Acute gastrointestinal infections (AGI);-a group of infectious diseases of different etiology (viral, bacterial, fungal, parasitic), characterized by fecal-oral route of transmission, primarily involving the gastrointestinal tract. Among infectious diseases in children acute intestinal infections require special attention. Only acute respiratory illness exceed them by the spread of morbidity, and in the structure of mortality from infectious causes in Ukraine AGI take 2-3 place. According to the WHO classification, all human diarrheal diseases are  divided into infectious and noninfectious. Infectious diarrhea are divided into invasive (inflammatory, blood) and secretory (noninflammatory, watery).

1. MPH OF UKRAINE
IVANO-FRANKIVSK NATIONAL MEDICAL
UNIVERSITY
DEPARTMENT OF CHILDREN
INFECTIOUS DISEASES

2. On skin On mucosa
EXANTHEM ENANTHEM
Rash – focal skin or mucosa reaction to the
impact of microorganisms or their toxins,
including the effect of histaminelike
substances (allergic rash).

3. Exanthem
infectious
non-
infectious

4. Rash is the most spread but not the only one symptom of
children infectious diseases. It appears on the background
of other syndromes.
Infectious
diseases, that are
always with rash
Measles
Chickenpox
Herpes zoster
Scarlet fever
Roseola infantum
(erythema of Rosenberg)
Infectious erythema of
Tschamer
Infectious
diseases, that are
often accompanied
by rash
Rubella
Typhoid fever, paratyphoid
Pseudotuberculosis
Infectious
diseases, that may
be accompanied by
rash (25-30 %)
Ebstein-Barr infection
Enteroviral infection
Brucellosis
Toxoplasmosis

5. Mechanisms of infectious
exanthems development
metastatic
• Pathogen through
blood gets into
skin
• Herpes simplex,
herpes zoster,
enteroviral
infection,
meningococcemia
infectious-
allergic
• The reaction of pathogen
with circulating immune
factors
• Measles, rubella,
iyersiniosis
• Or without pathogen -
Lyell's syndrome, Stevens-
Johnson syndrome
toxic
• Action of
bacterial toxins
• Scarlet fever,
pseudotuberculo
sis

6. Primary lesions
roseola
macule
erythema
hemorrhage
papule
tubercle
node
vesicle
bulla
pustule
wheal
Secondary lesions
squama
crust
pigmentation
ulcer
scar

7. SKIN STRUCTURE

8. Primary skin lesions

9. Secondary skin lesions

10. Roseola
a pale pink, red or purple spot
size is from 1 to 5 millimeters
doesn’t arise above the skin level
 appears as a result of papillary skin
layer vasodilatation.

11. Macule (spot)
 the lesion the same colour with roseola,
 but it’s larger (from 5 to 20 millimeters)
 doesn’t arise above skin level,
 often irregularly shaped
small macules
(5-10 mm)
big macules
(more then 10 mm)

12. Erythema
macules over 20 mm in
diameter that may become
confluent

13. Haemorrhage
 the bleeding into skin
 the result of diapedesis or destruction
of skin vessels
petechiae
(droplet
hemorrhages)
ecchymosis
(largher than
5 mm)
purpura
(from 2 to 5
mm)
petechiae
(droplet
hemorrhages)
ecchymosis
(largher than
5 mm)
purpura
(from 2 to 5
mm)

14. Papule
more or less solid element without
cavity,
arises above skin level
 sizes are from 1 to 20 mm
 color and shape are different

15. Tubercle
element without cavity
appears as a result of the
inflammatory granulomas
formation in deep derma layers

16. Node
limited, deeply permeating the skin
dense formation
the result of cellular infiltrate in the
dermis and adipose tissue

17. Vesicle
a cavity located in the epidermis
contains liquid
arises slightly above the skin level
Diameter - 1 to 5 mm

18. Bulla
a formation, equivalent to vesicles,
but larger than 5 mm to 10-15 mm

19. Pustule
exudative cavitary element with
pus, located on the infiltrated
base

20. Wheal
is an exudative cavitary element which
is formed by the swelling of the
papillary skin layer, it is a solid round
or oval projection, ranging in size
from several millimeters to 10-15-20
cm, accompanied by severe itching

21. Squama
consists of separated keratic
epidermis plates, it’s color can
be different: white, gray, yellow,
brown

22. Crust
the formation that appears as
a result of the skin serous
fluid, pus or blood drying on
serous crust
(translucent or
gray)
hemorrhagic
(dark red, brown )
pus crust
(yellow or
orange-yellow)

