Food Borne Illness
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Transcript of Food Borne Illness
Food Borne IllnessFood Borne Illness
Infections that require large infective dosage
Infections that require large infective dosage
Infections that require large infective dosage
Infections that require large infective dosage
Bacteria Salmonella spp. Yersinia enterocolitica and Yersinia pseudotuberculosis Vibrio parahaemolyticus and other vibrios Escherichia coli - Enterotoxigenic (ETEC) Enterohemorrhagic HUS Campylobacter jejuni Listeria
Bacteria Salmonella spp. Yersinia enterocolitica and Yersinia pseudotuberculosis Vibrio parahaemolyticus and other vibrios Escherichia coli - Enterotoxigenic (ETEC) Enterohemorrhagic HUS Campylobacter jejuni Listeria
EnterobacteriaceaeEnterobacteriaceae Classification – more than15 different
genera Classification – more than15 different
generaLactoes Ferm +ve
EscherichiaEnterobacterCitrobacterKlebsiellaPectinobacterium
Lactoes Ferm –ve
ShigellaEdwardsiellaSalmonellaHafniaSerratiaProteusProvidenciaMorganellaYersiniaErwinia
EnterobacteriaceaeEnterobacteriaceae
Morphology and General Characteristics Gram-negative, non-sporing, rod shaped
bacteria Oxidase – Ferment glucose and may or may not
produce gas in the process (aerogenic vs anaerogenic)
Reduce nitrate to nitrite (there are a few exceptions)
Morphology and General Characteristics Gram-negative, non-sporing, rod shaped
bacteria Oxidase – Ferment glucose and may or may not
produce gas in the process (aerogenic vs anaerogenic)
Reduce nitrate to nitrite (there are a few exceptions)
EnterobacteriaceaeEnterobacteriaceae
Are facultative anaerobes If motile, motility is by peritrichous flagella Many are normal inhabitants of the
intestinal tract of man and other animals Some are enteric pathogens and others are
urinary or respiratory tract pathogens Differentiation is based on biochemical
reactions and and differences in antigenic structure
Are facultative anaerobes If motile, motility is by peritrichous flagella Many are normal inhabitants of the
intestinal tract of man and other animals Some are enteric pathogens and others are
urinary or respiratory tract pathogens Differentiation is based on biochemical
reactions and and differences in antigenic structure
EnterobacteriaceaeEnterobacteriaceae
Most grow well on a variety of lab media including a lot of selective and differential media originally developed for the the selective isolation of enteric pathogens. Most of this media is selective by
incorporation of dyes and bile salts that inhibit G+ organisms and may suppress the growth of nonpathogenic species of Enterobacteriaceae.
Many are differential on the basis of whether or not the organisms ferment lactose and/or produce H2S.
Most grow well on a variety of lab media including a lot of selective and differential media originally developed for the the selective isolation of enteric pathogens. Most of this media is selective by
incorporation of dyes and bile salts that inhibit G+ organisms and may suppress the growth of nonpathogenic species of Enterobacteriaceae.
Many are differential on the basis of whether or not the organisms ferment lactose and/or produce H2S.
Antigenic Structure of Enterobacteriaceae
Antigenic Structure of Enterobacteriaceae
Escherichia coliEscherichia coli
Normal inhabitant of the G.I. tract. Some strains cause various forms of
gastroenteritis. Is a major cause of urinary tract
infection and neonatal meningitis and septicemia.
Normal inhabitant of the G.I. tract. Some strains cause various forms of
gastroenteritis. Is a major cause of urinary tract
infection and neonatal meningitis and septicemia.
E. coliE. coli
May be hemolytic on CBA – more common in pathogenic strains
KEY tests for the normal strain:TSI is A/A + gasLIA K/KUrea – Indole +Citrate –Motility +
There is an inactive biotype that is anaerogenic, lactose – , and nonmotile.
May be hemolytic on CBA – more common in pathogenic strains
KEY tests for the normal strain:TSI is A/A + gasLIA K/KUrea – Indole +Citrate –Motility +
There is an inactive biotype that is anaerogenic, lactose – , and nonmotile.
