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INTESTINAL INFECTIONS. MUDr. RNDr. František Stejskal , Ph.D. November 19, 2007 Department of T ropic al M edic ine 1 st F a c ult y of Medicine Charles U niversity and Hospital Bulovka Studničkova 7, 128 00 Praha 2. DIARRHEA - DEFINITION. DIARRHEA
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INTESTINAL INFECTIONS MUDr. RNDr. František Stejskal, Ph.D. November 19, 2007 Department ofTropicalMedicine 1stFaculty of Medicine Charles University and Hospital Bulovka Studničkova 7, 128 00 Praha 2
DIARRHEA - DEFINITION • DIARRHEA • Increase in fluidity, volume or frequency of bowel movement • Normal bowel habit varies greatly from person to person • Above 12 mo age, more than 3 loose stools per day are abnormal • ACUTE DIARRHEA • Subside spontaneously within a few days • PERSISTENT AND CHRONIC DIARRHEA • Persist for more than 2 – 3 weeks
INFECTIVE DIARRHEA VIRUSES • Rotaviruses • Norwalk virus (Noroviruses) • Caliciviruses • Astroviruses • Enteric adenoviruses
INFECTIVE DIARRHEA - BACTERIA • Enterotoxicoses (preformed toxin) • Bacillus cereus • Staphylococcus aureus • Clostridium perfringens C • Cholera and other Vibria • Enterotoxigenic E. coli (ETEC) • Salmonellosis • Campylobacter jejuni • Yersinia enterocolitica • Shigellosis • Enteroinvasive (EIEC) and enteroadherent E. coli • Aeromonas hydrophila • Plesiomonas shigelloides
INFECTIVE DIARRHEA - PARASITES • Protozoa • Giardiasis • Amebiasis • Cryptosporidium • Cyclospora • Isospora • Helminths • Ascariasis • Trichuriasis • Ancylostomosis • Strongyloidosis • Taeniasis
PATHOGENESIS OF INFECTIVE DIARRHEA • Toxin production • Staphylococcus pyogenes, St. aureus (preformed toxin) • Vibrio cholerae, ETEC toxin (↑cAMP – inhibition of Na+ absorption) • Enterocytes adhesion and colonisation • E.coli • Giardia intestinalis • Destruction of intestinal mucous membrane at the bacterial or parasite attachment place • Enteropathogenic E. coli, viruses • Cryptosporidium • Mucous membrane and submucose invasion • Salmonella, Campylobacter jejuni, Yersinia enterocolitica • Isospora, Cyclospora • Colonic wall invasion and ulcers formation • Shigella, enteroinvasive E.coli (EIEC) • Entamoeba histolytica
PATHOGENESIS OF DIARRHEA II • Host defense mechanism: • Increased risc: • - Treatment with anacides, proton pump inhibitors, H2 inhibitors • - Immunity defects – IgA deficiency • Infective dose: • Low (less than 103 bacteria cells) • - shigellosis, Campylobacter (contagious infections) • High (more than 103 bacteria cells) • - salmonellosis
SOURCE OF INFECTION EPIDEMIOLOGY • Contaminated water • Undercoched or roh meat, fish or seafood • Fruits and vegetabele • Milk products
ACUTE DIARRHEA – DIFFERENTIAL DIAGNOSIS • With fever and with blood • Shigellosis, Campylobacter, EIEC, Cl. perfringens C – enteritis necroticans, (salmonellosis - 50%, typhoid) • With fever and without blood • Rotaviruses, Norwalk, salmonellosis (50 %); any localized infection at small children (otitis, tonsillitis, pneumonia), malaria • Without fever and with blood • Amoebiasis, intestinal schistosomiasis, balantidiosis, trichuriasis • Without fever and without blood • cholera, ETEC, enterotoxicosis (stafylococcal, B. cereus), cryptosporidiosis, isosporiasis, cyclosporiasis
CHRONIC DIARRHEA • With fever • Intestinal tuberculosis, visceral leishmaniasis, yersiniosis, HIV infection, CMV • Without fever and with blood • Amoebiasis, intestinal schistosomiasis, balantidiosis, trichuriasis, Crohn disease, idiopatic proctocolitis • Without fever and without blood • Giardiasis, tropical sprue, coeliacal sprue, lactase deficiency, strongyloidosis, cryptosporidiosis, Whipple disease, intestinal malignant lymphoma, mucoviscidosis
INVESTIGATION IN DIARRHEA • Fecal smear: fecal leucocytes • Stool culture • Parasitic stool investigation (persistantdiarrhea, for more than 2-3 weeks)
DIRECT FAECAL SMEAR • Place a drop of sterile saline on the left hand site of the slide; place a drop of iodine on the right hand site of the slide and add a small portion of stool to each drop and mix to form suspension • Cover with a coverslip and examine with the x10 objective first Mr. Brown X 10/12/04
FECAL LEUCOCYTES • Mucus (pus) from stool is stained with 2 drops of Lőffler’s methylen blue
DIRECT FAECAL SMEAR - RESULTS • Cysts (Giardia, amoebas, etc.) • Trophozoites (amoebas, Giardia, trichomonads, other flagellates, etc) • Oocysts (Isospora, Cyclospora) of parasitic protists • Blastocystis hominis • Yeasts (Candida, Saccharomyces) • Ova of parasitic helmints • Vibrio cholerae Negative in cryptosporidiosis, special staining
STOOL CULTURE • Routine: Salmonella sp., Shigella, Citrobacter, Proteus sp., Morganella sp. and other enterobacteria • Special: Campylobacter, Vibrio cholerae, Yersinia enterocolitica • Yeasts • Virus isolation (enteroviruses) • Parasites – special culture media: • Amoebas, trichomonads, other flagellates
ORAL REHYDRATATION SOLUTION • NaCl 3,5 g • KCl 1,5 g • Na-bicarbonate 2,5 gor Na-citrate 2,9 g • glucose 20 g or saccharose 40 g • in 1 L of boiled water • Add 1 tsp of salt and 2-3 tsp of sugar or honey and 1 lemon to 1 liter of water.
