A 57-year old man was hospitalized in New York with a 2-day history of severe, watery diarrhea. The illness had begun 1 day after his return from Ecuador. The patient was dehydrated and suffering from an electrolyte imbalance (acidosis, hypokalimea).

The patient made an uneventful recovery after fluid and electrolyte replacement was instituted to compensate for the losses resulting from the watery diarrhea.

Stool cultures were positive for ….

Vibrio and Pseudomonas

Vibrio cholerae

Vibrio parahaemolyticus

Vibrio vulnificus

Pseudomonas aeruginosa

Vibrio

V. cholerae V. parahaemolyticus Gram-negativeComma-shapedFacultatively anaerobicCan grow in the absence of saltSingle polar flagellum

Vibrio

The O polysaccharide of the LPS is used to subdivide Vibrio species into serogroups:

V. cholerae O1 and O139 > classic cholera

V. cholerae O1 serogroup is divided further into biotypes

"el tor”classical (cholerae)

Protective gearagainst cholerain early 19thcentury Germany

PathogenesisCholera toxin ("choleragen”) encoded by

bacteriophage CTXø A-B structure5 B subunits bind to gangliosides on

mucosal cells (ctxB gene)A subunit ADP-ribosylates the Gs protein

(ctxA gene)Activates adenylate cyclase

Vibrio

Pathogenesis

Accumulation of cAMP

Secretion of chloride, bicarbonate and water into the intestinal lumen

Fluid loss in severely infected patients1 liter of fluid per hour

Vibrio

Pathogenesis

Toxin co-regulated pilus (tcp gene)Adherence to intestinal mucosal cellsBinding site for bacteriophage CTXø

Colonization factor (cep gene)Adhesin molecules mediate adhesion to the

mucosal cell surface

Pathogenesis

Accessory cholera entereotoxin (ace gene)Increased fluid secretion

Zonula occludens toxin (zot gene)Loosens the tight junctions of the small

intestine mucosa

Hemagglutinin-protease (hap gene) Mucinase: Dissolves the protective

glycoprotein coating over intestinal cells

Attachment ofV. choleraeto the brush border

Attachment ofV. choleraeto M cells in human ileal mucosa

Pathogenesis

Vibrio parahaemolyticus

Thermostable direct hemolysin“Kanagawa hemolysin”Induces chloride ion secretion by increasing

intracellular calciumCauses ß-hemolysis on agar media with

human blood (Kanagawa-positive)

TransmissionVibrio Grow in estuarine and marine environments,

particularly those with chitinous shellfish

Transmitted by contaminated water and food

Seven major pandemics since 1817

Transmission

V. parahaemolyticus and V. vulnificusVia improperly cooked seafood (oysters!) and exposure to contaminated seawater

V. parahaemolyticusMost common cause of bacterial gastroenteritis in Japan and Southeast AsiaMost common Vibrio species responsible for gastroenteritis in the US

From Todar’s Online Textbook of Bacteriology

Spread of O1 El Tor starting in 1961 in the Philippines

Spread of pandemicV. cholerae O1 El Tor in the Americas

1991-1994

Clinical syndromesVibrio choleraeWatery diarrhea and vomitingRice-water stoolsFluid loss

> dehydration> metabolic acidosis (bicarbonate loss)> hypovolemic shock (abnormally decreased

plasma volume)> cardiac arrhythmia> renal shock

Rice water stool in cholera

London 1932: Bundling up of cholera patient

Science sleeps on aNew York dock as Cholera floats across the ocean from Europe

Epidemic in Marseille, 1895

Clinical syndromes

Vibrio parahaemolyticusWatery diarrheaHeadacheAbdominal crampsNauseaVomitingLow grade feverMay persist for 72 h or more

Clinical syndromes

Vibrio vulnificusRapidly progressive wound infections after exposure to contaminated seawater

Initial swelling, erythema, painDevelopment of vesicles, tissue necrosis

Septicemia after exposure to contaminated raw oystersMortality can be as high as 50% if antimicrobial treatment is not started promptly

