 |
Gorgas Case 2026-3 |
 |
|
The following patient was seen on the inpatient ward of Cayetano Heredia Hospital in Lima by participants in the 2026 Gorgas Course.
 History: A 54-year-old man presented with a 3-month history of abdominal pain, weight loss, fever, and jaundice. Symptoms began with nausea and scleral/mucosal jaundice, and one month later, fatigue, poor appetite, postprandial epigastric pain, and bloating. He later developed pale stools, dark urine, night sweats, and fevers up to 38 °C. During the third month, he was empirically treated at a GI clinic with steroids (prednisone 40 mg/qd for one week) for a presumptive diagnosis of IgG4 disease. A week and a half later, he developed generalized lymphadenopathy and a papular skin rash. Worsening symptoms prompted an ED presentation and hospital admission for further evaluation. Epidemiology: The patient has a history of cutaneous leishmaniasis diagnosed and treated in 2022, which recurred in 2023 and healed with residual scarring. He was born in Yurumarca, Chachapoyas, in the high jungle of Peru. In adolescence, he moved to Lima. From 2020 to 2024, he lived and worked on a farm in Vituya, in the high jungle, where he cultivated dragon fruit, lemons, bananas, and oranges, and harvested coffee. He frequently swam in nearby rivers, visited caves while resting from farm work, raised multiple domestic animals, including guinea pigs, cattle, chickens, pigs, and donkeys, and reported exposure to rodents and bats. He consumed home-produced foods, including unpasteurized dairy products, and experienced frequent insect and mosquito bites. He denied known sick contacts, though neighbors reportedly had untreated skin lesions compatible with leishmaniasis. His home lacked electricity and potable water. Physical examination: HR: 103x’, RR: 21x’, BP: 120/80, Temp: 38°C, SatO2: 95% on room air. Clinical examination revealed jaundice of the skin, sclerae, and mucous membranes, along with pallor (Image A). Papular and crusted skin lesions were present on the face, submental region, and upper and lower extremities (Image B). An atrophic, hypopigmented scar was noted on the posterior left upper extremity. Oral examination revealed a full dentition without thrush or ulcers. Bilateral lymphadenopathy was noted, predominantly tender and soft, affecting the retroauricular, submandibular/submaxillary, axillary, and inguinal regions, with most nodes mobile and dry. The abdomen was distended, with right upper quadrant tenderness on palpation. The liver was palpable 3 cm below the right costal margin, and splenomegaly was noted. The rest of the exam was unremarkable. Laboratory: Basic analysis showed mild normocytic normochromic anemia with hemoglobin in 10.5 g/dL, with 8700 leukocytes (86% neutrophils, 8.6% lymphocytes, 1% eosinophils, 0.1% basophils, 4.3% monocytes). Glucose was 79 mg/dL. Renal function remained preserved (creatinine 0.7 mg/dL, urea 29–25 mg/dL), with normal electrolytes. Liver function tests were increased, with alkaline phosphatase of 920 U/L (Normal range: 40 to 129 U/L) and gamma-glutamyl transferase 1142 U/L (Normal range: 5-40 U/L), associated with total bilirubin of 17.4 mg/dL (Normal range: 0.1 to 1.2 mg/dL), with direct predominance (15 mg/dL). Liver transaminases were elevated AST/ALT: 119/120. Coagulation studies showed prolonged PT 25.6 and INR 2.07 and PTT 62. Lipid profile revealed hypercholesterolemia 219 mg/dL and hypertriglyceridemia 224 mg/dL. Amylase was 50 U/L (normal range: 30–140 U/L), lipase was 23 U/L (normal range: 0 to 160 U/L). Imaging: A chest X ray revealed mild bilateral accentuation of the bronchovascular markings, with no other significant findings (Image C), a magnetic resonance cholangiography showed marked dilation of the intrahepatic bile ducts secondary to diffuse mural thickening of the extrahepatic bile ducts, along with signs of hepatosplenomegaly, retroperitoneal lymphadenopathy, and gallbladder hydrops with minimal biliary sludge (Images D and E). UPCH Case Editors: Carlos Seas, Course Director / Paola Nakazaki, Associate Coordinator |
