Varicella-Zoster Virus
Varicella-zoster virus (VZV) causes primary, latent, and recurrent infections. The
primary infection is manifested as varicella (chickenpox) and results in
establishment of a lifelong latent infection of sensory ganglion neurons.
Reactivation of the latent infection causes herpes zoster (shingles). Although often a
mild illness of childhood, varicella can cause substantial morbidity and mortality in
otherwise healthy children. Morbidity and mortality are higher in immunocompetent
infants, adolescents, and adults as well as in immunocompromised persons.
Etiology
:
VZV is a neurotropic human herpesvirus with similarities to herpes simplex virus.
Epidemiology
:
Most children were infected by 10 yr of age, with fewer than 5% of adults
remaining susceptible. This pattern of infection at younger ages remains
characteristic in all countries in temperate climates. Varicella is a more serious
disease in young infants, adults, and immunocompromised persons, in whom there
are higher rates of complications and deaths than in healthy children. Within
households, transmission of VZV to susceptible individuals occurs at a rate of 65-
86%; more casual contact, such as occurs in a school classroom, is associated with
lower attack rates among susceptible children. Persons with varicella may be
contagious 24-48 hr before the rash is evident and until vesicles are crusted, usually
3-7 days after onset of rash. Susceptible persons may also acquire varicella after
close, direct contact with adults or children who have herpes zoster.
Herpes zoster is caused by the reactivation of latent VZV. It is not common in
childhood and shows no seasonal variation in incidence. Zoster is not caused by
exposure to a patient with varicella; in fact, exposures to varicella boost the cell-
mediated immune response to VZV in individuals with prior infection, decreasing
the likelihood of reactivation of latent virus. Herpes zoster in children tends to be
milder than herpes zoster in adults, is less frequently associated with acute pain, and
postherpetic neuralgia generally does not occur in healthy children.
Pathogenesis
:
VZV is transmitted by contact with oropharyngeal secretions and the fluid of skin
lesions of infected individuals, either by airborne spread or through direct contact.
Primary infection (varicella) results from inoculation of the virus onto the mucosa
of the upper respiratory tract and tonsillar lymphoid tissue. During the early part of
the 10-21 day incubation period, virus replicates in the local lymphoid tissue, and
spreads to T lymphocytes, causing a viremia that delivers the virus to skin where
innate immunity controls VZV replication for some days. After innate immunity is
overcome in skin, widespread cutaneous lesions develop as the incubation period
ends.
In the immunocompromised child, the failure of adaptive immunity, especially
cellular immune responses, results in continued viral replication that may lead to
prolonged and/or disseminated infection with resultant complications in the lungs,
liver, brain, and other organs.
The skin lesions of varicella and herpes zoster have identical histopathology, and
infectious VZV is present in both.
Clinical Manifestations:
Varicella in Unvaccinated Individuals:
The illness usually begins 14-16 days after exposure, although the incubation period
can range from 10-21 days. Subclinical varicella is rare; almost all exposed,
susceptible persons experience a rash, albeit so mild in some cases that it may go
unnoticed. Prodromal symptoms may be present, particularly in older children and
adults. Fever, malaise, anorexia, headache, and occasionally mild abdominal pain
may occur 24-48 hr before the rash appears. Temperature elevation is usually 37.8-
38.9°C (100-102°F) but may be as high as 41.1°C (106°F); fever and other systemic
symptoms usually resolve within 2-4 days after the onset of the rash.
Varicella lesions often appear first on the scalp, face, or trunk. The initial exanthem
consists of intensely pruritic erythematous macules that evolve through the papular
stage 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. The distribution of the rash is predominantly
central or centripetal with the greatest concentration on the trunk and proximally on
the extremities. Ulcerative lesions involving the mucosa of the oropharynx and
vagina are also common; many children have vesicular lesions on the eyelids and
conjunctivae, but corneal involvement and serious ocular disease are rare.
The exanthem may be much more extensive in children with skin disorders, such as
eczema or recent sunburn. Hypopigmentation or hyperpigmentation of lesion sites
persists for days to weeks in some children, but severe scarring is unusual unless the
lesions were secondarily infected.
