Abstract
Background
Cervicofacial cellulitis (CCF) is a severe deep neck infection involving the cervical fascial spaces, most commonly of odontogenic origin. It may rapidly extend to adjacent compartments and lead to life-threatening complications such as mediastinitis, necrotizing fasciitis, and septic shock. In immunocompromised patients, particularly those infected with human immunodeficiency virus (HIV), the clinical course may be more aggressive due to impaired cellular immunity.
Aim
This study aims to report two cases of severe cervicofacial cellulitis revealing previously undiagnosed HIV infection and to emphasize the importance of early diagnosis and multidisciplinary management.
Cases
We describe two patients who presented with extensive cervicofacial cellulitis complicated by mediastinal extension and systemic involvement. Both required urgent contrast-enhanced computed tomography, broad-spectrum intravenous antibiotics, and extensive surgical drainage. In the first case, the infection progressed to septic shock and necrotizing fasciitis. The causal tooth was extracted during surgery. Microbiological cultures isolated Klebsiella pneumoniae and α-hemolytic Streptococcus. In both cases, HIV infection was diagnosed during hospitalization.
Conclusion
Cervicofacial cellulitis may represent the first clinical manifestation of undiagnosed HIV infection. Severe or atypical deep neck infections should prompt systematic HIV screening. Early imaging, targeted antimicrobial therapy guided by microbiological findings, and coordinated surgical and medical intervention are essential to improve patient outcomes.
Keywords: Cervicofacial cellulitis, HIV, Immunosuppression, Mediastinitis, Odontogenic infection
Introduction
Cervicofacial cellulitis (CCF) is a severe form of deep neck infection characterized by diffuse inflammation and suppuration of the cervical fascial planes, with the potential for rapid progression to deep cervical spaces, necrotizing soft-tissue infection, and mediastinal extension if not promptly recognized and treated [1], [2]. Odontogenic infections represent the most common etiology, particularly those originating from mandibular molars, whose anatomical proximity to the submandibular and parapharyngeal spaces facilitates rapid spread [3]. In severe cases, infection may evolve into necrotizing fasciitis and descending necrotizing mediastinitis, both of which are associated with substantial morbidity and mortality and require urgent surgical and medical management.
Human immunodeficiency virus (HIV) infection causes progressive impairment of cell-mediated immunity, increasing susceptibility to severe, rapidly progressive, and polymicrobial bacterial infections [4]. Clinical studies have demonstrated that immunocompromised patients, particularly those with HIV infection, are at increased risk of extensive deep neck infection, mediastinal extension, necrotizing complications, prolonged hospitalization, and mortality compared with immunocompetent individuals [5], [6], [7]. Despite advances in cross-sectional imaging, antimicrobial therapy, and surgical techniques, HIV-associated deep neck infections remain diagnostically and therapeutically challenging, particularly when the underlying immunosuppression has not yet been recognized [5].
Although cervicofacial cellulitis has been reported as an initial presentation of previously undiagnosed HIV infection [6], [8], the occurrence of exceptionally severe necrotizing cervicofacial infection in this setting, particularly when associated with necrotizing fasciitis, polymicrobial infection, and descending necrotizing mediastinitis, represents a clinically challenging presentation. The identification of organisms such as Klebsiella pneumoniae in a polymicrobial infection further illustrates the complexity of bacterial infections that may occur in the context of unrecognized immunosuppression. Moreover, severe infection may precede the recognition of HIV status, highlighting the importance of considering underlying immunodeficiency when the extent or progression of a cervicofacial infection appears disproportionate to the initial clinical presentation.
The present report describes two patients presenting with severe cervicofacial infections as the first clinical manifestation of previously undiagnosed HIV infection, characterized by necrotizing complications, polymicrobial infection including Klebsiella pneumoniae, and, in particular, descending necrotizing mediastinal extension. By reporting these cases from an African tertiary-care setting, we aim to highlight the diagnostic challenges associated with delayed recognition of HIV infection and to emphasize the importance of early imaging, microbiological investigation, aggressive surgical source control, appropriate antimicrobial therapy, and coordinated multidisciplinary management involving otorhinolaryngology, surgery, intensive care, radiology, microbiology, and infectious diseases.
