LECTURE Flashcards
(298 cards)
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
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.
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
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
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
6
Q
Non-motile Enterobacters
A
Klebsiella
Shigella
Yersinia
7
Q
Yersinia are nonmotile at [?]
A
35-37 oC
8
Q
Yersinia are motile at [?]
A
room temperature
9
Q
(somatic antigen or cell wall antigen)
A
O antigens
10
Q
(capsular antigen or fimbrial antigen)
A
K antigen
11
Q
(flagellar antigen)
A
H antigen
12
Q
most external part of the cell wall lipopolysaccharide
A
O antigens
13
Q
consisting of repeating units of polysaccharide
A
O antigens
14
Q
usually are detected by bacterial agglutination
A
O antigens
15
Q
each genus of Enterobacteriaceae is associated with specific O groups – a single organism may carry several O antigens
A
O antigens
16
Q
HA-S
A
O antigens
17
Q
H-L
A
K antigen
18
Q
HA-L
A
H antigen
19
Q
external to the O antigens on some but not all Enterobacteriaceae
A
K antigen
20
Q
found on the surface of flagella.
A
H antigen
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
22
Q
organism tends to change from one phase to the
other; this is called phase variation.
A
H antigen
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
24
Q
ferment lactose at either 35 or 37 oC
include the normal enteric flora
A
COLIFORMS
25
COLIFORMS spp
o Escherichia
o Klebsiella
o Enterobacter
o Citrobacter
26
differ from coliforms by their inability to ferment lactose; NLF
NONCOLIFORMS
27
Fecal coliforms
o most common facultative bacterium in feces of man and warm-blooded animals
o indicator organism of choice for fecal contamination
Escherichia coli
28
ferments lactose at 44.5 oC
Fecal coliforms
29
Non fecal coliforms
Klebsiella, Enterobacter, Citrobacter
30
Fecal coliforms spp
o most common facultative bacterium in feces of man and warm-blooded animals
o indicator organism of choice for fecal contamination
Escherichia coli
31
do NOT ferment lactose at 44.5 oC
Non fecal coliforms
32
Non fecal coliforms spp
Klebsiella, Enterobacter, Citrobacter
33
Opportunistic, normal gut flora spp
Proteus
Providencia
Morganella
Serratia
Hafnia
Edwardsiella
34
Pathogenic enterics (true enteropathogens) spp
Salmonella
Shigella
Yersinia enterocolitica
Y. pseudotuberculosis
35
Pathogenic, non-enteric spp
Yersinia pestis
36
Escherichia coli was first described by [?] in 1885
Theodor Escherich
37
Escherichia coli common name
“colon bacillus”
38
Infections with E. coli and the other enteric bacteria depend on the [?] and cannot be differentiated by [?] from processes caused by other bacteria.
site
symptoms or signs
39
accounts for approximately 90% of first urinary tract infections in young women
Uropathogenic E. coli
40
Strains of E. coli that cause UTIs usually originate in the large intestine as resident biota.
Uropathogenic E. coli
41
Infection is more common in women because of their relatively short urethras that promote ascending infection to the bladder (cystitis) and occasionally, the kidneys.
Uropathogenic E. coli
42
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
Uropathogenic E. coli
43
Uropathogenic strains possess O antigen types that have specifically elaborated virulence factors that facilitate colonization and subsequent clinical infections
Uropathogenic E. coli
44
most common cause of UTIs;
E. coli
45
most common cause of UTIs
E. coli
46
primary virulence factor associated with the ability of E. coli to cause UTIs
Pili (P fimbrae)
47
allow the bacteria to attach to the urinary epithelial
| mucosa and not be washed out with urine flow
Pili (P fimbrae)
48
binds to P blood group antigen
Pili (P fimbrae)
49
cytolysins which can kill immune effector cells and inhibit
| chemotaxis and phagocytosis of certain white blood cells
Hemolysins
50
allows the bacterial cell to chelate iron; free iron is
| generally unavailable within the host for use by bacteria
Aerobactin
51
Enterovirulent E. coli
Diarrheagenic E. coli
52
E. coli may cause several different GI syndromes
Diarrheagenic E. coli
53
based on virulence factors, clinical manifestation, epidemiology, and different O and H serotypes, there are five major categories of diarrheagenic E. coli:
Enteropathogenic E. Coli (EPEC)
Enterotoxigenic E. coli (ETEC)
Enterohemorrhagic E. coli (EHEC)
Enteroinvasive E. coli (EIEC)
54
associated with diarrheal outbreaks occurring in hospital nurseries and daycare centers, but cases in adults are rarely seen
EPEC
55
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.
