Search

Chagas disease, caused by the parasite Trypanosoma cruzi, can cause a potentially life-threatening cardiomyopathy in approximately 10-40% of afflicted individuals. The decline in cardiac function characteristically progresses over the course of many years. We report a case of Chagas disease in which the patient experienced an atypical rapid deterioration to severe cardiomyopathy over the course of 16 months. This case argues the need for increased routine surveillance for patients with confirmed T. cruzi infection, who are determined to be at high-risk for worsening cardiomyopathy., (© The American Society of Tropical Medicine and Hygiene.)

We analyzed the intensity of inflammation and parasitism in BALB/c mice infected with Trypanosoma cruzi I stocks from Mexico with and without benznidazole treatment in the acute phase of disease. Heart and skeletal muscles were evaluated for parasites and inflammation and blood was evaluated for persistence of circulating parasites. Parasitemia was influenced by T. cruzi stocks used and benznidazole treatment. This treatment cleared circulating parasites three days after starting treatment when monitored by direct microscopy. There was a significant reduction of inflammation in skeletal muscles after benznidazole treatment in animals infected with Mexican T. cruzi I stocks (P < 0.05), but this reduction was not significant in the heart (P > 0.05). Trypanosoma cruzi I parasites from Mexico were demonstrated by polymerase chain reaction in tissues and blood of animals after benznidazole treatment.

Chagas cardiomyopathy remodeling is based on the presence of Trypanosoma cruzi in heart tissue and on the complex inflammatory response leading to a myocardium fibrosis and alterations in conductive and functional heart parameters. This study aims to evaluate Simvastatin on the inflammatory response and heart functionality using dogs infected with Y strain of T. cruzi. Animals were treated daily with Simvastatin (20 mg) for 6 months and submitted to clinical and immunopathological evaluations. Simvastatin reduced heart expression and serum levels of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) but not interleukin-10 (IL-10), possibly favoring blood parasitism but reducing inflammation and fibrosis in the left ventricle and right atrium. Simvastatin also ameliorated ejection fraction, diastolic diameter, and mass index of the left ventricle 6 months after infection. This study suggests that more investigation should be performed on the use of statins as a prophylactic therapy against cardiac remodeling because of their effects on modifying immune response and benefiting functional parameters in dogs with T. cruzi-induced ventricular dysfunctions.

We report a case of an adult who developed superior vena cava syndrome because of cardiac hydatidosis. A 37-year-old man from Morocco developed progressive dyspnoea and cough. Cardiac hydatidosis was diagnosed because of both the typical radiological findings and the positive serology for echinococcosis. The patient was treated by surgery and albendazole without complications.

Like domestic cats, wild felids are involved in the complete infective cycle of Toxoplasma gondii because they can host in their gastrointestinal tract sexually mature parasites and shed infective oocysts in their feces. We report, to our knowledge, the first isolation and molecular characterization of a T. gondii strain from the heart tissue of a free-living jaguar (Panthera onca) in French Guiana. Sequencing at six polymorphic markers indicated that the jaguar isolate had an atypical genotype, including an allele at TgM-A previously found only in isolates from South America, and an allele at GRA6, which was previously reported only in Californian sea otter isolates. These findings are consistent with the recent description of atypical T. gondii strains involved in severe toxoplasmoses in immunocompetent patients in French Guiana that seemed to be linked to a neotropical forest-based cycle involving wild cats and their prey.

Plasmodium falciparum is a significant cause of morbidity and mortality in travelers to areas where the parasite is endemic. Non-specific clinical manifestations may result in failure to recognize malaria until autopsy, when it is often too late to obtain whole blood for microscopic evaluation. The use of immunohistochemical (IHC) assays in the detection of three P. falciparum antigens, histidine rich protein-2 (HRP-2), aldolase, and Plasmodium lactate dehydrogenase (pLDH), was evaluated in formalin-fixed paraffin-embedded autopsy tissues from five travelers to malaria-endemic areas, whose deaths were initially suspected to have been caused by other bacterial or viral hemorrhagic fevers. The HRP-2 assay was specific for P. falciparum, whereas the aldolase and pLDH assays also reacted with P. vivax. Immunostaining patterns were predominately cytoplasmic and membranous. P. falciparum antigens were detected in a variety of organs but were most abundant in the blood vessels of brain, heart, and lung tissues.

