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Salmonella infections

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SALMONELLA INFECTIONS (salmonelloses) CHOLERA An acute infection by Vibrio cholerae involving the entire small bowel characterized by profuse watery diarrhea ... – PowerPoint PPT presentation

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Title: Salmonella infections


1
Salmonella infections
  • (salmonelloses)

2
  • The Enterobacteraceae comprise Salmonella,
    Shigella, Escherichia, Klebsiella, Enterobacter,
    Serratia, Proteus, Morganella, Yersenia, and
    other less common genera. This oxidase-negative,
    Gr. (-), catalase-positive organisms are readily
    cultured on ordinary media, ferment glucose and
    reduce nitrates to nitrites.

3
The 2200 known serotypes of Salmonella may be
grouped into these
  • highly adapted to human hosts
  • adapted to non-human hosts
  • unadapted to specific host

4
  • The first group includes S. typhi and S.
    paratyphi A, B and C, which are pathogenic only
    in humans and commonly cause enteric fever.
  • The second group causes disease almost
    exclusively in animals, although 2 strains within
    this group, S. dublin and S. choleraesuis also
    cause disease in humans.
  • The third group designated S. enteritidis,
    includes gt than 2000 serotypes that cause
    gastroenteritis.

5
Typhoid fever
  • A systemic disease caused by S. typhi and
    characterized by fever, prostration, abdominal
    pain, and a rose-colored rash

6
Pathogenesis
  • S. typhi invades first the alimentary tract by
    ingestion, then via the lymphatic system, via the
    thoracic duct into the blood stream.
  • This first septicemic phase leads to infection of
    the reticuloendothelial system and the gall
    bladder.
  • Infection of the gall bladder causes discharge of
    organisms into the intestine, with heavy
    infection of the Peyers pathes and septicemia
    and the onset of symptoms.

7
Symptoms and signs
  • IP 8-14 (14-21 days)
  • Onset is usually gradual, with fever, headache,
    arthralgias, pharyngitis, constipation, anorexia,
    and abdominal pain and tenderness.
  • If no therapy is began the temperature raises in
    steps over 2 to 3 days, remains elevated (usually
    to 39-40?C) for another 10 to 14 days, begins to
    fall gradually at the end of the 3rd wk, and
    reaches normal levels during the fourth week.
  • Prolonged fever is often accompanied by relative
    bradycardia and prostration and CNS symptoms such
    as delirium, stupor, or coma occur in severe
    cases.

8
  • In about 10 of the patients discreet pink,
    blanching lesions (rose spots) appear in crops on
    the chest and abdomen during the 2nd wk and
    resolve in 2 to 5 days.
  • Intestinal perforation, usually involving the
    distal ileum, occurs in 1-2 of patients.
  • Splenomegaly, leucopenia, anemia, liver function
    abnormalities, proteinuria, and a mild
    consumption coagulopathy are common
  • Diarrhea is a late symptom, usually in the third
    week of illness and still may contain blood. In
    about 2 of patients, severe bleeding occurs
    during the third week with a mortality rate of
    about 25.

9
  • In addition bacteriemia, occasionally leads to
    focal infections, such as osteomyelitis,
    endocarditis, menengitis, soft tissue abscesses,
    glumerulonephritis, or GU tract involvement.

10
Complications
  • Relapse, intestinal perforation and hemorrhage
    are the most serious. Relapse is common, with
    recrudescence of symptoms about a week after the
    end of the primary illness
  • Carriers around 2-5 of patients with typhoid
    fever become chronic carriers, owing to
    persistent infection of the gall bladder.

11
Diagnosis
  • Best made by isolation of the infecting organism
    from feces, blood and urine. Blood culture is
    positive in over 80 of patients in the first
    week of illness.
  • Blood and urine Mac Conkey medium
  • Feces use selective and enrichment media

12
  • Identification biochemical reactions S
    typhi, unlike other salmonellae, produces no gas
    on fermentation of sugars.
  • serological preliminary identification
    with salmonella polyvalent H and O antisera
  • phagotyping

13
  • Serology the classic test is the Widal test
    agglutination test for antibodies to flagellar H
    antigens and somatic O antigens of S. typhi and
    S. paratyphi A and B, but the results are
    difficult to interpret, especially if the
    patients has been immunized with typhoid vaccine.
    This test is no longer used in routine diagnostic
    laboratories.

