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Year : 2008  |  Volume : 51  |  Issue : 2  |  Page : 294-295
Cytomegalovirus pneumonia with pulmonary mucormycosis

Department of Pathology, M. S. Ramaiah Medical College, Bangalore, Karnataka, India

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Solid organ transplantation is becoming increasingly common in the treatment of end-stage organ failure. However, despite improvements in patient and allograft survival, immunosuppression-induced compromised cell-mediated immunity predisposes transplant recipients to opportunistic infections. We describe a case of mixed opportunistic lung infection in the form of cytomegalovirus pneumonia and mucormycosis in a renal transplant recipient. Prompt recognition and treatment of infection is imperative for successful transplantation.

Keywords: Cytomegalovirus, mucormycosis, pneumonia, post-transplant infections, renal transplantation

How to cite this article:
Mysorekar VV, Rao SG. Cytomegalovirus pneumonia with pulmonary mucormycosis. Indian J Pathol Microbiol 2008;51:294-5

How to cite this URL:
Mysorekar VV, Rao SG. Cytomegalovirus pneumonia with pulmonary mucormycosis. Indian J Pathol Microbiol [serial online] 2008 [cited 2020 Oct 24];51:294-5. Available from: https://www.ijpmonline.org/text.asp?2008/51/2/294/41704

   Introduction Top

Since the dawn of the age of transplantation, opportunistic infections have become common, as well as crucial, life-threatening complications in transplant recipients. Two major factors which affect the risk of infection among transplant patients are the environmental exposure to infective agents and the net immunosuppressive effect present. [1] Urinary tract infection ranks first in frequency, followed by pulmonary infection. [2] In one study, the incidence of pulmonary infections after kidney transplantation was 19%. [3]

We describe a case of mixed opportunistic lung infection in the form of cytomegalovirus (CMV) pneumonia and mucormycosis in a renal transplant recipient.

   Case History Top

A 29-year-old man who had received a renal transplant 3 months back and was on immunosuppressant therapy (cyclosporin with steroids) presented with fever and breathlessness of 1 week's duration. Chest X-ray showed consolidation of the entire right lung. Hematological investigations revealed leukopenia, the total leukocyte count being 3.8 10 9 /L, with severe neutropenia. The platelet count was 80 10 9 /L. Blood urea nitrogen (BUN) and serum creatinine levels were within normal limits, indicating that there were no signs of renal allograft rejection. The patient was seronegative for antibodies to CMV. As the right lung was found to be nonfunctional, pneumonectomy was performed and the specimen was sent for histopathological examination. Postoperatively, his renal parameters continued to be normal. The patient developed respiratory failure and expired on the second postoperative day. The relatives of the patient did not consent for an autopsy.

Pathological findings

The lung weighed 800 g and was firm in consistency. The external and cut surfaces showed multiple grayish white areas and foci of hemorrhage. Extensive areas of consolidation were present. Microscopic examination of the lung showed pulmonary edema, along with an interstitial and intra-alveolar inflammatory exudate composed of neutrophils, lymphocytes and macrophages. Scattered throughout were enlarged alveolar lining cells with intranuclear amphophilic-to-eosinophilic, prominent, sharply demarcated CMV inclusions. Many cells also showed intracytoplasmic inclusions, which appeared as clustered, small, granular, basophilic bodies [Figure 1]. Adjacent areas showed a large number of hyphae of mucor fungus, which appeared basophilic, broad, irregular, nonseptate with right-angled branching. The hyphae were also seen invading blood vessels which showed thrombi [Figure 2]. Large areas of hemorrhagic necrosis were seen in the lung tissue. A diagnosis of mixed opportunistic infection, viz., CMV pneumonia with mucormycosis, was made.

