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354 Part two Host Defense Mechanisms and Inflammation

INFECTIOUS DISEASES ASSOCIATED
WITH EOSINOPHILIA

Eosinophilia is encountered only with specific infectious diseases.
With active bacterial or viral infections, eosinopenia is charac-
teristic. This suppression of blood eosinophils is, in part, caused
by heightened endogenous corticosteroid production as well as
by inflammatory mediators released during these infections. This
suppression of eosinophilia, with either serious bacterial infections
or marked inflammation, accounts for the absence of otherwise
expected eosinophilia in some patients with helminth infections,
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including those with hyperinfection strongyloidiasis. As a general
clinical guideline, patients with a febrile illness and an increased
or even normal blood eosinophilia are not likely to have common
bacterial or viral infections, unless they have adrenal insufficiency
FIG 24.3 Eosinophil Endomyocardial Disease. A large thrombus or a confounding medication-elicited eosinophilia.
is present in the apex of the left ventricle and the chordae Helminth Parasites
tendineae are entrapped, leading to severe mitral valve
regurgitation. Helminth parasites are multicellular metazoan organisms—the
“worm” parasites. Infections with diverse helminths elicit
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eosinophilia (Chapter 31). Although eosinophilia may provide
a hematological clue to the presence of helminth infection, the
heightened numbers of eosinophils and some activating events, absence of blood eosinophilia does not exclude such infections.
as yet ill-defined, that promote eosinophil-mediated tissue damage. The eosinophilic response to helminths is determined both by
Cardiac damage progresses through three stages. In the first the host’s immune response and by the parasite, including its
stage, there is damage to the endocardium and infiltration of distribution, migration, and development within the infected
the myocardium with eosinophils and lymphocytes, with host. The level of eosinophilia tends to parallel the magnitude
eosinophil degranulation and myocardial necrosis. Elevated and extent of tissue invasion by helminth larvae or adults. In
plasma levels of troponin can be a sensitive assay of early several helminth infections, the migration of infecting larvae or
eosinophil-mediated cardiac damage. A similar acute eosinophilic subsequent developmental stages through tissues is greatest early
myocarditis can develop with drug hypersensitivity reactions in infection, and hence the magnitude of the elicited eosinophilia
and may be more fulminant. The first stage is frequently clinically will be the greatest in these early phases. In established infections,
occult, although subungual splinter hemorrhages may be local eosinophil infiltration will often be present around helminths
prominent. Elevations of serum troponins as a measure of within tissues, without significant blood eosinophilia. Eosinophilia
myocardial injury should be evaluated. Echocardiography usually may be absent in those helminth infections that are well contained
detects no abnormalities at this stage, although cardiac magnetic within tissues (e.g., intact echinococcal cysts) or are solely
resonance imaging (MRI) is evolving as a technique to potentially intraluminal within the intestinal tract (e.g., Ascaris, tapeworms).
detect cardiac involvement at an earlier stage. Uncommonly, In some established infections, increases in blood eosinophilia
death due to acute progressive cardiac disease can occur. Cor- may be episodic. Intermittent leakage of cyst fluids from echi-
ticosteroid therapy during the acute stage may help control and nococcal cysts can transiently stimulate increases in blood
prevent the evolution of myocardial fibrosis. eosinophilia and also cause symptoms attributable to allergic or
The second stage of heart disease, the formation of thrombi anaphylactic reactions (urticaria, bronchospasm). For tissue-
along the damaged endocardium, affects either or both ventricles dwelling helminths, increases in eosinophilia may occur principally
and occasionally the atrium. Outflow tracts near the aortic and in association with migration of adult parasites, as in loiasis and
pulmonic valves are usually spared. These thrombi can embolize gnathostomiasis.
to the brain and elsewhere. Finally, in the fibrotic stage, progressive Helminth infections more likely to elicit prolonged hypereo-
scarring leads to entrapment of chordae tendineae with the sinophilia in adults include filarial and hookworm infections
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development of mitral and/or tricuspid valve regurgitation and and strongyloidiasis (Table 24.1). Trichinellosis can elicit an
to endomyocardial fibrosis, producing a restrictive cardiomy- acute hypereosinophilia. Strongyloides stercoralis infection, difficult
opathy. Echocardiography and MRI are valuable in detecting to diagnose solely by stool examinations, is especially important
intracardiac thrombi and the manifestations of fibrosis. Patients to exclude, not only because it elicits modest to even marked
with sustained eosinophilia should be monitored by using eosinophilia but also because, unlike other helminths, it can
echocardiography and serum troponin assays for evidence of develop into a disseminated, often fatal, disease (hyperinfection
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cardiac disease. In an older series of patients referred to the syndrome) in patients given immunosuppressive corticosteroids.
National Institutes of Health (NIH), much of the mortality among Enzyme-linked immunosorbent assay (ELISA) serology has proved
these patients with hypereosinophilia was attributable to end-stage valuable in detecting strongyloidiasis and should be obtained
congestive heart failure. In contemporary times, earlier recognition for patients with eosinophilia likely to receive corticosteroids.
of cardiac involvement, mitral valve replacement with biopros- Some tissue- or blood-dwelling helminths that are not diagnosable
theses and additional therapeutic options for hypereosinophilic by stool examinations but that can cause marked eosinophilia
syndromes (see below) have largely minimized the morbidity require diagnostic examination of blood or biopsied tissues or
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and mortality attributable to end-stage eosinophilic endomyo- specific serological tests. Infections with these organisms include
cardial disease. filarial infections, trichinellosis, and visceral larva migrans. In