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2000
Volume 17, Issue 1
  • ISSN: 1874-4672
  • E-ISSN: 1874-4702

Abstract

Brucellosis is an infectious disease caused by different species of bacteria. It is also known as Malta fever, one of the neglected diseases that can cause infection in both animals and humans. Although human-to-human infection is rare, it can spread through the inhalation of airborne agents, and if left untreated, it can lead to serious health complications. In this review, we aim to highlight the pathophysiology, prevention, epidemiology, mitigation, cure, targets for drug development, and vaccine development against human brucellosis. Human brucellosis is mainly caused by consuming unpasteurized milk or dairy products, uncooked meat, and contact with infected animals. Human brucellosis outbreaks are mainly associated with developing and low- to middle-income countries. Brucella is present all over the world, and only some of the regions are at high risk, including Asia, Africa, Eastern Europe, Mexico, South and Central America, the Caribbean, the Mediterranean Basin, and the Middle East. Because of intracellular survival, inhibition of apoptosis, and immune evasion, Brucella can survive and multiply inside the host cell, which can cause chronic disease. By using proteomics approaches, several new drug targets were reported for human brucellosis that can be used for the development of novel drugs. We can also develop an efficient vaccine against human brucellosis by exploring previously reported vaccine candidates against animal brucellosis. The information provided through this review will facilitate research to control and cure human brucellosis and its complicated symptoms.

This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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