Case Reports

Hyperhemolysis syndrome is a form of atypical hemolytic transfusion reaction (HTR). It is characterized by a significant drop in hemoglobin (Hb) after seemingly compatible red blood cell transfusions, suggesting destruction of both transfused and autologous red blood cells. Its pathophysiology is not well understood, and a serologic cause is often not identified.14 In contrast, delayed HTRs are typically characterized by a positive direct antiglobulin test (DAT), suggesting that the patient's red blood cells are coated by immunoglobulin G and/or complement components and by the appearance of previously undetected red blood cell alloantibody or antibodies that developed from a secondary anamnestic response; however, autologous red cells are not destroyed.

CASE

A 48‐year‐old African American woman with sickle cell disease (SCD) was readmitted for pain crisis. Her medical history included stroke, pulmonary hypertension, and congestive heart failure. She had received several transfusions and consequently had developed antibodies to seven clinically significant red blood cell antigens. A week prior to readmission, she was discharged from the hospital with an Hb of 6.9 g/dL after a sickle cell crisis precipitated by pneumonia. She was treated with hydration, pain medications, antibiotics, and a unit of cross‐match‐compatible red blood cells (RBCs) that was antigen negative for her antibodies.

On readmission, she had an Hb of 5.6 g/dL and an uncorrected reticulocyte count of 17.6%. Her reticulocyte production index, a reticulocyte count corrected for the degree of anemia and reticulocyte maturation time, was elevated at 2.6. She was transfused with 1 unit of phenotypically matched and cross‐match‐compatible RBCs. Three hours after transfusion, she developed dark‐colored urine. The transfusion reaction investigation revealed no clerical error or incompatibility, a negative DAT, and an antibody panel identical to that from pretransfusion testing. During hospitalization, the hemolytic anemia worsened (Fig. 1). On the 10th hospital day, she became severely dyspneic as her Hb reached its nadir of 3.6 g/dL despite ongoing erythropoiesis. She developed decompensated heart failure and renal insufficiency, precipitated by the acutely worsening anemia. Along with diuretic and vasodilator therapies, she was treated with methylprednisolone at 125 mg twice daily for 3 days followed by tapering doses of prednisone for 2 weeks, intravenous immunoglobulin (IVIG) at 400 mg/kg a day for 5 days, and 4 cross‐match‐compatible RBC transfusions that were antigen negative for her antibodies. The hemolysis resolved and the patient improved. Throughout hospitalization, her DAT remained negative. The Hb remained stable at 7 g/dL until she was discharged. Ten months of follow‐up showed no new red blood cell antibody in her serum or recurrence of hyperhemolysis syndrome despite receiving subsequent transfusions.

Figure 1

DISCUSSION

Hyperhemolysis syndrome has been described in patients with SCD,14, 6, 7 suggesting that an underlying hemoglobinopathy may be a risk factor; however, a patient with anemia of chronic disease was recently described in the literature to have developed hyperhemolysis syndrome.5 Possible mechanisms include innocent bystander hemolysis through complement‐mediated lysis and/or formation of red blood cell alloantibody or autoantibody;1, 2 and hyperactive macrophages of the reticuloendothelial system that recognize Hb S RBCs of patients with SCD more avidly than normal RBCs because of the exposure of aminophosphatides in the outer layer of the sickled RBC membrane.3 In effect, red blood cells may be destroyed regardless of whether they are autologous or transfused. Additionally, transfusion‐related suppression of erythropoiesis may worsen the severity of anemia.2 Recent studies of patients with SCD suggest that the presence of free plasma Hb, as a consequence of hemolysis, reduces nitric oxide bioavailability, promotes endothelial dysfunction, and contributes to the development of pulmonary hypertension and the varying presentations of vasoocclusion.6 A common observation among patients who experience hyperhemolysis syndrome is that withholding transfusion seems beneficial, probably because immunologic reactions are not exacerbated, whereas treatment with steroids1, 2, 4 and/or IVIG3, 7 resolves hemolysis because of their immunomodulatory effects.

CONCLUSIONS

Hyperhemolysis syndrome is a potentially life‐threatening complication of RBC transfusion. It is important to recognize this syndrome when managing patients with SCD who present with worsening anemia after RBC transfusions. Although further transfusions can exacerbate hemolysis4, 7 and may be relatively contraindicated, in severe and desperate situations, simultaneous treatment with steroids and IVIG, together with RBC transfusions, may be lifesaving.

Hyperhemolysis syndrome is a form of atypical hemolytic transfusion reaction (HTR). It is characterized by a significant drop in hemoglobin (Hb) after seemingly compatible red blood cell transfusions, suggesting destruction of both transfused and autologous red blood cells. Its pathophysiology is not well understood, and a serologic cause is often not identified.14 In contrast, delayed HTRs are typically characterized by a positive direct antiglobulin test (DAT), suggesting that the patient's red blood cells are coated by immunoglobulin G and/or complement components and by the appearance of previously undetected red blood cell alloantibody or antibodies that developed from a secondary anamnestic response; however, autologous red cells are not destroyed.

CASE

A 48‐year‐old African American woman with sickle cell disease (SCD) was readmitted for pain crisis. Her medical history included stroke, pulmonary hypertension, and congestive heart failure. She had received several transfusions and consequently had developed antibodies to seven clinically significant red blood cell antigens. A week prior to readmission, she was discharged from the hospital with an Hb of 6.9 g/dL after a sickle cell crisis precipitated by pneumonia. She was treated with hydration, pain medications, antibiotics, and a unit of cross‐match‐compatible red blood cells (RBCs) that was antigen negative for her antibodies.

On readmission, she had an Hb of 5.6 g/dL and an uncorrected reticulocyte count of 17.6%. Her reticulocyte production index, a reticulocyte count corrected for the degree of anemia and reticulocyte maturation time, was elevated at 2.6. She was transfused with 1 unit of phenotypically matched and cross‐match‐compatible RBCs. Three hours after transfusion, she developed dark‐colored urine. The transfusion reaction investigation revealed no clerical error or incompatibility, a negative DAT, and an antibody panel identical to that from pretransfusion testing. During hospitalization, the hemolytic anemia worsened (Fig. 1). On the 10th hospital day, she became severely dyspneic as her Hb reached its nadir of 3.6 g/dL despite ongoing erythropoiesis. She developed decompensated heart failure and renal insufficiency, precipitated by the acutely worsening anemia. Along with diuretic and vasodilator therapies, she was treated with methylprednisolone at 125 mg twice daily for 3 days followed by tapering doses of prednisone for 2 weeks, intravenous immunoglobulin (IVIG) at 400 mg/kg a day for 5 days, and 4 cross‐match‐compatible RBC transfusions that were antigen negative for her antibodies. The hemolysis resolved and the patient improved. Throughout hospitalization, her DAT remained negative. The Hb remained stable at 7 g/dL until she was discharged. Ten months of follow‐up showed no new red blood cell antibody in her serum or recurrence of hyperhemolysis syndrome despite receiving subsequent transfusions.