Differential Diagnosis:
+ Herpes simplex
+ Enterovirus
+ Monkey pox
+ Rickettsial pox
+ Staph. Aureus
+ Drug reactions
+ Disseminated herpes simplex
+ Contact dermatitis
+ Insect bites
Varicelliform Rashes in Vaccinated Individuals:
Varicelliform rashes that occur after vaccination could be a result of wild-type
VZV, vaccine strain VZV, or other etiologies (e.g., insect bites, coxsackievirus). In
the early stages of a vaccine program, rash within 1-2 wk is still most commonly
caused by wild-type VZV, reflecting exposure to varicella before vaccination could
provide protection. Rash occurring 14-42 days after vaccination is a result of either
wild-type or vaccine strains, reflecting exposure and infection before protection
from vaccination or an adverse event of vaccination (vaccine-associated rash),
respectively.
Breakthrough varicella is disease that occurs in a person vaccinated more than 42
days before rash onset and is caused by wild-type virus. The rash in breakthrough
disease is frequently atypical and predominantly maculopapular, vesicles are seen
less commonly. The illness is most commonly mild with <50 lesions, shorter
duration of rash, fewer complications, and little or no fever.
Neonatal Varicella:
Mortality is particularly high in neonates born to susceptible mothers who
contracted varicella around the time of delivery. Infants whose mothers demonstrate
varicella in the period from 5 days prior to delivery to 2 days afterward are at high
risk for severe varicella. These infants acquire the infection transplacentally as a
result of maternal viremia, which may occur up to 48 hr prior to onset of maternal
rash. The infant’s rash usually occurs toward the end of the 1st wk to the early part
of the 2nd wk of life (although it may be as soon as 2 days).
Newborns whose mothers develop varicella during the period of 5 days before
to 2 days after delivery should receive VZIG as soon as possible. Although
neonatal varicella may occur in about half of these infants despite administration of
VZIG, it is usually milder than in the absence of VZIG administration. All
premature infants born <28 wk of gestation to a mother with active varicella at
delivery (even if the maternal rash has been present for >1 wk) should receive
VZIG.
Because perinatally acquired varicella may be life threatening, the infant should be
treated with acyclovir (10 mg/kg every 8 hr IV) when lesions develop.
Neonates with community-acquired varicella who experience severe varicella,
especially those who have a complication such as pneumonia, hepatitis, or
encephalitis, should also receive treatment with intravenous acyclovir (10 mg/kg
every 8 hr). Infants with neonatal varicella who receive prompt antiviral therapy
have an excellent prognosis.
Complications:
# Asymptomatic transient varicella hepatitis( in otherwise healthy child)
# Mild thrombocytopenia with petechiae
# Progressive varicella
# Acute cerebellar ataxia
# Encephalitis
# Pneumonia
# Nephrotic syndrome, nephritis
# HUS
# Arthritis, myocarditis, pericarditis, pancreatitis, orchitis, and acute retinal
necrosis.
Bacterial Infections:
Secondary bacterial infections of the skin, usually caused by group A Streptococcus
and S. aureus, may occur in up to 5% of children with varicella. These range from
impetigo to cellulitis, lymphadenitis, and subcutaneous abscesses. The more
invasive infections, such as varicella gangrenosa, bacterial sepsis, pneumonia,
arthritis, osteomyelitis, cellulitis, and necrotizing fasciitis, account for much of the
morbidity and mortality of varicella in otherwise healthy children.
Diagnosis:
o Varicella and herpes zoster have been diagnosed primarily by their clinical
appearance.
o Leukopenia is typical during the 1st 72 hr after onset of rash; it is followed by
a relative and absolute lymphocytosis.
o Results of liver function tests are also usually (75%) mildly elevated.
o Direct fluorescence assay of cells from cutaneous lesions (vesicular fluid) in
15-20 min, by PCR amplification testing (vesicular fluid, crusts)
o Rapid culture with specific immunofluorescence staining
o Scrapings of maculopapular lesions can be collected for PCR or direct
fluorescence assay testing.
o PCR is the most sensitive and allows for differentiation of wild-type and
vaccine strains.
o A 4-fold or greater rise in IgG antibodies is confirmatory of acute infection.
