A case of Bartonellosis presenting as a puzzling multisystem
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A previously well 60-year-old man was admitted with a 10-day history of chest pain, influenza-like symptoms, sore throat, fatigue, myalgia, night sweats and arthralgia. He had worsening pleuritic chest pain in the 2?days prior to presentation. He had no recent travel outside the UK and was not known to be immunocompromised. He had a pet dog but reported no contact with cats; however, he did report a severe dog bite 2?years prior to presentation, which had required surgical intervention. He is a regular gardener but cannot recall any injuries and is normally fit and well with no significant medical history.

There was no palpable lymphadenopathy on examination or other notable findings. He was started on intravenous piperacillin-tazobactam for possible lower respiratory tract infection. He developed a urticarial-type rash on day 1 of his admission.

On admission, he was feverish and had raised inflammatory markers including white cell count of 20.3×109/L (normal value 3.2–10.5×109/L) and C reactive protein of 328?mg/L (normal value 0–5?mg/L).

CT pulmonary angiogram imaging of the chest showed enlarged mediastinal and pretracheal lymph nodes in addition to a pericardial effusion. He underwent endobronchial ultrasound (EBUS) with transbronchial needle aspiration of the mediastinal lymph nodes and endobronchial washings were taken from right lower lobe. EBUS showed lymphadenopathy with benign features and cytology was reported as an excess of lymphoid blasts.

For the pericardial effusion noted on CT imaging, the patient underwent multiple transthoracic echocardiograms and one transoesophageal echocardiogram, which demonstrated no evidence of infective endocarditis but demonstrated growth followed by resolution of the pericardial effusion. MRI of his spine excluded spondylodiscitis and a subsequent CT of his head showed no acute intracranial abnormalities. CT imaging of the abdomen revealed no intra-abdominal source of infection.

Urine dipstick showed proteinuria, and on day 6 of admission, urine microscopy showed cellular and granular casts with simultaneous blood workup showing acute kidney injury (AKI).

Despite six previous negative swab results during this admission, he swabbed positive for COVID-19 on day 12 of admission, therefore, thought to be nosocomial. Throughout admission, nine blood cultures were carried out, all of which showed no growth. Procalcitonin levels were carried out and initially showed a level of 3.57?ng/mL (normal value <0.10?ng/mL), indicative of bacterial infection, which warranted further microbiology testing. Multiple screens were sent for ongoing fever including Mycoplasma, Legionella, hepatitis B, hepatitis C, HIV, Epstein-Barr virus, cytomegalovirus, parvovirus 19, syphilis, gonorrhoea, acid-fast bacilli culture, Aspergillus, beta D-glucan, toxoplasma, Coxiella burnetii, Brucella, Bartonella and respiratory viral screen.

He was discharged with outpatient follow-up on day 14 to await pending investigation results and a positron emission tomography scan.

He was readmitted on day 15 with low oxygen saturations, cough and worsening shortness of breath. Serological tests confirmed the diagnosis of active Bartonellosis and the presence of strongly positive Bartonella antibodies had, by this time, been detected. However, further information regarding subspecies was not available. All other microbiology tests were unremarkable except for a single sputum culture demonstrating Mycobacterium chimaera but this was not reproduced in any other sample. Procalcitonin level on day 18 of admission was 106.15?ng/mL and he was treated with meropenem and doxycycline.

Additionally, he was given intravenous dexamethasone and then swapped to a weaning regime of prednisolone for COVID-19 pneumonia. He was also noted to have intermittent fevers, some associated with rigours, during this admission. On day 19 of admission, he developed stage 2 AKI requiring intravenous fluids. Unfortunately, he deteriorated from COVID-19 and was started on non-invasive ventilation 12 days after swabbing positive and was transferred to the intensive care unit. He developed melena which was managed with intravenous proton pump inhibitors and ablation of the causative duodenal ulcer at oesophagogastroduodenoscopy.

Repeat CT imaging of his chest towards the end of his admission showed extensive multifocal consolidation and ground-glass changes consistent with COVID-19 pneumonitis. There was a small amount of reactive mediastinal lymphadenopathy. He recovered well on the ward with oxygen saturations above 94% in room air and was discharged once clinically improved.

Source: https://casereports.bmj.com/content/14/8/e244002?rss=1
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