Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (519 page)

   In congenital infection, IgM is usually present, but a negative result does not rule out toxoplasmosis. IgG in the absence of infection, due to transplacental transfer, should disappear within 6–12 months. In retinochoroiditis, IgG is positive and IgM is negative. In reactivation of latent disease in immunocompromised patients, IgG is positive but IgM typically negative. In acute toxoplasmosis in immunocompromised patients, positive IgG and IgM reactions, or an increased IgG titer, usually develop. A negative reaction for IgG in serum occurs in 3% of AIDS patients with toxoplasma encephalitis.

   ANAs and RF may cause false-positive IgM-IFA tests. IgM antibodies may be detectable for more than a year after acute infection. IgG reactivity remains detectable for life.

   A number of tests may be needed to determine the timing of infection. If IgG is positive and IgM is negative, it is likely that infection was acquired >6 months previously. If IgG and IgM are both positive, primary infection may have been only as recent as the previous 2 years. An IgG avidity test may be helpful. Low avidity suggests acute infection within the prior 3 months.

Molecular tests
: PCR techniques have proven to be sensitive for the diagnosis of toxoplasmosis, especially for prenatal diagnosis. PCR of amniotic fluid has a sensitivity >97% and NPV >99% for intrauterine toxoplasmosis.

Core laboratory
: Atypical lymphocytosis, increased or decreased WBC, anemia, and decreased platelets. Increased globulin concentration and signs of specific organ dysfunction occur in severe disease.

CSF findings
: Pleocytosis and increased protein.

TRICHINOSIS (TRICHINELLOSIS;
TRICHINELLA SPIRALIS
)

   Definition

Trichinosis is caused by
Trichinella spiralis
and related species. A foodborne zoonotic infection with a global distribution, trichinosis most commonly occurs in Europe and North America. All mammals are susceptible to disease. Swine and rats form the major host reservoir for
T. spiralis
. When infected meat is ingested, the capsule is digested, allowing the larvae to emerge and invade into the epithelium of the small intestine.

   Who Should Be Suspected?

Clinical infection shows two phases.

   The first phase, correlated with the entry and activity of adult worms in the small intestine, is often mild.

   The second phase, caused by the circulation of larvae, is associated with fever, myalgias, weakness, malaise, diarrhea, and periorbital and facial edema (approximately 50% of cases) and other symptoms.

Headache is very common. Neurologic symptoms occur in 10–20% of patients and suggest a more severe course. Myalgias, fatigability, headache, and ocular symptoms may persist for decades in chronic infection.

   Laboratory Findings

Diagnosis is usually made on the basis of clinical symptoms, dietary history, and serologic testing.

Direct detection
: Definitive diagnosis, if needed, is achieved by demonstration of larvae in striated muscle. The deltoid muscle is often biopsied. Muscle biopsy may show the encysted larvae beginning 10 days after ingestion. Direct microscopic examination of compressed specimen is superior to routine histologic preparation. Stool O&P examination is rarely contributory, but adult worms may be seen in acute illness with diarrhea.

Serology
: Useful, but seroconversion may not occur for several weeks after acute infection. Serologic tests become positive 1 week after onset of symptoms in only 20–30% of patients and reach a peak in 80–90% of patients by 4th to 5th week. Rise in titer in acute and convalescent phase sera is diagnostic. Titers may remain negative in overwhelming infection. False-positive results may occur in polyarteritis nodosa, serum sickness, penicillin sensitivity, infectious mononucleosis, malignant lymphomas, and leukemia. EIA is method of choice; it peaks in 3 months and may still be detected at 1 year. Specificity is >95%. IHA is also used. Previously used tests include CF, bentonite flocculation, precipitin, and latex fixation.

Core laboratory:

   Eosinophilia develops in >50% of patients and may be one of the earliest laboratory abnormalities supporting a clinical diagnosis. Eosinophilia appears with values of ≤85% on differential count and 15,000/μL on absolute count. It occurs about 1 week after the eating of infected meat and reaches maximum after 3rd week. It usually subsides in 4–6 weeks but may last up to 6 months and occasionally for years.

   Laboratory signs indicating muscle damage (e.g., increased concentrations of creatine phosphokinase, LDH, aldolase, aminotransferases) are frequently seen.