Radiology of Infectious Diseases

: 2021  |  Volume : 8  |  Issue : 3  |  Page : 125--129

Fortuitous discovery of pulmonary tuberculosis in an asymptomatic, SARS-CoV-2 positive, Moroccan patient

Kaoutar Cherrabi, N Benmansour, NM El Alami 
 Department of ENT and Cervico-Facial Surgery, Fez, Morocco

Correspondence Address:
Dr. Kaoutar Cherrabi
Department Head and Neck Surgery, Hassan II Hospital, Fez


The COVID-19 pandemic has created worldwide change in screening, management, and deadlines for the treatment of tuberculosis, among other latent diseases. Safe access to health-care structures, drug interactions, and ongoing changes in treatment guidelines are the main challenges. The first published cohort of 45 patients with both tuberculosis and SARS-CoV-2 infection presented three different scenarios regarding the timing of these diagnoses, both diagnoses being made within the same week in only nine of these patients. Thus far, tuberculosis has not been shown to influence the pathophysiology of SARS-CoV-2 infection. The association between these two diseases may be incidental. Tuberculosis remains the leading lethal infection worldwide. 2In patients with preexisting pulmonary tuberculosis and COVID-19, management priorities, drug interactions, and optimal frequency of clinical, biological, and radiological check-ups require clarification. We here report an asymptomatic young patient who had both COVID-19 and pulmonary tuberculosis, raising challenging questions regarding diagnostic tools, treatment, and follow-up.

How to cite this article:
Cherrabi K, Benmansour N, El Alami N M. Fortuitous discovery of pulmonary tuberculosis in an asymptomatic, SARS-CoV-2 positive, Moroccan patient.Radiol Infect Dis 2021;8:125-129

How to cite this URL:
Cherrabi K, Benmansour N, El Alami N M. Fortuitous discovery of pulmonary tuberculosis in an asymptomatic, SARS-CoV-2 positive, Moroccan patient. Radiol Infect Dis [serial online] 2021 [cited 2022 Dec 4 ];8:125-129
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In morocco, SARS-CoV-2 pandemic has made the management of several chronic diseases difficult, especially tuberculosis. Limited data is available concerning de novo co-infection with tuberculosis and SARS-CoV2.[1],[2],[3],[4] With the pandemic reaching into countries where Tuberculosis-HIV co-infection have been creating a major public health issue, the installation of recommendations and consensuses is an imperative measure.

 Case Report

This 36-year-old patient was admitted for screening for SARS-CoV-2 infection after close contact with an infected family member.

On physical examination, he was eupnoeic and had right apical crackles. He was afebrile and had no evidence of hemodynamic abnormalities. Blood tests on admission showed evidence of inflammation, including a high white blood cell count of 17,000 with neutrophils = 12000, C-reactive protein = 236, and lactic acid dehydrogenase = 145 U/L. The patient had no preexisting conditions, including no diabetes mellitus, chronic obstructive pulmonary disease, or a family history of atopy.

Reverse transcription-polymerase chain reaction (RT-PCR) testing of a combined nasopharyngeal and oropharyngeal swab revealed positivity for SARS-CoV-2 RNA.

A thoracic computed tomography (CT) scan showed minor lesions compatible with SARS-CoV-2 infection in up to 50% of the pulmonary parenchyma. In addition, he had cavitating right apical lesions, which are not typical of SARS-CoV-2 infection but are typical of pulmonary tuberculosis [Figure 1], [Figure 2], [Figure 3].{Figure 1}{Figure 2}{Figure 3}

A sputum smear and Xpert Ultra assay were both positive for Mycobacterium tuberculosis. Ehrlich–Ziehl–Neelsen staining of a smear revealed acid-fast bacilli.

All individuals who had had close contact with the patient were screened for both COVID-19 and tuberculosis.

An initial fasting blood sugar was normal and a complete serology panel came back negative. There was no evidence of a compromised immune system or any other viral infection. A screening electrocardiogram and hepatic and renal blood tests showed no abnormalities.

