Download Enterobacteriaceae: Intestinal Infection Escherichia coli

ENTEROBACTERIACEAE
Dr. Rouchelle
Dept of Microbiology
Characteristics of the Enterobacteriaceae
•
Gram-negative bacilli
Four major features:
1. Ferment glucose
2. Reduce nitrates to nitrites
3. Oxidase negative
4. All except Klebsiella, Shigella and Yersinia are
motile by peritrichous flagella
• Grow readily on
– MacConkey (MAC) agar
– Eosin methylene blue (EMB) agar
• Grow readily at 35oC except Yersinia (25o-30oC)
• Do not form spores
• Natural Habitat:
– Environment (soil, water, and plants)
– Intestines of humans and animals
Classification of Enterobacteriaceae:
• Very large number of organisms in Family
Enterobacteriaceae, species are grouped into - TRIBES
•
•
•
•
•
Tribe 1 – Escherichieae
Tribe 2 – Klebsiellae
Tribe 3: Proteae
Tribe 4 : Yersiieae
Tribe 5 : Erwinieae
• Within each Tribe, species are further subgrouped under
genera
Major Genera of family Enterobacteriaceae:
1. Escherichia
2. Shigella
3. Salmonella
4. Yersinia
5. Klebsiella
6. Proteus
Antigenic Factors of Enterobactericeae:
• Ability to colonize, adhere, produce various toxins and
invade tissues
• Some possess plasmids that may mediate resistance to
antibiotics
• Imp antigens used to identify the organisms:
– O antigen – somatic, cell wall, heat-stable Ag
– H antigen – flagellar, heat labile Ag
– K antigen – capsular, heat-labile Ag
Clinical Significance of Enterics:
• Ubiquitous in nature
• Except for Salmonella, Shigella and Yersinia, most are
present in the intestinal tract of animals and humans as
commensal flora; “fecal coliforms”
• Some live in water, soil and sewage
Clinical Significance of Enterics:
• Based on clinical infections produced, enterics are divided
into two categories:
1. Opportunistic pathogens – normally part of the usual
intestinal flora, that may produce infection outside the
intestine
2. Primary intestinal pathogens – Salmonella, Shigella,
and Yersinia sp.
Enterobacteriaceae: Modes of Infection
1. Contaminated food and water (Salmonella spp.,
Shigella spp., Yersinia enterocolitica, Escherichia coli
O157:H7)
2. Endogenous infection (urinary tract infection, primary
bacterial peritonitis, abdominal abscess)
3. Abnormal host colonization (nosocomial pneumonia)
4. Transfer between debilitated patients
5. Insect (flea) vector: unique for Yersinia pestis
1. Urinary tract infection: Escherichia coli, Klebsiella
pneumoniae, Enterobacter spp., and Proteus mirabilis
2. Pneumonia: Klebsiella pneumoniae; Enterobacter spp.,
3. Wound Infection: Escherichia coli, Enterobacter spp.,
Klebsiella pneumoniae, and Proteus mirabilis
4. Bacteremia: Escherichia coli, Enterobacter spp.,
Klebsiella pneumoniae, and Proteus mirabilis
Enterobacteriaceae: Intestinal Infection
• Escherichia coli
• Shigella
• Salmonella
• Yersinia enterocolitica
Identification of Enterobacteriaceae:
• IMViC Test
• Indole, Methyl Red, Voges-Prosakaur, Citrate
(IMViC) Tests:
– The IMViC series of reactions allows for the
differentiation of the various members of family
Enterobacteriaceae.
A) Indole –Positive, B) MR –Positive
C) VP- Positive, D) Citrate- Negative
Methyl Red-Voges Proskauer (MR-VP) Tests
Principle
Glucose
Acidic pathway
Or
Acety methyl carbinol
(ACETOIN)
Mixed acids
 pH less than 4.4
Barrit’s A
Barrit;s B
Methyl Red
indicator
Red color
Neutral pathway
MR positive
E. coli
VP positive
Klebsiella
Pink color
MR/VP test
Methyl Red test
Red: Positive MR (E. coli)
Yellow or orange: Negative MR (Klebsiella)
Voges-Proskauer test
Pink: Positive VP (Klebsiella)
No pink: Negative VP (E. coli)
Result
Example
Reaction on TSI
Butt
color
Red
Slant
color
Red
H2 S
Negative
Negative
Yellow
Yellow
Yellow
Red
Red
Yellow
Positive
black in
butt
Negative
Result
Alk/Alk/(No action on
sugars)
A/Alk/(Glucose fermented
without H2S)
A/Alk/+
(Glucose fermented
with H2S)
A/A/(three sugars are
fermented)
Non fermenter
e.g.
