Mostly introduced about food toxic infection, Infectious toxic shock, Clinical and diagnostical algorithm. Principles of emergency aid with position of evidence-based medicine.

1. Semey 2015

2.  Introduction
 Food toxic infection
 Infectious toxic shock
 Clinic and diagnostic algorithm
 Principles of emergency aid with position of evidence-based
medicine.

3.  Infectious diseases of children is one of the most common reasons for
seeking emergency care. Under these conditions, in addition to aid, it is
necessary to solve questions the need for hospitalization.
 The absolute indications for hospitalization of children in the presence of
infectious diseases:
• all infectious diseases in newborns;
• all infectious diseases in children of the first two years of severe intoxication;
• diphtheria;
• intoxication;
• typhoid, paratyphoid diseases;
• especially dangerous infections;
• Meningococcal disease;
• meningitis various etiology;
• intestinal infections with intestinal toxemia and exsicosis;
• viral hepatitis.

4.  Food toxic infection - a group of acute intestinal
infections resulting from consumption of foods
containing opportunistic microbes and
enterotoxins. Food toxic infection in children are
characterized by transient phenomena of
intoxication and acute gastritis or gastroenteritis.
 There are two kinds of food poisoning: poisoning
by toxic agent or by infectious agent.

5. • Food poisoning is caused by bacteria that synthesize enterotoxins. Most
disease is caused by the following pathogens:
• - Klebsiella,
• - Proteus,
• - Tsitrobakter,
• - Escherichia coli,
• - Streptococcus,
• - Staphylococcus aureus,
• - Halophilic vibrio,
• - Clostridia.
• Most of these foodborne pathogens are quite stable in the environment
and is also capable multiply in foods.

6.  The source of the pathogen in the food poisoning
are often people who are engaged in cooking,
sometimes animals and birds - sick or healthy
bacillicarriers. They identify pathogens in the
environment with the faeces. Since these bacteria
are widely distributed in nature, often the source
of their origin can not be established. In some
cases, they may be persons with pustular skin
diseases, sore throat, bacterial nasopharyngitis,
pneumonia.

7.  The mechanism of transmission of food poisoning - fecal-
oral. Most often it is realized by food. Food contaminated as
a result of non-compliance with sanitary conditions of their
preparation and storage. Especially dangerous is the
contamination of the products, not heat-treated immediately
before use (jelly, salads, jelly, sour cream, etc.).
 Susceptibility to foodborne diseases not high. It is believed
that mostly sick people with chronic pathology of the
digestive system (gastritis, gastric ulcer and duodenal ulcer,
cholecystitis, colitis, etc.), As a consequence, reduced local
immunity.

8.  The disease occurs by ingestion of child a substantial
amount of bacterial enterotoxins. Therefore, an important
condition for the occurrence of food poisoning is an intense
pre-multiplication of bacteria in the food. Having a tropism
for the intestinal cells (enterocytes), toxins cause
inflammation of the mucous membrane of the stomach and
intestines, stimulates the synthesis of biologically active
substances, the motility of the digestive tract. This gives rise
to diarrhea and vomiting, loss of fluid may cause
dehydration. General toxic syndrome also develop with the
changes of the cardiovascular and nervous systems.

9.  Food poisining diseases caused by various pathogens, have similar symptoms.
 The incubation period is short, usually 5-6 hours, sometimes shortened to 1 hour or
extended to 12 hours. Clinic foodborne diseases cause lesions of the gastrointestinal tract
as gastritis, gastroenteritis, or, occasionally, gastroenterocolitis, intoxication and
dehydration. Symptoms occur suddenly and rapidly growing. There are coldness,
cramping abdominal pain, often epigastric and around the navel.
 Nausea and repeated vomiting that brings relief to the sick child. Later joined by
diarrhea. The stools are loose or watery, fetid, up to 10 times a day or more, sometimes
with mucus. Urging to stool are mostly mandatory.
 The body temperature with food poisoning often low-grade or normal, rarely rises to
high numbers. The skin is pale, dry and in severe cyanosis of the lips and there is toe.
Tongue coated white or gray coating. Pulse frequent, blood pressure is lowered. When
reusable vomiting and diarrhea symptoms of dehydration: dry and decreased skin
turgor, decrease in urine output, muscle cramps limbs, tachycardia, hypotension.

10. First aid for food poisoning is needed immediately after the
appearance of symptoms of the disease.
Emergency assistance with food poisoning include:
• Gastric lavage to remove residual food that caused the poisoning;
• Reception means that are able to adsorb toxin in the alimentary tract, and
bacteria, e.g., smectite or activated charcoal;
• Reinforced drinking mode of use of the solution rehydron;
• The use of broad-spectrum antimicrobial action (ftalazol, furazolidone);
• A strict diet;
• If repeated vomiting can be taken Reglan to suppress the vomiting reflex.
Do not use the medication immediately after the procedure, gastric lavage.

