Transcript Microbiology: A Systems Approach, 2nd ed. Chapter 22: The Gastrointestinal Tract and Its Defenses.

Microbiology: A Systems
Approach, 2nd ed.
Chapter 22: The Gastrointestinal
Tract and Its Defenses
22.1 The Gastrointestinal Tract and Its
Defenses
• GI tract is composed of eight main sections and
augmented by four accessory organs
• Eight sections: mouth, pharynx, esophagus, stomach,
small intestine, large intestine, rectum, and anus
• Accessory organs: salivary glands, liver, gallbladder,
and pancreas
• Also known as the digestive tract or alimentary canal
• The GI tract is an internal tube (lumen) that passes
through the body; only chemicals absorbed through
the GI tract actually gain entrance to the internal
portions of the body
Figure 22.1
Defenses
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Mucus
Secretory IgA
Peristalsis
Fluids with antimicrobial properties: saliva,
stomach fluid, bile
• GALT tissues: tonsils, adenoids, lymphoid tissue
in the esophagus, Peyer’s patches, appendix
• Microbial antagonism
22.2 Normal Biota of the
Gastrointestinal Tract
• Large variety of normal biota
• Oral cavity alone: more than 550 known
species of microorganisms
• Esophagus and stomach much more sparsely
populated
• Large intestine: billions of microorganisms
22.3 Gastrointestinal Tract Diseases
Caused by Microorganisms
• Tooth and Gum Infections
– If left undisturbed, normal biota biofilm eventually
contains anaerobic bacteria that can damage the
soft tissues and bones (periodontium)
surrounding the teeth
– Introduction of carbohydrates to the oral cavity
can result in breakdown of dentition
Dental Caries (Tooth Decay)
• Most common infectious disease of human
beings
• Symptoms: often not noticeable, but range
from minor disruption in the enamel to
complete destruction of the enamel and
deeper layers
• Deeper lesions can result in infection to soft
tissue inside the tooth leading to a toothache
Figure 22.2
Figure 22.3
Figure 22.4
Periodontal Disease
• 97% to 100% of the population has some
manifestation of it by age 45
• Most are due to bacterial colonization and
varying degrees of inflammation
Periodontitis
• Initial stage: gingivitis (swelling, loss of
normal contour, patches of redness, and
increased bleeding of the gingival)
• If persists, periodontitis develops
– Extension of gingivitis into the periodontal
membrane and cementum
– Increases the size of pockets between the tooth
and the gingival and can cause bone resorption
enough to loosen and possible lose the tooth
Figure 22.5
Figure 22.6
Necrotizing Ulcerative Gingivitis and
Periodontitis
• Syntergistic infections infolving Treponema
vincentii, Prevotella intermedia, and
Fusobacterium species
• Together they produce several invasive factors
that cause rapid advancement into the
periodontal tissues
• Severe pain, bleeding, pseudomembrane
formation, and necrosis
Mumps
• Incubation period 2o to 3 weeks
• Initial symptoms: fever, nasal discharge, muscle
pain, and malaise
• May be followed by inflammation of the salivary
glands, producing gopherlike swelling of the
cheekcs (parotitis)
• Multiplication in the salivary glands followed by
invasion of other organs, especially testes,
ovaries, thyroid gland, pancreas, meninges, heart,
and kidneys
Figure 22.7
Figure 22.8
Gastritis and Gastric Ulcers
• Heliobacter pylori thrives in the acidic environment of
the stomach and has been linked to a variety of
gastrointestinal ailments
• Gastritis: sharp or burning pain emanating from the
abdomen
• Gastric ulcers are actual lesions in the mucosa of the
stomach
• Duodenal ulcer: lesion in the uppermost portion of the
small intestine
• Severe ulcers can be accompanied by bloody stools,
vomiting, or both
• Long-term infection with H. pylori might be a
contributing factor to stomach cancer
Figure 22.9
Acute Diarrhea
• In the U.S., up to a third of all cases
transmitted by contaminated food
• Most cases are self-limiting and do not require
treatment
• Some (E. coli O157:H7) can be devastating
Acute Diarrhea Caused by Salmonella
• Salmonellosis: can be severe (elevated body
temperature and septicemia) or mild (vomiting,
diarrhea, and mucosal irritation); symptoms
usually spontaneously subide after 2 to 5 days
• Typhoid fever: fever, diarrhea, and abdominal
pain; the bacterium infiltrates the mesenteric
lymph nodes and the phagocytes of the liver and
spleen; progressive and invasive that leads
eventually to septicemia
Figure 22.10
Acute Diarrhea Caused by Shigella
• Causes the most severe form of dysentery
• Uncommon in the U.S.
