Gastro-intestinal infections

Clinical manifestations - according to the segment concerned of the digestive

tract
Acute gastritis - which affects the stomach and is evidenced by nausea,
vomiting, pain in epigastrium.
Acute gastroenteritis - which affects the stomach and small intestine include,
clinical manifestations including further colicative abdominal pain and diarrhea
Acute gastroenterocolitis -affects the stomach, small intestine and colon.
Acute enterocolitis - affected the small intestine and colon.
 ETIOLOGY

Noninvasive acute enterocolitis pattern can be produced by Vibrio

cholerae, enterotoxic E. coli, Enterobacter, Klebsiella, Clostridium
perfringens, Bacillus cereus, Staphylococcus aureus, Citrobacter, Arizona
and the following viruses: Rotavirusuri, Norwalk, Baltimore, Parvovirus,
Minireovirus, Astrovirus, Adenovirus, Calicivirus, enteroviruses.
Invasive acute enterocolitis pattern may be caused by Shigella,
Salmonella, enteropathogen and enteroinvasive E. coli , Yersinia
enterocolitica, Campylobacter jejuni, Vibrio parahemolyticus, B hemolytic
streptococci group A and group D enterococci, Proteus, Piocianic
Systemic enterocolitis may be caused by Enterobacteriaceae: Salmonella,
E. coli, Yersinia enterocolitica, Campylobacter, Shigella, Klebsiella,
Enterobacter, Yersinia, Proteus, Arizona, Citrobacter.
 Epidemiology

Reservoir of infection can be the sick man / carriers or an animal

Almost all domestic and wild animals can eliminate Salmonella.
E. coli is found more frequently in cattle, and Vibrio cholerae in crustaceans and
molluscs. Foods containing these animal products can cause illness (milk,
milk products, especially duck eggs, meat products).
Route of transmission is fecal-oral.
Contamination may be direct (direct contact with patients or carriers of germs
from dirty hands) or indirectly (contamination of various objects, food, water).
 THE ORGANISMS
DEFENCE

Age
infants - intestinal microbial flora is not fully Normal intestinal microflora
developed and specific immunological factors in Loss of the normal intestinal flora, or
the intestinal tract are poor changes in its balance, caused by
antibiotics, often leads to its replacement by
Personal Hygiene other pathogenic microbes that can cause
Enterocolitica outbreak depends on the number developing severe infections.
of seeds ingested---> necessary  number of
germs (100,000 - 100 million) to trigger disease.
Endogenous intestinal flora has been shown
An exception is infection with Shigella, which to attach to receptors of intestinal mucosa
can produce only 10 to 100 seeds. and acting through a competitive
mechanism preventing attachment of
Gastric juice acidity and other physical barriers pathogens.
This barrier may be neutralized by antiacids,
hypoacid gastritis, increased liquid ingestion
(as happens in summer) . Another physical
Local specific immunity
barrier is the integrity of gastrointestinal mucosa Disorders of humoral immunity, particularly
and biochemical composition of intestinal mucus in the production of Ig A, and cellular
immunity, favor the onset of gastrointestinal
Intestinal motility infections
a) Inhibition of intestinal motility leads to inhibition
of Na + and water absorption. Protective factor in milk and serum
The mother's milk are a number of factors
b) Intestinal stasis favors excessive development such as lactoferrin, lysozyme, phagocytes,
of bacteria. acting bacteriostatic and bactericidal.
Microorganism's
aggresion
Enterotoxins are attached to specific receptors in the intestine ---> a massive loss of
water and electrolytes in the faeces leading to isotonic dehydration and metabolic
acidosis. Intestinal mucosa do not show inflammatory changes remain intact. Therefore
stools are watery, no mucus, blood and leukocytes. Thus Vibrio cholerae produces
enterotoxin secretion of water and electrolytes through activation of adenylcyclase
increasing the intracellular cyclic ATP, which stimulates the secretion to the intestinal
lumen Na, Cl, K, bicarbonate and water. The mechanism acts like thermolabile
enterotoxin of E. coli. Thermostable enterotoxin of E. coli acts on guanyl cyclase with
increasing concentrations of cyclic GMP, with similar effects . Some strains of Shigella,
Salmonella, Clostridium perfringens, Klebsiella, Enterobacter, Citrobacter enterotoxin
which can cause the exact mechanism of action is not elucidated causes noninvasive
enterocolitis--- prototype model is cholera
Cytotoxin products of different intestinal pathogens act mainly in the large intestine and
are responsible for inflammation at this level. After penetrating the intestinal mucosa,
germs multiply, have cytolytic effects and cytotoxins are released. The intestinal mucosa
is an ulcerative colitis with pathological factors: mucus, blood, pus, white blood cells and
destroyed epithelial cells . -causes invasive enterocolitis-- prototype model is dysentery
There is a third pathogenic mechanism that is systemic mechanism. Bacilli reach the
small intestine where they multiply penetrates the intestinal mucosa ----> in the blood
causing a secondary metastatic sepsis and systemic toxicity. Systemic enterocolitis
model is the typhoid infection
 Microorganism's
aggresion
Neurotoxins are usually ingested as preformed toxins in food, stimulates vagal receptors in
the intestinal tract, which then transmittes/(or act directly) the excitation to the vomiting
center. These neurotoxins are produced by Staphylococcus and Bacillus cereus. With
short incubation period (30 minutes to 6 hours) and began with nausea and vomiting.
Endotoxin is a lipopolysaccharide (or LPS). Pyrogens are in the wall of all Gram negative. The
lipid A( part of LPS) is responsible for biological properties of endotoxins. They are:
---- initial leukopenia as a result of margination of circulating leukocytes and leukocytosis
by stimulating bone marrow.
---- thrombocytopenia
---- disseminated intravascular coagulation
---- complement activation by alternate pathway
---- damages of the vascular endothelium leading to release of histamine, kinin, serotonin
---- depress myocardial function by direct action
---- alters the metabolism of carbohydrates, fat, protein
----ACTH promotes the release site and growth hormone
----is responsible for generalized Shwartzman phenomenon
Shwartzman reaction, is a rare reaction of a body to endotoxins, which cause thrombosis in
the affected tissue.
 Clinical
Dyspeptic digestive syndrome
- manifested by loss of appetite by anorexia, nausea, vomiting,colicative diffuse
abdominal pain tenesmus in small children can lead to prolapse of the anal
mucosa, in dysentery you can feel the descending colon spastic, a sign called
"colic rope” .
Noninvasive diarrhea is watery, without mucus or blood,the microscopic
examination shows no leukocytes, red blood cells, skin cells exfoliate. The stools
are very numerous in cholera – can lose tens of liters of fluid per 24 hours ,
containing mucus with the appearance of white grain "rice soup"
The invasive enterocolitic stools contains mucus, blood or pus, had a musty
odor and microscopic examination shows the presence of white blood cells, red
cells, epithelial cells. In dysentery stools are numerous, in small quantity and are
emptied by faeces. Salmonellosis stool is green "mashed peas “appearance and
in E. coli infection looks yellowish.
Febrile syndrome
Dehydration syndrome manifested as thirst, dry mucous membranes, sunken
eyes with prominent nose, dry skin with reduced or persistent skin fold. Biological
Ht is increased, leukocytosis
 Clinical