EPEC
56
Diarrhea is usually self-limited but can be prolonged or chronic.
EPEC
57
EPEC adhere to intestinal epithelial cells in localized microcolonies producing characteristic histopathologic lesions known as
“attaching and effacing lesions”
58
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
Attachment
59
occurs after attachment where there is loss of microvilli
Effacement
60
formation of filamentous actin pedestals or cup-like structures
Effacement
61
occasionally, entry of the EPEC into the mucosal cells.
Effacement
62
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”).
ETEC
63
Infection is spread commonly via consumption of
contaminated food or water; poor hygiene, reduced
availability of sources of potable water, and inadequate
sanitation.
ETEC
64
Produces a typically mild, self-limiting disease which has an abrupt onset with short incubation period.
ETEC
65
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.
ETEC
66
facilitates colonization of ETEC on the proximal small intestine by binding to specific receptors on the intestinal microvilli
Fimbrae
67
is similar in action and amino acid sequence to cholera toxin from Vibrio cholerae.
Heat-labile toxin (LT)
68
Consists of two fragments (A and B), which follow the A/B model of bacterial toxins
Heat-labile toxin (LT)
69
enzymatically actie portion
A moeity
70
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 moeity
71
accumulation of cAMP results to hypersecretion of both electrolytes and fluids into the intestinal lumen, resulting in watery diarrhea similar to cholera
A moeity
72
also known as binding portion
B moeity
73
confers specificity to the LT
B moeity
74
associated with hemorrhagic diarrhea, colitis, and
| hemolytic uremic syndrome (HUS)
EHEC
75
characterized by low platelet count, hemolytic anemia, and kidney failure
hemolytic uremic syndrome (HUS)
76
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
EHEC
77
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
EHEC
78
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
EHEC
79
EHEC produces 2 cytotoxins
verotoxin I and verotoxin II
80
verotoxin I and verotoxin II are identical to the
Shiga toxin (Stx) produced by Shigella dysenteriae type I
81
African green monkey kidney cells; "verotoxin"; damaged by verotoxin I and verotoxin
Vero cells
82
phage-encoded cytotoxin
Verotoxin I
83
is biologically similar to, but immunologically different from, both Stx and verotoxin I.
Verotoxin II
84
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
O157:H7
85
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
EIEC
86
Infections seem to occur in children in developing
| countries and in travelers to these countries.
EIEC
87
Direct transmission of EIEC from person to person via the [?] has been reported.
fecal-oral route
88
Clinical infection is characterized by fever, colitis, severe abdominal cramps (tenesmus), malaise, and watery diarrhea with blood, mucus and leukocytes in stool.
EIEC
89
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.
EAEC
90
Adhere to epithelial cells in a pattern resembling a pile of stacked bricks.
EAEC
91
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.
EAEC
92
Pathology has been associated with production of ST-like toxin, an LT toxin, and fibril colonization factors called “AAFs” (aggregative adherence fimbriae).
EAEC
93
fibril colonization factors
“AAFs” (aggregative adherence fimbriae)
94
E. coli remains one of the most common causes of septicemia and meningitis among neonates.
Extraintestinal Infections
95
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
Extraintestinal Infections
96
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.
Extraintestinal Infections
97
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.
Extraintestinal Infections
98
Klebsiella species common name
“Friedlander’s bacillus”
99
have been associated with various opportunistic and hospitalacquired infections, particularly pneumonia, wound infections, and UTIs.