14
Treatment
  • Ciprofloxacin 500mg po q12h is the drug of
    choice, especially with the emergence of
    multiresistance involving other antibiotics but
    care is needed with children. Ceftriaxone is a
    useful alternative in such cases.
  • Ceftriaxone 30mg/kg/day im or iv in 2 divided
    doses for 2 week (eg. 1 g iv q 12h for adults).
  • Cefoperazone is given 60mg/kg/day iv in 2 divided
    doses for 2 weeks.
  • Co-trimoxazole.

15
Paratyphoid fever
  • Causal organisms S. paratyphi A, B and C
  • Clinically a milder febrile illness than typhoid
    fever, with a shorter duration and incubation
    period. Transient diarrhea and symptomless
    infection are common.
  • Carriers patients become carriers less
    frequently than after typhoid fever.
  • Diagnosis best made by isolation of the
    infecting organism from feces, blood and urine.
    Blood culture is positive in over 80 of patients
    in the first week of illness.
  • Treatment Ciprofluxacin is the drug of choice,
    but care is needed with children. Ceftriaxone is
    a useful alternative in such cases.
    Chloramphenicol is as effective, but resistance
    is now a problem. Co-trimoxazole is less good
    than Chloramphenicol, but has less serious side
    effects.

16
Non-typhoidal Salmonella infections
  • Formerly the commonest cause of diarrhea in
    Europe and the USA.
  • Diarrhea due to Salmonella is traditionally
    called food poisoning, although this term is
    somewhat misleading. Infected meat-producing
    animals, poultry, raw milk, eggs and egg products
    are common sources of Salmonella.
  • There are more than 2000 serotypes of Salmonella,
    but only about 14 are important or common causes
    of infection.
  • In recent years the commonest serotype has been
    S. enteritidis. Other common Salmonellae are S.
    typhi murium, S. heidelberg, S. Newport, S. agona

17
Pathogenesis
  • Sight of infection is the small or large
    intestine. Many strains produce enterotoxins
    similar to those of toxigenic strains of E.
    colli. NB! The Salmonella enterotoxins are still
    poorly defined. Other Salmonellae invade the
    mucosa of the small intestine like Shigellae.

18
Symptoms and signs
  • Salmonella infection may present clinically as
    gastroenterits, enteric fever (S. paratyphi A, B
    and C), a bacteremic syndrome, or focal disease.
  • IP is short around 12-36-48 hours.
  • Main symptoms are acute onset of abdominal pain
    and diarrhea, sometimes with fever and vomiting.
    Dehydratation may require correction, especially
    in babies.
  • Usually the stool is watery, but made be paste
    like semisolid. Rarely, mucus or blood is
    present.

19
Bacteremia
  • (S. choleraesuis, S. typhimurium, S. heidelberg).
    Although blood cultures are positive, stool
    cultures are generally negative.

20
Focal manifestation
  • of Salmonella infections may occur with or
    without sustained bacteriemia. In patients with
    bacteriemia localized infection may occur,
    involving the GI tract (liver, gall bladder and
    appendix), endothelial surfaces.(heart valves),
    pericardium, meninges, lungs, joints, bones, GU
    tract.

21
Diagnosis
  • Is made by isolating the organism from stool or
    another infected site. The prognosis is usually
    good unless severe underlying disease is present.
    Asymptomatic carriage is usually self-limited and
    antibiotics treatment is rarely required.
    Eradication may be attempted with Ciprofluxacin
    500 mg po q12h for 1 month, but follow up stool
    cultures should be obtained in the weeks after
    drug administration to document elimination of
    Salmonella.

22
Treatment
  • Rarely necessary rehydratation may be required
    in babies oral isotonic fluid replacement can be
    life-saving in infants with diarrhea.
  • Antibiotics are contraindicated except in
    septicemia cases they do not affect symptoms and
    may prolong convalescent carriage of the
    organism they also contribute to the emergence
    of antibiotic resistant strains.
  • Trimethoprim-Sulphamethaxazole (TMP-SMX) 5mg/kg
    of TMP component po every 12h for children, or
    Ciprofluxacin 500mg po q12 hours for adults.
  • Neledix 50mg/kg
  • Gentamycin - 2-5mg/kg
  • Amikacin 5-15mg/kg.

