SESSION TYPE: AIDS/ Immunocompromised Patients PostersPRESENTED ON: Wednesday, October 24, 2012 at 01:30 PM - 02:30 PM

PURPOSE:

The CURB-65 pneumonia severity scoring system has been validated for predicting mortality in several studies. It is used as a clinical prediction rule for stratifying patients into outpatient, inpatient, and intensive care treatment strategies. Previous studies have excluded patients with human immunodeficiency virus (HIV) infection. As a result, the validity of CURB-65 in predicting mortality and ICU admission in HIV patients with community acquired pneumonia (CAP) is unknown.

METHODS:

A retrospective chart review of 230 patient admissions, age 18-50 years, with CAP to the Saskatoon Health Region in 2010. 139 admissions fully satisfied all inclusion and exclusion criteria. Thirty-five HIV patients were compared to 104 non-HIV patients with respect to mortality, ICU admission, ICU and hospital length of stay, and CURB-65 score.

RESULTS:

The mortality rate and ICU admission rate in the HIV population was 11.4% and 28.6% versus 4.8% and 27.9% in the non-HIV population. The ICU and hospital length of stay in the HIV population was 19.7 days (95% CI 10.2 to 29.2) and 18.7 days (95% CI 12.2 to 25.2) versus 7.3 days (95% CI 4.8 to 9.8) and 7.1 days (95% CI 5.8 to 8.4) in the non-HIV population. The CURB-65 score in the HIV population was 1.23 (95% CI 0.96 to 1.5) versus 1.41 (95% CI 1.21 to 1.61) in the non-HIV population.

CONCLUSIONS:

The CURB-65 pneumonia severity scoring system may underestimate the mortality rate and need for ICU admission in CAP patients with HIV infection. Further prospective studies are required to determine the validity of CURB-65 in stratifying CAP patients with HIV infection into different treatment strategies.

CLINICAL IMPLICATIONS:

At the present, no pneumonia severity scoring system has been validated in patients with CAP and HIV infection. We currently do not recommend the use of CURB-65 in patients with HIV infection.DISCLOSURE: The following authors have nothing to disclose: Jordan Olfert, Stuart SkinnerNo Product/Research Disclosure InformationUniversity of Saskatchewan, Saskatoon, SK, Canada.

SESSION TYPE: Critical Care Student/Resident Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Acinetobacter baumannii is generally considered an opportunistic nosocomial pathogen and is rarely encountered as a pathogen causing community-acquired soft tissue infection.

CASE PRESENTATION:

A 54 year old female presented with bilateral hand pain followed by all four extremity weakness and urinary incontinence over a period of two months. She has h/o well controlled hypertension, diabetes mellitus type 2 and arthritis. No h/o previous surgery. She denied smoking, alcohol drinking and illicit drug use. Here vitals were stable and neuro examination showed loss of touch sensations on right side of the face and body, right flaccid hemiplegia and left spastic hemiplegia. There was lymphadenopathy. Her routine blood workup was with in normal limits with negative HIV testing. PPD was positive, AFB sputum smear time three came back negative and chest Xray was negative. There was an extradural circumferential mass causing compression at the level of C1, C2 and C3 on contrast enhanced MRI of the cervical spinal cord. CT guided core biopsy of the mass was done. Gram staining showed rare WBC and gram negative rods, AFB smear was negative while culture grew abundant gram negative rods- Acinetobacter baumanii. After treatment with antibiotics clinically patient improved.

DISCUSSION:

Acinetobacter baumannii is an aerobic gram-negative coccobacillary rod with a natural reservoir in soil and water sources around the world. It is generally considered an opportunistic nosocomial pathogen , affecting especially patients receiving treatment in the intensive care unit setting and immunocompromised patients. This is the first reported case of community-acquired A. baumannii denovo soft tissue infection causing higher cervical spinal cord compression resulting in quadriplegia. The evidence is now mounting that A. baumannii can no longer be exclusively considered a nosocomial pathogen, and is capable of causing profound clinical disease in the absence of traditional nosocomial risk factors.

