MaternalChild Ch 18 Immunologic Infections

Germs, including bacteria and viruses, are foreign invaders, or

antigens

Antigens

which the immune system recognizes and responds to by producing proteins called antibodies to fight them

Antibodies

fight the antigens

Memory cells

are cells that recall the original antigen and bring up the body’s defenses if it invades the body again, and this level of protection is known as immunity

Leukocytes are produced or stored in the

lymphoid organs: lymph nodes, bone marrow, thymus, spleen, and tonsils

Mature B lymphocytes

independently identify foreign antigens and differentiate into antibody-producing plasma cells (memory cells). Once they have produced antibodies, these antibodies remember the invader so if the same antigen is presented to the immune system again, the antibodies can respond

Innate (natural) immunity

is a general protection and includes the physical barriers of the body, like the skin and mucous membranes

Adaptive (or active) immunity

develops as children are exposed to diseases or immunized against diseases through vaccination

Passive immunity

is acquired by the introduction of preformed antibodies into an unprotected individual, and it lasts for a short period of time

What type of immunity can occur from antibodies that pass from the mother to the fetus through the placenta or newborns that acquire immunity through breastfeeding?

passive

Immune response

The body’s second line of defense

The skin

is the first line of defense in preventing diseases from entering the body

regulates body temp, prevents water loss, helps produce vitamin D

IgM

is the first type of antibody made by the body in response to an infection. This antibody helps other immune system cells destroy foreign substances

IgG

antibodies are important in fighting bacterial and viral infections; most common

IgA

antibodies protect the body’s surface from foreign substances

IgE

causes the body to react against foreign substances such as fungus spores, animal dander, and pollen, allergic reactions

Why children are more vulnerable to infections

Children have thinner skin that can more easily become irritated and absorb microorganisms.

Children younger than 5 have less resistance to infectious organisms than older children and adults because of lower levels of immunoglobulin A (IgA).

Children younger than three have more difficulty regulating body temperature than older children and adults because of immature endocrine (sweat) glands.

Largest organ in the body

the skin

Mechanical barriers

tears, urine vaginal secretions, semen

Chemical barriers

acidic secretions of the stomach and digestive enzymes that serve to neutralize organisms taken into the body through the mouth. Chemical barriers in the gastrointestinal (GI) system can be maintained with good nutrition

Antibody Deficiency: B-Cell Disorders

inadequate immunoglobulins are present. Maternal antibodies naturally protect newborns during the first few months of life; thus B-cell disorders do not become apparent until after 3 to 6 months of age, and some do not occur until later childhood or adulthood.

In B-cell disorders, the child usually has recurrent infections, beginning with respiratory infections, sinus infections, and pneumonia.

Some children have chronic GI malabsorption syndromes and inflammatory bowel disease (Crohn’s disease and ulcerative colitis)

Combined Deficiency T- and B-Cell Disorders

Diseases affecting B and T lymphocytes usually manifest before 6 months of age. Babies may have failure to thrive and suffer from severe infections, including septicemia and meningitis.

Other features of this disorder cluster include recurrent candidiasis and prolonged diarrhea, both of which may cause severe diaper dermatitis.

In these disorders, opportunistic infections caused by Pneumocystis jiroveci pneumonia and Toxoplasma gondii are seen

Phagocyte Defect Disorders

These disorders also can occur very early in a child’s life. They are manifested with dermatitis, impetigo, mouth ulcers, pneumonia, suppurative adenitis (infected lymph nodes), abscesses, and osteomyelitis. Wounds in children with this immune disorder do not heal properly

Complement Defect Disorders

This group of disorders can arrive at any age in childhood. Severe infections including meningitis, septicemia, and sinus or pulmonary infections are common.

Associated autoimmune disorders may occur, including systemic lupus erythematosus, dermatomyositis, and scleroderma

Other Congenital Immunodeficiency Disorders

X-linked agammaglobulinemia

The onset occurs after 4 months of age, typically in males with low or absent IgM, IgG, and IgA antibodies and B lymphocytes.

“Low or no b cells and antibodies”

Treatment of these congenital immunodeficiency disorders is lifelong with the administration of intravenous immune globulin (IVIG) or (IV IgG)

Wiskott-Aldrich syndrome*

an X-linked immunodeficiency syndrome occurring from genetic mutation but only occurring in males.