23
Shigellosis(Dysenteriae)
  • Shigellosis is an acute infectious inflammatory
    colitis due to one of the members of the genus
    Shigella. The less severe illness predominates in
    industrialized countries, whereas more severe,
    often fatal dysenteria occurs in patients in
    developing countries.

24
The four species of Shigella are
  • ? S. dysenteriae
  • ? S. flexneri
  • ? S. boydii
  • ? S. sonnei
  • All the species except S. sonnei contain several
    distinguishable serotypes.
  •  

25
Pathogenesis and pathology
  • Shigella are orally ingested and because they
    survive low pH better than other enteric
    pathogens, they seem to have little difficulty in
    passing the gastric acid barrier
  • An essential step in pathogenesis is invasion of
    colonic epithelial cells and cell-to-cell spread
    of infection.
  • Invasion and cell-to-cell spread involve the
    initial attachment of the organism to colonic
    cells, entry by and an endocytic mechanism, in
    which organisms are initially incased in and then
    escape from plasma membrane-enclosed vesicles,
    and a jet propulsion-like movement to the
    epithelial cell surface that is powered by
    bacteria-induced actin polymerization at the
    trailing end of the bacterium

26
  • A second property of apparent importance in
    virulence, at least for S. dysenteriae type I is
    the ability to produce cytotoxic proteins. Shiga
    toxin composed of two distinct peptide subunits,
    each with highly conserved active regions.

27
  • Shigella organisms penetrate the mucosa of the
    lower intestini, causing mucous secretion,
    hyperemia, leucocytic infiltration, edema and
    often superficial mucosal ulceration. The watery
    diarrhea associated with shigella infection may
    be mediated by an enterotoxin that causes
    increased intestinal secration.

28
  • S. dysenteriae has invasive properties and
    produces a powerful neurological exotoxin, but
    this probably does not play a role in shiga
    dysenteriae. An enterotoxin and cytotoxin are
    also produced their role is uncertain, but they
    may be partly responsible for invasiveness. Shiga
    toxin, is very closely related to E. colli
    verocytotoxin 1(VT1). Cytotoxins, which cause
    destruction of mucosal cell and associated
    inflammatory diarrhea and neurotoxins, which act
    directly on the central or peripheral nervous
    system.

29
Symptoms and signs
  • IP 1-9 days.
  • Diarrhea with blood, mucus and often pus in the
    stools, which varies from a severe life
    threatening to a mild and symptomless infection.
  • In young children onset is sudden, with fever,
    irritability or drowsiness, anorexia, nausea or
    vomiting, diarrhea, abdominal pain and distention
    and tenesms. The number of stools may increase to
    more than 20/day, and weight loss and
    dehydratation may become severe.
  • In adults first symptoms may be episodes of
    abdominal pain, urgency to defecate and little or
    no tenesms.

30
Complications
  • severe mucosal ulcerations may cause significant
    acute blood loss.
  • Intestinal perforation
  • Hemolytic-uremic syndrome in children
  • Arthritis, myocarditis, toxic neuritis

31
Laboratory findings and diagnosis
  • ? Diagnosis isolation culture feces and rectal
    swabs on MacConckey medium and selective media.
    Identify by biochemical tests, then serology.
  • ? WBC count is often reduced at onset
    hemoconcentration is common, as is
    diarrhea-induced metabolic acidosis.
  • ? The mucosal surface, as seen through a
    prostoscope, is diffusely erithematous with
    numerous small ulcers.

