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examination he was cachectic with palpable inguinal lymph nodes.

Neurological examination revealed myoclonic jerks of the arm and

reduced upwards gaze but normal power and reflexes. The patient

complained of ocular pain, photophobia and floaters in the vision.

Examination of the eyes revealed a non-descript intermediate uveitis.


Numerous investigations were performed including an

upper gastrointestinal endoscopy and biopsy. Histology of the

duodenal biopsy showed features highly suggestive of Whipple


disease. Fixed paraffin curls from the duodenal biopsy were positive

for Tropherymawhipplei by 16S rRNA PCR. PCR of CSF was also weakly



The patient was treated with 2 weeks of intravenous co-

trimoxazole due to penicillin allergy, then oral co-trimoxazole

planned for at least 1 year. His symptoms started improving and

weight increased by day 10 of treatment.

Discussion and/or Conclusion(s):


s disease is extremely rare

and difficult to recognise. This patient fit the characteristic demo-

graphics being a middle-aged Caucasian male. He did not complain of

diarrhoea, the most common feature of Whipple

s disease, but this

may have beenmasked by opioids taken for back pain. His neurological

and ocular symptoms are recognised but rarer features of Whipple



This case highlights the importance of taking appropriate biopsy

samples, clinical awareness of Whipple

s disease and identifying

pathognomonic features on histology.

ID: 4742

An uncommon complication of a common infection

Aneeka Chavda, Poonam Kapila, Abhinav Kumar.

Sherwood Forest

Hospitals NHS Foundation Trust, King

s Mill Hospital


We report a case of a 55 year old Turkish male with a

background of ulcerative colitis who presented with a two week

history of increasing shortness of breath. He progressively deteriorated

despite being treated with broad spectrum antibiotics and unfortu-

nately died. Evidence of phagocytosis on blood film along with high

serum ferritin (14,519 microgram/mL) and multi organ failure led to

diagnosis of haemophagocytic syndrome (HPS). Four days after his

death, the respiratory samples tested positive for



. HPS due to

Mycobacterium tuberculosis

is uncommon and

only a handful of cases have been reported predominantly in the



HPS is an aggressive and life-threatening syndrome of excessive

immune activation; the excessive inflammation is thought to be

caused by a lack of normal down regulation of activated macrophages

and lymphocytes.


Infection is a common trigger, both in those with a

genetic predisposition and in sporadic cases. Prompt initiation of

treatment is essential for the survival of affected patients. Often the

greatest barrier to a successful outcome is a delay in diagnosis, which

is difficult because of the rarity of this syndrome, the variable clinical

presentation and the lack of specificity of the clinical and laboratory



1. Brastianos PK

et al.

Tuberculosis-associated haemophagocytic


The Lancet Infectious Diseases

. 2006;6:447


2. Larroche C. Pathogenesis of hemophagocytic syndrome (HPS).

Autoimmun Rev

. 2004;3:69


ID: 4749

The drugs don

t work; linezolid + rifampicin

Fiona Robb, Lee Stewart, Nitish Khanna, Erica Peters.

NHS Greater

Glasgow & Clyde


Patient JJ was admitted to NHS Greater Glasgow & Clyde

(NHSGGC) with confusion, fever and acute kidney injury requiring

dialysis. He had a complex medical history including Type II diabetes

and heart failure requiring previous coronary artery bypass graft,

metalic aortic valve (AV) replacement and a pacemaker. Two sets of

blood cultures grew

Staphylococcus aureus

; resistant to penicillin but

sensitive to flucloxacillin, rifampicin, linezolid and clindamycin. A

transthoracic echocardiogram revealed an AV vegetation and aortic

root abscess. Cardio-thoracic surgeons decided surgery was not

possible. The patient was referred to the infection consult team who


Staphylococcus aureus

endocarditis and recommended 6

weeks intravenous (IV) antibiotics (IV flucloxacillin, IV synergistic

gentamicin and oral rifampicin) followed by life-long oral antibiotics;

rifampicin and linezolid. However there was concern that rifampicin

may interact with linezolid resulting in sub-therapeutic plasma



The aim was to identify if recommended thera-

peutic steady-state linezolid plasma concentrations were obtained

when co-administered with rifampicin.


Linezolid was introduced whilst Patient JJ was still

receiving the initial IV antibiotic therapy plan. Linezolid levels, 2 hr

post dose (Cmax) and trough (Cmin), were obtained and sent to the

antimicrobial reference laboratory for analysis.


Linezolid plasma concentrations were reported; Cmax-

8.9 mg/L and Cmin-0.8 mg/L. The recommended optimal steady-

state Cmax and Cmin linezolid concentrations for the treatment

of endocarditis are approximately 15

27 mg/L and 2

7 mg/L


Discussion and/or Conclusion(s):

As a result linezolid was stopped

due to concerns of possible clinical failure. Following completion of IV

antibiotic therapy Patient JJ was discharged home on indefinite oral

rifampicin and clindamycin.

ID: 4755

A rare case of

Ureaplasma urealyticum

pulmonary infection

Harish Reddy


, Samuel Julie




Freeman Hospital, Newcastle Upon Tyne

Hospitals NHS Foundation Trust,


Newcastle Upon Tyne Hospitals NHS

Foundation Trust


U. urealyticum

is a commensal of genito-urinary tract

and sometimes causally linked to disseminated infections in new-

borns, patients with hypogammaglobulinemia, renal transplant,

lymphoma or those undergoing rituximab treatments.


To highlight the rarity of disseminated infection,

in this case of lung abscess possibly secondary to epidydimo-orchitis

in a patient with follicular lymphoma receiving rituximab.


Case: A 51-year old male with follicular lymphoma,

on chemotherapy, was admitted with right groin infection and

pelvic collection following orchidectomy secondary to epidydimo-

orchitis/ruptured testis/scrotal abscess 3 weeks earlier. Urology team

performed incision and drainage of abscess. Patient failed to respond

on standard antibiotics requiring ITU admission for sepsis. He

developed right lung consolidation/cavitation and abscess.


U. urealyticum

was detected by 16S PCR from pleural fluid.

Antibiotics were changed to moxifloxacin for 8 weeks, followed by

complete resolution of clinical symptoms.

Discussion and/or Conclusion(s):

Ureaplasmas are well-known

agents of non-gonococcal urethritis, post-partum fever/abortion,

chorioamnionitis and neonatal sepsis. Infection outside urogenital

tract is extremely rare in adults. Hypogammaglobulinemia seems to be

a risk factor for invasive ureaplasma infection, as demonstrated

by various case reports, especially following rituximab treatment.

Because Ureaplasma was isolated only from pleural fluid, it is impos-

sible to determine the primary source of infection. It is plausible

that the combination of immunosuppression, epidydimoorchitis and

surgery (orchidectomy and scrotal abscess drainage) could have led

to haematogenous dissemination, resulting in lung abscess/pleural


This case highlights a few diagnostic issues:

Ureaplasma is a very rare cause of lung abscess, hence often not

included in the differential diagnosis.

Consider 16S PCR in IC patients with negative routine cultures.

Abstracts of FIS/HIS 2016

Poster Presentations / Journal of Hospital Infection 94S1 (2016) S24