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    Gitmicro Gitmicro Presentation Transcript

    • 25
      Microbial Diseases of the Digestive System
    • Introduction 
      Diseases of the digestive system are the second most common illnesses in the United States.
    • Microbial Diseases of the Digestive System
      Transmitted in food and water
      Fecal-oral cycle can be broken by
      Proper sewage disposal
      Disinfection of drinking water
      Proper food preparation and storage
    • The Digestive System
      Figure 25.1
    • Structure and Function of the Digestive System
       The gastrointestinal (GI) tract, or alimentary canal, consists of the mouth, pharynx, esophagus, stomach, small intestine, and large intestine.
      In the GI tract, with mechanical and chemical help from the accessory structures, large food molecules are broken down into smaller molecules that can be transported by blood or lymph to cells.
      Feces, the solids resulting from digestion, are eliminated through the anus.
    • Normal Microbiota
      >700 species in mouth
      Large numbers in large intestine, including
      Bacteroides
      E. coli
      Enterobacter
      Klebsiella
      Lactobacillus
      Proteus
    • Normal Microbiota of the Digestive System
      Large numbers of bacteria colonize the mouth.
      The stomach and small intestine have few resident microorganisms.
      Bacteria in the large intestine assist in degrading food and synthesizing vitamins.
      Up to 40% of fecal mass is microbial cells.
    • protective
      Waldeyer’s ring
      Mucus lining and high acid (stomach)
      Paneth cells (small intestine)
      Phagocyte
      Release defensin and lysozymes
      Normal miocrobiota (large intestine)
    • Dental Caries
      Figure 25.3
    • Dental Caries (Tooth Decay)
       Dental caries begin when tooth enamel and dentin are eroded and the pulp is exposed to bacterial infection.
      Streptococcus mutans-uses sucrose to form dextran from glucose and lactic acid from fructose.
      Bacteria adhere to teeth and produce sticky dextran, forming dental plaque.
      Acid produced during carbohydrate fermentation destroys tooth enamel at the site of the plaque.
    • Dental Caries (Tooth Decay)
       Gram-positive rods and filamentous bacteria ( Actinomycosis ) can penetrate into dentin and pulp.
      Carbohydrates such as starch, mannitol, sorbitol, and xylitol are not used by cariogenic bacteria to produce dextran and do not promote tooth decay.
      Caries are prevented by restricting the ingestion of sucrose and by the physical removal of plaque.
    • Dental Caries (Tooth Decay)
       lactic acid
      Saliva(lysozyme)
      Crevicular fluid
    • Tooth Decay
      Figure 25.4
    • Periodontal Disease
       Caries of the cementum and gingivitis are caused by streptococci, actinomycetes, and anaerobic gram-negative bacteria.
      Chronic gum disease (periodontitis) can cause bone destruction and tooth loss; periodontitis is due to an inflammatory response to a variety of bacteria growing on the gums.
      Acute necrotizing ulcerative gingivitis is often caused by Prevotellaintermedia.
    • Periodontal Disease
      Figure 25.5
    • Bacterial Diseases of the Lower Digestive System
       A gastrointestinal infection is caused by the growth of a pathogen in the intestines.
      Incubation times range from 12 hours to 2 weeks. Symptoms of infection generally include a fever.
    • Bacterial Diseases of the Lower Digestive System
      A bacterial intoxication results from the ingestion of preformed bacterial toxins.
      Symptoms appear 1–48 hours after ingestion of the toxin. Fever is not usually a symptom of intoxication.
      Infections and intoxications cause diarrhea, dysentery, or gastroenteritis.
      These conditions are usually treated with fluid and electrolyte replacement.
    • Staphylococcal Food Poisoning
      Staphylococcus aureusenterotoxin is a superantigen.
      Figure 25.6
    • Staphylococcal Food Poisoning (Staphylococcal Enterotoxicosis)
      ingestion of an enterotoxin (improperly stored foods)
      bacteria grow and produce enterotoxin (room temperature)
      Heat stable, 30 minutes of boiling
      Temperature abuse
      Foods with high osmotic pressure and those not cooked immediately before consumption (most common often source)
    • Staphylococcal Food Poisoning (Staphylococcal Enterotoxicosis)
      Higher osmotic pressure/ low moisture food (cream pies, custard and hams).
