Adenovirus: Epidemiology, Global Spread of Novel Types, and Approach to Treatment

2021 ◽  
Vol 42 (06) ◽  
pp. 800-821
Author(s):  
Joseph P. Lynch ◽  
Adriana E. Kajon

AbstractAdenoviruses (AdVs) are DNA viruses that typically cause mild infections involving the upper or lower respiratory tract, gastrointestinal tract, or conjunctiva. Rare manifestations of AdV infections include hemorrhagic cystitis, hepatitis, hemorrhagic colitis, pancreatitis, nephritis, or meningoencephalitis. AdV infections are more common in young children, due to lack of humoral immunity. Epidemics of AdV infection may occur in healthy children or adults in closed or crowded settings (particularly military recruits). The vast majority of cases are self-limited. However, the clinical spectrum is broad and fatalities may occur. Dissemination is more likely in patients with impaired immunity (e.g., organ transplant recipients, human immunodeficiency virus infection). Fatality rates for untreated severe AdV pneumonia or disseminated disease may exceed 50%. More than 100 genotypes and 52 serotypes of AdV have been identified and classified into seven species designated HAdV-A through -G. Different types display different tissue tropisms that correlate with clinical manifestations of infection. The predominant types circulating at a given time differ among countries or regions, and change over time. Transmission of novel strains between countries or across continents and replacement of dominant viruses by new strains may occur. Treatment of AdV infections is controversial, as prospective, randomized therapeutic trials have not been done. Cidofovir has been the drug of choice for severe AdV infections, but not all patients require treatment. Live oral vaccines are highly efficacious in reducing the risk of respiratory AdV infection and are in routine use in the military in the United States but currently are not available to civilians.

2020 ◽  
Vol 41 (01) ◽  
pp. 099-114 ◽  
Author(s):  
Gail Reid ◽  
Joseph P. Lynch ◽  
Michael C. Fishbein ◽  
Nina M. Clark

AbstractMucormycosis is an infection caused by a group of filamentous molds within the order Mucorales. Infections may result from ingestion of contaminated food, inhalation of spores into the nares or lungs, or inoculation into disrupted skin or wounds. In developed countries, mucormycosis occurs primarily in severely immunocompromised hosts (e.g., those with hematological malignancies, organ transplantation, neutropenia, autoimmune disorders, or other impairments in immunity). Only 6 to 10% of cases occur in subjects with no underlying disease. In contrast, in developing countries, most cases of mucormycosis occur in persons with poorly controlled diabetes mellitus or in immunocompetent subjects following trauma. Mucormycosis exhibits a marked propensity to invade blood vessels, leading to thrombosis, necrosis, and infarction of tissue. Mortality associated with invasive mucormycosis is high (> 30–50%), with 90% mortality associated with disseminated disease. Mortality rates are much lower, though still significant (10–30%), among patients with localized cutaneous disease.The diagnosis of mucormycosis relies upon histopathology and culture. Blood tests are of limited diagnostic value. Even with disseminated disease, blood cultures are usually negative. Mucorales have a distinct histological appearance, with irregular, nonseptate hyphae that branch at right angles. Cultures and/or polymerase chain reaction (PCR) are important to identify the genera.Based on anatomic localization, mucormycosis can be classified as one of six forms: (1) rhino-orbital-cerebral mucormycosis (ROCM), (2) pulmonary, (3) cutaneous, (4) gastrointestinal (GI), (5) disseminated, and (6) mucormycosis of uncommon sites. Among diabetics, ROCM is the most common clinical presentation, whereas lung involvement is uncommon. In contrast, among organ transplant recipients or patients with hematological malignancies (HemeM), pulmonary and disseminated diseases are most common. Mucormycosis can progress rapidly, and delay in initiation of treatment by even a few days markedly worsens outcomes.Due to the rarity of mucormycosis, randomized controlled therapeutic trials have not been performed. Lipid formulations of amphotericin B (LFAB) are the mainstay of therapy, but the newer triazoles, posaconazole (POSA) and isavuconazole (ISAV) (the active component of the prodrug isavuconazonium sulfate), may be effective in patients refractory to or intolerant of LFAB. Early surgical debridement or excision plays an important adjunctive role. Additional studies are required to assess the optimal duration of therapy as well as the specific roles of LFAB and the triazoles in the treatment of mucormycosis.


