Enterobacteriaceae Lec 26,27 Micro Exam 2

Front 1

What are some organisms you would find on the skin?

Back 1

S. aureus, Corynebacterium, various streptococci, Pseudomonas aeruginosa, anaerobes (e.g. Propionibacterium), yeasts (e.g. Candida albicans)

Front 2

In teh stomach, what is an important organism?

Back 2

Helicobacter pylori, Lactobacillus spp. and Streptococcus spp.

Front 3

Colon organisms?

Back 3

Bacteroides fragilis, E. coli

Bifidobacterium, Eubacterium, Fusobacterium, Lactobacillus, various aerobic Gram-negative rods, Enterococcus faecalis, streptococci, Clostridium

Front 4

Vagina organisms?

Back 4

Lactobacillus, E. coli3, group B streptococci3

Various streptococci, various Gram-negative rods, B. fragilis, Corynebacterium, Candida spp.

Front 5

Urtertha organisms?

Back 5

S. epidermidis, coag-neg Staph., Corynebacterium, various streptococci, various Gram-negative rods, e.g. E. coli3

Front 6

What are some sites of infection of enterobacteriaceae?

Back 6

central nervous system (escherichia)
lower respiratory tract (klebsiella pneumonia - usually in those wiht preexisting conditions; eneterobacter ; escherichia)

blood stream (escherichia, lkelbsiella, enterobacter)

GI tract (salmonella, shigella, escherichia)

Urinary tract (escherichia, proteus)

Front 7

Remember the differences in the cell wall of

Back 7

Gram - and Gram + walls.

Gram - rods are often part of our normal flora. Gram - : LPS, has an outer membrane and able to live in GI tract with harsh environment. has periplasmic space that may confer antibiotic resistance.

Front 8

What antigens in the structure of enterobacteriaceae are used in serum testing? What is this used for?

Back 8

reference antibodies can be mixed with the antigens and form agglutinations = indicative of recognition.

Kauffman white scheme: flagella recognition (H antigen); Capsule (K or Vi antigens) ; all of these bacteria have a common antigen (core of LPS) ; O antigen (part of long polysaccharide chain)

all important in determining strains.

Front 9

Phase variation

Back 9

Use the mechanisms of capsules to conserve energy; also used to evade immune response.

Front 10

What can you vary to make the endotoxin less toxic?

Back 10

Can vary the O antigen to different structures in order to make it less toxic.

Front 11

Describe Type 3 secretion systems

Back 11

Its a multiprotein complex found in a pathogenicity islands. protein structures serve as a giant syringe; factors are injected into host and help bacteria cause disease.

Front 12

What are some mechanisms that bacteria and enterobactericea have for competing nutrients in a host?

Back 12

. Production of bacterial siderophores that bind iron
ii. Production of hemolysins that lyse host cells and release iron

Front 13

How can bacteria enhance their virulence?

Back 13

Genetic acquistion of antibiotic resistance by mutation, plasmids, etc.

Can secrete factors that inhibit binding of complement (known as serum resistance)

Front 14

What is MacConkey Agar?

Back 14

a selective and differential medium. selective = has antibiotics and other factors that select for growth of Gram - and select against grwoth of gram +.
differential = Gram + rods that grow are based on whether or not they can ferment lactose will form pinkish colonies. Those that do not ferment lactose form whitish colonies.

Front 15

2 mechanisms by which bacteria cause diarrhea

Back 15

1) toxin mediated
2) invasion/inflammatory

fever generation is usually through organisms that use the invasive/inflammatory mechanisms. Ex. salmonella, shigella, C. jejuni, E coli (EHEC)

white blood cells are indicative of the invasic/inflammatory mechanism in the stool. They stain it with methyelene blue to detect blood cells.

-organisms vary in infective dose in terms of how much is needed to cause disease

Front 16

Name 4 important properties and structure part of E. Coli

Back 16

1. The most common and medically-relevant species in the genus, Escherichia; many
serotypes and strains.
2. Facultative anaerobe.
3. Encapsulated.
4. Motile.

Front 17

How is E. Coli transmitted?

Back 17

1. Part of normal flora; most common facultative anaerobe in GI tract in humans.
2. Most infections due to endogenous infections when immune system/barriers become
compromised.
3. Strains that cause gastroenteritis are usually acquired by exogenous infection.

Front 18

Describe the role of adhesins and exotoxins in E Coli.

Back 18

1. E. coli has all the virulence factors described in general for the Enterobacteriaceae, but
strains that cause urinary tract infections (UTIs) and gastroenteritis also have a variety
of adhesins and produce exotoxins.
a. Adhesins: there are a variety of adhesin proteins produced by various strains of E.
coli that allow these bacteria to “stick” to tissues in the urinary and GI
tracts and resist “washing away” by urine flow and peristalsis,
respectively; found on pili.
b. Exotoxins: E. coli strains produce a variety of enterotoxins (exotoxins that act in
the enteric tract) that promote disease production, as well. See Table 1.