|
  Discussion: KOH examination of an induced sputum sample (Image F) revealed large, oval, double-walled yeast cells with multiple budding daughter cells, characteristic of Paracoccidioides species. Our patient underwent ERCP, during which a biliary sphincterotomy with balloon sweep was performed, and a biliary stent was placed. Nodular erosive lesions were observed in the duodenum, and a biopsy was obtained. Histopathologic evaluation of duodenal mucosa reported glandular architectural changes and moderate chronic inflammation with the presence of yeasts; no granulomas were reported (Image G), and a lymph node biopsy (Image H) demonstrated a mixed necrotizing granulomatous inflammatory process with abundant yeast-like fungal structures of variable size on hematoxylin and eosin staining. Paracoccidioidomycosis is an endemic mycosis caused by fungi of the genus Paracoccidioides, predominantly Paracoccidioides brasiliensis. It primarily affects rural populations in Latin America, particularly in tropical regions such as Brazil, Peru, Venezuela, Ecuador, and Colombia (1). It is strongly associated with agricultural work, where exposure to soil is important. Paracoccidioides species reside in the environment in their mycelial form and are acquired through inhalation; once inside the host, the fungus undergoes thermal dimorphism, transforming into its yeast form (2). Paracoccidioidomycosis presents with diverse clinical manifestations and is generally categorized into two main forms: the acute/subacute (juvenile) form and the chronic (adult) form. In severely immunocompromised patients, it may present with features of both forms (3). The juvenile form is the least common, occurring in 5% to 25% of cases, and it primarily affects children and young adults under 35 years, with equal gender distribution. It progresses rapidly, typically presenting with fever, weight loss, and generalized lymphadenopathy. Hepatosplenomegaly, abdominal symptoms, skin lesions, and, occasionally, bone involvement may occur, while pulmonary involvement is uncommon (2,3). The chronic form accounts for 75% to 95% of cases and typically affects men aged 30 to 60 years. It has a slow onset and may be localized or disseminated. Pulmonary involvement is most common, presenting with chronic respiratory symptoms and weight loss. Mucocutaneous oral lesions are frequent, and adrenal involvement may occur. Fever and significant lymphadenopathy are uncommon (2,3). Although our patient is outside the typical age range for the juvenile form, he meets clinical criteria consistent with this presentation. Additionally, high-dose corticosteroids may have contributed to accelerated clinical progression. Paracoccidioidomycosis is diagnosed by demonstrating P. brasiliensis in clinical specimens. The fungus can be identified by direct microscopy of sputum, skin scrapings, or biopsy material, including tissue sections stained with hematoxylin and eosin or Gomori–Grocott. Serologic assays for antibodies or antigens may support the diagnosis, although their sensitivity varies and cross-reactivity with other endemic mycoses can occur. Additional diagnostic tools include PCR techniques and fungal culture (4). All patients with the juvenile form should receive amphotericin B. The deoxycholate formulation is administered at 0.5–0.7 mg/kg/day (maximum 50 mg/day). Once clinical stabilization is achieved, the regimen is transitioned to an oral azole derivative or trimethoprim–sulfamethoxazole (3, 5). Our patient is currently receiving amphotericin B and is showing clinical and laboratory improvement, with a significant decrease in previously elevated liver function tests. References |
|
Gorgas Case 2026-2 |
|
|
The following patient was seen on the inpatient ward of Cayetano Heredia Hospital in Lima by the 2026 Gorgas Course participants.