Author(s):  
Mohammad Soleimani ◽  
Ahmad Masoumi ◽  
Sadegh Khodavaisy ◽  
Mostafa Heidari ◽  
Ali A. Haydar ◽  
...  

AbstractNocardia species are an uncommon but important cause of keratitis. The purpose of this review is to discus previous published papers relation to the epidemiology, etiology, diagnosis and management of Nocardia keratitis. Nocardia asteroides is the most frequently reported from Nocardia keratitis. Pain, photophobia, blepharospasm and lid swelling are mainly clinical manifestations. Usual risk factors for Nocardia keratitis are trauma, surgery, corticosteroids, and contact lens wear. Several antibiotics were used for treatment of Nocardia infection but according to studies, topical amikacin is the drug of choice for Nocardia keratitis. Topical steroid should not prescribe in these patients. In conclusion, although Nocardia keratitis is rare, early diagnosis and treatment are essential to prevent any scar formation and preserve a good visual acuity.


2016 ◽  
Author(s):  
James H. Diaz

Herpes zoster can plague anyone who has had varicella or has received the varicella or chickenpox vaccine. The incidence of herpes zoster increases with age and rises exponentially after 60 years of age. Postherpetic neuralgia (PHN) may occur after herpes zoster at any age but typically occurs after 50 years of age, with over 40% of persons over 60 years of age suffering from PHN after a shingles attack. Up to 1 million new cases of herpes zoster and 200,000 new cases of PHN may now be anticipated in the United States every year, with the incidence rate increasing as the population grows and ages with prolonged life expectancies. Although new antiviral medications will improve and shorten the course of herpes zoster, they do not guarantee the prevention of PHN. Given the high prevalence of PHN in an aging population and the availability of primary prevention by vaccination, the objectives of this review are to describe the epidemiology, pathophysiology, and clinical manifestations of zoster and PHN and to recommend a combination of strategies for the clinical management and prevention of PHN. This review contains 6 figures, 4 tables and 13 references Key words: evidence-based pain medicine, herpes zoster, neuropathic pain, postherpetic neuralgia


PEDIATRICS ◽  
1994 ◽  
Vol 94 (5) ◽  
pp. 741-742
Author(s):  
Sandeep K. Gupta ◽  
Ben Z. Katz

Mycobacterium tuberculosis (MTB) is a well described human pathogen.1 Less commonly, atypical or nontuberculous mycobacteria (NTM) can cause disease in humans. Recent studies report that NTM account for one-third of all pathogenic mycobacterial isolates in the United States.2 Mycobacterium avium-intracellulare complex (MAI) is the most common NTM causing human disease.2 It is also the most common mycobacterial cause of cervical lymphadenitis in children in areas with low endemic rates of MTB infection.3 MAI/NTM infection other than cervical adenitis is unusual in children, except in those that are immunosuppressed.4 Rarely, MAI presents as mediastinal or endobronchial disease in otherwise healthy children.


2021 ◽  
Author(s):  
Anne Gershon

A live attenuated vaccine against varicella (later also used to prevent zoster) was developed in 1974 by Takahashi and colleagues. Varicella vaccine was licensed for universal immunization of healthy children in the United States in 1995. It is also now used for this purpose in at least 15 additional countries all over the world. Varicella is disappearing in the US. Varicella vaccine has proven extremely safe and side effects are unusual, mild, and less serious than varicella or its complications. 85% of children are protected completely after 1 dose; the 15% who develop varicella despite immunization usually (but not always) have mild infections. These 15%, however, can transmit the wild type virus to others. Therefore, for optimal effect, 2 doses are required, mostly to address children who did not have an optimal primary immune response after the first dose. Waning immunity does not seem to pose a serious problem, but surveillance of vaccinees is continuing. It was demonstrated in 2005 that at a high dose of vaccine – 15 times higher than that used for prevention of varicella in children - zoster in adults can also be safely prevented. The live attenuated zoster vaccine is effective in approximately 50% of healthy individuals over age 60 who have had varicella in the past, and therefore have latent infection with varicella-zoster virus. It is given as one dose, but its effect runs out about 8 years after vaccination. In 2017, a new vaccine against zoster was also introduced. This is a subunit vaccine which does not contain contagious virus. It is even more effective than the older zoster vaccine and is over 95% effective in adults 50–≥70 years of age in preventing zoster and post herpetic neuralgia.


