Society in general at present is considerably misinformed about zoophilia, its stereotypes, and its meaning. The distinction between zoophilia and zoosadism is a critical one to these researchers, and is highlighted by each of these studies. Masters (1962), Miletski (1999) and Weinberg (2003) each comment significantly on the social harm caused by misunderstandings regarding zoophilia: "This destroy[s] the lives of many citizens".Beetz also states the following:

The phenomenon of sexual contact with animals is starting to lose its taboo: it is appearing more often in scholarly publications, and the public are being confronted with it, too. ... Sexual contact with animals – in the form of bestiality or zoophilia – needs to be discussed more openly and investigated in more detail by scholars working in disciplines such as animal ethics, animal behavior, anthrozoology, psychology, mental health, sociology, and the law. More recently, research has engaged three further directions: the speculation that at least some animals seem to enjoy a zoophilic relationship assuming sadism is not present, and can form an affectionate bond.Beetz described the phenomenon of zoophilia/bestiality as being somewhere between crime, paraphilia and love, although she says that most research has been based on criminological reports, so the cases have frequently involved violence and psychiatric illness. She says only a few recent studies have taken data from volunteers in the community.
When MNGCs lyse, they form plaques (a central clear area with a ring of fused cells) that provide shelter for the bacteria for further replication or latent infection. This same process in infected neurons can allow bacteria to travel through nerve roots in the spinal cord and brain, leading to inflammation of the brain and spinal cord. In addition to spreading from cell to cell, the bacteria can also spread through the bloodstream, causing sepsis. The bacteria can survive in antigen-presenting cells and dendritic cells. Thus, these cells act as vehicles that transport the bacteria into the lymphatic system, causing widespread dissemination of the bacteria in the human body.While B. pseudomallei can survive in phagocytic cells, these cells can kill B. pseudomallei by several mechanisms. Macrophages activated by interferon gamma (IFN) have improved the killing of B. pseudomallei via the production of inducible nitric oxide synthase. Acidification of the endosome and degradation of the bacteria is also possible, however, the bacterial capsule and LPS makes B. pseudomallei resistant to lysosomal degradation. Once B. pseudomallei escapes into the host cytosol it can be recognized by pattern recognition receptors such as NOD-like receptors, triggering the formation of the inflammasome and activation of caspase 1, which induces death of the host cell by pyroptosis and further activation of the immune system. Several systemic host defenses also contribute to the immune response.