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Gorgas Case 2025-7 |
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The following patient was seen on the inpatient ward of Cayetano Heredia Hospital (HCH) in Lima by the 2025 Gorgas Course participants.
 History: A 52-year-old male patient presented to the outpatient clinic in HCH with a seven-year history of swelling, changes in coloration, and discomfort while walking on the right foot. The patient reports that seven years before admission, during a trip to the jungle (Juanjui, San Martin), after playing soccer barefoot, he noticed a small laceration on the sole of his right foot. He did not experience significant discomfort; however, the lesion persisted. Five years before admission, the lesion progressively increased in volume, became edematous, and adopted a tumor-like appearance. Symptoms continued, and two years before admission, he noticed that the tumor-like lesion acquired a dark-brown discoloration and began intermittently discharging white-to-yellowish granules. Epidemiology: He was born in Bagua, Amazonas but moved to Lima 25 years before admission. He previously worked as a rice harvester before coming to Lima and, since moving, has been a handcrafter. Seven years ago, he traveled to Juanjui, San Martín, where he played soccer barefoot. He has not traveled to the jungle ever since. Physical Examination on admission: BP: 120/70 mmHg; RR: 18; HR: 77; T: 26.8°C, Sp02 99% on room air. He was in regular general condition. He presented with a tumor-like lesion on the right foot with grain discharge (Image A), edema with fovea extending from the ankle to the foot (Image B), and a single enlarged right inguinal lymph node measuring 2x1 cm, mobile, and non-tender to palpation. His respiratory and abdominal examinations were non-contributory. The musculoskeletal evaluation showed muscle contraction on the inner part of the thigh with preserved strength in the right lower limb. Neurologically, he was alert with a Glasgow Coma Scale score of 15/15, without focal or meningeal signs. The rest of the exam was normal. Laboratory: Hb 10.7 g/dL, MCV 88.2 fL, MCH 28.4 pg, WBC 7.46 ×10³/µL (Neut 5.33 ×10³/µL, Lymph 1.4 ×10³/µL, Mono 0.46 ×10³/µL, Eos 0.20 ×10³/µL, Baso 0.07 ×10³/µL), Plt 506 ×10³/µL, Glu 93 mg/dL, Urea 35 mg/dL, Cr 0.84 mg/dL, AST 17 U/L, ALT 13 U/L, T. Bili 0.41 mg/dL (D. Bili 0.16 mg/dL, I. Bili 0.25 mg/dL). Serology tests for HIV, HTLV, HBsAg, and RPR were negative. Imaging: A foot MRI revealed lytic lesions in the tarsus and metatarsus and a soft tissue abscess in the Achilles heel and foot sole (Image C). Microbiology: Gram stain from the grains revealed the following structures (Image D) and culture revealed the following colonies (Image E). UPCH Case Editors: Carlos Seas, Course Director / Mario Suito, Associate Coordinator |
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Discussion: Gram stain from the grains revealed gram-positive 0.5-1-μm-wide filamentous structures compatible with an agent of actinomycetoma, later identified through MALDI-TOF as Nocardia farcinica. Mycetoma (also known as Madura foot) is the most common worldwide subcutaneous tropical infection first described in 1842 in Madras, India. The latest reports indicate over 8,700 cases globally, with approximately 127 new cases per year across 23 countries, the most affected being India, Sudan, and Mexico (1). Males are disproportionately affected (6:1), and the disease primarily occurs in adolescents and young adults under 40 (2). Actinomycetoma, which predominates in the Americas, is caused by various species of aerobic filamentous bacteria, including Nocardia, Actinomadura, and Streptomyces. Eumycetoma, by contrast, is a fungal infection most commonly caused by Madurella mycetomatis and is more prevalent in Africa and Asia (3).Clinically, mycetoma is characterized by tumor-like swellings, sinus tracts, and grain discharge. The lower extremities are affected in 80% of cases. While the disease is usually localized, actinomycetomas more frequently extend deeper into bones and joints than eumycetomas. Actinomycetoma grains tend to be smaller than those of eumycetomas, are composed of filamentous bacteria, and function as biofilms, limiting antibiotic penetration. Actinomycetoma grains are typically white or pale yellow, except for those caused by Actinomadura pelletieri, which appear red to pink. Eumycetoma grains, on the other hand, are usually black, brown, yellow, or white, depending on the causative fungal species. In this case, the presence of white granules ruled out Madurella mycetomatis, which typically produces black granules (4). Diagnosis is primarily clinical, based on the triad of swelling, sinus tracts, and grain drainage. Imaging assesses disease extent, while culture and molecular methods confirm the causative organism (5). Grains, either spontaneously extruded or aspirated, can be cultured on blood or Sabouraud agar, and drug susceptibility testing is recommended for all cases (6, 7). Among Nocardia species, the most common causative agent is Nocardia brasiliensis. A recent study from China found Nocardia farcinica the most common species among all nocardiosis cases and was, as most Nocardia species, susceptible to TMP-SMX, Amikacin, and Linezolid (8). Combination antibiotic therapy is recommended to prevent antimicrobial resistance. Treatment typically involves a trimethoprim-sulfamethoxazole (TMP-SMX) backbone combined with an aminoglycoside, rifampin, or dapsone for 6–24 months. While surgery is commonly used for eumycetomas, it is less frequently required for actinomycetoma due to the high effectiveness of medical therapy (3, 9). Our patient was started on a combination regimen of TMP-SMX and amikacin. References |
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Gorgas Case 2025-6 |
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The following patient was seen in Cuzco by the 2025 Gorgas Course participants.