Treatment:
Varicella:
The only antiviral drug available in liquid formulation that is licensed for treatment
of varicella for pediatric use is acyclovir. However, acyclovir therapy is not
recommended routinely by the American Academy of Pediatrics for treatment of
uncomplicated varicella in the otherwise healthy child because of the marginal
benefit, the cost of the drug, and the low risk for complications of varicella. Oral
therapy with acyclovir (20 mg/kg/dose; maximum: 800 mg/dose) given as 4
doses/day for 5 days can be used to treat uncomplicated varicella in individuals at
increased risk for moderate to severe varicella: nonpregnant individuals older than
12 yr of age and individuals older than 12 mo of age with chronic cutaneous or
pulmonary disorders; individuals receiving short-term, intermittent, or aerosolized
corticosteroid therapy; individuals receiving longterm salicylate therapy; and
possibly secondary cases among household contacts. To be most effective,
treatment should be initiated as early as possible, preferably within 24 hr of the
onset of the exanthem. There is less clinical benefit if treatment is initiated more
than 72 hr after onset of the exanthema.
Some experts recommend the use of famciclovir or valacyclovir in older children
who can swallow tablets.
Intravenous therapy is indicated for severe disease and for varicella in
immunocompromised patients (even if begun more than 72 hr after onset of rash).
Any patient who has signs of disseminated VZV, including pneumonia, severe
hepatitis, thrombocytopenia, or encephalitis, should receive immediate treatment.
IV acyclovir therapy (500 mg/m2 every 8 hr) initiated within 72 hr of development
of initial symptoms decreases the likelihood of progressive varicella and visceral
dissemination in high-risk patients. Treatment is continued for 7-10 days or until no
new lesions have appeared for 48 hr.
Acyclovir-resistant VZV has been identified primarily in children infected with
HIV. These children may be treated with intravenous foscarnet (120 mg/kg/day
divided every 8 hr for up to 3 wk).
Herpes Zoster:
Treatment of uncomplicated herpes zoster in the child with an antiviral agent may
not always be necessary, treatment with oral acyclovir (20 mg/kg/dose; maximum:
800 mg/dose) to shorten the duration of the illness(start antiviral therapy as soon as
possible, delay beyond 72 hr from onset of rash limits its effectiveness).
Patients at high risk for disseminated disease should receive IV acyclovir (500 mg/
m2 or 10 mg/kg every 8 hr.
Use of corticosteroids in the treatment of herpes zoster in children is not
recommended.
Prognosis:
Primary varicella has a mortality rate of 2-3 per 100,000 cases, with the lowest case
fatality rates among children 1-9 yr of age. Compared with these age groups, infants
have a 4 times greater risk of dying and adults have a 25 times greater risk of dying.
Herpes zoster among healthy children has an excellent prognosis and is usually self-
limited. Severe presentation with complications and sometimes fatalities can occur
in immunocompromised children.
Prevention:
VZV transmission is difficult to prevent, especially from persons with varicella,
because a person with varicella is contagious for 24-48 hr before the rash is
apparent.
Vaccine:
Varicella is a vaccine-preventable disease. Varicella vaccine contains live,
attenuated VZV and is indicated for subcutaneous administration. Varicella vaccine
is safe and well tolerated.
In the United States, varicella vaccine is recommended for routine administration as
a 2 dose regimen. Vaccination with 2 doses is recommended for all persons without
evidence of immunity. The minimum interval between the 2 doses is 3 mo for
persons 12 yr of age or younger and 4 wk for older children, adolescents, and adults.
Postexposure Prophylaxis:
= Vaccine given to healthy children within 3 or 5 days after exposure (as soon as
possible is preferred) is effective in preventing or modifying varicella.
= Oral acyclovir administered late in the incubation period may modify subsequent
varicella in the healthy child; however, its use in this manner is not recommended
until it can be further evaluated.
= High-titer anti-VZV immune globulin as postexposure prophylaxis is
recommended for immunocompromised children, pregnant women, and newborns
exposed to varicella.
Leishmaniasis
The leishmaniases are a diverse group of diseases caused by intracellular
protozoan parasites of the genus Leishmania, which are transmitted by
phlebotomine sand flies. Multiple species of Leishmania are known to cause human
disease involving the skin and mucosal surfaces and the visceral reticuloendothelial
organs. Cutaneous disease is generally mild but may cause cosmetic disfigurement.
