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\begin{document}

\title{Atypical presentation of \emph{Abiotrophia defectiva} infective
endocarditis in an octogenarian}



\author[1]{Gerard Forde}%
\author[1]{Mary Lucey}%
\author[1]{Paula O Shea}%
\author[1]{Ramadan Shatwan}%
\author[1]{Julie Okiro}%
\author[2]{Eamon Mulkerin}%
\affil[1]{University Hospital Galway}%
\affil[2]{Saolta University Hospital Group}%


\vspace{-1em}



  
  \date{May 25, 2024}


\begingroup
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\selectlanguage{english}
\begin{abstract}
\emph{Abiotrophia defectiva (A defectiva)}, a rare cause of bacterial
infective endocarditis(IE) often presents with pyrexia and florid
sepsis. This case highlights that \emph{A defectiva} IE can present
non-specifically in older frail patients without classical clinical
findings. \emph{A. defectiva} may be associated with a high proportion
of culture-negative IE.%
\end{abstract}%



\sloppy


\textbf{Atypical presentation of \emph{Abiotrophia defectiva} infective
endocarditis in an octogenarian}

\textbf{Gerard Forde, Mary Lucey*, Paula M O Shea**, Julie Okiro,
Ramadan Shatwan*** and Eamon C Mulkerrin}

\textbf{Department of Geriatric Medicine, University Hospital, Galway}

\textbf{*Department of Microbiology, University Hospital, Galway}

\textbf{**Department of Clinical Biochemistry, University Hospital,
Galway}

\textbf{*** Department of Pathology, University Hospital, Galway}

\textbf{Keywords:} infective endocarditis, \emph{Abiotrophia defectiva}
, nutritionally-variant Streptococci, older patients, atypical
presentation

\textbf{Key} \textbf{Clinical Message}

Blood cultures should be performed in non-specifically unwell older
adults following non\textbf{-s} pecific presentations.

Prompt diagnosis and commencement of targeted antimicrobial therapy is
essential in older patients with \emph{A. defectiva} IE.

\textbf{Introduction:}

\emph{A. defectiva,} is an organism which is part of the normal flora of
the intestinal tract, oral cavity and urogenital tract {[}1{]}. It
accounts for up to 6\% of streptococcal infective endocarditis (IE) and
has also been proposed as a possible pathogen in culture-negative
endocarditis {[}2{]}.

Classified as a nutritionally variant streptococcus
(NVS),\emph{A.defectiva} can have devastating implications if missed due
to its high frequency of septic embolisation {[}3{]}. A case of aortic
valve infective endocarditis in an 87-year-old lady with a background
history of severe aortic stenosis (AS) who presented atypically with
bleeding per rectum (PR) and functional decline is described. The
patient gave written informed consent to reporting her clinical and
laboratory data as well as her radiographic images.

\textbf{Case History:}

An 87-year-old lady self-presented to the emergency department (ED) with
a three-day history of bleeding PR associated with general malaise,
subacute weight loss of 5 kg over three months and functional decline
over a five-week period.

This octogenarian was frail (Clinical Frailty Scale score: 8)
pre-admission with known severe aortic stenosis. Past medical history
was otherwise significant for IHD with percutaneous coronary
intervention five months previously, diverticular disease, anal squamous
cell carcinoma (treated definitively with radiotherapy), dystonic
tremor, hypertension and an 80 pack-year smoking history.

The patient denied any significant abdominal pain and had stable
exertional dyspnoea without any recent deterioration in symptoms.
Initial physical examination revealed a blood pressure of 116/50mmHg and
heart rate of 82 beats per minute, an ejection systolic and early
diastolic murmur consistent with mixed aortic valve disease and none of
the stigmata of IE such as splinter haemhorrages, janeway lesions etc.
There was no recorded pyrexia with a temperature of 36.7degrees C and
the patient denied any recent history of rigors. There was pallor and
mild generalised abdominal tenderness on palpation. In the ED, she had
blood cultures as part of her unwell adult (without obvious clinical
cause) investigations, part of the protocol within our service.
Intravenous (IV) co-amoxiclav 1.2g three times daily was commenced for
suspected acute diverticulitis. This lady was anaemic on admission, with
a haemoglobin of 7.7g/dL (reference range 12 - 15 g/dl), necessitating
transfusion of one unit of red cell concentrate (RCC).