Figure 1

DISCUSSION

Hyperhemolysis syndrome has been described in patients with SCD,14, 6, 7 suggesting that an underlying hemoglobinopathy may be a risk factor; however, a patient with anemia of chronic disease was recently described in the literature to have developed hyperhemolysis syndrome.5 Possible mechanisms include innocent bystander hemolysis through complement‐mediated lysis and/or formation of red blood cell alloantibody or autoantibody;1, 2 and hyperactive macrophages of the reticuloendothelial system that recognize Hb S RBCs of patients with SCD more avidly than normal RBCs because of the exposure of aminophosphatides in the outer layer of the sickled RBC membrane.3 In effect, red blood cells may be destroyed regardless of whether they are autologous or transfused. Additionally, transfusion‐related suppression of erythropoiesis may worsen the severity of anemia.2 Recent studies of patients with SCD suggest that the presence of free plasma Hb, as a consequence of hemolysis, reduces nitric oxide bioavailability, promotes endothelial dysfunction, and contributes to the development of pulmonary hypertension and the varying presentations of vasoocclusion.6 A common observation among patients who experience hyperhemolysis syndrome is that withholding transfusion seems beneficial, probably because immunologic reactions are not exacerbated, whereas treatment with steroids1, 2, 4 and/or IVIG3, 7 resolves hemolysis because of their immunomodulatory effects.

CONCLUSIONS

Hyperhemolysis syndrome is a potentially life‐threatening complication of RBC transfusion. It is important to recognize this syndrome when managing patients with SCD who present with worsening anemia after RBC transfusions. Although further transfusions can exacerbate hemolysis4, 7 and may be relatively contraindicated, in severe and desperate situations, simultaneous treatment with steroids and IVIG, together with RBC transfusions, may be lifesaving.

Hyperhemolysis syndrome is a form of atypical hemolytic transfusion reaction (HTR). It is characterized by a significant drop in hemoglobin (Hb) after seemingly compatible red blood cell transfusions, suggesting destruction of both transfused and autologous red blood cells. Its pathophysiology is not well understood, and a serologic cause is often not identified.14 In contrast, delayed HTRs are typically characterized by a positive direct antiglobulin test (DAT), suggesting that the patient's red blood cells are coated by immunoglobulin G and/or complement components and by the appearance of previously undetected red blood cell alloantibody or antibodies that developed from a secondary anamnestic response; however, autologous red cells are not destroyed.

CASE

A 48‐year‐old African American woman with sickle cell disease (SCD) was readmitted for pain crisis. Her medical history included stroke, pulmonary hypertension, and congestive heart failure. She had received several transfusions and consequently had developed antibodies to seven clinically significant red blood cell antigens. A week prior to readmission, she was discharged from the hospital with an Hb of 6.9 g/dL after a sickle cell crisis precipitated by pneumonia. She was treated with hydration, pain medications, antibiotics, and a unit of cross‐match‐compatible red blood cells (RBCs) that was antigen negative for her antibodies.

On readmission, she had an Hb of 5.6 g/dL and an uncorrected reticulocyte count of 17.6%. Her reticulocyte production index, a reticulocyte count corrected for the degree of anemia and reticulocyte maturation time, was elevated at 2.6. She was transfused with 1 unit of phenotypically matched and cross‐match‐compatible RBCs. Three hours after transfusion, she developed dark‐colored urine. The transfusion reaction investigation revealed no clerical error or incompatibility, a negative DAT, and an antibody panel identical to that from pretransfusion testing. During hospitalization, the hemolytic anemia worsened (Fig. 1). On the 10th hospital day, she became severely dyspneic as her Hb reached its nadir of 3.6 g/dL despite ongoing erythropoiesis. She developed decompensated heart failure and renal insufficiency, precipitated by the acutely worsening anemia. Along with diuretic and vasodilator therapies, she was treated with methylprednisolone at 125 mg twice daily for 3 days followed by tapering doses of prednisone for 2 weeks, intravenous immunoglobulin (IVIG) at 400 mg/kg a day for 5 days, and 4 cross‐match‐compatible RBC transfusions that were antigen negative for her antibodies. The hemolysis resolved and the patient improved. Throughout hospitalization, her DAT remained negative. The Hb remained stable at 7 g/dL until she was discharged. Ten months of follow‐up showed no new red blood cell antibody in her serum or recurrence of hyperhemolysis syndrome despite receiving subsequent transfusions.

Figure 1

DISCUSSION

Hyperhemolysis syndrome has been described in patients with SCD,14, 6, 7 suggesting that an underlying hemoglobinopathy may be a risk factor; however, a patient with anemia of chronic disease was recently described in the literature to have developed hyperhemolysis syndrome.5 Possible mechanisms include innocent bystander hemolysis through complement‐mediated lysis and/or formation of red blood cell alloantibody or autoantibody;1, 2 and hyperactive macrophages of the reticuloendothelial system that recognize Hb S RBCs of patients with SCD more avidly than normal RBCs because of the exposure of aminophosphatides in the outer layer of the sickled RBC membrane.3 In effect, red blood cells may be destroyed regardless of whether they are autologous or transfused. Additionally, transfusion‐related suppression of erythropoiesis may worsen the severity of anemia.2 Recent studies of patients with SCD suggest that the presence of free plasma Hb, as a consequence of hemolysis, reduces nitric oxide bioavailability, promotes endothelial dysfunction, and contributes to the development of pulmonary hypertension and the varying presentations of vasoocclusion.6 A common observation among patients who experience hyperhemolysis syndrome is that withholding transfusion seems beneficial, probably because immunologic reactions are not exacerbated, whereas treatment with steroids1, 2, 4 and/or IVIG3, 7 resolves hemolysis because of their immunomodulatory effects.

CONCLUSIONS

Hyperhemolysis syndrome is a potentially life‐threatening complication of RBC transfusion. It is important to recognize this syndrome when managing patients with SCD who present with worsening anemia after RBC transfusions. Although further transfusions can exacerbate hemolysis4, 7 and may be relatively contraindicated, in severe and desperate situations, simultaneous treatment with steroids and IVIG, together with RBC transfusions, may be lifesaving.

