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 Table of Contents  
CASE REPORT
Year : 2020  |  Volume : 7  |  Issue : 2  |  Page : 88-91

Mycoplasma pneumoniae-induced cerebral venous sinus thrombosis with autoimmune hemolytic anemia


Department of Pediatrics, Bharati Hospital, Pune, Maharashtra, India

Date of Submission31-Jan-2020
Date of Decision07-Mar-2020
Date of Acceptance10-Mar-2020
Date of Web Publication10-Apr-2020

Correspondence Address:
Dr. Venkat Sandeep Reddy
Department of Pediatrics, Bharati Hospital, Pune, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JPCC.JPCC_20_20

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  Abstract 

Mycoplasma pneumoniae (MP) is a common organism causing pneumonia in school-going children. Although the disease is usually mild, it can rarely lead to severe extrapulmonary complications which may be life-threatening. We hereby report a case of an 8-year-old male child who presented with fever, cough, a maculopapular rash, and difficulty in breathing for 8 days who, after initially receiving treatment as community-acquired pneumonia with synpneumonic effusion, went on to develop severe autoimmune hemolytic anemia and cerebral venous thrombosis with features of vasculitis. With utilization of DNA polymerase chain reaction along with other laboratory parameters, the diagnosis of MP infection was made. The child was treated with oral clarithromycin, pulse dose methylprednisolone, low-molecular-weight heparin, and intravenous immunoglobulin while he also required mechanical ventilation, transfusions, and vasopressor support. He responded to these measures and survived with no neurological sequelae.

Keywords: Autoimmune hemolytic anemia, cerebral venous sinus thrombosis, low-molecular-weight heparin, methyl prednisolone, Mycoplasma pneumoniae


How to cite this article:
Deshpande S, Sarangi B, Reddy VS, Walimbe A. Mycoplasma pneumoniae-induced cerebral venous sinus thrombosis with autoimmune hemolytic anemia. J Pediatr Crit Care 2020;7:88-91

How to cite this URL:
Deshpande S, Sarangi B, Reddy VS, Walimbe A. Mycoplasma pneumoniae-induced cerebral venous sinus thrombosis with autoimmune hemolytic anemia. J Pediatr Crit Care [serial online] 2020 [cited 2020 May 31];7:88-91. Available from: http://www.jpcc.org.in/text.asp?2020/7/2/88/282219




  Introduction Top


Mycoplasma pneumoniae (MP) is a common cause of community-acquired pneumonia most frequently affecting school-going children. Extrapulmonary complications due to Mycoplasma are rare, most common being hematological manifestations such as hemolytic anemia. Central nervous system (CNS) manifestations such as meningoencephalitis, thrombosis, optic neuritis, transverse myelitis, and stroke have also been occasionally reported apart from dermatological, gastrointestinal, connective tissue, cardiac, ocular, and renal complications.

MP have specialized transmembrane proteins (e.g., P1 and P30) that help in adherence and gliding motility along the respiratory epithelium. These adherence proteins of MP have an affinity for respiratory tract epithelium, and after attachment, they produce hydrogen peroxide and superoxide radicals, causing injury to epithelial cells and cilia. The clinical manifestations of MP infection are determined by the immune competency and response of the host, indicating that some of the pathogenic features of MP infection, particularly extrapulmonary manifestations (e.g., hemolysis and encephalitis), are immune mediated. The antibodies produced against the glycolipid antigens of MP cross-react with human red cells and brain cells and may act as autoantibodies.


  Case Report Top


An 8-year-old male child was referred to our hospital with complaints of fever and cough for 8 days, maculopapular rash and difficulty in breathing for 2 days, and having received treatment for community-acquired pneumonia (intravenous [IV] ceftriaxone and oral doxycycline). Chest X-ray showed left lung consolidation with synpneumonic effusion [Figure 1]. Diagnostic tap revealed lymphocytic predominant cell count. On admission to our hospital, his sensorium was normal (Glasgow Coma Scale [GCS]: 15/15) with the only significant findings on examination being tachypnea (respiratory rate: 48/min), decreased oxygen saturation (90% in room air), mild intercostal retractions, and decreased air entry over the left side.
Figure 1: Chest X-ray done on admission