Both anaerobic and aerobic bottles of admission blood cultures flagged
positive at 14 hours with Gram-positive cocci in pairs and chains, which
later cultured on chocolate agar and identified as \emph{A.
defectiva}(Figure 1) Other laboratory values on admission included:
white blood cell count (WBC) of 11.6 x 10\textsuperscript{9}/L
(reference range 4 - 10 x 10\textsuperscript{9}/L), absolute neutrophil
count of 9.24 x 10\textsuperscript{9}/L (reference range 2 - 7 x
10\textsuperscript{9}/L), mean corpuscular volume 85.0 fl (reference
range 84 - 96 fl), platelet count of 320 x 10\textsuperscript{9}/L
(reference range 150 - 400 x 10\textsuperscript{9}/L), serum C-reactive
protein of 62 mg/L (reference range 0 -- 5 mg/L), blood urea nitrogen of
8.6 mmol/L (reference range 2.9 -- 8.2 mmol/L), serum creatinine of 108
\selectlanguage{greek}µ\selectlanguage{english}mol/L (reference range 49 -- 90 \selectlanguage{greek}µ\selectlanguage{english}mol/L), serum albumin 31 g/L
(reference range 39 -- 51 g/L), and serum ferritin 1015 ng/mL (reference
range 10 - 200 \selectlanguage{greek}µ\selectlanguage{english}mol/L). The haematological and biochemical parameters of
the patient are tabulated in Table 1.

Thereafter, the patient had two episodes of bleeding PR with associated
fall in haemoglobin and RCC transfusion. She underwent an
oesophagogastroduodenoscopy on day five of admission, which did not
reveal any active/recent bleeding or ulceration.

The patient stabilised over the next 48 hours with clinical improvement
but then had further bleeding PR, although remaining haemodynamically
stable. She was unfit for bowel preparation and/or colonoscopy. Computed
tomography (CT) scans of the abdomen and pelvis were performed to
investigate ongoing gastrointestinal(GI) blood loss against a background
of subacute weight loss. This revealed appearances consistent with
multiple splenic infarcts (Figure 2) and diverticular disease.
Concurrently with the identification of splenic infarcts, the patient
had further bleeding PR with requirement for 2 further units of RCC
transfusion and developed clinical sepsis, evidenced by fluctuating
consciousness, mild hypoactive delirium, tachycardia and low-grade
pyrexia.

The combination of \emph{A. defectiva} bacteraemia with ongoing pyrexia,
known aortic murmur and apparent splenic infarcts on CT scan prompted
the decision to treat as infective endocarditis (IE), as advised by
Clinical Microbiology. Ceftriaxone 2 grams once daily was started
empirically while sensitivity tests were pending. Transthoracic
echocardiogram revealed a large mobile echo-density suggestive of a
vegetation on a stenotic (maximum gradient 74mmHg) aortic valve with
evidence of aortic regurgitation (Figure 3A). A diagnosis of \emph{A.
defectiva} IE was made. The Infectious Disease team was consulted and
intravenous antimicrobial therapy was switched to amoxicillin 1 gram
every four hours and gentamicin 50 milligrams three times daily, with
monitoring of gentamicin serum levels as per protocol. A CT scan of the
brain revealed no radiographic evidence of septic emboli in the brain
parenchyma, a complication frequently associated with \emph{A.
defectiva} endocarditis {[}4{]}.

The patient was deemed not to be a candidate for valve replacement given
her frailty and significant pre-morbid co-morbidities. However, an
initial clinical and biochemical response to antimicrobial therapy was
noted.

