LESSON № 4
Topics:
1. Infectious diseases of childhood.
2. Immunization of children’s infectious diseases.
Infectious diseases of childhood.
Rash (exanthem) = an acute cutaneous eruption in more parts of the body. It can arise due to the systemic effects of a microorganism on the skin.
Exanthematic infection = an infection where the rash is an obligatory, prominent, and fairly characteristic symptom.
According to the morphology the rashes are classified usually to five (or more) groups
· maculopapular
· vesiculobullous
· petechial or purpuric
· erythematous
· nodular
MEASLES
an acute communicable disease, is characterized by three stages: (1) an incubation stage of approximately 10–12 days with few, if any, signs or symptoms; (2) a prodromal stage with an enanthem (Koplik spots) on the buccal and pharyngeal mucosa, slight to moderate fever, mild conjunctivitis, coryza, and an increasingly severe cough; and (3) a final stage with a maculopapular rash erupting successively over the neck and face, body, arms, and legs and accompanied by high fever.
ETIOLOGY. Measles is an RNA virus of the family Paramyxoviridae, genus Morbillivirus. Only one antigenic type is known. During the prodromal period and for a short time after the rash appears, it is found iasopharyngeal secretions, blood, and urine. It can remain active for at least 34 hr at room temperature.
Measles virus may be isolated in cultures of human embryonic or rhesus monkey kidney tissue. Cytopathic changes, visible in 5–10 days, consist of multinucleated giant cells with intranuclear inclusions. Circulating antibody is detectable when the rash appears.
INFECTIVITY. Maximal dissemination of virus is by droplet spray during the prodromal period (catarrhal stage). Transmission to susceptible contacts often occurs prior to diagnosis of the original case. An infected person becomes contagious by the 9th–10th day after exposure (beginning of prodromal phase), in some instances as early as the 7th day. Isolation precautions, especially in hospitals or other institutions, should be maintained from the 7th day after exposure until 5 days after the rash has appeared.
EPIDEMIOLOGY. Measles is endemic over most of the world. In the past, epidemics tended to occur irregularly, appearing in the spring in large cities at 2- to 4-yr intervals as new groups of susceptible children were exposed. Measles is very contagious; approximately 90% of susceptible family contacts acquire the disease. It is rarely subclinical. Prior to the use of measles vaccine, the age of peak incidence was 5–10 yr; most adults were immune. At present in the
The many similarities among the biologic features of measles and smallpox suggest the possibility that measles may be eradicable. These features are (1) a distinctive rash, (2) no animal reservoir, (3) no vector, (4) seasonal occurrence with disease-free periods, (5) no transmissible latent virus, (6) one serotype, and (7) an effective vaccine. A prevalence of more than 90% immunization of infants has been shown to produce disease-free zones. In 1980, three fourths of all counties in the
Infants transplacentally acquire immunity from mothers who have had measles or measles immunization. This immunity is usually complete for the first 4–6 mo of life and disappears at a variable rate. Although maternal antibody levels are generally undetectable in the infant by the usual tests performed after 9 mo of age, some protection persists, which may interfere with immunization administered prior to 15 mo. Most women of child-bearing age in the
PATHOLOGY. The essential lesion of measles is found in the skin; in the mucous membranes of the nasopharynx, bronchi, and intestinal tract; and in the conjunctivae. Serous exudate and proliferation of mononuclear cells and a few polymorphonuclear cells occur around the capillaries. There is usually hyperplasia of lymphoid tissue, particularly in the appendix, where multinucleated giant cells of up to 100 mmin diameter (Warthin-Finkeldey reticuloendothelial giant cells) may be found. In the skin, the reaction is particularly notable about the sebaceous glands and hair follicles. Koplik spots consist of serous exudate and proliferation of endothelial cells similar to those in the skin lesions. A general inflammatory reaction of the buccal and pharyngeal mucosa extends into the lymphoid tissue and the tracheobronchial mucous membrane. Interstitial pneumonitis resulting from measles virus takes the form of Hecht giant cell pneumonia. Bronchopneumonia may be due to secondary bacterial infection.
In fatal cases of encephalomyelitis, perivascular demyelinization occurs in areas of the brain and spinal cord. In
CLINICAL MANIFESTATIONS.
The incubation period is approximately 10–12 days if the first prodromal symptoms are selected as the time of onset, or approximately 14 days if the appearance of the rash is selected; rarely it may be as short as 6–10 days. A slight rise in temperature may occur 9–10 days from the date of infection and then subside for 24 hr or so.
The prodromal phase, which follows, usually lasts 3–5 days and is characterized by low-grade to moderate fever, a hacking cough, coryza, and conjunctivitis. These nearly always precede Koplik spots, the pathognomonic sign of measles, by 2–3 days. An enanthem or red mottling is usually present on the hard and soft palates. Koplik spots are grayish white dots, usually as small as grains of sand, with slight, reddish areolae; occasionally they are hemorrhagic. They tend to occur opposite the lower molars but may spread irregularly over the rest of the buccal mucosa. Rarely they are found within the midportion of the lower lip, on the palate, and on the lacrimal caruncle. They appear and disappear rapidly, usually within 12–18 hr. As they fade, red, spotty discolorations of the mucosa may remain. The conjunctival inflammation and photophobia may suggest measles before Koplik spots appear. In particular, a transverse line of conjunctival inflammation, sharply demarcated along the eyelid margin, may be of diagnostic assistance in the prodromal stage. As the entire conjunctiva becomes involved, the line disappears.
Conjunctivitis in measles
Koplik spots
Enanthema
Occasionally, the prodromal phase may be severe, being ushered in by sudden high fever, at times with convulsions and even pneumonia. Usually the coryza, fever, and cough are increasingly severe up to the time the rash has covered the body.
The temperature rises abruptly as the rash appears and often reaches 40–40.5º C (104–105º F). In uncomplicated cases, when the rash appears on the legs and feet, within about 2 days, the symptoms subside rapidly; the subsidence includes a usually abrupt temperature drop. Patients up to this point may appear desperately ill, but within 24 hr after the temperature drop, they appear essentially well.
The rash usually starts as faint macules on the upper lateral parts of the neck, behind the ears, along the hairline, and on the posterior parts of the cheek. The individual lesions become increasingly maculopapular as the rash spreads rapidly over the entire face, neck, upper arms, and upper part of the chest within approximately the first 24 hr
Fig. Maculopapular rash of measles, the first day of the eruption
Fig. Maculopapular rash of measles, the second day of the eruption
Fig. Maculopapular rash of measles, the third day of the eruption
Fig. Hemorrhagic rash of measles
The rash pigmentation
During the succeeding 24 hr it spreads over the back, abdomen, entire arms, and thighs. As it finally reaches the feet on the 2nd–3rd day, it begins to fade on the face. The fading of the rash proceeds downward in the same sequence in which it appeared. The severity of the disease is directly related to the extent and confluence of the rash. In mild measles the rash tends not to be confluent, and in very mild cases there are few, if any, lesions on the legs. In severe measles the rash is confluent, the skin being completely covered, including the palms and soles, and the face is swollen and disfigured.
The rash is often slightly hemorrhagic; in severe cases with a confluent rash, petechiae may be present in large numbers, and there may be extensive ecchymoses. Itching is generally slight. As the rash fades, branny desquamation and brownish discoloration occur and then disappear within 7–10 days.
The rash may vary markedly. Infrequently a slight urticarial, faint macular, or scarlatiniform rash may appear during the early prodromal stage and disappear in advance of the typical rash. Complete absence of rash is rare except in patients who have received human antibodies during the incubation period, in some patients with human immunodeficiency syndrome (HIV) infection, and possibly in infants younger than 8 mo who have appreciable levels of maternal antibody. In the hemorrhagic type of measles (black measles), bleeding may occur from the mouth, nose, or bowel. In mild cases the rash may be less macular and more nearly pinpoint, somewhat resembling that of scarlet fever or rubella.
Lymph nodes at the angle of the jaw and in the posterior cervical region are usually enlarged, and slight splenomegaly may be noted. Mesenteric lymphadenopathy may cause abdominal pain. Characteristic pathologic changes of measles in the mucosa of the appendix may cause obliteration of the lumen and symptoms of appendicitis. Changes of this type tend to subside with the disappearance of Koplik spots. Otitis media, bronchopneumonia, and gastrointestinal symptoms, such as diarrhea and vomiting, are more common in infants and small children (especially malnourished ones) than in older children.
The diagnosis of measles is frequently delayed in adults because practitioners providing health care for adults are not used to encountering the disease and rarely include it in the differential diagnosis. The clinical picture is similar to that seen in children. Liver involvement, with abdominal pain, mild to moderate elevation of aspartate aminotransferase (AST) levels, and occasionally jaundice, is common in adults. In developing countries and in recent outbreaks in the
DIAGNOSIS.
This is usually made from the typical clinical picture; laboratory confirmation is rarely needed. During the prodromal stage multinucleated giant cells can be demonstrated in smears of the nasal mucosa. Virus can be isolated in tissue culture, and diagnostic rises in antibody titer can be detected between acute and convalescent sera. The white blood cell count tends to be low with a relative lymphocytosis. Lumbar puncture in patients with measles encephalitis usually shows an increase in protein and a small increase in lymphocytes. The glucose level is normal.
DIFFERENTIAL DIAGNOSIS.
The rash of rubeola must be differentiated from exanthem subitum, rubella, infections resulting from echovirus, coxsackie virus, and adenovirus, infectious mononucleosis, toxoplasmosis, meningococcemia, scarlet fever, rickettsial diseases, serum sickness,
Koplik spots are pathognomonic for rubeola, and the diagnosis of unmodified measles should not be made in the absence of cough.
Roseola infantum (exanthem subitum) is distinguished from measles in that the rash of the former appears as the fever disappears. The rashes of rubella and of enteroviral infections tend to be less striking than that of measles, as do the degree of fever and severity of illness. Although cough is present in many rickettsial infections, the rash usually spares the face, which is characteristically involved in measles. The absence of cough or the history of injection of serum or administration of a drug usually serves to identify serum sickness or drug rashes. Meningococcemia may be accompanied by a rash that is somewhat similar to that of measles, but cough and conjunctivitis are usually absent. In acute meningococcemia the rash is characteristically petechial purpuric. The diffuse, finely papular rash of scarlet fever with a “goose flesh” texture on an erythematous base is relatively easy to differentiate.
The milder rash and clinical picture of measles modified by gamma globulin or by partial immunity induced by measles vaccine, or in infants by maternal antibody, may be difficult to differentiate.
COMPLICATIONS.
The chief complications of measles are otitis media, pneumonia, and encephalitis. Noma of the cheeks may occur in rare instances. Gangrene elsewhere appears to be secondary to purpura fulminans or disseminated intravascular coagulation following measles.
Pneumonia (see Chapter 170) may be caused by the measles virus itself; the lesion is interstitial. Measles pneumonia in patients with HIV infection is often fatal and not always accompanied by rash. Bronchopneumonia is more frequent, however; it is due to secondarily invading bacteria, particularly the pneumococcus, streptococcus, staphylococcus, and Haemophilus influenzae. Laryngitis, tracheitis, and bronchitis are common and may be due to the virus alone.
One of the potential dangers of measles is exacerbation of an existing tuberculous process. There may also be a temporary loss of hypersensitivity to tuberculin.
Myocarditis is an infrequent serious complication; transient electrocardiographic changes are said to be relatively common.
