Gram Positive Rods Corynebacteria, Bacillus, Listeria, Lactobacillus, Propionibacteria, Erysipelothrix

Corynebacteria, Bacillus, Listeria, Lactobacillus, Propionibacteria, Erysipelothrix

Gram-positive

Non-acid-fast

Bacillus

Spore-forming

Corynebacteria, Listeria, Lactobacillus, Propionibacteria, Erysipelothrix

Non-spore-forming

Corynebacteria, Bacillus

Aerobic or facultative anaerobic

Listeria

Facultative anaerobe, obligate intracellular

Lactobacillus, Erysipelothrix

Facultative anaerobe, microaerophilic

Propionibacteria

Aerotolerant anaerobe

C. diphtheriae

Microbiology

Aerobic, facultatively anaerobic, nonmotile, toxin-producing

Gram positive bacill

Disease producing strains carry a B-phage encoding a gene for toxin production (tox+ )

Bacteriophage

Viruses that infect and replicate in bacterial cells

Ubiquitous in nature, found in soil, water, and even the human gut (virome)

Can transfer virulence and antibiotic resistance genes via transduction

C. Diphtheriae

Epidemiology

Humans are the only reservoir

Spread by droplet

C. diphtheriae

Pathogenesis

Exotoxin (classic two-component toxin)

B and A

Exotoxin (classic two-component toxin)

B (binds), which binds to specific receptors on susceptible cells, and A (active), the active segment

STOPS PROTEIN SYNTHESIS

Toxin ADP-ribosylates Elongation Factor-2

C. diphtheriae

Pathogenesis

responsible for tRNA translocase acivity resulting in cessation of protein synthesis (ADP-ribosylation is also seen with cholera and pertussis toxin).

Diphtheria – Clinical Manifestations

The expression of tox+ depends on the physiologic state of C. diphtheria

Low iron conditions induce toxin expression 

High iron conditions repress toxin production

Diphtheria – Clinical Manifestations

targets 

Targets heart (myocarditis), nerves (demyelination), and kidneys (tubular necrosis). 

Very potent. Nanogram quantities of toxin can kill.

Clinical Summmary

Symptoms 

Diphtheria

Weakness

redness of skin and swelling

grey membrane covered ulcers

thraot ache 

Clinical Summary

complications

Diphtheria  

Destruction of throat lining

Lymph node augmentation

Neuropathy

Kidney failure

Clinical Summary

Treatment

Diphtheria

Antibiotics

Antitoxin targeting

C. diphtheriae

Clinical Summmary

prevention 

Diphtheria

three in one vaccine

DTap and DT vaccines for children

Tdap vaccines for adults

Good hygiene

Diphtheria

greek word for “leather”

Bull neck:Associated with massive lymphadenopathy

Diphtheria:Immunity and Prevention

Toxoid vaccine

3 injections in the initial series, prior to high school

Diphtheria: Treatment

◦ Penicillin and erythromycin

Antitoxin will deactivate circulating toxin but not if it has already bound to or entered the cell

Bacillus anthracis

etiologic agent of anthrax

Bacillus anthracis

microbiology

Gram positive

Non-motile rods with blunt ends 

Sporulates in culture 

Aerobic or facultative anaerobic 

Non-hemolytic growth on blood agar 

Catalase positive

Bacillus anthracis

endospores

Enable bacteria to survive in environments where normal bacterial cells would die 

Highly resistant to disinfectants, heat, radiation, and drying. 

When spores are inhaled or ingested, they can germinate and cause anthrax infection

Main Anthrax Virulence Factors

Encoded on two plasmids: pX01 and pX02

pX02

encodes poly-d-γ-glutamic acid (PGA) capsule

pX01

plasmid encodes three components

protective antigen (PA), edema factor (EF), and lethal factor (LF)

Edema toxin

composed of PA combined with EF, produces local skin edema

Lethal toxin

composed of the same PA together with LF, highly lethal

combination of all three components (PA, EF, LF)

most lethal

Anthrax Factors Combine to Make Two Toxins

Protective Antigen (PA)

