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Microbiology > 30- Enterobacteriaceae > Flashcards

30- Enterobacteriaceae Flashcards

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Biology 101 flashcards
1
Q

What are enteric bacteria?

A

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.

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2
Q

FIl in the chart

A
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3
Q

What is an endotoxin?

A

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.

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4
Q

What is the type III sectretion system?

A

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.

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5
Q

What genera have the type III secretion system?

A

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

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6
Q

What is the function of siderophores?

A

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.

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7
Q

What is enteritis?

A

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

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8
Q

What is septicemia?

A

bacteria in the blood. Often occurs with severe infections.

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9
Q

What is enteric fever?

A

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

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10
Q

What is an urban plague?

A

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.

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11
Q

What is an sylvatic plague?

A

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

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12
Q

ETEC- diseases

A

Traveler’s diarrhea; infant diarrhea in developing countries

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13
Q

ETEC- virulence factors

A

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

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14
Q

ETEC- clinical presentation

A

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

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15
Q

ETEC- epidemiology

A

Fecal-oral of contaminated food or water

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16
Q

ETEC- pathogenesis

A
  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.
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17
Q

EPEC- diseases

A

Infant diarrhea in underdeveloped countries

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18
Q

EPEC- virulence factors

A

Adhesions: Bundle-forming pili (Bfp); intimin

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19
Q

EPEC- clinical presentation

A

watery diarrhea and vomiting, nonbloody stools

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20
Q

EPEC-epidemiology

A

Person-person, fecal-oral

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21
Q

EPEC- pathogenesis

A

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

22
Q

EHEC- diseases

A

Hemmoragic colitis, Hemolytic uremic system (HUS)

23
Q

EHEC- virulence factors

A

Shiga toxins

24
Q

EHEC- clinical presentation

A

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

25
Q

EHEC- epidemiology

A

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

26
Q

EIEC- diseases

A

Disease in developing countries

27
Q

EIEC- virulence factors

A

Invasive plasmid antigen (Ipa)

28
Q

EIEC- clinical presentation

A

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

29
Q

EIEC- epidemiology

A

Fecal-oral of contaminated food or water

30
Q

EIEC- pathogenesis

A

Plasmid-mediated invasion and destruction of epithelial cells lining colon

31
Q

Shigella- diseases

A

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

32
Q

Shigells- virulence factors

A

Shiga toxins

33
Q

Shigella- clinical presentation

A

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

34
Q

Shigella- epidemiology

A

fecal-oral, person-person

35
Q

Shigella- pathogenesis

A

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.

36
Q

Salmonella- diseases

A

S. Typhi- Typhoid fever, Nontyphoidal-gastroenteritis

37
Q

Salmonella- clinical presentation

A

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

38
Q

Salmonella- epidemiology

A

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

39
Q

Salmnonella- pathogenesis

A

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.

40
Q

Yersinia- diseases

A

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

41
Q

Yersinia-virulence factors

A

Antiphagocytic protein capsule, plasminogen activator (Pla) protease

42
Q

Yersinia- clinical presentation

A

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.

43
Q

Yersinia- epidemiology

A

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

44
Q

Yersinia- pathogenesis

A

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

45
Q

Klebsiella- diseases

A

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

46
Q

Klebsiella- virulence factors

A

Prominent capsule

47
Q

Klebsiella- clinical presentation

A

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

48
Q

Klebsiella- epidemiology

A

Donovanosis: STD

49
Q

Proteus- diseases

A

Urinary tract infections (P. mirabilis)

50
Q

Proteus- virulence factors

A

Urease

51
Q

Proteus- clinical presentation

A

Kidney stones

52
Q

Proteus- pathogenesis

A

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.

Microbiology (35 decks)

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