Micro Made Simple Chapter 9 Enterics

Front 1

What are enterics?

Back 1

Gram negative bacteria. Part of the normal intestinal flora OR cause GI disease.

Usually the genus name is enough since there are so many different species within each genus:

Front 2

Main groups (genus) of the enterics

Back 2

1. Enterobacteriaceae
2. Vibrionaceae
3. Pseudomonoadacaea
4. Bacteriodaceae

These organisms are also divided into groups based upon biochemical and antigenic properties.

Front 3

Biochemical classification of enteric organisms biochemically.

Back 3

1. Ability to ferment lactose- and convert to gas (which can be visualized with a dye that changes color with pH). E.coli and most of the enterobacteriaceae ferment lactose while SSS (Salmonella, Shigellak, and pSeudomonas aeruginosa) DO NOT!

2. The production of H2S, ability to hydrlyze urea, liquefy gelatin, and decarboxylate specific amino acids. (the first of these being the one we need to know)

IF YOU KNOW NOTHING ELSE KNOW THIS:

Some growth media kill 2-birds w/one stone: 1)They contain chemicals that inhibit growth of gram + bacteria that may be contaminants 2) They have indicators that change color when lactose ferments.

KNOW THESE 2 MEDIA:
1) EMB agar (Eosine Methylene Blue): inhibits gram+ bacteria, and colonies of lactose fermenters become deep purple to black in this medium. E. coli takes on a metallic green sheen.

2. MacConkey agar: Bile salts in the medium inhibit gram+ bacteria, and lactose fermenters develop a pink-purple coloration

Front 4

MacConkey agar

Back 4

MacConkey agar: Bile salts in the medium inhibit gram+ bacteria, and lactose fermenters develop a pink-purple coloration

Front 5

When working in Uruguay w/ many cases of diarrhea from patients drinking from a common water supply, you suspect the water is contaminated with E.coli. How might you prove the water is fecally contaminated?

Back 5

E. coli is coliform= colon (normal GI inhabitant). E. coli contamination in water proves fecal contamination, but not necessarily that e. coli is the agent causing diarrhea.

Run the following tests:
1. (presumptive test) Add river water to test tubes containing nutrient broth that contains LACTOSE. An inverted vial above the tubes collect gas and dye indicator that changes color if acid production ocurrs. Tubes w/ color changes suggest that water has e.coli or non-enteric bacteria.

2.(confirmed test) Streak EMB (eosine methylene blue) agar w/ water samples. E. coli should form colonies with metal green sheen. E. coli can grow at 45.5oc.

3. (completed test): Colonies that were metallic green are placed in broth again. If they produced acid and gas, then you know the river water contains e. coli.

Front 6

3 major surface antigens of enterics

Back 6

Antigenic determinants are cell surface structures that bind antibodies).

1. O antigen: most external component of LPS of gram (-) bacteria. The O antigen differs from organism to organism. depending on different sugars and different side-chain substitutions.
Remember "O for outer"

2. K antigen: This is a capsule (Kapsule) that covers the O antigen

3. H antigen: this antigenic determinant makes up the subunits of the bacterial flagella, so only bacteria that are motile will possess this antigen.

SHIGELLA (no H antigen)

SALMONELLA (has H that changes from time to time)

Front 7

Pathogenesis of enterics

Back 7

2 types of diseases:

1. Diarrhea with or without systemic invasion
2. Various other infections: including UTI, pneumonia, bacteremia, sepsis (especially in debilitated hospitalized patients)

Front 8

Various Clinical Manifestations of Diarrhea

Back 8

1. No cell invasion: The bacteria bind to intestinal epithelial cells--do not enter cells. Diarrhea is caused by exotoxin release (called enterotoxins in GI) which cause electrolyte and fluid loss from intestinal epithelial cells or epithelial cell death. Water diarrhea wo systemic symptoms is usual. Think E.coli and Vibrio cholera.

2. Invasion of intestinal epithelial- the bacteria have virulence factors that allow binding and invasion. Toxins are released that destroy cells--> results in systemic immune response with local WBC infiltrate (leukocytes in stool) and fever. The cell death results in RBC leakage into stool. Examples: Enteroinvasive E. Coli, Shigella and Salmonella enteritidis

3. Invasion of Lymph nodes and bloodstream: Along with ab pain and diarrhea containing W and R cells, this deeper invasion results in systemic sxs: fever, headache, WBC elevation. Also mesenteric lymph enlargement, bacteremia, and sepsis.