23. Pigmentation
is the skin color changing at the rash
site due to enhanced melanin
pigment deposition after the primary
rash elements disappearing or as a
result of the red blood cells
hemoglobin collapse

24. Ulcer
a defect of the skin,which is
spread on tissues lying below

25. Scar
is a formation of coarse-
fibered connective tissue at
the site of skin defects

26. Examining of patient with rash
Type of element
Number
Size
Colour
Localization
Order of appearance
and disappearence

27. The rash types
Punctate
Scarlet fever
Pseudotuberc
ulosis
Staphylococcal
infection
Varicella
Sudamen
Roseolous
Typhoid fever
Typhus
Maculous
Measles
Rubella
Enteroviral
infection
Infectious
erythema
Allergic
eruption
Vesiculous
Varicella
Streptoderma
Strophulus
Lyell’s
syndrom
Stevens-
Johnson
syndrom
Mixed
Meningococcal
infection
Infectious
mononucleosis

28. Measles
• Duration is 9 -17 days
Incubative period
• lasts 3-4 days
• Cough, corryza, conjunctivitis
• fever to 38-39 ° C and above
• pathognomonic symptom – Belsky-Filatov-Koplik spots
Prodromal or
catarrhal period
• starts on the 4-5 day of illness and lasts for 3-4 days
• catarrhal phenomena of eyes and respiratory tract
mucosa intensify
• Exanthem appears
Rash period
• on-the site of rash elements
• this process goes in the same order as the rash and up to
6 days from onset of rash / to the 11-22th day of the
disease
Pigmentation
period

29. Features of rash in measles
 rash stages from top to bottom for 3 days
 maculopapulous,
 located on the normal skin background
 with a tendency to become confluent
 There is no selective localization of exanthem - it
is equally intense on the inner and outer surfaces
of the upper limbs, chest, back, abdomen,
buttocks.
 In some cases, the rash becomes hemorrhagic
 Step by step for 3 days on the site of rash elements
pigmentation develops

30. Measles: 2nd day of illness
Koplik’s spots

31. Rubella
 Incubation period – 11 – 21 days
 The first day of rash is the first day of illness.
 Rash is monomorphic / smallmaculous /,separate
elements can be maculopapular, pale pink, with
cyanotic tint, very rare confluent, on normal skin
background.
 rash is concentrated on the extensor surfaces of the
upper extremities, in the back, buttocks, outer
surface of thighs
 generalized lymphadenopathy, mainly of back
neck and occipitallymph nodes

32. Rubella: 1st day of the disease

34. Varicella (Chickenpox)
 Causative agent – Varicella zoster virus, from
Herpesviridae family, type III
 Incubation period – 11 – 21 days
 Prodromal period - poor appetite, disturbance of the
general condition, fever up to 37,5-38 ° C, dyspeptic
disorders.
 Period of eruption :
macule papule vesicle crust

35.  Rash covers the whole body, even on the scalp,
conjunctiva, mouth mucosa, genitals, with a
primary distribution on the trunk
 Lasts 4-5 days, lesions at all stages of
development are present simultaneously
(false polymorphism) and crops of new
lesions continue to appear,that is
accompanied by temperature increasing

36. Varicella

38. Complications
 Excoriation often lead to bacterial superinfection, vesicles
become pustules and as a result scars are formed.
 Adults with immunosuppression may develop generalized
infection with high fever, encephalitis, pneumonia, DIC.
 Infection in the I half of pregnancy in 60% of cases leads to
miscarriage, and 2% - to "congenital varicella syndrome "
with skin scars, lesions of eyes and central nervous system, limb
hypoplasia.
 Infection in the II half of pregnancy 2 weeks before birth is
not associated with risk. If woman is infected 5 days before
delivery or up to 2 days after them or a child gets infection up to
10 days of life, then fulminant form of disease occurs with
high mortality (30%). This is due to the lack of transplacental
transfer of maternal antibodies in that period.

39. Scarlet fever:
pharyngeal enanthem
Scarlet fever: bright hyperemia
of the pharynx, membranous tonsillitis

40. Herpes zoster
 sporadic disease, the result of the latent varicella-
zoster virus activation in patients with
immunodeficiency
 is characterized by inflammation of the posterior
roots of the spinal cord and intervertebral ganglia
 fever, general intoxication and vesicular exanthema
along sensory nerves
 people who previously had chickenpox become ill,
mostly adults and elderly (60-80 years). Incidence of 5
to 10 per 1000 people.