.

Unfortunately, on day 15, the patient had further bleeding PR with a
drop in Hb necessitating further RCC transfusion. Later that day, she
was found pulseless and unresponsive and, being declared Not for Active
Resuscitation, she died peacefully on the ward. She had a post-mortem
which confirmed severe aortic stenosis with calcification and vegetation
of the valve leaflets grossly and microscopically (Figure 3B-D) and
severe widespread critical coronary atherosclerosis adjacent to coronary
stents associated with 90\% occlusion involving the three coronary
vessels (Figure 4). There was no evidence of acute ischaemic changes
within the heart. The entire aorta showed severe calcified atheroma.
There was no bleeding focus found in the upper gastrointestinal(GI)
tract, small bowel or large bowel which demonstrated mild diverticular
disease. No evidence of recurrent tumour within the anal area which
revealed evidence of internal haemorrhoids (Figure 5).

Unexpectedly, the spleen showed no evidence of infarction on detailed
examination grossly and microscopically. Kidneys showed granular
cortical surfaces with evidence of hypertensive changes represented by
thickened blood vessels. Lethal cardiac arrhythmia secondary to severe
triple coronary atheroma was the most likely cause of death.

\textbf{Discussion:}

This frail octogenarian presented non-specifically, with relatively
limited haematological and biochemical derangement of acute phase
reactants associated with symptoms of bleeding PR, functional decline
and anaemia. The initial working diagnosis was acute diverticulitis with
associated sepsis. While the patient had initial clinical improvement on
IV co-amoxiclav, she had further bleeding PR and evidence of sepsis
following a switch to oral antibiotics prompting further imaging of the
abdomen and subsequently the heart. The confirmation of \emph{A.
defectiva} bacteraemia with known AS and evidence of potential
embolisation prompted the investigations which lead to a diagnosis of
aortic valve IE. Following the initiation of penicillin-based
antimicrobial therapy repeat blood cultures were sterile. Post-mortem
examination confirmed evidence of aortic valve IE with the likely cause
of intermittent major PR bleeding being haemorrhoids. It is possible
that the source of bacteraemia was secondary to bowel translocation in
the context of recurrent haemorrhagic episodes.

\emph{A. defectiva} is an NVS considered part of the normal flora of the
oral cavity, GI and urogenital tract in humans. In 1961, Fenkel and
Hirsch first isolated a series of satellite streptococci growing
adjacent to larger bacteria on agar media. The larger colonies were
noted to be supplementing the growth of the satellite bacteria, later
termed NVS {[}1{]}. NVS was further speciated in 1991 by Bouvet et al.
to \emph{Streptococcus defectivus} and \emph{Streptococcus
adjacens}{[}5{]}. In 1995 a new genus of NVS was identified through 16S
rRNA sequencing, named \emph{Abiotrophia} {[}6{]}. Further sequencing
carried out by Collins et al. brought about the reclassification of a
number of\emph{Abiotrophia} strains in 2000 and the
\emph{Granulicatella} genus was named {[}7{]}.

Fastidious in nature, NVS characteristically require the addition of
L-cysteine or pyridoxal to grow on blood agar {[}1,7{]}. Due to the
variation in Gram stains, colony morphology and difficulty culturing by
routine laboratory methods, NVS must be considered a potential pathogen
in all culture negative endocarditis {[}1{]}. However, the introduction
of molecular methods of identification such as matrix assisted laser
desorption ionization-time of flight (MALDI-TOF) mass spectrometry has
made it increasingly possible to identify these pathogens in the
clinical laboratory by providing a rapid, accurate and cost effective
means of bacterial identification {[}9--11{]}. Following ionization of
samples, isolates are separated according to mass and analysed by their
`time of flight' to the detector where sample analysis is cross
referenced to a data base and the bacteria is matched and identified
{[}8{]}.