Ex: Salmonella typhi, Yersinia enterocolitica, and cympylobacter jejuni

Front 9

E. coli and Vibrio cholera diarrhea

Back 9

Watery diarrhea w/o clinical manifestations due to exotoxin release

Front 10

Enteroinvasive E. coli diarrhea

Back 10

Invasion of intestinal epithelial- the bacteria have virulence factors that allow binding and invasion. Toxins are released that destroy cells--> results in systemic immune response with local WBC infiltrate (leukocytes in stool) and fever. The cell death results in RBC leakage into stool.

Front 11

Shigella and Salmonella enteritidis diarrhea

Back 11

Invasion of intestinal epithelial- the bacteria have virulence factors that allow binding and invasion. Toxins are released that destroy cells--> results in systemic immune response with local WBC infiltrate (leukocytes in stool) and fever. The cell death results in RBC leakage into stool.

Front 12

Salmonella typhi, yersinia, enterocolitica, and cympylobacteria can cause what type of invasion and diarrhea?

Back 12

Invasion of lymph nodes and blood stream

Front 13

Hospital-acquired gram negatives or nosocomial gram-negatives

Back 13

These are enterics that usually live with us peacefully, but in hospital, they can require antibiotic resistance and cause disease.

E. coli, Klebsiella pneumoniae, proteus mirabalis, enterobacter, serratia, and pseudoomonas aeruginosa.

Front 14

Escherichia coli

Back 14

Normally resides in colon w/o disease, but DNA is swapped via conjugation with plasmid exchange, lysogenic conversion by temperate bacteriophages, and direct transposon mediated DNA insertion).

NON-pathogenic e.coli (normal flora) + Virulence factors= DISEASE

Front 15

Escherichia Coli virulence factors:

Back 15

Virulence factors acquired via some means of genetic transfer include:

1. Mucosal interaction- mucosal adherance w/ pili (colonization factor) or ability to invade intestinal epithelial cells.

2. exotoxin production : either heat labile and stable (LT and ST) or Shiga-like toxin

3. Endotoxin: Lipid A portion of LPS.

4. Iron binding siderophore: obtains iron from human transferrin or lactoferrin.

Front 16

Diseases caused by E. coli in presence of virulence factors include:

Back 16

1. diarrhea
2. UTI
3. Neonatal meningitis
4. Gram-negative sepsis, occuring commonly in debilitated hospitalized patients

Front 17

The virulence of E. coli diarrhea depends

Back 17

Which virulence factors the strain of e.coli possesses.

Front 18

Traveler's diarrhea

Back 18

when citizens from developed countries travel they are susceptible because they haven't developed antibodies to strains of e.coli in these underdeveloped region.

Front 19

3 groups of diarrhea-producing E.coli

Back 19

The 3 groups are named according to which virulence factors and diarrheal diseases they cause.

1. Enterotoxigenic Eschericia coli (ETEC): Heat labile toxin (LT) which is cholera toxin, and heat stable toxin (ST)

2. Enterohemorrhagic E. coli (EHEC): Have a pili colonization factor like ETEC but can secrete powerful Shiga-like-toxin (AKA VEROTOXIN). can cause Hemolytic uremic Syndrome (HUS): strain O157:H7

3. Enteroinvasive E Coli (EIEC): Same as caused by Shigella. Virulence factor is encoded in a plasmid shared by shigella and e. coli. This plasmid gives the bacteria the ability to invade the epithelium.

Front 20

Enterotoxigenic E. coli (ETEC)

Back 20

1. Causes traveler's diarrhea
2. Has pili (colonization factor)--helps bind to intestinal epithelia where it releases exotoxins similar to cholera exotoxins.
3. Exotoxins are heat labile (LT)--just like cholera toxin--and heat stable toxin (ST). These exotoxins inhibit reabsorption of Na+ and Cl- and stimulate secretion of Cl- and HCO3- into lumen. Water follows pull of ions, producing watery diarrhea.

The stool looks like rice water--just like cholera!

