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[8] BACTERIAL SPECIES > Spore-forming Gram-positive Bacilli > Flashcards

Spore-forming Gram-positive Bacilli Flashcards

1
Q

are found in the soil

A

Spores

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2
Q

remain viable in soil for decades. Although spores are naturally in soil from around the world, the organisms are not regularly cultivated from soils.

A

Spores

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3
Q

Animals, esp. livestock (?), become infected while grazing on grass contaminated with spores which germinate.

A

goats, sheep, cattle, horses

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4
Q

The vegetative cells multiply and elaborate toxins, which spread in the body cause fatal (?). When the organisms are returned to the soil in animal excrement or carcasses, they sporulate and become a long-term reservoir of infection.

A

septicemia and toxemia

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5
Q

Transmission to humans is by

A

direct inoculation, ingestion, or inhalation of spores

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6
Q

Most common form of anthrax in humans, accounting for more than 95% of cases, but the least dangerous form

A

Cutaneous Anthrax (malignant pustule)

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7
Q

Acquired by inoculation of spores through cut or abrasion of the skin, either from soil or infected animal products

A

Cutaneous Anthrax (malignant pustule)

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8
Q

begins with a small, itchy lesion resembling an insect bite; in 1-2 days, it develops into a non-painful papule that changes rapidly into a vesicle, then a pustule filled with blue-black edema fluid.

A 
Cutaneous Anthrax (malignant pustule) : 
Signs and symptoms: Skin infection
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9
Q

blackened crater, typically 1-3 cm in diameter, surrounded by edem.

A

“black eschar”

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10
Q 
Cutaneous Anthrax (malignant pustule) : 
Signs and symptoms
A

Lymphangitis and lymphadenopathy

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11
Q 
Cutaneous Anthrax (malignant pustule) : 
Signs and symptoms
A

fever, malaise, and headache may occur.

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12
Q

is fully developed. Eventually, it dries, loosens, and separates; healing is by granulation and leaves a scar. It may take many weeks for the lesion to heal and the edema to subside.

A

Eschar

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13
Q

Can lead to sepsis, the consequences of systemic infection—including meningitis—and death in 20% of untreated cases.

A

Cutaneous Anthrax (malignant pustule)

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14
Q

Extremely rare in humans (accounts for less than 1% of cases)

A

Gastrointestinal Anthrax (violent enteritis)

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15
Q

Acquired from ingestion of the organism’s spores from contaminated or uncooked meat.

A

Gastrointestinal Anthrax (violent enteritis)

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16
Q

Characterized by an acute inflammation of the intestinal tract.

A

Gastrointestinal Anthrax (violent enteritis)

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17
Q

Death occurs in 60% of untreated cases.

A

Gastrointestinal Anthrax (violent enteritis)

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18
Q 
Gastrointestinal Anthrax (violent enteritis) :
Signs and symptoms:
A
  • Initially, nausea, loss of appetite, vomiting, and fever

- Followed by abdominal pain, vomiting of blood, and severe (often bloody) diarrhea.

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19
Q

Acquired by inhalation of airborne spores while handling animal products

A

Pulmonary or Inhalation Anthrax (Woolsorter’s disease)

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20
Q

it develops in handlers of raw animal hair, wool or hides

A

Pulmonary or Inhalation Anthrax (Woolsorter’s disease)

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21
Q

The incubation period in inhalation anthrax may be as long as 6 weeks.

A

Pulmonary or Inhalation Anthrax (Woolsorter’s disease)

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22
Q

The fatality rate in inhalation anthrax is high in the setting of known exposure

A

Pulmonary or Inhalation Anthrax (Woolsorter’s disease)

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23
Q

it is higher when the diagnosis is not initially suspected.

A

Pulmonary or Inhalation Anthrax (Woolsorter’s disease)

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24
Q
  • First symptoms are flu- or common cold-like symptoms including a sore throat, mild fever, and muscle aches.
  • Followed by coughing, chest discomfort, shortness of breath, and tiredness — which are manifestations of toxemia, marked hemorrhagic necrosis, edema of the mediastinum, and substernal pain. Sepsis occurs, and there may be hematogenous spread to the gastrointestinal tract, causing bowel ulceration, or to the meninges, causing hemorrhagic meningitis.
A

Pulmonary or Inhalation Anthrax (Woolsorter’s disease):

Signs and symptoms

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25
Q

has been considered as an agent for bioterrorism. It has been classified as Category A (highest priority) biological agent because it is easily disseminated, can cause high mortality, and can generate public panic.

