Sunday, February 24, 2013
Candida glabrata Prosthetic Hip Infection.
Candida glabrata Prosthetic Hip Infection.
2012
Bartalesi F, Fallani S, Salomoni E, Marcucci M, Meli M, Pecile P, Cassetta MI, Latella L, Bartoloni A, Novelli A.
Source
Consultant Physician, Infectious and Tropical Diseases Department, Azienda Ospedaliero-Universitaria Careggi, Florence, Italy. bartalesif@aou-careggi.toscana.it.
Abstract
We present a case of a 60-year-old Caucasian woman carrying a 2-year-old hip prosthesis infected by Candida glabrata dose-dependent susceptible to fluconazole and voriconazole. Resection arthroplasty was performed. Six weeks of caspofungin plus liposomal amphotericin combination therapy achieved joint sterilization and allowed a successfully reimplantation arthroplasty. In addition we review 9 cases of C. glabrata prosthetic joint infection described to date in the literature.
Labels: arthroplasty, Candida glabrata, caspofungin, Infection, liposomal amphotericin, Prosthetic Hip
# posted by Pat O'Connor @ 8:32 AM
Wednesday, February 13, 2013
Evaluation of diagnostic value of procalcitonin as a marker of neonatal bacterial infections.
Evaluation of diagnostic value of procalcitonin as a marker of neonatal bacterial infections.
2012
Source
Pathology department, Hamadan University of Medical Sciences, Hamadan, Iran.
Abstract
KEYWORDS: Infection, Newborn, Predictive Value of Tests, Procalcitonin, Sensitivity, Specificity
OBJECTIVE:
This study tried to assess sensitivity, specificity, positive and negative predictive value of procalcitonin for diagnosis of neonatal bacterial infections.
METHODS:
This prospective cross sectional study was carried out during an 18-month period in NICU and neonatal wards of Besat Hospital in Hamedan province, Iran. 39 symptomatic infants with clinical and laboratory findings in favor of bacterialinfection with a positive blood, CSF, and/or supra pubic urine culture entered the study; 32 newborns without any bacterialinfection served as control group. Quantitative procalcitonin level ≥0.5 ng/ml was accepted as pathological. Finally sensitivity, specificity, positive (PPV) and negative predictive value (NPV) were calculated for procalcitonin test.
FINDINGS:
20 blood cultures, 17 urine cultures and 8 CSF cultures were positive. Sensitivity, specificity, PPV and NPV for procalcitonin test was 76.9%, 100%, 100% and 78% respectively. Diagnostic value of procalcitonin test in accordance with blood culture for mentioned items was 85%, 100%, 100% and 91.4% respectively. Its diagnostic value according to urine culture was: sensitivity 70.6%, specificity 100%, PPV 100% and NPV 86.4%, and according to CSF culture was: sensitivity 75%, specificity 100%, PPV 100% and NPV 94.1% respectively.
CONCLUSION:
The results show that the procalcitonin test has high sensitivity, specificity, PPV and NPV for diagnosis of neonatal infections.
Labels: blood cultures, Infection, newborn, Predictive Value of Tests, Procalcitonin, Sensitivity, Specificity, urine cultures
# posted by Pat O'Connor @ 7:57 AM
Thursday, February 07, 2013
A case of mycoplasma hominis infection on chronic refractory lower leg ulceration caused by livedo vasculopathy
A case of mycoplasma hominis infection on chronic refractory lower leg ulceration caused by livedo vasculopathy
2012
[Article in Japanese]
Source
Clinical Laboratory Department, St. Luke's International Hospital, Chuo-ku, Tokyo 104-8560, Japan. yamaji@luke.or.jp
Abstract
Mycoplasma hominis is a common inhabitant of the human urogenital tract and most frequently causes diseases of the genitourinary tract. Extragenital M. hominis infections are uncommon, with almost all occurring in immunosuppressed persons or those predisposed due to surgery or trauma. We report a case of non surgical, non-traumatic wound infectioncaused by M. hominis. A 28-year-old immunocompetent woman with livedo vasculopathy had an open wound on dorsum of her right foot with signs and symptoms of infection. However, gram staining of the wound swab demonstrated no microorganisms, and initial bacterial cultures did not reveal any microbial growth. After 2 days of culture, minute translucent colonies were appeared and subsequently identified as M. hominis. She was successfully treated with levofloxacin(LVFX). For the patient's being immune-competent, this infection seems to need a substantial bacterial transfer from the inhabitant organ. The transfer is likely mediated by the fluid's drop, for anatomical locations of vagina and the infection site on leg. Namely, the hinder leg infection is suspected to be caused by continual and heavy bacterial exposure originated from the vaginal M. hominis. This clinical case suggests that infections may occur even in normal immunological status if the site is close to, and lacks anatomical barrier from, the M. hominis inhabitant organ. Especially in infection at chronic refractory lower leg ulceration, M. hominis should be considered as a causative organism.