 History: A 43-year-old male patient presented to the emergency department at Cuzco with a 6-month history of productive cough, fever and 3 months of disseminated cutaneous lesions. Six months before admission the patient presented productive cough with blood-tinged sputum, subjective fevers and night sweats. Symptoms persisted and 3 months before admission multiple umbilicated papules first appeared in the palms and soles and progressed to affect the rest of the body. Lesions were painful, non-pruriginous and had no discharge. Three days before admission he developed shortness of breath for which he attended the ED and was admitted. Epidemiology: The patient was born in the city of Cuzco and worked as an agricultural technician. He lived with his female partner, denied polygamy, MSM or contact with sexual workers. He traveled to the low jungle in two occasions, 1 year and 7 months, before admission where he had significant exposure to animals including birds and bird guano. Physical Examination on admission: BP: 120/70 mmHg; RR 26; HR 91; T: 36.5°C, Sp02 92% on room air. He appeared to be tachypneic and in mild respiratory distress. On the skin, multiple erythematous umbilicated papular lesions on the palms, soles, upper and lower extremities, trunk, face and tongue were noted (Image A). There was no palpable lymphadenopathy. There were decreased breath sounds bilaterally with bibasilar crackles. The rest of the exam was normal. Laboratory: WBC 12,910/µL with Seg 10,700 (82.9%), Lin 1,110 (8.6%), Mon 750 (5.8%), Bands 0.9%; Hb 12.6 g/dL with MCV 76.1 fL, MCH 25.7 pg; Platelets 332,000/µL, CRP: 19.44 mg/L. Creatinine 0.91 mg/dL, Urea 40.9 mg/dL, AST 34 U/L, ALT 73 U/L, TB 7.2 mg/dL (DB 1.79 mg/dL), Alk. Phos 298 U/L, GGT 335 U/L. Na+ 139 mmol/L, K+ 5.4 mmol/L. TSH 1.91 µIU/mL, free T4 1.45 ng/dL, T3 0.26 ng/mL. HIV, HTLV-1, VDRL, HBsAg, anti-HBc, HCV, HAV were negative. Anti-MPO (ANCA P), Anti-PR3 (ANCA C) negative. Blood cultures came back negative, as well as AFB sputum, urine, and stool. Sputum GeneXpert was negative, but a BAL sample GeneXpert was positive for MTB with indeterminate rRifampicin resistance. Imaging: A CT chest revealed alveolar consolidation in the right lower lobe with peripheral air bronchogram along withnd other scattered ground-glass opacities in both lungs and in the left lower lobe, cavitary-appearing lesions with peripheral alveolar consolidation (Image B). Both head and Abdominopelvic CT were normal. Pathology: : A skin biopsy (Image C, H&E stain) and culture (Image D) from the lesions were performed, revealing the following structures. UPCH Case Editors: Carlos Seas, Course Director / Mario Suito, Associate Coordinator |
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Discussion: Histopathology revealed budding yeasts and culture demonstrated fungal colonies compatible with Cryptococcus sp. Cryptococcosis is caused by the ubiquitous yeasts of Cryptococcus neoformans, C. gattii, and, less commonly, C. laurentii and C. albidus. C. neoformans is most commonly isolated from soil contaminated with bird (pigeons, turkeys and chickens) guano. Humans are infected after inhalation of the Cryptococcus sp. Propagule, which in normal hosts is eliminated, but in certain cases and more frequently in immunosuppressed patients, can proliferate and cause invasive disease. Of all affected patients, 80-85% have a predisposing condition, the most common being HIV infection (1). Although less frequently affected, the remaining 20-25% of non-HIV and non-transplant (NHNT) patients have more lung involvement, higher mortality (2), and longer duration of symptoms (34 days vs 81 days, p < 0.001) (3). Pulmonary involvement is the second most common location after CNS and includes well-defined single or multiple parenchymal nodules, masses, parenchymal infiltrates, hilar lymphadenopathy, pleural effusions, and cavitary lesions (4). Cutaneous cryptococcosis almost exclusively represents disseminated disease and is the third most affected organ with protean manifestations. Papules with an ulcerated center are the most common manifestation and may resemble the umbilicated papules of molluscum contagiosum (5). Diagnosis involves either direct observation of the encapsulated yeasts, culture and antigen detection. Classically, the use of the inverse contrast staining of India ink has been used with high specificity (100%) low sensitivity in non-HIV (50%) compared to moderate to high (80%) in HIV infected patients (4). Yeasts surrounded by apparently empty spaces may be seen in H&E stains from affected tissues. The polysaccharide capsule can by identified with mucicarmine and alcian blue stains and the yeasts as well as the narrow budding can be identified using silver fungal stains such as Gomori methenamine stain. Culture from CSF and peripheral blood can give positive results in 3-7 days and the quantitative analysis of the colony count can be used to evaluate antifungal therapy effectiveness. Glucuronoxylomannan (GXM) polysaccharide antigen detection using the latex agglutination test is highly sensitive and specific when used in serum and CSF. Recently, a cheap, rapid, and simple lateral flow assay (LFA) has been developed with comparable test characteristics, widely replacing latex agglutination in routine clinical practice (6-9). Antigen titer measurement is inaccurate and should not be used for treatment decisions. Treatment of non-CNS cryptococcosis is extrapolated from CNS data. Induction therapy with liposomal amphotericin B (3-4 mg/kg IV) daily plus flucytosine (100 mg/kg PO daily in four doses) should be continued for at least 2 weeks. Before switching to consolidation therapy, the patient should have clinical improvement and CSF sterilization, the latter being demonstrated by a repeat LP for fungal culture at the 2-week mark before switching to Fluconazole 400-800 mg PO daily consolidation therapy for at least 8 weeks, after which patients can be switched to maintenance therapy with Fluconazole 200mg PO daily for at least 1 year (10, 11). In cases of CNS Cryptococcosis, management of increased intracranial pressure with either repeat LP’s or lumbar drain decreases mortality and should be pursued aggressively (12). Our patient was started on both antifungal and drug-sensitive tuberculosis treatment. GeneXpert Ultra detects M. tuberculosis (LOD: 16 CFU/mL) and rifampicin resistance (LOD: ~100 CFU/mL) via rpoB mutations. In trace-level paucibacillary TB, resistance cannot be determined, requiring confirmation with MGIT culture or Line Probe Assays (13). References |
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Gorgas Case 2025-5 |
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The following patient was seen in Cuzco by the 2025 Gorgas Course participants.
