Immune system in infancy and in toddlers icon

Immune system in infancy and in toddlers

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Bukovinian State Medical University

Department of Developmental Pediatrics


to the practical class for medical students of 3-rd years

Modul 1: Child’s development

Submodul 2:

Topic 4:



It is completed by:

MD, MSc, PhD Strynadko Maryna

Chernivtsy – 2007

To understand immunologic deficiency disorders and their serious, often life-threatening consequences. It is helpful to review the normal functioning of the immune system. In simple terms the function of the immune system is to recognize "self" from "non-self" and to initiate responses to eliminate the "non-self" or the foreign substance known as antigen. However, the specific processes involved in this function are complex and interrelated. The following is a review of the major responses.

The immune system includes the primary lymphoid organs (thymus, bone marrow, and probably liver) and the secondary lymphoid organs (lymph nodes, spleen, and gut-associated lymphoid tissue). The functions of the immune system are basically two types: nonspecific and specific. Nonspecific immune defenses are activated on exposure to any foreign substance but react similarly regardless of the type of antigen; they are unable to identify the antigen. The principal component of this system is phagocytosis, the process of ingesting and digesting foreign substances. Phagocytic cells are composed of neutrophils and monocytes.

Specific defenses are those that have the ability to recognize the antigen and respond selectively. The components of adaptive immunity are humoral immunity and cell-mediated immunity. The cells responsible for these two forms of immunity are the lymphocytes, specifically B-lymphocytes and T-lymphocytes.

^ Humoral immunity

Humoral immunity is involved with antibody production and complement. The principal cell involved in antibody production is the B-lymphocyte. In humans the exact site of production of the B-lymphocyte is speculative, although it is probably the bone marrow. In chickens the site is clearly identified as a hind-gut organ known as the bursa of Fabricius, hence the term "B-lymphocyte," or "B-cell." When challenged with an antigen, B-cells divide and differentiate into plasma cells. The plasma cells produce and secrete large quantities of antibodies specific to the antigen. Five classes of antibodies or immunoglobulins (IG) have been identified - G, M, A, D, and E, each serving a specific function.

On initial exposure to an antigen, the B-lymphocyte system begins to produce antibody, predominantly IgM, which appears in 2 to 3 days. This process is referred to as the primary antibody response.

With subsequent exposure to the antigen, a secondary antibody response occurs. Antibody, chiefly lgG, is produced in much greater quantities within 1 to 2 days. An example of the secondary response is consecutive administration of immunizations, often called boosters. Memory B-cells allow the immune system to recognize the same antigen for months or years.

When antibody reacts with antigen, they bind to form an antigen-antibody complex. This binding serves several functions. Antibody aids in the phagocytosis of antigen by sensitizing it in such a manner that it is more readily destroyed by phagocytes, a process known as opsonization.

Antibody also activates or fixes complement, the second component of humoral immunity. The complement system is a series of nine major factors (CI and C9) present in serum that results in a cascade of enzymatic actions and death of a viable antigen. It also serves to bridge cellular and humoral immunity. After being activated by antibody, complement produces a chemotactic factor that summons T-lymphocytes and macrophages to the antigen site.

^ Cell-mediated immunity

Cell-mediated immunity is involved in a variety of specific functions mediated by the T-lymphocyte. The T-lymphocyte is so named because it passes through the thymus during the differentiation process, which leads to the mature T-cell. T-lymphocytes do not carry typical immunoglobulins on their surfaces as do the B-cells. However, they are functionally heterogenous in that several subsets have been iden­tified, including cytotoxic T-cells, memory T-cells, helper T-lymphocytes, and regulator T-lymphocytes.

Specific functions of T-lymphocytes include: protection against most viral, fungal, and protozoan infections and slow-growing bacterial infections, such as tuberculosis, rejection of hystoincompatible grafts, mediation of cutaneous delayed hypersensitivity reactions, such as in tuberculin testing, and probably immune surveillance for malignant cells. In addition, they also have regulatory functions within the immune system. For example, helper T-lymphocytes assist B-lymphocytes and other types of T-cells to mount an optimum immune response. The cellular immune response is initiated when a T-lymphocyte is sensitized by antigen. In response to this contact the T-cell releases numerous humoral factors called lymphokines, which eventually bring about death of the antigen. For example, chemotactic factor promotes the migration of phagocytes and other T-lymphocytes to the antigenic area, migratory inhibitor factor prevents their leaving the site, transfer factor transforms nonsensitized T-cells into sensitized T-lymphocytes, blastogenic factor initiates the rapid mitosis of sensitized T-cells, and macrophage activation factor transforms local macrophages to highly phagocytic cells. Another lymphokine is interferon, which nonspecifi-cally inhibits viral replication, promotes phagocytosis, and stimulates the killer activity of sensitized lymphocytes.

