Keywords
HIV - acute retroviral syndrome - Bell’s palsy - facial palsy - oral hairy leukoplakia
Introduction
Acute retroviral syndrome (ARS) refers to signs and symptoms of acute human immunodeficiency
virus (HIV) infection.[1] Clinical suspicion for ARS is often based on signs and symptoms believed to be typical
of ARS. However, 70% of patients present with typical ARS and 30% present with atypical
ARS,[1] which both include a broad range of signs and symptoms. [Fig. 1] illustrates data from 12 studies that assessed frequencies of 19 signs and symptoms
believed to be typical of ARS. Yet, frequencies of these typical signs and symptoms
differed greatly across studies and the most frequent signs and symptoms are nonspecific
(e.g., fever, malaise/fatigue, pharyngitis, myalgia, headache). [Table 1] lists data from a study of 70 patients with atypical ARS.[1] Among just 70 patients, there were 32 unique presentations and seven patients were
entirely asymptomatic. The variety of signs and symptoms, or lack thereof, associated
with typical and atypical ARS makes the clinical diagnosis of ARS challenging.
Table 1
Diverse presentations associated with atypical acute retroviral syndrome
|
System
|
Presentation
|
n
|
|
Abbreviations: CMV, cytomegalovirus; HSV-1, herpes simplex virus 1.
Note: Data are from a study in which 70 patients presented with atypical ARS.
Source: Adapted with permission from Braun and Kouyos.1
|
|
Asymptomatic
|
7
|
|
Cardiovascular
|
Acute atrial fibrillation
|
1
|
|
Pancytopenia
|
3
|
|
Thrombophlebitis
|
1
|
|
Constitutional
|
Weight loss or night sweats
|
7
|
|
Ocular
|
Herpes keratitis
|
1
|
|
Gastrointestinal
|
Acalculous cholecystitis
|
1
|
|
Anal abscess
|
1
|
|
Appendicitis-like illness
|
1
|
|
Diarrhea
|
1
|
|
HSV-1 stomatitis, esophagitis, and anitis
|
1
|
|
Gastritis with bleeding
|
1
|
|
Tonsillitis
|
4
|
|
Neurological
|
Acute psychiatric disorder
|
1
|
|
HSV-1 meningitis
|
1
|
|
Paresis (e.g., faciobrachial)
|
2
|
|
Paresthesias and aphasia
|
1
|
|
Vertigo
|
1
|
|
Encephalitis
|
2
|
|
Opportunistic
|
Autoimmune thrombocytopenia
|
1
|
|
Candida stomatitis and esophagitis
|
12
|
|
CMV gastritis
|
1
|
|
CMV hepatitis
|
2
|
|
Multisegmental herpes zoster
|
1
|
|
Peripheral polyradiculoneuritis
|
1
|
|
Diarrhea (>30 days)
|
1
|
|
Respiratory
|
Pneumonia
|
3
|
|
Upper respiratory tract infection
|
2
|
|
Skin and soft tissue
|
Impetigo contagiosa
|
1
|
|
Dermatitis
|
2
|
|
Soft tissue infection
|
3
|
|
Urogenital
|
Acute renal failure
|
1
|
|
Epididymitis
|
1
|
|
Total
|
|
70
|
Fig. 1 Diverse signs and symptoms associated with typical acute retroviral syndrome. Data
are from a study that describes primary data and reviews 11 published studies.[1] Black dots represent frequencies of signs and symptoms as reported by the studies.
Red bars represent median frequencies of the signs and symptoms. Note that median
frequencies do not give weight to the number of patients included in each study (range:
12–378, median = 32).
Case Report
First Encounter
A 30-year-old man presented to the primary care clinic with tongue numbness and left-sided
facial droop for 6 days, and flu-like symptoms 1 month before the visit. He reported
a family history of Bell’s palsy but did not report a social history suggesting increased
risk for HIV infection. On his left side, he lacked forehead folds and had decreased
ability to clench his jaw, inflate his cheek, close his eye, and smile. On both sides,
he had decreased forehead, infraorbital, and chin sensation. A computed tomography
scan of the head was normal and the consulting neurologist confirmed our primary diagnosis
of Bell’s palsy (i.e., idiopathic facial palsy), which resolved with prednisone.
Second Encounter
The patient returned 2 and a half years later, reporting white spots on the right
side of his tongue for 1 year and left side of his tongue for several weeks. Physical
examination revealed a corrugated, white plaque on the right side of his tongue ([Fig. 2A]) and circular, white plaque with a 5 mm diameter on the left side of his tongue
([Fig. 2B]). A punch biopsy of the left-sided tongue lesion was positive for squamous hyperplasia
and negative for dysplasia and neoplasm, suggesting oral hairy leukoplakia. An HIV-1
antibody immunoassay was positive, HIV-1 polymerase chain reaction revealed 5.52 log10 copies/mL (reference, < 1.30 log10 copies/mL), and CD4 cell count was 101 cells/μL (reference, 365–2087 cells/μL). He
was referred to an infectious disease specialist and started on antiretroviral therapy.
Fig. 2 Photos of the patient’s tongue lesions taken several months after the second encounter.
(A) The right lesion remained unchanged since the second encounter. (B) During the second encounter, a punch biopsy removed the entire left lesion. The
pictured lesion developed during the following months.
Discussion
Because of the broad range of presentations, clinical examination has limited capacity
to identify acute HIV infection.[2] Thus, organizations like the Centers for Disease Control and Prevention and United
States Preventive Services Taskforce call for extensive HIV screening (i.e., at least
one lifetime test and repeat testing for those with increased risk).[3]
[4] Still, some HIV-positive patients will slip through cracks in screening guidelines.
It falls on primary care providers to catch these patients, preferably during acute
HIV infection, to interrupt transmission and reduce HIV-related morbidity and mortality.[5]
During the first encounter, our patient presented with left-sided facial weakness
and left- and right-sided facial sensory deficits. The latter finding suggests involvement
of both trigeminal nerves, which is consistent with reports of additional cranial
nerve deficits in patients with Bell’s palsy.[6] However, no risk factors or symptoms suggested HIV infection. Although we did not
investigate the potential for an HIV infection at this time, the patient likely had
an acute HIV infection, as he experienced flu-like symptoms (i.e., typical ARS) before
the visit and soon after developed the facial palsy (i.e., atypical ARS). By the second
encounter, his HIV infection had progressed to acquired immunodeficiency syndrome
(AIDS), at which time he presented with oral hairy leukoplakia. The majority of facial
palsies are idiopathic (i.e., Bell’s palsy),[7] but ~0.1% are caused by HIV.[8] Although few reports describe facial palsies at the time of ARS, there is a clear
connection between facial palsies and HIV infections.[8]
[9]
[10]
Conclusion
We suggest that facial palsies should pique clinical suspicion for HIV, especially
in the context of recent or concurrent flu- or mononucleosis-like illness.