      Refrigeration is important (prevention)
    • Staphylococcal Food Poisoning (Staphylococcal Enterotoxicosis)
      1million bacteria/gram of food
      Diagnosis is based on symptoms. Nausea, vomiting, and diarrhea begin 1–6 hours after eating and last about 24 hours.
      Laboratory identification of S. aureus isolated from foods is used to trace the source of contamination.
      Serological tests are available to detect toxins in foods.
    • Shigellosis
      Shigellaspp. Gram negative facultative bacilli producing Shiga toxin
      Shiga toxin causes inflammation and bleeding.
      Families, daycare facilities
      Figures 25.7, 25.8
    • Shigellosis (Bacillary Dysentery)
       Shigellosis is caused by any of four species of Shigella.
      Shigellasonnei- most cpommon in US, mild dysentery, traveller’s diarrhea
      Symptoms severe dysentery and prostation
      blood and mucus in stools, abdominal cramps, and fever. Infections by S. dysenteriae result in ulceration of the intestinal mucosa. With “Shiga toxin)
      Shigellosis is diagnosed by isolating and identifying the bacteria from rectal swabs.
    • Rex Karl S. Teoxon, R.N, M.D
      24
    • 25
      BACILLARY DYSENTERY/SHIGELLOSIS
      Shiga bacillus: dysenteriae (fatal), flexneri (Philippines), boydii, sonnei; gram (-)
      Shiga toxin destroys intestinal mucosa
      Humans are the only hosts
      Not part of normal intestinal flora
      IP: 1-7 days
      MOT : oral fecal route
    • 26
      SIGNS AND SYMPTOMS
      Fever
      abdominal pain
      diarrhea is watery to bloody with pus
      tenesmus
    • 27
      DIAGNOSIS
      stool culture
    • 28
      MANAGEMENT
      Oresol
      Ampicillin
      Trimethoprim-Sulfamethoxazole, Chloramphenicol, Tetracycline, Ciprofloxacin
      Flouroquinolones
    • Salmonellosis
      Salmonella entericaserovars such as S. typhimurium
      Mortality (<1%) due to septic shock caused by endotoxin
      Figure 25.9
    • Salmonellosis (Salmonella Gastroenteritis)
       Salmonellosis, or Salmonella gastroenteritis, is caused by many Salmonella entericaserovars.
      Symptoms include nausea, abdominal pain, and diarrhea and begin 12–36 hours after eating large numbers of Salmonella.
      Septic shock can occur in infants and in the elderly.
      Fever might be caused by endotoxin.
    • Salmonellosis (Salmonella Gastroenteritis)
       Mortality is lower than 1%, and recovery can result in a carrier state.
      Cooking food will usually kill Salmonella.
      Laboratory diagnosis is based on isolating and identifying Salmonella from feces and foods.
    • Salmonellosis and Typhoid Fever Incidence
      Figure 25.10
    • Typhoid Fever
      Salmonella typhi
      Frequent cause of death in the world with poor sanitation
      Bacteria is spread throughout body in phagocytes. Lysed and released to the bloodstream
      incubation period of 2-3 weeks
      High grade fever 40C and headache
      Diarrhea and fever decline 2nd or 3rd week
      Severe cases fatal ulceration and perforation of intestine
    • Typhoid Fever
      1-3% becomes Chronic carrier (gallbladder)
      1 to 3% recovered patients become carriers, harboring Salmonella in their gallbladder.
    • Typhoid Fever
       Salmonella typhi causes typhoid fever; the bacteria are transmitted by contact with human feces.
      Fever and malaise occur after a 2-week incubation period. Symptoms last 2–3 weeks.
      S. typhi is harbored in the gallbladder of carriers.
      Typhoid fever is treated with quinolones and cephalosporins; vaccines are available for high-risk people.
