Capnocytophaga canimorsus Infection

Waterhouse-Friderichsen Syndrome Following a Dog Bite in an Asplenic Patient: Case Report and Review of the Literature

“…In our patient, although the cultures remained negative after three weeks of incubation, the MALS can be likely ascribed to a C. canimorsus infection due to the asplenia, the recent dog bite, the stormy course and the gram-bacilli visible inside the neutrophils that were identical to those described in other cases of septic shock due to same organism [14]: thus, is conceivable that this nding could be ascribed either to the antibiotic treatment initiated some days before the ICU admission and/or to the use of a medium not allowing the growth of this germ [15].…”

“…The clinical course is characterized by a septic shock complicated by a DIC that is responsible of the diffuse microvascular thromboses accounting for (a) the rapidly extending skin infarctions 9; (b) the occurrence of HBD and AKI; and (c) the adrenal failure caused by the plugging of the adrenal venules draining the medullary sinusoids and the subsequent increase of the venous pressure leading to the intraglandular hemorrhage. The rapid deterioration of the clinical conditions alongside with the widespread involvement of the skin account for the denomination of "purpura fulminans" (PF) that is often used as a synonymous of the syndrome [9][10][11][12][13][14]. The underlying causes are not fully understood, and include (a) the capsular polysaccharide that affect the host-pathogen interaction by blocking the complement and the phagocytosis; (b) the presence of catalase making them resistant to the H2O2 produced by the macrophages; and (c), in asplenic subjects, the lack of an adequate number of B1a cells due to the absence of the splenic marginal zone B [10].…”

Waterhouse-Friderichsen syndrome following a dog bite in an asplenic patient: case report and review of the literature

“…The clinical course is characterized by a septic shock complicated by a DIC that is responsible of the diffuse microvascular thromboses accounting for (a) the rapidly extending skin infarctions 9, (b) the occurrence of HBD and AKI, and (c) the adrenal failure caused by the plugging of the adrenal venules draining the medullary sinusoids and the subsequent increase of the venous pressure leading to the intraglandular hemorrhage. The rapid deterioration of the clinical conditions alongside with the widespread involvement of the skin accounts for the denomination of “purpura fulminans” (PF) that is often used as a synonymous of the syndrome [ 9 – 14 ]. The underlying causes are not fully understood and include (a) the capsular polysaccharide that affects the host–pathogen interaction by blocking the complement and the phagocytosis, (b) the presence of catalase making them resistant to the H2O2 produced by the macrophages, and (c), in asplenic subjects, the lack of an adequate number of B1a cells due to the absence of the splenic marginal zone B [ 10 ].…”

Cellulitis and transient bacteremia by Capnocytophaga canis after a cat scratch in an immunocompetent patient

“…In relation to the risk factors in the patients from the cases described above, at least three of them presented risk factors that had already been related to C. canimorsus infections, as chronic and heavy alcohol consumption or splenectomy (one patient presented both) [13][14][15][16]. C. canimorsus infections have also been reported in immunocompetent patients [17][18][19].…”