Labels: human urogenital tract, immunocompetent, Infection, levofloxacin, livedo vasculopathy, lower leg ulceration, LVFX, mycoplasma hominis
# posted by Pat O'Connor @ 7:01 AM
Wednesday, January 30, 2013
Infections Succumbs to Blue Light
Infections Succumbs to Blue Light
January 2013
Blue light can selectively eradicate Pseudomonas aeruginosa infections of the skin and soft tissues, while preserving the outermost layer of skin, according to a proof-of-principle study led by Michael R. Hamblin of the Massachusetts General Hospital, and the Harvard Medical School in Boston. The research is published online ahead of print in the journal Antimicrobial Agents and Chemotherapy.
"Blue light is a potential non-toxic, non-antibiotic approach for treating skin and soft tissue infections, especially those caused by antibiotic resistant pathogens," says Hamblin.
In the study, animal models were infected with P. aeruginosa. All of the animals in the group treated with blue light survived, while in the control, 82 percent (9 out of 11) of the animals died.
Skin and soft tissue infections are the second most common bacterial infections encountered in clinical practice, and represent the most common infection presentation—more than 3 percent—in patients visiting emergency departments, says Hamblin. The prevalence of skin and soft tissue infections among hospitalized patients is 10 percent, with approximately 14.2 million ambulatory care visits every year and an annual associated medical cost of almost $24 billion (equivalent to $76 for every American), says Hamblin.
Treatment of skin and soft tissue infections has been significantly complicated by the explosion of antibiotic resistance, which may bring an end to what medical scientists refer to as the antibiotic era, says Hamblin. "Microbes replicate very rapidly, and a mutation that helps a microbe survive in the presence of an antibiotic drug will quickly predominate throughout the microbial population. Recently, a dangerous new enzyme, NDM-1, that makes some bacteria resistant to almost all antibiotics available has been found in the United States. Many physicians are concerned that several infections soon may be untreatable."
Besides harming public health, antibiotic resistance boosts health care costs. "Treating resistant skin and soft tissue infections often requires the use of more expensive, or more toxic drugs, and can result in longer hospital stays for infected patients," says Hamblin.
Reference: Dai T, Gupta A, et al. 2013. Blue light rescues mice from potentially fatal Pseudomonas aeruginosa burn infection: efficacy, safety, and mechanism of action. Antim. Agents Chemother. Published ahead of print Dec. 21, 2012 ,doi:10.1128/AAC.01652-12)
Labels: Antibiotic resistance, blue light, enzyme, Infection, NDM-1, Pseudomonas aeruginos, skin infections, soft tissue infections, treatment
# posted by Pat O'Connor @ 9:46 AM
Saturday, December 29, 2012
A genomic analysis of Clostridium difficile infections in blunt trauma patients.
A genomic analysis of Clostridium difficile infections in blunt trauma patients.
Jan 2013
Efron PA, Liu H, Lottenberg L, Cuenca AG, Gentile LF, Miggins MV, Bihorac A, Baker HV, Moore FA, Moldawer LL, Ang DN.
Source
From the Departments of Surgery (P.A.E., H.L., L.L., A.G.C., L.F.G., M.V.M., F.A.M., L.L.M., D.N.A.), Anesthesia (A.B.), and Molecular Genetics and Microbiology (H.V.B.), University of Florida, Gainesville, Florida.
Abstract
BACKGROUND:
Evidence demonstrates that susceptibility to Clostridium difficile infection is related to host risk factors as much as bacterial potency. Using blood leukocyte genome-wide expression patterns of severe blunt trauma patients obtained by the National Institute of General Medical Sciences-sponsored Glue Grant Inflammation and the Host Response to Injury, we examined leukocyte genomic profiles of patients with C. difficile infection to determine preinfection and postinfection gene expression changes.
METHODS:
The genomic responses of 21 severe trauma patients were analyzed (5 C. difficile, 16 controls matched for age and severity of injury). After elimination of probe sets whose expression was below baseline or were unchanged, remaining probe sets underwent hierarchical clustering and principal component analysis. Molecular pathways were generated through Ingenuity Pathways Analysis.
RESULTS:
Supervised analysis demonstrated 118 genes whose expression in patients with C. difficile infection varied before and after their infection. Supervised analysis comparing patients with C. difficile infection with matched non-C. difficile patients before infection suggested that the expression of 501 genes were different in the two groups with up to 87% class prediction (p < 0.05). Many of these genes are related to cell-mediated immune responses, signaling, and interaction.