After a multidisciplinary meeting, it was decided to postpone antibacterial treatment for a week. He was started on hydroxychloroquine 200 mg twice a day for one day and 200 mg daily for 9 days thereafter, azithromycin 500 mg for 1 day and 250 mg daily for 6 days thereafter, and preventive doses of enoxaparin sodium 4000 UI once a day, Vitamin C, and zinc. Routine blood tests were scheduled every 48 h.

The patient lacked energy, was anorexic, and lost five kilograms in weight in the first 2 weeks of hospitalization. There was no specific evidence of intolerance to treatment. An electrocardiogram was normal. Routine blood tests showed hepatic dysfunction with glutamic-oxaloacetic transaminase six times normal values, glutamate pyruvate transaminase six times normal values, gamma-glutamyl transferase three times normal values, and normal TP of 97%. No other biochemical abnormalities were noted.

Having achieved respiratory stability, hydroxychloroquine was stopped. With the completion of macrolide treatment, only vitamin therapy was continued with checking of hepatic function every 48 h until liver enzyme concentrations were normal.

Antibacterial treatment was started uneventfully. Twenty days after admission, RT-PCR testing of a combined nasopharyngeal and oropharyngeal swab for SARS-CoV-2 RNA was negative. The patient was transferred to a dedicated center for the treatment of patients with tuberculosis.


In Morocco, the COVID-19 pandemic has complicated the management of several chronic diseases, especially tuberculosis.

Limited data are available concerning de novo co-infection with tuberculosis and SARS-CoV-2.[1],[2],[3],[4] With the COVID-19 pandemic reaching countries in which tuberculosis–HIV co-infections have already created major public health issues, it is imperative that consensus is reached on recommendations for the management of combinations of infectious diseases.[5]

During previous coronavirus pandemics, co-infections with tuberculosis and SARS-CoV-1 and MERS-CoV were reported in 2003 and 2012, respectively.[6] More research into pathophysiological aspects and therapy of co-infections with tuberculosis and SARS-CoV-2 infections is required, data in this field remains limited.[1],[3]

Similarities between the transmission modes and symptoms of tuberculosis and COVID-19 have already been established.[1] In addition, there are theories about possible overlaps in physio-pathological mechanisms.[1]

The protective role of the previous bacillus-Calmette-Guérin vaccine on SARS-CoV-2 infection is still contentious.[4] The transient decrease in cellular immunity caused by SARS-CoV-2 and tuberculosis infections may account for this co-infection, either by leading to a new infection or reactivation of a latent one.[5] Further, experience with previous coronaviruses has highlighted correlations between this association and poor outcomes related to SARS-CoV-2.[6]

Approximately one in three people worldwide have latent tuberculosis infections.[7] Tuberculosis still has the highest mortality rate of all infectious diseases.[1] The presence of debilitating conditions like advanced age and comorbidities such as diabetes mellitus and chronic respiratory diseases contribute to the poor outcomes of co-infection with SARS-CoV-2.[2]

The combination of HIV infection and tuberculosis in patients with SARS-CoV-2 infection has a high death rate.[4] Infection disease control measures and contact tracing for SARS-CoV-2 infection and tuberculosis are similar. Additional measures for tuberculosis include appropriate treatment for active and latent forms, with the goal of making the tuberculosis noncontagious.[6],[8],[9]

The mild clinical course of our patient may be attributable to his youth and the absence of comorbidities.[2] The most curious aspects of our case are the total absence of symptoms and normal laboratory findings at the time of diagnosis.

Diagnosing a SARS-CoV-2 infection is frequently difficult in individuals who are HIV-positive.[1]

High C-reactive protein concentrations are found in 60% of such patients, high in 33%, and low albumin in 75%. However, lymphopenia (lymphocyte count >109/L) is the most frequent abnormality found in patients with SARS-CoV-2 infection (83%). Additionally, coagulopathy with a prolonged prothrombin time occurs in more than 5% of patients, mild thrombocytopenia in 30%, high D-dimer concentrations in 43%–60%, high alanine aminotransferase in 25%, high aspartate aminotransferase,[10] and high lactate dehydrogenase in 50%–60%. More severe abnormalities have been associated with super-infection. High D-dimer concentrations and lymphopenia are prognostic indicators.[11],[12]

