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Akpaka et al. Journal of Medical Case Reports 2011, 5:157
http://www.jmedicalcasereports.com/content/5/1/157

CASE REPORT

JOURNAL OF MEDICAL

CASE REPORTS
Open Access

Methicillin sensitive Staphylococcus aureus
producing Panton-Valentine leukocidin toxin in
Trinidad & Tobago: a case report
Patrick E Akpaka1*, Stefan Monecke2, William H Swanston1,3, AV Chalapathi Rao1,3, Renee Schulz4 and
Paul N Levett4

Abstract
Introduction: Certain Staphylococcus aureus strains produce Panton-Valentine leukocidin, a toxin that lyses white
blood cells causing extensive tissue necrosis and chronic, recurrent or severe infection. This report documents a
confirmed case of methicillin-sensitive Staphylococcus aureus strain harboring Panton-Valentine leukocidin genes
from Trinidad and Tobago. To the best of our knowledge, this is the first time that such a case has been identified
and reported from this country.
Case presentation: A 13-year-old Trinidadian boy of African descent presented with upper respiratory symptoms
and gastroenteritis-like syptoms. About two weeks later he was re-admitted to our hospital complaining of pain
and weakness affecting his left leg, where he had received an intramuscular injection of an anti-emetic drug. He
deteriorated and developed septic arthritis, necrotizing fasciitis and septic shock with acute respiratory distress
syndrome, leading to death within 48 hours of admission despite intensive care treatment. The infection was
caused by S. aureus. Bacterial isolates from specimens recovered from our patient before and after his death were
analyzed using microarray DNA analysis and spa typing, and the results revealed that the S. aureus isolates
belonged to clonal complex 8, were methicillin-susceptible and positive for Panton-Valentine leukocidin. An
autopsy revealed multi-organ failure and histological tissue stains of several organs were also performed and
showed involvement of his lungs, liver, kidneys and thymus, which showed Hassal’s corpuscles.
Conclusion: Rapid identification of Panton-Valentine leukocidin in methicillin-sensitive S. aureus isolates causing
severe infections is necessary so as not to miss their potentially devastating consequences. Early feedback from the
clinical laboratories is crucial.

Introduction
Staphylococcus aureus has a variety of different virulence
factors. Among these, there are hemolysins and leukocidins [1]. A minority of S. aureus strains carry bi-component leukocidin. Its genes, lukS-PV and lukF-PV, are
encoded on prophages and can be found in diverse
genetic lineages of S. aureus. This toxin lyses white
blood cells, causing extensive tissue necrosis and severe
infection. Strains which are positive for this leukocidin
are usually associated with community-acquired infections which generally affect previously healthy children
* Correspondence: peakpaka@yahoo.co.uk
1
Microbiology/Pathology Unit, Department of Para-Clinical Sciences, Faculty
of Medical Sciences, University of the West Indies, St Augustine, Trinidad
Full list of author information is available at the end of the article

and young adults. It was first described in 1932 by Panton and Valentine [2] and is therefore known as Panton-Valentine leukocidin, or PVL.
Recently the issue of the emergence of novel, community-acquired methicillin-resistant S. aureus (MRSA)
strains being positive for PVL has been emphasized.
However, PVL is also common in methicillin-susceptible
S. aureus (MSSA) and can be detected in as much as
30% of abscess isolates [3]. In MSSA, it is frequently not
diagnosed as there are no phenotypic features or rapid,
non-molecular assays available. For that reason, clinical
isolates from cases with suspected PVL-associated disease (chronic, recurrent or unusually severe skin and
soft tissue infections, necrotizing pneumonia or fasciitis)

© 2011 Akpaka et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in
any medium, provided the original work is properly cited.

Akpaka et al. Journal of Medical Case Reports 2011, 5:157
http://www.jmedicalcasereports.com/content/5/1/157

may further be analyzed using rapid molecular tools
whether they were MRSA or MSSA.
There are no previously documented cases of infection
by S. aureus producing PVL in Trinidad and Tobago
and the Caribbean regions. Although the prevalence of
MRSA have been reported in Trinidad and Tobago [4],
there has never been any report of S. aureus carrying
PVL genes in this country. We describe here the first
confirmed case from Trinidad and Tobago, or, in fact,
from any English speaking Caribbean island, of a fatal
multi-organ failure caused by a PVL-producing MSSA
infection in a previously healthy child. This report stresses the fact that invasive infections due to MSSA could
have innocuous symptoms, should not be treated lightly
since such infections may have a high mortality rate,
and that PVL in MSSA still remains a clinically important issue.