A 72‐year‐old man had been suffering from low‐grade fever, minimally productive cough, and shortness of breath for 1 week when he experienced sudden, moderately severe right‐sided chest pain. His local primary care physician found no abnormalities on physical exam and laboratory testing. A chest x‐ray, however, did reveal a small right‐sided pleural effusion. The patient was empirically started on levofloxacin but noticed no improvement. Two weeks into his illness, he was referred to our institution for further management. By this time, he reported a rapid 10‐pound weight loss and a daily low‐grade fever. Chest examination revealed dullness to percussion along with decreased breath sounds in the right posterior lung fields. A complete blood count showed an elevated white count of 17,000/mL with 14,000 neutrophils. Hemoglobin was 13.5 g/dL. A repeat chest x‐ ray and then a CT scan showed a multiloculated pleural effusion in the right lower hemithorax. Ultrasound‐guided tap of this effusion showed cloudy fluid consistent with pus, with a protein of 4.8 g/dL and total nucleated cells of 6000/mL. A gram stain on this fluid was negative.

The patient had a history remarkable for severe underlying chronic obstructive pulmonary disease (COPD). His forced expiratory volume in 1 second (FEV1) was 21%, and his diffusing capacity of carbon monoxide (DLCO) was 27%. Therefore, decortication under general anesthesia was not an option. So the largest pus pocket was drained under CT guidance, and the patient was dismissed home on levofloxacin.

He returned for follow‐up after 3 weeks and reported daily low‐grade fever, night sweats, and an additional weight loss of 14 pounds. His white count had risen to 18,300/mL with a neutrophil count of 16,600. Hemoglobin had fallen to 11.9 g/dL. A repeat CT scan showed that although the previously drained fluid pocket had resolved, a moderate amount of fluid had reaccumulated in other pockets. Delayed anaerobic culture results from the hospitalization 3 weeks earlier were now available and, interestingly, showed 2+ growth of Campylobacter jejuni, broadly sensitive to all antibiotics including penicillin. Piperacillin/tazobactam was started intravenously, and CT‐guided drainage of the largest pus pocket was again performed.

We carefully reexamined the patient's CT scan, and there appeared to be a lesion in the right main‐stem bronchus. We decided to perform a bronchoscopy, which revealed a foreign body in the right main‐stem bronchus. The foreign body turned out to be a piece of chicken and a peanut. On specific questioning of the patient again, he admitted that at times he coughed after eating too quickly. Specifically, he remembered that a few days before falling sick he was at a village fair, where he had had chicken, and he thought he might have coughed after eating it. He denied any diarrheal illness in the recent past. We obtained a swallow study and upper gastrointestinal endoscopy, both of which were unremarkable.

He improved remarkably after removal of the foreign body and was sent home on amoxicillin‐clavulanic acid for 3 weeks.

DISCUSSION

Campylobacter is one of the most common zoonoses in the world.1 Commercially raised poultry is nearly always colonized with Campylobacter jejuni, and therefore, not surprisingly, 50% to 70% of C. jejuni infection in humans is caused by undercooked poultry.2 The most common presentation of C. jejuni in humans is acute enteritis or colitis, but it can have numerous extraintestinal manifestations.3 Bacteremia occurs in fewer than 1% of patients, but C. jejuni meningitis and endocarditis have been reported. Hepatitis, interstitial nephritis, hemolytic‐uremic syndrome, and IgA nephropathy are other reported complications. Our patient probably aspirated a piece of undercooked chicken that likely was the source of the C. jejuni, causing a persistent empyema.

Most patients fully recover from C. jejuni infections without medications, but if illness is severe or prolonged, antibiotics are recommended. Macrolides are usually the first‐line treatment, but their increasing veterinary use is leading to their being resistant to these drugs.4 Most isolates are not susceptible to cephalosporins or penicillins, except amoxicillin or ticarcillin plus clavulanic acid. The C. jejuni isolated in culture in our lab from this patient was unusual in being broadly sensitive.

Our patient aspirated a foreign body in the form of chicken and a peanut without even realizing it. This is extremely uncommon, although foreign‐body aspiration in otherwise healthy and alert adults sometimes does occur. The most common presentation is sudden choking, coughing, and vomiting, followed by wheezing and breathlessness. Patients may also present with persistent cough, hemoptysis, fever, breathlessness, or wheezing. Children may present with cyanosis.

Inorganic foreign bodies tend to be from dental accidents, and organic aspirated foreign bodies tend to depend on the types of food eaten in a particular population, with bones, nuts, and apple pips the most common. In adults, all foreign bodies tend to lodge in the right bronchial tree. Aspiration of organic material is usually diagnosed later than aspiration of nonorganic material.5 In either case, airway foreign‐body aspiration is a common cause of recurrent bacterial pneumonia, and long delays in diagnosis are quite typical.6

Plain x‐rays may be entirely normal. A CT may demonstrate an aspirated foreign body in the lumen of the tracheobronchial tree. Other common findings are atelectasis, hyperlucency, bronchiectasis, lobar consolidation, ipsilateral pleural effusion, and lymphadenopathy and a thickened bronchial wall adjacent to the foreign body.7 Newer methods such as CT virtual bronchoscopy are being evaluated for use in selected cases when clinical suspicion is high.8 0

Figure 1

A 72‐year‐old man had been suffering from low‐grade fever, minimally productive cough, and shortness of breath for 1 week when he experienced sudden, moderately severe right‐sided chest pain. His local primary care physician found no abnormalities on physical exam and laboratory testing. A chest x‐ray, however, did reveal a small right‐sided pleural effusion. The patient was empirically started on levofloxacin but noticed no improvement. Two weeks into his illness, he was referred to our institution for further management. By this time, he reported a rapid 10‐pound weight loss and a daily low‐grade fever. Chest examination revealed dullness to percussion along with decreased breath sounds in the right posterior lung fields. A complete blood count showed an elevated white count of 17,000/mL with 14,000 neutrophils. Hemoglobin was 13.5 g/dL. A repeat chest x‐ ray and then a CT scan showed a multiloculated pleural effusion in the right lower hemithorax. Ultrasound‐guided tap of this effusion showed cloudy fluid consistent with pus, with a protein of 4.8 g/dL and total nucleated cells of 6000/mL. A gram stain on this fluid was negative.

The patient had a history remarkable for severe underlying chronic obstructive pulmonary disease (COPD). His forced expiratory volume in 1 second (FEV1) was 21%, and his diffusing capacity of carbon monoxide (DLCO) was 27%. Therefore, decortication under general anesthesia was not an option. So the largest pus pocket was drained under CT guidance, and the patient was dismissed home on levofloxacin.