41. Vesicles dry up and turn into crust. Pain can stay for months.
After 3-5 days (sometimes 10-12 days) characteristic rash appears.
Pain and eruption are localized along the affected nerves (most
often intercostal or trigeminal). In this place infiltration and
hyperemia first appear, than vesicles with clear, then cloudy
content unilaterally along the nerves.
Beginning is acute, with fever, symptoms of intoxication,
expressed excruciating pain at the site of future eruption
(ganglionitis, neuritis).

43. Herpes zoster
1. Herpes Zoster in more than one
dermatome in a 30 year old HIV
positive man.
2. Herpes Zoster as the first sign
of HIV infection in a 3 1/2 year
old boy.

44. Scarlet fever
• from several hours to 7 days, it’s average duration
is 2-4 days.Incubative period
• β-hemolytic streptococcus group A,
• which also causes tonsillitis, acute respiratory
disease, erysipelas.
Causative agent
• a time of first symptoms occurrence until the
rash appears /few hours - to 1-2 days /
Initial
/prodromal/
period
• airborne
Way of
transmission

45. Clinical manifestation
The classical triad of illness is fever, sore throat, vomiting.
Body temperature rises to 38° -39° C,
Tonsillitis is represented by tonsils enlargement, their hypertrophy,
inflammation spreads on palatine uvula, arches, where hyperemia has clear
paths in the form of semicircular lines.
The rash period

46. Rash in scarlet fever
 appears first on the neck, then - on the trunk, chest,
abdomen, proximal extremities
 lasts for 3-5 days
 It is punctate rash, located on hyperaemic skin,
abundant, skin becomes dry, rough due to hypertrophy
of hair follicles.
 Symmetry is characteristic for this rash /in the axillary
and inguinal areas/.
 Never appears in the nasolabial triangle , there is
so called, scarlet fever mask of Filatov.
 Pastia symptom (bright rash in the skin folds in the
form of lines).

47. Other symptoms of scarlet fever
 intoxication, tonsillitis with regional lymphadenitis,
changes of the tongue, white dermographism.
 On the day when rash appears tongue is cleaned from fur,
first from the tip, then on the side surfaces /day of illness to
4-5/, the tongue papillas increase in size, swell /"raspberry
tongue"/. Papillae hypertrophy remains to the 10-12th day
of illness. The patient’s lips become bright red or cherry,
thicken and crack easely.
 the initial period is marked by relative tachycardia,
moderate increase of blood pressure, reducing heart tones
(it’s so called sympatycus phase), on the 4-5th day relative
bradycardia, hypotension appears (vagus phase).

48. Recovery period of scarlet fever
 In the first — early second week
 largeplate skin shelling may occur. It begins from the
fingertips of hand and feet, spreads on palms and
soles. The epidermis is desquamated like flakes,
sometimes it is removed like a glove. Shelling ends in
2-3 weeks.
 During this period the patient feels well, the main
clinical symptoms are absent.

49. complications
 Without antibiotics, scarlet fever may be complicated
by otitis, sinusitis, cervical lymphadenitis arising
at 1-2 weeks of illness.
 The most dangerous late complication - rheumatic
fever, glomerulonephritis, heart disease
(myocarditis), which develop at 3-4 weeks of illness.
 also possible pneumonia, synovitis.

50. Scarlet fever pin-point exanthema
on abdomen
Scarlet fever exanthema in
skin folds

51. Scarlet fever Filatov’s mask
Scarlet fever, strawberry tongue,
coated in the centre (4th day from
the disease beginning)

54. Infectious erythema of Tshamer (erythema
infectiosum, slapped cheek syndrome)
• Parvovirus B19
Causative
agent
• airborne
• parenteral
• transplacental
way of
transmission
• 4-14 days
• patient is most contagious at 1 week
of illness
Incubation
period
• occurs mainly in the winter months,
affects school children.
• 60% of adults have antibodies to
parvovirus.
epidemiology

55. Clinical manifestation
large maculous rash on face, where it becomes
confuent in the form of butterfly, captures nose bridge
and cheeks / "Wings" /. Than rash spreads on extensor
surfaces of extremities / shoulder, hip / , rarely on the
trunk.
First rash is brightly hyperaemic, then
enlightenment appears in the center of each element,
periphery remains hyperaemic, flows into garlands,
rings.
In 10-12 days rash disappears without pigmentation
and shelling

57. Exanthema subitum (meaning sudden rash),
as roseola infantum or three-day fever
 Pathogen - human herpesvirus type 6
 In most cases the primary infection develops in the
first years of life and occurs as a sudden rash or
feverish illness.
 Peak incidence occurs in age from 6 to 12 months.
Like other herpesvirus, HSV 6 for life persists in the
body in the form of latent infection.

