A 13-year old male patient was admitted to hospital with complaint of bloody diarrhea along with tenesmus, cramping abdominal pain and fever. The amount of feces passed was scanty. The mucus was blood tinged, feces was not foul smelling and was adherent to the container.

What is your diagnosis?
It could be a case of bacillary dysentery.

Which are the pathogens that can cause dysentery?
Among bacteria that can cause dysentery include Shigella sps and Enteroinvasive E. coli. Bloody diarrhea can be caused by Salmonella sps, Campylobacter sps, Enterohemorrhagic E.coli etc. Among protozoa, Entamoeba histolytica and Balantidium coli can cause dysentery. Differential diagnoses should also include Crohn Disease and Ulcerative Colitis.

What are the differences between bacillary and amoebic dysentery?

	Amoebic dysentery	Bacillary dysentry
Number of motions per day	6-8	>10
Amount of feces	copious	scanty
Odour	Offensive	odourless
Colour	Dark red	Bright red
Nature	Blood and mucus mixed with feces	Blood and mucus, little feces
pH	Acid	Alkaline
Consistency	Not adherent to container	Adherent to the bottom of container
RBCs	Clumps	Rouleaux
Macrophages	Very few	Large and numerous
Pus cells	Scanty	Many
Pyknotic bodies	Common	Nil
Charcot Leydon crystals	Present	Absent
Ghost cells	Nil	Numerous

What is the pathogenesis of dysentery?
Shigellosis is basically an enteric disease and the transmission involves feco-oral route. Shigella is transmitted via food, fingers, fomites or flies. Ingestion of small numbers of bacilli (approximately 10²) can initiate infection in a susceptible person. As few as 10 S. dysenteriae bacilli can cause clinical disease, whereas 100-200 bacilli are needed for S. sonnei or S. flexneri infection. Once they survive the gastric juices, they reach large intestine and  penetrate the cells of the epithelial lining. Incubation period can be short (1-7 days) but can be very short in people with achlorhydria. Pathogenesis requires invasion and toxin production. The characteristic virulence factor is encoded on a large (220 kb) plasmid that is responsible for synthesis of polypeptides that cause cytotoxicity. Shigella also produce siderophores that are coded on plasmid can chelate iron from host cells from its protein-bound state. Shiga toxin (Stx) is not essential for virulence of S dysenteriae type 1 but contributes to the severity of dysentery. The chromosomally encoded enterotoxin are are potent cytotoxins that are responsible for many pathogenic features of Shigella infection. Lipopolysaccaharide plays an important role in resistance to nonspecific host defense encountered during tissue invasion. The bacilli multiplies in the epithelia and spreads laterally to adjacent tissue and penetrate lamina propria. Inflammatory response ensues which ultimately leads to capillary thrombosis and sloughing off of epithelium due to necrosis leaving behind superficial ulcers. Some strains produce enterotoxin (Shiga toxin) that has neurotoxic, cytotoxic and enterotoxic action. The accumulation of inflammatory cells leads to the formation of microabscesses, which spread and coalesce to form larger abscesses. Bleeding occurs from superficial ulcerations. Bacterial shedding usually ceases within 4 weeks of the onset of illness. Chronic carriers are extremely rare.

What is the specimen collected and how is the condition diagnosed with the aid of laboratory?
Freshly passed feces is collected in a sterile wide mouthed container, if no feces is available rectal swabs may also be taken. A saline wet mount may be performed to observe pus cells, RBCs and their arrangement, or presence of any parasitic forms. In case of delay, the feces may be transported in transport medium such as Sach's buffered glycerol saline. Direct gram stained smear or hanging drop preparation is not useful. Feces is inoculated on to MacConkey's agar, and on to selective media such as XLD (xylose-lysine-deoxycholate) agar, DCA (deoxycholate citrate agar) or SS (Salmonella-Shigella) Agar and incubated at 37^oC overnight. The sample may also be inoculated into enrichment broth such as selenite F broth and later subcultured on to MacConkey's agar for subsequent overnight incubation. An enzyme immunoassay for Shiga toxin is used to detect S. dysenteriae type 1 in the stool.

What is your observation?
Pale (non-lactose fermenting), smooth, low convex, circular colonies of a single type is seen on MacConkey's agar. Gram stained smear of the colony shows gram negative bacilli, hanging drop shows non-motile bacilli, and catalase test is positive. Results of biochemical reactions are negative indole test, negative urea hydrolysis, negative citrate utilization, positive MR test and negative VP test. TSI agar shows alkaline slant/acid butt with no gas or H₂S. The isolate ferments mannitol with acid production. The isolate is identified as Shigella sps other than S. dysenteriae, which does not ferment mannitol.

How do you identify the species?
Sigella dysenteriae (Group A) does not ferment mannitol while the rest three serogroups ferment. Shigella sonnei (group D) is a late lactose fermenter and can be identified by a positive ONPG test. It is difficult to differentiate S. flexineri (group B) from S. boydii (group C). Confirmation of their identities can be made by slide agglutination using specific antisera.

Is it necessary to identify the species?
Identity of the species is not important for treatment. S. dysenteriae is known to cause severe form of dysentery than other species because it produces shiga toxin. Species identification is also epidemiologically significant. it is believed that S. dysenteriae is common in underdeveloped countries, S. flexineri in developing countries and S. sonnei is developed countries.

How is Shigella classified?
Shigella are grouped into 4 species: Shigella dysenteriae, Shigella flexneri, Shigella boydii, and Shigella sonnei, also known as groups A, B, C, and D, respectively. Group A has 13 serotypes, group B has 6 serotypes, group C has 18 serotypes, and group D has 1 serotype.

Which are the pathogenicity tests?
Pathogenicity tests to demonstrate Shigella's invasiveness include Sereny's test (development of keratoconjunctivitis in guinea pig), penetration of HeLa/Hep-2 cells in vitro or congo red binding test.

What are the complications of Shigella dysentery?
Complications include bacteremia, hemolytic uremic syndrome (microangiopathic hemolytic anemia, thrombocytopenia, and renal failure), septic arthritis, toxic neuritis, conjunctivitis, intussusception in children, intestinal perforation, and septicemia.

Is antibiotic treatment necessary?
Mild cases of dysentery are self limiting, but in pediatric cases or severe dysentery antibiotic administration is necessary. Resistance of Shigella species to sulfonamides, tetracyclines, ampicillin, and trimethoprim-sulfamethoxazole (TMP-SMX) has been reported worldwide, and these agents are not recommended as empirical therapy. Since Shigella are acquiring resistance to multiple antibiotics, antibiotic susceptibility testing must be performed along with culture.