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Possible varicella, pneumonia in an 8-month-old febrile male
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An 8-month-old febrile male infant was referred for admission by a regional hospital emergency department with the diagnosis of varicella with pneumonia and a fever of 103°F. The history of the illness began 5 days earlier with the onset of some minor discomfort in the inguinal and lower abdominal area with a rash.
James H. Brien
The evening before admission, the child had the onset of intermittent fever spikes up to 104°F. His past medical history is unremarkable, and his immunizations are up to date. There were no known sick contacts, but he does attend day care. He has had a good appetite prior to the onset of fever, with no weight loss or other complaints on review of systems, including cough.
Examination upon admission revealed normal weight and vital signs, with a temperature of 99°F and a rash (Figures 1 and 2).
Source: Brien JH
Examination upon admission revealed normal weight and vital signs, with a temperature of 99°F and a rash (Figures 1 and 2), which revealed discrete vesicular lesions on slightly erythematous bases and with some denuded areas of skin, consistent with larger blisters having previously ruptured. The lesions seemed to be confined to the right lower abdominal and inguinal area. The rest of the skin was essentially normal. The rest of his exam was also normal, including clear breath sounds.
Lab tests performed included a complete blood count with a white blood cell count of 24,300, with 47% segmented neutrophils, 31% lymphocytes and 20% monocytes, with a normal hemoglobin and hematocrit. A blood culture is pending. Rapid testing for influenza and respiratory syncytial virus (RSV) were both negative. Vesicular fluid was sent for herpes simplex virus (HSV) and varicella virus PCR and standard bacterial culture. A Gram stain was not obtained.
A chest radiograph revealed a right middle lobe density (Figure 3).
A chest radiograph revealed a right middle lobe density (Figure 3), and upon arrival, the patient was placed in airborne precautions in a private room with negative air flow. Treatment was begun with intravenous acyclovir, ceftriaxone and vancomycin, and the next morning the Infectious Disease Service was consulted.
Case Discussion
The next morning, the clinical diagnosis of bullous impetigo (B) with coincident, community-acquired pneumonia was made, and reasonably confirmed the following day with a positive skin lesion culture for Staphylococcus aureus. Since the child had no more fever spikes, he was discharged home the following day on oral clindamycin, as a reasonable choice for both conditions. He had no more fevers and was essentially well on follow-up 48 hours later. By that time, the microbiology lab had reported the S. aureus to be resistant only to penicillin and ampicillin, which, of course, extends the choices of therapy to include anti-staphylococcal penicillins and cephalosporins if needed.
These bullous skin infections are usually caused by phage group II S. aureus that produces a low molecular weight protein that causes the lysis of cells high up in the granular layer of the epidermis, forming a blister with a very thin roof of skin (Figure 4, from the J.W. Bass collection). This epidermolytic toxin-producing S. aureus can be recovered from the blister fluid of the individual lesion, as it is a local site of infection, whereas in the case of staphylococcal scalded skin syndrome, the toxin is circulating, with a specific focus of a staphylococcal infection, such as a wound, resulting in diffuse erythroderma and large areas of bullous formation (Figure 5). In that case, the blister fluid is sterile.
The lysis of cells high up in the granular layer of the epidermis form a blister with a very thin roof of skin (Figure 4, from the J.W. Bass collection). The toxin is circulating, with a specific focus of a staphylococcal infection such as a wound, resulting in diffuse erythroderma and large areas of bullous formation (Figure 5).
PLEVA is an acronym meaning “pityriasis lichenoides et varioliformis acuta.” This is an uncommon, papulosquamous dermatological condition of school-age children. It is not an infectious disease at all. However, I have seen several cases; each being referred for evaluation of “atypical varicella.” It starts with the eruption of maculopapular lesions that occur in crops in a generalized distribution, much like varicella, and progresses to a crusting stage (Figures 6 and 7). There is no fever or other associated findings.
It starts with the eruption of maculopapular lesions that occur in crops in a generalized distribution, much like varicella, and progresses to a crusting stage (Figures 6 and 7).
One of the key differentiating features is a lack of true vesicles, like one sees in varicella (Figure 8). But, as one can see from the images, the lesions may appear to be vesicular from a distance. The cause is unknown, and the duration may be many months, but ultimately it is self-limiting, requiring no treatment. However, some dermatologists may choose to try a prolonged course of erythromycin and/or ultraviolet B phototherapy. If one chooses to use erythromycin, the parents need to be aware of the association with the gastrointestinal stimulus effect. While this may not be very significant in the toddler, if an infant receives erythromycin, there is an increased risk for pyloric stenosis.
One of the key differentiating features is a lack of true vesicles, like one sees in varicella (Figure 8). Bullous varicella was not uncommon when varicella was commonly seen (Figure 9 from the J.W. Bass collection).
With regard to leukemia: this would be an unusual presentation of a new leukemic patient, but possible. The clues against that diagnosis would be the essentially normal complete blood count with no anemia or unusual cells reported. Also, the lesions seen are not visually consistent with the typical varicella rash, or the distribution, which is normally generalized.
Having said that, children with cancer who happen to have a varicella infection can have lesions that appear atypical, and if it becomes disseminated to the lungs, it can be rapidly fatal. Bullous varicella was not uncommon when varicella was commonly seen (Figure 9 from the J.W. Bass collection). This condition results from varicella lesions individually becoming infected with the same staph that causes bullous impetigo noted above. It typically responds well to oral anti-staph antibiotics and hygiene. The antimicrobial agent selected should be effective for the strains of MRSA and methicillin-sensitive S. aureus (MSSA) that is most commonly seen in the patient community. My choice is oral clindamycin at about 30 mg/kg/day in three divided doses. I also always recommend obtaining a culture from one of the lesions.
Diaper rashes are frequently secondarily infected with Candida albicans, often producing a bright red rash with satellite lesions (Figure 10).
If it turns out to be a methicillin-sensitive strain, then an anti-staphylococcal penicillin or a first-generation cephalosporin may be used. However, from a practical standpoint, getting a child to take oral dicloxacillin suspension is very difficult due to the taste. I learned this lesson the hard way 34 years ago when I tried to get my daughter to take it. It turned this pleasant, happy and normally very cooperative 6-year-old girl into the possessed child seen in the movie The Exorcist. So I tasted it myself and learned why she protested.
With proper counseling of the parents and persistence, it can be done, but most people will have too much trouble and give up, both from a taste and frequency of dosing standpoint. I’ve found that oral cephalexin is a reasonable choice for these young children with MSSA infections. Once they can take capsules, then I may use dicloxacillin, but because of the frequency of dosing required, it remains an unlikely choice without enhanced counseling of the importance of compliance.
Lastly, diaper rashes are frequently secondarily infected with Candida albicans, often producing a bright red rash with satellite lesions (Figure 10). While they may also have some pustular lesions, it is not likely to appear bullous or blistering, making the diagnosis fairly easy.
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James H. Brien, DO, is with the department of infectious diseases at McLane Children’s Hospital, Baylor Scott & White Health, Texas A&M College of Medicine in Temple, Texas. He is also a member of the Infectious Diseases in Children Editorial Board. Brien can be reached at: jhbrien@aol.com.
Disclosure: Brien reports no relevant financial disclosures.