Colonic Leishmaniasis Mimicking a Malignant Stricture: Initial Presentation of HIV Infection – A Case Report

First Report of Visceral Leishmaniasis In An Orthotopic Heart Transplant Recipient

Parasitic Infections in Solid Organ Transplant Recipients

Visceral leishmaniasis treated with liposomal amphotericin B.

Detection of Leishmania parasites in a clinical sample is necessary to confirm a suspected case of leishmaniasis. We compared the sensitivity of internal transcribed spacer 1-PCR (ITS 1-PCR) assay for parasite diagnosis with that of microscopic detection in clinical samples from kala-azar (KA) or post-kala-azar dermal leishmaniasis (PKDL) suspects in Mymensingh. Of 39 specimens collected from 35 KA and four PKDL suspects, 26 were positive by microscopic examination of smears from bone marrow and skin exudates; 38 specimens spotted on filter paper and 27 of the 28 Giemsa-stained slides tested by PCR proved positive by ITS1-PCR.

Visceral leishmaniasis in three children with leukemia.

Visceral leishmaniasis (VL), also known as kala-azar, is a life-threatening systemic disease caused by the obligate intracellular protozoan, Leishmania, and transmitted to humans by the female phlebotomine sand fly (Phlebotomus argentipes). The disease is fatal, if left untreated. We report a case of a patient clinically suspected of disseminated tuberculosis, but fine needle aspiration cytology of cervical and axillary lymph nodes yielded a diagnosis of leishmaniasis. Diagnosis of VL was challenging as the disease closely mimicked tuberculosis in the setting of extensive lymphadenopathy including conglomerate of mesenteric lymph nodes, on and off fever, and granulomatous lymphadenitis on aspiration. Bone marrow examination was further performed. A detailed workup revealed patient to be severely immunocompromised and newly diagnosed human immunodeficiency virus (HIV) positive. Worldwide, India has the largest number of VL cases, accounting for 40%–50% of world's disease burden and the second largest HIV-infected population, accounting for approximately 10% of the global disease burden. HIV increases the risk of developing VL by 100–2320 times in endemic areas and concurrently VL promotes the clinical progression of HIV disease. Co-infection with HIV alters the body's immune response to leishmaniasis thus leading to unusual presentations. This case highlights the diagnostic problem in the aforesaid setting. Moreover, co-infection with HIV in VL can be a potential source of drug resistance. An early diagnosis and intensified treatment is the key to patient management.

