Cardiovascular Pathology 23 (2014) 358–362

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Cardiovascular Pathology

Clinical Case Report

Multiple and atypical opportunistic infections in a HIV patient with

Toxoplasma myocarditis

Amanjit Bal a, Sahajal Dhooria b, Ritesh Agarwal b, Mandeep Garg c, Ashim Das a,⁎a Department of Histopathology, Post Graduate Institute of Medical Education & Research, (PGIMER), Sector-12, Chandigarh 160012, Indiab Department of Pulmonary Medicine, Post Graduate Institute of Medical Education & Research, (PGIMER), Sector-12, Chandigarh 160012, Indiac Department of Radiodiagnosis, Post Graduate Institute of Medical Education & Research, (PGIMER), Sector-12, Chandigarh 160012, India

a b s t r a c ta r t i c l e i n f o

Financial disclosure: The authors have no funding, finof interest to disclose.⁎ Corresponding author. Department of Histopath

160012, India.E-mail address: ashim126@gmail.com (A. Das).

http://dx.doi.org/10.1016/j.carpath.2014.06.0021054-8807/© 2014 Elsevier Inc. All rights reserved.

Article history:Received 13 May 2014Received in revised form 12 June 2014Accepted 12 June 2014

Keywords:ToxoplasmaMyocarditisNecrotizing Pneumocystis pneumoniaCMV

Opportunistic infections cause significant morbidity and mortality in patients infected with the humanimmunodeficiency virus (HIV). Multiple opportunistic infections can occur in a patient in the setting of severeimmunodeficiency and can have atypical clinicoradiological presentation. Cardiac involvement has also beenobserved on autopsy in HIV-infected patients in the form of myocarditis, dilated cardiomyopathy,endocarditis, neoplasms, and drug-related cardiotoxicity. Mostly, the cardiac opportunistic infections areclinically asymptomatic, and sudden death due to these is extremely rare. We report a case of 44-year-oldgentleman who presented with cough, pleuritic chest pain, and breathlessness and died of refractory shockdue to myocarditis. At autopsy, he was found to have Toxoplasma myocarditis, Pneumocystis jiroveciipneumonia, and cytomegalovirus adrenalitis.

ancial relationships, or conflicts

ology, PGIMER, Chandigarh-

© 2014 Elsevier Inc. All rights reserved.

1. Introduction

Over the past two decades, with the development of antiretroviraltherapy, there has been a change in the spectrum of human immuno-deficiency virus (HIV)-related diseases. However, despite advances of thetherapeutics, the HIV-related mortality continues to be a significantproblem in the developing countries possibly due to poor compliance. OfHIV-related diseases, the opportunistic infections cause significantmorbidity and mortality [1]. In a large autopsy series, the cardiacinvolvement has also been observed in HIV-infected patients in the formof myocarditis, dilated cardiomyopathy, endocarditis, neoplasms, anddrug-related cardiotoxicity [2]. Multiple opportunistic infections canoccur in the samepatient in a setting of severe immunodeficiency and canalso present with atypical manifestations. We report a patient withrecently diagnosed HIV infection, who had multiple opportunisticinfections, with atypical manifestations and dominant cardiac involve-ment which was the cause of demise of the patient.

2. Case report

2.1. Clinical findings

A 44-year-old male presented with history of dry cough and right-sided pleuritic chest pain for the preceding 2 months. He also

complained of anorexia and weight loss during this period, but therewas no history of fever. He had no known comorbidities. He was anonsmoker, did not consume alcohol, and denied any history ofunprotected sexual intercourse, blood transfusion, intravenous drugabuse, or tattooing. On initial evaluation in the clinic, the physicalexamination was normal apart from pallor and bilateral multipleanterior cervical lymph nodes. Laboratory investigations revealedanemia (hemoglobin 8.8 g/dl), leukocyte count 6800 cells/μl, andplatelet count of 171,000/μl. Liver function tests were deranged(aspartate transaminase 107 U/l, alanine transaminase 82 U/l, andalkaline phosphatase 134 U/l, with a normal bilirubin 0.5 mg/dl).Serum urea and creatinine and fasting glucose were within normallimits. Ultrasound of the abdomen showed fatty liver. Tuberculin skintest was negative (0 mm). A chest radiographwas normal; however, acomputed tomogram (CT) of the chest and abdomen along with high-resolution CT revealed the presence of a 2.9×1.4-cm pleural-basedlesion with central hypodensity along the inferior aspect of rightanterior costal pleura (Fig. 2A), mild hepatomegaly, and enlargedabdominal lymph nodes (less than 1 cm in short axis). Blood wasdrawn for HIV testing, and he also underwent a fine needle aspiration(FNA) from the lung lesion under ultrasound guidance.