Front 21

Enterohemorrhagic E. coli (EHEC)

Back 21

1. like ETEC, have pili colonization factor, but are distinct due to 2. Shiga-like toxin production (verotoxin)--which is just like the Shigella toxin. They inhibit protein syntehsis by inhibiting 60S ribosome, which results in intestinal epithelial cell death.

These cells grasp onto epithelial cells and shoot away with Shiga-like toxins leading to bloody (hemorrhagic) diarrhea accompanied by severe abdominal cramps, and is called hemorrhagic colitis.

3. Hemolytic uremic Syndrome (HUS) with anemia, thrombocytopenia (decrease in platelets), and renal failure (thus uremia), is associated with infxn by O157:H7. outbreaks secondary to infected hamburger meat occured suggesting EHEC reservoir in cattle.

Front 22

Enteroinvasive Escherichia coli (EIEC)

Back 22

Same as disease caused by Shigella. Main virulence factor encoded in plasmid shaEscherischia coli.

This plasmid allows bacteria to invade epithlium along w/ small production of shiga-like toxin.

The host tries to get rid of this inasion resulting in inflammatory rx with fever. WBCs invade intestinal wall, and the diarrhea is bloody with White cells (like shigellosis)!

Front 23

Vibrio cholera, echerichia coli, and shigella dysenteriae

Back 23

All are holding hands. E. coli, can causes diarrhea JUST LIKE SHIGELLOSIS AND CHOLERA, and it's impossible to tell.

The point is e. coli causes diarrhea by acquiring virulence from plasmids. If it looks like rice water it's either from cholera (or e. coli with virulence acquired from cholera--enterotoxigenic) or like shigeloosis (with diarrhea w/ wbcs and blood).

Front 24

UTIs and escherichi coli

Back 24

acquisition of pili virulence factors allow e.coli to now travel up urethra and infect:
1. bladder (cystitis)
2. Kidney (pyelonephritis)

Front 25

What is the most frequent cause of UTIs? Who gets them usually?

Symptoms?

Back 25

Escherichia coli: which usually occur in women and hospitalized patients with catheters in the urethra

Symptoms:
1. dysuria--burning on urination
2. frequency (elevated)

Front 26

E. coli meningitis

Back 26

second most common of neonatal meningitis second to group B streptococcus. Neonates especially vulnerable during 1st month of life

Front 27

E. coli sepsis

Back 27

most common cause of gram-negative sepsis. Septic shock due to lipid A of LPS (usually the cause of death)

Front 28

E. coli Pneumo

Back 28

E. coli is a common cause of hospital acquired pneumonia

Front 29

Klebsiella pneumoniae

Back 29

An enteric that is encapsulated (O antigen) but is nonmotile (no H antigen). Klebsiella is common in hospitals causing sepsis (second most common next to e. coli), UTIs (in patients with foley catheters).

Hospitalized patients and alcoholics (debilitated patients) are prone to K. pneumo pneumonia, which features bloody sputum in about 50% of cases.

This pneumonia is violent and frequently destroys lung tissue, producing cavities. Thick sputum coughed up with K. pneumoniae clasically looks like red jelly, which is the color of the O antigen capsule. Mortaility rate is high despite antibiotic therapy.

Front 30

This pneumonia is violent and frequently destroys lung tissue, producing cavities. Sputum can appear like red currant jelly.

Back 30

Pneumonia secondary to Klebsiella pneumonia.

Front 31

Proteus mirabilis

Back 31

A very motile organism. Won't grow as round colonies due to this, but as a confluence of colonies.

Since this bacteria can break down urea, it is often known as urea-splitting proteus.

3 strains cross react with Rickettsia.

Proteus can cause UTIs and nosocomial infections. The splitting of urea into NH3 and CO2 by proteus leads to alkaline urine (primarily due to ammonia content)

Front 32

3 strains of proteus mirabilis that have cross-reacting antigens with some Rickettsia.

Back 32

1. OX-19, OX-2, and OX-K. This is purely coincidental but serves as a useful tool to determine if a person has been infected with Rickettsia.

Serum is mixed with these proteus strains to determine whether there are antibodies in the serum that cross react with proteus antigens. If these antibodies are present, this suggests that the patient has been infected with Rickettsia.

