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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 Prevotella intermedia.
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 aureus
enterotoxin 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 Shigella spp. 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.
Shigella sonnei- 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 enterica serovars 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 enterica serovars.
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.
39
TYPHOID FEVER Salmonella typhii, gram (-) Carried only by humans Enteric Fever Active Immunization Carrier state – harbor in gallbladders
IP: 1-3 weeksMOT: oral fecal route
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
42
PATHOPHYSIOLOGY
Oral ingestion
Bloodstream
Reticuloendothelial system (lymph node, spleen, liver)
Bloodstream
Gallbladder
Peyer’s patches of SI necrosis and ulceration
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
Vibrio cholerae 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
Vibrio cholerae 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 daysMOT: 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
NONCHOLERA VIBRIOS
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
Enterohemorrhagic E. 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 DIARRHOEAA B C
CONDITION Well, alert Restless, irritable
Lethargic, unconcsious
EYES normal sunken sunken
THIRST Drinks NNot thirsty
ThirstyDrinks eagerly
Drinks poorlyNot able to drink
SKIN PINCH Goes back quickly
Goes back slowly
Goes back very slowly
DECIDE No signs of dehydration
If pt. has 2 or more signs B (C)Some Dehydration
If pt. has 2 or more signs CSevere Dehydration
TREAT Tx plan A Tx plan B Tx plan C
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 bilateralOophoritisStimulating food cause severe painaseptic meningitis
Dx: serologic testing, ELISAMgmt: 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
Transmission Causative agent Chronic liver disease?
Vaccine?
Hepatitis A Fecal-oral Picornaviridae No Inactivated virus
Hepatitis B Parenteral, STD
Hepadnaviridae Yes Recombinant
Hepatitis C Parenteral Filoviridae Yes No
Hepatitis D Pareteral, HBV coinfection
Deltaviridae Yes HBV vaccine
Hepatitis E Fecal-oral Caliciviridae No No
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.
101
HEPATITIS A RNA, Hepa A virus Infectious hepa Poor sanitation Worldwide distribution Mortality 1%, with full recovery
IP: 3 - 5 weeksMOT: Fecal oral route, food handlers
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 infectionAnti HAV IgG – old infection; no active diseaseLiver 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.
109
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)
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 daysAnorexia, nausea and vomiting, LBM, weight loss RUQ pain, fatty food intolerance, fever, chills and headache
Stage II icteric for 2-6 weeksJaundice, pruritus, weight gain, ascites, dark-tea colored urine (urobilirubin), S/sx of ADEK deficiency
Stage III pre comaNH3 level increases with decreasing LOC, Flapping tremors or 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 encephalopathy2. 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 Giardia lamblia 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 surgeryFigure 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
Trichinella spiralis 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