 History: A 60-year-old male from Lima presented with a 6-year history of a progressively enlarging left nasal lesion and dysphagia. The lesion initially appeared as a painless papule with mild pruritus that gradually increased in size. By the fifth year of disease, the lesion became pustular after self-manipulation, with progressive growth and blood-tinged discharge. The nasal lesion became crusted and extended bilaterally, causing partial nasal obstruction, sleep-related breathing difficulty, nasal discharge, hoarseness, and dysphagia. In the last seven months, he noticed worsening of the symptoms. Due to the burden and progression of symptoms, he sought medical attention and was subsequently hospitalized. Epidemiology: The patient was born in Lima and currently resides in the district of Carabayllo, where he works as a construction worker. Travel history includes Aguaytia, a city in the high jungle of Peru, where he went thirty-two years ago and stayed for two years, working as a farmer harvesting bananas and cassava. In his second year, he developed a painless, ulcerative lesion with regular, elevated borders on the elbow. He didn’t seek medical care, and it self-limited in approximately three months, leaving an atrophic, hypochromic scar with irregular edges. He reports that during his stay, many of his co-workers presented similar lesions. Past medical history is notable for pulmonary tuberculosis, diagnosed seven months prior to admission after he developed cough, dyspnea, and weight loss. He completed treatment. Physical examination: HR: 81 x’, RR: 17 x’, BP: 102/66, Temp: 36.5, SatO2: 97%, FiO2: 0.21. The patient presents with marked nasal abnormalities, including an infiltrative, ulcerated lesion with irregular borders measuring approximately 3 × 3 cm in the left nasal cavity, associated with deformity, partial amputation of the left nostril, and a nasal septum perforation. Oral examination reveals a granulomatous lesion involving the hard palate and a nodular lesion at the apex of the tongue (Images A and B). Cutaneous findings include an atrophic, hypopigmented scar with irregular borders measuring approximately 6 × 2 cm on the elbow (Image C). A mobile left cervical lymph node measuring approximately 1 × 1 cm was also noted. The rest of the exam was unremarkable. Laboratory: Initial laboratory findings included hemoglobin of 9.9 g/dL, a white blood cell count of 5.8 ×10⁹/L with 68.8% neutrophils, and a platelet count of 576 ×10⁹/L. The metabolic panel was normal (urea 35 mg/dL, creatinine 0.5 mg/dL, sodium 137 mEq/L, potassium 4 mEq/L, chloride 95 mEq/L, and glucose of 88 mg/dL). Liver function tests and coagulation tests were also normal. Serologic testing for HIV was negative. A Montenegro skin test was positive (15x15mm). Imaging: A chest X-ray showed a nodular bilateral pattern, predominantly. Marked laryngeal thickening and narrowing. A neck lateral X ray showed thickening of the oropharyngeal region with visible obstruction (Image D). A CT scan showed similar findings along with cervical lymph nodes (Image E). UPCH Case Editors: Carlos Seas, Course Director / Paola Nakazaki, Associate Coordinator |
|
 Discussion: The patient was diagnosed with extensive mucosal leishmaniasis. Significant clinical findings were noted after fiberoptic bronchoscopy, revealing a congested pharynx, epiglottis, and larynx with multiple friable granulomatous lesions, edematous vocal cords, and approximately 10% patency of the surrounding mucosal opening (Image F). A nasal mucosal biopsy demonstrated inflammatory infiltrates with fibrosis and intracellular structures morphologically consistent with amastigotes (Image G), confirming the diagnosis of mucosal leishmaniasis. Leishmaniasis is a vector-borne parasitic disease caused by Leishmania species, transmitted by infected female sandflies (Phlebotomus and Lutzomyia). It is endemic in tropical and subtropical regions. The World Health Organization reports an estimated annual incidence of 700,000 to 1 million new leishmaniasis cases, with the majority occurring in the African region and the Americas (1). It is an endemic infectious disease in Peru, Leishmania (Viannia) braziliensis is the principal etiologic agent of mucocutaneous leishmaniasis, with L. (V.) guyanensis, L. (V.) peruviana, and rarely L. (L.) amazonensis also reported (2). With more than 4,000 cases reported annually, it is predominant in rural areas of the jungle and highlands. The highest incidence is observed in the departments of Madre de Dios, Cuzco, Loreto, Ucayali, and Huanuco (3). This disease manifests in three main clinical forms: cutaneous, mucocutaneous, and visceral, with the cutaneous