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Bacterial, Mycobacterial, and Spirochetal (Nonvenereal) Infections
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Laboratory studies: Investigations include bacterial culture from skin, blood, urine, or umbilical cord sample (in a newborn baby). A Tzanck smear (scraping of an ulcer base to look for acantholytic cells, dyskeratosis, no or little inflammation, cocci, and absence of abundant neutrophils) can be a useful, simple, low-cost rapid test to aid diagnosis.
Microbiological Diagnosis of Viral Diseases
Published in Nancy Khardori, Bench to Bedside, 2018
Cutaneous viral lesions like vesicles can be tested for a suspected viral etiology (e.g., HSV 1 and 2, VZV, etc.) by collecting the vesicular fluid using a swab and transporting the latter in VTM. A Tzanck smear can be prepared by scraping the base of such a lesion.
How to master MCQs
Published in Chung Nen Chua, Li Wern Voon, Siddhartha Goel, Ophthalmology Fact Fixer, 2017
Lipschutz bodies, also called Cowdry type A inclusions, are seen in cells infected with herpes simplex or varicella zoster virus. They are best seen with the infected epithelial cells fixed in Bouin's solution and stained with Papanicolaou method. Giemsa stain shows up cells infected by the herpetic virus. The infected cells show multi-nucleation with balloon degeneration. Immunofluorescence can identify cells infected with herpes virus. Henderson Patterson bodies refer to eosinophilic cytoplasmic inclusion bodies seen in molluscum contagiosum. Tzanck smear involves scraping the base of a vesicle and inoculating it onto a microscopic slide. The syncytial giant cells which are characteristic of cells infected with the herpes virus can be demonstrated with Wright's or Giemsa stain.
Self-limited acne agminate-like granulomatous reaction to facial laser rejuvenation in a patient with comedonal acne vulgaris
Published in Journal of Cosmetic and Laser Therapy, 2020
Kamran Balighi, Robabeh Abedini, Alireza Ghanadan, Amir Abbas Peymanfar, Marwa Akhdar, Ifa Etesami
A 41-year-old female patient presented to our laser clinics requesting rejuvenation laser. At the time of presentation, she had mild inflammatory acne limited to her neck and chin (Figure. 1a). Her past medical history was unremarkable, except for a history of acne during her adolescence, for which she was treated with isotretinoin for 8 months. Perioperatively, she was asked to clean her face with a facial cleanser; then, the treatment area was cleaned by 70% ethanol solution. She underwent Fotona 4D laser for one session and herpes prophylaxis was prescribed for her. Three days after laser therapy, she developed erythematous papules on the face and neck. The lesions turned into monomorphic pustules 1 week after laser therapy (Figure. 1b). The pustules were checked for herpes by Tzanck smear that was negative and also gram stains and culture for bacterial infection. Gram stain revealed a few gram-positive cocci and staphylococcus epidermidis in culture was detected which is mainly considered as normal flora of the skin. Her lesions did not respond to different antibiotics such as cyclins, cephalexin, and ciprofloxacin. These lesions started to scale off after about 2 weeks and changed to infiltrated edematous erythematous papules on the face and neck.
A case of herpes simplex virus reactivation after fractional ablative carbon dioxide laser to treat a burn scar
Published in Journal of Cosmetic and Laser Therapy, 2019
Anissa Zaouak, Rym Benmously, Houda Hammami, Samy Fenniche
A 48-year-old woman with Fitzpatrick skin type III presented with a scar in her perioral area desiring esthetic improvement of her burn scar. She did not have a history of recurrent herpes simplex virus (HSV) infection periorally. A fractionated resurfacing laser Quadralase (Candela) was used to treat her perioral burn scar. Laser was performed under local anesthesia using 125 mm handpiece, 10 mm spot, 25% density, and energies between 8 and 10 W. One single pass was performed. Two sessions were performed with a month interval. Five days after the second session of laser therapy even after she took antiviral prophylaxis based on valacyclovir 500 mg twice daily 24 hours before the laser session and 3 days after, she presented with a rash on the perioral area preceded by pain. Physical examination revealed pinpoint erosions and vesicles in a scattered distribution over the entire chin and the two nasolabial folds (Figure 1). A Tzanck smear taken from the base of a freshly opened vesicle was examined for virally induced cytopathological features by light microscopy and was positive. Correlation of the history and the clinical presentation was consistent with HSV reactivation. Treatment was initiated with acyclovir 10 mg/kg/8 h administered intravenously for 10 days with a clearing of her vesicular eruption. Physical examination at the follow-up visit revealed residual hypopigmented and hyperpigmented areas with hypertrophic scarring (Figure 2). She noticed improvement of the quality of her scar after the second resurfacing treatment and received further fractional resurfacing treatments without complications.
Corneal Involvement in HIV-infected Individuals
Published in Ocular Immunology and Inflammation, 2021
Naveen Radhakrishnan, Derrick Smit, N Venkatesh Prajna, Rathinam S.R.
Keratitis caused by DNA viruses is the most common corneal opportunistic infection associated with HIV. Herpes zoster ophthalmicus in a young adult (<50 years) is considered an early indicator for HIV infection.7 The incidence of HZO is higher in HIV-infected individuals compared to non-HIV individuals. Although 5–15% of HIV positive patients are coinfected with Varicella-Zoster virus (VZV), only 50% develop ocular lesions.8 VZV may cause a vesiculobullous skin rash, dendritiform keratitis, stromal keratitis, conjunctivitis, retinitis, scleritis, uveitis, hemorrhagic hypopyon and secondary glaucoma.9 In HIV-infected individuals, the disease is more severe and has a longer duration with a higher rate of ocular complications.10,11 Similarly, the rate of hospitalization is higher in patients with HZO in HIV infection along with a higher rate of recurrence and longer duration of post-herpetic neuralgia.10 A dendritic keratitis in an HIV patient is more likely to be due to HZV than HSV.12 Naseri et al reported VZV-associated immune recovery stromal keratitis in a patient with HIV after initiation of HAART. Multiple anterior stromal infiltrates were seen in this patient which resolved with topical steroids and oral acyclovir.13 Late dendritic ulcer by VZV has also been documented in a post-HZO infection patient with HIV. The dendrites were linear without terminal bulbs.14 Diagnosis of HZO is mainly clinical. Tzanck smear and PCR for viral DNA can aid in confirmation. HZO in a HIV-infected individual can progress to viremia complicated with neurologic and visceral infection associated with high morbidity and mortality.4 Treatment of HZO in HIV-infected individuals requires intravenous acyclovir 10 mg/kg body weight every 8 hours for 7 days followed by prolonged course of oral acyclovir 800 mg five times a day for 3–6 weeks.4