 History: A 17-year-old male patient with a history of epilepsy presented to the outpatient clinic in Cuzco with a 10-year history of a progressive lesion on his right earlobe. Ten years before admission, he noticed a non-painful, non-pruritic, papule-like lesion on his right earlobe. The lesion increased significantly in size, prompting surgical removal seven years before admission. Unfortunately, the lesion recurred after surgery with a faster growth rate, developing a tumor-like, verrucous appearance, associated with burning pain and pruritus.. The lesion was non-anesthetic, had no drainage or fistulation, and was not associated with systemic symptoms or evidence of metastatic disease. Epidemiology: The patient was born and raised in Cuzco, a highland city in Peru. Fourteen years before admission, he traveled with his father to Madre de Dios in the low jungle of Peru, where he stayed for two years. He returned to Madre de Dios for two weeks one year before admission. He also reported contact with a cousin who had tuberculous meningitis. Physical Examination on admission: BP 100/60 mmHg, RR 18 breaths per minute, HR 71 bpm, Temp 36.4°C, SpO₂ 92% on room air. A tumor-like exophytic lesion with multiple nodules and superficial crusting was noted on the helix and lobule of the right earlobe (Image A). The lesion was firm and hard to touch, with no discharge, regional lymphadenopathy, or sinus tracts. The rest of the physical exam was within normal limits. Laboratory: Hb: 18.7 g/dL (Hematocrit: 54%); Leukocytes: 10,260/µL (Neutrophils: 7,120/µL, Eosinophils: 120/µL, Lymphocytes: 2,370/µL); Platelets: 397,000/µL; Glucose: 97 mg/dL; Urea/Creatinine: 30/1.16 mg/dL; AST/ALT: 27/37 U/L; Alkaline Phosphatase: 119 U/L; Albumin: 4.5 g/dL; Sputum AFB x2: Negative. HIV, HTLV-1, Syphilis, HBsAg, Anti-HBc, and HCV non-reactive. UPCH Case Editors: Carlos Seas, Course Director / Mario Suito, Associate Coordinator |
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Discussion: Both KOH-stained light microscopy and histopathology revealed fungal structures compatible with Paracoccidioides loboi. Lobomycosis is an exceedingly rare subcutaneous mycosis caused by the yet unculturable and recently renamed Paracoccidioides loboi (formerly Lacazia loboi). Accidental trauma, particularly involving plants and thorns, is thought to be the primary transmission mode, although not in all cases (1). The latest prevalence estimates report 907 total cases of lobomycosis, with 55% of cases originating in Acre State, Brazil (2). The remaining cases come from the Amazonian rainforest regions of Brazil, Peru, and Colombia. Cases in developed countries such as the United States have been reported in migrants or tourists returning from endemic areas (3). Notably, bottlenose dolphins have also been found to be affected by this disease. Lobomycosis remains restricted to the skin and typically follows a decades-long progression. The classical lesions are red, hard, shiny keloidal plaques or nodules that may ulcerate with secondary crusting or develop a verrucous appearance over time. Local extension is the norm, and there have been no reported cases of metastatic disease. The most common sites of involvement are the lower extremities, followed by the ears, upper extremities, and head. Disseminated cases have been described, presenting with multifocal lesions, intense pruritus, and marked ulceration. The diagnosis is confirmed by direct visualization of fungal cells in KOH-stained light microscopy or histopathological analysis of clinical specimens, revealing round 9-µm single or short-chain yeast cells with thick double cell walls. Specimens for light microscopy can be obtained using the “Scotch tape test,” where vinyl adhesive tape is applied to the crusted lesion and transferred to a glass slide for KOH staining. Histopathology (Hematoxylin-eosin or Grocott-Gomori staining) is the gold standard diagnostic test (3). Since P. loboi has not been successfully cultured, 18S ribosomal analysis has revealed its close relation to Paracoccidioides brasiliensis (4) The main differential diagnosis includes bacterial infections such as cutaneous TB (Tuberculosis verrucosa cutis), non-tuberculous mycobacteria (NTM) infections, actinomycetoma, and botryomycosis; fungal infections such as paracoccidioidomycosis, eumycetoma, sporotrichosis, and chromoblastomycosis; and parasitic infections such as cutaneous leishmaniasis (5) There is no curative treatment for lobomycosis. Surgery is an option, though primarily for cosmetic purposes. Case reports have described successful treatment with posaconazole, clofazimine, and itraconazole (6-8). Our patient was treated with 1 month of TMP/SMX and itraconazole, but no significant clinical response was observed, leading to surgical removal of the lesion. References |
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Gorgas Case 2025-4 |
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The following patient was seen in the inpatient ward of Cayetano Heredia Hospital in Lima by the 2025 Gorgas Course participants.