Escherichia coliEscherichia coli Virulence factors
Toxins
Enterotoxins and Shigella like Toxins
Enterotoxins causes a movement of water and ions from the tissues to the bowel resulting in watery diarrhea.
There are two types of enterotoxin: LT and ST
Virulence factorsToxins
Enterotoxins and Shigella like Toxins
Enterotoxins causes a movement of water and ions from the tissues to the bowel resulting in watery diarrhea.
There are two types of enterotoxin: LT and ST
E. Coli EnterotoxinsE. Coli Enterotoxins LT – is heat labile and LT – is heat labile
and alters the activity of sodium and chloride transporters producing an ion imbalance that results in fluid transport into the bowel.
ST – is heat stable and binds to specific receptors with the same results as with LT.
LT – is heat labile and LT – is heat labile and alters the activity of sodium and chloride transporters producing an ion imbalance that results in fluid transport into the bowel.
ST – is heat stable and binds to specific receptors with the same results as with LT.
Shiga-type toxinsShiga-type toxinsShiga-type toxin – also called the
verotoxin -produced by enterohemorrhagic strains of E. coli (EHEC)
– is cytotoxic, enterotoxic, neurotoxic, and may cause diarrhea and ulceration of the G.I. tract.
Shiga-type toxin – also called the verotoxin -produced by enterohemorrhagic strains of E. coli (EHEC)
– is cytotoxic, enterotoxic, neurotoxic, and may cause diarrhea and ulceration of the G.I. tract.
E. coli infectionsE. coli infections
Gastroenteritis – there are several distinct types of E. coli that are involved in different types of gastroenteritis:
enterotoxigenic E. coli (ETEC), enteroinvasive E. coli (EIEC), enteropathogenic E. coli (EPEC) , enteroaggregative E. coli (EAEC), and enterohemorrhagic E. coli (EHEC).
Gastroenteritis – there are several distinct types of E. coli that are involved in different types of gastroenteritis:
enterotoxigenic E. coli (ETEC), enteroinvasive E. coli (EIEC), enteropathogenic E. coli (EPEC) , enteroaggregative E. coli (EAEC), and enterohemorrhagic E. coli (EHEC).
ShigellaShigella
Shigella Contains four species that differ
antigenically and, to a lesser extent, biochemically.
Shigella Contains four species that differ
antigenically and, to a lesser extent, biochemically.
Shigella speciesShigella species
S. dysenteriae (Group A) S. flexneri (Group B) S. boydii (Group C) S. sonnei (Group D)
Biochemistry TSI K/A with NO gas LIA K/A Urea – Motility - All ferment mannitol except S. dysenteriae S. sonnei may show delayed lactose fermentation
S. dysenteriae (Group A) S. flexneri (Group B) S. boydii (Group C) S. sonnei (Group D)
Biochemistry TSI K/A with NO gas LIA K/A Urea – Motility - All ferment mannitol except S. dysenteriae S. sonnei may show delayed lactose fermentation
Shigella speciesShigella species
Virulence factorsShiga toxin – is produced by S.
dysenteriae and in smaller amounts by S. flexneri and S. sonnei.
Acts to inhibit protein synthesis This plays a role in the ulceration of the intestinal mucosa.
Virulence factorsShiga toxin – is produced by S.
dysenteriae and in smaller amounts by S. flexneri and S. sonnei.
Acts to inhibit protein synthesis This plays a role in the ulceration of the intestinal mucosa.
ShigellaShigella Clinical significance
Causes shigellosis or bacillary dysentery. Transmission is via the fecal-oral route. The infective dose required to cause infection is
very low (10-200 organisms). There is an incubation of 1-7 days followed by
fever, cramping, abdominal pain, and watery diarrhea (due to the toxin)for 1-3 days.
This may be followed by frequent, scant stools with blood, mucous, and pus (due to invasion of intestinal mucosa).
