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TASHKENT MEDICAL ACADEMY Infectious and children infectious diseases department Theme: Early and Comparative diagnosis of diseases with the syndrome of diarrhea Lecturer: Definition Bacillary dysentery is a type of dysentery caused by Shigellosis. Bacillary dysentery is associated with species of bacteria from the Enterobacteriaceae family. The term is usually restricted to Shigella infections. Shigellosis is caused by one of several types of Shigella bacteria. Three species are associated with bacillary dysentery : Shigella sonnei, Shigella flexneri and Shigella dysenteriae. One study in China indicated that Shigella flexneri was the most common serotype. Salmonellosis caused by Salmonella enterica (serovar Typhimurium) has also been described as a cause of bacillary dysentery, though this definition is less common. It is sometimes listed as an explicit differential diagnosis of bacillary dysentery, as opposed to a cause. Bacillary dysentery should not be confused with diarrhea caused by a bacterial infection. One characteristic of bacillary dysentery is blood in stool which is the result of invasion of the mucosa by the pathogen. Synonyms • Shigella • Shigella infection • Salmonella infection Morphological Description of Biologic Agent • Shigella is a genus of gram-negative, non-spore forming rodshaped bacteria closely related to Escherichia Coli and Salmonella. The causative agent of human shigellosis, Shigella cause disease in primates, but not in other mammals. It is only naturally found in humans and apes. During infection, it typically causes dysentery. Mode of Transmission • Shigella infection is typically via ingestion (fecal–oral contamination); depending on age and condition of the host as few as ten bacterial cells can be enough to cause an infection. Signs and Symptoms • Most people who are infected with Shigella develop diarrhea, fever, and abdominal cramps. Severity of the disease ranges from mild to very severe diarrhea. Diarrhea is bloody 25-50 percent of the time and most often contains mucus. Rectal spasms are common. The illness starts 12 hours to 6 days, usually 1-2 days, after exposure. Dehydration is also a common symptom of Shigella infection. Nausea or vomiting may also be experienced. Muscle aches also occur. In some cases, white blood cell count is lower than normal at the onset. Diagnostics/Lab Tests • Your own observation of symptoms. • Medical history and physical exam by a doctor. • Laboratory stool culture. • Blood counts. Period of Communicability • Shigellosis is spread during the acute infection and until the infectious agent is no longer present in feces. This can last as long as four weeks. Asymptomatic carriers have the ability to transmit disease. The duration of carriage may be reduced with the use of antibiotics. Incubation Period • The incubation period may range from 12 to 96 hours (one to three days). Outcome of Disease • Most shigella infections are mild and don't require drastic treatment. However, in a severe attack, excessive dehydration can be fatal (especially in infants and young children) if treatment is unsuccessful. Treatment • Fluids and electrolyte replacement if excessive fluid loss through diarrhea or vomiting. • Agents are not recommended as they may prolong the course of disease. • Treatment is recommended for most symptomatic patients. Use of antibiotics will shorten the period of fecal excretion of the infecting strain and will shorten the clinical course of disease often to a few days. • Antibiotics - for adults and children, if the strain is susceptible, are ciprofloxacin or TMP/SMX or azithromycin. • Antibiotic resistance frequently develops after treatment. Control Measures • • • • • Good personal hygiene Toilet hygiene Wash soiled clothing and bed linen Handling food While you are suffering from diarrhea you should not go to work/school. • Sanitation of food utensils General Characteristics of Salmonella Coliform bacilli (enteric rods) Motile gram-negative facultative anaerobes Non-lactose fermenting Resistant to bile salts H2S producing Classification and Taxonomy of Salmonella (Confused) Old: Serotyping & biochemical assays used to name individual species within genus (e.g., Salmonella enteritidis, S. choleraesuis, S. typhi) Over 2400 O-serotypes (referred to as