Neurologic complications are more common in measles than in any of the other exanthems. The incidence of encephalomyelitis is estimated to be 1-2/1,000 reported cases of measles. There is no correlation between the severity of the measles and that of the neurologic involvement or between the severity of the initial encephalitic process and the prognosis. Rarely, encephalitis has been reported in association with measles modified by gamma globulin or by live attenuated measles virus vaccine. Infrequently, encephalitic involvement is manifest in the pre-eruptive period, but more often the onset occurs 2–5 days after the appearance of the rash. The cause of measles encephalitis remains controversial. It is suggested that when encephalitis occurs early in the course of the disease, viral invasion plays a large role, although measles virus has rarely been isolated from brain tissue; encephalitis that occurs later is predominantly demyelinating and may reflect an immunologic reaction. In this demyelinating type the symptoms and course do not differ from those of other parainfectious encephalitides. Fatal encephalitis has occurred in children receiving immunosuppressive treatment for malignancies. Other central nervous system complications, such as Guillain-Barré{acute-e} syndrome, hemiplegia, cerebral thrombophlebitis, and retrobulbar neuritis, are rare.
Subacute sclerosing panencephalitis is due to measles virus.
PROGNOSIS.
Case fatality rates in the
When measles is introduced into a highly susceptible population, the results may be disastrous. Such an occurrence in the
PROPHYLAXIS.
Quarantine is of little value because of the contagiousness during its prodromal stage, when measles may not be suspected.
The initial measles immunization may be given at 12 to 15 mo but may be given earlier in areas where disease is occurring. Because the seroconversion rate following immunization is not 100% and there may be some waning of immunity with time, a second immunization against measles, usually given as measles-mumps-rubella (MMR), is indicated. This dose can be given when the child enters school or later on entry to middle school. Adolescents entering college should also have received a second measles immunization.
The response to live measles vaccine is unpredictable if immune globulin has been administered in the 3 mo preceding immunization. Anergy to tuberculin may develop and persist for 1 mo or longer after administration of live, attenuated measles vaccine. A child with active tuberculous infection should be receiving antituberculosis treatment when live measles vaccine is administered. A tuberculin test prior to or concurrent with active immunization against measles is desirable.
Use of live measles vaccine is not recommended for pregnant women or for children with untreated tuberculosis. Live vaccine is contraindicated in children with leukemia and in those receiving immunosuppressive drugs because of the risk of persistent, progressive infection such as giant cell pneumonia. After exposure of these susceptible children to measles, measles immune globulin (human) should be given intramuscularly in a dose of 0.25 mL/kg as soon as possible. A larger dose may be advisable in children with acute leukemia, even those in remission. Children with HIV infection should receive measles vaccine because mortality from measles is high in this group and they tolerate the vaccine well. Despite a history of having received measles immunization, these children should receive gamma globulin after exposure to measles in a dose of 0.5 mL/kg (maximum 15 mL). This is twice the usual recommended dose. Measles vaccine can be given following exposure to the disease. Reactions are not increased, and measles may be prevented.
The use of inactivated (killed) virus vaccine is not recommended.
Passive Immunization.
Passive immunization with pooled adult serum, pooled convalescent serum, placental globulin, or gamma globulin of pooled plasma is effective for prevention and attenuation of measles. Measles can be prevented by using immune serum globulin (gamma globulin) in a dose of 0.25 mL/kg given intramuscularly within 5 days after exposure but preferably as soon as possible. Complete protection is indicated for infants, for children with chronic illness, and for contacts in hospital wards and children’s institutions. Attenuation may be accomplished by the use of gamma globulin in a dosage of 0.05 mL/kg. Gamma globulin is approximately 25 times as potent in antibody titer as pooled adult serum, and it avoids the risk of hepatitis. Attenuation is variable, and the modified clinical patterns may vary from those with few or no symptoms to those with little or no modification. Encephalitis may follow measles modified by gamma globulin.
After the 7th–8th day of incubation the amounts of antibody administered must be increased greatly for any degree of protection. If the injection is delayed until the 9th, 10th, or 11th day, slight fever may already have started and only slight modification of the disease may be expected.
TREATMENT.
Sedatives, antipyretics for high fever, bed rest, and an adequate fluid intake may be indicated. Humidification of the room may be necessary for laryngitis or an excessively irritating cough, and it is best to keep the room comfortably warm rather than cool. The patient should be protected from being exposed to strong light during the period of photophobia. The complications of otitis media and pneumonia require appropriate antimicrobial therapy.
With complications such as encephalitis, subacute sclerosing panencephalitis, giant cell pneumonia, and disseminated intravascular coagulation, each case must be assessed individually. Good supportive care is essential. Gamma globulin, hyperimmune gamma globulin, and steroids are of limited value. Currently available antiviral compounds are not effective. Treatment with oral vitamin A (400,000 IU) reduces morbidity and mortality in children with severe measles in the developing world.
Short statement of the material
Measles is a viral infection that is passed by an air-droplet way, is characterized by cyclic course, syndromes of intoxication, catarrhal inflammation of respiratory tract, conjunctiva, and rashes on the skin.
Etiology: the measles virus is a member of the family Paramyxoviridae, genus
Morbillivirus.
Epidemiology:
1. Source of infection – infected person during last 2 days of incubation period, catarrhal period, and 4 days period of eruption (in case of complications –10 days period of eruption).
2. Infection is transmitted by inhalation of large and small airborne droplets.
3. Susceptible organism – no immunized people, older than 6 month, which never had measles.
Pathogenesis:
• The primary site of infection is the respiratory epithelium and conjunctiva.
• Local replication of the virus is followed by viremia (primary).
• During this phase virus is spread by leukocytes to the reticuloendothelial systemwhere it replicates.
• Following necrosis of white blood cells, a secondary viremia occurs.
• Than:
– morphological changes in CNS, mucus membrains of the trachea, bronchi,
intestinum;
– inflammation, destruction, liberation of virus;
– secondary immune deficiency, and growth of the bacterial microflora;
– forming of complications.
• With the development of specific antibody and cell-mediated responses, viremia is terminated and the illness resolves.
Clinical presentation
1. The incubation period is 9-17 days, in those who has received specific immunoglobulin for prevention – it may be longer (up to 21 days).
4. Prodromal period is the next, lasting 3 to 5 days. The classic three “C’s” (cough, corryza, conjunctivitis) make their appearance. The enanthema of measles occurs, Koplick’s spots (small, bluish-gray papules on a red base) localized on entire oral mucosa. They usually disappear by the second day of the exanthema. Temperature is usually high at first day.
5. Exanthema period: Second increase of temperature. Initial lesions are noted behind the ears on the forehead and face. During 3-4 days they spread downward, involve the trunk and extremities. The rashes consist of an erythematosus maculopapular eruption. They are initially discrete but then became confluent on the areas of initial involvement.
6. Pigmentation period progresses in the same fashion as the appearance of the rashes. As the rashes resolves, a brownish desquamation may occur.
Classification
By the form:
Typical, by the severity:
– mild;
– moderate;
– severe (without hemorrhagic syndrome, with hemorrhagic syndrome);
Atypical:
– abortive;
– mitigious;
– hyperreactive;
– subclinical;
– asymptomatic;
– measles in vaccinated;
– measles in person who receive antibiotics and hormones.
By the course:
– smooth (uncomplicated);
– not smooth, uneven (complicated).
Complications:
By the etiology:
– primary (due to measles virus);
– secondary (bacterial).
By the time of development:
– early (in prodromal and rushes period);
– late (in pigmentation period).
By the localization:
– respiratory system (laryngitis, laryngotracheobronchitis, pneumonia);
– digestive system (enterocolitis, colitis);
– nervous system (encephalitis, serous meningitis, encephalomyelitis);
– eyes (keratitis);
– ears (otitis media);
– skin (staphylo- or streptodermia);
– urinary system (pyelonephritis).
Complications:
viral – laryngotracheitis (croup), bronchitis, encephalitis, Giant-cell pneumonia, and diarrhea is common in infants;
secondary bacterial – otitis media, pneumonia, gingivostomatitis, pyelonephritis, diarrhea, dermatitis.
Peculiarities of measles in infants
1. Atypical (mitigious) forms.
2. Reduction of the disease periods.
3. Unexpressed clinical signs (catarrhal phenomena, fever, small unabundant rashes with the shortened staging and pigmentation).
4. Complications are more frequent.
Laboratory work-up
• Common laboratory tests are non-specific, CBC – leucopenia, lymphocytosis, eosynophylia, and thrombocytopenia (may be).
• Cytoscopic examination of smears from the pharynx – presence of typical multinuclear giant cells.
• Viral isolation is technically difficult.
• Immune enzyme analysis (ELISA) – presence of Ig M antibodies in acute period.
• Serology (DHAR, PHAR) is confirmed when fourfold or greater rise in antibody titre or the presence of specific Ig M antibodies.
Diagnosis example:
• Measles, typical form, period of exanthema, moderate severity, uncomplicated.
• Measles, typical form, period of pigmentation, severe (with hemorrhagic
syndrome), complicated by the leftside polysegmental (S4–S6) pneumonia with
obstruction syndrome, Respiratory insufficiency 2nd degree.
Differential diagnose should be performed between scarlet fever, Epstein-Barr viral infection, meningococcal sepsis, pseudotuberculosis, Kawasaki syndrome, Stevens-Johnson syndrome, adenovirus, enterovirus infection, diaper rashes (photo 1), Rheumathoid arthritis systemic form (photo 2), and allergic rashes (photo 3-10).
During prodromal period – between other upper respiratory tract viral infections.
Heat rash
Drug allergy
Food allergy (urticaria)
Cool allergy
Evidences for obligatory hospitalization of patients with infectious exanthema
1. The severe form of disease, when appears need in undertaking of intensive therapy; patients with moderate forms at age before 3 years.
2. Sick children from families with bad social-home conditions, especially in the event of impossibility of their isolation to prevent infections transmission.
3. Absence of conditions for examination and treatment at home.
4. Sick children from closed children institutions.
Advantages of the home treatment
1. Possibility of additional infection by hospital bacteria is completely excluded.
2. Realization of individual care principle for sick child is more full.
3. Avoiding stressful reactions, which could appear in case of hospital treatment.
Treatment in home conditions is possible
1. In conditions of isolated flat.
2. In case of satisfactory material position of the parents.
3. In case of parents desire to organize individual care and treatment at home.
Treatment
Noncomplicated mild, moderate measles and atypical forms do not need medicine.
1. Bed rest up to the normalization of body temperature.
2. Regular ventilation of the room.
3. Adequate rehydration with oral fluids (lemon tea, raspberry tea, warm alkalic
5. drinks).
4. Vitaminized milk-vegetable food.
5. Control of fever (when the temperature is more than 38.5-
6. Nasal drops (in infants before 6 mo – physiologic saline solutions as Salin; in elder children – naphtizin, rhinasolin, nasivin for children 1-2 drops 3 t.d. in the nostrils, not more than 3 days).
7. In case of dry cough – cough suppressors (such as dextramethorphan, synecod).
8. Mucolytics in case of the moist nonproductive cough (ambroxol, acetylcystein etc.).
9. Looking after oral cavity (gurgling with boiled water, antiseptic fluids).
10. Looking after conjunctiva (washing with boiled water, concentrated tea, sulfacyl Na in drops).
11. Vitamin A orally.
• In case of bacterial complication – antibacterial therapy should be used.
• In case of severe episodes – corticosteroids (1-2 mg/kg for 2-3 days).
• In case of croup: mist tent with 25-30 % oxygen inhalation, antianxiety medicines, steroids and mechanical ventilation in severe cases.
• In case of meningitis:
Base therapy:
1. Bed regimen till body temperature normalization, disappearance of general cerebral and considerable improvement of focal neurological signs, not less than 14-16 days.
2. A diet (before stable vital functions is due to adequate parenteral infusion therapy),
3.
4. A milk vegetable diet (№5) is appointed for preschoolers or school children, 5-6 times per day with the next passing to the diet №2 whether №15 (depending the age) in the recovery period;
5. Oral fluids intake corresponds to age norms (with including the IV fluids).
6. Antibacterial therapy: for infants at presence of concomitant bacterial infection, chronic infection, inflammatory changes in the CBC (by the broadspectrum antibiotic in average therapeutic doses, a short course).