2021 ◽  
Vol 12 ◽  
Author(s):  
Marcia M. L. Kho ◽  
Stefan Roest ◽  
Dominique M. Bovée ◽  
Herold J. Metselaar ◽  
Rogier A. S. Hoek ◽  
...  

BackgroundStudies on herpes zoster (HZ) incidence in solid organ transplant (SOT) recipients report widely varying numbers. We investigated HZ incidence, severity, and risk factors in recipients of four different SOTs, with a follow-up time of 6–14 years.MethodsRecords of 1,033 transplant recipients after first heart (HTx: n = 211), lung (LuTx: n = 121), liver (LiTx: n = 258) and kidney (KTx: n = 443) transplantation between 2000 and 2014 were analyzed for VZV-PCR, clinical signs of HZ, and complications.ResultsHZ was diagnosed in 108 of 1,033 patients (10.5%): 36 HTx, 17 LuTx, 15 LiTx, and 40 KTx recipients. Overall HZ incidence rate after HTx (30.7 cases/1,000 person–years (PY)), LuTx (38.8 cases/1,000 PY), LiTx (22.7 cases/1,000 PY) and KTx (14.5 cases/1,000 PY) was significantly higher than in the general 50–70 year population. Multivariable analysis demonstrated age ≥50 years at transplantation (p = 0.038, RR 1.536), type of organ transplant (overall p = 0.002; LuTx p = 0.393; RR 1.314; LiTx p = 0.011, RR 0.444; KTx p = 0.034, RR 0.575), CMV prophylaxis (p = 0.043, RR 0.631) and type of anti-rejection therapy (overall p = 0.020; methylprednisolone p = 0.008, RR 0.475; r-ATG p = 0.64, RR1.194) as significant risk factors. Complications occurred in 33 of 108 (31%) patients (39% of HTx, 47% of LuTx, 20% of LiTx, 20% of KTx): post-herpetic neuralgia, disseminated disease, and cranial nerve involvement.ConclusionHZ incidence and severity in SOT recipients are most pronounced after heart and lung transplantation, in older patients, and when CMV prophylaxis is lacking.


2009 ◽  
Vol 51 (6) ◽  
pp. 337-339 ◽  
Author(s):  
Ismael A. Conti-Díaz ◽  
Jonas Moraes-Filho ◽  
Richard C. Pacheco ◽  
Marcelo B. Labruna

We report three new rickettsiosis human cases in Uruguay. The three clinical cases presented clinical manifestations similar to previous reported cases of Rickettsia parkeri in the United States; that is mild fever (< 40 ºC), malaise, headache, rash, inoculation eschar at the tick bite site, regional lymphadenopathy, and no lethality. Serological antibody-absorption tests with purified antigens of R. parkeri and Rickettsia rickettsii, associated with immunofluorescence assay indicated that the patients in two cases were infected by R. parkeri. Epidemiological and clinical evidences, coupled with our serological analysis, suggest that R. parkeri is the etiological agent of human cases of spotted fever in Uruguay, a disease that has been recognized in that country as cutaneous-ganglionar rickettsiosis.