It is rare for the organism to disseminate. The severity of the disease depends upon the
species one is infected with. S. dysenteria is the most pathogenic followed by S.
flexneri, S. sonnei and S. boydii.
Clinical significance Causes shigellosis or bacillary dysentery. Transmission is via the fecal-oral route. The infective dose required to cause infection is
very low (10-200 organisms). There is an incubation of 1-7 days followed by
fever, cramping, abdominal pain, and watery diarrhea (due to the toxin)for 1-3 days.
This may be followed by frequent, scant stools with blood, mucous, and pus (due to invasion of intestinal mucosa).
It is rare for the organism to disseminate. The severity of the disease depends upon the
species one is infected with. S. dysenteria is the most pathogenic followed by S.
flexneri, S. sonnei and S. boydii.
SalmonellaSalmonella
Salmonella Classification has been changing in the
last few years. There is now 1 species: S. enteritica,
and 7 subspecies: 1, 2 ,3a ,3b ,4 ,5, and 6.
Subgroup 1 causes most human infections
2000 sub species
Salmonella Classification has been changing in the
last few years. There is now 1 species: S. enteritica,
and 7 subspecies: 1, 2 ,3a ,3b ,4 ,5, and 6.
Subgroup 1 causes most human infections
2000 sub species
SalmonellaSalmonellaClinically Salmonella isolates are often
still reported out as serogroups or serotypes based on the Kauffman-White scheme of classification.
Based on O and H (flagella) antigensThe H antigens occur in two phases; 1
and 2 and only 1 phase is expressed at a given time.
Polyvalent antisera is used followed by group specific antisera (A, B, C1, C2, D, and E)
Salmonella typhi also has a Vi antigen which is a capsular antigen.
Clinically Salmonella isolates are often still reported out as serogroups or serotypes based on the Kauffman-White scheme of classification.
Based on O and H (flagella) antigensThe H antigens occur in two phases; 1
and 2 and only 1 phase is expressed at a given time.
Polyvalent antisera is used followed by group specific antisera (A, B, C1, C2, D, and E)
Salmonella typhi also has a Vi antigen which is a capsular antigen.
SalmonellaSalmonella
Biochemistry TSI K/A + gas and H2S: S. typhi produces only a small
amount of H2S and no gas , and S. paratyphi A produces no H2S
LIA K/K with H2S with S. paratyphi A giving K/A results Urea – Motility + Citrate +/- Indole -
Virulence factors Endotoxin – may play a role in intracellular survival Capsule (for S. typhi and some strains of S. paratyphi) Adhesions – both fimbrial and non-fimbrial
Biochemistry TSI K/A + gas and H2S: S. typhi produces only a small
amount of H2S and no gas , and S. paratyphi A produces no H2S
LIA K/K with H2S with S. paratyphi A giving K/A results Urea – Motility + Citrate +/- Indole -
Virulence factors Endotoxin – may play a role in intracellular survival Capsule (for S. typhi and some strains of S. paratyphi) Adhesions – both fimbrial and non-fimbrial
SalmonellaSalmonella
Clinical Significance – causes two different kinds of disease: enteric fevers and gastroenteritis. Both types of disease begin in the same
way, but with the gastroenteritis the bacteria remains restricted to the intestine and with the enteric fevers, the organism spreads
Transmission is via a fecal-oral route, i.e., via ingestion of contaminated food or water.
Clinical Significance – causes two different kinds of disease: enteric fevers and gastroenteritis. Both types of disease begin in the same
way, but with the gastroenteritis the bacteria remains restricted to the intestine and with the enteric fevers, the organism spreads
Transmission is via a fecal-oral route, i.e., via ingestion of contaminated food or water.