The immunologic properties of the mucosal lining of the gastrointestinal tract are immature, which predisposes this system, like the respiratory system, to increased risk of infection and inflammation. The immunologic system undergoes numerous changes during the first year. The newborn receives significant amounts of maternal lgG, which confers immunity for about 3 months against antigens to which the mother was exposed. During this time the infant begins to synthesize his own lgG, and about 40% of adult levels are reached by 1 year of age. Significant amounts of lgM are produced at birth, and adult levels are reached by 9 months of age. The production of IgA, lgD, and lgE is much more gradual, and maximum levels are not attained until early childhood.

The defense mechanisms of the tissues and blood, particularly phagocytosis, are much more efficient in the toddler than in the infant. The production of antibodies is well-established. Immunoglobulin G (IgG), which neutralizes microbial toxins, reaches adult levels by the end of the second year of life. Passive immunity from maternal transfer disappears by the beginning of toddlerhood, necessitating the use of artificial immunizations. Immunoglobulin M (lgM), which responds to artificial immunizing techniques and combats serious infection, attains adult levels during late infancy. Immunoglobulins A, D, and E increase gradually, not reaching eventual adult levels until later childhood. Many young children demonstrate a sudden increase in colds and minor infections when entering nursery school or kindergarten because of the exposure to new antigens.


Severe combined immunodeficiency disease is characterized by absence of both humoral and cell-mediated immunity. The terms "Swiss type lymphopenic agammaglobulinemia," an autosomal-recessive form of disease, and "x-linked lymphopenic agammaglobu­linemia" have been used to describe this disorder, which, as the names imply can follow either mode of inheritance.


The exact cause of SCID is unknown. The theories include (1) a defective stem cell that is incapable of differentiating into B- or T-cells, (2) defective organs responsible for the differentiating process, primarily the thymus and lymphoid complex, or (3) an enzymatic defect that supresses lymphocytic cell function.

The consequence of the immunodeficiency is an overwhelming susceptibility to infection and to the graft reaction. The latter occurs when any histoincompatible tissue from an immunocompetent donor is infused into the immunodeficient recipient. Because of its immunodeficiency, the body is unable to reject the foreign incompatible tissue. Therefore, the antigenic donor cells attack the host's tissues. The graft-host reaction is a serious complication in the only known treatment for SCID, bone marrow transplant.

^ Clinical manifestations

Obviously the most common manifestation is susceptibility to infection early in life, most often by 3 months of age when maternal immunity is low. Specifically the disorder in children is characterized by chronic infection, failure to completely recover from an infection, frequent reinfection, and infection with unusual agents. In addition, the history reveals no logical source of infection. Failure to thrive is a consequence of the persistent illnesses.

If the child should receive a foreign tissue, such as blood supplements, signs of graft-vs-host reaction, such as fever, skin rash, alopecia, hepatosplenomegaly, and diarrhea, are expected. Since the reaction requires 7 to 20 days for tissue damage to become evident, the symptoms may be mistaken for an infection. However, the presence of a graft-vs-host reaction increases the child's susceptibility to overwhelming infection and, therefore, is a grave complication.

^ Diagnostic evaluation

Diagnosis is usually based on a history of recurrent, severe infections from early infancy, a familial history of the disorder, and specific laboratory findings, which include lymphopenia, lack of lymphocyte response to antigens, and absence of plasma cells in the bone marrow. Documentation of immunoglobulin deficiency is difficult during infancy because of the normally delayed response of the infant to produce his own immunoglobulins and maternal transfer of im­munoglobulin G.

