Unraveling Complexity: Mycoplasma Pneumonia Complicated by Hemolytic Anemia, Renal Failure, and Venous Thromboembolism; A Case Report

doi:10.21203/rs.3.rs-5103871/v1

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Case Report

Unraveling Complexity: Mycoplasma Pneumonia Complicated by Hemolytic Anemia, Renal Failure, and Venous Thromboembolism; A Case Report

https://doi.org/10.21203/rs.3.rs-5103871/v1

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Introduction:

Mycoplasma pneumoniae, a common respiratory pathogen, is a leading cause of atypical pneumonia, often presenting with a nonproductive cough, fever, and malaise. While typically causing mild upper respiratory symptoms, M. pneumoniae can lead to severe complications, including hemolytic anemia, acute renal failure, and venous thromboembolism. These complications are relatively uncommon but highlight the pathogen's capacity to affect multiple organ systems. Here, we present a rare and complex case of M. pneumoniae infection complicated by hemolytic anemia, renal failure, and venous thromboembolism in an adult patient.

Case Presentation:

A 58-year-old man with no prior comorbidities presented to the emergency department (ED) with complaints of fever for 12 days, cough, shortness of breath, and generalized fatigue for 10 days. On examination, he was icteric and exhibited coarse breath sounds, and his urine was dark in colour. Despite an initial treatment regimen consisting of ceftriaxone, doxycycline, and methylprednisolone, the patient's condition deteriorated. Investigations revealed pneumonia, hemolytic anemia, and acute renal failure. A respiratory panel identified mycoplasma pneumoniae leading to a diagnosis of complicated mycoplasma pneumonia; his antibiotic regimen was subsequently to azithromycin. The patient was discharged after a week but returned the same day with symptoms indicative of venous thromboembolism. Further evaluation revealed bilateral venous thrombosis and bilateral acute pulmonary embolism, necessitating heparin anticoagulation and a subsequent transition to oral apixaban therapy. The patient was stabilized and discharged, with no complications noted at follow-up.

Discussion

This case underscores the rare but potentially severe extrapulmonary manifestations of M. pneumoniae infection. Hemolytic anemia associated with this pathogen is believed to be due to cold agglutinin antibodies targeting erythrocyte antigens, while renal failure may result from acute tubular injury secondary to hemolysis. Venous thromboembolism, although rare, is increasingly recognized as a complication of M. pneumoniae, particularly in cases where vascular endothelium is directly affected or systemic hypercoagulability is induced.

Conclusion

This case illustrates the complexity of diagnosing and managing severe complications of M. pneumoniae infection, including hemolytic anemia, renal failure, and venous thromboembolism. Early recognition and appropriate management of these complications are crucial to improving patient outcomes and avoiding fatal sequelae.

Mycoplasma Pneumoniae

Deep Venous thrombosis

Pulmonary Embolism

Hemoglobinuria

Renal Failure

Hemolytic Anemia

Reticulocytosis

Case Report

Complications

Mycoplasma pneumoniae is a respiratory pathogen initially known as an “Eaton agent," causing disease of varied severity and being the most important causative organism for atypical pneumonia. With a size of only 150–350 nm, mycoplasmas are the smallest free-living organisms. M. pneumonia occurs worldwide with no seasonal pattern. Infection is acquired by inhalation of aerosols, with an incubation period of 2–4 weeks. M. pneumonia accounts for ~ 23% of cases of community-acquired pneumonia in adults. It primarily affects young adults with no underlying disease [1, 2, 3, 4]. M. pneumonia is infrequent, and an enhanced host cellular immune response is considered as the reason for the development of severe cases. M. pneumonia causes small airways disease, including cellular bronchiolitis and obliterans, with or without organizing pneumonia [3, 5, 6, 7]. Acute M. pneumonia infection manifests as a nonspecific upper respiratory syndrome with pharyngitis, tracheobronchitis, and wheezing. The most common presenting symptom is a nonproductive cough. Headache, malaise, chills, and fever are common [8]. Extrapulmonary manifestations of M. pneumonia infection are relatively uncommon but include acute renal failure, neurologic manifestations (e.g., encephalitis, Guillain-Barré syndrome), and hematologic manifestations (e.g., hemolytic anaemia, coagulopathies) [9, 10]. One of the extra-respiratory symptoms linked to an infection with Mycoplasma pneumoniae is thrombosis [11]. The number of case reports of thrombosis linked to Mycoplasma pneumoniae infection is rising as our understanding of the condition deepens [12, 13]. Thrombosis is a leading global cause of death and disability. While venous thromboembolism is linked to endothelial dysfunction and blood stasis, which results in fibrin- and erythrocyte-rich thrombus, arterial thrombosis is typically associated with plaque rupture, which causes platelets to form platelet-rich clots [14, 15]. Thrombosis may develop in a different area of the body after contracting Mycoplasma pneumoniae, which might occasionally have an impact on the prognosis of the illness [16, 17].