Etiologic therapy: specific therapy is absent.
Pathogenetic therapy:
• Glucocrticoids 3-5 mg/kg (by prednisolon), course not more than 10 days.
• Vascular medicine (penthoxyphyllin, nicergolin and others like that).
• In posthypoxia period – nootrops, vitamins group B.
• In case of CSF hypertension – dehydration by 25 % MgSO4 IM, lasix 1-3 mg/kg IV or IM, acethazolamid orally
• In case of seizures – Anticonvulsant therapy: benzodiasepins (seduxenum, sibasonum) 0.3-0.5 mg/kg IV, if they are ineffective – 1 % hexenalum or thiopenthalum sodii in 3-5 mg/kg IV. Dehydration therapy: lasix 2-3 mg/kg IM or IV.
Prevention
1. Specific active immunization by MMR vaccine (measles, mumps, rubella) at age 12 months. Revaccination at 4 to 6 years or at 10 to 11 years (in
2. Specific passive prophylaxis with immune serum globulin in a dose of 0.25 ml/kg as a postexposure prophylaxis.
3. Nonspecific: – isolation of ill person until 5th day of the exanthema period (if complicated by pneumonia, encephalitis – up to 10th day), isolation of contact person from 8 to 17 days (in case of the specific immunoglobulin prevention – up
to 21 day).
Key words and phrases: measles, Morbillivirus, prodromal period, exanthema period, enanthema, Koplick’s spots, maculopapular rashes, spread downward, cleaning (pigmentation) period, brownish desquamation, giant-cell pneumonia, specific and nonspecific prophylaxis.
Rubella
Rubella is a viral infection, that has the acquired form (with the air-droplet mechanism of transmission, mild clinical signs and benign completion) and innate (with the transplacental mechanism of transmission and development of severe fetal defects).
Etiology: an agent is a RNA-containing Rubivirus from the Togaviruses.
Rubivirus
Epidemiology:
– the source of infection is a patient or carrier;
– the mechanism of transmission is air-droplet, transplacental;
– receptivity is common, especially high in children 2-9 years.
Pathogenesis
Acquired Rubella:
1. An entrance gate is the mucus membranes of nasopharynx, where virus is replicating.
1. Hematogenous distribution (viremia).
2. Damage of organs and systems.
3. Immunological answer, recovery.
Innate Rubella:
1. Transplacental infection of the fetus.
4. Destruction of the cells by the virus, violation of the correct organs’ development.
5. Forming of the development defects.
Diagnostic criteria of the acquired Rubella:
• Latent period – 18-23 days.
• Prodromal period – 1-2 days:
– mild toxic syndrome;
– mild catarrhal syndrome (rhinitis, pharyngitis, catarrhal tonsillitis);
– increase of posterior cervical, occipital lymph nodes.
• Period of exanthema (rashes, erruption) – 3-4 days:
– rashes (maculous, pinky, on face, trunk, extensor surfaces of extremities, on the unchanged background, arises during one day) (photo 11);
– toxic syndrome (mild);
– increase of cervical, occipital lymph nodes (rarely – polyadenopathy).
Rubella, throat and skin changes
The rashes in acquired Rubella
VARICELLA (Chickenpox)
Primary infection with varicella-zoster virus (VZV) causes varicella (chickenpox). The virus establishes latent infection in dorsal root ganglia; its reactivation causes herpes zoster (shingles).
ETIOLOGY.
VZV is a human herpesvirus; it is classified as an alpha herpesvirus because of its similarities to the prototype for this group, which is herpes simplex virus (HSV). VZV is an enveloped, double-stranded DNA virus; the viral genome encodes more than 70 proteins, including proteins that are targets of immunity and a viral thymidine kinase, which makes the virus sensitive to inhibition by acyclovir and related antiviral agents.
VZ-Virus
PATHOLOGY.
Varicella begins with mucosal inoculation of virus transferred in respiratory secretions or by direct contact with skin lesions of varicella or herpes zoster. Inoculation is followed by an incubation period of 10–21 days, during which subclinical viral spread occurs. Widespread cutaneous lesions result when the infection enters a viremic phase; peripheral blood mononuclear cells carry infectious virus, generating new crops of vesicles for 3–7 days. VZV is also transported back to respiratory mucosal sites during the late incubation period, permitting spread to susceptible contacts before the appearance of rash. The transmission of infectious virus by respiratory droplets distinguishes VZV from other human herpes viruses. Visceral dissemination of the virus follows the failure of host responses to terminate viremia, which results in infection of lungs, liver, brain, and other organs. VZV becomes latent in dorsal root ganglia cells in all individuals who experience primary infection. Its reactivation causes a localized vesicular rash that usually involves the dermatomal distribution of a single sensory nerve; necrotic changes are produced in the associated ganglia, sometimes extending into the posterior horn. The histopathology of varicella and herpes zoster lesions is identical; infectious VZV is present in herpes zoster lesions, as it is in varicella lesions, but is not released into respiratory secretions. Varicella elicits humoral and cell-mediated immunity that is highly protective against symptomatic reinfection. Suppression of cell-mediated immunity to VZV correlates with an increased risk of VZV reactivation as herpes zoster.
EPIDEMIOLOGY.
In the
CLINICAL MANIFESTATIONS OF VARICELLA.
Although the incubation period of varicella ranges from 10–21 days, the illness usually begins from 14–16 days after exposure. Almost all exposed, susceptible children experience a rash, but it may be limited to fewer than 10 lesions. Prodromal symptoms are common, particularly in older children; fever, malaise, anorexia, headache, and occasionally mild abdominal pain occur 24–48 hr before the rash appears. Temperature elevation is usually moderate, ranging from 100–102º F but may be as high as 106º F; fever and other systemic symptoms persist during the first 2–4 days after the onset of the rash. Varicella lesions appear first on the scalp, face, or trunk. The initial exanthem consists of intensely pruritic erythematous macules that evolve to form clear, fluid-filled vesicles. Clouding and umbilication of the lesions begin in 24–48 hr. While the initial lesions are crusting, new crops form on the trunk and then the extremities; the simultaneous presence of lesions in various stages of evolution is characteristic of varicella.
Typical rash in varicella
Pustular rashes and hemorrhagic rashes
Hemorrhagic form of varicella
Ulcerative lesions involving the oropharynx and vagina are common; many children have vesicular lesions on the eyelids and conjunctivae, but serious ocular disease is rare. The average number of varicella lesions is about 300, but healthy children may have from fewer than 10 to more than 1,500 lesions. In secondary household cases and cases involving older children, more days of new lesion formation and more lesions are likely. The exanthem is more extensive in children with skin disorders, such as eczema or recent sunburn. Hypopigmentation of lesion sites persists for days to weeks in some children, but scarring is unusual.
An element on the palate
Varicella Convalescent
The differential diagnosis of varicella includes vesicular rashes caused by other infectious agents, such as enterovirus or Staphylococcus aureus, drug reactions, contact dermatitis, and insect bites.
COMPLICATIONS OF VARICELLA.
Secondary bacterial infections, usually resulting from S. aureus or Streptococcus pyogenes (group A b{beta}-hemolytic streptococcus), are the most common complication of varicella. Cellulitis, lymphadenitis, and subcutaneous abscesses also occur. Varicella gangrenosa, usually resulting from S. pyogenes, is a rare but potentially life-threatening consequence of secondary infection. Acute bacterial sepsis is uncommon, but transient bacteremia may cause focal infections, including staphylococcal or streptococcal pneumonia, arthritis, or osteomyelitis. Encephalitis and cerebellar ataxia are well-described neurologic complications of varicella; the incidence of central nervous system morbidity is highest among patients younger than 5 yr and older than 20 yr. Meningoencephalitis is characterized by seizures, altered consciousness, and nuchal rigidity; patients with cerebellar ataxia have a more gradual onset of gait disturbance, nystagmus, and slurred speech. Neurologic symptoms usually begin from 2–6 days after the onset of the rash but may occur during the incubation period or after resolution of the rash. VZV-related encephalitis and cerebellar ataxia may be immune mediated; the severe hemorrhagic encephalitis caused by HSV is very rare in children with varicella. Clinical recovery is typically rapid, occurring within 24–72 hr, and is usually complete. Before the association of salicylates was documented, some children with varicella had neurologic symptoms caused by the encephalopathy associated with Reye syndrome. Varicella hepatitis is relatively common and is usually subclinical, but some children have severe vomiting, which must be differentiated from that associated with Reye syndrome. Acute thrombocytopenia, accompanied by petechiae, purpura, hemorrhagic vesicles, hematuria, and gastrointestinal bleeding, is a rare complication that is usually self-limited. Other rare complications of varicella include nephritis, nephrotic syndrome, hemolytic-uremic syndrome, arthritis, myocarditis, pericarditis, pancreatitis, and orchitis.
Progressive disease caused by primary VZV infection occurs in otherwise healthy adolescents and adults, immunocompromised children, pregnant women, and newborn infants. Varicella pneumonia is very rare in children, but this complication accounts for most of the increased morbidity and mortality in high-risk populations. Respiratory symptoms, which may include cough, dyspnea, cyanosis, pleuritic chest pain, and hemoptysis, usually begin within 1–6 days (average, 3 days) after the onset of the rash. Hypoxemia is often much more severe than is suggested by the physical findings; the chest radiograph may be normal or may show diffuse bilateral infiltrates. Varicella pneumonia is often transient, resolving completely within 24–72 hr, but in severe cases, the interstitial pneumonitis progresses rapidly to cause respiratory failure. Hemorrhage into the cutaneous lesions is a sign of severe varicella in high-risk patients, as is severe abdominal or back pain, although its pathogenesis is uncertain.
The risk of progressive varicella is highest in children with malignancy if chemotherapy was given during the incubation period and the absolute lymphocyte count is less than 500 cells. In one large series, the mortality rate without antiviral therapy was 7%, and all varicella-related deaths occurred within 3 days after the diagnosis of varicella pneumonia. Hepatitis, encephalitis, and disseminated intravascular coagulopathy are other frequent complications. The syndrome of inappropriate antidiuretic hormone secretion may accompany disseminated varicella with or without clinical encephalitis. Children who acquire varicella after organ transplantation are also at risk for progressive VZV infection. Children on long-term, low-dose steroid therapy usually have no complications, but fatal varicella has occurred in patients receiving high-dose steroids. Untreated varicella is severe or fatal in children with congenital immunodeficiency disorders, especially involving cell-mediated immunity. Unusual clinical findings of varicella, including lesions that develop a unique hyperkeratotic appearance and chronic new lesion formation for weeks or months, have been described in children with HIV infection.
In rare instances, maternal varicella results in the congenital varicella syndrome, associated with unusual cutaneous defects, atrophy of an extremity, microcephaly, ocular defects, and damage to the autonomic nervous system. Infants who are born within 4 days after or 2 days before the onset of maternal varicella may acquire progressive varicella.
CLINICAL MANIFESTATIONS OF HERPES ZOSTER.
VZV reactivation is rare in childhood. When it occurs, it causes vesicular lesions clustered unilaterally in the dermatomal distribution of one or more adjacent sensory nerves, which are preceded or accompanied by localized pain, hyperesthesias, pruritus, and low-grade fever.
The rash is mild, with new lesions appearing for a few days, symptoms of acute neuritis are minimal, and complete resolution usually occurs within 1–2 wk. Immunocompromised children have more severe dermatomal disease and may experience viremia, causing pneumonia, hepatitis, encephalitis, and disseminated intravascular coagulopathy. Severely immunocompromised children, particularly those with HIV infection, may have unusual, chronic, or relapsing cutaneous disease, retinitis, or central nervous system disease without rash. Transverse myelitis with transient paralysis is a rare complication of herpes zoster. In contrast to adults, postherpetic neuralgia is very unusual in children.
