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To date, the pathogenesis of VZV infection is not fully understood because VZW is an exclusively human pathogen and is difficult to replicate in animal models (Breuer & Whitley, 2007).
Among immunocompromised populations, herpes zoster rashes typically are more severe and prolonged and may become disseminated, indicating VZV viremia.
VZV rashes typically are presented by a well-defined dermatomal distribution in immunocompetent individuals, so the diagnosis can be established by characteristic clinical presentation.
Acyclovir, famciclovir, and valacyclovir are nucleoside analogs that inhibit replication of human herpesviruses and are approved by the U.S.
Since VZV prophylaxis has been shown to effectively decrease the incidence of VZV reactivation and reduce disseminated VZV infection in BMT recipients, VZV prophylaxis should be considered for hematologic patients without BMT with severe myelosuppression. Among high-risk patients without transplantation, reactivation and disseminated VZV infection also can occur. Disseminated herpes zoster, and check out Disseminated herpes zoster on Wikipedia, Youtube, Google News, Google Books, and Twitter on Digplanet. The diseases that most often require respiratory protection include Mycobacterium tuberculosis, rubeola, varicella, disseminated herpes zoster and severe acute respiratory syndrome (SARS). BOSTON a€” The herpes zoster vaccine can be safely used in patients with rheumatoid arthritis, psoriatic arthritis, and spondyloarthropathies who are being treated with biologic agents, according to the results of a new study.
Sir,65-year-old male, known case of non-hodgkin lymphoma completed four cycles of chemotherapy (CHOP) two months back, presented with generalized vesicular eruption and constitutional symptoms of five days.
Human herpes virus 8 (HHV-8) is mainly responsible for the development of Kaposi's sarcoma and multicentric Castleman's disease in immunocompromised patients with untreated human immunodeficiency virus. A 25-year-old man of West African origin with HIV complained of asthenia, weight loss, fever, and abdominal pain. We analyzed the HHV-8 deoxyribonucleic acid in two other plasma samples (one from six months earlier and the other was 10 days after the positive test) and both yielded negative results.
We describe the case of a patient with HIV who tested positive for asymptomatic HHV-8 replication during an opportunistic disease suggestive of multicentric Castleman's disease.
IntroductionHuman herpes virus 8 (HHV-8) is associated with the development of Kaposi's sarcoma (KS) and multicentric Castleman's disease (MCD) mostly in immunocompromised patients with untreated human immunodeficiency virus (HIV).
Case presentationA 25-year-old man of West African origin was diagnosed with HIV in August 2006. A computed tomography scan revealed multiple mediastinal, retroperitoneal and pelvic lymphadenopathies, hepatosplenomegaly, and disseminated pulmonary micronodules.
DiscussionThe clinical presentation of fever, weight loss, generalized lymphadenopathy and enlargement of the liver and spleen in our patient was suggestive of tuberculosis. ConclusionThis case report underlines the need to clarify the quantification as well as the full clinical meaning and implication of a positive HHV-8 viral load in patients with HIV. ConsentWritten informed consent was obtained from the patient for publication of this case report and any accompanying images.
Competing interestsThe authors declare that they have no competing interests.Authors' contributionsSI and EB were the major contributors in writing the manuscript. However, the clinical presentation may be atypical or may have disseminated disease without rashes in immunocompromised patients; as a result, laboratory tests, including polymerase chain reaction, direct fluorescent antibody, and viral culture are needed to confirm the diagnosis. Monitoring CD4 counts may be useful for clinicians in determining the need for VZV prophylaxis among high-risk populations, such as (a) hematologic patients with cancer following cytotoxic chemotherapy who fail to recover from myelosuppression over a prolonged period of time, (b) patients with myelodysplastic syndrome who have severe leukopenia refractory to granulocyte-colony-stimulating factor or granulocyte- macrophage-colony-stimulating factor, and (c) patients anticipating a prolonged course of immunosuppressive therapy who also are VZV seropositive (indicting a latent VZV state). Two patients with solid cancers in the first author's practice developed disseminated VZV infections -- one patient with breast cancer receiving standard adjuvant chemotherapy and one patient with metastatic colorectal cancer who received chemotherapy over four years. Co-reactivation of varicella zoster virus and herpes simplex virus with disseminated cutaneous lesions in a lymphoma patient.
Disseminated herpes Simplex virus and varicella zoster virus coinfection in a patient taking thalidomide for relapsed multiple myeloma. Simultaneous reactivation of herpes simplex virus and varicella-zoster virus in a patient with idiopathic thrombocytopenic purpura.