Here, we report a complicated presentation of mycoplasma pneumonia in a young adult who has a history of pneumonia but with no known comorbidities. This case report emphasizes the challenges in diagnosis and treating the complications induced by Mycoplasma pneumoniae infection in order to understand complications better. This case report adheres to the CARE 2013 Guidelines [18].

A 58-year-old man with no known comorbidities presented to our ED with complaints of fever for 12 days, shortness of breath, cough, and generalized fatigue for 10 days. According to the patient, he was in his usual state of health until 12 days ago, when he felt feverish but initially disregarded it, as his family was experiencing similar symptoms. His condition worsened after five days, leading him to contact his primary care physician, who ruled out COVID-19 and ordered a rapid strep test, which returned positive. He was subsequently prescribed antibiotics and benzonatate, but there was no improvement in his condition. After further assessment by his primary care physician, a chest X-ray revealed pneumonia, and he was advised to monitor his condition at home using a pulse oximeter. His oxygen saturation levels were marginal, dropping as low as 89% with movement but occasionally recovering to 95%. As his condition continued to worsen, he presented to the ED. Upon physical examination, the patient had a temperature of 98.4°F (36.9°C), a heart rate of 73 beats per minute, a respiratory rate of 18 breaths per minute, blood pressure of 156/80 mm Hg, and transcutaneous oxygen saturation of 96% without oxygen administration. He exhibited coarse breath sounds, and his skin was icteric. Additionally, his urine appeared black with a reddish tinge.

Routine blood tests revealed anemia, leukocytosis, thrombocytosis, reticulocytosis, and acute renal failure with a creatinine level of 6 mg/dl (see Table 1). An abnormal urinalysis was also noted (see Table 2). A computed tomography (CT) scan of the chest revealed extensive lingular and left lower lobe pulmonary infiltrates, suggestive of pneumonia (see Fig. 1). An abdominal ultrasound indicated a coarse liver texture with mild increased echogenicity. The patient was empirically treated with ceftriaxone, doxycycline, methylprednisolone, pantoprazole, fluticasone inhalations, and subcutaneous heparin. On the second day of admission, he experienced an episode of bloody diarrhea, and his complete blood count showed a hemoglobin level of 6.4 g/dL. He was subsequently transfused to maintain hemoglobin levels above 7 g/dL.

Table 1

Blood tests showing anemia, leukocytosis, thrombocytosis, reticulocytosis, and acute renal failure with a high creatinine level.
Complete blood count with differential
WBC	23.18×10^3/µl
Hb	11.0 g/dl
Hematocrit	31.8%
Platelet count	539×10^3/µl
RBC	3.35×10^6/µl
MCV	94.9 fL
MCH	32.8 pg
MCHC	34.6 g/dl
nRBC %	0.1/100 WBC
Absolute nRBC	0.02×10^3/µl
Preliminary absolute neutrophil count	17.45×10^3/µl
Neutrophils	75.3%
Lymphocytes	12.9%
Monocytes	5.9%
Eosinophils	0.6%
Basophils	0.5%
Immature granulocytes	4.8%
Absolute neutrophils	17.45×10^3/µl
Lymphocytes absolute	2.98×10^3/µl
Absolute monocytes	1.37×10^3/µl
Absolute Eosinophils	0.14×10^3/µl
Absolute basophils	0.12×10^3/µl
Absolute immature granulocytes	1.12×10^3/µl
Reticulocyte count	2.2%
Automated absolute reticulocyte count	0.0287×10^6/µl
Immature retic fraction	18.9%
Comprehensive Metabolic Profile
Glucose	86 mg/dl
BUN	56 mg/dl
Creatinine	6.0 mg/dl
Sodium	134 mEq/l
Potassium	6 mEq/l
Chloride	105 mEq/l
CO2	19 mEq/l
Calcium	8.7 mEq/l
GFR	10.2 ml/min/1.73 m^2
AST	21 U/l
ALT	28 U/l
ALP	71 U/l
Albumin	3.3 g/dl
Total protein	6.3 g/dl
Globulin	3.0 g/dl
Total bilirubin	0.4 mg/dl

