Group G streptococcal lymphadenitis in rats

Abstract

Group G streptococci which have been isolated from the oral fora of rats are also normal inhabitants of the human skin, oropharynx, gastrointestinal tract, and female genital tract. This group of streptococci can cause a wide variety of clinical diseases in humans, including septicemia, pharyngitis, endocarditis, pneumonia, and meningitis. Ten days after oral gavage with 7,12-dimethylbenz[a]anthracene, 12 of 22 two-month-old, female, outbred, viral-antibody-free rats presented with red ocular and nasal discharges and marked swelling of the cervical region. Various degrees of firm, nonpitting edema in the region of the cervical lymph nodes and salivary glands as well as pale mucous membranes and dehydration were observed. Pure cultures of beta-hemolytic streptococci were obtained from the cervical lymph nodes of three rats that were necropsied. A rapid latex test system identified the isolates to have group G-specific antigen. These streptococcal isolates fermented trehalose and lactose but not sorbitol and inulin and did not hydrolize sodium hippurate or bile esculin. A Voges-Proskauer test was negative for all six isolates. Serologic tests to detect the presence of immunoglobulin G antibody to rat viral pathogens and Mycoplasma pulmonis were negative. Histopathologic changes included acute necrotizing inflammation of the cervical lymph nodes with multiple large colonies of coccoid bacteria at the perimeter of the necrotic zone. To our knowledge, this is the first report of naturally occurring disease attributed to group G streptococci in rats.

Homophilic protein interactions facilitate bacterial aggregation and IgG-dependent complex formation by theStreptococcus canisM protein SCM

“…Rather, Plg (a further ligand of SCM), co-precipitated with SCM and IgG (Figure 4(b), lanes 3 and 11). We next incubated a constant amount of IgG (20 µg) with different amounts of SCM (1,10,20,40, and 80 µg) and analysed complex formation qualitatively by SDS-PAGE. As depicted in Figure 4(c), increasing concentrations of SCM concomitantly led to an increase in recruited IgG, suggesting that complex formation follows a strict stoichiometrical ratio.…”

“…Streptococcus canis is a frequent colonizer of mucosal surfaces and the skin of dogs and cats, and occasionally identified in various other host species such as cows, rats, minks, mice, rabbits, and foxes [1][2][3][4][5][6]. As an opportunistic pathogen, S. canis infections generally lead to local and self-limiting alterations of skin and mucosa, but in some cases can proceed to severe and life-threatening diseases, such as streptococcal toxic shock-like syndrome (STSLS), necrotizing fasciitis (NF), meningitis and septicemia [7][8][9][10].…”

Microbiological Quality Control for Laboratory Rodents and Lagomorphs

“…Homologous reactions, indicating that an immune serum contains antibodies to the C antigen, can be demonstrated by precipitation or by the agglutination of antibody-coated latex particles (Fig. 2) (Corning et al, 1991;Patterson, 1996;Washington, 1996).…”

The type-2 Streptococcus canis M protein SCM-2 binds fibrinogen and facilitates antiphagocytic properties

“…The group G beta-hemolytic Streptococcus canis commonly colonizes the skin and mucosal surfaces of dogs and cats. Furthermore, S. canis was also identified in various other animal hosts, such as cows, rats, minks, mice, rabbits and foxes ( Corning et al, 1991 ; Iglauer et al, 1991 ; Chaffer et al, 2005 ; Verkühlen et al, 2016 ; Nikolaisen et al, 2017 ; Timoney et al, 2017 ). As an opportunistic pathogen, S. canis infections generally lead to local and self-limiting alterations of skin and mucosa, but in some cases it can proceed to severe and life-threatening diseases, such as streptococcal toxic shock-like syndrome (STSLS), necrotizing fasciitis (NF), meningitis and septicemia ( Miller et al, 1996 ; DeWinter et al, 1999 ; DeWinter and Prescott, 1999 ; Lamm et al, 2010 ).…”