A

B. anthracis

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26
Q

Occurs after the intravenous injection of drugs contaminated with spores

A

Injectional anthrax

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27
Q

May result to soft tissue infections, may result in death of shock, coma, organ failure, and necrotizing fasciitis.

A

Injectional anthrax

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28
Q

Found in virulent strains of B. anthracis.

A

Capsule

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29
Q

Consists mainly of a polypeptide, poly-D-glutamic acid

A

Capsule

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30
Q

Instrumental in the adherence of the organism to host’s cells and tissue and is an anti-phagocytic factor.

A

Capsule

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31
Q

Antibodies formed against the capsule do not protect against the disease.

A

Capsule

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32
Q

Plasmid-encoded protein complex made up of 3 components

A

Anthrax exotoxins

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33
Q

binds to specific cell receptors, and after proteolytic activation, it forms a membrane channel that mediates entry of EF and LF into the host’s cell.

A

Protective antigen (PA)

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34
Q

It is so called because it induces protective antitoxins

A

Protective antigen (PA)

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35
Q

is an adenylate cyclase.

A

Edema factor (EF)

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36
Q

Together with PA, it forms a toxin known as edema toxin.

A

Edema factor (EF)

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37
Q

This most likely impairs host defenses and is responsible for the fluid accumulation seen in anthrax.

A

Edema factor (EF)

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38
Q

combines with PA to form lethal toxin, responsible for cytolysis of macrophages.

A

Lethal factor (LF)

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39
Q

This is a major virulence factor and cause of death in infected animals and humans. When injected into laboratory animals (eg, rats), the lethal toxin can quickly kill the animals.

A

Lethal factor (LF)

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40
Q

Control soil contamination is key to preventing anthrax, measures include:

A

(1) disposal of animal by burning or by deep burial in lime pits (2) decontamination (usually by autoclaving) of animal products (3) protective clothing and gloves for handling potentially infected materials
(4) active immunization of domestic animals with live attenuated vaccines

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41
Q

Vaccination is recommended for the following high-risk groups:

A

(1) laboratory workers handling the B. anthracis routinely
(2) persons who handle potentially infected animals/animal products (e.g., hides and furs) esp. in high incidence areas
(3) military personnel deployed to areas with high risk for exposure

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42
Q

The first-generation human vaccine to be licensed for use in the United States

A

BioThrax

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43
Q

a cell-free formulation prepared from a culture filtrate of a toxigenic, nonencapsulated, avirulent strain of B. anthracis , which contains PA, LF, and EF, with PA being the major component.

A

BioThrax

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44
Q

It consists of 3 subcutaneous injections given 2 weeks apart, followed by 3 additional SC injections given at 6, 12, and 18 months; annual booster injections are recommended thereafter to maintain protective level of immunity.

A

BioThrax

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45
Q

Two vaccines using highly purified recombinant (?) have been manufactured in the United States and the United Kingdom.

A

PA (rPA)

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46
Q

is recommended in the setting of potential exposure to B. anthracis as an agent of biologic warfare

A

Chemoprophylaxis

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47
Q

Similar to B. anthracis, but B. cereus are motile with peritrichous flagella, and are non-encapsulated.

A

Bacillus cereus

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48
Q

Spores are found in the soil (also considered as an airborne and dust-borne contaminant that multiplies very readily in cooked foods such as rice, potato, and meat dishes)

A

Bacillus cereus: HABITAT

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49
Q

Transmission to humans is by ingestion or direct inoculation.

A

Bacillus cereus: TRANSMISSION

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50
Q

Food poisoning

•Has two distinct forms:

A

Emetic form

Diarrheal form

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51
Q

Associated with eating fried rice, and occasionally, pasta dishes that are contaminated with the organism’s toxin.

A

Emetic form

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52
Q

Has incubation period of 1–6 hours

A

Emetic form

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53
Q

Manifestations include nausea, vomiting, abdominal cramps, and occasionally diarrhea (clinically resembles staphylococcal food poisoning)

A

Emetic form

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54
Q

Recovery occurs within 24 hours after the onset.

