In essence, the reputation of vancomycin as a nephrotoxin is overstated, and it has not been demonstrated that maintaining vancomycin serum levels within certain ranges will prevent its nephrotoxic effects, when they do occur. Ototoxicity
Attempts to establish rates of vancomycin-induced ototoxicity are even more difficult due to the scarcity of quality evidence. The current consensus is that clearly related cases of vancomycin ototoxicity are rare. The association between vancomycin serum levels and ototoxicity is also uncertain. While cases of ototoxicity have been reported in patients whose vancomycin serum level exceeded 80 µg/mL, cases have been reported in patients with therapeutic levels, as well. Thus, whether therapeutic drug monitoring of vancomycin for the purpose of maintaining "therapeutic" levels will prevent ototoxicity also remains unproven. Interactions with other nephrotoxins
Another area of controversy and uncertainty concerns the question of whether, and if so, to what extent, vancomycin increases the toxicity of other nephrotoxins. Clinical studies have yielded variable results, but animal models indicate some increased nephrotoxic effect probably occurs when vancomycin is added to nephrotoxins such as aminoglycosides. However, a dose- or serum level-effect relationship has not been established. Dosing considerations
The recommended parenteral dosage in adults is 500 mg iv every 6 hours or 1000 mg every 12 hours, with modification to achieve a therapeutic range as needed. The recommended oral dosage in the treatment of antibiotic induced pseudomembranous enterocolitis is 125 to 500 mg every 6 hours for 7 to 10 days.
In adults, infection is asymptomatic, which means that the patient is a carrier of the infection, but experiences no symptoms or only mild feverish illness.The mortality rate is less than 1% and most patients with encephalitis clinical symptoms recover completely. Up to 20% of patients develop behavioral problems or recurrent seizures. Pathophysiology
Initial infection by the virus and primary spread of the virus causes the onset of non-specific symptoms such as headache and fever. Secondary spread and the multiplication of the virus in the CNS (central nervous system) causes symptoms such as stiff neck, lethargy and seizures. It then can result in encephalitis, when inflammation of the brain, produced by infection by the virus, damages nerve cells, which affects signaling of the brain to the body. After the virus enters the body via a mosquito bite, the virus undergoes local replication at the skin site where virus entered the body. A primary spread of virus occurs, with seeding of the reticuloendothelial system, mainly in the liver, spleen, and lymph nodes. With the ongoing replication of the virus a secondary spread occurs, with the seeding of the CNS. Not all the cases reach this stage, depending on the efficiency of viral replication at the different stages and the degree of virus spread. The California encephalitis virus invades the CNS through either the cerebral capillary endothelial cells or the choroid plexus. Treatment
Treatments are given to manage the symptoms the patient is having. In patients who are very sick, supportive treatment, such as mechanical ventilation, is equally important.