EnterobacteriaceaeEnterobacteriaceae
Proteus, Providencia, and Morganella Are all part of the NF of the GI tract (except
Providencia). All motile, with Proteus swarming PA + Lysine deamination + (LIA R/A) Urea + for most, strongly + for Proteus TSI variable (know the reactions for each in
the lab!) Indole – only P. mirabilis is -
Proteus, Providencia, and Morganella Are all part of the NF of the GI tract (except
Providencia). All motile, with Proteus swarming PA + Lysine deamination + (LIA R/A) Urea + for most, strongly + for Proteus TSI variable (know the reactions for each in
the lab!) Indole – only P. mirabilis is -
Proteus, Providencia, and Morganella
Proteus, Providencia, and Morganella
Virulence factorsUrease – the ammonia produced may
damage the epithelial cells of the UT
Clinical SignificanceUT infections, as well as pneumonia,
septicemia, and wound infections
Virulence factorsUrease – the ammonia produced may
damage the epithelial cells of the UT
Clinical SignificanceUT infections, as well as pneumonia,
septicemia, and wound infections
Enterobacter sakazakii Enterobacter sakazakii Enterobacter sakazakii a Gram-negative rod-shaped pathogenic
bacterium. It is a rare cause of invasive infection with
historically high case fatality rates (40–80%) in infants.
From contaminated infant formulas E. sakazakii as a now classified into a new
genus, Cronobacter, comprising five species
For survivors, severe lasting complications can result including neurological disorders.
Enterobacter sakazakii a Gram-negative rod-shaped pathogenic
bacterium. It is a rare cause of invasive infection with
historically high case fatality rates (40–80%) in infants.
From contaminated infant formulas E. sakazakii as a now classified into a new
genus, Cronobacter, comprising five species
For survivors, severe lasting complications can result including neurological disorders.
Three ways infant formula get contaminated with Cronobacter
sp. ?
Three ways infant formula get contaminated with Cronobacter
sp. ? a) Through the raw material used for producing
the formula; b) through contamination of the formula or
other dry ingredients after pasteurization; and c) through contamination of the formula as it is
being reconstituted by the caregiver just prior to feeding.
Can other foods also be contaminated? Cronobacter sp. has been detected in other
types of food, but only powdered infant formula has been linked to outbreaks of disease.
a) Through the raw material used for producing the formula;
b) through contamination of the formula or other dry ingredients after pasteurization; and
c) through contamination of the formula as it is being reconstituted by the caregiver just prior to feeding.
Can other foods also be contaminated? Cronobacter sp. has been detected in other
types of food, but only powdered infant formula has been linked to outbreaks of disease.
CampylobacterCampylobacter
CampylobacteriosisMost frequent notified enteric
disease
The organism – G-ve, motile, spiral rod
C. jejuni & C. coli Thermophile (25 to 43 deg. C)
CampylobacteriosisMost frequent notified enteric
disease
The organism – G-ve, motile, spiral rod
C. jejuni & C. coli Thermophile (25 to 43 deg. C)
CampylobacterCampylobacter
Exponential Slender, curved shaped growth
morphology
Exponential Slender, curved shaped growth
morphology
CampylobacterCampylobacter
Characteristics
- thermophile, survives > 1 hour on
hands & moist surfaces - survives refrigeration
- can revert to VBNC
Characteristics
- thermophile, survives > 1 hour on
hands & moist surfaces - survives refrigeration
- can revert to VBNC
CampylobacterCampylobacter
The illness
- incubation – 2 to 5 days - febrile prodrome - watery/bloody diarrhoea, abdominal pain & nausea
The illness
- incubation – 2 to 5 days - febrile prodrome - watery/bloody diarrhoea, abdominal pain & nausea
CampylobacterCampylobacter The illness, continued
- infective dose – 1 000 to 10 000 cells - any age group; infants < 1 year &
young adults; males up to 45 years - Rx – fluids, ? erythromycin (resistance)
The illness, continued
- infective dose – 1 000 to 10 000 cells - any age group; infants < 1 year &
young adults; males up to 45 years - Rx – fluids, ? erythromycin (resistance)