Case presentation
A. Case 1
A 45-year-old man from sub-Saharan Africa presented to the emergency department with a painful cervical swelling and high-grade fever for six days, following dental pain self-treated with non-steroidal anti-inflammatory drugs. He had no known medical history. On admission, the patient was confused. Clinical examination revealed an indurated, tender swelling extending from the right submandibular region to the anterior cervical area and spreading to the upper chest, with multiple fistulas discharging pus (Fig. 1). No respiratory distress was observed. Oral examination revealed poor dental hygiene with multiple caries.
Fig. 1.
Rapidly progressive cervicofacial swelling extending from the cervical region to the upper thoracic area (red arrow).
Laboratory tests showed leukocytosis and an elevated C-reactive protein (CRP) of 214 mg/L. Given the severity of infection and lymphopenia, HIV testing was performed and was positive, with a CD4 count of 312 cells/µL. HIV viral load and WHO clinical staging were not available at the time of initial management. Screening for associated infections, including syphilis and hepatitis B and C, was negative. (Table 1). Contrast-enhanced cervical CT revealed a sizable 6 × 3.5 cm rim-enhancing fluid collection in the left submandibular region, extending into the parapharyngeal and sublingual spaces. Extensive surrounding inflammatory changes were noted, including diffuse cervicofacial cellulitis and fascial plane disruption with multiple gas locules, highly suggestive of necrotizing soft tissue infection. Inferior spread into the mediastinum was observed, consistent with descending necrotizing mediastinitis. Associated pulmonary parenchymal infiltrates compatible with pneumonia were also present. (Fig. 2).
Table 1.
Laboratory investigations and reference ranges of both patients.
| Test | Case 1 | Case 2 | Reference Range | Interpretation |
|---|---|---|---|---|
| White Blood Cell count (×10⁹/L) | 14.2 | 11.8 | 4.0 – 10.0 | Leukocytosis |
| Neutrophils (%) | 82 | 79 | 40 – 75 | Elevated |
| Lymphocytes (/µL) | 910 | 820 | 1000 – 4800 | Normal |
| C-Reactive Protein (mg/L) | 214 | 190 | < 5 | Highly elevated |
| Hemoglobin (g/dL) | 11.5 | 12.2 | 12 – 16 | Mild anemia |
| Platelets (×10⁹/L) | 410 | 395 | 150 – 400 | Mild thrombocytosis |
| Blood glucose (mmol/L) | 5.4 | 5.1 | 3.9 – 6.1 | Normal |
| Creatinine (µmol/L) | 85 | 78 | 50 – 110 | Normal |
| HIV status | Newly diagnosed | Newly diagnosed | ||
| CD4 T-cell count (cells/µL) | 312 | 340 | 500 – 1500 | Decreased (immunosuppression) |
| HIV serology | Positive | Positive | Negative | Confirmed infection |
| Hepatitis B serology | Negative | Negative | Negative | Normal (no infection) |
| Hepatitis C serology | Negative | Negative | Negative | Normal (no infection) |
| Syphilis serology (VDRL/RPR) | Negative | Negative | Negative | Normal (no infection) |
Fig. 2.
(A) Contrast-enhanced cervico-thoracic scan (axial view) showing a large hypodense collection with gas formation extending through the deep cervical fascia (red arrow), consistent with cervicofacial cellulitis complicated by mediastinal extension. (B) Axial thoracic section demonstrating mediastinal spread of the infection with multiple air bubbles within the superior mediastinum (red arrow).
