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[9b] MODULE 6 UNIT 2: Curved, Gram-negative Bacilli > LECTURE > Flashcards

LECTURE Flashcards

1
Q

V. cholerae: common name

A

“Kommabacillus”

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2
Q

V. cholerae: habitat

A

human colon

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3
Q

Man is the only known reservoir of V. cholerae. Human carriage may persist after untreated infection for months after infection; however, permanent carrier state is rare. They can survive and grow in fresh and brackish water.

A

V. cholerae

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4
Q

V. cholerae: transmission

A

fecal-oral route.

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5
Q

The most common source of infection is contaminated water. Food, especially shellfish (contaminated from contaminated waters) eaten
raw, have also been a source of infection.

A

V. cholerae

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6
Q

Cholera, which is also known as

A

Asiatic cholera or epidemic cholera

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7
Q

The incubation period of Cholera is [?] depending on the size of the inoculum ingested.

A

12 hours up to 3 days

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8
Q

Symptoms include sudden onset of nausea, vomiting, abdominal cramps and profuse “rice water” diarrhea (stool resembles water in which the rice has been boiled) that may be as many as 10 to 30 per day, containing mucus, epithelial cells, and large numbers of species

A

Cholera

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9
Q

In severe cholera, infected individual can lose several liters of fluid, as much as [?]. If left untreated, it can result in a rapid fluid and electrolyte loss that leads to dehydration, hypovolemic shock, metabolic acidosis, and death in a matter of hours.

A

20-30 liters per day

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10
Q

To cause disease, cells of V. cholerae must adhere to the gastric and intestinal mucosal epithelial cells of the host; two properties that aid in the penetration of the protective mucin layer that coats the surface of the gastroenteric mucosa.

A

Motility and mucinase

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11
Q

The cholera toxin is a heat-labile enterotoxin, the genes for which are encoded in a lysogenic phage.

A

Choleragen (cholera toxin)

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12
Q

Cholera is consists of 2 subunits:

A

A (active) subunits and binding (B) subunits

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13
Q

The A subunit is composed of two peptides:

A

A1 with toxin activity

A2

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14
Q

it activates adenylate cyclase, causing increased levels of cyclic adenosine monophosphate (cAMP) and hypersecretion of electrolytes (Na+, K+, HCO3−) and water out of the cell and into the lumen of the intestine. The net effect is that the gastrointestinal tract’s absorptive ability is overwhelmed, resulting in the massive outpouring of watery stools

A

A1 with toxin activity

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15
Q

facilitates penetration of the A1 subunit into the enterocyte

A

A2

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16
Q

[?] binds the A2 subunit to the GM1 ganglioside receptor on the cell membrane of the enterocytes. There are five B subunits per toxin molecule, arranged in a ring around a central core that contains the enzyme A1.

A

B subunit

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17
Q

Heat-labile substances that are found in all V. cholerae strains

A

H antigen

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18
Q

Cell wall lipopolysaccharides that confer serologic specificity to the bacterial cells

A

O antigen

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19
Q

V. cholerae strains are designated into 3 major serogroups based on agglutination with V. cholerae O1 polyvalent antiserum.

A

Serogroups of V. cholerae

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20
Q
  • Is agglutinated by V. cholerae O1 antiserum
A

V. cholerae O1

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21
Q
  • Is NOT agglutinated by V. cholerae O1 antiserum
A

V. cholerae non-O1

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22
Q
  • Is NOT agglutinated by V. cholerae O1 antiserum
A

V. cholerae O139

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23
Q

There are two biotypes of V. cholerae serogroup O1 based on their differences in biochemical characteristics, which is associated with how they differ with respect to the severity of the disease they can cause.

A

Biotypes of V. cholerae O1

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24
Q

caused the epidemic cholera from early 1800s to early 1900 – during this time, there were 6 waves of cholera pandemic that spread across the world.

A

Classical strain of V. cholerae

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25
Q

was isolated in the early 1900s from Meccabound pilgrims at the El Tor Quarantine Station in Sinai Peninsula.

