Tick-Borne Rickettsiosis in Traveler Returning from Honduras

To the Editor: Although tick-borne rickettsioses are widespread globally, few reports document their presence in Central America (1). Serosurveys detected rickettsial antibodies in humans in Central America in 1971 in Costa Rica, Honduras, Nicaragua, and Panama (2,3). An outbreak of rickettsial illness was reported to have occurred in Costa Rica in 1974, where 2 case clusters affected 6 of 15 family members (4). A rickettsial organism was isolated from a patient who died in Panama in 1950 (5), and more recently Rickettsia rickettsii was confirmed in a fatal case in Panama (6). We report a patient with serologic evidence of rickettsiosis after a tick bite sustained during travel in Honduras. 
 
A 51-year-old man sought medical evaluation after returning from travel to Roatan, Honduras, where he was bitten by a tick in the lower abdomen. He reported erythema and induration at the site of the tick bite with associated central necrosis. He described an illness with headache, fever, weakness, dizziness, abdominal discomfort, diarrhea, flu-like symptoms, and respiratory symptoms affecting him 1–2 weeks after the tick bite. He was evaluated while still traveling and received multiple diagnoses, including malaria, respiratory infection, and parasites, and was given chloroquine, primaquine, penicillin, and mebendazole. His condition improved. He returned to the United States 2 months after the tick bite. 
 
His travel history included Thailand, Jamaica, Aruba, the Bahamas, Belize, Germany, Spain, Hungary, the Netherlands, and New Zealand. The patient recalled removing ticks from his body as a child in Maryland but had no associated illness. He denied any recent tick bite other than the one in Honduras, where he had close contact with a horse and dogs and was frequently outdoors. 
 
Results of his physical examination were unremarkable; routine laboratory studies showed values within reference ranges. No antibodies to Borrelia burgdorferi or Plasmodium spp. were detected. 
 
Serologic analysis for rickettsia, performed by a commercial laboratory (Focus Diagnostics, Cypress, CA, USA) and the Centers for Disease Control and Prevention (Atlanta, GA, USA), showed elevated titers (Table). The patient took doxycycline (100 mg 2×/d) for 10 days and subjectively improved. 
 
 
 
Table 
 
Rickettsia spp. serologic titers for a man who returned from Honduras, 2005* 
 
 
 
On the basis of infections documented in the Americas, R. rickettsii, R. africae, and other less well-known rickettsial pathogens such as R. parkeri or R. massiliae (1) are possible etiologic agents in our case. The most common human-biting tick in Central America is Amblyomma cajennense, which is a known vector of R. rickettsii. Serosurveys have suggested the presence of R. rickettsii infection in the Yucatan (7), and PCR has confirmed a case of R. rickettsii in that region (8). Rhipicephalus sanguineus, the vector of R. conorii (boutonneuse fever) in the Mediterranean, is also found in Mexico, but to date no transmission of R. conorii has been documented in the Americas. R. sanguineus was implicated in a cluster of human Rocky Mountain spotted fever cases in the United States in 2002–2004 (9). 
 
Our patient had not traveled to the areas of the Caribbean where transmission of R. africae has been documented, but he had lived in areas of the United States with potential transmission of rickettsial infections. R. parkeri is a newly recognized pathogen in the Americas (10). Its vectors (A. maculatum and A. triste) are found in parts of North, Central, and South America. The illness caused by R. parkeri appears to be less severe than Rocky Mountain spotted fever and could be consistent with our patient’s illness. Because antibodies against R. parkeri and R. rickettsii cross-react, serologic analysis is of little use for differentiating these 2 organisms. 
 
The history and serologic findings for our patient suggest a recent tick-borne rickettsiosis, most likely acquired in Honduras. However, we can neither confirm that infection was recent nor confirm the species. The history of a tick bite and description of the skin lesion are consistent with an eschar, but no physical evidence of the tick or eschar remained at the time of evaluation. Diagnosis of rickettsial infection can be confirmed by demonstrating at least a 4-fold increase in titers between acute-phase and convalescent-phase serum samples, by identification of rickettsiae in an acute-phase serum or tissue sample, or by culture. Use of an immunofluorescent antibody assay alone does not identify the specific agent causing spotted fever. 
 