32
DD
  • Should include invasive E. colli, Salmonella,
    Yersenia, Campylobacter, Amebiasis, and viral
    diarrheas.

33
Treatment
  • Fluid therapy. Diarrhea usually causes isotonic
    dehydratation (equal salt and water loss), with
    metabolic acidosis and significant potassium
    loss. Thirst from dehydratation can lead to a
    proportionately excessive water intake, causing
    hypotonicity.
  • Antibiotics. The decision to use antibiotics
    requires consideration of disease severity, age
    of the patient and other factors. In children,
    TMP-SMX at 4mg/kg/po of the TMP component q12h is
    the treatment of choice.
  • In adults the dose is one double strand tablet
    q12h (320 mg TMP). An alternative for adults is
    norfluxacin or ciprofluxacin 500mg po bid (two
    times a day). Many shigella isolates are likely
    to be resistant to Ampicillin and Tetracyclin

34
Cholera
  • An acute infection by Vibrio cholerae involving
    the entire small bowel characterized by profuse
    watery diarrhea, vomiting muscular cramps,
    dehydratation, oliguria, and collapse.

35
Etiology
  • ? The causative organism, V. cholerae, serogroups
    01 and 1039. Epidemic cholera is caused by V.
    cholerae serogroup 01. which is divided into
    three serotypes, Ogava, Inaba, Hikojima. However,
    antigenic structure may change within the human
    gut.
  • ? Biotypes two biotypes of V. cholerae 01,
    classic and El Tor. Any serotype can be of either
    classic or El Tor biotype.
  • ? Non-01 vibrios, deficient in the 01 antigen,
    were classified as non-cholera vibrios but a
    cholera epidemic in Bangladesh in 1992 was due to
    serogroup 0139.

36
Pathogenesis
  • V. cholerae produces a potent exotoxin cholera
    toxin (CT), vary similar to the LT enterotoxin of
    ETEC, which is plasmid coded. The toxin
    stimulates the activity of the enzyme
    adenylcyclase, which raises the concentration of
    cyclic AMP is cell this causes an increase in
    the flow of water and electrolytes into the bowel
    lumen. The fluid lost has relatively high
    concentration of bicarbonate and potassium.
  • V. cholerae is not invasive and does not
    penetrate the gut mucose membrane, although
    adhesion to gut epithelium plays a part in its
    pathogenesity.

37
Clinical feature
  • ? IP 6h to 5 days.
  • ? Acute onset of abdominal pain and diarrhea
    the diarrhea being typically of exceptional
    severity, progressing to the continuous passage
    of rice-water stools.
  • ? Vomiting, dehydratation, acidosis and collapse
    may follow.
  • Some cases are much les severe with only mild
    diarrhea. Two forms of disease are recognized
  • severe classic cholera
  • milder cholera associated with the 01 El Tor
    biotype.

38
CHOLERA
39
Diagnosis
  • Culture feces on alkaline selective medium.
    Observe for typical colonies, which can be
    identified by slight agglutination, with
    polyvalent antiserum.

40
Treatment
  • ? Correction of dehydratation by intravenous
    administration of fluid and electrolytes to
    restore the acid-base balance. Mortality can be
    reduced from more the 50 to 0 with fluid
    replacement treatment.
  • ? Tetracycline, given orally or intravenously,
    may help to limit the duration of diarrhea and
    reduce fluid loss.

41
  • ? Composition of World Health Organization oral
    rehydratation solution (WHO ORS).
  • In 1000ml pre-boiled water
  • 20g glucose
  • 3.5g NaCl
  • 2.5g NaHCO3
  • 1.5g KCl
  • Concentration (mmol/l) Na 90, K 20, HCO3 30
  • ex tempore
  • Rehydrin
  • - Phillips solution

42
Esherichioses intestinales
  • (Colibacilloses)

43
  • Enteric infections are common cause of diarrhea
  • infantile gastroenteritis
  • travelers diarrhea
  • hemorrhagic diarrhea
  • hemorrhagic colitis
  • hemolytic-uremic syndrome

44
  • ETEC enterotoxigenic E. coli travelers
    diarrhea (Delhi belly, Tokyo two step etc)
  • EPEC enteropathogenic (eneteroadherent) E. coli
    childhood diahhrea.
  • EIEC enteroinvasive E. coli a dysentery-like
    disease
  • EHEC enterohemorrhagic E. coli hemorrhagic
    colitis and HUS in children.

