Brucellosis

Table of Contents

  1. Overview
  2. Epidemiology
  3. Pathophysiology
  4. Etiology and Risk Factors
  5. Clinical Presentation
  6. Diagnosis
  7. Treatment
  8. Complications
  9. Prognosis
  10. Prevention
  11. Recent Research
  12. References
  13. Featured Videos

1. Overview

Brucellosis is the most common zoonotic infection worldwide, caused by gram-negative, facultatively intracellular coccobacilli of the genus Brucella. With approximately 500,000 new human cases reported annually — and significant underreporting in endemic regions — the true global burden may exceed 2 million cases per year. The disease was first described by Sir David Bruce in 1887, who isolated the causative organism from the spleens of British soldiers dying of "Malta fever" on the island of Malta; subsequently Bernhard Bang identified Brucella abortus in cattle (1897), giving rise to the common name "Bang's disease."

The cardinal clinical feature is "undulant fever" — waves of fever that characteristically rise in the afternoon and evening, remit, and return — accompanied by profuse sweating with a distinctive musty or "wet hay" odor, profound fatigue, and musculoskeletal pain. Brucellosis can affect virtually every organ system and is notorious for its protean manifestations and capacity to produce focal complications including sacroiliitis, spondylitis, neurobrucellosis, and endocarditis that mimic other serious diseases.

The infection is acquired primarily through consumption of unpasteurized dairy products or undercooked meat from infected animals, direct contact with infected animal tissues (especially placental material during abortions), or inhalation of infectious aerosols in occupational settings. Despite effective antibiotic regimens, brucellosis remains a significant public health problem in developing regions, a persistent occupational hazard for those working with livestock, and an ongoing concern as a potential bioterrorism agent.

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2. Epidemiology

Brucellosis has a worldwide distribution but is highly endemic in specific geographic regions. The highest burden is found in the Mediterranean basin (Spain, Italy, Greece, Turkey), the Middle East (Iraq, Iran, Saudi Arabia, Syria, Kuwait), Central Asia, South and Latin America (Mexico, Peru, Colombia, Argentina, Brazil), Sub-Saharan Africa, and the Indian subcontinent. The WHO estimates approximately 500,000 cases per year are formally reported globally; the true burden is likely 5–20 times higher due to widespread underdiagnosis in resource-limited settings and significant underreporting even in countries with mandatory notification.

In the United States, brucellosis is relatively rare, with approximately 100–200 confirmed cases reported annually to the CDC. The majority are travel-related — acquired during visits to endemic countries — or linked to consumption of imported unpasteurized dairy products such as Mexican-style soft cheeses (queso fresco, queso de mano). Highest incidence in the US is in California, Florida, and Texas, reflecting both the Hispanic-immigrant population (cultural consumption of traditional dairy) and proximity to the US-Mexico border. Brucella melitensis is the species most commonly imported.

Occupational exposure represents a significant risk category: livestock handlers, veterinarians, slaughterhouse and meat-packing workers, dairy farmers, and laboratory personnel are all at elevated risk. In laboratory settings, Brucella is classified as a BSL-3 pathogen; a notable number of laboratory-acquired infections have resulted from inadvertent aerosol generation during processing of clinical specimens before the organism was identified. Male sex and middle age show higher reported incidence, likely reflecting occupational exposure patterns rather than intrinsic susceptibility.

Transmission routes in order of frequency: ingestion of unpasteurized milk, soft cheeses, butter, ice cream, or yogurt from infected goats, sheep, or cattle; direct contact with infected animal tissues (blood, urine, vaginal secretions, aborted fetuses, placentas) through skin abrasions or mucous membranes; inhalation of infectious aerosols in abattoirs or on farms; and, rarely, person-to-person transmission (sexual contact, breastfeeding, blood transfusion, bone marrow transplantation — all documented but uncommon). Human-to-human transmission is not a practical concern for isolation precautions.

