GUIDELINE for Streptococcal infections

Published: 01/01/2015
Last updated: 21/05/2024
Last reviewed:

The Streptococcal infections guidelines were first published in the Journal of Feline Medicine and Surgery (2015) 17:620-625 by Tadeusz Frymus et al. The present update was authored by Tadeusz Frymus.

Key points

  • Streptococcus canis, part of the commensal mucosal flora in cats, can cause disease as a result of predisposing factors.
  • These conditions include neonatal septicaemia, cervical lymphadenitis, abscesses, pneumonia, discospondylitis, osteomyelitis, polyarthritis, urogenital infections, necrotizing fasciitis/myositis, streptococcal toxic shock syndrome, sinusitis, meningitis, and endocarditis.
  • Streptococcus equi zooepidemicus can induce severe haemorrhagic pneumonia, mostly in canine shelters, but occasionally also in cats. Clinical signs of feline pneumonia and sinusitis included purulent nasal discharge, cough, dyspnoea, otitis media-interna, meningoencephalitis and death.
  • High incidence of e. subsp. zooepidemicus infections have been reported in cats from a hoarding environment suffering from pneumonia or other conditions.
  • A tentative diagnosis of a streptococcal infection can be made basing on the presence of gram-positive coccus chains in the lesions or exudates and confirmed by culture and identification of the bacteria.
  • All streptococcal strains isolated from animals were sensitive to penicillin and amoxicillin. First-generation cephalosporin is a treatment alternative.
  • There are no vaccines against streptococcal infections for cats.
  • Proper cattery hygiene and management, including stress reduction and regular core vaccinations can reduce the risk of secondary streptococcal complications.


Though different streptococci have been isolated occasionally from cats, including S. agalactiae, S. pneumoniae, S. suisS. pyogenes, the most prevalent one is S. canis, for which dogs and cats are the natural host (Prescott et al., 2023). In addition, Streptococcus equi subsp. zooepidemicus became an emerging pathogen in dogs, and later also in cats (Blum et al., 2010; Polak et al., 2014).

Agent properties and epidemiology

Streptococcus canis infection

Historically this beta-haemolytic Lancefield group G gram-positive bacterium was considered a canine pathogen, being part of the skin and mucosal microbiota of healthy individuals, but sometimes inducing disease ranging from mild superficial inflammation to severe invasive conditions (Pagnossin et al., 2022). Now S. canis is known to cause disease in a variety of other mammals, including cats and humans.

In cats, this bacterium is also considered part of the commensal mucosal flora of the oral cavity, upper respiratory tract, genital organs and perianal region. The infection seems to be sporadic in single-cat households, especially in older cats (Prescott et al., 2023). In contrast, up to 70-100% of young queens (up to 2 years of age) in breeding catteries may carry this bacterium in the vagina, resulting in infection of the kittens, but also in the transfer of passive immunity against S. canis via colostrum. The level of maternally derived antibodies, immune response, age, infection pressure, stress, and probably also the strain virulence, determine whether the bacteria cause disease or not.

In up to 10% of cats suffering from chronic upper respiratory tract disease, S. canis can be isolated from the nasal cavity (Pesavento and Murphy, 2014; Fig. 2).  Outbreaks in cats with fatal disease have been reported in shelters and breeding colonies (Pesavento and Murphy, 2014), as all the conditions mentioned above may result in septicaemia and embolic lesions, especially of the lung and heart (Prescott et al., 2023).

S. canis infections are believed to be very rare in humans compared to those caused by other bacteria, but their real incidence might be underestimated (Pagnossin et al., 2022).

More information on S. canis can be found in the reviews by Prescott  et al. (2023) as well as by Pagnossin et al. (2022).

