Bacterial Gastrointestinal Infection 2-Year Medical Students Prof.Dr. Asem Shehabi Faculty of Medicine University of Jordan.

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Bacterial Gastrointestinal Infection 2-Year Medical Students Prof.Dr. Asem Shehabi Faculty of Medicine University of Jordan

Introduction  Worldwide, At least one billion of children & adults are affected by diarrhea each year. In developing countries, where general sanitation is low, epidemics of bacterial gastroenteritis cause high morbidity  The commonest clinical manifestations of bacterial gastrointestinal infections are diarrhea, vomiting, abdominal pain, fever.. Few percentage mortality.  Bacterial intestinal infection..followed water/Food contamination.. incubation period 8-24 hrs.. rarely involve other organs and systems.. Recovery h  Watery diarrhea..involved small and large intestines  Bloody-diarrhea (Dysentery ) mostly Large intestine  Enterocolitis inflammation of mucosa of both small & large intestines.. due to bacterial cytotoxin

Bacteria Food poisoning  Bacterial food poisoning..Food intoxication.. is another common cause GI illness associated with the presence of a pre-formed toxin in food by toxigenic bacteria.. Mostly associated first with vomiting & later diarhea.. No fever.. Short incubation period..2-8 hours  In many cases the toxin may be produced in the food by bacteria during storage or preparation, hand or environmental contamination.  Common Gram-ve :Salmonella spp., Various types diarrheagenic E. coli, Campylobacter spp., V. cholerae.. Listeria & Aeromonas  Gram-positive : Cl. perfingens, Cl.difficile, Staphylococcus aureus, Bacillus cereus

Salmonella Group  Salmonellae: Gram-negative bacilli, Facultative anaerobes.. By current classification there is only one major species of Salmonella: S. enterica.. but there are numerous serovars.. about  A serovar is classified by presence of a specific set of O (cell wall),H (flagellar), Vi (Virulence) antigens.  Human Salmonellosis is divided into: 1) Enteric Fever Salmonellas.. Typhoid Fever.. 1) Enteric Fever Salmonellas.. Typhoid Fever.. 2) Gastroenteritis/Food-poisoning Salmonellosis. 2) Gastroenteritis/Food-poisoning Salmonellosis.  Typhoid Salmonella infect only humans.. Gastroenteritis Salmonellas infect both humans & Animals..Birds.. Widely distributed in nature

Salmonella-Typhoid Fever -1  S. enterica subtypeTyphi & Paratyhi A, B, C cause severe human systemic diseases, including enteric fever/ Typhoid fever..blood sepsis..may be associated with bloody enterocolitis, meningitis, pneumonia, endocarditis, osteomyelitis, septic arthritis, hepatic abscesses, soft tissue abscesses in any body part.  Typhoidal Salmonella develop following invading GI S.typhi with few cells..often by contaminated water..Less Food.. Less direct contact.. highly virulence factors.. Proteinous capsule (Vi antigen), Cell wall Lipopolysaccharides, cytotoxin.. Incubation period 1-3 weeks.. Over disease or recovery. S.typhi with few cells..often by contaminated water..Less Food.. Less direct contact.. highly virulence factors.. Proteinous capsule (Vi antigen), Cell wall Lipopolysaccharides, cytotoxin.. Incubation period 1-3 weeks.. Over disease or recovery.

Typhoid fever-2  Typhoid fever is a severe multisystemic illness.. invasion and multiplication within intestinal mucosa.. Peyer patches.. Enter intestinal lymphoid follicles.. Macrophages carry cells to Reticulo-endothelial system..Causing Lymphoid hyperplasia & hypertrophy.. Spread to Blood and other internal organs..  Typhoid Fever is characterized by the prolonged & high fever, headache, Malaise, Liver-Spleen enlargement..Skin rash (Rose spots)..Mostly watery- bloody diarrhoea /constipation at the beginning.  Host responded by production of specific antibodies (Anti-O & anti-H) which can be detected after 2 weeks. (Anti-O & anti-H) which can be detected after 2 weeks.

Typhoid fever-3  Necrosis of liver, spleen, gallbladder. lymph tissues, Peyer patches.. Salmonella re-enter intestinal tract.. causing severe mucosa inflammatory.. More Bloody diarrhea.. intestinal perforation & toxic shook % ended with death.. without antibiotic treatment.  Up to 5% of infected persons become healthy carriers later..Females more than Males..Infection becomes chronic.. Carry the bacteria in their Gallbladder.. Less in Peyer patches.. execrate bacteria in their feces long live.  Healthy carriers maintain the cycle of Typhoid disease in the community.