species) (Kauffman-White antigenic schema) Bioserotyping (e.g., S. typhimurium) DNA homology shows only two species Salmonella enterica (six subspecies) and S. bongori New: Most pathogens in S. enterica ssp. enterica Epidemiology of Salmonella Infection Annual Reported Incidence of Salmonella Infection (excluding typhoid fever) Clinical Syndromes of Salmonella Salmonellosis = Generic term for disease Clinical Syndromes Enteritis (acute gastroenteritis) Enteric fever (prototype is typhoid fever and less severe paratyphoid fever) Septicemia (particularly S. choleraesuis, S. typhi, and S. paratyphi) Asymptomatic carriage (gall bladder is the reservoir for Salmonella typhi) Epidemiology and Clinical Syndromes of Salmonella (cont.) Enteritis Most common form of salmonellosis with major foodborne outbreaks and sporadic disease High infectious dose (108 CFU) Poultry, eggs, etc. are sources of infection 6-48h incubation period Nausea, vomiting, nonbloody diarrhea, fever, cramps, myalgia and headache common S. enteritidis bioserotypes (e.g., S. typhimurium) Pathogenesis of Salmonella Enteritis (cont.) Virulence attributable to: Invasiveness Intracellular survival & multiplication Endotoxin Exotoxins: Effects in host have not been identified Several Salmonella serotypes produce enterotoxins similar to both the heat-labile (LT) and heat-stable enterotoxins (ST), but their effect has not been identified A distinct cytotoxin is also produced and may be involved in invasion and cell destruction Pathogenesis of Salmonella (cont.) Invasiveness in Enteritis (cont.) Penetrate mucus, adhere to and invade into epithelial layer (enterocytes) of terminal small intestine and further into subepithelial tissue Bacterial cells are internalized in endocytic vacuoles (intracellular) and the organisms multiply PMN’s confine infection to gastrointestinal (GI) tract, but organisms may spread hematogenously (through blood, i.e., septicemia) to other body sites Inflammatory response mediates release of prostaglandins, stimulating cAMP and active fluid secretion with loose diarrheal stools; epithelial destruction occurs during late stage of disease Clinical Progression of Salmonella Enteritis Lamina propria = thin membrane between epithelium & basement layer Hyperplasia = abnormal increase in # of normal cells Hypertrophy = abnormal increase in normal tissue/organ size Prostaglandins = potent mediators of diverse set of physiologic processes Epidemiology & Clinical Syndromes (cont.) Enteric Fevers S. typhi causes typhoid fever S. paratyphi A, B (S. schottmuelleri) and C (S. hirschfeldii) cause milder form of enteric fever Infectious dose = 106 CFU Fecal-oral route of transmission Person-to-person spread by chronic carrier Fecally-contaminated food or water 10-14 day incubation period Initially signs of sepsis/bacteremia with sustained fever (delirium) for > one week before abdominal pain and gastrointestinal symptoms Pathogenesis of Salmonella (cont.) Enteric Fevers (cont.) Virulence attributable to: Invasiveness Pass through intestinal epithelial cells in ileocecal region, infect the regional lymphatic system, invade the bloodstream, and infect other parts of the reticuloendothelial system Organisms are phagocytosed by macrophages and monocytes, but survive, multiply and are transported to the liver, spleen, and bone marrow where they continue to replicate Second week: organisms reenter bloodstream and cause prolonged bacteremia; biliary tree and other organs are infected; gradually increasing sustained fever likely from endotoxemia Second to third week: bacteria colonize gallbladder, reinfect intestinal tract with diarrheal symptoms and possible necrosis of the Peyer’s patches Clinical Progression of Enteric Fever (Typhoid fever) Lumen (intraluminal); ileocecal area = see above - Anatomy of Digestive Tract (RES) Liver, spleen, bone marrow (10-14 days) RES = sum total of strongly phagocytic Gastrointestinal cells; primarily found in lymph nodes, blood, Symptoms liver, spleen and bone marrow Hyperplastic changes = see hyperplasia above - Clinical Progression of Enteritis Microbial Defenses Against Host Immunological Clearance ENCAPSULATION and ANTIGENIC MIMICRY, MASKING or SHIFT CAPSULE, GLYCOCALYX or SLIME LAYER Polysachharide capsules Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, etc. Polypeptide capsule of Bacillus anthracis