NVS account for 5-6\% of all streptococcal endocarditis {[}1{]}.\emph{A.
defectiva} is rarely cultured successfully and has been attributed to
\textless{}1\% of all bacterial endocarditis {[}9{]}. The organism has a
number of virulence factors such as the production of exopolysaccharide
and the ability to bind with fibronectin which may account for its
propensity to adhere to heart valves and produce the associated embolic
phenomenon which have been previously described {[}13,15,16{]}

Evidence suggests that resistance of \emph{A. defectiva} to penicillin
is increasing {[}10{]}. Alberti et al. carried out an extensive
investigation of susceptibility patterns of a number of NVS. One third
of the isolates examined in the study were susceptible to penicillin,
14\% were resistant and the remaining 53\% were of intermediate
sensitivity. In general \emph{A. defectiva} was found to be more
resistant than \emph{G. adiacens} with 18.9\% of \emph{A.
defectiva}resistant to penicillin. No resistance of \emph{A. defectiva}
to third generation cephalosporins was observed whereas 50\% of \emph{G.
adiacens} isolates were resistant to cefotaxime. All isolates were fully
susceptible to meropenem and vancomycin {[}11{]}. Choice of
antimicrobial treatment in the setting of NVS IE is often not
straightforward, as guidelines on treatment vary and results of
susceptibility testing can often be delayed if isolates are sent to
reference laboratories for work-up. The European Society of Cardiology
(ESC) recommend a number of antimicrobial treatment options including
benzylpenicillin, ceftriaxone and vancomycin combined with an
aminoglycoside for the first 2 weeks of treatment {[}12{]}. However the
British Society of Antimicrobial Chemotherapy do not advise the use of
ceftriaxone with gentamicin in the setting of prosthetic valve
endocarditis or if there is an extra-cardiac focus of infection or if
the person is deemed a candidate for surgery. This is due the risk of
nephrotoxicity and \emph{Clostridium difficile} infection {[}12{]}. The
isolate in this case report was sensitive to both penicillin and
ceftriaxone with minimum inhibitory concentrations of 0.125 mg/L and
0.5mg/L respectively. Despite the sensitivity of this organism the
clinical outcome was poor, reflecting the frequent presence of life
threatening comorbidities in older patients, such as severe IHD in this
case as well as the high pathogenicity and virulence of NVS which is
independent to its antimicrobial sensitivity.

There are over one hundred-case reports of \emph{A defectiva}deep-seated
infection in the literature. These range from quadruple-valve
endocarditis, vertebral osteomyelitis to endophthalmitis and peritonitis
{[}15, 21--23{]}. This pathogen affects all age groups from young
children to very old patients {[}13{]}. However outcomes in children are
much better as surgical intervention is generally successful despite the
presence of embolic complications {[}14{]}. The sudden mortality of this
case is consistent with other case reports of this age-group and is
often a reflection of the high rates of valvular endothelial damage
observed in patients over the age of 60, or severe comorbidities as in
this case {[}19,26{]}.

The vast majority of NVS endocarditis cases evaluated in the literature
refer to presentations with pyrexia associated with features of septic
shock and heart failure {[}15{]}. Cases of \emph{A. defectiva} IE
reported often involve immunocompromised patients and/or the presence of
non-native or structurally defective valves. ?need reference

The atypical presentation of this older patient with non-specific
symptoms represents an unusual manifestation of infection with a rare
organism which classically presents with more florid signs of sepsis
often with devastating consequences. Given the difficulty with culture
and identification of this organism, it is likely that \emph{A.
defectiva} may be associated with a higher proportion of
culture-negative IE than previously reported {[}16{]}. Moreover, it is
conceivable that the prevalence of \emph{A. defectiva} infection in
older patients is higher than reported in the literature.

