In April 2007, a 30-year-old man from Bahia sought care for a 6-day febrile illness that began 9 days after he found a tick attached to his right wrist while hiking and camping in the Chapada Diamantina National Park in Paty Valley (12°48′26′′S, 41°19′53′′W), a semiarid region in Bahia. Primary signs and symptoms were fever (39–40°C), severe myalgia, and swelling and pain at the site of the tick bite. Two days after onset of illness, the man noticed a scab forming on his right wrist and painful swelling in his right axillary region, followed 2 days later by a generalized rash and painful ulcerative lesions in the mouth. The patient sought medical care, and an outpatient physician prescribed acetaminophen and cefadroxil, which did not reduce symptoms.
On day 6 of his illness, the patient sought care from an infectious disease specialist, who noted a 2.5-cm eschar on the patient’s wrist (, panel A); disseminated papular rash on his face, trunk, and upper extremities (, panel B); and several small erosions on his tongue, buccal mucosa, and lips (, panels C, D). The mucosal erosions were painful, and some skin papules formed small pustules (, panel E). In the right axilla was a tender, enlarged, 3-cm lymph node. Results of a hemogram and blood biochemistry were unremarkable except for a high level (425 U/L) of lactic dehydrogenase. A rickettsial disease was considered, and the patient was given doxycycline (100 mg 2×/d) for 14 days. The fever and generalized rash resolved within 2 days, and the eschar healed completely within 2 weeks after initiation of therapy.
Figure 1 Lesions on day 6 of illness of patient with eschar-associated rickettsial disease, Bahia, Brazil, 2007. A) Eschar on right wrist; B) papular skin rash on left elbow; C) ulcerated lesion on lower lip; D) erosions on tongue mucosa; E) vesicular papular (more ...)
Acute-phase and convalescent-phase serum samples were evaluated by microimmunofluorescence assay for antibodies to spotted fever group rickettsiae (SFGR) (4
). Before antimicrobial drug therapy was started, biopsy specimens of the papule and the scab from the eschar were collected, preserved in 10% formol, and evaluated by routine histopathology, immunohistochemical staining, and PCR (4
Serum collected on day 6 of the illness was nonreactive with R. rickettsii and R. parkeri antigens (class-specific immunoglobulin G [Ig] and IgM <32 for both assays, cutoff >64). Subsequent testing determined IgG/IgM titers on day 12 to be 128/<32 against R. parkeri and 128/32 against R. rickettsii antigens and on day 19 to be 128/64 and 512/32, respectively.
Hematoxylin and eosin–stained sections of the papule biopsy specimen demonstrated lymphohistiocytic perivascular inflammatory cell infiltrates in the superficial to middle dermal layers. Immunohistochemical staining for SFGR showed rare antigens in a few small foci of perivascular inflammation.
The sequences for omp
A (632-bp, GenBank accession no. GQ853063) from the scab and glt
A (382-bp, GenBank accession no. GQ900666) from the papule specimen each had 100% identity to homologous gene sequences of SFGR detected recently in an eschar specimen from a patient from Peruibe, São Paulo (3
). The sequences from both organisms were most related to SFGR strain S previously reported from Armenia (6
) but were not identical to R. sibirica
, and R. africae
(). The nucleotide sequence of a 928-bp sca
4 fragment (GenBank accession no. GQ853064) had 99% identity to the homologous fragment of R. parkeri
(GenBank accession no. AF155059), and the conserved 17-kDa protein gene amplicon (GenBank accession no. GQ853062) was similar to those of many SFGR.
Figure 2 Genetic relationships of the spotted fever group rickettsiae (SFGR) detected in tissue of patient with eschar-associated rickettsial disease, Bahia, Brazil, 2007. Sequence comparison was conducted with MEGA version 4 (www.megasoftware.net). The phylogenetic (more ...)