Shock Syndrome
by adding a component of endotoxin shock due to Gram-negative bacilli
endotoxins.
Renal Syndrome
-if the shock is prolonged acute renal failure may occur--oliguria, -with albuminuria,
cilindruria and blood urea and creatinine are elevated.
Disorders of ionic and acid-base balance
- hypo-K + with muscular asthenia and cardiac rhythm disorders, hypo Na + with
muscle pain, hypo Ca + + - muscle cramps and metabolic acidosis. If vomiting
predominate metabolic alkalosis may occur by loss of Cl-.
Syndrome of nervous intoxication
Manifested by headache, meningism, drowsiness.
 Laboratory

Blood : Serum ionogram and Astrup parameters, CBC, proteinemia, urea,

creatinine, urinalysis.
Leukocytes in stool examination
Coprocultures establishing etiologic diagnosis-- at least 3 and collected before
antibiotic administration.
Serological tests - determin bacterial serotype and highlights the enterotoxin.
 Minimal or no Mild to Moderate Severe
Symptom Dehydration (<3%) (3%-9%) (>9%)
Management
Mental Status Alert Normal, restless, Lethargic,
irritable unconscious
Thirst Normal PO or Thirsty Drinks poorly or
refuses unable
Heart Rate Normal Normal to increased Tachycardia

Quality of pulses Normal Normal to Weak or impalpable

decreased
Breathing Normal Normal to fast Deep

Eyes Normal Slightly sunken Deeply sunken

Tears Present Decreased Absent

Oral mucosa Moist Dry Parched

Skin fold Instant recoil Recoil in < 2 sec Recoil > 2sec

Capillary refill Normal Prolonged Prolonged; minimal

Extremities Warm Cool Cool, mottled,

cyanotic
Urine output Normal to decrease Decreased Minimal
 Management of diahrrea


Breastfed infants with acute diarrhea should be continued on breast milk
without any need for interruption- Breast milk contains many substances that
promote bowel growth and antagonize bacteria

The BRAT diet (ie, bananas, rice, applesauce, toast) - is adequate during
early convalescence, but, as the patient tolerates solid food, advance the
diet to provide adequate protein and caloric intake
 Lactose ingestion- a very transient use of lactose-free formulas (5-6 days)
can be considered.