CONCLUSIONS:

We described a patient who is from community, non smoker, and non alcoholic, had well controlled DM -2 and had no h/o trauma/surgery. The case raises concerns that this highly adaptable organism may soon evolve into a significant community pathogen, too.1) Glew, R. H., Jr., R. C. Moellering, and L. J. Kunz. 1977. Infection with Acinetobacter calcoaceticus (Herellea vaginicola): clinical and laboratory studies. Medicine 56:79-95.2) Jimenez, P., A. Torres, R. Rodriguez-Roisin, J. P. de la Bellacasa, R. Aznar, J. M. Gatell, and A. Agusti-Vidal. 1989. Incidence and etiology of pneumonia acquired during mechanical ventilation. Crit. Care Med. 17:882-885.DISCLOSURE: The following authors have nothing to disclose: Qammar Abbas, Hafiz Imran, Ameer RasheedNo Product/Research Disclosure InformationTBHC New York, Brooklyn, NY.

SESSION TYPE: Infectious Disease Global Case Report PostersPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Community acquired pneumonia is one of the leading cause of hospitalization worldwide. Parapneumonic pleural effusions are seen in approximately 35-40% of patients, and almost 10% require drainage. The number of all cases of pneumonia in the world rises as well as the rate of unusual etiological agents including opportunistic pathogens, such as Canida Albicans. Immune response is vital for surviving the pneumonia, which remains potentially fatal even in 21st century.

CASE PRESENTATION:

55 years old woman with no significant medical history had been admitted to our pulmonary department because of community acquired pneumonia. Despite of combined antibiotic therapy the health state of the patient worsened and loculated pleural effusions occur. The change of antibiotics and drain insertion followed by local application of fibrinolytics lead to little improvement and another drain had to be inserted. Other sources of infection and pulmonary embolism were excluded. The sputum, blood samples and BAL show only Candida albicans. After switching the antibiotics to fluconazole the patient recovers very quickly.

DISCUSSION:

The gastroscopy shows huge mucous candidosis, which is considered not to be a focus, but a part of systemic infection. Although Candida Albicans is an opportunistic pathogen, largely harmful to immunocompromised patients. No immunodeficiency including HIV infection and tumor was discovered in this case. Immunologist assumes role of CARS syndrome in development of overwhelming systemic Candida infection.

CONCLUSIONS:

CARS syndrome (Compensatory Anti-inflammatory Response Syndrome) qualifies counter-regulatory mechanisms initiated to limit the overzealous inflammatory process in patients with infectious (sepsis) or non-infectious systemic inflammatory response syndrome (SIRS). The major consequence of CARS is the modification of the immune status that could favor the enhanced susceptibility of patients to nosocomial infections. This seems to be the scenario of our case too, where initial CAP of unknown origin lead to SIRS followed by huge Candida infection due to suppressed immune response according to CARS syndrome.1) Compensatory anti-inflammatory response syndrome Minou Adib-Conquy; Jean-Marc Cavaillon, Unit Cytokines & Inflammation, Institut Pasteur, Paris, France, www.thrombosis-online.com2) A prospective observational study of candidemia: epidemiology, therapy, and influences on mortality in hospitalized adult and pediatric patients. Clin Infect Dis. 2003; 37(5):634-43 (ISSN: 1537-6591) Pappas PG; Rex JH; Lee J; Hamill RJ; Larsen RA; Powderly W; Kauffman CA; Hyslop N; Mangino JE; Chapman S; Horowitz HW; Edwards JE; Dismukes WE; University of Alabama at Birmingham3) Trends in hospitalizations for pneumonia among persons aged 65 years or older in the United States, 1988-2002. Fry AM, Shay DK, Holman RC, Curns AT, Anderson LJ. Source Respiratory and Enteric Viruses Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Ga 30333, USA. afry@cdc.gov JAMA, Dec 7 2005DISCLOSURE: The following authors have nothing to disclose: Michal Svarc, Vratislav Sedlak, Vladimir Koblizek, Frantisek Salajka, Jakub NovosadNo Product/Research Disclosure InformationFakultni Nemocnice Hradec Kralove, Hradec Kralove, Czech Republic.

SESSION TYPE: Infectious Disease Student/Resident Case Report Posters IPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Pulmonary nocardiosis is a rare gram-positive bacterial infection that usually occurs in immunocompromised individuals. Our patient had a history of solid organ transplantation.

