(88% of the time) and less frequently from bite wounds. In incidents where the patient is in full septic shock, whole blood smears may be effective. Treatment Immediate cleansing of wounds caused by canines and felines can be successful in keeping C. canimorsus infections at bay. Irrigation of wounds with saline is recommended and individuals are encouraged to seek medical help for the administration of antibiotics. Antibiotics are recommended if wounds are deep or individuals postpone seeking medical attention. Antibiotics that contain beta-lactamase inhibitors (i.e., oral Augmentin or parenteral Unasyn) cover C. canimorsus, as well as other organisms common in bites. Penicillin G is the drug of choice, although some isolates have been found to show resistance. C. canimorsus is susceptible to ampicillin, third-generation cephalosporins, tetracyclines, clindamycin, and chloramphenicol. It has shown resistance to gentamicin. Treatment is recommended for a minimum of three weeks. Hospitalization is required in more severe infections. For cases of sepsis, high doses of penicillin are required. Third-generation cephalosporins are often given prior to diagnosis because they cover a broad range of Gram-negative bacteria. After diagnosis, provided the strain is not beta-lactamase-producing, medication should be switched to penicillin G. Presumably, penicillin G could be given with a beta-lactamase inhibitor combination, such as Unasyn, for patients with a beta-lactamase-producing strain. Mortality of meningitis-related infections is much lower than mortality associated with sepsis. Because C. canimorsus induces fulminant sepsis, earlier diagnosis is associated with greater survival. Evasion of immune system C. canimorsus has been observed to multiply in the presence of mouse J774.1 macrophages. Macrophages recognize and kill pathogens by engulfing them. They also secrete cytokines necessary to begin the immune pathway cascade. C. canimorsus bacteria are not internalized by macrophages; in fact, macrophage monolayers break down in their presence, suggestive of a cytotoxin. In the presence of C. canimorsus, cytokine activity is greatly downregulated, because the macrophages fail to produce TNF-α, IL-8, IL-6 and IL-1α, interferon-γ, and nitric oxide. In addition, toll-like receptor 4 (TLR4 ) normally recognizes pathogens and begins a signalling cascade to induce production of proinflammatory cytokines via the NF-κB pathway. In cells infected with C. canimorsus, TLR4 did not activate the signalling pathway, so did not elicit an inflammatory response by the immune system. Because this species does not elicit a strong inflammatory response, the bacteria have ample time for replication before detection by the host immune system. Electron micrographs of J774.1 monolayers