Pseudomonas
LNF
e.g. Shigella
LNF
e.g. Salmonella
& Proteus
LF
e.g. E. coli,
Klebsiella,
Enterobacter
TSI Reactions of the Enterobacteriaceae
•
•
•
•
•
•
•
A/A + g = acid/acid plus gas (CO2)
A/A = acid/acid
A/A + g, H2S = acid/acid plus gas, H2S
Alk/A = alkaline/acid
Alk/A + g = alkaline/acid plus gas
Alk/A + g, H2S = alkaline/acid plus gas, H2S
Alk/A + g, H2S (w) = alkaline/acid plus gas, H2S (weak)
A/A + g
• Escherichia coli
• Klebsiella
A/A + gas, H2S
• Citrobacter freundii
• Proteus vulgaris
• Non-lactose, sucrose fermenter
Alk/A
– Shigella
– Providencia
Alk/A + g
– Salmonella serotype Paratyphi A
Alk/A + g, H2S
– Salmonella
– Proteus mirabilis
– Edwardsiella tarda
Lactose fermenting
colonies
Non lactose fermenting
colonies
Escherichia coli
•
•
•
•
Most significant species in the genus
Important potential pathogen in humans
Common commensal in the intestine
Pink (lactose positive) colony with surrounding pink area on
MacConkey
– Ferments glucose, lactose, trehalose, & xylose
– Usually motile
– Positive indole and methyl red tests
– Does NOT produce H2S
– Simmons citrate negative
– Voges-Proskauer test negative
Infections caused by E.coli:
– Meningitis, gastrointestinal, urinary tract, wound, and
bacteremia
– Gastrointestinal Infections :
1. Enteropathogenic (EPEC)
– Primarily in infants and children;
– Outbreaks in hospital nurseries and day care
centers
– Stool has mucous but not blood
– Identified by serotyping
Enteropathogenic E.coli
Destruction of surface microvilli
• Fever
Gut lumen
• Diarrhea
• Vomiting
• Nausea
• Non-bloody stools
25
Enterotoxigenic E. coli
• Diarrhea resembling cholera
• Travelers diarrhea
26
Enterotoxigenic E. coli
• Heat labile toxin
– Like cholera toxin
– Adenyl cyclase activated
– Cyclic AMP
– Secretion water/ions
• Heat stable toxin
– Guanylate cyclase activated
– cyclic GMP
– uptake water/ions
27
Enteroinvasive E. coli (EIEC )
•Dysentery
- Resembles shigellosis
Enterohemorrhagic E. coli
• Usually O157:H7
Flagella
Transmission electron
micrograph
29
O157:H7 transmitted- through meat products or
sewage-contaminated vegetables
• Hemorrhagic diarrhea
– Bloody, copious diarrhea
– Few leukocytes
– Afebrile
• Hemolytic-uremic syndrome (HUS)
– Hemolytic anemia
– Thrombocytopenia (low platelets)
– Kidney failure
30
Enterohemorrhagic E. coli
• Vero toxin- “shiga-like”
• Hemolysins
Enteroaggregative (EaggEC)
Cause diarrhea by adhering to the mucosal surface of the
intestine; watery diarrhea; symptoms may persist for over
two weeks
31
Urinary Tract Infections
• E. coli is most common cause of UTI and pyelo-nephritis
in humans
• Usually originate in the large intestine
• Able to adhere to epithelial cells in the urinary tract
Septicemia & Meningitis
• Most common causes of septicemia and meningitis
among neonates
• Acquired in the birth canal before or during delivery
• E. coli also causes bacteremia in adults, secondary to
genitourinary tract infection or a gastrointestinal
source
Klebsiella, Enterobacter
• Usually found in intestinal tract
• Wide variety of infections, primarily pneumonia, wound,
and UTI
• General characteristics:
– Non-motile
– Simmons citrate positive
– H2S negative, Weakly urease positive
– MR negative; VP positive
• Usually found in Gastro-intestinal tract
• K. pneumoniae is most commonly isolated species
• Possesses a polysaccharide capsule - which protects
against phagocytosis and antibiotics
• Makes the colonies moist and mucoid
– Frequent cause of nosocomial pneumonia
– Significant biochemical reactions
• Lactose positive
• Most are urease positive
• Non-motile
• Nosocomial pneumonia: Spread by health care
personnel and equipment
• Frequently caused by K. pneumoniae
• Often seen in middle-aged males who abuse alcohol
• Difficult to diagnose due to commensals in sputum
Proteus, Morganella & Providencia species
• All are normal intestinal flora
• Opportunistic pathogens
