Gram+ Rods Flashcards
of the Gram+ rods, name 2 non-spore forming species and 3 spore-forming species
non-spore forming:
1. Corynebacterium (C. diphtheriae)
2. Listeria monocytogenes
spore-forming:
1. Bacillus (B. anthracis, B. cereus)
2. Clostridial (C. perfringens, C. botulinum, C. tetani)
3. Clostridioides difficile
Where does Corynebacterium diphtheriae come from and how does it spread? (Gram+ rod)
humans are only reservoir, spread via respiratory droplets or contact
only clinically significant in areas lacking vaccination, otherwise rare
What is the effect of the exotoxin produced by Corynebacterium diphtheriae? (Gram+ rod)
B fragment delivers A by binding to cell membrane proteins CD-9 and Heparin-binding EGF
A toxin ADP-ribosylates elongation factor EF-2 to inactive —> protein synthesis disrupted
just 1 exotoxin molecule completely terminates cell protein synthesis!
[Step 1 note: low iron induces toxin expression, high iron suppresses]
what are the clinical characteristics of infection by Corynebacterium diphtheriae? (Gram+ rod)
infects throat/ nasopharynx —> respiratory illness, typically beginning with sore throat
dense/grey layer of cell debris forms pseudomembrane, “bull neck” due to lymphadenopathy
systemic toxin —> myocarditis (major cause of mortality) and neurologic toxicities
how can Corynebacterium diphtheriae be cultured and identified? (Gram+ rod)
Tinsdale’s agar: selective medium with potassium tellurite to inhibit respiratory flora
organisms produce black colonies with halos
microscope: “coryneform” (club-shaped)
diagnosis requires confirmation of toxin production
how is Corynebacterium diphtheriae (Gram+ rod) treated?
!neutralize toxin! with Diphtheria anti-toxin
Rx: Erythromycin or penicillin
prevention: immunization using inactivated toxin
where does Listeria monocytogenes (Gram+ rod) come from and what populations are especially at risk?
only Listeria that infects humans, usually food born (poultry, cheese, ice cream)
very serious for pregnant women, neonates, infants, immunocompromised
how does Listeria monocytogenes (Gram+ rod) invade the body?
- escape phagolysosome via Listeriolysin O toxin
- reorganize actin to create tail and pushes into adjacent cells (direct transfer evades immune response)
facultative intracellular pathogen - immunity is therefore cell-mediated
describe the clinical manifestations of Listeria monocytogenes (Gram+ rod)
most commonly mild diarrhea with fever
in at risk populations:
- neonates —> meningitis, septic arthritis
- pregnant women —> flu-like, pre-term delivery
- defects in cell mediated immunity —> generalized infection
how can Listeria monocytogenes (Gram+ rod) be cultured and distinguished?
beta-hemolytic with blue-green sheen on blood agar
tumbling motility on LM in hanging drop culture (culture in tube)
can survive with or without oxygen
produces catalase
how is Listeria monocytogenes (Gram+ rod) treated?
Ampicillin
prevent with proper food handling (contracted via poultry, cheese, ice cream)
of these spore-forming Gram+ rods, which is an aerobe?
a. Bacillus
b. Clostridia
c. Clostridioides
a. Bacillus (B. anthracis, B. cereus) is aerobe
b. Clostridia (C. perfringens, C. tetani, C. botulinum) and (c.) Clostridioides are anaerobes
how is Bacillus anthracis (spore-forming Gram+ rod) contracted?
zoonotic (sheep, goats, etc) transmitted to humans via contaminated dust or contact with animal products
what is essential for virulence of Bacillus anthracis (spore-forming Gram+ rod), and what is unique about it?
anti-phagocytic capsule composed of proteins (NOT polysaccharides)
essential for full virulence!
[B. anthracis also produces Edema toxin and Lethal toxin, which require protective antigen for cell entry]
what 2 toxins does Bacillus anthracis (spore-forming Gram+ rod) produce, and what do they require?
