Vibrio and Friends Flashcards
1
Q
Vibrio bacteriology
A
- 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
2
Q
vibrio bacteriology 2
A
- 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
3
Q
What is the pathogenesis of Cholera?
A
- 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
4
Q
tell me about Cholera toxin
A
- 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
5
Q
more cholera pathogenesis
A
- 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
6
Q
epidemiology of Cholera
A
- 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
7
Q
how do you diagnose cholera on exam?
A
- 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%
8
Q
mild dehydration on exam
A
- 3-5% down from normal weight
- excessive thirst
9
Q
moderate dehydration on exam
A
- 5-8% decreased BW
- hypotension, tachycardia, weakness
- fatigue
- prolonged skin tenting after a longitudinal pinch
- acidosis
10
Q
severe dehydration on exam
A
- 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
11
Q
other aspects of cholera on exam
A
- hypoglycemia
- acidemia
- hypokalemia- crash with treatment from acidosis
- peds-very drowsy, coma, fever, hypoglycemic convulsions
12
Q
cholera diagnosis on lab
A
- 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
13
Q
treatment for cholera
A
- 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
14
Q
prevention of cholera
A
- 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
15
Q
vibrio parahaemolyticus bacteriology
A
- 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
16
Q
pathogenesis of parahaemolyticus
A
- 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
17
Q
diagnosis of parahaemolyticus on exam
A
- 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
18
Q
parahaemolyticus diagnosis on lab
A
- 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.
19
Q
treatment for parahaemolyticus
A
- in a previously healthy patient, will be self limited, oral rehydration
- if complicating factors on high fever, doxy or quinolone, IV rehydration
20
Q
vibrio vulnificus bacteriology
A
- 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
21
Q
vulnificus pathogenesis
A
- 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
22
Q
vulnificus pathogenesis 2
A
- 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
23
Q
vulnificus diagnosis on exam
A
- 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
24
Q
vulnificus on lab
A
- 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
25
treatment for vulnificus
- 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
26
campylobacter bacteriology!
- 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!)
27
pathogenesis of campylobacter
- 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
28
campylobacter jejuni pathogenesis 2
- infection strongly predisposing for guillain Barre syndrome
- can alternatively trigger reactive arthritis
- rarely, bloody diarrhea strains are associated with hemolytic uremic syndrome
29
diagnosis of campylobacter on exam
-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+
-
30
campylobacter on sigmoidoscopy
- abnormal but variable
- focal mucosal edema
- hyperemia
- patchy petechiae
- ulceration
- rule out toxic megacolon by sonogram if distended
31
campylobacter on lab
- 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
32
treatment for campylobacter
- 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
33
H pylori bacteriology
- 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
34
h pylori pathogenesis
- 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
35
h pylori pathogenesis 2
- 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
36
h pylori on exam
- 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
37
h pylori on lab
- 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
38
h pylori treatment
- 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
39
triple therapies for h pylori
- omeprazole, amox, clarithromycin
- bismuth subsalicyclate, metronidazole, tetra
- lansoprazole, amox, clarith
