead to death by obstruction of airway or toxemia d/t myocardial/neuro damage
C. diphtheriae virulence factor
Diphtheria toxin: two polypeptide protein A-B exotoxin produced at site of infxn, blood dissemination
A vs. B polypeptide in diphtheria toxin
A: catalytic region that shuts off host protein synthesis by binding eEF-2 on small ribosomal subunit
B: receptor-binding region to bind surface HB-EGF of heart, nerve, other cells & translocation region to help move toxin into cell
Location of diphtheria toxin gene
Lysogenic bacteriophage encodes tox gene
Prevention for diphtheria
Vaccine with diphtheria toxoid (formalin treatment of exotoxin) given with pertussis, tetanus Ags to induce Abs that neutralize the binding and activity of the exotoxin
Treating diphtheria
Antitoxin (Ab to exotoxin), passive immunity via maternal IgG in newborns, antibiotics (penicillin, erythromycin), remove pseudomembrane
Corynebacterium jeikeium: who affects, diseases
Opportunistic, in immunocompromised
Comm and hosp-acquired bacteremia/sepsis, endocarditis, meningitis, ventriculitis, pneumonia, pyelonephritis, osteomyelitis
Resistance in C. jeikeium
Multi-drug resistant (beta-lactams, ahminoglycosides, variable to macrolides, tetracyclines, rifampin, Qs)
Chromosomal-assc resistance