Front 19

What are 2 diseases that E coli often cause?

Back 19

especially may cause neonatal meningitis. women are usually screened for this.

also is the most common cause of UTIs

Front 20

What's another common cause of UTIs?

Back 20

Staph. saprophydicus

Front 21

What are the symptoms of diarrheal disease?

Back 21

Symptoms: vomiting, diarrhea, abdominal pain, fever

Front 22

What are some predisposing factors to different strains of E.Coli infection?

Back 22

age, present state of health, site of action (small vs. large intestine).

Front 23

Enteropathogenic E. coli (EPEC)

Back 23

Infants in developing countries.

Watery, nonbloody stools, vomiting; lasts 5-15 days; dehydration, electrolyte imbalance can cause death.

Small intestine

Attaches to mucosal epithelial cells & produces cytoskeletal changes and cell death; Type III secretion system involved.

Front 24

Enterotoxigenic E. Coli (ETEC)

Back 24

Most common cause of Traveler’s Diarrhea; serious disease in infants in developing countries; Need large inoculum to produce disease-usually acquired by ingestion of fecally contaminated food or water; no person-to-person spread.

Watery, nonbloody stools, nausea & vomiting are rare; abdominal cramps, low-grade fever; lasts 1-3 days in adults; more serious disease in infants.

Small intestine

ETEC in gut produces heat-labile or heat-stable enterotoxins (encoded on plasmid) that cause hypersecretion in small intestine; no evidence of tissue damage or inflammation.

Front 25

Enterohemorrhagic E Coli (EHEC)

Back 25

These strains are the most common cause of gastroenteritis in developed countries; ingestion of < 100 organisms can cause disease; typically acquired by ingestion of undercooked meat (especially beef; part of normal flora of cattle), unpasteurized milk or fruit juice, uncooked vegetables or fruit. The most common strain associated with disease in U.S. is O157:H7.

Starts with watery, nonbloody diarrhea, but can progress to bloody diarrhea (hemorrhagic colitis) with abdominal cramps; no or low-grade fever; with O157:H7 strains, can progress to hemolytic uremic syndrome if organisms enter bloodstream.

Large intestine

Organism produces cytotoxic Shiga toxins (Stx-1, and 2) which inhibit protein synthesis and lead to death of absorptive cells in intestine; Stx-2 destroys glomerular endothelial cells.

Front 26

Enteroinvasive E Coli (EIEC)

Back 26

Rare, but more common in developing countries. Starts with watery diarrhea, fever, & cramping, but may progress to dysentery with low volume, bloody stools. Large intestine Bacterial genes carried on a plasmid mediate invasion of epithelial cells; cell destruction & inflammation lead to ulceration in colon.

Front 27

How is Salmonella transmitted to humans?

Back 27

Salmonella is acquired by humans by ingesting food or water contaminated by human
and/or animal feces, except S. typhi which is transmitted only by humans.
a. The most frequent animal sources are poultry and eggs; inadequately cooked
meats are another source; contact with certain pets (dogs, turtles, snakes, lizards)
is also a risk.

b. Humans may excrete Salmonella before or after an episode of enterocolitis or may
be chronic carriers who excrete bacteria for years.

Front 28

Salmonella can make 3 types of disease..

Back 28

Enterocolitis, Typoid/Enteric fevers, and Septicemia

Front 29

Describe enterocolitis

Back 29

i. Characterized by invasion of epithelial and subepithelial tissue of the small and large
intestines.
ii. Inflammation and diarrhea occurs; bacteremia does not usually occur.
iii. Large inoculum, >100,000 organisms required to produce disease in
immunocompetent host. Gastric acid is important host defense.

Has a 12-48 hr incubation period.
b. Begins with nausea and vomiting, the progresses to abdominal pain and diarrhea,
which can be mild or severe, +/- blood.

c. S. typhimurium is most common Salmonella species to cause enterocolitis in U.S.
d. Usually self-limiting within a few days.

Front 30

Describe typhoid/enteric fevers

Back 30

i. Infection starts in small intestine, but few GI symptoms occur. Organisms replicate in
phagocytes, then spread to liver, gallbladder, and spleen, and then enter
bloodstream.
ii. Bacteremia is associated with fever and other endotoxin-associated symptoms.
iii. Carrier state can establish with chronic infection in gall bladder and excretion of
bacteria in feces for years.


