Bacillary dysentery is a gastrointestinal disease. Bacillary means related to bacteria, and dysentery is severe diarrhea containing blood or mucus. With bacillary dysentery, a bacterial infection becomes more invasive and severe, causing inflammation in the intestines. Symptoms can range from mild to life-threateningDysentery is an infection of the intestines that causes diarrhoea containing blood or mucus. Other symptoms of dysentery can include: painful stomach cramps. feeling sick or being sick (vomiting)Transmission is fecal-oral and is remarkable for the small number of organisms that may cause disease (10 ingested organisms cause illness in 10% of volunteers, and 500 organisms cause disease in 50% of volunteers). Shigella bacteria invade the intestinal mucosal cells but do not usually go beyond the lamina propria. Dysentery is caused when the bacteria escape the epithelial cell phagolysosome, multiply within the cytoplasm, and destroy host cells. Shiga toxin causes hemorrhagic colitis and hemolytic-uremic syndrome by damaging endothelial cells in the microvasculature of the colon and the glomeruli, respectively. In addition, chronic arthritis secondary to S. flexneri infection, called reactive arthritis, may be caused by a bacterial antigen; the occurrence of this syndrome is strongly linked to HLA-B27 genotype, but the immunologic basis of this reaction is not understoodSpecimen: Fresh stool is collected. Culture: Specimen is inoculated on selective media like MacConkey's agar, DCA, XLD agar. Selenite F broth(0.4%) is used as enrichment medium which permits the rapid growth of enteric pathogens while inhibiting the growth of normal flora like E. coli for 6–8 hours. Subculture is done on the solid media from selenite F broth. All the solid media are incubated at 37 degrees for 24 hours. Cultural characteristics: Colorless (NLF) colonies appear on MacConkey's agar which are further confirmed by gram staining, hanging drop preparation and biochemical reactions.Dysentery is initially managed by maintaining fluid intake using oral rehydration therapy. If this treatment cannot be adequately maintained due to vomiting or the profuseness of diarrhea, hospital admission may be required for intravenous fluid replacement. Ideally, no antimicrobial therapy should be administered until microbiological microscopy and culture studies have established the specific infection involved. When laboratory services are not available, it may be necessary to administer a combination of drugs, including an amoebicidal drug to kill the parasite and an antibiotic to treat any associated bacterial infection. Anyone with bloody diarrhea needs immediate medical help. Treatment often starts with an oral rehydrating solution—water mixed with salt and carbohydrates—to prevent dehydration. (Emergency relief services often distribute inexpensive packets of sugars and mineral salts that can be mixed with clean water and used to restore lifesaving fluids in dehydrated child

1. Bacillary Dysentery
Prepared by Dr.Maryam

2. Introduction
 Shigellosis infection by shigella species is an acute invasive enteric infection
 Bacillary dysentery is a term often used to distinguish dysentery caused by
shigella from amoebic dysentery caused by Entamoeba histolytica.
 Clinically manifested by diarrhea that is often bloody
 The term dysentery describes a syndrome of bloody diarrhea with
 Fever
 Abdominal cramps
 Rectal pain
 Mucoid stool

3. Etiology
 Four species of shigella are responsible for shigellosis
 Shigella dysenteriae (group A)
 Shigella flexneri (group B)
 Shigella boydii (group C)
 Shigella sonnei (group D)
 Serotypes are use to distinguish members of each group 15, 19 ,19 ,and 1 in
groups A-D respectively.

4. Epidemiology
 WHO estimated 80 to 165 million cases of shigellosis each year world wide
 600,000 deaths annually
 Shigella spp are endemic to temperate and tropical climates
 Most of the cases and deaths occur in developing countries where public
health sanitation and hygiene are inadequate
 Infection can occur at any age, children less than 10 year of age have the
highest incidence rates
 Males having an approximately 1.3 fold higher incidence than females.

5.  Approximately 70% of all episodes and 60% of all shigella related deaths involve
children less than 5 year old
 Infection in the first 6 months of life is rare for reasons that are not clear
 Breastfeeding might partially explain the age related incidence.
 Infection with shigella occurs most often during warm months in temperate climates
and during the rainy season in tropical climates.
 Contaminated food and water are important vectors.