CASE PRESENTATION:

A 60-year-old male, ex-smoker, presented with fever, dry cough and night sweats of 2 weeks duration. History was significant for diabetes mellitus and cardiac transplantation 6 months prior. His medications included mycophenolate, tacrolimus and prednisone. Vital signs were significant for temperature of 100.5 F. Rest of the physical examination was unremarkable. Laboratory data showed a leukocyte count of 8800/µL (neutrophils-84%). Chest X-ray and chest computed tomography (CT) showed multifocal pneumonia (Fig. 1, 2). CT-guided biopsy and culture identified Nocardia asteroides. Head CT showed no central nervous system (CNS) involvement. Patient was treated with intravenous imipenem and oral minocycline and discharged with plan to continue treatment for one year.

DISCUSSION:

Nocardiosis typically occurs in immunocompromised patients with deficiency in cell-mediated immunity as in solid organ or hematopoietic stem cell transplant, HIV infection, steroid therapy, diabetes mellitus or malignancy. CNS dissemination is common in nocardiosis. Relapse or progression despite appropriate therapy is frequent. Pulmonary nocardiosis usually presents with fever, night sweats, dyspnea, cough, hemoptysis and pleuritic chest pain. Radiological findings seen include solitary/multiple nodules, lung masses (with or without cavitation), reticulonodular and interstitial infiltrates, lobar consolidation and pleural effusions [1]. Hence, initial misdiagnosis as mycobacterial/fungal infections, or malignancy is common. Nocardia species are not naturally found in the respiratory tract and isolation in sputum almost always indicates infection. Due to slow growth in the laboratory, invasive procedures to obtain adequate samples are often mandated. A presumptive diagnosis of nocardiosis can be made if partially acid-fast filamentous branching rods are visualized in clinical specimens. All immunocompromised patients and those with CNS involvement should be treated for at least one year, with the exception of isolated cutaneous infections. Clinical and radiographic response to therapy should be monitored and the duration of treatment modified based on these factors [2]. Individuals without reversible immunosuppression should be placed on indefinite therapy with trimethoprim-sulfomethoxazole, doxycyline, or minocycline [2].

CONCLUSIONS:

Pulmonary nocardiosis can present as multifocal pneumonia in a patient with suppressed cell-mediated immunity. Timely diagnosis and appropriate duration of therapy are cornerstones for recovery.1) Kanne J,Yandown D, Mohammed TL. CT Findings of Pulmonary Nocardiosis. AJR. 2011; 197:W266-W272.2) Martínez R, Reyes S, Menéndez R. Pulmonary nocardiosis: risk factors, clinical features, diagnosis and prognosis. Curr Opin Pulm Med. 2008 May;14(3):219-27.DISCLOSURE: The following authors have nothing to disclose: Anupam Kumar, Veena Panduranga, Shine Raju, Ranjit Joseph, Michael LawlorNo Product/Research Disclosure InformationUniversity of Connecticut Health Center, Farmington, CT.

SESSION TYPE: Infectious Disease Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

A. xylosoxidans is a catalase-positive, oxidase-positive, gram-negative bacillus that inhabits a variety of aqueous environments. It has been described as small outbreaks as well as in immunocompromised hosts. We describe a case of disseminated A. xylosoxidans infections in patient on Rituximab treatment.

CASE PRESENTATION:

56 year old woman was admitted to the hospital for fever and progressive dyspnea over 2 weeks. Her past medical history was significant for Mantle cell lymphoma status post autologous stem cell transplant (SCT) in 2009 and haploidentical SCT in 2010. She was on Rituximab through her right chest port for recurrence of lymphoma in her right hip. Her temperature was 103 degree fahrenheit and she had a leucocytosis of 14,000/microL. Chest roentgenogram showed a new left loculated effusion. Initial blood cultures were positive for gram negative rods. Echocardiogram showed a large pericardial effusion. She was started on intravenous vancomycin and aztreonam (she was penicillin allergic). Her respiratory status deteriorated quickly requiring mechanical ventilation. Left sided thoracentesis was performed, the fluid was exudative and grew A. Xylosoxidans. Blood cultures finalized to be A. Xylosoxidans as well. The organism was oxidase positive and grew in anaerobic bottle only. It was resistant to aztreonam and ciprofloxacin, while sensitive to gentamicin, ceftazidime, meropenem and tobramycin. The patient was managed with switching aztreonam to intravenous meropenem. A video assisted thoracoscopic surgery, left chest decortication, pericardial window and port removal was done in the operating room. Pericardial fluid also grew A. xylosoxidans. A right pleural effusion later developed which was managed with therapeutic thoracentesis; fluid was sterile. Further ICU course included tracheostomy and gastrostomy tube placement followed by a prolonged hospitalization and discharge to rehabilitation.