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3. Pathophysiology

Brucella species are small (0.6–1.5 × 0.5–0.7 μm), gram-negative, non-motile, non-spore-forming coccobacilli. They are obligate intracellular pathogens that survive and replicate within host phagocytes — primarily macrophages, monocytes, and dendritic cells — by establishing a specialized replication compartment called the "Brucella-containing vacuole" (BCV). The BCV evades lysosomal fusion through a precisely orchestrated trafficking pathway, ultimately maturing into an endoplasmic reticulum (ER)-derived compartment where bacterial replication proceeds unchecked.

Several virulence mechanisms underpin this intracellular survival strategy. The smooth lipopolysaccharide (sLPS) of virulent Brucella strains possesses an unusual lipid A structure with longer fatty acid chains and lower acylation that poorly stimulates TLR4 — in stark contrast to the highly immunostimulatory LPS of enteric gram-negatives — allowing early immune evasion. The Type IV secretion system (T4SS/VirB), encoded by the virB operon, acts as a molecular syringe injecting bacterial effector proteins into the host cell cytoplasm; these effectors modulate vesicular trafficking, suppress pro-apoptotic signaling, and redirect the BCV away from bactericidal endolysosomal pathways toward the ER. The BvrR/BvrS two-component regulatory system controls outer membrane permeability and modulates expression of lipoproteins that interact with host innate immune sensors. Additional virulence factors include Cu-Zn superoxide dismutase and alkyl hydroperoxide reductase that neutralize reactive oxygen species generated during the respiratory burst of infected phagocytes.

After entry via the gastrointestinal mucosa (most common route), the respiratory epithelium (occupational inhalation), or skin/conjunctival mucosa (direct contact), Brucella organisms are phagocytosed by local macrophages and dendritic cells, then transported via lymphatics to regional lymph nodes. Bacteremia follows as infected phagocytes circulate in the bloodstream; organisms are rapidly taken up by tissue macrophages in the liver (Kupffer cells), spleen, bone marrow, and lymph nodes — explaining the hepatosplenomegaly and lymphadenopathy characteristic of systemic disease. The host mounts a predominantly Th1 immune response (IFN-γ, TNF-α, IL-12) essential for macrophage activation and eventual bacterial clearance, but this response is chronically dysregulated by the organism's immune-evasion mechanisms, permitting persistent infection. Granuloma formation — collections of activated macrophages and epithelioid cells — is a pathologic hallmark in liver, spleen, bone marrow, and lymph nodes.

In animals, Brucella preferentially replicates in the gravid uterus and fetal trophoblasts because erythritol — a four-carbon sugar present in high concentrations in animal placentas — serves as an energy source that preferentially stimulates growth. This explains the reproductive pathology (abortion storms) central to animal brucellosis. Humans lack high-erythritol concentrations in reproductive tissues, which explains why human fetal loss, while documented with B. melitensis infection in particular, is less common and less severe than in animals.

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4. Etiology and Risk Factors

The genus Brucella contains multiple species, four of which cause the great majority of human infections:

Additional species with very rare human cases include B. pinnipedialis and B. ceti (marine mammals) and the recently described B. inopinata.

Key risk factors for acquiring brucellosis: consumption of unpasteurized dairy products (milk, soft cheeses, butter, yogurt, ice cream) — the single most important modifiable risk in non-occupational settings; occupational exposure (veterinarians, livestock farmers, abattoir and meat-processing workers, laboratory personnel); travel to endemic regions; contact with animals that abort (placental material is extraordinarily infectious — a single inadvertent mucosal or conjunctival exposure can transmit disease); accidental inoculation with live attenuated animal vaccines (Rev-1, S19) in veterinary personnel; and, very rarely, blood transfusion or organ transplantation from an infected donor.

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5. Clinical Presentation

The incubation period is typically 2–4 weeks, but may range from 1 week to 2 months depending on the infectious inoculum, route of exposure, and species involved. Onset may be insidious (gradual, over 1–2 weeks) or acute (abrupt, within days). Three clinical phases are recognized.