Oral or iv rehydration therapy
 Antimicrobial therapy is indicated for some bacterial gastroenteritis
infections.
 Bacillary dysentery
Etiology
Dysenteric bacilli belong to the genus Shigella, the family Enterobacteriaceae.
They are immobile, unsporulated Gram-negative bacilli of the intestinal habitat.
Genus Shigella is divided into 4 subgroups: A, B, C, D, each containing
several serotypes.
Subgroup A is the species of Shigella dysenteriae serotypes 10 (1
Shigella Shigae, 2 Shigella Schmitzii, 3.10 Large-Sachs).
Subgroup B - Shigella flexneri, with 6 serotypes.
Subgroup C - Shigella boydii, with 15 serotypes
Subgroup D - Shigella sonne one serotype
 Shiga invasion

Shiga toxin (Stx) - true Shiga toxin is produced by Shigella

dysenteriae.Shiga toxins act to inhibit protein synthesis within target cells
All virulent strains of Shigella flexneri possess a plasmid that mediates its
virulence properties. This so-called the invasion plasmid has been shown
to encode the genes for several aspects of Shigella virulence, including
- Adhesins that are involved in the adherence of bacteria on the surface of target
epithelial cells
- The production of invasion plasmid antigens (Ipa) that have a direct role in the
Shigella invasion process
 Bacillary dysentery
Pathophysiology
Bacilli ingested with food pass without difficulty gastric acid barrier, reach the large
intestine where it multiplies. Colonic epithelial cell invasion --->spread infection
from one cell to another, acting through pyrogens (possibly citotoxin or
enterotoxin), causing epithelial cell damage and local nerve irritation (tenesmus).
impaired intestinal motility and inhibition of intestinal secretion promotes the
proliferation of dysenteric bacilli.
the intestinal mucosa with areas of necrosis and ulceration predominently involved
the sigmoid and rectum. When ulceration is not too large is healing without scars,
but when is infected and extended ---->scar healing, fibrosis and even intestinal
stenosis. Dezenteric bacilli enters the bloodstream only exceptionally.
Immunity is serotype specific but appears to be protective.
 Bacillary dysentery
Clinical

Incubation is 2-4 (1-7) days.

Onset is sudden, manifested by abdominal cramps, tenesmus, diarrheal
watery stools, fever.

Dyspeptic digestive syndrome is characterized by typical small stool amounts

(as a spoon) – sputum like -empty of faeces, composed of mucus, blood and
pus, smelling musty, 20-50 stools / 24h.Typical appear tenesmus and
intestinal cramps.
Febrile syndrome is versatile (can miss), manifested by fever 38-39 ° C.
Nervous syndrome occurs mainly in dysentery on Sh. dizenteriae - neurotoxin

Syndromes of dehydration, shock and renal failure are rare, because although
the stools are very common in dysentery, their amount is small.
 Bacillary dysentery
Lab Diagnosis
Coprocitogram
Fecal leukocytes ( confirming the presence of colitis)
Fecal blood
Stool culture- positive in the first phase, the index of positivity decreased in
convalescence.
Blood
leukocytosis with neutrophilia
changes in blood ionogram with hypo Na, K, Ca and Astrup parameters
changes with metabolic acidosis.
Serological diagnosis is used only for epidemiological studies
 Bacillary dysentery
Clinical forms
After severity :
After clinical status :
mild - as a ordinary enterocolitis
Typical forms
medium
Atypical forms that simulate
severe caused mainly by food or ordinary enterocolitis
Shigella dizenteriae,
characterized by severe nervous Chronic dysentery occurs
symptoms, dehydration and following an
shock ignored/untreated/acute
dysentery with elements of
After age appear: reactivity
infant forms (atypical with fetal
evolution)
small child forms (with more
frequent atypical manifestations)
adult forms
old forms ( more frequent toxic
form and severe evolution)
 Bacillary dysentery
Prognosis

treated correctly for both clinical and bacteriological cure ---- excellent
Dysentery untreated can develop into a slow recovery, but long convalescence
and many recrudescent, or to a state of chronic carriers of dysenteric bacilli.
Another possible evolution is chronic, which may occur in 2-4% of cases.
 Bacillary dysentery
Differential diagnosis
WITH the acute invasive enterocolitis caused by
E. coli enteroinvasive Shiga toxin producing E Coli 0157:H7
Salmonella
Yersinia enterocolitica
Campylobacter jejuni
Paratifoid fevers,
Entamoeba histolytica
WITH lower gastro-intestinal bleeding :ulcero-hemorrhagic colitis, rectal polyps,
rectal cancer, mesenteric infarction, hemorrhoids, intestinal invagination.
 Bacillary dysentery
Complications
Dehydration – most common
chronic colitis, paresis and paresthesia ,sd. Fissinger-Leroy- Reiter
(reactive arthritis)
Other complications are the consequence of intestinal lesions of chronic
colitis, anemia, malabsorbtion with avitaminosis occurring in dysentery in
infants with chronic or long evolution of the disease.
Cholestatic hepatitis
Pneumonia
S.dysenteriae serotype 1 – Shiga Toxin- produces hemolysis, anemia-->
hemolytic uremic syndrome
 Bacillary dysentery
Treatment
Proper rehydration and diet
Because shigellosis is self-limiting, some authorities recommend withholding
antibiotic therapy. However, even if not fatal, the untreated illness may cause
chronic or recurrent diarrhea, this may lead to malnutrition The risk of continued
shedding of organisms in stool increases the risk of transmission of further disease
among contacts argues against withholding antimicrobial treatment.
Antibiotic treatment
effective for susceptible strains Ampicillin 50-100 mg/kg/d PO divided q4-6h and
TMP-SMZ >40 kg: 160 mg/dose PO bid and children >2 months: 8-10 mg/kg/d PO
divided bid for 5 d
If ampicillin and TMP-SMZ resistant strain is isolated or if susceptibility is unknown,
parenteral ceftriaxone sodium adult 2 g IV/IM, child 50-100 mg/kg/d IV/IM for 5 d ,
a fluoroquinolone (eg, ciprofloxacin, ofloxacin), or azithromycin dihydrate are the
drugs of choice
 Cholera