Concurrent reactivation of varicella zoster virus and herpes simplex virus in an immunocompetent child. Identification and characterization of 20 immunocompetent patients with simultaneous varicella zoster and herpes simplex virus infection.
Positive viral loads have been described in cases of Kaposi's sarcoma and multicentric Castleman's disease, with higher values found in the latter. Physical examination revealed that the patient had adenopathies and hepatosplenomegaly, but no skin or mucosal lesions were seen. A search for latent and lytic HHV-8 antibodies confirmed that the patient was seropositive for HHV-8 before this episode.
The initial analysis was nullified by the diagnosis of a disease that was unrelated to HHV-8. MCD is an atypical lymphoproliferative disease characterized by systemic symptoms that include fever, weakness, severe weight loss, generalized lymphadenopathy and hepatosplenomegaly.
In January 2007, the patient started complaining about multiple bouts of asthenia, weight loss, fever, and abdominal pain. A tuberculin skin test and whole blood interferon gamma assay were both positive.Cultures for mycobacteria in sputum, bronchoalveolar lavage fluid, urine and blood were performed, but no acid-fast bacilli were seen. However, as the search for mycobacteria was initially negative, the diagnosis was expanded to include MCD.
The potential for diagnosing MCD needs to be studied further to determine its sensitivity and specificity.
A copy of the written consent is available for review by the Editor-in-Chief of this journal. The data provided represent the methods employed in the detection and quantification of HHV-8 viral load in the plasma, whole blood and PBMC. EO analyzed and interpreted the patient's data regarding the HHV-8 infection and strong suspicion of MCD.


Primary infection with VZV results in varicella or chickenpox, which largely affects children with a mild, self-limiting course (Wharton, 1996).
Women have a slightly higher risk than men, and African Americans have a lower incidence of herpes zoster (Opstelten, Van Essen, Schellevis, Verheij, & Moons, 2006). During initial viraemia, infected CD4 T cells cause down regulation of the histocompatibility complex class I expression and allow VZV to escape from the immune system (Ku, Padilla, Grose, Butcher, & Arvin, 2002). The most common rash sites are the thoracic and lumbar dermatomal zones (Yawn et al., 2007). Therefore, considering VZV prophylaxis is clinically reasonable to reduce the risk of deadly disseminated VZV infection among high-risk patients with cancer without BMT. History of vesicular eruption over lips was recorded for over two years with three episodes at intervals of six months, each lasting for 4-5 days. We describe the case of a patient with HIV in whom a high level of HHV-8 replication was detected and who contracted an opportunistic disease other than multicentric Castleman's disease or Kaposi's sarcoma. This case report underlines the need to clarify the full clinical meaning and implication of a positive HHV-8 viral load in patients with AIDS. The pathological examination of lymph nodes reveals angiofollicular hyperplasia, atrophic germinal centers surrounded by concentric layers of small B cells with a typical onion skin feature, and intense interfollicular plasma cell hyperplasia. This was supported by the clinical presentation and the high HHV-8 viral load measured in the patient's blood plasma. Finally, when faced with the dilemma of urgently starting chemotherapy in a patient whose condition is deteriorating and whose clinical presentation suggests MCD, high whole blood and plasmatic HHV-8 viral loads should be interpreted with caution and histological analysis of lymph nodes should be obtained first in order to establish the definitive diagnosis of MCD.
GC performed the histological examination of the adenopathies and measured the HHV-8 levels. After clinical resolution of primary infection, viral latent infection is established when VZV retrogrades into the sensory dorsal roots of ganglia (Breuer & Whitley, 2007).
In addition, infected T cells transport VZV via T-cell trafficking from tonsillar tissue to the skin, where VZV replicates and produces cell-free VZV, resulting in highly infectious skin lesions. The rashes initially are erythematous and maculopapular, then progress to coalescing clusters of clear vesicles that contain high concentrations of VZV, which are contagious for VZV seronegative individuals. However, direct fluorescent antibody offers rapid diagnosis and is highly sensitive (Chan, Brandt, & Horsman, 2001). Therapy should be initiated within 72 hours of rash onset or as soon as possible (Dworkin et al.) (see Table 1). A retrospective analysis of 192 allogeneic peripheral blood stem cell transplantation recipients indicated that a very low dose of acylovir (200 mg daily) protected against VZV reactivation (Kim et al., 2008).
In addition, the prophylaxis regimen may decrease patients' physical suffering and associated hospitalizations.
