Shigelosis

Shigellosis = inflammation of intestines (especially the colon) with accompanying severe abdominal cramps, tenesmus and frequent, low-volume stools containing blood, mucus and fecal leukocytes.

1. ShigellosisShigellosis
Infectious Diseases, AIDS & Clinical Infectious Diseases, AIDS & Clinical
Immunology Research Center TbilisiImmunology Research Center Tbilisi

2. Shigellosis = inflammation of intestines Shigellosis = inflammation of intestines
(especially the colon) with (especially the colon) with
accompanying severe abdominal accompanying severe abdominal
cramps, tenesmus and frequent, low-cramps, tenesmus and frequent, low-
volume stools containing blood, mucus volume stools containing blood, mucus
and fecal leukocytes.and fecal leukocytes.

3. Shigella causes abdominal pain Shigella causes abdominal pain
(Intestinal cramps) and bloody (Intestinal cramps) and bloody
diarrhea ± sudden fever, headache diarrhea ± sudden fever, headache
and occasionally neck stiffness. and occasionally neck stiffness.

4. EtiologyEtiology
Gram-negative non-spore forming, Gram-negative non-spore forming,
nonmotile bacteria;nonmotile bacteria;
Primarily parasite of the digestive tract of Primarily parasite of the digestive tract of
humans;humans;
Infective dose is small;Infective dose is small;
Cause a severe form of dysentery called Cause a severe form of dysentery called
shigellosis;shigellosis;
Resistant to bile salts;Resistant to bile salts;
Discovered by a Japanese scientist K. Discovered by a Japanese scientist K.
Shiga.Shiga.

5. Four well-defined speciesFour well-defined species
·Shigella sonneiShigella sonnei (most common in industrial (most common in industrial
world)world)
·Shigella flexneri Shigella flexneri (most common in (most common in
developing countries)developing countries)
·Shigella boydiiShigella boydii
·Shigella dysenteriae Shigella dysenteriae – produces a more – produces a more
serious disease than the other species.serious disease than the other species.

6. Shigella dysenteriae produces an Shigella dysenteriae produces an
exotoxin (Shiga Toxin) which acts as exotoxin (Shiga Toxin) which acts as
an enterotoxin, a neurotoxin an enterotoxin, a neurotoxin
(meningismus and coma) and a (meningismus and coma) and a
cytotoxin. cytotoxin.
Shiga Toxin is similar to the Shiga-like Shiga Toxin is similar to the Shiga-like
toxin of enterohemorrhagic E. coli toxin of enterohemorrhagic E. coli
(EHEC).(EHEC).

7. EpidemiologyEpidemiology
Low infectious dose (10Low infectious dose (10
22
-10-10
44
CFU) CFU)
The human intestinal tract represents the The human intestinal tract represents the
major reservoir of Shigella.major reservoir of Shigella.
Transmission Transmission – – person to person, person to person,
primarily fecal-oral by contaminated hands.primarily fecal-oral by contaminated hands.
Although onsumption of contaminatedAlthough onsumption of contaminated
water or food. water or food.

8. Who is at risk?Who is at risk? – Anyone exposed to – Anyone exposed to
carrier, particularly young children. carrier, particularly young children.
In a review of WHO, the total annual In a review of WHO, the total annual
number of cases in 1966-1997 wasnumber of cases in 1966-1997 was
estimated at 165 million and 69% of theseestimated at 165 million and 69% of these
cases occurred in children < 5 years of cases occurred in children < 5 years of
age.age.

9. Shigella is common in developing
countries or refugee camps.
Outbreaks of shigellosis are
associated with poor sanitation,
contaminated food and water, and
crowded living conditions.


10. Pandemics of ShigellosisPandemics of Shigellosis

11. More recent data (2000-2004) from six More recent data (2000-2004) from six
Asian countries (Bangladesh, China, Asian countries (Bangladesh, China,
Pakistan, Indonesia, Vietnam and Thailand) Pakistan, Indonesia, Vietnam and Thailand)
indicate that even though the incidence of indicate that even though the incidence of
shigellosis remain stable.shigellosis remain stable.
Epidemics follow a cyclic pattern in areas Epidemics follow a cyclic pattern in areas
such as the Indian subcontinent and sub-such as the Indian subcontinent and sub-
Saharan Africa.Saharan Africa.

