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Brucella abortus is a small, gram-negative, non-motile, facultative intracellular coccobacillus that primarily infects cattle, causing late-term abortion, retained placenta, and infertility, while also serving as a major zoonotic pathogen in humans leading to brucellosis with symptoms like undulant fever, joint pain, and organ involvement. It survives and replicates within host macrophages by deploying a type IV secretion system (T4SS) to manipulate host vesicular trafficking, inhibit phagosome-lysosome fusion, and modulate ER stress responses via effectors like TcpB and Bsp proteins, thereby evading innate and adaptive immunity. Virulence factors include acid-fast cell walls, exopolysaccharide transporters like ExsA for intracellular persistence, and stress-response enzymes such as catalases for resisting oxidative bursts. In disease, it spreads hematogenously to spleen, liver, bone marrow, and joints, establishing lifelong chronic infections if untreated. Treatment relies on prolonged antibiotic combinations like doxycycline plus rifampin to reduce relapse, though vaccine strains like RB51 pose challenges due to drug resistance; no direct host molecular targets exist, but research explores disrupting bacterial UPR modulation or T4SS for novel therapies. Overall, B. abortus exemplifies a stealth pathogen reliant on host cell hijacking rather than a conventional druggable receptor or enzyme.
Antibiotics inhibit bacterial protein synthesis (tetracyclines), RNA synthesis (rifampin), or folate synthesis (TMP-SMZ); vaccines like S19 and RB51 induce protective immunity by attenuating bacterial replication
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