Radiological imaging, specifically chest radiographs and CT, contributes to making a diagnosis and evaluation of disease severity.[6]

Typical imaging findings in SARS-CoV-2 pulmonary infection are ground-glass nodules, patchy consolidation, and interstitial abnormalities.[6] However, primary tuberculosis also occurs in adolescents and adults, the most frequent imaging findings being parenchymal lesions in the upper lobes or superior segments of the lower lobes, pleural effusion, and lymph node enlargement. Cavitation in areas of consolidation is typically found in adults with primary tuberculosis.[13]

The optimal tool for identifying SARS-CoV-2 is PCR performed on nasopharyngeal swabs, the sensitivity being 71%.[12] When false-negative findings are suspected, clinical, biological, and radiological data can contribute to making a definitive diagnosis.[10]

Tuberculosis is most frequently diagnosed by examination of sputum or broncho-alveolar lavage.[1],[6] In addition, staining for TB bacilli, phenotypic culture methods, and rapid diagnostic tests such as the GeneXpert test can be helpful.[1],[6]

While awaiting the development of a vaccine, control measures are required to control the spread of SARS-CoV-2.[6] However, implementation of lockdown may increase the risk of transmission of tuberculosis in close social gatherings.[9]

Conservative care, including oxygen therapy and monitoring of vital functions, are the mainstays of treatment in most patients. Dexamethasone may decrease mortality in patients who require oxygen and are symptomatic for more than a week.[10],[14]

The places of chloroquine and hydroxychloroquine remain contentious.[15] Hepatotoxicity related to administering chloroquine or hydroxychloroquine to patients with SARS-CoV-2 infection has been reported, making checks of hepatic function important throughout any such treatment.[16]

Several protocols have been proposed for treating SARS-CoV-2 infection. These include antibiotics such as azithromycin, antivirals such as ritonavir/lopinavir and darunavir/cobicistat, protease inhibitors[4] remdesivir,[9] anticoagulants such as enoxaparin,[4] and N-acetyl-cysteine.[4] Clinical trials are still ongoing.[1],[2],[4],[5],[10],[16]

The American Thoracic Society, Center for Disease Control and Prevention, and Infectious Diseases Society of America have jointly developed treatment guidelines for patients with drug-susceptible tuberculosis.[7]

These guidelines recommend an initial phase for treating tuberculosis comprising rifampicin 10 mg/kg (maximum 600 mg), isoniazid 5 mg/kg (maximum 300 mg), pyrazinamide 15–30 mg/kg (maximum 2 g), and ethambutol 15–20 mg/kg (maximum 1.6g) given daily for 8 weeks, followed by a continuation phase of isoniazid 15 mg/kg (maximum 900 mg) and rifampicin 10 mg/kg (maximum 600 mg) administered 2–3 times/week for 18 weeks.[7] Researchers investigating the treatment of COVID-19 and HIV infection recommend substituting rifabutin for rifampicin and considering antivirals such as ritonavir and lopinavir to minimize adverse effects, especially regarding liver function.[17] There are too few data on patients with mild forms of SARS-CoV-2 infection and tuberculosis to determine the benefit/risk balance.[3],[10] Assessing the clinical relevance of drug interactions requires further clinical studies.[10]

Early diagnosis and control of these two diseases are the main means of preventing transmission and decreasing the mortality and morbidity associated with this combination of infections.[1],[3],[10],[17]


The COVID-19 pandemic has reached countries in which tuberculosis is endemic. This combination has a poor prognosis depending on the extent of lesions and the presence of comorbidities. Controlling the spread of these two contagious conditions raises questions about diagnostic tools and timing, consensus on optimal therapy, evaluation of prognosis, and the management of contacts.

The most important features of our case are the mismatch between clinical and radiological presentations, hydroxychloroquine and azithromycin drug-induced hepatocellular toxicity, and the achievement of complete remission with no sequelae.


We thank Dr. Trish Reynolds, MBBS, FRACP, from Liwen Bianji (Edanz) (, for editing the English text of a draft of this manuscript.

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.

Ethic statement

Not applicable.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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