Pulmonary arterial disease in cats seropositive for Dirofilaria immitis but lacking adult heartworms in the heart and lungs

Browne, Leanne E.; Carter, Todd D.; Levy, Julie; Snyder, Patti S.; Johnson, Calvin M.

doi:10.2460/ajvr.2005.66.1544

Cited by 43 publications

(34 citation statements)

References 15 publications

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“…The result is diminished pulmonary function, hypoxemia, dyspnea, and cough; in some cats, this can lead to chronic respiratory disease. These findings provide evidence that pulmonary disease occurs in heartworminfected cats, even when the infection does not progress to the adult worm stage, by inducing a strong vascular and parenchymal inflammatory response (53,69,114). This pronounced bronchoreactivity has been hypothesized to be due to the activity of pulmonary intravascular macrophages, a component of the reticuloendothelial system that cats, but not normal dogs, possess (118).…”

Section: Clinical Features Of Human and Animal Dirofilariasis Heartwomentioning

confidence: 81%

Human and Animal Dirofilariasis: the Emergence of a Zoonotic Mosaic

et al. 2012

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SUMMARY Dirofilariasis represents a zoonotic mosaic, which includes two main filarial species ( Dirofilaria immitis and D. repens ) that have adapted to canine, feline, and human hosts with distinct biological and clinical implications. At the same time, both D. immitis and D. repens are themselves hosts to symbiotic bacteria of the genus Wolbachia , the study of which has resulted in a profound shift in the understanding of filarial biology, the mechanisms of the pathologies that they produce in their hosts, and issues related to dirofilariasis treatment. Moreover, because dirofilariasis is a vector-borne transmitted disease, their distribution and infection rates have undergone significant modifications influenced by global climate change. Despite advances in our knowledge of D. immitis and D. repens and the pathologies that they inflict on different hosts, there are still many unknown aspects of dirofilariasis. This review is focused on human and animal dirofilariasis, including the basic morphology, biology, protein composition, and metabolism of Dirofilaria species; the climate and human behavioral factors that influence distribution dynamics; the disease pathology; the host-parasite relationship; the mechanisms involved in parasite survival; the immune response and pathogenesis; and the clinical management of human and animal infections.

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Section: Clinical Features Of Human and Animal Dirofilariasis Heartwomentioning

confidence: 81%

Human and Animal Dirofilariasis: the Emergence of a Zoonotic Mosaic

et al. 2012

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“…Research has demonstrated that the early immature adult infection is associated with an intense inflammatory response Dillon, 2008;Holmes et al, 1992;Selcer et al, 2005). In addition, clinical experience and a prospective clinical study of cats with suspected heartworm disease has indicated that some cats will get the early infection, the worm(s) will die, but the cat will continue to develop chronic inflammatory lung disease , and lung pathology continue to be present after the infection (Browne et al, 2005).…”

Section: Introductionmentioning

confidence: 94%

“…Sections were scored on a scale of 0-3 individually for interstitium, bronchus, bronchioles, pulmonary arterioles, and major pulmonary artery areas (Browne et al, 2005;Dillon et al, 2013). The right caudal lung at the mid-lobar cross-section, corresponding to a plane and location of CT slice, was used for section for evaluation.…”

Section: Histopathologymentioning

confidence: 99%

Effect of pre-cardiac and adult stages of Dirofilaria immitis in pulmonary disease of cats: CBC, bronchial lavage cytology, serology, radiographs, CT images, bronchial reactivity, and histopathology

