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CASE REPORT Table of Contents   
Year : 2010  |  Volume : 53  |  Issue : 3  |  Page : 555-557
A fulminant case of acute respiratory distress syndrome associated with Mycoplasma pneumoniae infection

Department of Microbiology, All India Institute of Medical Sciences, New Delhi-110 029, India

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Date of Web Publication22-Oct-2010


Acute respiratory distress syndrome (ARDS) caused by mycoplasmas is very rare. This report describes a severe case of atypical pneumonia due to M. pneumoniae in a formerly healthy young woman who developed high grade fever and cough leading to severe disseminated lung disease and finally to fatal ARDS. This case came into picture when killer atypical pneumonia, namely, SARS (severe acute respiratory syndrome), spread very fast from South-Asian countries to the rest of the world. Moreover, the clinical presentation and radiologic features of SARS bear resemblance to the syndrome of atypical pneumonia, which lead us to investigate this case into detail. We suggest that M. pneumoniae infections should be included in the differential diagnosis of pathogens causing ARDS, establishing an early diagnosis may have important therapeutic implications.

Keywords: Acute respiratory distress syndrome, atypical pneumonia, mycoplasma, M.pneumoniae

How to cite this article:
Chaudhry R, Tabassum I, Kapoor L, Chhabra A, Sharma N, Broor S. A fulminant case of acute respiratory distress syndrome associated with Mycoplasma pneumoniae infection. Indian J Pathol Microbiol 2010;53:555-7

How to cite this URL:
Chaudhry R, Tabassum I, Kapoor L, Chhabra A, Sharma N, Broor S. A fulminant case of acute respiratory distress syndrome associated with Mycoplasma pneumoniae infection. Indian J Pathol Microbiol [serial online] 2010 [cited 2021 Dec 7];53:555-7. Available from: https://www.ijpmonline.org/text.asp?2010/53/3/555/68283

   Introduction Top

M. pneumoniae is an important cause of community-acquired pneumonia. Although severe-to-life threatening courses of mycoplasma pneumonia appear to be rare, they can cause pulmonary disease such as ARDS as well as multiple organ failure. We describe a case of ARDS due to M. pneumoniae.

   Case Report Top

A 35-year-old female was referred to our hospital because of progressive respiratory distress. Ten days prior to admission she developed high-grade fever and cough, treated with steroids for two days by a private practitioner. Her condition deteriorated and she was admitted to a nursing-home where she was diagnosed as a case of bilateral pneumonia with sepsis, administered levofloxacin, amoxicillin+clavulanic acid and metronidazole and put on artificial ventilation. She deteriorated further and was admitted to our referral hospital intensive care unit (ICU) on 17 March 2003, in a disoriented, agitated and tachypnoeic state, coughing blood-tinged secretions. There was no history of travel to other South East Asian countries and contact with a patient of SARS could not be elicited. Her chest radiograph revealed diffuse bilateral infiltrates. The peripheral white blood cell (WBC) count was 15-20,000 cells / mm 3 with a markedly low absolute lymphocyte count (15-20 / mm 3 ). A battery of tests was performed on different samples received [Table 1]. The sera were also found to be highly reactive with recombinant P1 and P116 protein of M. pneumoniae (FH) as demonstrated by immunoblot analysis for specific IgG antibodies [Figure 1].
Table 1: Results of microbiological and molecular investigations performed

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Figure 1: Immunoblot analysis of purifi ed P1 or P116 protein with patient sera- Lane 1: Prestained standard protein marker, Lane 2: P1 (39.8kDa) recombinant protein detected using positive serum, Lane 3:P116 (27 kDa) recombinant protein detected using positive serum

