Spore-forming Gram-positive rods Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

What are the spore-forming bacteria of clinical interest?

A
  • Bacillus anthracis
  • Bacilluscereus
  • Clostridium difficile
  • Clostridium tetani
  • Clostridium botulinum
  • Clostridium perfringens (rarely)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the morphologic features of bacterial spores?

A
  • Contain a complete copy of the chromosome
  • Contain minimum concentrations of essential proteins and ribosomes
  • Have a high concentration of calcium bound to dipicolinic acid
  • The spore has an inner membrane, two peptidoglycan layers, and an outer keratin–like protein coat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the growth requirements of Bacillus spp.?

A

Aerobic or facultative anaerobic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the morphology of Bacillus spp.?

A
  • Large, Gram-positive rods
  • Occur in chains, single or paired rods, or as long, serpentine chains
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is human anthrax acquired?

A
  • Inoculation: the main natural route. Inoculation of Bacillus spores through exposed skin from contaminated soil or infected animal products
  • Ingestion
  • Inhalation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the virulence factors of anthrax?

A
  • Capsule: inhibits phagocytosis; made up of poly-ᴅ-glutamic acid
  • Edema toxin: has adenylate cyclase activity, leading to fluid accumulation
  • Lethal toxin: a zinc MMP that stimulates macrohphages to release TNF-α, IL-1β, and other pro-inflammatory cytokines leading to a cytotoxic effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the types of anthrax disease?

A
  • Cutaneous anthrax
  • Gastrointestinal anthrax
  • Inhalation anthrax
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the features of cutaneous anthrax?

A
  • Starts with development of a painless papule at the site of inoculation
  • Rapidly progresses to an ulcer surrounded by vesicles and then a necrotic eschar
  • Systemic signs, painful lymphadenopathy, and massive edema may develop
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the features of gastrointestinal anthrax?

A
  • Infection of upper GI tract: ulcers form in the mouth or esophagus, leading to regional lymphadenopathy, edema, and sepsis
  • Infection of cecum/terminal ileum: nausea, vomiting, and malaise, which rapidly progress to systemic disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the features of inhalation anthrax?

A
  • Associated with a prolonged latent period (2+ months) in which spores remain latent in the nasal passages
  • In active disease, the spores reach the lower airways, in which alveolar macrophages ingest the spores and transport them to the mediastinal lymph nodes
  • The initial symptoms are fever, myalgias, nonproductive cough, and malaise
  • Later, there is rapid worsening of fever, edema, massive lymphadenopathy, respiratory failure, and sepsis
  • Almost all cases progress to shock and death within 3 days of initial symptoms unless specific treatment is given
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

When were the anthrax attacks?

A

2001

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the diseases associated with Bacillus cereus?

A
  • Vomiting disease (emetic food poisoning)
  • Diarrheal disease (diarrheal food poisoning)
  • Ocular diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is emetic form B. cereus food poisoning acquired?

A

Consumption of contaminated rice, in which heat-resistant spores survive. If the cooked rice is not refrigerated, the spores germinate and the bacteria multiply rapidly. The heat-stable enterotoxin is not destroyed when the rice is reheated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the features of emetic form B. cereus food poisoning?

A
  • Intoxication, not infection
  • Short incubation period (1–6 hours)
  • Short duration of illness (<24 hours)
  • Nausea, vomiting, and abdominal cramps
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is diarrheal form B. cereus food poisoning acquired?

A

Ingestion of the bacteria in contaminated meat, vegetables, or sauces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the features of diarrheal form B. cereus food poisoning?

A
  • True infection with a longer incubation period
  • Release of heat-labile enterotoxin follows, which is responsible for diarrhea, nausea, and abdominal cramps
  • Course of 1 day or longer
17
Q

How are ocular infections with B. cereus acquired?

A

Traumatic, penetrating injuries of the eye with a soil-contaminated object

18
Q

What are the clostridia of clinical significance?

A
  • C. tetani
  • C. botulinum
  • C. difficle
  • C. perfringens
19
Q

What are the morphologic and growth features of clostridia?

A

Gram-positive, spore-forming, anaerobic rods

20
Q

How are C. difficile infections acquired?

