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Table of Contents
Year : 2023  |  Volume : 19  |  Issue : 1  |  Page : 32-35

Eyes cannot see what the mind does not know!

1 Department of Respiratory Medicine, Amrita Institute of Medical Sciences, Kochi, Kerala, India
2 Department of Microbiology, Amrita Institute of Medical Sciences, Kochi, Kerala, India

Date of Submission22-Feb-2023
Date of Acceptance07-Mar-2023
Date of Web Publication28-Mar-2023

Correspondence Address:
Asmita Anilkumar Mehta
Department of Respiratory Medicine, Amrita Institute of Medical Sciences, Ponekkara, Kochi 682041, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/AMJM.AMJM_6_23

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We present a previously healthy female who presented with life-threatening bilateral pneumonia causing respiratory failure associated with severe hemolysis. Because of their endemicity in India, malaria, dengue, and leptospirosis top the list of differential diagnosis in such cases. However, we found an alternate cause.

Keywords: Autoimmune hemolytic anemia, bilateral pleural effusion, Mycoplasma pneumonia, systemic steroids

How to cite this article:
Mehta AA, Shashindran N, Kunoor A, Theja L. Eyes cannot see what the mind does not know!. Amrita J Med 2023;19:32-5

How to cite this URL:
Mehta AA, Shashindran N, Kunoor A, Theja L. Eyes cannot see what the mind does not know!. Amrita J Med [serial online] 2023 [cited 2023 Jun 4];19:32-5. Available from: https://ajmonline.org.in/text.asp?2023/19/1/32/372708

  Introduction Top

Respiratory tract involvement due to Mycoplasma pneumonia is generally benign and only 3%–10% of patients develop clinical pneumonia.[1] It is uncommon to see fatalities caused by it.[2]Mycoplasma pneumoniae infections are often asymptomatic but can involve multiple organ systems. 25% of the patients develop extra-pulmonary complications, involving the central nervous system as well as the cardiovascular, gastrointestinal, and hematological systems.[3] Formation of cold agglutinins is frequently observed during M. pneumoniae infections. Cold agglutinins were presumed to cause antibody mediated hemolysis in 10% of the patients.[4] We hereby report a case of severe autoimmune hemolytic anemia secondary to M. pneumoniae infection in a 32-year-old lady. The significance of reporting this case is to highlight the fact that M. pneumoniae infections should be considered in the differential diagnosis of autoimmune hemolytic anemia.

  Case Report Top

A 32-year-old-lady was admitted to our hospital, complaining of difficulty in breathing. Her previous medical history was uneventful. The present illness began 7 days before admission with general malaise, sore throat, and high-grade fever. She became increasingly breathless and 5 days before admission was admitted in another hospital. Because of gradual worsening of her condition, she was referred to our hospital. She denied any history of hemoptysis, chest pain, cough, joint pain, vomiting, and diarrhea. There was history of similar illness in family and her 3-year-old son also received treatment for upper respiratory tract infection. She received oral clarithromycin and injection crystalline penicillin before presenting to us without any relief in her symptoms.

  On Examination Top

She was distressed, ill-looking woman with the oxygen saturation of 92% on breathing 4 L oxygen via nasal prongs. There was pallor, but there was neither icterus nor lymphadenopathy. Her vitals were as follows: temperature—101°F, pulse—130/minute, blood pressure—120/80 mmHg, and respiratory rate—34/min. She had tachycardia. Respiratory system examination revealed absence of breath sounds in right infra-axillary and infra scapular region with left sided basal crepitations and diminished breath sounds. Other systems appeared normal.