Klebsiella
100
the most commonly isolated Klebsiella species
Klebsiella pneumoniae
101
In addition to inhabiting the intestines of humans and animals
Klebsiella pneumoniae
102
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.
Klebsiella pneumoniae
103
found in the respiratory tract and feces of about 5% of normal individuals
Klebsiella pneumoniae
104
Also produces urinary tract infection, wound infections, meningitis, bacteremia with focal lesions (e.g., abscesses) in debilitated patients.
Klebsiella pneumoniae
105
Pathology has been associated with a large polysaccharide capsule that confers protection against phagocytosis and antimicrobial absorption.
Klebsiella pneumoniae
106
Produces infections similar to those caused by K. pneumoniae.
Klebsiella oxytoca
107
Isolates have also been linked to antibiotic/antimicrobial-associated hemorrhagic colitis (AAHC)
Klebsiella oxytoca
108
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.
antibiotic/antimicrobial-associated hemorrhagic colitis (AAHC)
109
Has been isolated from cerebral abscesses and nasal mucosa in ozena
Klebsiella pneumoniae subspecies ozaenae
110
cerebral abscesses and nasal mucosa in ozena,
Klebsiella pneumoniae subspecies ozaenae
111
a fetid, progressive atrophy of mucous membranes (atrophic rhinitis and tissuedestructive disease restricted to the nose).
ozena
112
rhinoscleroma
Klebsiella pneumoniae subspecies rhinoscleromatis
113
a destructive granuloma of the nose and pharynx that manifests as an intense swelling and malformation of the entire face and neck.
rhinoscleroma
114
Klebsiella granulomatis formerly called
Calymmatobacterium granulomatis
115
causes, granuloma inguinale, a chronic genital ulcerative disease and an uncommon sexually transmitted disease.
Klebsiella granulomatis
116
Resembles Klebsiella in terms of growth and most biochemical characteristics except that they motile.
Enterobacter species
117
Pathology is associated with capsule production for some strains.
Enterobacter species
118
are the two most common isolates of Enterobacter species
Enterobacter cloacae and Enterobacter (now Klebsiella) aerogenes
119
cause a broad range of hospital-acquired infections such as pneumonia, urinary tract infections, and wound and device infections, on occasion, septicemia, and meningitis
Enterobacter cloacae and Enterobacter (now Klebsiella) aerogenes
120
derived from a Greek word meaning “of all sorts and sources,” — describing these bacteria that come from diverse geographic and ecologic sources.
Pantoea
121
was responsible for an outbreak of septicemia caused by contaminated intravenous fluids
Enterobacter (now Pantoea) agglomerans
122
typically produces a yellow pigment and is sometimes
| referred to as "yellow-pigmented E. cloacae”
Enterobacter (now Cronobacter) sakazakii
123
linked with several cases of neonatal meningitis and
sepsis associated with contaminated powdered infant
formula
Enterobacter (now Cronobacter) sakazakii
124
has also been isolated from cultures taken from brain abscesses and respiratory and wound infections.
Enterobacter (now Cronobacter) sakazakii
125
has been found in respiratory samples and is rarely isolated from blood cultures
Enterobacter gergoviae
126
has been isolated from human sources such as blood, wounds, and sputum
Enterobacter hormaechei
127
was earlier classified within the tribe Salmonelleae but has been designated its own tribe
Citrobacter species
128
All species grow on Simmons citrate medium, hence the genus name.
Citrobacter species
129
are associated with hospital-acquired infections, most frequently UTIs
Citrobacter species
130
Although has been known as an extra intestinal pathogen, can also be isolated in stool cultures
Citrobacter freundii
131
Other than UTI, it has been associated with nosocomial infectious diseases including pneumonias, and intraabdominal abscesses as well as endocarditis in intravenous drug abusers.
Citrobacter freundii
132
is a pathogen documented as the cause of nursery outbreaks of neonatal meningitis and brain abscesses
Citrobacter koseri
133
Their control measures are not feasible as far as the normal endogenous flora is concerned.