Mucosal and visceral leishmaniasis is associated with significant morbidity and
mortality.
Etiology
Leishmania organisms are members of the Trypanosomatidae family and include 2
subgenera, Leishmania (Leishmania) and Leishmania (Viannia). The parasite is
dimorphic, existing as a flagellate promastigote
in the insect vector and as an aflagellate amastigote that resides and replicates
within mononuclear phagocytes of the vertebrate host.
Epidemiology
The leishmaniases are estimated to affect 10-20 million people in endemic tropical
and subtropical regions on all continents except Australia and Antarctica. With only
rare exceptions, the Leishmania organisms that primarily cause cutaneous disease
do not cause visceral disease.
The emergence of the leishmaniases in new areas is the result of (1) movement of a
susceptible population into existing endemic areas, usually because of agricultural
or industrial development or timber harvesting; (2) increase in vector and/or
reservoir populations as a result of agriculture development projects or climate
change; (3) increase in anthroponotic transmission owing to rapid urbanization in
some focuses; and (4) increase in sandfly density resulting from a reduction in
vector control programs.
Pathology
Histopathologic analysis of the Localized cutaneous leishmaniasis (LCL) and
disseminated leishmaniasis (DL) lesion shows intense chronic granulomatous
inflammation involving the epidermis and dermis with relatively few amastigotes.
Occasionally, neutrophils and even microabscesses can be seen.
In Visceral leishmaniasis (VL) there is prominent reticuloendothelial cell
hyperplasia in the liver, spleen, bone marrow, and lymph nodes. Amastigotes are
abundant in the histiocytes and Kupffer cells. Late in the course of disease, splenic
infarcts are common, centrilobular necrosis and fatty infiltration of the liver occur,
the normal marrow elements are replaced by parasitized histiocytes, and
erythrophagocytosis is present.
Pathogenesis
Cellular immune mechanisms determine resistance or susceptibility to infection
with Leishmania. Resistance is mediated by interleukin(IL)-12 driven generation of
a T helper 1 cell response, with interferon-γ inducing classical macrophage (M1)
activation and parasite killing.
Within endemic areas, people who have had a subclinical infection
can be identified by a positive delayed-type hypersensitivity skin
response to leishmanial antigens (Montenegro skin test) or by antigen-induced
production of interferon-γ in a whole blood assay. Subclinical infection occurs
considerably more frequently than does active cutaneous or visceral disease.
Individuals with prior activedisease or subclinical infection are usually immune to a
subsequent clinical infection; however, latent infection can lead to active disease if
the patient is immunosuppressed.
Clinical Manifestations
Visceral Leishmaniasis:
VL (kala-azar) typically affects children < 5 yr of age in the New World and
Mediterranean region (L. infantum/chagasi) and older children and young adults in
Africa and Asia (L. donovani).
After inoculation of the organism into the skin by the sandfly, the child may have a
completely asymptomatic infection or an oligosymptomatic illness that either
resolves spontaneously or evolves into active kala-azar.
Children with asymptomatic infection are transiently seropositive but show no
clinical evidence of disease. Children who are oligosymptomatic have mild
constitutional symptoms (malaise, intermittent diarrhea, poor activity tolerance) and
intermittent fever; most will have a mildly enlarged liver. In most of these children
the illness will resolve without therapy, but in approximately 25% it will evolve to
active kala-azar within 2-8 mo.
Extreme incubation periods of several years have rarely been described. During the
first few wk to months of disease evolution the fever is intermittent, there is
weakness and loss of energy and the spleen begins to enlarge.
The classic clinical features of high fever, marked splenomegaly, hepatomegaly,
and severe cachexia typically develop 3-6 mo after the onset of the illness, but a
rapid clinical course over 1 mo has been noted in up to 20% of patients in some
series.
At the terminal stages of kala-azar the hepatosplenomegaly is massive, there is
gross wasting, the pancytopenia is profound, and jaundice, edema, and ascites may
be present.