Infections most severe in patients with hepatic disease, hematopoietic disease, and those receiving immunosuppressive drugs

Treatment and controlVibrio cholerae

Fluid and electrolytes before hypovolemic shock

Doxycyline, tetracycline: reduce exotoxin productionFurazolidone for pregnant womenTrimethoprim-sulfamethoxazole for children

Improved sanitation: sewage; water purification

Killed cholera vaccine: short lived protection

Treatment and control

Vibrio parahaemolyticusUsually self-limitingFluid and electrolyte therapyAntibiotics

Vibrio vulnificus Immediate treatment with Minocyline, and a fluoroquinolone or cefotaxime

Aerobic, Gram-negative bacilli

In soil, decaying organic matter, vegetation and water

In hospitals: food, cut flowers, sinks, toilets, floor mops, equipment for respiratory therapy and dialysis

In hexachlorophene-containing soap solutions and disinfectant solutions

Pseudomonas aeruginosa

From Todar’s Online Textbook of Bacteriology

Pyocyanin production in culture

Pathogenesis

AdhesinsBacterial neuraminidasePolysaccharide capsuleEndotoxinExotoxin A

Blocks protein synthesisADP-ribosyltransferase

Tissue damage in burn wound, chronic pulmonary and ocular infections

Pseudomonas aeruginosa

Pathogenesis

Exoenzymes S and T ADP-ribosyltransferaseInterferes with phagocytic killingCause epithelial cell damage, via actin rearrangement

Elastases > lung parenchymal damage, hemorrhagic lesions (ecthyma gangrenosum)Degrade complement, inhibit PMN chemotaxis

Phospholipase C

Pathogenesis

PyocyaninImpairs ciliary functionStimulates IL-8 release (neutrophil migration)Mediates tissue damage via production of

superoxide and hydrogen peroxide (in the presence of pyochelin, a siderophore)

Antibiotic resistanceMutation of porin proteins-lactamase production

Transmission

Ubiquitous opportunistic pathogen

Persistent carriage common in hospitalized patients

Pseudomonas aeruginosa

Transmission

Risk factorsPrior treatment with broad-spectrum antibioticsRespiratory therapyProlonged hospitalizationCompromised immune functionExposure to contaminated waterDiabetesOld ageiv drug use

Pseudomonas aeruginosa

Clinical syndromes

Most commmon infections

Urinary tract infectionsPneumonia (in Cystic Fibrosis)Wound infections (burns)

Pseudomonas aeruginosa

Clinical syndromes

Pulmonary infectionsFrom benign tracheobronchitis to severe

necrotizing bronchopneumoniaCystic fibrosis > involvement of pulmonary

parenchyma Cystic fibrosis > P. aeruginosa initiates a rapid

mutation rate

Pseudomonas aeruginosa

Clinical syndromes

Primary skin infectionsMostly in burn woundsLocalized vascular damageTissue necrosisBacteremia

Pseudomonas aeruginosa

Ecthymagangrenosum in a child with Pseudomonassepticemiaassociated with immunodeficiency

Due to degradation of elastin by bacterial elastase

Clinical syndromes

Ear infectionsExternal otitis

Most frequently caused by P. aeruginosa Swimming is a risk factor

Malignant external otitis (elderly and diabetics) Damage to nerves and bone

Chronic otitis media

Pseudomonas aeruginosa

Clinical syndromes

Eye infections

Bacteremia Mostly in patients with neutropenia, diabetes, extensive burns and hematological malignanciesMortality rate > 50%

Endocarditis Mostly in iv drug users

Pseudomonas aeruginosa

Treatment and control

Resistant to most antibioticsResistance can develop during therapy

ß-lactamases, plasmid-mediated transferCombination of aminoglycosides (poor activity in the

acidic environment of an abscess) and ß-lactam antibiotics (e.g., ticarcillin or piperacillin)

Hyperimmune serumGranulocyte transfusions

Pseudomonas aeruginosa

Treatment and control

Avoid contamination of sterile equipment

Avoid contamination of patients by medical personnel

Remove indwelling catheters promptly

Take special care of burned skin

Pseudomonas aeruginosa