Enteric Gram-Negative Rods

Demissew sh.
ENTERIC GRAM-NEGATIVE RODS

(ENTEROBACTERIACEAE)
June 11, 2024 Dep MLS

Introduction
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 The Enterobacteriaceae is a large family of Gm-ve rods

 Natural habitat: the intestinal tract of humans & animals
 They are facultative anaerobes in the large intestine but are present in relatively small
numbers compared with anaerobes such as Bacteroides.
 Although the members of the Enterobacteriaceae are classified together taxonomically, they
cause a variety of diseases with different pathogenetic mechanisms
 Some enteric pathogens, e.g. E. coli, are part of the normal flora & incidentally cause disease
(like, UTI).
Demissew sh. June 11, 2024
 Others: Salmonella & Shigella are regularly pathogenic for humans.
Morphology General features
3
 All Enterobacteriaceae
 Gram negative rods
 Ferment glucose with/without acid production
 Reduce nitrates nitrite
 Oxidase negative
 Catalase positive
 Facultative anaerobes and non-spore forming
 All motile by peritrichous flagella except Shigella, Klebsiella and Yersinia
 Non -capsulated except Klebsiella
 Non -fastidious
 Grow on bile containing media (MacConkey)
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 ≈ 50 genera have been known

 The most common includes:
 Escherichia coli Providencia
 Klebsiella Edwardsiella
 Proteus Yersinia
 Serratia Salmonella
 Enterobacter Shigella
 Citrobacter
 Morganella
Enterobacteriaceae
5
Culture:
 Grow on ordinary media - e.g. Blood, MacConkey, Eosin methylene blue (EMB)
 Typical colonies on most bacteriologic media are - circular, convex & glistening or mucoid.
 The loss of capsules produce rough colonies that are flat, irregular & granular in appearance.
 Most are non-pigmented, although a few spp include strains that produce red, pink, yellow or
blue pigments
 Some are highly motile with unique swarming pattern on agar cultures.... Proteus
 Biochemically they active & ferment a large number of carbohydrates (eg: glucose, lactose...)
General characteristics….
Antigenic Structure
 Possess a wide variety of antigens which are used in serotyping,
particularly salmonellae, shigellae, and E.coli.
1. O antigens: Are also called somatic antigen: is the O-specific

polysaccharide of the Lipo-polysaccharide (LPS) component of the cell
wall and are heat stable. The O-specific polysaccharide protects some species
against host resistance factors.
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2. K antigens: capsular polysaccharide antigens, surround the cell wall. The K

polysaccharide also provides a barrier to phagocytosis because of its ability to resist
activation of the alternative complement path way.
3. H antigens: flagellar protein antigens possessed by motile enterobacteria. They are
heat labile (destroyed at 60-100 ºC).

4. Colicins (Bacteriocins)
 Colicins are bactericidal substances produced by certain strains of bacteria active
against some other strains of the same or closely related species. Their production is
controlled by plasmids. Colicins can be used for typing “organisms”.
5. Toxins and Enzymes: In many bacterial infections thesh.characteristic
Demissew June 11, 2024 pathology is caused
by toxins.
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Two major types of toxins:
1. Endotoxin: also called LPS, is a component of the outer membrane of gram

negative bacteria and released from the bacterial surface following natural
lysis of the bacterium.
2. Exotoxins: are diffusible proteins secreted into the external medium by the
pathogen

Antigenic structure

Pathogenesis
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 Cause both intestinal and extraintestinal diseases

 Some strain E.coli have evolved to be strictly
intestinal pathogen
 Extraintestinal infections are the predominant
presentation of disease caused by enteric GNB
 Depending on both the host and pathogen, nearly
every organ or cavity can be infected with GNB.

Disease caused by GNR
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In GIT
 The enteric bacteria generally do not cause diseases
 In the intestine, they may even contribute to normal flora function and nutrition
 When clinically important infection occur, they are usually caused by E. coli
 In general, the invasive and cytotoxic strains
 Produce an inflammatory diarrhoea called dysentery with white blood
cells(WBCs) and/or blood in stool. Demissew sh. June 11, 2024
Diseases caused by GNR
12
 The enterotoxin-producing strains

 Cause a watery diarrhoea in which fluid loss is the primary pathophysiological
features
 But the other enteric bacteria are causes of hospital –acquired infection
occasionally cause community -acquired infection.

