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Methicillin-Resistant Staphylococcus Aureus
Methicillin-resistant Staphylococcus aureus (MRSA) is a
strain of staphylococcus that causes skin infections and has
become resistant to common broad-spectrum antibiotics.
When an infection occurs in a health care setting, it is re-
ferred to as health care–associated MRSA or HA-MRSA. If
it occurs in a community setting, it is CA-MRSA. Children
with weakened immune systems are at most risk of con-
tracting the infection.
An infection usually begins as a boil. It can spread to be-
come a painful abscess or invade deeper body structures such
as joints and heart valves. Children who are identified as
having MRSA are isolated to help prevent spread of the bac-
teria to others. Vancomycin is the drug of choice for treat-
ment of hospital based lesions because the bacteria are still
susceptible to its design. Trimethoprim-sulfamethoxazole is
commonly used with community infections. Use strict stan-
dard infection precaution measures when caring for a child
with an MRSA infection. Teach children that the best way
to prevent staphylococcal infections of the skin is good
handwashing and reporting skin wounds to a health care
provider before an open wound can become infected (Pallin
et al., 2008).
Scalded Skin Disease
Scalded skin disease (Ritter’s disease) is a staphylococcal infec-
tion seen primarily in newborns. Children develop rough-tex-
tured skin and general erythema. Large bullae (vesicles), filled
with clear fluid, form. The epidermis separates in large sheets,
leaving a red, glistening, scalded-looking surface. Children
need intensive intravenous antibiotic therapy to survive this
extreme infection (Painter, Trevillion, & Snape, 2007).
Other Bacterial Infections
Diphtheria
• Causative agent: Corynebacterium diphtheriae (Klebs-
Löffler bacillus)
• Incubation period: 2 to 6 days
• Period of communicability: Rarely more than 2 weeks to
4 weeks in untreated persons; 1 to 2 days in children
treated with antibiotics
• Mode of transmission: Direct or indirect contact
• Immunity: Contracting the disease gives lasting natural
immunity.
• Active artificial immunity: Diphtheria toxin given as part
of DTaP vaccine
• Passive artificial immunity: Diphtheria antitoxin
Assessment. Although diphtheria is an illness that should be
extinct because of available immunization, it still occurs in
isolated outbreaks. When diphtheria bacilli invade and grow
in the nasopharynx of children, they produce an exotoxin (a
potent protein poison) that causes massive cell necrosis and
inflammation. The necrosing material lends itself well to the
growth of the bacilli, so the bacilli reproduce rapidly. The in-
flammation and necrosing cells form a characteristic gray
membrane on the nasopharynx. This may extend up into the
nose and down into the major bronchi, causing a purulent
nasal discharge and a brassy cough. The toxin is absorbed
from the membrane surface and spread systemically by the
bloodstream to affect major organs, such as the heart and
nervous system. If untreated, myocarditis with heart failure
and conduction disturbances may occur. Central nervous
system involvement can include severe neuritis with paralysis
of the diaphragm and pharyngeal and laryngeal muscles. The
diagnosis of diphtheria is made based on clinical appearance
and on a throat culture, which reveals the presence of the
bacilli (Chambers, 2009).
Therapeutic Management. Treatment involves intravenous
administration of antitoxin in large doses. In addition, chil-
dren are given penicillin or erythromycin intravenously.
Complete bedrest is crucial during the acute stage of the ill-
ness. Droplet precautions must be followed until cultures are
negative. Children need careful observation at all times to
prevent airway obstruction. If obstruction occurs, endotra-
cheal intubation may be necessary.
Because the diphtheria vaccine is included in routine im-
munizations for infants, diphtheria is almost extinct in the
United States. However, isolated instances do occur, and when
they do, prompt recognition and treatment are necessary.
Whooping Cough (Pertussis)
• Causative agent: Bordetella pertussis
• Incubation period: 5 to 21 days
• Mode of transmission: Direct or indirect contact
• Period of communicability: Greatest in catarrhal (respira-
tory illness) stage
• Immunity: Contracting the disease offers lasting natural
immunity.
