2.  Shigella organisms cause bacillary dysentery, a
disease that has been described since early
recorded history.

3. The disease is due to Enterobacteriaceae, the genus
Shigella, that includes more than 100 serotypes
Classification- There are four groups of shigellae
described as follows:
Group A: Shigella dysenteriae (10 serotypes)
Group B: Shigella flexneri (6 serotypes)
Group C: Shigella boydii (15 serotypes)
Group D: Shigella sonnei.

4. Insufficient data exists, but conservative estimates
suggest that Shigella causes approximately 90 million
cases of severe dysentery annually, with at least
100,000 of these resulting in death, mostly among
children in the developing world. Shigella also causes
approximately 580,000 cases annually among travelers
and military personnel from industrialized countries.
An estimated 18,000 cases of shigellosis occur annually
in the United States. Infants, the elderly, and the infirm
are susceptible to the severest symptoms of disease,
but all humans are susceptible to some degree.
Individuals with acquired immune deficiency
syndrome (AIDS) are more frequently infected
with Shigella. Shigellosis is a more common and
serious condition in the developing world; fatality
rates of Shigellosis epidemics in developing countries
can be 5–15%.

5. Epidemiology of shigellosis

6.  Shigellae are released from the patient or carrier
with excrements. The microorganisms can survive
in soil for 3 months, on soiled utensils, dishes,
moist linens for weeks or even months, for several
days on food (bread, meat); in milk they persist for
30 days or longer, in running water they can
survive from several hours to 5-9 days.
 S sonnei and S flexneri cause 90% of the cases of
shigellosis.
 S dysenteriae has produced epidemic shigellosis.

7.  Shigella species (eg, Shigella dysenteriae, Shigella flexneri,
Shigella sonnei, Shigella boydii) are aerobic, nonmotile,
glucose-fermenting, gram-negative rods that are
highly contagious, causing diarrhea after ingestion of
as few as 180 organisms.
 Shigella species cause damage by 2 mechanisms, as
follows:
(1) invasion of the colonic epithelium, which is
dependent on a plasmid-mediated virulence factor,
and
(2) production of enterotoxin, which is not essential for
colitis but enhances virulence.
 The organism is spread by fecal-oral contact; via
infected food or water; during travel; or in long-term
care facilities, day care centers, or nursing homes.

8. Invasion of shigella
In addition to the toxins, the invsasive properties of shigellae
are also very important for the development of pathology in the
intestine. Intracellular parasites cause degenerative changes,
desquamation and destruction of the epithelial cells .
Toxaemia affects the CVS and CNS, causes disorders in the
alimentary canal and in the first instance upsets the secretory,
motor and absorption functions; water, mineral, protein,
carbohydrate, fat and vitamin metabolisms are also affected.

9.  Acute bloody diarrhea
 Crampy abdominal pain
 Tenesmus
 Passage of mucus
 Fever (1-3 d after exposure)
 Occasionally vomiting (35% prevalence)
 Self-limited course (3 d to 1 wk and rarely lasts as long as 1
mo)

10.  Lower abdominal tenderness
 Normal or increased bowel sounds
 Dehydration (occasional)

11. Abdominal tenderness in shigellosis

12.  Symptoms may range from mild abdominal discomfort to
full-blown dysentery characterized by cramps, diarrhea,
fever, vomiting, blood, pus, or mucus in stools
or tenesmus. Onset time is 12 to 96 hours, and recovery
takes 5 to 7 days.
 Infections are associated with mucosal ulceration, rectal
bleeding, and drastic dehydration. Reiter's
disease and hemolytic uremic syndrome are possible
sequelae that have been reported in the aftermath of
shigellosis.
 Shigella can be transmitted through food,
including salads (potato, tuna, shrimp, macaroni, and
chicken), raw vegetables, milk and dairy products, and
meat. Contamination of these foods is usually through the
fecal-oral route. Fecally contaminated water and unsanitary
handling by food handlers are the most common causes of
contamination. Apart from hand-to-mouth infection,
Shigellosis is transmitted through fomites, water and
mechanical vectors like houseflies.
 The most common neurological symptom includes
seizures.

13.  Amebiasis
 Campylobacter Infections
 Cholera
 Clostridium Difficile Colitis
 Colon Cancer, Adenocarcinoma
 Crohn Disease
 Cryptosporidiosis
 Escherichia Coli Infections
 Gastroenteritis, Bacterial
 Gastroenteritis, Viral
 Pseudomembranous Colitis
 Salmonellosis
 Ulcerative Colitis
 Yersinia Enterocolitica

14. 1. Laboratory Studies: Fecal leukocytes and erythrocytes
 Mildly elevated hematocrit, sodium, and urea nitrogen are
indicative of volume depletion in cases of shigellosis.
 Leukocytosis is rare.
 Positive findings on stool culture of a fresh fecal specimen
 In patients who are immunocompromised (eg, HIV), blood
cultures are rarely helpful in cases of shigellosis.