Table 2

Showing an abnormal urinalysis.
Urinalysis
Urine colour	red
Urine clarity	Hazy
Urine specific gravity	1.016
Urine pH	6.5
Urine leucocyte esterase	trace
Urine nitrite	negative
Urine protein	2+
Urine Glucose	negative
Urine urobilinogen	4.0 mg/dl
Urine bilirubin	negative
Urine blood	large
RBC	0–2/hpf
Urine WBC	0–5/hpf
Urine squamous epithelial cells	0–5/hpf

Further testing, including a Group A Streptococcus rapid antigen test, glucose-6-phosphate dehydrogenase assay, mononucleosis screen, COVID-19 test, influenza test, urine Legionella antigen test, and hepatitis A, B, and C serology, all returned negative results. His haptoglobin levels were below 8 mg/dl, and the direct Coombs test was positive for the presence of non-specific cold antibodies. The respiratory panel confirmed the presence of Mycoplasma pneumonia. Complement levels were normal, and the workup for antinuclear antibodies returned negative results. He was ultimately diagnosed with Mycoplasma pneumonia complicated by hemolytic anemia and renal failure. His antibiotic regimen was changed to azithromycin. He was medically stabilized and discharged a week later on oral antibiotics.

The patient returned to the emergency room the same day after discharge, reporting dizziness and lightheadedness. Upon arrival, he was tachycardic, with a heart rate of 107 beats per minute, and hypotensive, with a systolic blood pressure of 86 mm Hg. He was saturating only 88% on 2 litres of nasal cannula oxygen. Laboratory results revealed a hemoglobin level of 6.0 g/dL, leukocytosis with a white blood cell count of 16.86 x 10^3/µL, a sodium level of 133 mEq/L, a procalcitonin level of 0.32 ng/mL, total bilirubin of 6.4 mg/dL, direct bilirubin of 2.1 mg/dL, blood urea nitrogen (BUN) of 32 mg/dL, creatinine of 1.4 mg/dL, a glomerular filtration rate (GFR) of 58.3 mL/min/1.73 m², and a D-dimer level of 29.03 µg/mL. Urinalysis indicated hemoglobinuria (see Table 3), and an ultrasound showed bilateral peroneal and soleus venous thrombosis. A CT angiogram of the chest revealed acute pulmonary embolism (PE) (see Fig. 2). He was started on heparin, and his hemoglobin and hematocrit were monitored closely. The infectious disease team recommended completing a two-week course of azithromycin. He was weaned off the nasal canula once stabilized, and his anticogualtion was changed to apixaban. He was discharged after four days of hospitalization with a prescription of apixaban 5 mg daily and advised to follow up in four days. During the follow-up visit, he reported feeling well.

Table 3

Urinalysis indicating hemoglobinuria.
Urinalysis
Urine Color	Yellow
Urine Clarity	Clear
Urine Specific Gravity	1.025
Urine pH	6.0
Urine Leukocyte Esterase	Negative
Urine Nitrite	Negative
Urine Protein	1+
Urine Glucose	1+
Urine Ketones	Negative
Urine Urobilinogen	3.0 mg/dL
Urine Bilirubin	Negative
Urine Blood	Large
RBC, UA	3–5/hpf
Urine WBC	0–5/hpf
Urine Squamous Epithelial Cells	0–5/hpf
Urine Mucus	Present