The word cholera is derived from a Greek term

that means "flow of bile." Cholera is caused by
Vibrio cholerae, the most feared epidemic
diarrheal disease because of its severity.
Dehydration and death can occur within hours of
infection.
 Cholera
History
The modern era has seen 7 cholera pandemics .

Top 6 developed between 1817-1923 and were caused by VH (Vibrio

cholerae) classic O1-serotype . They have evolved from Asian (Indian
subcontinent), with further expansion in Europe and America

7th cholera pandemic is driven by the VH O1 biotype El Tor, a biotype which

was originally isolated in Egypt (the early twentieth century) and was associated
with sporadic cases until 1961.
 Cholera
Etiology
The organism is a comma-shaped, gram-negative aerobic bacillus whose size
varies from 1-3 µm in length by 0.5-0.8 µm in diameter, belongs to genus Vibrio,
the gamma subdivision of the Proteobacteria.
Its antigenic structure consists of a flagellar H antigen and a somatic O antigen.
The species V. cholerae can be sub-classified into 200 serogroups based on
the O antigen of LPS (lipopolysaccharide).
Only O1 and O139 strains - implicated in the cholera syndrome.
 Cholera
Antigenic structure
Vibrio cholerae serogroup O1, containing 13 antigenic factors, noted with
the first 13 capital letters of the alphabet: A-M.
V cholerae O1 is classified into 2 major biotypes: classic and El Tor.
Currently, El Tor is the predominant cholera pathogen.
Organisms in both biotypes are subdivided into serotypes according to the
structure of the O antigen, as follows:
Serotype Inaba - O antigens A and C
Serotype Ogawa - O antigens A and B
Serotype Hikojima - O antigens A, B, and C
 Cholera
Epidemiology
Habitat - Vibrions live in sea water or surface water. The diseases they
produce appear on the sea coast, in summer-autumn seasons or in
connection with the consumption of seefood. Seasonality is another
characteristic of cholera. Epidemics tend to occur in warm seasons and in
countries where there is more than 1 hot season / year.
Transmission- fecal-oral route. Owing to the relatively large infectious dose,
transmission occurs almost exclusively via contaminated water or food.
Receptivity is general. Pregnant women are serious forms of disease-abortion or
premature birth. Direct transmission through inter-human contact is possible.
Immunity from the disease is fairly effective and long lasting.
Sensitivity to antibiotics: Classical Vibrio cholerae is highly sensitive to
Tetracycline, and is sensitive to Chloramphenicol, Ampicillin, Erythromycin,
Neomycin, Furazolidone.
 Cholera Pathogenesis
Low infectious dose is required :103 -106 organisms to produce disease.
V cholerae O1 and V cholerae O139 cause clinical disease by producing an
enterotoxin - promotes the secretion of fluid and electrolytes into the lumen of the
small intestine. The enterotoxin is a protein molecule composed of 5 B subunits
and 2 A subunits. The B subunits are responsible for binding to a ganglioside
(monosialosyl ganglioside, GM1) receptor located on the surface of the cells that
line the intestinal mucosa.
The activation of the A1 subunit by adenylate cyclase is responsible for the net
increase in cyclic adenosine monophosphate (cAMP). cAMP blocks the absorption
of sodium and chloride by the microvilli and promotes the secretion of chloride and
water by the crypt cells. The result is watery diarrhea with electrolyte
concentrations isotonic to those of plasma.
Fluid loss originates in the duodenum and upper jejunum; the ileum is less affected.
The colon is usually in a state of absorption because it is relatively insensitive to
the toxin. However, the large volume of fluid produced in the upper intestine
overwhelms the absorptive capacity of the lower bowel, resulting in severe
diarrhea.The enterotoxin acts locally and does not invade the intestinal wall. As a
result, few neutrophils are found in the stool.
 Cholera
Clinical
The amount of fluid loss and the
After a 24- to 48-hour incubation period corresponding clinical signs of cholera
are as follows:
- sudden onset of painless watery diarrhea
that may quickly become voluminous * With 3-5% loss of normal body weight -
and is often followed by vomiting. The Excessive thirst
diarrhea has a "rice water" appearance
and a fishy odor. In patients with severe * With 5-8% loss of normal body weight -
disease, the stool volume can exceed Postural hypotension, tachycardia,
250 mL/kg in the first 24 hours. Without weakness, fatigue, and dry mucous
replacement of fluids and electrolytes--> membranes or dry mouth
hypovolemic shock and death . * With greater than 10% loss of normal
- accompanying abdominal cramps. body weight - Oliguria; glassy or sunken
eyes; sunken fontanelles in infants;
-Fever is typically absent. Full recovery is weak, thready, or absent pulse; wrinkled
achieved within 5-8 days. "washerwoman" skin; somnolence; and
coma
 Cholera Lab studies
Hypovolemia
Elevated hematocrit
Neutrophil leukocytosis
Elevated blood urea nitrogen and creatinine levels consistent with prerenal
azotemia.
Hypovolemia may cause hyperglycemia secondary to systemic release of
epinephrine, glucagon, and cortisol.
Diagnosis may be confirmed via identification of V cholerae in the stool. The
organism may be detected directly with dark-field microscopy examination of a wet
mount of fresh stool; chaotic motility is observed.
Laboratory isolation requires a selective medium. V cholerae grows as a flat, yellow
colony on thiosulfate-citrate-bile salts-sucrose agar or taurocholate-tellurite-gelatin
agar.
PCR has been used with a high degree of sensitivity and specificity.
 Cholera
Differential diagnosis
Food intoxication
Severe infant diarrhea
Clostridium enterocolitis after antibiotic therapy
Enterocolitis with E. coli enteropathogens
Diahorrea with hormonal disorder
 Cholera
Complications and Prognosis
If a patient is adequately treated with fluid and electrolytes, complications are
averted and the self-limited process resolves in a few days.
Potential complications include dehydration and volume loss that lead to
acute tubular necrosis and renal failure. Hypovolemic shock and death
ensue. Relapses are possible in convalescence.