COLIFORMS
134
Enteropathogenic E. coli serotypes should be controlled like
salmonellae
135
Some of the enterics constitute a major problem in hospital infection. Within hospitals or other institutions, these bacteria commonly are transmitted by
personnel, instruments, or parenteral medications.
136
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).
COLIFORMS
137
are widely recognized human pathogens and have been isolated from urine, wounds, and ear and bacteremic infections.
P. mirabilis and P. vulgaris
138
They produce urease, resulting in rapid hydrolysis of urea with liberation of ammonia.
Proteus species
139
In urinary tract infections with Proteus species, rapid hydrolysis of urea causes the urine to become alkaline, making acidification virtually impossible and promoting
struvite kidney stone formation/calculi
140
struvite kidney stones formed are [?] of infection in urinary tract
nidus
141
Proteus species are famous for their [?] on solid culture media.
swarming
142
This was first observed in 1946 by Dienes
Dienes phenomenon
143
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.
line of inhibited growth
144
If two strains were able to detect different [?] produced by a neighbor, there would be growth inhibition and the formation of a Dienes
line.
proticines
145
Alternatively, if no proticine difference were detected, the neighboring swarmer would be recognized as [?] and the swarms would interact.
"self"
146
Morganella morganii previously designated [?] was reassigned to the new genus Morganella as M. morganii.
Proteus morganii
147
The genus Morganella has only one species
M. morganii
148
is a documented cause of UTI and wound infections and has also been identified as a cause of neonatal sepsis.
M. morganii
149
it also produces [?] and is motile
urease
150
unlike Proteus species, it does not swarm
M. morganii
151
Providencia spp that has been associated with human
| infections
P. rettgeri and P. stuartii
152
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
P. rettgeri
153
has been implicated in outbreaks in burn units and has been isolated from urine cultures
P. stuartii
154
Infections caused by these spps especially in immunocompromised patients, are particularly difficult to treat because of their resistance to antimicrobials
P. stuartii and P. rettgeri
155
most commonly found in the feces of children with diarrhea; however, its role as a cause of diarrhea has not been proven.
P. alcalifaciens
156
Is the only recognized human pathogen in the genus Edwarsiella
Edwardsiella tarda
157
The chief reservoirs in nature are reptiles (especially snakes, toads, and turtles) and freshwater fish.
Edwardsiella tarda
158
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.
hydrogen sulfide
159
an opportunist, causing a variety of extraintestinal infections, the most common are wound infections resulting from trauma, often related to aquatic accidents.
Edwardsiella tarda
160
The organism has also been implicated in abscesses that may lead to bacteremia or myonecrosis.
Edwardsiella tarda
161
Its pathogenic role in cases of diarrhea is controversial.
Edwardsiella tarda
162
The Serratia species are unique among the Enterobacteriaceae in producing three hydrolytic enzymes:
lipase, gelatinase, and DNase
163
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.
Serratia species
164
non-water-soluble, and non-diffusible pigment
Prodigiosin
165
water-soluble and diffusible pigment
Pyrimine
166
most important member of the genus Serratia and is a common opportunistic pathogen in hospitalized patients
S. marcescens
167
associated with a variety of human infections, particularly pneumonia, bacteremia, and endocarditis, especially in narcotics addicts and hospitalized patients
non-pigmented S. marcescens
168
Currently, based on [?], the genus Salmonella comprises only two species
DNA homology and sequencing
169
is the type species of the genus Salmonella
S. enterica
170
six subspecies of S. enterica
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
Most human illness is caused by
S. enterica subsp. enterica (subspecies I)
172
Nearly all former Salmonella spp. have been placed as serotypes below the level of
S. enterica subsp. enterica
173
For named serotypes, to emphasize that they are not separate species, the serotype name is [?], and the first letter is [?]
not italicized
capitalized
174
rarely isolated species that is named after the town of Bongor in Chad, Africa
S. bongori
175
primarily infective for humans, and infection with these organisms implies acquisition from a human source
Salmonella Typhi
S. Choleraesuis
S. Paratyphi A
S. Paratyphi B
176
The organisms almost always enter via the oral route, usually with contaminated food or drink.