Acute Brucellosis: The hallmark is undulant fever — temperature rises to 38–40°C, characteristically in the afternoon and evening, followed by drenching sweats and then defervescence, cycling over days to weeks. The sweating has a distinctive musty, hay-like, or goat-like odor that experienced clinicians in endemic regions recognize as nearly pathognomonic. Profound fatigue and malaise are often the dominant complaints and may persist long after fever resolves. Headache is nearly universal. Diffuse myalgias and arthralgias, anorexia, and weight loss are common. Hepatomegaly, splenomegaly, or both occur in 20–30% of patients. Peripheral lymphadenopathy is present in 10–20%. Psychological symptoms — depression, irritability, sleep disturbance — are a recognized feature and may antedate or overshadow the somatic presentation, leading to diagnostic delay when the infectious etiology is not considered.

Subacute and Chronic Brucellosis: Symptoms persisting from 2 months to 1 year are termed subacute; symptoms lasting more than 1 year, chronic brucellosis. The clinical course is fluctuating, with periods of apparent improvement alternating with relapse. Focal complications develop in this phase and can dominate the clinical picture.

Focal Complications develop in approximately 30% of cases and may affect any organ system:

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6. Diagnosis

Diagnosis requires integration of epidemiological exposure history, clinical presentation, and laboratory confirmation. Because brucellosis is uncommon in non-endemic countries and mimics many other febrile illnesses, a high index of suspicion and targeted questioning about dietary history, travel, and occupational exposures is essential.

Culture: Blood culture is the gold standard for diagnosis during acute brucellosis, with positivity rates of 50–70% in the acute phase. Brucella grows slowly (requiring 7–21 days of incubation) and may not trigger automated blood culture system alerts; the laboratory must be specifically informed of suspected brucellosis so that bottles are held for extended incubation and manipulated under BSL-3 conditions. Bone marrow culture has the highest yield of any specimen (~80–90%) and is the preferred diagnostic method in subacute or chronic disease, or when blood cultures are negative. Bone marrow culture positivity is maintained even after initiation of antibiotic therapy in some cases. Safety note: Brucella is one of the most common causes of laboratory-acquired infection worldwide — all manipulations beyond initial plating should be performed in a BSL-2 or BSL-3 cabinet; gram stains and subcultures must be conducted with appropriate respiratory protection.

Serology: The Standard Agglutination Test (SAT/Wright's agglutination test) detects IgM and IgG antibodies against smooth-LPS antigens. A single titer of ≥1:160 is considered diagnostically significant in a clinically consistent presentation; a four-fold rise between acute and convalescent sera (collected 4 weeks apart) is confirmatory. The Rose Bengal plate agglutination test (RBPT) is a rapid, inexpensive field screening test with high sensitivity (>97%) but lower specificity — a negative RBPT strongly argues against active brucellosis. The prozone effect (false-negative agglutination due to antibody excess at low dilutions) can cause erroneously low SAT titers — laboratories must routinely test sera at dilutions beyond the zone of inhibition. The Brucellacapt (FELISA/blocking ELISA) detects non-agglutinating antibodies (primarily IgA and some IgG subclasses) that are missed by SAT; it is particularly valuable in chronic brucellosis where the prozone effect is most problematic.

PCR: Real-time PCR targeting conserved sequences in the Brucella genome (e.g., bcsp31, IS711) provides rapid, highly sensitive diagnosis with the advantage of species identification and the ability to work on blood, CSF, joint fluid, or tissue. Sensitivity of blood PCR in acute disease approaches 85–95% in published series. PCR is increasingly used in the diagnosis of neurobrucellosis (CSF PCR), monitoring treatment response (serial blood PCR), and distinguishing relapse from reinfection. Standardization between laboratories remains a limitation.