Front 33

Enterobacter

Back 33

highly motile gram negative rod. (normal flora). It is occasionally responsible for hospital-acquired infections.

Front 34

Serratia

Back 34

1. Production of bright red pigment. can cause UTIs, wound infection, or pneumonia

Front 35

Shigella

Back 35

1. non-motile
2. (Shigella holds hands with e.coli) and has NO FLAGELLA!
3. Does not ferment lactose or produce H2S. So you can use this to distinguish Shigella from E.coli and Salmonella

Front 36

Shigella mediated disease

Back 36

Humans are the only host, and the dysentery it causes usually strikes preschool kids and nursing home populations.

It is not a part of flora, always a pathogen, and is transmitted in fecally contaminated water and hand-to-hand.

The disease is similar to enteroinvasive ecoli (EIEC) due to invasion and release of Shiga toxin causing cell death/destruction. White cells arrive.

Upon colonoscopy, the colon has shallow ulcers where cells have sloughed off.

Illness begins with fever (unlike ETEC and cholera which don't invade epithelia and thus don't cause a fever), abdominal pain, and diarrhea.

The diarrhea may contain flecks of bright-red blood and pus (white cells).

Patients develop diarrhea because the inflamed colond, amaged by shiga toxin, is unable to resorb fluid and electrolytes.

So Shazam Shigella with his Shiga Laser blasts the 60 S ribosome, causing epithelial cell death.

Front 37

Shiga Toxin

Back 37

Same toxin as EHEC and EIEC, and its mechanism is the same.

It's an A toxin bound to 5 B subunits.

The B subunits bind to microvillus in the colon, allowing the entry of deadly A (action) which inactivate 60S ribosome. You know the rest.

Front 38

Salmonella ("The Salmon")

Back 38

A non-lactose fermenter, is motile (like a salmon), and produces H2S.

Has a Vi antigen ( a polysaccharide capsule that surrounds the O-antigen, thus protecting the bacteria from antibody attack on the O antigen. Just like K antigen, but with Salmonella they named it Vi for virulence).

Front 39

Salmonella serotypes divided into 3 groups for convenience:

Back 39

1. salmonella typhi
2. Salmonella cholera
3. Salmonella enteritidis

named according to diseases:
It's different from ALL other enterics because it lives in GI tract of animals and infects human when contamination of food or water with animal feces.

Front 40

Salmonella transmission, pathology, and subtypes

Back 40

Many animals carry Salmonella (like a salmon). Pet turtles caused an epidemic in U.S. one time. Salmonella often comes from eating uncooked chicken eggs.

1. Salmonella typhi- esception: not zoonoti. It's carried only by humans.

Salmonella (and Shigella) never considered part of the normal GI flora! Always pathogenic. Cause 4 diseases:

1. typhoid fever
2. carrier state
3. sepsis
4. gastroenteritis (diarrhea)

Front 41

Typhoid fever

Back 41

Caused by salmonella typhi (enteric fever). Moves one step beyond EIEC and Shigella-->after invading intestinal epithelial cells, it invades regional lymph nodes and can seed multiple organ systems.

Bacteria are phagocytosed by monocytes and survive inside cells.

So salmonella typhi is a facultative intracellular parasite.

Front 42

Typhoid fever clinical findings

Back 42

Think about the salmon with a fever (thermometer) and rose spots on belly. Salmonellosis 1-3wks after exposure includes:
1. fever
2. headache
3. abdominal pain (diffuse or localized to right lower quadrant over terminal ilium)
4. mimicking appendicitis.

Inflammation of involved organs may occur, the spleen may enlarge and the patient may develop diarrhea and rose spots on abdomen.

Front 43

Diagnosis of typhoid fever:

Treatment.

Back 43

diagnose by cultring blood, urine or stool. Ciprofloxacin or ceftriaxone are considered appropriate therapy.

Front 44

Salmonella transmission post-active infection

Back 44

Some people recovering become chronic carriers, harboring salmonella typhi in gallbladders and excrete the bacteria constantly.

Typhoid Mary, a swiss cook, spread the disease to dozens in NYC). Wash hands after toilte use.

Some carriers may require surgical removal of gallbladders.

Front 45

Salmonella sepsis

Back 45

Salmon cruise the bloodstream to infect lungs, brain or bone.