- Edema toxin: adenylate cyclase, increase in cAMP —> widespread leak of fluid from capillaries
- Lethal toxin —> tissue necrosis
both require protective antigen for cell entry
what are the clinical manifestations of Bacillus anthracis (spore-forming Gram+ rod) infection?
mostly cutaneous - painless, swollen pustule with black eschar (“malignant pustule”), sepsis if untreated
inhalation of spores —> hemorrhagic mediastinitis (100% mortality without treatment)
how can Bacillus anthracis (spore-forming Gram+ rod) be cultured and how does it appear morphologically?
non-hemolytic on blood agar with “comma shape” colonies
blunt-ended in chains with centrally-located endospores - appearance of bamboo
facultative or strictly aerobic
how is Bacillus anthracis (spore-forming Gram+ rod) treated? specify for cutaneous and inhalation anthrax
cutaneous anthrax: Doxycycline, ciproflaxin, erythromycin
inhalation anthrax: Ciprofloxacin + clindamycin
aggressive and fast treatment
prevention: cell-free vaccine available for high risk individuals
where does Bacillus cereus (aerobic Gram+ rod, spore-forming) infection come from?
food born (think “cereal”)
*intoxication rather than infection
emetic form associated with spore-contaminated rice
Of Clostridia (obligate anaerobe Gram+ rods, spore-forming), which of these species is invasive?
a. C. tetani
b. C. botulinum
c. C. perfringens
c. C. perfringens - invasive
C. tetani and C. botulinum are toxin-forming
*note that all these species synthesize potent exotoxins
what genus of bacteria does this describe?
- spore-forming
- obligate anaerobes
- form endospores
- synthesize potent exotoxins
- produce large, raised colonies on blood agar
- single or double zones of hemolysis
- can ferment sugar or digest proteins
Clostridia: Gram+ rod
where can Clostridium perfringens (spore-forming Gram+ rod) be found?
normal flora of large intestine, skin, vagina
spores found in soil
*note Clostridium are obligate anaerobes (damaged by oxygen) and can ferment sugar or digest protein
what is the purpose of alpha toxin of Clostridium perfringens (spore-forming Gram+ rod)?
alpha toxin (phospholipase C): lyses WBCs, RBCs, platelets
also produces heat-resistant enterotoxin (loss of fluids, proteins), degradative enzymes (DNAase, hyaluronidase, collagenase, protease)
what are the clinical characteristics of Clostridium perfringens (spore-forming Gram+ rod) infection?
myonecrosis when spores introduced to soft tissue - fermentation yields gas, gas gangrene, life-threatening
food poisoning: no fever, self-limited
clostridial endometritis: complication of incomplete abortion
how is Clostridium perfringens (spore-forming Gram+ rod) cultured?
anaerobically on blood agar - unique double zone of hemolysis (complete + partial ring of hemolysis)
how is Clostridium perfringens (spore-forming Gram+ rod) treated?
early aggressive debridement of devitalized tissue, hyperbaric oxygen therapy, combo antibiotics
where is Clostridium botulinum (spore-forming Gram+ rod) found?
soil, aquatic sediments, spores in vegetables and meat (especially home-canned) - most cases due to toxin ingestion (food poisoning)
produce toxin in anaerobic and neutral/basic pH environment —> toxin is what causes disease
(“toxin-forming” type of Clostridia, versus invasive)
how does Clostridium botulinum (spore-forming Gram+ rod) cause disease?
via neurotoxic exotoxin - cleaves SNARE proteins that allow vesicle docking and NT release
light chain blocks Ach release (toxin is active at neuron end plates) —> flaccid paralysis
affects skeletal muscle and parasympathetic nervous system
[recall that somatic/skeletal muscle and parasympathetic nerves have Ach presynaptically, and all postsynaptic are Ach]
how does Botulism, caused by Clostridium botulinum (spore-forming Gram+ rod), present?