• Deaminate phenylalanine
• Non lactose fermenters
Proteus species
• P. mirabilis and P. vulgaris are widely recognized
human pathogens
• Isolated from urine, wounds, and ear and bacteremic
infections
• Both produce swarming colonies and have a distinctive
“burned chocolate” odor
• Both are strongly urease positive
• Both are phenylalanine deaminase positive
• Exhibits characteristic “swarming”
Laboratory Diagnosis of Enterics
Specimen collection:
• Specimens collected and transported in Cary-Blair,
Amies, or Stuart media
Isolation and Identification
– Site of origin must be considered
– Enterics from sterile body sites are highly significant
– Routinely cultured from stool
Media for Isolation and Identification of
Enterics:
– Blood agar and a selective/differential medium such
as MacConkey
– On MacConkey, lactose positive are pink; lactose
negative are clear and colorless
– For stool, highly selective media, such as Hektoen
Enteric (HE), XLD, or SS is used along with
MacConkey agar
• Identification: All enterics are
 Oxidase negative
 Ferment glucose
 Reduce nitrates to nitrites
SHIGELLA &
SHIGELLOSIS
Characteristics of Shigella:
–
–
–
–
–
–
Short gram negative bacilli
Non-motile
Do not produce gas from glucose
Fragile organisms
Non-lactose fermenting
Resistant to bile salts
CLASSIFICATION:
• Shigellae are classified into 4 subgroups (A, B,
C, D) based on biochemical and serological
specificity
• Subgroup A – Mannitol fermentation negative
• Subgroup B, C, D – Mannitol positive
SERO
GROUP
ORGANISM
REACTIONS
DISTRIBUTION
A
S. dysenteriae
(Sh.shigae)
12 serotypes
-Catalase
negative
- mannitol
negative
Developing
Countries Africa,
Latin America, Asia
B
S.flexneri
6 serotypes
Few biotypes
form acid & gas
Common in
developing countries
C
S.boydii
18 serotypes
Bacillary
dysentery
Indian subcontinent
D
S.sonnei
Late lactose
fermenter
Developed countries
Clinical Infections
– Dysentery (bloody stools, mucous, and numerous
WBC)
– S. sonnei and S. flexneri common
– Humans are only known reservoir
– Oral-fecal transmission
– Low infectious dose (102-104 CFU)
• Incubation period = 1-3 days
• Watery diarrhea with fever; changing to dysentery
• Outbreaks in daycare centers, nurseries,
institutions
Pathogenesis of Shigellosis (2 stages)
 Early stage:
• Watery diarrhea - Enterotoxic activity of Shiga
toxin
• Following ingestion and noninvasive colonization,
multiplication, and production of enterotoxin in the
small intestine
 Second stage:
• Adherence and tissue invasion of large intestine symptoms of dysentery
• Cytotoxic activity of Shiga toxin increases
severity of dysentry
Virulence attributable to:
1. Invasiveness
•
Attachment (adherence) and internalization
•
Large multi-gene virulence plasmid regulated by
multiple chromosomal genes
2. Exotoxin (Shiga toxin)
3. Intracellular survival & multiplication
Invasiveness in Shigella-Associated Dysentery
•
Penetrate through colonic mucosa, invade and multiply
in the colonic epithelium but do not typically invade
beyond the epithelium into the lamina propria
•
Preferentially attach to and invade into M cells in
Peyer’s patches (lymphoid tissue, i.e., lymphatic system)
of small intestine
Invasiveness in Shigella-Associated Dysentery
 M cells - transport foreign antigens from the intestine to
underlying macrophages,
 Shigella can lyse the phagocytic vacuole (phagosome)
and replicate in the cytoplasm
 Note: This contrasts with Salmonella which multiplies in the
phagocytic vacuole
 Actin filaments propel the bacteria through the
cytoplasm and into adjacent epithelial cells with cell-tocell passage, thereby effectively avoiding antibodymediated humoral immunity (similar to Listeria
monocytogenes)
In
Shigella pathogenesis
Toxins produced by Shigella:
1. Endotoxin
2. Exotoxin: acts as Enterotoxin & Neurotoxin
3. Shiga toxin: (Verocytotoxin) produced by Sh.dysentriae
type 1.
