(7) Etiological structure and epidemiology of the

pg ­ 1 Report on Etiological structure and epidemiology of the acute intestinal infections. Pathogenesis of dearrhoeas caused by infectious agents. ­ Acute intestinal infections can be due to bacteria, virus, parasitic, toxic or nonspecific/uncertain in etiology.

Factors influencing the growth of bacteria ­ (a) Bacterial features ­1) Size of Inoculum ­ Eg (1) Salmonella 105 (2) V.cholorea, E­coli 108 (3) Shigella 10 ­100 bacteria (4) Giadria, Entamoeba 10­100 cysts 2) Intestinal adherence factors ­ Eg, V.cholerae ­ Toxin co­regulated Pilus (TOP) ETEC ­ colonization factor antigen (CFA) EPEC ­ virulance determinants EHEC ­ Fimbriae 3) Toxin production – (a) Enterotoxins ­ produces secretory watery dearrhoea Eg, I V.cholerae toxin composed of A&B subunit. B subunit binds to enterocyte ­ to ganglioside GMI receptors& thus a subunit which enters the enterocyteactivates adenyl cyclase increase cAMP increase Cl secretion & decrease Na+ absorption from intestinal mucosaeFluid accumilation into lumen diarrhoea. 2. ETEC(LT) – simillar to cholera toxins.(via activation of adenyl cyclase) 3. ETEC(ST) – activates guanyl cyclase cGMPincrease cl excretion , decrease Na + absorptionfluid accumilationwatery diarrhoea (b) Bacterial cytotoxins ­ destroys intestinal mucose & produces bloody stools containing inflammatory cells Eg, ­ shigella, c.difficile, v.parahaemoliticus. (c) Neurotoxins ­ Eg, ­ S.aureus, B.aureus acts on CNS to produce vomiting.

4) Invasion Eg – 1. Shigella, ETECenter enterocytes ­­>multiplicationspread to adjacent cells. 2.

S.typhi, Y.enerocolitica ­ penetrate mucosamultiple in peyers patches & LN & disseminate through blood. (b) Host factors – (1) Normal intestinal microflora ­ Normal intestial microflora acts as antagonists to pathogenic microflora. 99% of normal microflora is anaerobic and produce an acidic media which is antagonists to pathogenic microorganism. Infants who are not yet developed normal. colonization of intestines and pt receiving antibiotics are at higher risk of developing infections.

Normal flora ­ anaerobes – 1. Bactereoides species Bactereoides fragilis, fusobacterium ,2.

Lactobacilus Species ­ Bifidobacterium 3 Clostridium Species ­ C.perfringens, 4. Peptostreptococcus Facultative aerobes (1) cocci (2) Pseudomonas, proteus, klebsiella Aerobes (1) E.coli (2) Gastric acidity ­ high gastric acidity is antagonists to pathogenic colonization pt having gastrectomy or receiving H2 antagonists are prone to intestinal infections.

(3) Intestinal motility ­ Peristalsis is the major mechanism of clearing bacteria from upper small intestines. If this is lost bacterial overgrouth leading to infections occurs.

Eg ­ 1) Opiate treatment 2) Anatomic abnormalities ­ fistulas, deverticulas, afferent loop stasis after surgery. 3) Hypomatility states ­ D.M, sclerodema.

(4) Immunity­ Viruses (Adeno,Rota) causes acute intestinal infections by infecting the enterocytes within the villous epithelium of small intestines. Destruction or cells in this layer causes transudation of fluids & salts into the intestinal lumen. Malabsorption of carbohydratesosmotic dearrhoea.

Diarrhoea Increase in stool weight > 300g/24hrs . Pt may describe as increase in liquidity/loose stools & frequency.)

Classification ­ (A) Acute ­ < 2weeks in duration (B) Chronic ­ > 2weeks in duration, may have history of same condition, may have a relapsing & remitting course.