Two days later, he presented to the emergency department withprogressively increasing breathlessness. On evaluation, he wasafebrile and had tachycardia, tachypnea, hypotension, hypoxemia,and bilateral jugular venous distension. Lab investigations revealednormal renal function with hyponatremia (serum sodium128 mEq/l).Arterial blood gases initially revealed hypoxemia with metabolicacidosis and respiratory alkalosis (pH 7.45, PaO2 76 mmHg, PaCO2

25 mmHg, HCO3 17 mEq/l, FiO2 0.5). Electrocardiogram showed sinus

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tachycardia, right axis deviation, ST depression, and T wave inversionsin leads 2, 3, aVF, and V3–V6. Myocardial fraction of creatine kinase(CK-MB) was 257 ng/ml; troponin I kit test was negative. Enzyme-linked immunosorbent assay was positive for HIV by Comb AIDS andsignal HIV kits, and for HIV-1 by the PrkTriline kit test. FNA from thelung lesion revealed presence of granulomatous inflammation.Ultrasound abdomen showed mild ascites, mild hepatomegaly,gallbladder wall edema, dilated inferior vena cava, and hepaticveins. Compression ultrasound of lower limb veins did not showany deep vein thrombosis. A chest radiograph showed presence ofhomogenous opacity over both lung fields. CT pulmonary angiographydid not reveal any thromboemboli. High-resolution CT of the chestrevealed an increase in size of the lesion and new soft tissue densitiesin the lower lobe of the left lung. It also showed the appearance ofbilateral peribronchovascular thickening and ground-glass opacitieswith moderate bilateral pleural effusion. A diagnosis of acquiredimmunodeficiency syndrome (AIDS) was made. A request was sent tothe cytopathologist for special stains on the cytology material. Thepatient was also suspected to have Pneumocystis jirovecii pneumonia(PJP) in view of the diffuse pulmonary involvement along withpulmonary tuberculosis with possible tuberculous myocarditis caus-ing cardiogenic shock. He was started on vasopressors (vasopressinand noradrenaline), intravenous piperacillin–tazobactum and azi-thromycin, along with intravenous hydrocortisone, and oral cotri-moxazole. He was also administered antituberculosis treatment withisoniazid, rifampicin, pyrazinamide, and ethambutol. However, hedeveloped progressive respiratory distress and hypoxemia for whichhe was intubated and mechanically ventilated. However, he contin-ued to deteriorate and, after 20 h of hospital stay, developedcardiopulmonary arrest from which he could not be revived.Grocott–Gomori methenamine silver staining of the cytology speci-men performed postmortem showed organisms with morphologyconsistent with Pneumocystis jirovecii. After an informed writtenconsent from patient’s relatives, an autopsy was performed.

2.2. Autopsy findings

On autopsy, the peritoneal cavity yielded 1 l of hemorrhagic fluid,pericardial cavity yielded 150 ml, and each pleural cavity yielded100 ml of serous fluid. Mediastinal and abdominal lymph nodessampled showed mixed stage of follicular hyperplasia and involution.In addition, there was extensive apoptosis of lymphoid cells. On

Fig. 1. Photomicrographs showing (A) lymph nodes showing mixed stage of follicimmunohistochemsitry, (C) CD20-positive lymphoid follicles, (D) relative depletion of CDCD8-positive T cells, (G) the follicular dendritic cells of germinal center showing expression

immunohistochemsitry, there was marked depletion of CD4+ Tcells, and the follicular dendritic cells of germinal center showedexpression of HIV p24 protein. In addition, a few macrophages alsoshowed p24 expression (Fig. 1A–H). Similarly, the lymphoid tissue ofthe small intestine showed depletion of lymphoid cells withapoptosis and HIV p24 protein expression in follicular dendriticcells of germinal center.

The lungs were heavy and weighed 800 g. The pleurae were dulland had fibrinous tags. On slicing, the right lower lobe in thesubpleural location showed a grayish white nodular area ofconsolidation with central breakdown measuring 3.5×2.5 cm(Fig. 2B). The remaining lung parenchyma was subcrepitant andoozed edema fluid. Microscopic examination from nodular areashowed eosinophilic foamy intraalveolar exudates punctuated byround basophilic dots (Fig. 2C). Exudates are infiltrating alveolar septacausing septal lysis and infiltrating the walls of blood vessels, causingvasculitis. Focal areas of macrophage collection and giant cells werealso seen. Grocott’s stain highlighted 5–7-μm round and collapsedcrescent or boat-shaped cyst forms of Pneumocystis (Fig. 2D). Adjacentareas showed pulmonary edema. Hilar and carinal lymph nodes wereenlarged (0.5–2 cm) and showed necrotic areas which on microscopyshowed foamy exudates containing Pneumocystis.