On examination, discrete and grouped vesicles were seen on the face, trunk and upper extremities with relative sparing of lower extremities and acral regions. The diagnosis of multicentric Castleman's disease needs to be studied further to determine its sensitivity and specificity. Immunohistochemistry using antibodies against latent nuclear antigen of HHV-8 allows the detection of B cells infected with HHV-8. On physical examination, he had fever (38.9A°C), multiple inguinal and axillary adenopathies, and hepatosplenomegaly.
A polymerase chain reaction (PCR) search revealed neither the presence of Mycobacterium tuberculosis complex DNA nor clonal B or T cells.At this point, due to the absence of mycobacteria in all samples and because the patient's presentation was also compatible with MCD, his HHV-8 DNA was measured. Finally, the histology and positive PCR assay of the second lymph node biopsy firmly established the diagnosis of disseminated tuberculosis. Vaccination in children to prevent primary VZV has reduced chickenpox cases in the United States (Marin, Guris, Chaves, Schmid, & Seward, 2007). Uninfected T cells also arrive at the infection sites, become primed with cell-free VZV, and mount a systemic immune response to control the initial infection (Ku et al., 2005). In immunocompetent people, the rashes crust in 7-10 days and are no longer infectious (Harpaz et al., 2008). The specimen is obtained by scraping the bases of uncrusted vesicular skin lesions and placing the scrapings on a plain glass slide. Similarly, 137 BMT recipients who were given long-term acylovir of 200 mg daily until the end of immune suppression and at least one year following BMT had significantly decreased incidence of VZV reactivation, and visceral dissemination and serious complications were completely eliminated (Asano-Mori et al., 2008). However, the histology and positive polymerase chain reaction assay for Mycobacterium tuberculosis complex of a second lymph node biopsy enabled us to conclude that the patient had disseminated tuberculosis and we started the patient on antituberculosis treatment. Finally, when faced with the dilemma of urgently starting chemotherapy on a patient whose condition is deteriorating and whose clinical presentation suggests multicentric Castleman's disease, high HHV-8 viral loads should be interpreted with caution and histological analysis of lymph nodes or liver biopsies should be obtained first. These cells have undergone plasma cell differentiation and are mainly located in the mantle zone. This was further supported by the fact that the patient was apparently cured by antituberculosis treatment.
Herpes zoster, the second clinical condition of VZV infection, results from the reactivation of this latent neurotropic virus and commonly presents with painful, unilateral vesicular skin eruption distributing within the dermatomal zones (Gnann & Whitley, 2002).
Following initial infection, the VZV-specific cell-mediated immunity keeps VZV in latency and prevents its reactivation (Breuer & Whitley).
Although VZV cutaneous dissemination may start with a dermatomal rash, it presents without any primary dermatomal involvement in some cases.
This method of staining is particularly useful when typical features such as onion skin lesions are lacking and when intense interfollicular hyperplasia may be considered as non-specific or secondary to HIV infection. Physical examination did not reveal any mucocutaneous signs of KS.The patient underwent a second lymph node biopsy, which revealed areas of necrosis surrounded by giant cell granulomas. This evolution, as well as two lymph node biopsies without evidence of MCD made it unlikely that the patient had both tuberculosis and MCD.
When an individual's immune system is compromised, such as in older adults or people with cancer undergoing chemotherapy or transplantation, his or her VZV-specific cell mediated immunity also is likely to be impaired, leading to VZV reactivation.


The most common complication following herpes zoster infection is postherpetic neuralgia, a persistent pain that can last months to years and occasionally becomes permanent. The results of Ziehl-Neelson staining were again negative, but the PCR search for Mycobacterium tuberculosis complex was positive, which enabled us to conclude that the patient had disseminated tuberculosis. Large bullous lesions and grouped vesicles in a zosteriform pattern were seen on left upper back over multiple dermatomes (C7, C8, and T1) [Figure 1]a. There was no evidence for MCD or any other lymphoproliferative processes.The patient was then started on isoniazid, rifampicin, ethambuthol and pyrazinamide treatments, and his condition subsequently improved.
Positive values in PBMCs have been found in up to 73.2% of reported patients with KS [6] and in all patients with MCD or primary effusion lymphomas [7]. The patient was started on highly active antiretroviral therapy (HAART) two months later and once the antituberculosis treatment had been simplified.
Adjunct therapy for pain and postherpetic neuralgia often is required for patients with herpes zoster. Based on clinical findings, possibility of disseminated zoster or disseminated herpes simplex infection or co-infection of both at different anatomical sites was considered. Positive values are found during KS and MCD, but levels rise in magnitude during active MCD [3a€“5].We describe the case of a patient with HIV infection and severe constitutional symptoms. In between these two periods, the patient had received methyprednisolone 250 mg three times daily for two days. It is also important to note that two of the 12 patients with asymptomatic HHV-8 infection had low detectable levels of 2,91 log copies [5].