The patient underwent emergency surgical drainage of cervical and mediastinal collections with debridement under general anesthesia, in collaboration with thoracic surgeons. The causal tooth was identified as the right mandibular second molar presenting advanced caries with periapical infection. Extraction was performed during surgical drainage. Intravenous amoxicillin–clavulanate and metronidazole were administered. The postoperative course was complicated by septic shock, requiring mechanical ventilation and intensive care. Perioperative cultures isolated Klebsiella pneumoniae and α-hemolytic Streptococcus (sensitive strains) from the cervical abscess (Table 2, Table 3). Histopathological examination of debrided tissue confirmed extensive necrosis consistent with necrotizing fasciitis, without evidence of a specific invasive fungal or mycobacterial infection. The patient required 10 days of mechanical ventilation and 30 days of intravenous antibiotics. He was eventually discharged in stabilized condition and referred to the Infectious Diseases department for initiation of HIV treatment and follow-up.
Table 2.
Microbiological culture results (Case 1).
| Parameter | Findings (Case 1) |
|---|---|
| Sample source | Cervical abscess pus |
| Organisms isolated | Klebsiella pneumoniae and α-hemolytic Streptococcus |
| Gram stain | Mixed flora: Gram-negative bacilli and Gram-positive cocci in chains |
| Culture media | Blood agar and MacConkey agar |
| Observed growth | Lactose-fermenting colonies of K. pneumoniae on MacConkey agar; α-hemolytic streptococci on blood agar |
| Final identification | Klebsiella pneumoniae and α-hemolytic Streptococcus |
Table 3.
Antibiotic susceptibility results (Case 1).
| Antibiotic | Klebsiella pneumoniae | α-hemolyticStreptococcus | Interpretation |
|---|---|---|---|
| Ampicillin | Resistant | – | Klebsiella is intrinsically resistant to ampicillin |
| Amoxicillin–clavulanate | Sensitive | – | Effective β-lactam/β-lactamase inhibitor against Klebsiella |
| Ceftriaxone | Sensitive | – | Third-generation cephalosporin effective vs. Klebsiella |
| Cefotaxime | Sensitive | – | Similar spectrum to ceftriaxone |
| Gentamicin | Sensitive | – | Aminoglycoside effective against Klebsiella |
| Amikacin | Sensitive | – | Active aminoglycoside against Klebsiella |
| Ciprofloxacin | Sensitive | – | Fluoroquinolone effective against Klebsiella |
| Cotrimoxazole | Resistant | – | Klebsiella is resistant to folate pathway inhibitors |
| Imipenem | Sensitive | – | Carbapenem highly active against Klebsiella |
B. Case 2
A 35-year-old woman with no significant medical history was admitted to the otolaryngology department for a rapidly progressive right lateral cervical swelling associated with intense pain and torticollis. On examination, there was a large inflammatory mass (∼8 cm) on the right side of the neck. Laboratory tests showed marked inflammatory syndrome. Cervico-thoracic CT imaging revealed two adjacent 4 cm jugulocarotid abscess collections with diffuse involvement of deep cervical spaces, consistent with extensive cervicofacial cellulitis (Fig. 3). HIV testing was also positive in the second patient, with a CD4 count of 340 cells/µL. HIV viral load and WHO clinical staging were not available at the time of initial management. Screening for syphilis and hepatitis B and C was negative (Table 1).
Fig. 3.
Contrast-enhanced cervico-thoracic scan (coronal view) showing cervicofacial cellulitis with two contiguous abscess collections (red asterisks).
The patient underwent urgent surgical drainage of both abscesses and extraction of the 47 causal tooth was performed during surgical drainage, combined with broad-spectrum intravenous antibiotics, followed by daily wound care. Perioperative cultures isolated Streptococcus mitis, a viridans group streptococcus (Table 4, Table 5). The clinical course was favorable, with marked improvement after 10 days of hospitalization. The patient was subsequently discharged and referred to the Infectious Diseases department for ongoing HIV management. This case is particularly notable as cervicofacial cellulitis led to the diagnosis of previously unknown HIV infection in a young patient without known immunodeficiency.