^ Therapeutic management

The only definitive treatment is a histocompatible bone marrow transplant. The perfect donor is an identical twin because the human lymphocyte antigens (HLA) are exactly the same. The second best choice is a sibling. The procedure consists of aspirating several samples of bone marrow from the donor and infusing the marrow intravenously into the host. However, bone marrow transplants are usually done at medical centers where measures to control posttransplantation infection, such as a sterile environment, and other specialized facilities are available. Since the host's immunologic system is incompetent, graft inejection is not a problem. However, a graft-vs-host reaction is always a possibility in a nonidentical twin graft, and once it occurs, little can be done to reverse the process.

Other approaches to SCID are providing passive immunity with lrntnune globulin and maintaining the child in a sterile environment.

The latter is effective if instituted before the existence of any infectious process in the infant. Other investigational transplant procedures include nonidentical HLA bone marrow grafts and fetal liver or thymus transplants. However, the results are still uncertain, although they provide potential hope for future children born with the disorder.

Nursing considerations

Since the prognosis for SCID is very poor if a compatible bone marrow donor is not available, nursing care is directed at supporting the family in caring for a fatally ill child. Genetic counseling is essential because of the modes of transmission in either form of the disorder. Nursing goals are directed at helping parents prevent sources of infection in the child, such as cautious isolation from crowded facilities and individuals with active infection, meticulous skin and mouth care, good general nutrition, and careful supervision during periods of activity to prevent skin trauma. However, even with exacting environmental control, these children are prone to opportunistic infection. Chronic fungal infections of the mouth and nails with Candida albicans are frequent problems despite vigorous efforts at prevention or treatment. A hoarse voice may result from repeated esophageal and vocal cord eroisons from the fungus. It is important to stress to parents that such conditions are not a result of laxity on their part in preventing them but are the result of the severe immunologic disorder. Parents should be encouraged to immediately notify a physician regarding any evidence of a worsening infection.

Children who receive frequent injections of immune serum globulin (ISG, or IG) need support during the procedure because the injections are painful. Infants are best comforted by their parents, but toddlers and preschoolers may benefit from needle play. Immune globulin is injected deeply into a large muscle mass, usually the vastus lateralis. To prevent tissue damage and provide maximum absorption, the total amount may be divided into two injections and given in two different sites. A record is kept of the sites to ensure a rotating schedule for future injections. An intravenous preparation of ISG (intravenous modified ISG [MISG]) is available that reportedly is more effective and causes less distress.

A rare complication of long-term ISG administration is mercury toxicity (acrodynia, or pink disease) caused by a mercury-containing bacteriostatic agent in the commercial preparation. Nurses working vvith these paftients should be aware of signs of this unusual reaction, including pink, scaling, pruritic palms and soles, photophobia, sweating, irritability, and insomnia.

Care of the child undergoing bone marrow transplantation is mainly directed at preventing infection. Because it takes 7 t& 20 days before evidence of bone marrow functioning becomes evident, hospitalization is long. It is not the purpose of this discussion to detail the care of the child with a bone marrow transplant because of the specialized care involved, except to emphasize that the psychologic needs of the parents and child are tremendous. For the parents it represents the last hope for successful therapy and survival. For the child it means sensory deprivation because of isolation, numerous blood tests, and the possibility of more pain and suffering if a graft-vs-host reaction occurs. To meet these needs, a sensitive, consistent team of nurses who function effectively as members of the total health team is essential.


The Wiskott-Aldrich syndrome is an X-linked recessive disorder characterized by a triad of abnormalities: thrombocytopenia, eczema, and immunodeficiency of selective functions of B- and T-lymphocytes.


The exact defect is unknown, although recent evidence suggests a basic hematopoietic cell abnormality specifically elated to cell energy metabolism. A variety of pathologic findings are evident. The platelets are abnormally small in size and have a shortened life span, possibly because of a metabolic defect in their synthesis. The primary immunologic defect consists of the inability of phagocytes (macrophages) to process foreign antigens, particularly polysaccharides such as pneumococcus. As a result, immunologically competent cells fail to produce normal immunoglobulin patterns. Early in life the immuno­globulin levels may be normal, but later low levels of lgM are observed. Typically isohemagglutinins (anti-A and anti-B agglutinins in the blood) are decreased or absent.

The thymus and lymph nodes are normal at birth but become progressively dysfunctional with age until a profound cellular immunodeficiency results. Consequently these children are highly susceptible to infection and malignancy, especially of the lymphoreticular system.

