Vibrio and Friends

Question 1

Vibrio bacteriology

Answer 1

• curved, comma shaped, motile gram negative rod
• stains aerobic, is facultatively anaerobic
• microscopic discovery of Koch (from those postulates)
• causing human epidemics for at least a milennium
• epidemic in london in 1854- john snow and the pump
• 2 reservoirs-humans and plankton ecosystem of Indian ocean

Question 2

vibrio bacteriology 2

Answer 2

• 7 pandemics since 1817, spread from the Indian Ocean
• 7th began in 1961 and is still in progress
• O cell wall antigen indicates pathogenicity, O1 and O139 groups cause epidemic disease
• two O1 biotypes: El Tor and cholera
• three O1 serotypes- Ogawa, Inaba, Hikojima
• non-O1 causes sporadic or no disease, occasional shellfish food poisoning

Question 3

What is the pathogenesis of Cholera?

Answer 3

• fecal oral
• shed by asymptomatic carriers in incubation or convalescence
• travels to untreated water or undercooked shellfish
• usually killed by stomach acid, high infectious dose (1000-1,000,000)
• people on antacids or with gastrectomy or coincident H pylori infection are more susceptible
• surviving bacteria reach small intestine, secrete mucinase to clear path to brush border
• attach by toxin-coregulated pilus (TCP), growing bacteria secrete cholera toxin

Question 4

tell me about Cholera toxin

Answer 4

• secreted by bacteria
• enterotoxin
• A-B subunit
• B binds ganglioside receptor GM1 on intestinal lining
• A causes persistent activation of adenylate cyclase, leads to loss of water and ions
• blocks absorption by microvilli while also promotes secretion by crypt
• massive watery diarrhea
• toxin carried by lysogenic bacteriophage CTX

Question 5

more cholera pathogenesis

Answer 5

• local acting, little penetration of the gut wall by O1, occasional bacteremia from O139
• morbidity and death result from dehydration and electrolyte balance
• severe cases can kill in hours
• surviving patients run the self limited course in 7 days

Question 6

epidemiology of Cholera

Answer 6

• rare in US, 50 cases a year, mostly returning travelers
• cases from Haiti may be more antibiotic resistant
• some local: O1 biotype El Torm serotype Inaba is now endemic to Gulf of Mexico

Question 7

how do you diagnose cholera on exam?

Answer 7

• 24-48 h incubation
• mild cases don’t present
• 5% proceed to rice water stool: large volumes of watery diarrhea
• more diarrhea than any other infectious gasteroenteritis
• no pain, blood, or neutrophils in stool
• some vomiting, no fever
• acidosis and hypokalemia from loss of bicarb and potassium
• dehydration leading to cardac and renal failure in hourse, >40% untreated mortality
• treatment is primarily rehydration, begin before dx
• mortality with IV hydration is about 1%

Question 8

mild dehydration on exam

Answer 8

• 3-5% down from normal weight

- excessive thirst

Question 9

moderate dehydration on exam

Answer 9

• 5-8% decreased BW
• hypotension, tachycardia, weakness
• fatigue
• prolonged skin tenting after a longitudinal pinch
• acidosis

Question 10

severe dehydration on exam

Answer 10

• 10% BW
• glassy/sunken eyes
• sunken fontanelles in infants
• pulse weak, thready, absent
• wrinkled skin, can’t wake up, coma
• may be hard to catch in a child

Question 11

other aspects of cholera on exam

Answer 11

• hypoglycemia
• acidemia
• hypokalemia- crash with treatment from acidosis
• peds-very drowsy, coma, fever, hypoglycemic convulsions

Question 12

cholera diagnosis on lab

Answer 12

• lab techniques seldom used for diagnosis during an epidemic, may only be useful for epidemiology
• for sporadic cases in US, isolate on buffered media, find oxidase positive, only slightly lactose fermenting
• ferments sucrose, grows on bile salts agar (halophile)
• gives acid reaction on triple sugar iron agar
• addition of specific antisera to sample will halt motility
• can retroactively dx by serology
• darkfield microscopy of stool sample reveals motile vibrios
• bloodwork for dehydration