The rash in herpes Zoster
LABORATORY FINDINGS AND DIAGNOSIS.
Laboratory evaluation is not necessary for appropriate management of healthy children with varicella or herpes zoster. Abnormal laboratory values are common during varicella. Leukopenia is typical during the first 72 hr; it is followed by a relative and absolute lymphocytosis. Liver function tests are also often moderately elevated. Patients with neurologic complications of varicella or uncomplicated herpes zoster have a mild lymphocytic pleocytosis and a slight to moderate increase in protein; the cerebrospinal fluid glucose is usually normal. Rapid laboratory diagnosis of VZV is often important in high-risk patients and can be accomplished by direct immunohistochemical staining of cells from cutaneous lesions. Multinucleated giant cells can be detected with nonspecific stains, but false-negative results are common, and these methods do not differentiate VZV and HSV infections. The definitive diagnosis of VZV infection requires the recovery of infectious virus using tissue culture. VZV immunoglobulin G (IgG) antibodies can be detected by several methods, but serologic diagnosis is retrospective; testing for VZV IgM antibodies is not useful for clinical diagnosis because commercially available methods are unreliable. VZV IgG antibody tests are valuable to determine the immune status of individuals whose clinical history of varicella is unknown or equivocal.
TREATMENT.
Acyclovir—9-[(2-hydroxyethoxy) methyl] guanine—is the drug of choice for varicella and herpes zoster when specific therapy is indicated. Any patient who has signs of disseminated VZV including pneumonia, hepatitis, thrombocytopenia, or encephalitis should receive immediate treatment with intravenous acyclovir. Acyclovir therapy given within 72 hr prevents progressive varicella and visceral dissemination in high-risk patients; the dosage is 500 mg/m2 every 8 hr, administered intravenously for 7 days or until no new lesions have appeared for 48 hr. Delaying antiviral treatment until prolonged new lesion formation is evident is not an option because visceral dissemination occurs during the same time period. Recent large, placebo-controlled clinical studies have shown that oral acyclovir diminishes the clinical symptoms of varicella in otherwise healthy children, adolescents, and adults when it is administered within 24 hr after the appearance of the initial cutaneous lesions. Drug efficacy was established for all groups, but the clinical benefit may be considered more significant in older children and in secondary household cases. Acyclovir therapy does not interfere with the induction of VZV immunity.
Acyclovir is also effective for treatment of herpes zoster in healthy and immunocompromised patients. Patients at high risk for disseminated disease should receive 500 mg/m2 or 10 mg/kg every 8 hr intravenously. Onset of VZV reactivation reduces the duration of new lesion formation to only about 3 days. Oral acyclovir is an option for immunocompromised patients who are considered at low risk for visceral dissemination. Antiviral drug resistance is rare but has occurred in children with HIV infection; foscarnet is the only drug now available for the treatment of acyclovir-resistant VZV infections.
PREVENTION.
VZV transmission is difficult to prevent because the infection is contagious for 24–48 hr before the rash appears. Infection control practices, including caring for infected patients in isolation rooms with filtered air systems, are essential in hospitals that treat immunocompromised children. Susceptible health care workers who have had a close exposure to varicella should not care for high-risk patients during the incubation period.
Varicella-zoster immune globulin (VZIG) prophylaxis is recommended for immunocompromised children, pregnant women, and newborn infants exposed to maternal varicella. VZIG is distributed by the American Red Cross Blood Services; the dosage is one vial per
Acyclovir should not be given as prophylaxis against varicella. Acyclovir prophylaxis for herpes zoster is not essential because the prompt initiation of acyclovir for the treatment of recurrent VZV infections is very effective in reducing morbidity and mortality among immunocompromised patients. Prolonged low-dose administration of acyclovir should be avoided to minimize the emergence of drug-resistant VZV.
The live, attenuated varicella vaccine, made from the
Short statement of the material
Chicken pox is an acute viral disease caused by the virus from herpes virus family, is
characterized by the moderate fever, appearance on a skin, mucus membranes small vesicles
with transparent content.
Etiology: DNA containing Varicella-Zoster virus.
Epidemiology:
• Source of infection – ill person with chicken pox, (rare – herpes zoster).
• Chickenpoxis is transmitted from person to person by respiratory route or by the direct contact.
• Susceptible organism – everyone, who didn’t ill before.
• Infection confers lifetime immunity – in 3 % of patients it may develop for the 2nd
time.
Pathogenesis:
1. Inoculation of virus and it’s replication in epithelial cells of upper respiratory tract.
2. With lymph it enters to the blood and viremia develops.
3. Damage of the skin epithelium and mucosa epithelium.
4. Damage of the nervous system – (intravertebral ganglia, brain and cerebellum cortex, subcortical region).
5. Generalization of the infection (damage of liver, kidneys, lungs) in immunosupressed people.
Clinical presentation
• The incubation period ranges from 11 to 21 days (most cases 14-17 days).
• The contagious period extends from 1 to 2 days before the rashes erupt until all of the lesions have crusted (5 days after the last rashes have appeared).
• The prodrome consists of 1 to 2 days of fever, headache, malaise, and anorexia.
• The rashes, often pruritic, begin as a maculae and progresses rapidly through the stages of papule, vesicle (photo 12), and crusted lesion (photo 13). The spots first appear on the face or trunk, obvious on the scalp (photo 14) and, at the height of the illness, are more numerous centrally than distally (photo 15). In severe cases may be present on palms and soles (as spots and papules) (photo 16). The lesions erupt in crops for 3 to 4 days (sometimes to 7 days) and it is characteristic of the rashes that lesions in different stages of development may be found on one area (false polymorphism) (photo 17). The vesicle is a 2 to
stages of papule, vesicle
crusted lesion
crusted lesion on the scalp
Lesions are more numerous centrally than distally
spots and papules on soles
Rashes polymorphism
Rashes on the oral mucosa
Posterior neck lymphadenitis
Work-up. Laboratory tests are rarely needed. In CBC: leucopenia, relative lymphocytosis, normal ESR. Vesicle scrapings contain multinucleated giant cells, and vesicle fluid contains virus in the first days of illness. It could be detected by the:
• Immune Fluorescent method;
• Serological reactions: CBR, Immune-enzyme reaction, IHAR to find antibodies
against viruses with fourfold increasing of antibodies title in 10-14 days may be
used;
• CSF investigation (signs of serous meningitis) – in case of meningoencephalitis;
• Virological separation of the VZ-virus on embryonic cells.
Diagnosis example: Chickenpox, typical form, moderate severity, complicated by
the bilateral medial otitis.
Differential diagnosis should be performed among early impetigo, insect bites, scabies,
and urticarial lesions.
Features of chicken pox in infants
·Beginning from a general infectious signs (malaise, anxiety, absence of appetite), dyspepsia phenomena.
·Body t° is normal or subfebrile, grows when rashes appear.
·Rashes appear on 2nd-5th day, massive, sometimes remain in one phase of development (gradual development of illness).
·Neurotoxicosis (cramps, meningeal symptoms).
· Possible visceral signs.
· Frequent is secondary bacterial infection.
Evidences for obligatory hospitalization of patients with infectious exanthema
· The severe form of disease, when appears need in undertaking of intensive therapy; patients with moderate forms at age before 3 years.
7. Sick children from families with bad social-home conditions, especially in the event of impossibility of their isolation to prevent infections transmission.
8. Absence of conditions for examination and treatment at home.
9. Sick children from closed children institutions.
Advantages of the home treatment
1. Possibility of additional infection by hospital bacteria is completely excluded.
2. Realization of individual care principle for sick child is more full.
3. Avoiding stressful reactions, which could appear in case of hospital treatment.
Treatment in home conditions is possible
Treatment
In most cases only symptomatic (Basic therapy) up to disappear of clinical signs
• Antiseptic fluids for skin lesions to prevent secondary bacterial infection (1 % brilliant green, 1-2 % KMnO4);
• Gurgling with oral antiseptic fluids after the food intake;
• Antihistamines for itching;
• Acetaminophen for fever control.
Etiological therapy by Acyclovir (IV 10 mg/kg 3 t.d. for 7 days or up to 48 hours the last elements appear) – for immunocompromised children:
n Patients with oncohematologic diseases;
n Patients after bone marrow or inner organs transplantation;
n Patients who achieve corticosteroids;
n Patients with the primary immune deficit;
n Patients with HIV-infection;
n Inborn Chicken pox;
n Chicken pox complicated by the damage of CNS, hepatitis, thrombocytopenia, pneumonia;
n And Severe forms of Chicken pox (Acyclovir orally 80 mg/kg/day 4 t.d. for children elder than 2 years and teenagers).
Also for severe cases ieonates – Varicella-Zoster immune globulin (0.2 ml/kg).
In case of encephalitis:
Base therapy:
• Bed regimen till body temperature normalization, disappearance of general cerebral and considerable improvement of focal neurological signs, not less than 14-16 days;
• A diet (before stable vital functions is due to adequate parenteral infusion therapy);
• Brest feeding or bottle feeding by adopted formulas for infants, in the first day 1/2-1/3 of average volume with a next increase to the complete volume during 2-3th days;
• A milk vegetable diet (№5) is appointed for preschoolers or school children, 5-6 times per day with the next passing to the diet №2 whether №15 (depending the age) in the recovery period;
• Oral fluids intake corresponds to age norms (with including the IV fluids);
• Antibacterial therapy: for infants at presence of concomitant bacterial infection, chronic infection, inflammatory changes in the CBC (by the broadspectrum antibiotic in average therapeutic doses, a short course).
Etiologic therapy:
• In encephalitis without the expressed general cerebral symptoms – IV acyclovir 10 mg/kg 3 times per day during 7-10 days; in the case of encephalitis with the expressed general cerebral symptoms (violation of consciousness, cramps) –15-30 mg/kg 3 times per day during 10-14 days, then continue 200-400 mg 5 times per day PO during 14 days;
• In meningitis IV acyclovir 10-15 mg/kg 3 times per day during 5-7 days.
Pathogenetic therapy:
• Glucocrticoids 3-5 mg/kg (by prednisolon), course not more than 10 days;
• vascular medicine (penthoxyphyllin, nicergolin and others like that);
• In posthypoxia period – nootrops, vitamins group B.
• In case of CSF hypertension – dehydration by 25 % MgSO4 IM, lasix 1-3 mg/kg IV or IM, acethazolamid orally.
• In case of seizures – Anticonvulsant therapy: benzodiasepins (seduxenum, sibasonum)
0.3-0.5 mg/kg IV, if they are ineffective – 1 % hexenalum or thiopenthalum sodii
in 3-5 mg/kg IV. Dehydration therapy: lasix 2-3 mg/kg IM or IV.
Prevention:
1. To isolate ill person until the 5 day after the last vesicles has appeared.
2. To isolate contacts from 11 till 21 day after exposure.
3. VZ immune globulin in immunocompromised children (not later than 72 hours
after exposure).
Key words and phrases: Varicella-Zoster, chickenpox, polymorphism, congenital
varicella syndrome, bullous varicella, multinuclear giant cells, acyclovir, Varicella-Zoster
immune globulin, immunocompromised children.
Scarlet Fever.
This disease is the result of infection by streptococci that elaborate one of three pyrogenic (erythrogenic) exotoxins.
Β-hemolytic streptococcus group A
The incubation period ranges from 1–7 days, with an average of 3 days. The onset is acute and is characterized by fever, vomiting, headache, toxicity, pharyngitis, and chills. Abdominal pain may be present; when this is associated with vomiting prior to the appearance of the rash, an abdominal surgical condition may be suggested. Within 12–48 hr the typical rash appears.
