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[9a] MODULE 6 UNIT 1: Enterobacteriaceae and Other Related Enterobacteria > LECTURE > Flashcards

LECTURE Flashcards

1
Q

Enterobacteriaceae is the most common group of [?] cultured in clinical laboratories both as normal flora and as agents of disease.

A

gram-negative rods

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2
Q

The taxonomy of the Enterobacteriaceae is complex and rapidly changing since the introduction of techniques that measure evolutionary distance, such as [?] and [?]

A

nucleic acid hybridization and nucleic acid sequencing.

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3
Q

Revisions in bacterial taxonomy and nomenclature, and recognition and acknowledgement of novel bacteria are published in the

A

International Journal of Systematic and Evolutionary Microbiology

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4
Q

Changes published in the years [?]include the major reorganization of the family Enterobaceriaceae and the revisions within the genus Enterobacter.

A

2016 and 2017

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5
Q

GENERAL CHARACTERISTICS OF ENTEROBACTERIACEAE

  • Gram reaction and shape
  • spore
  • motility
  • capsule
  • oxygen requirement
  • oxidase
  • carbohydrate fermentation
  • nitrate reduction enzyme, which to what
A
  • Gram-negative bacilli
  • Non-spore forming
  • Motile (peritrichous)
  • capsule
  • oxygen requirement
  • oxidase
  • carbohydrate fermentation
  • nitrate reduction enzyme, which to what
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6
Q

Non-motile Enterobacters

A

Klebsiella
Shigella
Yersinia

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7
Q

Yersinia are nonmotile at [?]

A

35-37 oC

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8
Q

Yersinia are motile at [?]

A

room temperature

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9
Q

(somatic antigen or cell wall antigen)

A

O antigens

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10
Q

(capsular antigen or fimbrial antigen)

A

K antigen

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11
Q

(flagellar antigen)

A

H antigen

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12
Q

most external part of the cell wall lipopolysaccharide

A

O antigens

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13
Q

 consisting of repeating units of polysaccharide

A

O antigens

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14
Q

 usually are detected by bacterial agglutination

A

O antigens

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15
Q

 each genus of Enterobacteriaceae is associated with specific O groups – a single organism may carry several O antigens

A

O antigens

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16
Q

HA-S

A

O antigens

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17
Q

H-L

A

K antigen

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18
Q

HA-L

A

H antigen

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19
Q

external to the O antigens on some but not all Enterobacteriaceae

A

K antigen

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20
Q

found on the surface of flagella.

A

H antigen

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21
Q

within a single serotype, flagellar antigens may be present in either or both of two forms, called phase 1 (designated by lower-case letters) and phase 2 (designated by Arabic numerals).

A

H antigen

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22
Q

organism tends to change from one phase to the

other; this is called phase variation.

A

H antigen

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23
Q 
 aerobic and facultative anaerobic
 non-sporeforming
 gram-negative rods
 cytochrome-oxidase negative
 capable of growth in the presence of bile salts
A

COLIFORMS

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24
Q

 ferment lactose at either 35 or 37 oC

 include the normal enteric flora

A

COLIFORMS

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25
Q

COLIFORMS spp

A

o Escherichia
o Klebsiella
o Enterobacter
o Citrobacter

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26
Q

differ from coliforms by their inability to ferment lactose; NLF

A

NONCOLIFORMS

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27
Q

Fecal coliforms

o most common facultative bacterium in feces of man and warm-blooded animals
o indicator organism of choice for fecal contamination

A

 Escherichia coli

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28
Q

ferments lactose at 44.5 oC

A

Fecal coliforms

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29
Q

Non fecal coliforms

A

Klebsiella, Enterobacter, Citrobacter

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30
Q

Fecal coliforms spp

o most common facultative bacterium in feces of man and warm-blooded animals
o indicator organism of choice for fecal contamination

A

 Escherichia coli

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31
Q

do NOT ferment lactose at 44.5 oC

A

Non fecal coliforms

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32
Q

Non fecal coliforms spp

A

Klebsiella, Enterobacter, Citrobacter

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33
Q

Opportunistic, normal gut flora spp

A

 Proteus
 Providencia
 Morganella

 Serratia
 Hafnia
 Edwardsiella

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34
Q

Pathogenic enterics (true enteropathogens) spp

A

 Salmonella
 Shigella
 Yersinia enterocolitica
 Y. pseudotuberculosis

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35
Q

Pathogenic, non-enteric spp

A

 Yersinia pestis

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36
Q

Escherichia coli was first described by [?] in 1885

A

Theodor Escherich

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37
Q

Escherichia coli common name

A

“colon bacillus”

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38
Q

Infections with E. coli and the other enteric bacteria depend on the [?] and cannot be differentiated by [?] from processes caused by other bacteria.

A

site

symptoms or signs

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39
Q

accounts for approximately 90% of first urinary tract infections in young women

A

Uropathogenic E. coli

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40
Q

Strains of E. coli that cause UTIs usually originate in the large intestine as resident biota.

A

Uropathogenic E. coli

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41
Q

Infection is more common in women because of their relatively short urethras that promote ascending infection to the bladder (cystitis) and occasionally, the kidneys.