• Frequent, watery stools, fever, and intense
abdominal pain
• Nausea and vomiting are common
• Often bloody stools
Figure 22.11
Acute Diarrhea Caused by E.coli
O157:H7 (EHEC)
• Most virulent strain of E. coli
• Enterohemorrhagic E. coli
• Symptoms range from mild gastroenteritis
with fever to bloody diarrhea
• About 10% of patients develop hemolytic
uremic syndrome (can cause kidney damage
and failure)
• Can also cause neurological symptoms such as
blindness, seizure, and stroke
Figure 22.12
Acute Diarrhea Caused by Other E.
coli
• Four other categories:
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Enterotoxigenic
Enteroinvasive
Enteropathogenic
Enteroaggregative
Enterotoxigenic E. coli (ETEC)
• Presentation varies depending on which type
of E. coli is causing the disease
• Traveler’s diarrhea: watery diarrhea, lowgrade fever, nausea, and vomiting
Enteroinvasive E. coli (EIEC)
• Cause a disease similar to Shigella dysentery
• Invade gut mucosa and cause widespread
destruction
• Blood and pus found in stool
• Significant fever
Enteropathogenic E. coli (EPEC)
• Profuse, watery diarrhea
• Fever and vomiting also common
• Produce effacement of gut surfaces
Enteroaggregative E. coli (EAEC)
• Can cause chronic diarrhea in young children
and in AIDS patients
Acute Diarrhea Caused by
Campylobacter
• Most common bacterial cause of diarrhea in the
U.S.
• Frequent watery stools, fever, vomiting,
headaches, and severe abdominal pain
• Symptoms may last beyond 2 weeks
• Symptoms may subside then recur over a period
of weeks
• In a small number of cases, can lead to a serious
neuromuscular paralysis called Guillain-Barré
syndrome (GBS)
Figure 22.13
Acute Diarrhea Caused by Yersinia
Species
• Y. enterocolitica and Y. pseudotuberculosis
• Uncommon in U.S.
• Inflammation of the ileum and mesenteric
lymph nodes gives rise to severe abdominal
pain
• Infection occasionally spreads to the
bloodstream
Acute Diarrhea Caused by Clostridium
difficile
• Causes pseudomembranous colitis
• Major cause of diarrhea in hospitals
• Able to superinfect the large intestine when
drugs have disrupted the normal biota
• Produces two enterotoxins (toxins A and B) that
cause areas of necrosis in the wall of the intestine
• Diarrhea
• Severe cases exhibit abdominal cramps, fever,
and leukocytosis
Figure 22.14
Acute Diarrhea Caused by Vibrio
cholera
• Incubation period of a few hours to a few days
• Symptoms begin abruptly with vomiting
• Followed by copious watery feces called
secretory diarrhea
• Can lose up to 1 liter of fluid an hour in severe
cases
Figure 22.15
Acute Diarrhea Caused by
Cryptosporidium
• Headache, sweating, vomiting, severe
abdominal cramps, and diarrhea
• In AIDS patients may develop into chronic
persistent cryptosporidial diarrhea
Figure 22.16
Figure 22.17
Acute Diarrhea Caused by Rotavirus
• Effects of infection vary with age, nutritional state,
general health, and living conditions of the patient
Figure 22.18
Acute Diarrhea Caused by Other
Viruses
• Many other viruses can cause gastroenteritis
• For example adenoviruses, noroviruses, and
astroviruses
• Common in the U.S. and around the world
• Profuse, water diarrhea of 3 to 5 days duration
Acute Diarrhea with Vomiting (Food
Poisoning)
• Symptoms in the gut that are caused by a
preformed toxin of some sort
• If the symptoms are violent and the
incubation period is very short, intoxication
rather than infection should be considered
Food Poisoning by Staphylococus
aureus Exotoxin
• Associated with food such as custards, sauces,
cream pastries, processed meats, chcken salad, or
ham that have been contaminated and then left
unrefrigerated for a few hours
• Toxins do not noticeably alter the food’s taste or
smell
• Heating the food after toxin production may not
prevent disease
• Symptoms: cramping, nausea, vomiting, and
diarrhea
• Rapid recovery- usually within 24 hours
Food Poisoning by Bacillus cereus
Exotoxin
• Two exotoxins: one causes diarrheal-type
disease, the other cause an emetic disease
• The type of disease that takes place is influenced
by the type of food that is contaminated
• Emetic form frequently linked to fried rice,
especially when cooked and kept warm for long
periods of time
• Diarrheal form associated with cook mats or
vegetables that are held at a warm temperature
for long periods of time
Food Poisoning by Clostridum
perfringens Exotoxin
• Animal flesh and vegetables such as beans