Usually this is caused by Salmonella choleraesuis and not involving Gi tract.

Front 46

Who may be especially susceptible to salmonella osteomyelitis?

tx.

Back 46

Patients with sickle-cell anemia and/or are asplenic can't clear encapsulated bacteria via opsonization w/ macrophages and neutrophils in the spleen (reticulo-endothelial system).


Vigorous and prolonged antibiotic therapy.

Front 47

Salmonella diarrhea

Back 47

1. caused by a type of salmonella enteritidis
2. nausea, abdominal pain, diarrhea (watery sometimes w/ mucous + trace blood)
3. and fever in 50% of patients

Caused by uncharacterized cholera toxin (watery) or ileal inflammation (mucous)

Front 48

Tx. of Salmonella diarrhea

Back 48

fluid or electrolyte replacement only. Diarrhea is acute and >1 week in duration

Front 49

Yersinia enterocolitica

Back 49

1. gram - rod that causes gastroenteritis (as the name indicates). it's not really an enteric bacteria.

2. Closely related to yersinia pestis

3. animals a major source, but transmitted fecal-oral (not flea like pestis) --milk or contaminated water

4. symptoms include: fever, diarrhea, abdominal pain, w/mucosal ulceration in right lower quadrant (terminal ileum)

Front 50

Pathogenesis of Yersinia enterocolitica

Back 50

1. Invasion (like s. typhi) can bind intestinal walls--> gain systemic access via regional lymph nodes into blood stream. Mesenteric nodes can swell and sepsis can develop

2. Enterotoxin: organism can secrete enterotoxin (much like HS toxin from e.coli) that causes diarrhea

Isolate in either feces or blood. Unlike other enterics, it can survive and grow in cold (fridge etc.)

Front 51

Treatment of Y. enterocolitca

Back 51

isolate either in feces or blood. Tx won't alter course, but septic patients need antibiotics.

Front 52

Enterobacteriaceae family

Back 52

1. e coli
2. klebsiella pneumo
3. proteus miribalis
4. enterobacter
5. serratia
6. shigella
7. salmonella
8. y. enterocolitica
9. others : (edswardsiella, citrobacter, hafnia, and providencia)

Front 53

Vibrio cholera

Back 53

1. Like the picture in micro made simple, it's a curved, gram (-) rod w/ single, polar flagellum.
2. Diarrheal disease, causes cholera, fecal-oral transmission.

Front 54

Vibrio cholera pathogenesis

Back 54

1. multiplies intestinally to cause same disease as ETEC w/ no colonic invasion.

2. Attaches to epithelial cells and releases A-B-toxin, which is basically cholera toxin that binds to GM1 ganglioside on epithelial cell surface-->activates adenylate cyclase--> upregulates cAMP.

Front 55

Dx of vibrio cholera

Back 55

Stool slide microscopy reveals curved rods w/ polar flagellum w/ fast darting movements

Front 56

Tx. of vibrio cholera

Back 56

fluid/electrolytes + doxy

shortens illness duration

Front 57

Vibrio parahaemolyticus

Back 57

1. marine bacterium, causes gastroenterotis (like vibrio c.) but it loves seafood and sushi

Front 58

Campylobacter jejuni

Back 58

( camps in jejunum w/ nothing better to do than cause diarrhea)
1. looks like vibrio cholera
2. campylobacter jejuni, ETEC, and Rotavirus are 3 most common causes of diarrhea on the planet (2 mill cases in US alone/year)

Front 59

Campylobacter Jejuni transmission

Back 59

Zoonic, like Salmonella (but not s. typhi which is human only)

1. reservoirs in wild/poultry
2. fecal-oral transmission as well
3. drinkin' up some unpasteurized milk
4. children most commonly affected, as with many diarrheal diseases

Front 60

Campylobacteria jejuni diarrhea

Back 60

1. fever headache starts as prodome, followed 1/2 day later w/ abdominal cramps and BLOODY/LOOSE diarrhea.

This diarrhea is caused by invading the lining of small intestine and systemic spreading (like s. typhi, and y. enterocolitica)

-LT toxin similar to e.coli and an unspecified cytotoxin that destroys intestinal mucosal cells.

Front 61

H. pylori (campylobacter jejuni)

1. disease
2. tx.