A

Uropathogenic E. coli

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42
Q

Strains that cause lower urinary tract and acute pyelonephritis in otherwise healthy hosts are designated as uropathogenic E. coli and are
different from strains causing disease in the urinary tracts of individuals who are immunocompromised

A

Uropathogenic E. coli

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43
Q

Uropathogenic strains possess O antigen types that have specifically elaborated virulence factors that facilitate colonization and subsequent clinical infections

A

Uropathogenic E. coli

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44
Q

most common cause of UTIs;

A

E. coli

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45
Q

most common cause of UTIs

A

E. coli

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46
Q

primary virulence factor associated with the ability of E. coli to cause UTIs

A

Pili (P fimbrae)

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47
Q

allow the bacteria to attach to the urinary epithelial

mucosa and not be washed out with urine flow

A

Pili (P fimbrae)

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48
Q

binds to P blood group antigen

A

Pili (P fimbrae)

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49
Q

cytolysins which can kill immune effector cells and inhibit

chemotaxis and phagocytosis of certain white blood cells

A

Hemolysins

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50
Q

allows the bacterial cell to chelate iron; free iron is

generally unavailable within the host for use by bacteria

A

Aerobactin

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51
Q

Enterovirulent E. coli

A

Diarrheagenic E. coli

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52
Q

E. coli may cause several different GI syndromes

A

Diarrheagenic E. coli

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53
Q

based on virulence factors, clinical manifestation, epidemiology, and different O and H serotypes, there are five major categories of diarrheagenic E. coli:

A

Enteropathogenic E. Coli (EPEC)
Enterotoxigenic E. coli (ETEC)
Enterohemorrhagic E. coli (EHEC)
Enteroinvasive E. coli (EIEC)

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54
Q

associated with diarrheal outbreaks occurring in hospital nurseries and daycare centers, but cases in adults are rarely seen

A

EPEC

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55
Q

Infection is characterized by low-grade fever, malaise, vomiting, and profuse, watery diarrhea. Stool typically contains large amounts of mucus, but apparent blood is not present. Fecal leukocytes are seen only
occasionally.

A

EPEC

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56
Q

Diarrhea is usually self-limited but can be prolonged or chronic.

A

EPEC

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57
Q

EPEC adhere to intestinal epithelial cells in localized microcolonies producing characteristic histopathologic lesions known as

A

“attaching and effacing lesions”

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58
Q

facilitated by bundle-forming pilus encoded by a plasmid EPEC adherence factor (EAF) and the chromosomal locus of enterocyte effacement (LEE) pathogenicity island that promote the tight adherence, characteristic of EPEC

A

Attachment

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59
Q

occurs after attachment where there is loss of microvilli

A

Effacement

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60
Q

formation of filamentous actin pedestals or cup-like structures

A

Effacement

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61
Q

occasionally, entry of the EPEC into the mucosal cells.

A

Effacement

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62
Q

Associated with two clinical syndromes: “weanling diarrhea” among children in tropical and subtropical climates, especially in developing countries and “Traveler’s diarrhea” (also referred to as “Montezuma’s revenge”; “Delhi belly”).

A

ETEC

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63
Q

Infection is spread commonly via consumption of
contaminated food or water; poor hygiene, reduced
availability of sources of potable water, and inadequate
sanitation.

A

ETEC

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64
Q

Produces a typically mild, self-limiting disease which has an abrupt onset with short incubation period.

A

ETEC

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65
Q

Symptoms include profuse watery diarrhea (similar with V. cholerae), usually without blood, mucus, or pus; accompanied by mild abdominal cramps; usually without vomiting or fever.

A

ETEC

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66
Q

facilitates colonization of ETEC on the proximal small intestine by binding to specific receptors on the intestinal microvilli

A

Fimbrae

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67
Q

is similar in action and amino acid sequence to cholera toxin from Vibrio cholerae.

A

Heat-labile toxin (LT)

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68
Q

Consists of two fragments (A and B), which follow the A/B model of bacterial toxins

A

Heat-labile toxin (LT)

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69
Q

enzymatically actie portion

A

A moeity

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70
Q

activates cellular adenylate cyclase, causing an increase in the conversion of adenosine
t r i p h o s p h a t e t o c y c l i c adenosine monophosphate (cAMP)

A

A moeity

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71
Q

accumulation of cAMP results to hypersecretion of both electrolytes and fluids into the intestinal lumen, resulting in watery diarrhea similar to cholera

A

A moeity

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72
Q

also known as binding portion

A

B moeity

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73
Q

confers specificity to the LT

A

B moeity

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74
Q

associated with hemorrhagic diarrhea, colitis, and

hemolytic uremic syndrome (HUS)

A

EHEC

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75
Q

characterized by low platelet count, hemolytic anemia, and kidney failure

A

hemolytic uremic syndrome (HUS)

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76
Q

produces a watery diarrhea that progresses to bloody
diarrhea with abdominal cramps and low-grade fever or an absence of fever but the stool does not contain
leukocytes which distinguishes it from dysentery caused by Shigella spp. or EIEC infections