Table 4.
Microbiological culture results (Case 2).
| Parameter | Findings (Case 2) |
|---|---|
| Sample source | Cervical abscess aspirate |
| Organism isolated | Streptococcus mitis |
| Gram stain | Gram-positive cocci in chains |
| Culture medium | Blood agar |
| Observed growth | α-hemolytic colonies |
| Final identification | Streptococcus mitis (viridans group streptococci) |
Table 5.
Antibiotic susceptibility results (Case 2).
| Antibiotic | Streptococcus mitis | Interpretation |
|---|---|---|
| Ampicillin | – (Not tested) | – |
| Amoxicillin–clavulanate | – (Not tested) | – |
| Ceftriaxone | – (Not tested) | – |
| Cefotaxime | – (Not tested) | – |
| Gentamicin | Low-level resistance | Reduced susceptibility to aminoglycosides |
| Amikacin | – (Not tested) | – |
| Ciprofloxacin | – (Not tested) | – |
| Cotrimoxazole | Resistant | Resistance to folate pathway inhibitors |
| Imipenem | – (Not tested) | – |
| Tetracycline | Sensitive | Good susceptibility |
| Erythromycin | Sensitive | Macrolide-sensitive |
| Lincomycin | Sensitive | Lincosamide-sensitive |
| Pristinamycin | Sensitive | Streptogramin-sensitive |
| Levofloxacin | Sensitive | Fluoroquinolone-sensitive |
| Vancomycin | Sensitive | Glycopeptide-sensitive |
| Teicoplanin | Sensitive | Glycopeptide-sensitive |
Discussion
Deep neck infections remain a significant cause of morbidity despite advances in diagnostic and therapeutic strategies. Large retrospective analyses from tertiary centers have demonstrated that delayed presentation, inadequate initial management, and comorbid conditions significantly increase the risk of severe complications [1], [2], [6]. Our cases illustrate the aggressive evolution that cervicofacial cellulitis may follow, particularly when systemic involvement is already established at the time of admission.
One of the most feared complications of deep neck infections is descending necrotizing mediastinitis. The anatomical continuity between cervical fascial planes and the mediastinum facilitates rapid downward spread of infection. Multidisciplinary management involving otolaryngologists, maxillofacial surgeons, thoracic surgeons, and intensivists is essential in such cases [3], [8]. Mortality rates remain considerable, especially when diagnosis is delayed. In our first case, early recognition of mediastinal extension on contrast-enhanced CT and immediate surgical drainage were decisive in preventing further deterioration.
Radiological imaging plays a central role in the management of deep neck infections. Clinical examination alone may underestimate the true extent of disease, particularly in deep anatomical compartments. Contrast-enhanced computed tomography (CT) is considered the gold standard for evaluating abscess formation, detecting gas in soft tissues suggestive of necrotizing fasciitis, and identifying mediastinal spread or vascular complications [7], [8]. Imaging findings directly influence surgical planning and prognosis.
Odontogenic infections remain the primary source of cervicofacial cellulitis worldwide [4], [5]. Mandibular molars are especially implicated because their root apices lie close to the mylohyoid line, allowing infection to spread into submandibular and parapharyngeal spaces. In our first patient, tooth 47 was identified as the causal focus and extracted during surgical drainage. Several surgical series emphasize that eradication of the dental source in combination with incision and drainage significantly reduces recurrence and hospital stay [1], [9]. Failure to address the primary focus may lead to persistent infection and repeated surgical interventions.
Necrotizing fasciitis represents a rare but devastating complication of deep neck infections. It is characterized by rapid fascial necrosis, gas formation, and systemic toxicity. Although it may occur in immunocompetent individuals, immunosuppression and delayed treatment increase the risk of severe evolution [10]. Early recognition and aggressive surgical debridement remain the cornerstone of management.