DISCUSSION:

A. Xylosoxidans is a very uncommon cause bacteremia. The mortality is reportedly low with catheter related bacteremia but high with clinical syndromes like pneumonia and endocarditis. In our case, the infection was likely port related but resulted in acute respiratory distress syndrome from pneumonia; and empyema, requiring surgical treatment. Pericarditis with A. xylosoxidans bacteremia has not been previously reported. The organism is known to be resistant to aminoglycosides but was sensitive in our case. The severity of illness, development of pericarditis, sensitivity pattern and good clinical outcome are unique to our case.

CONCLUSIONS:

A. Xylosoxidans bacteremia in an immunocompromised host can be life threatening. Pneumonia, empyema and pericarditis are potential complications. Choice of intravenous antibiotics and surgical management as appropriate are important for a favorable outcome.1) Duggan et al, Achromobacter xylosoxidans bacteremia: Report of four cases and review of literature. Clin Inf Dis 1996;23 569-76DISCLOSURE: The following authors have nothing to disclose: Naveed Hasan, Mani KavuruNo Product/Research Disclosure InformationThomas Jefferson University Hospital, Philadelphia, PA.

SESSION TYPE: Infectious Disease Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Pulmonary mucormycosis, a rare fungal infection with a high mortality rate, has been reported in patients with diabetic ketoacidosis, diabetes mellitus, and immunosupression due to chemotherapy, steroids, and hematological malignancies. Without early recognition and management, it can be ultimately fatal. We report a rare case of isolated pulmonary mucormycosis.

CASE PRESENTATION:

65-year-old Caucasian male presented with shortness of breath for 2 days associated with chills, nonproductive cough, right upper pleuritic chest pain, and 4 days of polyuria and polydipsia. Patient was recently admitted and discharged on tapering prednisone for COPD exacerbation. Patient had 30 pack year smoking history. On presentation he was febrile, tachycardic, tachypneic and normotensive with physical findings consistent with right upper lobe (RUL) infiltrate. Lab investigations showed leukocytosis. Serum chemistry showed acute kidney injury (AKI) and hyperglycemia with a normal anion gap. Chest x-ray demonstrated RUL infiltrate. Patient was started on IV fluids, insulin drip, and piperacillin-tazobactam, vancomycin and ciprofloxacin. In ICU, patient's vitals deteriorated requiring mechanical ventilation. Initially all cultures showed no growth. Ciprofloxacin and vancomycin were changed to moxifloxacin and linezolid with addition of tobramycin. RUL infiltrate steadily worsened with suspicion of cavitation or abscess formation. CT chest showed necrotizing RUL infiltrate. Patient developed multi-organ failure and DIC requiring aggressive management. Bronchoscopy and BAL of the RUL showed mucosal edema and dark brown secretions . Few weeks later BAL results yielded a mold with cultures positive for Rhizopus species. Posaconazole and amphoterocin B were used to treat Rhizopus. Surgery for lobectomy could not be performed due to multilobar involvement. Gradually necrotizing pneumonia resulted in right sided pneumothorax. Chest tube was placed with non-resolving severe air leak. Repeat bronchoscopy showed bronchopleural fistula and necrotizing tissue. After multiple family meetings, comfort care decision was made, after which patient passed away.

DISCUSSION:

Rhizopus is genus of class Zygomycetes. It can cause tissue infarctions ranging from cutaneous, rhinocerebral, and sinopulmonary to disseminated and frequently fatal infections, especially in immunocompromised hosts. Ischemic necrosis of tissues can prevent delivery of antifungal agents to the foci of infection. Surgical debridement is critical for treatment but is only possible if disease is localized. Combination of posaconazole, amphotericin B and capsofungin is used for medical management.