(not in infants or from wounds)
botulism —> loss of somatic motor nerves and parasympathetic motor nerves (toxin affects somatic and parasympathetic nerves)
symmetric neurological deficits - double vision, difficulty swallowing, flaccid paralysis (progressive, can lead to respiratory failure), ptosis, pupillary dilation, loss of intestinal peristalsis, etc
preserved cognitive responsiveness and sensation
Dyplopia, Dysarthria, Dysphagia, Dyspnea
what is the most common form of Botulism in the US?
infant botulism: constipation, lethargy, hypotonia
associated with honey
caused by Clostridium botulinum (spore-forming Gram+ rod)
how is Clostridium botulinum (spore-forming Gram+ rod) infection diagnosed?
by detecting the toxin (not the organism), either in serum/stool/leftover food
how is Clostridium botulinum (spore-forming Gram+ rod) infection treated?
immediate antitoxin! Botulinum toxin is super potent
infection never results in immunity
where is Clostridium tetani (spore-forming Gram+ rod) found and contracted?
barnyard, garden, other soils
common infection from puncture wounds (spores need to be deeply inoculated into tissue because C. tetani is strictly anaerobic)
what causes illness by Clostridium tetani (spore-forming Gram+ rod)? how does it present?
toxin-producing type of Clostridium - growth of bacteria is local but neurotoxin spreads to CNS
single gene product (tetanospasm) cleaved into A and B fragments - B delivers A into neuron cytoplasm
A fragment blocks GABA or glycine release at inhibitory synapses —> spastic paralysis, lockjaw, autonomic hyperactivity, respiratory failure
[incubation period 4 days to several weeks]
how does paralysis caused by Clostridia botulinum compare to that caused by Clostridia tetani? explain why these differences occur
C. botulinum: Botulinum toxin blocks Ach release at somatic and parasympathetic motor nerve terminals —> flaccid paralysis
C. tetani: Tetanus toxin blocks GABA/glycine release at inhibitory synapses —> spastic paralysis (disinhibition of motor nerves)
what is the shape of Clostridium tetani?
Clostridium tetani: spore-forming Gram+ rod, obligate anaerobic
racquet-shaped bacillus
what is recommended regarding immunization against Clostridium tetani (spore-forming Gram+ rod)?
immunization with tetanus toxoid + booster every 10 years
can also give tetanus immune globulin if no history of immunization with toxoid (or ineffective immune system)
infection does not confer immunity because lethal dose is lower than immunogenic dose
what bacteria species does this describe?
- spore-forming
- strictly anaerobic
- aggressive nosocomial pathogen
- causes antibiotic-associated colitis
- minor component of GI flora
Clostridioides difficile: anaerobic Gram+ rod, spore-forming
spores acquired via fecal-oral route but doesn’t typically germinate until antibiotic use disrupts normal GI flora
associated with use of proton pump inhibitors (decreased acid production in stomach = more spore survival)
what do the toxins of Clostridioides difficile (Gram+ rod, spore-forming) do?
produce Toxin A and B: glycosylate/inactive Rho family proteins —> damage epithelial cells, producing pseudomembrane
toxin levels correspond to severity of disease
what is the clinical manifestation of Clostridioides difficile (Gram+ rod, spore-forming) infection?
Clostridioides difficile is toxin-producing (rather than invasive), so illness is due to Toxin A and B (inactive Rho proteins)
causes watery diarrhea following antibiotic therapy (disrupts GI flora, allowing C. difficile germination)
“antibiotic-associated colitis” with high WBC count and sepsis
how is Clostridioides difficile (Gram+ rod, spore-forming) diagnosed?
hard to culture, very sensitive to oxygen (anaerobic)
pseudomembranes in large intestine, antigen detection in stool
NAAT (nucleic acid amplification test) used to detect gene that encodes Toxin B
what type of Gram+ bacteria grow as branching filaments? (2)
Nocardia: aerobic (N. asteroides)
Actinomyces: anaerobic (A. israelii)
where is Nocardia asteroides (branching Gram+) found, how is it transmitted, and where does it infect the body?
exogenous: soil, water
transmitted via respiratory route, contamination of skin lesion
infects lung, brain
where is Actinomyces israelii (branching Gram+) found, how is it transmitted, and where does it infect the body?
endogenous: normal flora
transmitted via endogenous source
infects oral cavity, abdomen, female GU tract
what is the typical clinical manifestation of infection with either Nocardia asteroides or Actinomyces israelii?
tend to cause abscesses - masses of bacteria in pus are yellow (“sulfur granules”)
culture required to identify species