(A) Acute diarrhoea – causes a) Infections Mechanism Location Inness Stool findings Eg/

1)Noninflamma tory (enterotoxins) 2)Inflammatory (Invasive / destructive/cyto toxic) 3) Penetrating

Proximal Watery small bowel dearrhoea

Nofecal leukocytes

­V.cholerae –ETEC ­C.perfringes ­B.cereus ­ Staph.aureus ­Rota virus ­Giardia lamblia

Colon

FecalPMN leukocytes

­Shigella ­Salmonella enteritis ­C.jejuni ­V.parahaemolyticus ­ETEC –EHEC ­Entamoeba histolytica

dysentery

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distalsmall Enteric fever Faecal S:typhi bowel mononuclear Y.enterocolitica monocytes b) Drugs ­ 1) GIT ­ Mg containing antacids, laxatives, misoprostol 2) Cardiac ­ Digitalis, Quinidine, diuretics 3) Hypolipidemic ­ Clofibrates, Geinfibrozil, levostatin 4) Antibiotics ­ Clindamycin, ampicillin, cephalosporin, erythromycin 5) Psychiatric ­ Lithium, valproic acid 6) Others ­ theophylline, Thyroid drugs c) Dietary indiscretion d) Male homosexual e) Prostitutes f) Toxic stuff – FoodMushrooms, shellfish chemicals Organi Poisons,arsenic g) Food poisoning (1) mainly caused by B.cereus (emetic) & Staph.aureus (1­6 hrs IP) (2) C.perfringers, B.cereus (dearrheal) (IP 8­16 hrs) ( B) Chronic diarrhoea ­ causes a) Inflammatory bowel disease b) Parasitic / fungal infections c) Malabsorption d) Gut resection e) Colonic neoplasia f) Endocrine ­ (1) Pancreatic tumours, Gastrinoma(2) Medullary carcinoma of the thyroid.

(3) Thyrotoxicosis(4) Diabetic neuropathy g) Faecal impaction ­ elderly Mechanism of dearrhoea Mechanism Clinical features Example 1) Inflammatory ­Fever, Abdominal pain, ­Dysentery due to shigella ­Salmonella ­ ­Damage to intestinal mucosal ­Blood &/or ­WBC in faeces UC, crohns ­Radiation colitis cells. Thus defective absorption of ­ ESR ­ CRP ­Eosinophilic gastroenteritis fluid & electrolytes 2) Osmotic ­Gut mucosa acts as semipermeable membrane and fluid enters the bowel if there are large quantaties of non absorbed or non digested hypertonic substances

­Improvement of dearrhoea with fasting ­Bulky, greasy, foul smelling stools ­ weight loss

3) Secretory ­watery diarrhoea ­Active intestinal secretion of fluid ­Continues during fasting and electrolytes as well as decrease ­Dehydration may occur absorption. This stools volumes may be very high . Food does not affect the deahoea so will continue during fasting

4) Abnormal motility ­Volume & weight of stools (usually not true dearrhoea) Due to is not that high

­Pancreatic insufficiency ­Celiac disease ­Lactase insufficiency ­Whipples disease ­Bacterialovergrowth (most of these causes leads to malabsorption so that high concentrations of solute remain in the gut) ­Enterotoxins ­ Eg, cholera, ­ETEC (LT/ST) ­Hormones ­ Eg, VIP ­Secretion in non Bcell pancreatic tumor ­Bile salts (in the colon) following ileal resection ­Fatty acids (in the colon) following ileal resection ­Staphylococcus aureus B.cereus ­Diabetic dearrhoea ­Postvagotomy diarrhoea

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abnormal motility in the upper gut 5) Self induced / Purgative abuse most in chronic dearrhoea

­Frequency ­Hyperthyroid dearrhoea ­Altering dearrhoea & ­Irritable bowel syndrome & constipation may occur ­Neurological diseases ­High volume (>1l/d) ­Low serum potassium (Sigmoidoscopy  mela nosis coli/pigmented mucosa.

Barium enema  loss of haustral pattern. Absorption test abnormalities)

Report on Etiological structure and epidemiology of the acute intestinal infections. Pathogenesis of diarrohea caused by infectious agents.

Report prepared by 1. Dr. Sajid Mahmood, MD (EU), Accident & Emergency Department, NHS Royal infirmary Liverpool United Kingdom.

2. Dr. Adnan Akram, MD (EU), Department of Infectious Diseases. University Hospital Riga Latvia.

3. Dr. Aftab Ahmed, MD (EU), Infection Control Department, Kaunas Medical University Clinic. Kaunas. Lithuania.

Contact: publications [at] infekcijas.eu 12.02.2008