He returned for follow‐up after 3 weeks and reported daily low‐grade fever, night sweats, and an additional weight loss of 14 pounds. His white count had risen to 18,300/mL with a neutrophil count of 16,600. Hemoglobin had fallen to 11.9 g/dL. A repeat CT scan showed that although the previously drained fluid pocket had resolved, a moderate amount of fluid had reaccumulated in other pockets. Delayed anaerobic culture results from the hospitalization 3 weeks earlier were now available and, interestingly, showed 2+ growth of Campylobacter jejuni, broadly sensitive to all antibiotics including penicillin. Piperacillin/tazobactam was started intravenously, and CT‐guided drainage of the largest pus pocket was again performed.

We carefully reexamined the patient's CT scan, and there appeared to be a lesion in the right main‐stem bronchus. We decided to perform a bronchoscopy, which revealed a foreign body in the right main‐stem bronchus. The foreign body turned out to be a piece of chicken and a peanut. On specific questioning of the patient again, he admitted that at times he coughed after eating too quickly. Specifically, he remembered that a few days before falling sick he was at a village fair, where he had had chicken, and he thought he might have coughed after eating it. He denied any diarrheal illness in the recent past. We obtained a swallow study and upper gastrointestinal endoscopy, both of which were unremarkable.

He improved remarkably after removal of the foreign body and was sent home on amoxicillin‐clavulanic acid for 3 weeks.

DISCUSSION

Campylobacter is one of the most common zoonoses in the world.1 Commercially raised poultry is nearly always colonized with Campylobacter jejuni, and therefore, not surprisingly, 50% to 70% of C. jejuni infection in humans is caused by undercooked poultry.2 The most common presentation of C. jejuni in humans is acute enteritis or colitis, but it can have numerous extraintestinal manifestations.3 Bacteremia occurs in fewer than 1% of patients, but C. jejuni meningitis and endocarditis have been reported. Hepatitis, interstitial nephritis, hemolytic‐uremic syndrome, and IgA nephropathy are other reported complications. Our patient probably aspirated a piece of undercooked chicken that likely was the source of the C. jejuni, causing a persistent empyema.

Most patients fully recover from C. jejuni infections without medications, but if illness is severe or prolonged, antibiotics are recommended. Macrolides are usually the first‐line treatment, but their increasing veterinary use is leading to their being resistant to these drugs.4 Most isolates are not susceptible to cephalosporins or penicillins, except amoxicillin or ticarcillin plus clavulanic acid. The C. jejuni isolated in culture in our lab from this patient was unusual in being broadly sensitive.

Our patient aspirated a foreign body in the form of chicken and a peanut without even realizing it. This is extremely uncommon, although foreign‐body aspiration in otherwise healthy and alert adults sometimes does occur. The most common presentation is sudden choking, coughing, and vomiting, followed by wheezing and breathlessness. Patients may also present with persistent cough, hemoptysis, fever, breathlessness, or wheezing. Children may present with cyanosis.

Inorganic foreign bodies tend to be from dental accidents, and organic aspirated foreign bodies tend to depend on the types of food eaten in a particular population, with bones, nuts, and apple pips the most common. In adults, all foreign bodies tend to lodge in the right bronchial tree. Aspiration of organic material is usually diagnosed later than aspiration of nonorganic material.5 In either case, airway foreign‐body aspiration is a common cause of recurrent bacterial pneumonia, and long delays in diagnosis are quite typical.6

Plain x‐rays may be entirely normal. A CT may demonstrate an aspirated foreign body in the lumen of the tracheobronchial tree. Other common findings are atelectasis, hyperlucency, bronchiectasis, lobar consolidation, ipsilateral pleural effusion, and lymphadenopathy and a thickened bronchial wall adjacent to the foreign body.7 Newer methods such as CT virtual bronchoscopy are being evaluated for use in selected cases when clinical suspicion is high.8 0

Figure 1

A 72‐year‐old man had been suffering from low‐grade fever, minimally productive cough, and shortness of breath for 1 week when he experienced sudden, moderately severe right‐sided chest pain. His local primary care physician found no abnormalities on physical exam and laboratory testing. A chest x‐ray, however, did reveal a small right‐sided pleural effusion. The patient was empirically started on levofloxacin but noticed no improvement. Two weeks into his illness, he was referred to our institution for further management. By this time, he reported a rapid 10‐pound weight loss and a daily low‐grade fever. Chest examination revealed dullness to percussion along with decreased breath sounds in the right posterior lung fields. A complete blood count showed an elevated white count of 17,000/mL with 14,000 neutrophils. Hemoglobin was 13.5 g/dL. A repeat chest x‐ ray and then a CT scan showed a multiloculated pleural effusion in the right lower hemithorax. Ultrasound‐guided tap of this effusion showed cloudy fluid consistent with pus, with a protein of 4.8 g/dL and total nucleated cells of 6000/mL. A gram stain on this fluid was negative.

The patient had a history remarkable for severe underlying chronic obstructive pulmonary disease (COPD). His forced expiratory volume in 1 second (FEV1) was 21%, and his diffusing capacity of carbon monoxide (DLCO) was 27%. Therefore, decortication under general anesthesia was not an option. So the largest pus pocket was drained under CT guidance, and the patient was dismissed home on levofloxacin.

He returned for follow‐up after 3 weeks and reported daily low‐grade fever, night sweats, and an additional weight loss of 14 pounds. His white count had risen to 18,300/mL with a neutrophil count of 16,600. Hemoglobin had fallen to 11.9 g/dL. A repeat CT scan showed that although the previously drained fluid pocket had resolved, a moderate amount of fluid had reaccumulated in other pockets. Delayed anaerobic culture results from the hospitalization 3 weeks earlier were now available and, interestingly, showed 2+ growth of Campylobacter jejuni, broadly sensitive to all antibiotics including penicillin. Piperacillin/tazobactam was started intravenously, and CT‐guided drainage of the largest pus pocket was again performed.

We carefully reexamined the patient's CT scan, and there appeared to be a lesion in the right main‐stem bronchus. We decided to perform a bronchoscopy, which revealed a foreign body in the right main‐stem bronchus. The foreign body turned out to be a piece of chicken and a peanut. On specific questioning of the patient again, he admitted that at times he coughed after eating too quickly. Specifically, he remembered that a few days before falling sick he was at a village fair, where he had had chicken, and he thought he might have coughed after eating it. He denied any diarrheal illness in the recent past. We obtained a swallow study and upper gastrointestinal endoscopy, both of which were unremarkable.

He improved remarkably after removal of the foreign body and was sent home on amoxicillin‐clavulanic acid for 3 weeks.

