Capnocytophaga canimorsus Capsular Serovar and Disease Severity, Helsinki Hospital District, Finland, 2000-2017.

We assembled a collection of 73 Capnocytophaga canimorsus isolates obtained from blood cultures taken from patients treated at Helsinki University Hospital (Helsinki, Finland) during 2000-2017. We serotyped these isolates by PCR and Western blot and attempted to correlate pathogen serovar with patient characteristics. Our analyses showed, in agreement with previous research, that 3 C. canimorsus serovars (A-C) caused most (91.8%) human infections, despite constituting only 7.6% of isolates found in dogs. The 3 fatalities that occurred in our cohort were equally represented by these serovars. We found 2 untypeable isolates, which we designated serovars J and K. We did not detect an association between serovar and disease severity, immune status, alcohol abuse, or smoking status, but dog bites occurred more frequently among patients infected with non-A-C serovars. Future research is needed to confirm serovar virulence and develop strategies to reduce risk for these infections in humans.

T cell epitope mimicry between Sjögren's syndrome Antigen A (SSA)/Ro60 and oral, gut, skin and vaginal bacteria.

This study was undertaken to test the hypothesis that Sjogren's syndrome Antigen A (SSA)/Ro60-reactive T cells are activated by peptides originating from oral and gut bacteria. T cell hybridomas generated from HLA-DR3 transgenic mice recognized 3 regions on Ro60, with core epitopes mapped to amino acids 228-238, 246-256 and 371-381. BLAST analysis identified several mimicry peptides, originating from human oral, intestinal, skin and vaginal bacteria, as well as environmental bacteria. Amongst these, a peptide from the von Willebrand factor type A domain protein (vWFA) from the oral microbe Capnocytophaga ochracea was the most potent activator. Further, Ro60-reactive T cells were activated by recombinant vWFA protein and whole Escherichia coli expressing this protein. These results demonstrate that peptides derived from normal human microbiota can activate Ro60-reactive T cells. Thus, immune responses to commensal microbiota and opportunistic pathogens should be explored as potential triggers for initiating autoimmunity in SLE and Sjögren's syndrome.

Smoking-related cotinine levels and host responses in chronic periodontitis.

BACKGROUND AND OBJECTIVE: Smoking has been reported to increase the risk of periodontal disease by disrupting the balance of immune responses and tissue repair processes; however, this risk varies among smokers. Cotinine levels in saliva are routinely used to measure the level of smoking, and reflect the quantity of nicotine, and other smoking-related xenobiotics that challenge host systems. This study delineated characteristics of inflammatory mediators in saliva and serum antibody responses to both periodontal pathogens and commensal bacteria in smokers as they related to cotinine levels. MATERIALS AND METHODS: This case-control study (n = 279) examined salivary inflammatory mediator responses [interleukin (IL)-1ß, IL-10, prostaglandin E2, myeloperoxidase and plasminogen activator inhibitor-1], and serum IgG antibody responses to three periodontal pathogens (Aggregatibacter actinomyce-temcomitans, Porphyromonas gingivalis, Treponema denticola) and five commensal oral microorganisms (Veillonella parvula, Streptococcus sanguis, Prevotella loescheii, Actinomyces naeslundii, Capnocytophaga ochracea). RESULTS: The patients were stratified into health (n = 30), gingivitis (n = 55) and periodontitis (n = 184); cotinine levels correlated with reported smoking habits in health, less so with gingivitis, and were not correlated in periodontitis. Of the inflammatory mediators/acute phase proteins, only IL-1ß levels were positively associated (p < 0.001) with the pack years and cotinine levels. As might be predicted, patients with periodontitis smoked more (p < 0.001) and had higher levels of cotinine. IL-1ß and antibody to A. actinomycetemcomitans, P. gingivalis and T. denticola were significantly higher in the patients with periodontitis than either patients with gingivitis or who were healthy. CONCLUSIONS: Generally, antibody to the pathogens and commensals was lower with decreased cotinine levels. Smoking exacerbated differences in both inflammatory mediators and three antibody in periodontal disease compared to healthy subjects.

Resistance of Capnocytophaga canimorsus to killing by human complement and polymorphonuclear leukocytes.