•
Made of 2 subunits: A & B
• Subunit B binds to intestinal cells
• Subunit A inhibits protein synthesis
Shiga toxin (3 effects)
1. Enterotoxic
2. Cytotoxic
3. Inhibits protein synthesis
Enterotoxic Effect:
– Adheres to small intestine receptors
– Blocks uptake of electrolytes, glucose, and amino
acids from the intestinal lumen
57
Shigellosis:
• Incubation: 1 to 2 days (up to 7 days)
• Duration: 4 days to 2 weeks (shedding!)
Clinical Signs:
• Mild watery diarrhea
• Severe dysentery
• Abdominal pain,
• Fever
• Bloody stools with mucus, tenesmus
• Dehydration, acidosis and death – in young, old,
immunocompromised & malnourished
Complications of Shigellosis
•
•
•
•
•
•
Intestinal perforation
Septicemia
Toxic megacolon
Seizures
Reactive Arthritis
HUS (S. dysenteriae)
Laboratory diagnosis:
1. Specimen collection:
• Stool
• Rectal swabs
Transport medium used- Sach’s buffered glycerol saline
2. Microscopy (wet mount)
•
Fecal leucocytes are found in large No. (>50
cells/HPF) in Shigellosis
*Clumps of fresh leucocytes, RBCs & Macrophages
typical of Shigellosis
STOOL IN SHIGELLOSIS
3. Inoculation of primary isolation media
• MA- convex, colorless NLF colonies
• XLD- red, smooth colonies
• SSA- colourless, transluscent colonies
• Selinite F broth – enrichment medium
Confirmtion is by :
4. Biochemical identification
5. Serological identification
– Polyvalent antisera for Group A, B, C and D
serogroups – slide agglutination test
Treatment:
• Proper hydration - generally a self-limiting disease
• Sever disease – treated with antibiotics (children)
• Nalidixic acid , Norfloxacin - used
• Effective antibiotic treatment
– Reduces duration of illness from 5-7 days to 3 days
– Reduces period of Shigella excretion after symptoms
subside.
• Antimicrobial resistance a worldwide problem
Prevention of Shigellosis:
• Proper sanitation, cooking and storage of food
• Identification of carriers, especially food
handlers
SALMONELLA
Genus: SALMONELLA
Clinically important species
• S. typhi
• S. paratyphi A, B, C
• Other Salmonella species
Diseases caused:
• Enteric fever
• Gastroenteritis
• Septicemia
Normal habitat:
• Intestines of animals - especially pigs, cattle, rodents,
shellfish (contaminated meat and fish)
• S.typhi and S. paratyphi - found only in humans
• Excreted in faeces & urine of patients , and present in the
gall bladder of long term carriers.
• Mode of Infection - By ingestion organism in food/water
or contaminated hands.
• S. typhi causes typhoid – spread mainly by water
• S. paratyphi by food.
General Characteristics of Salmonella:
 Coliform bacilli (Enteric rods)
 Motile gram-negative facultative anaerobes
 Non-lactose fermenting
 H2S producing (except S.paratyphi A &
S.cholersuis))
Biochemical reactions:
• Salmonellae ferment glucose, Mannitol and maltose –
producing acid and gas.
• ( S.typhi does not produce gas)
• Utilise citrate (except S.typhi & S.paratyphi A)
• Indole negative
• Do not ferment lactose
• Most produce H2S in TSI agar. (except S.paratyphi A
& S.cholersuis)
Antigenic structure:
• Salmonellae possess 3 types of antigens based on which
they are classified
1. Flagellar antigen ‘H’
2. Somatic antigen ‘O’
3. Surface antigen ‘Vi’
Flagellar antigen ‘H’
• Present on the flagella
• Heat labile protein
• Destroyed by boiling, alcohol & acids
• Strongly immunogenic
• When mixed with antisera, H agglutination occursproducing large , loose. Fluffy clumps
• Flagellar antigens present in 2 phases – phase 1 &
phase 2
Somatic antigen ‘O’
•
•
•
•
LPS – part of the cell wall
Heat stable
Resistant to boiling, alcohol & acids
Less immunogenic than H antigen – Titre of ‘O’ Ab in
serum after infection / immunisation.