The prognosis is severe cholera. Mortality in untreated cases is 50-80%, but

may be decreased by early treatment, even below 1%.
 Cholera
Treatment
The primary goal of therapy is to replenish fluid losses caused by diarrhea and
vomiting
Rehydration is accomplished in 2 phases, rehydration and maintenance.
Treatment with an antibiotic to which the organism is susceptible diminishes the
duration and volume of the fluid loss and hastens clearance of the organism
from stool.
Pharmacotherapy plays a secondary role in the management of cholera.
Treatment of choice is Tetracycline 2 g / day for 3 days or Doxycycline 300 mg
PO once
In areas of known tetracycline resistance, therapeutic options include
Ciprofloxacin 250 mg PO qd for 3 d or 1 g once, Erythromycin 40 mg/kg PO
divided tid for 3 d, Chloramphenicol.
FOOD poisoning
FOOD INTOXICATION (FOOD POISONING)

- NO INFECTION (no viable bacteria need to

encounter the host)

- toxin preformed in the food as a result of

bacterial contamination (soil or human)
correlation symptoms ------- food borne
illness etiology (1)
1) Nausea and vomiting occurred in 30 min - 6 hours of food intake
Etiology:
Staphylococcus aureus
Bacillus cereus ( release thermostable toxin ). Short incubation period reflects the fact
that these conditions are caused by enterotoxins preformed in food. Ingested with
food they trigger the disease. Watery diarrhea occurs in a smaller percent. Disease
duration is short, until 12 h
2) Abdominal cramps and diarrhea in 8-16 hours after ingestion of food
Etiology:
Clostridium perfringens (which release a thermolabile enterotoxin)
Bacillus cereus (which release a thermolabile enterotoxin)
nausea may occur, but vomiting and fever are rare. Toxinfection usually resolve in 24
hours.
3) Fever, abdominal cramps, invasive diarrhea in 16-48 hours after ingestion of the food.
Etiology:
Salmonella Shigella E Coli V. Parahaemolytious Campylobacter jejuni
Diarrhea is of invasive pattern with mucus, blood and leukocytes. Toxinfection may
take up to a week and relapses may occur in untreated patients.
 correlation symptoms ------- food
borne illness etiology (2)
4) Colic, watery diarrhea 16-72 hours after ingestion of food
Etiology:
Enterotoxigenic E. coli, V. cholerae, V. parahaemolyticus, Sometimes, Salmonella,
Shigella, Norwalk virus
Fever and vomiting are rare. It takes 3-4 days, except VH non-O1, which can take 2-
12 days and 1-2 days Norwalk virus.
5) Fever, abdominal cramps 16-48 hours after ingestion of food
Etiology:
Yersinia enterocolitica (producing a thermostable toxin)
Abdominal cramps often mimic an acute appendicitis. Diarrhea is common. It takes
24 hours - 4 weeks.
6) Bloody diarrhea without fever in 72-120 hours after food intake
Etiology:
E. coli O157: H7 that produces a cytotoxin.
Originally diarrhea is watery, with blood and mucus and accompanied by abdominal
cramps.
It takes 1-12 days.
 SALMONELLA
Salmonella is a rod-shaped,
facultative anaerobe in the family
Enterobacteriaceae
• Gram-negative
• Facultative anaerobes
• Glucose-fermenting
• Straight, rod
• 2-3 µm in length
• Flagellated
• Many serovars
• Typhi
• Typhimurium
• Enteriditis
 Different types of Salmonella
Three clinical forms of salmonellosis