 History: A 43-year-old male patient with no significant past medical history presented to the emergency department of Cayetano Heredia Hospital (HCH) with 2.5 months of diarrhea, vomiting, and abdominal pain. Two months and fifteen days before admission, he presented with watery diarrhea without mucus or blood, 3-4 times every other day, associated with postprandial abdominal pain. Two months before admission, he attended a Primary Care Center, where he tested positive for HIV and was promptly started on ART (tenofovir, lamivudine, dolutegravir). His symptoms remained stable with marginal improvement, and one month before admission, he developed marked abdominal distention associated with postprandial vomiting. This was aggravated by the appearance of lower extremity edema. On the day of admission, he presented with worsening abdominal pain. An ambulatory colonoscopy revealed multiple ulcers in the descending, sigmoid, and ascending colon and cecum, including fistulizing ulcers in the descending and sigmoid colon. Of note, he had a 15 kg involuntary weight loss in the last 6 months and 2.5 months of asthenia. He denied headaches, visual symptoms, fever, dyspnea, cough, or chest pain. Epidemiology: The patient was born in Cerro de Pasco, a city located in the central highlands of Peru, but currently lives in northern Lima, where he moved 25 years ago after working for one year as a coffee farmer in the jungle of Chanchamayo. He denies any known TB contacts and has no pets. He has had five male sexual partners with inconsistent condom use and was previously treated for genital herpes one year ago. Physical Examination on admission: BP: 110/70 mmHg, RR: 18, HR: 115, Temp: 36.1°C, SpO₂: 96% on room air. He appeared malnourished but was ventilating spontaneously and in no acute distress. An approximately 2 × 2 cm ulcer in the right upper hard palate and 2-4 smaller ulcers in the left internal cheek were found (Image A). Pitting edema up to his knees was noted, and had multiple palpable 0.5 × 0.5 cm mobile, non-tender cervical lymph nodes. He had normal breath sounds with diffuse wheezing but no rales or crackles. His abdomen was markedly distended, with increased bowel sounds and shifting dullness. The rest of the exam was normal. Laboratory: Hemoglobin 9.9 g/dL (MCV 79.6 fL, MCHC 35.6 g/dL), WBC 8,300/uL (0% bands, 77.2% neutrophils, 0.1% eosinophils, 0.1% basophils, 8.6% monocytes, and 14% lymphocytes), platelets 380,000/uL. Urea 31 mg/dL, creatinine 0.64 mg/dL. AST 31 U/L, ALT 28 U/L, alkaline phosphatase 108 U/L, total bilirubin 0.5 g/dL, LDH 211 U/L. INR 1.23. A repeat HIV test was positive, and RPR, hepatitis B, and C serologies were negative. An initial HTLV-1 ELISA test at a reference lab was positive, but an in-house repeat ELISA was negative, confirmatory Western Blot is pending. A thorough TB workup was negative, including sputum AFB and GeneXpert ultra, urinary TB LAM, and tuberculin skin test. The serum cryptococcal lateral flow assay was negative, as were serial stool O&P’s. Lastly, a urinary Histoplasma sp. antigen was found to be positive. Imaging: An abdominal ultrasound revealed an estimated 1-1.5 L free intraperitoneal fluid collection and hepatomegaly. An abdominal X-ray showed dilated small and large bowel loops and multiple air-fluid levels (Image B). An abdominal CT scan showed dilated intestinal loops associated with bowel wall edema. A chest CT showed multiple bilateral nodules associated with areas of ground-glass opacities and multiple thin-walled cavitary lesions (Image C). A KOH stain from a BAL sample was performed (Image D). Results from biopsies obtained from the colonoscopy are shown (Image E, H&E stain; Image F, Grocott stain). UPCH Case Editors: Carlos Seas, Course Director / Mario Suito, Associate Coordinator |
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Discussion: Both the direct BAL smear and the large intestine biopsies revealed variable-sized yeasts with narrow-based budding and birefringent walls, findings compatible with Paracoccidioides sp. infection. PCM is an endemic mycosis of Latin America’s rainforests caused by the thermally dimorphic fungus Paracoccidioides brasiliensis and, less commonly, by Paracoccidioides lutzii (1). Brazil reports 80% of all cases, with the remainder being from Argentina, Bolivia, Colombia, Ecuador, Venezuela, Mexico, and Peru (2). Transmission occurs through the respiratory route, with an estimated 10 million people infected in Latin America, most of them being over 30 years old, with no racial predominance but with a male-to-female ratio of around 14:1 (3). The most associated risk factor is working as a farmer in coffee or tobacco crops (4). PCM can be clinically divided into asymptomatic infection, active disease, and sequelae or residual form. Active PCM disease can be further classified into an acute/subacute or juvenile form, a chronic progressive or adult form that can be unifocal or multifocal, or a mixed form with characteristics of both the juvenile and chronic progressive forms. The juvenile form develops in days to weeks and commonly presents with fever and reticuloendothelial system involvement (generalized lymphadenopathy, liver and spleen enlargement). At-risk populations are those less than 30 years old and immunosuppressed patients, such as those with advanced HIV (5). The chronic progressive form develops over months to years and commonly presents with bilateral, apical-sparing pulmonary involvement, localized lymphadenopathy, and oral mucosal lesions. Pulmonary