| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
One month later, a study nurse visited the patient at home for follow-up. His fever had relapsed 2 weeks after the initial visit to the fever clinic, but he did not seek medical care or take antibiotics. His fever resolved spontaneously. The results of the MAT panel from the first visit showed a titer of 1/1,600 against a newly identified leptospiral serovar, provisionally delineated Var102 (Matthias MA and others, manuscript in preparation; Segura ER and others, in press). ELISA for IgM was negative, but testing of the stored serum and urine samples using a TaqMan-based real-time PCR3 revealed the presence of Leptospira in the urine sample at an estimated concentration of 868 leptospires/mL, confirming that the patient indeed had had acute leptospirosis. Repeat testing of serum by ELISA for leptospira and serum and urine by real-time PCR at follow-up were negative while the MAT titer decreased to 1/100, consistent with resolving infection.
Five months later, the patient returned to the same hospital because of sudden onset of fever, jaundice, edema below the umbilicus, and odynophagia. Remarkable findings on admission physical exam included oral mucosal candidiasis and severe wasting, as well as hepatomegaly and splenomegaly. These findings suggested advanced HIV infection. After he gave oral and written consent, the stored serum from the first fever clinic visit was found to be positive for anti–human immunodeficiency virus I antibodies by ELISA and Western blot. The underlying medical reason for the second admission remained undiagnosed but was not related to leptospirosis, as serologic, culture, and nucleic acid tests for Leptospira infection were negative, indicating complete resolution of the previous infection. CD4 count was not performed due to lack of resources. He recovered progressively with supportive care and was discharged home. He died at home several months later; autopsy was not performed.
This case is particularly notable because previously reported patients with acute leptospirosis and HIV coinfection had severe clinical courses. Clinical manifestations differed between patients, variably including meningitis, renal insufficiency, acute respiratory distress syndrome, and hypotension as main manifestations.4–7 All patients recovered fully from leptospirosis, except one who had residual renal insufficiency. In contrast, the patient reported here experienced a clinical course of leptospirosis consistent with the more common presentation of acute self-resolving undifferentiated fever. Many believe that humoral immunity, primarily against leptospiral lipopolysaccharide (LPS), mediates recovery from acute leptospirosis and protects against reinfection.8 As a T-independent antigen, leptospiral LPS would be predicted to induce antibodies in the absence of CD4+ T cell help,9 explaining the high MAT titer during acute infection despite likely advanced HIV-driven immunodeficiency. The high MAT titer cannot be dismissed as HIV-related B cell polyclonal proliferation with hypergammaglobulinema, as an etiologic diagnosis (real-time PCR) definitely demonstrated infection. The patient recovered from acute leptospirosis without antibiotic treatment, without acute complications or sequelae, and without requiring hospitalization. Acute leptospirosis was retrospectively confirmed by a molecular diagnostic technique conducted on-site in the Peruvian Amazon, which has been demonstrated to be very sensitive and specific, detecting pathogenic Leptospira to ~10 organisms per specimen without cross-detecting other pathogens or non-pathogenic Leptospira.3
We conclude that acute leptospirosis in HIV coinfection is not inevitably severe and that there is probably wide variation in clinical manifestations similar to what occurs in immuno-competent hosts. Clinical presentations and complications likely depend on a combination of virulence potential differences that vary between pathogenic Leptospira and host genetics of non–T-cell-dependent innate immune responses. A prospective cohort study in an HIV and leptospirosis dually endemic area would be necessary to establish definitively whether HIV infection alters the course of leptospiral infection, either acutely or in chronic infection, as it does for Treponema pallidum, the agent of another spirochetal disease, syphilis, which lacks the T-independent LPS antigen.10
Received December 8, 2004. Accepted for publication January 22, 2005.
Acknowledgments: The study was approved by the UCSD Institutional Review Board and the Ethical Committee of the Universidad Peruana Cayetano Heredia.
Financial support: This work was supported by NIH/Fogarty International Center grants R01-TW05860 and D43TW007120.
* Address correspondence to Joseph M. Vinetz, Division of Infectious Diseases, University of California San Diego School of Medicine, 9500 Gilman Drive, 0640, La Jolla, California. E-mail: jvinetz{at}ucsd.edu 
Authors’ addresses: Christian A. Ganoza, Eddy R. Segura, and Edu-ardo Gotuzzo, Instituto de Medicina Tropical Alexander von Hum-boldt, Universidad Peruana Cayetano Heredia, A.P. 4314, Lima 100, Peru. E-mail: cganoza{at}hotmail.com, cganoza{at}hotmail.com, eddysegura{at}hotmail.com, and egh{at}upch.edu.pe., and egh{at}upch.edu.pe Mark A. Swancutt and Joseph M. Vinetz, Division of Infectious Diseases, University of California San Diego School of Medicine, 9500 Gilman Drive, 0640, LaJolla, CA 92093-0640. E-mail: mswancutt{at}ucsd.edu and jvinetz{at}ucsd.edu
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
