30- Enterobacteriaceae

Question 1

What are enteric bacteria?

Answer 1

a. Enteric bacteria are the bacteria of the intestines. It refers to both the normal flora of the intestines that do not cause any harm, as well as the pathogenic bacteria of the intestines.

Question 2

FIl in the chart

Answer 2

Question 3

What is an endotoxin?

Answer 3

a. Endotoxin is a virulence factor that all the enterobacteriacae share. The activity of the toxin depends on lipid A component of LPS, which is released at cell lysis.

Question 4

What is the type III sectretion system?

Answer 4

It’s an effector system for delivering their virulence factors into targeted eukaryotic cells. It’s like a molecular syringe consisting of approximately 20 proteins that facilitate secretion of bacterial virulence factors when the bacteria comes into contact with the host cells.

Question 5

What genera have the type III secretion system?

Answer 5

Yersina, Salmonella, Shigella, Eschericia, Pseudomonas, Chlamydia.

Question 6

What is the function of siderophores?

Answer 6

a. These are iron-chelating compounds secreted by bacteria to free the iron that is bound by transferrin or lactoferrin of eukaryotic cells. The iron is an essential growth factor required by bacteria.

Question 7

What is enteritis?

Answer 7

inflammation of the small intestine. Symptoms include abdominal pain, cramping, diarrhea, dehydration and fever.

Question 8

What is septicemia?

Answer 8

bacteria in the blood. Often occurs with severe infections.

Question 9

What is enteric fever?

Answer 9

this is also called “typhoid fever.” Involves diarrhea and a rash, and most commonly due to an infection of Salmonella typhi.

Question 10

What is an urban plague?

Answer 10

maintained in rat populations and is spread among rats. It can also be spread to humans from rats through a flea vector. Easy to control because you can control rat populations.

Question 11

What is an sylvatic plague?

Answer 11

difficult to eliminate because mammalian reservoirs and flea vectors are widespread. Infections occur with contact of the reservoir populations.

Question 12

ETEC- diseases

Answer 12

Traveler’s diarrhea; infant diarrhea in developing countries

Question 13

ETEC- virulence factors

Answer 13

Heat-labile toxin (LT-1); Heat-stable toxin (STa)

Question 14

ETEC- clinical presentation

Answer 14

watery diarrhea, vomiting, cramps, nausea, low-grade fever

Question 15

ETEC- epidemiology

Answer 15

Fecal-oral of contaminated food or water

Question 16

ETEC- pathogenesis

Answer 16

1. LT-1 is similar to the cholera toxin and has the same pathogenesis. A-B toxin that is structurally and functionally similar to the heat-labile enterotoxin of E. coli. A ring of 5 identical B subunits binds with the host glycoprotein, A subunit is internalized and interacts with G proteins. This increases cAMP in the cells and hypersecretion of water and electrolytes 2. STa binds to membrane guanylate cyclase receptors, leading to an increase in cGMP. This causes a hypersecretion of fluids.

Question 17

EPEC- diseases

Answer 17

Infant diarrhea in underdeveloped countries

Question 18

EPEC- virulence factors

Answer 18

Adhesions: Bundle-forming pili (Bfp); intimin

Question 19

EPEC- clinical presentation

Answer 19

watery diarrhea and vomiting, nonbloody stools

Question 20

EPEC-epidemiology

Answer 20

Person-person, fecal-oral

Question 21

EPEC- pathogenesis

Answer 21

Plasmid-mediated attachment histopathology with disruption of normal microvillus structure, resulting in malabsorption and diarrhea

Question 22

EHEC- diseases

Answer 22

Hemmoragic colitis, Hemolytic uremic system (HUS)

Question 23

EHEC- virulence factors

Answer 23

Shiga toxins

Question 24

EHEC- clinical presentation

Answer 24

Initial watery diarrhea followed by grossly bloody diarrhea (hemorrhagic colitis) with abdominal cramps; little or no fever; may progress to renal failure (HUS)

Question 25

EHEC- epidemiology

Answer 25

Comsumption of undercooked meat, water, underpasturized milk or fruit juices, and undercooked veggies and fruit. Fecal-oral, person-person