    • TYPHOID FEVER
      Salmonella typhii, gram (-)
      Carried only by humans
      Enteric Fever
      Active Immunization
      Carrier state – harbor in gallbladders
      IP: 1-3 weeks
      MOT: oral fecal route
      39
    • 40
      SIGNS AND SYMPTOMS
      Rose spot (abdominal rashes), Step ladder fever 40-41 deg, headache, abdominal pain, constipation (adults), mild diarrhea (children)
    • Rex Karl S. Teoxon, R.N, M.D
      41
    • PATHOPHYSIOLOGY
      Oral ingestion
      Bloodstream
      Reticuloendothelial system (lymph node, spleen, liver)
      Bloodstream
      Gallbladder
      Peyer’s patches of SI necrosis and ulceration
      42
    • 43
      TYPHOID FEVER
      1st week
      step ladder fever (BLOOD)
      2nd week
      rose spot and fastidial
      typhoid psychosis (URINE & STOOL)
      3rd week
      (complications) intestinal bleeding, perforation, peritonitis, encephalitis,
      4th week
      (lysis) decreasing S/SX
      5th week
      (convalescent)
    • 47
      DIAGNOSIS
      Blood culture (typhi dot) 1st week
      Stool and urine culture 2nd week
      Widal test (Ab to O and H Ag) - nonspecific
      Mgmt: Chloramphenicol, Amoxicillin, Sulfonamides, Ciprofloxacin, Ceftriaxone
    • Cholera
      Vibriocholerae serotypes that produce cholera toxin.
      Toxin causes host cells to secrete Cl–, HCO–, and water.
      SEVERE diarrhea and violent vomiting with severe dehydration, no fever
      12-20 liters (3-5gallons) fluid lost- shock, collapse and death
      Figure 25.11
    • Cholera
      Brackish (salty) waters- copepods, algae, aquatic plants and plankton
      Sensitive to stomach acid
      Epidemic :
      serotype O:1
      Serotype O:1 Eltor/ El Tor
      Serotype O:139
      None serotype O:1/ O:139
      100 million of bactreia per gram of stool
      Tx. doxycycline ``
      Figure 25.11
    • Cholera
       Vibriocholerae O:1 and O:139 produce an exotoxin that alters the membrane permeability of the intestinal mucosa; the resulting vomiting and diarrhea cause a loss of body fluids.
      The symptoms last for a few days. Untreated cholera has a 50% mortality rate.
      Fluid and electrolyte replacement provide effective treatment..
    • 53
      CHOLERA
      Vibrio coma (inaba, ogawa, hikojima), vibrio cholerae, vibrio el tor; gram (-)
      Choleragen toxin induces active secretion of NaCl
      Active Immunization
      IP: few hours to 5 days
      MOT: oral fecal route
    • 54
      SIGNS AND SYMPTOMS
      Rice watery stool with flecks of mucus (mucus and epithelial cells)
      s/sx of severe dehydration i.e. Washerwoman’s skin, poor skin turgor
      Dx: stool culture
    • 55
      MANAGEMENT
      IV fluids, Tetracycline, Doxycycline, Erythromycin, Quinolones, Furazolidone and Sulfonamides (children)
    • Noncholera Vibrios
      Usually from contaminated crustaceans or mollusks
      V. cholerae serotypes other than O:1, O:139, and eltor
      V. parahaemolyticus
      V. vulnificus
    • NoncholeraVibrios 
       Ingestion of other V. cholerae serotypes can result in mild diarrhea.
      Vibrio gastroenteritis can be caused by V. parahaemolyticus and V. vulnificus.
      These diseases are contracted by eating contaminated crustaceans or contaminated mollusks.
    • Escherichia coli Gastroenteritis
      Occurs as traveler's diarrhea and epidemic diarrhea in nurseries.
      50% of feedlot cattle may have enterohemorrhagic strains in their intestines.
      Enterohemorrhagic strains such as E. coli O157:H7 produce Shiga toxin.
      O = cell wall antigen
      H = flagellar antigen
    • Escherichia coli Gastroenteritis
       Traveler’s diarrhea may be caused by enterotoxigenic or enteroinvasive strains of E. coli.
      The disease is usually self-limiting and does not require chemotherapy.
    • Escherichia coli Gastroenteritis
       EnterohemorrhagicE. coli, such as E. coli O157:H7
      produces Shiga toxins that cause inflammation and bleeding of the colon, including hemorrhagic colitis and hemolytic uremic syndrome.
      Shiga toxins can affect the kidneys to cause hemolytic uremic syndrome.
    • Campylobacter Gastroenteritis
      Campylobacter jejuni
      Campylobacter is the second most common cause of diarrhea in the United States.