A

Emetic form

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55
Q

Associated with meat dishes and sauces contaminated with spores

A

Diarrheal form

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56
Q

Has an incubation period of 8-16 hours

A

Diarrheal form

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57
Q

Manifestations include profuse diarrhea with abdominal pain and cramps; fever and vomiting are uncommon (clinically resembles C. perfringens food poisoning)

A

Diarrheal form

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58
Q

Recovery occurs within 12 hours after the onset.

A

Diarrheal form

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59
Q

Occurs when the organisms are introduced into the eye by foreign bodies in association with trauma.

A

Eye Infections

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60
Q

Clinical presentation may be in the form of severe keratitis, endophthalmitis, and panophthalmitis.

A

Eye Infections

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61
Q

B. cereus has also been associated with localized infections and with systemic infections, including:

A

endocarditis, meningitis, osteomyelitis, and pneumonia.

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62
Q

are released during spore germination, and may be preformed in the food or produced in the intestine.

A

Enterotoxins

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63
Q

Responsible for the clinical presentation of the emetic form of the disease.

A

Heat-stable enterotoxin

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64
Q

Produced when spores survive cooking rice, and keeping the rice warm results in germination of spores and enterotoxin formation

A

Heat-stable enterotoxin

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65
Q

this pre-formed toxin remains in the food despite reheating.

A

Heat-stable enterotoxin

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66
Q

Responsible for the clinical presentation of the diarrheal form of the disease. •Produced after ingestion of the B. cereus spore-contaminated vegetables,

A

Heat-labile enterotoxin

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67
Q

Produced after ingestion of the B. cereus spore-contaminated vegetables, meat, and cream sauces.

A

Heat-labile enterotoxin

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68
Q

Acute diarrheal disease caused by B. cereus may be prevented by?

A

proper cooking and refrigeration of foods prepared in bulk to prevent proliferation of vegetative forms of the bacteria and formation of the enterotoxin.

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69
Q

may be gram-variable on prolonged incubation.

A

Gram-positive bacilli

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70
Q

Spores are larger than the diameter of the organism in which they are formed; may be placed centrally, subterminally, or terminally.

A

Spore-forming

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71
Q

Sporangia are swollen.

A

Spore-forming

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72
Q

Most are motile with peritrichous flagella EXCEPT

A

C. perfringens, C. innocuum, C. ramosum

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73
Q

Groups of anaerobes based on aerotolerance test: Each colony type from the anaerobic isolation plate is subcultured to an aerobic (5% to 10% CO2) and anaerobic blood agar plate for overnight incubation.

A

Anaerobic

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74
Q

NOT capable of growth on agar surfaces exposed to O2 levels above 0.5%.

A

Strict obligate anaerobes

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75
Q

e.g., C. heamolyticum, C. novyi type B, C. tetani, C. botulinum, Clostridioides (formerly Clostridium) difficile

A

Strict obligate anaerobes

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76
Q
  • Can grow when exposed to oxygen levels ranging from about 2% to 8% (average, 3%) e.g., C. perfringens
A

Moderate obligate anaerobes

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77
Q

Show limited or scant growth on agar in room air or in a 5% to 10% CO2 incubator, but grow best under anaerobic conditions.

A

Aerotolerant anaerobes

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78
Q

e.g., C. histolyticum, C. tertium and C. carnis

A

Aerotolerant anaerobes

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79
Q

Catalase (-)

A

CLOSTRIDIUM SPECIES

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80
Q

Can be part of the normal flora of the GI tract; these are clinically relevant as the cause of both endogenous and exogenous infections.

A

CLOSTRIDIUM SPECIES

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81
Q

causes 80% of gas gangrene (myonecrosis)

A

C. perfringens

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82
Q

also associated with food poisoning, necrotizing skin infection, or bacteremia.

A

C. perfringens

83
Q

Other causes of Gas Gangrene / Histotoxic Group

A

C. novyi, C. septicum, C. histolyticum, C. sordellii, C. sporogenes, C. bifermentans.

84
Q

causes tetanus (commonly known as lock jaw)

A

C. tetani

85
Q

a disease characterized by spastic paralysis.