DISCUSSION

Campylobacter is one of the most common zoonoses in the world.1 Commercially raised poultry is nearly always colonized with Campylobacter jejuni, and therefore, not surprisingly, 50% to 70% of C. jejuni infection in humans is caused by undercooked poultry.2 The most common presentation of C. jejuni in humans is acute enteritis or colitis, but it can have numerous extraintestinal manifestations.3 Bacteremia occurs in fewer than 1% of patients, but C. jejuni meningitis and endocarditis have been reported. Hepatitis, interstitial nephritis, hemolytic‐uremic syndrome, and IgA nephropathy are other reported complications. Our patient probably aspirated a piece of undercooked chicken that likely was the source of the C. jejuni, causing a persistent empyema.

Most patients fully recover from C. jejuni infections without medications, but if illness is severe or prolonged, antibiotics are recommended. Macrolides are usually the first‐line treatment, but their increasing veterinary use is leading to their being resistant to these drugs.4 Most isolates are not susceptible to cephalosporins or penicillins, except amoxicillin or ticarcillin plus clavulanic acid. The C. jejuni isolated in culture in our lab from this patient was unusual in being broadly sensitive.

Our patient aspirated a foreign body in the form of chicken and a peanut without even realizing it. This is extremely uncommon, although foreign‐body aspiration in otherwise healthy and alert adults sometimes does occur. The most common presentation is sudden choking, coughing, and vomiting, followed by wheezing and breathlessness. Patients may also present with persistent cough, hemoptysis, fever, breathlessness, or wheezing. Children may present with cyanosis.

Inorganic foreign bodies tend to be from dental accidents, and organic aspirated foreign bodies tend to depend on the types of food eaten in a particular population, with bones, nuts, and apple pips the most common. In adults, all foreign bodies tend to lodge in the right bronchial tree. Aspiration of organic material is usually diagnosed later than aspiration of nonorganic material.5 In either case, airway foreign‐body aspiration is a common cause of recurrent bacterial pneumonia, and long delays in diagnosis are quite typical.6

Plain x‐rays may be entirely normal. A CT may demonstrate an aspirated foreign body in the lumen of the tracheobronchial tree. Other common findings are atelectasis, hyperlucency, bronchiectasis, lobar consolidation, ipsilateral pleural effusion, and lymphadenopathy and a thickened bronchial wall adjacent to the foreign body.7 Newer methods such as CT virtual bronchoscopy are being evaluated for use in selected cases when clinical suspicion is high.8 0

Figure 1

A 37‐year‐old man presented to an ophthalmologist in July 2004 with a history of slowly decreasing vision in both eyes for several weeks. His vision on presentation was 20/400 in the right eye and 20/200 in the left eye. Slit‐lamp examination showed a bilateral anterior uveitis with 360 degrees of posterior synechiae (adhesions) and a dense vitritis (posterior uveitis) that obscured the view of the retina in both eyes. He was diagnosed with panuveitis and started on topical steroid and cycloplegic drops. He was referred to a uveitis specialist for investigation but missed his appointments.

One year later he presented to the emergency room with fever and severe pain in his left eye. On initial assessment he had no complaints of mouth or genital ulcers, recent or remote rashes, joint symptoms, or penile discharge. He denied any prior eye trauma or surgery. He reported that his last sexual encounter had been 8 months prior with a male and that his most recent HIV screen was negative 6 months ago. His family history was negative for autoimmune disorders.

On inspection, he appeared cachectic, lethargic, and very ill. He was febrile and tachycardic; the remainder of his vital signs were normal. There was no lymphadenopathy. His neck was supple with no meningismal signs. There were no heart murmurs, oral ulcers, swollen joints, mucosal eschar, or skin lesions. Respiratory and abdominal examinations were unremarkable.

His visual acuity was light perception in right eye and no light perception in the left eye. There was significant eyelid edema, erythema and purulent discharge with mild proptosis of the left eye (Fig. 1). Pupils were 3 mm and fixed, with 360 of posterior synechiae. Intraocular pressure was elevated in the left eye (42 mm Hg, where normal is 20 mm Hg). There was moderate uveitis in both eyes, with a 1‐mm hypopyon in the left eye and forward bowing of the iris (iris bomb). A dense vitritis was present in both eyes, preventing visualization of the retina. B‐scan ultrasound examination showed bilateral retinal detachments, worse in the left eye.

Figure 1

Because of the high intraocular pressure in the left eye, the patient was given topical Cosopt (dorzolamide hydrochloride‐timolol maleate), bromonidine 0.15%, and oral acetazolamide to lower intraocular pressures. He was started on a preliminary treatment of hourly topical prednisolone acetate 1%, atropine 1% 4 times daily, and topical moxifloxacin 0.5%. He was admitted to hospital to investigate the source of his panophthalmitis (suppurative infection of the eye and sclera, extending to involve the orbit).

Blood and urine cultures, HIV, rapid plasma reagin test (RPR), HLA B27, toxoplasmosis serology, and ANA rheumatoid factor were sent. Overnight, he developed classic Janeway lesions on his palms and soles, and both blood and urine cultures grew gram‐positive cocci in clusters. Repeat blood cultures were taken. He was started on IV vancomycin empirically. Ultimately, all 3 blood cultures grew Staphylococcus aureus.

A transesophageal echocardiogram diagnosed endocarditis with a pedunculated mobile mass identified on the posterior mitral valve leaflet. Mild mitral regurgitation was noted. The aortic valve was normal, as were ventricular size and function. Antibiotics were modified to cloxacillin and gentamicin IV 2 days later, once sensitivities were reported.

A CT scan of the orbits revealed diffuse orbital inflammation with no evidence of an orbital abscess (Fig. 2). The inflammation and proptosis of the left eye continued to worsen, and a vitreous paracentesis of the left eye was performed for 1.5 mL of dark brown fluid. The aspirated sample was sent for C&S, PCR (for HSV, CMV), acid‐fast stain, and fungal, viral, and mycobacterial cultures. Intravitreal injections of vancomycin and ceftazidime were given. Bacterial cultures showed a heavy intraocular growth of S. aureus, giving the diagnosis of endophthalmitis (bacterial or fungal infection of the vitreous or aqueous humor); all remaining stains and cultures were negative.

Figure 2

Over the next several days, the initial blood work returned with the following abnormal results: CD4 count was 70/L, and HIV serology was positive. The rapid plasma reagin test (RPR) was positive (titer 1:64). The enzyme immunoassay (EIA) and Treponema pallidum particle agglutination (TPPA) were also positive.