In this case an intra-abdominal source of sepsis was thought to be
likely. Persistent bleeding PR during the patient's admission against a
background of apparent septic splenic emboli, raised the possibility of
colonic septic embolisation with associated bowel ischaemia. However,
the patient's serum lactate level was always within normal parameters
and her clinical status was not consistent with extensive bowel
ischaemia. Unfortunately, she was unfit for proctoscopy, sigmoidoscopy
or colonoscopy but acute diverticulitis and/or colonic carcinoma were
the most plausible clinical causes for bleeding PR. However, at
post-mortem, haemorrhoids were the likely actual source, with no
pathological evidence of bowel ischaemia, tumour or diverticulitis. This
suggests that bacterial translocation from the lower GI tract was the
most likely source of bacteraemia.

This pathogen is rarely identified clinically and can have devastating
complications often associated with septic embolisation in up to one
third of cases {[}17{]}. This case highlights the importance of
performing blood cultures in non-specifically unwell older adults and
cardiac imaging, especially with known or suspected valvular disease.
The patient, albeit frail and unfit for invasive tests, responded to IV
antibiotics and was returning towards her baseline functional status,
emphasising the importance of accurate diagnosis and definitive
treatment in this frequently encountered population. Her pre-existing
established severe IHD was the likely attributable cause of death,
probably resulting in fatal arrythmia.

Prompt diagnosis, pathogen isolation and commencement of targeted
antimicrobial therapy is essential in older patients with \emph{A.
defectiva} IE. This is particularly important in order to prevent
potentially fatal complications, since presenting symptoms are highly
variable and, non-specific especially in older patients.

\textbf{Author Contribution:}

\textbf{Gerard Forde:} Conceptualization (lead); writing -- original
draft (lead); writing -- review and editing (equal)

\textbf{Mary Lucey:} Conceptualization (secondary); writing -- original
draft (secondary)

\textbf{Paula M O Shea:} Data curation (lead); formal analysis (lead)

\textbf{Ramadan Shatwan:} Writing -- original draft (secondary);
resources (lead)

\textbf{Julie Okiro:} Conceptualization (secondary); writing -- review
and editing (equal)

\textbf{Eamon C Mulkerrin:} Supervision (lead); concetualization
(secondary); writing -- review and editing (equal)

\textbf{Conflict of Interest Statement:}

The authors have no conflicts of interest to disclose.

\textbf{References}

1. Ruoff, K.L., \emph{Nutritionally variant streptococci.} Clinical
microbiology reviews, 1991. \textbf{4} (2): p. 184-190.

2. Senn, L., et al., \emph{Bloodstream and endovascular infections due
to Abiotrophia defectiva and Granulicatella species.} BMC Infectious
Diseases, 2006. \textbf{6} (1): p. 1-6.

3. Stein, D.S. and K.E. Nelson, \emph{Endocarditis due to nutritionally
deficient streptococci: therapeutic dilemma.} Reviews of infectious
diseases, 1987. \textbf{9} (5): p. 908-916.

4. Bajaj, A., et al., \emph{Aortic valve endocarditis by a rare
organism: Abiotrophia defectiva.} J Clin Exp Cardiolog, 2013.\textbf{4}
(276): p. 2.

5. Bouvet, A., F. Grimont, and P. Grimont, \emph{Intraspecies variations
in nutritionally variant streptococci: rRNA gene restriction patterns of
Streptococcus defectivus and Streptococcus adjacens.} International
Journal of Systematic and Evolutionary Microbiology, 1991.\textbf{41}
(4): p. 483-486.

6. Kawamura, Y., et al., \emph{Transfer of Streptococcus adjacens and
Streptococcus defectivus to Abiotrophia gen. nov. as Abiotrophia
adiacens comb. nov. and Abiotrophia defectiva comb. nov.,
respectively.}International Journal of Systematic and Evolutionary
Microbiology, 1995.\textbf{45} (4): p. 798-803.

