Dysentery

Dysentery comes from Greek, that is dys (= trouble) and enteron (= intestine), is meaning chafes intestine generating symptom to extend, mixed mucus faeces of blood [ 1]. Dysentery symptoms for example is:


Defecation with bloody faeces


Watery diarrhoea with volume a few

Defecation with mixed faeces of lender(mucus)


Pain in bone when defecation ( tenesmus)

Etiology


Bacterium ( Dysentery basilar)

Shigella, all important dysentery cause and often (± 60% dysentery case referred and most all heavy dysentery cases and menaces soul because of Shigella [ 2].
Escherichia coli enteroinvasive ( EIEC)
Salmonella


Campylobacter jejuni, especially at baby
Amoeba ( Dysentery amoeba), caused Entamoeba hystolitica, a more regular at child of age > 5 year

Pathogenesis

Transmission : fecal-oral, through : food / water contamination, person-to-person contact.
Dysentery basiler

Shigella and EIEC


MO --> colonization in ileum terminal’s / colon, especially distal colon ? invasion to cell epitel intestine mucosa --> multiplication --> spreading of intracellular and intercell --> produce of enterotoxin --> ? cAMP --> persecretion of intestine ( liquid diarrhoea, secretion diarrhoea). --> produce of exotoxin ( Shiga toxin) --> cytotoxic --> infiltration of cell chafes --> cell necrosis epitel mucosa --> small ulkus-ulkus --> erythrocyte and plasma go out to gut lumen --> mixed faeces of blood. --> invasion to lamina propia ? --> bacteremia ( especially at infection Sdysenteriae serotype 1)

Salmonella


MO --> colonization in jejunum/ileum/kolon --> invasion to cell epitel intestine mucosa --> invasion to lamina propia --> infiltration of cells chafes --> synthesis Prostaglandin --> produce of heat-labile cholera-like enterotoxin --> invasion to Plak Peyeri --> spreading to KGB mesentery --> hypertrophy --> degradation of blood stream to mucosa --> mucosa necrosis --> ulkus chasm --> erythrocyte and plasma go out to lumen --> mixed faeces of blood.


Campylobacter jejuni


MO --> colonization in jejunum/ileum/kolon --> invasion to cell epitel intestine mucosa --> invasion to lamina propia --> infiltration of cells chafes --> Prostaglandin --> produce of heat-stabile cholera-like enterotoxin --> produce of cytotoxin ?? --> mucosa necrosis --> ulkus --> erythrocyte and plasma go out to lumen --> mixed faeces of blood. --> steps into circulation ( bacteremia).

Dysentery amoeba


Form of histolitika ( trophozoite) --> invasion to cell epitel intestine mucosa --> produce of enzyme histolisin ? intestine mucosa network necrosis --> invasion to stibmucosa network --> ulkus amoeba --> wide ulkus and interaction forms stibmucosa sines --> imbibition surface damage ? malabsorption --> ? mass intraluminal --> osmotic pressure intraluminal --> diarrhoea osmotik.

Manifests clinics

Dysentery basiler


Sudden diarrhoea accompanied by blood and mucus in faeces. At dysentery shigellosis, at pain start, can there is watery diarrhoea without blood in first 6-24 hours, and after 12-72 hours after pain start, got blood and mucus in faeces.

High temperature ( 39,50 - 400 C), appear toxic.

Pukings.


Anorexia.


Muscle-bound pain in stomach and ill in anus when CHAPTER.


Sometime is accompanied with symptom to look like encephalitis and sepsis ( spastic, headache, lethargy, scruff rigid, hallucination).


Dysentery amoeba


Diarrhoea is accompanied [by] blood and mucus in faeces.


Chapter Frequency generally slimmer than dysenteries basiler (= 10x/hari)


Excitement stomachache ( colic)

Constitutional symptom usually not exist ( hot only found by 1/3 cases).