CampylobacterCampylobacter
Sources
- human – faecal-oral person-to-person
- animal – ruminants, cats, dogs, flies,
birds
Sources
- human – faecal-oral person-to-person
- animal – ruminants, cats, dogs, flies,
birds
Campylobacter jejuniCampylobacter jejuni
CampylobacterCampylobacter
Sources - food – raw poultry, raw milk, offal, red
meat
- environment – faeces from infected
animals contaminate soil &
water
Sources - food – raw poultry, raw milk, offal, red
meat
- environment – faeces from infected
animals contaminate soil &
water
Yersinia enterocoliticaYersinia enterocolitica
Yersiniosis
The organism – small G-ve rods of family Enterobacteriaceae
Geographical variation in pathogenic serotypes
Serotype O:3 in NZ
Yersiniosis
The organism – small G-ve rods of family Enterobacteriaceae
Geographical variation in pathogenic serotypes
Serotype O:3 in NZ
Yersinia enterocoliticaYersinia enterocolitica
Characteristics
- grows at wide range of temperatures
(0 to 44 0 C), aerobically & anaerobically - withstands freezing & survives in damp soil
Characteristics
- grows at wide range of temperatures
(0 to 44 0 C), aerobically & anaerobically - withstands freezing & survives in damp soil
Yersinia enterocoliticaYersinia enterocolitica
The illness
- incubation – 7 days - abdominal pain (confused with appendicitis) - headache, fever, diarrhoea, nausea & vomiting (children – watery, mucoid
diarrhoea)
The illness
- incubation – 7 days - abdominal pain (confused with appendicitis) - headache, fever, diarrhoea, nausea & vomiting (children – watery, mucoid
diarrhoea)
Yersinia enterocoliticaYersinia enterocolitica
The illness, continued - infective dose – unknown - children < 4 years & adults 20-34
years - Rx – antibiotics when serious
The illness, continued - infective dose – unknown - children < 4 years & adults 20-34
years - Rx – antibiotics when serious
Yersinia enterocoliticaYersinia enterocolitica
Sources - human – person-to-person, hospitals
- animal – primary source is pigs (tongue &
tonsils), companion animals, rats & insects
- food – pork & pork products
- environment – drinking & surface water,
sewage sludge
Sources - human – person-to-person, hospitals
- animal – primary source is pigs (tongue &
tonsils), companion animals, rats & insects
- food – pork & pork products
- environment – drinking & surface water,
sewage sludge
Yersinia enterocoliticaYersinia enterocolitica
Yersiniosis cases in NZ from 1996 to 2004
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Listeria monocytogenesListeria monocytogenes
Listeriosis(invasive disease & non-
invasive enteritis)
The organism – G+ve ovoid to rod-shaped bacterium
Widespread in environment
Listeriosis(invasive disease & non-
invasive enteritis)
The organism – G+ve ovoid to rod-shaped bacterium
Widespread in environment
Listeria monocytogenesListeria monocytogenes
Characteristics - grows in wide range of
temperatures (1 to 45o C)
- survives freezing - aerobic & anaerobic conditions
Characteristics - grows in wide range of
temperatures (1 to 45o C)
- survives freezing - aerobic & anaerobic conditions
Listeria monocytogenesListeria monocytogenes
The illness – invasive form
- incubation – 30 days
- flu’-like symptoms, diarrhoea, vomiting, meningitis,
septicaemia, spontaneous abortion
The illness – invasive form
- incubation – 30 days
- flu’-like symptoms, diarrhoea, vomiting, meningitis,
septicaemia, spontaneous abortion
Listeria monocytogenesListeria monocytogenes
The illness – invasive form, continued
- infective dose – 100 to 1 000 cells
- pregnant women, newborn babies, the elderly & AIDS patients
- Rx – penicillin, ampicillin +/- gentamicin
The illness – invasive form, continued
- infective dose – 100 to 1 000 cells
- pregnant women, newborn babies, the elderly & AIDS patients
- Rx – penicillin, ampicillin +/- gentamicin
Listeria monocytogenesListeria monocytogenes
The illness – non-invasive
- incubation – 18 hours - diarrhoea, fever, muscle pain, headache, abdominal cramps & vomiting
The illness – non-invasive
- incubation – 18 hours - diarrhoea, fever, muscle pain, headache, abdominal cramps & vomiting
Listeria monocytogenesListeria monocytogenes
The illness – non-invasive - infective dose – > 100 thou.