This disorder includes thrombocytopenia and eczema, so the symptoms include potential bloody diarrhea, cerebral hemorrhage, and later malignancies and autoimmune syndromes

Wiskott-Aldrich diagnosis

leukemia and idiopathic thrombocytopenic purpura (ITP)

Wiskott-Aldrich treatment

includes antibiotic prophylaxis with trimethoprim sulfamethoxazole (Bactrim or Septra) for Pneumocystis jiroveci pneumonia and IgG replacement therapy.

Splenectomy is a possibility to decrease thrombocytopenia, and stem cell transplant can offer a cure

Modell’s 10 Warning Signs of Primary Immunodeficiency*

Eight or more ear infections per year

Two or more serious sinus infections per year

Two or more months on antibiotics with little effect

Two or more pneumonias within 1 year

Failure of infant to gain weight or grow normally

Recurrent, deep skin or organ abscesses

Persistent thrush in the mouth or on the skin after 1 year of age

Need for IV antibiotics to clear infections

Two or more deep-seated infections

Family history of primary immunodeficiency

Most primary or congenital immunodeficiency disorders are __, but good prenatal care and education regarding care can decrease the associated clinical manifestations

genetic and not preventable

Lab tests for congenital immunodeficiency disorders

CBC) with differential, immunoglobulin levels (IgA, IgG, IgM), T and B lymphocyte tests, and protein electrophoresis is drawn to determine types of immunoglobulin disorders.

Additionally, pre- and postimmunization titers for routine immunizations (tetanus, diphtheria, mumps, and rubella) are drawn

May not be considered safe for kids with congenital immunodeficiency disorders*

live vaccines; or the sibling may not receive live vaccines as well

Nursing education for kids with congenital immunodeficiency disorders

continued monitoring of growth and development on standardized growth charts is done to assess for failure to thrive or weight loss patterns

need early detection

HUMAN IMMUNODEFICIENCY VIRUS (HIV [AIDS])

Attacks and destroys the immune system by targeting the CD4 (helper T cells)

Opportunistic infections

infect the body when the immune system us weak

When CD4 levels drop, symptoms begin to appear and the change from

HIV to AIDS begins

Infant HIV risk factors

Advanced maternal disease, High maternal viral load, Low maternal CD4+ count

Prematurity

In utero transmission

High viral load in the first 2 months of life

Lack of neutralizing antibodies

Presence of p24 antigen

AIDS-defining illnesses

Early cytomegalovirus infection

Early neurological disease

Mycobacterium avium complex and anemia

Failure to thrive

Early-onset diarrhea

Signs of HIV in children

Lymphadenopathy (enlarged painful lymph nodes)

Hepatosplenomegaly and hepatitis

Chronic diarrhea, with malabsorption

Failure to thrive

Oral thrush

Skin infections

Fevers

Recurrent infections, including mucous membrane and skin infections

Thrombocytopenia

Developmental delay and loss of milestone achievements

Pancytopenia

an issue for children with HIV that may cause thrombocytopenia (low platelet count)

Epoetin alfa (Erythropoietin)

a newer medication that increases RBC and WBC production in cases of WBC abnormalities also, including neutropenia, leukopenia, and lymphopenia

Can result from pancytopenia

Cardiomyopathy

Nephropathy

In kids older than 13*

HIV antibody testing is the same as for adults, using the enzyme-linked immunosorbent assay (ELISA) test that identifies the presence of HIV antibodies.

If the initial ELISA antibody test is positive, it merits repeating, and if the repeat test is still positive, it is necessary to add the Western blot test, which is a confirmatory indirect fluorescent antibody test

Other ways to test for HIV for kids older than 13

They include an oral fluid (not saliva) antibody test that needs a confirmatory Western blot, a urine test that needs a confirmatory Western blot, a rapid test that uses blood from a finger stick or oral fluid, and home testing kits.

Only one kit, Home Access HIV Test System, using a finger prick, is approved by the Food and Drug Administration

Pneumocystis jiroveci pneumonia

is the most common opportunistic infection in children

Caring for children with HIV or AIDS - infections

The nurse must be ready to manage these infections, often with prompt and vigorous antimicrobial therapy, all infants born to HIV-infected mothers are routinely started on a prophylactic antibiotic regimen for this organism.

Trimethoprim sulfamethoxazole (Bactrim or Septra) is the agent of choice for this treatment. Intravenous immune globulin (IVIG) has also been used to prevent bacterial infections in young children.