The heart weighed 250 g and was flabby with fibrinous tags onpericardium. All chambers were markedly dilated, and the cardiacvalves were normal (Fig. 3A). The coronary arteries and aorta showedgrade I atherosclerotic changes. On microscopy, there were extensivediffuse myocardial necrosis, edema, and a mixed inflammatoryinfiltrate comprising of neutrophils, lymphocytes, and macrophages.A few true cysts and numerous pseudocysts composed of clumps oftachyzoites of Toxoplasma were seen in myocardial fibres. Theintracellular Toxoplasma cysts were 50–200 μm in diameter, andtheir wall was unstained by PAS; however, the bradyzoites andtachyzoites were PAS positive. Immunohistochemistry by anti-Toxoplasma gondii antibody highlighted the cysts with bradyzoitesand intracellular tachyzoites.

The brain did not reveal any meningeal exudates, and the vesselsof the circle of Willis were of normal caliber. On slicing, no focallesions were seen. However, on microscopy, focal areas of collectionsof macrophages were seen in both gray and white matter along withcysts containing bradyzoites and pseudocyts of tachyzoites ofToxoplasma. Immunohistochemistry by anti-Toxoplasma gondii anti-body highlighted the cysts with bradyzoites and tachyzoites. Pituitaryalso showed areas of necrosis, nuclear debris, and cysts of Toxoplasma.

ular hyperplasia and involution, (B) extensive apoptosis of lymphoid cells. On3-positive T cells, (E) marked depletion of CD4+ T cells, (F) excess of intrafollicularof HIV p24 protein. (H) In addition, a fewmacrophages also showed HIVp24 expression.

Fig. 2. (A) CT scan of the chest showing pleural-based lesion (arrow) along the inferior aspect of the right anterior costal pleura, (B) grayish white nodular area of consolidation withcentral breakdown measuring 3.5×2.5 cm, (C) eosinophilic foamy intraalveolar exudates punctuated by round basophilic dots. (D) Grocott’s stain highlighting 5–7-μm round andcollapsed crescent or boat-shaped cyst forms of Pneumocystis.

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Adrenals showed extensive necrosis with CMV inclusionshighlighted by immunostaining (Fig. 4). Bone marrow was normo-cellular for age and had evidence of secondary hemophagocytosis.Liver showed centrizonal sinusoidal dilatation and necrosis ofhepatocytes without reticulin condensation indicative of terminalevent. Spleen and pancreas were within normal limits. Renal tubulesshowed shedding of lining epithelium with granular casts indicativeof acute tubular necrosis.

A 44-year-old HIV-positive male had evidence of HIV infection inlymph nodes and mucosa-associated lymphoid tissue. The final

Fig. 3. (A) Gross of flabby heart with dilated left ventricle; (B) extensive diffuse myocalymphocytes, and macrophages; (C) numerous pseudocysts composed of clumps of tachybradyzoites and tachyzoites; (E) immunohistochemistry by anti-Toxoplasma gondii antibparenchyma showing focal areas of collections of macrophages and tachyzoites of Toxoplanuclear debris, and cysts of Toxoplasma [inset in (G) and (H): immunohistochemistry by an

autopsy diagnosis of necrotizing Pneumocystis jiroveci pneumonia(right lower lobe) with dissemination to hilar nodes; Toxoplasmamyocarditis, encephalitis, and hypophysitis; cytomegalovirus adre-nalitis; pulmonary edema; acute tubular necrosis; and secondaryhemophagocytosis was made.

3. Discussion

There are several learning points from this case. First is thedocumentation of HIV infection and clue about CD4 counts in the

rdial necrosis, edema, and mixed inflammatory infiltrate composed of neutrophils,zoites of Toxoplasma were seen in myocardial fibres; (D) PAS stain highlighting theody highlighting the cysts with bradyzoites and intracellular tachyzoites; (F) brainsma; (G) brain cysts containing bradyzoites; (H) pituitary showing areas of necrosis,ti-Toxoplasma gondii antibody highlighting the Toxoplasma cysts].

Fig. 4. Photomicrographs from adrenals showing (A) extensive necrosis with CMV inclusions and (B) inclusions highlighted by CMV immunostaining.