A

C. tetani

86
Q

causes botulism (foodborne, infant, wound, intestinal)

A

C. botulinum

87
Q

a disease characterized by flaccid paralysis; listed by the Centers for Disease Control and Prevention (CDC) as a potential agent of bioterrorism.

A

C. botulinum

88
Q

Other botulinum neurotoxin-producing species:

A

C. baratii, C. butyricum, C. argentinense.

89
Q

cause bacteremia or other infections.

A

C. clostridioforme group, C. ramosum, C. innocuum, C. tertium

90
Q

causes antibioticassociated diarrhea (AAD) to pseudomembranous colitis (PMC) and associated complications

A

Clostridioides (formerly Clostridium) difficile

91
Q

normal colonizers of the GIT in 3% of healthy adults.

A

Clostridioides (formerly Clostridium) difficile

92
Q

Formerly Clostridium welchii

A

Common name: Welch’s bacillus

93
Q

Spores are found in the soil, and the intestinal tract of animals and humans

A

Clostridium perfringens: HABITAT

94
Q

Transmission occurs by direct inoculation of organisms’ spores through breaks in the skin, or by ingestion.

A

Clostridium perfringens: TRANSMISSION

95
Q

Characterized by extensive necrosis of muscle and connective tissue

A

Gas gangrene (or anaerobic myonecrosis)

96
Q

Acquired by wound contamination with spores of C. perfringens (or other clostridia within the same histotoxic group, such as C. septicum); most cases occur following trauma (e.g., gunshot) or surgical procedures (e.g. septic abortion)

A

Gas gangrene (or anaerobic myonecrosis)

97
Q

Initial trauma to host tissue damages muscle and impairs blood supply resulting in hypoxia or anoxia. This lack of oxygenation allows spore germination and growth of anaerobic clostridia, and elaboration of exotoxins.

A

Gas gangrene (or anaerobic myonecrosis)

98
Q

Initially, generalized fever, pain, edema, and blood-tinged exudate in the infected tissue.

A

Gas gangrene (or anaerobic myonecrosis): Signs and symptoms

99
Q

Tissue becomes discolored, purple, then black, general tissue destruction and bubbles caused on the skin by gas formation in underlying tissue.

A

Gas gangrene (or anaerobic myonecrosis): Signs and symptoms

100
Q

Tissue becomes filled with bubbles of gas, as CO2 and H2 accumulate during the growth of the organisms.

A

Gas gangrene (or anaerobic myonecrosis): Signs and symptoms

101
Q

Occurs by ingestion of vegetative cells of C. perfringens in contaminated food.

A

Perfringens food poisoning

102
Q

Signs and symptoms occur in 8 to 16 hours up to 24 hours after ingesting the suspected food.

A

Perfringens food poisoning

103
Q
  • Crampy abdominal pain
  • Foamy, foul-smelling diarrhea
  • Nausea
  • Fever and vomiting re uncommon
A

Perfringens food poisoning: Signs and symptoms

104
Q

Recovery is rapid and death is extremely rare.

A

Perfringens food poisoning

105
Q

An inflammation of both the small intestines and the colon

A

Necrotizing Enterocolitis (or necrotizing bowel disease)

106
Q

Acquired from contaminated food — food-borne, or it may be transmissible by inanimate objects.

A

Necrotizing Enterocolitis (or necrotizing bowel disease)

107
Q

Characterized by the sudden onset of abdominal cramps and abdominal distention, vomiting, bloody diarrhea, shock related to fluid and electrolyte problems and acute inflammation with focal to widespread necrosis of the intestinal mucosa.

A

Necrotizing Enterocolitis (or necrotizing bowel disease)

108
Q

Referred to by other names in some countries, such as “fire in the bowel” (Germany) or “pig bel” (Papua, New Guinea).

A

Necrotizing Enterocolitis (or necrotizing bowel disease)

109
Q

Results when C. perfringens gains access to necrotic products of conception retained in the uterus, commonly after an incomplete abortion with inadequately sterilized instruments.

A

Endometritis

110
Q

Necrosis of uterine tissue and bacteremia with massive intravascular hemolysis due to toxin then follow.

