MPH OF UKRAINE IVANO-FRANKIVSK NATIONAL MEDICAL

UNIVERSITY DEPARTMENT OF CHILDREN

INFECTIOUS DISEASES

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).

Exanthem

infectious non-

infectious

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

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, pseudotuberculosis

Primary lesions

roseola

macule

erythema

hemorrhage

papule

tubercle

node

vesicle

bulla

pustule

wheal

Secondary lesions

squama

crust

pigmentation

ulcer

scar

SKIN STRUCTURE

Primary skin lesions

Secondary skin lesions

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.

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)

Erythema macules over 20 mm in

diameter that may become confluent

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)

Papule more or less solid element without

cavity,

arises above skin level

sizes are from 1 to 20 mm

color and shape are different

Tubercle

element without cavity

appears as a result of the inflammatory granulomas formation in deep derma layers

Node

limited, deeply permeating the skin dense formation

the result of cellular infiltrate in the dermis and adipose tissue

Vesicle

a cavity located in the epidermis

contains liquid

arises slightly above the skin level

Diameter - 1 to 5 mm

Bulla

a formation, equivalent to vesicles, but larger than 5 mm to 10-15 mm

Pustule

exudative cavitary element with pus, located on the infiltrated base

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

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

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)

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

Ulcer

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

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

Examining of patient with rash

Type of element

Number

Size

Colour

Localization

Order of appearance and disappearence

The rash types

Punctate

Scarlet fever

Pseudotuberculosis

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

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

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

Measles: 2nd day of illness

Koplik’s spots

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

Rubella: 1st day of the disease

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

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

Varicella

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.

Scarlet fever: pharyngeal enanthem

Scarlet fever: bright hyperemia of the pharynx, membranous tonsillitis

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.

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).

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.

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

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

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).

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).

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.

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.

Scarlet fever pin-point exanthema on abdomen

Scarlet fever exanthema in skin folds

Scarlet fever Filatov’s mask

Scarlet fever, strawberry tongue, coated in the centre (4th day from the disease beginning)

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

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

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.

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.

Urticaria

Meningococcemia: hemorrhagic rash

Thank You for Attention!

MPH OF UKRAINE IVANO-FRANKIVSK NATIONAL MEDICAL

UNIVERSITY DEPARTMENT OF CHILDREN INFECTIOUS

DISEASES

Lecturer: assistant

Horbal Natalia Bogdanivna

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."

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 .

• tonsillitis • diphtheria • infectious mononucleosis • tularemia • listeriosis • scarlet fever • adenoviral infection • typhoid and paratyphoid • syphilis • candidiasis of the oropharynx

Infe

cti

ou

s d

ise

as

es

• acute leukemia • agranulocytosis • radiation sickness

No

n-i

nfe

cti

ou

s

dis

ea

se

s

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

• 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

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.

• 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 gaps lacunar

• suppuration of the tonsils spreads into neighboring tissue phlegmonous

• formation of superficial ulcers, tonsillitis Symanovsky-Plaut-Vincent as an independent nosological form

necrotic-ulcerative

Catarrhal tonsillitis

Lacunar tonsillitis

Folicular tonsillitis

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

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.

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/

• 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

contagiousness

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

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

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

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

Depending on the degree of intoxication

and the intensity of local inflammation

Localized form

Spread form

Toxic form

Type of local

changes

catarrhal

insular

membraneous

According to the

localization

Tonsillar diphtheria

nasopharyngeal diphtheria

anterior nasal diphtheria

laryngeal diphtheria

diphtheria of other (rare) localization

(cutaneous, ocular, genital)

Combinated

Forms by severity

subclinic

mild

moderate

severe

hypertoxic

carryering

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

• 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

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.

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.

• swelling spreads to the middle of the neck

Іst degree

• swelling spreads to the clavicle

ІInd degree

• swelling spreads below the clavicle

ІIIrd degree

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.

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)

• 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

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.

• 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

• 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

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.

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

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

• 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

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

(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.

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

tissue .

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