Capnocytophaga canimorsus is a bacterium of the canine oral flora known since 1976 to cause rare but severe septicemia and peripheral gangrene in patients that have been in contact with a dog. It was recently shown that these bacteria do not elicit an inflammatory response (H. Shin, M. Mally, M. Kuhn, C. Paroz, and G. R. Cornelis, J. Infect. Dis. 195:375-386, 2007). Here, we analyze their sensitivity to the innate immune system. Bacteria from the archetype strain Cc5 were highly resistant to killing by complement. There was little membrane attack complex (MAC) deposition in spite of C3b deposition. Cc5 bacteria were as resistant to phagocytosis by human polymorphonuclear leukocytes (PMNs) as Yersinia enterocolitica MRS40, endowed with an antiphagocytic type III secretion system. We isolated Y1C12, a transposon mutant that is hypersensitive to killing by complement via the antibody-dependent classical pathway. The mutation inactivated a putative glycosyltransferase gene, suggesting that the Y1C12 mutant was affected at the level of a capsular polysaccharide or lipopolysaccharide (LPS) structure. Cc5 appeared to have several polysaccharidic structures, one being altered in Y1C12. The structure missing in Y1C12 could be purified by classical LPS purification procedures and labeled by tritiated palmitate, indicating that it is more likely to be an LPS structure than a capsule. Y1C12 bacteria were also more sensitive to phagocytosis by PMNs than wild-type bacteria. In conclusion, a polysaccharide structure, likely an LPS, protects C. canimorsus from deposition of the complement MAC and from efficient phagocytosis by PMNs.

Capnocytophaga canimorsus resists phagocytosis by macrophages and blocks the ability of macrophages to kill other bacteria.

Capnocytophaga canimorsus is a commensal bacterium from the canine oral flora, which can cause septicemia or meningitis in humans upon bite wound infections. C. canimorsus 5 (Cc5), a strain isolated from a patient with fatal septicemia, was used to investigate the interaction between C. canimorsus and J774.1 mouse macrophages. J774.1 cells infected at high multiplicity with Cc5 did not phagocytose nor kill Cc5 within 120 min of infection, unless the bacteria were opsonized with specific antibodies. Opsonization with complement, however, did not increase phagocytosis. Moreover, infection of J774.1 cells with live Cc5 led to the release of a soluble factor, which interfered with the ability of macrophages to kill other phagocytosed bacteria. These results provide an example of how C. canimorsus neutralizes the innate immune system.

Capsular serovars of virulent Capnocytophaga canimorsus are shared by the closely related species C. canis and C. cynodegmi.

Capnocytophaga canimorsus is a dog oral commensal bacterium that causes rare but life-threatening generalized infections in humans who have been in contact with its animal hosts. Two other dog commensals, Capnocytophaga canis and Capnocytophaga cynodegmi, cause rare, mild local infections. To date, nine capsular serovars have been described in C. canimorsus. Here, we serotyped 112 strains of Capnocytophaga spp. isolated from human infections. The C. canimorsus strains (86 of 96, 89.6%) belonged to serovars A, B, or C with relative frequencies of approximately 30% for each serovar. The high prevalence of the A, B, and C serovars in strains isolated from humans, compared to the previously described low prevalence of these serovars among dog isolates (7.6%), confirms that these three serovars are more virulent to humans than other serovars and suggests that the low incidence of disease may be linked to the low prevalence of the A, B, and C serovars in dogs. We serotyped six strains of C. canis and ten strains of C. cynodegmi and, surprisingly, found one C. canis and three C. cynodegmi strains to be of capsular serovar B. This observation prompted us to test 34 dog-isolated C. canis and 16 dog-isolated C. cynodegmi strains. We found four C. canis strains belonging to serovar A and one belonging to serovar F. In contrast, no dog-isolated C. cynodegmi strain could be typed with the available antisera. This work demonstrates that virulence-associated capsular polysaccharides (A, B, and C) are not specific to the C. canimorsus species.

In vitro killing of oral Capnocytophaga by granule fractions of human neutrophils is associated with cathepsin G activity.