Because our patient was examined 2 months after the exposure, options for making a diagnosis were limited. Extensive serologic cross-reactivity exists among the rickettsial species, which precludes the determination of species in our case. Although antibodies to rickettsiae can be long-lived, the extremely high levels of immunoglobulin (Ig) G and IgM suggest a recent rickettsial infection in our patient. Testing was unavailable for other rickettsiae (e.g., R. parkeri, R. massiliae). 
 
Our patient likely had rickettsial infection acquired in Honduras. We present this case to alert clinicians to consider the diagnosis of rickettsial infections in the Americas, even if infections have not been previously documented in a specific country or region. Because rickettsial infections can be severe and are treatable, the clinician should consider rickettsial infections in returned travelers with compatible clinical findings. Our case also demonstrates the potential role of travelers as sentinels of emerging infectious diseases.

Hospital Medical Center in Flushing, New York, with complaints of headache, fever, and vomiting, which she had experienced for ≈1 week. She had no photophobia, confusion, or rash; neurologic examination found no abnormalities. CSF contained 81 leukocytes with 82% lymphocytes, 3 erythrocytes, protein at 194 mg/dL, and glucose at 67 mg/dL. CSF was positive for HSV-1 viral DNA by PCR. A computed tomography (CT) scan of the head showed unilateral temporal lobe edema. Intravenous acyclovir 10 mg/kg every 8 hours was administered. HIV test was negative. On day 5, a repeat CT scan showed worsening edema and hemorrhage, despite clinical improvement (Figure). CSF contained 490 leukocytes with 99% lymphocytes and protein at 336 mg/dL. After continued treatment with parenteral acyclovir, the patient's symptoms resolved. On day 12, the patient was discharged after a final CT scan showed resolution of hemorrhage and edema and CSF contained decreased leukocytes and protein.
Although this patient had classic signs of meningitis without encephalitis, the CT scan of the head showed cerebral involvement. These factors can be explained by the location of cerebral inflammation in the nondominant lobe of the brain, thereby masking signs of encephalitis. The classic teaching that viral meningitis may not need treatment may miss the occasional viral encephalitis if brain imaging and CSF PCR are not performed. Failure to perform these tests may lead to illness and death from HSV encephalitits if this disease is not considered as a possible diagnosis.