CONCLUSIONS:

Pulmonary mucormycosis is a rapidly progressive rare disease that carries a high mortality over a short period of time. Dissemination, multiorgan failure and invariably death follows, if not recognized early.1) Francis Y. Pulmonary Mucormycosis Arch Intern Med. 1999;159:1301-1309DISCLOSURE: The following authors have nothing to disclose: Muhammad Ali, Hasan Zaidi, Aasiya Haroon, Nader Mahmood, Mourad IsmailNo Product/Research Disclosure InformationSt. Josephs's Regional Medical Center/Seton Hall Universtiy, Paterson, NJ.

SESSION TYPE: Infectious Disease Student/Resident Case Report Posters IPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Cryptococcosis primarily causes meningoencephalitis or pneumonia in immunocompromised patients. In the absence of impaired immunity, clinical disease is rare. The following report describes a case of pulmonary cryptococcosis presenting as multiple pulmonary masses in an otherwise healthy adult male.

CASE PRESENTATION:

A 26 year-old man with no medical history presented with cough, fevers, shortness of breath, and chest discomfort for 10 days. Prior to admission, he was treated for community-acquired pneumonia at another hospital but failed to improve. The patient denied sick contacts or unusual environmental exposures. The patient's vital signs and cardiopulmonary examination were normal. However, his chest radiograph showed multiple bilateral lung opacities. A chest CT confirmed large pulmonary masses, some with cavitation, in multiple lung fields. The largest lesion measured 7.9 x 4.9 x 4.4 cm. A rapid HIV antibody test, respiratory cultures, and AFB smears of the sputum were negative. The patient had a diagnostic bronchoscopy, but the transbronchial biopsies and bronchoalveolar lavage were non-diagnostic. He then underwent a CT-guided biopsy of one of the lung lesions, which revealed encapsulated organisms consistent with Cryptococcus. The serum cryptococcal antigen titer was 1:512. Blood cultures and a lumbar puncture were negative for disseminated cryptococcosis. The patient was started on oral fluconazole for cryptococcal pneumonia.

DISCUSSION:

Pulmonary cryptococcosis in immunocompetent patients is uncommon, and its presentation differs from that in immunocompromised patients. Immunocompetent patients are less likely to exhibit typical symptoms of infectious pneumonia. Radiographically, they are more likely to demonstrate discrete pulmonary nodules, masses, and infiltrates. Given the nonspecific findings on presentation, the diagnosis of pulmonary cryptococcosis is often made by bronchoscopy or surgical lung biopsy. Immunocompetent patients with isolated pulmonary cryptococcosis have a good prognosis and frequently improve with or without antifungal therapy. Their risk of disease progression and systemic dissemination is low.

CONCLUSIONS:

While cryptococcosis is most commonly an opportunistic infection in immunocompromised patients, this case highlights the need to also include it in the differential diagnosis for non-resolving pneumonias in immunocompetent patients.1) Chang WC, Tzao C, Hsu HH, Lee SC, Huang KL, Tung HJ, Chen CY. Pulmonary cryptococcosis: comparison of clinical and radiographic characteristics in immunocompetent and immunocompromised patients. Chest. 2006;129;333-340.2) Nadrous HF, Antonios VS, Terrell CL, Ryu JH. Pulmonary cryptococcosis in nonimmunocompromised patients. Chest. 2003;124;2143-7.DISCLOSURE: The following authors have nothing to disclose: Christopher Yee, Dong ChangNo Product/Research Disclosure InformationHarbor-UCLA Medical Center, Torrance, CA.

SESSION TYPE: Critical Care Student/Resident Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Enterovirus (EV) and Human rhinovirus(HRV), belong to the Picornaviridae family and most commonly cause acute respiratory tract illness(RTI) in the pediatric age group. Chronic airway disease and immunocompromise predispose to pneumonia, bronchitis, bronchiolitis and trachietis. For community acquired pneumonia (CAP), their disease spectrum ranges from mild upper RTI most commonly to severe lower RTI requiring mechanical ventilation. So far, only a handful of adult cases have been reported, all of whom had either chronic lung disease or were immunocompromised.