Imaging: Plain radiographs of the spine and sacroiliac joints are insensitive in early osteoarticular brucellosis and may be normal for weeks to months after symptom onset. MRI is the investigation of choice for suspected sacroiliitis or spondylitis, demonstrating bone marrow edema, joint effusion, and paraspinal soft tissue changes that direct diagnosis and extent-of-disease assessment. CT is useful for detecting paraspinal abscess formation and guiding percutaneous biopsy. Echocardiography (transthoracic and transesophageal) is mandatory in any patient with clinical features suggesting brucella endocarditis — TEE is more sensitive for detecting vegetations and perivalvular extension.

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7. Treatment

Critical principle: Brucellosis must be treated with combination antibiotic therapy — monotherapy is associated with a relapse rate of 30% or higher. Minimum treatment duration for uncomplicated brucellosis is 6 weeks; focal complications require 3–6 months or longer.

Uncomplicated Brucellosis — first-line regimens per WHO and IDSA guidelines:

Spondylitis and Sacroiliitis: Doxycycline plus rifampin for a minimum of 3 months, often extending to 6 months depending on clinical and MRI response. Some experts advocate an initial 2-week course of an aminoglycoside alongside doxycycline before transitioning to doxycycline plus rifampin for the maintenance phase. Surgical intervention is rarely needed unless spinal cord compression, epidural abscess, or severe vertebral instability develops.

Neurobrucellosis: Triple-drug therapy for CNS penetration is recommended: Doxycycline plus Rifampin plus Trimethoprim-sulfamethoxazole (TMP-SMX, 480 mg twice daily) for 3–6 months. Doxycycline achieves adequate CSF levels; rifampin and TMP-SMX enhance CNS penetration. Duration is guided by clinical response and normalization of CSF parameters — serial lumbar punctures every 4–6 weeks are advisable. Corticosteroids may be considered as adjunctive therapy for meningoencephalitis with raised intracranial pressure, though evidence is limited.

Endocarditis: Doxycycline plus Rifampin plus an aminoglycoside (gentamicin) for the initial phase, transitioning to doxycycline plus rifampin for prolonged maintenance — total duration at least 6 months after valve surgery, or longer if surgery is not performed. Valve surgery (repair or replacement) is necessary in virtually all cases of aortic valve endocarditis and in mitral valve disease complicated by severe regurgitation, large vegetations, heart failure, or perivalvular extension. The decision to operate — and its timing relative to antibiotic therapy — should involve cardiac surgery, infectious disease, and cardiology teams.

Pregnancy: Doxycycline is contraindicated. Recommended regimens: TMP-SMX plus Rifampin for the first trimester (aminoglycosides avoided due to fetal ototoxicity risk); after the first trimester, Rifampin alone or TMP-SMX plus Rifampin are options. B. melitensis infection during pregnancy has been associated with spontaneous abortion; treatment may reduce but not eliminate this risk.

Children under 8 years: Doxycycline is relatively contraindicated due to dental staining risk. TMP-SMX plus Rifampin, with or without an aminoglycoside for initial 5–7 days, is the preferred pediatric regimen. For children aged 8 and older, adult doxycycline-based regimens apply.

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8. Complications

Relapse is the most common adverse outcome, occurring in 5–15% of patients treated with optimal combination therapy. The risk is higher with rifampin-based regimens compared to doxycycline-aminoglycoside. Relapse typically occurs within 3–6 months of completing antibiotic therapy and must be distinguished from reinfection (repeat exposure in an endemic setting). Crucially, relapsing isolates remain antibiotic-susceptible — relapse represents failure to eradicate intracellular bacteria, not the emergence of drug resistance. Re-treatment with the original regimen, or with an enhanced combination including an aminoglycoside, is effective in most cases.