A

EHEC

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77
Q

produces a watery diarrhea that progresses to bloody
diarrhea with abdominal cramps and low-grade fever or an absence of fever but the stool does not contain
leukocytes which distinguishes it from dysentery caused by Shigella spp. or EIEC infections

A

EHEC

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78
Q

food and food products such as processed meats, unpasteurized dairy products and apple cider, bean sprouts, and spinach have been implicated in the spread of infection

A

EHEC

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79
Q

EHEC produces 2 cytotoxins

A

verotoxin I and verotoxin II

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80
Q

verotoxin I and verotoxin II are identical to the

A

Shiga toxin (Stx) produced by Shigella dysenteriae type I

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81
Q

African green monkey kidney cells; “verotoxin”; damaged by verotoxin I and verotoxin

A

Vero cells

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82
Q

phage-encoded cytotoxin

A

Verotoxin I

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83
Q

is biologically similar to, but immunologically different from, both Stx and verotoxin I.

A

Verotoxin II

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84
Q

Of the E. coli serotypes that produce Shiga toxin, [?] is the most common and is the one that can be identified most readily in clinical specimens

A

O157:H7

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85
Q

produce a diarrheal illness which is very similar to that produced by Shigella spp — dysentery with direct penetration, invasion, and destruction of the epithelial cells that make up the large intestinal mucosa

A

EIEC

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86
Q

Infections seem to occur in children in developing

countries and in travelers to these countries.

A

EIEC

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87
Q

Direct transmission of EIEC from person to person via the [?] has been reported.

A

fecal-oral route

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88
Q

Clinical infection is characterized by fever, colitis, severe abdominal cramps (tenesmus), malaise, and watery diarrhea with blood, mucus and leukocytes in stool.

A

EIEC

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89
Q

Causes acute and chronic diarrhea (>14 days in duration) in persons in developing countries; it also is the cause of food-borne illnesses in industrialized countries and have been associated with traveler’s diarrhea and persistent diarrhea in patients with HIV.

A

EAEC

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90
Q

Adhere to epithelial cells in a pattern resembling a pile of stacked bricks.

A

EAEC

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91
Q

Illness is characterized by watery, mucoid diarrhea with low grade fever and little or no vomiting, white blood cells and red blood cells are typically absent from the stool.

A

EAEC

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92
Q

Pathology has been associated with production of ST-like toxin, an LT toxin, and fibril colonization factors called “AAFs” (aggregative adherence fimbriae).

A

EAEC

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93
Q

fibril colonization factors

A

“AAFs” (aggregative adherence fimbriae)

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94
Q

E. coli remains one of the most common causes of septicemia and meningitis among neonates.

A

Extraintestinal Infections

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95
Q

A newborn usually acquires the infection in the birth canal just before or during delivery, when the mother’s vagina is heavily colonized or may also result if the amniotic fluid occurs becomes contaminated

A

Extraintestinal Infections

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96
Q

Sepsis may occur when normal host defenses are inadequate (e.g., newborns may be highly susceptible to E. coli sepsis because they lack IgM antibodies); or secondary to urinary tract infection.

A

Extraintestinal Infections

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97
Q

Approximately 75% of E. coli from meningitis cases have the K1 antigen which is said to cross-react with the group B capsular polysaccharide of N. meningitidis.

A

Extraintestinal Infections

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98
Q

Klebsiella species common name

A

“Friedlander’s bacillus”

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99
Q

have been associated with various opportunistic and hospitalacquired infections, particularly pneumonia, wound infections, and UTIs.

A

Klebsiella

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100
Q

the most commonly isolated Klebsiella species

A

Klebsiella pneumoniae

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101
Q

In addition to inhabiting the intestines of humans and animals

A

Klebsiella pneumoniae

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102
Q

It causes a small proportion (~1%) of bacterial pneumonias characterized as extensive hemorrhagic necrotizing consolidation of the lung resulting in the production of sputum that may be thick, mucoid, and brick red, or thin and “currant jelly-like” in appearance.

A

Klebsiella pneumoniae

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103
Q

found in the respiratory tract and feces of about 5% of normal individuals

A

Klebsiella pneumoniae

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104
Q

Also produces urinary tract infection, wound infections, meningitis, bacteremia with focal lesions (e.g., abscesses) in debilitated patients.

A

Klebsiella pneumoniae

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105
Q

Pathology has been associated with a large polysaccharide capsule that confers protection against phagocytosis and antimicrobial absorption.

A

Klebsiella pneumoniae

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106
Q

Produces infections similar to those caused by K. pneumoniae.

A

Klebsiella oxytoca

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107
Q

Isolates have also been linked to antibiotic/antimicrobial-associated hemorrhagic colitis (AAHC)

A

Klebsiella oxytoca

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108
Q

a distinct form of antibiotic-associated diarrhea, in which C. difficile is absent and where patients experience a sudden onset of bloody diarrhea often in combination with severe abdominal cramps.