form being the most frequent. The clinical expression and severity of the disease are influenced by parasite, host, and vector-related factors (4). Mucocutaneous leishmaniasis most commonly presents as a late sequela of the cutaneous form, although concurrent presentation may occur (1). Approximately 90% of cases are associated with a history of prior cutaneous lesions, often evidenced by residual scarring, as in our patient’s case (Image C). Mucocutaneous leishmaniasis most commonly presents with nasal involvement, and as the disease progresses, lesions may extend to the oral cavity, palate, pharynx, or larynx; presenting with erythema, edema, infiltration, nodular or ulcerative lesions, and, in advanced cases, destructive changes (2). Diagnosis is based on clinical manifestations and epidemiologic factors, and is confirmed by identification of the species through microscopic examination of lesion aspirates or biopsies, culture, and molecular methods (5). Differential diagnosis includes paracoccidioidomycosis, tuberculosis, histoplasmosis, syphilis, rhinoescleroma, granulomatosis with polyangiitis, or extranodal T-cell lymphoma. Hospitalization was required for systemic treatment and observation due to our patient’s severe clinical presentation. Amphotericin B deoxycholate 0.7-1 mg/kg IV is recommended for extensive mucosal compromise and laryngeal and pharyngeal involvement (5, 6, 7). Despite the lack of large, randomized trials to guide dosing or duration, adjunctive short-term steroids may be recommended for patients with severe inflammatory disease and airway-threatening edema, with tapering guided by clinical response (2). ENT evaluation is also advised to manage and follow airway involvement (5). Our patient is receiving systemic treatment with Amphotericin B deoxycholate with a target of a cumulative dose of 25 mg/kg, and a course of steroids with significant clinical improvement. References |
|
Gorgas Case 2026-1 |
|
|
The Gorgas Course in Clinical Tropical Medicine is held at the Institute of Tropical Medicine at Universidad Peruana Cayetano Heredia in Lima, Peru. Now in its 30th consecutive year, we are delighted to present a selection of intriguing cases encountered by course participants during the February/March sessions. The 9-week Gorgas Course in Clinical Tropical Medicine is currently underway. New cases will be distributed via email each week for the 9 weeks. Each case features a concise clinical history and relevant digital images, followed by the diagnosis and a brief discussion.
The following patient was seen on the inpatient ward of Cayetano Heredia Hospital in Lima by the 2026 Gorgas Course participants.  History: A 55-year-old male from the port of Callao, Lima, presented with a 2-day history of a painful vesiculobullous lesion on the right lower extremity. Symptoms began abruptly upon waking with sudden, intense pain in the posterior right thigh. Several hours later, he developed localized pruritus and burning and self-medicated with an unspecified antibiotic. The pain progressively worsened to severe intensity (10/10), was exacerbated by pressure, and was only minimally responsive to analgesics. One day prior to admission, he noted increased local warmth and persistent pain, followed by a violaceous bullous lesion and yellowish skin discoloration. On the day of admission, ongoing symptoms were accompanied by dark-colored urine, prompting presentation to the emergency department. He denies fever, prior skin trauma, nausea, vomiting, and generalized muscle cramps. Epidemiology: The patient had been temporarily working as a miner in Nazca and was residing in a rudimentary wooden structure without basic services or flooring, with reported exposure to rodents and spiders. Physical Examination on admission: HR: 100x’, RR: 20x’, Temperature: 37°C, BP: 104/71 mmHg, SatO2: 97% on room air. Skin examination revealed a confluent violaceous plaque measuring approximately 8 × 8 cm with associated violaceous bullae on the affected extremity (Image A,B), and jaundice. The patient was alert, well appearing, and in no acute distress. There was no peripheral edema or lymphadenopathy. Cardiopulmonary examination was unremarkable with clear lung fields and regular heart rate and rhythm. The abdomen was soft and non-tender, without hepatosplenomegaly. There was no costovertebral angle tenderness. Neurologic examination showed no focal deficits, and there were no meningeal signs. Laboratory: Initial laboratory evaluation was notable for leukocytosis with neutrophilia (WBC 11.9 ×10⁹/L, ANC 9.77), marked azotemia (creatinine 4.2 mg/dL, urea 136 mg/dL), a decline in hemoglobin from 12.1 g/dL to 8.8 g/dL was observed. And predominantly indirect hyperbilirubinemia (total 8.3 mg/dL; direct 1.5 mg/dL; indirect 6.8 mg/dL), consistent with hemolysis, along with AST-predominant transaminitis (AST 184 U/L, ALT 29 U/L), GGT was 35 U/L, and alkaline phosphatase was 71 U/L. There were marked elevations of LDH and CPK (2418 U/L and 673 U/L, respectively). PT was 15.3, INR 1.17 and PTT was 26.9. Urinalysis showed 3+ bacteria and granular casts, and arterial blood gas revealed respiratory alkalosis (pH 7.47, PCO₂ 27.1 mmHg). UPCH Case Editors: Carlos Seas, Course Director / Paola Nakazaki, Associate Coordinator |