Case presentation
This is a report of a previously active and healthy 13year-old Trinidadian boy of African descent with no
past medical history, significant history of trauma or travel abroad. He suddenly presented with flu-like symptoms, vomiting and diarrhea of four days duration at a
community health center. There was no history of
known contact with S. aureus infection either at school
or with family. He was assessed as a case of viral illness,
possibly gastroenteritis, and was treated symptomatically
with anti-emetic and analgesic intramuscular injections.
Laboratory tests were not pursued and he was discharged with instructions for home care and, if necessary, oral rehydration therapy. About two weeks later he
was admitted to the hospital complaining of fever,
increasing pain, weakness and inability to lift or to move
his left leg where he received an intramuscular injection
of the anti-emetic drug.
On admission, his physical examination revealed
tender and warm erythematous swelling of his left
thigh extending to his upper thigh and hip joint. An
ultrasound scan of his left hip, a chest X-ray, electrocardiography and Doppler ultrasound of his popliteal
pulses detected no abnormality. Blood cultures, samples of pus from a skin rash and samples for clinical
chemistry were taken. Initial laboratory results are
given in Table 1.
On further review, the child was assessed as having
septic arthritis with a high suspicion of necrotizing fasciitis and septicemia or infective endocarditis. Thus,
treatment with clindamycin, ceftriaxone, vancomycin
and cloxacillin was started. Later the same day, the cellulitic area around his right knee was noticed to increase
rapidly and a computed tomography scan revealed a collection or abscess around his left hip but not involving
the capsule of the joint. An immediate exploratory

Page 2 of 5

Table 1 Laboratory clinical chemistry results of a fatal
case of methicillin-sensitive Staphylococcus aureus
producing PVL gene in Trinidad and Tobago
Indices

Referral Center

On admission

Normal values

WBC

3.2

1.5

4-11 × 109/L
11.5 -13.5 g/dL

Hemoglobin

11.2

2.3

HCT

30.7

23.8

40-45%

ESR

NT

89

0-15 mm/L

Platelet
Calcium

148
7.6

81
7.5

150 -400 × 109/L
8.4-11.5 mg/dL

Chloride

103

110

92-118 mmol/L

Creatinine

0.9

1.9

0.2- 1.7 mg/dL

CRP

15

90

0-10 mg/dL

Potassium

3.8

7

3.6-5.8 mmol/L

Sodium

138

140

130-148 mmol/L

BUN

13

40

4-24 mg/dL

Uric acid
Phosphorus

5.6
4.3

13
15.1

2.5- 9.0 mg/dL
2.5- 6.5 mg/dL

ALT

34

1211

4- 48U/L

ALP

215

241

38-151U/L

Total Protein

4.9

4.4

6.3-8.6 g/dL

WBC = white cell count; HCT = hematocrit %; ESR = erythrocyte segmentation
rate; NT = not tested; CRP = C-Reactive Protein; BUN = Blood Urea Nitrogen;
ALT = Alanine transaminases, ALP = Alkaline phosphatase

laparotomy and drainage of the pelvic wall abscess
under general anesthesia was arranged. During the
operation, 200 ml of straw colored fluid was collected
and a deep pelvic wall abscess was found, measuring 8
× 6 × 4 cm, adjoining his hip joint capsule and near to
the obturator canal. There was thick shiny brown pus in
the cavity extending superiorly towards the inlet of his
iliac bone, inferiorly to the superior and inferior ramus
of his left pelvic bone. The thick joint capsule was intact
and there was no evidence of gluteal abscess, but there
was a compression from the external and greater tuberosity of the hip bone by the thick pus collection. The
pus was drained. Our patient was transferred to the
intensive care unit (ICU) although the post-operative
condition was very satisfactory. While in the ICU, our
patient started to have persistent cough productive of
white sputum and was observed to have bilateral crepitations in all his lung fields. A chest X-ray was suggestive of acute respiratory distress syndrome with ground
glass appearance. He required inotropes, and had difficulty ventilating resulting in the need for intubation and
artificial ventilation. However, our patient’s condition
deteriorated rapidly and he died 48 hours after admission. An autopsy was remarkable for necrotizing multiorgan failure involving his lungs, kidneys, thymus and
other organs. It also revealed congestion, edema and
hemorrhage of his lung alveoli, necrosis of his kidney
epithelia and Hassall’s corpuscles and microabscesses of
his thymus gland.

Akpaka et al. Journal of Medical Case Reports 2011, 5:157
http://www.jmedicalcasereports.com/content/5/1/157

Laboratory results received after the death of our
patient revealed grossly abnormal data. These are also
shown on Table 1.