• Active artificial immunity: Pertussis vaccine given as part
of DTaP vaccine
• Passive artificial immunity: Pertussis immune serum
globulin
Pertussis is a serious disease of childhood. Like diphthe-
ria, pertussis has become quite rare because of required im-
munizations, but it still occurs sporadically and is actually
making a comeback in some locales and in adolescents
(Judelsohn & Koslap-Petraco, 2007). Those most suscepti-
ble are children who have not been immunized because a
previous vaccine had possible side effects that led parents to
refuse immunization.
Assessment. Pertussis manifests itself in three stages: ca-
tarrhal, paroxysmal, and convalescent. The catarrhal stage
begins with upper respiratory symptoms such as coryza, sneez-
ing, lacrimation, cough, and a low-grade fever. Children are
irritable and listless. In some children, a mild cough is the
only symptom during this stage. It lasts from 1 to 2 weeks
(Knox, 2008).
The paroxysmal stage lasts 4 to 6 weeks. During this time,
the cough changes from a mild one to a paroxysmal one, in-
volving 5 to 10 short, rapid coughs, followed by a rapid in-
spiration, which causes the “whoop,” or high-pitched crow-
ing sound, of whooping cough. Children are in obvious
distress while coughing. They may become cyanotic or red-
faced, and their nose may drain thick, tenacious mucus. They
often vomit after a paroxysm of coughing, and they are ex-
hausted afterward from the effort. Attacks of coughing tend
to be more severe at night.
During the convalescent stage, there is a gradual cessation
of the coughing and vomiting. The cough may be present for
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CHAPTER 43 Nursing Care of a Family When a Child Has an Infectious Disorder
some time, but as single, not paroxysmal, coughs. During the
next year, if children develop an upper respiratory infection,
they may again have a return of the paroxysmal coughing
with vomiting.
Pertussis is diagnosed by its striking symptoms, although
in children younger than 6 months of age, the “whoop” of
the cough may be absent, making it more difficult to diag-
nose. The B. pertussis bacillus may be cultured from na-
sopharyngeal secretions during the catarrhal and paroxysmal
stages. The white cell count, particularly the lymphocyte
count, increases with whooping cough: it may be as high as
20,000 to 30,000/mm3 at the end of the catarrhal stage (nor-
mal is 5000 to 10,000/mm3).
Therapeutic Management. Children with pertussis are
maintained on bedrest until the paroxysms of coughing sub-
side. They need to be secluded from environmental factors,
such as cigarette smoke, dust, and strenuous activity, that ini-
tiate coughing episodes. Nutrition may be a problem if the
child is constantly coughing and vomiting. As a rule, fre-
quent small meals are vomited less than larger meals. Infants
with pertussis may be admitted to a health care facility for
observation because they may have such tenacious secretions
with coughing episodes that they need airway suction. Place
an intercom in the infant’s room so personnel can listen for
paroxysms of coughing.
A full 10-day course of erythromycin or azithromycin
may be prescribed as these drugs have the potential to
shorten the period of communicability and may shorten the
duration of symptoms. Droplet precautions are used until 5
days after a child starts effective therapy. Complications of
pertussis include pneumonia, atelectasis, or emphysema from
plugged bronchioles. Seizures from asphyxia as a result of se-
vere paroxysms of coughing may occur. Epistaxis, subcon-
junctival and subarachnoid bleeding from the force of cough-
ing, may occur. If sufficient fluid intake cannot be
maintained, alkalosis and dehydration from persistent vom-
iting can occur.
Prevention. Little passive immunity is transferred to the
newborn, so children in their early months are particularly
susceptible to this disease. This is why pertussis vaccine is
one of the first immunizations scheduled. Infants who have
not yet been immunized or are immunocompromised and
are exposed may be given pertussis immune serum globulin
to protect them from contracting the disease (Wood et al.,
2008).
What if... An adolescent with pertussis vomits after an
episode of coughing? Should you urge him to try to
eat again immediately, or do you think he would be
too nauseated to do so?