   Discussion Top

In spite of progress in transplantation procedures, infection remains a significant cause of morbidity and mortality in renal transplant recipients. Infections are most common during the first 6 months post-transplant. [1],[4] Data from blood donors and seroprevalence studies indicate that more than 50% of adults have been infected with CMV, with active excretion of the virus in about 10%. [5] CMV infection in the transplant recipient may occur by reactivation of latent endogenous infection during the immunosuppressed state. CMV is known to remain latent within leukocytes, which are the major reservoirs. [6] Alternatively, CMV infection in transplant patients may be acquired exogenously - from the environment, transfusions, or even the donor organ itself. [6]

Apart from the direct effects of invasive disease, CMV produces immunomodulatory effects, resulting in further immunosuppression and increased risk of other opportunistic infections. [7] Multiple mechanisms that play a role in CMV-induced immunomodulation have been suggested. [8] CMV impairs the ability of lymphocytes and monocytes to produce cytokines such as interleukin (IL)-1 and IL-2 and impairs the function of antigen-specific cytotoxic T lymphocytes and natural killer (NK) cells. CMV also impairs the oxidative respiratory burst and phagocytic function of macrophages. [8] CMV infection may induce a deleterious immunologic shift towards T helper cell-2 responses in the lung, [9] predisposing patients to invasive fungal infections. Thus in our patient, mucormycosis has occurred secondary to the immunosuppression caused by CMV and is likely to have been acquired within the hospital environment. Neutropenia, as seen in our patient, is a predisposing condition for mucormycosis. As an autopsy could not be performed, it is not known whether there were opportunistic infections in multiple organs.

Studies have proved that two paradoxical responses to CMV infections are seen in transplant patients. [6] In the relatively immunocompetent patient, the infection is associated with renal allograft rejection, a prompt antibody response to the virus and recovery. The severely immunosuppressed patient cannot make an antibody response, does not exhibit allograft rejection as a cause of renal malfunction, may be further immunosuppressed by the viral infection and is susceptible to sequential opportunistic infections leading to death. Our patient falls into the latter category.

The present case emphasizes the importance of early diagnosis and treatment of opportunistic infections in transplant recipients.

   References Top

1.Locnen SR, Pena AC, Abrihan-Arce Y, Cerezo CU. Infectious disease complications of renal transplantation at the University of the East Ramon Magsaysay Memorial Medical Center (UERMMMC). Phil J Microbiol Infect Dis 2000;29:119-22.  Back to cited text no. 1    
2.Rao KH, Jha R, Narayan G, Sinha S. Opportunistic infections following renal transplantation. Indian J Med Microbiol 2002;20: 47-9.  Back to cited text no. 2    
3.Jha R, Narayan G, Jaleel MA, Sinha S, Bhaskar V, Kashyap G, et al. Pulmonary infections after kidney transplantation. J Assoc Physicians India 1999;47: 779-83.  Back to cited text no. 3    
4.Fishman JA, Rubin RH. Infection in organ transplant recipients. N Eng J Med 1998;338:1741-51.  Back to cited text no. 4    
5.Hinrichs SH, Harrison CJ, Haggerty S. Viral diseases. In : Damjanov I, Linder J, editors. Anderson's Pathology. 10 th ed. St. Louis: Mosby; 1996. p. 886-950.  Back to cited text no. 5    
6.Simmons RL, Lopez C, Balfour H Jr, Kalis J, Rattazzi LC, Najarian JS. Cytomegalovirus: Clinical virological correlations in renal transplant recipients. Ann Surg 1974;180:623-32.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Kotton CN, Fishman JA. Viral infection in the renal transplant recipient. J Am Soc Nephrol 2005;16:1758-74.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Boeckh M, Nichols WG. Immunosuppressive effects of beta-herpesviruses. Herpes 2003;10:12-6.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Sparrelid E, Emanuel D, Fehniger T, Andersson U, Andersson J. Interstitial pneumonitis in bone marrow transplant recipients is associated with local production of TH2-type cytokines and lack of T cell-mediated cytotoxicity. Transplantation 1997;63:1782-9.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]

Correspondence Address:
Vijaya V Mysorekar
89, A.G.'s Office Colony, 5th Main, 6th Cross, New BEL Road, Bangalore - 560 054, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.41704

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