A

antibiotic/antimicrobial-associated hemorrhagic colitis (AAHC)

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109
Q

Has been isolated from cerebral abscesses and nasal mucosa in ozena

A

Klebsiella pneumoniae subspecies ozaenae

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110
Q

cerebral abscesses and nasal mucosa in ozena,

A

Klebsiella pneumoniae subspecies ozaenae

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111
Q

a fetid, progressive atrophy of mucous membranes (atrophic rhinitis and tissuedestructive disease restricted to the nose).

A

ozena

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112
Q

rhinoscleroma

A

Klebsiella pneumoniae subspecies rhinoscleromatis

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113
Q

a destructive granuloma of the nose and pharynx that manifests as an intense swelling and malformation of the entire face and neck.

A

rhinoscleroma

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114
Q

Klebsiella granulomatis formerly called

A

Calymmatobacterium granulomatis

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115
Q

causes, granuloma inguinale, a chronic genital ulcerative disease and an uncommon sexually transmitted disease.

A

Klebsiella granulomatis

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116
Q

Resembles Klebsiella in terms of growth and most biochemical characteristics except that they motile.

A

Enterobacter species

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117
Q

Pathology is associated with capsule production for some strains.

A

Enterobacter species

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118
Q

are the two most common isolates of Enterobacter species

A

Enterobacter cloacae and Enterobacter (now Klebsiella) aerogenes

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119
Q

cause a broad range of hospital-acquired infections such as pneumonia, urinary tract infections, and wound and device infections, on occasion, septicemia, and meningitis

A

Enterobacter cloacae and Enterobacter (now Klebsiella) aerogenes

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120
Q

derived from a Greek word meaning “of all sorts and sources,” — describing these bacteria that come from diverse geographic and ecologic sources.

A

Pantoea

121
Q

was responsible for an outbreak of septicemia caused by contaminated intravenous fluids

A

Enterobacter (now Pantoea) agglomerans

122
Q

typically produces a yellow pigment and is sometimes

referred to as “yellow-pigmented E. cloacae”

A

Enterobacter (now Cronobacter) sakazakii

123
Q

linked with several cases of neonatal meningitis and
sepsis associated with contaminated powdered infant
formula

A

Enterobacter (now Cronobacter) sakazakii

124
Q

has also been isolated from cultures taken from brain abscesses and respiratory and wound infections.

A

Enterobacter (now Cronobacter) sakazakii

125
Q

has been found in respiratory samples and is rarely isolated from blood cultures

A

Enterobacter gergoviae

126
Q

has been isolated from human sources such as blood, wounds, and sputum

A

Enterobacter hormaechei

127
Q

was earlier classified within the tribe Salmonelleae but has been designated its own tribe

A

Citrobacter species

128
Q

All species grow on Simmons citrate medium, hence the genus name.

A

Citrobacter species

129
Q

are associated with hospital-acquired infections, most frequently UTIs

A

Citrobacter species

130
Q

Although has been known as an extra intestinal pathogen, can also be isolated in stool cultures

A

Citrobacter freundii

131
Q

Other than UTI, it has been associated with nosocomial infectious diseases including pneumonias, and intraabdominal abscesses as well as endocarditis in intravenous drug abusers.

A

Citrobacter freundii

132
Q

is a pathogen documented as the cause of nursery outbreaks of neonatal meningitis and brain abscesses

A

Citrobacter koseri

133
Q

Their control measures are not feasible as far as the normal endogenous flora is concerned.

A

COLIFORMS

134
Q

Enteropathogenic E. coli serotypes should be controlled like

A

salmonellae

135
Q

Some of the enterics constitute a major problem in hospital infection. Within hospitals or other institutions, these bacteria commonly are transmitted by

A

personnel, instruments, or parenteral medications.

136
Q

Their control depends on handwashing, rigorous asepsis, sterilization of equipment, disinfection, restraint in intravenous therapy, and strict precautions in keeping the urinary tract sterile (ie, closed drainage).

A

COLIFORMS

137
Q

are widely recognized human pathogens and have been isolated from urine, wounds, and ear and bacteremic infections.

A

P. mirabilis and P. vulgaris

138
Q

They produce urease, resulting in rapid hydrolysis of urea with liberation of ammonia.

A

Proteus species

139
Q

In urinary tract infections with Proteus species, rapid hydrolysis of urea causes the urine to become alkaline, making acidification virtually impossible and promoting

A

struvite kidney stone formation/calculi

140
Q

struvite kidney stones formed are [?] of infection in urinary tract

A

nidus

141
Q

Proteus species are famous for their [?] on solid culture media.

A

swarming

142
Q

This was first observed in 1946 by Dienes

A

Dienes phenomenon

143
Q

When different Proteus species swarm towards each other, a [?] results where strains meet. This line of inhibited growth results from the production of and sensitivity to different types of bacteriocins, namely, proticines, produced by different strains of Proteus species.

A

line of inhibited growth

144
Q

If two strains were able to detect different [?] produced by a neighbor, there would be growth inhibition and the formation of a Dienes
line.

A

proticines

145
Q

Alternatively, if no proticine difference were detected, the neighboring swarmer would be recognized as [?] and the swarms would interact.