Clinical manifestations

At birth the major effect of the disorder is bleeding because of the thrombocytopenia. As the child grows older, recurrent infection and eczema become more severe and the bleeding becomes less frequent.

Eczema is typical of the allergic type and readily becomes superinfected. Chronic infection with herpes simplex is a frequent problem and may lead to chronic keratitis of the eye with loss of vision. From infection, chronic pulmonary disease, sinusitis, and otitis media result. In those children who survive the bleeding episodes and overwhelming infections, malignancy presents an additional risk to survival.

Diagnostic evaluation

Diagnosis can usually be made during the neonatal period because of the thrombocytopenia. Specific tests for immunologic function confirm the diagnosis. Carrier detection is also possible.

Therapeutic management

Medical treatment mainly involves (1) counteracting the bleeding tendencies with platetet transfusions, (2) using immune globulin to provide passive immunity, and (3) administering prophylactic antibiotics to prevent and control infection. Bone marrow transplants have been attempted but, even if successful, do not reverse all the defects of this disorder. Overall median survival is only to 6.5 years of age, with death most often resulting from infection (pneumonia or sepsis) or bleeding.

Nursing considerations

Because of the grave prognosis for these children, the main nursing consideration is "supporting the family in the care of a fatally ill child. Physical care is directed at controlling the problems imposed by the disorder - control bleeding, preventing or controlling infection, treat eczema.

The genetic implications of this X-linked recessive disorder differ little from those of hemophilia. However, because of the multiplicity of defects, the emotional adjustment and physical care required for these children are greater than those of many other conditions. The nurse can be especially supportive by providing short-term goals during Periods of hospitalization and by focusing on long-range needs through coordinated efforts with a public health nurse.


One of the most dramatic advances in pediatrics has been the decline of infectious diseases over the past 30 years because of the widespread use of immunization for preventable diseases. Although many of the presently available immunizations can be given to individuals of any age, the recommended primary schedule begins during infancy and, with the exception of boosters, is completed during early childhood. Therefore, the discussion of childhood immunizations for diptheria, tetanus, pertussis, polio, measles, mumps, and rubella is included under health promotion during the first year.

In order to facilitate one's understanding of immunization, the following terms are defined for reference throughout the next section:

• immunity: an inherited or acquired status in which an individual is resistant to the occurrence or the effects of a specific disease, particularly an infectious agent.

• natural immunity Innate immunity or resistance to infection

or toxicity.

• acquired immunity: immunity from exposure to the invading agent, either bacteria, virus, or toxins.

• active immunity: individual actively forms immune bodies against specific antigens, either naturally by his having had the disease clinically or subclinically or articifically by the introduction of an antigen (vaccine) into the individual.

• passive immunity: temporary immunity by transfusing plasma proteins either artificially from another human or an animal that has been actively immunized against an antigen or naturally from the mother to the fetus via the placenta.

• antibody: a protein found mostly in serum that is formed in response to exposure to a specific antigen.

• antigen: a variety of foreign substances, including bacteria, viruses, toxins, and foreign proteins that stimulate the formation of antibodies.

• antitoxin: antibody formed in response to a toxin (antigen): a poisonous substance usually produced by the invading microorganism.

• toxoid: a toxin that has been treated to destroy its toxic properties but retain its antigenic quality.

• vaccine: collectively a term to denote any type of active, immunization, such as toxoids or attenuated live viruses, specifically a suspension of disease-causing bacteria or viruses that acts like an antigen, stimulates antibody production, and produces active acquired immunity.

• attenuate: reduction of the virulence (infectiousness) of a pathogenic microorganism by such measures as treating it with heat, chemicals, or cultivating it on a certain media

Immunodeficient conditions, or deficiency of immune response, include a wide group of independent diseases (nosologic forms) and concomitant syndromes with such common signs as deficiency of the immune system, inability of an organism to resist an alien antigens' agression.

Primary immunodeficient conditions. Classification of primary immunodeficient conditions

1. Prevalence of antibodies deficiency:

a) sex-linked agammaglobulinemia;

b) sex-linked agammaglobulinemia and growth hormone deficiency;

c) autosomal recessive agammaglobulinemia;

d) selective immunoglobulin deficiency:

- with elevated level of IgM and IgD;

- IgA deficiency.

e) selective -deficiency of other isotypes of Ig;

f) kappa-chains deficiency;

g) immunodeficiency on the background of thymoma;

h) transitory hypogammaglobulinemia in children.