Key component of anthrax toxins that binds to the host cells

The toxins are then taken into the cytosol, where they mediate cellular damage

PA heptamer complexes with EF

forms edema toxin

PA heptamer complexes with LF

forms lethal toxin

Anthrax types

Cutaneous

Inhalational

Gastrointestinal

CNS anthrax 

Cutaneous Anthrax

Local inoculation of organism or spores

No purulence (oozing puss) and not terribly painful

Hallmark is classic black eschar (scab)

Development of significant local disease

Swelling and erythema

Inhalational Anthrax

Rapid disease progression

Mortality ~100% if untreated

Pleural fluid and widened mediastinum

Enlarging and hemorrhagic mediastinal nodes

Treatment for anthrax

Antibiotics:

Ciprofloxacin: A first-line treatment for anthrax Doxycycline: A first-line treatment for anthrax

Antitoxins:

injectable antibody medications 

Prevention

for anthrax

Vaccines

BioThrax: A vaccine that prevents anthrax infection and treats infected people (durable protection)

Cyfendus: A vaccine that prevents anthrax infection after exposure (faster as it has a second adjuvant)

Inhalational anthrax treatment

Treated with 60 days of antimicrobial drugs

Anthrax meningitis treatment

Treated with at least three antimicrobial drugs

Systemic anthrax treatment

Treated with antibiotics and antitoxin

Cutaneous anthrax treatment

Treated with antibiotics for 3–7 days

Listeria monocytogenes

Gram positive rod

Catalase positive

Beta-hemolytic

Obligate intracellular pathogen

Listeria monocytogenes frequencies 

More frequently seen in immunocompromised patients, neonates, and the elderly

High frequency of infections in pregnancy

Frequently causes infections in the central nervous system

Listeria monocytogenes

Microbiology

Tumbling motility in culture:flagella

Jet motility in cells by actin formation:Actin polymerization

Listeria monocytogenes Microbiology

Flagella

Tumbling motility in culture 

Jet motility in cells by actin formation

Listeria monocytogenes

Pathogenesis

Replicates intracellularly

 Attaches to intestinal epithelial cell and macrophages

Once in phagolysosome secretes a listeriolysin which allows escape from the phagosome and replication in the cytoplasm

Protein called ActA on its surface triggers actin polymerization at the bacterial membrane allowing bacteria to surf on the newly formed actin filaments!

Listeria monocytogenes Microbiology

(cont.)

Listeria can multiply at 4˚C and survive frozen

Requires thorough pasteurization

Listeria monocytogenes

Epidemiology

Zoonosis (infection in humans acquired from animals)

Associated with milk and milk products, particularly soft cheese

Any failure in pasteurization can lead to organisms that then multiply at 4˚C or survive in freezer

L. Monocytogenes

Major Clinical Syndromes

Meningitis 

Bacteremia

Placenta and fetus 

L. Monocytogenes

Prevention

Thoroughly cook raw food from animal sources, such as beef, pork, or poultry.

Wash raw vegetables thoroughly before eating.

L. Monocytogenes

Prevention - High Risk Patients

Do not eat hot dogs, luncheon meats, or deli meats, unless they are reheated until steaming hot

Avoid getting fluid from hot dog packages on other foods, utensils, and food preparation surfaces, and wash hands after handling hot dogs, luncheon meats, and deli meats.

Do not eat soft cheeses such as feta, Brie, and Camembert, blue-veined cheeses, or Mexican-style cheeses such as queso blanco, queso fresco, and Panela, unless they have labels that clearly state they are made from pastuerized milk.

Lactobacillus

Gram-positive, facultative anaerobic (or microaerophilic) rod-shaped bacteria

Lactic acid bacteria group

L. acidophilus

Used in yogurt and some types of cheese

Beer spoilage organisms

L. brevis is the most common, also L. lindneri, L. casei and others

Vaginal flora

Common species: L. crispatus, L. gasseri, L. jensenii, and L. iners 

Important in maintaining vaginal pH at ~4.5 which prevents yeast growth

Propionibacteria bad

able to synthesize propionic acid

•Implicated in acne vulgaris

Propionibacteria good

Propionibacterium freudenreichii is used in cheesemaking

Erysipelothrix rhusiopathiae

Uncommon Gram-positive rod in human

Erysipeloid (mild cutaneous form in humans)

Common organism in animals

Zoonosis