The Capnocytophaga are inhabitants of the hypoxic human gingival crevice that are normally prevented by neutrophils from causing periodontal and systemic infection. To identify potential nonoxidative bactericidal mechanisms against Capnocytophaga within human neutrophils, gel filtration chromatography was used to fractionate neutrophil granule extracts. Seven granule fractions, designated A through G, were obtained. The Capnocytophaga were most sensitive to killing by fraction D. Fraction D exhibited substantial bactericidal activity under aerobic and anaerobic conditions. The bactericidal activity associated with ion-exchange subfractions D8-D11, which contained primarily cathepsin G as assessed by enzymatic activity, amino acid composition, and NH2-terminal sequence. Heat-inactivation, diisopropylfluorophosphate, PMSF, and N-benzyloxycarbonylglycylleucylphenylalanyl-chloromethyl ketone inhibited bactericidal activity against Capnocytophaga sputigena but not Escherichia coli. We conclude that (a) human neutrophil cathepsin G is an important antimicrobial system against the Capnocytophaga, (b) the bactericidal activity of cathepsin G against Capnocytophaga is oxygen independent, and (c) an intact enzyme active site is involved in the killing of C. sputigena but not E. coli. We suggest that human neutrophil cathepsin G is an important antimicrobial system against certain oral bacteria and that cathepsin G kills bacteria by two distinct mechanisms.

Evidence for a LOS and a capsular polysaccharide in Capnocytophaga canimorsus.

Capnocytophaga canimorsus is a dog's and cat's oral commensal which can cause fatal human infections upon bites or scratches. Infections mainly start with flu-like symptoms but can rapidly evolve in fatal septicaemia with a mortality as high as 40%. Here we present the discovery of a polysaccharide capsule (CPS) at the surface of C. canimorsus 5 (Cc5), a strain isolated from a fulminant septicaemia. We provide genetic and chemical data showing that this capsule is related to the lipooligosaccharide (LOS) and probably composed of the same polysaccharide units. A CPS was also found in nine out of nine other strains of C. canimorsus. In addition, the genomes of three of these strains, sequenced previously, contain genes similar to those encoding CPS biosynthesis in Cc5. Thus, the presence of a CPS is likely to be a common property of C. canimorsus. The CPS and not the LOS confers protection against the bactericidal effect of human serum and phagocytosis by macrophages. An antiserum raised against the capsule increased the killing of C. canimorsus by human serum thus showing that anti-capsule antibodies have a protective role. These findings provide a new major element in the understanding of the pathogenesis of C. canimorsus.

Association Between Serum Antibodies to Periodontal Bacteria and Rheumatoid Factor in the Third National Health and Nutrition Examination Survey.

OBJECTIVE: Alterations in the microbiome, including the periodontal microbiome, may be a risk factor for rheumatoid arthritis (RA). Most studies that have analyzed this association are relatively small, focus primarily on a single periodontal pathogen (Porphyromonas gingivalis), and are not population based. This study was undertaken to investigate the association between elevated serum levels of IgG antibodies to 19 periodontal species and the prevalence of rheumatoid factor (RF) in a large nationally representative sample of adults. METHODS: The Third National Health and Nutrition Examination Survey (NHANES-III) is a cross-sectional sample of the noninstitutionalized US population (n = 33,994). Our study population included all dentate participants who were 60 years and older, did not have RA as defined by a modified version of the American College of Rheumatology 1987 criteria, and had complete data for both serum IgG antibodies against periodontal bacteria and serum RF antibody titer (n = 2,461). RESULTS: Adjusted odds ratios (ORs) and 95% confidence intervals (95% CIs) summarizing the relationship between the 19 periodontal serum IgG antibodies and RF seropositivity ranged from 0.53 (95% CI 0.29-0.97) to 1.27 (95% CI 0.79-2.06), and 17 of the 19 observed ORs were <1.0. The ORs for RF seropositivity among participants with elevated Prevotella intermedia (0.53 [95% CI 0.29-0.97]) and Capnocytophaga ochracea (0.54 [0.31-0.95]) IgG levels were statistically significant. CONCLUSION: Our findings indicate that elevated levels of IgG antibodies to periodontal bacteria are mostly unassociated with RF seropositivity in the nationally representative NHANES-III. Elevated levels of antibodies to P intermedia and C ochracea are associated with lower odds of RF seropositivity.

Purification of immunosuppressive factor from Capnocytophaga ochracea.

Capnocytophaga, one of the genera of oral bacteria, has been implicated in the pathogenesis of several diseases, including endocarditis, septicaemia and disorders of the oral cavity such as abscesses and periodontal disease. This study examined sonic extracts (SE) of Capnocytophaga strains for their ability to alter lymphocyte function. The SE of tested Capnocytophaga caused dose-dependent suppression of spleen cells in response to mitogen. This suppressive effect was heat-labile and sensitive to the proteolytic enzyme pronase E. The suppressive factor (SF) was purified from SE of C. ochrasea by a combination of ultrogel-AcA34, high-pressure liquid DEAE ion-exchange chromatography and hydroxyapatite columns, which revealed a single band of 14 kDa by SDS-PAGE. Rabbit anti-serum against the purified SF inhibited the immunosuppression induced by SE of C. ochracea with the recovery of lymphocyte proliferation.