A

Endometritis

111
Q

Clostridium perfringens produces multiple exotoxins that have different pathogenic significance in different animal species

A

Exotoxins

112
Q

A necrotizing, hemolytic exotoxin

A

Alpha toxin (lecithinase, phospholipase C)

113
Q

Hydrolyzes lecithin and sphingomyelin, thus disrupting the cell membranes of various host cells, including erythrocytes, leukocytes, and muscle cells.

A

Alpha toxin (lecithinase, phospholipase C)

114
Q

Oxygen-labile cytolysin; contributes to rapid tissue destruction — has pore-forming activity similar to streptolysin O

A

Theta (θ) toxin

115
Q

Alters capillary permeability and is toxic to heart muscle.

A

Theta (θ) toxin

116
Q

Responsible for the symptoms of food poisoning with C. perfringens

A

Enterotoxin

117
Q

Released during sporulation of the organisms in the intestines

A

Enterotoxin

118
Q

Inserts into enterocyte membranes to form pores leading to alterations in intracellular calcium and membrane permeability. This leads to loss of cellular fluid and macromolecules.

A

Enterotoxin

119
Q

are liberated into the surrounding tissue, causing more local tissue necrosis and systemic toxemia.

A

Collagenase, protease, and lipase

120
Q

one of the most effective ways to prevent clostridial wound infections along with prophylactic antibiotic therapy.

A

Immediate and rigorous cleansing and surgical of deep wounds, compound fractures, and infected incisions

121
Q

Immediate and rigorous cleansing and surgical of deep wounds, compound fractures, and infected incisions, is one of the most effective ways to prevent clostridial wound infections along with prophylactic antibiotic therapy.

A

PREVENTION AND CONTROL of Clostridium perfringens

122
Q

Prevention of food poisoning involves good cooking hygiene and adequate refrigeration.

A

PREVENTION AND CONTROL of Clostridium perfringens

123
Q

Debridement (removal) of diseased tissue eliminate the conditions that promote the spread of gangrenous infections. This surgical treatment is supplemented by large doses of broad-spectrum antimicrobial agents in the intestines or body cavity, where only limited amount of tissue can be removed.

A

PREVENTION AND CONTROL of Clostridium perfringens

124
Q

Surgical removal or amputation of the affected site in cases wherein there is extensive myonecrosis.

A

PREVENTION AND CONTROL of Clostridium perfringens

125
Q

is being used to treat patients with clostridial wound infections and diabetic ulcers. This hyperbaric therapy involves breathing higher levels of oxygen. The increased oxygen content of the tissues presumably blocks further bacterial multiplication and toxin production, thereby promoting healing.

A

large decompressor chamber

126
Q

Common names: Drumstick bacillus, lollipop bacillus, tennis racquet bacillus, tack head bacillus

A

Clostridium tetani

127
Q

Spores are found in the soil, and in the intestinal tract of humans or animals

A

Clostridium tetani: HABITAT

128
Q

Transmission occurs by wound contamination with spores from the soil (or soiled objects) or feces

A

Clostridium tetani: TRANSMISSION

129
Q

Tetanus

Gk. tetanos means?

A

to stretch

130
Q

Acquired by spore contamination of wound; Necrotic tissue and poor blood supply in the wound favor spore germination and growth of anaerobic clostridia, and elaboration of exotoxins.

A

Tetanus

131
Q

Some common types of wounds that can lead to tetanus infection include cuts from a rusty can, tattoos, animal bites, splinters, surgical wounds, injection drug use, body piercing, or lacerations.

A

Tetanus

132
Q

The incubation period varies from 4 to 10 days, and shorter incubation period signifies a more serious condition.

A

Tetanus

133
Q

whereby muscles contract uncontrollably

A

muscular spasm

134
Q

is an early effect of the disease due to the rigid contraction of the masseter muscle of the face, resulting to difficulty in opening the jaw.

A

Trismus (or lockjaw)

135
Q

is described as sustained trismus. The patient looks eerily as though he is smiling.

A

Risus sardonicus (sarcastic grin)

136
Q

caused by involvement of spinal musculature

A

Opisthotonus

137
Q

is characterized by continuous back spasms causing extreme arching of the back, flexion of the arms, and extension of the legs. Contractions are intermittent and extremely painful and may be forceful enough to break the vertebrae.

A

Opisthotonus

138
Q

Respiratory failure ensues, and without treatment, results in high mortality rate up to how many %?