11.  Toxic shock syndrome (TSS) is a multisystem disease manifested
by sudden onset of fever, chills, hypotension, and rash.
Multisystem involvement may cause vomiting, diarrhea, myalgia,
mucous membrane hyperemia, mental confusion, renal
dysfunction, hepatic abnormalities, and thrombocytopenia.
 TSS is caused by toxin-producing strains of staphylococci
(staphylococcal TSS) and streptococci (streptococcal TSS). Both
causes are discussed in this article. Todd et al first described
staphylococcal toxic shock syndrome in 1978. The association of
TSS with menstruation and tampon use was established in 1980.
Cases of TSS caused by streptococci were first reported in the mid-
1980s.

12. Findings
Staphylococcal Toxic
Shock Syndrome
Streptococcal Toxic
Shock Syndrome
Age 15-35 y 20-50 y
Sex More common in females Males and females
Local invasive disease Absent Present
Generalized
erythroderma
Present Absent
Nausea, vomiting, or
diarrhea
>90% of patients Uncommon
Bacteremia Uncommon 60% of patients
Toxins implicated
TSST-1; enterotoxins B
and C
Streptococcal pyrogenic
exotoxins A and B
Mortality rate 3.3% 30%
The following table summarizes key
distinctions between staphylococcal and
streptococcal TSS.

13.  Toxic shock syndrome starts suddenly, often with high fever
(temperature at least 102°F [38.8°C]), a rapid drop in blood
pressure (with lightheadedness or fainting), confusion,
vomiting, diarrhea, headache, or muscle aches.
 A sunburn-like rash may appear anywhere on the body,
including the palms of the hands and the soles of the feet. A
person also might have bloodshot eyes and an unusual
redness under the eyelids or inside the mouth (and in the
vagina in females). The area around an infected wound can
become swollen, red, and tender, but might not even appear
infected.

14.  Other symptoms can include confusion or
other mental changes, decreased urination,
fatigue and weakness, and thirst.
 If TSS is untreated, organs such as the liver and
kidneys may begin to fail, and problems such
as seizures, bleeding, and heart failure can
develop.

15. Using the criteria for case definition of Staphylococcal Toxic Shock Syndrome4 in paediatric practice
is complicated by communication difficulties, diminished prodromal period in children and the
requirement to include desquamation in the diagnosis (this occurs up to two weeks later and only if
the illness is allowed to progress).
 Pragmatic criteria for diagnosis of Staphylococcal TSS in children1 include:-
1. Pyrexia . 39oC
2. Irritability
3. Diarrhoea +/- vomiting
4. Lymphopaenia with a commonly normal total white cell count
5. Rash (commonly non-specific diffuse maculopapular)
Not all of these features need to be present to make the diagnosis.
Hyponatraemia is commonly seen. Other haematological changes such as thrombocytopaenia and
coagulopathy may be late developments in children.

16. Streptococcal TSS commonly arises from invasive soft tissue infections viz. necrotising fasciitis,
cellulitis and myositis. Diagnosis is confirmed by the isolation of Group A Streptococcus from a
normally sterile site (blood, CSF, peritoneal fluid, tissue biopsy) together with clinical signs of
severity :-
• Hypotension / shock
• Two or more of the following:-
 Renal impairment
 Coagulopathy (thrombocytopaenia or disseminated intravascular coagulation)
 Hepatic involvement (elevated transaminases and bilirubin)
 Respiratory Distress Syndrome
 Generalised erythematous, macular rash (may desquamate)
 Soft tissue necrosis (gangrene, necrotising fasciitis, myositis)
In children, coagulopathy and rash may be late signs and should not be relied upon.

17.  TSS is rapidly progressive with high mortality. Suspected
cases should be managed on the Paediatric Intensive Care
Unit. Consultant advice and support should be sought from
the PICU, Burns and Paediatric Renal teams.
 Management as per standard septic shock guidelines6
should be commenced including active fluid resuscitation,
early use of vasopressors and inotropes, establishment of
central access and intubation mechanical ventilation if
required. Note that unlike “warm shock” TSS usually
displays high systemic vascular resistance and may be
refractory to inotropes.

18. In general, after the history and physical, if the
patient has low blood pressure and multiorgan
involvement characterized by two of the above listed
symptoms of organ dysfunction (renal, lung, liver,
skin, or blood), the clinical diagnosis of TSS is made,
according to CDC criteria. A confirmation of the
diagnosis is done by isolation of bacteria from a
normally sterile site; the bacteria should be identified
as capable of producing exotoxin that either is, or
functions like, TSST-1.