Salmonella species
177
The mean infective dose to produce clinical or subclinical infection in humans is
10^5–10^8 salmonellae
(may be as few as 10^3 S. Typhi).
178
result from the ingestion of food contaminated with the organisms originating from infected individuals or carriers
Enteric fevers and gastroenteritis
179
does not have a known animal reservoir — humans are the only known source of infection
Salmonella Typhi
180
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
Typhoid fever
181
important sources of infection by Salmonella species
Carriers - food handlers
| direct transmission - fomites
182
is a major cause of bacterial enteric illness in both humans and animals
Salmonellosis
183
Factors responsible for the virulence of salmonellae include
Fimbriae
ability to traverse intestinal mucosa
Enterotoxin
Vi antigen (virulence or capsular antigens)
184
used in adherence and in initiating intestinal infection by Salmonella species
Fimbriae
185
produced by certain Salmonella strains that cause gastroenteritis.
Enterotoxin
186
This syndrome is produced by only a few of the salmonellae
Enteric Fevers (Typhoid Fever)
187
Typhoid fever develops approximately [?] days after ingestion of the organisms.
9 to 14
188
most important agent for Enteric Fevers
S. Typhi
189
Onset of symptoms depends on the number of
organisms ingested
190
relationship between inoculum and incubation period
inversely proportional
191
After the organisms are ingested and reach the proximal end of the small intestine, they subsequently invade and penetrate the intestinal mucosa
First week of Enteric Fevers
192
The patient develops a fever accompanied by malaise, anorexia, lethargy, myalgia, and a continuous dull frontal headache and constipation instead of diarrhea.
First week of Enteric Fevers
193
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.
mononuclear phagocytes
194
- 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.
They are later released into the bloodstream — for the second time
195
The organisms invade the gallbladder and Peyer’s patches of the bowel. They also reach the intestinal tract via the biliary tract.
Second and Third week of Enteric Fevers
196
The px generally experiences sustained fever with prolonged bacteremia.
Second and Third week of Enteric Fevers
197
During the second week of fever, blanching, rose-colored papules (called [?]) appear around the umbilical region.
rose spots
198
The involvement of biliary system sites initiates GI symptoms as the organisms reinfect the intestinal tract.
Second and Third week of Enteric Fevers
199
The bacteria now exists in large numbers in the bowel and may be isolated from the stool.
Second and Third week of Enteric Fevers
200
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.
Second and Third week of Enteric Fevers
201
Complications of typhoid fever include:
‣ necrosis in the gallbladder leading to necrotizing cholecystitis
‣ necrosis of the Peyer’s patches leading to hemorrhage
‣ perforation of the bowel
202
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.
Salmonella bacteremia
203
It may occur with and without extraintestinal foci of infection and is characterized primarily by prolonged fever and intermittent bacteremia.
Bacteremia with Focal Lesions
204
After oral infection, there is early invasion of the bloodstream
possible focal lesions in lungs, bones, meninges; intestinal manifestations are often absent
Bacteremia with Focal Lesions
205
Blood culture results of Bacteremia with Focal Lesions are
positive
206
The most common manifestation of salmonella infection
Enterocolitis
207
are prominent causes, but can be caused by any of the more than 1400 group I serotypes of salmonellae.
S. Typhimurium and S. Enteritidis
208
Nausea, headache, vomiting, and profuse diarrhea, becomes apparent 8 to 48 hours after ingestion of salmonellae.
Enterocolitis
209
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.
Enterocolitis
210
Blood culture results of Enterocolitis are
negative
211
Stool culture results of Enterocolitis are
positive
212
may remain so for several weeks after clinical recovery
Stool culture results of Enterocolitis
213
Individuals who recover from infection may harbor the organisms in the gallbladder
Carrier state
214
site of chronic carriage in Enterocolitis
gallbladder
215
Carriers excrete the organisms in their feces either continuously or intermittently; nevertheless, they become an important source of infection for susceptible persons.