PEDIATRICS ◽  
1994 ◽  
Vol 94 (5) ◽  
pp. 774-775 ◽  
Author(s):  

This statement describes a modification of the recommended routine schedule for administering trivalent oral poliomyelitis vaccine (OPV). The American Academy of Pediatrics previously has recommended that healthy children receive a three-dose primary series of OPV at 2, 4, and 15 to 18 months of age and a fourth dose at the time of school entry (4 to 6 years of age).1 Available data indicate that the response rates to the third dose of OPV administered at 6 months of age are as good as the rates following administration of this dose at 15 to 18 months of age. Completion of the three-dose primary series at an earlier age will help health care providers induce immunity against poliomyelitis at an early age. Although wild type poliomyelitis has not caused disease in the United States for many years, the virus remains prevalent in many countries. Continued introduction of the virus into the United States by travelers could result in transmission and disease if high levels of immunity are not maintained in preschool age children. For example, wild type poliovirus type 3 was recently introduced into Canada by a religious sect that did not believe in immunization.2 The virus was probably imported from the Netherlands, where a small epidemic of poliomyelitis occurred in members of the same sect in 1992 and 1993.3 SERUM ANTIBODY RESPONSE FOLLOWING OPV ADMINISTRATION After two doses of OPV are administered at 2 and 4 months of age, 89 to 100% of children vaccinated in the United States have evidence of humoral immunity to poliomyelitis types 1 and 3, and 99 to 100% have immunity to type 2 (Table).


2018 ◽  
Author(s):  
Raghu V Durvasula ◽  
Jonathan Himmelfarb

Chronic kidney disease (CKD) is a clinical syndrome arising from progressive kidney injury, formerly known as chronic renal failure, chronic renal disease, and chronic renal insufficiency. It is classified into five stages based primarily on glomerular filtration rate (GFR). This article discusses the epidemiology of CKD and end-stage renal disease (ESRD), as well as etiology and genetics, pathophysiology, and pathogenesis. The section on diagnosis looks at clinical manifestations and physical findings, laboratory (and other) tests, imaging studies, and biopsy. A short section on differential diagnosis is followed by a discussion of treatment, including hemodialysis and peritoneal dialysis. Long-term complications of patients on dialysis include cardiovascular disease, renal osteodystrophy, dialysis-related amyloidosis, and acquired cystic disease (renal cell carcinoma). The final section addresses prognosis and socioeconomic burden. Figures include the classification system for CKD, prevalence of CKD in the United States, rising prevalence, risk of, and leading causes of ESRD in the United States, plus the changing prevalence of ESRD over time, clinical manifestations of uremia, and an overview of hemodialysis circuit. Tables look at the burden of CKD relative to other chronic disorders, the specific hereditary causes of kidney disease, and situations when serum creatinine does not accurately predict GFR. Other tables list equations for estimating GFR, the causes of CKD without shrunken kidneys, and clinical features distinguishing chronic kidney disease from acute kidney injury. ESRD and indications for initiation of dialysis are presented, as well as typical composition of dialysate and reasons for failure of peritoneal dialysis. This chapter contains 71 references.


2017 ◽  
Author(s):  
Raghu V Durvasula ◽  
Jonathan Himmelfarb

Chronic kidney disease (CKD) is a clinical syndrome arising from progressive kidney injury, formerly known as chronic renal failure, chronic renal disease, and chronic renal insufficiency. It is classified into five stages based primarily on glomerular filtration rate (GFR). This article discusses the epidemiology of CKD and end-stage renal disease (ESRD), as well as etiology and genetics, pathophysiology, and pathogenesis. The section on diagnosis looks at clinical manifestations and physical findings, laboratory (and other) tests, imaging studies, and biopsy. A short section on differential diagnosis is followed by a discussion of treatment, including hemodialysis and peritoneal dialysis. Long-term complications of patients on dialysis include cardiovascular disease, renal osteodystrophy, dialysis-related amyloidosis, and acquired cystic disease (renal cell carcinoma). The final section addresses prognosis and socioeconomic burden. Figures include the classification system for CKD, prevalence of CKD in the United States, rising prevalence, risk of, and leading causes of ESRD in the United States, plus the changing prevalence of ESRD over time, clinical manifestations of uremia, and an overview of hemodialysis circuit. Tables look at the burden of CKD relative to other chronic disorders, the specific hereditary causes of kidney disease, and situations when serum creatinine does not accurately predict GFR. Other tables list equations for estimating GFR, the causes of CKD without shrunken kidneys, and clinical features distinguishing chronic kidney disease from acute kidney injury. ESRD and indications for initiation of dialysis are presented, as well as typical composition of dialysate and reasons for failure of peritoneal dialysis. This chapter contains 71 references.


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