Osteoarticular complications — sacroiliitis and spondylitis — may cause prolonged morbidity. Spondylitis with vertebral destruction, epidural abscess formation, or spinal cord compression can require surgical decompression and stabilization; delayed diagnosis and treatment significantly worsen outcomes. Peripheral arthritis generally responds to antibiotic therapy without permanent joint damage.

Neurobrucellosis has a variable prognosis. Most patients with brucella meningitis recover completely with prolonged triple antibiotic therapy; encephalitis and myelitis carry higher risk of permanent neurological deficits (cognitive impairment, weakness, cranial nerve palsies). Psychiatric complications — depression, anxiety, personality change — may persist as post-infectious sequelae beyond bacterial clearance.

Infective endocarditis is the most feared complication of brucellosis, responsible for the majority of brucellosis-related deaths. Even with combined medical-surgical management, mortality is 5–10%; without surgery, mortality exceeds 80% for aortic valve endocarditis. Embolic complications (stroke, visceral infarction) and perivalvular abscess are frequent.

Additional complications include: splenic abscess (uncommon; may require percutaneous drainage or splenectomy); hepatic granulomas and hepatic abscess (rare); epididymo-orchitis (usually responds to antibiotics, testicular infarction or abscess requiring surgery is rare); uveitis (posterior segment involvement reported in neurobrucellosis); brucellosis in pregnancy associated with spontaneous abortion, premature delivery, and intrauterine fetal death — particularly with B. melitensis infection; and chronic brucellosis, a poorly defined syndrome of persistent symptoms (fatigue, musculoskeletal pain, cognitive symptoms) lasting more than 1 year, whose relationship to ongoing active infection versus post-infectious immunological dysregulation remains controversial.

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9. Prognosis

The overall mortality of brucellosis with appropriate antibiotic treatment is low — less than 2% in most modern series. Untreated, mortality may approach 5%, predominantly from undiagnosed endocarditis. The prognosis is substantially worse in specific high-risk subgroups:

Endocarditis carries the worst prognosis of all brucellosis complications. Surgical intervention combined with prolonged combination antibiotics reduces but does not eliminate mortality (5–10% in treated series). Patients who cannot undergo surgery due to comorbidities or delayed diagnosis face very high mortality (>80% for aortic valve endocarditis managed medically alone).

Neurobrucellosis is associated with full recovery in most patients with meningitis treated promptly with triple therapy; encephalitis and myelitis carry higher risk of permanent deficits. Long-term neuropsychiatric sequelae are underrecognized — studies of brucellosis survivors document higher rates of depression, anxiety, and cognitive complaints compared to controls, even after apparent microbiological cure.

Relapse occurs in 5–15% of appropriately treated patients within the first 6 months post-therapy. Relapsing strains remain susceptible to first-line antibiotics; re-treatment is effective in the majority of cases. Serial serology (SAT titers) can help distinguish relapse from serological scar — a four-fold rise in titer or persistent high titers with clinical symptoms warrants re-treatment. It is important to note that SAT titers may remain elevated for years after successful treatment and clinical cure (so-called "serological scar"), and this must not be interpreted as treatment failure in the absence of clinical symptoms.

Long-term musculoskeletal outcomes are generally favorable with prompt diagnosis and adequate antibiotic duration. Sacroiliitis and peripheral arthritis resolve completely in most patients; spondylitis may leave residual vertebral deformity, disc space collapse, or fusion, but neurological recovery is usually achieved if spinal cord compression is treated before irreversible damage occurs.

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10. Prevention

Pasteurization of dairy products is the single most effective and impactful public health intervention for the prevention of human brucellosis. Heating milk to sufficient temperature (63°C for 30 minutes or 72°C for 15 seconds in high-temperature short-time pasteurization) reliably kills Brucella. The dramatic reduction in human brucellosis in Western Europe and North America over the 20th century is directly attributable to mandatory milk pasteurization programs. Conversely, the persistence of raw-milk consumption traditions — and the importation of unpasteurized cheeses — continues to drive cases in countries that have otherwise achieved low livestock prevalence.