The extent of inflammation, fibrosis, and progression of chronic Chagas heart disease (cChHD) was associated with persistence of parasite DNA in cardiac lesions of necropsies or explants from Argentinean cChHD patients. A Trypanosoma cruzi-based polymerase chain reaction showed a positive result in 1) 15% of cardiac sections with less than 10 mononuclear inflammatory cells/high-power field (440x) (MNC/HPF), 89% with 10-19 MNC/HPF, and 100% with more than 20 MNC/HPF (P < 0.0001); 2) 33% with less than 10% fibrosis, 79% with 10-19% fibrosis, and 100% with more than 20% fibrosis (P < 0.01); 3) 25% of specimens from patients classified in Kuschnir groups 0 and I, 70% in group II and 90% in group III (P < .001); and 4) 45% and 90% of the specimens from cChHD patients without or with heart failure, respectively (P < 0.01). These findings stress the role of the parasite in pathogenesis and disease progression of cChHD.

Different stages of Trypanosoma cruzi are seen during mammalian infection. Histologic sections of infected hearts have shown amastigotes and, when using immunohistochemistry (IHC), parasite antigens; however, demonstration of trypomastigotes in these tissues has proven elusive. Using a mouse strain that develops chagasic cardiomyopathy (histologically similar to human infection) 70 days after injecting T. cruzi-Brazil strain, we studied the distribution of parasite stages and the extent of inflammation. All organs had varying amounts of mononuclear inflammation by day 10, which peaked between day 20 and day 30, and decreased by day 50. Amastigotes were detected in myocytes, histiocytes, acinar pancreatic cells, astrocytes and ependymal cells by day 10, and the number of amastigotes peaked on day 30. Immunohistochemistry demonstrated trypomastigotes in sinusoids, vessels and interstitial tissues of several organs between day 15 and 50. Abundant parasite antigens (granular staining) were detected in connective tissues throughout the infection. The burden of amastigotes and trypomastigotes during the acute phase seems to correlate with the degree of inflammation and granular staining in the chronic stage.

Heart sections from 16 mongrel dogs, two normal controls and 14 infected with Trypanosoma cruzi, were submitted to immunohistochemical staining with either rabbit anti-cow S100 Protein monoclonal antibody or rabbit anti-T. cruzi purified specific antibody, using the peroxidase technique to investigate the participation of the interstitial dendritic cells of the heart (IDCs) in myocarditis of Chagas disease. Trypanosoma cruzi antigens were revealed as granular and dense deposits in IDC membrane in the heart of infected dogs both during acute and chronic myocarditis, but not in normal controls. Anti-S100 Protein labeled the IDCs, both in normal and infected dogs and a significant increase in the numbers of IDCs occurred in the myocardium, proportionally to the intensity of the inflammatory infiltration. These findings suggest that IDCs, probably by presenting T. cruzi antigens to immune-competent cells, play an important role in the pathogenesis of Chagas disease.

We tested four isolates of Trypanosoma cruzi to assess parasite virulence and ability to cause myocarditis, cardiac sympathetic denervation, and histopathologic alterations in organs of the digestive system. The susceptibility of rats depends on the population of T. cruzi, with the ABC strain and the CL-Brener clone killing all animals, regardless of the parasitemic pattern. All tested T. cruzi populations caused acute myocarditis, but failed to induce histologic alterations in the intestine. The Cl-Brener and ABC isolates caused esophageal myositis. The myocarditis caused by the ABC, CL-Brener, and Y isolates was severe, but resolution started at the end of the acute phase. In contrast, the Col 1.7 G2 clone induced mild and sustained myocarditis. Our results also showed that T. cruzi populations able to induce severe acute myocarditis caused marked sympathetic denervation, but recovery of normal cardiac histology and innervation occurred. The sustained myocarditis induced by Col 1.7 G2 clone failed to cause sustained denervation.

The persistence of Trypanosoma cruzi tissue forms was detected in the myocardium of seropositive individuals clinically diagnosed as chronic chagasic patients following endomyocardial biopsies (EMBs) processed by immunohistochemical (peroxidase-anti-peroxidase [PAP] staining) and molecular (polymerase chain reaction [PCR]) techniques. An indirect immunofluorescent technique revealed antigenic deposits in the cardiac tissue in 24 (88.9%) of 27 patients. Persistent T. cruzi amastigotes were detected by PAP staining in the myocardium of 22 (84.6%) of 26 patients. This finding was confirmed with a PCR assay specific for T. cruzi in 21 (91.3%) of 23 biopsy specimens from the same patients. Statistical analysis revealed substantial agreement between PCR and PAP techniques (k = 0.68) and the PCR and any serologic test (k = 0.77). The histopathologic study of EMB specimens from these patients revealed necrosis, inflammatory infiltrates, and fibrosis, and made it possible to detect heart abnormalities not detected by electrocardiogram and/or cineventriculogram. These indications of myocarditis were supported by the detection of T. cruzi amastigotes by the PAP technique or its genome by PCR. They suggest that although the number of parasites is low in patients with chronic Chagas' disease, their potential for heart damage may be comparable with those present during the acute phase. The urgent necessity for testing new drugs with long-term effects on T. cruzi is discussed in the context of the present results.