Question 26

EIEC- diseases

Answer 26

Disease in developing countries

Question 27

EIEC- virulence factors

Answer 27

Invasive plasmid antigen (Ipa)

Question 28

EIEC- clinical presentation

Answer 28

Fever, cramping, watery diarrhea; may progress to dysentery with scant, bloody stools. Similar to Shigella

Question 29

EIEC- epidemiology

Answer 29

Fecal-oral of contaminated food or water

Question 30

EIEC- pathogenesis

Answer 30

Plasmid-mediated invasion and destruction of epithelial cells lining colon

Question 31

Shigella- diseases

Answer 31

most common form of disease is gastroenteritis (shigellosis); severe form of disease is caused by S. dysenteriae (bacterial dysentery)

Question 32

Shigells- virulence factors

Answer 32

Shiga toxins

Question 33

Shigella- clinical presentation

Answer 33

Shigellosis- an initial watery diarrhea progressing within 1 to 2 days to abdominal cramps, tenesmus, bloody stools with pus. HUS

Question 34

Shigella- epidemiology

Answer 34

fecal-oral, person-person

Question 35

Shigella- pathogenesis

Answer 35

The Shiga toxin has 1 A subunit and 5 B subunits. The B subunit binds to the host cell glycolipid and facilitates transfer of the A subunit into the cell. The A subunit disrupts protein synthesis in the host cell and damages the host cell.

Question 36

Salmonella- diseases

Answer 36

S. Typhi- Typhoid fever, Nontyphoidal-gastroenteritis

Question 37

Salmonella- clinical presentation

Answer 37

Typhoidal- fever, headache, rose-spots, constipation, shock. Non-typhoidal- nausea, vomiting, nonbloody diarrhea.

Question 38

Salmonella- epidemiology

Answer 38

Typhi by fecal-oral. Nontyphoidal by reptiles and uncooked poultry, eggs and dairy products.

Question 39

Salmnonella- pathogenesis

Answer 39

Attach to the mucosa of the small intestine and invade into the M cells in the Peyer patches. Don't lyse the cell, just trigger immune response. Both strains increase cAMP.

Question 40

Yersinia- diseases

Answer 40

Bubonic plague and pneumonic plague (Y. pestis), gastroenteritis by other strains

Question 41

Yersinia-virulence factors

Answer 41

Antiphagocytic protein capsule, plasminogen activator (Pla) protease

Question 42

Yersinia- clinical presentation

Answer 42

Bubonic plague- high fever, bubo (swollen lymph nodes) in groin or axilla, bacteremia. Pneumonic plague- fever, mailaise, pulmonary signs. Gastroenteritis- diarrhea, fever, abdominal pain, pseudoappendicitis.

Question 43

Yersinia- epidemiology

Answer 43

Bubonic- Zoonotic infection from rodents, transmitted by flea bites or direct contact with infected tissues. Pneumonic- person-person by inhalation of infectious aerosols from a patient with pulmonary disease. Gastroenteritis- fecal-oral

Question 44

Yersinia- pathogenesis

Answer 44

The protein capsule allows evasion of phagocytosis. Pla degrades complement components C3b and C5a, which prevents opsonization and phagocytic migration.

Question 45

Klebsiella- diseases

Answer 45

Lobar pneumonia (K. pneumoniae and K. oxytoca). Granuloma inguinale/Donovanosis (K. granulomatis)

Question 46

Klebsiella- virulence factors

Answer 46

Prominent capsule

Question 47

Klebsiella- clinical presentation

Answer 47

Lobar: Necrotic destruction of alveolar spaces, formation of cavities, production of blood-tinged sputum Donovanosis: subcutaneous nodules on genitalia

Question 48

Klebsiella- epidemiology

Answer 48

Donovanosis: STD

Question 49

Proteus- diseases

Answer 49

Urinary tract infections (P. mirabilis)

Question 50

Proteus- virulence factors

Answer 50

Urease

Question 51

Proteus- clinical presentation

Answer 51

Kidney stones

Question 52

Proteus- pathogenesis

Answer 52

Urease splits urea into CO2 and urea, which raises the urine pH. This precipitates Mg and Ca in the form of struvite and apatite crystals --\> kidney stones.