Gastrointestinal Tract Infections               Reading pg. 277 – 310

p     Alimentary tract

p     Passageway from mouth to anus

p     Path by which food is broken down

p     Divided into upper and lower tracts

p     Focus on infections of the lower tracts

Normal Flora

p    Important in protecting body from invasion

p    Stomach

n    Lysozyme, IgA, HCl

n    Bile is antimicrobial

n    Peristalsis – moves bacteria along preventing colonization

p    Intestines

n    few bacteria colonize upper small intestine

n    very high numbers in large intestine

p   ~10¹¹ bacteria per gram of feces (100 billion bacteria!!!!)

p   bacterial population:

§    Escherichia coli, Bacteriodes, Enterobacter faecalis, klebsiella pneumoniae

Infectious intestinal infections

Pathogens contracted via fecal-oral route.

p          transmitted from fecal contaminated

n         fingers of unsanitary food handlers

n         flying or crawling insects

n         Food or water.

 •            Primary cause = ingested food

•            For infection to occur, pathogens must be:

•          Ingested in sufficient

•          Able to evade host defenses

•            Food poisoning (intoxication) vs. food-associated poisoning (infection)

•          Intoxication - ingestion of a toxin present in food

•          Infection - ingestion of live microorganisms

•            gastrointestinal tract infection types (fig. 22.1)

§          toxins responsible for most of the symptoms

Diarrhea

•             Results from an increase in fluid and electrolyte loss into gut lumen à liquid feces

•             means used by host to forcibly expel pathogen

•            Aids dissemination of pathogen

•             major cause of mortality in children in developing countries

p           Fig. 22.2 pathogens that infect gastrointestinal tract

Diarrheal diseases

p    hard to diagnosed

p    Information that can help include:

n    Patient’s recent food

n    Travel history

n    Macroscopic and microscopic examination of feces for blood and pus

n    Lab tests – especially important in outbreak cases

Bacterial causes of diarrhea

•             Escherichia coli

p           Part of normal gut flora

p           Become pathogenic by:

n           acquiring virulence genes

n           entering places where it does not belong

n           encountering compromised host.

p           Cause of most traveler’s diarrhea

p           Strains that cause GI infections (fig. 22.6)

Enteropathogenic E. coli (EPEC)

p    cause diarrhea in children under 1 year of age.

p    generally do not produce enterotoxins

p    Possess adherence factor on plasmids:

n    pili, adhesins, and associated proteins

p   allow attachment to intestinal mucosa

n    subsequent destruction of brush border microvilli

p   Results in diarrhea and attachment-effacement lesions

Enterotoxigenic E. coli (ETEC)

§      contain plasmids that carry genes for:

n   Enterotoxins

n   factors (fimbriae and pili) for attachment.

n   two different enterotoxins:

p  Heat-labile (LT) - identical to cholera toxin

p  Heat-stable (ST) – activate guanylate cyclase activity à fluid loss

Enterohemorrhagic E. coli (EHEC)

p   Prototype strain is O157:H7

p   possess plasmid encoding:

n   fimbriae for attachment to cells

n   a verotoxin (identical to Shiga toxin)

p  Toxin destroys colon cells à dysentery symptoms

p  kidney problems (hemolytic-uremic syndrome).

§    survivors may require dialysis later in life.

Enteroinvasive E. coli (EIEC)

§       Do not produce enterotoxins

§       Possess enteroinvasive plasmids

§     allow bacteria to attach and invade mucosal cells by endocytosis

§     lyse endocytic vacuole, enter cytoplasm and multiply and spread to other adjacent cells.

§       Causes tissue damage, inflammation, necrosis, and ulceration

§     Results in blood and mucus in stool

Enteroaggregative E. coli (EAEC)

p    Display aggregative adherence to cells

p    Plasmids encodes for:

n    fimbriae

n    enterotoxin/cytotoxin

p    distinguishing clinical feature:

n    persistent diarrhea that last more than 14 days.

Diffuse-aggregative E. coli (DAEC)

p   Produces

n    a-hemolysins

n   Cytotoxic necrotizing factor

p   Role of these are uncertain

Escherichia coli

p     Epidemiology

n     Person-to-person spread

n     Contaminated food and water

n     Unpasteurized milk and juices

p     Treatment

n     Antibacterial therapy – not indicated

p    Infants may require antibiotics

n     Replacement of fluids and electrolytes

n     Dialysis - hemolytic uremic syndrome

n     Traveler’s diarrhea controlled with bismuth preparations

p    Pepto-Bismal

p     Prevent diseases by:

n     clean water supply

n     adequate sewage system

n     Hand washing

n     Pasteurization of drinks

n     Proper food preparation

•       Salmonellae

•       most common cause in developed countries

•       large animal reservoir contributes to food associated poisoning

p     Fig. 22.10 Transmission to humans

•          argument over number of species and nomenclature

p      2400 or more Salmonella serovars (serotypes)

p       2 species recognized

§       S. enterica

§       S. bongori – rarely isolated from humans

•          normal pathogenic process causes diarrhea but may cause septicemia à Fig 22.11

•            laboratory diagnosis is by selective media

•            Treatment:

•          antibiotic treatment not usually needed

•          fluid and electrolyte replacement

p          Transmission

p         Present on outside of eggs, chicken, strawberries

p         Most cases have an animal source

§        Exception: Enteric fevers caused by Salmonella typhi

§        Systemic à fever, shock - fatal

§        Human à human, fecal-oral

§        often spread by food handlers

•        organism may be shed for weeks following infection

§        “Typhoid Mary” notorious carrier – in gall bladder

§        Caused at least 53 cases over 15 years

n           Prevention

p         Hand washing before handling food

p         public health and education

•         Campylobacter jejuni {microaerophile, thermophile (42° C)

n       Bacteria recognized in 1972

n       Transmitted by fowl (raw chicken) and other animals

p      Fecal/oral, or waterborne

p      seldom spread person to person or by food handlers

n       most common cause of bacterial diarrhea in United States

p      affects young children, elderly and immunocompromised

p      Death rates low – death due to dehydration

n       laboratory diagnosis by gram stain (fig. 22.13) and selective media

Helicobacter pylori

p       Gram negative, spiral

p       Multiple polar flagella

p       Like acidic environment

n       Produces urease – break down urea to ammonia

p      Neutralizes acid creating a less acidic microenvironment

n       Causes gastritis, gastric ulcers, gastric

p       Symptoms

n       Abdominal pain

n       Tenderness

n       Bleeding

Helicobacter pylori Gastritis

p    Infection results in decrease in mucus production

n    stomach lining not protected from acidic environment

p    Epidemiology

n    Transmission through fecal-oral route

p   Flies also capable of transmission

n    20% of US population infected

p   Incidence increases with age

§    Almost 80% of those over 75 infected

p   Rates highest in lower socioeconomic groups

p     Prevention and Treatment

n    No proven prevention measures

n    Infection eradicated with 2 antibiotic combo treatment

•       Vibrio cholera

•       free-living, found in aquatic environments

•       comma shaped gram negative bacteria (fig. 22.15)

•       Antigenic structure

p     Common heat-labile flagellar H antigen

p     O lipopolysaccharide confers serologic specificity

•    2 serotypes:

•     O1 most important – divided into biotypes classical and El Tor

•     Non-O1

•    serosub groups

•    Other Vibrio: fish and seafood

•         Vibrio cholera

n      Pathogenesis

p     Requires large numbers ingested to cause infection

§      Highly sensitive to stomach acid

p     Bacteria adhere to epithelial cells of  small intestine and multiply.

p      Disease symptoms caused by enterotoxin (cholera toxin) (fig. 22.17)

§      Encoded by a prophage

§      regulates activation of adenlyate cyclase

§      Result is persistent increase in cAMP levels

§      Hyper secretion of Na, Cl, K, bicarbonate and H₂0

Cholera

•         Shigellosis (Shigella dysenteriae)

•        bacillary dysentery

p      Symptoms

§      Dysentery and Vomiting

§      Flu symptoms

§      Fever, stiff neck

§      Joint pain

§      Convulsions (rare)

•        symptoms dependent on species and health of host

•       Shigella sonnei – mild infections

•       Shigella flexner and Shigella boydii – moderately severe disease

•       Shigella dysenteriae – most severe disease

p      All cause shigellosis by producing Shiga Toxin

§      Acts much like cholera toxin

§      Toxin associated with fatal hemolytic uremic syndrome

•        primarily a pediatric disease

p      a problem in day-care centers.

•            no animal reservoir and not found in the environment

•            person to person transmission only

p         Fecal-oral route

p         Not easily killed by stomach acid

§        As few as 10 organisms to cause infection

p         invade epithelial cells and multiply

§        Move from cell to cell via actin tails

§        Kills cells and dead cells slough off

§        Initiates intense inflammatory response

§        stool initially watery then full of pus and blood

•            Treatment:

•          self-limiting; fluid and electrolyte replacement

•          rarely treated with antibiotics

•            proper public health and education could eliminate disease

Other bacterial causes of diarrheal disease

•             Vibrio parahaemolyticus (Halophile, foodborne)

–           found in fish and shellfish

–           disease results from uncooked or poorly cooked food

–           pathogenic mechanism unknown

–           produces a hemolytic cytotoxin

–           laboratory analysis requires special media

–          Biochemical tests and specific antisera

–           prevention is properly cooked food

–          Fish and seafood

•             Yersinia enterocolitica 

–           found in colder regions, likes 22-25°C

–           vast animal reservoir

–          Rodents, rabbits, pigs, sheep, cattle, horses, domestic pets

–           dog to human transmission has been reported

–           can survive and multiply in refrigerator, milk contamination occurs

–           pathogenic mechanism unknown

–           invades terminal ileum

–          causes necrosis in Peyer’s patches

–          inflammation in mesenteric lymph nodes (fig. 22.20)

–           laboratory analysis requires special media

–          Isolation, biochemical tests, serological tests to confirm

•             Clostridium perfringens (fig. 22.21)

–           transmitted in spore contaminated food

–           enterotoxin producing strains

–           rare b toxins produced in persons not used to a high protein diet

•             Clostridium perfringens (fig. 22.21)

–           grows on routine anaerobic media

–           enterotoxin can be detected by latex agglutination

–           antibacterial treatment is rarely required

–           Also causes wound and soft tissue infections

–           prevention through thorough cooking and rapid consumption

•             Bacillus cereus (fig. 22.22)

•            Normal soil inhabitant

•            vegetative and spores contaminate food (grains and spices)

•            Two different toxins involved

–         enterotoxin à diarrhea

–      abdominal cramps and diarrhea

–      incubation period of 8 to 16 hours

–         emetic toxin à vomiting; heat stable

–      nausea, vomiting, & abdominal cramps

–      incubation period of 1 to 6 hours (ingestion of toxin).

–         prevention through thorough cooking, rapid consumption and refrigeration

–         rare antibacterial treatment

•             Clostridium difficile

–           arises in aftermath of broad spectrum antibiotic treatment

–           antibiotic associated diarrhea

–           drugs disrupt normal intestinal flora

–           pseudomembranous colitis

p        severe inflammation of the colon (large intestine).

p         Due to cytotoxin and enterotoxin

–           commonly found in children and some adults in small normal numbers

–           can be acquired from other patients