45
EPEC (055 0111) strains
  • cause childhood diarrhea, especially in
    underdeveloped countries and in nursery
    outbreaks. These bacteria bind to the membranous
    cells of Peyers patches and disrupt the
    overlying mucous gel of the host cell.
  • EPEC do not produce toxins and are non-invasive,
    but produce an attaching end effacing lesion in
    the small intestine

46
  • ETEC there are more than 100 0 serogroups.
    Important examples are 06, 078.
  • ETEC produce heat-labile toxin (LT) or
    heat-stabile toxin (ST) or both. They also posses
    colonization factors, which facilitate the
    attachment of the organism to the epithelium of
    the small intestine.
  • EIEC (0124, 0164) invade the host cell and
    provoke significant inflammatory response.
    Manifestations are those of bacterial dysentery
    with fever and bloody diarrheal stool, containing
    polymorphonuclear leukocytes.

47
EHEC strains
  • all belong to the serotype 0157H7, cause
    hemorrhagic colitis.
  • These strains produce shiga-like toxins that kill
    certain cells in tissue culture.
  • Although the typical patient is afebrile the
    sequel can be severe. In the elderly the disease
    is often confused with ischemic colitis. It can
    lead to death. Children (1-4 years) and
    occasionally adults with EHEC infection can
    develop HUS, which also can lead to death. HUS is
    seen occasionally with bacteria other than
    0157H7, including other E.coli serotypes and
    Shigella.

48
  • ? HUS in children diarrheal prodrome, followed
    by uremia, throbocytopenia and hemolytic anemia.
  • ? Shiga-like toxins have a cytopathic effect on
    Vero (monkey kidney) cells. There are two Vero
    cytotoxins, VT1 and VT2, which are antigenically
    distinct from each other. Vero cytotoxin
    producing E.coli strains are known as VTEC. Over
    80 phagotypes of serogroup 0157 can be
    distinguished.

49
Diagnosis
  • ? Culture feces on MacConckey medium.
  • ? Identify by serology and biochemical tests.

50
Treatment
  • Rehydratation with correction of fluid loss and
    electrolyte and acid base balance
  • Antibiotics therapy is of doubtful value,
    although it may be useful in severe cases
  • Treatment may be started empirically, than
    modified on the basis of antibiotic sensitivity
    studies. Although many strains are still
    sensitive to Ampicillin (Piperacillin,
    cephalosporins, amynoglucosides, TMP-SMX, and
    quinolons in adults).

51
Dehydration syndrome
  • Rehydration
  • ? oral rehydratation WHO ORS
  • In 1000ml pre-boiled water
  • 20g glucose
  • 3.5g NaCl
  • 2.5g NaHCO3
  • 1.5g KCl
  • Concentration (mmol/l) Na 90, K 20, HCO3 30,
    Cl 80
  • ex tempore
  • Rehydrin a commercial solution

52
i.v. fluids
  • Classification of dehydratation in infants
  • Ist grade up to 5 loss of body weight (infuse
    with 80-100ml/kg/24h)
  • IInd grade between 5-10 loss of body weight
    (120-150ml/kg/24h)
  • IIIrd grade more than 15 loss of body weight
    (150-170ml/kg/24h)

53
  • At the end of the rehydratation period (about 4
    hours), the patient should be reassessed. If
    signs of dehydratation persist, rehydratation
    therapy should be repeated until dehydratation is
    corrected

54
Metabolic acidosis phlt7.37
  • The amount of NaHCO3 can be approximated by the
    formula
  • NaHCO3 required (mEq) BE(base excess) x 0.4 x
    body wt(kg)
  • First 1/3rd of the received quantity is applied
    and if fails to correct the acidosis, the rest is
    added.

55
Hypokaliemia
  • a decrease in the serum potassium concentration,
    below 3.5 mEq/l. It is a result of excessive
    losses of K from GI tract. It is characterized my
    muscle weakness and can lead to paralysis and
    respiratory failure. ECG ST depression.
  • Treatment i.v. KCl amp.15 10ml 2mEq/kg
    slowly!

56
  • The use a antibiotics therapy in bacterial
    diarrheas is controversial and generally not
    necessary in patients with mild or resolving
    disease, but should be considered in patients
    with Shigellosis, travelers diarrhea, cholera.

57
  • Reference
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