In a retrospective study involving eight patients with HIV and with either KS or KS and MCD, Boivin et al. However, just before the patient was initiated on chemotherapy for presumed MCD, high levels of HHV-8 DNA were detected.
Uniplex and nested polymerase chain reaction (PCR) for both VZV (Varicella Zoster Virus) and HSV-1 (Herpes Simplex Virus 1) from the vesicular fluid obtained from discrete as well as grouped vesicles over trunk was positive and thus confirmatory of acute co-infection. On the contrary, it must be noted that the negative predictive value of HHV-8 DNA in PBMCs, when associated with the clinical and biological symptoms of MCD, is quite high. IgG antibody titres done on parallel specimen of acute sera (obtained on 5 th day of vesicular eruption) and convalescent sera (obtained on 18 th day) showing four-fold rise denoted recent and past infection.
In our patient, the high viral concentration found in his plasma may suggest the replication and non-specific activation of a latent HHV-8 infection in the context of inflammatory dysregulation associated with another infection, instead of a reactivation associated with MCD or KS [8].There are few published examples of HHV-8 reactivation without evidence of MCD or KS.
IgM (Immunoglobulin M) antibody titre was not done as PCR confirmed the acute co-infection. Complete blood counts, renal and liver parameters, chest radiograph, ultrasound abdomen and pelvis were found normal. Half of the patients with HHV-8 reactivation had concomitant cytomegalovirus (CMV) infections [9]. This experimental evidence tends to imply that increased plasmatic levels of HHV-8 are not exclusively indicative of the presence of MCD or KS, but could simply reflect inflammatory dysregulation associated with HIV infection, for example.In non-HIV immunosuppressed patients such as transplant recipients, other herpes viruses such as CMV or Epstein-Barr virus are known to reactivate. In 2% to 10% of immunocompromised patients with zoster, disseminated cutaneous disease occurs.
A regular follow-up of the DNA load is thus suggested to detect continuous replication and elevated values in order to prevent the development of the disease and to adapt the immunosuppressive treatment [14].
In an immunosuppressed host severe, extensive, widespread eruption of vesicles, pustules and erosions can occur.
Disseminated herpes simplex virus infections may resemble varicella; however, there is often an obvious concentration of lesions at and surrounding the site of the primary or recurrent infection and there may be associated pneumonia, hepatitis and encephalitis. Clinically, the widespread infection lesions at varying stages in few areas on the back, sparing of distal areas seemed suggestive of varicella in an immunosuppressed patient, in whom reinfection is possible.
Grouped lesions on the face and upper back, unlikely to be seen in varicella aroused suspicion of disseminated zoster or herpes simplex.
Since the zosteriform lesion over the back satisfied the criteria of disseminated herpes zoster which is defined as more than 20 vesicles outside the area of primary or adjacent dermatomes producing a varicella-like eruption, [2] clinically the diagnosis of disseminated zoster was made. Disseminated herpes simplex was also considered as an alternative diagnosis based on the grouped lesions preferentially involving perioral and nasal area, not in a zosteriform pattern. Usually disseminated herpes simplex in an immunosuppressed host presents with systemic involvement, our patient was stable with no systemic complications.The lesions of varicella, herpes zoster and herpes simplex are indistinguishable by Tzanck smear or histopathology. Detection of viral DNA in clinical specimens after amplifications by PCR provides the greatest assay sensitivity, very high specificity, and rapid turn-around time. A four-fold rise in IgG antibody titres in the convalescent sera was also seen, for both VZV and HSV-1. Past history of chicken pox and labial vesiculation suggested reactivation of dormant viruses. A final diagnosis of co-reactivation of disseminated zoster and disseminated herpes simplex infection was made. In our case, coinfection with VZV and HSV-1 presented with lesser morbidity and severity and responded readily to treatment with no recurrence even after 6 months of follow up. Development of varicella in the intern 10 days post-exposure indicates high infectivity of disseminated zoster as compared to that of zoster. VZV can also be transmitted through an air-borne route, particularly in patients with disseminated zoster increasing the secondary attack rate manifold.As far as known, around 30 cases of similar co-infection occurring in immunosuppressed as well as immunocompetent patients have been reported worldwide.
Another probable explanation is that reactivation of a neurotropic herpes virus can reactivate another neurotropic virus if both types are present in the same ganglion.




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