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Enterbacteriaceae Flashcards

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Biology 101 flashcards
1
Q

Enterobacteriaceae

E. Coli (Shiga toxin producing) aka enterohemorrhagic E. Coli

Gram:
shape:
invasion type:
epidemiology:
serology:
clinical manifestation:
treatment:
testing:
virulence factor:
A

Gram: Neg
Shape: Short thick rods, peritrichous (spread all over) flagella.
Hardiness: Survives gastric acid, intestinal motility, normal flora, mucosal immunity (IgA), and inflammation from phagocytes/ complement
Testing: Oxidase NEG
Epidemiology: Lives in intestine, oral/fecal transmission
Feces, Fingers, Flies, Food (and water). Screws up water quality and food sanitation
Mode of action: Attaches enterocytes and M cells (trancytosis of antigens to underlying lymphoid tissue….pathogens use these m cells to hitch ride out of the intestine)

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2
Q

Vibrio cholerae

Gram:
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virulence factor
A

Gram: Neg
Shape: curved rods
invasion type: non invasive
epidemiology:
serology: O1 caused outbreaks 1 to 6. O139 did pandemic 7
clinical manifestation: massive diarrhea…death by loss of fluid/salts
treatment: oral hydration therapy + tetracycline or ampicillin)
testing: blood/chocolate/macconkey/tcbs agar plate (plate is green…virbrio cholera growth on it turns it yellow)
virulence factor: cholera toxin made of AB5 subunits. (subunit = enzymatically active and actually enters the cell. B subunit bindes to enterocyte, mediating endocytosis into the cell. A subunit activates Adenylate cyclase, increases cAMP, which pumps Cl- into the lumen and causes diarrhea). Otherwise, other virulence factors include the the toxin coregulated pilus (type IV), which mediates attachment to the endothelium

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3
Q

Escherichia coli (Enterotoxigenic)

Gram:
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A

Gram: Neg
shape: Rods
invasion type: Type III secretion
epidemiology:
serology:
clinical manifestation: Traveler’s diarrhea..those who live in the area are immune, but those visiting in the new area are subject to the illness
treatment:
testing:
virulence factor: Similar to vibrio cholera. adhere to intestinal mucosa enterocytes via pili, but uses 2 exotoxins (heat sensitivity distinguishes them): Labile toxin (like cholera toxin, but in smaller amounts) and Stable toxin: gut peptide hormone analogue that stimulates gGMP coupled receptors. Increase cAMP or cGMP = increase in diarrhea. No where near as severe as Vibrio cholera.
In addition: type III secretion system export proteins to cytosol of enterocyte, causing cytoskeleton rearrangement, and removing the brushborder. Pedastals are created

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4
Q

Shigella (flexneri (most virulent, least common), boydii, sonnei (least virulent, most common))..only difference between the 4 is the O antigen

Gram:
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Gram: Neg
shape: Rod. Virtually identical genetically to E. coli
invasion type: Trancytosis by M cells. Invades and kills cells of intestinal mucosa enterocytes. Uses Type III system. bacteria works by lysing phagocytic vacuole and entering the cytosol of the enterocyte, instead of staying outside like E. coli enteropathogenic). When actin is produced inside cell through Type III, it pushes bacteria through plasma membrane into adjacent cells. Spreads infections laterally
epidemiology: Humans only (person to person, never animal to person)
serology:
clinical manifestation: frequent, painful, low-volume stools containing blood, wbcs, mucus…note abdominal cramps
treatment:
testing:
virulence factor: Shiga toxin (AB5 structure). A subunit cleaves RNA of large ribosomal subunit, rendering ribosome inactive. Systemically, can lead to hemolytic-uremic synderom (HUS), which is microvascular damage in kidney + rbc lysis

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5
Q

E. Coli (Shiga toxin producing) aka enterohemorrhagic E. Coli

Gram:
shape:
invasion type:
epidemiology:
serology:
clinical manifestation:
treatment:
testing:
virulence factor:
A

Gram: Neg
shape: rod
invasion type:
epidemiology: Principally found in cattle. leads to outbreaks from fecal contamination of hamburgers, ice cream, apple cider, and water
serology:
clinical manifestation: bloody diarrhea. Inflammatory enteritis, hemmorrage.
treatment:
testing: Sorbitol neg. on sorbitol-MAC plate
virulence factor: verotoxin. predominantly idetified with O157:H7 serotype

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6
Q

Salmonella (non-typhoid) (named by serotype, not by genus…)

Gram:
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virulence factor:
A

Gram: Neg
shape: rod
invasion type: Exits lumen via M cells, invades enterocytes, multiplies locally. Induces macrophage apoptosis via Type III invasion system. Causes ruffling on enterocyte membrane
epidemiology: Transferred from other vertebrates to humans. Usually through eggs or meat. Can rarely come from reptiles/other pets
serology:
clinical manifestation: gastroenteritis (enterocolitis), NON BLOODY diarrhea, fever, nausea, vomiting
treatment:
testing:
virulence factor:

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7
Q

Campylobacter jejuni

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A

Gram: Neg, but Gullwing morphology
shape: Rod, curved
invasion type: Transferred from infected chicken (note that the bacteria grows best at 42 degrees C, just like chickens)
epidemiology:
serology:
clinical manifestation: Gullian Barre syndrome (ascending paralysis…acute in onset)
treatment: Antigen and molecular testing.
testing:
virulence factor: cytotoxin

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8
Q

Helicobacter (pylori)

Gram:
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A

Gram:
shape:
invasion type: Type IV (similar to type III)invasion system, which exports ctytoxin
epidemiology: Chronic infection of gastric mucosa. escapes stomach acid since it lives below mucus layer. also secretes urease, converting urea to ammonia (basic envrionment)
serology:
clinical manifestation: peptic ulcers AND MALT lymphoma (H pylori is reacting with T cells in GI tract, hence why the illness can last for years or decades). Can become malignant. in cases of chronis infection/inflammation (stomach cancer, gastric lymphoma develops)
treatment: surgery, stress relief, antacids. Can use antibiotics + bismuth salt (pepto-bismol) + proton pump inhibitor to reduce gastric acid and speed up healing
testing: Diagnose with gastric biopsy or breath test to see presence of ammonia (since pylori has urease). can also use stool antigen assays
virulence factor:

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9
Q

Salmonalla typhi

Gram:
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A

Gram: Neg
shape: Rod. HAS A CAPSULE, type Vi (virulence)
invasion type:
epidemiology: Human to human transfer. penetrates M cells, and DOES NOT cause macrophage apoptosis. Multiplies inside phagocytic vacuole, spreads throughout body. Cultured from blood/bone marrow. Can lead to chronic carrying in person’s gallbladder, and can shed salmonella for years. Colonizes int heir gall bladder
serology:
clinical manifestation:
treatment:
testing:
virulence factor: HAS A CAPSULE, type Vi (virulence)

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10
Q

Yersinia enterocolictica/ Yersinia pseudotuberculosis

A

Gram: Neg
shape: Rod
invasion type: Type III, translocates proteins that inhibit phagocytosis
epidemiology: Resides in local lymph nodes of intestine. Grows at 4 degrees C. (refrigerated food like milk or BLOOD PRODUCTS)
serology:
clinical manifestation: Painful inflammation of lymph nodes. Mimics appendicitis
treatment:
testing:
virulence factor:

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11
Q

E. coli. (UTI)

Gram:
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invasion type:
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A 
Gram: Neg
shape: rod
invasion type:
epidemiology:
serology:
clinical manifestation: UTI's and systitis. Note urgency, freq, and painful urination (dyuria)
treatment:
testing:
virulence factor: P fimbrae...bacteria adhere specifically to urinary tract transitional epithelium
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12
Q

E. coli (K1)

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A 
Gram Neg
shape: rod
invasion type:
epidemiology: Neonatal infections
serology:
clinical manifestation: spesis and meningitis
treatment:
testing:
virulence factor: S. fimbra, which attaches to endothelium, choroid plexus. Also has K1 capsule, which is not immunogenic, resemble the host (how it evades immune system), and does not activate complement. Acquires iron from host.
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13
Q

Haemophilus influenzae

Gram:
shape:
invasion type:
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virulence factor:
A

Gram: Neg
shape: Rod, slender and pleiomorphic (not all the same size or shape)
invasion type:
epidemiology: Grows only in NAD (V) and hemin (X), only found in chocolate agar. Without these guys, it WILL NOT grow. Only colonizes and infects humans. Those encapsulated spread disease through coughing, sinusitis, sever upper respiratory tract infections, pneumonia, meningitis, septic arthritis, OTITIS MEDIA, acute hypozia
serology:
clinical manifestation: respiratory tract colonization and infections. ear infections.Respiratory
treatment: HiB conjugate vaccine (given to all kiddies at 2 months of age. )
testing:
virulence factor: Capsule (when present..normally not) (type B), IgA protease, Fe acquisition mechs. 25% pf haemophilus influenza produces beta-lactamsse, which resists ampicillin. All susceptible to cephalosporins (cefotaxime)

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14
Q

Haemophilus ducreyi

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A 
Gram: Neg
shape: Rod , school of fish gram stain morphology
invasion type:
epidemiology:
serology:
clinical manifestation: chancroid (genital infection)
treatment:
testing:
virulence factor:
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15
Q