Back 61

Most common causes of ulcers and chronic gastritis

tx: pepto-bismol w/bismuth salts, w/ metronidazole, ampicillin, and/or tetracycline

Front 62

Vibrionaceae family

Back 62

1. vibrio cholera
2. vibrio parahaemolyticus
3. campylobacter jejuni
4. H. pylori

Front 63

Psuedomonas Aeruginosa

Back 63

(You will be so sick of hearing about this guy). It's an obligate aerobic (non-lactose fermenter) gr (-) rod.

It loves sick immunocompromised hospital patients, and it's basically resistant to almost every antibiotic--reps will always mention psuedomonas coverage.

Front 64

Psuedomonas metabolism

Back 64

obligate aerobe (non-lactose ferment), gram negative rod, produces pigments (pycyanin and fluorescein) which gives wounds and dressings a greenish-blue color.

grape like scene which can be detected in wounds or dressings.

Front 65

Bacteria that produces green fluorescent pigment (fluorescein) and a blue pigment (pyocyanin)

Back 65

p. aeroginosa

Front 66

P. aeruginosa pathogenesis

Back 66

1. weak ability to invade, but deadly once inside. It elaborates exotoxins (like exo A) that acts like diptheria toxin to stop protein synthesis, but it's antigenically distinct from this toxin.

2. Possess antiphagocytic capsule to target cells (like lungs)

Front 67

P. aeruginosa infections

Back 67

1. Pneumonia: CF patients colonized w/ it--> chronic pneumonia-->progressive lung destruction.

2. osteomyesltis: especially diabetes patients who have ulcers that can become infected-->penetrate to bone
IV users-->inc in ostemy of vetrbrae or clvicle. Children who develop osteomyletis 2^o to puncture wounds of foot.

3. Burn wound infxns: organism can set in burn wounds-->fatal sepsis. Sepsis with p aurigonosa is deadly. UTI--> pyelonephritis (urethral foley catheters)

4. Endocarditis (staph aureus and p. aug)

5. Malignant external otitis (burrows into mastoid bone from external ear canal).

6. Corneal infxns: (Contact lens wearers)

Front 68

Tx. of pseudomonas

Back 68

Anti-pseudomonal peniccilin + aminoglycoside for synergy.

Aminoglycosides include: piperacillin and gentamycin (Bind 30S ribosomal subunit)

Front 69

Psuedomonas cepacia

Back 69

key pathogen in burn CF and hospital patients

Front 70

family pseudomonadaceae

Back 70

1. Pseudomonas aurigonsa
2. Pseudomonas cepacia

Front 71

Bacteroidacea family

Back 71

1. obligate anaerobic, gram (-) rods found in GI tract, mouth, and vagina.
2. 99% of the flora of our intestinal tract is made up of bacteroidacea.

Front 72

Bacteroides fragilis

Back 72

1. Gram (-) bacteria w/o lipid A (endotoxin) in outer cell membrane.
2. encapsulated. it's main importance is in surgery. It's generally low virulence and resides in intestines, but intestinal penetration can lead to "fragile" peritoneal extravasation -->abscesses. (which is basically a collection of bacteria, white cells, and dead tissue).

This leads to fever-->systemic spread.

Because of low prevalance in oral cavity-->rarely implicated in aspiration pneumo.

Front 73

Tx. of bacteroides fragilis

Back 73

1. after Abdominal surgery, antibiotics covering anaerobes given as prophylaxis

(a) clindamycin (bacteriostatic--binds 50S)
b) metronidazole (prodrug, disrupts DNA synthesis)
c) chloramphenicol (broad spec. bacteriostatis, inhibits peptidyl transferase + ribosome)

lastly, d) abscesses need to be drained surgically.

Front 74

Bacteroides melaninogenicus

Back 74

1. produces black pigment on blood agar
2. resides in oral cavity, vagina, and intestine. Necrotizing aerobic pneumonias caused by aspiration of sputum during a drunken or seizure state.

Cause of periodontal disease.

Front 75

Fusobacterium

Back 75

Just like bacteroides melaninogenicus (caauses gum disease and aspiration pneumonia

but can cause abdominal and pelvic abscesses and otitis media

Front 76

Anaerobig gram + cocci (enterics)

Back 76

peptostreptococcus and peptococcus. They are gram+ aerobes and are part of normal flora of mouth, vagina, and intestine.