cells/gm - all individuals susceptible - Rx - penicillin, ampicillin +/-
gentamicin
The illness – non-invasive - infective dose – > 100 thou.
cells/gm - all individuals susceptible - Rx - penicillin, ampicillin +/-
gentamicin
Listeria monocytogenesListeria monocytogenes
Sources - human – person-to-person rare
- animal – diseased animals shed in faeces,
contamination of red meat; silage
- food – ready-to-eat cooked food with long
shelf-life
- raw foods
- environment – widespread in soil, water & sewage
(Hospitals & occupational exposure)
Sources - human – person-to-person rare
- animal – diseased animals shed in faeces,
contamination of red meat; silage
- food – ready-to-eat cooked food with long
shelf-life
- raw foods
- environment – widespread in soil, water & sewage
(Hospitals & occupational exposure)
Listeria monocytogenesListeria monocytogenes
Listeriosis cases in NZ from 1980 to 2004
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Vibrio, Aeromonas & Plesiomonas
Similarities to Enterobacteriaceae Gram-negativeFacultative anaerobesFermentative bacilli
Differences from EnterobacteriaceaePolar flagella Oxidase positive
Formerly classified together as VibrionaceaePrimarily found in water sourcesCause gastrointestinal diseaseShown not closely related by molecular methods
General Characteristics of Vibrio, Aeromonas and Plesiomonas
Comma-shaped (vibrioid) bacilli V. cholerae, V. parahaemolyticus, V. vulnificus
are most significant human pathogens Broad temperature & pH range for growth on media
18-37C pH 7.0 - 9.0 (useful for enrichment)
Grow on variety of simple media including: MacConkey’s agar TCBS (Thiosulfate Citrate Bile salts Sucrose) agar
V. cholerae grow without salt Most other vibrios are halophilic
Morphology & Physiology of Vibrio
Vibrio spp. (Family Vibrionaceae) Associated with Human Disease
Vibrio spp. (including V. cholerae) grow in estuarine and marine environments worldwide
All Vibrio spp. can survive and replicate in contaminated waters with increased salinity and at temperatures of 10-30oC
Pathogenic Vibrio spp. appear to form symbiotic (?) associations with chitinous shellfish which serve as an important and only recently recognized reservoir
Asymptomatically infected humans also serve as an important reservoir in regions where cholera is endemic
Epidemiology of Vibrio spp.
Taxonomy of Vibrio cholerae >200 serogroups based on somatic O-antigen O1 and O139 serogroups are responsible for
classic epidemic cholera O1 serogroup subdivided into
Two biotypes: El Tor and classical (or cholerae)Three serotypes: ogawa, inaba, hikojima
Some O1 strains do not produce cholera enterotoxin (atypical or nontoxigenic O1 V. cholerae)
Other strains are identical to O1 strains but do not agglutinate in O1 antiserum (non-cholera (NCV) or non-agglutinating(NAG) vibrios) (non-O1 V.cholerae)
Several phage types
Epidemiology of Vibrio cholerae
Cholera recognized for more than two millennia with sporadic disease and epidemics
Endemic in regions of Southern and Southeastern Asia; origin of pandemic cholera outbreaks
Generally in communities with poor sanitation Seven pandemics (possible beginning of 8th)
since 1817 attributable to increased world travel Cholera spread by contaminated water and food Human carriers and environmental reservoirs
Recent Cholera Pandemics7th pandemic: V. cholerae O1 biotype El Tor Began in Asia in 1961 Spread to other continents in 1970s and 1980s Spread to Peru in 1991 and then to most of
South & Central America and to U.S. & Canada By 1995 in the Americas, >106 cases; 104 dead8th pandemic (??) V. cholerae O139 Bengal is first non-O1 strain
capable of causing epidemic cholera Began in India in 1992 and spread to Asia,
Europe and U.S. Disease in humans previously infected with O1
strain, thus no cross-protective immunity
Pathogenesis of V.cholerae Incubation period: 2-3 days High infectious dose: >108 CFU
103 -105 CFU with achlorhydria or hypochlorhydria (lack of or reduced stomach acid)
Abrupt onset of vomiting and life-threatening watery diarrhea (15-20 liters/day)
As more fluid is lost, feces-streaked stool changes to rice-water stools: Colorless Odorless No protein Speckled with mucus
Pathogenesis of V.cholerae (cont.)