A lumbar puncture was performed, and CSF analysis indicated CSF fluid was clear, 2 erythrocytes and 2 leukocytes in the fourth tube, CSF glucose of 2.7 mmol/L (serum glucose 8.2 mmol/L), and CSF total protein of 1100 mg/L. There were no bacteria seen on the gram stain, and a rapid agglutination test for cryptococcal antigen was negative. The CSF RPR titer was 1:2, and the Treponema pallidum particle agglutination assay (TP‐PA) was reactive. The MRI of the brain indicated diffuse white matter disease but no meningeal enhancement. In combination, these results were indicative of neurosyphilis, and penicillin G IV therapy was initiated. He received a total of 14 days of IV therapy, followed by 3 weekly IM doses of benzathine penicillin. He also received a total of 28 days of IV cloxacillin therapy with 5 days of concomitant IV gentamicin for endocarditis treatment.

Over 8 weeks, the patient's panophthalmitis slowly improved. However, he maintained only light perception in the right eye and did not regain any vision in the left eye. He was discharged home to follow‐up with the infectious diseases and ophthalmology departments. The issue of initiating antiretroviral therapy, deferred during hospital admission because of his poor compliance history and the threat of immune reconstitution symptoms, was to be readdressed at this time. He missed both appointments and returned to the emergency room several months later with widespread Kaposi's sarcoma.

DISCUSSION

One of the key learning points from this case underlines that panuveitis carries a broad differential including inflammatory and infectious conditions, as well as lymphoma. Systemic infections include tuberculosis, syphilis, and in cases of severe immunosuppression, toxoplasmosis. Cytomegalovirus and candidiasis are less likely as they are not associated with intraocular inflammation. HIV is also on the differential, although it rarely causes severe panuveitis on its own. Inflammatory disorders such as Behcet syndrome, sarcoidosis, and, rarely, lens‐associated uveitis (if presented with a history of lens trauma or surgery) are also included on the differential. A systematic approach to the history and physical examination must be undertaken to narrow the search. A syphilis screen should always be included in the differential when investigating uveitis,1 especially given the resurgence of syphilis since 2000.2

Our patient presents an interesting study as he was coinfected with both syphilis and HIV. The progression of syphilis is far more aggressive in this scenario,3 as there is a higher frequency of initial presentation as secondary syphilis4 and with multiple persisting chancres.5 Secondary‐stage skin lesions are also more aggressive in coinfected patients (nodular or ulcerative lesions with necrotic centers), although the same dermatological presentations can be seen in HIV‐negative patients.6 It has not been definitively established whether HIV‐positive patients develop neurological complications of syphilis more frequently or earlier in disease, but most patients present with early neurosyphilis at the time of diagnosis.7 In keeping with these findings, our patient's initial presentation included both ocular and neurosyphilis as diagnostic features.

An atypical link highlighted by our case is that of endogenous, bacterial endophthalmitis secondary to endocarditis. Although traumatic or surgical complications are the most common causes of endophthalmitis, seeding from an endogenous infective source, although rare, is possible.810 Staphylococcus aureus endocarditis is one of the most common causes of endogenous spread.9 In our patient, his chronic uveitis and decompensated blood‐ocular barrier may have contributed to S. aureus seeding of his eye. As is the case with many patients diagnosed with S. aureus endocarditis, the source of infection was unknown, although several risk factors for S. aureus bacteremia have been documented. These risk factors include hospitalization, dialysis, transplantation, HIV‐positive status, heart disease, cancer, diabetes, and intravenous drug use. In a population‐based surveillance study from 1999 to 2000, 550 invasive isolates of S. aureus were obtained; the relative risk in HIV‐positive patients was 23.7.11 In a similar study, the source of the S. aureus bacteremia/endocarditis was not identified in 26% of patients with underlying medical conditions such as HIV infection.12

This case has demonstrated several intertwined disease presentations in a patient coinfected with multiple organisms. In an immunocompromised patient, Occam's razor does not necessarily hold true, and the possibility of multiple diagnoses must be entertained. Thus, clinicians must maintain a high index of suspicion for atypical presentations of typical diseases if their patients are to survive in the eye of the storm.

A 37‐year‐old man presented to an ophthalmologist in July 2004 with a history of slowly decreasing vision in both eyes for several weeks. His vision on presentation was 20/400 in the right eye and 20/200 in the left eye. Slit‐lamp examination showed a bilateral anterior uveitis with 360 degrees of posterior synechiae (adhesions) and a dense vitritis (posterior uveitis) that obscured the view of the retina in both eyes. He was diagnosed with panuveitis and started on topical steroid and cycloplegic drops. He was referred to a uveitis specialist for investigation but missed his appointments.

One year later he presented to the emergency room with fever and severe pain in his left eye. On initial assessment he had no complaints of mouth or genital ulcers, recent or remote rashes, joint symptoms, or penile discharge. He denied any prior eye trauma or surgery. He reported that his last sexual encounter had been 8 months prior with a male and that his most recent HIV screen was negative 6 months ago. His family history was negative for autoimmune disorders.

On inspection, he appeared cachectic, lethargic, and very ill. He was febrile and tachycardic; the remainder of his vital signs were normal. There was no lymphadenopathy. His neck was supple with no meningismal signs. There were no heart murmurs, oral ulcers, swollen joints, mucosal eschar, or skin lesions. Respiratory and abdominal examinations were unremarkable.

His visual acuity was light perception in right eye and no light perception in the left eye. There was significant eyelid edema, erythema and purulent discharge with mild proptosis of the left eye (Fig. 1). Pupils were 3 mm and fixed, with 360 of posterior synechiae. Intraocular pressure was elevated in the left eye (42 mm Hg, where normal is 20 mm Hg). There was moderate uveitis in both eyes, with a 1‐mm hypopyon in the left eye and forward bowing of the iris (iris bomb). A dense vitritis was present in both eyes, preventing visualization of the retina. B‐scan ultrasound examination showed bilateral retinal detachments, worse in the left eye.

Figure 1

Because of the high intraocular pressure in the left eye, the patient was given topical Cosopt (dorzolamide hydrochloride‐timolol maleate), bromonidine 0.15%, and oral acetazolamide to lower intraocular pressures. He was started on a preliminary treatment of hourly topical prednisolone acetate 1%, atropine 1% 4 times daily, and topical moxifloxacin 0.5%. He was admitted to hospital to investigate the source of his panophthalmitis (suppurative infection of the eye and sclera, extending to involve the orbit).

Blood and urine cultures, HIV, rapid plasma reagin test (RPR), HLA B27, toxoplasmosis serology, and ANA rheumatoid factor were sent. Overnight, he developed classic Janeway lesions on his palms and soles, and both blood and urine cultures grew gram‐positive cocci in clusters. Repeat blood cultures were taken. He was started on IV vancomycin empirically. Ultimately, all 3 blood cultures grew Staphylococcus aureus.

A transesophageal echocardiogram diagnosed endocarditis with a pedunculated mobile mass identified on the posterior mitral valve leaflet. Mild mitral regurgitation was noted. The aortic valve was normal, as were ventricular size and function. Antibiotics were modified to cloxacillin and gentamicin IV 2 days later, once sensitivities were reported.