Lab Diagnosis  Definitive diagnosis Typhoid Fever: Requires culture & isolation of the organism from blood, Feces, CSF, Urine Acute- sub-acute cases.  Chronic cases.. bone marrow, Gallbladder.. Healthy Carriers.. execrate bacteria in stool.  Presence bacteria only in stool without clinical disease indicates often carriage state.  Selective culture media: S-S agar, Heckton-enteric agar… Lactose-non-fermenter bacteria growth  Serological test: Widal test is used for the diagnosis of Typhoid fever.. measures levels of antibodies against (O, H ) antigens.. Titer > 160 or rising titers.. positive (Vi ) antigen indicate S. typhi.. acute infection.

Treatment & Prevention  Antibiotic therapy is essential and should begin empirically if clinical evidence is strong.. Ciprofloxacin 4 weeks.. Ceftriaxone for pregnant women & Children.. Chloramphenicol & Amoxacillin/Ampicillin is not more used.  Fatality is high without antibiotic treatment  In endemic countries.. Most developing countries.. public health measures to ensure safe drinking water, proper sewage disposal.. Detection of human carries.. Education programs on food hygiene  Vi antigen is used in preparation of oral & injectable vaccine.. short protection..endemic region..Used in Endemic area.

Gastroenteritis/ Food-Poisoning Salmonellas-2  S. enterica var Typhimurium and S. enterica var Enteritidis.. are most common serotypes of GI Salmonellosis in humans, chicken, Rats.. Million of cases each year. Worldwide  Contaminate commonly human fresh food.  After Salmonella ingestion.. invade epithelial cells of small intestine.. multiply in lymphoid follicles.. cause inflammatory response.. Mediates release of prostaglandines.. stimulates cAMP.. Fluid secretion.. inhibition Na-absorption. Incubation 8-24 hrs, Watery- bloody diarrhea, abdominal pain, fever.. Less vomiting.. Rare complications: septicemia, meningitis developed in neonates, infant, immune- suppression.

GastroenteritisSalmonellas-2  No antimicrobial drugs treatment.. For normal healthy persons.. Only Rehydration.. Antimicrobial drugs used for very young infants & immuno- suppressed patients.  Rarely human healthy carriers in intestine.. Clinical cases execrate salmonella for few days-weeks..  No human vaccine available.  Prevention hand-food contamination.. often Chicken eggs & meat /Grounded meat.. Dairy Products.  Stool culture.. S-S agar, Heckton-enteric agar  Widal test is not significant in diagnosis of infection.

Shigellosis-1  Shigella spp continue to be a major health problem worldwide, causing an estimated 1 million deaths and about 150 million cases of diarrhea annually. Shigella are Gram-negative, Lactose-ve bacilli.. Facultative Anaerobes.. Highly susceptible to dryness.. Acidity.. killed within 1 hour in stool. There are 4 species of Shigella: S. dysenteriae, S. sonnei, S.boydii, S. flexneri  Clinical disease ranges from mild diarrhea to dysentery.. Most deaths occur in Jung children or elderly persons due to dehydration.. Infection Limited to human..Incub period within 24 hours.. highly communicable..Person to person contact.. contaminated Water, fresh green leaf vegetables.

Shigellosis-2  Shigellae invade, multiply in mucosa of large intestine.. necrosis.. Fluid secretion.. Due to cytotoxin & endotoxin.. Bloody diarrhea with few-numerous WBCs & mucus, severe abdominal cramps  Dysenteriae is the classic cause of bacillary dysentery.. severe mucopurulent bloody diarrhoea with severe abdominal pain & fever..more severe bloody diarrhea & dehydration & Death if not treated.. septicemia is rare..  S. dysenteriae produces heat-labile Shiga enterotoxin (neurotoxin).. Toxin affects small intestine.. Carried to blood.. CNS.. Causes mild-severe Meningism & Comma.. Few cases hemolytic-uremic syndrome.

Diagnosis & treatment  Acute case.. Direct stool examination for presence of numerous WBCs and blood cells  Direct rectal swab.. or rapid stool culture of feces on S-S agar, Heckton-enteric agar.. Shigella Isolation & conformation by biochemical tests and serotyping.  Antibiotics is recommended.. ciprofloxacin, doxycycline, cotrimoxazole.. Shorten the diarrhea duration.... Rehydration is important but not enough..  Most person develop non-protective specific antibodies.. No healthy carrier stage..Prevention concentrate on hygiene control of water, milk, fresh food..Vaccine used in wars and endemic area.