6. Pathogenesis
 Shigella has specialized mechanisms to survive the low gastric pH.
 The basic virulence trait shared by all shigella is the ability to invade colonic
epithelial cells
 Turning on a series of temperature regulated and host dependent proteins.
 Shigella that lose the virulence plasmid are no longer pathogenic.
 Enteroinvasive Escherichia coli (EIEC) behave clinically similar to shigella.
 The virulence plasmid encodes a type 3 secretion system required to trigger entry
into epithelial cells and apoptosis in macrophages

7.  Translocates effector molecules from the bacteria cytoplasm to the membrane
 And cytoplasm of target host cells through a needle like appendage.
 Type 3 secretion system is composed of approximately 50 proteins and 30
effector proteins
 Chromosomally encoded factors are also required for full virulence.
 The pathologic changes of shigellosis take place primarily in the colon
 Most intense in the distal colon

8.  Shigellae cross the colonic epithelium through M cells in the follicle associated
epithelium
 Overlying the peyer patches
 Diffuse mucosal edema, ulcerations, friable mucosa bleeding and exudate may
be seen
 After shigella transcytosis through M cells it encounters resident macrophages
 Subverts macrophage killing by activating the inflammasome and inducing
pyroptosis , apoptosis
 Free bacteria invades the epithelial cells from the basolateral side

9.  Some shigella makes toxins including shiga toxin and enterotoxins
 Shiga toxin is a Potent exotoxin
 Inhibits protein synthesis to injure vascular endothelial cells and trigger the
severe complications of haemolytic uremic syndrome

10. Immunity
 In symptomatic infection shigella activates an intense innate immune response
 Triggering extra and intracellular pathogen recognition systems.
 Massive recruitment of PMNs produces intensive local tissue destruction.
 In rectal biopsies of infected patients :
 Acute phase proinflammatory cytokines
 Interleukin IL 1beta, IL 6 , IL 8
 Tumor necrosis factor alpha and beta
 Induction of humoral response
 IgA IgG

11. Clinical Manifestations
 Shigellae produce intra and extraintestinal symptoms
 Incubation period of 12 hours to several days
 Severe abdominal pain, emesis, anorexia, generalized toxicity, urgency and painful
defection
 High fever with shigellosis distinguishes it from EHEC
 Diarrhea may be watery and of large volume initially
 Evolving into small volume bloody mucoid stools.
 Significant dehydration
 Neurological findings are among the most common extraintestinal manifestation
 Seizures associated with hypocalcemia and hyponatremia

12. Complications
 Intestinal complications:
 Rectal prolapse
 Toxic megacolon
 Intestinal perforation and obstruction
 Appendicitis
 Persistent diarrhea
 Extraintestinal complications:
 Dehydration
 Severe hyponatremia, hypoglycaemia
 Focal infections e.g meningitis, osteomyelitis, arthritis, splenic abscesses, vaginitis
 Sepsis, seizure or encephalopathy

13.  Postinfectious manifestations:
 Hemolytic uremic syndrome
 Reactive arthritis
 Irritable bowel syndrome
 malnutrition

14. Differential Diagnosis
 Infection by campylobacter jejuni
 Salmonella spp,
 Shiga toxin producing E coli
 Yersinia enterocolitica
 Clostridium difficile
 Entameoba histolytica
 IBS

15. Diagnosis
 Finding of fecal leukocytes usually greater than 50 or 100 PNMs per high power
field
 Fecal blood
 Total peripheral white blood cell count is usually 5000-15000 cells/l
 Culture of both stool and rectal swab
 PCR

16. Treatment
 Fluid and electrolyte correction and maintenance
 Nutrition
 Single dose of vit A
 Zinc supplementation
 Shigella antimicrobial susceptibility varies by species and geography
 Empirical therapy
 Azithromycin 12mg/kg/24 or ciprofloxacin 20-30mg/kg/24
 Ceftriaxone 50-100mg/kg/24
 Cefixime 8mg/kg/24

17. Prevention
 Mothers should be encouraged to prolong breastfeeding of infants
 Families and daycare personnel should be educated in proper handwashing tecniques
 Children with diarrhea should be excluded from childcare facilities
 Safe water supply and appropriate sanitation system
 Measles immunization can substantially reduce the incidence and severity of diarrheal
diseases including shigellosis