Clinical Infectious Diseases
BRIEF REPORT
Identification of a Novel Mycoplasma
Species in a Patient With Septic
Arthritis of the Hip and Seal Finger
Benjamin P. Westley,1 Ryan D. Horazdovsky,2 Dina L. Michaels,3 and Daniel R. Brown3
Departments of 1Internal Medicine, and 2Orthopedics, Alaska Native Tribal Health Consortium,
Anchorage; and 3Department of Infectious Diseases and Pathology, University of Florida,
Gainesville
An Alaska Native hunter developed fever, swollen finger, and
septic hips after harvesting seals. Evaluation of hip tissue by
16S rRNA gene polymerase chain reaction and sequencing revealed a putative novel mycoplasma species. We report the
identification of this organism and describe the first known
case of disseminated seal finger mycoplasmosis.
Keywords. septic arthritis; mycoplasma; seal finger.
A previously healthy 38-year-old Alaska Native man presented
in November 2014 for evaluation of high fever and abdominal
pain of 7-days duration. Symptoms began 2 days after walking
for 24 hours across frozen tundra when his all-terrain vehicle
broke down in freezing temperatures during a subsistence seal
hunt. Further history revealed that his right middle finger had
become swollen, red, and tender with mild drainage from a lesion overlying the proximal interphalangeal joint several days
after returning home. He was admitted to a regional hospital
in northwest Alaska where his initial temperature of 37.5°C
rose to 38.8°C on the following hospital day. His blood pressure
was 124/73 mm Hg, his pulse was 88 beats per minute, and his
respiratory rate was 14 breaths per minute with an oxygen saturation of 98% while breathing room air. Examination revealed
moderate lower abdominal tenderness, a tender swollen right
middle finger, and severe pain in the inguinal region bilaterally.
The white blood cell count was 14 × 103 cells/µL, hemoglobin was
12.9 g/dL, and platelets were 236 × 103 cells/µL. The C-reactive
protein was elevated at 29.4 mg/dL. Urinalysis and comprehensive metabolic panel were normal. A computed tomography
(CT) scan of the abdomen and pelvis performed after the administration of intravenous contrast demonstrated left psoas
muscle inflammation, which was concerning for early abscess
formation and small bilateral hip effusions. Blood cultures
Received 26 August 2015; accepted 24 September 2015; published online 8 October 2015.
Correspondence: B. P. Westley, 4320 Diplomacy Dr, Ste 2800, Anchorage, AK 99508
([email protected]).
Clinical Infectious Diseases® 2016;62(4):491–3
© The Author 2015. Published by Oxford University Press for the Infectious Diseases Society
of America. All rights reserved. For permissions, e-mail [email protected].
DOI: 10.1093/cid/civ875
were obtained, and intravenous vancomycin plus ceftriaxone
was administered. Severe bilateral hip pain developed 48 hours
later; repeat CT scan was compatible with increased fluid collecting in the bilateral hip capsules (Figure 1). Blood cultures
remained negative. Ceftriaxone was broadened to piperacillin/
tazobactam, and the patient was transferred to the Alaska Native Medical Center in Anchorage, Alaska.
On examination he was found to have significant groin pain
with any motion of the hip bilaterally. A magnetic resonance
imaging scan confirmed inflammatory fluid in the distal psoas
musculature, contiguous with bilateral hip joint effusions. He
was taken to the operating room for hip irrigation and debridement, where purulent turbid fluid was noted in both hip capsules. The synovial fluid white blood cell count was 107 × 103
cells/µL (95% polymorphonuclear) with 47 × 10 3 red blood
cells/µL. Gram stains and cultures for bacterial and acid-fast bacilli were negative. A transthoracic echocardiogram showed no
valvular vegetations or regurgitation. He was continued on vancomycin alone, but after brief improvement, pain and drainage
from the hip incisions recurred, requiring repeat debridements
on days 7, 9, and 20.
Due to the suspected infectious origin of inflammation but
negative cultures, tissue from the left hip collected at debridement
on hospital day 7 was sent to the University of Washington in
Seattle for broad-range polymerase chain reaction (PCR) detection of generic bacteria, fungal, and acid-fast bacilli organisms.
On hospital day 20, results returned a high-quality signal for bacteria of the Mycoplasmataceae family but with a previously undescribed partial 16S rRNA sequence. Further questioning revealed
that 1 week prior to the onset of symptoms, the patient had harvested 3 ringed seals (Pusa hispida) without wearing protective
gloves. In addition, in the year 1997, he had been treated with tetracycline for swelling and pain of a finger after butchering a walrus. Given the known association of mycoplasma species with
seal finger, an infection normally restricted to the fingers and
hand [1], the patient now was presumed to have hematogenous
spread of infection from his right middle finger to his hips. Vancomycin was discontinued, and oral doxycycline 100 mg twice a
day was initiated on day 20. Pain and drainage from the hip incisions rapidly improved, and the C-reactive protein fell from
16.9 mg/dL to 0.74 mg/dL after 13 days of therapy. The patient
completed 6 weeks of orally administered doxycycline, with complete normalization of his inflammatory markers and uneventful
healing of his previously draining hip incisions. Follow-up imaging with plain x-ray of the hips 6 months after presentation revealed only mild degenerative joint disease, and the patient was
able to ambulate well but does have persistent bilateral hip pain,
which limits his subsistence activities.