2. Combined immunodeficiency: a) total variable immune deficiency:

- with primary antibody deficiency;

- with primary deficiency of cellular immunity.

b) severe combined immunologic deficiency:

- reticular dysgenesis;

- deficiency of T- and B-lymphocytes (earlier the Swiss of IDC).

c) T-lymphocyte deficiency (earlier Nezelof syndrome);

d) adenosindeaminase deficiency;

e) purine-nucleotide-phosphorylase deficiency;

f) absence of HLA-antigens of the 1st class (syndrome of "naked" lymphocytes);

g) absence of HLA-antigens of the 2nd class.

3. Immunodeficiency in combination with other congenital defects:

a) Wiscott-Aldrich syndrome;

b) ataxia-telangiectasia (Louis-Bar, syndrome);

c) syndrome of 3nd-4th pockets of branchial arch (Di George syndrome);

d) transcobalamin-2 deficiency;

e) immunodeficiency due to congenital anomalous reaction at Epstein-Barr virus.

^ Diagnostic criteria


A. Suggestive T-cell deficit:

a) systemic illness following vaccination with any alive virus or BCG;

b) unusual life-threatening complication following infection caused by ordinary benign viruses (e.g., giant rubella pneumonia; varicella pneumonia);

c) chronic oral candidiasis after 6 months of life;

d) chronic mucocutaneous candidiasis;

e) fine, thin hair, short-limbed dwarfism with characteristic radiographic features of cartilage-hair hypoplasia (CHH);

f) intrauterine graft-versus-host disease - the most characteristic feature is scaly erythroderma and total alopecia (absence of eyebrows is quite striking);

g) graft-versus-host disease after blood transfusion;

h) hypocalcemia in newborn (Di George anomaly, especially with characteristic faces, ears and cardiac lesions);

i) small (less than 10 mm in diameter) lymphocytes count persistently less than 1500/mm3, must rule out gastrointestinal loss of them or loss from the lymphatic vessels.

B, Suggestive B-cell defect

a) recurrent proved bacterial pneumonia, sepsis or meningitis;

b) nodular lymphoid hyperplasia

C. Suggestive B- and T-cell deficiency (combined immunodeficienj; disease - CID)

a) all the above mentioned features except chronic mucocutaneous candidiasis and nodular lymphoid hyperplasia;

b) features of Wiskott-Aldrich syndrome (draining ears, trombocytopenia and eczema);

c) features of ataxia-telangiectasia.

P. Suggestive immunodeficiency without clearly implicat T- or B-cell defect

a) Pneumocystis carinii pneumonia;

b) intractable eczema;

c) ulcerative colitis in infants less than 1 year old;

d) intractable diarrhea;

e) unexplained hematological deficiency (RBC, WBC, platelet);

f) severe generalized seborrheal dermatitis (Leiner's disease) suggests C5 deficiency; seborrhea is common in combined immunodeficient disease;

g) recurrent pyogenic infections seen in C3 deficiency.

E. Suggestive biochemical defect

a) features of combined immunodeficiency with characteristic bony lesions (adenosine deaminase deficiency);

b) features of Blackfan-Diamond aplastic anemia (nucleoside phosphorylase deficiency).

F. Suggestive abnormality of polymorphonuclear leukocytes

a) primary skin infections (if associated with asthma, eczema and coarse faces, think of Buckley syndrome);

b) chronic osteomyelitis caused by Klebsiella or Serratia species, draining lymph nodes (chronic granulomatous disease).

G. Suggestive secondary deficiency

a) concomitant or preceding viral infection;

b) lymphoid malignancy (chronic lymphatic leukemia, Hodgkin s disease, myeloma).


a) genealogical anamnesis;

b) common blood analysis (not only total but absolute quantity of different leukocytes);

c) investigation of numeral link of immunity:

- gammaglobulin concentration;

- immune serum globulins by Manchini;

- Immunoelectrophoresis of serum proteins

- tilers of different antibodies, blood group, liter of isohernagglu-tinins;

- secretory immunoglobulins;

- surface immunoglobulins of antiserum lymphocytes feiarked with fluoroscein;

- EAC-rosellas.

d) investigation of cellular link of immunity:

- E-rosellas;

- reaction of blast transformation (in unspecific stimulation with FHA, in stimulation with antigens, in mixed lymphocyts culture);

- depression of macrophages migration;

- reaction of hypersensitivity of a delayed type (intracuta­neous tests with 2,4-dinitroftorbenzol, streptokinase, odoriase, antigen; Shieck's reaction).

e) special investigations:

- functions of T-helpers and T-suppressors;

- hystochemical determination of adenosine-deaminase's activity;

- transcobalamin's content.