A CT scan of the orbits revealed diffuse orbital inflammation with no evidence of an orbital abscess (Fig. 2). The inflammation and proptosis of the left eye continued to worsen, and a vitreous paracentesis of the left eye was performed for 1.5 mL of dark brown fluid. The aspirated sample was sent for C&S, PCR (for HSV, CMV), acid‐fast stain, and fungal, viral, and mycobacterial cultures. Intravitreal injections of vancomycin and ceftazidime were given. Bacterial cultures showed a heavy intraocular growth of S. aureus, giving the diagnosis of endophthalmitis (bacterial or fungal infection of the vitreous or aqueous humor); all remaining stains and cultures were negative.

Figure 2

Over the next several days, the initial blood work returned with the following abnormal results: CD4 count was 70/L, and HIV serology was positive. The rapid plasma reagin test (RPR) was positive (titer 1:64). The enzyme immunoassay (EIA) and Treponema pallidum particle agglutination (TPPA) were also positive.

A lumbar puncture was performed, and CSF analysis indicated CSF fluid was clear, 2 erythrocytes and 2 leukocytes in the fourth tube, CSF glucose of 2.7 mmol/L (serum glucose 8.2 mmol/L), and CSF total protein of 1100 mg/L. There were no bacteria seen on the gram stain, and a rapid agglutination test for cryptococcal antigen was negative. The CSF RPR titer was 1:2, and the Treponema pallidum particle agglutination assay (TP‐PA) was reactive. The MRI of the brain indicated diffuse white matter disease but no meningeal enhancement. In combination, these results were indicative of neurosyphilis, and penicillin G IV therapy was initiated. He received a total of 14 days of IV therapy, followed by 3 weekly IM doses of benzathine penicillin. He also received a total of 28 days of IV cloxacillin therapy with 5 days of concomitant IV gentamicin for endocarditis treatment.

Over 8 weeks, the patient's panophthalmitis slowly improved. However, he maintained only light perception in the right eye and did not regain any vision in the left eye. He was discharged home to follow‐up with the infectious diseases and ophthalmology departments. The issue of initiating antiretroviral therapy, deferred during hospital admission because of his poor compliance history and the threat of immune reconstitution symptoms, was to be readdressed at this time. He missed both appointments and returned to the emergency room several months later with widespread Kaposi's sarcoma.

DISCUSSION

One of the key learning points from this case underlines that panuveitis carries a broad differential including inflammatory and infectious conditions, as well as lymphoma. Systemic infections include tuberculosis, syphilis, and in cases of severe immunosuppression, toxoplasmosis. Cytomegalovirus and candidiasis are less likely as they are not associated with intraocular inflammation. HIV is also on the differential, although it rarely causes severe panuveitis on its own. Inflammatory disorders such as Behcet syndrome, sarcoidosis, and, rarely, lens‐associated uveitis (if presented with a history of lens trauma or surgery) are also included on the differential. A systematic approach to the history and physical examination must be undertaken to narrow the search. A syphilis screen should always be included in the differential when investigating uveitis,1 especially given the resurgence of syphilis since 2000.2

Our patient presents an interesting study as he was coinfected with both syphilis and HIV. The progression of syphilis is far more aggressive in this scenario,3 as there is a higher frequency of initial presentation as secondary syphilis4 and with multiple persisting chancres.5 Secondary‐stage skin lesions are also more aggressive in coinfected patients (nodular or ulcerative lesions with necrotic centers), although the same dermatological presentations can be seen in HIV‐negative patients.6 It has not been definitively established whether HIV‐positive patients develop neurological complications of syphilis more frequently or earlier in disease, but most patients present with early neurosyphilis at the time of diagnosis.7 In keeping with these findings, our patient's initial presentation included both ocular and neurosyphilis as diagnostic features.

An atypical link highlighted by our case is that of endogenous, bacterial endophthalmitis secondary to endocarditis. Although traumatic or surgical complications are the most common causes of endophthalmitis, seeding from an endogenous infective source, although rare, is possible.810 Staphylococcus aureus endocarditis is one of the most common causes of endogenous spread.9 In our patient, his chronic uveitis and decompensated blood‐ocular barrier may have contributed to S. aureus seeding of his eye. As is the case with many patients diagnosed with S. aureus endocarditis, the source of infection was unknown, although several risk factors for S. aureus bacteremia have been documented. These risk factors include hospitalization, dialysis, transplantation, HIV‐positive status, heart disease, cancer, diabetes, and intravenous drug use. In a population‐based surveillance study from 1999 to 2000, 550 invasive isolates of S. aureus were obtained; the relative risk in HIV‐positive patients was 23.7.11 In a similar study, the source of the S. aureus bacteremia/endocarditis was not identified in 26% of patients with underlying medical conditions such as HIV infection.12

This case has demonstrated several intertwined disease presentations in a patient coinfected with multiple organisms. In an immunocompromised patient, Occam's razor does not necessarily hold true, and the possibility of multiple diagnoses must be entertained. Thus, clinicians must maintain a high index of suspicion for atypical presentations of typical diseases if their patients are to survive in the eye of the storm.

A 37‐year‐old man presented to an ophthalmologist in July 2004 with a history of slowly decreasing vision in both eyes for several weeks. His vision on presentation was 20/400 in the right eye and 20/200 in the left eye. Slit‐lamp examination showed a bilateral anterior uveitis with 360 degrees of posterior synechiae (adhesions) and a dense vitritis (posterior uveitis) that obscured the view of the retina in both eyes. He was diagnosed with panuveitis and started on topical steroid and cycloplegic drops. He was referred to a uveitis specialist for investigation but missed his appointments.

One year later he presented to the emergency room with fever and severe pain in his left eye. On initial assessment he had no complaints of mouth or genital ulcers, recent or remote rashes, joint symptoms, or penile discharge. He denied any prior eye trauma or surgery. He reported that his last sexual encounter had been 8 months prior with a male and that his most recent HIV screen was negative 6 months ago. His family history was negative for autoimmune disorders.

On inspection, he appeared cachectic, lethargic, and very ill. He was febrile and tachycardic; the remainder of his vital signs were normal. There was no lymphadenopathy. His neck was supple with no meningismal signs. There were no heart murmurs, oral ulcers, swollen joints, mucosal eschar, or skin lesions. Respiratory and abdominal examinations were unremarkable.