-can cause osteomyelitis especially with those who have preexisiting conditions.

a. Typhoid fever is caused by S. typhi; enteric fever is caused by S. paratyphi A, B, C
b. Slow onset, with fever and constipation.
c. Bacteremia becomes sustained within a week, leading to high fever, delirium,
tender abdomen, and enlarged spleen; leukopenia and anemia, abnormal liver
function may occur.
d. Resolution of disease usually starts by 3rd week, but complications can occur and
some patients become chronic carriers (<3%).

Front 31

Describe septicemia

Back 31

i. Occurs in only 5-10% of Salmonella infections in patients with either preexisting
chronic disease (e.g. sickle cell anemia or cancer) or a child with enterocolitis.
ii. Bacteremia leads to infection of many organs; osteomyelitis, pneumonia, and
meningitis are the most common resulting diseases.


a. Usually caused by S. cholerasuis.
b. Begins with fever, little or no enterocolitis, then organ-specific (bone, lung).

Front 32

Describe the lab diagnosis of enterocolitis, salmonella

Back 32

1. In enterocolitis, isolation of organism from stool; in enteric or typhoid fevers, from blood
specimen; in septicemia, from bone marrow, or other relevant target organ.
2. Salmonella form non-lactose-fermenting colonies on MacConkey agar (colorless).
3. Slide agglutination tests are done to identify isolates based on O, H, and Vi antigens.
4. Salmonellosis is a reportable disease.

Front 33

What are some treatments for enetrocolitis and typhoid

Back 33

1. enterocolitis: use fluids and electrolytes to prevent dehydration.
2. can use antibitocs only for neonates
3. Typhoid fever: 2 vaccines
-oral vaccine: has S. typhi strain
- parenterally administeered vaccine with capsular polysaccharidie given for most.

Front 34

How is Shigella transmitted?

Back 34

1. Cause disease (shigellosis) only in humans; no animal reservoir.
2. Transmitted by the fecal-oral route; fingers, flies, food, and feces (“the four F’s”) play
major roles in transmission.
3. Shigella has a very low ID50, ~100 organisms are sufficient to cause disease.
4. Foodborne outbreaks are most common.
5. Outbreaks occur in day-care centers and similar institutions where fecal-oral
transmission is hard to control. Very common in children <10 years old.

Front 35

In shigella, what is disease limited to? What does it invade?

Back 35

1. Disease is limited to the GI tract.
2. Organism invades mucosal cells of the distal ileum and colon; inflammation and
ulceration occurs, but organisms rarely enter bloodstream.

Front 36

Describe the clinical findings of shigella.

Back 36

1. dysentery (bloody diarrhea)
2. incubation is 1-4 days. starts as watery diarrhea and may turns bloody and w/ mucus
3. severity depends on age and preexisiting conditions (younger age and elderly have more severe).

b. S. dysenteriae causes the most severe disease; usually occurs in developing
countries or in travelers to these areas.
c. S. sonnei causes a milder disease and is the most common cause of disease in the
U.S.
d. Diarrhea is usually self-limiting within 2-3 days.
e. No protective immune response is generated.

Front 37

How can Shigella be diagnosed in the lab?

Back 37

1. Isolation of organism from stool.
2. Shigella form non-lactose-fermenting colonies on MacConkey agar (colorless).
3. Slide agglutination tests are done to confirm identification.

Front 38

How is Shigella treated?

Back 38

1. Supportive treatment usually sufficient: fluids and electrolytes to prevent dehydration.
2. Antibiotics may be given for severe cases, but resistance is a problem.
3. Prevention depends on interrupting fecal-oral route of transmission; there is no vaccine
or recommended prophylaxis.

Front 39

Describe structure, transmission, clnical findings, lab diagnosis and treatment of Proteus

Back 39

A. Important Properties/Structure
1. Many species are motile and “swarm” on agar plates.

B. Epidemiology and Transmission
1. Proteus species are found in the soil and water, and as part of the normal flora of
humans in the colon.

C. Clinical Findings
1. Very common cause of UTIs, especially P. vulgaris and P. mirabilis.
2. Also cause pneumonia, wound infections, septicemia.

D. Laboratory Diagnosis
1. Swarm on agar plates—hard to isolate colonies.
2. Isolation in culture; non-lactose fermenting colonies on MacConkey agar.
3. Urease-positive.

E. Treatment and Prevention
1. Treat with antibiotics.
2. No specific preventative measures, but catheter care and prompt removal in
hospitalized patients helps.

Front 40

Describe the structure, transmission, pathogenesis, lab diagnosis of vibrio cholerae

Back 40

A. Important Properties/Structure
1. Curved, comma-shaped.
2. Facultative anaerobe.

B. Epidemiology and Transmission
1. Acquired by ingestion of water or food contaminated with human feces (usually).
2. Humans in incubation or convalescence periods often excrete organisms
asymptomatically.
3. Outbreaks occur under conditions of overcrowding, poor sanitation, malnutrition, etc.

