Chapter 85: Pneumocystosis

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Pneumocystis carinii is a saprophyte of low virulence that is found primarily in the mammalian lung. Clinical pneumonia has been reported to occur spontaneously in dogs in association with a suspected immunodeficiency. Airborne transmission is suspected because healthy animals become infected when they are housed with infected animals. It is presumed that the organism may have a dormant life stage in the environment. The taxonomy of P. carinii is uncertain. It has been classified as a unicellular protozoan belonging to the phylum Sarcomastigophora, subphylum Sarcodina. However, its reproductive behavior is similar to that of yeast cells. On the other hand, phylogenetic classification based on 16S-like ribosomal RNA sequences indicates that P. carinii is related most closely to fungi of the class Ascomycetes, yet it behaves like a protozoan because it is sensitive to drugs used to treat protozoan infections.

The morphology of P. carinii and the histopathologic features of the lesions produced by both human and animal isolates throughout the world are similar. Only a single species name has been assigned to the genus Pneumocystis, but antigenic differences suggest that there may be several strains. Although it currently is controversial, four species have been described: two species that infect dogs and rats, P. carinii and Pneumocystis wakefieldiae; Pneumocystis murina, which infects mice; and Pneumocystis jiroveci, which infects humans. Biologic differences among isolates from different hosts are suggested by the relative difficulty of experimental interspecies transmission. Phylogenetic analysis of the dihydrofolate reductase and dihydropteroate synthase genes in different P. carinii strains obtained from different host species (human, mouse, rat, ferret, owl monkey, dog, and rabbit) showed that all P. carinii strains were confined within a distinct group that was closely related to ascomycete fungi and that human-derived P. carinii was most closely related to monkey-derived P. carinii.


P. carinii appears to be maintained in nature by transmission from infected to susceptible animals within a species. The primary mode of spread is thought to be airborne droplet transmission between hosts. The contagious nature of pneumocystosis is suggested by the epidemic spread that has occurred in institutionalized humans. Sporadic cases may represent an activation of latent infection by stress, crowding, and immunosuppressive therapy during hospitalization of latent carriers. Clinical disease also has been activated experimentally after cortisone therapy, cytotoxic chemotherapy, and irradiation. A higher prevalence of infection has been found in dogs with canine distemper than in a corresponding control population.

The entire life cycle of P. carinii is completed within the alveolar spaces, where organisms adhere in clusters to the pneumocytes. Two main forms, the trophozoite and the cyst, are found. Although Pneumocystis infections usually are limited to the lung, in humans and in a single dog organisms have been reported in extrapulmonary sites. Severe immunodeficiency states in humans such as acquired immunodeficiency syndrome (AIDS) can be associated with lymphatic or hematogenous dissemination of the organisms from the lungs to other tissues. Transmission of infection to an offspring may occur via aspiration of amniotic fluid contaminated by placental infection.


Pneumocystis can be inhaled from the environment and can colonize the lower respiratory tract of clinically healthy mammals; however, organisms rarely multiply to large numbers in the lungs of clinically healthy hosts. Under conditions in which there is impaired host resistance or preexisting pulmonary disease, proliferation of organisms can occur. Alveolocapillary blockage and decreased gaseous exchange result secondary to the overgrowth and clustering of P. carinii within the alveolar spaces. Intraalveolar organisms often are accompanied by thickening of alveolar septa, but organisms seldom invade the pulmonary parenchyma and rarely are found in alveolar macrophages. The inflammatory response that the organism provokes contributes to the pulmonary alveolar damage and clinical pathophysiology.

Clinical Findings

Most reported canine cases have been in miniature dachshunds younger than 1 year, although cases of pneumocystosis have been reported in a Shetland sheepdog, a Yorkshire terrier, and cavalier King Charles spaniels. The syndrome of common variable immunodeficiency, in which there is an absence of B cells resulting in little or no antibody production in association with defective T cells, appears to occur in affected miniature dachshunds and is likely a risk factor for clinical disease in these dogs. More recently Pneumocystis pneumonia was diagnosed in two cavalier King Charles spaniel littermates, which further supports the possibility of an underlying inheritable immunodeficiency in this breed.

The typical clinical history in dogs with pneumocystosis is that of gradual weight loss and variable polypnea progressing over time. Weight loss, which occurs in spite of a good appetite in most dogs, may be associated with diarrhea and occasional vomiting. Coughing is not always present, but exercise intolerance is present consistently. Infected animals may show some response to antibiotic or cortisone therapy.

Affected dogs generally remain relatively alert and afebrile. Abnormalities on clinical examination include polypnea, tachycardia, and pulmonary crackles on thoracic auscultation. Animals usually are in poor condition, are cachectic, and often show dermatologic changes such as superficial bacterial pyoderma and demodicosis. Although the mucous membranes generally are of normal color, in severely affected animals they may be cyanotic.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Chapter 85: Pneumocystosis
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