Mycoplasma pneumonia typically causes upper respiratory tract infections but can also cause pneumonia, making it one of the most common causes of atypical pneumonia in the United States [19]. Even if there is no respiratory illness, approximately 25% of patients may experience extrapulmonary complications [3]. Many extrapulmonary infections have been linked to M pneumoniae infections, including pericarditis, myocarditis, venous thromboembolism, aseptic meningitis, encephalitis, transverse myelitis, hemolytic anaemia, erythema nodosum, myalgia, septic arthritis, hepatitis, and glomerulonephritis [19]. To our knowledge, these cases have been reported separately. This is the first case to report mycoplasma pneumonia complicated by hemolytic anaemia, renal failure, and venous thromboembolism, three complications in the same patient. Mycoplasma pneumoniae-associated cold agglutinin antibody hemolytic anaemia is classified as an autoimmune disorder. It is caused by cold agglutinin antibodies that target the I antigen. This is a carbohydrate antigen found on both erythrocytes and respiratory epithelial cells, where it serves as a receptor for mycoplasma infection. Mycoplasma's interaction with the receptor, in which the microbe acts as an adjuvant, is most likely responsible for the formation of antibodies against the I antigen [20]. Antibodies against Sia-b1 on erythrocytes have also been reported, and the presence of antibodies directed at both of these epitopes is thought to be highly specific for M. pneumoniae infection [21]. In our case, a positive direct Coombs test with the presence of nonspecific cold antibodies, reticulocytosis, decreased haptoglobin and continuously dropping haemoglobin confirmed the hemolysis. In our patient, hemolytic anaemia was complicated by acute kidney injury. Mycoplasma infection can cause a variety of tubulointerstitial nephritis and glomerulonephritis, including mesangioproliferative glomerulonephritis, endocapillary proliferative glomerulonephritis, and acute tubular injury [22, 23]. In our case glomerulonephritis was ruled out by normal complement levels and no red blood cell casts in urinalysis. Increased creatinine and BUN were due to acute kidney injury. The pathophysiology of acute tubular injury during intravascular hemolysis is due to accumulation of heme and heme proteins in the tubules [24], as evidenced by reddish urine, positive blood on urinalysis, and proteinuria which is possibly due to haemoglobin excretion. Two cases of hemolytic anemia complicated by acute kidney injury during the course of mycoplasma infection have been reported in 1980 and 2017 [25, 26]. Thromboembolism is a rare complication of mycoplasma and is more common in children than adults [27]. Recent studies have supported the link between infection and thromboembolism. Thromboembolism can be caused by a variety of pathogens, including viruses, as demonstrated during the COVID-19 pandemic [28]. In a case series conducted in children in 2023, pulmonary vascular thromboembolism was most common in 35 of 49 cases and 13 had in other anatomic locations. The majority of pulmonary artery embolism cases were in situ pulmonary artery thrombosis (ISPAT), not classic thromboembolic PE, These indicated that the vasculitis caused by the direct invasion contributed to the local thromboembolism [27]. Without causing systemic hypercoagulability, Mycoplasma pneumonia may directly cause local thrombosis occlusion by impacting the vascular wall [29]. During an autopsy on a patient who had suffered an acute myocardial infarction, it was discovered that the unstable segments of the intima contained Mycoplasma pneumoniae [30]. Furthermore, thrombotic vessel occlusion may be caused by systemic hypercoagulability resulting from the activation of chemical mediators, such as complement [29]. In our case, the patient had bilateral lower extremity thrombosis complicated by acute pulmonary embolism, as venous thromboembolism can be due to many factors, but all were ruled out as patient was not immobilised for a long time, had no family history of thromboembolism, and had no congenital protein C or S deficiency and was on a heparin anticoagulation profile.

This case highlights the importance of considering Mycoplasma pneumoniae as a potential cause of severe extrapulmonary manifestations, including hemolytic anemia, acute renal failure, and venous thromboembolism. Comprehensive diagnostic evaluation and prompt therapeutic intervention are essential in managing these complex cases to prevent significant morbidity and mortality. This report adds to the growing body of evidence on the multifaceted nature of Mycoplasma pneumoniae infection, emphasizing the need for heightened clinical awareness and a multidisciplinary approach in cases with atypical presentations.

emergency department

computed tomography

BUN

blood urea nitrogen

GFR

glomerular filtration rate

pulmonary embolism

ISPAT

in situ pulmonary artery thrombosis

Funding: The authors received no financial support for the research, authorship, and/or publication of this article.

Competing Interests: The authors declared no potential conflicts of interest concerning the research, authorship, and/or publication of this article.

Ethical Approval: Ethical approval is not applicable since we do not disclose any patients’ information.

Consent to Participate: Informed consent was obtained from the patient’s parents for participation.

Consent for publication: Written consent was obtained from the patient for publication of this case report and accompanying images.

Availability of data and materials: Not applicable.

Code Availability: Not applicable.

Author Contributions: Data collection was done by AK, HM, SK and ZZ. Literature Review and Manuscript writing was done by AK, HM, SK, ZZ, SO and MF. Review-Editing was done by AK, and SO. Referencing and formatting were done by AK and SO.

Acknowledgments: None to Declare.

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No competing interests reported.

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Unraveling Complexity: Mycoplasma Pneumonia Complicated by Hemolytic Anemia, Renal Failure, and Venous Thromboembolism; A Case Report

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Abstract

Introduction:

Case Presentation:

Discussion

Conclusion

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Introduction

Case presentation

Discussion

Conclusion

Abbreviations

Declarations

References

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