Anemia may be severe enough to precipitate heart failure. Bleeding episodes,
especially epistaxis, are frequent. The late stage of the illness is often complicated
by secondary bacterial infections, which frequently are a cause of death. A younger
age at the time of infection, HIV co-infection, and underlying malnutrition may be
risk factors for the development and more rapid evolution of active VL. Death
occurs in > 90% of patients without specific antileishmanial treatment and in 4-10%
of treated patients.
Leishmaniasis may also result from reactivation of a longstanding subclinical
infection. Frequently there is an atypical clinical presentation of VL in HIV-infected
individuals with prominent involvement of the gastrointestinal tract and absence of
the typical hepatosplenomegaly.
Laboratory findings
Laboratory findings associated with classic kala-azar include anemia (hemoglobin
5-8 mg/dL), thrombocytopenia, leukopenia (2,000-3,000 cells/μL), elevated hepatic
transaminase levels, and hyperglobulinemia (>5 g/dL) that is mostly
immunoglobulin G.
Differential diagnosis
malaria, typhoid fever, miliary tuberculosis, schistosomiasis, brucellosis, amebic
liver abscess, infectious mononucleosis, lymphoma, andleukemia.
Diagnosis
Serologic testing by enzyme immunoassay, indirect fluorescence assay, or direct
agglutination is very useful in VL because of the very high level of antileishmanial
antibodies.
An immunochromatographic strip test using a recombinant antigen (K39) has a
diagnostic sensitivity and specificity for VL of 80-90% and 95%, respectively.
Serodiagnostic tests have positive findings in only about half of the patients who are
co-infected with HIV.
Definitive diagnosis of leishmaniasis is established by the demonstration of
amastigotes in tissue specimens or isolation of the organism by culture.
In patients with VL, smears or cultures (by using Novy-McNeal-Nicolle (NNN)
biphasic blood agar medium ) of material from splenic, bone marrow, or lymph
node aspirations are usually diagnostic.
Treatment
All patients with VL should receive therapy.
The pentavalent antimony compounds (sodium stibogluconate (Pentostam,)and
meglumine antimoniate have been the mainstay of antileishmanial chemotherapy
for >40 yr.
These drugs have similar efficacies, toxicities, and treatment regimens.
the recommended regimen is
20 mg/kg/day intravenously or intramuscularly for
28 days.
An initial clinical response to therapy usually occurs in the 1st wk of therapy, but
complete clinical healing ( regression of splenomegaly and normalization of
cytopenias ) is usually not evident for weeks to a few months after completion of
therapy.
Cure rates with this regimen 80-100% for VL were common in the 1990s, but
clinical resistance to antimony therapy has become common.
Adverse effects of antimony therapy are dose and duration dependent and
commonly include fatigue, arthralgias and myalgias (50%), abdominal discomfort
(30%), elevated hepatic transaminase level (30-80%), elevated amylase and lipase
levels (almost 100%), mild hematologic changes (slightly decreased leukocyte
count, hemoglobin level, and platelet count) (10-30%), and nonspecific T-wave
changes on electrocardiography (30%). Sudden death due to cardiac toxicity is
extremely rare and is usually associated with use of very high doses of pentavalent
antimony.
Amphotericin B desoxycholate at doses of 0.5-1.0 mg/kg every day or every other
day for 14-20 doses achieved a cure rate for VL of close to 100%, but the renal
toxicity associated with amphotericin B was common.
Aminoglycoside paromomycin (aminosidine) has efficacy (
∼95%) similar to that
of amphotericin B.
Miltefosine, a membrane-activating alkylphospholipid 50-100 mg/day for 28 days,
has been recently developed as the 1st oral treatment for VL and has a cure rate of
95% . needed, especially in children.
Prevention
Personal protective measures should include avoidance of exposure to
the nocturnal sandflies and, when necessary, the use of insect repellent
and permethrin-impregnated mosquito netting.
Where peridomiciliary transmission is present, community-based residual
insecticide spraying has had some success in reducing the prevalence of
leishmaniasis, but long-term effects are difficult to maintain.
Control or elimination of infected reservoir hosts (e.g., seropositive domestic
dogs) has had limited success.
Where anthroponotic transmission is thought to occur, early recognition and
treatment of cases are essential.