Anthrax
• Causative agent: Bacillus anthracis, a bacteria
• Incubation period: 1 to 7 days (inhalational), 1 to 12 days
(cutaneous), 1 to 7 days (gastrointestinal)
• Mode of transmission: Originally contracted from contact
with cow or sheep feces; not transmissible from person to
person
• Immunity: Unstudied
1281
• Active artificial immunity: A vaccine is available for peo-
ple in high-risk occupations, such as veterinarians, but it
is not recommended for children.
• Passive artificial immunity: Not available
Anthrax is an acute infectious disease that is contracted
from exposure to the bacteria or its spores (Bravata et al.,
2007). Such bacteria live in the feces of infected cows or
sheep. As the organism grows inside the human body, a toxin
is produced that is the actual source of the symptoms.
Children, like adults, may be affected by all three clinical
forms: cutaneous, inhalational, or gastrointestinal.
Inhalational anthrax begins with a brief prodromal pe-
riod of flulike symptoms, followed shortly by dyspnea, se-
vere systemic shock, and marked evidence of mediastinal
widening and pleural effusion on radiography. The mortal-
ity for this form is over 90%. Because it can be fatal and
spread through coughing, inhalational anthrax has been
proposed as bacteria that could be used in bioterrorism
(Place et al., 2007).
Cutaneous anthrax is characterized by a skin lesion that
begins as a papule, then passes through a vesicle stage to a
painless depressed black eschar. Fever, malaise, and headache
and regional swollen lymph nodes may accompany the skin
lesion. The mortality of cutaneous anthrax is as low as 1%
with antibiotic therapy.
Gastrointestinal anthrax is contracted by eating under-
cooked meat infected with the organism. The child develops
severe abdominal pain, fever, bloody diarrhea, and sep-
ticemia. Mortality is about 25%.
If a child is exposed to anthrax, prophylaxis with
ciprofloxacin (Cipro) for those over 18 years and doxycycline
for younger patients should be started. Drug therapy is con-
tinued for 60 days because of the potential persistence of
spores.
Tetanus (Lockjaw)
• Causative agent: Clostridium tetani
• Incubation period: 3 days to 3 weeks
• Period of communicability: None
• Mode of transmission: Direct or indirect contamination
of a closed wound
• Immunity: Development of the disease gives lasting nat-
ural immunity.
• Active artificial immunity: Tetanus toxoid contained in
DTaP vaccine
• Passive artificial immunity: Tetanus immune globulin
Tetanus, a highly fatal disease if untreated, is caused by an
anaerobic, spore-forming bacillus. The bacillus, found in soil
and the excretions of animals, enters the body through a
wound. If the wound is deep, such as a puncture wound,
where the distal end of the wound is shut off from an oxygen
source, the tetanus bacilli begin to reproduce. The organism
may also enter through a burn site, which crusts, creating an
anaerobic environment. As the bacilli grow, they produce ex-
otoxins that cause the disease symptoms by affecting the
motor nuclei of the central nervous system (Ogle &
Anderson, 2008).
The entrance site of the bacillus does not appear infected
(no pus or reddened area is present unless a secondary infec-
tion also exists). After the incubation period, the exotoxins
have developed to such an extent, however, that they are ca-
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1282 UNIT 7 The Nursing Role in Restoring and Maintaining the Health of Children and Families With Physiologic Disorders
pable of disrupting the nervous system. In the United States
most children are vaccinated against tetanus; in developing
countries it continues to have a high incidence, caused by in-
fection of an entry point such as the umbilical cord at birth
(Roper, Vandelaer, & Gasse, 2007).
Assessment. The first symptoms that are noticeable are stiff-
ness of the neck and jaw (lockjaw). Within 24 to 48 hours,
muscular rigidity of the trunk and extremities develops. The
back becomes arched (opisthotonos), the abdominal muscles
are stiff and boardlike, and the face assumes an unusual ap-
pearance, with wrinkling of the forehead and distortion of
the corners of the mouth (a “sardonic grin” sign). Any stim-
ulation, such as a sudden noise, a bright light, or a touch,
causes painful, paroxysmal spasms. The sensorium is clear
throughout the course of the disease, so the child is aware of
the pain associated with muscle spasms. As these spasms
begin to include laryngospasm, respiratory obstruction, and
a collection of secretions in the respiratory tract, death by as-
phyxiation may occur.