They mix w/ preceding organisms in abscesses and aspiration pneumonia. ex: strep: viridans

Front 77

E. coli appearnce on EMB and MacConkey's

Back 77

Ferments lactose, colonies appear deep purple on EMP and pink-purple on MacConkey's

Front 78

Which bacterial contains urease?

Back 78

P. miribalis

Front 79

Haemophilus influenza, bordatella pertussis, and legionalla all are:

Back 79

1. acquired through respiratory tract.

h. flu (flu is upper respiratory illness)

Pertussis (means cough)

Pneumophilia (lung loving)

Front 80

Haemophilus influenzae:

Back 80

Haemophilus influenzae:
* Haemophilus- "blood loving" blood containing medium, required for growth due to hematin and NAD+ in blood) and influenzae refers to h. influenza's ability to attack lungs of a person debilitated w/ a viral influenza. This led to confusion in 1890/1918 flu pandemics that h. influenza was the actual cause of flu.

Front 81

h. influenza pathogenesis

Back 81

1. obligate human parasite (transmission= inhalation)

2. Two means of causing disease: (1) polysaccharide capsules of 6 types a->f, but "b" is bad and causes meningitis, epiglottis, and septic arthritis

2) no capsular antibodies 6 mos-->3 years

Front 82

H. influenza type b meningitis, acute epiglottitis, and septic arthritis + sepsis (describe how h. flu causes these)

Back 82

1. meningitis: most serious. inhalation-->local lymph node invasion-->blood-->meningeal penetration. Mortality is <5%, but 50% of infected kids can retian residual deficits. Antibiotics cause killed bacteria to lyse-->release antigens like lipid A endotoxin-->violent immune rx. that destroys neurons and bacteria (systemic steroids can reduce this adverse rx)

2. Acute epiglottitis (Cherry @ base of tongue). Hflu-b can cause swelling of epiglottis/sorethroat & fever-->stridor + upper airway wheeze-->xs saliva that can't pass epiglottis-->drooling

3. Septic arthritis- Most comon cause of septic arthritis in infants is h. flu b. It usually affects single joint with accompanying fever, pain, and decreased mobility of joint. Exam of joint fluid shows pleomorphic gram - rods.

4. sepsis--fever, lethargy, anorexia, and no localized disease.

Front 83

Tx. of H. influenza

Back 83

Meningitis, epiglottitis, and bacterial sepsis all require:

1. 3rd gen cephalosorpin for serious infxns (cefotaxime , ceftriaxone)

2. Ampicillin or Amoxicillin for less serious (like otitis media)

Ampicillin is old tx. because of plasmid mediated resistance from other H.Flu's

Front 84

Haemophilus influenza vaccine?

Back 84

Hib capsular vaccine (Haemphils influenza b= HIB) B =bad

1. goal: early generation of capsular antibodies. The vaccine actually has type b (Hib) capsule & dipth. toxin.

The diptheria toxin activates t-lymphocytes and anti-b capsule antibodies.

-immunizing women in month 8 of preg. can lead to pasive immunity via breast-feed

Front 85

Haemophilus decreyi and differential

Back 85

1. causes STD chancroid which is charcterized by PAINFUL genital ulcer, swollen inguinal nodes (50%) which can become matted and release pus.

Must be differentiated from other chancroid-like disease states that are in the differential including...

1. syphilis (treponema pallidum) the ulcer is painless with non-supparitive (pus) adenopathy

2. Herpes (HSV1/2) vesicles break and can be mischaracterized as chancroid because they're painful too. Herpes, though, usually has myalgias and fevers.

3. Lymphogranula venereum (chlamydia trachomotis)

Front 86

Tx. for chancroid (H. ducreyi)

Back 86

tx: erythromycin or trimethoprim/sulfamethoxazole.

Front 87

Gardnerella vaginilas:

Back 87

1. Bacterial vaginitis in conjunct w/ anaerobic vaginal bacteria.
2. women w/ vaginitis-->prutitis (itching) of labia, dysuria (pain), &foul-smelling, FISHY vaginal discharge

Front 88

Gardnerella culture

Back 88

* rule/o other causes of vaginitis (candida/trichomonas) by slidemicroscopy looking for "clue cells"

Front 89

clue cells

Back 89

what you like for in a microscopy of vaginal epithelium when trying to rule/i gardnerlla vaginalis.