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abscess [5]. Its presumed spread from the patient’s finger to his
hips is remarkable because such dissemination is unprecedented
in prior reports of seal finger zoonotic mycoplasmal infection of
the hand [6–9]. There was no indication of any other kind of
mycoplasma in the specimens. No mycoplasma could be cultured from the predoxycycline peripheral blood or biopsy material on modified SP-4 (with fetal bovine serum, glucose, and
arginine), Hayflick’s (with horse serum, glucose, and arginine),
or Frey’s medium (with pig serum, plus cysteine and nicotinamide adenine dinucleotide) [2].
DISCUSSION
Figure 1. Contrast-enhanced computed tomography imaging of the abdomen and
pelvis of our patient demonstrated rim-enhancing fluid collections in the right iliopsoas muscle extending into the groin (arrowheads) and a large rim-enhancing fluid
collection in the right hip capsule (arrows).
Samples of hip joint fluid and tissue as well as peripheral blood
collected on day 20 were sent for evaluation to the Mollicutes
Collection reference laboratory at the University of Florida,
where the presence of mycoplasmal DNA in solid and sterile
processed hip tissue and hip joint exudates was independently
confirmed by conventional PCR employing genus-specific primers (5′-AGAGTTTGATCCTGGCTCAGGA-3′ upstream and 5′TGCACCATCTGTCACTCTGTTAACCTC-3′ downstream) that
target the 16S rRNA gene [2]. The same mycoplasmal 16S rRNA
sequence (GenBank accession KP292569) was present in each of
those specimens, but peripheral blood samples were PCR negative. Phylogenetic analysis indicated the sequence represents a
putative novel species, taxonomically affiliated with the Mycoplasma equigenitalium/Mycoplasma elephantis cluster in the
Mycoplasmataceae (Figure 2), a clade previously related to polyarthritis in elephants and raccoons [3, 4] and a domestic cat bite
Figure 2. Balanced minimum evolution phylogram [17] of all GenBank accessions
(shown in parentheses) having ≥90% nucleotide sequence identity over ≥94% of
the 1417 bp novel 16S rRNA sequence detected in this patient. Boldface indicates
the novel sequence situated in the Mycoplasma equigenitalium/Mycoplasma elephantis phylogenetic cluster [2]. Scale bar = substitutions per nucleotide.
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BRIEF REPORT
In 1907 Bidenknap described the first known case of seal finger
[10]. Also known as sealer’s finger, spekkfinger, or blubber
finger, this little-known entity is well described in the Canadian
and Scandinavian literature and is most often seen in subsistence seal harvesters and those handling pinnipeds for research
or occupational purposes. A seminal review of 224 cases by
Candolin in 1953 suggests that the middle finger is the most
commonly affected digit, generally on the nondominant hand,
and that nearly 90% of patients recall an inoculation injury [11].
Etiology was initially unknown and thought possibly to be due
to micrococcus species [12] until 1998 when Mycoplasma phocacerebrale was isolated from the infected finger of a seal trainer
from the New England Aquarium as well as the mouth of the
seal that bit her [13]. Several mycoplasma species have been
implicated in outbreaks of illness among seals, both along the
New England seaboard and in the Baltic Sea and North Sea
[14]. Interestingly, our patient noted that in the previous
months a greater-than-normal proportion of ringed seals appeared to be diseased in the areas that he regularly hunted.
Case series suggest that outcome is good when tetracyclinebased therapy is promptly initiated [15, 16]. The lack of a
peptidoglycan-containing cell wall among Mycoplasmataceae
renders glycopeptides and beta-lactams ineffective, explaining
the persistent symptoms seen in our patient prior to doxycycline initiation. Fever and lymphangitis are felt to be rare in uncomplicated cases and likely to represent super-infection with
Gram-positive bacteria [11, 16]. However, our patient had no
evidence of bacterial infection other than mycoplasmosis. To
our knowledge, systemic dissemination following seal finger
or due to M. phocacerebrale in the absence of finger infection
has not been described. Our patient has no known immune deficit and is otherwise healthy. Whether his severe presentation
was due to unknown virulence factors related to this putative
newly discovered organism or due to host factors is unclear
but merits further investigation, especially given the frequency
of human exposure to cats and raccoons.
Notes
Acknowledgments. The seals were legally subsistence harvested. Preliminary molecular diagnostics were performed by Dhruba J. SenGupta of the
University of Washington Medical Center, Seattle, Washington.
Potential conflicts of interest. All authors: No reported conflicts and no
sources of funding. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider
relevant to the content of the manuscript have been disclosed.
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