- Gastroenteritis (S. typhimurium) Food poisoning

- Septicemia (S. enterica)
- Enteric Fevers (i.e. S. typhi – Typhoid Fever)
 Antigenic structure of Salmonella
Over 2000 strains are grouped into S. enterica.
- divided into six subgroups based on three surface antigens, O, H and Vi.
I- enterica
II - salamae
IIIa -arizonae
IIIb -diarizonae
IV - houtenae
V - bongori
VI - indica
Somatic or 0 Antigens contain long chain polysaccharides ( LPS )
comprises of heat stable polysaccharide commonly.

• Flagellar or H Antigens are strongly immunogenic and induces antibody

formation rapidly and in high titers following infection or immunization
• Surface antigen - the Vi antigen. The Vi antigen occurs in only three
Salmonella serovars: Typhi, Paratyphi C, and Dublin. Important for
epidemiological reason: germ carriers
All strains that are pathogenic to humans are in species S. enterica, subgroup
1 (also called enterica).
 Pathology and Pathogenesis of
Salmonellosis
• Caused by
S. typhi
S.paratyphi
A BC
The organisms penetrate ileal mucosa--> reach mesentric lymph nodes via
lymphatics , multiply, invade blood stream via thoracic duct

In 7 – 10 days through blood stream infects:

Liver, Gall Bladder, Spleen, Kidney, Bone marrow.
After multiplication bacilli pass into blood causing secondary and heavier
bactermia
Virulence factors responsible for pathogenicity in enteric bacteria are often
encode by plasmids, as in E Coli, Yersinia spp, and Shigella spp.
Salmonella spp. The virulence plasmid of Salmonella is important for
bacterial multiplication in the rethiculoendotelial system.
 Typhoid fever
History
 “Typhoid Mary” Mallon was the first famous carrier
of typhoid fever in the U.S.

 Some individuals have natural immunity to

Salmonella. Known as “chronic carriers”, they
contract only mild or asymptomatic disease, but still
carry the bacteria in their body for a long time.
These cases serve as natural reservoir for the
disease.

 One such case was Mary Mallon, who was hired as

a cook at several private homes in the new York
area in the early 1900’s.
 Salmonellosis - epidemiology
RESERVOIR
a) multiple animal reservoirs

b) mainly from poultry and eggs (80%

cases from eggs)
c) fresh produce and exotic pets are also a
source of contamination (> 90% of
reptile stool contain salmonella
bacterium); small turtles,lizards
TRANSMISSION - improperly prepared,
previously contaminated food or water -
contaminated eggs, medical products of
animal origin (billiary salt, tisular extract
of thyroid)
RECEPTIVITY Everyone, especially:
CRONIC CARRIER -excreted in feces up the elderly, infants, achlorhydia,
to 5 weeks immunocompromised patients
HIGH RISK -veterinarians, contaminated
 Clinical forms
Nontyphoidal enterocolitis
Infection with nontyphoidal salmonellae usually causes enterocolitis similar to
that caused by other bacterial enteric pathogens.
The incubation period depends on the host and the inoculum is generally 12-36
hours (4-48h). In most cases, stools quantitatively rich, watery with mucus
and streaks of blood, yellow-green, with fetid odor.
Febrile syndrome remains at high values of 2-5 days The diarrhea is
typically self-limiting and resolves within 3-7 days.
Fever, abdominal cramping, chills, headache, and myalgia are common.
Nontyphoidal focal disease
Focal disease is due to transient or persistent bacteremia. Almost any organ can
be affected, with sites of preexisting structural abnormalities being the
most vulnerable.
 Clinical patterns
As a particular form, salmonella can take appearance of:
septicemia (blood poisoning form)
influenza (flu-like shape)
dysentery (as disenteric)
typhoid fever (typhoid form)
nosocomial form that appears on the background of other conditions
holeriform form (with watery stools riziforme)
Depending on the severity are:
mild (as an acute gastritis)
medium disease
severe disease (with dehydration and shock)
toxic disease (with algid collapse, nervous system involvement,
hypothermia)
Depending on age, are:
form that appears in infants, which often can give sepsis with secondary
outbreaks (otitis, bronhopneumonia, meningitis, angiocolitis, abscesses,
osteomyelitis)
elderly - more severe symptoms.
 Typhoid fever
Clinical
The incubation period is 10-14 days