Diseases caused by GNR
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 Extra –intestinal sites

 The bacteria become pathogenic
 When they reach tissues outside of their normal intestinal or other less
common normal microbiota sites
 some of the enteric bacteria (eg. Serratia marcescens, Enterobacter aerogenes)
are opportunistic pathogen
 Infancy or old age
 In the terminal stages of other diseases
 After immunosuppression
 With indwelling venous or urethral catheter Demissew sh. June 11, 2024
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 Enterobacteria classified as Lactose fermenting and Non- Lactose fermenting.

 Lactose fermenting Enterobacteria includes
 Escherichia
 Enterobacter Coliforms
 Klebsiella
 Citrobacter

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 2. Non-lactose fermenting enterobacteria

 Salmonella
 Shigella
 Serratia
 Proteus
 Providencia
 Yersinia
 Morganella
 Edwardsiella
 Hafnia
GENUS: ESCHERICHIA
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 Main species of medical importance is Escherichia coli.

 The genus is named after Theodor Escherich, discoverer of E.coli.
 Escherichia is a genus of Gram-negative, non-spore forming, facultative
anaerobic,
 rod-shaped bacteria from the family Enterobacteriaceae.
 In those species which are inhabitants of the gastrointestinal tracts of warm-
blooded animals,
General characteristics
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 Escherichia coli is a commensal found in the intestinal tract of humans and animals.
 One gram of faces may contain from 1x107 to 1x108 organism.
 It is the most abundantly found bacteria in colon and faeces.
 Found in soil, water and vegetation.
 Most are motile; some are capsulated.
 Despite being commensals, some strains of E. coli are pathogenic and cause
diarrheal disease and extra-intestinal infections.
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 Extra intestinal disease caused by E. coli is usually the result of person-to-person contact.
 The infection may also be endogenous in which the organism travels from the intestine to the urinary tract →
UTI.
 E. coli is implicated in approximately 20% of all urinary tract infections in hospital.
 Hospital-associated infections represent another group of extra intestinal infection caused by E. coli.
 E. coli possesses a broad range of virulence factors General factors possessed by all members of the
family Enterobacteriaceae,
 Escherichia strains possess specialized virulence factors that can be placed into two general
 categories:
 – adhesins and exotoxins.
Antigenic structure and Virulence factor
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1. Antiphagocytic surface properties: capsules, K antigens and LPS.
2. Adhesins: fimbriae / pili , Intimin (non-fimbrial adhesin)
3. Invasins: hemolysisn, siderophores and siderophore uptake
systems and Shigella-like "invasins" for intracellular invasion and spread.

 Strains of E. coli that are associated with UTI often possess adhesins called P
pili.
 More P pili containing strains are reported in more severe forms of urinary
tract disease such as pyelonephritis (inflammation
Demissewof
sh. the
Junekidney
11, 2024 usually arising
from infection ascending from the ureter).
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4. Hemolysin: E. coli produces an alpha hemolysin that lyses erythrocytes.
5. K antigen or capsular polysaccharide: the K antigens are anti-phagocytic.
The polysaccharide also blocks opsonisation by interfering with complement
deposition.
6. Toxins: Heat labile(LT) toxin , heat stable (ST) toxin , Shiga like toxin ,
Epidemiology
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 Large numbers of E. coli are present in the GI tract.

 Opportunistic pathogens when the intestines are perforated and the bacteria enter the
peritoneal cavity, most E. coli that cause GI and extraintestinal disease do so because they
have acquired specific virulence factors
– encoded on plasmids or in bacteriophage DNA.
 Most infections are endogenous;
– with the exception of neonatal meningitis and gastroenteritis
– the E. coli that are part of the patient’s normal microbial flora are able to establish infection
Clinical features
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Pathogenesis and clinical manifestations
E. coli causes:
1.Urinary tract infections (UTI). E. coli is the commonest pathogen isolated from patients with cystitis.
Recurring infections are common in women.
 Uropathogenic E. coli colonize the vagina & peri urethral region from where they ascend to the bladder or kidney
causing cystitis or pyelonephritis.
 The symptoms and signs include urinary frequency, dysuria, hematuria, and pyuria.
 UTI can result in bacteremia with clinical signs of sepsis.
 Infections of wounds, peritonitis, sepsis and endotoxin induced shock.
 Meningitis and bacteraemia in neonates. E. coli capsularDemissew
type K1 sh. antigen is associated with neonatal
June 11, 2024
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2.Intestinal diseases:
 Different strains of E. coli can cause diarrhoea through different
mechanisms:
 Diarrhoeal disease: infantile gastroenteritis, traveller’s diarrhoea, dysentery,
and haemorrhagic diarrhoea which may progress to haemolytic uraemic
syndrome.
 E. coli strains associated with diarrhoeal disease
 More than 180 different O serotypes of E.coli have been described, but only
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1.Enterotoxigenic E. coli (ETEC): Causes watery (secretory) diarrhoea due to