A

El Tor strain of V. cholerae

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26
Q
  • Includes virulent strains producing cholera toxin
A

V. cholerae O1

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27
Q
  • Associated with epidemic cholera
A

V. cholerae O1

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28
Q
  • Includes V. cholerae O2 up to V. cholerae O138
A

V. cholerae non-O1

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29
Q
  • Does NOT produce cholera toxin; but, they appear to produce an enterotoxin different from cholera toxin.
A

V. cholerae non-O1

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30
Q
  • Has been associated with isolated cases of diarrheal disease (NOT epidemic-associated)
A

V. cholerae non-O1

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31
Q
  • Represented a new serogroup, as it is a strain that could not be identified as any of the 138 known types of V. cholerae
A

V. cholerae O139

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32
Q
  • Is also known as “Bengal strain” to indicate its first isolation from the coastal areas of the Bay of Bengal; it caused large epidemics of cholera in Bangladesh, India, and neighboring countries in 1992.
A

V. cholerae O139

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33
Q
  • Produces cholera toxin in quantities similar to that produced by V. cholerae O1
A

V. cholerae O139

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34
Q
  • Makes polysaccharide capsule like other non-O1 strains (V. cholerae O1 does not make a capsule.)
A

V. cholerae O139

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35
Q
  • Has spread in epidemic proportions across the Indian subcontinent.
A

V. cholerae O139

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36
Q

These vibrios resembled classical V. cholerae in many way but caused lysis of goat or sheep erythrocytes in a test known as the Greig test.

A

El Tor strain of V. cholerae

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37
Q

has been found to be hardier and better capable of surviving in the environment

A

El Tor strain of V. cholerae

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38
Q

epidemic in the Phil in 1961 that has started the 7th pandemic. Currently, the El Tor biotype of V, cholerae O1 is the predominant ch

A

El Tor strain of V. cholerae

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39
Q

A number of tests differentiate them from classical V. cholerae

A

El Tor strain of V. cholerae

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40
Q

V. cholerae serogroup, in both the classical and the El Tor biotypes, are separated into 3 serotypes based on differences in antigen determinants on the O side chain of the lipopolysaccharide (LPS) antigen. These serotypes are important for epidemiological studies. These can be detected by agglutination with specific antiserum

A

Serotypes of V. cholerae O1

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41
Q

has determinants A, and B

A

Ogawa

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42
Q

has determinants A, and C

A

Inaba

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43
Q

produces all 3 antigens (A, B, C))

A

Hikojima

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44
Q

are considered the predominant epidemic strains.

A

Ogawa and Inaba

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45
Q

has been isolated in outbreaks , but its occurrence has been rare

A

Hikojima

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46
Q

Control rests on education and on improvement of sanitation, particularly of food and water.

A

PREVENTION AND CONTROL of Vibrio cholerae

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47
Q

Patients should be isolated, their excreta disinfected, and contacts followed up

A

PREVENTION AND CONTROL of Vibrio cholerae

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48
Q

Repeated injection of a vaccine containing either
lipopolysaccharides extracted from vibrios or [?] can confer limited protection to heavily exposed persons (eg, family contacts) but is not effective as an epidemic control measure.

A

dense Vibrio suspensions

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49
Q

inhabits seawaters

A

Vibrio parahaemolyticus

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50
Q

first recognized as a pathogen in Japan in 1950, when it caused a large food poisoning outbreak

A

Vibrio parahaemolyticus

51
Q

causes gastroenteritis — it is the second most common Vibrio species implicated in gastroenteritis after V. cholerae

A

Vibrio parahaemolyticus

52
Q

Infection results from consumption of raw, improperly cooked, or recontaminated seafood, particularly oysters

A

Vibrio parahaemolyticus

53
Q

After an incubation period of 12–24 hours, nausea and vomiting, abdominal cramps, fever, and watery to bloody diarrhea occur and fecal leukocytes are often observed.

A

Vibrio parahaemolyticus

54
Q

The enteritis tends to subside spontaneously in 1–4 days with no treatment other than restoration of water and electrolyte balance.

A

Vibrio parahaemolyticus

55
Q

halophilic organism of Vibrio parahaemolyticus requiring [?] and grows slowly on nonselective media

A

2-4% NaCl

56
Q

No enterotoxin has yet been isolated from this organism

A

Vibrio parahaemolyticus

57
Q

there is an association between hemolysin production and virulence, known as the

A

Kanagawa phenomenon

58
Q

a high-salt (7%) blood agar (defibrinated human or rabbit blood) medium containing D-mannitol as the carbohydrate source

A

Wagatsuma agar

59
Q

Kanagawa phenomenon is well recognized to be closely associated with human pathogenicity of V. parahaemolyticus due to the expression of

it damages the erythrocyte membrane by acting as a pore-forming toxin

A

Thermostable Direct Hemolysin (TDH).

60
Q

Most [?] of V. parahaemolyticus do NOT manifest Kanagawa phenomenon.