Chagas' disease is caused by the hemoflagellate protozoan Trypanosoma cruzi. The most common, serious manifestation of Chagas' disease is a progressive inflammatory cardiomyopathy, which occurs decades after primary infection. The inability to consistently demonstrate T. cruzi by histologic techniques in inflammatory cardiac lesions has suggested that the parasites' persistence may not be required for the pathology of the chronic phase. In this report we further analyze the persistence and localization of T. cruzi DNA in the hearts of seven patients with chronic chagasic cardiomyopathy, along with four indeterminate patients and seven control patients seronegative for T. cruzi infection. In the seven patients with chronic chagasic cardiomyopathy, we extracted DNA from selected inflammatory foci-positive (IFP) and inflammatory foci-negative (IFN) areas of' hematoxylin and eosin-stained cardiac tissue. We then used polymerase chain reaction methodology to amplify three different T. cruzi sequences (a minicircle sequence [MCS], a satellite repetitive sequence [RS], and, a low copy number sequence within the gene coding for a flagellar protein [FPS]). The MCS was detected in approximately 100% of both the IFP and IFN areas analyzed. The RS was detected in 37.5% and 23% of the IFP and IFN areas, respectively (difference not statistically significant; P > 0.10, degrees of freedom = 1, G test of independence = 1.9522). The FPS was rarely detected (2%), and was only present in DNA extracted from IFP areas. The MCS was also detected in most indeterminate cases (none of whom had inflammatory lesions) although with a markedly diminished amplification signal relative to cardiomyopathy cases. The MCS was not amplified from the cardiac tissues from seronegative controls. These results suggest that the quantity of T. cruzi DNA persisting in hearts of patients with Chagas' disease correlates with cardiomyopathy, but may not be preferentially associated with inflammatory foci.

Chagas' disease is caused by the hemoflagellate protozoan Trypanosoma cruzi, which is predominantly found in South and Central America and Mexico. Although the parasite is present in the United States, confirmed cases of human disease are rare. The most serious manifestation of chronic Chagas' disease is a progressive inflammatory cardiomyopathy. However, T. cruzi has not been consistently demonstrated with histologic techniques in inflammatory cardiac lesions. In this study, we used both polymerase chain reaction (PCR) amplification of extracted DNA from hematoxylin and eosin-stained tissue scrapings, and in situ hybridization to detect the presence of T. cruzi in infected murine cardiac tissue sections. Three T. cruzi-specific DNA sequences were used: a 122-basepair (bp) sequence localized within the minicircle network (MCS), a 188-bp nuclear repetitive sequence (RS), and a 177-bp sequence within the open reading frame of a gene coding for a flagellar protein (FPS). We found that all three sequences are amplifiable from scrapings of murine cardiac tissue. The MCS and RS are detected at 0.167 and 0.24 amastigote DNA equivalents, while FPS is barely detected at 0.24 amastigote DNA equivalents. On the other hand, in situ hybridization with all three sequences allowed for the detection of T. cruzi amastigotes within the tissue. The MCS and FPS, however, consistently yielded a more intense signal. These results indicate that PCR and in situ hybridization may prove useful in establishing the prevalence of T. cruzi in human chagasic cardiomyopathy.

Three cases of cysticercosis in black bears (Ursus americanus) in three northern California counties between 1990 and 1994 have been identified as due to the tapeworm Taenia solium. Both morphologic characteristics as well as the presence of T. solium mitochondria cytochrome oxidase I gene sequences, as detected by the polymerase chain reaction, confirmed the diagnosis. The number and geographic separation of the cases suggests that infection of the bears was not due to a single contamination. Humans infected with the definitive stage of T. solium are the probable source of cysticercosis for bears, as well as other humans. This is the first confirmation of cysticercosis due to T. solium in a black bear in North America.

