30- Enterobacteriaceae Flashcards
What are enteric bacteria?
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.
FIl in the chart
What is an endotoxin?
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.
What is the type III sectretion system?
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.
What genera have the type III secretion system?
Yersina, Salmonella, Shigella, Eschericia, Pseudomonas, Chlamydia.
What is the function of siderophores?
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.
What is enteritis?
inflammation of the small intestine. Symptoms include abdominal pain, cramping, diarrhea, dehydration and fever.
What is septicemia?
bacteria in the blood. Often occurs with severe infections.
What is enteric fever?
this is also called “typhoid fever.” Involves diarrhea and a rash, and most commonly due to an infection of Salmonella typhi.
What is an urban plague?
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.
What is an sylvatic plague?
difficult to eliminate because mammalian reservoirs and flea vectors are widespread. Infections occur with contact of the reservoir populations.
ETEC- diseases
Traveler’s diarrhea; infant diarrhea in developing countries
ETEC- virulence factors
Heat-labile toxin (LT-1); Heat-stable toxin (STa)
ETEC- clinical presentation
watery diarrhea, vomiting, cramps, nausea, low-grade fever
ETEC- epidemiology
Fecal-oral of contaminated food or water
ETEC- pathogenesis
- 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.
EPEC- diseases
Infant diarrhea in underdeveloped countries
EPEC- virulence factors
Adhesions: Bundle-forming pili (Bfp); intimin
EPEC- clinical presentation
watery diarrhea and vomiting, nonbloody stools
EPEC-epidemiology
Person-person, fecal-oral
EPEC- pathogenesis
Plasmid-mediated attachment histopathology with disruption of normal microvillus structure, resulting in malabsorption and diarrhea
EHEC- diseases
Hemmoragic colitis, Hemolytic uremic system (HUS)
EHEC- virulence factors
Shiga toxins
EHEC- clinical presentation
Initial watery diarrhea followed by grossly bloody diarrhea (hemorrhagic colitis) with abdominal cramps; little or no fever; may progress to renal failure (HUS)
EHEC- epidemiology
Comsumption of undercooked meat, water, underpasturized milk or fruit juices, and undercooked veggies and fruit. Fecal-oral, person-person
EIEC- diseases
Disease in developing countries
EIEC- virulence factors
Invasive plasmid antigen (Ipa)
EIEC- clinical presentation
Fever, cramping, watery diarrhea; may progress to dysentery with scant, bloody stools. Similar to Shigella
EIEC- epidemiology
Fecal-oral of contaminated food or water
EIEC- pathogenesis
Plasmid-mediated invasion and destruction of epithelial cells lining colon
Shigella- diseases
most common form of disease is gastroenteritis (shigellosis); severe form of disease is caused by S. dysenteriae (bacterial dysentery)
Shigells- virulence factors
Shiga toxins
Shigella- clinical presentation
Shigellosis- an initial watery diarrhea progressing within 1 to 2 days to abdominal cramps, tenesmus, bloody stools with pus. HUS
Shigella- epidemiology
fecal-oral, person-person
Shigella- pathogenesis
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.
Salmonella- diseases
S. Typhi- Typhoid fever, Nontyphoidal-gastroenteritis
Salmonella- clinical presentation
Typhoidal- fever, headache, rose-spots, constipation, shock. Non-typhoidal- nausea, vomiting, nonbloody diarrhea.
Salmonella- epidemiology
Typhi by fecal-oral. Nontyphoidal by reptiles and uncooked poultry, eggs and dairy products.
Salmnonella- pathogenesis
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.
Yersinia- diseases
Bubonic plague and pneumonic plague (Y. pestis), gastroenteritis by other strains
Yersinia-virulence factors
Antiphagocytic protein capsule, plasminogen activator (Pla) protease
Yersinia- clinical presentation
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.
Yersinia- epidemiology
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
Yersinia- pathogenesis
The protein capsule allows evasion of phagocytosis. Pla degrades complement components C3b and C5a, which prevents opsonization and phagocytic migration.
Klebsiella- diseases
Lobar pneumonia (K. pneumoniae and K. oxytoca). Granuloma inguinale/Donovanosis (K. granulomatis)
Klebsiella- virulence factors
Prominent capsule
Klebsiella- clinical presentation
Lobar: Necrotic destruction of alveolar spaces, formation of cavities, production of blood-tinged sputum Donovanosis: subcutaneous nodules on genitalia
Klebsiella- epidemiology
Donovanosis: STD
Proteus- diseases
Urinary tract infections (P. mirabilis)
Proteus- virulence factors
Urease
Proteus- clinical presentation
Kidney stones
Proteus- pathogenesis
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.