Streptococcus equi subsp. zooepidemicus

Streptococcus equi subsp. equi (commonly referred to as S. equi) and Streptococcus equi subsp. zooepidemicus (S. zooepidemicus), both beta-haemolytic gram-positive Lancefield group C bacteria, are the most important equine streptococci worldwide (Timoney et al., 1998). S. equi is an obligate agent causing strangles, the most frequently diagnosed infectious disease of horses, and one which is both devastating and highly contagious. S. equi is host-restricted, infecting almost exclusively equines.

S. zooepidemicusis regarded a mucosal commensal, most notably in equines, with a potential to cause serious opportunistic disease secondary to viral infections, heat exposure, transportation or other stressful situations (Hoffman et al., 1993). Believed to be part of the normal microflora of the upper respiratory airways and lower reproductive tract, this bacterium is frequently isolated from suppurative discharge in horses including complications of viral infections of the upper airways (Hoffman et al., 1993; Timoney et al., 1998). However, in contrast to S. equiS. zooepidemicusstrains are highly diverse and are not restricted to causing disease in horses. These strains have been found in a wide range of other species including pigs, cattle, sheep, goats, poultry, dogs, cats, guinea pigs, seals, dolphins, monkeys, llama and farmed red deer (de Lisle et al., 1988; Sharp et al., 1995; Soedarmanto et al., 1996; Hewson and Cebra, 2001; Las Heras et al., 2002; Akineden et al., 2007; Timoney, 2008; Pisoni et al., 2009; Blum et al., 2010; Lamm et al., 2010; Priestnall and Erles, 2011; Venn-Watson et al., 2012). Occasionally glomerulonephritis, rheumatic fever, meningitis or purulent arthritis caused by S. zooepidemicus have been reported in humans (Kuusi et al., 2006; Abbott et al., 2010; Pelkonen et al., 2013). Many of these zoonotic conditions resulted from contact with horses or from the consumption of unpasteurized milk of cows or goats. In addition, transmission of S. zooepidemicus from a dog to a handler has been documented (Abbott et al., 2010), and a human case of an acute S. zooepidemicus infection (with cellulitis and bacteraemia), resulting from a bite by a feral cat with nasal discharge, has been described (Dolapsakis et al., 2023).

There is increasing evidence that the veterinary role of S. zooepidemicus may be underestimated, and concern has been expressed that this bacterium may be “potentially more than just an opportunist” (Björnsdóttir et al., 2012). Several outbreaks in species other than horses have been described. In Asia, pandemics have occurred in pigs (Feng and Hu, 1977; Soedarmanto et al., 1996). Also, in companion animals, the incidence of infections by this agent has apparently increased. Since 2003, several outbreaks of an acute S. zooepidemicus related severe haemorrhagic canine pneumonia have been described in many countries (Chalker et al., 2003; Kim et al., 2007; Gibson and Richardson, 2008; Pesavento et al., 2008; Byun et al., 2009). This disease is highly contagious and often fatal. The most prominent signs were a sudden onset, fever, dyspnoea, and haemorrhagic nasal discharge. Haemorrhagic pneumonia and pleural effusion were recognized post mortem. Most outbreaks occurred in shelters, where S. zooepidemicus infection caused many deaths. Additionally, kennels and research facilities were involved (Garnett et al., 1982), but individually housed dogs were occasionally affected too (Gibson and Richardson, 2008; Abbott et al., 2010).

It is generally considered that, in contrast to S. canisS. zooepidemicus is not a part of the normal flora of dogs and cats (Smith, 1961; Bailie et al., 1978; Biberstein et al., 1980; Devriese et al., 1992). Nevertheless, both canine and feline subclinical infections have been observed (Chalker et al., 2003; Abbott et al., 2010; Acke et al., 2010; Blum et al., 2010). S. zooepidemicus-related diseases secondary to viral infections have been described in dogs, especially in cases with distemper, canine influenza virus (CIV) infections and other conditions (Yoon et al., 2005). The bacterium may also act as a primary cause of canine pneumonia, sometimes with a peracute course, although experimental infections have not been performed (Gower and Payne, 2012).