Bordetella pertussis

Gram:
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virulence factor:
A

Gram: Neg
shape: rod
invasion type:
epidemiology: Only colonizes and infects humans. Lives short period of time in environment. Poor growth, small colonies on blood agar. Spread via respiratory route, 2 week incubation. Found in the kiddies
serology:
clinical manifestation: WHOOPING COUGH, followed by vomiting, cyanosis, convulsions
treatment: take s 4 to 6 weeks to clear. otherwise, use DDTwP (Dipheria, tetanus, whole cell pertussis) vaccine, but tend to use acellular version (DTaP)
testing: NAAT
virulence factor: adhesins…promotes attachment and prevents clearance by phagocytes. Uses:
1. filamentous hemagglutinin (binds integrins on ciliated epithelial cells)
2. fimbriae (phase variation..even after immune system recognizes it)
3. BrkA (resists complement), tracheal
4. Tracheal cytotoxin (stimulates IL-1 mediated killing of ciliated epithelial cells.)
5. Adenylatescyclase toxin (inhibits phagocyte function)
6. pertussis toxin (effects LYMPHOCYTES, sensitization to histamine and enhanced insulin secretion)

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16
Q

Legionella pnemonphila

Gram:
shape:
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virulence factor:
A

Gram: neg
shape: slender rod
invasion type:
epidemiology: Transmitted from environment to people. Naturally in warm water. Multiplies in protozoa (amoebae) hosts, and in macrophages (blocking phagocytic and lysosome funciton). Exposure is usually from
serology:
clinical manifestation: Respiratory. Pontiac fever, in lesser form
treatment: Hyperchlorination and high heat control its growth
testing: Highly fastidious, but will grown in BYCE (buffer, charcoal, yeast extract) with Iron, cysteine, and antibiotics agar. Use Urine Ag test to locate serotype 1 infection. Also do a direct fluorescent antibody stain.
virulence factor:

17
Q

Zoonoses

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virulence factor:
A

Transmitted from animals directly or by insect

Gram: Neg
shape: cocci bacillus (shape between a rod and a coccus)
invasion type:
epidemiology: multiplies in phagocytes
serology:
clinical manifestation:
treatment:
testing:
virulence factor:
18
Q

Brucella species (zoo)

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A 
Gram: Neg
shape: coccobacillus
invasion type:
epidemiology: Travels via livestock, unpasteurized dairy
serology:
clinical manifestation: systemic febrile illness. Likely laboratory worker subjection
treatment:
testing:
virulence factor:
19
Q

Pasteurella multocida (zoo)

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A

Gram: Neg
shape: cocobacillus
invasion type:
epidemiology: Lives in normal oral flora of domestic animals (cats, dogs). Infections caused by animal bites.
serology:
clinical manifestation: snuffles in rabbits, rapidly progressive soft tissue infection
treatment: antibiotics are pretty effective
testing:
virulence factor:

20
Q

Francisella tularensis (zoo)

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A 
Gram: Neg
shape: coccobacillus
invasion type:
epidemiology: Transmitted by wild animals, such as rabbits, by direct contact or through insects. Seen mainly in central US. Highly infectious, and is a high risk to laboratory workers.
serology:
clinical manifestation:
1. Ulceroglandular (ulcer at site of infection)
2. Oculogladular
3. oral or pharyngeal
4. Respiratory infections
treatment:
testing:
virulence factor:
21
Q

Yersinia pestis (zoo)

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A

Gram: Neg
shape: rod…looks like a safety pin
invasion type:
epidemiology: Spread from rodents to humans via flea bite. Need travel history in order to get this diagnosis. Specifically ingests blood in the flea gut. When the flea feeds on human, it is sent back out to host. Multiplies in lymph nodes which become enlarged (buboes). Spreads to blood, lungs, and meninges of the human
serology:
clinical manifestation: Bubonic plague, pneumonic plague if present in the lungs, leading to human-human transmission
treatment:
testing: Wayson stain, but grows in a variety of media. use NAAT test.
virulence factor: Capsule, iron acquisition, phagocyte paralysis

22
Q

Pseudomonas aeruginosa

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Antibiotics:
Aerobicity:
A

Gram: Neg
shape: rod, has flagella
invasion type: Type III
epidemiology: Opportunistic. Found everywhere in environment (rocks, soil, vegetation) in biofilms (complex structure where bacteria adheres to surface and forms 3d structure. Bacteria is heterogenious in metabolic activity between those closer to outside and these on inside of biofilm). Found mostly in patients with cystic fibrosis (dumb hard to get rid of in these patients)
serology:
clinical manifestation otitis externa, sever infection in burn victims, further screws up cystic fibrosis, screws up intubated people, and can cause hot tub folliculitis
treatment:
testing:
virulence factor: Extracellular polysach, pili, LPS, extracellular enzymes, exotoxin A, and Type III seceetion system
Antibiotics: very resistant
Aerobicity: Obligate oxidizer, no acids from sugars on test media. Produces siderophores (pyoverdin)

Microbiology (11 decks)

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