58. Clinical manifestation
Disease begins with fever that lasts 3-5 days and is
often accompanied by febrile convulsions.
Temperature quickly becomes normal
than spotted or macule-papulous rash appears on
the trunk, which lasts 3-4 days.
 Because of high fever (over 39 ° C) and its difficult
differential diagnosis, children are often
prescribe antibiotics. Normalization of
temperature and rash often are mistakenly
regarded as an allergic reaction to the antibiotic.

60. Urticaria

62. Meningococcemia:
hemorrhagic rash

63. Thank You for Attention!

64. MPH OF UKRAINE
IVANO-FRANKIVSK NATIONAL MEDICAL
UNIVERSITY
DEPARTMENT OF CHILDREN INFECTIOUS
DISEASES
Lecturer: assistant
Horbal Natalia Bogdanivna

65.  Acute tonsillitis (angina) is very
frequent disease in childhood. In
practice, the doctor must
distinguish tonsillitis, as an
independent disease, and
tonsillitis occurring on the
background of other infectious
diseases.
 Diphtheria is one of the most
dangerous infectious diseases.
Urgency of the problem can be
shown by the fact that low
immunization coverage of
population (less than 95%) may
increase the incidence of
diphtheria, even epidemics with
serious consequences, up to
lethal.
The word "angina" comes from
the Latin "angere" meaning "to
choke or throttle."

66.  1. Characterize tonsillitis, their etiological structure and
clinical forms .
 2. Epidemiological features of diphtheria nowadays.
 3.To characterize the features of diphtheria (morphology
, pathogenic properties).
 4. Characterize clinical forms of diphtheria (paying
particular attention to the diphtheria of oropharynx).
 5. Discuss clinical and laboratory diagnosis methods of
diphtheria.
 6. Make differential diagnosis of tonsils diphtheria.
 7.To learn the principles of treatment of diphtheria.
 8.To learn the basics of diphtheria prevention.
 9.To learn the tactics of the physician in case of
identifying tonsillitis, diphtheria, and in cases of
suspected diphtheria .

67. • tonsillitis
• diphtheria
• infectious
mononucleosis
• tularemia
• listeriosis
• scarlet fever
• adenoviral
infection
• typhoid and
paratyphoid
• syphilis
• candidiasis of the
oropharynx
Infectiousdiseases
• acute leukemia
• agranulocytosis
• radiation sickness
Non-infectious
diseases
size
color
relief
the state of the palatine arches,
soft palate, uvula, posterior
pharyngeal wall
lymph nodes
subcutaneous tissue
neck
character of breathing, changes
of the voice, supporting muscles
involved in breathing

68. • Mild enlargement of
the tonsils - they don’t
extend beyond the
anterior palatal arches
I degree
• Moderate enlargement
- they extend beyond
the arches
II
degree
• Severe - tonsils
almost meet one
another
III degree

69. pain when swallowing
hyperemia and edema of the
tonsils
small pustular elements
(follicles) with a diameter of 2-
3 mm , which can be seen
through the mucous membrane
presence of pus in the lacunas
fibrinous deposits on their
surface
Hypertrophic tonsils - can be caused by recurrent pharyngitis and local
inflammation, especially in children and young adults.
Inspection of the oral cavity reveals hypertrophy of the palatine tonsils, so called
“kissing tonsils” when they meet in the midline or overlap.Tonsilloliths may be
lodged in the crypts. May be asymptomatic, massive tonsils sometimes fall back and
occlude the oropharynx, particularly when the patient is recumbent. Most cases of
obstructive sleep apnea in children are associated with hypertrophic tonsils.

