Article information
La Brucellosis es una zoonosis de elevada incidencia en España, sobretodo en zonas rurales. Aunque la afectación neurológica es infrecuente tiene importancia clínica por la morbilidad asociada.
To the editor: Brucellosis is a zoonosis with a high incidence rate in Spain, particularly in rural areas. While neurological involvement is uncommon, it has clinical significance due to the associated morbidity.
Full Text
To the editor: Brucellosis is a zoonosis with a high incidence rate in Spain, particularly in rural areas. While neurological involvement is uncommon, it has clinical significance due to the associated morbidity.
We report the case of a 29-year-old male born in Senegal with an unremarkable epidemiological history. His clinical
history included arterial hypertension and chronic kidney disease (CKD) from an unknown cause on chronic hemodialysis for one year. Patient reported low grade fever and fatigue for the past 15 days. During hemodialysis, he experienced headache, lethargy, and projectile vomiting. Physical examination revealed sleepiness and flapping, temperature of 37.4 ºC, blood pressure of 180/120 mmHg, rhythmic heart sound with panfocal systolic murmur (III/VI), and unremarkable pulmonary auscultation and abdominal examination. Normal neurological examination, with no meningeal signs. Laboratory test results included: blood glucose 82 mg/dL, urea 158 mg/dL, creatinine 14.16 mg/dL, GOT 61 U/L, GPT, 279 U/L, LDH 864 U/L, GGT 298 U/L, CRP 42.9, hemoglobin 12.0 g/dL, WBCs 5.38 10(9)/L with normal differential, and platelet count 167 10(3)/L. All other laboratory parameters were within normal ranges. Ophthalmoscopy: right eye with normal disc and macula, nasal bleeding, and temporal superior arcade with cotton wool exudates; left eye with normal disc. Patient was diagnosed of grade III hypertensive retinopathy. No pathological findings were made in CT and MRI of the brain. Diagnosis of accelerated arterial hypertension led to
start intravenous antihypertensive treatment that achieved optimal control of pressure values, but neurological symptoms persisted. Cerebrospinal fluid (CSF) pressure was increased to 33 mg (normal, up to 20 mmHg), with leukocytosis (36 WBCs/mm3) with a predominance of lymphocytes (70%), increased protein levels (87 g/dL), and low glucose (84 mg/dL). Serologic testing was positive for Brucella, Bengal rose, agglutination with anti-brucella antibodies 1/160, and immune capture with anti-brucella antibodies > 1/5120. CSF and blood cultures were positive
for Brucella spp. Neurobrucellosis was diagnosed, and specific antibiotic therapy was started with doxycycline, rifampin, and trimethoprim-sulfamethoxazole. After five days of treatment, patient experienced a clear improvement, showing no fever or symptoms.
Incidence of brucellosis in Europe is low. In Spain, however, brucellosis is the main zoonosis, and endemic areas continue to exist, particularly in rural cattleraising areas.1 Clinical signs of brucellosis are very diverse, and genitourinary, gastrointestinal, and cardiological manifestations are most common. Central nervous system involvement by brucellosis (neurobrucellosis) is uncommon and mainly causes meningeal signs, although
papilledema, optic neuropathy, radiculitis, and stroke may also occur.2,3 Cases of neurobrucellosis have been reported in patients with CKD living in endemic areas.4 In our patient, the condition occurred as intracranial hypertension and fever.
Diagnosis of neurobrucellosis should be considered in a patient with CKD who also has fever of unknown origin and
neurological signs. When the disease is suspected based on clinical signs, serologic tests allow for confirming diagnosis, and germ isolation from culture is an even more definitive evidence, as in the reported case. While this is an uncommon condition, it should be kept in mind because early diagnosis and treatment decrease the high mortality associated to neurobrucellosis. Long-term treatment should be administered with two or three antibiotics able to cross the blood-brain barrier. Our patient received treatment for three months and has no neurological sequelae.
We report the case of a 29-year-old male born in Senegal with an unremarkable epidemiological history. His clinical
history included arterial hypertension and chronic kidney disease (CKD) from an unknown cause on chronic hemodialysis for one year. Patient reported low grade fever and fatigue for the past 15 days. During hemodialysis, he experienced headache, lethargy, and projectile vomiting. Physical examination revealed sleepiness and flapping, temperature of 37.4 ºC, blood pressure of 180/120 mmHg, rhythmic heart sound with panfocal systolic murmur (III/VI), and unremarkable pulmonary auscultation and abdominal examination. Normal neurological examination, with no meningeal signs. Laboratory test results included: blood glucose 82 mg/dL, urea 158 mg/dL, creatinine 14.16 mg/dL, GOT 61 U/L, GPT, 279 U/L, LDH 864 U/L, GGT 298 U/L, CRP 42.9, hemoglobin 12.0 g/dL, WBCs 5.38 10(9)/L with normal differential, and platelet count 167 10(3)/L. All other laboratory parameters were within normal ranges. Ophthalmoscopy: right eye with normal disc and macula, nasal bleeding, and temporal superior arcade with cotton wool exudates; left eye with normal disc. Patient was diagnosed of grade III hypertensive retinopathy. No pathological findings were made in CT and MRI of the brain. Diagnosis of accelerated arterial hypertension led to
start intravenous antihypertensive treatment that achieved optimal control of pressure values, but neurological symptoms persisted. Cerebrospinal fluid (CSF) pressure was increased to 33 mg (normal, up to 20 mmHg), with leukocytosis (36 WBCs/mm3) with a predominance of lymphocytes (70%), increased protein levels (87 g/dL), and low glucose (84 mg/dL). Serologic testing was positive for Brucella, Bengal rose, agglutination with anti-brucella antibodies 1/160, and immune capture with anti-brucella antibodies > 1/5120. CSF and blood cultures were positive
for Brucella spp. Neurobrucellosis was diagnosed, and specific antibiotic therapy was started with doxycycline, rifampin, and trimethoprim-sulfamethoxazole. After five days of treatment, patient experienced a clear improvement, showing no fever or symptoms.
Incidence of brucellosis in Europe is low. In Spain, however, brucellosis is the main zoonosis, and endemic areas continue to exist, particularly in rural cattleraising areas.1 Clinical signs of brucellosis are very diverse, and genitourinary, gastrointestinal, and cardiological manifestations are most common. Central nervous system involvement by brucellosis (neurobrucellosis) is uncommon and mainly causes meningeal signs, although
papilledema, optic neuropathy, radiculitis, and stroke may also occur.2,3 Cases of neurobrucellosis have been reported in patients with CKD living in endemic areas.4 In our patient, the condition occurred as intracranial hypertension and fever.
Diagnosis of neurobrucellosis should be considered in a patient with CKD who also has fever of unknown origin and
neurological signs. When the disease is suspected based on clinical signs, serologic tests allow for confirming diagnosis, and germ isolation from culture is an even more definitive evidence, as in the reported case. While this is an uncommon condition, it should be kept in mind because early diagnosis and treatment decrease the high mortality associated to neurobrucellosis. Long-term treatment should be administered with two or three antibiotics able to cross the blood-brain barrier. Our patient received treatment for three months and has no neurological sequelae.