|
 Discussion: Although the patient did not identify the culprit spider, he had noticed several brown spiders in his cabinet. The history and clinical presentation in this case are typical of loxoscelism, which is caused by envenomation from a Loxosceles species bite. These are cosmopolitan arachnids, with over 140 species described worldwide. The species of greatest clinical relevance in South America are L. intermedia, L. laeta, and L. gaucho, commonly known as violin spiders for the violin-shaped marking on the cephalothorax (1). However, the violin mark is not distinctive of the genus Loxosceles; correct identification includes the disposition of its six eyes and the lack of spines on its legs (2), Image C. Spider bites occur most frequently during warmer months, particularly spring and summer. Loxosceles bites usually occur at night in dry, dark indoor environments. The pathophysiology of the disease relies on the venom component, sphingomyelinase D, that causes endothelial damage, activates the complement system, and exerts direct cytotoxic effects that amplify the inflammatory response, leading to severe local or systemic reactions (1). A recent analysis of the components of the Peruvian L. laeta indicates that 69% of the venom contains Phospholipase-D, followed by metalloproteases (20,72 %), sicaritoxins (6,03 %), serine-proteases (2,28 %), hyaluronidases (1,80 %), and Translationally Controlled Tumor Protein (TCTP) (0,56 %) (3). During 2024, the Ministry of Health in Peru reported 1315 cases, with a cumulative number of more than 10,000 in the last 10 years. The jungle of the country concentrated most of the cases, followed by Lima (4). There are two clinical forms: cutaneous and systemic. The first is the most frequent and least severe, characterized by local and regional findings at the bite site, usually associated with skin necrosis appearing as an irregular area of ecchymosis or a livedoid plaque, along with erythema, edema, pain, and pruritus (1,5). The less frequently seen clinical manifestation is the viscerocutaneous or systemic presentation; it is potentially life-threatening and can present with fever, jaundice, disseminated intravascular coagulation, hemolysis, thrombocytopenia, and acute renal failure. Systemic symptoms can appear within 24 to 48 hours and are usually nonspecific (5,6). Loxoscelism is diagnosed clinically by integrating epidemiologic factors, clinical history, and characteristic cutaneous manifestations. Laboratory evaluation may be useful in identifying complications associated with systemic or viscerocutaneous presentation (7,8). Differential diagnosis includes accidents caused by other venomous animals, such as scorpions, snakes, or other spiders; vasculitis; hematologic or coagulation disorders, for example, hemolytic uremic syndrome and autoimmune hemolytic anemia; and other infectious causes, including ecthyma gangrenosum, cutaneous anthrax, or toxic shock syndrome (1)/. Management is primarily supportive and includes local wound care and symptomatic treatment with analgesics and antihistamines. Hospitalization is indicated for patients with systemic manifestations or rapidly progressive lesions. Our patient received one vial of heterologous antivenom and analgesics. Data on the use of antivenom or other medications for Loxosceles bites are conflicting; recommendations may vary. No therapy has demonstrated benefit beyond supportive care, and no medications have been shown to shorten healing time (1,4). Administration of specific anti-Loxosceles antivenom might be recommended, preferably within the first 24 hours or as soon as it is recognized; it is not advised after 72 hours (4,9). In other regions where the antivenom may not be available, short courses of systemic steroids are frequently used (4,7). The patient significantly improved; hemolysis stopped by the third day of hospitalization, but renal damage was established. A non-oliguric form of AKI remains, with no need for dialysis. Plastic surgeons have evaluated the patient for further intervention. References |