the production of plasmid mediated toxins in infants and adults.
 → Pathogenic serogroups includes O6 ,O8, O15, O25, O27, O63, O119,
O125 - O128 and O142.
 They are responsible for community-acquired diarrhoeal disease in areas
of poor sanitation and are the commonest causes of traveller’s diarrhoea.

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 ETEC produces heat-stable(ST) enterotoxin or heat-labile(LT) enterotoxin, or both.

 In addition, they usually express fimbriae that are specific for the host animal
species and that enable the organisms to adhere to the epithelium of the small
intestine.
 2. Enteropathogenic E. coli (EPEC): Causes vomiting, fever, and prolonged
diarrhoea mainly in infants (less than 2 year).
 Due to bacteria adhering to epithelial cells, multiplying and causing lesions.
. Demissew sh. June 11, 2024

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Enteropathogenic E. coli (EPEC) :

 Cause infantile enteritis, especially in tropical countries.
 Pathogenic sero-groups includes: O26,O55, O86,O111, O114, O125- O128 and
O142.
 Colonisation of the upper part of the small intestine occurs in infantile enteritis
associated with EPEC

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3. Entero-invasive E. Coli (EIEC): Causes dysentery (similar to shigellosis),

fever and colitis, with blood, mucus, and many pus cells in faecal specimens.
Due to bacteria invading and multiplying in epithelial cells. Pathogenic sero-
groups includes: O78,O115, O148,O153, O159 and O167.
 EIEC, like Shgella cause disease by invading intestinal epithelium.
 Infection is mainly by ingestion; only a small number of bacteria need to be
swallowed as they are relatively resistant to gastric acid and bile, and pass
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4.Enterohaemorrhagic E. coli (EHEC): Causes life-threatening haemorrhagic

diarrhoea (colitis) in all ages, without pus cells, and often without fever. It can
progress to haemolytic uraemic syndrome with renal failure.
→ EHEC is due to cytotoxins damaging vascular endothelial cells, and is mainly

associated with the serogroup O157:H7. It is sometimes referred to as VTEC
(verocytotoxin-producing E. coli, because it is toxic to vero monkey cells in culture).
→ Infection occurs by ingesting contaminated meat products, un pasteurized milk

and dairy products. Demissew sh. June 11, 2024
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5.Enteroaggregative E. coli ( Eagg EC)
 have been implicated as a cause of persistent, watery diarrhea with dehydration

in infants in developing countries and in travellers to these countries.

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3. Neonatal meningitis
• E. coli causes 40% of neonatal meningitis followed by group B streptococci.
4. It causes bacteraemia & endotoxic shock in immunocompromised host.
5. It causes hospital-acquired infections

Lab diagnosis
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 Specimen: Urine, pus, blood, stool, body fluid

 Pathologic material is inoculated on MacConkey media; LF colonies are further identified by
their morphology & biochemical reactions.

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 Treatment : will be best, based on results of AST.

 Cipro, cotri,Cefotaxime, Ampicillin
 PREVENTION AND CONTROL
• Restricting use of antibiotics and avoiding unnecessary use of urinary catheters.
• Maintenance of high hygienic standards to reduce risk of gastroenteritis.