that have not been cooked thoroughly enough
to destroy endospores
• Acute abdominal pain, diarrhea, and nausea in
8 to 16 hours
• Rapid recovery
Chronic Diarrhea
• Lasting longer than 14 days
• Infectious or noninfectious
• AIDS patients suffer from it due to
opportunistic infections
• Several microbes can be responsible
Chronic Diarrhea by Enteroaggregative
E. Coli (EAEC)
• Adheres to human cells in aggregates rather
than as single cells
• Stimulates large amounts of mucus in the gut
Figure 22.19
Chronic Diarrhea by Cyclospora
• Incubation period of about 1 week
• Watery diarrhea, stomach cramps, bloating,
fever, and muscle aches
• If prolonged, also experience anorexia and
weight loss
Figure 22.20
Chronic Diarrhea by Giardia
• Diarrhea of long duration, abdominal pain,
and flatulence
• Stools have a greasy, malodorous quality
• Fever usually not present
Figure 22.21
Chronic Diarrhea by Entamoeba
• Clinical amoebiasis exists in intestinal and extraintestinal
forms
• Intestinal targets: cecum, appendix, colon, and rectum
– Secretes enzymes that dissolve tissues
– Leaves erosive ulcerations as it penetrates deper layer of
mucosa
– Dysentery, abdominal pain, fever, diarrhea, weight loss
– Can also manifest hemorrhage, perforation, appendicitis, and
amoebomas
• Extraintestinal: common target is the liver
– Amoebic hepatitis
– Rarer complication- pulmonary amoebiasis
Figure 22.22
Figure 22.23
Figure 22.24
Hepatitis
• Inflammatory disease marked by necrosis of
hepatocytes and a mononuclear response that
swells and disrupts the liver architecture
• Occurs when certain viruses infect the liver
• Causes jaundice when bilirubin accumulates
in the blood and tissues
Hepatitis A Virus (HAV)
• In general, far milder and shorter term than
the other forms
• Either subclinical or vague, flulike symptoms
• In some cases, may include jaundice and
swollen liver
• Darkened urine often seen
• Not oncogenic
• Complete uncomplicated recovery
Hepatitis B Virus (HBV)
• May include fever, chills, malaise, anorexia,
abdominal discomfort, diarrhea, and nausea
• Rashes may appear
• Arthritis may occur
• Can be serious and life-threatening
• Some patients develop glomerulonephritis and
arterial inflammation
• Complete liver regeneration and restored
function occur in most patients
• Small number of patients develop chronic liver
disease (necrosis or cirrhosis)
Hepatitis C Virus (HCV)
• “silent epidemic”
• Takes many years to cause noticeable
symptoms
• Shares many symptoms of HAB but is more
likely to become chronic
• Cancer may also result
Helminthic Intestinal Infections
• Usually provoke an increase in granular
leukocytes called eosinophils (eosinophilia)
• Most spend part of their life cycle in the
intestinal tract
Figure 22.25
General Clinical Considerations
• Pathogenesis and Virulence Factors
– Most do not have sophisticated virulence factors
– Have numerous adaptations that allow them to
survive in their hosts
• Specialized mouthparts
• Enzymes
• Cuticial or other covering
– Organ systems are reduced to the essentials
– Damage caused to host is usually the result of the
host’s response to the presence of the worm
– Many have more than one host- the host in which the
adult worm is found is the definitive host
Diagnosis
• Differential blood count showing eosinophilia
• Serological tests indicating sensitivity to
helminthic antigens
• Discovery of eggs, larvae, or adult worms in
stools or other tissues
Prevention and Treatment
• Prevention- minimizing human contact with
parasite or interrupting its life cycle
• Treatment- antihelminthic drugs or in some
cases removal of the worms or larvae
Intestinal Distress as the Primary
Symptom
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Trichuris trichiura
Enterobius vermicularis
Taenia solium
Diphyllobothrium latum
Hymenolepis species
Trichuris trichiura
• Localized hemorrhage of the bowel caused by
worms burrowing and piercing intestinal
mucosa
• Heavier infections can cause dysentery, loss of
muscle tone, and rectal prolapsed
Enterobius vermicularis
• Pronounced anal itching when the mature
female emerges from the anus and lays eggs
• Can also suffer from disrupted sleep, nausea,
abdominal discomfort, and diarrhea
Taenia solium
• Few symptoms
• Occasionally proglottids in the stool
• Sometimes vague abdominal pain and nausea
Figure 22.26
Diphyllobothrium latum
• Possible abdominal discomfort or nausea