Fever is an ominous sign accompanying tetanus. Children
who survive the disease rarely have more than a low-grade
fever.
Therapeutic Management. A child needs to be cared for in
a quiet, stimulation-free room. If the wound has necrotic tis-
sue, it may be débrided to ensure that no secondary infec-
tions arise. Enteral or total parenteral nutrition may be nec-
essary to prevent aspiration from laryngeal spasm. Tetanus
immune globulin (human) is administered to supply passive
antitoxins to combat the growing organisms.
Parenteral penicillin G or erythromycin is administered to
reduce the number of growing forms of the bacillus. Sedation
and a muscle relaxant may be necessary to reduce the sever-
ity and pain of the muscle spasms. A child may need to be in-
tubated and mechanical ventilation begun to maintain respi-
ratory function.
Prevention. Tetanus is a serious disease, but it can be pre-
vented through active immunization and suitable booster im-
munization. Children routinely receive tetanus immuniza-
tion as part of routine DTaP immunization and a booster
dose at school age; thereafter they should receive a booster
dose every 10 years. At the time of a wound, the wound site
should be cleaned well with soap and water and a suitable an-
tiseptic. If the wound is deep, such as a knife stab, a nail
puncture, or a dog bite, it should not be sutured but should
be left open to heal by secondary intention. This reduces the
possibility of an anaerobic pocket forming in the wound. If
the child received basic immunization against tetanus and it
has been fewer than 10 years since the last injection, no
booster or antitoxin management is needed at the time of the
wound.
If a child’s immunization record cannot be obtained, or if
it has been more than 10 years since the child received a
booster injection or an initial injection for tetanus, a child
will probably be treated with a booster injection and tetanus
immune globulin. A booster injection provides tetanus anti-
gen to the child. If the child received initial immunization for
this disease, the booster will cause the body to “remember”
how to make tetanus antibodies, and the body will begin to
produce them rapidly. By the time the invading tetanus or-
ganisms from the wound have passed their long incubation
period (3 days to 3 weeks), the child will have antibodies in
the system prepared to eradicate the organisms. If the initial
immunizations were incomplete or are unknown, in addition
to tetanus antigen the child will also receive the passive anti-
bodies included in tetanus immune globulin (Ogle &
Anderson, 2008).
Lyme Disease
• Causative agent: Borrelia burgdorferi, a spirochete
• Incubation period: 3 to 30 days
• Period of communicability: Not communicable from one
person to another
• Mode of transmission: Deer tick
• Active artificial immunity: Lyme disease vaccine
Lyme disease is caused by a spirochete, Borrelia burgdor-
feri, that is transmitted by a tick often carried on deer (Philip
& Jacobs, 2009). The disease is the most frequently reported
vector-borne infection in the United States, occurring most
often in the summer and early fall. Almost immediately after
the tick bite, an erythematous papule is noticeable at the site,
which spreads over the next 3 to 30 days (the incubation pe-
riod) to become a large, round ring with a raised swollen bor-
der (erythema chronicum migrans; Fig. 43.13). This is fol-
lowed by systemic involvement that leads to cardiac,
musculoskeletal, and neurologic symptoms. Cardiac involve-
ment may be so severe that it includes heart block from atri-
oventricular conduction abnormalities. Neurologic symp-
toms commonly include stiff neck, headache, and cranial
nerve palsy. Musculoskeletal symptoms occur in 50% of chil-
dren and include painful swollen arthritic joints, particularly
the knee.
Amoxicillin or penicillin V is administered at the time of
the bite to young children. Doxycycline is given to those
older than 8 years of age. A vaccine for the disease has been
approved for use in adults who live or work in high-risk areas
but not yet for children.
Parents should be cautioned to inspect the skin of chil-
dren who have been playing in wooded areas for tick bites to
help identify the disorder before debilitating symptoms
occur. Other suggestions for avoiding Lyme disease are
shown in Box 43.8.
FIGURE 43.13 The rash of Lyme disease. (© Larry
Mulvehill/Science Source/Photo Researchers.)