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Clinicians are well aware of the fact that patients with Parkinson's disease may significantly deteriorate following a systemic infection or, in its most severe case, may even develop an akinetic crisis. Although this phenomenon is widely observed and has a major impact on the patients' condition, the knowledge about the underlying mechanisms behind is still sparse. Possible explanations encompass changes in the pharmacodynamics of the dopaminergic drugs, altered dopamine metabolism in the brain, alterations in the dopaminergic transmission in the striatum or an enhancement of neurodegeneration due to remote effects of peripheral inflammatory processes or circulating bacterial toxins. This article provides possible explanatory concepts and may hence support formulating hypothesis for future studies in this field.