7. Collins, M.D. and P.A. Lawson, \emph{The genus Abiotrophia (Kawamura
et al.) is not monophyletic: proposal of Granulicatella gen. nov.,
Granulicatella adiacens comb. nov., Granulicatella elegans comb. nov.
and Granulicatella balaenopterae comb. nov.} International journal of
systematic and evolutionary microbiology, 2000. \textbf{50} (1): p.
365-369.

8. Dingle, T.C. and S.M. Butler-Wu, \emph{MALDI-TOF mass spectrometry
for microorganism identification.} Clinics in laboratory medicine,
2013.\textbf{33} (3): p. 589-609.

9. Roberts, R.B., et al., \emph{Viridans streptococcal endocarditis: the
role of various species, including pyridoxal-dependent
streptococci.}Reviews of infectious diseases, 1979. \textbf{1} (6): p.
955-966.

10. Tuohy, M.J., G.W. Procop, and J.A. Washington, \emph{Antimicrobial
susceptibility of Abiotrophia adiacens and Abiotrophia
defectiva.}Diagnostic microbiology and infectious disease, 2000.
\textbf{38} (3): p. 189-191.

11. Alberti, M.O., J.A. Hindler, and R.M. Humphries, \emph{Antimicrobial
susceptibilities of Abiotrophia defectiva, Granulicatella adiacens, and
Granulicatella elegans.} Antimicrobial agents and chemotherapy,
2016.\textbf{60} (3): p. 1411-1420.

12. Habib, G., et al., \emph{ESC Committee for Practice Guidelines.
Guidelines on the prevention, diagnosis, and treatment of infective
endocarditis (new version 2009): the Task Force on the Prevention,
Diagnosis, and Treatment of Infective Endocarditis of the European
Society of Cardiology (ESC). Endorsed by the European Society of
Clinical Microbiology and Infectious Diseases (ESCMID) and the
International Society of Chemotherapy (ISC) for Infection and
Cancer.}Eur Heart J, 2009. \textbf{30} (19): p. 2369-2413.

13. Kohok, D.D., et al., \emph{Subarachnoid hemorrhage in a patient with
Abiotrophia defectiva endocarditis.} The American Journal of the Medical
Sciences, 2011. \textbf{341} (2): p. 157-159.

14. Song, S.H., et al., \emph{Abiotrophia defectiva as a cause of
infective endocarditis with embolic complications in
children.}Infection, 2020.

15. Pinkney, J.A., et al., \emph{Abiotrophia defectiva
endocarditis.}Case Reports, 2014. \textbf{2014} : p. bcr2014207361.

16. Garc\selectlanguage{ngerman}ía-Granja, P.E., R. Ladrón, and J. López, \emph{Nutritionally
variant streptococci infective endocarditis: Report of 5 cases.}Medicina
clinica, 2019. \textbf{152} (5): p. 201-202.

17. Giuliano, S., et al., \emph{Endocarditis caused by nutritionally
variant streptococci: a case report and literature review.} sepsis,
2012. \textbf{1} : p. 2.