Enterocolitis
216
The carrier state may be terminated by [?] if gallbladder infection is not evident
antimicrobial therapy
217
has been the only solution to the chronic state of enteric carriers
cholecystectomy
218
Sanitary measures must be taken to prevent contamination of food and water by rodents or other animals that excrete salmonellae.
Prevention and Control of Salmonella species
219
Infected poultry, meats, and eggs must be thoroughly cooked.
Prevention and Control of Salmonella species
220
Carriers must not be allowed to work as food handlers and should observe strict hygienic precautions.
Prevention and Control of Salmonella species
221
Vaccination is recommended for travelers to endemic regions, especially if the traveler visits rural areas or small villages where food choices are limited.
Prevention and Control of Salmonella species
222
Two typhoid vaccines are currently available in the United States
- oral live, attenuated vaccine
| - Vi capsular polysaccharide vaccine for intramuscular use
223
The genus Shigella is named after the Japanese microbiologist [?], who first isolated the organism in 1896.
Kiyoshi Shiga
224
not members of the normal GI microbiota
Shigella species
225
can cause bacillary dysentery that can vary in severity, mortality rate, and epidemiology
Shigella species
226
what classification system separates the genus Shigella into four serogroups or species based on their antigen types
Ewing’s classification
227
four serogroups or species od Shigella spp based on their antigen types
S. dysenteriae, S. flexneri, S. sonnei, and S. boydii.
228
the four serogroups of shigella spp are further subdivided into serotypes based on the
O-antigen structure of their LPS.
229
A - Shiga’s bacillus / Japanese dysentery bacillus
Shigella dysenteriae
230
B - Flexner’s bacillus or Strong’s bacillus /Philippine dysentery bacillus
Shigella flexneri
231
C - Boyd’s bacillus / British dysentery bacillus
Shigella boydii
232
D - Sonne-Duval’s bacillus / US dysentery bacillus
Shigella sonnei
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Humans and other large primates are the only known reservoir of
Shigella spp
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Transmission of Shigella spp
direct person-to-person contact
fecal-oral route
flies, fingers, and food or water contaminated by infected persons
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is highly communicable because of the low infective dose required to produce the disease
Shigellosis
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infective dose of Shigellosis
(approximately less than 100 bacilli)
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Clinical manifestations of [?] vary from asymptomatic to severe forms of the disease
shigellosis
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released upon autolysis of all shigellae and probably contribute to the irritation of the bowel wall
Endotoxin
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Shigella dysenteriae Exotoxin is produced by
S. dysenteriae type I
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An antigenic protein (stimulates antitoxin production).
Shigella dysenteriae Exotoxin
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produces diarrhea as does the E coli Shigalike toxin, perhaps by the same mechanism, inhibits sugar and amino acid absorption in the small intestine.
Shigella dysenteriae Exotoxin as enterotoxin
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contributes to the extreme severity and fatal nature of S dysenteriae infections and to the central nervous system reactions observed.
Shigella dysenteriae Exotoxin as neurotoxin
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After ingestion, the organisms multiply in the small intestine, move toward the colon.
shigellosis
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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).
shigellosis
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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.
shigellosis
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was used by Hippocrates to indicate a condition characterized by frequent passage of stool containing blood mucus accompanied by straining and painful defecation.
“dysentery”
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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.
Bacillary dysentery
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Severe cases of shigellosis may become life threatening as extraintestinal complications develop including:
Rectal prolapse
| Ileus
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an obstruction of the intestines, with marked abdominal dilation, possibly leading to toxic megacolon
Ileus
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may result from excessive straining during defecation
Rectal prolapse
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are transmitted by “food, fingers, feces, and flies” from person to person.
Shigellae
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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.