Generally, temperature increases abruptly and may peak at 39.6–40º C (103–104º F) on the 2nd day and gradually returns to normal within 5–7 days in the untreated patient; it is usually normal within 12–24 hr after initiation of penicillin therapy. The tonsils are hyperemic and edematous and may be covered with a gray-white exudate.
Group A streptococcal pharyngitis with inflammation of the tonsils and uvula.
The pharynx is inflamed and covered by a membrane in severe cases. The tongue may be edematous and reddened. During the early days of illness the dorsum of the tongue has a white coat through which the red and edematous papillae project (i.e., white strawberry tongue). After several days the white coat desquamates; the red tongue studded with prominent papillae persists (i.e., red strawberry tongue, raspberry tongue). The palate and uvula may be edematous, reddened, and covered with petechiae.
Note inflammation of the oropharynx with petechiae on the soft palate, small red spots caused by group A streptococcal pharyngitis.
The exanthem is red, is punctate or finely papular, and blanches on pressure. In some individuals, it may be palpated more readily than it is seen, having the texture of gooseflesh or coarse sandpaper. The rash appears initially in the axillae, groin, and neck but within 24 hr becomes generalized. Punctate lesions generally are not present on the face. The forehead and cheeks appear flushed, and the area around the mouth is pale (i.e., circumoral pallor). The rash is most intense in the axillae and groin and at pressure sites. Petechiae may occur owing to capillary fragility. Areas of hyperpigmentation that do not blanch with pressure may appear in the deep creases, particularly in the antecubital fossae (i.e., pastia lines). In severe disease, small vesicular lesions (miliary sudamina) may appear over the abdomen, hands, and feet.
Flushed face, circumoral pallor (Filatov’s sign),
Pastia lines in skin folds
Desquamation begins on the face in fine flakes toward the end of the 1st wk and proceeds over the trunk and finally to the hands and feet. The duration and extent of desquamation vary with the intensity of the rash; it may continue for as long as 6 wk.
Desquamation on the skin (fine flakes)
Desquamation on the palms and soles (macrolamellar)
Scarlet fever may follow infection of wounds (i.e., surgical scarlet fever), burns, or streptococcal skin infection. Clinical manifestations are similar to those just described, but the tonsils and pharynx generally are not involved. A similar picture may be observed with certain strains of staphylococci that produce an exfoliative toxin.
Scarlet fever must be differentiated from other exanthematous diseases, including measles (characterized by its prodrome of conjunctivitis, photophobia, dry cough, and Koplik spots), rubella (disease is mild, postauricular lymphadenopathy usually is present, and throat culture is negative), and other viral exanthems. Patients with infectious mononucleosis, have pharyngitis, rash, lymphadenopathy, and splenomegaly as well as atypical lymphocytes. The exanthems produced by several enteroviruses can be confused with scarlet fever, but differentiation can be established by the course of the disease, the associated symptoms, and the results of culture. Roseola is characterized by the cessation of fever with the onset of rash and the transient nature of the exanthem.
Septic or severe scarlet fever associated with bacteremia or toxemia may manifest high fever and may be complicated by arthritis, jaundice, and hydrops of the gallbladder. Scarlet fever may be differentiated from
DIAGNOSIS. Although 30% of children with sore throat have a positive throat culture for group A streptococci, only 50% of these have a positive antibody response indicative of active infection rather than colonization. Streptococcal pharyngitis is suggested by age greater than 5 yr, high fever, exudates, tender anterior cervical lymphadenopathy, scarlatiniform rash, and a history of exposure. However, only 15% of children with pharyngitis and 25% of those with exudates have streptococcal infection; 50% of those with streptococcal pharyngitis do not have tonsillar exudates. Clinical judgment does not predict which children may have streptococcal infection, which must be diagnosed by throat culture or antigen detection.
Throat culture is the most useful laboratory aid in reaching a diagnosis in patients with acute tonsillitis or pharyngitis. Selective media give a higher yield than sheep blood agar plates. A positive result for a throat culture may indicate streptococcal pharyngitis, but hemolytic streptococci are common inhabitants of the nasopharynx in well children. Isolation of a group A streptococcus from the pharynx of a child with pharyngeal infection does not necessarily indicate that the disease is caused by this organism. When streptococci are isolated from children with moderate or severe exudative pharyngitis who have petechiae on the palate and cervical adenitis, the diagnosis is more secure. Rapid antigen detection tests are not sufficiently sensitive to be used without a back-up culture. Treatment is, however, recommended for all children with pharyngitis and a positive throat culture or rapid antigen test for group A streptococci, even though in some cases the streptococci represent colonization.
The immunologic response of the host after exposure to streptococcal antigen can be assessed by measuring antistreptolysin O (ASO) titers. An increase in ASO titer to greater than 166 Todd units occurs in more than 80% of untreated children with streptococcal pharyngitis within the first 3–6 wk following infection. This response may be modified or abolished by early and effective antibiotic therapy. ASO titers may be very high in patients with rheumatic fever; in contrast, they are weakly positive or not elevated at all in patients with streptococcal pyoderma; responses in patients with glomerulonephritis are variable. Group A b-hemolytic streptococci also may be recovered from the pharynx of asymptomatic individuals who develop an antibody response to this organism, indicating that subclinical infection has occurred.
Individuals with impetigo may react strongly to stimulation by other streptococcal extracellular products. Anti-DNase (deoxyribonuclease) B provides the best serologic test for streptococcal pyoderma; it begins to rise 6–8 wk after infection. Most patients with streptococcal pharyngitis also develop elevated titers to this enzyme. Patients with pyoderma and pharyngitis also may develop antibody responses to hyaluronidase, but antihyaluronidase (AH) titers are elevated with less regularity than are ASO titers.
A 2-min, inexpensive Streptozyme slide test (Wampole Laboratories,
The white blood cell count may or may not be elevated. Because leukocytosis may occur in many bacterial and viral diseases, this finding is nonspecific. Similarly, elevations in the erythrocyte sedimentation rate and C-reactive protein do not help to establish a specific diagnosis.
DIFFERENTIAL DIAGNOSIS.
Acute pharyngitis that is indistinguishable clinically from that caused by group A b-hemolytic streptococci may be caused by many viruses, including Epstein-Barr virus (infectious mononucleosis). A viral cause may be suggested by failure to isolate streptococci and can be identified specifically by viral culture and serologic studies. Infectious mononucleosis may be suggested by the clinical manifestations, the presence of atypical lymphocytes in the peripheral blood, and a rise in heterophil and Epstein-Barr viral antibody titers. Acute pharyngitis similar to that caused by b-hemolytic streptococci may occur in patients with diphtheria, tularemia, toxoplasmosis, infection with Mycoplasma or A. haemolyticum, and, rarely, in individuals with tonsillar tuberculosis, salmonellosis, and brucellosis or infections caused by Neisseria gonorrhoeae, Neisseria meningitidis, and Yersinia enterocolitica. These diseases can be differentiated by appropriate cultures and serologic tests.
Streptococcal pyoderma must be differentiated from staphylococcal skin disease. Often these bacterial species coexist. The lesions produced are clinically indistinguishable; distinction is made only by culture.
Streptococcal septicemia, meningitis, septic arthritis, and pneumonia present signs and symptoms similar to those produced by other bacterial organisms. The offending pathogen can be established only by culture.
COMPLICATIONS. Complications generally reflect extension of streptococcal infection from the nasopharynx. This may result in sinusitis, otitis media, mastoiditis, cervical adenitis, retropharyngeal or parapharyngeal abscess, or bronchopneumonia. Hematogenous dissemination of streptococci may cause meningitis, osteomyelitis, or septic arthritis. Nonsuppurative late complications include rheumatic fever and glomerulonephritis.
PREVENTION. Administration of penicillin will prevent most cases of streptococcal disease if the drug is provided prior to the onset of symptoms. Except for rheumatic fever (see Chapter 175), indications for prophylaxis are not clear. Oral penicillin G or V (400,000 U/dose) is provided four times each day for 10 days. Alternatively, 600,000 U of benzathine penicillin in combination with 600,000 U of aqueous procaine penicillin may be given as a single intramuscular injection. This approach should be used for institutional epidemics. Children exposed to an individual case at school may be observed carefully.
Management of carriers of group A b{beta}-hemolytic streptococci is controversial. It has been suggested that treatment of the carrier precludes the development of type-specific immunity, thereby leaving the individual susceptible to reinfection later in life. It is probably unnecessary to re-treat asymptomatic convalescent patients with persistently positive throat cultures for group A streptococci, since they are generally carriers who do not have persistent or recurrent streptococcal infections. Children thought to have recurrent streptococcal infections may be carriers who have frequent viral respiratory infections masquerading as streptococcal infections. Parental anxiety may be high after several such episodes. Treatment with a non-penicillin antibiotic (e.g., cephalosporin, erythromycin, clindamycin) may be useful in eradicating the carrier state but should be reserved for the rare problem case.
No streptococcal vaccines are available for clinical use.
TREATMENT. The goals of therapy are to decrease symptoms and prevent septic, suppurative, and nonsuppurative complications. Penicillin is the drug of choice for the treatment of streptococcal infections. All strains of group A b{beta}-hemolytic streptococci isolated to date have been sensitive to concentrations of penicillin achievable in vivo.
Blood and tissue levels of penicillin sufficient to kill streptococci should be maintained for at least 10 days. Children with streptococcal pharyngitis should be treated with penicillin (125–250 mg/dose three times a day) for 10 days. Penicillin G or penicillin V may be employed; the latter is preferable because satisfactory blood levels are achieved even when the stomach is not empty. A single intramuscular injection of a long-acting benzathine penicillin G (600,000 U for children <
Erythromycin (40 mg/kg/24 hr), clindamycin (30 mg/kg/24 hr), or cefadroxil monohydrate (15 mg/kg/24 hr) may be used for treating streptococcal pharyngitis in patients who are allergic to penicillin. Generally, relapse rates are lower with regimens other than penicillin. Tetracyclines and sulfonamides should not be used for treatment, although sulfonamides may be used for prophylaxis of rheumatic fever.
Treatment failure, defined as persistence of streptococci after a complete course of penicillin, occurs in 5–20% of children and is more common with oral than with intramuscular therapy. It may be due to poor compliance, reinfection, the presence of b{beta}-lactamase–producing oral flora, tolerant streptococci, or presence of a carrier state. Persistent carriage of streptococci predisposes a small number of patients to symptomatic relapse. Repeating the throat culture after a course of penicillin therapy is indicated only in high-risk situations, such as in patients with a history of previous rheumatic fever. If the throat culture is again positive for group A streptococci, some clinicians recommend a second course of treatment. Persistence after a second course of antibiotics probably indicates a carrier state, which has a low risk for the development of rheumatic fever and does not require further therapy.
Patients with severe scarlet fever, streptococcal bacteremia, pneumonia, meningitis, deep soft tissue infections, erysipelas, streptococcal toxic shock syndrome, or complications of streptococcal pharyngitis should be treated parenterally with penicillin, preferably intravenously. The dose and duration of therapy must be tailored to the nature of the disease process, with daily doses as high as 400,000 U/kg/24 hr required in the most severe infections. Severe, necrotizing infections may require the addition of a second antibiotic (e.g., clindamycin) to ensure complete bacterial killing.
PROGNOSIS. The prognosis for adequately treated streptococcal infections is excellent; most suppurative complications are prevented or readily treated. When therapy is provided promptly, nonsuppurative complications are prevented and complete recovery is the rule. In rare instances, particularly ieonates or in children whose response to infection is compromised, fulminant pneumonia, septicemia, and death may occur despite usually adequate therapy.
Short statement of the material
Scarlet fever is an acute infectious disease, that is caused by group A b-hemolytic streptococcus, transmitted by an air-droplet way, characterized by intoxication, rashes on a
skin, tonsillitis, regional lymphadenitis, and strawberry tongue.