Horses are common carriers of this bacterium, and so contact with horses is a potential source of infection (Acke et al., 2010). Dogs experimentally infected with CIV and then kept together with healthy horses acquired S. zooepidemicus pulmonary infection (Yamanaka et al., 2012). Indirect transmission should also be taken into consideration, as equine streptococci may survive outdoors for up to several days, and indoors probably longer (Weese et al., 2009). It has been speculated that contact with staff members could explain outbreaks in canine research facilities and urban kennels, where direct contact with horses was excluded (Priestnall and Erles, 2011). Certainly S. zooepidemicus is able to spread between dogs through direct contact, and outbreaks in shelters usually affect large numbers of animals within a short time.

The same probably applies to cats. It has been postulated that close confinement of animals, such as in shelters, research laboratories and other facilities, appears to be the major risk factor for the development of S. zooepidemicus-associated disease in dogs and cats (Chalker et al., 2003; Britton and Davies, 2010). Co-infection with other respiratory pathogens, as well as age and health of the animal on entry to the facility has been shown to be unrelated to later colonization of the respiratory tract by S. zooepidemicus in dogs (Garnett et al., 1982; Chalker et al., 2003). Though it has been shown that strains with the same clonal complex are pathogenic for both dogs and cats (Britton et al., 2018), the role of dogs as a source of feline infections is not known; however, in one shelter, canine haemorrhagic pneumonia caused by this bacterium did not spread to cats located in an adjacent building of the same facility (Byun et al., 2009).

Pathogenesis of streptococcal infections in cats

The pathogenesis of streptococcal infections infection in small animals is poorly understood. Rare but apparently highly lethal results of streptococcal infections in cats are necrotizing fasciitis/myositis and toxic shock syndrome.

Necrotizing fasciitis/myositis usually begins with a skin wound. Proteolytic enzymes produced by S. canis contribute to penetration of the infection, within 24-78 hours, deep into subcutaneous tissue and fascia with extensive gangrene, and sometimes toxic shock syndrome.

In many cats the rapid onset of streptococcal disease and progression of the clinical signs are similar to human toxic shock syndrome caused by Streptococcus pyogenes (Taillefer and Dunn, 2004; Priestnall et al., 2010; Prescott  et al., 2023). Toxic shock is characterized by a hyper-reactive inflammatory response resulting in increased vascular permeability, vasodilatation, increased coagulation and migration of inflammatory cells to the site of infection (Lappin and Ferguson, 2009). Pyrogenic exotoxins produced by some streptococci act as superantigens by binding simultaneously to major histocompatibility complex (MHC) class II receptors on macrophages and T-cell receptors, bypassing conventional antigen presentation, and leading to the activation of a large proportion of T lymphocytes (Fraser and Proft, 2008). The resulting overproduction of proinflammatory cytokines has been linked to increased virulence and has also been suggested to contribute to the pathogenesis of some streptococcal diseases. Marked elevation of the mRNA of some proinflammatory cytokines was also observed in dogs with S. zooepidemicus-induced pneumonia, and three superantigen genes were prevalent among canine isolates of the bacterium (Priestnall et al., 2010). Various typing methods have been used to determine the virulence factors and genetic relationships among different S. zooepidemicus isolates; M-like protein, IgG-binding proteins and fibronectin binding protein appear to be the main virulent factors of this bacterium (Jonsson et al., 1995; Timoney et al., 1995; Hong, 2005).

To date, the factors underlying the differences in pathogenicity between isolates/genotypes of S. canis and S. zooepidemicus in cats remain unknown.

Clinical signs

Feline S. canis-related disease

The clinical course and symptoms of S. canis related disease vary significantly depending on the anatomic site(s) of infection and predisposing factors. The infection is usually opportunistic as a result of wounds, including surgery, immunosuppression or viral infections (Fig. 1). One of the clinical outcomes can be a quickly progressing general illness, associated with a wound that often shows erythema, swelling, and pain around (Sura et al., 2008).