Onset period lasts one week and is characterized by a prodromic phase - with
progressive alteration of the general condition and prolonged low-grade fever,
frontal headache, malaise, myalgia, dry cough, anorexia, nausea , confusion, stupor
 Typhoid fever with atypical symptoms may start and an organ affected by
making the clinical picture of: pneumotyphos, pleurotyphos, meningotyphos,
colotyphos, nefrotyphos. During the natural evolution of disease, fever has
characteristic febrile "trapeze” curve described by Wunderlich, rarely seen
today.
Average period lasts 14 days and is characterized by:
a) febrile syndrome
fever remains high at values of 39 - 40 ° C, the entire period with
insignificant thermal oscillations, “plateau fever”

b) nervous syndrome -apathy, obnubilation, lying immobile, with disregard to

the entourage. Maintain of headache and insomnia. Mild forms of the
present stage is characterized by discrete nerve symptoms: headache,
 Typhoid fever
Clinical
c.)Digestive Syndrome
- loss of appetite, thirst, dry mucous membranes. Tongue with roasted aspect
"parrot tongue” the sabural deposit, with red edges .The lips are burned, dry,
cracked. Pharynx present Duguet angina sometimes consisting of ovalar
gray painless ulceration.The abdomen is sensitive to palpation, especially in
right iliac fossa with flatulence, garguiments. Constipation is present in 1 / 3 of
cases. Diarrhea in typhoid fever is characterized by liquid stools looking like”
mashed peas” yellow greenish , with epithelial exfoliate.

d.)Cardiovascular syndrome
is characterized by decreases in blood pressure, dicrot pulse, sphygmo-
thermal dissociation (also known as relative bradycardia or pulse-temperature
deficit).Transition from bradycardia to tachycardia and cardiac noise changes,
changes in ECG instalation of thyphos miocarditis
 Typhoid fever
Clinical
e.)Hepatic-splenic syndrome:
hepato-splenomegaly especially in children
f.)Eruptive syndrome
-3rd week: rose spots (1-2 mm diameter on the skin), blanchable: duration: 2-5
days occurring mainly on the flanks and chest, especially between day 6th
and 9th of disease "lenticular spots" (rozeola typhous) can be seen as well in
disseminated TB or septicemia. Disappear within 3-4 days without a trace.

Decline of disease is characterized by gradual reduction of fever. Sometimes

fever decreases in crisis with sweating and polyuria.
Convalescence is prolonged, there is the possibility of complications. Clinical
and bacteriological recovery are not simultaneous. Relapses usually occur
within 8-15 days of convalescence.
 Typhoid fever Lab studies
Stool culture - special medium MacConkey agar, eosin-methylene blue
agar, agar HE
S.typhi-isolated from stool, urine, roseole, gastric or intestinal secretions,
blood, bone marrow
Salmonella species are differentiated by conventional biochemical tests,
serological patterns and patterns fagica
The Widal test is used to measure antibodies against O and H antigens
of S typhi. Newer diagnostic tests (Typhidot, Tubex) allow direct
detection of immunoglobulin M (IgM) antibodies against specific S
typhi antigens
Blood : leukopenia, neutropenia, anemia
 Typhoid fever
Complication
Until the introduction of chloramphenicol to treat typhoid fever, complications
were alarming, every organ may be interested in:
pneumonia, pleuritis, meningo-encephalitis, myelitis, phlebitis,
arthritis, cholecystitis, hepatitis, nephritis, endocarditis, pericarditis,
purulent arthritis, hemolytic uraemic, skin suppurative
complications.

Intestinal bleeding
Intestinal perforation mimic an acute abdomen
 Typhoid fever
Differential diagnosis
➲ Non invasive disease ➲ Invasive disease
 E. Coli enterohemoragic
 Viral enterocolitis  E. Coli enterotoxic
 E. Coli enteropatogen  Shigella
 Campylobacter
 Arizona, Citrobacter  Yersinia enterocolitica
 Clostridium perfrigens  Vibrio parahaemoliticus
 Klebsiella
 Cholera
Typhoid fever is distinguished from other diseases:
tuberculosis, septicemia, malaria, brucellosis, subacute
endocarditis, infectious mononucleosis etc
 Treatment
➲ Mild disease- self limited disease- simptomatic treatment -NO
ATB - supress normal enteric flora,extends bacterial clearance
and predispose to chronic portage
Severe disease -CIPROFLOXACIN
Gastrointestinal nontyphoidal salmonellosis requiring
therapy: 500 mg PO bid for 3-7 d
Typhoid fever: 400 mg IV bid (switch to PO when
tolerated) for a total course of 7-10 d
CEFOTAXIM,CEFTRIAXON Typhoid fever: 2-3 g IV qd for 7-14 d
AZITROMICIN,CLORAMFENICOL 7-14 days
Sometimes chronic portage- colecistectomy- GALLBLADDER
REZERVOIR
 Vaccines for Typhoid Prevention

Two types of vaccines are available

Oral and Inject able
Oral – A live oral vaccine , one capsule on 1, 3, 5 days ( three
doses )
The inject able vaccine, contains purified Vi polysaccharide
antigen derived from S.typhi strain ty21
Given as single subcutaneous or intramuscular injection
Staphylococcus spp. gastrointestinal
infections
 Staphylococcus spp. gastrointestinal
infections
Acute enterocolitis caused by
Staphylococcus food poisoning occurs
staphylococcus can take other 2
following the ingestion of food with
pathogenic models:
preformed staphylococcal
ENTEROTOXIN Acute diarrheal disease as a
result of pre-existing
2 types of enterotoxin: A and B staphylococcal infection
(staphylococcal skin, otitis,
a polypeptide structure
angina, bronchopneumonia,
its production is enhanced by the arthritis). Appears only in the
presence of microorganisms in the neonate and small infant to 3
intestine as E. coli, Proteus months.

