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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 - PowerPoint PPT Presentation
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INTESTINAL INFECTIONS
MUDr. RNDr. František Stejskal, Ph.D.
November 19, 2007
Department of Tropical Medicine1st Faculty of Medicine
Charles Universityand 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
TERMINOLOGY OF DIARRHEAL DISEASESTerminology Symptoms/signs Example/etiology
Gastritis Vomiting, nausea, no fever Food poisoning, preformed toxins (Staphylococcus aureus, Bacillus cereus)
Gastroenteritis Vomiting, nausea, diarrhea usually watery without blood, abdominal pain/cramps, fever may be present
Food poisoning, preformed toxins
CholeraSalmonellosis, giardiasis
Enteritis No vomiting Salmonellosis, giardiasis, cryptosporidiosis
Enterocolitis No vomiting, diarrhea often with blood, abdominal pain/cramps
Campylobacter, Yersinia enterocolitica
Colitis - ulcerative
- pseudomembranose
Diarrhea with blood and pus, abdominal cramps, tenesm, fever may be present
Bacillary, amoebic dysentery
Intestinal schistosomiasisUlcerative colitis
Bloody diarrhea, abdominal cramps, usually without fever
Clostridium perfringens C (pigbel), Cl. difficile
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
• Protozoa– Giardiasis– Amebiasis– Cryptosporidium– Cyclospora– Isospora
• Helminths– Ascariasis– Trichuriasis– Ancylostomosis– Strongyloidosis– Taeniasis
INFECTIVE DIARRHEA - PARASITES
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
• 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
PATHOGENESIS OF DIARRHEA II
SOURCE OF INFECTION EPIDEMIOLOGY
• Contaminated water
• Undercoched or roh meat, fish or seafood
• Fruits and vegetabele
• Milk products
• 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
ACUTE DIARRHEA – DIFFERENTIAL DIAGNOSIS
• 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
CHRONIC DIARRHEA
INVESTIGATION IN DIARRHEA
• Fecal smear: fecal leucocytes
• Stool culture
• Parasitic stool investigation (persistant diarrhea, 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
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FECAL LEUCOCYTES• Mucus (pus) from stool is stained with 2 drops of Lőffler’s methylen blue
Infection/disease White blood cells (WBC)
Viral gastroenteritis NO
Cholera, ETEC, enterotoxicosis NO
Giardia, Cryptosporidium NO
Salmonella typhi Monocytes
Salmonellosis (S. enteritidis) PMN
Shigellosis, EIEC PMN
Campylobacter, Yersinia enterocolitica
PMN
Entamoeba histolytica, Balantidium coli
PMN
Ulcerative colitis, Crohn disease PMN
• 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 choleraeNegative in cryptosporidiosis, special staining
DIRECT FAECAL SMEAR - RESULTS
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
THERAPY OF DIARRHEA
ORAL REHYDRATATION SOLUTION
• NaCl 3,5 g• KCl 1,5 g• Na-bicarbonate 2,5 g or 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
COMPARISON OF ORS and Valík solution
Original ORS g/L
Valík solution g/L
NaCl 3,5 2,36
KCl 1,5 1,12
Na-bicarbonate 2,5 1,68
Glucose 20 27,0
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
Seventh pandemic of cholera, 1961-1971 (CDC)
CHOLERA PANDEMIC
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!
CHOLERA PANDEMIC IN SOUTH AMERICA
CHOLERA OUTBREAK IN 2005
Shigella – species and serogroups
SPECIES SEROGROUP SEROTYPE
S. dysenteriae A 1 – 15
S. flexneri B 1 – 6 (15 subtypes)
S. boydii C 1 - 18
S. sonnei D 1
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. boydii are causind ussually mild disease with watery or bloody diarrhea, they are more common in developed countries of temperate climate
• S. flexneri is 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)