The pig is a vital link in the transmission cycle of Taenia solium, the cestode responsible for human-porcine cysticercosis. Infected pigs also represent an important source of economic loss to farmers in developing countries. Past efforts to find an adequate therapeutic regimen to treat this parasite disease in swine have failed because of low efficacy, high cost, side effects, or the need for multiple doses. In this randomized, no treatment-controlled study, the efficacy and safety of oxfendazole and praziquantel for the treatment of porcine cysticercosis were evaluated in 16 naturally infected pigs. Four groups of four pigs were treated with oxfendazole, praziquantel, oxfendazole plus praziquantel, or untreated. The pigs were humanely killed 12 weeks post-treatment, the number of cyst was counted, and parasite viability was assessed by cyst evagination. No detectable side effects were seen in any of the pigs. Praziquantel treatment alone appeared to reduce the number of cysts, but did not decrease the viability of the remaining parasites. Treatment with oxfendazole alone or oxfendazole plus praziquantel killed all of the parasites, and left only microcalcifications in the meat. Oxfendazole provides, for the first time, a practical, effective, inexpensive, and single-dose therapy for porcine cysticercosis.

In a randomized, controlled study, the efficacy and safety of two different schemes of albendazole therapy for treatment of porcine cysticercosis were tested. Seventeen naturally infected pigs were divided into three groups and treated per os with albendazole (50 mg/kg single dose), albendazole (30 mg/kg every day for three days), or given no treatment, respectively. Serologic responses were monitored with the enzyme-linked electroimmunotransfer blot assay. Pigs were humanely killed 12 weeks after treatment, necropsied, and the number of parasites was recorded. Scolex evagination was used to assess viability of the cysts. Both albendazole-treated groups had significant side effects (anorexia, lethargy). Only a single viable cyst was recovered from the brain of one animal after therapy in the multiple-dose group, and the single-dose therapy left 11% of the cysts viable. In contrast, more than 90% of muscle cysts were found to be viable in the untreated group. Although albendazole therapy for three days was found to be highly effective, side effects and the need for multiple doses would still prevent its widespread use.

Lyme borreliosis is a newly recognized systemic infection with protean clinical manifestations. Because the localization of the causative spirochete (Borrelia burgdorferi) in infected tissues is unknown, we used electron microscopy to find spirochetes in the hearts of chronically infected mice. There were three predominant locations for the spirochete in the hearts. In mice infected for one month or less, the spirochetes were mostly in or around blood vessels. They were either in the lumen or in the perivascular space. Mice infected for more than one month had B. burgdorferi in cardiac myocytes as well, often with clear spaces around them. The third area in which spirochetes were common was collagen fibers; the borreliae were wrapped around fibers with their long axis parallel to the fibers. The number of spirochetes was relatively low, but there was no appreciable decrease in numbers of spirochetes with increasing time postinfection. Inflammatory infiltrates were primarily in the endocardium and pericardium, but spirochetes were generally not in or near areas of inflammation. These data are consistent with previously published information that have identified the heart as a site of chronic infection and inflammation in the mouse. The studies extend our understanding of the behavior of the spirochete in vivo by identifying common locations of B. burgdorferi and by noting the disparity between infection and inflammation.

The paper reviews a previously published case of hydatid disease in the human heart of a Brazilian person who died of tetanus. Based on present knowledge about the distinguishing characteristics of Echinococcus granulosus, E. vogeli, and E. oligarthrus, it was recognized that the infection was due to E. oligarthrus, mainly based the morphologic features of the hooklets of the protoscolex. This is the second human infection due to E. oligarthrus and the first showing wall features of cysts. Therefore, some human infections of polycystic hydatid disease observed outside the range of the bush dog, the only definitive host of E. vogeli (Panama to Northern Argentina), may be due to E. oligarthrus rather than to E. vogeli.

One hundred consecutive patients who died of the acquired immunodeficiency syndrome (AIDS) were studied with an emphasis on the heart. Thirty-two patients showed pathologic changes. The pathologic findings included infection by Histoplasma capsulatum, Toxoplasma gondii, Mycobacterium tuberculosis, cytomegalovirus. Cryptococcus neoformans, and atypical mycobacteria. Noninfectious pathologic findings included nonspecific myocarditis, focal necrosis, focal fibrosis, and acute subendocardial infarction.