CONCLUSION:
Genomic analysis of severe blunt trauma patients reveals a distinct leukocyte expression profile of C. difficile both before and after infection. We conclude that an association may exist between a severe trauma patient's leukocyte genomic expression profile and subsequent susceptibility to C. difficile infection. Further prospective expression analysis of this C. difficile population may reveal potential therapeutic interventions and allow early identification of C. difficile-susceptible patients.
LEVEL OF EVIDENCE:
Prognostic/diagnostic study, level III.
Labels: bacterial potency, blunt trauma patient, Clostridium difficile, Genomic analysis, Infection
# posted by Pat O'Connor @ 8:48 AM
Saturday, September 01, 2012
Seven year old boy dies from flesh eating bacterial disease
Seven year old boy dies from flesh eating bacterial disease
Sept 1, 2012
MailOnline
Sept 1, 2012
A seven-year-old boy from Texas who developed a rash under his arm during a July trip to San Diego, California, died after contracting a flesh-eating bacterial infection, the Medical Examiner’s Office announced on Thursday
Tevita Alatini’s official cause of death was listed as bacterial necrotizing myositis, which means that infection spread into muscle tissue.
Officials listed autoimmune hemolytic anemia - a malfunction of the immune system - as a contributing condition.
Alatini passed away on July 10 at Rady Children’s Hospital, three days after arriving in San Diego with his family from Spring, Texas, for a family reunion, the San Diego Union-Tribune reported.
Shortly after the boy’s death, his uncle Sione Niko told the North County Times that the family had traveled to Lake O’Neill Recreational Park on the Camp Pendleton Marine Corps base on July 9 when his nephew fell ill and developed a rash.
Helen Niko, one of Tevita's aunts, told San Diego's 10News.com: 'He was happy and climbing light poles and running around and having a good time just like any other seven-year-old would.
'At first we thought it was nothing to worry about as he was born with a weak immune system but then the rash came.'
Flesh-eating infections are often contracted while swimming in a lake or pond, and the boy's parents told the press in July that their son ventured into the water during the camping trip.
However, Niko insisted that his nephew did not even go near the lake.
'He was sitting down and just hanging out with everybody, just having family time. Then he was complaining about a pain on his side, and it started off just like a little rash, and then it just became bigger,' Niko said.
He was just laying there not feeling well, and he was throwing up again, and he just became real sick. He wasn’t really responding to his mother, so that’s when they decided that he needed to go straight to the ER.'
The autopsy conducted on the seven-year-old’s body did not address how the boy might have developed the rare disease.
Tevita’s parents noticed a large red spot under his left arm after their lake outing and took their son to the base hospital, where doctors recognized the signs of a severe infection and had the child airlifted to Rady Children’s Hospital.
The boy went into medical arrest shortly after arriving at the hospital and was pronounced dead early the next morning.
The day after he died, the family held a memorial for the seven-year-old at the beach at Camp Pendleton.
The bacteria that led to Tevita’s death is known to release toxins which destroy tissue, thus earning it the term ‘flesh-eating.’
According to the National Necrotizing Fasciitis Foundation, it can be caused by various types of germs which usually enter the body through a wound in the skin, sometimes as small as a paper cut. They can also be swallowed or inhaled.
One drop of untreated water can contain millions of bacteria. It is possible to develop skin infections, ear infections, eye infections, diarrhea, and respiratory infections from contaminated lake water.
If caught early, the rapidly progressing disease can be stopped with the use of antibiotics, according to the foundation.
MailOnline
Labels: autoimmune hemolytic anemia, bacterial necrotizing myositis, flesh eating bacteria, immune system, Infection
# posted by Pat O'Connor @ 9:34 AM
Monday, August 27, 2012
Alpha-Toxin Promotes Staphylococcus aureus Mucosal Biofilm Formation.
Alpha-Toxin Promotes Staphylococcus aureus Mucosal Biofilm Formation.
2012
Source
Department of Experimental and Clinical Pharmacology, University of Minnesota Minneapolis, MN, USA.
