These considerations suggest that models of a potential smallpox attack should incorporate an aerobiological perspective to predict how the infection might propagate in the modern environment. It is particularly important to examine smallpox transmission in hospitals because hospitals have previously been identified as the major site of transmission in developed countries and ill patients will inevitably gravitate to hospitals, at least early in the outbreak before alternatives exist (Mack, 1972 (Mack, , 2003 . Additional attention to prevention of airborne transmission in hospitals from unrecognized cases may not only be an important aspect of public health preparedness for smallpox, but may also benefit society by reduced morbidity and disruption from SARS and other emergent airborne infections. Chitinase Dependent Control of Protozoan Cyst Burden in the Brain Chronic infections represent a continuous battle between the host's immune system and pathogen replication. Many protozoan parasites have evolved a cyst lifecycle stage that provides it with increased protection from environmental degradation as well as endogenous host mechanisms of attack. In the case of Toxoplasma gondii, these cysts are predominantly found in the immune protected brain making clearance of the parasite more difficult and resulting in a lifelong infection. Currently, little is known about the nature of the immune response stimulated by the presence of these cysts or how they are able to propagate. Here we establish a novel chitinase-dependent mechanism of cyst control in the infected brain. Despite a dominant Th1 immune response during Toxoplasma infection there exists a population of alternatively activated macrophages (AAMØ) in the infected CNS. These cells are capable of cyst lysis via the production of AMCase as revealed by live imaging, and this chitinase is necessary for protective immunity within the CNS. These data demonstrate chitinase activity in the brain in response to a protozoan pathogen and provide a novel mechanism to facilitate cyst clearance during chronic infections. The brain has unique structures in place to limit access of immune cells and molecules. Although this can provide protection against an overambitious inflammatory response it may also lead to the high prevalence of latent and chronic infections that can persist at this site. Removal of such pathogens has its own particular problems in an organ dense with sensitive neurons and stringent gateways for immune cell infiltration. Toxoplasma gondii is a common intracellular protozoan parasite that forms a chronic infection in the brain for the lifetime of the host. The infection is controlled, in part, through the effector mechanisms of macrophages that result in the conversion of fast replicating tachyzoites to the slow replicating, cyst forming bradyzoites [1] [2] [3] . Cysts can form in all tissues but exist predominantly in the brain for the lifetime of the host requiring a continuous immune response to prevent cyst reactivation and Toxoplasmic encephalitis, a common cause of AIDS related fatalities [4, 5] . The infection-induced immune response in the brain consists of activated CNS resident cells including astrocytes and microglia, infiltrating CD4+ and CD8+ T cells, peripheral macrophages and substantial tissue remodeling [6] [7] [8] . Such immune activity in the brain is often associated with a pathological outcome yet despite the high prevalence of infection Toxoplasma is seemingly controlled without adverse neurological damage. The mechanisms that are involved in the trafficking and control of such a potentially pathological immune response within the CNS are only beginning to be understood [6, [8] [9] [10] [11] . The cyst and cyst-forming bradyzoites are poorly immunogenic [12, 13] and although we have known for some time that T cells are required to prevent cyst reactivation [4, 5, 14] , very little is understood about the biology of this structure in the brain. Although anti-Toxoplasma drugs are available that efficiently control the tachyzoite, there are as yet no therapies available that can effectively remove the cyst form of the parasite. Thus, the continuous presence of Toxoplasma cysts in the brain presents a critical and constant danger for the immune compromised patient.