ORS WITH REDUCED OSMOLARITY • ORS solution does not reduce stool output or duration of diarrhoea • This solution, which is slightly hyperosmolar when compared with plasma, may cause hypernatraemia or an osmotically driven increase in stool output, especially in infants and young children • For this reason paediatricians in some developed countries recommended the ORS with reduced osmalarity containing about 60 mEq/l sodium and having a total osmolarity of 250 mOsm/l
ORS WITH REDUCED OSMOLARITY • Na+: 60-75 mEq/l (original ORS 90 mEq/l) • Glucose: 75-90 mmol/l • Total osmolarity: 215 - 260 mOsm/l (original ORS 311 mOsm/l)
USE OF ANTIMICROBIAL DRUGS • Bloody diarrhea with fever (dysentery) which does not improve after 2-3 days or rehydratation • Cholera with severe dehydratation • Bacterial diarrhea at immunocompromised patients • Diarrhea with high fever in small children • Parasitic diarrhea
CHOLERA PANDEMIC Seventh pandemic of cholera, 1961-1971 (CDC)
CHOLERA • Humans are the only known natural host • Large infective dose – contaminated food or water • Incubation period: a few hours to 5 days • Severe watery diarrhea (up to 30 L per day), painless, without fever • Electrolyte imbalances, metabolic acidosis, prostration, dehydration • Management: ORS, doxycyclin 300 mg in single dose in the severe cases
DIAGNOSIS OF CHOLERA • In epidemics based on clinical grounds alone • In non-epidemic periods, acute watery diarrhea resulting in severe dehydration: • Dark-field microscopy of faecal material • Transportation of samples in alkaline peptone water and kept cool • Culture in selective media such as TCBS agar • Bio- and serotyping in the reference laboratory • Notify the infection!
EPIDEMIOLOGY OF SHIGELLOSIS • Shigella is causing 80 mil. of symptomatic infections and 700 000 deaths each year • 99% of infections are in developing countries • 70% of cases and 60% of deaths at children under 5 years • The recent epidemics: • 1969 – 73: Central America – 0,5 mil. of cases, 20 000 of deaths • 1993 – 95: countries of central and south Africa • 1994: Rwandian refugies to DR of Congo (20 000 of deaths during the first month) • 1999 – 03: Sierra Leone, Liberien, Guinea, Senagal, … • 2000: India a Banglades – resistance to FQ
EPIDEMIOLOGY OF SHIGELLOSIS • S. sonnei and S. boydiiare causind ussually mild disease with watery or bloody diarrhea, they are more common in developed countries of temperate climate • S. flexneriis the main cause of endemic shigellosis in developing countries • S. dysenteriae typ 1 (Sd1, Shiga bacillus) is causing the most serious disease, it is causing epidemies in developing countries
Shigella dysenteriae serotype 1 • It deffer from other species: • It produces a potent cytotoxin (Shiga toxin) • It is causing more severe, long-lasting, potentially deadly diarrhea • The resistance to antibiotics is more common • It may cause large, often regional epidemics: • „high attack rates“ • „high case fatality rates“
DYSENTERY SYNDROME • Diarrhea with blood and pus • Abdominal pain and cramps • Tenesms
DIFFERENTIAL DIAGNOSTICS • Entamoeba histolytica • Campylobacter jejuni • Entheroinvasive E. coli • Enthero-hemorrhagic E. coli • Salmonella sp. • Intentestinal schistosomosis (Schistosoma mansoni, S. japonicum)