To the Editor: In Argentina, 14 autochthonous human cases of visceral leishmaniasis (VL) were reported during 1925–1989. These cases occurred in different localities in Salta, Jujuy, Santiago del Estero, and Chaco Provinces of northwestern Argentina (Figure A1), where cutaneous leishmaniasis (CL) caused principally by Leishmania (Viannia) braziliensis is endemic. It had been postulated that scattered/sporadic VL cases could be caused by visceralization of dermatrophic Leishmania spp. because of 1) absence of already recognized L. (Leishmania) infantum vector species; 2) geographic overlap with the region where CL is endemic; 3) simultaneous symptoms of CL; or 4) lack of detailed parasitic characterization at the molecular level for cases of suspected VL (1). However, during recent decades, urban outbreaks of VL have spread to southern regions of South America (Mato Grosso do Sul, Brazil, and Asuncion, Paraguay) near the northern border with Argentina. In May 2006, an autochthonous human case of VL was reported in Posadas (northeastern Argentina); it was associated with the canine visceral form of the disease. In addition, the presence of Lutzomyia longipalpis sandflies was also reported (2). Currently, 58 human VL cases have been reported in Posadas (3), and >7,000 infected dogs, Lu. longipalpis sandflies, and canine VL have been found 350 km south of Posadas (4). During 2007–2008, new VL cases in 4 children and 7 dogs were reported clustering in time and space in La Banda-Santiago del Estero in the dry Chaco region of Argentina. This focus showed a different pattern from that found in the only urban outbreak of VL reported (nearly the same number of cases in humans and dogs, and the suspected vector was Lu. migonei sandflies instead of Lu. longipalpis sandflies) (5). We report a case of autochthonous human VL in Salta Argentina that was caused by L. (L.) infantum. This parasite was characterized by cytochrome b (cytb) gene sequencing. Sequencing of this gene has been validated for precise characterization of Leishmania spp (6,7). On September 9, 2009, a 44-year-old man from Salta, Argentina (Figure A1), was admitted to the Infectious Disease Service at Hospital Senor del Milagro in Salta. The patient had fever, weight loss, dyspepsia, and splenomegaly that evolved over 3 weeks. Physical examination showed cutaneous and mucosal paleness. His general condition was feverish and rapidly deteriorating. Laboratory tests at the time of final diagnosis showed anemia, leukocytopenia, thrombocytopenia, and increased levels of lactate dehydrogenase. Results of urinalysis and coproculture were negative for parasites. Electrophoresis of serum proteins showed increased levels of gamma globulins. The differential diagnosis was negative for malaria, mycosis, autoimmune hepatitis, and lymphoma. A bone marrow smear showed abundant amastigotes by Giemsa staining (Figure, panel A). The patient was treated with liposomal amphotericin B, 3 mg/day for 7 days, and recovered (8). After a comprehensive interview, we verified that this patient had not been in the VL-endemic area in Argentina. However, he had worked (deforestation activities) during January–February 2009 on a farm in Finca Las Maravillas (22o3′29.30″S, 63o14′28.17″W), where he had been bitten by phlebotomines and acquired the disease. This farm was situated in the dry Chaco region near the border with Bolivia and Paraguay (zones with VL) (9), a region with intensive deforestation and agricultural activities. For species identification, DNA was extracted from a bone marrow aspirate and peripheral blood. We amplified by nested PCR and sequenced the cytb gene (Figure, panel B) (6). The aligned 817-bp sequence obtained showed 100% homology with the cytb gene of the MHOM/TN/80/IPT1 L. (L.) infantum World Health Organization reference strain (Tunisian strain) and 99.3% homology with the MHOM/BR/74/PP75 L. (L.) chagasi strain (Brazilian strain) (7). L. (L.) infantum was identified as the causative agent of this VL case in Salta, Argentina, where VL cases had not been seen for 50 years. Our findings indicate that this case was not caused by visceralization or a dermatropic Leishmania spp. We suggest that the scattered pattern of VL incidence in the dry Chaco region is caused by an enzootic cycle with accidental human transmission (5). There are no reports of Lu. longipalpis sandflies in the study area or surrounding areas (10). Nevertheless, studies on natural infections of vector sandflies and reservoir-host animals (especially dogs) are needed. Therefore, the search for naturally infected sandflies and reservoirs of this infection should be intensified. Epidemiologic surveys of dogs are needed to identify spread of VL foci in areas of deforestation. Deforestation could alter vector and reservoir range and parasite density in the enzootic cycle and increase human exposure to infected vectors. Figure Case of autochthonous human visceral leishmaniasis in a 44-year-old man, identified by parasitologic diagnosis and molecular detection of the causative species, Salta, Argentina. A) Leishmania amastigotes in a bone marrow smear. N, nucleus; K, kinetoplast; ...

PCR identification of Leishmania in diagnosis and control of canine leishmaniasis

Visceral leishmaniasis is a parasitic disease transmitted by sandflies, with 0.5 million new cases annually.1 It is most commonly seen in India, Bangladesh, Brazil, Sudan, and around the Mediterranean. About...

Objective: To evaluate the hematological and clinical features of Visceral and Cutaneous Leishmaniasis.
 Materials and Methods: This was hospital-based retrospective study which included all cases of Cutaneous leishmaniasis and Visceral leishmaniasis that were diagnosed from Jan 2018 till December 2019 at Pathology Department, Rehman Medical Institute, Peshawar. The diagnosed cases were analyzed for clinical and laboratory profile in details, results of CBC, demographic information and physical signs at presentation were noted as well as bone marrow aspirations were performed for LD bodies.
 Results: Out of 104 cases, 36 (34.61%) visceral leishmaniasis and 68 (65.38%) cutaneous leishmaniasis were observed during the study period, in which 82 (78.85%) were male and 22 (21.15%) were females. Age range was from 03-40 years with mean of 23 + 4.21 years. Intermittent fever was observed in almost all the cases of visceral leishmaniasis and 52 (76.47%) of cutaneous leishmaniasis. All patients with visceral leishmaniasis had hepatomegaly and splenomegaly. Patients with CL presented as lesions on face and foot region. In VL all patients were male, while in CL 46 were males and only 22 were females. Majority (83.33%) of patients in VL were children (age group 1-10 years), in cutaneous leishmaniasis 34 (50%) were in age group 31-40 years.
 Conclusion: Our study concludes that leishmaniasis mainly affecting age group 10-20 years. Patients with visceral Leishmaniasis presented with pallor, weight loss fever and splenomegaly while those with cutaneous leishmaniasis presented with lesions on the foot and face especially nose. Anemia and thrombocytopenia were most common hematological parameters. It is essential that the Public Health authorities be more aware of the condition in order to improve environmental sanitation and personal protective measures and to establish diagnostic laboratories for early and correct diagnosis and treatment.