A

70%

139
Q

is due to fecal contamination of the umbilical cord, or use of contaminated instruments (e.g., umbilical stumps).

A

Tetanus neonatorum (neonatal tetanus)

140
Q

showing spastic paralysis of the paravertebral muscles, which locks the back into a rigid, arched position. Also note the abnormal flexion of the arms and the legs.

A

Baby with neonatal tetanus

141
Q

A potent, heat-stable, plasmid-mediated neurotoxin and one of the most poisonous substances; only a small amount is required to initiate symptoms.

A

Tetanospasmin

142
Q

Released by vegetative cells at the site of infection, and spread throughout the body by the blood stream. (The bacilli remain at the site of infection.)

A

Tetanospasmin

143
Q

Binds to receptors on the presynaptic membranes of motor neurons, then travels along the nerves to the central nervous system (CNS).

A

Tetanospasmin

144
Q

Binds to gangliosides, blocking the release of inhibitory neurotransmitters (glycine and γaminobutyric acid – GABA), so muscles are released from inhibition and begin to contract uncontrollably — spastic paralysis.

A

Tetanospasmin

145
Q

is irreversible, so recovery requires the generation of new axon terminals.

A

Binding of the toxin

146
Q

a) After traumatic injury, bacilli infecting the local tissue secrete tetanospasmin, which is absorbed by the peripheral axons and is carried to target neurons in the spinal column.
(b) In the spinal cord, the toxin attaches to the junction of regulatory neurons that inhibit inappropriate contraction. Released from inhibition, the muscles, even the opposing members of a muscle group, receive constant stimuli and contract uncontrollably.
(c) Muscles contract spasmodically, without regard to regulatory mechanisms of conscious control. Note the clenched jaw, typical of risus sardonicus.

A

The events in tetanus

147
Q

that causes local tissue necrosis at sites of vegetative growth, thereby lowering oxygen tension in tissue.

A

hemolysin

148
Q

Routine active immunization with tetanus toxoid, usually combined with diphtheria toxoid and pertussis vaccine (DPT) for primary immunization in childhood, and DT for adults, can completely prevent tetanus.
Five doses of DT are recommended, to be given at the ages of 2, 4, 6, and 18 months, and once again between the ages of 4 and 6 years. Thereafter, a booster of adulttype tetanus diphtheria toxoid should be given every 10 years.

A

PREVENTION AND CONTROL of Clostridium tetani

149
Q

A patient with symptoms of tetanus should immediately receive antitoxin therapy with human tetanus immune globulin (TIGH). It neutralizes the circulating toxin, but is ineffective against toxin already fixed in the central nervous system. Active immunization with tetanus toxoid should accompany antitoxin prophylaxis.

A

PREVENTION AND CONTROL of Clostridium tetani

150
Q

Prevention of tetanus also depends on aggressive wound care. Surgical debridement is vitally important because it removes the necrotic tissue that is essential for proliferation of the organisms.

A

PREVENTION AND CONTROL of Clostridium tetani

151
Q

Antibiotic (penicillin) strongly inhibits the growth of C. tetani and stops further toxin production.

A

PREVENTION AND CONTROL of Clostridium tetani

152
Q

Common name: Canned good bacillus

A

Clostridium botulinum

153
Q

Spores are found in the soil, and vegetation.

A

Clostridium botulinum: HABITAT

154
Q

Transmission is by ingestion preformed toxin or spores in food, or by wound contamination with spores.

A

Clostridium botulinum: TRANSMISSION

155
Q

L. botulis = sausage: the disease was earlier associated with spoiled sausage

A

Classical Botulism or Food-borne botulism

156
Q

Acquired by ingestion of preformed toxin, often traced to improperly canned (also vacuum-packed) food.

  • The foods most often implicated are home-canned, low acid foods such as vegetables, fruits, condiments and fish.
  • Most cases are due to inadequate sterilization, failing to kill the spores during the canning process. Canning creates an environment with little or no air which favors anaerobic germination of spores into vegetative cells that produce exotoxins.
A

Classical Botulism or Food-borne botulism

157
Q

Signs and symptoms:

-Onset is 12 to 72 hours after ingestion, depending on the size of the dose (amount of toxin ingested).