symptoms are usually mild, with hemoptysis being rare. Radiological findings can include alveolar, interstitial, and/or nodular patterns. Cavitary lesions and pleural effusions are less common. Pulmonary fibrosis is the eventual common endpoint for severe and/or untreated PCM pulmonary disease (6). Mucosal lesions are more common in the chronic form and usually involve the oral mucosa. Lesions tend to be painful, destructive, and ulcerative, accompanied by gingival infiltration causing tooth loss. Skin lesions are more common in the juvenile form, are pleomorphic, and frequently affect the face. Intestinal involvement can affect any segment of the GI tract but most commonly affects the ascending colon, cecum, and ileum, followed by the small intestine. Symptoms include abdominal pain, weight loss, and chronic diarrhea (7). Patients with advanced HIV and CD4 counts less than 200 are at risk for the reactivation of latent foci. These patients tend to present with disseminated, multi-organ involvement, exhibiting characteristics of both the chronic multifocal and juvenile forms (8). Of note, HTLV-1 coinfected patients have also been described with a predominance of juvenile and/or mixed forms and intestinal involvement (9). The fastest, most cost-effective, and clinically applicable diagnostic method is the direct examination of round yeast cells with peripheral budding in KOH-prepared samples from affected tissues, such as oral or skin lesions, sputum, lymph node aspirates, and CSF (10). The same yeast cells can be seen in histopathological samples, which can be enhanced by silver stains, PAS, and/or immunofluorescence techniques. Culture is the second standard diagnostic method but requires cool temperatures of 18-24°C and takes up to 20-30 days to grow. Serological tests remain an area of ongoing research, being utilized in endemic countries like Brazil but unavailable in most settings. Antibody detection using the double immunodiffusion method (DID) with the 43 kDa antigen is the most used method but remains positive years after exposure, limiting its use in detecting active disease (11). For mild to moderate cases of PCM, the preferred treatment option is itraconazole, with a variable duration of treatment from 9 to 18 months. Cotrimoxazole can also be used for 18 to 24 months. In cases of severe and disseminated presentation, the preferred therapeutic choice is 2 to 4 weeks of Amphotericin B until clinical stabilization, followed by a switch to oral maintenance therapy (11). Our patient was started on amphotericin B 1.0 mg/kg. References |
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Gorgas Case 2025-3 |
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The following patient was seen in the inpatient ward of Cayetano Heredia Hospital (HCH) in Lima by the 2025 Gorgas Course participants.
 History: A 70-year-old male patient with no significant past medical history presented to the outpatient clinic at HCH with a six-year history of expanding, painless skin lesions on his left foot. Six years before admission, he developed a painless, non-pruritic, 1 x 1.5 cm non-healing papule that became ulcerated on the dorsum of his left foot. At that time, he sought care at a local health center, where he received three intralesional pentavalent antimonial injections over three consecutive days, with partial clinical improvement. Five years before admission, the lesion increased in size to 5 x 5 cm and was accompanied by localized swelling. The lesion continued to expand, and four months before admission, it became moderately painful, impairing his daily activities. Due to persistent symptoms, he attended the dermatology clinic and was admitted for further workup and management. Epidemiology: The patient was born and resides in La Merced, a city located in the high jungle of Peru, where he works in agriculture cultivating coffee and fruits. He frequently walks barefoot in the jungle soil and experiences numerous mosquito bites. He denies any travel outside his place of birth. He has no known tuberculosis (TB) contacts but reports that multiple neighbors throughout his lifetime have presented with similar non-healing cutaneous ulcers. Physical Examination on admission: BP: 110/80 mmHg, HR: 70 bpm, RR: 20 breaths per minute, T: 36.5°C, SpO2: 98% on room air. The skin examination revealed multiple tumor-like, verrucous, confluent hyperkeratotic plaques with irregular and poorly defined borders in the middle and lateral malleolar regions and on the heel of the left foot, with hyperpigmentation and scaling (Image A). The rest of the examination was normal. Laboratory: Hemoglobin: 9.4 g/dL (MCV 92 fL, MCHC 33 g/dL), Hematocrit: 29%, WBC: 4,400/µL (0% bands, 65.1% neutrophils, 8.7% eosinophils, 0.5% basophils, 11.3% monocytes, 14.4% lymphocytes), Platelets: 433,000/µL, Creatinine: 0.81 mg/dL, Sodium: 140 mEq/L, Potassium: 4.9 mEq/L, Chloride: 104 mEq/L. Serology for HIV, HTLV-1, RPR, and Hepatitis B and C were all negative. A foot X-ray showed no bone involvement (Image B). A Giemsa-stained scraping from the border of a lesion was performed (Image C; reference image, original of low quality). UPCH Case Editors: Carlos Seas, Course Director / Mario Suito, Associate Coordinator |