In addition, the nurse teaches the family signs and symptoms of infection and encourages them to limit the child’s exposure to large crowds of people and to those with notable infections

An antibiotic used for prophylaxis and treatment of infection is TMP-SMZ (Bactrim or Septra)

used in the prevention of Pneumocystis jiroveci pneumonia; major toxicities are thrombocytopenia and neutropenia

can result in Stevens-Johnson syndrome, a potentially fatal syndrome

Stevens-Johnson syndrome

begins with high fever, sore throat, cough, arthralgias, vomiting, and diarrhea. Next, erythematous macules begin to spread from head and neck down to the trunk. These may develop into hemorrhagic blisters and even involve the mucosa of the nose, mouth, and eyes.

Associated disorders include GI bleeding, renal problems, sepsis, pneumonitis, and ophthalmological issues

Children with Stevens-Johnson syndrome must be

admitted rapidly to the pediatric intensive care unit for wound care, hydration, electrolyte issues, pain management, and nutritional assistance. IVIG is the treatment of choice for this sometimes-fatal reaction

HIV nursing care

watch for s/s of infection, manage pain, support nutrition growth and development, monitor when patient receives vaccinations

HIV education

large crowds and sick people

stay consistent with medications

learn to recognize and look for symptoms of illness

get plenty of rest

HIV pain

results from inflammation or from systemic manifestation of AIDS such as cardiomyopathy, drug toxicities, invasive secondary infections, and medical procedures used to monitor and treat the HIV infection

HIV and nutrition

monitor for chronic diarrhea, GI symptoms

Obesity occurs as a result of side effects from some of the medications commonly used to treat HIV coupled with decreased physical activity

Oral supplementation is recommended to proactively meet nutritional goals of underweight children

Causes of HIV chronic diarrhea include

Mycobacterium avium-intracellulare, Giardia, and Cryptosporidium

Live vaccines in HIV + children

now children can receive these vaccinations if their immunity is good, depending on their CD4 counts (T-cell counts)

HAART

as become the cornerstone of medical treatment for HIV. Although these regimens keep changing as new drugs are created, currently, combining at least three drugs from two different classes is recommended

Systemic Lupus Erythematosus

a multisystem chronic autoimmune disorder of the blood vessels and connective tissue. The basic pathophysiology of SLE includes autoantibodies that attach to the body proteins, creating antigen-antibody complexes. These antigen-antibody complexes are then deposited throughout the body, causing widespread tissue damage. The exact cause of SLE is unknown, although it is tied to genetic predisposition coupled with unidentified trigger(s) that cause the disease to activate

Systemic Lupus Erythematosus triggers

estrogen, infections, sunlight, ultraviolet light, pregnancy, and certain drugs

Lupus s/s

Fever

Malaise

Chills

Fatigue

Weight loss

As the disease progresses, symptoms may include a characteristic malar photosensitive rash (butterfly rash on the face); arthritis; photosensitivity; serositis; proteinuria; immunological and hematological disorders such as hemolytic anemia, lymphocytopenia, thrombocytopenia, and vasculitis; and an abnormal antinuclear antibody (ANA)

Lupus diagnosis

include a complete blood cell count with differential, metabolic chemistry panel, urinalysis, ANA, anti-DNA antibody, complement 3 (C3), complement 4 (C4), quantitative immunoglobulins, rapid plasma reagin, lupus anticoagulant, erythrocyte sedimentation rate, cardioreactive protein, and antiphospholipid antibodies.

A negative ANA test excludes SLE diagnosis, while a positive ANA test does not definitively indicate SLE

Spondyloarthropath

Pain at tendon insertions—heel, tibial tubercle; low back pain; sacroiliitis

Enteropathic arthritis; includes Reiter’s syndrome, celiac and inflammatory bowel disease (IBD)-associated arthritis

Uveitis (a form of eye inflammation affecting the uvea, the middle layer of the eye wall), stomatitis (aphthous ulcers in mouth), hepatitis, erythema nodosum

Polyarteritis nodosa: vasculitis, caused by streptococcus, hepatitis B, parvovirus

Fever, painful nodules, purpura, myalgias/arthralgias, hypertension, proteinuria, hematuria, cardiac and CNS disease

Fibromyalgia: chronic pain syndrome

Fatigue, sleep disturbance, headache, musculoskeletal pain, trigger point pain, “fuzzy brain”

Treatment of pain and inflammation in mild SLE is generally accomplished with

nonsteroidal anti-inflammatory medications (NSAIDs)

Antimalarial medications

are also used in mild SLE to control symptoms of arthritis, skin rashes, mouth ulcers, fever, and fatigue

In SLE, Corticosteroids in forms such as

prednisone, prednisolone, or Medrol are highly effective in reducing inflammation and symptoms, although they also have the serious side effect of immunosuppression.

