OUTLINE :

 INTRODUCTION
 CAUSATIVE ORGANISM
 PATHOGENESIS
 CLINICAL PRESENTATION
 MANAGEMENT
 PREVENTION

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INTRODUCTION
Shigellosis is an infection of the intestine caused by the gram-negative Shigella
spp. it encompasses the whole spectrum of disease ranging from mild diarrhea to
the severe Bacillary dysentery caused by the bacteria. In general the infection is
limited to the intestinal mucosa rarely does it invade the blood. This disease is
known as a major burden in public health care.
CAUSATIVE ORGANISM: Shigella spp. The Shigella causing disease in humans
include s. dysenteriae, s. flexneri, s.boydii, s.sonnei. Of these s.dysenteriae cause
more severe disease.
EPIDEMIOLOGY
Shigellosis occurs worldwide. Estimated 150million cases occur Annually
worldwide. The incidence of shigellosis in developing Countries is nearly 20 times
more than in developed countries. It is estimated that ;
30% of these infections are caused by S. dysenteriae.
S. flexneri is the most common cause of shigellosis in developing countries
S. sonnei is the most common cause in the industrial world.
PATHOGENESIS
Infection is initiated by ingestion of Shigella usually via faecal-oral route or
contaminated food and formites. Because Shigella are relatively resistant to
gastric acid, ingestion of as few as 10-100 organisms can cause disease. The
organism enters the host and travels through the digestive system until it reaches
the colon. Upon reaching the colon, Shigella is taken up in vacuoles by microfold
cell (M cells) which are specialized epithelial cells that overlie the mucosal
lymphoid follicles. The organism escapes from the vacuole and finally travels to
underlying M cell-associated lymphoid follicles. Macrophages in these follicles
phagocytose the bacteria. Upon phagocytosis, shigella induces apoptosis of
macrophage resulting in death of macrophage and escape of the pathogen. Death
of the macrophage causes the release of proinflammatory cytokine interleukin-1
that ultimately leads to recruitment of polymorphonuclear leucocytes (PMN) to
the site of infection and the onset of inflammation . Meanwhile, the bacteria
induce their own uptake into colonic epithelial cells and spread laterally through

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the cells of the epithelium by a process known as actin based motility (ABM)
through the comet tail formation. This actin based filamentous tail propels the
Shigella into the protrusions on the contiguous enterocytes. During cell-cell
spread the plasma membrane that envelops the bacteria are lysed which results
in intracellular replication, production of toxin (endotoxin and exotoxin) and
intercellular bacterial spread potentiating the infection. As the inflammation
persists and expands, the infiltration of the PMNs facilitates the entry of
additional bacteria into the epithelium. Ultimately, it is the cells of the host’s
immune system that cause inflammation and ulceration to the mucosa of the
colon and develops the symptoms associated with shigellosis.
CLINICAL PRESENTATION
With a short incubation period(1-2days), the symptoms vary from mild watery
diarrhea to severe inflammatory dysentery(BACILLARY DYSENTERY) which
manifests with a sudden onset of high-grade fever along with abdominal cramp,
tenesmus, urgency, and passage of loose, scanty feces containing frank blood and
mucus. In a small number of patients, asymptomatic colonization of shigella
occurs in the colon, which makes the patient a persistent reservoir for infection.
Complications
Complications are most often associated with S. dysenteriae type1 infection.
These include:
■ Arthritis, toxic neuritis, conjunctivitis, and, in children, intussusception.
■ Hemolytic uremic syndrome may also occur following infection with S.
dysenteriae because of vasculopathy mediated by Shiga toxin.
■ Shigella septicemia is rare, except in malnourished children with S. dysenteriae
infection.
■ Disseminated intravascular coagulation, bronchopneumonia, and multiple
organ failure may occur in lethal cases of Shigella septicemia.
DIAGNOSIS
Diagnosis of shigellosis is made by isolating Shigella spp. from feces. For optimal
organism recovery, fecal specimens should be collected during the early stages of

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the illness. Specimens Include fresh stool, mucus flecks, and rectal swabs for
culture(produces Pale non–lactose-fermenting colonies on MacConkey agar and
colorless colonies on SS agar). While whole stool is usually the preferred specimen
for laboratory workup of diarrhea, rectal swabs with visible fecal staining present
may be the preferred specimen for the isolation of shigella.
IDENTIFICATION OF ORGANISM
1. Produces nonlactose-fermenting pale colonies on MacConkey Agar and SS
agar; and green Colonies on HE agar.
2. Nonmotile.
3. Ferments glucose with exception of some strains producing acid Only, but no
gas.
4. Mannitol fermentation test is used to classify shigellae into mannitol-
fermenting and -nonfermenting species.
5. Do not ferment lactose, sucrose, salicin, adonitol, or inositol.
6. Catalase positive with exception of S. dysenteriae type 1
7. H2S negative, urease positive, citrate negative, and oxidase negative.
MANAGEMENT
Uncomplicated shigellosis is a self-limiting condition and patients usually recover
spontaneously in a few days. Hence, no antibiotics are recommended for these
cases.
Antibiotic treatment for Shigella infection is recommended for;
 severe or toxic cases
 the Very young, debilitated, and the aged individuals
 The immunocompromised
Trimethoprim–sulfamethoxazole, ampicillin, tetracycline, and the quinolones,
such as ciprofloxacin, are frequently used antibiotics. it is important to do a
susceptibility test before initiation of Antibiotic therapy as there are resistant
strains of shigella.
The dehydration caused by the diarrhea, particularly in infants and young
Children, needs adequate replacement with fluids and electrolytes.

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Avoid the use of antimotility agents, because they have the potential to worsen
the symptoms and may predispose to toxic dilatation of the colon.
PREVENTION
A vaccine for shigellosis is not currently available, hence prevention centers
around improving personal And environmental sanitation, use of safe drinking
water, Refrigeration and proper preparation and cooking of food.

REFERENCE
1. Jawertz, Melnick & Adelberg’s Medical Microbiology
2. Text book of microbiology and immunology
3. https://microbiologyjournal.org/shigellosis-a-conformity-review-of-the-
microbiology-pathogenesis-and-epidemiology-with-consequence-for-
prevention-and-management-issues-2/