CASE PRESENTATION:

20 year old male presented with worsening cough for 2 weeks. He presented a week prior with gastrointestinal (GI)symptoms and had been diagnosed with gastroenteritis. This visit prompted a workup for Legionella pneumonia among other pathogens. CXR showed patchy infiltrates over bilateral lung fields and pneumomediastinum. Lab work was within normal limits on admission. He rapidly decompensated requiring emergent intubation. Repeat CXR was suggestive of ARDS and hypoxic respiratory failure on arterial blood gas. Workup included Sputum stain and culture including acid fast bacilli, respiratory virus panel, PCR for pertussis, urine legionella and strep antigen, blood cultures, ricketsial antibody screen and leptospira antibody, HIV Elisa. Patient was covered with broad spectrum antibiotics empirically: Piperacillin-tazobactum, Vancomycin, Gentamycin and Azithromycin. Positive labwork included an escalating neutrophilic leucocytosis and positive PCR for HRV/Enterovirus. Antibiotics were discontinued and patient improved dramatically within 72hours. Patient was successfully extubated with no subsequent complications and diagnosed with EV-HRV CAP with ARDS. The pneumomediastinum present on admission was likely secondary to violent coughing that the patient had presented with.

DISCUSSION:

In the United States, 2 systems are commonly used for detection of multiple viral pathogens from pharyngeal swabs: Luminex xTAG Respiratory Virus panel and Idaho Technologies. These systems use PCR for detection of Influenza viruses, Respiratory syncytial virus, Human metapneumovirus , Adenovirus and HRV/EV. Both systems utilize reactive primers for RNA amplification from HRV or EV reporting the results as a combined positive in contrast to Reverse transcription- polymerase chain reaction which identifies Human EV 68 separately. As stated earlier, these viruses commonly affect the pediatric age group, patients with chronic lung disease and those who might be immunocompromized likeHIV positive, transplant patients or those with leukemias. Disease spectrum is variable but severe disease requiring mechanical ventilation is rare, even more so in healthy young adults, like the case we present.

CONCLUSIONS:

As Above1) Clusters of Acute Respiratory Illness Associated With Human Enterovirus 68-Asia, Europe, and USA, 2008-2010. Centers for Disease Control and Prevention. September 2011.DISCLOSURE: The following authors have nothing to disclose: Pratik Dalal, Divyashree VarmaNo Product/Research Disclosure InformationSUNY-Upstate Medical University, Syracuse, NY.

SESSION TYPE: Infectious Disease Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Blastomycosis is unique since it usually affects healthy, non-immunocompromised individuals. Lung involvement is the most frequent clinical manifestation; however, extrapulmonary manifestations involving skin (most common), bone, genitourinary tract and central nervous system are also described. Clinical presentation can vary from mild self limiting pulmonary infection to fulminant pneumonia and rarely, ARDS.

CASE PRESENTATION:

A 63 year old caucasian nonsmoker male farmer presented with dyspnea on exertion, dry cough, weight loss, skin ulcers and low grade fever for 3 months. He noted painful skin ulcers over his elbows and ankles that kept enlarging and increasing in number. Laboratory data revealed WBC count of 14,700/cumm(normal differential), otherwise normal CBC, electrolytes, renal and liver function tests. Blastomyces antibody by complement fixation, Blastomyces antibody test by immunodiffusion and Blastomyces urinary antigen were negative. Chest X-ray revealed diffuse interstitial infiltrates bilaterally and Chest CT with contrast revealed extensive bilateral multiple reticulo-nodular densities with hilar lymphadenopathy. Biopsies of skin lesions confirmed the presence of Blastomyces. Patient was intubated for respiratory distress and placed on mechanical ventilation; requiring high FiO2 and PEEP. Patient was initially treated with Amphotericin B IV but had a severe allergic reaction and was switched to itraconazole. Patient improved and was discharged on itraconazole.