They are tiny, pleiomorphic bacilli inside "clue" vaginal epithelium cells

Front 90

Gardnerall vaginialis tx:

Back 90

Metronidazole (covers gardnerella and co-infections)

Front 91

Bordetella pertussis pathogenesis and toxins

Back 91

(gram negative, with a negative/violent attitude)

Causes whooping cough via 4 major virulence factors which allow: attachment to ciliated epithelial cells of trachea and bronchi, evasion of host defenses, and destruction of ciliated cells.

Toxins:

1) pertussis toxin: A-B toxin with A unit activating membrane G proteins-->adenylate cyclase--> up cAMP--> protein kinase activation --> histamine sensitation, increase in insulin synth, and increase in lymphocyte production and inhibition of phagocytosis.

2. Extracytoplasmic adenylate cyclase--> when attacking bronchi, bordetella throws adenylate cyclase grenades swallowed by host immune cells. In host immune cells--> up cAMP--> impairs chemotaxis and H2O2/superoxide radical generation

3. FHA (filamentous hemagglutinin): bordatella contains a pili rod that aids in attachment. Bordatella does not invade, it just attaches, so FHA Ab's are preventatively protective.

4. Tracheal cytotoxin: destroys ciliated epithelium and impairs bacterial clearnce-->mucous, exudate, and may explain the violent cough.

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Bordatella pertussis culture

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Will not grow on cotton, so specimens are collected from posterior pharynx w/ calcium alginate swab. Swab inserted to poste. nares and patient coughs,.

The swab is wiped on the nasiest thing ever: POTATO, BLOOD, AND GLYCEROL AGAR (Bordet-Gengou medium). Rapid ELISA is usually test of choice.

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Bordatella pertussis tx:

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tx. is primarily supportive. Infants need oxygen, suction of secretions, respiratory islation.

Tx. w/ ERYTHROMYCIN (during prodromal or catarrhal may prevent disease)

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Vaccination:

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Heat-killed organisms. Includes pertussis toxin, FHA, and adenylate cyclase.

Generally combined with DPT (formalin inactivated tetanus and diptheria toxoids).

In an effort to reduce adverse affects, new vaccines only contain inactivated proteins such as pertussis toxin, FHA, and others (such as pertactin and fimbrial antigens).

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Legionella pneumophilia

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Aerobic gram negative famous for pneumonia at American legion convention in Philadelphia.

Ubiquitous in made-made water environments.

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Legionella transmission

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Aeroslized contaminated water inhaled-->infxn.

Air conditioning systems, cooling towers, and whirlpools have all caused outbreaks. Even with shower heads and misters at super-markets! no transmission human-human

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Legionalla pneumophilia pathogenesis

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It's a facultative intracellular parsite that settles in lower respiratory tract and is gobbled up by macrophages. But once it's taken up, it inhibits phagosome-lysosome fusion, surviving and replicating intracellularly.

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What pathogen is taken up by macrophages, inhibits phagosome-lysosome fusion, then survives/replicates intracellularly?

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Legionalla pneumophilia

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Legionella is also responsible for diseases ranging from asymptomatic to:

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1. Pontiac fever (a flu-like illness): Like influenza, this disease involves heache, muscle aches, fatigue, followed by fever and chills. Pontiac fever strikes suddenly and completely resides in less than one week. Named for illness that struck Pontiac car employees in Michigan. Cause was legionella in A/C system.

or

2. Legionnaire's disease:VERY high fevers+ severe pneumonia. Legionella pneumophila is one of the most common causes of community acquired pneumonia-->correctly diagnosed 3% of the time.

Suspect if patient has pneumonia and is >50 y.o. and if they are smokers.

Sputum gram steam revealing neutrophils and few organisms is very suspicious

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Sputum gram steam revealing neutrophils and few organisms is very suspicious for what organism in a pneumonia patient?

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Legionalla pneuophila, which is so small and very hard to see on gram stain.)

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Legionella pneumophila tx.

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Erythromycin (bacteriocidal) because this organism has a beta-lactamase making it resistant to peniccillins.

Determine the source of the legionella.