• Anemia
Hymenolepis species
• Mild symptoms
• Most common tapeworm infections in the
world
Intestinal Distress Accompanied by
Migratory Symptoms
• Inflammatory reactions along migratory
routes inside the human
• Can result in eosinophilia and pneumonia
Ascaris lumbricoides
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Larvae and adult stages in humans
Releases eggs in feces which are then spread to other humans
Ingested eggs hatch in intestine
Larvae then penetrate intestinal wall, enter the lymphatic and
circulatory systems, sweep into the heart, arrive at the
capillaries of the lungs
Then larvae migrate up the respiratory tree to the glottis
Worms are swallowed and returned to the small intestine,
reach adulthood, and reproduce
Can also invade biliary channels of the liver and gallbladder,
and sometime emerge from the nose and mouth
Severe inflammatory reactions mark the migratory route
Necator americanus and Ancylostoma
duodenale
• Larvae hatch outside the body
• Infect by penetrating the skin (usually through bare feet)
• Actively burrow into the skin, reach the lymphatic or
blood circulation, carried to the heart and lungs
• Larvae proceed up the bronchi and trachea to the throat
• Swallowed and arrive in the small intestine, where they
anchor, feed on blood, and mature
• Eggs appear in the stool about 6 weeks after the time of
entry
• Symptoms follow the progress of the worm in the body
Figure 22.27
Strongyloides stercoralis
• Can complete its life cycle either inside the
human body or outside in moist cell
• Larvae penetrate the skin
• Worm enters the circulation, carried to the
respiratory tract and swallowed, enters the
small intestine to complete development
• Eggs are laid in the gut, eggs hatch into larvae
in the colon
Figure 22.28
Liver and Intestinal Disease
• Opisthorchis sinensis and Clonorchis sinensis
• Fasciola hepatica
Opisthorchis sinensis and Clonorchis
sinensis
• Chinese liver flukes
• Complete their sexual development in mammals;
intermediate development in snail and fish hosts
• Ingest cercariae in inadequately cooked or raw
freshwater fish
• Larvae hatch and crawl into the bile duct
• Mature and shed eggs into the intestinal tract
• Feces containing eggs passed into standing water
• Eggs infect snails that release cercariae that invade fish
• Symptoms are slow but include thickening of the lining
of the bild duct and possible granuloma formation in
the liver
Fasciola hepatica
• Occasionally transmitted to humans, common
in sheep, cattle, goats, and other mammals
• Complex life cycle
• Symptoms of vomiting, diarrhea,
hepatomegaly, and bile obstruction
Figure 22.29
Muscle and Neurological Symptoms
• Trichinosis
• Life cycle spent entirely within the body of a mammalian host
• Human eats undercooked pork; cyst envelope digested in the
stomach and small intestine, and larvae is liberated
• Larvae burrows into the intestinal mucosa and reach adulthood
and mate
• Larvae then penetrate the intestine and enter the lymphatic
channels and blood]
• Final development occurs when the coiled larvae are encystsed in
the skeletal muscle
• Symptoms may be unnoticeable or life-threatening, depending on
how many larvae were ingested
• First symptoms mimic influenza or viral fevers with diarrhea,
nausea, abdominal pains, fever, and sweating
• Second phase produce puffiness around the eyes, intense muscle
and joint pain, shortness of breath, and pronounced eoisinophilia
Liver Disease
• Schistosomiasis
• First symptoms: itchiness in the area where
the worm enters the body
• Followed by fever, chills, diarrhea, and cough
• Chronic infection can lead to hepatomegaly
and liver disease and splenomegaly
Life Cycle
• Infected humans release eggs into irrigated fields or ponds through
defecation or urination
• Egg hatches in water and gives off a miracidium
• Miracidium swims to a snail and burrows into a vulnerable site,
shedding its covering
• Multiplies into a larger larva called a cercaria
• Infected snails give off thousands of cercariae into the water
• Cercaria attach themselves to human skin and penetrate into hair
follicles
• Pass into small blood and lymphatic vessels
• Carried to the liver where they achieve sexual maturity and mate in
permanently attached pairs
• The pair migrates to and lodges in small blood vessels at specific
sites, feed upon blood and the female lays eggs
Figure 22.30
Figure 22.31