The main pathologic findings in 23 patients with acquired immunodeficiency syndrome (AIDS) and Chagas' disease are reviewed; five are from our own experience and 18 from the literature. The presence of Trypanosoma cruzi parasites and/or T. cruzi antibodies in blood and cerebrospinal fluid was recorded and computerized tomograms of the brain were evaluated. Twenty (87%) of the 23 subjects developed severe, multifocal or diffuse meningoencephalitis with necrosis and hemorrhage associated with numerous tissue parasites. The second most severely affected site was the heart. Seven (30.4%) of the 23 cases had myocarditis on pathologic examination. It was acute in four patients, chronic in two, and simultaneously acute and chronic in one. Acute myocarditis and meningoencephalitis are interpreted as being caused by relapses of chronic T. cruzi infections. An AIDS permissive role is suggested for these conditions since immunologic defense against T. cruzi is mediated mainly by T lymphocytes, whose CD4 subpopulation is depleted in patients with this disease. Consequently, AIDS is a factor that may favor the reactivation of T. cruzi infections. The lesions reported in the association of Chagas' disease with AIDS were compared with those reported from patients without AIDS having fatal, acute, vector-transmitted infections, contaminated blood transfusions, or accidental exposures in the laboratory. For the latter three, meningoencephalitis is uncommon. Only immunosuppressed cases of Chagas' disease have been described as having a pseudotumoral presentation that shows expanding lesions with a mass effect in the cranial cavity that causes intracranial hypertension and simulates neoplasms (tumors such as gliomas, lymphomas, metastases, etc.).

Cobalt-60 gamma irradiation was used to kill the larvae of Angiostrongylus cantonensis in four groups of snails that were irradiated at a rate of 15.4 Gy/min for 16.23 min (0.25 kGy), 32.47 min (0.50 kGy), 48.70 min (0.75 kGy), and 64.94 min (1.00 kGy), respectively. Third-stage (infected stage) larvae were isolated from these snails and 50 were administered to each experimental animal via an esophageal tube. At a dosage of 0.25 kGy, the mean +/- SD number of worms recovered from 30 rats and 30 mice was 15.6 +/- 6.5 and 11.3 +/- 6.2, respectively. These were significantly different from the number of worms recovered from the nonirradiated (control) groups, which were 28.9 +/- 9.6 (P < 0.05) and 16.6 +/- 10.3 (P < 0.05) for rats and mice respectively. Worms and cellular infiltrations in lung tissue of rats were histopathologically identified in the 0.25-kGy-irradiated group as well as in the control group. Worms and eosinophilic meningitis were also noted in the brain tissue of mice in control groups. No worms or pathologic findings were observed in the heart, lung, or brain tissue of rats or mice infected with larvae irradiated at or exceeding 0.50 kGy. It is therefore concluded that a dosage of 0.50 kGy is sufficient to prevent successful infection in mice and rats.

The major cause of morbidity and mortality in Chagas' disease is a chronic inflammatory cardiomyopathy, which presents ten or more years following initial infection. Demonstration of Trypanosoma cruzi in cardiac tissue by routine microscopy or culture is difficult in these patients, which has suggested that persistent organisms are not required for chronic disease. Consequently, studies have focused on elucidating an autoimmune pathogenesis of chronic injury. To further assess the persistence of T. cruzi in host tissue, DNA extracted from formalin-fixed, paraffin-embedded autopsy specimens from seronegative or seropositive patients was amplified by the polymerase chain reaction using T. cruzi-specific primers. Trypanosoma cruzi DNA sequences were not consistently amplified from four seropositive patients who lacked evidence of fatal chronic chagasic cardiomyopathy (CCC) (0 positive of 12 heart samples, 0 positive of four gonadal samples, and 0 positive of four adrenal samples) or nine seronegative patients (0 positive of 27 heart samples, 0 positive of nine gonadal samples and 0 positive of nine adrenal samples). In seven seropositive patients with severe CCC, cardiac tissue adjacent to inflammatory infiltrates yielded amplified T. cruzi DNA sequences in 18 of 21 heart samples. Parallel testing of gonadal and adrenal tissues from these same patients produced detectable T. cruzi DNA in none of the gonadal tissue samples and one of the seven adrenals. Our studies demonstrate that T. cruzi, or a portion of its genome, is present in the inflammatory lesion of chronic cardiac Chagas' disease.