Question 13

treatment for cholera

Answer 13

• rehydrate and rebalance electrolytes
• IV lactated ringer solution 50-100 ml/kg/ hr (normal saline doesn’t correct acidosis) for up to 4 hours- watch overhydration in kids
• maintenance- oral rehydration solution 500-1000ml/hr, more if requested
• watch for the return of urine output every 3-4 hours beginning 6-8 h after rehydration
• asymptomatic close contacts should be sent home with ORS
• can treat with short course of tetracycline, doxy, furazolidone, cipro after IV rehydration to shorten course and reduce shedding

Question 14

prevention of cholera

Answer 14

• public health- treat water, cook food, reduce overcrowding
• killed vaccine is 50% effective for 3-6 mo
• neither vaccine recommended for routine use in travelers
• prophylactic tetracycline can protect close contacts

Question 15

vibrio parahaemolyticus bacteriology

Answer 15

• oxidase positive, gram negative, curved motile rod
• saltwater borne, particularly warm ocean water
• halophile
• freq of non-cholera vibrio infections appears to be increasing in US
• more common than vulnificus
• usually causes gastroenteritis, but can also cause cellulitis

Question 16

pathogenesis of parahaemolyticus

Answer 16

• leading cause of gastroenteritis in those who eat undercooked seafood, esp shellfish
• secretes hemolysin and an enterotoxin similar to choleragen
• causes a diarrhea of varied severity

Question 17

diagnosis of parahaemolyticus on exam

Answer 17

• nausea, vomiting
• abd cramps, diarrhea
• fever
• usually self limited
• check for dehydration
• obtain history of factors predisposing to complications:
• immunodef
• liver disease
• iron overload
• kidney disease

Question 18

parahaemolyticus diagnosis on lab

Answer 18

• bloodwork for DIC, HBV, HCV, iron
• culture in 8% NaCl
• ideally, culture from stool on thiosulfate-citrate-bile salts sucrose
• stool smear for blood, leukocytes, bacteria, parasites.

Question 19

treatment for parahaemolyticus

Answer 19

• in a previously healthy patient, will be self limited, oral rehydration
• if complicating factors on high fever, doxy or quinolone, IV rehydration

Question 20

vibrio vulnificus bacteriology

Answer 20

• oxidase positive, gram negative curved motile rod
• some encapsulated
• saltwater borne, particularly warm ocean water
• found in Gulf Coast, some in new england and northern pacific
• concentrated by filter feeding mollusks
• halophile
• infections in gulf coast jumped after hurricane katrina

Question 21

vulnificus pathogenesis

Answer 21

• infects shellfish- contaminated wounds: cellulitis progressing to necrotizing fasciitis in shellfish market workers
• can also infect wounds exposed to seawater (shark/alligator bites, fish hook punctures)
• produces hemolysin and protease exotoxins
• produces siderophores, infection exacerbated by iron overload

Question 22

vulnificus pathogenesis 2

Answer 22

• causes rapidly fatal septicemia in immunocompromised people who eat raw shellfish
• septicemia mortality 35-50%
• highest case fatality rate (39%) fir foodborne disease
• preexisting liver diseases predisposes to poor outcome

Question 23

vulnificus diagnosis on exam

Answer 23

• cellulitis with history of handling raw shellfish
• foot injuries from stepping on seashells, crustaceans, stingrays
• severe pain progressing to numbness
• septicemia with hemorrhagic bullae
• obtain history of factors predisposing to complications:
• immunodef, liver disease, iron overload, kidney disease
• dramatic clinical progression in wound infection/septicemia
• high fever, shaking chills, severe pain in feet
• CXR may diagnose ARDS
• radiography of wound site may reveal shells, fish hooks, etc

Question 24

vulnificus on lab

Answer 24

• bloodwork for DIC, HBV, HCV, iron
• gram stain and culture from aspirate of wound site and adjacent blood
• biopsy demonstrates gram neg bacilli, acute inflammation, tissue necrosis, fat infarction

Question 25

treatment for vulnificus

Answer 25

• surgical care at wound site- debride early and often, necrotizing fasciitis or compartment syndrome may develop
• treat sepsis, septic shock, DIC, ARDS, renal failure as needed
• ceftazidime and doxy or antipseudomonal penicillin
• alternative- cefotaxime or fluoroquinolones

Question 26

campylobacter bacteriology!

Answer 26

• comma or s shaped gram neg rod
• non-spore forming
• motile (flagella)
• oxidase and catalase positive
• microaerophilic
• multiple species are common causes of diarrhea, occasional complications
• reservoir in guts of domestic animals, 100% of poultry
• transmitted fecal oral- raw milk, sexual contact, sick pets (the puppies!)