A

Classical Botulism or Food-borne botulism

158
Q

Signs and symptoms:
-Initial neuromuscular symptoms involve the muscles of the head: ‣diplopia (double vision)
‣dysphagia (difficulty in swallowing), dysphonia (difficulty in speech) ‣dizziness, but there is no sensory or mental lapse.

A

Classical Botulism or Food-borne botulism

159
Q

Later symptoms are descending muscular paralysis; cardiac arrhythmias and blood pressure instability are also evident; death results from respiratory paralysis unless there is proper respiratory intensive care, including mechanical ventilation.

A

Classical Botulism or Food-borne botulism

160
Q

Commonly occurs in infants between the ages of 3 weeks and 8 months is now the most commonly diagnosed form of botulism.

A

Infant botulism

161
Q

Acquired by ingestion of spores C. botulinum in honey, also from the soil, household dust, or another source; spores yield vegetative bacteria, which multiply and produce exotoxin in the infant’s colon.

A

Infant botulism

162
Q

Signs and symptoms include constipation, poor muscle tone, lethargy, and feeding problems and may have ophthalmic and other paralyses similar to those in food-borne botulism, and respiratory arrest.

A

Infant botulism

163
Q

Has accounted for a small number of sudden infant death syndrome (SIDS), also known as “crib death”.

A

Infant botulism

164
Q

Occurs when spore of C. botulinum enter a wound or a puncture, germinate and produce botulinum toxins.

A

Wound botulism

165
Q

The symptoms are similar to those of food borne botulism.

A

Wound botulism

166
Q

Cases have increasingly been reported in injecting drug users.

A

Wound botulism

167
Q

Among most potent exotoxins known (together with tetanospasmin)

A

Botulinum toxin (botulin)

168
Q

Heat-labile, phage-mediated neurotoxin

A

Botulinum toxin (botulin)

169
Q

Of seven (7) types — serotypes A to G

A

Botulinum toxin (botulin)

170
Q

Is absorbed into the blood circulation, and binds to receptors of presynaptic membranes of motor neurons of the cranial nerves initially, followed by the peripheral nervous system.

A

Botulinum toxin (botulin)

171
Q

Blocks the release of excitatory neurotransmitter acetylcholine at the peripheral nerve endings, including neuromuscular junctions, resulting in lack of muscle contraction —flaccid paralysis.

A

Botulinum toxin (botulin)

172
Q

are associated with botulism in man, with type F as the least common.

A

Botulinum toxin Types A, B, E, and F

173
Q

are associated with botulism in birds and mammals.

A

Botulinum toxin Types C and D

174
Q

produced by what is now reclassified C. argentinense; it is not clear to what extent these organisms cause botulism in humans.

A

Botulinum toxin Type G

175
Q

The botulinum toxin in controlled doses can be used to temporarily minimize wrinkles.

A

Cosmetic injection of botulinum toxin (botox)

176
Q

depends on educating the public about the proper methods of preserving and handling canned foods. Home canners should be aware of the types of foods and conditions that are likely to cause botulism.

A

Prevention of botulism

177
Q

The administration of large doses of horse C. botulinum antitoxin is said to be useful in neutralizing free toxin.

A

PREVENTION AND CONTROL of Clostridium botulinum

178
Q

A recommended prevention measure for infant botulism is to avoid giving honey to infants less than 12 months of age, as botulinum spores are often present. In older children and adults the normal intestinal bacteria suppress development ofC. botulinum

A

PREVENTION AND CONTROL of Clostridium botulinum

179
Q

Formerly Clostridium difficile

A

Clostridioides difficile

180
Q

It is part of the normal gastrointestinal flora in 2–10% of humans, sometimes at higher rates among hospitalized persons and infants.

A

Clostridioides difficile: HABITAT

181
Q

Disease is acquired endogenously.

A

Clostridioides difficile: TRANSMISSION

182
Q

Develops as drug-resistant C. difficile super infect the intestine when the normal flora has been disrupted by antibiotics.

A

Antibiotic-associated diarrhea (AAD) and Pseudomembranous colitis (PMC, a.k.a. Antibioticassociated colitis)

183
Q

The predominant symptom is diarrhea commencing late (usually 5 - 10 days) into the antimicrobial therapy or even after the therapy has stopped.