• When mixed with antisera- agglutination produces
compact, chalky, granular clumps.
Surface antigen ‘Vi’:
• Surface antigen, Interferes with agglutination of freshly
isolated strains
• Poorly immunogenic - Induces production of low titres of
Ab following infection- not useful for diagnosis
• Total absence of Vi antibody in a typhoid case- poor
prognosis
• Persistence of Vi Ab indicates- CARRIER STATE
Classification:
• The Kaufmann-White system used to classify Salmonella
based on identifying the O and H antigens by agglutination
• The detection of Vi antigen is also used in the detection of
Salmonella typhi and other species.
2nd bacteremia
(mononuclear
phagocytes )
liver、spleen、gall、
Bone Marrow
early stage (1-3W）
Bacilli. In gall
Bac. In
Bac. In
feces
feces
peyer's patches &
mesenteric lymph nodes
Enterorrha
gia,intestin
al
perforation
LN Proliferate,swell
necrosis defervescence
stage
（3-4w）
1st bacteremia
(Incubation stage)
10-14d
S.Typhi eliminated
convalvescence stage
(4-5w)
Pathogenecity
S. Typhi causes : Typhoid fever.
Symptoms –
 Fever with low pulse rate,
 Headache,
 Spleenomegaly
 Mental confusion,
 Rashes [rose spots] on light colored skin,
 In uncomplicated typhoid, total WCC is low with
relative lymhocytosis and anaemia.
S. Paratyphi A&B
• Paratyphoid or enteric fever - milder than typhoid fever.
• Diarrhea and vomitting
Other Salmonella species cause:
• Food poisoning [enterocolitis]
• Food poisoning strains can also cause bacteremia,
inflammation of the gall bladder, ostitis and occasionally
abscesses.
Laboratory diagnosis of enteric fever:
•
Specimens: Blood, Bone marrow, Urine, Stools, Intestinal
contents by enterotube
•
Commonly Blood, urine & feces for culture.
• Blood Culture– positive in 75-90% of patients during first
10 days of infection
• Faeces – S.typhi can be isolated from 80% of patients in the
3rd week.
Microscopy:
• Gram negative motile bacilli
• Faeces may contain blood and few pus cells
Culture
• Enrichment & selective media for enrichment of
Salmonella from faeces –Selenite F broth.
• Differential media is XLD and BSA
• XLD-pink colonies with black centers
• BSA- black colonies with silver metallic sheen.
XLD Agar
XLD - Red pink black
centered colonies Salmonella
BSA- Black colonies
with silver metallic
sheen.
Biochemical reactions
TSI
• K/Ag+ Salmonella species
• K/A+ (H2S) Salmonella typhi
Lysine
Salmonella typhi Salmonella species +
Shigella
-
Indole
-
Mannitol
+
+
-
O Antigens
• Cell wall heat stable antigens.
• Groups are designed A- Z
• Medically important Salmonella belong to groups A to G.
• Each group has a group factor, which is an O antigen
common to all members of the group and not possessed
by Salmonella belonging to other groups.
H Antigens
• Flagella – heat stable antigens
• Serotyped by their H antigens
• Many Salmonella are diphasic, i.e. occur in 2 antigen
forms referred to as phase l and phase ll.
• Phase l antigens are given in alphabetical letters and
phase ll are either numbered or given a letter if known
to occur in both phases.
Vi Antigen:
• Surface or capsule antigen can be found in S. typhi, S.
paratyphi C and a few other Salmonella.
• Associated with virulence and can be detected using Vi
antiserum.
• It can interfere with O antigen testing
• Saline suspension of organism should be heated in water
bath for 20 mins and after being allowed to cool, the
bacterial cells should be retested with the O antiserum.
Grouping and serotyping of Salmonella
• Specific O, H and Vi antisera to identify the S. typhi.
• The following sera are required to identify S. typhi:
 Salmonella O antiserum Factor 9 [Group D]
 Salmonella H antiserum
 Salmonella Vi antiserum
Widal Test
• This tests for presence of O & H antibodies in the
patients serum.