0 X-ray of the chest including side positions and tomo-gram of mediastinum for revealing the thymus;

g) biopsy of the lymph nodes with the use of hystotogical and hystochemical methods;

h) investigation of complement's system (total complement, its Actors);

i) investigation of phagocytosis function (opsonization bacteria's killing, a test with blue tetrazolium, cytochemical methods of termination of enzyme's activity etc.)

^ Acquired immunodeficiency syndrome (AIDS)

AIDS is caused by human immunodeficiency virus (HIV) of type 1 (HIV-l). HIV-1 infects CD4+ T-lymphocytes predominantly Depletion of CD4+ lymphocytes results in immunodeficiency.

The clinical picture of AIDS is the final phase of HIV infection and its manifestation, with a wide spectrum of clinical disorders. The majority of them is nonspecific.

^ Clinical manifestations of HIV infection in children



Persisting generalized lymphadenopathy

One or more nodes have size more than 1 cm and exist longer than 1 month (especially substantial is enlargement of auxiliary lymph nodes)

Persisting hepatome­galy

Enlargement of the liver, registered for 3 months and more

Persisting splenom­egaly

Enlargement of the spleen, registered for 3 months and more

Persisting diarrhea

Stool is three times a day for more than 1 month


t = 38 °C for 4 weeks and more, 2 and more episodes of fever of obscure nature

Persisting enlargement of salivary glands

For 3 months and more


Amount of thrombocytes is less than 100 000 per ml twice and more times

Serious bacterial infec­tions

2 and more episodes of exacerbation or chronization of an infection (for more than 3 days in spite of the treatment)

Retardation of develop­ment

Progressing hypotrophy, encephalopathy

Persisting or recurring oral candidiasis

It lasts for 2 months and more or relapses after the course of treatment


Signs of heart insufficiency


Nephrotic syndrome (proteinuria, hypoalbuminemia)

Children with HIV infection present to the ED with a wide spectrum of initial presentations and associated complications. Many who live in chaotic social environments use the ED as their primary source of medical care. The typical case of pediatric HIV infection is a child born to a mother at risk who develops recurrent bacterial infections, thrush, failure to thrive, lymphadenopathy, and hepatosplenomegaly in the first few years of life. However, both those who acquire HIV perinatally and those who acquire infection by transfusion may not present with symptoms until several years of age.


The types of infections are similar to those in patients with hypogammaglobulinemia. Infections with the encapsulated organisms, Haemophilus influenzae type B, Streptococcus pneumoniae, and enteric gram-negative rods are common and can cause chronic or recurrent otitis media, pneumonia, lymphadenitis, bacteremia, mastoiditis, and meningitis. Malignant external otitis, a disease usually seen in older patients, also occurs. Other common conditions include dermatitis, particularly eczema; in those patients Staphylococcus aureus also an important pathogen. Salmonella infections can be quite severe and may cause prolonged gastroenteritis or bacteremia; frequent relapses may occur. Many of the usual childhood infections are seen in HIV-infected patients, but they may present in a more severe form. Oral candidiasis (thrush) is extremely common, particularly in infancy. HIV-infected patients often have extensive thrush, in the absence of previous antibiotic therapy. Infection may extend to the esophagus or the larynx and is resistant to the "usual forms of therapy. Viral diseases such as herpes simplex, varicella, and measles can be quite aggres­sive in HIV-infected children. Herpes simplex may cause prolonged °r recurrent ulcerations and varicella may disseminate to cause pneumonia.

A unique feature in pediatric HIV infection is the development °f parotitis. This can be chronic, with slow progressive, painless growth, or it can be acute, xiated with rapid enlargement, fever, and pain. The etiology is unknown.