Prevention and Control of Shigellae
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Of the many Yersinia species isolated in man, only three are considered as human pathogens
Y. pestis
Y. enterocolitica
Y. pseudotuberculosis
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zoonoses caused by Yersinia
yersinioses
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the causative agent of plague
Y. pestis
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Have been found in a wide variety of animals, including domestic swine, cats, and dogs.
Yersinia enterocolitica
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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.
Yersinia enterocolitica
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Food refrigeration is an ineffective preventive measure because of its ability to survive in cold temperatures.
Yersinia enterocolitica
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An inoculum of [?] yersiniae must enter the alimentary tract to produce infection.
10^8–10^9
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Yersinia enterocolitica infections manifest in several forms:
- an acute gastroenteritis
- an appendicitislike syndrome,
- septicemia, arthritis, and erythema nodosum
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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
acute gastroenteritis
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associated with the transfusion of contaminated packed red blood cells has also been reported
Sepsis
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The incidence of [?] is higher among elderly adults or those with underlying diseases
systemic infection
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Is pathogen primarily of rodents, particularly guinea pigs
Yersinia pseudotuberculosis
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Yersinia pseudotuberculosis is derived from the disease it produces in animals which is characterized by caseous swellings called
pseudotubercles
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Human infections caused by Yersinia pseudotuberculosis, which are rare, are associated with
- close contact with infected animals or their fecal material
- ingestion of contaminated drink and foodstuff
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Yersinia pseudotuberculosis when ingested, the organisms spread to the [?], producing a generalized infection that is usually self-limiting.
mesenteric lymph nodes
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Clinical manifestations can include septicemia accompanied by mesenteric
lymphadenitis, a presentation similar to appendicitis.
Yersinia pseudotuberculosis
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Yersinia pestis common name
“plague bacillus”
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caused the great pandemic of “black death” in 1800s.
Yersinia pestis
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Plague is a disease primarily of rodents.
Yersinia pestis
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most common and effective vectors of Yersinia pestis
bites of fleas
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Humans can develop plague through contact with:
- wild animals - ?
- domestic or semi domestic animals - ?
- infected humans.
(syllabic plague)
| urban plague
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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.
(Xenopsylla cheopsis)
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results from inhalation of infective droplets .
Primary pneumonic plague
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The most common form of plague
Bubonic/glandular form
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Usually results form the bite of an infected flea
Bubonic/glandular form
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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)
Bubonic/glandular form
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Occurs when the bacteria spread to the bloodstream.
Septicemic form
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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.
Septicemic form
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signs of pneumonia and meningitis can appear, and
| Y. pestis multiplies intravascularly and can be seen in blood smears
Septicemic form
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May occur as a primary infection if the bacteria are inhaled
Pneumonic form
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Secondary to bubonic plague or the septicemic form
when organisms proliferate in the bloodstream and
respiratory tract.
Pneumonic form
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Patients often have a fulminant course with chest pain, cough, hemoptysis, and severe respiratory distress.
Pneumonic form
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Has a high fatality rate— essentially 100%—in untreated patients.
Pneumonic form
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All yersiniae possess lipopolysaccharides that have endotoxic activity when released
Endotoxin
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consisting of a membrane-spanning complex that allows the bacteria to inject proteins directly into cytoplasm of the host cells
Type III secretion systems
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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.
V and W antigens
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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.
pPCP1
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(20°–28°C, the temperature of the flea)
coagulase activity
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(35°–37°C, the temperature of the host)
fibrinolytic activity
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plasmid encodes the capsular protein n (fraction F1)
| and phospholipase D
pFra/pMT
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produced mainly at 37°C and confers anti-phagocytic properties
capsular protein n (fraction F1)
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required for organism survival in the flea midgut
phospholipase D
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encoded by a pathogenecity island (PAI), is an iron-scavenging siderophore.
Yersiniabactin
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requires surveys of infected animals, vectors, and human
| contacts.
control of plague
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if a human case is diagnosed, health authorities must be notified promptly
control of plague
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All patients should be isolated, particularly if pulmonary involvement has not been ruled out and all specimens must be treated with extreme caution.
control of plague