From a microbiological perspective, deep neck infections are typically polymicrobial, involving aerobic and anaerobic bacteria originating from the oral cavity [4], [11]. However, recent studies have demonstrated evolving bacteriological profiles and increasing antimicrobial resistance patterns [11], [12]. This underscores the importance of systematic bacteriological sampling and antibiotic susceptibility testing. In our cases, culture-guided therapy enabled targeted antibiotic adjustment, which is particularly important in severe infections with systemic involvement.
Predictors of poor outcome identified in retrospective cohorts include delayed hospital admission, comorbidities, immunosuppression, and inadequate initial antibiotic therapy [2], [6], [13], [14]. Efficient surgical management and multidisciplinary coordination have been shown to improve survival and reduce complications [9], [14]. Structured management protocols, such as those described in prospective observational studies of complicated odontogenic infections, highlight the importance of early intervention pathways [15].
Our cases reinforce several key clinical lessons. First, cervicofacial cellulitis may progress rapidly to systemic complications, including mediastinitis and septic shock. Second, early contrast-enhanced CT imaging is indispensable for accurate assessment and surgical planning. Third, eradication of the odontogenic focus must be performed simultaneously with surgical drainage. Finally, microbiological confirmation and culture-guided antibiotic therapy are essential in the context of emerging antimicrobial resistance.
Overall, these observations emphasize that cervicofacial cellulitis remains a potentially life-threatening condition requiring early diagnosis, aggressive surgical intervention, and coordinated multidisciplinary management to optimize outcomes. Our cases reinforce that cervicofacial cellulitis may act as a sentinel event revealing undiagnosed HIV infection and support systematic HIV screening in patients with severe or atypical presentations.
Conclusion
Cervicofacial cellulitis in HIV-positive patients may present as a rapidly progressive and life-threatening condition. Severe deep neck infection can reveal previously undiagnosed HIV infection. Early imaging, aggressive surgical management, microbiological evaluation, and systematic HIV screening in severe cases are essential. Multidisciplinary coordination significantly reduces morbidity and mortality.
CRediT authorship contribution statement
Wejdan Mohamed TRABELSI: Writing – original draft, Investigation, Data curation, Conceptualization. Nadia Romdhane: Validation, Supervision. Imen Zoghlami: Project administration, Investigation, Formal analysis. Chiraz Mbarek: Supervision. Ines Hariga: Validation, Supervision. Dorra Chiboub: Visualization, Supervision.
Ethics declaration
Written informed consent to take part in the study and to publish the article has been obtained from all participants or their legal representatives. The privacy rights of participants have been observed.
This study was performed in compliance with relevant laws, regulatory frameworks and guidelines where the research took place. Ethics committee approval was not required under relevant laws and institutional guidelines. Ethics committee approval was not required for this case report according to the applicable institutional guidelines and regulations. Written informed consent was obtained from both patients for publication of the case report and accompanying images.
This research follows the CARE guidelines and the CARE checklist.
Ethical approval
Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal on request.
Funding
No funding was made available for this manuscript.
Declaration of Competing Interest
All authors declare that they have no financial or personal relationships with any individuals or organizations that could inappropriately influence (bias) this work. There are no conflicts of interest to declare.
Acknowledgement
There are no additional acknowledgements and no source of funding was available for the preparation of this manuscript.
Contributor Information
Wejdan Mohamed Trabelsi, Email: trabelsiwejdanmohamed@gmail.com.
Imen Zoghlami, Email: zoghlamiimen48@gmail.com.
Nadia Romdhane, Email: docteurnadia2016@gmail.com.
Dorra Chiboub, Email: chdorra@hotmail.com.
Ines Hariga, Email: ineshriga@gmail.com.
Chiraz Mbarek, Email: chirazmbarekchaouch@gmail.com.
Data availability
The data supporting the findings of this study are available from the corresponding author upon reasonable request.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The data supporting the findings of this study are available from the corresponding author upon reasonable request.