Tick-Borne Rickettsiosis in Traveler Returning from Honduras
To the Editor: Although tickborne rickettsioses are widespread globally, few reports document their presence in Central America (1). Serosurveys detected rickettsial antibodies in humans in Central America in 1971 in Costa Rica, Honduras, Nicaragua, and Panama (2,3). An outbreak of rickettsial illness was reported to have occurred in Costa Rica in 1974, where 2 case clusters affected 6 of 15 family members (4). A rickettsial organism was isolated from a patient who died in Panama in 1950 (5), and more recently Rickettsia rickettsii was con- firmed in a fatal case in Panama (6). We report a patient with serologic evidence of rickettsiosis after a tick bite sustained during travel in Honduras.
A 51-year-old man sought medical evaluation after returning from travel to Roatan, Honduras, where he was bitten by a tick in the lower abdomen. He reported erythema and induration at the site of the tick bite with associated central necrosis. He described an illness with headache, fever, weakness, dizziness, abdominal discomfort, diarrhea, flu-like symptoms, and respiratory symptoms affecting him 1-2 weeks after the tick bite. He was evaluated while still traveling and received multiple diagnoses, including malaria, respiratory infection, and parasites, and was given chloroquine, primaquine, penicillin, and mebendazole. His condition improved. He returned to the United States 2 months after the tick bite.
His travel history included Thailand, Jamaica, Aruba, the Bahamas, Belize, Germany, Spain, Hungary, the Netherlands, and New Zealand. The patient recalled removing ticks from his body as a child in Maryland but had no associated illness. He denied any recent tick bite other than the one in Honduras, where he had close contact with a horse and dogs and was frequently outdoors.
Results of his physical examination were unremarkable; routine laboratory studies showed values within reference ranges. No antibodies to Borrelia burgdorferi or Plasmodium spp. were detected.
Serologic analysis for rickettsia, performed by a commercial laboratory (Focus Diagnostics, Cypress, CA, USA) and the Centers for Disease Control and Prevention (Atlanta, GA, USA), showed elevated titers (Table). The patient took doxycycline (100 mg 2×/d) for 10 days and subjectively improved.
On the basis of infections documented in the Americas, R. rickettsii, R. africae, and other less well-known rickettsial pathogens such as R. parkeri or R. massiliae (1) are possible etiologic agents in our case. The most common human-biting tick in Central America is Amblyomma cajennense, which is a known vector of R. rickettsii. Serosurveys have suggested the presence of R. rickettsii infection in the Yucatan (7), and PCR has confirmed a case of R. rickettsii in that region (8). Rhipicephalus sanguineus, the vector of R. conorii (boutonneuse fever) in the Mediterranean, is also found in Mexico, but to date no transmission of R. conorii has been documented in the Americas. R. sanguineus was implicated in a cluster of human Rocky Mountain spotted fever cases in the United States in 2002-2004 (9).
Our patient had not traveled to the areas of the Caribbean where transmission of R. africae has been documented, but he had lived in areas of the United States with potential transmission of rickettsial infections. R. parkeri is a newly recognized pathogen in the Americas (10). Its vectors (A. maculatum and A. triste) are found in parts of North, Central, and South America. The illness caused by R. parkeri appears to be less severe than Rocky Mountain spotted fever and could be consistent with our patient's illness. Because antibodies against R. parkeri and R. rickettsii cross-react, serologic analy-sis is of little use for differentiating these 2 organisms.
The history and serologic findings for our patient suggest a recent tick-borne rickettsiosis, most likely acquired in Honduras. However, we can neither confirm that infection was recent nor confirm the species. The history of a tick bite and description of the skin lesion are consistent with an eschar, but no physical evidence of the tick or eschar remained at the time of evaluation. Diagnosis of rickettsial infection can be confirmed by demonstrating at least a 4-fold increase in titers between acute-phase and convalescent-phase serum samples, by identification of rickettsiae in an acute-phase serum or tissue sample, or by culture. Use of an immunofluorescent antibody assay alone does not identify the specific agent causing spotted fever.
Because our patient was examined 2 months after the exposure, options for making a diagnosis were limited. Extensive serologic cross-reactivity exists among the rickettsial species, which precludes the determination of species in our case. Although antibodies to rickettsiae can be long-lived, the extremely high levels of immunoglobulin (Ig) G and IgM suggest a recent rickettsial infection in our patient. Testing was unavailable for other rickettsiae (e.g., R. parkeri, R. massiliae). Our patient likely had rickettsial infection acquired in Honduras. We present this case to alert clinicians to consider the diagnosis of rickettsial infections in the Americas, even if infections have not been previously documented in a specific country or region. Because rickettsial infections can be severe and are treatable, the clinician should consider rickettsial infections in returned travelers with compatible clinical findings. Our case also demonstrates the potential role of travelers as sentinels of emerging infectious diseases.

KI and WU Polyomaviruses in Patients Infected with HIV-1, Italy
To the Editor: Before 2007, two human polyomaviruses were known to infect humans: BK virus and JC virus (1,2). Recently, 2 novel polyomaviruses, KI polyomavirus (KIPyV) and WU polyomavirus (WUPyV), were identified in the respiratory secretions of children with signs of acute respiratory signs (3,4); little evidence exists to suggest that these viruses are causative agents of respiratory tract disease (5). To determine the prevalence of WUPyV and KIPyV in the plasma of HIV-1-infected patients, we screened 62 persons who were HIV-1 positive by using PCR to detect the 2 viruses. We also conducted phylogenetic analysis of the identified strains.
Plasma specimens were collected at Istituto di Ricovero e Cura a Carattere Scientifico Instituto Fisioterapico Ospetaliere-San Gallicano Institute and Tor Vergata University Hospital, Rome, Italy, from April 2005 through September 2008. Patients were adults (37-54 years of age, median age 45.5 years) and were being treated with antiretroviral drugs. HIV-1 viral load determination, CD4+ counts, and HIV-1 genotyping were performed as part of the routine investigation. Plasma viremia levels ranged from <50 to 2,877,764 copies/mL, and CD4+ counts ranged from 150 to 1,218. Most patients (64.5%) were infected by HIV-1 subtype B. Other subtypes found were F, G, and C.