Streptococcus canis is a common skin commensal (particularly in the peri-anal region), upper respiratory tract (URT), oropharynx, rectum, and urogenital tract of clinically normal cats. It is also known to cause outbreaks of severe disease in group-housed cats.17,18 Prevalence is particularly high in the caudal reproductive tract of breeding colony queens <2 years of age, with rates of 70% to 100% reported.¹⁹ Outbreaks of disease in kittens may be seen when subclinical carriers are introduced into naïve breeding colonies.

The dichotomy of S. canis as both a harmless common commensal and the causative agent of devastating epizootics has prompted researchers to explore potential strain-related differences in virulence. Streptococcus canis lacks the phagocytosis-inhibiting capsular proteins of Lancefield A and C organisms and appears to be readily engulfed by neutrophils. Several Streptococcus species, including S. canis, can express M-protein on their surface. Variants of the M-protein can bind host mini-plasminogen, a cleavage product of serine protease plasmin. Active plasmin can thence be recruited, which enhances the ability of the bacterium to invade host tissues via the degradation of fibrinogen, and to survive in the blood by inhibition of complement opsonization. Streptococcus canis M-protein can also bind host-specific immunoglobulin G, which may interfere with antibody-mediated killing of the organism.²⁰ A study has shown that isolates of S. canis associated with feline disease are mostly biotype 1 and express M-protein encoded by a particular allelic variant.²¹ Biotypes suspected to be less virulent were only isolated from healthy cats (e.g., biotype 2). Host factors such as suboptimal passive transfer of maternal antibodies, genetic predisposition, or stressful events such as concurrent infectious diseases, overcrowding, poor hygiene, and inadequate nutrition may all contribute to enhanced disease prevalence and morbidity.

Streptococcus canis is a significant problem in kittens that acquire the infection from the genital tract of the queen during birth or via the oropharynx during grooming. The organism gains entry via the umbilical cord and then either directly infects the peritoneal cavity and/or enters the systemic circulation. Neonatal kittens may suffer overwhelming peritonitis and/or sepsis and this agent may be a cause of the so-called “fading kitten” syndrome or peracute deaths (Fig. 40.1). Swelling and exudate may be observed at the umbilicus (omphalophlebitis), and peripheral lymphadenopathy, joint effusion, or pneumonia may also be clinical features. The organism can cause pyometra in queens.²²

Older cats may also be sporadically affected, typically due to a breach in the host’s normal defense mechanisms (e.g., cutaneous wounds, immunosuppressive conditions, viral infections, etc.). Clinical conditions associated with S. canis in adult cats include chronic rhinosinusitis,23 otitis media and meningitis,²⁴ discospondylitis,²⁵ osteomyelitis, endocarditis,²⁶ and myocarditis.²⁷

There are occasional reports of streptococcal toxic shock syndrome (STSS), necrotizing fasciitis (NF), and multiple organ dysfunction in cats caused by S. canis.28–30 Streptococcal toxic shock syndrome is a multisystem syndrome characterized by the sudden onset of shock and organ failure that was first recognized in humans in 1978. In humans, STSS is typically caused by group A streptococci (especially Streptococcus pyogenes) and about half of patients have concurrent NF.

Feline and canine cases of STSS and NF bear striking similarity to human cases although not enough cases have been studied to determine predisposing factors. In human medicine, scoring systems have been developed to help physicians distinguish early NF lesions from other less aggressive infections. However, no scoring systems have been developed for veterinary patients. Therefore, NF in cats is initially suspected based on the physical findings (e.g., local erythema, edema, severe pain, sometimes with signs of shock) and surgical findings (e.g., easy separation of fascia from other tissues, copious exudate that is thin and malodorous).³¹ Tissue for culture and histopathology should be taken from the leading edge of the lesion.