Etiology: group A b-hemolytic streptococcus (GABHS).
Epidemiology:
– source of infection – ill persoot only with scarlet fever, but other forms of GABHS infections (sore throat, erysipelas, streptodermia).
– infection is transmitted by inhalation of infected airborne droplets, rare with food and direct contact.
– susceptible organism – children 2-9 years old.
Pathogenesis An entrance gate is the mucus membrane of the throat, seldom damaged skin, and maternity ways (at delivery).
Pathogenesis has three lines:
· Toxic (toxically damage of cardiovascular, central nervous, endocrine systems).
· Septic – primary inflammation in the place of infection (tonsillitis, secondary bacterial complication).
· Allergic – sensibilization by GABHS proteins (depression of immunity leads to allergic complications – nephritis, arthritis, myocarditis, rheumatism).
Clinical presentation: Onset is usually acute and is characterized by a sore throat (often with dysphagia), fever (often above
The eruption is characterized by dusky red, blanching tiny papules that have a rough texture. Papules are usually absent on the face, palms, and soles, but the face characteristically shows flushing with circumoral pallor. On the body, the rashes are intensified in skin folds and at sites of pressure. In the antecubital and axillary fosses, linear petechias are seen with accentuation of the erythema (Pastia’s lines).
The exanthema usually lasts 4 to 5 days and then begins to desquamate, first on the face last on the palms and soles. Pharyngitis usually resolves in 5 to 7 days.
Clinical diagnostic criteria:
1. Latent period: a few hours – 7 days.
2. Initial or prodromal period (from the first signs of illness to rashes appearance):
up to 1-2 days
• acute beginning;
• toxic syndrome, hyperthermia;
• in the throat: pain, bright hyperemia, pin-point enanthema,
• catarrhal regional lymphadenitis (photo).
3. Period of exanthema (rashes):
а) Phase of height (1 – 2 days)
• maximal intoxication, fever up to 39-
• tonsillitis: bright hyperemia of the throat marked off a hard palate (photo 31), pinpoint enanthema, hypertrophied tonsils, catarrhal, lacunar (photo 32, 33), follicle (photo 34, 35) or necrotizing (photo 36) tonsillitis;
• regional lymphadenitis;
• pin-point rashes for a few hours spread all over the body, intensified on the front and lateral surface of neck, lateral surfaces of trunk (photo 37), abdomen (photo 38, 39), lumbar region (photo 40, 41), iatural skin folds (photo 42), on the red background of skin, typical intensified in skin folds with hemorrhagic elements (Pastia’s lines) (photo 43), a skin is rough (“sand paper” sign), pale perioral triangle (Filatov’s sign) (photo 44, 45);
• white dermatographia;
• coated tongue (photo 46) within 2-3 days clears up (photo 47, 48), on 4th – 5th day becomes “strawberry” (photo 49, 50);
• sympatic phase of “scarlet fever” heart (tones are loud, tachycardia, BP is elevated).
bright hyperemia of the throat marked off a hard palate
pin-point enanthema
Follicular tonsillitis
Lacunar tonsillitis
Necrotizing tonsillitis
pin-point rashes
Typical rashes localization in skin folds
Coated tongue
Strawberry tongue
b) Fading phase:
• normalization of body temperature till 3rd – 4th day of the disease, decrease of the toxic syndrome;
• rashes and redness of the skin from 2nd – 3rd up to 6th day turns pale;
• throat: enanthema disappears from 2nd – 3rd day, hyperemia turns pale till 6-7 day;
• the sizes of lymphnodes normalized till 4th – 5th day;
• vagus-phase of scarlet fever heart (bradycardia, dilation of the cardiac dullness borders, systolic murmur on the apex, low BP);
• a tongue turns pale till 10th – 12th day, with enlarged follicles.
4. Period of recovery: from 2nd week (for 10-14 days)
• changes on the skin: flakes-like desquamation all over the body except palms and soles (where it is larger) (photo 51);
• tongue with enlarged follicles;
• the vagus-phase of scarlet fever heart continue for 2-4 weeks;
• rise sensitivity to the streptococcus infection, possibility of complications.
Classification
1. Form:
a) typical;
b) atypical:
• without rashes;
• effaced;
• extra pharyngeal (burns, wounds, post-natal, after operations, delivery);
• with aggravated symptoms (hypertoxic, hemorrhagic).
2. Severity:
a) mild;
b) moderate;
c) severe: toxic, septic, toxic-septic.
3. Course:
a) smooth;
b) uneven (relapses, complications).
Complications
By the character:
• are infectious (streptodermia (photo 50, 52), necrotizing tonsillitis (photo 36), secondary tonsillitis (photo 54), peritonsilitis (photo 53) peritonsilar abscess (photo 55), otitis, purulent lymphadenitis, sepsis);
• and allergic (rheumatism, myocarditis, arthritis, glomerulonephritis).
By the time of development:
• early (first week of the disease);
• late (2nd – 3rd week).
By the etiology:
• specific or primary (caused by the same streptococcus);
• secondary (caused by the other bacteria).
Laboratory tests
1. The diagnose is confirmed by throat culture with group A b-hemolytic streptococcus.
2. Serology (antistreptolysin O, antidesoxyribonuclease B) with their grows in 2 weeks may be useful for documenting recent GABHS infection.
3. The complete blood cell count is helpful: usually white blood cell count higher 12500 cells/mm3, neutrophyllosis, left shift, eosynophylia, elevated ESR ECG, CBC and urinanalysis on the 10th day after the disease began, and on 21th day for possible late complications diagnostic (nephritis, myocarditis).
Diagnosis example:
• Scarlet fever, typical form, exanthema period, severe (toxic) degree, complicated by the right side peritonsilar abscess.
• Scarlet fever, typical form, recovery period, moderate degree, complicated by the myocarditis.
Differential diagnosis: tonsillitis may be seen with diphtheria, mononucleosis, adenovirus, and micoplasm; rashes may be seen with measles, rubella, and pseudotuberculosis.
Evidences for obligatory hospitalization of patients with infectious exanthema
– The severe form of disease, when appears need in undertaking of intensive therapy; patients with moderate forms at age before 3 years.
– Sick children from families with bad social-home conditions, especially in the event of impossibility of their isolation to prevent infections transmission.
– Absence of conditions for examination and treatment at home.
– Sick children from closed children institutions.
Advantages of the home treatment
1. Possibility of additional infection by hospital bacteria is completely excluded.
2. Realization of individual care principle for sick child is more full.
3. Avoiding stressful reactions, which could appear in case of hospital treatment.
Treatment in home conditions is possible
1. In conditions of isolated flat.
2. In case of satisfactory material position of the parents.
3. In case of parents desire to organize individual care and treatment at home.
Treatment
1. Bed regime during an acute period.
2. Etiological treatment for scarlet fever is:
a. In the mild case penicillin orally (penicillin V) for 10 days 50,000-100,000 EU/kg/day divided in 3-4 doses. Erythromycin (or another macrolides) is alternative antibiotic (30-50 mg/kg/day). The course of treatment is 10 days.
b. In the moderate case penicillin intramuscularly (penicillin G), the same dose as in the mild case. The course of treatment is 10-14 days.
c. In the severe case: cefalosporins of the 1st-2nd generation, klindamycin, vancomycin intravenously for 10-14 days.
3. Detoxication therapy:
a. In the mild case large amount of oral fluids.
b. In the moderate and severe cases – Glucose and saline solutions IV.
4. Antihistamines (in average doses) – pipolphen, suprastin, claritin, cetirizin.
5. Medicine which strengthens vascular wall (vit. C and PP: ascorutin, galascorbin)
6. Control of fever (when the temperature is more than 38.5-
7. Local treatment with antiseptic fluids (gurgling), UV-insolation. Patient may go home from infection department not earlier the 10th day of the illness, in 10 days blood analysis, urinalyses, ECG must be done.
Prevention: isolation of the patient on the 10 days, but he mustn’t visit school until 22 day of the disease. Contact person (children before 8 years) must be isolated for 7 days (period of incubation).
Key words and phrases: scarlet fever, three lines of pathogenesis, Group A b-hemolytic streptococcus(GABHS), ”doughnut” lesions on the soft palate, rashes “sandpaper”, dusky red, blanching tiny papules, circumoral pallor. Pastia‘s lines, desquamate, purulent and allergic complications.
Diphtheria
Diphtheria is an acute toxic infection caused by toxigenic strains of Corynebacterium diphtheria, characterized by a local lesion consisting of a membrane. The constitutional symptoms are due to circulation exotoxin, which has a special affinity for nerve tissue, heart muscle and kidneys.
Etiology: Corynebacterium diphtheria
· Corynebacterium species are aerobic, no encapsulated, non-sporeforming, mostly no motile, gram-positive bacilli.
Sensitive to high temperature and disinfection
· Stabile to freezing and dryness
· Three biotypes –
1. mitis
2. gravis
3. intermedius
C.diphtheriae colonies
Epidemiology:
Transmission is from person-to-person (from a patient or carrier)
· through direct contact
· or airborne respiratory droplets
These materials include discharge from the nose, throat, and lesions on the skin, eyes and even the vagina.
Contagious index – 10-15%
Seasonality – autumn-winter
Immunity – instable
Pathogenesis:
· Entrance for the infection: throat, nose, larynx, sex organs, wound.
· Dissemination of the Corynebacterium, production of exotoxin.
· Local toxin effects with membranous inflammation.
· Toxemia.
· Diffuse toxic effects on kidneys, suprarenal glands, cardiovascular system, and peripheral nervous system.
Fibrinous inflammation
• Diphtheritic (on flat multilayer epithelium)
• Crupose (on cylindrical single layer epithelium)
Incubation period is short (from one to seven days)
Clinical features: diphtheria may be localized, spread, toxic (with edema of subcutaneous tissue), hypertoxic, hemorrhagic.
Classification of Diphtheria
Classification of Diphtheria by localization
1. Diphtheria of tonsills
• localized (catarrhal, islet-like, membranous)
• spread form
• toxic form:
1. I grade
2. II grade
3. III grade
4. hypertoxic
• hemorrhagic form
• gangrenous form
Diphtheria of the pharynx: The clinical onset is generally insidious with low-grade fever, cough, hoarseness, and mild sore throat. Intensity of the body temperature and intoxication increases proportionally to the square of damages (localized, spread, toxic forms). While examining the throat you could see a gray adherent membranous exudates on the tonsils (localized forms), extending to soft palate, cheeks, even tongue (spread form). The exudates bleed when removed. Hyperemia of throat has cyanotic color with edema of mucous membrane. Regional lymph nodes are enlarged and tenderness appears. In case of toxic forms you could see “bull neck” due to the neck subcutaneous tissue edema which may extend even to the thorax. Hypertoxic form has sudden onset with hard intoxication (nausea, vomiting, seizures, unconsciousness, body temperature is more than 40o C) which exceeds local symptoms. Hemorrhagic form is characterized by hemorrhages, bleeding, membranous exudates consists blood.
Tonsillar diphtheria, localized (moderate)
Tonsillar diphtheria, spread (moderate)
Tonsillar diphtheria, toxic (severe)
Tonsillar diphtheria, toxic (“bull neck” sign)
2. Diphtheria of the larynx (laryngotracheitis, croup)
· Localized croup
· Spread croup
1. laryngotracheitis
2. laryngotracheobronchitis
· Stages of croup
1. Catarrhal croup
2. Stenosis
1. Compensated
2. Subcompensated
3. Decompensated
3. Asphyxia
Diphtheria of the upper respiratory tract demonstrates clinical features of croup. It has slow development, intoxication usually is absent because between membranous exudates and mucous membrane of larynx, trachea and bronchi mucous is present. That’s why toxemia is absent. Croup has catarrhal, stenotic stages and asphyxia.