A

“self”

146
Q

Morganella morganii previously designated [?] was reassigned to the new genus Morganella as M. morganii.

A

Proteus morganii

147
Q

The genus Morganella has only one species

A

M. morganii

148
Q

is a documented cause of UTI and wound infections and has also been identified as a cause of neonatal sepsis.

A

M. morganii

149
Q

it also produces [?] and is motile

A

urease

150
Q

unlike Proteus species, it does not swarm

A

M. morganii

151
Q

Providencia spp that has been associated with human

infections

A

P. rettgeri and P. stuartii

152
Q

is a documented pathogen of the urinary tract and has caused occasional outbreaks in health care settings and also been implicated in diarrheal disease among travelers

A

P. rettgeri

153
Q

has been implicated in outbreaks in burn units and has been isolated from urine cultures

A

P. stuartii

154
Q

Infections caused by these spps especially in immunocompromised patients, are particularly difficult to treat because of their resistance to antimicrobials

A

P. stuartii and P. rettgeri

155
Q

most commonly found in the feces of children with diarrhea; however, its role as a cause of diarrhea has not been proven.

A

P. alcalifaciens

156
Q

Is the only recognized human pathogen in the genus Edwarsiella

A

Edwardsiella tarda

157
Q

The chief reservoirs in nature are reptiles (especially snakes, toads, and turtles) and freshwater fish.

A

Edwardsiella tarda

158
Q

A key feature of E. tarda is the production of abundant amounts of [?]. Except for this feature, the biochemical properties of the bacterium are similar to those of E. coli.

A

hydrogen sulfide

159
Q

an opportunist, causing a variety of extraintestinal infections, the most common are wound infections resulting from trauma, often related to aquatic accidents.

A

Edwardsiella tarda

160
Q

The organism has also been implicated in abscesses that may lead to bacteremia or myonecrosis.

A

Edwardsiella tarda

161
Q

Its pathogenic role in cases of diarrhea is controversial.

A

Edwardsiella tarda

162
Q

The Serratia species are unique among the Enterobacteriaceae in producing three hydrolytic enzymes:

A

lipase, gelatinase, and DNase

163
Q

produce red pigments which are easily seen when grown on blood-free media such as nutrient agar especially when the cultures are incubated at room temperature.

A

Serratia species

164
Q

non-water-soluble, and non-diffusible pigment

A

Prodigiosin

165
Q

water-soluble and diffusible pigment

A

Pyrimine

166
Q

most important member of the genus Serratia and is a common opportunistic pathogen in hospitalized patients

A

S. marcescens

167
Q

associated with a variety of human infections, particularly pneumonia, bacteremia, and endocarditis, especially in narcotics addicts and hospitalized patients

A

non-pigmented S. marcescens

168
Q

Currently, based on [?], the genus Salmonella comprises only two species

A

DNA homology and sequencing

169
Q

is the type species of the genus Salmonella

A

S. enterica

170
Q

six subspecies of S. enterica

A

S. enterica subsp. enterica (subspecies I)
S. enterica subsp. salamae (subspecies II)
S. enterica subsp. arizonae (subspecies IIIa)
S. enterica subsp. diarizonae (subspecies IIIb)
S. enterica subsp. houtenae (subspecies IV)
S. enterica subsp. indica (subspecies VI)

171
Q

Most human illness is caused by

A

S. enterica subsp. enterica (subspecies I)

172
Q

Nearly all former Salmonella spp. have been placed as serotypes below the level of

A

S. enterica subsp. enterica

173
Q

For named serotypes, to emphasize that they are not separate species, the serotype name is [?], and the first letter is [?]

A

not italicized

capitalized

174
Q

rarely isolated species that is named after the town of Bongor in Chad, Africa

A

S. bongori

175
Q

primarily infective for humans, and infection with these organisms implies acquisition from a human source

A

Salmonella Typhi
S. Choleraesuis
S. Paratyphi A
S. Paratyphi B

176
Q

The organisms almost always enter via the oral route, usually with contaminated food or drink.

A

Salmonella species

177
Q

The mean infective dose to produce clinical or subclinical infection in humans is

A

10^5–10^8 salmonellae

(may be as few as 10^3 S. Typhi).

178
Q

result from the ingestion of food contaminated with the organisms originating from infected individuals or carriers

A

Enteric fevers and gastroenteritis

179
Q

does not have a known animal reservoir — humans are the only known source of infection

A

Salmonella Typhi

180
Q

occurs more often in tropical and subtropical areas, where outbreaks has been associated with improper disposal of sewage, poor sanitation, and lack of a modern potable water system

A

Typhoid fever

181
Q

important sources of infection by Salmonella species

A

Carriers - food handlers

direct transmission - fomites

182
Q

is a major cause of bacterial enteric illness in both humans and animals

A

Salmonellosis

183
Q

Factors responsible for the virulence of salmonellae include

A

Fimbriae
ability to traverse intestinal mucosa
Enterotoxin
Vi antigen (virulence or capsular antigens)

184
Q

used in adherence and in initiating intestinal infection by Salmonella species

A

Fimbriae

185
Q

produced by certain Salmonella strains that cause gastroenteritis.