Pulmonary infection is a common and serious manifestation of infection. The most commonly diagnosed infection is Pneumocystis carinii pneumonia (PCP), which can present acutely with respiratory distress or with a history of progressive cough and respiratory symptoms over days to weeks. Clinically, it may be difficult to distinguish PCP from more typical causes of childhood pneumonia. The chest X-ray typically shows a diffuse interstitial pneumonitis, although almost every pattern of infiltrate has been seen with PCP. A second common pneumonitis is lymphoid interstitial pneumonitis (LIP); the cause is unknown. Children with LIP often have a longstanding history of pulmonary symptoms, particularly cough. They are usually not febrile or acutely dyspneic, and rarely have significant auscultatory findings. A concomitant infection can cause a child with pre-existing LIP to present acutely. LIP is most often seen in children with other lymphoproliferative manifestations of HIV such as lymphadenopathy and parotitis; these patients may have signs of chronic pulmonary disease such as clubbing. The chest X-ray shows a diffuse interstitial infiltrate similar to that seen with PCP, but in some longstanding cases there may be a diffuse nodular pattern with widening of the superior mediastinum and hilus. LIP is currently a diagnosis of exclusion.

In addition to PCP and LIP, other routine and opportunistic infections must be considered in an HIV-infected child with respiratory distress. Bacterial pathogens are frequent. Another common pathogen is respiratory syncytial virus (RSV), an extremely common viral infection in young infants and children, which can cause giant cell pneumonia in the compromised host. Cytomegalovirus can be cultured from the lung in these patients, although it is not always clear that it is the primary pathogen. Other opportunistic pulmonary infections are also in the differential diagnosis, including atypical mycobacteria and fungi.

CENTRAL NERVOUS SYSTEM DISORDERS CNS disorders are a prominent part of the clinical spectrum of HIV infection in children. Encephalopathy, either static or progressive, is often noted. Manifestations often include acquired microcephaly, progressive motor dysfunction, loss of developmental milestones, ataxia, and extrapyramidal rigidity. Isolated seizures are unusual but may occur with a concomitant febrile illness. Focal neurologic signs are uncommon in pediatric AIDS and should suggest possible CNS lymphoma. Opportunistic infections, particularly cryptococcal menin­gitis, may be present in the child with CNS symptoms. However, in ixiost series of children dying with HIV encephalopathy, opportunistic infection of the CNS is rare, and most signs and symptoms are secondary to HIV infection of the nervous system.


Gl illnesses, especially diarrhea, are a major problem for HIV-infected patients. Salmonella can be a persistent problem, particularly in patients with blood or mucus in the stool. Severe or prolonged diarrhea in pediatric AIDS patients also occurs with parasitic enteric pathogens, most notably Glardia lamblia, and Cryptosporidium. In some instances, even after extensive evaluation, no specific etiology can be found to account for the diarrhea.

Clinical Evaluation and Ancillary Data Use an aggressive diagnostic approach, because many of the acute illnesses are treatable. For example, a child with HIV infection who presents with fever is quite likely to have a bacterial infection; obtain a complete blood count (CBC), blood culture, urinalysis, and chest X-ray if there is no obvious source of fever on examination. Other imaging studies such as sinus films may be indicated. If the child has a history of neutropenia or is receiving azidothyrnidine (AZT), the absolute neutrophil count may be depressed, which would influence therapeutic decisions. The new onset of pulmonary symptoms requires a thorough evaluation. Although many of these patients may not have an easily treated form of pulmonary disease, early therapy is important Because it is difficult to differentiate clinically the common forms of pneumonia in pediatric AIDS patients, hospitalization is often required. In such patients, the initial diagnostic tests include chest X-ray, WBC count, blood culture, and, in the appropriate epidemiologic setting, nasopharyngeal swabs for immunofluorescence or culture.

Weight loss and diarrhea may be acute or chronic and are often quite severe. In addition to routine bacterial culture, obtain stool for ova and parasites. Assess the patient's state of hydration clinically and measure serum electrolytes, blood urea nitrogen, and creatinine, since enormous fluid losses and profound electrolyte imbalances are sometimes present. CNS symptoms and physical signs will determine whether lumbar puncture or scanning is appropriate. If a spinal tap is performed, obtain more fluid than necessary to diagnose bacterial meningitis, because additional tests are often indicated, such as a culture for acid-fast organisms, viral culture, and cryptococcal antigen. If focal neurologic signs apt present arrange for a CT scan to evaluate for lymphoma or toxoplasmosis.