Catarrhal stage: – duration 2-3 days; intoxication is small or moderate; barking cough, voice becomes hoarse; slow development of signs and symptoms/
Stenotic stage: – duration 2 hours – 2-3 days; moderate intoxication; stenotic breathing appears; signs of hypoxia (peripheral, then general cyanosis, tachycardia, anxiety).
Asphyxia: – pallor or grayness of skin; sleepiness; superficial breathing; arrhythmia, hypotonia, hypothermia, other signs of coma, then – death of the patient.
3. Diphtheria of the nasopharynx (nasopharyngitis, pharyngitis)
• difficulty of the nasal breathing;
• nasality of voice;
•throat pain with an irradiation in ears;
• nasal dyscharge is bloody-purulent;
• visible inflammation in the nasal cavity is absent;
• during posterior rhinoscopic examination edema and moderate hyperemia of adenoid tonsill mucus and (or) fibrinous membranes on its surface;
• “spear-shaped” coat which slips down by the back pharyngeal wall;
• regional (posterior cervical) lymphadenitis;
• the signs of general intoxication are moderate or severe (fatigue, pallor, anorexia, increase of temperature).
4. Diphtheria of the anterior part of a nose
• Localized:
– Catarrhal,
– Islet-like,
– Membranous.
• Spread;
• Toxic.
Diphtheria of the anterior part of a nose also may be localized, spread and toxic. Signs of it: slow development; minimal toxic signs; it is hard to breathe by nose; purulent and bleed discharges from the nose; maceration of the perinasal area; rhinoscopy reveals gray adherent membranous exudates on the mucous membranes or ulcers; in case of spread form they extend to additional cavities; in case of toxic form – perinasal edema appears, intoxication enlarges.
Diphtheria of the nose
5. Diphtheria of other localization: diphtheria of the eye, ear, sex organs, umbilical, wounds, lip, and cheek.
diphtheria of the lip
The course of disease
· With complication
· Without complication
Complications
– early:
toxic shock syndrome;
DIC syndrome
suprarenal glands insufficiency;
Kidneys insufficiency
Respiratory insufficiency
Plural organs insufficiency
(in the end of 1st to 2nd week) nephritis; myocarditis; peripheral cranial nerves palsies;
Late (on the 3rd to 7th week): myocarditis; peripheral spinal nerves palsies.
Laboratory tests. Diphtheria can be confirmed with isolation of C.diphtheriae from the pharyngeal membrane, nose (bacterioscopic or bacteriologic method); serologic reactions, fluorescent antibody techniques are available.
Treatment: all the patients are hospitalized into infectious or resuscitative department (for severe forms and in case of laryngeal diphtheria).
• Absolute bed regime (2-3 wks);
• Diphtheritic antitoxin therapy (etiological) (Doses see in table);
• Antibacterial therapy for 10-14 days
– In moderate or severe cases:
n Semisynthetic penicillines 50-100 mg/kg/day
n or cefalosporins 100 mg/kg/day
– In mild cases:
n Erythromycin 40-50 mg/kg/day or
n Rifampicin 10-15 mg/kg/day
• Antiseptic fluids locally (in spray or for gurgling);
• Disintoxication therapy (50-100 ml/kg/day) with glucose, crystalloid and colloid fluids IV in moderate or severe cases;
• Corticosteroids therapy by prednisolone 2-3 mg/kg/day in moderate form, 10-20 mg/kg/day in severe form.
Prompt treatment with diphtheria antitoxin (DAT) from horse serum is mandatory following tests for hypersensitivity.
In case of toxic shock syndrome:
– Immediately intravenous infusion of DAT with prednisone intravenously 30-50 mg before DAT;
– Prednisone 10-20 mg/kg/day in equal doses 2-4 times per day;
– Detoxication, correction of acid-base balance and electrolytes;
– Dopamine, trental, corglicon.
In case of diphtheria of the larynx (except DAT):
– Inhalation of antiedematous drugs (2 % NaHCO3, hydrocortisone, euphyllin, and mucolithics);
– suctioning of membranes and mucus;
– inhalation of oxygen;
– in the III stage of stenosis – intubation;
– In case of spread croup, combined with diphtheria of pharynx – tracheotomy.
Treatment of complications
Myocarditis:
• needs bed regimen on 35-50 days;
• cardiomonitoring;
• prednisone 2 mg/kg/ day per os;
• rhiboxin or ATPh,
• per oral potassium (panangin);
• diuretics.
Neuritis:
• proserin;
• galanthamin;
• strychnine nitric;
• vitamins group B (B1, B6, B12), C;
• diuretics.
Discharge of the patient:
• Clinically healthy;
– Mild and moderate in 14-21 days;
– Severe – in 30-60 days.
• With two documented negative pharyngeal and nasal cultures taken 48 hrs apart in 3 days after stopping antibacterial treatment;
• Dispensarization not less than 6 months (in uncomplicated cases).
Treatment of healthy infected by C. diphtheria person:
– Erythromycin 40-50 mg/kg/day, or
– Roxitromycinum 5-8 mg/kg, or
– Rifampicin 10-15 mg/kg/day;
• Antiseptic fluids locally;
• Vitamins B-group, C;
• Immune modulators in case of chronic site of infection;
• Tonsillectomy, adenotomy in case of chronic carrying.
Prophylaxis
Specific:
• by DTP vaccine from 3 months age 3 times with 30 days interval (3, 4, 5 months), revaccination in 18 months (DTaP), 6, 14, 18 years (DT), later – every 10 years.
Combined vaccines
Nonspecific:
• Close contacts who were previously immunized longer than 5 years before should receive booster dose of diphtheria toxicoid;
• Antibiotic (erythromycin, rifampin) orally for 7 days;
• Revealing, sanation of healthy infected persons;
• Looking after contacts for 10 days;
• Disinfection of epidemic focus.
MUMPS (INFECTIOUS PAROTITIS).
Mumps is an acute, generalized viral disease in which painful enlargement of the salivary glands, chiefly the parotids, is the usual presenting sign.
ETIOLOGY.
The virus is a member of the paramyxovirus group, which also includes the parainfluenza, measles, and
EPIDEMIOLOGY.
Mumps is endemic in most urban populations; the virus is spread from a human reservoir by direct contact, airborne droplets, fomites contaminated by saliva, and possibly by urine. It is distributed worldwide and affects both sexes equally; 85% of infections occurred in children younger than 15 yr prior to widespread immunization. Now disease often occurs in young adults, producing epidemics in colleges or in the work place. Epidemics appear to be primarily related to lack of immunization rather than to waning of immunity. Epidemics occur at all seasons but are slightly more frequent in late winter and spring. Sources of infection may be difficult to trace because 30–40% of infections are subclinical. There has been a decrease in the incidence since the introduction of mumps vaccine in 1968.
Virus has been isolated from saliva as long as 6 days before and up to 9 days after appearance of salivary gland swelling. Transmission does not seem to occur longer than 24 hr before appearance of the swelling or later than 3 days after it has subsided. Virus has been isolated from urine from the 1st–14th day after the onset of salivary gland swelling.
Lifelong immunity usually follows clinical or subclinical infection, although second infections have been documented. Transplacental antibodies seem to be effective in protecting infants during their first 6–8 mo. Infants born to mothers who have mumps in the week prior to delivery may have clinically apparent mumps at birth or experience illness in the neonatal period. Severity ranges from mild parotitis to severe pancreatitis. The serum neutralization test is the most reliable method for determining immunity but is cumbersome and expensive. A complement-fixing antibody test is available (see Diagnosis). The presence of V antibodies alone suggests previous mumps infection.
PATHOGENESIS.
After entry and initial multiplication in the cells of the respiratory tract, the virus is blood-borne to many tissues, among which the salivary and other glands are the most susceptible.
CLINICAL MANIFESTATIONS.
The incubation period ranges from 14–24 days, with a peak at 17–18 days. In children, prodromal manifestations are rare but may be manifest by fever, muscular pain (especially in the neck), headache, and malaise. The onset is usually characterized by pain and swelling in one or both parotid glands. The parotid swells characteristically; it first fills the space between the posterior border of the mandible and the mastoid and then extends in a series of crescents downward and forward, being limited above by the zygoma. Edema of the skin and soft tissues usually extends further and obscures the limit of the glandular swelling, so that the swelling is more readily appreciated by sight than by palpation. Swelling may proceed extremely rapidly, reaching a maximum within a few hours, although it usually peaks in 1–3 days. The swollen tissues push the ear lobe upward and outward, and the angle of the mandible is no longer visible. Swelling slowly subsides within 3–7 days but occasionally lasts longer. One parotid gland usually swells a day or two before the other, but swelling limited to one gland is common. The swollen area is tender and painful, pain being elicited especially by tasting sour liquids such as lemon juice or vinegar. Redness and swelling about the opening of the Stensen duct are common. Edema of the homolateral pharynx and soft palate accompanies the parotid swelling and displaces the tonsil medially; acute edema of the larynx has also been described. Edema over the manubrium and upper chest wall may occur probably because of lymphatic obstruction. The parotid swelling is usually accompanied by moderate fever; normal temperatures are common (20%), but temperatures of 40º C (104º F) or more are rare.
Although the parotid glands alone are affected in the majority of patients, swelling of the submandibular glands occurs frequently and usually accompanies or closely follows that of the parotid glands. In 10–15% of patients only the submandibular gland(s) may be swollen. Little pain is associated with the submandibular infection, but the swelling subsides more slowly than that of the parotids. Redness and swelling at the orifice of the Wharton duct frequently accompany swelling of the gland.
Least commonly the sublingual glands are infected, usually bilaterally; the swelling is evident in the submental region and in the floor of the mouth.
A maculopapular erythematous rash, most prominent on the trunk, occurs infrequently; rarely it is urticarial.
OTHER ORGANS DAMAGE
Meningoencephalomyelitis. This is the most frequent complication in childhood. The true incidence is hard to estimate because subclinical infection of the central nervous system, as evidenced by cerebrospinal fluid pleocytosis, has been reported in more than 65% of patients with parotitis. Clinical manifestations occur in over 10% of patients. The incidence of mumps meningoencephalitis is approximately 250/100,000 cases; 10% of these cases occurred in patients older than 20 yr. The mortality rate is about 2%. Males are affected three to five times as frequently as females. Mumps is one of the most common causes of aseptic meningitis
The pathogenesis of mumps meningoencephalitis has been described as (1) a primary infection of neurons and (2) a postinfectious encephalitis with demyelination. In the first type, parotitis frequently appears at the same time or following the onset of encephalitis. In the latter type, encephalitis follows parotitis by an average of 10 days. Parotitis may in some cases be absent. Aqueductal stenosis and hydrocephalus have been associated with mumps infection. Injecting mumps virus into suckling hamsters has produced similar lesions.
Mumps meningoencephalitis is clinically indistinguishable from meningoencephalitis of other origins. Moderate stiffness of the neck is seen, but the remainder of the neurologic examination is usually normal. The cerebrospinal fluid (CSF) usually contains fewer than 500 cells/mm3, although occasionally the count may exceed 2,000. The cells are almost exclusively lymphocytes, in contrast to enteroviral aseptic meningitis, in which polymorphonuclear leukocytes often predominate early in the disease. Mumps virus can be isolated from cerebrospinal fluid early in the illness.
Orchitis, Epididymitis. These complications rarely occur in prepubescent boys but are common (14–35%) in adolescents and adults. The testis is most often infected with or without epididymitis; epididymitis may also occur alone. Rarely, there is a hydrocele. The orchitis usually follows parotitis within 8 days or so; it may also occur without evidence of salivary gland infection. In about 30% of patients both testes are affected. The onset is usually abrupt, with a rise in temperature, chills, headache, nausea, and lower abdominal pain; when the right testis is implicated, appendicitis may be suggested as a diagnostic possibility. The affected testis becomes tender and swollen, and the adjacent skin is edematous and red. The average duration is 4 days. Approximately 30–40% of affected testes atrophy. Impairment of fertility is estimated to be about 13%, but absolute infertility is probably rare.