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2. Non-lactose fermenting enterobacteria

 Salmonella
 Shigella
 Serratia
 Proteus
 Providencia
 Yersinia
 Morganella
 Edwardsiella
 Hafnia
Genus Shigella
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 Enteric rods
 Non motile gram-negative facultative anaerobes
Based on antigenic structure and biochemical reactions, Shigella organisms are divided into four
subgroups.
1. Subgroup A: Shigella dysenteriae

- Contains 13 distinct serotypes
- Serotype 1 was formerly called S. shiga→ produce Shiga toxins and most important as a cause of severe
bacillary dysentery.
2. Subgroup B: Shigella flexneri

- Contains 6 related serotypes
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3. Subgroup C: Shigella boydii
→ Contains 18 distinct serotypes
4. Subgroup D: Shigella sonnei
→ Contains one serotype

Characteristics of shigella
37
 Gram-negative
 Non-motile
 Non-spore forming
 Rod-shaped bacteria
 Possess O and some have K antigens
 Do not produce gas from glucose
 Do not produce H2S on TSI
 Non-lactose fermenters
 Oxidase negative
Habitat and Transmission
38
 Shigella species are found only in the human intestinal tract

 Humans are the only reservoir
 Transmitted by the fecal-oral route
 The incidence of shigellosis highest in children
Mode of spread: person-to-person, contaminated fingers, food, flies, fomites etc.

 Infective dose: 10-100 viable bacilli
 Incubation period: 1 to 7 days Demissew sh. June 11, 2024
Virulence factors
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1.Endotoxin: irritate the bowel wall.
2. Exotoxin (Shiga toxin): Enterotoxin and neurotoxin and cytotoxin activity
3.Long chain LPS - preventing the effect of serum complement.
4.Intracellular survival & multiplication

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Acid resistance gene and Invasion gene

 As they exit from infected host in stool, shigellae are acid resistant. This
facilitates their survival during passage though the acidic environment of the
stomach and accounts for their low oral infections dose of shigellae
 Shigellae in the acid resistant state are less invasive. As the result, once they
passed the stomach the acid resistant gene is down regulated and the invasive
gene is up regulated thereby producing invasive shigellae.
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 Shigellosis is an infectious disease caused by various species of Shigella.

 The clinical entity is characterized by the frequent passage of blood-stained
mucoprulent stools.
 Shigella infections are almost always limited to the gastrointestinal tract,
bloodstream invasion is quite rare.
 Shigellae are highly communicable
 The essential pathologic process is invasion of the mucosal epithelial cells (eg,
M cells) by induced phagocytosis, escape from the phagocytic vacuole,
multiplication and spread within the epithelial cell cytoplasm, and passage to
adjacent cells.
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 Pathogenesis of Shigella: Shigellosis

1.Early stage
Watery diarrhea attributed to the enterotoxic activity of Shiga toxin following
ingestion and noninvasive colonization, multiplication, and production of
enterotoxin in the small intestine Fever attributed to neurotoxic activity of toxin
Second stage
Adherence to and tissue invasion of large intestine with typical symptoms of
dysentery Cytotoxic activity of Shiga toxin increases
Demissew sh. severity
June 11, 2024
Pathogenesis …..
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Characteristics of Shiga Toxin

 Enterotoxin, neurotoxic and cytotoxic
 Encoded by chromosomal genes
 Similar to the Shiga-like toxin of enterohemorrhagic E. coli (EHEC)
• Note: except that Shiga-like toxin is encoded by lysogenic bacteriophage

Clinical Features of Shigellosis
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 Persistent diarrhoea with frequent and painful passage of stools consisting mostly of
blood, mucus and pus
• Accompanied by fever and stomach cramps
 Cause breaks (ulcers) in mucous membrane lining of intestine:-
 Inflammation and tissue damage
• Causes painful straining to pass stools
• Ulcers commonly in the rectum
• Results in increased production of mucus
• Loss of blood and serum proteins into intestinal cavity

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 Physical signs are those of dehydration beside fever, lower abdominal

tenderness & normal or increased bowel sounds
 The severity of the disease depends upon the species one is infected
– S. dysenteria is the most pathogenic followed by S. flexneri, S. sonnei and
S. boydii.
 Case fatality rates of 5-15%

Laboratory diagnosis
47
 Specimen: Fresh stool or rectal swabs

 Gram reaction: Gram-negative non-motile rods.
 Culture
The following media can be used:

