Staphylococcus pseudintermedius necrotizing fasciitis in a dog

Abstract

Staphylococcus pseudintermedius was implicated as the cause of rapidly progressive and fatal necrotizing fasciitis in a dog. The isolate was methicillin-susceptible and did not contain genes encoding the Panton-Valentine leukocidin. While Streptococcus canis is typically considered to be the main cause of necrotizing fasciitis in dogs, staphylococci should also be considered.

A 15-year-old female, spayed, mixed breed dog was presented to the Ontario Veterinary College as an emergency for evaluation of a red and edematous lesion on the left caudo-ventral abdomen. The dog had been previously diagnosed with intracranial meningioma and insulinoma, and had been treated with high doses of dexamethasone over the preceding week. There was no history of recent antimicrobial therapy. On presentation, the dog was depressed, poorly responsive to stimuli, tachypneic, and pyrexic (40.5°C). A red edematous and warm skin lesion was present on the left caudo-ventral abdomen over an area of approximately 10 × 15 cm. A complete blood (cell) count (CBC) was submitted and a leukocytosis (21.2 × 10⁹/L; reference range: 4.9–15.4 × 10⁹/L) characterized by neutrophilia (18.7 × 10⁹/L; reference range: 2.9–10.6 × 10⁹/L) and left shift (band neutrophils 0.64 × 10⁹/L; reference range: 0–0.3 × 10⁹/L) was present. Severe metabolic acidosis (pH 7.22; reference range: 7.32–7.38), adjusted base excess −15.3 (reference range: −6.4 to −0.4), was identified by venous blood gas analysis.

Case description

The dog was admitted to the intensive care unit and treatment with antimicrobials (cefoxitin, clindamycin), analgesics (fentanyl, ketamine constant rate infusion) and intravenous fluids (crystalloids and colloids) was initiated. Because of progressive hypotension, vasopressors were administered. Over the next few hours, the soft tissue inflammation extended dramatically to include the entire left side of the ventral abdomen and proximal half of the left pelvic limb. The center of the lesion progressively changed in color from red to purple, then black. The clinical presentation was consistent with necrotizing fasciitis. Because of the severity of disease and poor response to initial treatment, the dog was euthanized 15 h after admission.

At necropsy, there was a large area of cyanotic and thickened skin over the ventral abdomen and inguinal area. The subcutaneous tissues were thickened, edematous, and hemorrhagic. An intracranial meningioma and a pancreatic endocrine tumor were also confirmed. Histological examination of tissues confirmed the clinical diagnosis of necrotizing fasciitis. There was extensive diffuse subcutaneous and deep dermal necrosis and inflammation, with large numbers of neutrophils. Abundant cellular debris, pyknotic cells, and coccoid bacteria were present throughout.

Bacterial culture was performed on a tissue sample from the lesion. Heavy and pure growth of a coagulase-positive Staphylococcus species was obtained, which is consistent with the observation of abundant cocci histologically. The isolate was classified biochemically as S. intermedius and subsequently re-classified as S. pseudintermedius based on sequencing of the sodA gene (1). The isolate was susceptible to cefoxitin and clindamycin, the 2 antimicrobials that were administered. It was also methicillin-susceptible, as confirmed by PBP2a latex agglutination test (MRSA Latex Agglutination Test; Oxoid, Hants, United Kingdom). Genes encoding the Panton-Valentine leukocidin (PVL) were not detected by real-time polymerase chain reaction (PCR) (2). No anaerobes were isolated.

Discussion

Necrotizing fasciitis is a rapidly progressive necrotizing infection of skin, soft tissue and deep fascia, and is often fatal. While rare, with an estimated 500–1500 cases per year in humans in the United States (3), it gathers significant attention because of the severity of disease, rapid progression, high mortality, and colloquial description as “flesh-eating disease.” In humans, it is most commonly caused by group A streptococci (3), although there are increasing reports of cases caused by community-associated methicillin-resistant Staphylococcus aureus (MRSA) (4). There is a single report of isolation of S. intermedius from a human with necrotizing fasciitis (5); however, the relevance of the organism was unclear as MRSA was also isolated. While the incidence of necrotizing fasciitis in dogs has not been described, it is a rare condition. Streptococcus canis, a group G Streptococcus, has been implicated in most cases (6,7). Staphylococci have not been implicated as causes of necrotizing fasciitis in dogs, although there is a report describing toxic shock and cellulitis caused by S. intermedius in a dog (8) and it is possible that the cited case was actually necrotizing fasciitis.

Staphylococcus pseudintermedius is a coagulase-positive Staphylococcus that was first described in 2005 (9). While there is a limited number of reports describing S. pseudintermedius infection or colonization in dogs (10,11), there is recent evidence that many, if not all, canine isolates that have been classified biochemically as S. intermedius are actually S. pseudintermedius and that S. pseudintermedius may be an important canine pathogen (1,12). In dogs, S. intermedius typically causes pyoderma and similar skin and soft tissue infections, but can also cause opportunistic infections at other body sites (13).

The public health risks with S. pseudintermedius are currently unclear. Staphylococcus pseudintermedius has also been isolated from the nares of veterinary personnel (10) and was the cause of a soft tissue infection in a human (14). While it is currently unclear whether S. pseudintermedius poses a zoonotic risk, it has been suggested that S. pseudintermedius is likely a zoonotic pathogen because of the genetic similarity between canine and human isolates (12) and because zoonotic transmission of S. intermedius has been documented (15).

This is the first reported case of necrotizing fasciitis in a dog caused by the newly described and poorly understood S. pseudintermedius. The origin of infection was unclear. There was no history of previous skin disease or trauma to the infected site; however, this is not uncommon (7). The reason that severe invasive disease developed in this case is unclear. The pathophysiology of necrotizing fasciitis is not well understood and may relate to bacterial factors, patient factors, or both. Bacterial factors associated with staphylococcal necrotizing fasciitis are not known. Strains of MRSA most commonly associated with necrotizing fasciitis in humans produce PVL (4); however, there is considerable debate about the actual role of this toxin in disease (16). This isolate did not contain genes encoding PVL; however, it is possible that the isolate possessed other virulence factors that were not tested for or which are unknown. Fluoroquinolone administration has been implicated as an inciting factor in S. canis necrotizing fasciitis in dogs (17); however, a similar relationship between drug administration and staphylococcal necrotizing fasciitis has not been reported in any species. The comorbidities and immunosuppressive therapy may have played a role in development of severe invasive disease. The role of S. pseudintermedius in disease in dogs and other species is currently unclear and evaluation is complicated by the need for sequence-based identification. Ongoing investigation of the role of this organism in animal disease and the potential for zoonotic transmission is required. CVJ