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.
An uncommon complication of a common infection
Aneeka Chavda, Poonam Kapila, Abhinav Kumar.
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
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
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
The Lancet Infectious Diseases
2. Larroche C. Pathogenesis of hemophagocytic syndrome (HPS).
The drugs don
t work; linezolid + rifampicin
Fiona Robb, Lee Stewart, Nitish Khanna, Erica Peters.
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
; 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
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
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.
A rare case of
, Samuel Julie
Freeman Hospital, Newcastle Upon Tyne
Hospitals NHS Foundation Trust,
Newcastle Upon Tyne Hospitals NHS
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.
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