A

Enterotoxin

186
Q

This syndrome is produced by only a few of the salmonellae

A

Enteric Fevers (Typhoid Fever)

187
Q

Typhoid fever develops approximately [?] days after ingestion of the organisms.

A

9 to 14

188
Q

most important agent for Enteric Fevers

A

S. Typhi

189
Q

Onset of symptoms depends on the number of

A

organisms ingested

190
Q

relationship between inoculum and incubation period

A

inversely proportional

191
Q

After the organisms are ingested and reach the proximal end of the small intestine, they subsequently invade and penetrate the intestinal mucosa

A

First week of Enteric Fevers

192
Q

The patient develops a fever accompanied by malaise, anorexia, lethargy, myalgia, and a continuous dull frontal headache and constipation instead of diarrhea.

A

First week of Enteric Fevers

193
Q

Through the lymphatic system, the bacteria eventually reach the bloodstream and spread to the liver, spleen, and bone marrow, where they are immediately engulfed by [?] — where they multiple intracellularly.

A

mononuclear phagocytes

194
Q
  • Febrile episode becomes more evident during this release of the organisms into the circulatory system.
  • At this time, the organisms may be isolated easily from the blood.
A

They are later released into the bloodstream — for the second time

195
Q

The organisms invade the gallbladder and Peyer’s patches of the bowel. They also reach the intestinal tract via the biliary tract.

A

Second and Third week of Enteric Fevers

196
Q

The px generally experiences sustained fever with prolonged bacteremia.

A

Second and Third week of Enteric Fevers

197
Q

During the second week of fever, blanching, rose-colored papules (called [?]) appear around the umbilical region.

A

rose spots

198
Q

The involvement of biliary system sites initiates GI symptoms as the organisms reinfect the intestinal tract.

A

Second and Third week of Enteric Fevers

199
Q

The bacteria now exists in large numbers in the bowel and may be isolated from the stool.

A

Second and Third week of Enteric Fevers

200
Q

The gallbladder becomes the foci of long-term carriage of the organism which may cause occasional reseeding (reinfection) of the intestinal tract and shedding the organisms in the feces.

A

Second and Third week of Enteric Fevers

201
Q

Complications of typhoid fever include:

A

‣ necrosis in the gallbladder leading to necrotizing cholecystitis
‣ necrosis of the Peyer’s patches leading to hemorrhage
‣ perforation of the bowel

202
Q

is commonly associated with S. choleraesuis but may be caused by any salmonella serotype such as Typhimurium, and Paratyphi — collectively referred to as nontyphoidal Salmonella.

A

Salmonella bacteremia

203
Q

It may occur with and without extraintestinal foci of infection and is characterized primarily by prolonged fever and intermittent bacteremia.

A

Bacteremia with Focal Lesions

204
Q

After oral infection, there is early invasion of the bloodstream

possible focal lesions in lungs, bones, meninges; intestinal manifestations are often absent

A

Bacteremia with Focal Lesions

205
Q

Blood culture results of Bacteremia with Focal Lesions are

A

positive

206
Q

The most common manifestation of salmonella infection

A

Enterocolitis

207
Q

are prominent causes, but can be caused by any of the more than 1400 group I serotypes of salmonellae.

A

S. Typhimurium and S. Enteritidis

208
Q

Nausea, headache, vomiting, and profuse diarrhea, becomes apparent 8 to 48 hours after ingestion of salmonellae.

A

Enterocolitis

209
Q

Commonly, there is low grade fever which resolves within 2 - 3 days; inflammatory lesions are present in the small and large intestinal mucosa and stools have few leukocytes.

A

Enterocolitis

210
Q

Blood culture results of Enterocolitis are

A

negative

211
Q

Stool culture results of Enterocolitis are

A

positive

212
Q

may remain so for several weeks after clinical recovery

A

Stool culture results of Enterocolitis

213
Q

Individuals who recover from infection may harbor the organisms in the gallbladder

A

Carrier state

214
Q

site of chronic carriage in Enterocolitis

A

gallbladder

215
Q

Carriers excrete the organisms in their feces either continuously or intermittently; nevertheless, they become an important source of infection for susceptible persons.

A

Enterocolitis

216
Q

The carrier state may be terminated by [?] if gallbladder infection is not evident

A

antimicrobial therapy

217
Q

has been the only solution to the chronic state of enteric carriers

A

cholecystectomy

218
Q

Sanitary measures must be taken to prevent contamination of food and water by rodents or other animals that excrete salmonellae.

A

Prevention and Control of Salmonella species

219
Q

Infected poultry, meats, and eggs must be thoroughly cooked.

A

Prevention and Control of Salmonella species

220
Q

Carriers must not be allowed to work as food handlers and should observe strict hygienic precautions.

A

Prevention and Control of Salmonella species

221
Q

Vaccination is recommended for travelers to endemic regions, especially if the traveler visits rural areas or small villages where food choices are limited.