EVASION or INCAPACITATION of PHAGOCYTOSIS and/or IMMUNE CLEARANCE PHAGOCYTOSIS INHIBITORS: mechanisms enabling an invading microorganism to resist being engulfed, ingested, and or lysed by phagocytes/ phagolysosomes RESISTANCE to HUMORAL FACTORS RESISTANCE to CELLULAR FACTORS See Chpt. 19 Methods That Circumvent Phagocytic Killing , Salmonella typhi See Chpt. 19 Epidemiology & Clinical Syndromes (cont.) Septicemia Can be caused by all species, but more commonly associated with S. choleraesuis, S. paratyphi, S. typhi, and S. dublin Old, young and immunocompromised (e.g., AIDS patients) at increased risk Epidemiology & Clinical Syndromes (cont.) Asymptomatic Carriage Chronic carriage in 1-5% of cases following S. typhi or S. paratyphi infection Gall bladder usually the reservoir Chronic carriage with other Salmonella spp. occurs in <<1% of cases and does not play a role in human disease transmission Treatment, Prevention and Control of Salmonella Infections Enteritis: Antibiotics not recommended for enteritis because prolong duration Control by proper preparation of poultry & eggs Enteric fever: Antibiotics to avoid carrier state Identify & treat carriers of S. typhi & S. paratyphi Vaccination can reduce risk of disease for travellers in endemic areas Botulism • • • • • • • Organism History Epidemiology Transmission Disease in Humans Disease in Animals Prevention and Control Organism • Clostridium botulinum – Gram positive – Obligate anaerobic bacillus – Spores • Ubiquitous • Resistant to heat, light, drying and radiation • Specific conditions for germination – Anaerobic conditions – Warmth (10-50oC) – Mild alkalinity Neurotoxins • Seven different types: A through G – Different types affect different species – All cause flaccid paralysis – Only a few nanograms can cause illness – Binds neuromuscular junctions • Toxin: Destroyed by boiling • Spores: Higher temperatures to be inactivated Neurotoxins Neurotoxin A B Human X X Horses Cattle Sheep D E F X X X X X X Dogs X X Avian X X X X Mink & Ferret X X C X G History • 1793, Justinius Kerner – “Wurstgift” • “Botulus” = Latin for sausage • 1895, Emile von Ermengem – Isolated organism during Belgium outbreak • U.S. outbreaks led to improved industry processing Transmission • Ingestion – Organism – Spores – Neurotoxin • Wound contamination • Inhalation • Person-to-person not documented Epidemiology • In U.S., average 110 cases each year – Approximately 25% food-borne – Approximately 72% infant form – Remainder wound form • Case-fatality rate – 5-10% • Infective dose- few nanograms Epidemiology • 1977, Largest botulism outbreak – Michigan - 59 people – Poorly preserved jalapeno peppers • Alaska – 27% of U.S. foodborne botulism cases – 1950-2000 • 226 cases from 114 outbreaks Human Disease • Three forms – Foodborne – Wound – Infant • All forms fatal and a medical emergency • Incubation period: 12-36 hours Foodborne Botulism • Preformed toxin ingested from contaminated food • Most common from home-canned foods – Asparagus, green beans, beets, corn, baked potatoes, garlic, chile peppers, tomatoes; type A – Improperly fermented fish (Alaska); type E Infant Botulism • Most common form in U.S. • Spore ingestion – Germinate then toxin released and colonize large intestine • Infants < 1 year old – 94% < 6 months old • Spores from varied sources – Honey, food, dust, corn syrup Wound Botulism • Organism enters wound – Develops under anaerobic conditions – From ground-in dirt or gravel – It does not penetrate intact skin – Associated with addicts of black-tar heroin Adult Clinical Signs • • • • Nausea, vomiting, diarrhea Double vision Difficulty speaking or swallowing Descending weakness or paralysis – Shoulders to arms to thighs to calves • Symmetrical flaccid paralysis • Respiratory muscle paralysis Infant Clinical Signs • • • • • • Constipation Lethargy Poor feeding Weak cry Bulbar palsies Failure to thrive Diagnosis • Clinical signs • Toxin in serum, stool, gastric aspirate, suspected food • Culture of stool or gastric aspirate – Takes 5-7 days • Electromyography also diagnostic • Mouse neutralization test – Results in 48 hours Treatment • Intensive care immediately – Ventilator for respiratory failure • Botulinum antitoxin – Derived from equine source – CDC distributes – Used on a case-by-case basis • Botulism immune globulin – Infant cases of types A and G