12. pathogenesispathogenesis
Bacteria shigella are able to invade intestinal Bacteria shigella are able to invade intestinal
epithelial cells. epithelial cells.
Shigella attaches to epithelial cell of colon;Shigella attaches to epithelial cell of colon;
Shigella triggers phagocytosis;Shigella triggers phagocytosis;
Shigella multiplies in cytosol;Shigella multiplies in cytosol;
Shigella invades neighboring epithelial cells, thus Shigella invades neighboring epithelial cells, thus
avoiding immune defenses;avoiding immune defenses;
An mucosal abscess forms as epithelial cells are An mucosal abscess forms as epithelial cells are
killed by the infection;killed by the infection;
Shigella that enters the blood is quickly Shigella that enters the blood is quickly
phagocytized.phagocytized.

13. pathogenesispathogenesis

14. Clinical ManifestationsClinical Manifestations
Incubation periodIncubation period: : 1-4 days, but may be as 1-4 days, but may be as
long as 8 days.long as 8 days.
Watery diarrhea period: Watery diarrhea period:
–Transient feverTransient fever
–Watery diarrheaWatery diarrhea
–MalaiseMalaise
–AnorexiaAnorexia
(Unlike most diarrheal syndromes, dysenteric (Unlike most diarrheal syndromes, dysenteric
syndromes do not have dehydration as a syndromes do not have dehydration as a
major feature).major feature).

15. Dysentery period: Dysentery period:
–Small volumes of bloody mucopurulent Small volumes of bloody mucopurulent
stools with increased tenesmus and stools with increased tenesmus and
abdominal cramps. abdominal cramps.
–At this stage, Shigella produces acute At this stage, Shigella produces acute
colitis involving mainly the distal colon colitis involving mainly the distal colon
and the rectum. and the rectum.

16. ComplicationsComplications
Most often in children <5 years of ageMost often in children <5 years of age
Intestinal:Intestinal:
Toxic megacolonToxic megacolon
Intestinal perforationsIntestinal perforations
Rectal prolapseRectal prolapse
Metabolic:Metabolic:
HypoglycemiaHypoglycemia
HyponatremiaHyponatremia
dehydrationdehydration

17. The postinfectious immunologic complication known as The postinfectious immunologic complication known as
reactive arthritis (Reiter’s syndrome) can develop weeks reactive arthritis (Reiter’s syndrome) can develop weeks
or months after shigellosis. or months after shigellosis.
About 3% of patients infected with S. flexneri later About 3% of patients infected with S. flexneri later
develop Reiter’s syndrome, with arthritis, ocular develop Reiter’s syndrome, with arthritis, ocular
inflammation and urethritis – a condition that can last for inflammation and urethritis – a condition that can last for
months or years and progress to difficult-to-treat chronic months or years and progress to difficult-to-treat chronic
arthritis. arthritis.
Postinfectious arthropathy occurs only after infection with Postinfectious arthropathy occurs only after infection with
S. flexneri and not after the other Shigella serotypes.S. flexneri and not after the other Shigella serotypes.

18. Laboratory DiagnosisLaboratory Diagnosis
The “gold standard” for the diagnosis The “gold standard” for the diagnosis
of Shigella infection is the isolation of Shigella infection is the isolation
and identification of the pathogen from and identification of the pathogen from
fecal material. fecal material.

19. TreatmentTreatment
Antibiotic treatmentAntibiotic treatment
Rehydration and nutritionRehydration and nutrition
Non-specific, symptom-based therapyNon-specific, symptom-based therapy
Treatment of complicationsTreatment of complications
(Beause of the ready transmissibility of Shigella, (Beause of the ready transmissibility of Shigella,
current public health recommendations in the current public health recommendations in the
United States are that every case be treated with United States are that every case be treated with
antibiotics).antibiotics).

20. Antibiotic treatmentAntibiotic treatment
Antimicrobial agent In Children In adults
First line
Ciprofloxacin 15mg/kg 2 times per day
for 3 days PO
500 mg 2 times per day for
3 days PO
Second line
Ceftriaxon 50-100 mg/kg – Once a
day IM for 2-5 days
Azithromycin 6-20 mg/kg
Once a day for 1-5 days,
PO
1-1,5 g
Once a day for 1-5 days,
PO