DISCUSSION:

ARDS develops in <10% of patients with pulmonary blastomycosis and is associated with high mortality rate of 50 to 89% despite adequate antifungal therapy. Exaggerated cellular immune response is postulated has likely reason for clinical deterioration in blastomycosis induced ARDS. Antibody assays remain nonspecific and insensitive, and the confirmatory diagnostic test is growth of the organism in culture. In patients with severe ARDS with hypoxemia refractory to conventional modes of ventilation, ECMO can provide temporary pulmonary assistance to prolong the time for antifungals to work. The role of corticosteroids remains arguable. More than a third of patients who develop respiratory failure die within several days of hospitalization. Early diagnosis and treatment may help prevent significant morbidity and mortality.

CONCLUSIONS:

This case serves as a reminder to add exotic fungal infection to the list of differential diagnoses in patients with refractory pneumonia and ARDS.1) Lemos, LB. Acute respiratory syndrome and blastomycosis. Presentation of nine cases and review of literature. Ann Diagn Pathol 2001;5:1-9.DISCLOSURE: The following authors have nothing to disclose: Pushan Jani, Ankit Upadhyay, Carlos Ramirez-IcazaNo Product/Research Disclosure InformationUniversity of Texas Health Science Center, Houston, TX.

SESSION TYPE: Infectious Disease Cases IPRESENTED ON: Monday, October 22, 2012 at 01:45 PM - 03:00 PM

INTRODUCTION:

Immunocompromised hosts are at increased risk of infection from endemic mycoses such as Histoplasma capsulatum, a fungus pervasive in the southeastern U.S. Physicians should be knowledgeable of unique presenting features of progressive disseminated histoplasmosis.

CASE PRESENTATION:

41 year old AA female with AIDS having a CD4 cell count of 6, noncompliance with HAART, and prior Pneumocystis jirovecii pneumonia presents to the emergency department after being found unresponsive. She reports three weeks of fatigue, weight loss, and fever. On examination she is noted to be febrile, tachycardic, and tachypneic with a spO2 of 94% on room air. She is somnolent and oriented only to person. Pulmonary auscultation reveals rales, and a diffuse papular rash is present on her trunk and upper extremities. Her labs show evidence of acute kidney injury, pancytopenia, and an elevated LDH of 6438 with a normal haptoglobin. An initial review of her peripheral smear shows no abnormalities. Her initial chest roentgenogram demonstrates mild peribronchial thickening without infiltrates. On hospital day #2 her peripheral smear reveals intracellular and extracellular yeast and Amphotericin B is initiated. Dermatology is consulted for a biopsy of the rash which demonstrates budding yeast forms consistent with histoplasmosis, confirmed by strongly positive urine quantitative histoplasma antigen. Despite all efforts, her clinical condition continues to deteriorate and she expires on hospital day #6.

DISCUSSION:

This patient demonstrates some of the findings that may be encountered in an immunocompromised patient with progressive disseminated histoplasmosis (PDH). Fever and weight loss are the most commonly encountered symptoms seen in up to 75% of patients. 25% of individuals with PDH may not present with pulmonary symptoms, and when present usually only have mild interstitial infiltrates on chest roentgenogram. Physical examination is typically unrevealing except for hepatosplenomegaly; however, in rare cases a papular rash containing abundant yeast may be present. On laboratory evaluation pancytopenia is present in approximately a quarter of patients. Additionally, case series have shown that infection with histoplasma can produce an LDH greater than 600. The diagnosis of PDH can frequently be made first by a review of a peripheral smear which displays intracellular yeast within phagocytes.

CONCLUSIONS:

Classic findings of fever and weight loss combined with an elevated LDH and characteristic rash point to the diagnosis of PDH in this patient. A review of a peripheral smear and skin biopsy showing yeast combined with a positive urine histoplasma antigen confirm the diagnosis.1) Sarosi GA, Davies SF: Endemic mycosis complicating human immunodeficiency virus infection. West j Med 1996;164:335-3402) Butt, A. Serum LDH level as a clue to the diagnosis of histoplasmosis. AIDS Read. 2002 Jul;12(7):317-21.DISCLOSURE: The following authors have nothing to disclose: Jennifer Trevor, Michael Brown, Victor John ThannickalNo Product/Research Disclosure Information, Birmingham, AL.