Microbiological diagnosis and molecular analysis
of bacterial isolates
Blood, pus and post-mortem specimens yielded growth
of S. aureus as identified by Gram stain, catalase and
coagulase reactions and by biochemistry (MicroScan
Walk Away 96 SI, Siemens). The isolates were susceptible to several antibiotics including oxacillin as shown on
Table 2. Swab materials from the autopsy also yielded S.
aureus with same anti-microbial susceptibility pattern.
Blood cultures also yielded S. aureus.
The isolates from blood specimens and from swab and
tissue specimens at autopsy were further analyzed using
spa typing [5] and microarray analysis [6]. This allowed
us to detect virulence- and resistance-associated genes
as well as to assign the isolates to clonal complexes
(CC).
The two genotyped isolates were identical and their
overall hybridization profile allowed assignation to CC8.
Species markers or regulatory genes, including 23SrRNA gene, katA (encoding catalase), coA (coagulase)
and spa (Protein A) were all positive. The isolates did
not harbor mecA nor did any other genes associated
with staphylococcal chromosomal cassette mec elements.
Genes blaZ (beta lactamase) and associated regulatory
genes blaI and blaR as well as fosB (putative resistance
Table 2 Antimicrobial susceptibility test results of a
methicillin sensitive Staphylococcus aureus producing PVL
gene in Trinidad and Tobago
Drug

MIC (μ/mL)

Interpretation

Ampicillin

>8

R

Amoxycilin/Clavulanic

< 4/2

S

Cefazolin

<2

S

Ciprofloxacin

<1

S

Clindamycin

<1

S

Erythromycin

>4

R

Gentamicin

>8

R

Imipenem
Levofloxacin

<1
<2

S
S
S

Linezolid

<4

Oxacillin

< 0.25

S

Penicillin

>8

R

Piperacillin/Tazobactam

<1

S

Rifampin

<1

S

Synercid

0.5

S

Tetracycline
Trimethoprim/Sulfamethoxazole

<4
< 2/38

S
S

Vancomycin

<2

S

S = susceptible; R = resistant

Page 3 of 5

marker for fosfomycin, bleomycin) were detected. The
isolates carried the hemolysin gamma locus (lukF, lukS,
hlgA) as well as the genes encoding PVL (lukF-PV, lukSPV). The enterotoxin genes entD, entJ, entK, entQ and
entR (sed, sej, sek, seq, ser) were found, but other enterotoxin genes were not present. The isolates belonged to
agr group I and capsule type 5. Genes encoding adhesion factors (microbial surface components recognizing
adhesive matrix molecules) such as bone sialoproteinbinding protein (bbp), clumping factor A and B (clfA
and clfB), cell-wall associated fibronectin-binding protein (ebh), immune invasion genes isaB (immunodominant antigen B), isdA (heme/transferin-binding protein),
lmrP (putative transporter protein) and genes encoding
staphylococcal superantigen-like proteins were also present in these isolates, and their allelic variants were in
accordance to CC8 affiliation.
The spa typing analysis revealed the isolate to be spa
type t400. This is quite an uncommon spa type, and has
only previously been reported from northern Europe [7].
It has also been observed in a PVL-negative mutant of
the MRSA strain USA300 (P N Levett, personal communication). Since this strain also belongs to CC8, this
confirms the assignment of our isolates to that complex.
The repeat pattern of spa type t400 (11-19-12-21-17-3434-22-25) is related to other clonal complex 8 spa types
(such as t008, 11-19-12-21-17-34-24-34-22-25 or t009,
11-12-21-17-34-24-34-22-24-34-22-33-25).

Discussion
This case showed an unusually severe clinical presentation. This is similar to previous reports on PVL-producing S. aureus [8] causing conditions such as necrotizing
pyogenic skin infections, cellulitis, tissue necrosis, septic
arthritis, bacteremia, purpura fulminans (typically characterized by disseminated intravascular coagulation and
purpuric skin lesions) and community-acquired necrotizing pneumonia.
PVL disease often can be observed in young and
healthy people without previous medical history, who
might be in close contact to others due to accommodation in barracks or dormitories, or who might be
engaged in close contact sport. These risk factors are
conceivable in a school child. PVL-positive S. aureus
have also been transmitted by contaminated articles like
sharing towels, razors, poor hand hygiene or illicit drug
use. In our case, a transmission by intramuscular injection appears possible, but cannot be proven
retrospectively.
The causative strain belonged to CC8. It lacked some
of the most prevalent enterotoxins (egc-cluster) as well
as exfoliative toxins (etA, etB or etD) and epidermal cell
differentiation inhibitors (edinA, edinB or edinC). On
the other hand, it carried, beside PVL, several different