70. • redness and swelling of the mucous
membrane of the tonsils without formation of
deposits
catarrhal
• inflammation runs deep in the tonsils, follicles
are with pus, like “star sky"follicular
• pus is formed in the gapslacunar
• suppuration of the tonsils spreads into
neighboring tissuephlegmonous
• formation of superficial ulcers, tonsillitis
Symanovsky-Plaut-Vincent as an independent
nosological form
necrotic-ulcerative

71. Catarrhal tonsillitis
Lacunar tonsillitis
Folicular tonsillitis

72.  acute bacterial anthroponosis infection, caused by Corynebacterium
diphtheria and characterized by inflammation with the formation of
fibrinous exudates on the place of pathogen invasion (diphtheritic or
croupous inflammation), symptoms of intoxication and toxic lesions of
the cardiovascular, nervous system, adrenal glands and kidneys.
Corynebacterium diphtheria
(Klebs-Löffler bacillus)
• Gram-positive
• does not form spores
• resistant on dryness and freezing
• sensitive to high temperature and
disinfectants
• characteristic feature of the
pathogen - is toxin formation

73.  The ability to toxin
formation of different
strains of the pathogen
varies, perhaps its loss
can even happen. Under
the influence of
bacteriophages
nontoxigenic strains can
become toxigenic.
 The most important toxin
– is exotoxin (histotoxin),
which determines the
pathogenicity of
corynebacterium
diphtheria.
 The pathogens produce
other biologically active
substances to, including
hyaluronidase, due to
which they penetrate into
the surrounding tissues
from areas of specific
local process and
facilitates the absorption
of toxin into lymph and
blood; neuraminidase –
decreases pain because of
nerves endings damaging
Stained Corynebacterium cells.The "barred"
appearance is due to the presence of
polyphosphate inclusions called metachromatic
granules. Note also the characteristic "Chinese-
letter" arrangement of cells.

74.  Diphtheria takes its name from the Greek word
‘dipthera’ meaning leather and was named in
1826 by French physician Pierre Bretonneau.
This is because it refers to the leathery, sheath-
like membrane that grows on the tonsils, throat
and in the nose.
 In the (early) 1900s it was the most common
cause of death from an infectious disease with
rates as high as 400 cases per 100,000 people.
In 1932 vaccination against the infection began
and by the late 1950s rates had plummeted
 There's a risk that an outbreak could occur if the
number of people who are vaccinated falls
below a certain level. This risk was
demonstrated by the diphtheria epidemic that
struck the countries of the former Soviet Union
between 1990 and 1998. It resulted in 157,000
cases and 5,000 deaths. The epidemic was
caused by an increase in the number of children
who were not vaccinated against the disease.
Number of
reported cases
2010 2011
Ukraine 17 8
Russian
Federation
9 5
Germany 8 4
India 3123 3485
Ghana 47 -
Turkey 0 1
Nigeria - 0
http://www.who.int/countries/en

75. • patients with diphtheria
(are contagious from the
illness beginning to the
15-25th day of illness)
• carriers of toxigen
strains
Source of
infection
• Droplet (airborne) is
the main
• Contact transmission is
also possible due to
pathogen resistance
The
mechanism of
infection
transmission
• 0.15-0.2
Index of
contagiousnes
s
4'489 reported cases in 2012
25'00 estimated deaths (in 2011)
83% estimated DTP3 coverage
32% of countries reached >=80%
DTP3 coverage in all districts

77. In the area of gateway
bacteria multiplies
and secretes exotoxin
exotoxin penetrates
into the blood,
leading to
toxemia
in the gate area - the
local inflammatory
process
The period of circulation of toxins in the
blood is not longer than 12-24 hours
because of their intense fixation on the
cells (primarily the nervous system).
• heart (cardiomyocytes,
intra-and extracardial
inervative apparatus,
interstitial tissue),
• sympathetic ganglia of the
autonomic nervous system,
• adrenal glands
• kidneys (mainly tubules)
THE TOXIN INJURES

78. Violation of protein
synthesis in cells
specific inhibition of
aminoacetyltransfera
sis
coagulation necrosis
of the epithelium
local vessels paresis,
increased
permeability of the
walls of small vessels
in the lesion focus
In the intercellular
space the etravasate
rich in fibrinogen is
forming
With the participation
of necrotic tissue
trombocinaze
fibrinogen is
converted to fibrin
with the formation of
fibrinous deposits on
the affected surface