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Considering persistent pneumonia, the child was continued on oxygen therapy with injection piperacillin-tazobactam and injection vancomycin as antibiotic cover after sending cultures. Computed tomography chest showed consolidatory changes in both lungs predominantly on the left [Figure 2]. He continued to remain intermittently febrile with gradual improvement in respiratory findings and radiological improvement. On day 8 of admission, he was noticed to have significant pallor followed by a steady fall in his GCS score from 15/15 to 12/15 and subsequently to 10/15 over a period of 4 h. Examination revealed poor sensorium, tachycardia, and severe pallor with CNS examination showing signs of pyramidal tract dysfunction. On investigation, his hemoglobin had shown a fall from 9.1 g/dl to 2.1 g/dl [Table 1]. He was electively intubated and put on mechanical ventilation. Due to drastic fall in hemoglobin. suspecting hemolysis, direct and indirect coombs test were done which were both positive (4+) with cold agglutination. The child was transfused with packed cells of blood group O negative due to inability to cross-match compatible blood type, and IV methylprednisolone pulse therapy was started to suppress the autoimmune hemolysis. Magnetic resonance imaging (MRI) brain done showed thrombosis of the left transverse and sigmoid sinus, part of the left internal jugular vein, and partial thrombosis of the right transverse sinus with restricted diffusion in both frontal regions suggesting cytotoxic edema/venous infarcts [Figure 3].
Figure 2: Consolidatory changes noted on computed tomography

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Table 1: Laboratory investigations

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Figure 3: First magnetic resonance imaging brain showing thrombosis of the left transverse and sigmoid sinus, visualized part of the left internal jugular vein, and partial thrombosis of the right transverse sinus

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With evidence of vasculitis on MRI, IV immunoglobulin (IVIG) (at 2 g/kg) was also added along with low-molecular-weight heparin. Considering possible causes for hypercoagulability and the child's clinical presentation, polymerase chain reaction (PCR) of tracheal aspirate for MP was done and was positive while blood specimen tested positive for Mycoplasma IgM antibodies. Following this, oral clarithromycin was added. Antiphospholipid antibodies (beta-2 glycoprotein-1 IgM) and cardiolipin antibody anticardiolipin (ACL) IgM were found to be positive. The child responded to the above measures, and his sensorium improved. He was extubated after 4 days of ventilation. Repeat MRI brain done after 10 days showed findings similar to previous MRI with near-total recanalization of the right transverse sinus [Figure 4] and [Figure 5]. Serial investigations showed reducing evidence of hemolysis. The child was discharged on oral steroid and clarithromycin after complete clinical resolution of respiratory and neurological signs with a plan to repeat thrombotic workup after 3 months.
Figure 4: Repeat magnetic resonance imaging showing near total recanalization of the right transverse sinus. Few collateral vessels are seen along the surface of the sinus

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Figure 5: Repeat magnetic resonance imaging brain showing hyperintense signals on T2- and fluid-attenuated inversion recovery images

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  Discussion Top


MP, acquired through respiratory secretions of an infected person, usually presents with symptoms including fever, malaise, sore throat, and cough and becomes noticeable after the first 1–3 weeks of exposure. Often referred to as “walking pneumonia,” most cases of MP are uncomplicated. However, extensive pulmonary disease in the form of massive lobar pneumonia with pleural effusions as well as necrotizing pneumonia has been reported.[1],[2],[3] Pleural fluid data available from these reports have shown the pleural effusion to be lymphocyte predominant rather than polymorphonuclear leukocyte predominant as was the case with our child. While all of these children have protracted periods of fever and respiratory distress, early-stage diagnosis is difficult due to the lack of obvious symptoms.

MP can be detected by PCR, including multiplex PCR panels which can be performed rapidly and have a high sensitivity and specificity. They can be done on a respiratory specimen (e.g., nasopharyngeal or throat swab). The yield from cerebrospinal fluid is low. Culture can take as long as 3 weeks and does not take on gram stain as it lacks a cell wall. If PCR is not available, MP IgM and IgG enzyme immunoassay can be done.