      Usually transmitted in cow's milk
    • Helicobacter Peptic Ulcer Disease
      Treated with antibiotics
      H. pylori causes stomach cancer
      Figure 11.12
    • Helicobacter Peptic Ulcer Disease
       Helicobacter pylori produces ammonia, which neutralizes stomach acid; the bacteria colonize the stomach mucosa and cause peptic ulcer disease.
      Bismuth and several antibiotics may be useful in treating peptic ulcer disease.
    • Helicobacter Peptic Ulcer Disease
      Figure 25.14
    • Yersinia Gastroenteritis
      Y. enterocolitica and Y. pseudotuberculosis
      Can reproduce at 4°C
      Usually transmitted in meat and milk
    • Clostridium Infections
      Clostridium perfringens Gastroenteritis
      Grow in intestinal tract, producing exotoxin
      Clostridium difficile–associated diarrhea
      Grow following antibiotic therapy
      Associated with hospitalized patients and nursing home residents
    • Clostridium Perfringens Gastroenteritis
      C. perfringens causes a self-limiting gastroenteritis.
      Endospores survive heating and germinate when foods (usually meats) are stored at room temperature.
      Exotoxin produced when the bacteria grow in the intestines is responsible for the symptoms.
      Diagnosis is based on isolation and identification of the bacteria in stool samples.
    • Clostridium Difficile–Associated Diarrhea
       Growth of C. difficile following antibiotic therapy can result in mild diarrhea or colitis.
      The condition is usually associated with hospitalized patients and nursing home residents.
    • Bacillus cereus Gastroenteritis
      Ingesting food contaminated with the soil saprophyte Bacillus cereus can result in diarrhea, nausea, and vomiting.
      Ingestion of bacterial exotoxin produces mild symptoms.
    • ASSESMENT OF DIARRHOEA
    • Mumps
      Mumps virus
      Enters through respiratory tract
      Infects parotid glands
      Prevented with MMR vaccine
      Figure 25.15
    • Mumps
       Mumps virus enters and exits the body through the respiratory tract.
      About 16–18 days after exposure, the virus causes inflammation of the parotid glands, fever, and pain during swallowing. About 4–7 days later, orchitis may occur.
    • Mumps
       After onset of the symptoms, the virus is found in the blood, saliva, and urine.
      A measles, mumps, rubella (MMR) vaccine is available.
      Diagnosis is based on symptoms or an ELISA test is performed on viruses cultured in embryonated eggs or cell culture.
    • 93
      MUMPS
      RNA, Mumps virus
      Mumps vaccine - > 1yo
      MMR – 15 mos
      Lifetime Immunity
      IP: 12-16 days
      MOT: Droplet, saliva, fomites
    • 94
      SIGNS AND SYMPTOMS
      Unilateral or bilateral parotitis
      Orchitis - sterility if bilateral
      Oophoritis
      Stimulating food cause severe pain
      aseptic meningitis
      Dx: serologic testing, ELISA
      Mgmt: supportive
    • Hepatitis
      Inflammation of the liver.
      Inflammation of the liver is called hepatitis. Symptoms include loss of appetite, malaise, fever, and jaundice
      Hepatitis may result from drug or chemical toxicity, EB virus, CMV, or the hepatitis viruses.
    • 96
      HEPATITIS
      Hepa A – fecal oral route
      Hepa B – body fluids
      Hepa C – non A non B, BT, body fluids
      Hepa D – hypodermic, body fluids
      Hepa E – fecal oral route, fatal and common among pregnant women
      Hepa G – BT, parenteral
    • Hepatitis
    • Hepatitis A 
      Hepatitis A virus (HAV) causes hepatitis A; at least 50% of all cases are subclinical.
      HAV is ingested in contaminated food or water, grows in the cells of the intestinal mucosa, and spreads to the liver, kidneys, and spleen in the blood.
      The virus is eliminated with feces..
    • Hepatitis A 
      The incubation period is 2–6 weeks; the period of disease is 2–21 days, and recovery is complete in 4–6 weeks.
      Diagnosis is based on tests for IgM antibodies.
      A vaccine is available; passive immunization can provide temporary protection.