19.  The treatment for TSS varies from patient to patient; however, the
following treatments are fairly common. Patients with TSS usually
will be treated with two or more of the following treatments:
 Intravenous fluids to treat shock
 IV antibiotics
 Deep surgical cleaning of any infected wounds
 Cardiac medications to help treat low blood pressure
 Oxygen and/or mechanical ventilation as needed
 Blood products if needed
 Dialysis for patients with kidney failure
 Hospitalization in an intensive-care unit

20.  It is possible to reduce the chances of developing
TSS. Menstruating females should minimize use of
items like tampons, diaphragms, and sponges.
Tampons should be changed frequently, and
superabsorbent tampons should be avoided.
Anyone diagnosed with TTS has a higher risk of
reinfection; women diagnosed with TSS should
avoid tampon use in the future. Early treatment of
wounds, especially deep wounds, can help
prevent

21. Causes and Source Control
 Ensure a careful survey for infectious focus. Any
surgical wounds should be considered potential
sources of infection. If evidence of wound infection,
wide debridement is suggested. Do not delay surgical
intervention for medical imaging. Necrotising fasciitis
or necrotising myositis is a surgical emergency
requiring aggressive debridement. In females, vaginal
examination for foreign bodies such as tampons should
be considered.

22. Antimicrobial Therapy
 Inadequate initial antimicrobial therapy markedly increases mortality and
discussion with microbiology at the earliest availability is important.
Empirical therapy to cover both Staphylococcal TSS and Group A
Streptococcal disease is advised, for example high-dose flucloxacillin.
Clindamycin should also be included in all initial antimicrobial regimes
due to demonstrated reduction in toxin production.
 Vancomycin is not advised as a first-line antibiotic due to the low
prevalence of MRSA in the paediatric population while flucloxacillin has
better bactericidal efficacy. For patients with history of non-severe
penicillin allergy, cefuroxime and clindamycin are recommended. For
patients with history of severe penicillin allergy, clindamycin with
vancomycin or linezolid is advised.

23. Intravenous Immunoglobulin (IVIG)
 IVIG is recommended as an adjunctive therapy in children with severe toxin-
related infection showing failure to improve despite best standard care7.
Intravenous immunoglobulin should be considered in patients in whom there has
been no clinical response within the first six hours of aggressive therapy8. IVIG for
this indication should be at the request of a PICU Consultant only. An IVIG request
form must be submitted to the immunoglobulin panel. There is no conclusive
evidence or guideline for IVIG dosage for this indication. Therefore adoption of the
recommended dose for PVL-SA / adult TSS is recommended. Total dose of 2g/kg
is suggested (rounded down to the nearest whole vial). It is reasonable to consider
repeat administration after 48 hours if there remains a poor response to treatment.
Human Intravenous Immunoglobulin (IVIG) may rarely induce thromboembolic
events including myocardial infarction, cerebrovascular accident, pulmonary
embolism and deep vein thrombosis. Caution is therefore advised in the
prescription and administration of high dose immunoglobulin in patients with pre-
existing risk factors for arterial or venous thrombotic events.

24.  Results of trials on intravenous immunoglobulin (IVIG) as adjunctive
therapy for sepsis have been conflicting. A prospective single-centre case-
control study suggested IVIG conferred a significant reduction in
mortality in PICU sepsis patients9; adjunctive use of IVIG in sepsis and
septic shock is advocated in the 2008 Surviving Sepsis guidelines6.
However, meta-analysis in adults and children has failed to conclusively
support the use of IVIG in sepsis and septic shock10,11. There is growing
evidence that IVIG therapy has no effect upon the outcome of suspected
or proven neonatal sepsis11,12. Evidence for the use of IVIG in
Staphylococcal Toxic Shock Syndrome in children is graded as III on the
basis of case reports, in vitro studies and extrapolation from adult
studies7 and is recommended for use as a short-term therapy of medium
(blue) priority in the event of clinical rationing.

25.  Young A and Thornton K. Toxic Shock Syndrome in Burns: Diagnosis and Management.
Arch Dis Child Educ Pract Ed 2007; 92: 97-100
 2. Descloux E et al. One in Five Mortality in Non-Menstrual Toxic Shock Syndrome
Versus No Mortality in Menstrual Cases in a Balanced French Series of 55 Cases. Eur J
Clin Microbiol Infect Dis 2008; 27: 37-43
 3. Lamagni T et al. Epidemiology of Severe Streptococcus pyogenes disease in Europe. J
Clin Microbiol 2008; 46: 2359-2367
 4. Wharton M et al. Case Definitions for Public Health Surveillance. MMWR Recomm
Rep 1990; 39: 1-43
 5. Working Group on Severe Streptococcal Infections. Defining the Group A
Streptococcal Toxic Shock Syndrome: Rationale and Consensus Definition. JAMA 1993;
269: 390-391
 6. Dellinger R et al. Surviving Sepsis Campaign: International Guidelines for the
Management of Severe Sepsis and Septic Shock: 2008. Crit Care Med 2008; 36: 296-327
 7. Department of Health Clinical Guidelines for Intravenous Immunoglobulin Use. 2011
www.ivig.nhs.uk
 Medically Reviewed by a Doctor on 12/9/2014 Joseph S Bushra, MD, FAAEM Charles
Patrick Davis, MD, PhD
 Paediatr Drugs. 2005;7(1):11-25. Toxic shock syndrome in children: epidemiology,
pathogenesis, and management. Chuang YY1, Huang YC, Lin TY.