79. DIPHTHERITIC
INFLAMMATION
If fibrinous deposits
are formed on the
mucous membranes
covered with
multilayer flat
epithelium, it
penetrates the entire
mucous membrane and
closely associats with it
specific for
diphtheria of
tonsils
CROUPOUS
INFLAMMATION
If fibrinous deposits are
formed on the mucous
membranes covered with
single layer of cylindrical
epithelium, it does not
bind to it tightly and can
be easily separated
specific for
diphtheria of
larynx, trachea,
bronchi

80. Depending on the
degree of intoxication
and the intensity of local
inflammation
Localized
form
Spread
form
Toxic form
Type of
local
changes
catarrhal
insular
membraneou
s
According to
the
localization
Tonsillar
diphtheria
nasopharyngea
l diphtheria
anterior nasal
diphtheria
laryngeal
diphtheria
diphtheria of other
(rare) localization
(cutaneous, ocular,
genital)
Combinated
Forms by
severity
subclini
c
mild
moderate
severe
hypertoxic
carryering

81.  low or moderate intoxication
 local inflammation is limited by area of the tonsils, mild pain when
swallowing, moderate enlargement of lymph nodes, which are not very
painful
• is detected in the focuses of diphtheria in contact persons
• moderate enlargement of the tonsils, slight hyperemia with
cyanotic shade, low-grade fever and mild symptoms of intoxication.
• Diagnosis is confirmed by the detection of toxigenic type of C.
diphtheria
Catarrhal
(atypical)
form
• most common in vaccinated children
• tightly bound to the surface of moderately enlarged tonsils
islands of whitish or whitish-gray color fur, from 1 to 3-4 mm,
which can be removed without difficulty, their removing may not
be accompanied by bleeding.
• low-grade fever, mild pain on swallowing, slightly enlarged
regional lymph nodes.
Insular form
Membraneous
form

82. • sharp rise in temperature to 38-390C, headache, weakness,
loss of appetite, sometimes vomiting.
• mucosa is edematous, hyperemic with cyanotic shade
• Tonsils are enlarged, with whitish, whitish-gray deposits
with smooth or wavy surface. They are tightly linked to
surrounding tissues, it is difficult to remove them with a
spatula, after removing the bleeding is observed.The
removed memrane is fibrinous (elastic, can not be grinded
between spatulas).
• swelling of the mucous membrane of palatal arches, tongue,
and even paratonsillar tissues.
• this form lasts for 6-7 days: the temperature is reduced on
the 2-3 day, deposits are kept up to 6-7th day
MEMBRANEOUS
FORM

83.  expressed intoxication: temperature is
380C and higher, pallor, malaise,
anorexia, mild sore throat, especially
when swallowing.
 Thick greyish-white or dirty gray
deposits with wavy surface extending to
the anterior palatine arches, uvula,
nasopharynx. Deposits can not be
removed with a spatula, after their
rejection surface under them bleeds,
they are fibrinous (elastic, not grinded,
keep their shape)
 The mucosa is slightly hyperemic with
cyanotic shade, there is a clear-cut
swelling of the mucous membrane
around the site with deposits (perifocal
edema). Swelling may involve
neartonsillar tissue.
 Regional lymph nodes are enlarged,
moderately painful
 There are symptoms of the
cardiovascular system injury from the
first days of illness .
Pharyngeal diphtheria with membranes
covering the tonsils and uvula in a 15-year-
old girl.

84.  begins acutely
 temperature is 400C, there is severe headache, vomiting,
anorexia, pallor, growing malaise
 mucosa is edematous, hyperemic with cyanotic shade.
 tonsils are enlarged expressively, their surface is covered
with thick whitish-gray, dirty-gray, gray deposits with the
rough surface.
 The deposits extend to the anterior palatine arches, uvula,
soft and hard palate, the back wall of the pharynx.
 The voice has nasal tone. Breathing becomes noisy.
 Face is pale, lips are dry, cracked. The mouth is half-
opened, there is rotten sweet sugary smell from the mouth.
During examination of oropharynx intense perifocal edema
is observed, swelling extends to the neck subcutaneous
adipose tissue.