A

environmental strains

61
Q

Causes the second most serious types of Vibrio associated infections after cholera

A

Vibrio vulnificus

62
Q

Causes the second most serious types of Vibrio associated infections after cholera

A

Vibrio vulnificus

63
Q

Infections of Vibrio vulnificus generally fall into two categories

A

Bacteremia

Wound infections

64
Q

Thought to occur through the gastrointestinal route after the consumption of shellfish, especially raw oysters and in persons who have alcoholism or liver disease.

A

Bacteremia

65
Q

Often proceeds rapidly, with development of severe disease and about 50% of the patients die.

A

Bacteremia

66
Q

May occur among normal or immunocompromised persons who are in contact with water where the bacterium is present.

A

Wound infections

67
Q

Infections may be mild but often proceed rapidly (over a few hours), with development of bullous skin lesions, cellulitis, and myositis with necrosis

A

Wound infections

68
Q

Vibrio vulnificus are halophilic organism requiring [?]; shows good growth on blood agar

A

1% NaCl

69
Q

formerly classified with the vibrios because of their positive oxidase and characteristic microscopic morphology but has been reclassified because of DNA homology studies.

A

campylobacters

70
Q

campylobacters are primarily zoonotic organisms causing diseases collectively referred to as

A

campylobacterioses

71
Q

They have been known to cause abortion in domestic animals, such as cattle, sheep, and swine.

A

Campylobacter species

72
Q

are found worldwide as inhabitants of the GI tract and oral cavity of humans and animals including wild or domesticated cattle, sheep, swine, goats, dogs, cats, and fowl, especially turkeys and chickens.

A

Campylobacter species

73
Q

Campylobacter species: transmission

A

fecal-oral route

74
Q

Infections are acquired by ingestion of contaminated beverages and improperly cooked foods, especially poultry; or direct contact with infected animals or animal products and their excreta.

A

Campylobacter species

75
Q

is known as the most common cause of bacterial gastroenteritis worldwide

A

C. jejuni

76
Q

When ingested, the bacteria multiply in the mucosa of the last segment of the small intestine (ileum); they invade the epithelium, and produce inflammation.

A

Gastroenteritis

77
Q

Symptoms become apparent after an incubation period of 1 to 7 days which include headache, fever, chills, abdominal pain followed by cramps and bloody or watery diarrhea; and rarely accompanied by nausea and vomiting.

A

Gastroenteritis

78
Q
  • Stools often contain red and white blood cells.
A

Gastroenteritis

79
Q

In most patients, the illness is self-limited and usually resolves in 5 to 8 days.

A

Gastroenteritis

80
Q

Occasionally, the bloodstream is invaded, and a clinical picture of enteric fever develops.

A

Gastroenteritis

81
Q

Localized tissue invasion; Endotoxin

A

Gastroenteritis

82
Q

A heat-labile enterotoxin that stimulates a secretory diarrhea like that of cholera.

A

Campylobacter jejuni toxin (CJT)

83
Q

is an autoimmune disorder characterized by acute ascending paralysis caused by damage to the peripheral nervous system.

A

Guillain-Barré syndrome (GBS)

84
Q

Strong evidence suggests that Campylobacter infection plays a role in GBS since many patients with GBS test positive for [?] to Campylobacter,

A

antibodies

85
Q

It is believed that antibodies produced during a Campylobacter infection bind to [?] found on peripheral nerves.

A

gangliosides

86
Q

[?] with these nerve cells in an autoimmune response may be responsible for this debilitating nerve disorder.

A

Cross-reactivity

87
Q

an opportunistic pathogen that causes systemic

infections in immunocompromised patients and elderly patients

A

C. fetus subspecies fetus

88
Q

may be the portal of entry of C. fetus subspecies fetus

A

gastrointestinal tract

89
Q

has been isolated most frequently from blood cultures and is occasionally associated with gastrointestinal illness

A

C. fetus subspecies fetus

90
Q

is a rare cause of human disease

A

C. fetus subspecies venerealis

91
Q

Disease is associated with several surface array proteins

A

Campylobacter fetus

92
Q

form a capsule-like structure on the surface of the organism

A

Campylobacter fetus

93
Q

has been compared with the polysaccharide capsules of pathogens such as Neisseria meningitidis and Streptococcus pneumoniae

A

Campylobacter fetus

94
Q

presence of which is correlated with the ability of the bacteria to cause bacteremia after oral challenge and cause death in a high percentage of the animals

A

Campylobacter fetus

95
Q

initial name of Campylobacter pylori

A

Campylobacter pyloridis

96
Q

Colonizes mucous lining mainly of the antrum of the stomach (also the duodenum) in 25% of healthy middle-aged adults and in >60% of adults over 60 years of age. The major, if not exclusive, reservoir is humans.

