Infection of the desert toad, Scaphiopus couchii, by the monogenean Pseudodiplorchis americanus involves 2 principal sites: post-invasion juveniles reside in the respiratory tract for 1 month before migrating to the urinary bladder where they reach sexual maturity and may live up to 4 years. While previous work has demonstrated the long-term impact on host condition of the blood-feeding adults, this study assesses pathological effects of the short-term pulmonary infection. Lung ultrastructure was compared in toads (i) maintained in captivity for 1 year without invasion, and (ii) experimentally infected with 50–300 juveniles/host, equivalent to burdens in the wild, and examined 23–44 days p.i. Typically, the alveolar lining of S. couchii is composed of a single cell type with characteristics of both Type I and Type II pneumocytes. However, infected lung tissue exhibited an inflammatory reaction with epithelial cell vacuolation, interstitial oedema, and an increase of alveolar exudate, leucocytes and fibrous tissue. Accompanying a post-infection increase in host immune cells in the lungs, there was evidence of reciprocal tegumental damage to the parasites. Lung epithelium of toads free of infection for 1 year exhibited scar tissue representing a residual effect of past infection. The pathological consequences of P. americanus infection therefore have 2 components. Acute lung infection coincides with the host's brief activity season: impaired respiratory function could compromise feeding and accumulation of reserves and hence ability to survive following a 10 month period of hibernation. Additionally, adult toads are normally exposed annually to re-infection and may accumulate chronic lung damage with extended effects on host survival.