Treatment and Disposition

The treatment plan and the decision to hospitalize the patient must be made in conjunction with the family; many families want aggressive diagnostic and therapeutic plans, while others may prefer to keep medical intervention limited, with the goal of making the patient comfortable.

Consider hospitalizing HIV-infected patients with fever without a focus of infection, recent onset of pulmonary or CNS manifestations, or severe failure to thrive or diarrheal disease.

Patients who are not acutely ill and do not require hospitalization may require antibiotic therapy. If a focal infection is identified, such a sinusitis or otitis media, and there is no evidence of bacteremia, the patient can ordinarily be managed as an outpatient. However, a longer duration of therapy is required; for example, treat sinusitis for a minimum of 3 weeks.

In cases of possible bacteremia, the antimicrobials must be effective against the encapsulated organisms and the enteric gram-negative rods.

For any HIV-infected patient who does not require hospitalization, arrange for the necessary follow-up of the acute problem with the primary physician and make appropriate referrals for long-term management. Because of the chronic and complex nature of pediatric HIV infection, non-urgent problems are best handled in the calmer, more familiar outpatient office or clinic, not the ED.

Isolation techniques are based upon the mode of transmission of the disease.


A report of certain communicable diseases must be filed with the city health department upon the admission of the child Personnel giving direct care to the child with a communicable disease should seek protection when immunization measures are available. Frequent handwashing is essential.

Isolation Gowns

When isolation gowns are used, a fresh gown should be used for each patient contact Organization of activities is essential for the economical use of supplies.

Isolation Masks

If a mask is used, it should cover both the nose and the mouth, be worn no longer than 30 minutes, and be discarded immediately after use.

Disposal of Wastes

Paper bags for the disposal of tissues should be available within the unit. All contaminated waste should be wrapped securely and discarded in a special receptacle marked "isolation."

Bedpans may be emptied into the community sewage system, using the bedpan flusher. The flusher should be handled with paper barriers. Waste cans should be lined with paper and kept covered.

All reusable equipment should be cleaned, wrapped, labeled "isolation," and sterilized before routine reprocessing. Infusion bottles should be discarded after use

Care of Dishes

Disposable dishes maybe requested through the dietary department. If regular dishes are used, they should be returned to the kitchen for processing in the dishwashing machine. Formula bottles should be washed and returned to the reception area of the formula kitchen.


Care of Linen

All used linen should be placed in a special laundry bag and labeled. Diapers should be placed in a covered receptacle Laundry bags should be closed, tied, and labeled "isolation."

Laundry bags which have been contaminated on the outside should be placed in a separate, clean bag. The technique for doing this is:

1. Have a "clean" nurse hold the clean bag with the top cuffed over her hands.

2. The "contaminated" nurse places the full bag into the clean bag. 3 The "clean" nurse then ties and labels the bag for pickup by laundry personnel.

Use of Clean Equipment in a Contaminated Area

A stretcher may be protected from contamination by covering the stretcher pad with a sheet and folding the sheet over the child.

Stretchers used to transport deceased patients who had a communicable disease should be washed and aired before reuse.



Make a general conclusion on a theme of a class №1 and conducted practical work.



Situation tasks.


1. Nursing care of Infants and Children / editor Lucille F. Whaley and I. Wong. Donna L. - 2nd ed. - The C.V. Mosby Company. - 1983. - 1680 p.

2. Nykytyuk S.O. et al. Manual of Propaedeutic Pediatrics. – Ternopil: TSMU, 2005. – P. 6-22.

3. Pediatric Nurse Practitioner Certification Review Guide / editor, Virgina layng Milloing: contributing authors, Ellen Rudy Clore and all. - 2nd ed. - Health Leadership Associates,Inc.,1994. - 628 p.

4. Nelson Textbook of Pediatrics / edited by Richard E. Behrman, Robert M. Kliegman, Ann M. Arvin; senior editor, Waldo E. Nelson - 15th ed. - W.B.Saunders Company, 1996. - 2200 p.

5. Whaley L.F., Wong D.L.: Nursing care of infants and children, St. Louis, Toronto, London, 1983.


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