Shigella Flashcards
1
Q
• Shigellae are enterobacterieceae
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They are non sporing and non capsulated
Non motile and non flagellate
2
Q
• Possess capsule (K antigen) and O antigen
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Also non lactose fermenting
3
Q
• Reduce Nitrates and are Oxidase
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4
Q
• Aerobes and facultative anaerobes
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with a growth
5
Q
temperature range of 10-40oC and optima of 37oC and pH 7.4.
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6
Q
They grow well on conventional media:
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7
Q
• Nutrient Agar and Blood Agar
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8
Q
• MacConkey Agar:
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9
Q
• Deoxycholate Citrate Agar (DCA)
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10
Q
• Xylose Lysine Deoxycholate (XLD):
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11
Q
best selective medium for shigellae.
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12
Q
Colonies are red
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13
Q
Salmonella-Shigella (SS) Agar:
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14
Q
•Colorless colonies with no blackening
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15
Q
•While those of Salmonella are colorless with
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16
Q
black centers.
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17
Q
Hektoen Enteric (HE) Agar:
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18
Q
•Direct plating medium for fecal specimen.
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19
Q
•Colonies of Shigella are green while those of
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20
Q
Salmonella are blue green with black centers
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21
Q
due to H2S production.
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22
Q
Peptone Water and Nutrient Broth:
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23
Q
•Growth with uniform turbidity
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24
Q
Classification of Shigella
A
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• Based on somatic O polysaccharide antigen
Shigella
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species are classified into 4 species:
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•S. dysenteriae
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•S. flexneri
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•S. boydii and
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•S. sonnei
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• Which are also designated as serogroups A
B
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respectively.
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1. S. dysenteriae (group A):
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• They are mannitol non-fermenting bacilli
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• Consists of 12 serotypes
each characterized by a different type antigen.
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• Among all
S. shigae (Serotype 1) is the only Shigella which produces a
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powerful exotoxin (Shiga toxin)
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• Shiga toxin acts as enterotoxin as well as neurotoxin.
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As enterotoxin
it acts on the intestinal mucosa causing transdation of
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fluid in the lumen
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As neurotoxin
it damages endothelial cells of small blood vessels of the
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CNS which results in neurological complications like polyneuritis
coma and
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meningism.
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• S. dysenteriae also produces an cytotoxin which is active on vero cells
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and is known as Verotoxin.
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2. S. flexneri (group B):
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• The most complex species antigenically.
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• Typed into 6 serotypes
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• Serotype 6 is always indole negative
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3. S. boydii (group C):
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• It has 19 serotypes.
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• Isolated least frequently from cases of bacillary dysentery.
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4. S. sonnei (group D):
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• It is antigenically homogeneous and has only 1 serotype.
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• It can be typed by colicin typing into 26 colicin types.
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Other Antigens of Shigellae
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• K antigen may be present in some serotypes which may not be
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visible as capsule
but it covers the O antigen and makes it
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inagglutinable by homologous antisera.
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• Fimbrial antigens may be found in some strains
especially in
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S. flexneri.
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• Crossreactivity:
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o Antigens of many Shigella serotype (other than S. sonnei)
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cross-react with serotypes of E. coli.
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o Antigens of S. sonnei cross-react with Plesiomonas shigelloides.
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Mode of transmission:
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• Infection occurs by ingestion through contaminated fingers
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(most common)
food
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• It can also be transmitted sexually homosexuals.
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• The infection is highly communicable because of:
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✔ The low infective dose(10 - 100 bacilli initiate the disease) is
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required to produce the disease (Highly infectious)
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✔ Their ability to survive the gastric acidity.
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✔ Shigella can survive up to 30 days in milk
eggs and cheese
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▪ Outbreak of shigella can are common in place where sanitation is poor
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Pathogenesis
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• Shigellae cause bacillary dysentery.
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• Humans are the only reservoir.
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• Bacteria are acquired by fecal-oral spread.
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• Penetrate the mucosa and epithelial cells of the colon (but do not
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invade beyond the epithelium).
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• Survive the passage through the host defences due to the O antigens
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and Lipopolysaccharide (LPS)
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Invasiveness:
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• Exotoxin (shiga toxin): help to penetrate and multiply in colonic mucosa
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• Large plasmids: responsible for cell penetration.
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These proteins are called ‘virulence marker antigens’ (VMA).
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Pathogenesis ctn
…
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• Bacilli enter the mucosa via M cells and cross M cells to reach
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the sub-mucosa where they are engulfed by macrophages and
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cause the released of cytokines which attract and increased the
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number of inflammatory cells to the infected site and cell death
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(due to cytotoxic properties of shiga toxin).
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Polymorphonuclear leukocytes which can be seen on microscopic
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examination of stool
together with red cells.
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• Leading to the acute colitis that characterizes shigellosis.
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o Most common form is an initial watery diarrhea
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o Severe form of disease is caused by S. dysenteriae.
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Clinical manifestation
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• Bacillary dysentery has a short incubation period (1-7 days
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usually 48 hours).
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• The clinical manifestations of shigellosis vary from asymptomatic
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to severe forms of the disease.
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• The main clinical features are: frequent passage of loose
scanty
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feces containing blood and mucus
along with abdominal cramps.
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• Fever and vomiting may be present.
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▪ Infection is usually self-limited
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▪ Although antibiotic treatment is recommended to reduce the
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risk of secondary spread to family members and other contacts
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Diagnosis
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• To identify the causative agent; stool samples can be cultured.
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• Fresh feces should be inoculated without delay or
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• Transported in a suitable medium such as cary-Blair medium
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• The best sample for culture is rectal swab.
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• Microscopy: show numerous erythrocytes and polymorphs and
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some macrophages.
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• Commonly used primary isolation media include MacConkey
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Hektoen Enteric Agar and Salmonela-Shigella(SS) agar
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• Biochemical test: urease
citrate
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• Identification is confirmed by slide agglutination
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Treatment
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• Routine antibacterial treatment is not indicated in dysentery.
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• Treatment with a suitable antibiotic is necessary in the very
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young
the aged or the debilitated
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▪ Ampicillin
cotrimoxazole
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antibiotics such as nalidixic acid and ciprofloxacin are
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appropriate choices.
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• Multiple drug resistance plasmids are widely prevalent in shigellae.
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The choice of antibiotic should be based on the sensitivity
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of the prevailing strain.
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Control
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• Improving personal hygiene (hands)
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• Environmental sanitation (proper sewage disposal)
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• Water chlorination
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• Insect control (flies)
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• No effective vaccine is available