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tissue samples. Following entry of HIV-1 into the body, the virusinfects dendritic cells of mucosa or skin and CD4+ T lymphocytes. It isthen carried to lymphoid tissue where it resides in follicular dendriticcells (FDCs) within the germinal centers of lymphoid tissue. It remainshere as a stable reservoir until the FDC meshwork is destroyed interminal HIV disease [3]. Viral burden on FDCs within lymphoid tissuecorrelates with the various clinical phases of disease. Also, this caseshowed lot of apoptosis of CD4 T lymphocytes due to HIV and is thusindicative of disease progression.

The other important highlight of this case is the presentation ofPneumocystis jirovecii as a solitary pleural-based nodule withcytological examination erroneously showing presence of granulo-matous inflammation due to the presence of some giant cells whichwere evident in the autopsy sections. PJP generally presents withbilateral diffuse lung involvement with ground glass opacities or aninterstitial pattern [4]. Presentation with a single nodule/mass isdistinctly rare. In a series of 150 cases of PCP, presentation with asingle lung nodule was seen in only two patients [5]. In our patient,granulomatous inflammation was reported in a lung nodule and wasinitially thought to be due to tuberculosis. However, after Grocott’sstain, it became evident that the nodule was in fact caused by PJP. Onautopsy, the findings were consistent with necrotizing Pneumocystispneumonia as evidenced by septal lysis, associated vasculitis, anddissemination to hilar lymph nodes. This highlights the importance ofperforming special stains in histology or cytology samples of HIVpatients even when a diagnosis is not suspected on clinico–radiologicgrounds. Pneumocystis pneumonia is the second most common AIDS-defining event in North American and European cohorts but has beenreported to be a less common infection in India due to high burden oftuberculosis [6–8]. In some series, it does not appear among thediagnosed opportunistic infections [9,10] It is probable that PJPremains under recognized in India because it is not usually looked for.

Another peculiarity in this patient was the occurrence oftoxoplasmosis without any clinical evidence of cerebral involvement.It has been observed that extracerebral toxoplasmosis is often notsuspected during life and is usually identified at autopsy, the heartbeing the commonest extracerebral site involved [11]. The autopsy ofour patient revealed not only Toxoplasma myocarditis but alsocerebral and pituitary involvementwhich remained subclinical duringlife. Myocarditis itself is a frequent finding at autopsy of patients dyingof AIDS who have not received highly active antiretroviral therapy(HAART) [12,13]. Viruses are the commonest cause of myocarditis inHIV patients, while Toxoplasma is the most common nonviral cause ofmyocarditis in HIV-infected patients seen in 8%–12% of patients dyingwith AIDS [14–17]. Overall, in most of the cases, myocarditis isattributable to direct infection by HIV itself [18,19]. Our patientpresented with an acute onset of biventricular failure and had a raisedCK-MB. We suspected the presence of myocarditis and attributed it totuberculosis because of the clinical presentation [20]. Toxoplasmamyocarditis was a surprise finding at autopsy because the patient did

not have any clinical evidence of encephalitis. Cardiac toxoplasmosisis a rare disease, and approximately 40 cases of toxoplasmosis of hearthave been reported in several necropsy series [11,12] and only 4 casesin Indian literature [21]. Also, cardiac toxoplasmosis generally occursduring the course of multivisceral dissemination; however, there are afew reported cases of Toxoplasmamyocarditis in which sudden deathis described, similar to our case [21].

Refractory shock in this patient was attributable primarily tomyocarditis. The presence of adrenal involvement with CMV mighthave contributed to adrenal insufficiency causing hyponatremia andrefractory shock. CMV is the most frequent agent identified in adrenalglands in autopsies of HIV patients [22]. CMV adrenalitis can causeadrenal failure in AIDS even in patients receiving steroids [23,24].Therefore, a high index of suspicion should be kept in HAART-naïvepatients with advanced AIDS who have features suggestive of adrenalinsufficiency. Such patientsmay respond to treatmentwith ganciclovirwhen picked up early in the reversible stage [25].

The case is notable for the occurrence of multiple opportunisticinfections in an AIDS patient with rare presentations of bothPneumocystis as well as toxoplasmosis. A similar patient has beenreported in the literature with presence of disseminated toxoplas-mosis, CMV adrenalitis, and PJP [26]. However, the presentations of allthese infections were typical in that case. There are a few limitationsof this report. The CD4 counts of the patient could not be obtained, asthe patient’s HIV status became known preterminally, when manyinvestigations could not be performed in the emergency setting.However, autopsy did reveal low CD4 cells in lymph nodes. We alsocould not measure the cortisol level of the patient.

To conclude, multiple opportunistic infections can coexist inpatients with AIDS, and they may have atypical presentations. Oneshould have a broad differential diagnoses to explain the clinicalfeatures in a given patient, and every effort should be made to achievethe accurate microbiological diagnosis with decreased reliance onempiricism.

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