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  Discussion: GeneXpert ultra and acid-fast bacilli (AFB) staining from the tissue biopsy were negative, as was the TB liquid media (MGIT) culture. KOH and fungal cultures were also negative. The Montenegro intradermal hypersensitivity test was positive (30 x 35 mm). A skin punch biopsy revealed parakeratosis and acanthosis associated with a lymphohistiocytic inflammatory infiltrate and epithelioid granulomas; however, no definitive amastigotes were seen. A kinetoplast DNA PCR (kDNA PCR) for Leishmania sp. was positive, confirming the diagnosis (Image D). Finally, the patient presented a remarkably positive therapeutic response after treatment with Amphotericin B, showing marked improvement of the lesion (Image E). Leishmaniasis is endemic in 88 countries, including Brazil, French Guiana, Colombia, Ecuador, Bolivia, and Peru (1). The most common manifestation is cutaneous leishmaniasis (CL), which affects 10 million people worldwide. Affected patients typically live in or have a history of travel to endemic areas. In Peru, over 7,000 cases are reported annually (2,3). CL in Peru is a zoonosis caused by Leishmania species, almost exclusively from the subgenus Viannia, particularly L. peruviana, L. braziliensis, L. guyanensis, and L. panamensis. Humans become infected when the sandfly vector (Lutzomyia sp.) inoculates promastigotes into the host’s bloodstream while taking a blood meal. These promastigotes are phagocytized by macrophages, where they develop into amastigotes that multiply until they are released and infect other cells. CL usually develops 2-8 weeks after inoculation. The most common presentations include the localized-ulcerative form, the nodular or sporotrichoid form, and the diffuse and disseminated cutaneous forms. Less common manifestations include plaque, psoriasiform, and verrucous leishmaniasis, which represent 2-5% of all CL cases (4). Verrucous leishmaniasis is a rare subtype of the already infrequent atypical cutaneous leishmaniasis subgroup. It is classically described as hyperkeratotic plaques covered by thick, adherent crusts. Diagnosis relies on identifying high-risk patients based on compatible clinical manifestations and the appropriate epidemiological exposure, followed by specific parasitological diagnostic tests. Most confirmatory tests require invasive tissue biopsies, where 1) direct microscopy with commonly used Giemsa stain reveals amastigotes, 2) culture from the lesion demonstrates promastigotes, and/or 3) PCR amplification detects genomic DNA from Leishmania sp. Serology has no role in the diagnosis of leishmaniasis. A positive Montenegro skin test demonstrates a delayed-type hypersensitivity reaction to Leishmania antigens but cannot differentiate between previous exposure and active disease. Speciation impacts treatment decisions regarding initiation, regimen selection, duration, and dosage. It can be performed using isoenzyme analysis requiring cultured promastigotes or molecular methods like PCR from a tissue sample (5). New World cutaneous leishmaniasis may be treated topically with paromomycin and gentamycin, intralesional injections of pentavalent antimonials, or physical methods such as thermal and cryotherapy (6). For patients with extensive (>5 cm) or multiple (≥ 5) lesions, immunosuppression, or species associated with mucosal disease (L. braziliensis, L. guyanensis), systemic treatment is recommended. Systemic options include intravenous pentavalent antimonials (SbV) (sodium stibogluconate, meglumine antimoniate) and Amphotericin B, as well as oral Miltefosine (7). Although no controlled randomized trials have demonstrated a significant statistical difference between amphotericin B and SbV, extensive cutaneous disease, such as in this case, is typically treated with Amphotericin B (8). References |
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Gorgas Case 2025-2 |
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The following patient was seen in the inpatient ward of the Cayetano Heredia Hospital (HCH) in Lima by the 2025 Gorgas Course participants.
 History: A 21-year-old male patient with no significant past medical history presented to the emergency department of HCH with a 5-month history of cough and chest pain. Five months before admission, he presented sporadic dry cough and occasional mild left pleuritic chest pain. He attended an occupational medicine consult where a routine chest X-ray was performed, revealing a radiopaque circular lesion in the left hemithorax (Image A), and a follow-up chest CT confirmed the presence of a 72x98x68mm left-sided pulmonary lesion and an additional right-sided 19x18x23mm hyperdense pulmonary lesion (Image B). Three weeks before admission his cough became productive with whitish sputum and was associated with shortness of breath on exertion. Ten days before admission, the pleuritic pain intensified and disrupted his sleep. Five days before admission, he presented a cough with blood-tinged sputum, generalized malaise, and subjective fever. Due to the persistence of symptoms, he traveled to Lima and attended the ED. Epidemiology: The patient was born and lives in Oyon, a city in northern Lima province at an altitude of 3600 meters above sea level. He lives in a rural area where he works as a mechanic and on his family’s farm, feeding, cleaning, and caring for sheep, cows, cats, and dogs. The dogs live inside the house and are fed on the dead sheep’s viscera. He has only traveled to rural areas nearby. He has no known TB contacts and no other family members have presented similar symptoms. Physical Examination on admission: BP was 100/60 mmHg, RR 28, HR 92, afebrile at 37°C with a Sp02 of 90% on room air. Breath sounds were abolished in the left hemithorax, and there was hyper