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The patient's condition deteriorated further; she was put on full support ventilation and given intravenous clarithromycin, metronidazole, cefepime, cotrimoxazole and cefoperazone. Once mycoplasma infection was established, she was started on chloramphenicol as she did not respond to clarithromycin. Despite intensive treatment, she developed progressive respiratory and multiorgan failure. At this stage, her blood urea was 220 mg / dl, serum creatinine 4.2 mg / dl and serum bilirubin 4.2 mg / dl. She was started on inhalational NO 2 and activated-protein-C-alpha. Her condition deteriorated after a brief period of stabilization. Finally, she went into renal shut down, became hemodynamically unstable and arrested on the 10 th day of ICU stay. Post-mortem lung histopathology showed marked interstitial widening, edema, inflammation and focal destruction of alveolar spaces, intra-alveolar hemorrhage and prominence of Type II pneumocytes and fibrin deposition lining the alveolar space with congested blood vessels. Features were compatible with ARDS.

Once the patient was diagnosed, her husband complained of symptoms of fever and cough, tested positive for agglutinating antibodies to M. pneumoniae (1:1280) and his condition improved with clarithromycin. The six-year-old son of the patient, as well as three of the patient's close contacts were also investigated and showed significant M. pneumoniae agglutination titers of 1:80.

Subsequently, samples of first patient were also subjected to polymerase chain reaction (PCR) to rule out common respiratory pathogens including SARS [Figure 2]a, b.
Figure 2a: Profi le of ethidium bromide-stained agarose gel showing PCR products(176bp) of multiplex PCR: Lane 1= Marker 100bp, Lanes 2,5,6=Negative control, Lane 3= sample 1(BAL), Lane 4= Sample 2 (throat swab), Lane 7= multiplex PCR positive control for RSV (~600 bp), Influenza A (~100 bp) and B (~500 bp), Lane 8=Multi plex PCR positive control for MPV (440bp), PIV 1 (84 bp), PIV 2(~200 bp) and PIV 3 (~300 bp)
Figure 2b: Profi le of ethidium bromide- stained agarose gel showing PCR products(176bp) for SARS virus: Lane 1= Marker 100bp, Lane 2=Negative control, Lane3-5= Positive control (176bp), Lane 6= Sample
(BAL), Lane 7= Sample2 (throat swab)

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   Discussion Top

We describe a case of fulminant atypical pneumonia due to M. pneumoniae in a formerly healthy young adult. She had a complicated course and required mechanical ventilation. Diagnosis of atypical pneumonia is often difficult since culture or direct detection of the suspected pathogen is time consuming and not readily available. In most cases, confirmation of diagnosis is based on serologic methods, requiring high acute antibody titers or paired serum samples for definitive diagnosis. Diagnosis in the present case was also confirmed by serologic methods. In conformity with findings of Takiguchi et al.[1] leucocytosis was a characteristic finding in the present case too. Another finding was marked lymphopenia (15-20 cells / mm 3 ) which is seen in most cases of ARDS. We could not establish sufficient evidence suggesting a close correlation between the deterioration of mental status and the acute M. pneumoniae infection which could be a possible cofactor. It remains unclear whether these complications were caused by or coincided with the acute M. pneumoniae infection. Hitherto unknown pathogenic mechanisms, which most probably involve immunological cell-mediated tissue damage, may be responsible or it may be due to more virulent organism. Noriega et al.[2] suggested that the host's cellular immune response to M. pneumoniae played a central role in severe pneumonitis, due to release of supranormal levels of mediators that cause tissue damage from previously sensitized lymphocytes.

The lack of response to adequate therapy with high doses of macrolides could be attributed to a delay in initiation of treatment. It is known that treatment of M. pneumoniae is effective only when administered early in the course of disease. [3] The frequency of fulminant pneumonia due to M. pneumoniae is relatively rare despite high prevalence of M. pneumoniae infection in general population. We searched MEDLINE database for articles published on ARDS due to M. pneumoniae within the last 25 years and came across 10 such reports . [1],[4],[5],[6],[7],[8],[9],[10] These reports are from various parts of the world and include patients of all age groups. An important feature in all the studies, including the present one, is that the patients were previously healthy and diagnosed mainly by serology. However, titers as high as 1: 20, 480 as seen in the present case have not been reported previously. Outcome of clinical course is available in seven of them with fatal outcome in three. The case of twins reported from Japan clearly highlights the crucial role of early treatment in determining the clinical course of M. pneumoniae pneumonia. [4] Establishing an early diagnosis may have important therapeutic implications, although it remains possible that ARDS is induced by a reinfection and is the expression of increasing host immune response to the organism. Only a few studies in India have reported M. pneumoniae community-acquired pneumonia, [3] sufficient epidemiological data for incidence of severe M. pneumoniae infections is lacking.