Several vaccines have been demonstrated to have efficacy in experimental models,
and vaccination of humans or domestic dogs may have a role in the control of the
leishmaniases in the future.
Pertussis (Bordetella pertussis and B. parapertussis
)
Bordetella organisms are small, fastidious, gram-negative coccobacilli. Bordetella
pertussis is the sole cause of epidemic pertussis and the usual cause of sporadic
pertussis. B. parapertussis is an occasional cause of pertussis. B. pertussis and B.
parapertussis are exclusive pathogens of humans. B. bronchiseptica is a common
animal pathogen.
Pertussis is extremely contagious, with attack rates as high as 100% in susceptible
individuals exposed to aerosol droplets at close range. Neither natural disease nor
vaccination provides complete or lifelong immunity against reinfection or disease.
Clinical Manifestations
Classically, pertussis is a prolonged disease, divided into catarrhal, paroxysmal, and
convalescent stages. The catarrhal stage (1-2 wk) begins insidiously after an
incubation period ranging from 3-12 days with nondistinctive symptoms of
congestion and rhinorrhea. As initial symptoms wane, coughing marks the onset of
the paroxysmal stage (2-6 wk). The cough begins as a dry, intermittent, irritative
hack and evolves into the inexorable paroxysms that are the hallmark of pertussis. A
well-appearing, playful toddler with insignificant provocation suddenly expresses
an anxious aura and may clutch a parent or comforting adult before beginning a
machine-gun burst of uninterrupted cough on a single exhalation, chin and chest
held forward, tongue protruding maximally, eyes bulging and watering, face purple,
until coughing ceases and a loud whoop follows as inspired air traverses the still
partially closed airway. Post-tussive emesis is common, and exhaustion is universal.
The number and severity of paroxysms escalate over days to a week and remain at
that plateau for days to weeks. At the peak of the paroxysmal stage, patients may
have more than 1 episode hourly. As the paroxysmal stage fades into the
convalescent stage (≥2 wk), the number, severity, and duration of episodes
diminish.{Protracted coughing (which in some cases is paroxysmal) is attributable
sporadically to Mycoplasma, parainfluenza viruses,
influenza
viruses,
enteroviruses, respiratory syncytial virus (RSV), or adenoviruses.
Infants <3 mo of age do not display the classic stages. The catarrhal phase lasts
only a few days or is unnoticed, and then, after the most insignificant startle from a
draft, light, sound, sucking, or stretching, a well-appearing young infant begins to
choke, gasp, gag, and flail the extremities, with face reddened. Cough may not be
prominent, especially in the early phase. Whoop infrequently occurs in infants
<3 mo of age who at the end of a paroxysm lack stature or muscular strength to
create sudden negative intrathoracic pressure. Apnea and cyanosis can follow a
coughing paroxysm, or apnea can occur without a cough as the only symptom.
Apnea and cyanosis both are more common with pertussis than with neonatal viral
infections. The paroxysmal and convalescent stages in young infants are lengthy.
Paradoxically, in infants, cough and whooping may become louder and more classic
in convalescence. “Exacerbations” of paroxysmal coughing can occur throughout
the first year of life with subsequent respiratory illnesses; these are not a result of
recurrent infection or reactivation of B. pertussis.
Adolescents and previously immunized children have foreshortening of all stages of
pertussis. Adults have no distinct stages. Classically, adolescents and adults
describe a sudden feeling of strangulation followed by uninterrupted coughs, feeling
of suffocation, bursting headache, diminished awareness, and then a gasping breath,
usually without a whoop. Post-tussive emesis and intermittency of paroxysms
separated by hours of well-being are specific clues to the diagnosis in adolescents
and adults. At least 30% of older individuals with pertussis have nonspecific cough
illness, distinguished only by duration, which is usually >21 days.
Findings on physical examination generally are uninformative. Signs of lower
respiratory tract disease are not expected unless complicating secondary bacterial
pneumonia is present. Conjunctival hemorrhages and petechiae on the upper body
are common.
Diagnosis
Pertussis should be suspected in any individual who has pure or predominant
complaint of cough, especially if the following are absent: fever, malaise or
myalgia, exanthem or enanthem, sore throat, hoarseness, tachypnea, wheezes, and
rales.