heat resistant and is not destroyed by Pseudomembranous colitis occurs

gastric juice following administration of broad
spectrum antibiotics for a long
a neurotoxin that acts on peripheral time. Is due to selection of
and central vomiting center. resistant strains of
staphylococcus, the destruction of
intestinal flora by antibiotics.
 Staphylococcus spp.
Gastrointestinal Clinical
The incubation period is short, from 30 min to 3-6 hours, because of the
preformed toxin
Onset is usually abrupt, adynamia, with nausea, vomiting, abdominal cramps,
dizziness, headache.
During the state period have repeated vomiting, abdominal cramps, and
watery diarrheal stools, seromucoase. In severe forms - shock. Seizures may
occur in young children, obnubilation, agitation. Fever is not common. The
total duration of illness is 1-2 up to 4 days.

The neonate and small infant presents with gastroenterocolitis- pasty

diarrheal stools, yellow gold, 3-5 per day, with mucositis. Diarrhea is
accompanied by abdominal cramps, vomiting, flatulence, food refusal,
agitation. There can progress to ulcerative colitis, which may be complicated
by intestinal perforation and peritonitis.
Staphylococcus spp Gastrointestinal
disease
Lab diagnosis -for the isolation of presumptive pathogenic staphylococci -
Chapman medium- incriminated food, vomiting, stool

Differential diagnosis
other model of noninvasive enterocolitis

Prognosis is good in adults, lethality is less than 1%. It is more severe in infants
less, because of the ulcero-suppurative and necrotic intestinal lesions.
Treatment
dietary recommandations- as all acute diarrheal diseases
drug therapy
Electrolite balance and antibiotic treatment if needed.
 Acute diarrhea with Escherichia coli

Escherichia coli is a Gram negative

bacillus
Belong to Enterobacteriaceae family
Antigenic structure is similar to the
germs of this family, containing
antigens A, H and K.
165 O serogroups, 54 H serotypes and
103 K serotypes .
The new nomenclature of each strain is
known by the initials A, K, H,
followed by a numer, indicating the
serogroup and serotype .
Enterotoxigenic E. coli

ETEC uses fimbrial adhesins to bind

enterocyte cells in the small intestine

ETEC can produce two enterotoxins:

* the larger of the two proteins, LT
enterotoxin, is similar to cholera toxin
* the smaller protein, ST enterotoxin causes
cGMP accumulation in the target cells and a
subsequent secretion of fluid and electrolytes
into the intestinal lumen
ETEC strains are non-invasive, and they do not
leave the intestinal lumen. ETEC is the leading
bacterial cause of diarrhea in children in the
developing world, as well as the most common
cause of traveler's diarrhea
Enteropathogenic E.coli
(EPEC)
Like ETEC, EPEC also causes diarrhea, but
the molecular mechanisms of colonization
and etiology are different. EPEC lack
fimbriae, ST and LT toxins, but they utilize
an adhesin known as intimin, a virulence
factor of EPEC and EHEC E. coli strains to
bind host intestinal cells. This virotype has
an array of virulence factors that are similar
to those found in Shigella and may possess
a shiga toxin. Adherence to the intestinal
mucosa causes a rearrangement of actin in
the host cell, causing significant
deformation. EPEC cells are moderately-
invasive (i.e. they enter host cells) and elicit
an inflammatory response. Changes in
intestinal cell ultrastructure due to
"attachment and effacement" is likely the
prime cause of diarrhea in those afflicted
with EPEC.
Enterohemorrhagic E. coli

The most famous member of this virotype is

strain O157:H7, which causes bloody diarrhea
and no fever. EHEC can cause hemolytic-
uremic syndrome and sudden kidney failure. It
uses bacterial fimbriae for attachment (E. coli
common pilus, ECP), is moderately-invasive and
possesses a phage-encoded Shiga toxin that
can elicit an intense inflammatory respons
Enteroinvasive E. coli

Enteroinvasive E. coli (EIEC) are able to

invade and multiply within intestinal
epithelial cells, resulting in cell destruction,
intense inflammation, and ulceration of the
intestinal lining. With symptoms of fever,
cramps, vomiting, and bloody diarrhea, the
disease closely resembles that caused by
Shigella spp.EIEC infection causes a
syndrome that is identical to Shigellosis
with profuse diarrhea and high fever.
Enteroaggregative
E. coli

So named because they have fimbriae which aggregate

tissue culture cells, EAEC bind to the intestinal mucosa
to cause watery diarrhea without fever. EAEC are non-
invasive. They produce a hemolysin and an ST
enterotoxin similar to that of ETEC.
Thank you