Question 27

pathogenesis of campylobacter

Answer 27

• sensitive to stomach acid, infectious dose is 10K
• both intestines are colonized and invaded
• bloody diarrhea with crypt abscesses and ulceration
• some strains produces a cholera-like enterotoxin–> watery diarrhea
• systemic infection can occur in neonates/ immunosuppressed

Question 28

campylobacter jejuni pathogenesis 2

Answer 28

• infection strongly predisposing for guillain Barre syndrome
• can alternatively trigger reactive arthritis
• rarely, bloody diarrhea strains are associated with hemolytic uremic syndrome

Question 29

diagnosis of campylobacter on exam

Answer 29

-common in kids
-incubation in 1 week
-initially watery, foul smelling diarrhea
-progresses to bloody stools with fever and abdominal pain
-rule out bacteremia, leads to meningitis, vascular infections, abscess
-infection also common in MSM, complications if HIV+
-

Question 30

campylobacter on sigmoidoscopy

Answer 30

• abnormal but variable
• focal mucosal edema
• hyperemia
• patchy petechiae
• ulceration
• rule out toxic megacolon by sonogram if distended

Question 31

campylobacter on lab

Answer 31

• stool sample culture, blood if bacteremia suspected
• blood agar plates with antibiotics to inhibit normal flora
• 42 and 25C, fails at low temp
• 5% oxygen, 10% Co2
• grows slowly in culture, may appear more coccoid as culture ages
• microscopic exam of fecal smear for darting motolity, leukocytes, erythrocytes
• gram stain fecal smear
• oxidase pos
• PCR tests for stool in pipeline

Question 32

treatment for campylobacter

Answer 32

• if simple- self limited, rehydrate
• antibiotics may be used if patient is a child or has high fever, bloody diarrhea, >8 stools a day, worsening sx, illness for >1 wk, pregnancy, HIV
• azithromycin in adults, erythromycin in pregnant woman and kids
• alt- tetra and clinda
• meningitis- meropenem, ampicillin, chloramphenicol
• do not use antimotility agents to treat the diarrhea

Question 33

H pylori bacteriology

Answer 33

• discovered in 1983
• curved gram neg rods (LPS)
• very similar to campylobacter but strongly urease pos
• causes peptic ulcer disease, associated with MALTomas, gastric lymphoma, adenocarcinoma of the stomach

Question 34

h pylori pathogenesis

Answer 34

• transmission mode unknown, probably person to person within households
• bacteria attach to mucus secreting cells of stomach with flagella virulence factor
• break down urea into ammonia with urease virulence factor
• ammonia neutralizes stomach pH, allowing bacterial growth and irritating stomach lining

Question 35

h pylori pathogenesis 2

Answer 35

• organism appears to create a niche in the lining where it multiplies, leading to infiltration by neutrophils, T and B cells, macrophages and mast cells
• appears to upregulate caspases, causing apoptosis in nearby cells
• disease may have AI component
• some strains produce Vac A vacuolating cytotoxin
• some produce Cag A, chemotactic for neutrophils
• irritation predisposes to gastritis, peptic ulcer, gastric ulcer, and MALToma

Question 36

h pylori on exam

Answer 36

• infection is very widespread, symptoms not
• obtain family history of gastric cancer
• gastritis, peptic ulcer
• recurrent pain, bleeding into GI
• imaging studies can diagnose ulcers, cancer
• esophagogastroduodenoscopy with biopsy visualizes damage to stomach lining and diagnosis cancer

Question 37

h pylori on lab

Answer 37

• culture is very difficult and not useful for diagnosis
• urea breath test, patient ingests radiolabeled urea, if infected, exhales radiolabeled CO2
• biopsy shows h pylori organisms, decreased mucus film, large IF infiltrate
• PCR test for stool is replacing breath test but UBT is still best for testing the cure

Question 38

h pylori treatment

Answer 38

• reduce irritation with bismuth salts
• PPIs may be used to relieve pain and help ulcers heal
• kill with triple therapy
• nausea and metallic taste are common side effects, stress importance of compliance to trt
• macrolide and clarithromycin resistance exist
• reinfection may occur

Question 39

triple therapies for h pylori

Answer 39

• omeprazole, amox, clarithromycin
• bismuth subsalicyclate, metronidazole, tetra
• lansoprazole, amox, clarith