Use of the polymerase chain reaction to assess the success of visceral leishmaniasis treatment

To explore current patterns of diagnosis and treatment, quantify household economic impact and identify household strategies to cover the costs of visceral leishmaniasis (VL) care in rural Bangladesh. Structured interviews with 113 VL patients from 87 households documenting all provider visits and expenditures for health care for VL, and the ways in which the expenditures were covered. Patients paid a median of 7 visits to six different providers before beginning VL treatment. All visited the subdistrict government hospital at least once. While health care, including antileishmanial drug therapy, is officially available free of charge at government facilities, 79% of patients reported making informal payments for provider access, diagnostics and drug administration; only 14% of patients received their full drug course from this source. For the 58% of patients who purchased the full treatment course, drug cost constituted 34% of direct expenditure. Median direct expenditure for one VL patient was US$87 and median income lost was $40; median total expenditure was 1.2 times annual per capita income of our study population. Households employed multiple coping strategies to cover expenditures, most commonly sale or rental of assets (62%) and taking out loans (64%). Visceral leishmaniasis treatment causes a major economic burden in affected families. Control strategies for VL should facilitate timely, affordable diagnosis and treatment of patients to decrease the infection reservoir and to alleviate the economic burden of VL on households.

Patient: Male, 69-year-oldFinal Diagnosis: LeishmaniasisSymptoms: Acute renal failure • purpuric skin lesionsMedication: —Clinical Procedure: Bone marrow biopsy • renal biopsy • ultrasonographySpecialty: NephrologyObjective:Rare co-existance of disease or pathologyBackground:Visceral leishmaniasis (VL) is an endemic systemic disease in the Mediterranean countries, including Spain. This vector-borne infection can present with several clinical presentations, from asymptomatic to severe forms. Renal impairment is frequently described in VL but is usually mild and related to interstitial nephritis, being that glomerular involvement is rarely found.Case Report:We describe a case of a 69-year-old Spanish male presenting with subacute renal failure due to membranoproliferative glomerulonephritis and mixed cryoglobulinemia accompanied by other autoimmune features (hypocomplementemia, antinuclear and antiDNA antibodies). No hepatosplenomegaly was found with abdominal ultrasound. Hepatotropic viruses and human immunodeficiency virus serological markers were negatives. We initially suspect the presence of an autoimmune disease and the patient was treated with steroids without improvement. After an extensive study including renal and bone marrow biopsy, a correct diagnosis of visceral leishmaniasis was made, and treatment with liposomal amphotericin B was initiated, achieving renal function recovery and normalization of immunological manifestations.Conclusions:Renal involvement can be an important feature of VL and it might be associated with increased morbidity and mortality. The association between mixed cryoglobulinemia and renal involvement in VL have rarely been described. VL is frequently associated with diverse autoimmune manifestations and it can be initially misdiag-nosed, which could lead to fatal consequences. The role of the immune system in the formation of cryoglobulins are discussed. In our case, an autoimmune disease was initially suspected, and starting treatment with steroids pulses was initiated. However, the presence of mixed cryoglobulinemia in this patient who was hepatitis C serological marker negative and who had poor renal function recovery after immunosuppressive treatment made us suspect other pathologies. The presence of cryoglobulinemia with renal disease in endemic areas of Leishmania should make us exclude this infection before starting immunosuppressive treatment.

Strongyloidiasis, caused by the gut nematode Strongyloides stercoralis, and visceral leishmaniasis (VL), caused by the protozoa Leishmania donovani and L. infantum, are two potentially fatal parasitic diseases with wide global distribution and close association with poverty. Although both infections are treatable, it is imperative to validate cure after treatment. Available diagnostics for both infections have reasonable to high sensitivity for current infection but cannot easily distinguish cure. There is a need for diagnostic tests that are rapid, simple to use and deployable in field conditions to diagnose infection and validate cure. This project aimed to identify candidate coproantigens of S. stercoralis and urine antigens of L. donovani, and to investigate the utility of IgG1 serology for determining cure versus relapse after treatment for VL. For Strongyloides coproantigen discovery, open access ‘omic’ data were analysed using computational tools. For Leishmania urine antigen discovery, antibodies were used to capture parasite antigens from VL urine, which were then identified by mass spectrometry. For Leishmania IgG1 serology, paired sera from preand post-treatment (cured) VL were compared with relapse sera in ELISA and with novel IgG1 specific rapid diagnostic tests (RDTs). This work identified over 40 candidate coproantigens of Strongyloides that satisfied the required characteristics. Seven L. donovani proteins were identified in VL urine, within which 22 protein sequences were indicated as having high epitope potential and specificity to L. donovani. In VL serology, IgG1 was able to differentiate between cure and relapse of VL in both ELISA and RDT assays. With development and optimisation, the candidate antigens and IgG1 assays presented here have potential to contribute to disease control for these parasitic infections. The computational method of antigen selection used here for S. stercoralis can be applied to multiple parasitic helminth infections using the wealth of open access ‘omic’ data.

Congenital Visceral Leishmaniasis