Dillon

Tillson

Wooldridge

et al. 2014

Veterinary Parasitology

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A controlled, blind study was conducted to define the initial inflammatory response and lung damage associated with the death of precardiac stages of Dirofilaria immitis in cats as compared to adult heartworm infections and normal cats. Three groups of six cats each were used: UU: uninfected untreated controls; PreS I: infected with 100 D. immitis L3 by subcutaneous injection and treated topically with selamectin 32 and 2 days pre-infection and once monthly for 8 months); IU: infected with 100 D. immitis L3 and left untreated. Peripheral blood, serum, bronchial lavage, and thoracic radiographic images were collected from all cats on Days 0, 70, 110, 168, and 240. CT images were acquired on Days 0, 110, and 240. Cats were euthanized, and necropsies were conducted on Day 240 to determine the presence of heartworms. Bronchial rings were collected for in vitro reactivity. Lung, heart, brain, kidney, and liver tissues were collected for histopathology. Results were compared for changes within each group. Pearson and Spearman correlations were performed for association between histologic, radiographic, serologic, hematologic and bronchoalveolar lavage (BAL) results. Infected cats treated with selamectin did not develop radiographically evident changes throughout the study, were heartworm antibody negative, and were free of adult heartworms and worm fragments at necropsy. Histologic lung scores and CT analysis were not significantly different between PreS I cats and UU controls. Subtle alveolar myofibrosis was noted in isolated areas of several PreS I cats and an eosinophilic BAL cytology was noted on Days 75 and 120. Bronchial ring reactivity was blunted in IU cats but was normal in PreS I and UU cats. The IU cats became antibody positive, and five cats developed adult heartworms. All cats with heartworms were antigen positive at one time point; but one cat was antibody positive, antigen negative, with viable adult females at necropsy. The CT revealed early involvement of all pulmonary arteries and a random pattern of parenchymal disease with severe lesions immediately adjacent to normal areas. Analysis of CT 3D reconstruction and Hounsfield units demonstrated lung disease consistent with restrictive pulmonary fibrosis with an interstitial infiltrate, absence of air trapping, and decrease in total lung volume in Group IU as compared to Groups UU and PreS I. The clinical implications of this study are that cats pretreated with selamectin 1 month before D. immitis L3 infection did not become serologically positive and did not develop pulmonary arterial hypertrophy and myofibrosis.

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“…In assays of each of these cats, in contrast to cats harboring adult heartworms, antibody concentration declined at subsequent time points and became negative or weak positive by day 270 p.i. Identification of cats that harbor immature worms with no evidence of adult worms is important because (Browne et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Temporal Pattern of Circulating Antigens and Antibody Responses in Cats Experimentally Infected with Dirofilaria immitis

et al. 2017

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Heartworm disease in cats has been attributed to immature adult heartworms reaching the pulmonary arteries approximately 2.5 -4 months post infection and the presence of mature adult worms in the cardiopulmonary system approximately 6 months after infection. The arrival and death of immature heartworms causes significant lung pathology, a condition referred to as heartwormassociated respiratory disease (HARD). To evaluate the humoral immune response to Dirofilaria immitis, 12 cats were each infected by subcutaneous injection of 100 third-stage larvae. Postinfection serum samples were collected weekly for 4 weeks, every other week for the following 4 weeks, then monthly to day 270 for evaluation of antibodies to D. immitis recombinant antigens HWAg-1 and HWAg-2 and circulating heartworm antigen (HWAg) using the PetChek ® HTWM PF Test Kit (IDEXX Laboratories). Necropsies were performed 278 -299 days post infection for collection of adult worms. Eleven cats were HWAg-1 antibody-positive 68 days post-infection, and the remaining cat became positive by day 140. Eleven cats were positive for HWAg-2 antibody 42 -84 days post infection; all 11 remained HWAg-2 antibodypositive through day 270. Circulating HWAg was detected in 10 cats, 2 by day 140 and 8 others by day 168. The 2 antigen-negative cats had no adult worms at necropsy. This study demonstrates that decomposition of immature adult heartworms can result in detectible levels of circulating antigen prior to sexual maturation. In this experimental Original Article S92EndoparasitEs model, D. immitis antigen was detectable in cats at time points (days 140 and 168) associated with HARD from dying immature adult heartworms.

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Pulmonary arterial disease in cats seropositive for Dirofilaria immitis but lacking adult heartworms in the heart and lungs

Cited by 43 publications

References 15 publications

Human and Animal Dirofilariasis: the Emergence of a Zoonotic Mosaic

Human and Animal Dirofilariasis: the Emergence of a Zoonotic Mosaic

Effect of pre-cardiac and adult stages of Dirofilaria immitis in pulmonary disease of cats: CBC, bronchial lavage cytology, serology, radiographs, CT images, bronchial reactivity, and histopathology

Temporal Pattern of Circulating Antigens and Antibody Responses in Cats Experimentally Infected with Dirofilaria immitis

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