 Salmonella Shigella agar
 MacConkey
 Eosin - methylene Blue agar
 Hektoen enteric agar Figure--- Non-lactose fermenting shigella colonies
 XLD agar
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Treatment
 Maintenance of hydration by use of oral rehydration salt solution (ORS).
 Ciprofloxacin, ampicillin, tetracycline, trimethoprim -sulfamethoxazole and chloramphenicol
Prevention & control
 Sanitary control of water, food, and milk.
 Proper sewage disposal.
 Disinfection of excreta.
 Early detection and treatment of carriers. e.g : Food handlers

Genus Salmonellae
50
 Ubiquitous human and animal pathogens

 Salmonellosis in humans usually takes the form of a self-limiting food
poisoning (gastroenteritis)
 But occasionally manifests as a serious systemic infection (enteric fever)

Characteristics of Salmonellae
51
 Gram-negative rods
 Motile (Peritrichous flagella)
 Non-sporulated
 Produce gas from glucose
 Produce H2S on TSI media
 Oxidase negative
 Non lactose fermenter
 Facultatively anaerobic

Antigenic Structure
52
1. Somatic (O) or cell wall antigens

 Somatic antigens, are lipopolysaccharide, used for serological tests and over 60 different O
antigens are recognized
2. Surface (Envelope) Antigens
 Includes: Capsular ( K) antigens, Vi antigen, Slime (mucus) or M antigen,
Fimbrial, or F antigen
3. Flagellar (H) Antigens subunits contain the epitope that form the basis of the
flagella-based serotyping scheme→H antigens.

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 The genus is comprised of two primary species

 S. enterica (human pathogen) and S. bongori (animal pathogen)
 • O antigen
• H antigen
. Vi antigen

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 Medically important includes (Serotype) :

 Salmonella typhi
 Salmonella paratyphi
 Salmonella choleriasis
 Salmonella typhimurium
 Salmonella enteritidis
 S. Typhi, S. Choleraesuis, and S. Paratyphi A and S. Paratyphi B are primarily

infective for humans.

Host range
55
 Strains of Salmonella enterica are widely distributed in nature.
 Most animal infections seem to range from those without symptoms to those resulting in
self-limiting gastero-enteritis of variable severity.
 Some strains, such as those belonging to serotype Typhimurium, show a wide host range
and can be isolated from many different animal species.
 Among the host-adapted serotypes, Typhi and Paratyphi A, B, and C are rarely, if ever,
isolated from animals other than man.
 Paratyphi B, although essentially a human pathogen, is occasionally isolated from cattle,
pigs, poultry, exotic reptiles and other animals
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 For human infection, the infective dose is uncertain.

 However, the accepted dictum for induction of illness varied 106 to 109 viable
organisms.
 But, investigation of outbreaks suggests that in natural infection the infective
dose might be below 103 viable organisms.
♦ Many factors are thought to influence the infective dose. There appears to be
considerable strain-to-strain variation in virulence even within a single serotype.
♦Host factors are also likely to be important, particularly the immune status of the
host.
Virulence factors
57
1.Lipopolysaccharide (endotoxin) - released into the bloodstream resulting in

septicemia.
2. Invasins – proteins that mediate adherence to, and penetration of intestinal

epithelial cells.
3. Factors involved in resistance to phagocytosis. Example: Catalase and super

oxide dismutase – protect the bacteria from intracellular killing by neutralizing
oxygen radicals. →Reactive oxygen species: H2O2, singlet oxygen etc
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4.Factors involved in resistance to acid pH
►Salmonellae are protected from stomach acid and acid pH phagosome by acid
tolerance response (ATR) genes of chromosome.
5. Vi (virulence ) antigen – This surface antigen of Salmonella typhi has anti

phagocytic properties. However, its exact role as a virulent factor is not clear.

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 In humans, Salmonella are the cause of two diseases called

salmonellosis:
– Enteric fever (typhoid), resulting from bacterial invasion of the
bloodstream E.g S. typhi and S. paratyphi
– Acute gastroenteritis (Non-typhoidal), resulting from a food borne
infection/intoxication. E.g S. typhimurium, S. enteriditis

60

Clinical Syndromes
61
1.Enteric fever
2..Gastro-enteritis
3.Bacteraemia with or without metastatic infection
►Asymptomatic carrier state
→Although uncommon, infection with salmonella can result in sequelae, including

reactive arthritis (Reiter’s syndrome).