During an exacerbation period, corticosteroids may be initiated in high doses.

After symptoms are under control, the dose is tapered down to the lowest therapeutic level. It is important to tell the parents that steroids must be tapered slowly when it is time to discontinue the medication

Immunosuppressive agents (in SLE)

may also be prescribed if there is a need to avoid corticosteroids. The decision to use immunosuppressives requires serious consideration because of significant side effects, primarily related to general immunosuppression

Examples of immunosuppressive agents used in treatment of SLE

azathioprine (Imuran), cyclophosphamide (Cytoxan), and methotrexate (Rheumatrex).

Each medication has unique and serious risks such as bone marrow depression and hepatotoxicity.

The nurse must reinforce information on the action of the medication as well as the side effects with the parents before administration of this medication

SLE discharge instructions

a balanced diet, low in salt (if the child becomes hypertensive or nephrotic), is encouraged. Rest and exercise include periods when the child is active during remissions and increases rest during exacerbation.

Avoidance of sun exposure is stressed because of the photosensitive rash that occurs with SLE. Use of sunscreen is important and planning outdoor activities in the shade or staying indoors may be necessary.

Because this condition may be difficult for the child and family to cope with and understand, encouraging the expression of feelings or joining a support group is encouraged. Parents should notify teachers, coaches, and others about their child’s condition so they can help monitor the child and obtain necessary treatment if needed.

It is also the nurse’s responsibility to help the child and family identify possible triggers, such as sunlight and emotional stress and assist the family in finding ways to avoid them

Dermatomyositis

a relatively uncommon autoimmune disorder found in children and adults, characterized by muscle weakness and a distinctive rash

no way to prevent it

Dermatomyositis s/s

Proximal muscle weakness, especially in shoulders and pelvis

Heliotropic violaceous (red-purple) rash around eyes and upper eyelids

Possible malar rash similar to SLE, with edema of face and eyes

Tenderness, stiffness of muscles, possible voice change, dysphagia

Dermatomyositis diagnosis

liver function tests (elevated), white blood cell count (elevated), lymphocyte count (depressed), hematocrit (low), albumin (low), creatine kinase (elevated), and erythrocyte sedimentation test (elevated).

Further testing includes electromyelogram testing, muscle biopsy, and MRI of muscles, specifically the quadriceps muscle

Dermatomyositis is treated with

long-term steroid administration. Steroids that are often used include methotrexate (Rheumatrex), cyclosporine (Sandimmune), hydroxychloroquine (Plaquenil), and IVIG when needed

Hypermobility Syndrome

also known as ligamentous laxity and may be a component of what is commonly termed “double-jointedness.”

Hypermobility associated problems

local or widespread pain, chronic fatigue, sleep problems, and early-age degenerative arthritis. Ehlers-Danlos syndrome and Marfan syndrome (elongated extremities and increased risk for aortic aneurysm) are two varieties of hypermobility syndromes.

Potential accompanying disorders include irritable bowel syndrome, mitral valve prolapse, easy bruising, and anemia

Hypermobility s/s

Arthralgias

Intermittent joint pain after exercise

Occasional joint edema after exercise

Criteria to be diagnosed with Hypermobility

(1) hyperextension of knee, (2) palms can be on floor with knees extended, (3) hyperextension of elbow, (4) passive opposition of thumb to flexor surface of forearm, and (5) passive hyperextension of fingers so they are parallel with extensor surface of forearm

Nursing care for Hypermobility

limitations on sports and repeated orthopedic and physical therapy appointments.

The nurse should inform the parents about the possibility of severe pain, poor balance, clumsiness, and early degenerative arthritis.

Nurses should be aware that children with this disorder may need to see physical therapists, occupational therapists, rheumatology physicians, and orthopedists

Anaphylaxis

considered a medical emergency as the most severe allergic reaction possible

Cascade of anaphylaxis

this cascade of events activates the heart, lungs, and vasculature in a detrimental manner, including vasodilation, hypotension, and resultant shock. Histamine can cause coronary artery vasospasm and shorten diastole. Histamine stimulates bronchial smooth muscle contraction, causing bronchospasm. Increased vascular permeability causes laryngeal edema, closing the airway down

Onset of anaphylaxis

food allergies can manifest from 25 minutes after exposure to several hours later. Insect stings and drug allergies cause the most rapid route to anaphylaxis, with an average of 5 to 20 minutes to onset

Anaphylaxis s/s

Wheezing, cyanosis, laryngospasm, nasal congestion

Tachycardia, Hypotension, Vascular collapse and cardiac arrest

Alteration in level of consciousness

Angioedema (swelling around mouth and oropharynx), facial edema

Anxiety, sense of impending doom

Hives and urticaria

Nausea and vomiting, abdominal pain

Diagnosis of anaphylaxis

must involve two body systems

Anaphylaxis basic life support

Basic life support must be initiated with support of airway, breathing, and circulation.