C. Pathogenesis and Immunity
1. Disease requires ingestion of large numbers of organisms, e.g 109 (sensitive to gastric
acid).
2. Organisms secrete a mucinase that helps them adhere to the cells in the brush border
of the gut.
3. Once organisms have colonized, they secrete an enterotoxin, an A-B exotoxin that
mediates the persistent stimulation of adenylate cyclase, resulting in loss of fluid and
electrolytes from cells.
4. Genes for the cholera toxin and other virulence factors are carried on a lysogenic
phage.

D. Clinical Findings
1. Large volumes of watery diarrhea; “rice water stool”. No blood or white bloo

Front 41

What is the treatment for vibrio cholera?

Back 41

1. Rapid, adequate fluid and electrolyte replacement is critical.
2. Antibiotic treatment usually not necessary.
3. There are 2 vaccines for cholera licensed for use in many countries, but not used in the
U.S.
a. Dukoral is an oral, killed whole-cell vaccine (01 strain) given with the nontoxic B
subunit of cholera toxin; it is licensed for use in the U.S., but is not routinely
recommended for most travelers because protection is incomplete and short-lived.
Travelers at risk are advised to take precautions and carry packets of oral
Rehydration salts if they will not have access to medical care. This vaccine is
also approved for use in the U.S. for protection against travelers’ diarrhea due to
ETEC.
b. Shanchol is an oral, bivalent (01 and 0139 strains), killed, whole-
cell vaccine licensed in India.

Front 42

Describe the structure, transmission, pathogensis, clinical findings, lab diagnosis and treatment of Campylobacter jejuni

Back 42

A. Important Properties/Structure
1. Curved, comma- or S-shaped.
2. Microaerophilic; grows well at 420C

B. Epidemiology and Transmission
1. Acquired by ingestion of water or food contaminated with animal feces. Domestic
animals, including cattle, chickens, and dogs are the source of organisms for humans.
2. Major cause of diarrhea in U.S.—more cases than Shigella or Salmonella.

C. Pathogenesis and Immunity
1. C. jejuni causes enterocolitis, but the mechanisms of pathogenesis are not well
understood.
2. No toxin has been identified; invasion does occur.

D. Clinical Findings
1. Enterocolitis begins with foul-smelling diarrhea, followed by bloody stools with fever and
severe abdominal pain.

E. Laboratory Diagnosis
1. Isolation of organism in culture; characteristic morphology by Gram staining;
MacConkey agar is not used.
2. Oxidase-positive, sensitive to nalidixic acid; urease-negative.

F. Treatment and Prevention
1. Treat with antibiotics.
2. No vaccine; prevent with good hygiene, fo

Front 43

Describe the structure, transmission, pathogensis, clinical findings, lab diagnosis and treatment of Helicobacter pylori

Back 43

A. Important Properties/Structure
1. Curved rods.

B. Epidemiology and Transmission
1. Present in the stomach of many people; probably acquired by ingestion, but has not
been isolated from food, water, stool or animals. Clustering of infection is observed in
families, suggesting person-to-person transmission.

C. Pathogenesis and Immunity
1. H. pylori attaches to mucus-secreting cells of the gastric mucosa.
2. This organism produces urease which breaks down urea and produces ammonia.
Ammonia neutralizes gastric acid and favors survival of the organism.
3. Ammonia production and inflammation results in damage to the mucosa and
predisposition to gastritis and peptic ulcers.
4. No bacteremia or disseminated disease occurs.

D. Clinical Findings
1. Carriage of H. pylori occurs and is usually asymptomatic, but gastritis and peptic ulcers
can result, if prolonged.

E. Laboratory Diagnosis
1. Gram staining of biopsy from gastric mucosa.
2. Isolation in culture.
3. Urease-positive (Campylobacter is

Front 44

Describe structure, transmission, pathogenesis, clinical finding, lab diagnosis and treatment of Klebsiella pneumoniae

Back 44

V. Klebsiella pneumoniae
A. Important Properties/Structure
1. Encapsulated.

B. Epidemiology and Transmission
1. Found in the respiratory tract of ~10% of healthy people.
2. Causes disease most often in people with predisposing conditions, including the elderly,
people with chronic respiratory disease, diabetes, or alcoholism.

C. Pathogenesis and Immunity
1. Anti-phagocytic capsule is an important virulence factor.


D. Clinical Findings
1. K. pneumoniae pneumonia is characterized by a thick, bloody sputum (“currant jelly”); can
progress to necrosis and formation of abscesses.

E. Laboratory Diagnosis
1. Isolation in culture; lactose fermenting colonies on MacConkey agar.
2. Biochemical tests to differentiate species.

F. Treatment and Prevention
1. Treatment with antibiotics; susceptibility testing is important.
2. No vaccine.