Leukocytosis (15,000–100,000 cells/mm
3
) due to absolute lymphocytosis is
characteristic in the catarrhal stage. Absolute increase in neutrophils suggests a
different diagnosis or secondary bacterial infection.
The chest radiograph appearance is mildly abnormal in the majority of hospitalized
infants. Parenchymal consolidation suggests secondary bacterial infection.
Pneumothorax, pneumomediastinum, and subcutaneous emphysema can be seen
occasionally.
Isolation of B. pertussis in culture remains the gold standard for diagnosis.
PCR testing on nasopharyngeal wash specimens is the lab.test of choice for
B.pertussis identification.
Treatment
Infants < 3 mo are usually hospitalized, as are many 3-6 mo old, unless witnessed
paroxysms are not severe, and at any age if significant complications occur.
Prematurely born young infants and children with underlying cardiac, pulmonary,
muscular, or neurologic disorders have a high risk for severe disease.
Typical paroxysms that are not life threatening have the following features:
a) duration less than 45 sec;
b) red but not blue color change;
c) tachycardia, bradycardia (not <60 beats/min in infants), or oxygen
desaturation that spontaneously resolves at the end of the paroxysm;
d) whooping or strength for self-rescue at the end of the paroxysm;
e) Self-expectorated mucus plug; and
f) post-tussive exhaustion but not unresponsiveness.
Hospital discharge is appropriate if over a 48 hr period disease severity is
unchanged or diminished, no intervention is required during paroxysms, nutrition is
adequate, no complication has occurred, and parents are adequately prepared for
care at home.
Antimicrobial agents
An antimicrobial agent is always given when pertussis is suspected or confirmed to
decrease contagiousnous and to afford possible clinical benefit. Azithromycin (10
mg/kg/day in a single dose for day1, then 5 mg/kg/day on days 2-5) is the drug of
choice in all age-groups for postexposure prophylaxis. Erythromycin (40–
50mg/kg/24hr divided qid PO; maximum: 2g/24hr) for 14 days can be used,
although not preferred in neonatal period(IHPS). Clarithromycin also can be used.
Trimethoprim-sulfamethoxazole (TMP-SMX)
is an alternative to azithromycin
for infants >2 mo old and children unable to receive azithromycin.
Patients are placed in respiratory isolation for 5 days after initiation of
azitthromycin therapy.
Care of Household and Other Close Contacts
Macrolide agent should be given promptly to all household contacts and other close
contacts, such as those in daycare, regardless of age, history of immunization, or
symptoms. Close contacts <7 yr of age who have received less than four doses of
pertussis-containing vaccines should have vaccination initiated or continued to
complete the recommended series.
Complications
The principal complications of pertussis are apnea, secondary infections, expected
pathogens include Staphylococcus aureus, S. pneumoniae, and bacteria of
oropharyngeal flora, (such as otitis media and pneumonia), and physical sequelae
of forceful coughing. Bronchiectasis has been reported rarely after pertussis.
Increased intrathoracic and intra-abdominal pressure during coughing can result in
conjunctival and scleral hemorrhages, petechiae on the upper body, epistaxis,
hemorrhage in the central nervous system (CNS) and retina, pneumothorax and
subcutaneous emphysema, and umbilical and inguinal hernias. Laceration of the
lingual frenulum is not uncommon. Rectal prolapse is distinctly unusual and should
elicit evaluation for underlying condition. Especially in infants in developing
countries, dehydration and malnutrition following post-tussive vomiting can have a
severe impact. Tetany has been associated with profound post-tussive alkalosis.
CNS abnormalities occur at a relatively high frequency and are almost always a
result of hypoxemia or hemorrhage associated with coughing or apnea in young
infants. Apnea or bradycardia or both may result from apparent laryngospasm or
vagal stimulation just before a coughing episode, from obstruction during an
episode, or from hypoxemia following an episode. Lack of associated respiratory
signs in some young infants with apnea raises the possibility of a primary effect of
PT on the CNS. Seizures are usually a result of hypoxemia, but hyponatremia from
excessive secretion of antidiuretic hormone during pneumonia can occur.