A

Helicobacter pylori

97
Q

Exact modes of transmission are not known.

A

Helicobacter pylori

98
Q

It is acquired early in life and carried asymptomatically.

A

Helicobacter pylori

99
Q

Person-to-person transmission by the oral-oral to oral-fecal route is likely because intrafamilial clustering of infection occurs.

A

Helicobacter pylori

100
Q

Since other animals are likewise susceptible, it has been proposed that the disease is a zoonosis transmitted to humans from an animal reservoir.

A

Helicobacter pylori

101
Q

It can also be spread by house flies acting as mechanical vectors

A

Helicobacter pylori

102
Q

Diseases of Helicobacter pylori

A 
Gastritis
Peptic ulcers (especially, duodenal)
103
Q

a protease, modifies the gastric mucus and aids in the penetration of the mucous layer of the gastric epithelium where physiologic pH (about 7.4) is present, and rapidly shifts down to neutral as it penetrates further.

A

Mucinase

104
Q

activity yields production of ammonia that neutralizes stomach acid. The ammonia produced is cytotoxic to gastric epithelial cells, too.

A

Urease

105
Q

even in mucus, enables the organism to find its way to the epithelial surface

A

Motility

106
Q

associated with injury to the gastric epithelium

A

Vacuolating cytotoxin

107
Q

There is also a strong evidence that H. pylori is linked to gastric adenocarcinoma and to the development of

A

gastric non-Hodgkin’s lymphoma

(i.e., mucosa associated lymphoid tissue [MALT] lymphomas).

108
Q

The genus Aeromonas previously resided in the family Vibrionaceae but phylogenetic evidence from molecular studies resulted in the proposal of a separate family,

A

Aeromonadaceae

109
Q

ubiquitous — they have been isolated in tap water, freshwater, estuarine, marine environments worldwide, soil, and food.

A

Aeromonas species

110
Q

They are frequently isolated from retail produce sources and animal meat products.

A

Aeromonas species

111
Q

Four categories of human infections have been described to be associated with Aeromonas species:

A

Gastroenteritis
Cellulitis and wound infections
Septicemia
Miscellaneous

112
Q
  • caused mostly by A. caviae complex
A

Gastroenteritis

113
Q
  • other Aeromonas species associated with diarrhea are A. hydrophila and A. veronii
A

Gastroenteritis

114
Q
  • manifestations ranges from acute watery diarrhea to less commonly a dysenteric type of illness
A

Gastroenteritis

115
Q

five diarrheal presentations are observed in patients in whom an Aeromonas has been isolated from their stools:

A

a. an acute, secretory diarrhea often accompanied by vomiting
b. an acute, dysenteric form of diarrhea (similar to shigellosis) with blood and mucus
c. a chronic diarrhea usually lasting more than 10 days
d. a cholera-like disease, including rice-water stools
e. Traveler’s diarrhea (similar to enterotoxigenic E. coli).

116
Q

Most cases are self-limiting, but in the pediatric, geriatric, and immunocompromised populations, supportive therapy and antimicrobials are often indicated.

A

Traveler’s diarrhea

117
Q

Invariably involves a recent traumatic

aquaticexposure and generally occurs on the extremities.

A

Cellulitis and wound infections

118
Q

The most common presentation is [?], although there have been a few cases of myonecrosis and necrotizing fasciitis and even a rare case of ecthyma gangrenosum associated with sepsis.

A

cellulitis

119
Q

are predominantly A. hydrophila subsp. hydrophilia

A

Aeromonad wound isolates

120
Q
  • Is one of the most invasive type of Aeromonas infection
A

Septicemia

121
Q
  • Has a strong association with the species A. veronii biovar sobria, and A. hydrophila.
A

Septicemia

122
Q

have also been implicated in cases of meningitis, osteomyelitis, pelvic abscesses, otitis, cystitis, endocarditis, peritonitis, cholecystitis, keratitis associated with contact lens wear, and endophthalmitis in healthy and immunocompromised individuals.

A

Aeromonas species

123
Q
  • Occurs in patients who are immunocompromised and have a history of liver disease or dysfunction, hematologic malignancies, hepatobiliary disorders, or traumatic injuries.
A

Septicemia

124
Q

Aeromonas species’ pathology has been associated with:

A
  • Production of hemolysins
  • Production of enterotoxins by some strains
  • The ability to invade cells

[9b] MODULE 6 UNIT 2: Curved, Gram-negative Bacilli (2 decks)

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