Most cases of STSS/NF documented in the veterinary literature involve canine patients. Canine STSS cases caused by S. canis were first identified in Ontario, Canada, in 1995.^32–34 Diagnosis of STSS was established if the animal had evidence of hypotensive shock and involvement of at least one organ or system in association with isolation of S. canis from a normally sterile site. Many cases had both STSS and NF, which appeared to increase mortality as it does in humans. Necrotizing fasciitis lesions often involve limbs and are characterized by intense pain with localized swelling that requires extensive drainage and débridement. Also similar to human cases, onset of clinical signs is sudden, disease progression is rapid, and the mortality rate is high.

A toxic shock–like syndrome associated with septicemia caused by a group G Streptococcus species was reported in three related kittens that presented with depression, pyrexia, respiratory signs, and limb swelling (although findings were not compatible with NF).²⁸ Two of the three kittens died. Sporadic case reports of NF in cats appear in the literature associated with various pathogens, including Prevotella bivia,³⁵ Acinetobacter baumannii,³⁶ and Fournier’s gangrene.^37,38 A few reported cases involved S. canis, including one fatal case of NF and necrotizing myositis with pneumonia³⁰ and another case that survived after extensive débridement and negative pressure wound management.²⁹

In contrast to individual case reports, reports of invasive streptococcal disease resembling STSS/NF affecting large numbers of intensively housed shelter cats have been reported in the United States with mortality rates up to 30%.¹⁷ Two distinct presentations have been noted. In two shelter outbreaks, skin ulceration and chronic respiratory infection progressed to necrotizing rhinitis/sinusitis and suppurative meningitis. Skin ulceration was most often found on distal limbs, and two or more limbs could be affected. Necrosis and perforation of the nasal bone overlying the frontal sinus were seen with subsequent cellulitis and edema of subcutaneous (SC) tissues causing the nasal bridge area to swell. In another shelter, rapid progression from NF with skin ulceration (Fig. 40.2) to toxic shock–like syndrome, sepsis, and death occurred.

These shelter outbreaks share some common and alarming characteristics. Although upper respiratory tract disease (URTD) was endemic in both shelters, S. canis was typically the sole pathogen reported in these cases. Although the S. canis isolates were sensitive to multiple antibiotics in vitro, treatment of patients was not always successful. Also, extensive environmental cleaning was often unable to prevent persistence of the bacteria in the environment. In an older report of an outbreak in a closed specific pathogen-free colony, only depopulating the affected building stopped the outbreak.39

The factors that allow a typically commensal organism to cause invasive life-threatening disease are not well-understood. Little is known about S. canis virulence factors in severe disease. All affected cats in one study carried almost identical isolates based on molecular typing, suggesting a clonal origin and spread of a virulent strain.⁴⁰ Other factors could include shelter management practices, stressors, and antibiotic therapy for other conditions. Control measures for shelter outbreaks are discussed later.

Reports of acute, fatal necrohemorrhagic pneumonia and septicemia associated with SEZ in dogs first appeared in racing kennels in the United Kingdom and in research colonies in the early 1980s.41,42 Since 2010, SEZ has been an important emerging pathogen in cats in shelters and large-scale hoarding situations. A large outbreak of upper and lower respiratory tract disease involving SEZ was reported in an Israeli cat shelter.¹⁰ Similarly, 55% of 81 cats with URTD rescued from four hoarding situations in the United States were positive for the organism (along with other common feline URT pathogens) on oropharyngeal and conjunctival swabs submitted for polymerase chain reaction (PCR) testing, and the authors speculated that this might have contributed to the particularly severe nature of the rhinosinusitis observed in these cats.⁴³ Isolated cases have occurred in Canada¹¹ and the United States.⁴⁴ None of the cats had known exposure to horses.

A surveillance study of the prevalence of Lancefield group C streptococci via oropharyngeal swabbing of healthy dogs, cats, and horses in New Zealand showed no tendency for cats to be colonized by this organism, regardless of contact with equines.⁴⁵

In cats, SEZ lacks the hemorrhagic component seen in dogs. Mild to severe rhinitis and sinusitis is a common feature (Fig. 40.3). Postmortem findings include severe acute diffuse bronchopneumonia; some cases also have pleuritis, peritonitis, or pyogranulomatous meningoencephalitis.¹⁰ Co-infection with other organisms (e.g., calicivirus, herpesvirus, Bordetella bronchiseptica, Mycoplasma felis) is common.