HLA-D types and serum IgG responses to Capnocytophaga in diabetes and periodontitis.

Serum IgG responses to the cell envelope proteins (CEPs) from Capnocytophaga sputigena, Capnocytophaga ochracea, and Capnocytophaga gingivalis were examined in periodontally healthy and periodontitis subjects, both with and without type 1 diabetes (n = 60). Serum IgG responses to CEPs were determined by immunoblotting with biotin-goat anti-human IgG and an alkaline phosphatase-streptavidin system. Reactivity was analyzed by transmission densitometry, digitization, and computer manipulation. The patients with diabetes showed significantly (p < 0.01) fewer responses to 14 CEPs (from 81 to 10 kDa) from C. sputigena, 5 CEPs (from 90 to 17 kDa) from C. gingivalis, and the 27-kDa CEP from C. ochracea than in the non-diabetic group. The periodontitis patients showed significantly (p < 0.01) fewer responses to the 25- and 11-kDa CEPs from C. sputigena, the 125- and 17-kDa CEPs from C. gingivalis, and the 42-kDa CEP from C. ochracea than in the periodontally healthy group. HLA-DR4, HLA-DR53, and HLA-DQw3 were associated with periodontitis, while only HLA-DR4 was associated with diabetes (p < 0.02). Significant (p < 0.01) correlations were found between HLA-DR2 and IgG reactivity patterns associated with non-diabetics, and between HLA-DR4 and IgG reactivity patterns associated with diabetic and periodontitis subjects. These results indicate that both type 1 diabetics and periodontitis subjects have a depressed IgG antibody profile to Capnocytophaga, which may account for an increased susceptibility to periodontitis infection. Periodontitis in type 1 diabetes may be related more to the HLA-D type and altered immune function than to the diabetes itself.

Humoral immune response to selected subgingival plaque microorganisms in insulin-dependent diabetic children.

Juvenile diabetics have been shown to have an increased susceptibility to gingivitis and periodontitis following puberty. However, little data are available on changes in the microbial flora that occur at the onset of puberty. This study was performed to determine if antibacterial antibody titers to selected periodontal disease-associated microorganisms might be helpful in revealing changes in plaque flora at the onset and conclusion of puberty. Sera was obtained from 35 subjects (ages 7 to 18 years) selected from a population of insulin-dependent diabetics. The subjects were given a thorough medical examination which included an assessment of sexual maturation and a dental examination which included the recording of onset and magnitude of bleeding according to the papillary bleeding score. Antibody titers to A. naeslundii (AN), B. intermedius (BI), B. gingivalis (BG), F. nucleatum (FN), A. actinomycetemcomitans (AA), C. ochracea (CO) and T. denticola (TD) were determined using the microELISA. Stratification of antibody titers by age groups (less than or equal to 12 years, 12 to 15 years, greater than 15 years) revealed that titers to AN increased significantly (P less than 0.025, ANOVA) and progressively (P less than 0.05, regression analysis) with increasing age. In contrast, the titers to FN were maximal in the under 12 year group and decreased with age (ANOVA, P less than 0.05; regression analysis, P less than 0.05). There were no significant variations in titers observed for the other microorganisms. Stratification by sexual maturity revealed a similar progressive decrease of the titer to FN (ANOVA, P less than 0.05; regression analysis, P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

HLA-D and T lymphocyte reactivity to specific periodontal pathogens in type 1 diabetic periodontitis.