A

Antibiotic-associated diarrhea (AAD) and Pseudomembranous colitis (PMC, a.k.a. Antibioticassociated colitis)

184
Q

The diarrhea may be mild and watery or bloody and accompanied by abdominal cramping, leukocytosis, and fever. The colon is inflamed and gradually sloughs off loose, membrane-like patches called pseudomembranes consisting of fibrin and inflammatory cells.

A

Antibiotic-associated diarrhea (AAD) and Pseudomembranous colitis (PMC, a.k.a. Antibioticassociated colitis)

185
Q

If the condition is not arrested, cecal (cecum) perforation and death can result.

A

Antibiotic-associated diarrhea (AAD) and Pseudomembranous colitis (PMC, a.k.a. Antibioticassociated colitis)

186
Q

An endoscope view of an inflamed colon caused by a C. difficile infection. The white plaques represent mucus and dead cells that have built up on the colon walls.

A

Pseudomembranous colitis

187
Q

Cause necrosis of the intestinal epithelium; both act in the cytoplasm of enterocytes which results in the disruption of intercellular tight junctions followed by altered membrane permeability and fluid secretion.

A

Polypeptide toxins: Toxin A (enterotoxin) and Toxin B (cytotoxin/ cytopathic toxin)

188
Q

Within hours of contact with enterocytes cell rounding and neutrophilic infiltration also appear.

A

Polypeptide toxins: Toxin A (enterotoxin) and Toxin B (cytotoxin/ cytopathic toxin)

189
Q

Because infected persons shed large number of spores in their stools, increased precautions are necessary to prevent spread of the agent to other patients who may be on anti-microbic therapy.

A

PREVENTION AND CONTROL of Clostridioides difficile

190
Q

Some new techniques include vaccination of C. difficile toxoid and restoration of normal flora by means of a mixed culture of lactobacilli and yeasts.

A

PREVENTION AND CONTROL of Clostridioides difficile

191
Q

Mild, uncomplicated cases respond to withdrawal of antibiotics and replacement therapy for lost fluids and electrolytes.

A

PREVENTION AND CONTROL of Clostridioides difficile

192
Q

is a microbial insect pathogen however, it is also capable of causing disease in humans occasionally — food poisoning, eye and other local infections.

A

B. thuringiensis

193
Q

Commercial preparations containing endospores and crystalline toxin (Bt) of this bacterium are sold in gardening supply shops to be sprayed on plants.

A

Bacillus thuringiensis

194
Q

The genes responsible for production of the Bt has been extracted and combined with those of plants to produce genetically - modified plants that are pest resistant (e.g. Bt corn).

A

Bacillus thuringiensis

195
Q

Are not easily distinguishable from B. cereus as to microscopic appearance, colonial characteristics, and identification tests.

A

Bacillus thuringiensis

196
Q
  • Crystal formation is used to differentiate B. thuringiensis from B. cereus.
  • After growth on sporulation agar or on nutrient agar for at least 48 hours, B. thuringiensis produces cuboid or diamond-shaped crystals adjacent to the spore (parasporal crystals).
  • The crystals, which consist of naturally produced insecticidal toxin, are demonstrated with phase contrast microscopy or staining with malachite green.
A

Bacillus thuringiensis

197
Q

Common name: hay bacillus

A

Bacillus subtilis

198
Q

is a harmless air contaminant.

A

B. subtilis

199
Q

When present in large numbers can cause lung and blood infections in people with weakened immunity.

A

Bacillus subtilis

200
Q

Gram-positive bacilli typically in chains, individual cells are less than 1µm wide, sporangia are not swollen, and spores are ellipsoidal.

A

Bacillus subtilis

201
Q

Nonmotile, non-encapsulated.

A

Bacillus subtilis

202
Q

Colonies on 5% sheep BAM: Large (2-7 mm), flat, dull, with “frosted-glass” or “ground-glass appearance”; may be pigmented (pink, yellow, orange, or brown); may be β-hemolytic.

A

Bacillus subtilis

203
Q

Colonies on PEMBA: Cream to light yellow with no zone of egg precipitation.

A

Bacillus subtilis

204
Q

Because it is a common laboratory contaminant; identification is not recommended unless isolated from a sterile site (e.g., blood) or found in large numbers in pure culture.

A

Bacillus subtilis

[8] BACTERIAL SPECIES (5 decks)

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