Using glycol methacrylate in conjunction with avidin-biotin-peroxidase complex techniques, we studied the contribution of T cell subsets to tissue inflammation during acute Trypanosoma cruzi infection. Two mouse/parasite model systems whose parasitology and pathology behaved differently were used. In C57Bl/6J mice infected with the T. cruzi Brazil strain, the levels of parasitism in blood and tissue (myocardial and skeletal muscle) reached a maximum at week 6 and decreased rapidly thereafter. Inflammatory responses in tissue corresponded with the parasitism, but decreased in intensity more gradually than that of parasitism. The T lymphocytes (Thy 1.2+) were found to be the major lymphocyte population in inflammatory cardiac and skeletal muscles (64.6-81.2%) at both three and six weeks postinfection. Among T cells, CD8+ cells (47.0-58.9%) significantly outnumbered CD4+ cells (9.3-18.6%). The number of B cells (0-1.0%) and macrophages was low. Experiments using C3H/HeSnJ mice infected with the Sylvio X10/4 clone of T. cruzi at 30 days postinfection resulted in similar findings except for a higher CD8+:CD4+ ratio. The primary finding of this study is that Thy 1.2+CD8+CD4- T lymphocytes are the major cell population in both heart and skeletal muscle in acute murine T. cruzi infection. The predominance of CD8+ T cells coincident with the decrease in the tissue parasite burden suggests a role for CD8+ T cells in the control of T. cruzi at the level of the infected cell.

Erythrocytes infected with Plasmodium fragile, like those infected with P. falciparum and P. coatneyi, adhere to vessels in heart, adipose tissue and, to a lesser ex00 nm knob protrusions on the plasma membrane of infected erythrocytes. The close apposition between knobs and endothelium (1 nm or less) excludes macromolecules such as fibrinogen or antibodies as the adhesive force. The components on the membrane responsible for adhesion at the knobs remain unknown.

Sarcocystis was identified in biopsy specimens of skeletal muscle from two adults in Singapore and one in Bombay, and in muscle obtained at autopsy from an adult in Uganda, and in the heart of a child in Costa Rica. Review of case reports revealed that in seven reported cases, including three reported by Lindemann, non-parasite objects were misinterpreted as sarcocysts; in four instances organisms of undetermined classification were described, and in 35 cases true sarcocysts were observed. Among the sarcocysts seen in the 40 cases (35 old, 5 new), seven morphological types were recognized, each representing one to several different species, all of which are zoonotic and none of which can be designated Sarcocystis lindemanni. Among the four types of sarcocysts found in skeletal muscle, three closely resembled a corresponding species found commonly in monkeys: one from a man in Uganda corresponding to a species in Ceropithicus talapoin, forms from India resembling one or two species in Macaca mulatta, and forms from Southeast Asia resembling a species in Macaca fascicularis. Among three types of sarcocysts found in the human heart, one resembled a species commonly seen in the heart of cattle. Of the 40 Sarcocystis infections in man, 13 probably were acquired in Southeast Asia, 8 in India, 5 in Central or South America, 4 each in Africa and Europe, 3 in USA, 1 IN China and 2 in unknown localities. Associated conditions include muscle soreness or weakness in 7 cases, subcutaneous swellings in 5, eosinophilia in 2, and periarteritis or polyarteritis nodosa in 2 cases. However, evidence of pathogenicity of the mature sarcocyst is inconclusive.

Two slender nematodes were incidentally found at autopsy in the heart and inferior vena cava of a 36-year-old Japanese man who died of liver cirrhosis. The parasite from the heart measured 29.5 cm by 0.87 mm, and that from the inferior vena cava 26.5 cm by 0.85 mm. The worms were identified as non-gravid adult female Dirofilaria immitis. This is the fourth case of infection with D. immitis in the heart and large vessels.

The effect of inoculum size and time on the distribution of Toxocara canis larvae in the mouse was investigated by recovering larvae from various body regions 7, 14, 28, and 56 days after administration of either 200, 600 or 1,000 infective eggs to groups of ten male mice. An analysis of variance of larval recoveries from the carcass, liver, brain and cardiopulmonary system suggests that inoculum size was a significant factor determining the proportional recovery for each of these sites. Length of infection was significant in relation to numbers of larvae in the anterior carcass, genitourinary system, brain and heart plus lungs, while length of infection and inoculum size acting in concert influenced the numbers of larvae recovered from the carcass, liver, brain, heart and lungs. Crowding effects, manifested as altered dispersion rates, were seen in the heavier infections.

Micronema, normally free-living in soil and humus, rarely invades and reproduces in the central nervous system, kidneys, lungs, maxillae and nasal cavity of equines. Two Micronema infections causing fatal meningoencephalomyelitis in man have been reported from Canada and Texas. Here we report a third infection in a 54-year-old black man, resident of Washington, D.C., who probably acquired the infection from decubitus ulcers. The worms in this patient were in the liver, heart and brain. The Micronema species was not identified.