Diagnosis

Diagnosis klinis can be upheld solely by finding mixed faeces of blood. Etiology diagnosis usually difficult to be upheld. Straightening of etiology diagnosis through image of klinis as of difficult eye, while inspection of faeces breeding to know causal agent often not necessarily be done by eating stripper time ( minimum of 2 day) and generally good symptom with therapy antibiotika empiric.


Inspection of supporter which can be done :


inspection of Faeces

Makroskopis : an dysentery amoeba can be upheld if found form of trophozoite in faeces


Benzidin test


Microscopic : fecal leucocyte ( petanda existence of colitis), fecal blood.


Faeces breeding :

Media : that MacConkey, xylose-lysine deoxycholate ( XLD), that SS.


Inspection of routine blood : leucocytosis ( 5000 – 15000 sel/mm3), sometimes detectable leucopenia.

Complicacy


Dehydration


Electrolyte trouble, especially hiponatremia


Spastic

Protein loosing enteropathy


Sepsis and DIC

Syndrome Hemolytic Uremia


Malnutrition / mal absorption


Hypoglycemia


rectal Prolapsed


Reactive arthritis

Syndrome Guillain-barre


Ameboma


Toxic megacolon


Perforation local


Peritonitis


How to do


1. Pays attention to child generality, if(when child of appear toxic, status gizi is less, does inspection of blood ( if possible is accompanied with blood culture) to detect existence of bacterium. If suspected existence of sepsis, gives therapy according sepsis at child. Takes heed existence of sepsis shock. 2. Dysentery therapy component : a. Corrective and maintenance dilution and electrolyte. b. Diet c. Antibiotic d. Sanitary landfill


a. Corrective and maintenance dilution and electrolyte


Like at acute diarrhoea case in general, first thing of which must be paid attention in dysentery after stable situation is assessment and corrective to hydration status and electrolyte balance.


b. Diet


Child of with dysentery must be continued giving of its(the food. Gives high slack diet of calorie and protein to prevent malnutrition. High unit dose of vitellarium ( 200000 IU) can be given to reduce level of hard of dysentery, especially to estimable child experiences deficiencies. To take a short cut disease journey, can be given biotic and preparat zinc oral8,9. In drugs giving, must be paid attention that drugs slowing down gut motility shall not be given caused by risk to lengthen a period of pain.


c. Antibiotic


• Child of with dysentery must be suspected suffers shigellosis and gets therapy appropriate. Therapy with correct antibiotic will lessen a period of pain and reduces risk complicacy and death. • Main choice for Shigelosis ( according to fomentation WHO) : Kotrimokasazol ( trimetoprim 10mg/kbBB/hari and sulfametoksazol 50mg/kgBB/hari) divided into 2 dose, during 5 day. • From result of research, is not got difference of giving benefit of kotrimoksazol compared to placebo10. • Alternative which can be given : o Ampisilin 100mg/kgBB/hari divided into 4 dose o Cefixime 8mg/kgBB/hari divided into 2 dose o Ceftriaxone 50mg/kgBB/hari, unit dose IV or IM o Nalidixic acid 55mg/kgBB/hari divided into 4 dose. • Repair ought to seen in 2 day, for example temperature downwards, ill and blood in faeces decreases, frequency CHAPTER decreases, etc. If(when in 2 day is not happened repair, antibiotic must be stopped and changed with other alternative. • Therapy antiamubik is given with indication : o is Found [by] trophozoite Entamoeba hystolistica in microscopic inspection of faeces. o permanent bloody faeces after therapy with 2 antibiotic successively ( each given for 2 day), effective usual for dysentery basiler. • Therapy selected as antiamubik intestinal at child of is Metronidazol 30-50mg/kgBB/hari divided into 3 dose during 10 days. If(when dysentery of course is because of E.


hystolistica, situation will be good in 2-3 days therapy.

d. Sanitary landfill


? Advises to old fellow child of always cleans hand with cleanness as of pot is clean cleans faeces child of prevent autoinfection.