Poliomyelitis should be considered in any unimmunized or incompletely immunized child with paralytic disease. VAPP should be considered in any child with paralytic disease occurring 7–14 days after receiving the orally administered polio vaccine (OPV). VAPP can occur at later times after administration, and should be considered in any child with paralytic disease in countries or regions where wild-type poliovirus has been eradicated and the OPV has been administered to the child or a contact. The combination of fever, headache, neck and back pain, asymmetric flaccid paralysis without sensory loss, and pleocytosis does not regularly occur in any other illness.

Identification of Poliovirus in Stool:

The World Health Organization (WHO) recommends that the laboratory diagnosis of poliomyelitis be confirmed by isolation and identification of poliovirus in the stool, with specific identification of wild-type and vaccine-type strains. In suspected cases of acute flaccid paralysis, 2 stool specimens should be collected 24–48 hr apart, as soon as possible after the diagnosis of poliomyelitis is suspected. Poliovirus concentrations are high in the stool in the 1st week after the onset of paralysis, which is the optimal time for collection of stool specimens. Polioviruses may be isolated from 80–90% of acutely ill patients, whereas <20% may yield virus within 3–4 wk after onset of paralysis. Because most children with spinal or bulbospinal poliomyelitis have constipation, rectal straws may be used to obtain specimens; ideally a minimum of 8–10 g of stool should be collected. In laboratories that can isolate poliovirus, isolates should be sent to either the Centers for Disease Control and Prevention or to 1 of the WHO-certified poliomyelitis laboratories where DNA sequence analysis can be performed to distinguish between wild poliovirus and neurovirulent, revertant OPV strains. With the current WHO plan for global Continue reading »

The signs and symptoms of CMV infection vary with age, route of transmission, and immunocompetence of the patient.

Congenital Infection.

Symptomatic congenital CMV infection was originally termed cytomegalic inclusion disease. Only 5% of all congenitally infected infants have severe cytomegalic inclusion disease, another 5% have mild involvement, and 90% are born with subclinical, but still chronic, CMV infection. The characteristic signs and symptoms of clinically manifested infections include intrauterine growth restriction, prematurity, hepatosplenomegaly and jaundice, blueberry muffin–like rash, thrombocytopenia and purpura, and microcephaly and intracranial calcifications. Other neurologic problems include chorioretinitis, sensorineural hearing loss, and mild increases in cerebrospinal fluid protein. Symptomatic newborns are usually easy to identify. The most severe symptomatic congenital infections and those resulting in sequelae are more likely to be caused by primary rather than reactivated infections in pregnant women. Reinfection with a different strain of CMV can lead to symptomatic congenital infection. Asymptomatic congenital CMV infection is likely the leading cause of sensorineural hearing loss, which occurs in approximately 7% of all infants with congenital CMV infection, whether symptomatic at birth or not.

Perinatal Infection.

Infections resulting from exposure to CMV in the maternal genital tract at delivery or in Continue reading »