Animal vaccination programs are the cornerstone of livestock disease control and represent the most sustainable long-term strategy for reducing the reservoir of human infection. The live attenuated B. abortus strain S19 vaccine (for cattle) and the B. melitensis Rev-1 vaccine (for sheep and goats) have been central to national eradication programs in Europe, North America, Australia, and New Zealand. These programs, combined with test-and-slaughter policies for seropositive animals, have effectively eliminated brucellosis from cattle herds in many developed countries. Gaps remain in developing regions where veterinary infrastructure, cold-chain logistics, and financial resources limit vaccination coverage.

Occupational protection: Workers at risk (veterinarians, livestock handlers, abattoir workers, laboratory staff) should wear appropriate PPE — gloves, gowns, face masks, and eye protection — when handling potentially infectious animal materials, conducting necropsies, or assisting in parturition. Vaccination with live animal vaccines (Rev-1, S19) should never be performed without proper protective equipment, as inadvertent inoculation or aerosol exposure can cause serious infection. In microbiology laboratories, all work with suspected Brucella cultures must be performed under BSL-2 conditions as a minimum, with BSL-3 procedures for activities generating aerosols (e.g., vortexing, sonication, subculture); the clinical laboratory must be informed when brucellosis is clinically suspected before specimen plating.

Traveler precautions: Travelers to endemic regions (Middle East, Mediterranean, Latin America, Central Asia, South Asia) should avoid all unpasteurized dairy products — including locally produced soft cheeses, fresh milk, yogurt, butter, and ice cream — and should avoid consumption of raw or undercooked meat. These precautions should be specifically communicated in pre-travel counseling for travelers to high-risk destinations.

Human vaccine: No licensed human vaccine is available in Western countries. A live attenuated human vaccine (derived from B. abortus strain 19-BA) has been used in the former Soviet Union and China for decades in high-risk occupational groups, but significant side effects (including disease resembling brucellosis at high doses) have limited its adoption elsewhere. Research into safer vaccine candidates — killed whole-cell vaccines, subunit vaccines targeting outer membrane proteins, and attenuated mutants lacking virulence factors such as the T4SS — is ongoing but no licensed product is expected in the near term.

Bioterrorism preparedness: Brucella species are classified as a CDC Category B bioterrorism agent. Their potential for weaponization via aerosol dispersal (extremely low infectious dose by inhalation — estimated <10–100 organisms in animal models), combined with their capacity to cause prolonged incapacitation of a workforce, makes them a biodefense concern. Preparedness planning includes stockpiling of doxycycline and rifampin for mass prophylaxis, laboratory surge capacity, and provider education on the clinical recognition of aerosol-acquired brucellosis (which may present predominantly with respiratory symptoms early in the course).

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11. Recent Research

Molecular diagnostics: PCR-based methods are increasingly supplanting culture as the primary diagnostic tool in well-resourced settings, offering results within hours rather than weeks. Real-time PCR targeting bcsp31, IS711, and omp2 loci achieves sensitivity of 85–97% on whole blood in acute brucellosis. Multiplex platforms that simultaneously identify species and screen for antibiotic resistance markers are under development. Matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF) has emerged as a rapid, accurate method for species-level identification directly from isolated colonies, dramatically reducing the time from positive culture to species confirmation in clinical laboratories.

Treatment optimization: A 2012 Cochrane systematic review (Yousefi-Nooraie et al.) and multiple meta-analyses continue to support the superiority of doxycycline-aminoglycoside combinations over doxycycline-rifampin for uncomplicated brucellosis, based on lower relapse rates. A key area of ongoing investigation is the optimal duration of aminoglycoside therapy — whether a 5-day versus 14-day course affects outcomes — given the nephrotoxicity concerns of prolonged aminoglycoside use. Clinical trials of fluoroquinolone-based regimens have generally been disappointing, with high relapse rates attributed to poor intracellular activity in the ER replication compartment.