Blood investigations were as follows: complete blood count: Hb—11.3 g/dL, total white blood cells—9850/mm3, 75% neutrophils, and 12% lymphocytes, platelets—275,000/mm3, ESR—80 mm/h, CRP—280 mg/L, urea—21.1 mg/dL, creatinine—0.75 mg/dL, Troponin I—0.0012 ng/mL, and creatinine kinase MB—34.9 U/L. Her liver function test was abnormal with total bilirubin—1.62 mg/dL, direct bilirubin—0.69 mg/dL, AST—523 IU/L, ALT—547 IU/L, and AlkP—354 IU/L, as well as total protein—6.38 g/dL, Alb–2.66 g/dL, and Glob—3.7 g/dL. Prothrombin time and activated partial thromboplastin time were mildly deranged. Her arterial blood gas taken on 4 L of oxygen was as follows: pH—7.49, PaCO2—24 mmHg, PaO2—77.6 mmHg, and HCo3— 21.8 mg/dL. At the time of presentation, X-ray chest showed bilateral lower zone consolidation with right sided loculated pleural effusion. Sputum culture and sputum smear for acid-fast bacilli for 2 days were negative. Computed tomography of chest showed bilateral lower lobe and right middle lobe pneumonia with bilateral pleural effusion left much greater than right. CT-guided pig tail insertion was done for left sided pleural effusion. Pleural fluid analysis: Prot—4.47 g/dL, glucose—94.4 mg/dL, lactate dehydrogenase—1852 U/L, and adenosine deaminase—27.6 U/L. Pleural fluid cytology showed lymphocyte-rich pleural fluid. Pleural fluid bacterial and acid-fast bacilli culture tests were negative. Ultrasonography abdomen was normal except with mild fatty liver. Advanced echocardiography was done, which showed ejection fraction of 60% with no other abnormality. She was started on betalactam-betalactamase inhibitors with fluroquinolone along with oseltamivir considering the diagnosis of viral/atypical pneumonia. However, even after effective drainage of pleural effusion and broad-spectrum antibiotics, she continued to have fever. Repeat chest X-ray [Figure 1] showed gradual worsening. Hb and PCV also showed gradual fall with simultaneous elevation of liver enzymes [Table 1]. So, she was evaluated further for other diseases. Her peripheral smear and serology for malaria parasite were negative. A tuberculin skin (100TU) test was negative. Blood culture, urine analysis, and urine culture were sterile. Her serology for dengue and leptospira were also found to be negative. Hepatitis A IgM antibodies, hepatitis C antibody, hepatitis B markers, and antibodies to human immunodeficiency virus were also negative. During her hospital stay, her Hb and PCV showed gradual fall every day along with increase in AST and ALT values [Table 1]. Peripheral blood smear showed leukocytosis with agglutination. Direct Coomb’s test was strongly positive. Her Mycoplasma pneumonia IgM was sent, which came positive with titer of 15.498 U (negative—<8, intermediate—8 to 12, positive—>12). Her serum heptaglobulin level was—223 U (NR 45—250 U/dL). She had an increase in the percentage of reticulocyte count with absolute reticulocyte count of 43,000/mm3 (26–126 K/µL). Final diagnosis of auto-immune hemolytic anemia secondary to Mycoplasma pneumonia was made. She was started on methyl prednisolone 40 mg intravenous twice daily. She was started on doxycycline 100 mg twice daily along with steroids and fluroquinolones. She required one packed red cell transfusion during the course of illness. She was given iron and folic acid supplementation. Her condition improved gradually with no further fall in Hb and normalization of liver function test [Table 1]. Left pleural pigtail catheter drained ~ 1.2 L yellow colored fluid, and once the daily drain was <10 mL, it was removed [Figure 2]. She was discharged in stable condition after 7 days of admission. She was continued on Levofloxacin 750 mg and Doxycycline 100 mg twice daily for total of 3 weeks. Her Mycoplasma IgM titer after 3 weeks of antibiotics was 8.487 U/mL. Six months later, she remains clinically well, with no recurrence of jaundice or anemia.
Figure 1: (a) Bilateral multiplobar consolidation and loculated pleural effusion. (b) and (c) CT chest showing right upper lobe and left lower lobe pneumonia with bilateral pleural effusion. (d) CT chest lung window showing bilateral multilobar consolidation

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Table 1: Serial laboratory values during the course of admission

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Figure 2: Chest X-ray at time of discharge showing resolution of effusion and pneumonia

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  Discussion Top

Mycoplasma pneumoniae is one of the most common causes of atypical pneumonia throughout the world.[1],[2]Mycoplasma pneumonia occurs in all age groups and is common in age group of 5–20 years. The most common presentation is symptoms of upper and lower respiratory tract infection.[3] The mode of transmission is inhalation of infected aerosols. It has an incubation period of two to three weeks, which is considerably longer than that of most other respiratory infections.[5] Infections with M. pneumoniae may occur throughout the year, with epidemics every few years. Infections in adults are often the result of contact with children as seen in our case.[6] The most common radiologic findings on chest radiograph are diffuse reticular infiltrates, unilateral hilar prominence, broncho pneumonia in perihilar regions or lower lobes usually with a unilateral distribution. Bilateral involvement may occur in 20% of cases.[7],[8] In one series by Pulziz et al.[9] pleural effusion was found in 8.84% of cases. Our patient had bilateral lobar pneumonia with bilateral pleural effusion. Clinical features are nonspecific and it is difficult to reliably distinguish M. pneumoniae from pneumoniae of any other etiology on the basis of it.[8] Extra pulmonary abnormalities can be an important part of Mycoplasma disease. These manifestations include skin rash, joint involvement, central nervous system, heart disease and hemolysis.[3],[4],[5] Our patient had sole extra-pulmonary manifestation in the form of auto-immune hemolytic anemia (AIHA). AIHA due to M. pneumoniae pneumonia is usually self-limiting and most patients recover with supportive care.[10],[11] Antibiotics have as such limited value; however, treatment of the underlying mycoplasma infection has been associated with more rapid resolution of the hemolytic process.[14] In the setting of an AIHA, packed red blood cell transfusions can potentiate hemolysis, and their use should be limited.[12] The coexistence of elevated serum levels of lactate dehydrogenase and bilirubin with low levels of haptoglobin is common in hemolytic anemia caused by cold agglutinins.[13] Our patient had all above mentioned features and probably the cause of hemolysis in our patient was mediated through cold agglutinin antibody. But unfortunately, we could not check the cold agglutinin level in our patient due to lack of availability of the test in our hospital.