Drugs used in treatment include erythromycin, azithromycin, clarithromycin, tetracyclines, chloramphenicol, aminoglycosides, and quinolones. The most commonly used is azithromycin given at 10 mg/kg/day on day 1, followed by 5 mg/kg/day for 4 days, while clarithromycin at 15 mg/kg/day is administered every 12 h for 10 days.[4]

Among the various extrapulmonary manifestations, hemolytic anemia has been frequently associated with MP pulmonary infection.[5] Steroids have been used in the management of encephalitis and hemolytic anemia. Splenectomy may be necessary if there is no response to steroids or if the remission is not maintained when the dose of prednisolone is reduced. Immunosuppressive drugs such as azathioprine and cyclophosphamide may be effective. Thrombosis occurs as a part of extrapulmonary complications and responds to anticoagulation. MP is known to cause prothrombotic state leading to the positivity of antiphospholipid antibodies. Antibody titers during the active infection and at a later date (~3 months) help to differentiate underlying autoimmune conditions from MP-related prothrombotic state.

IVIG (at 2 g/kg) has been used successfully in refractory MP infection, especially when there is suspicion of an autoimmune process with reports showing neurological improvement occurring within 48 h of administration of IVIG.[6],[7] Plasmapheresis remains another therapeutic intervention.[8]

In MP infections and other viral infections, lupus anticoagulant, ACL antibodies, and beta-2 glycoprotein antibody can be present transiently and require to be documented after a period of 3 months to confirm the prothrombotic state secondary to the infection.[9]


  Conclusion Top


Although often benign, MP can present with severe pulmonary and extrapulmonary complications. Newer diagnostic techniques such as DNA PCR for Mycoplasma for direct detection of the antigen are proving useful for rapid etiological diagnosis. Treatment of complications such as autoimmune hemolytic anemia includes administration of steroids while the CNS complications warrant the use of IVIG and plasmapheresis. Underlying autoimmune conditions should be differentiated from MP-related prothrombotic state by repeating antibody titers after a 3-month period.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Matsumoto M, Nagaoka K, Suzuki M, Konno S, Takahashi K, Takashina T, et al. An adult case of severe life-threatening Mycoplasma pneumoniae pneumonia due to a macrolide-resistant strain, Japan: A case report. BMC Infect Dis 2019;19:204.  Back to cited text no. 1
    
2.
Jo SY, Na KW, Kim SW, Hwang YH. Mycoplasma pneumoniae-associated necrotizing pneumonia in children: A case-report. Kosin Med J 2019;34:57-64.  Back to cited text no. 2
    
3.
Cha SI, Shin KM, Jeon KN, Yoo SS, Lee J, Lee SY, et al. Clinical relevance and characteristics of pleural effusion in patients with Mycoplasma pneumoniae pneumonia. Scand J Infect Dis 2012;44:793-7.  Back to cited text no. 3
    
4.
Costagliola ML. Pediatric Respiratory Diseases. In: Community-acquired pneumonia. Cham: Springer; 2020. p. 299-307.  Back to cited text no. 4
    
5.
Bell A, Hughes J, Williams C, Knox S. G547(P) Oh my… a very unusual coincidence! the case of a boy who developed haemolysis following a trip to the swimming pool. Archives of Disease in Childhood 2019;104:A221.  Back to cited text no. 5
    
6.
Attilakos A, Palaiologou P, Lagona E, Voutsioti A, Dinopoulos A. Mycoplasma pneumoniae encephalopathy: Recovery after intravenous immunoglobulin. Pediatr Neurol 2008;38:357-9.  Back to cited text no. 6
    
7.
Daba M, Kang PB, Sladky J, Bidari SS, Lawrence RM, Ghosh S. Intravenous immunoglobulin as a therapeutic option for Mycoplasma pneumoniae encephalitis. J Child Neurol 2019;34:687-91.  Back to cited text no. 7
    
8.
Hanzawa F, Fuchigami T, Ishii W, Nakajima S, Kawamura Y, Endo A, et al. A 3-year-old boy with Guillain-Barré syndrome and encephalitis associated with Mycoplasma pneumoniae infection. J Infect Chemother 2014;20:134-8.  Back to cited text no. 8
    
9.
Wang Chun K, See Wan Y, Poon Chuen W. Transient presence of lupus anticoagulant associated with Mycoplasma pneumonia. Asian Cardiovasc Thorac Ann 2016;24:286-7.  Back to cited text no. 9
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
 
 
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