His visual acuity was light perception in right eye and no light perception in the left eye. There was significant eyelid edema, erythema and purulent discharge with mild proptosis of the left eye (Fig. 1). Pupils were 3 mm and fixed, with 360 of posterior synechiae. Intraocular pressure was elevated in the left eye (42 mm Hg, where normal is 20 mm Hg). There was moderate uveitis in both eyes, with a 1‐mm hypopyon in the left eye and forward bowing of the iris (iris bomb). A dense vitritis was present in both eyes, preventing visualization of the retina. B‐scan ultrasound examination showed bilateral retinal detachments, worse in the left eye.

Figure 1

Because of the high intraocular pressure in the left eye, the patient was given topical Cosopt (dorzolamide hydrochloride‐timolol maleate), bromonidine 0.15%, and oral acetazolamide to lower intraocular pressures. He was started on a preliminary treatment of hourly topical prednisolone acetate 1%, atropine 1% 4 times daily, and topical moxifloxacin 0.5%. He was admitted to hospital to investigate the source of his panophthalmitis (suppurative infection of the eye and sclera, extending to involve the orbit).

Blood and urine cultures, HIV, rapid plasma reagin test (RPR), HLA B27, toxoplasmosis serology, and ANA rheumatoid factor were sent. Overnight, he developed classic Janeway lesions on his palms and soles, and both blood and urine cultures grew gram‐positive cocci in clusters. Repeat blood cultures were taken. He was started on IV vancomycin empirically. Ultimately, all 3 blood cultures grew Staphylococcus aureus.

A transesophageal echocardiogram diagnosed endocarditis with a pedunculated mobile mass identified on the posterior mitral valve leaflet. Mild mitral regurgitation was noted. The aortic valve was normal, as were ventricular size and function. Antibiotics were modified to cloxacillin and gentamicin IV 2 days later, once sensitivities were reported.

A CT scan of the orbits revealed diffuse orbital inflammation with no evidence of an orbital abscess (Fig. 2). The inflammation and proptosis of the left eye continued to worsen, and a vitreous paracentesis of the left eye was performed for 1.5 mL of dark brown fluid. The aspirated sample was sent for C&S, PCR (for HSV, CMV), acid‐fast stain, and fungal, viral, and mycobacterial cultures. Intravitreal injections of vancomycin and ceftazidime were given. Bacterial cultures showed a heavy intraocular growth of S. aureus, giving the diagnosis of endophthalmitis (bacterial or fungal infection of the vitreous or aqueous humor); all remaining stains and cultures were negative.

Figure 2

Over the next several days, the initial blood work returned with the following abnormal results: CD4 count was 70/L, and HIV serology was positive. The rapid plasma reagin test (RPR) was positive (titer 1:64). The enzyme immunoassay (EIA) and Treponema pallidum particle agglutination (TPPA) were also positive.

A lumbar puncture was performed, and CSF analysis indicated CSF fluid was clear, 2 erythrocytes and 2 leukocytes in the fourth tube, CSF glucose of 2.7 mmol/L (serum glucose 8.2 mmol/L), and CSF total protein of 1100 mg/L. There were no bacteria seen on the gram stain, and a rapid agglutination test for cryptococcal antigen was negative. The CSF RPR titer was 1:2, and the Treponema pallidum particle agglutination assay (TP‐PA) was reactive. The MRI of the brain indicated diffuse white matter disease but no meningeal enhancement. In combination, these results were indicative of neurosyphilis, and penicillin G IV therapy was initiated. He received a total of 14 days of IV therapy, followed by 3 weekly IM doses of benzathine penicillin. He also received a total of 28 days of IV cloxacillin therapy with 5 days of concomitant IV gentamicin for endocarditis treatment.

Over 8 weeks, the patient's panophthalmitis slowly improved. However, he maintained only light perception in the right eye and did not regain any vision in the left eye. He was discharged home to follow‐up with the infectious diseases and ophthalmology departments. The issue of initiating antiretroviral therapy, deferred during hospital admission because of his poor compliance history and the threat of immune reconstitution symptoms, was to be readdressed at this time. He missed both appointments and returned to the emergency room several months later with widespread Kaposi's sarcoma.

DISCUSSION

One of the key learning points from this case underlines that panuveitis carries a broad differential including inflammatory and infectious conditions, as well as lymphoma. Systemic infections include tuberculosis, syphilis, and in cases of severe immunosuppression, toxoplasmosis. Cytomegalovirus and candidiasis are less likely as they are not associated with intraocular inflammation. HIV is also on the differential, although it rarely causes severe panuveitis on its own. Inflammatory disorders such as Behcet syndrome, sarcoidosis, and, rarely, lens‐associated uveitis (if presented with a history of lens trauma or surgery) are also included on the differential. A systematic approach to the history and physical examination must be undertaken to narrow the search. A syphilis screen should always be included in the differential when investigating uveitis,1 especially given the resurgence of syphilis since 2000.2

Our patient presents an interesting study as he was coinfected with both syphilis and HIV. The progression of syphilis is far more aggressive in this scenario,3 as there is a higher frequency of initial presentation as secondary syphilis4 and with multiple persisting chancres.5 Secondary‐stage skin lesions are also more aggressive in coinfected patients (nodular or ulcerative lesions with necrotic centers), although the same dermatological presentations can be seen in HIV‐negative patients.6 It has not been definitively established whether HIV‐positive patients develop neurological complications of syphilis more frequently or earlier in disease, but most patients present with early neurosyphilis at the time of diagnosis.7 In keeping with these findings, our patient's initial presentation included both ocular and neurosyphilis as diagnostic features.

An atypical link highlighted by our case is that of endogenous, bacterial endophthalmitis secondary to endocarditis. Although traumatic or surgical complications are the most common causes of endophthalmitis, seeding from an endogenous infective source, although rare, is possible.810 Staphylococcus aureus endocarditis is one of the most common causes of endogenous spread.9 In our patient, his chronic uveitis and decompensated blood‐ocular barrier may have contributed to S. aureus seeding of his eye. As is the case with many patients diagnosed with S. aureus endocarditis, the source of infection was unknown, although several risk factors for S. aureus bacteremia have been documented. These risk factors include hospitalization, dialysis, transplantation, HIV‐positive status, heart disease, cancer, diabetes, and intravenous drug use. In a population‐based surveillance study from 1999 to 2000, 550 invasive isolates of S. aureus were obtained; the relative risk in HIV‐positive patients was 23.7.11 In a similar study, the source of the S. aureus bacteremia/endocarditis was not identified in 26% of patients with underlying medical conditions such as HIV infection.12

This case has demonstrated several intertwined disease presentations in a patient coinfected with multiple organisms. In an immunocompromised patient, Occam's razor does not necessarily hold true, and the possibility of multiple diagnoses must be entertained. Thus, clinicians must maintain a high index of suspicion for atypical presentations of typical diseases if their patients are to survive in the eye of the storm.