Administration of oxygen and initiation of an IV therapy with a NS solution as soon as possible are standard treatment.

Epinephrine (Adrenalin) injection is administered IM or IV to provide reversal of pulmonary bronchospasm and constriction of blood vessels, thereby improving respiratory status and blood pressure.

Ongoing assessment for shock is necessary and can be treated via IV fluid bolus.

Occasionally, antihistamines and corticosteroids may be added to further control symptoms after the initial stabilization

In case of an allergic reaction

instruct the parent to administer the medication exactly as directed and call 911 immediately

Viral infection

(influenza, common cold viruses, and HIV) are microorganisms that are smaller than bacteria and do not grow without having a living cell as a host. The virus replicates itself in other living cells of people, animals, or plants

Fungal infections

are pathological organisms including yeast and dermatophytes, such as tinea (athlete’s foot and candida yeast infections)

Fungal infections are most likely to occur in children with a compromised immune system

Bacterial infections

are caused by single-celled living microorganisms and include Streptococcus, Staphylococcus, and Escherichia coli

Bacteria can be found everywhere in the environment

Rubella

This disease is highly contagious. It is spread through placenta or nasopharyngeal secretions and fomites

Rubella s/s

mild fever, sore throat, arthralgia, eye pain, GI upset

Lymphadenopathy follows and is noted for the occurrence of postauricular nodes

Other lymph nodes, such as cervical and occipital nodes, can become inflamed

The rash is a fine, light-pink, maculopapular rash on the face then traveling to the chest and entire body

Rubella nursing care

give antipyretics

Isolate the child from others while disease is active, usually for up to 1 week after rash starts

Ruble complications

riskiest complications occur prenatally, in the first trimester to 16th week of pregnancy, and include mental retardation, deafness, eye disorders, cardiac defects, and stillbirth

Postnatal complications include arthritis, ITP, and encephalitis

Rubeola

transmission happens through the respiratory tract via droplets or direct contact with infectious secretions like blood or urine. This disease can also be transmitted via fomites

Infection Control—The incubation period is 8–12 days. Airborne and contact precautions are recommended from 2 days before onset of symptoms until 5 days after appearance of the rash (about 14 days total)

Rubella s/s

moderate fever, cough, coryza, and conjunctivitis

Koplik’s spots appear on the buccal mucosa 2 days before the onset of the rash (blue-white granules on erythematous base)

The rash stage usually lasts about 3–4 days with a rise in fever up to 105°F

The rash first appears on forehead and behind the ears and then spreads to face, trunk, and upper and lower extremities

After 4–7 days rash begins to fade, and the temperature begins to drop

Other common symptoms can include anorexia, malaise, fatigue, and generalized lymphadenopathy

If a child is given aspirin, it can cause

Reye's syndrome

Rubeola nursing care

antipyretics, bedrest, and increased fluids. Ensure the room is dark if photophobia occurs

Watch for complications and superinfections (otitis media and pneumonia)

Rubeola complications

pneumonia, otitis media, mastoiditis, encephalitis, and myocarditis

Younger children, medically fragile children, and children with underlying immunosuppression are at greater risk for complications

Chicken pox

highly contagious and is airborne, spread through contact with respiratory droplets and contact with lesions

Rash that is described as “tear drop on a rose”. Begins with a machine red base, then progresses to a clear vesicle in later forms a crust. The lesions are severely pruritic and may continue to occur for up to five days

The most common complications are bacterial superinfections with lesions, encephalitis, varicella, pneumonia, and immune thrombocytopenia purpura (ITP)

Use of aspirin-containing medications has been linked with Reye’s syndrome in children with Varicella-zoster (chickenpox)

Diphtheria

Low-grade fever, rhinorrhea, cough, sore throat, gray, adherent membrane in pharynx or trachea, possible skin ulcers, hoarseness, stridor, and pharyngitis are common

Hospitalization is required with IV antitoxin (hyperimmune equine antiserum) and antibiotics (erythromycin or penicillin)

All contacts are given prophylactic antibiotic treatment and immunization boosters