85. • swelling spreads
to the middle of
the neck
Іst
degree
• swelling spreads
to the clavicle
ІInd
degree
• swelling spreads
below the clavicle
ІIIrd
degree

86.  clinical symptoms are the
manifestations of infectious-toxic shock
with ultra-rapid rate of progression of
the pathological process
 the rapid development of DIC syndrome
(hemorrhagic form): hemorrhage in the
injection site, bleeding.
 Manifestations of ITSH can sometimes
ahead the development of local
inflammation. In some cases typical
fibrinous deposits have no time to be
formed
 Local changes are limited to expressed
swelling of soft tissues of oropharynx
and neck subcutaneous tissue.
 The prognosis is unfavorable
 At the toxic and hypertoxic forms
of diphtheria there is danger of
infectious-toxic shock (ITSH).
 Shock may also occur after gradual
complicating of the form (from
subtoxic to toxic of the III degree),
especially in combination with
other localizations (nasopharynx,
nose, throat) without treatment in
time.

87.  As an independent form is rare, often in combination with tonsillar
and/or nasopharyngeal diphtheria.
 Occurs in
 localized (only larynx) form
 spread (besides the larynx – trachea) form
 descending (if larynx, trachea and bronchi are involved) form
 The severity of hypoxia is caused by the airway occlusion by the films.
The toxin is absorbed poorly, so intoxication is not expressed.
CLASSICAL CROUP TRIAD
• hoarse voice
• rough barking cough
• stenotic noisy breathing
(stridor)

88. • at laryngoscopy only edema and hyperemia of the
mucosa are detected
• low-grade temperature, cough, hoarseness, barking
cough in 2 days
catarrhal
• After 2-3 days there is difficulty of breathing on
inspiration, aphonic voice, cough is soundless.
• Patients are unquiet. Cyanosis of the lips, the tip of the
nose, fingers. Heart sounds are muffled, tachycardia,
BP decreased.
• Stage lasts from a few hours to 2-3 days.
stenotic
• signs of respiratory failure - breathing is frequent,
superficial, arrhythmic, cyanosis increases. Pulse is
frequent, BP decreases. Confusion or loss of
counsciousness, seizures.
• Greatest threat - the presence of the films in the
trachea: during cough they can "sit" on the bifurcation
of the trachea, cause obstruction of the airways and
sudden death.
asphyxial

89. On 27 March 2012, a 68-year-old woman
presented to the Ear, Nose and Throat (ENT)
department in a hospital in Västra Götaland
Region, western Sweden, with a five-day
history of fever, coughing, hoarseness and
increasing pain in the throat.
Six days prior to the onset of fever and
throat symptoms she had returned from a
two-week holiday in western Africa
A laryngoscopy was performed on the
same day and revealed greyish
membranes on and surrounding the vocal
cords and the base of the tongue, and
swollen larynx.These changes could not
be seen by ordinary throat examination.

90. • myocarditis
cardiovascular system
• multiple parenchymal toxic neuritis (polyneuritis)
• Palsies are peripheral with hypotonia and muscle atrophy,
disappearance of tendon reflexes.
• Often there are incomplete paralysis - paresis
nervous system
• Nephrosis
• proteinuria, leucocyturia and cylinderuria
• acute renal failure with oliguria, anuria may develop
kidneys

91. • leukocytosis, neutrophilia , shift to the left,
accelerated ESR
Complete
blood count
• presence or absence of bacteria
morphologically similar to corynebacteria
diphtheria (colouring by Neisser) – typical
locating of rods, grains of volutin in bacterias
Bacterioscopy of
oropharyngeal
secretions and nasal
passages
• the culture of Corynebacterium diphtheria and
determining of its toxigenic properties
Bacteriological test
of oropharyngeal
mucus and biological
material from other
places of lesion
• PHAR with diphtheria diagnosticums - increase antitoxic
antibodies titre in serum in the dynamics of the disease.
• 5. IHAR with a commercial diphtheria antigen - detection
of diphtheria toxin in serum
• 6. PHAR of blood witherythrocyte diagnosticum before the
introduction of ADS - definition of diphtheria toxin level in
the serum
Serological
tests

92.  The first Nobel prize for medicine or physiology was awarded in 1901 to
German researcher Emil von Behring, for his work on serum therapy, a method
of treating disease by the injecting the blood serum of immune animals.
 In particular, the award committee honored von Behring's use of serum therapy
to treat the respiratory illness diphtheria and the nervous system infection
tetanus. "He has opened a new road in the domain of medical science and
thereby placed in the hands of the physician a victorious weapon against illness
and deaths," the committee said at the time.