Oophoritis. Pelvic pain and tenderness are noted in about 7% of postpubertal female patients. There is no evidence of impairment of fertility.
Pancreatitis. Severe involvement of the pancreas is rare, but mild or subclinical infection may be more common than is recognized. It may be unassociated with salivary gland manifestations and be misdiagnosed as gastroenteritis. Epigastric pain and tenderness, which are suggestive, may be accompanied by fever, chills, vomiting, and prostration. An elevated serum amylase value is characteristically present with mumps, with or without clinical manifestations of pancreatitis.
Nephritis. Viruria has been reported frequently. In one study of adults, abnormal renal function occurred at some time in every patient, and viruria was detected in 75%. The frequency of renal involvement in children is unknown. Fatal nephritis, occurring 10–14 days after parotitis, has been reported.
Thyroiditis. Although uncommon in children, a diffuse, tender swelling of the thyroid may occur about 1 wk after the onset of parotitis with subsequent development of antithyroid antibodies.
Myocarditis. Serious cardiac manifestations are extremely rare, but mild infection of the myocardium may be more common than is recognized. Electrocardiographic tracings revealed changes, mostly depression of the ST segment, in 13% of adults in one series. Such involvement may explain the precordial pain, bradycardia, and fatigue sometimes noted among adolescents and adults with mumps.
Mastitis. This is uncommon in each sex.
COMPLICATIONS.
Deafness. Unilateral, rarely bilateral, nerve deafness may occur; although the incidence is low (1:15,000), mumps is a leading cause of unilateral nerve deafness. The hearing loss may be transient or permanent.
Ocular Complications. These include dacryoadenitis, painful swelling, usually bilateral, of the lacrimal glands; optic neuritis (papillitis) with symptoms varying from loss of vision to mild blurring with recovery in 10–20 days; uveokeratitis, usually unilateral, with photophobia, tearing, rapid loss of vision, and recovery within 20 days; scleritis; tenonitis, with resultant exophthalmos; and central vein thrombosis.
Arthritis. Arthralgia associated with swelling and redness of the joints is an infrequent complication; complete recovery is the rule.
Thrombocytopenic Purpura. This sign is infrequent.
Mumps Embryopathy. There is no firm evidence that maternal infection is damaging to the fetus; a possible relationship to endocardial fibroelastosis has not been established. Mumps in early pregnancy does increase the chance of abortion.
DIAGNOSIS.
The diagnosis of mumps parotitis is usually apparent from the symptoms and physical examination. When the clinical manifestations are limited to those of one of the less common lesions, the diagnosis is not so clear but may be suspected, especially during an epidemic. The routine laboratory tests are nonspecific; there is usually leukopenia with relative lymphocytosis, but complications often result in polymorphonuclear leukocytosis of moderate degree. An elevation of serum amylase is common; the rise tends to parallel the parotid swelling and then to return to normal within 2 wk or so. The etiologic diagnosis depends on isolation of the virus from the saliva, urine, spinal fluid, or blood or the demonstration of a significant rise in circulating complement fixation antibodies during convalescence. Serum antibodies to the S antigen reach their peak early in about 75% of patients and are detectable at the time of the presenting symptoms. They gradually disappear within 6–12 mo; antibodies against the V or viral antigen usually reach a peak titer in about 1 mo, remain stationary for about 6 mo, and then slowly decline during the ensuing 2 yr to a low level, at which they persist. The presence of a high anti-S titer and a low anti-V titer during the acute stage of an otherwise undiagnosed meningoencephalitis, for example, strongly suggests a mumps infection, which would be confirmed if a convalescent serum (taken 14–21 days later) revealed a fourfold rise of anti-V antibodies accompanied by little change in the titer of anti-S antibodies.
DIFFERENTIAL DIAGNOSIS.
This includes parotitis of other origin, as in viral infections including human immunodeficiency virus (HIV) infection, influenza, parainfluenza 1 and 3, cytomegalovirus, or the rare instances of coxsackievirus A and lymphocytic choriomeningitis infections. These infections can be distinguished by specific laboratory tests; suppurative parotitis, in which pus can often be expressed from the duct; recurrent parotitis, a condition of unknown origin, but possibly allergic iature, which has frequent recurrences and a characteristic sialogram; salivary calculus, obstructing either a parotid or, more commonly, a submandibular duct, in which the swelling is intermittent; preauricular or anterior cervical lymphadenitis from any cause; lymphosarcoma or other rare tumors of the parotid; orchitis resulting from infections other than mumps, for example, the rare infections by coxsackievirus A or lymphocytic choriomeningitis viruses; and parotitis caused by cytomegalovirus in immunocompromised children.
TREATMENT.
Treatment of parotitis is entirely symptomatic. Bed rest should be guided by the patient’s needs, but no statistical evidence indicates that it prevents complications. The diet should be adjusted to the patient’s ability to chew. Orchitis should be treated with local support and bed rest. Mumps arthritis may respond to a 2-wk course of corticosteroids or a nonsteroidal anti-inflammatory agent. Salicylates do not appear to be effective.
PROPHYLAXIS
Passive. Hyperimmune mumps gamma globulin is not effective in preventing mumps or decreasing complications.
Active. The routine administration of live, attenuated mumps vaccine is discussed in Chapter 247. Vaccinated children usually do not experience fever or other detectable clinical reactions, do not excrete virus, and are not contagious to susceptible contacts. Rarely, parotitis can develop 7–10 days after vaccination. The vaccine induces antibody in about 96% of seronegative recipients and has a protective efficacy of about 97% against natural mumps infection. The protection appears to be long lasting. In one outbreak of mumps, several children who had been immunized with mumps vaccine in the past experienced an illness characterized by fever, malaise, nausea, and a red papular rash involving the trunk and extremities but sparing the palms and soles. The rash lasted about 24 hr. No virus was isolated from these children, but increases in the titer of mumps antibody were demonstrated
Short statement of the material
Mumps (parotid infection) is an acute viral disease, that is caused by a virus from Pramyxovirus family, is transmitted by droplet mechanism, is characterized by the predominant damage of salivary glands, rarer – other glandular organs (pancreas, testicles, ovaries, pectoral glands and other), and also nervous system.
Etiology: an RNA virus, myxovirus parotitis, pathogenic only in humans.
Epidemiology:
A source is a patient with clinical, effaced, subclinical forms of infection, contagiousness is up to 9 days from the beginning of disease;
the mechanism of transmission is droplet, the virus is transmitted primarily through saliva during speaking, breathing (air-droplet way), hand-to-hand (contact way);
the morbidity index does not exceed 50%, more frequent children 3-6 years are ill;
Immunity is persistent.
Pathogenesis:
Acquired through the mucous membrane of oral cavity, pharynx, respiratory tract, the virus proliferates locally and in regional lymph nodes;
Then occurs a viremia;
Dissemination of the virus to salivary glands,
Reproduction in them
Secretion of the virus by saliva
Secondary viremia
Damage of other organs: pancreas, testes, ovaries, thyroid, breasts and meninges.
Immune response, elimination of the virus.
Organs that are could be damaged by parotid infection
Classification
Typical forms
glandular (parotitis, submaxillitis, sublinguitis, pancreatitis, orchitis, oophoritis, mastitis, bartolonitis, prostatitis, tyroiditis);
nervous (serous meningitis, meningoencephalitis);
combined (parotitis + pancreatitis + serous meningitis).
Atypical forms
effaced;
subclinical (without clinical signs).
Severity: –
mild degree;
moderate degree;
severe degree.
Course:
acute;
further asthenic, hypertensive syndrome (in case of encephalitis);
complicated;
uncomplicated
Severity indexes:
degree of glands damage (swelling, tenderness, edema);
the CNS damage (meningeal and meningoencephalitis signs severity);
degree of toxic syndrome (body temperature, violation of the common state).
Clinical presentation
Incubation period range 11-21 days.
Prodromal symptoms are: general malaise, anorexia, and myalgia with a low-grade fewer. They are followed by parotitis; other manifestations may include pancreatitis, oophoritis, orchitis, mastitis, myocarditis, meningoencephalitis and cranial nerve involvement. These symptoms can occur singly, sequentially or concurrently.
Parotitis presents as an earache, parotid edema begins with erythema (or usually colorless) and tenderness above the angle of the mandible (during chewing, speaking) within 1-2 days. Edema increases over several days, may cause an upturning of the earlobe (photo). An examination of the buccal mucosa often reveals erytematous and edematous orifices of Wharton`s and Stensens ducts (Positive Moorson sign). Fever may increase to 40 oC. Another parotid gland usually inflamed in 1-2 days.
Other signs of mumps tend to occur 1 week or more after the onset of parotid edema.
Bylateral parotitis
Upturing of the earlobe
Moorson sign
Submaxillitis
Acute beginning from fever (temperature 38 – 39°С), toxic syndrome.
Pain in the area of the damaged gland.
Slight swelling in submandibular area.
Hyperemia and infiltration in the place of external duct of salivary gland.
Often comes with the damage of parotid glands.
Submaxillitis
Orchitis
Orchitis: symptoms include testicular edema and tenderness, nausea, vomiting and fever. In 25 % – is bilateral. Mild atrophy of one testis may develop in many cases.
Repeated rising of temperature on 7 – 14 day of illness, toxic syndrome.
Previous damage of salivary glands.
Pain in a groin increases at walking with an irradiation in a testicle.
A testicle is enlarged in sizes; thickened, very painful, skin of scrotum above him is red, shining.
In future is violation of testicles function, atrophy in 1/3
Treatment is symptomatic. In mild, moderate cases of isolate salivary glands damage home treatment is indicated.
Basic therapy in case of
Isolate salivary glands damage (parotitis, submaxillitis, and sublinguitis):
Bed regimen up to 7 days.
Mechanically sparing diet (liquid, semi liquid, soft food; exclude uncooked vegetables and fruits, juices, fatty and spicy food)
Care for oral cavity (gurgling with 2 % NaHCO3, 5% boric acid, and other antiseptic solutions).
Dry heat on the staggered glands.
In case of Pancreatitis additionally:
1 – 2 days hunger, diet №5 for 10 – 12 days.
Detoxication therapy (orally, IV: crioplasm, albumen, 5% glucose, physiologic sodium chloride solution).
Protease inhibitors (contrical 10-20 IU/kg/day)
Spasmolytics for the pain syndrome decrease (nospani, papaverini).
Enzymic preparations (pancreatin, creon, pangrol, digestin).
Bibliography
а) Basic
1. Jeffrey Bergelson. Pediatric Infectious Diseases: Requisites / Jeffrey Bergelson, Theoklis Zaoutis, Samir S. Shah. – Elsevier Health Sciences, 2008 – 448 p.Maureen R. Nelson. Pediatrics / Maureen R. Nelson. – NY: Demos Medical Publishing, 2010. – 259 p.
2. Elaine Landau. Chickenpox / Elaine Landau. – Marshall Cavendish, 2009. – 32 p.
3. Susan S. Aronson. Managing Infectious Diseases in Child Care and Schools: A Quick Reference Guide / Susan S. Aronson. – Amer Academy of Pediatrics, 2008. – 195 p.
b) Additional
http://www.netdoctor.co.uk/diseases/facts/childrensdiseases.htm
http://kidshealth.org/parent/growth/medical/immunization_chart.html
http://children.webmd.com/healthtool-childhood-immunizations-guide
Prepared by ass. prof. Luchyshyn N.Yu.. MD, PhD