Table 1: Routine haematological and biochemical investigations from
admission to day 15 of hospitalisation\selectlanguage{english}
\begin{longtable}[]{@{}lllllllll@{}}
\toprule
\begin{minipage}[b]{0.11\columnwidth}\raggedright\strut
\textbf{Laboratory parameter} \textbf{(Unitage)}\strut
\end{minipage} & \begin{minipage}[b]{0.11\columnwidth}\raggedright\strut
\textbf{Reference Interval}\strut
\end{minipage} & \begin{minipage}[b]{0.11\columnwidth}\raggedright\strut
\textbf{Day 1}\strut
\end{minipage} & \begin{minipage}[b]{0.11\columnwidth}\raggedright\strut
\textbf{Day 2}\strut
\end{minipage} & \begin{minipage}[b]{0.11\columnwidth}\raggedright\strut
\textbf{Day 5}\strut
\end{minipage} & \begin{minipage}[b]{0.11\columnwidth}\raggedright\strut
\textbf{Day 7}\strut
\end{minipage} & \begin{minipage}[b]{0.11\columnwidth}\raggedright\strut
\textbf{Day 8}\strut
\end{minipage} & \begin{minipage}[b]{0.11\columnwidth}\raggedright\strut
\textbf{Day 10}\strut
\end{minipage} & \begin{minipage}[b]{0.11\columnwidth}\raggedright\strut
\textbf{Day 15}\strut
\end{minipage}\tabularnewline
\midrule
\endhead
\begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
Admission Low Hb: 1 unit of RCC\strut
\end{minipage} & \begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
\textsuperscript{*}IV Coamoxiclav 1.2g tds for 5d\strut
\end{minipage} & \begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
OGD No active/ recent bleeding/ ulceration\strut
\end{minipage} & \begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
CTAP Revealed multiple splenic infarcts \& diverticula disease During
the afternoon the patient suffered an additional bleeding PR: 1unit of
RCC given overnight\strut
\end{minipage} & \begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
1 unit of RCC\strut
\end{minipage} & \begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
@08:00h Oral Coamoxiclav switched to IV Ceftriaxone 2g/d @ 14:00h TTE
Revealed a large echo density suggestive for vegetation @ 16:30h
*Amoxicillin 1g every 4h \& Gentamicin 50mg tds\strut
\end{minipage} & \begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
Further bleeding PR 1unit RCC Pulse-les, unresponsive, declared dead
(Rest in Peace)\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
White Cell Count ( 10\^{}9/L)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
4 - 10\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{11.6}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
9.8\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
8.6\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{10.6}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{9.9}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
9.2\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
8.9\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Neutrophil Count (10\^{}9/L)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
2 - 7\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{9.2}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{7.6}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
6.9\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{8.8}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{8.2}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{7.6}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
6.9\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Haemoglobin (g/dL)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
12 - 15\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{7.7}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{8.5}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{9.7}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{9.0}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{8.2}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{8.6}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{9.2}\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Mean corpuscular volume (fL)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
84 - 96\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
85\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
84\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
86\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
85\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
84\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
84\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
83\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Platelet count (10\^{}9/L)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
150 - 400\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
320\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
263\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
327\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
338\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
312\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
292\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
231\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
C-reactive protein (mg/L)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textless{}5\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{62}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n/r\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{52}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{37.8}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{33.3}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{25.7}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{19.6}\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Serum Urea (mmol/L)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
2.9-8.2\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{8.6}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n/r\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
4.3\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
5.2\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
4.1\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
3.8\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
2.7\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Serum Creatinine (\selectlanguage{greek}µ\selectlanguage{english}mol/L)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
49 - 90\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{108}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n/r\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
60\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
59\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
61\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
58\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
58\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Serum Albumin (g/L)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
39 - 51\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{31}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n/r\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{32}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{32}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{30}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{27}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{23}\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Serum Ferritin (ng/mL)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
10 - 200\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{1015}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n/r\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n/r\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n/r\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n/r\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n/r\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n/r\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Plasma Lactate (mmol/L)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
0.6-1.4\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n/r\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n/r\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
nr\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
nr\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
0.8\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
0.8\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n/r\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

\emph{Hb: Haemoglobin, RCC: red cell concentrate, *: Commencement of
antibiotic treatment, IV: intravenous,}

\emph{tds: three times daily, d: day, h: hour, OGD:
Oesophago-Gastro-Duodenoscopy,}

\emph{CTAP: Computed tomography of the abdomen and pelvis, TTE:
transthoracic echocardiogram}

\emph{n/r: not requested, Data in bold = abnormal values}

\textbf{Hosted file}

\verb`Pathology_figures_Abiotrophia_defectiva_case_report.docx`  available at \url{https://authorea.com/users/356385/articles/479261-atypical-presentation-of-abiotrophia-defectiva-infective-endocarditis-in-an-octogenarian}

\selectlanguage{english}
\FloatBarrier
\end{document}