A

Prevention and Control of Salmonella species

222
Q

Two typhoid vaccines are currently available in the United States

A
  • oral live, attenuated vaccine

- Vi capsular polysaccharide vaccine for intramuscular use

223
Q

The genus Shigella is named after the Japanese microbiologist [?], who first isolated the organism in 1896.

A

Kiyoshi Shiga

224
Q

not members of the normal GI microbiota

A

Shigella species

225
Q

can cause bacillary dysentery that can vary in severity, mortality rate, and epidemiology

A

Shigella species

226
Q

what classification system separates the genus Shigella into four serogroups or species based on their antigen types

A

Ewing’s classification

227
Q

four serogroups or species od Shigella spp based on their antigen types

A

S. dysenteriae, S. flexneri, S. sonnei, and S. boydii.

228
Q

the four serogroups of shigella spp are further subdivided into serotypes based on the

A

O-antigen structure of their LPS.

229
Q

A - Shiga’s bacillus / Japanese dysentery bacillus

A

Shigella dysenteriae

230
Q

B - Flexner’s bacillus or Strong’s bacillus /Philippine dysentery bacillus

A

Shigella flexneri

231
Q

C - Boyd’s bacillus / British dysentery bacillus

A

Shigella boydii

232
Q

D - Sonne-Duval’s bacillus / US dysentery bacillus

A

Shigella sonnei

233
Q

Humans and other large primates are the only known reservoir of

A

Shigella spp

234
Q

Transmission of Shigella spp

A

direct person-to-person contact
fecal-oral route

flies, fingers, and food or water contaminated by infected persons

235
Q

is highly communicable because of the low infective dose required to produce the disease

A

Shigellosis

236
Q

infective dose of Shigellosis

A

(approximately less than 100 bacilli)

237
Q

Clinical manifestations of [?] vary from asymptomatic to severe forms of the disease

A

shigellosis

238
Q

released upon autolysis of all shigellae and probably contribute to the irritation of the bowel wall

A

Endotoxin

239
Q

Shigella dysenteriae Exotoxin is produced by

A

S. dysenteriae type I

240
Q

An antigenic protein (stimulates antitoxin production).

A

Shigella dysenteriae Exotoxin

241
Q

produces diarrhea as does the E coli Shigalike toxin, perhaps by the same mechanism, inhibits sugar and amino acid absorption in the small intestine.

A

Shigella dysenteriae Exotoxin as enterotoxin

242
Q

contributes to the extreme severity and fatal nature of S dysenteriae infections and to the central nervous system reactions observed.

A

Shigella dysenteriae Exotoxin as neurotoxin

243
Q

After ingestion, the organisms multiply in the small intestine, move toward the colon.

A

shigellosis

244
Q

Initial symptoms appear approximately 24 to 48
hours after ingestion of the organisms and are
marked by high fever, chills, abdominal cramps,
and pain accompanied by tenesmus (rectal
spasms).

A

shigellosis

245
Q

Watery diarrhea progresses to bloody stools
containing mucus and numerous leukocytes
(dysenteric diarrhea) as the organisms invade the
colonic tissues and cause an inflammatory reaction.

A

shigellosis

246
Q

was used by Hippocrates to indicate a condition characterized by frequent passage of stool containing blood mucus accompanied by straining and painful defecation.

A

“dysentery”

247
Q

marked by penetration of intestinal epithelial cells after attachment of the organisms to mucosal surfaces, local inflammation, shedding of the intestinal lining, and formation of ulcers after epithelial penetration.

A

Bacillary dysentery

248
Q

Severe cases of shigellosis may become life threatening as extraintestinal complications develop including:

A

Rectal prolapse

Ileus

249
Q

an obstruction of the intestines, with marked abdominal dilation, possibly leading to toxic megacolon

A

Ileus

250
Q

may result from excessive straining during defecation

A

Rectal prolapse

251
Q

are transmitted by “food, fingers, feces, and flies” from person to person.

A

Shigellae

252
Q

control efforts must be directed at eliminating the organisms from this reservoir

(1) sanitary control of water, food, and milk; sewage disposal and fly control
(2) isolation of patients and disinfection of excreta
(3) detection of subclinical cases and carriers, particularly food handlers
(4) antibiotic treatment of infected individuals.

A

Prevention and Control of Shigellae

253
Q

Of the many Yersinia species isolated in man, only three are considered as human pathogens

A

Y. pestis
Y. enterocolitica
Y. pseudotuberculosis

254
Q

zoonoses caused by Yersinia

A

yersinioses

255
Q

the causative agent of plague

A

Y. pestis

256
Q

Have been found in a wide variety of animals, including domestic swine, cats, and dogs.

A

Yersinia enterocolitica

257
Q

Human infections most often occur after the ingestion of contaminated food, often pork, and vacuum packed deli meat, beef, lamb, chicken, and possibly chocolate milk and water, also from contact with household pets.

A

Yersinia enterocolitica

258
Q

Food refrigeration is an ineffective preventive measure because of its ability to survive in cold temperatures.

A

Yersinia enterocolitica

259
Q

An inoculum of [?] yersiniae must enter the alimentary tract to produce infection.