The mainstays of medical therapy possible for M. pneumoniae infection are azithromycin, doxycycline, erythromycin, or a fluoroquinolone.[13] Our patient was treated with levofloxacin and doxycycline. She was transfused one unit of packed red cells. Reduction of antibody production in AIHA is achieved by steroids (1 mg/kg).[14] Although, the effect of steroids in cold agglutinin disease is often limited[14]; our patient responded well. Intravenous immunoglobulin (1 g/kg for 2 consecutive days) may alter immune activity by interacting with anti-Fc-antibodies. It may also increase the number of T-suppressor cells. Plasmapheresis is used mainly to remove antibodies from plasma mainly IgM, leading to a reduction of the rate of hemolysis.[15]

  Conclusion Top

Although M. pneumoniae infection rarely warrants hospital admission, our case demonstrates that the combination of hypoxia due to bilobular interstitial pneumonia with bilateral pleural effusion and clinically significant hemolysis, can be severe and even lead to admission to the ICU. In a country like India, when a patient comes with pneumonia and AIHA with jaundice, the first possibilities thought are malaria, dengue, or leptospirosis. We found an alternate cause in our patient. It is rightly said: “Eyes cannot see what mind does not know.” Mycoplasma pneumonia is rarely considered in differential diagnosis of community acquired pneumonia due to lack of suspicion. Mycoplasma pneumoniae infection should be considered early on in patients with AIHA and pneumonia. Mycoplasma IgM titer should be done for such cases.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Foy HM Infections caused by Mycoplasma pneumoniae and possible carrier state in different populations of patients. Clin Infect Dis 1993;17:S37-46.  Back to cited text no. 1
Marrie TJ, Peeling RW, Fine MJ, Singer DE, Coley CM, Kapoor WN Ambulatory patients with community-acquired pneumonia: The frequency of atypical agents and clinical course. Am J Med 1996;101:508-15.  Back to cited text no. 2
Kano Y, Mitsuyama Y, Hirahara K, Shiohara T Mycoplasma pneumoniae infection-induced erythema nodosum, anaphylactoid purpura, and acute urticaria in 3 people in a single family. J Am Acad Dermatol 2007;57:S33-5.  Back to cited text no. 3
Kottayam R, Rozenberg G, Cohn RJ Unusual haematologic manifestations of Mycoplasma pneumoniae infection. J Paediatr Child Health 2007;43:80-2.  Back to cited text no. 4
Luby JP Pneumonia caused by Mycoplasma pneumoniae infection. Clin Chest Med 1991;12:237-44.  Back to cited text no. 5
Bartlett JG, Mundy LM Community-acquired pneumonia. N Engl J Med. 1995;333:1618-24.  Back to cited text no. 6
Kashyap S, Sarkar M Mycoplasma pneumonia: Clinical features and management. Lung India 2010;27:75-85.  Back to cited text no. 7
Hsieh SC, Kuo YT, Chern MS, Chen CY, Chan WP, Yu C Mycoplasma pneumonia: Clinical and radiographic features in 39 children. Pediatr Int 2007;49:363-7.  Back to cited text no. 8
Pulziz I, Kuman I, Dakovic-Rode O, Sconwald N, Mise B Chlamydia pneumonia and Mycoplasma pneumoniae pneumonia: Comparison of clinical, epidemiological characteristics and laboratory profiles. Epidemol Infect 2006;134:548-55.  Back to cited text no. 9
Pereyre S, Guyot C, Renaudin H, Charron A, Bebear C, Bebear CM In vitro selection and characterization of resistance to macrolides and related antibiotics in Mycoplasma pneumoniae. Antimicrob Agents Chemother 2004;48:460-5.  Back to cited text no. 10
Tsuruta R, Kawamura Y, Inoue T, Kasaoka S, Sadamitsu D, Maekawa T Corticosteroid therapy for hemolytic anemia and respiratory failure due to Mycoplasma pneumoniae pneumonia. Intern Med 2002;41:229-32.  Back to cited text no. 11
Gertz MA Cold hemolytic syndrome. Hematol Am Soc Hematol Educ Progr 2006:19-23. doi: 10.1182/asheducation-2006.1.19.  Back to cited text no. 12
Pereyre S, Guyot C, Renaudin H, Charron A, Bebear C, Bebear CM In vitro selection and characterization of resistance to macrolides and related antibiotics in Mycoplasma pneumoniae. Antimicrob Agents Chemother 2004;48:460-5.  Back to cited text no. 13
Tsuruta R, Kawamura Y, Inoue T, Kasaoka S, Sadamitsu D, Maekawa T Corticosteroid therapy for hemolytic anemia and respiratory failure due to Mycoplasma pneumoniae pneumonia. Intern Med 2002;41:229-32.  Back to cited text no. 14
Geurs F, Ritter K, Mast A, Van Maele V Successful plasmapheresis in corticosteroid-resistant hemolysis in infectious mononucleosis: Role of autoantibodies against triosephosphate isomerase. Acta Haematol 1992;88:142-6.  Back to cited text no. 15


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