resonance to percussion in the upper 2/3 and dullness in the lower 1/3 on the left hemithorax. The rest of the exam was normal. Laboratory: Hemoglobin was 17 g/dL (13-16 g/dL), WBC 17 100/uL (4-12 x 10^3/uL) with no bands, 51.6% neutrophils, 15.9% lymphocytes, 27% eosinophils (absolute count: 4 595, normal being less than 500/uL), 0% basophils, 4.9% monocytes. Platelets 391 000/uL. Urea 29 mg/dL, Creatinine 0.83 mg/dL, Sodium 142 mEq/L (135-145 mEq/L), Potassium 4.35 mEq/L (3.5-5.5 mEq/L), Chloride 107 mEq/L (96-106 mEq/L). Total bilirubin 0.53 g/dL with a direct of 0.32 g/dL. AST 14, ALT 24 IU/L (normal less than 40 IU/L). CRP 4.6 mg/dL (normal less than 0.3 mg/dL). PT 13.5 sec, PTT 29 sec with an INR of 1.15. HIV test was negative and VDRL was non-reactive. Imaging: A chest X-ray was performed on admission (Image C) followed by a normal abdominal ultrasound. UPCH Case Editors: Carlos Seas, Course Director / Mario Suito, Associate Coordinator |
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 Discussion: The chest X-ray on admission revealed a left side hydropneumothorax with a ruptured cyst on the left lung base showing the “water lily” sign (Image C, red arrow), which was more evident on chest imaging after chest tube insertion (Image D). Western Blot for Echinococcus granulosus was positive for the 21kDa, 16kDa, and 8kDa antigens, confirming the diagnosis. PHD is the second most common manifestation of cystic echinococcosis (CE) representing 20-30% of all cases (1). CE has an annual incidence in endemic areas of 1 to 200 per 100,000 and a mortality rate of 2-4% (2), affecting countries from South America, Eastern Africa, Central Asia, and the Mediterranean (1). It is commonly found in impoverished rural areas. Most affected individuals have one or more risk factors, including living in unsanitary conditions, raising livestock such as sheep, herding or guarding dogs often near homes that are fed offal, and slaughtering livestock close to humans and dogs (3). Echinococcus granulosus eggs are released by the adult tapeworms residing in the definitive hosts (canids, mainly dogs) GI tract that are ingested by humans who act as accidental hosts. Eggs hatch in the intestine, releasing oncospheres that enter the portal circulation or lymphatic system, reaching the liver, where they develop into hydatid cysts (metacestode larvae). The hydatid cyst is composed of an acellular laminar layer and an internal germinal layer that produces a clear hydatid fluid, protoscoleces, and daughter cysts, and is surrounded by a third membrane, the adventitial layer (pericyst), formed by the host immune reaction to the cyst and fibrous tissue. Oncospheres are usually trapped in the hepatic parenchyma, but some may travel through the liver sinusoids and pass through the hepatic veins and inferior vena cava, reaching the right heart and landing in the lungs or pass the lungs and through the left side of the heart reach other organs. PHD has a variable clinical presentation depending on location, size, and cyst wall integrity. It can be discovered incidentally since it can be asymptomatic until rupture, fistula development, mass effect, or other complications occur (4). Some symptoms and signs associated with cysts include shortness of breath, coughing, hemoptysis, pneumonia, atelectasis, and the expectoration of a salty fluid (‘’vomica’’) when a cystobronchial fistula is formed (5). Diagnosis is based on radiological findings and complementary confirmatory serology. Serology includes sensitive screening tests like enzyme immunoassays (EIA) and specific confirmatory tests like immunoblot (Western blot). Screening tests have a sensitivity of 80-100% for liver cysts but only 50-56% for lung cysts. Therefore, a high false-negative incidence rate must be considered, particularly for cyst stages where the host has not been exposed to the parasitic antigen (CE1) or for biologically inactive cysts (CE4, CE5) (6). Surgery is the cornerstone of therapy for PHD. It should be pursued first in the co-existence of pulmonary and liver cysts because of the higher risk of rupture and cystobronchial fistulas of the former (5). Treatment with albendazole 10-15 mg/kg divided into two doses can be started 1-3 days before surgery and continued 3 months postoperatively. In cases where the cyst contents spill into the pleural space either spontaneously or iatrogenically, as in our patient’s case, it is essential to begin antiparasitic treatment promptly alongside surgical intervention and thorough irrigation of the pleural space with isotonic saline to prevent secondary CE (5). Primary antiparasitic treatment without surgical involvement is usually avoided because of the risk of treatment-induced cyst membrane detachment, rupture, and opening of cystobronchial fistulas, except for small lung cysts less than 5 cm (7). References |
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Gorgas Case 2025-1 |
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The Gorgas Courses in Clinical Tropical Medicine are given at the Tropical Medicine Institute at Cayetano Heredia University in Lima, Perú. For the 29th consecutive year, we are pleased to share interesting cases seen by the participants that week during the February/March course offerings. Presently, the 9-week Gorgas Course in Clinical Tropical Medicine is in session. New cases will be emailed every Tuesday/Wednesday for 9 weeks. Each case includes a brief history and digital images pertinent to the case. A diagnosis and a short discussion follows.