Fig. 1. In adult cats, S. canis infection is usually opportunistic as a result of wounds, surgery, immunosuppression or viral infection. In this shelter cat, viral infection was severely complicated by secondary bacterial infection due to poor hygienic conditions. Courtesy of Tadeusz Frymus, Faculty of Veterinary Medicine, Warsaw University of Life Sciences, Poland

Fig. 1. In adult cats, S. canis infection is usually opportunistic as a result of wounds, surgery, immunosuppression or viral infection. In this shelter cat, viral infection was severely complicated by secondary bacterial infection due to poor hygienic conditions. Courtesy of Tadeusz Frymus, Faculty of Veterinary Medicine, Warsaw University of Life Sciences, Poland

Streptococcal involvement should be also considered in cats with severe purulent respiratory tract disease (Fig. 2), especially pneumonia.

Fig. 2. In some cats suffering from upper respiratory tract disease, S canis can be isolated from the nasal cavity. Courtesy of Tadeusz Frymus, Faculty of Veterinary Medicine, Warsaw University of Life Sciences, Poland

Fig. 2. In some cats suffering from upper respiratory tract disease, S canis can be isolated from the nasal cavity. Courtesy of Tadeusz Frymus, Faculty of Veterinary Medicine, Warsaw University of Life Sciences, Poland

Similarly, septicaemia, especially in cats housed in overcrowded facilities, can have streptococcal aetiology  (Prescott et al., 2023).

Other conditions associated with this pathogen include abscesses, pneumonia, discospondylitis, osteomyelitis, polyarthritis, urogenital infections, necrotizing fasciitis/myositis, streptococcal toxic shock syndrome, sinusitis, meningitis, and endocarditis.

Contamination of the umbilical vein may lead to a generalized infection resulting in neonatal septicaemia. Other reasons resulting in “fading” neonates and kittens are pneumonia, endocarditis, pyothorax, necrotizing fasciitis/myositis, toxic shock syndrome or other severe conditions. In 3 to 7-month-old kittens, a subclinical S. canis infection of the pharynx and tonsils may induce cervical lymphadenitis (Prescott et al., 2023).

Feline S. zooepidemicus-related disease

It was thought that this bacterium played no role in feline disease until an outbreak was described 2010 in a shelter in Israel (Blum et al., 2010). Early clinical signs included an effusive purulent nasal discharge and cough (Fig. 3), progressing to sinusitis, dyspnoea, pneumonia and death. The vaccination status of this cattery was unknown. Between June 2006 and January 2008, 78 dead cats from a shelter housing approximately 700 animals were submitted for post-mortem examination. In 39 of these, the major necropsy findings were severe, acute and diffuse bronchopneumonia (Fig. 4) or bronchioalveolar pneumonia, either suppurative or necrosuppurative in nature. Interstitial multifocal pyogranulomatous pneumonia was present in a few cats, pleuritis in 4 cases, and pyothorax in one animal. Pyogranulomatous meningoencephalitis was found in 4 cats. Necrosuppurative peritonitis was present in one case. The most common histopathological lesions were a diffuse mixed infiltrate of neutrophils, histiocytes and lymphocytes, thickening of the inter-alveolar septa and multifocal bacterial colonies with coccoid forms.