93.  specific antitoxic antidiphtherical serum (ADS)
 Before the introduction of therapeutic doses intracutaneous
test for sensitivity (Bezredko method) is done according to
the following scheme: 0.1 ml of diluted 1:100 ADS is
injected intradermally on the inner surface of the forearm,
in 30 minutes subcutaneously 0.1 ml of undiluted serum is
injected and in the absence of reaction therapeutic dose is
administered intramuscularly.
 ADS is injected intramuscularly (into one location to 8-10
ml of ADS, heated to 36 ° C).
 In the toxic forms intravenous serum (half dose) infusion is
possible.The calculated dose of serum is dissolved in a
solution of 5% glucose or saline in the ratio 1:2, is added to
2 mg / kg body weight prednisolone and put with speed of
40-60 drops per minute.
 The dose of ADS depends on the form and severity - from
30-50 thousand IU at the localized forms up to 100-120
thousand IU at toxic

94.  Immediate hospitalization
 Bed regimen (at localized forms - 10 days, at toxic - not less than 35-
45 days)
 Glucocorticoids (in toxic forms and croup)
 Antibiotics (penicilin, tetracyclin, erythromycin)
 In case of croup - inhalations, broncholitics, diuretics,
glucocorticoids, antibiotics, antihistamine, lytic admixture; if there
are indications - intubation, tracheotomy
DIPHTHERIA SEVERITY FIRST DOSE OF SERUM (in IU)
Mild form 20 000 – 40 000
Moderate form 50 000 – 80 000
Severe form 90 000 – 120 000
Hypertoxic form. ITSH 120 000 – 150 000

95. • Vaccination in 3, 4, 5 months. With DTP
vaccine, revaccination in 18 months
(DTaP); 6, 14, 18 (DT) years and adults
every 10 years)
Specific
• Close contacts who were previously
immunized longer than 5 years
before should receive booster dose
of vaccine
• Antibiotic orally for 7 days
• Revealing (bacteriological test) and
sanation of healthy infected persons
• Observation of contacts for 10 days
• Final disinfection
Nonspecific prophylaxis

96. lacunar or phlegmonous tonsillitis
group A streptococcal pharyngitis
Infectious mononucleosis, acute cytomegalovirus infection
paratonsillitis infiltrative or abscessed
necrotizing scarlet fever tonsillitis
Simanovsky-Plaut-Vincent’s tonsillitis
acute toxoplasmosis
thrush
post-tonsillectomy faucial membranes
tularemia
leukemia, agranulocytosis

97.  (glandular fever, Filatov –
Pfeyffer’s disease, monocytic
tonsillitis) -is an acute viral
disease with airborne droplets
transmission mechanism,
characterized by:
polyadenitis (especially
cervical),
fever
acute tonsillitis with deposits,
hepatosplenomegaly,
leukocytosis, limfomonocytosis,
the presence of atypical
mononuclear cells - vyrocytes.

99.  Vincent’s tonsillitis (angina) is usually
a mixed infection, caused by
Fusobacterium fusiformis and
spirochetal anaerobic bacteria.
 In most cases it is unilateral, but
described and bilateral lesions.The
disease begins quietly with swallowing
discomfort, passing then to pain.
Expressed changes in the throat are not
consistent with the overall satisfactory
condition of the patient .The body
temperature is subfebrile or normal.
 On the surface of tonsils gray or
yellowish-white films, like a spot of
stearic candles, round, of soft
consistency , sometimes extending to
the front arche.The film is surrounded
by a rim of inflammation, deposits are
relatively easy to remove with a cotton
swab. After removal of the film
bleeding from ulcerated surface occurs
First ulcer is superficial. If the
disease goes on for a long time,
ulcerative defect becomes deep,
crater-like shape, then it can
spread beyond the tonsil with
involvement in the process of deep

100.  In January 1925, Alaskan doctors feared a deadly diphtheria epidemic would spread
among the children of Nome. doctors needed to travel nearly a thousand miles to
Anchorage to get serum for treatment.With no trains running that far north and the
only available airplane sidelined by a frozen engine, the best chance of transporting the
medicine across the icy tundra was by sled dog.
 More than 20 sled teams coordinated to make the trip through blinding snow and sub-
zero temperatures. On the first of February, the package was handed off to the final team.
Lead by Balto, the team covered 53 treacherous miles back to Nome in 20 hours.
Newspapers and radio around the world followed the trek, fascinated by the brave team
whose efforts eventually helped end the epidemic.
 Balto became a national hero. Just 10 months after the successful mission, this statue by
animal sculptor Frederick G. R. Roth was dedicated in Central Park.
Balto with Gunnar Kaasen