Although M. pneumoniae infection is usually a benign self-limited disease, this case emphasizes its potentially serious nature even in normal healthy individuals. Also, M. pneumoniae infections should be included in the differential diagnosis of pathogens causing ARDS. Establishing an early diagnosis may have important therapeutic implications as suggested by the present case where the lung damage seems to have been induced early in the course of disease. Continuing studies which focus on the development of more sensitive and specific assays to detect M. pneumoniae infections and increase our understanding of the biology of this emerging human pathogen is essential.

   References Top

1.Daxboeck F, Eisl B, Burghuber C, Memarsadeghi M, Assadian O, Stanek G. Fatal Mycoplasma pneumoniae pneumonia in a previously healthy 18-year-old girl. Wien Klin Wochenschr 2007;12:379-84.   Back to cited text no. 1      
2.Noriega ER, Simberkoff MS, Gilroy FJ, Rahal JJ Jr. Life Threatening Mycoplasma pneumoniae pneumonia. JAMA 1974;229:1471-2.  Back to cited text no. 2  [PUBMED]    
3.Pandey A, Chaudhry R, Nisar N, Kabra SK. Acute Respiratory Tract Infections in Infections in Indian Children with Special Reference to Mycoplasma pneumoniae. J Trop Pediatr 2000;46:371-4.  Back to cited text no. 3      
4.Tanaka G, Nagatomo Y, Kai Y, Matsuyama M, Kuroki M, Sasaki T, et al. Mycoplasma pneumonia of identical twin sisters with different clinical courses depending on the treatment. Kansenshogaku Zasshi 2002;76:1040-4.   Back to cited text no. 4  [PUBMED]    
5.Halal F, Brochu P, Delage G, Lammarre A, Rivard G. Severe disseminated lung disease and bronchiectasis probably due to Mycoplasma pneumoniae. Can Med Assoc J 1977;117:1055-6.  Back to cited text no. 5      
6.Reigner P, Domenighetti G, Feihl F, Bonjour JP, Perret C. Acute respiratory distress syndrome after mycoplasma infection. Schweiz Med Wochenschr 1980;110:220-3.   Back to cited text no. 6  [PUBMED]    
7.Tomioka H, Umeda B, Nakai H. A case of adult respiratory distress syndrome likely due to measles and Mycoplasma pneumoniae. Kansenshogaku Zasshi 1992;66:1483-7.  Back to cited text no. 7  [PUBMED]    
8.Lo SC, Wear DJ, Green SL, Jones PG, Legier JF. Adult respiratory distress syndrome with or without systemic disease associated with infections due to Mycoplasma fermentans. Clin Infect Dis 1993;17:S259-63.  Back to cited text no. 8  [PUBMED]    
9.Shah DC, Muthiah MM. Adult respiratory distress syndrome due to Mycoplasma pneumonia. Postgrad Med J 1996;72:259-63.  Back to cited text no. 9      
10.Chian CF, Chang FY. Acute respiratory distress syndrome in Mycoplasma pneumoniae: a case report. J Microbiol Immunol Infect 1999;32:52-6.  Back to cited text no. 10  [PUBMED]    

Correspondence Address:
Rama Chaudhry
Department of Microbiology, All India Institute of Medical Sciences, New Delhi-110 029
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.68283

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  [Figure 1], [Figure 2]

  [Table 1]

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