the authors postulated that the parasite could mediate autoimmune damage to peripheral nerve myelin (Fasanaro et al. 1991).

Because L. infantum has been responsible for most cases of HIV-related VL (Russo et al. 2003), it might be particularly likely to persist in macrophages and monocytes. This organism was identified in one of the two cases of VL acquired in Afghanistan (CDC 2004a) but has not been identified in veterans of other conflicts. Of those two cases, one was diagnosed 14 months after deployment ended in Afghanistan, and the patient had symptoms of clinical recurrence. In addition, VL is estimated to be the third-most common opportunistic infection in HIV-infected persons in southern Europe, as detailed above (Russo et al. 2003).

Because the period of latent infection with VL organisms can be long (10 years is commonly cited), immune suppression can allow reactivation of a latent infection. In the description of the viscerotropic cases that occurred in the Gulf War, the authors stated that “if L. tropica is also capable of surviving in a latent state, visceral leishmaniasis will need to be included in the differential diagnoses of illness in veterans of Operation Desert Storm for years to come” (Magill et al. 1993). Although chronic infection is clearly plausible, no systematic studies have investigated the possibility prospectively, in part because there is no accurate and noninvasive screening test for the infection (Ohl et al. 1993). However, intensive evaluation among 150 Gulf War veterans with complaints was unable to identify prior or current infection with Leishmania spp. (Hyams et al. 1995).

Post-kala-azar dermal leishmaniasis (PKDL) is a well-documented long-term adverse health outcome of VL that occurs on the Indian subcontinent and in east Africa (Zijlstra et al. 2003). On the basis of the Indian experience, this health outcome may develop in 5-10% of patients several years after apparently successful treatment for VL (Zijlstra et al. 2003). PKDL has been mistaken for leprosy, and patients with this presentation remain infectious (Zijlstra et al. 2003). Nerve involvement (as is seen in leprosy) has been reported rarely with PKDL (El Hassan et al. 1992; Khandpur et al. 2004).

The committee concludes that

  • There is sufficient evidence of an association between infection with an etiologic agent of visceral leishmaniasis (VL) and delayed presentation of the acute clinical syndrome.

  • There is sufficient evidence of an association between infection with an etiologic agent of VL and the reactivation of VL in the context of future immunosuppression.

  • There is sufficient evidence of an association between VL and development of post-kala-azar dermal leishmaniasis (PKDL) if PKDL occurs generally within 2 years of the initial infection.


Human malaria is caused by infection with one or more of four species in the genus Plasmodium: P. falciparum, P. vivax, P. ovale, and P. malariae. Although estimates vary, there are probably 350-500 million clinical episodes of malaria each year and 0.7-2.7 million deaths (Breman 2001; WHO 2003). Malaria occurs worldwide in tropical and subtropical regions, typically affecting poor and developing areas most severely. P. falciparum predominates in tropical areas; P. vivax, in temperate regions. The two other species are less frequently

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