A

10^8–10^9

260
Q

Yersinia enterocolitica infections manifest in several forms:

A
  • an acute gastroenteritis
  • an appendicitislike syndrome,
  • septicemia, arthritis, and erythema nodosum
261
Q

the yersiniae multiply in the gut mucosa during the incubation period of 4-7 days. This leads to inflammation and ulceration, and leukocytes appear in feces

A

acute gastroenteritis

262
Q

associated with the transfusion of contaminated packed red blood cells has also been reported

A

Sepsis

263
Q

The incidence of [?] is higher among elderly adults or those with underlying diseases

A

systemic infection

264
Q

Is pathogen primarily of rodents, particularly guinea pigs

A

Yersinia pseudotuberculosis

265
Q

Yersinia pseudotuberculosis is derived from the disease it produces in animals which is characterized by caseous swellings called

A

pseudotubercles

266
Q

Human infections caused by Yersinia pseudotuberculosis, which are rare, are associated with

A
  • close contact with infected animals or their fecal material
  • ingestion of contaminated drink and foodstuff
267
Q

Yersinia pseudotuberculosis when ingested, the organisms spread to the [?], producing a generalized infection that is usually self-limiting.

A

mesenteric lymph nodes

268
Q

Clinical manifestations can include septicemia accompanied by mesenteric
lymphadenitis, a presentation similar to appendicitis.

A

Yersinia pseudotuberculosis

269
Q

Yersinia pestis common name

A

“plague bacillus”

270
Q

caused the great pandemic of “black death” in 1800s.

A

Yersinia pestis

271
Q

Plague is a disease primarily of rodents.

A

Yersinia pestis

272
Q

most common and effective vectors of Yersinia pestis

A

bites of fleas

273
Q

Humans can develop plague through contact with:

  • wild animals - ?
  • domestic or semi domestic animals - ?
  • infected humans.
A

(syllabic plague)

urban plague

274
Q

This flea feeds on a rodent infected with Y. pestis, the ingested organisms multiply in the gut of the flea and, helped by the coagulase, block its proventriculus so that no food can pass through.

A

(Xenopsylla cheopsis)

275
Q

results from inhalation of infective droplets .

A

Primary pneumonic plague

276
Q

The most common form of plague

A

Bubonic/glandular form

277
Q

Usually results form the bite of an infected flea

A

Bubonic/glandular form

278
Q

Symptoms begin appear 2 to 5 days after infection and include high fever with painful, swollen, and necrotic regional lymph nodes (typically in the groin, less often in the axilla) known as buboes (s.
bubo; G. boubon, the groin)

A

Bubonic/glandular form

279
Q

Occurs when the bacteria spread to the bloodstream.

A

Septicemic form

280
Q

Early manifestations include vomiting and diarrhea; disseminated intravascular coagulation leads to hypotension, altered mental status, and renal and cardiac failure occurs in the later stages.

A

Septicemic form

281
Q

signs of pneumonia and meningitis can appear, and

Y. pestis multiplies intravascularly and can be seen in blood smears

A

Septicemic form

282
Q

May occur as a primary infection if the bacteria are inhaled

A

Pneumonic form

283
Q

Secondary to bubonic plague or the septicemic form
when organisms proliferate in the bloodstream and
respiratory tract.

A

Pneumonic form

284
Q

Patients often have a fulminant course with chest pain, cough, hemoptysis, and severe respiratory distress.

A

Pneumonic form

285
Q

Has a high fatality rate— essentially 100%—in untreated patients.

A

Pneumonic form

286
Q

All yersiniae possess lipopolysaccharides that have endotoxic activity when released

A

Endotoxin

287
Q

consisting of a membrane-spanning complex that allows the bacteria to inject proteins directly into cytoplasm of the host cells

A

Type III secretion systems

288
Q

are encoded by genes on a plasmid and is essential for virulence. They yield the requirement for calcium for growth of the yersiniae at 37°C.

A

V and W antigens

289
Q

a plasmid that contains genes that yield plasminogen-activating protease that has temperature-dependent coagulase activity and fibrinolytic activity.

This factor is involved in dissemination of the organism from the flea bite injection site.

A

pPCP1

290
Q

(20°–28°C, the temperature of the flea)

A

coagulase activity

291
Q

(35°–37°C, the temperature of the host)

A

fibrinolytic activity

292
Q

plasmid encodes the capsular protein n (fraction F1)

and phospholipase D

A

pFra/pMT

293
Q

produced mainly at 37°C and confers anti-phagocytic properties

A

capsular protein n (fraction F1)

294
Q

required for organism survival in the flea midgut

A

phospholipase D

295
Q

encoded by a pathogenecity island (PAI), is an iron-scavenging siderophore.

A

Yersiniabactin

296
Q

requires surveys of infected animals, vectors, and human

contacts.

A

control of plague

297
Q

if a human case is diagnosed, health authorities must be notified promptly

A

control of plague

298
Q

All patients should be isolated, particularly if pulmonary involvement has not been ruled out and all specimens must be treated with extreme caution.

A

control of plague

[9a] MODULE 6 UNIT 1: Enterobacteriaceae and Other Related Enterobacteria (2 decks)

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