A

Long-term use of antibiotics permits overgrowth of the C. difficile population found in the normal flora or allows for exogenous infection

21
Q

How is C. difficile infection treated?

A

Fecal transplants from healthy donors to re-establish the normal flora

22
Q

What disease is associated with C. difficile infection?

A

Pseudomembranous colitis: formation of whitish plaques and friable erythematous mucosa content in the large intestine

23
Q

What are the morphologic features of C. tetani?

A
  • Large, motile, spore-forming rod
  • Produces round, terminal spores that give it the appearance of a drumstick
24
Q

What is the epidemiology of C. tetani?

A
  • Found in fertile soil and transiently colonizes the GI tract of humans
  • The vegetative forms are extremely susceptible to oxygen toxicity
25
Q

What are the toxins formed by C. tetani?

A
  • Tetanolysin: an oxygen-labile hemolysin
  • Tetanospasmin: a plasmid-encoded, heat-labile neurotoxin produced during the stationary growth phase and released when the bacterium is lysed
  • Tetanospasmin inactivates proteins that regulate the release of the inhibitory NTs glycine and GABA, leading to unregulated motor excitation and spastic paralysis
26
Q

What are the morphologic features of C. botulinum?

A
  • Large, fastidious, spore-forming, anaerobic rods
  • Subdivided into 4 groups based on phenotypic and genetic properties (and are technically 4 separate species)
  • Seven antigenically distinct toxins; human disease is caused by types A, B, E, and F
27
Q

Which types of botulism toxin cause disease in humans?

A

A, B, E, and F

28
Q

What are the types of botulism?

A
  • Classic/foodborne botulism: associated with consumption of home-canned foods containing toxins A and B, or contaminated preserved fish with type E toxin
  • Infant botulism: associated with consumption of foods (e.g. honey, infant milk powder) contaminated with botulinum or with ingestion of spore-contaminated soil and dust
  • Wound botulism
  • Inhalation botulism: important in bioterrorism
29
Q

What is the pathogenesis of botulism?

A

The botulism toxins are endopeptidases that inactivate the proteins that regulate release of ACh, blocking neurotransmission at peripheral cholinergic synapses, leading to flaccid paralysis

30
Q

What are the features of foodborne botulism?

A
  • Patients become weak and dizzy 1–3 days after consuming the contaminated food
  • Initial signs include blurred vision with fixed dilated pupils, dry mouth, constipation, and abdominal pain
  • Bilateral descending weakness of the peripheral muscles develops in patients progressing to flaccid paralysis
  • Respiratory paralysis leads to death
31
Q

What are the features of infant botulism?

A
  • The disease is caused by production of toxins in vivo by bacteria that colonize the GI tract
  • Does not occur in adults as C. botulinum cannot survive and proliferate in their intestines
32
Q

What are the morphologic features of C. perfringens?

A
  • Rectangular, Gram-positive rods
  • Spores are rarely observed
  • Colonies are distinctly rapid growing, with β-hemolysis
33
Q

What is the epidemiology of C. perfringens?

A
  • Type A commonly inhaits the intestines of humans and is widely distributed in nature, particularly in soil and feces-contaminated water
  • Strains of types B–E do not survive in soil but colonize the intestines of animals and sometimes humans
34
Q

What is the pathogenesis of C. perfringens infection?

A
  • The bacteria produce enterotoxin, primarily type A strains, whose activity is enhanced by exposure to trypsin
  • Enterotoxin is produced during the transition from vegetative cells to spores and is released in the alkaline environment of the small intestine when the cells sporulate
35
Q

What are the diseases caused by C. perfringens?

A
  • Cellulitis
  • Fasciitis or suppurative myositis
  • Myonecrosis with gas formation in the soft tissue (gas gangrene)
36
Q

What are the features of gas gangrene?

A
  • A life-threatening disease
  • The onset of the disease, characterized by intense pain, develops within a week of infection due to trauma or surgery
  • The α-toxin, which inserts into the plasma membrane and produces gaps
  • Gas is produced by the metabolism of the actively dividing bacteria
37
Q

What are the features of clostridial food poisoning?

A
  • Short incubation period
  • Abdominal cramps and watery diarrhea but no fever, nausea, or vomiting
  • Course lasting less than 24 hours