• Useful test when culturing facilities are not
available.
Buffy coat cultures
• A low yield is related to low numbers of Salmonella (<15
organisms per milliliter) in infected patients and/or to recent
antibiotic treatment.
• Centrifugation to isolate and culture the buffy coat, which
contains abundant blood mononuclear cells associated with
the bacteria, decreases time to isolation
Stools/intestinal secretions culture:
• 40-50- % positivity in 2nd week, 80 % in 3rd wk
Urine culture:
• 25 % in second week
• Excretion intermittent
• Multiple cultures needed
Bone marrow
• In long standing enteric fever more success in bone
marrow cultures than with blood especially if patient
on antimicrobials
• The test is extremely painful. Clinicians should try
to establish the diagnosis with less traumatic means.
Culture/blood/buffy coat/Bone marrow
• Blood collected in tryptic soy broth
Enrichment cultures of specimens like stool
/intestinal contents
• Stool/intestinal contents are put in selenite F broth /
tetrathionate broth before being cultured on to selective
/differential media
Selective /differential media for the isolation of salmonellae
from clinical samples including blood from
enrichment/selective broths
• Media of medium to high selectivity
• Inhibit gram positive and commensals including Gram
negative enterics
– DCA
– Brilliant green Agar
– Bismuth sulfite Agar
– XLD
Final identification
• By biochemical methods
• Slide and tube agglutination tests with
specific antiserum
DNA testing:
• Polymerase chain reaction assays for
identifying S typhi are available
Stools Microscopy/enteric fever
• Macrophages
• Blood
• Stools microscopy in other salmonellosis
• Pus cells and red cells
Widal
•
•
Detection of Abs against the organisms of enteric fever
Antigens known
• O antigens and H antigens
• Available commercially
• Qualitative
• Quantitative
• Qualitative slide method
• End point agglutination
Widal
• Quantitative, agglutination test
• Doubling dilutions of serum and addition of constant
quantity of antigen
• Incubation water bath
• Reaction
• Followed by settling time
• Examine the tubes with a hand lens against a dark
background
• End point carpet formation
• Granular agglutination
• Floccular agglutination
• Also look for clearing in supernatant fluid
Carpet
Larger flocules
Widal interpretation
• Active typhoid if titers above 1:180 or 1:200 against
O or H or both agglutinins is present
• High titer > 1:160 against O antigen suggestive of
infection
• High titer > 1:160 against H antigen alone suggests
past infection
Widal interpretation
• In acute infection, O Ab appears first
• H Ab appears slightly later but persists longer and
can be used to distinguish between various types of
enteric fever.
Limitations of Widal test:
• Titers against almost all the antigens raised
– TAB Vaccination
• Titers against o and H antigens may be raised in the
following diseases/conditions
• Other salmonellosis
• Chronic liver disease
• Immunological disorders
– rheumatic fever
– Nephrotic syndrome, Ulcerative colitis etc.
Prevention and control
• Prevent consumption of contaminated food and water
• Food like ice creams – can be contaminated with nontyphoidal Salmonella
• Boiling of milk before drinking
• Periodic check up of food handlers
• Exclude carriers
Antimicrobial treatment
• Chloramphenicol -emergence of resistant strains
• Co-trimoxazole, Ampicillin
• Amoxycillin
• Ciprofloxacin. Ofloxacin
• Ceftriaxone or some other third gen cephlosporins
• Emergence of MDR
Multidrug resistant strains
• These bacteria are resistant to chloramphenicol, ampicillin,
trimethoprim, sulfonamides, and tetracycline.
• Like chloramphenicol resistance, resistance to ampicillin
and trimethoprim is plasmid-encoded.
• Drug of choice for MDR treatment: Fluroquinolones
Chronic carrier state (stool & urinary carriers)
A small percentage become chronic carriers and continue to
have positive stool cultures for at least 1 year
• 1-4% of untreated patients become chronic carriers
• Bladder infection with Schistosoma haematobium
predisposes to urinary carriage.
• .
Typhoid Mary
•
Typhoid Mary's real name was Mary Mallon.
•
Irish immigrant who made her living as a cook
•
Mallon was the first person found to be a "healthy carrier"
of typhoid fever in the United States.
•
She herself was not sick – but over 30% of the bacteria in her
feces were S. typhi
•
Mallon is attributed with infecting 47 people with typhoid
fever, three of whom died.