Cholera toxin leads to profuse loss of fluids and electrolytes (sodium, potassium, bicarbonate) Hypokalemia (low levels of K in blood) Cardiac arrhythmia and renal failure
Cholera toxin blocks uptake of sodium & chloride from lumen of small intestine
Death attributable to: Hypovolemic shock (due to abnormally low
volume of circulating fluid (plasma) in the body) Metabolic acidosis (pH shifts toward acid side
due to loss of bicarbonate buffering capacity)
Treatment & Prevention of V. cholerae Untreated: 60% fatality Treated: <1% fatality Rehydration & supportive therapy
Oral Sodium chloride (3.5 g/L)+ Potassium chloride (1.5 g/L)+ Rice flour (30-80g/L)+ Trisodium citrate (2.9 g/L)
Intravenous (IV) Doxycycline or tetracycline (Tet resistance may
be developing) of secondary value Water purification, sanitation & sewage
treatment Vaccines
Laboratory Identification of Vibrios
Transport medium - Cary-Blair semi-solid agarEnrichment medium - alkaline peptone broth
• Vibrios survive and replicate at high pH
• Other organisms are killed or do not multiplySelective/differential culture medium - TCBS
agar
• V. cholerae grow as yellow coloniesBiochemical and serological tests
Characteristics and Epidemiology of Aeromonas (Family Aeromonadaceae)
Gram-negative facultatively anaerobic bacillus resembling members of the Enterobacteriaceae
Motile species have single polar flagellum (nonmotile species apparently not associated with human disease)
16 phenospecies: Most significant human pathogens A. hydrophila, A. caviae, A. veronii biovar sobria
Ubiquitous in fresh and brackish water
Acquired by ingestion of or exposure to contaminated water or food
Associated with gastrointestinal disease
Chronic diarrhea in adults
Self-limited acute, severe disease in children resembling shigellosis with blood and leukocytes in the stool
3% carriage rate
Wound infections
Opportunistic systemic disease in immunocompromised
Putative virulence factors include: endotoxin; hemolysins; eneterotoxin; proteases; siderophores; adhesins
Clinical Syndromes of Aeromonas
Afimbriated Aeromonas hydrophila
Nonadherent Afimbriated
Bacterial Cells and Buccal Cells
Adherent Fimbriated
Bacterial Cells and Buccal Cells
Fimbriated Aeromonas hydrophila
Characteristics of Plesiomonas Formerly Plesiomonadaceae Closely related to Proteus & now classified as
Enterobacteriaceae despite differences: Oxidase positive Multiple polar flagella (lophotrichous)
Single species: Plesiomonas shigelloides Isolated from aquatic environment (fresh or
estuarine) Acquired by ingestion of or exposure to
contaminated water or seafood or by exposure to amphibians or reptiles
Self-limited gastroenteritis: secretory, colitis or chronic forms
Variety of uncommon extra-intestinal infections
Epidemiological Features Aeromonas Plesiomonas
Natural HabitatSource of Infection
Fresh or brackish water
Contaminated water or food
Fresh or brackish water Contaminated
water or food
Clinical FeaturesDiarrheaVomiting
Abdominal CrampsFever
Blood/WBCs in Stool
PresentPresentPresentAbsentAbsent
PresentPresentPresentAbsentPresent
Pathogenesis Enterotoxin (??) Invasiveness
Characteristics of Aeromonas and Plesiomonas Gastroenteritis