In addition to severe upper and lower respiratory tract disease, SEZ has been isolated from two cats with acute, fatal meningitis, which was likely secondary to the rapid spread of contiguous rhinitis.11 Progression to the brain from otitis media/interna was also documented in one successfully treated indoor cat.⁴⁴

As in canine outbreaks of disease due to SEZ, contributing factors in feline outbreaks are not well-understood. There is evidence that some canine outbreaks may be due to virulent SEZ strains, and molecular analysis of feline isolates has demonstrated that members of the ST173 clonal complex are involved as in dogs.⁴⁶ Environmental and management factors, as well as coinfections, may also play a role in feline disease outbreaks as most cases are reported in intensively housed populations. Unfortunately, there is a lack of knowledge about the incubation period and ease of transmission outside of the shelter environment, as well as the frequency and manner of shedding after recovery for highly pathogenic S. canis and SEZ infections in dogs and cats.

Lancefield group G streptococci are typically sensitive to penicillins, erythromycin, and clindamycin. Systemic and/or CNS infections require high-dose antibiotic therapy (e.g., intravenous penicillin or ampicillin sodium, trimethoprim–sulfonamide, a cephalosporin, or clindamycin) along with intensive supportive therapy. Drug doses are listed in Table 40.3.

Prevention of neonatal infection in endemic environments has been described by treating the queen with 1.0 mL/cat SC injection of a combined benzathine/procaine penicillin (300,000 International Units/mL) at the time of delivery.48 Newborn kittens are treated with the same product (diluted 1 : 6 with sterile 0.9% saline, 0.25 mL/kitten, SC). It is important to note that this protocol will not eliminate the carrier state, but it may reduce the bacterial population enough to protect neonates. Affected juveniles and adults can be treated with penicillin or its derivatives at relatively high doses (as the organism can be harbored in the tonsils).

Successful treatment of NF and/or STSS in veterinary patients parallels recommendations for humans. Saving the patient’s life depends on prompt initiation of aggressive therapy that must be based on a presumptive diagnosis before test results are available. Treatment includes complete surgical débridement of necrotic tissue (often requiring multiple procedures or limb amputation), hemodynamic support, nutritional support, and analgesia. Antibiotic therapy is based on culture results, but broad-spectrum treatment is begun in the interim. Recommended drug regimens based on experience with human cases include a combination of penicillin, an aminoglycoside, and clindamycin.31 Fluoroquinolones are not recommended despite in vitro bacterial susceptibility. In fact, the use of enrofloxacin in dogs with S. canis infections is suspected to have contributed to the emergence of canine STSS/NF because fluoroquinolones may induce bacteriophages encoding superantigen genes and enhance virulence.⁴⁹ Wound management techniques such as active closed-suction drainage⁵⁰ and negative pressure wound therapy^29,51 have been associated with success in veterinary patients.

Control of SEZ and S. canis shelter outbreaks involves isolation of infected cats as the bacteria are shed in respiratory secretions.52 Clinically affected and exposed but apparently healthy individuals should be treated with an appropriate antibiotic as early as possible; duration of treatment is suggested to be 2 weeks.⁵³ If humane care and adequate housing cannot be provided (e.g., for feral cats), euthanasia is recommended. Recovered cats should be quarantined for 2 weeks following complete resolution of clinical signs. Steps should be taken to prevent fomite transmission; environmental cleaning and disinfection are very important. Streptococcal species are inactivated by commonly used quaternary ammonium compounds and oxidizing agents. They are also susceptible to phenol-based compounds, but they are toxic for cats. Although antibiotic choices for treatment of S. canis are predictable, little has been published about antimicrobial susceptabilities for SEZ in cats. In general, group C isolates are expected to be susceptible to penicillin, erythromycin, chloramphenicol (with complete blood count monitoring), and cephalosporins.