The Occurrence of Physaloptera hispida and a Mastophorus Sp. in Pulmonary Vessels of Hispid Cotton Rats (Sigmodon hispidus) from Georgia, U.S.A.

During 2017-2018, a survey for the rat lungworm, Angiostrongylus cantonensis (Nematoda: Metastrongyloidea), in rodents from Piedmont and Lower Coastal Plains physiographic regions of Georgia was conducted. On 4 occasions, a single worm was recovered from the pulmonary vessels of a single cotton rat (Sigmodon hispidis). One of these worms was identified as a Physaloptera sp. and the remaining 3 as a Mastophorus sp. by morphology. No A. cantonensis were found. Physaloptera (Nematoda: Physalopteroidea) and Mastophorus species (Nematoda: Spiruroidea) are stomach parasites of many wild and domestic animals. This is the first report of these species in the pulmonary vessels of a definitive host. To better characterize these parasites, representative specimens were collected from cotton rat stomachs and identified morphologically and molecularly. Based on partial cytochrome c oxidase subunit 1 (COI) gene sequences, Physaloptera hispida from stomachs were identical to the Physaloptera sp. from the pulmonary vessels. The COI sequences from the Mastophorus sp. from the stomach exhibited a higher degree of variability but confirmed that the pulmonary worms were the same Mastophorus species. Furthermore, sequences of Mastophorus from a coastal site clustered separately from a clade of Mastophorus sequences from cotton rats from a Piedmont site. Our data show that adult worms recovered from pulmonary vessels of cotton rats could be either Physaloptera or Mastophorus sp., indicating that these parasitic worms are not always restricted to the stomach and that worms from pulmonary vessels must be carefully examined to obtain a definitive diagnosis of A. cantonensis infection.

Effect of heartworm infection on in vitro contractile responses of canine pulmonary artery and vein.

OBJECTIVE: To test the effect of heartworm infection on agonist-induced constriction of canine pulmonary artery and vein in vitro. PROCEDURE: Cumulative concentration-response relations to norepinephrine, serotonin, histamine, prostaglandin F2 alpha, and the thromboxane A2 analog U-44069 were determined, using isolated rings of pulmonary artery and vein from control and heartworm-infected dogs. To determine the role of endothelial cells in histamine constriction, some rings were denuded of endothelial cells in both artery and vein. ANIMALS: Noninfected control and heartworm-infected dogs. RESULTS: There was no difference in constriction response to norepinephrine, serotonin, prostaglandin F2 alpha, or U44069 of pulmonary artery or vein from control or heartworm-infected dogs. Histamine-induced constriction of pulmonary artery from heartworm-infected dogs was not different from control values, however, when endothelial cells were removed from control, but not heartworm-infected pulmonary artery, histamine-induced constriction was enhanced. Histamine-induced constriction of pulmonary vein from heartworm-infected dogs was significantly depressed, compared with that of control pulmonary vein. However, removal of endothelial cells in pulmonary vein from heartworm-infected, but not control dogs significantly increased constriction. CONCLUSION: Heartworm infection alters histamine-induced constriction responses of pulmonary artery and vein. These changes may reflect high circulating histamine concentrations in heartworm-infected dogs, compared with that in controls. Increased circulating histamine concentrations in vivo could bring about decreased sensitivity of histamine receptors o decreases in the number of receptors expressed. CLINICAL RELEVANCE: Mast cells and histamine may be important factors in altered endothelium-mediated responses associated with heartworm disease.