Fig. 3. Purulent nasal discharge and cough may be early signs of S equi subsp. zoopidemicus-related diseases in cats. Courtesy of Tadeusz Frymus, Faculty of Veterinary Medicine, Warsaw University of Life Sciences, Poland

Fig. 3. Purulent nasal discharge and cough may be early signs of S equi subsp. zoopidemicus-related diseases in cats. Courtesy of Tadeusz Frymus, Faculty of Veterinary Medicine, Warsaw University of Life Sciences, Poland

Fig. 4. In cats succumbing to fatal S equi subsp. zooepidemicus infection, the major finding is severe acute and diffuse bronchopneumonia. Courtesy of Karolina Kozlowska, Warsaw, Poland

Fig. 4. In cats succumbing to fatal S equi subsp. zooepidemicus infection, the major finding is severe acute and diffuse bronchopneumonia. Courtesy of Karolina Kozlowska, Warsaw, Poland

S. zooepidemicus was the main pathogen isolated from both the dead cats with signs of respiratory disease, as well as from nasal and pharyngeal swabs or bronchoalveolar lavage obtained from sick animals. In the dead cats, S. zooepidemicus was isolated from the lungs of all cases, and also from the sinuses of a few. The bacterium was also cultured from the pleura in 2 of 4 cases of pleuritis, from the brain in 3 of 4 cases of meningoencephalitis and from the peritoneum in one case of peritonitis. Usually, S. zooepidemicus was isolated alone or was dominant in mixed cultures. However, the bacterium was not isolated from any of the 29 dead cats without clinical and pathological signs of respiratory disease, and only from 2 of 10 animals in which respiratory disease was suspected prior to death, but no gross pathological signs were found on necropsy. S. zooepidemicus could also be isolated from cats showing vague signs of respiratory disease, possibly meaning that cats shed the organism long before signs are detected. This could suggest subclinical carriage. In the few cases with lesions suggesting feline infectious peritonitis, the presence of feline coronavirus was ruled out by immunohistochemistry. Tests for feline herpesvirus (FHV) and feline calicivirus (FCV) were not performed but based on clinical signs, the authors suspected that the cat population in this shelter was infected with both of these viruses. The hygienic conditions and ventilation in this cattery were assessed as adequate and the facilities were not overcrowded. This suggests that S. zooepidemicus may have become persistent in the cattery despite sufficient hygienic practices and treatment. The authors speculated that the transfer to this shelter of a group of cats from another cattery (closed due to poor conditions) prior to the disease outbreak might have induced stress that facilitated the epidemic. However, the source of infection remained unknown. The cats had no contact with horses.

In 2010, a fatal S. zooepidemicus infection in two mature domestic cats housed in separate shelters was also described in Canada (Britton and Davies, 2010). Both animals had been resident for several months in the shelter prior to a sudden onset of a peracute disease with nonspecific clinical signs, and blindness in one cat, followed by death within 24 hours of both cats. Post-mortem examination revealed rhinitis as well as meningitis, and S. zooepidemicus was cultured from the nasal cavity and brain. Both cats had tested negative for feline leukaemia virus (FeLV) antigen and were seronegative for feline immunodeficiency virus (FIV) antibodies. Polymerase chain reaction (PCR) of lung, nasal mucosa and brain, performed post mortem, revealed that both cats were also negative for FCV and feline coronavirus (FCoV), and one was positive for FHV. Interestingly, other cats in these shelters remained normal. Neither of the succumbed cats, nor their shelter attendants, had had contact with horses.

A case of acute S. zooepidemicus meningoencephalitis was also described in an exclusively indoor cat in the USA in 2011 (Martin-Vaquero et al., 2011). It was likely secondary to otitis media/interna, as recognized by computed tomography. The patient presented with neurological signs of a central vestibular lesion and left Horner’s syndrome. From the cerebrospinal fluid, with marked neutrophilic pleocytosis, S. zooepidemicus was isolated in pure culture, but PCR results for Toxoplasma gondii, FCoV and FeLV were negative, as was Cryptococcus sp. antigen enzyme immunoassay testing. A bulla osteotomy and debridement were performed, and according to resistance profile results, the cat was treated with trimethoprim–sulfamethoxazole for 8 weeks. The patient recovered fully.