 History: A 34-year-old male patient with no significant PMH presented to the ED with a 2-week history of abdominal pain and subjective fevers. Two weeks before admission, he presented epigastric pain associated with nausea, decreased appetite, and fever quantified at 39 C. One week before admission, right pleuritic chest pain was added. Symptoms persisted, and on the day of admission, an abdominal US revealed hepatomegaly with a 13.4 x 3.6cm heterogeneous liver lesion. Epidemiology: The patient was born in Lima, Peru's capital, but currently lives in the city of Tumbes, in the northern part of the country’s coastline. He works as an independent vendor in the textile industry and constantly travels from Lima to Tumbes. While in Tumbes, he endorses eating raw vegetables, abundant seafood, including blood clam ceviche, from street vendors and drinking non-potable water. Two weeks before the onset of symptoms, he reported two weeks of self-limited watery diarrhea. Physical Examination on admission: BP: 120/80 mmHg; RR: 18; HR: 88; T: 38.4 °C, Sp02 97% on room air. The patient didn't appear to be in any acute distress. There was no skin rash or jaundice and no palpable lymphadenopathy. His abdomen was mildly distended, with epigastric tenderness on palpation. Hepatomegaly with point tenderness 3cm below the right costal margin was found. The rest of the exam was normal. Laboratory: Hemoglobin was 14.4 g/dL, WBC 26 000/uL with no bands, 22100/uL neutrophils, 1300/uL lymphocytes, no eosinophils, no basophils, and 1820/uL monocytes. Platelets were 429 000/uL. PT was 15 sec, PTT 30 sec with an INR 1.26. Total bilirubin was 2.9 g/dL with a direct bilirubin of 1.8 g/dL. Alkaline phosphatase was 307 UI/L (20-140 UI/L) with an albumin of 2.8 g/dL (3-4 g/dL). Sodium was 134 mEq/L (135-145 mEq/L), potassium 4.4 mEq/L (3.5-5.5 mEq/L), and chloride was 94 mEq/L (96-106 mEq/L). Imaging: A chest X-ray was performed, revealing elevation of the right hemidiaphragm (Image A). An abdominal CT scan without contrast revealed an approximately 12-15cm in diameter hypodense lesion with well-demarcated borders in the right hepatic lobe (Image B). Stool ova and parasite was performed (Image C). UPCH Case Editors: Carlos Seas, Course Director / Mario Suito, Associate Coordinator |
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 Discussion: US-guided percutaneous catheter drainage (PCD) of the liver lesion was performed (Video), revealing an anchovy paste-appearing fluid (Image D). Abscess direct microscopy for ova and parasites (O&P) was negative. Galactose/ Galactose- N-acetylcysteine (Gal/GalNAC) lectin antigen from the abscess was positive, as well as total serum anti-Gal/GalNAC antibodies for Entamoeba histolytica antibodies, confirming the diagnosis. Image C shows a cyst of E. histolytica in the stools, featuring a rounded structure with three nuclei (lugol stain). An amebic liver abscess (ALA) is the most common extra intestinal complication of Entamoeba histolytica infection. The disease remains prevalent in developing nations, particularly in rural areas with poor sanitation in India, South America, and Africa (1). ALA is 10 times more common in men between 30-50 years than in women and it tends to be more severe in older patients (2, 3). Alcohol consumption is a major risk factor (4), and the right lobe of the liver is involved in 80% of cases, usually solitary with variable size (5). ALA is the most common cause of liver abscesses in the developing world. This disease is caused by E. histolytica trophozoites that invade the liver through the portal circulation after ingestion of contaminated food or water by E. histolytica cysts, which hatch in the small intestine and penetrate the colonic mucosa, where they cause amebic colitis (5). Unlike pyogenic liver abscesses, ALA is non-suppurative and consists of necrotic hepatocytes and cellular debris caused by the phagocytic ingestion of cells in bites, also known as ‘’trogocytosis-like’’ (6). ALA is classified into three clinical forms: subacute mild, acute aggressive and chronic indolent. The most common (80%) is the subacute mild form, with moderate symptoms and good response to medical therapy. Acute aggressive ALA usually presents with a rapidly progressive course and high risk of rupture. Chronic indolent ALA shows prolonged symptoms, thick fibrotic walls, and potential for secondary bacterial infection (5). The classic clinical presentation includes fever, right upper quadrant pain, and hepatomegaly. Jaundice and pleuropulmonary symptoms occur in a minority of cases (7). Complications arise from rupture, secondary infections, or vascular events. Rupture occurs in 6–40% of cases and can lead to peritonitis, pleural empyema, hepatobronchial fistula, or pericardial tamponade (5, 8). Vascular complications include thrombosis of the hepatic and portal veins, leading to ischemia, portal hypertension, and Budd-Chiari syndrome (6). The differential diagnosis of the liver lesion includes pyogenic liver abscess, cystic echinococcosis, hypervirulent Klebsiella pneumoniae infection, and primary liver malignancy. Diagnosis is based on clinical presentation, imaging such as ultrasound or CT scan, and serological, antigenic, or molecular tests. Serology is of limited use in endemic countries due to the high seroprevalence (1, 8). Abscess drainage confirms the diagnosis by finding the classic “anchovy paste” aspirate and, more specifically, Gal/GalNAC lectin antigen detection. A possible alternative to diagnostic drainage is serum antigen detection, which is highly sensitive but not routinely available. Stool O&P is neither sensitive nor specific (5). The first-line treatment for ALA is metronidazole 500–750 mg TID for 7–10 days, followed by a luminal amebicide to prevent recurrence (6). Most uncomplicated cases respond to antibiotics alone. However, percutaneous drainage (PCD) is required for: 1) large abscesses (>5–10 cm), 2) non-resolving symptoms after 72–96 hours, 3) high-risk locations (left lobe, subcapsular, caudate lobe), 4) secondary infection or rupture. Surgical drainage is reserved for cases with extensive peritonitis or failure of PCD (1, 6). Our patient had a big abscess that merited drainage. He is receiving metronidazole with complete resolution of symptoms; fever disappeared after 2 days of antibiotic treatment. References |