15. 2. Histologic Findings: Intense neutrophilic and mononuclear
cells infiltrating the lamina propria
 Hemorrhage
 Ulcers
 Mucous depletion
 Occasional crypt abscesses
Endoscopic view of colitis caused by
shgellosis

16.  Treatment consists mainly of replacing fluids and salts lost
because of diarrhea. Oral replacement is satisfactory for most
people, but some may need to receive fluids intravenously. In
most cases, the disease resolves within four to eight days
without antibiotics. Severe infections may last three to six weeks.
Antibiotics, such as trimethoprim-sulfamethoxazole (Co-
Trimoxazole),norfloxacin, ciprofloxacin or furazolidone, may be
given when the person is very young or very old, when the
disease is severe, or when there is a high risk of the infection
spreading to other people. Additionally, ampicillin (but
not amoxicillin) is effective in treating this disease.
 The severity of the symptoms and the length of time the stool
contains Shigella are reduced with antibiotics. However, many
strains of Shigella are becoming resistant to common antibiotics,
and effective medications are often in short supply in developing
countries. Antidiarrheal drugs (such
as diphenoxylate or loperamide) may prolong the infection and
should not be used.

17.  1. Medical Care: General supportive care of
patients with shigellosis includes the following:
[5]
High fever in children should be treated.
 Narcotic-related antidiarrheals should be avoided.
 Antibiotic treatment is indicated in most patients.[6]
 Antimotility agents should be avoided. They have
the potential to worsen symptoms and may
predispose to toxic dilation of the colon.
 For fluid and electrolyte supplementation, oral
rehydration solutions are preferable.
2. Diet: Clear liquids followed by a low residue,
lactose-free diet are recommended until symptoms
of shigellosis resolve.

18.  Shigella infection produces a self-limited diarrheal illness that lasts 5-7
days and may not require antibiotics in individuals who are otherwise
healthy. Antibiotic treatment is recommended for infirm or older
patients, malnourished children, patients infected with HIV, food
handlers, health care workers, and children in day care centers.
 For public health reasons, most experts recommend treating any
person whose stool culture is positive for Shigella species. Moreover,
antibiotics have been shown to decrease the duration of fever and
diarrhea by about 2 days. The shorter duration of shedding with
antibiotic therapy can reduce the risk of person-to-person spread.
 Ampicillin was widely used in the past but is no longer an effective
empiric treatment in the United States because of antibiotic
resistance. In fact, antibiotic resistance to Shigella species is widespread
and increasing worldwide. Thus, antibiotic susceptibility testing is
essential for the management of patients with
suspected Shigella infection.
 Given the widespread resistance to ciprofloxacin as well as
trimethoprim-sulfamethoxazole and azithromycin, a third-generation
cephalosporin is appropriate empiric therapy in the setting of acute
illness. The treatment of choice for HIV-infected patients is a quinolone
for 5 days.

19. 1. Antibiotics: Empiric antimicrobial therapy must be comprehensive
and should cover all likely pathogens in the context of the clinical
setting.
- Ceftriaxone (Rocephin): Third-generation cephalosporin with
broad-spectrum, gram-negative activity; lower efficacy against
gram-positive organisms; higher efficacy against resistant
organisms. Bactericidal activity results from inhibiting cell wall
synthesis by binding to one or more penicillin binding proteins.
Exerts antimicrobial effect by interfering with synthesis of
peptidoglycan, a major structural component of bacterial cell wall.
Bacteria eventually lyse due to the ongoing activity of cell wall
autolytic enzymes while cell wall assembly is arrested.
Highly stable in presence of beta-lactamases, both penicillinase and
cephalosporinase, of gram-negative and gram-positive bacteria.
Approximately 33-67% of dose excreted unchanged in urine, and
remainder secreted in bile and ultimately in feces as
microbiologically inactive compounds. Reversibly binds to human
plasma proteins, and binding have been reported to decrease from
95% bound at plasma concentrations < 25 mcg/mL to 85% bound at
300 mcg/mL. (1-2 g IV/IM qDay or divided BID for 4-14 days
depending on type and severity of infection)

20. - Ciprofloxacin (Cipro): Fluoroquinolone that
inhibits bacterial DNA synthesis and,
consequently, growth. (Mild/Moderate/Severe:
500 mg PO q12hr for 5-7 days)
 - Trimethoprim-sulfamethoxazole (Bactrim,
Septra, Bactrim DS, Cotrim): Inhibits bacterial
growth by inhibiting synthesis of dihydrofolic
acid. Reasonable DOC in the United States due to
few resistant strains.
Dosing may be based on TMP component.
(Indicated for treatment of enteritis caused by
susceptible strains of Shigella flexneri and Shigella
sonnei DS tablet: 1 tab PO q12hr for 5 days
8-10 mg TMP/kg/day IV divided q6-12hr for up
to 5 days)

21.  - Azithromycin (Zithromax): Acts by binding to 50S
ribosomal subunit of susceptible microorganisms and
blocks dissociation of peptidyl tRNA from ribosomes,
causing RNA-dependent protein synthesis to arrest.
Nucleic acid synthesis is not affected.
Concentrates in phagocytes and fibroblasts as
demonstrated by in vitro incubation techniques. In
vivo studies suggest that concentration in phagocytes
may contribute to drug distribution to inflamed
tissues.
Treats mild-to-moderate microbial infections.
Plasma concentrations are very low, but tissue
concentrations are much higher, giving it value in
treating intracellular organisms. Has a long tissue half-
life.

22.  A vaccine for shigellosis is not currently available.
Until a vaccine is available, the following measures
can help prevent the dissemination of shigellosis:
 Use of safe drinking water
 Chlorination of unreliable water sources
 Strict handwashing
 Refrigeration and proper preparation and cooking of
foodFood handlers must be treated with antibiotics
and should not be involved in food preparation as
long as stool cultures are positive forShigella infection.
 At least 48 hours of antibiotic treatment are usually
required.

23.  Postinfection carriage is generally less than 3-4
weeks.
 Mild cramps and diarrhea may continue for
many days to weeks after treatment of
shigellosis.