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1. Salmonellosis: enteric fever (typhoid fever)
♦ Enteric fever is usually caused by strains of Salmonella typhi or

Salmonella paratyphi A, B, or C.
♦ The clinical features tend to be more severe with Salmonella typhi.
♦ After penetration of the ileal mucosa, the organisms pass via the lymphatics
to the mesentric lymph nodes, whence after a period of multiplication they
invade the bloodstream via the thoracic duct→resulting from bacterial
invasion of the bloodstream. Demissew sh. June 11, 2024
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♦The liver, gall bladder, spleen, kidney and bone marrow become infected
in the first 7-10 days of the incubation period.
♦.After multiplication in these organs, bacilli pass into the blood, causing a
second and heavier bacteraemia, the onset of which approximately
coincides with that of fever and other signs of clinical illness.

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 In the untreated case the temperature shows a step-ladder rise over the first week
of the illness, remains high for 7-10 days and then falls during the third or fourth
week.
 Apparent recovery can be followed by relapse in 5-10% of untreated cases.
 Severe intestinal haemorrhage and intestinal perforation are serious
complications that can occur at any stage of the illness.
 In endemic areas, it coexists with schistosomiasis
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2. Gastro-enteritis and food poisoning

♦ Acute gastro-enteritis is characterized by vomiting, abdominal pain, fever and
diarrhoea.
♦ Result from a food borne infection or intoxication. Salmonella strain produce a

thermo labile enterotoxin that bears a limited relatedness to cholera toxin both
structurally and antigenically.
♦ The term bacterial food poisoning is conveniently restricted to cases and epidemics
of acute gastro-enteritis that are caused by the ingestion of food contaminated by
bacteria or their toxins.
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3. Septicaemia (Bacteremia) and metastatic disease
♦Bacteraemia is a constant feature of enteric fever caused by Salmonella

typhi and Salmonella paratyphi.
♦ Osteomyelitis is most found in long bones, costochondral junctions and

the spine.
♦ Meningitis is a particularly serious complication of infection in neonates

and very young children.
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Salmonella carrier state

 Most people infected with Salmonella continue to excrete the organism in their
stool for days or weeks after clinical recovery.
 A few patients continue to excrete the Salmonellae for prolonged periods.
 The term chronic carrier is reserved for those who excrete Salmonellae
for a year or more.

Laboratory diagnosis
68
Specimen: Blood, Bone marrow, stool, urine , serum, left over food , and duodenal aspirates.
 Blood → 80% positive in the first week.
 Stool (gastroenteritis) → 70-80% positive in the second and third week.

 Urine → 20% positive in the third and fourth week.
 Serum - → for widal test- positive after the second week of illness.
 Gram reaction - Gram-negative rods Demissew sh. June 11, 2024
69
Figure 3. Salmonella sp. after 24 hours growth on XLD agar.

Xylose Lysine (XL) agar is used when trying to culture and
isolate Gram-negative enteric bacilli. When XL agar is
supplemented with sodium thiosulfate, ferric ammonium
citrate, and sodium deoxycholate, it is then termed XLD
agar, and is then an even more selective medium than XL
alone. The presence of any black colored area indicates the
deposition of hydrogen sulfide, (H2S) under alkaline
conditions. (CDC)
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Serological tests
♦ Infection with both invasive and non-invasive serotypes may induce specific serum
antibodies to salmonella surface antigens.
Widal test
♦The diagnostic value of the Widal test remains controversial. Most agree that the
test is not sufficiently sensitive or specific to be clinically useful when only a single
acute-phase serum sample is tested(common practice).
♦ Widal test is an agglutination test used for theDemissew

detection
sh.
of specific O, H and Vi
June 11, 2024
antigens.
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 The Widal test measures agglutinating antibody levels against O (somatic) and
H (flagellar) antibodies. In acute typhoid fever, O agglutinins can usually be
detected 6–8 days after the onset of fever and H agglutinins after 10-12 days.
Interpretation of results
1. Higher or rising titer of O ( > 1: 60) suggests active infection.
2. Higher titer of H ( > 1: 60) suggests past immunization or past infection.
3. Higher titer of antibody to Vi antigen occur in some carriers.