The pathogenic role of S. zooepidemicus in cat colonies was revealed following an investigation of cat hoarding (Polak et al., 2014). In this study, about 2000 cats were removed from four sanctuaries following reports consistent with animal hoarding. During shelter intake examination, 27% of the animals (366/1368) showed respiratory disease. A subset of 81 cats with respiratory signs was tested for infectious agents by PCR, and 55% were positive for S. zooepidemicus. In a recent study on cats from a hoarding environment suffering from otitis media-interna, S. zooepidemicus was cultured from 26/48 (54%) patients (Jacobson et al., 2023). In addition to the infections of domestic cats presented above, a fatal suppurative meningoventriculitis with intralesional S. zooepidemicus was also described in an elderly, captive snow leopard in Japan (Yamaguchi et al., 2012). This animal had had no contact with horses, but defrosted horse meat was fed routinely and was presumed to be the source of infection.


A tentative diagnosis of a streptococcal infection can be made basing on the history, clinical signs, lesions and the presence of gram-positive coccus chains in the lesions or exudates. In cats with respiratory disease, streptococci can be isolated from nasal and pharyngeal swabs, as well as from bronchoalveolar lavage, and from lung samples or other lesions in fatal cases (Blum et al., 2010). Species identification can be performed basing on colony morphology, haemolytic properties, grouping with Lancefield antisera, and biochemical methods such as the API20 Strep kit (BioMérieux). Quantitative PCR is helpful to detect streptococcal infections (Baverud et al., 2007; Cloet et al., 2023), and MALDI-TOF is also increasingly used for this (Ulrich et al., 2020; Van Tol et al., 2022) .

Assessment of antibiotic resistance of beta-haemolytic streptococci is not always performed, as all strains isolated from animals are sensitive to penicillin and amoxicillin (Prescott et al., 2023).


Early antibiotic application is the basis of therapy. The drugs of choice for streptococcal infections are beta-lactams, such as amoxicillin (6.6-20 mg/kg every 8-12 h po) or first-generation cephalosporin (cephazolin sodium 20-35 mg/kg every 8 h im or iv, or cephalexin 15-20 mg/kg every 12 h po) (Prescott et al., 2023).

In case of necrotizing fasciitis/myositis, a combination of penicillin G potassium or sodium 20 000 – 40 000 U/kg (or ampicillin sodium 10-20 mg/kg) iv or im every 6-8 h in combination with clindamycin 10 mg/kg every 12 h iv, im or sc should be considered. In addition, intensive surgical treatment of the wound is necessary, which is described in detail by Prescott et al. (2023), along with treatment of septic shock.

If S. zooepidemicus is recognized or suspected as the cause of severe pneumonia, amoxicillin with an aminoglycoside is indicated, as this combination has synergistic activity against this bacterium (Prescott et al., 2023).

In the case of streptococcal meningitis, trimethoprim-sulfamethoxazole (30 mg/kg every 12 h po or iv) can be an alternative to penicillin G. There is only one report of an effective treatment of an acute S. zooepidemicus meningoencephalitis in a cat (Martin-Vaquero et al., 2011). Trimethoprim–sulfamethoxazole administered over several weeks was the main antibiotic.

There are little data about the management of staphylococcal infections in catteries. However, if recognized or suspected, sick cats should be isolated, and staff should wear protective clothing when caring for them. Hands, premises and all contaminated equipment should be thoroughly cleaned and disinfected. Quaternary ammonium disinfectants, phenol-based solutions or oxidising agents are generally recommended.


There are no vaccines against streptococcal infections for cats.


Proper cattery hygiene and management, including stress reduction and regular vaccination against panleukopenia as well as FCV and FHV, can reduce the risk of secondary streptococcal infections. In shelters and other facilities, overcrowding should be avoided. Proper wound care is important in the prevention of necrotic fasciitis/myositis and other severe streptococcal complications, like septic shock, endocarditis, and septicaemia.


ABCD Europe gratefully acknowledges the support of Boehringer Ingelheim (the founding sponsor of the ABCD), Virbac and MSD Animal Health.


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