    • HEPATITIS A
      RNA, Hepa A virus
      Infectious hepa
      Poor sanitation
      Worldwide distribution
      Mortality 1%, with full recovery
      IP: 3 - 5 weeks
      MOT: Fecal oral route, food handlers
      101
    • 102
      SIGNS AND SYMPTOMS
      Flu like symptoms
      Diarrhea, fatigue and abdominal pain
      Loss of appetite
      Nausea, diarrhea and fever
      Jaundice and dark colored urine
      Pale stools
      Young children are asymptomtic
    • 103
      PATHOGENESIS
      Enters and infects the liver, interlobular infiltration with mononuclear cells
      Necrosis and hyperplasia of kuffer cells
      PERIOD OF COMMUNICABILITY – a week before and after the appearance of symptoms
    • 104
      DIAGNOSIS
      Anti HAV IgM – active infection
      Anti HAV IgG – old infection; no active disease
      Liver function test
      Mgmt: supportive
      Active Immunity (Havrix)
      Passive Immunity (HAIg)
    • Hepatitis B (
      Hepatitis B virus (HBV) causes hepatitis B, which is frequently serious.
      HBV is transmitted by blood transfusions, contaminated syringes, saliva, sweat, breast milk, and semen.
      Blood is tested for HBsAg before being used in transfusions.
      The average incubation period is 3 months; recovery is usually complete, but some patients develop a chronic infection or become carriers.
      A vaccine against HBsAg is available.
    • Hepatitis B Virus
      Figure 25.16
    • Hepatitis B (
      Hepatitis B virus (HBV) causes hepatitis B, which is frequently serious.
      HBV is transmitted by blood transfusions, contaminated syringes, saliva, sweat, breast milk, and semen.
      Blood is tested for HBsAg before being used in transfusions.
    • HEPATITIS B
      DNA, Hepa B virus
      Serum hepa
      Worldwide distribution
      Main cause of liver cirrhosis and liver cancer
      Blood recipients, hemodialysis, IV drug users, sexually active homosexual, tattoing and health care workers (high risk)
      109
    • 110
      HBV
      Active Immunity (hepavax-B)
      Passive Immunity (HBIg)
      Carrier state
      IP: 2-5 months
      MOT: Blood and other body fluids route, percutaneous, perinatal, sexual
    • 111
      MANIFESTATIONS
      Stage I pre-icteric for 1-21 days
      Anorexia, nausea and vomiting, LBM, weight loss RUQ pain, fatty food intolerance, fever, chills and headache
      Stage II icteric for 2-6 weeks
      Jaundice, pruritus, weight gain, ascites, dark-tea colored urine (urobilirubin), S/sx of ADEK deficiency
      Stage III pre coma
      NH3 level increases with decreasing LOC, Flapping tremorsor asterixis
      Stage IV recovery (lifetime carrier) or death
    • 112
      DIAGNOSIS
      Elevated AST or SGPT (specific) and ALT or SGOT
      Increased IgM during acute phase
      (+) or REACTIVE HBsAg = INFECTED, may be acute, chronic or carrier
      (+) HBeAg = highly infectious
      HBcAg = found only in the liver cells
    • 113
      DIAGNOSIS
      (+) Anti-HBc = acute infection
      (+) Anti-HBe = reduced infectiousness
      (+) Anti-HBs = with antibodies (from vaccine or disease)
      Blood Chem
      Liver biopsy (to detect progression to CA)
    • Rex Karl S. Teoxon, R.N, M.D
      114
    • Rex Karl S. Teoxon, R.N, M.D
      115
    • 118
      MANAGEMENT
      Prevention of spread – Immunization and Health Education
      Enteric and Universal precautions
      Assess LOC
      Bed rest
      ADEK deficiency intervention
      High CHO, Moderate CHON, Low fat
    • 119
      COMPLICATION
      1. Fulminant Hepatitis – s/sx of encephalopathy
      2. Chronic Hepatitis - lack of complete resolution of clinical sx and persistence of hepatomegaly
      3. HBsAg carrier
    • Hepatitis C
       Hepatitis C virus (HCV) is transmitted via blood.
      The incubation period is 2–22 weeks; the disease is usually mild, but some patients develop chronic hepatitis.
      Blood is tested for HCV antibodies before being used in transfusions.
    • Hepatitis D (Delta Hepatitis) 
      Hepatitis D virus (HDV) has a circular strand of RNA and uses HBsAg as a coat.