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Treatment
 Ampicillin, Cephalosporin, Chloramphenicol , co-trimoxazole.
 In salmonella meningitis Cefotaxime and ceftriaxone penetrate in to CSF

reasonably well and are highly active against most salmonellae.
 Resistance to any of the drugs can occur →treatment should be supported

by susceptibility test
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Prevention and Control

 Personal hygiene.
 Proper cooking and storage of food
 Use of pasteurized milk and milk products.
 Proper cooking of Vegetables and fruits
 Health education

Comparison of important features of Salmonella and shigella
74

Enterobacteriaceae clinical syndromes summary
75
demissew sh. June 11, 2024

76
THANK YOU!!!
STAY SAFE!
demissew sh. June 11, 2024

Enteric Gram-Negative Rods - PPTX Ho

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Demissew sh.

June 11, 2024 Dep MLS

 The Enterobacteriaceae is a large family of Gm-ve rods

 ≈ 50 genera have been known

1. O antigens: Are also called somatic antigen: is the O-specific

2. K antigens: capsular polysaccharide antigens, surround the cell wall. The K

3. H antigens: flagellar protein antigens possessed by motile enterobacteria. They are

heat labile (destroyed at 60-100 ºC).

Two major types of toxins:

1. Endotoxin: also called LPS, is a component of the outer membrane of gram

Demissew sh. June 11, 2024

Demissew sh. June 11, 2024

 Cause both intestinal and extraintestinal diseases

Demissew sh. June 11, 2024

 The enterotoxin-producing strains

Demissew sh. June 11, 2024

 Extra –intestinal sites

 Enterobacteria classified as Lactose fermenting and Non- Lactose fermenting.

Demissew sh. June 11, 2024

 2. Non-lactose fermenting enterobacteria

 Main species of medical importance is Escherichia coli.

1. Antiphagocytic surface properties: capsules, K antigens and LPS.

2. Adhesins: fimbriae / pili , Intimin (non-fimbrial adhesin)

3. Invasins: hemolysisn, siderophores and siderophore uptake

systems and Shigella-like "invasins" for intracellular invasion and spread.

4. Hemolysin: E. coli produces an alpha hemolysin that lyses erythrocytes.

5. K antigen or capsular polysaccharide: the K antigens are anti-phagocytic.

The polysaccharide also blocks opsonisation by interfering with complement

 Large numbers of E. coli are present in the GI tract.

Pathogenesis and clinical manifestations

1.Enterotoxigenic E. coli (ETEC): Causes watery (secretory) diarrhoea due to

Demissew sh. June 11, 2024

 ETEC produces heat-stable(ST) enterotoxin or heat-labile(LT) enterotoxin, or both.

. Demissew sh. June 11, 2024

Enteropathogenic E. coli (EPEC) :

Demissew sh. June 11, 2024

3. Entero-invasive E. Coli (EIEC): Causes dysentery (similar to shigellosis),

4.Enterohaemorrhagic E. coli (EHEC): Causes life-threatening haemorrhagic

→ EHEC is due to cytotoxins damaging vascular endothelial cells, and is mainly

→ Infection occurs by ingesting contaminated meat products, un pasteurized milk

5.Enteroaggregative E. coli ( Eagg EC)

 have been implicated as a cause of persistent, watery diarrhea with dehydration

Demissew sh. June 11, 2024

Demissew sh. June 11, 2024

4. It causes bacteraemia & endotoxic shock in immunocompromised host.

5. It causes hospital-acquired infections

Demissew sh. June 11, 2024

 Specimen: Urine, pus, blood, stool, body fluid

Demissew sh. June 11, 2024

 Treatment : will be best, based on results of AST.

Demissew sh. June 11, 2024

2. Non-lactose fermenting enterobacteria

1. Subgroup A: Shigella dysenteriae

2. Subgroup B: Shigella flexneri

3. Subgroup C: Shigella boydii

→ Contains 18 distinct serotypes

4. Subgroup D: Shigella sonnei

→ Contains one serotype

Demissew sh. June 11, 2024

 Shigella species are found only in the human intestinal tract

Mode of spread: person-to-person, contaminated fingers, food, flies, fomites etc.

1.Endotoxin: irritate the bowel wall.