Akpaka et al. Journal of Medical Case Reports 2011, 5:157
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enterotoxin genes (sed, sej, ser, seb, seq). The clinical
role of these toxins, a possible impact on the virulence,
and possible synergistic effects are not yet understood.
Thus it cannot be determined how much they contributed to the fatal course of the disease in addition to the
PVL. PVL alone is a potent virulence factor, especially
with regard to skin and/or soft tissue infections and
pneumonia. While enterotoxin genes sed, sej and ser are
common in that clonal complex [8], PVL appears to be
rare among CC8-MSSA. The majority of PVL-MSSA
infections from geographic areas other than Trinidad
and Tobago can be attributed to other clonal complexes,
such as CC1, CC5, CC22, CC30, CC80, CC121 and
CC152 [3,10]. This could suggest geographic differences
in the molecular epidemiology of the PVL-producing
MSSA. While PVL genes are uncommon in CC8-MSSA,
there is a common and widespread MRSA strain from
the same lineage, which is known as USA300. Interestingly, this strain has also been described in Colombia
[11], geographically close to Trinidad and Tobago. Thus
it is tempting to speculate on a possible phylogenetic
relationship between USA300 and the strain described
in this study. Further investigations on PVL-positive S.
aureus in the southern Caribbean and South America
are warranted.
Unfortunately, some symptoms, including the hypotension, tachycardia, leukocytopenia, and abnormal liver
function tests suggestive of shock, were not adequately
addressed until our patient was admitted into the ICU.
Some laboratory reports arrived at the ICU only after
the death of our patient. Information on the presence of
PVL was also obtained only after our patient died. Such
problems commonly plague health care providers in the
developing world where the facilities and technologies
are often not readily available.
The autopsy findings and histological reports proved
the involvement of the lungs and consequently their
failure. Except for the vague history of flu-like symptoms and the persistent productive cough of whitish
sputum noted during the last few hours of his life,
there were no major clinical features that suggested
pneumonia. An involvement of the kidneys was also
noted in this patient in the autopsy findings. These
findings emphasize the need for aggressive management of cases of infections by PVL producing S. aureus organisms since it appears that no organ or tissues
can be spared.
By both phenotypical and molecular methods, it was
shown that this strain was susceptible to several relevant
antibiotics. A combination of a bactericidal drug, such
as a beta-lactam, plus a compound that reduces toxin
synthesis, such as clindamycin or rifampicin, is strongly
advocated since beta-lactams alone have in vitro been
shown to increase PVL in synthesis studies [12].

Page 4 of 5

However, susceptibility tests need to be performed
urgently in order to assess the efficiency of the therapy
and to rule out PVL-MRSA. Thus, the initial choice of
antibiotics in the presented case appeared to be correct,
but nevertheless the case resulted in a fatal outcome.
This emphasizes the severity of PVL-associated disease.

Conclusion
Given the ability of PVL-producing S. aureus (either
MSSA or MRSA) to cause life-threatening disease, and
the absence of any rapid non-molecular tests for PVL,
the crucial role of awareness cannot be over-emphasized. This report provides timely and informative hints
to all health care facilities, on a local or regional level,
that clinical presentation of PVL-producing S. aureus
infections should not be underestimated. It is also the
first report of a confirmed case of PVL-producing S.
aureus in Trinidad and Tobago and in the English
speaking Caribbean islands.
Consent
A written informed consent was obtained from the
patient’s next-of-kin for the publication of this case
report and any accompanying images. A copy of the
written consent is available for review by the Editor-inChief of this journal.
Acknowledgements
PEA would like to specifically thank the University of the West Indies, St
Augustine for part financial support for the study.
Author details
1
Microbiology/Pathology Unit, Department of Para-Clinical Sciences, Faculty
of Medical Sciences, University of the West Indies, St Augustine, Trinidad.
2
Institute for Medical Microbiology and Hygiene, Carl Gustav Carus Faculty of
Medicine, Technical University of Dresden, Fetscherstrasse 74, D-01307
Dresden, Germany. 3Eric Williams Medical Sciences Complex, North Central
Regional Health Authority, Uriah Butler Highway, Champs Fleurs, Trinidad.
4
Saskatchewan Disease Control Laboratory, 5 Research Drive, Regina,
Saskatchewan, S4S 0A4, Canada.
Authors’ contributions
PEA and WHS carried out the clinical study of the patient. AVCR carried out
the autopsy and histological staining. SM, RS, PNL performed the molecular
analyses. PEA drafted the manuscript. All authors read and approved the
final manuscript.
Competing interests
The authors declare that they have no competing interests.
Received: 21 August 2010 Accepted: 20 April 2011
Published: 20 April 2011
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http://www.jmedicalcasereports.com/content/5/1/157

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doi:10.1186/1752-1947-5-157
Cite this article as: Akpaka et al.: Methicillin sensitive Staphylococcus
aureus producing Panton-Valentine leukocidin toxin in Trinidad &
Tobago: a case report. Journal of Medical Case Reports 2011 5:157.

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