Immune evasion mechanisms: Recent structural and functional studies of the Brucella T4SS have revealed how effector proteins BtpA and BtpB mimic host cell signaling proteins to suppress innate immune activation, and how VceC modulates ER stress responses to create a permissive replication compartment. These mechanistic insights are generating novel therapeutic targets for host-directed therapy strategies that could complement antibiotic regimens.

Vaccine research: Second-generation subunit vaccines targeting the outer membrane protein Bp26, lipopolysaccharide O-antigen conjugates, and live-attenuated Brucella mutants lacking T4SS components are in preclinical and early clinical development. The challenge remains achieving protective immunity without the side effects of the live attenuated strains used historically.

Brucellosis in pregnancy: A systematic review and meta-analysis published in 2014 (Vilchez et al.) examined outcomes of 68 reported cases and found a spontaneous abortion rate of approximately 40% in untreated infections and 14% in treated infections, supporting early antibiotic treatment despite the limitations of available regimens in the first trimester. Vertical transmission to the neonate has been confirmed in multiple reports.

Post-brucellosis fatigue syndrome: There is growing evidence that a subgroup of patients experience persistent fatigue, musculoskeletal pain, and cognitive difficulties for months to years after documented microbiological cure — a syndrome with similarities to post-Lyme disease syndrome and long COVID. The pathophysiology remains unclear; proposed mechanisms include residual immune activation, occult persistent infection, or neuroinflammation. Distinguishing this from chronic active infection requiring continued antibiotic therapy is a major clinical challenge and an active area of research.

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12. References

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  5. Solis Garcia del Pozo J, Solera J. Systematic review and meta-analysis of randomized clinical trials in the treatment of human brucellosis. PLoS One. 2012;7:e32090. PMID: 22355408. DOI: 10.1371/journal.pone.0032090
  6. Corbel MJ. Brucellosis in humans and animals. WHO/CDS/EPR/2006.7. World Health Organization; 2006. Available at: WHO Publication 9241547138
  7. Almendro-Vedia VG, Luengo JA, et al. Brucella endocarditis: clinical features and outcomes of 76 cases from a national database. J Infect. 2019;78:366–372. PMID: 30822509. DOI: 10.1016/j.jinf.2019.02.007
  8. Ducrotoy MJ, Bertu WJ, Matope G, et al. Brucellosis in sub-Saharan Africa: current challenges for management, diagnosis and control. Acta Trop. 2017;165:179–193. PMID: 26321469. DOI: 10.1016/j.actatropica.2015.10.011
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  10. Solera J. Update on brucellosis: therapeutic challenges. Int J Antimicrob Agents. 2010;36 Suppl 1:S18–20. PMID: 20951546. DOI: 10.1016/j.ijantimicag.2010.06.015
  11. Yousefi-Nooraie R, Mortaz-Hejri S, Mehrani M, Sadeghipour P. Antibiotics for treating human brucellosis. Cochrane Database Syst Rev. 2012;10:CD007179. PMID: 23076931. DOI: 10.1002/14651858.CD007179.pub2
  12. Dean AS, Crump L, Greter H, et al. Clinical manifestations of human brucellosis: a systematic review and meta-analysis. PLoS Negl Trop Dis. 2012;6:e1929. PMID: 23236528. DOI: 10.1371/journal.pntd.0001929

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Research Papers

The following PubMed topic searches retrieve current peer-reviewed literature on Brucellosis.

  1. Brucellosis review
  2. Brucella intracellular pathogen
  3. Brucellosis doxycycline treatment
  4. Brucella sacroiliitis
  5. Neurobrucellosis diagnosis
  6. Brucella endocarditis
  7. Brucellosis zoonosis global
  8. Brucella melitensis pathogenesis
  9. Brucellosis relapse treatment
  10. Brucella undulant fever
  11. Brucellosis pregnancy
  12. Brucella vaccine animal

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Connections

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