Bacterial antigen fragments complexed with class II major histocompatibility molecules (HLA-D) on antigen presenting cells (APCs) stimulate CD4+ T lymphocyte proliferation, presumably to protect the host. This study examined these responses to antigens of two periodontal pathogens in four groups (n = 15) of age- (young adult) and sex-matched Caucasian subjects with or without type 1 diabetes and moderate to severe periodontitis: Group DP = diabetics with periodontitis; Group DnP = diabetics without periodontitis; Group nDP = nondiabetics with periodontitis; and Group nDnP = nondiabetics without periodontitis. HLA-D phenotypes for each subject were determined by lymphocytotoxicity assays. T lymphocytes purified from peripheral blood were stimulated in cell culture with APC pulsed with various concentrations of tetanus toxoid, Porphyromonas gingivalis, and Capnocytophaga sputigena antigens. T lymphocyte reactivity (3H thymidine incorporation) was numerically lower in cultures from diabetics stimulated with unpulsed APC (not significant), and antigen-pulsed cultures showed low proliferation and no significant differences among groups. Stimulation indices in cultures from diabetic patients stimulated with P. gingivalis or C. sputigena, however, were significantly elevated at all antigen concentrations compared to nondiabetic cultures. The occurrence of HLA-DR4 was moderately associated with diabetes (P < 0.05) and highly associated with periodontitis (P < 0.001, log-linear model for categorical variables); and HLA-DR53 and HLA-DQ3 were significantly associated with periodontitis (P < or = 0.02). HLA-DR was crucial to lymphocyte stimulation (anti-HLA-DR blocking experiments), but the low peripheral blood T cell reactivity to antigens of periodontal pathogens could not be linked with HLA-D type or periodontitis susceptibility.(ABSTRACT TRUNCATED AT 250 WORDS)

Serum antibody responses in human periodontitis to cellular components of Capnocytophaga.

Serum levels of IgM, IgG and IgG-antibody subclasses directed against cell envelopes, lipopolysaccharides and cytoplasmic fractions from Capnocytophaga sputigena, C. gingivalis and C. ochracea were examined in age-, race- and sex-matched periodontally healthy (n = 25) subjects and subjects with adult periodontitis (n = 25). The envelopes and cytoplasmic fractions were obtained by ballistic disintegration of the cells and ultracentrifugation. Cell envelopes were treated with DNase, RNase and lysozyme. Lipopolysaccharides were obtained by hot phenol-water extraction and treated with DNase and RNase. The relative levels of the antibodies in response to the cell fractions were measured by the streptavidinbiotin micro enzyme-linked immunosorbent assay. Both groups showed IgM and IgG antibodies to each fraction of the three Capnocytophaga species, but the frequency of positive IgG subclass responses varied. The IgG4 responses were lower than the other subclasses. There were no significant differences between the IgM antibody levels of the two groups. However, the adult periodontitis group had significantly lower IgG antibody titres to the cell envelopes and cytoplasmic fractions of C. gingivalis and C. ochracea, and lipopolysaccharide of C. gingivalis. These results were reflected in the depressed levels of IgG1 and/or IgG2 to these cellular fractions from the same bacterial species. The adult periodontitis group also showed a lower level of IgG1 to the cytoplasmic fractions of C. sputigena without any depression in the total IgG antibody level. There were no significant differences between the groups in IgG3 and IgG4 antibody levels to any of the cellular fractions.(ABSTRACT TRUNCATED AT 250 WORDS)

Humoral immune responses in experimental gingivitis in rats.

Serum IgG, IgM, and IgA antibody levels to extracts of rat dental plaque and five oral bacteria (Haemophilus actinomycetemcomitans Y-4, Bacteroides gingivalis 381, Bact. intermedius ATCC 25261, Capnocytophaga sp. M-12, Eikenella corrodens ODU) were determined by ELISA. In addition, the presence of rat dental plaque and oral bacterial components in the inflamed gingival tissue was studied using immunofluorescence techniques. Serum and gingival tissue samples were obtained from ODU plaque-susceptible and plaque-resistant rats. In several susceptible rats, IgG, IgM, and IgA antibodies against dental plaque and oral bacteria were detected. There was a correlation between the levels of IgG antibody to dental plaque and pocket probing depth, but not between pocket probing depth and the levels of IgM and IgA. Furthermore, components of rat dental plaque and oral bacteria were detected in the inflamed gingival tissue.

Subgingival microflora and antibody responses against periodontal bacteria of young Japanese patients with type 1 diabetes mellitus.

Periodontal disease is a complication of patients with type 1 diabetes mellitus (T1DM), although the mechanisms responsible for this relationship remain unclear. The aim of this study was to examine oral manifestations and the prevalence of periodontal pathogens from subgingival plaque samples and serum IgG antibody levels against them in young Japanese type 1 diabetic subjects. One hundred and seventeen Japanese T1DM subjects (53 male, 64 female, mean age +/- SD, 16 +/- 6.5 years) participated in this study. Thirty-nine periodontally healthy, age-matched nondiabetics served as controls. T1DM subjects were clinically assigned into three groups: 12 periodontitis, 32 gingivitis and 73 periodontally healthy. Microbiological tests for four periodontal pathogens, Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Prevotella intermedia and Capnocytophaga ochracea were performed using 16S ribosomal RNA-based polymerase chain reaction methods. Serum IgG antibody levels against 12 periodontal bacteria including the four species assessed by polymerase chain reaction were measured by enzyme-linked immunosorbent assay. In the T1DM subjects, the Periodontitis group had a significantly longer mean duration of diabetes and a higher percentages of subjects harbouring P. gingivalis and P. intermedia than the Periodontally Healthy group. Serum IgG antibody levels against P. gingivalis were significantly elevated in the Periodontitis group compared with Gingivitis and Periodontally Healthy groups. These results indicate that Japanese T1DM subjects are a high-risk group for periodontal disease and both P. gingivalis infection and duration of T1DM are risk factors for the progression of periodontitis in patients with T1DM.