      Hepatitis E 
      Hepatitis E virus (HEV) is spread by the fecal–oral route.
      Other Types of Hepatitis 
      There is evidence of the existence of hepatitis types F and G.
    • Figure 25.17
      Viral Gastroenteritis
      Rotavirus:
      3 million cases annually
      1-2 day incubation; 1 week illness
      Norovirus:
      50% of U.S. adults have antibodies
      1-2 day incubation; 1-3 day illness
      Treated with rehydration
    • Mycotoxins
      Mycotoxins are produced by some fungi
      Claviceps purpurea
      Grows on grains
      Produces ergot
      Toxin restricts blood flow to limbs; causes hallucination
      Aspergillus flavus
      Grows on grains
      Produces aflatoxin
      Toxin causes liver damage; liver cancer
    • Giardiasis
      Giardialamblia
      Transmitted by contaminated water
      Symptoms of giardiasis are malaise, nausea, flatulence, weakness, and abdominal cramps that persist for weeks
      Diagnosed by microscopic examination of stool for ova and trophozoite
      Treated with metronidazole
      Figure 25.18
    • Cryptosporidiosis
      Cryptosporidium hominis
      Transmitted by oocysts in contaminated water
      Diagnosed by acid-fast staining of stool or presence of antibodies by FA or ELISA
      Treated with oral rehydration
      Figure 25.19
    • Cyclospora Diarrheal Infection
      Cyclospora cayetanensis
      Transmitted by oocysts in contaminated water
      Diagnosed by microscopic examination for oocysts
      Treated with trimethoprim and sulfamethoxazole
    • Amoebic Dysentery
      Entamoeba histolytica
      Amoeba feeds on RBCs and GI tract tissues
      Diagnosis by observing trophozoites in feces
      Treated with metronidazole
      Figure 12.18b
    • Helminthic Diseases of the Digestive System
      Figure 25.21
    • Tapeworms
      Taenia spp.
      Transmitted as cysticerci in undercooked meat
      Cysticerci may develop in humans
      Diagnosed by observing proglottids and eggs in feces
      Treatment with praziquantel
      Neurocysticercosis may require surgery
      Figure 12.27
    • Tapeworms 
      Tapeworms are contracted by the consumption of undercooked beef, pork, or fish containing encysted larvae (cysticerci).
      The scolex attaches to the intestinal mucosa of humans (the definitive host) and matures into an adult tapeworm.
      Eggs are shed in the feces and must be ingested by an intermediate host.
      Adult tapeworms can be undiagnosed in a human.
    • Tapeworms
      Figure 25.22
    • Hydatid Disease
      Echinococcus granulosus
      Definitive host: Dogs, wolves
      Intermediate host: Sheep and other herbivores; humans
      Transmitted by ingesting E. granulosis eggs
      Treatment is surgical
      Figure 25.23
    • Figure 12.28
      Echinococcus granulosus
    • Pinworms
      Enterobius vermicularis
      Definitive host: Humans
      Transmitted by ingesting Enterobius eggs
      Treatment with pyrantel pamoate or mebendazole
    • Pinworms
      Figure 12.29
    • Hookworms
      Larvae in soil hatched from eggs shed in feces
      Larvae bore through skin; migrate to intestine
      Treated with mebendazole
      Figure 12.30
    • Hookworms
      Figure 25.24
    • Ascariasis
      Ascaris lumbricoides
      Lives in human intestines
      Transmitted by ingesting Ascaris eggs
      Treated with mebendazole
      Figure 25.25
    • Trichinosis
      Trichinella spiralis
      Larvae encyst in muscles of humans and other mammals
      Transmitted by ingesting larvae in undercooked meat
      Treated with mebendazole to kill adults worms
      Figure 25.26a–b
    • Trichinellosis 
      Trichinellaspiralis larvae encyst in muscles of humans and other mammals to cause trichinellosis.
      The roundworm is contracted by ingesting undercooked meat containing larvae.
      Adult females mature in the intestine and lay eggs; the new larvae migrate to invade muscles.
    • Trichinellosis 
      Symptoms include fever, swelling around the eyes, and gastrointestinal upset.
      Biopsy specimens and serological tests are used for diagnosis.
    • Trichinosis
      Figure 25.26