Serum phenytoin concentration and IgG antibody titre to periodontal bacteria in patients with phenytoin-induced gingival overgrowth.

Epileptic patients taking phenytoin with gingival-overgrowth and those without gingival-overgrowth were compared for daily drug dose, plasma total phenytoin concentration, plasma free-phenytoin concentration and serum IgG antibody titre against 13 periodontal bacteria. Significantly higher daily drug dose was noted in patients with gingival overgrowth (P < 0.05) when compared with those without overgrowth. In addition, both total and free forms of plasma phenytoin concentration were significantly higher in sera of patients with gingival growth than of those without overgrowth (P < 0.01). Strong positive correlation was found between daily drug dose and serum phenytoin concentration in patients with gingival overgrowth, while weak correlation was found in patients without gingival overgrowth, suggesting a difference in drug metabolism in these two groups. However, no differences were found in serum IgG antibody titres to 13 periodontal bacteria examined between two groups. These results suggest that metabolic ability of phenytoin is one of the factors for developing gingival overgrowth, and that periodontal infection may not be a primary causative factor for gingival overgrowth but act as an additive factor which increase tissue mass for this unwanted side effect.

B-cell mitogenicity and IL-1 beta production of lipopolysaccharides from various Capnocytophaga strains.

To evaluate the etiological roles of Capnocytophaga species in the pathogenesis of periodontal disease, we examined the immunological activities of lipopolysaccharides (LPSs) from various Capnocytophaga strains. All LPSs from various Capnocytophaga species were mitogenic for BALB/c mouse spleen cells, although the responses were lower than those to reference LPSs from Escherichia coli or Salmonella typhimurium. LPSs of C. sputigena strains had polyclonal B cell activation and adjuvant activity and were comparable to reference LPSs. All LPSs from Capnocytophaga strains activated the interleukin-1 beta production from human peripheral monocytes, although the inducing activities of Capnocytophaga LPSs were lower than those of reference LPSs. It appears that LPSs from various Capnocytophaga strains activate certain immunological responses from lymphocytes and monocytes which may be important in the development and pathogenesis of periodontal disease.

Antibiotic treatment following a dog bite in an immunocompromized patient in order to prevent Capnocytophaga canimorsus infection: a case report.

BACKGROUND: Capnocytophaga canimorsus is a commensal bacterium found in the saliva of dogs and cats. Clinically significant infections in humans after a bite are often associated with the presence of immune deficiency. Early recognition and appropriate treatment are crucial for patient survival. In addition, patients with immune deficiency are susceptible to serious life-threatening nosocomial infections, which may also influence the prognosis of patients with Capnocytophaga canimorsus infection. CASE PRESENTATION: A 62-year-old Caucasian female was admitted with septic shock, acute respiratory distress syndrome, acute renal failure, metabolic acidosis and disseminated intravascular coagulation after suffering two small bites from her dog. She had received a splenectomy during childhood. The patient survived after early empiric treatment with antibiotics and intensive supportive care, including ventilation support, a high dose of noradrenalin, and continuous venovenous hemodialysis applied prior to the definitive diagnosis of Capnocytophaga canimorsus sepsis. She improved within 2 weeks but, despite all efforts to prevent nosocomial infection, her hospital course was complicated by Enterococcus species and Candida albicans pleuropneumonia that prolonged her stay in the intensive care unit, and necessitated ventilation support for 2 months. CONCLUSION: Severe Capnocytophaga canimorsus sepsis may be complicated by life-threatening nosocomial infection in immunocompromized patients. The prophylactic application of antibiotics after a dog bite should be considered in high-risk individuals with immune deficiency in order to prevent both Capnocytophyga canimorsus sepsis and serious nosocomial complications.