Abstract
Staphylococcus aureus causes many diseases in humans, ranging from mild skin infections to serious, life-threatening, superantigen-mediated Toxic Shock Syndrome (TSS). S. aureus may be asymptomatically carried in the anterior nares or vagina or on the skin, serving as a reservoir for infection. Pulsed-field gel electrophoresis clonal type USA200 is the most widely disseminated colonizer and the leading cause of TSS. The cytolysin α-toxin (also known as α-hemolysin or Hla) is the major epithelial proinflammatory exotoxin produced by TSS S. aureus USA200 isolates. The current study aims to characterize the differences between TSS USA200 strains [high (hla(+)) and low (hla(-)) α-toxin producers] in their ability to disrupt vaginal mucosal tissue and to characterize the subsequent infection. Tissue viability post-infection and biofilm formation of TSS USA200 isolates CDC587 and MN8, which contain the α-toxin pseudogene (hla(-)), MNPE (hla(+)), and MNPE isogenic hla knockout (hlaKO), were observed via LIVE/DEAD® staining and confocal microscopy. All TSS strains grew to similar bacterial densities (1-5 × 10(8) CFU) on the mucosa and were proinflammatory over 3 days. However, MNPE formed biofilms with significant reductions in the mucosal viability whereas neither CDC587 (hla(-)), MN8 (hla(-)), nor MNPE hlaKO formed biofilms. The latter strains were also less cytotoxic than wild-type MNPE. The addition of exogenous, purified α-toxin to MNPE hlaKO restored the biofilm phenotype. We speculate that α-toxin affects S. aureus phenotypic growth on vaginal mucosa by promoting tissue disruption and biofilm formation. Further, α-toxin mutants (hla(-)) are not benign colonizers, but rather form a different type of infection, which we have termed high density pathogenic variants (HDPV).
Labels: alpha toxin, bacterial denisty, colonizer, Infection, mucosal biofilm, skin, staphylocuccus, toxic shock syndrome, TSS
# posted by Pat O'Connor @ 9:52 AM
Thursday, September 24, 2009
Guidelines Issued for Management of Opportunistic Infections Among HIV-Exposed Children
Guidelines Issued for Management of Opportunistic Infections Among HIV-Exposed Children
News Author: Laurie Barclay, MDCME Author: Charles P. Vega, MD, FAAFP
September 8, 2009 — Children who either have been exposed to HIV or who are infected with HIV are at increased risk for certain opportunistic diseases, according to new recommendations published online August 26 in the Morbidity and Mortality Weekly Report.
The new guidelines were issued jointly by the US Centers for Disease Control and Prevention, the National Institutes of Health (NIH), the HIV Medicine Association of the Infectious Diseases Society of America, the Pediatric Infectious Diseases Society, and the American Academy of Pediatrics.
These guidelines update previous recommendations for clinicians and other healthcare practitioners providing medical care for HIV-exposed or HIV-infected children. Earlier guidelines were last published in 2002 and 2004, respectively.
"In the pre-antiretroviral era and before development of potent combination highly active antiretroviral treatment (HAART) regimens, opportunistic infections (OIs) were the primary cause of death in [HIV]-infected children," write Lynne M. Mofenson, MD, from the NIH in Bethesda, Maryland, and colleagues.
"Current HAART regimens suppress viral replication, provide significant immune reconstitution, and have resulted in a substantial and dramatic decrease in [AIDS]-related OIs and deaths in both adults and children.... Despite this progress, prevention and management of OIs remain critical components of care for HIV-infected children."
Development of Updated Guidelines
The Pediatric Opportunistic Infections Working Group, a panel of experts from the US government and academic institutions specializing in pediatric HIV infection and other infectious diseases, developed recommendations for the most effective strategies for diagnosis, prevention, and treatment of OIs.
For each OI, a pediatric specialist expert in that OI reviewed the literature for new information published since the previous guidelines were issued. In June 2007, revised recommendations were proposed at an NIH meeting, and the draft guidelines were revised further, reviewed and approved by the working group, and approved by the issuing organizations.
In addition to covering the management of opportunistic diseases encountered in the United States (Pneumocystis pneumonia, Toxoplasma gondii, Mycobacterium avium complex, Coccidioides species, Cryptococcus neoformans, Histoplasma capsulatum, microsporidiosis, cytomegalovirus, invasive bacterial infections, bartonellosis, Candida [esophageal], and herpes simplex virus), the guidelines also discuss malaria — an OI that could be acquired during international travel.
For each OI, the report summarizes epidemiology, clinical presentation, and diagnosis in children. Main topics include preventing exposure to OIs, using chemoprophylaxis and/or vaccination to prevent infection, discontinuing primary prophylaxis after immune reconstitution, treating OIs, monitoring for adverse effects during treatment, managing treatment failure, preventing recurrence of OIs, and discontinuing secondary prophylaxis after immune reconstitution.
A working group of experts specializing in adult HIV and infectious disease prepared a separate report on the prevention and treatment of OIs in HIV-infected adults and postpubertal adolescents, titled "Guidelines for the Prevention and Treatment of Opportunistic Infections in HIV-Infected Adults and Adolescents."
Populations Affected by OIs
Because HIV-infected women coinfected with opportunistic pathogens may be more likely than women uninfected with HIV to transmit these OIs to their infants, an infected mother is an important pathway for OI transmission, as well as for HIV infection, among children. Furthermore, mothers and other family members coinfected with HIV and certain opportunistic pathogens may be more likely to transmit these infections horizontally to young children, increasing the probability that the child will primarily acquire these infections.
OIs may therefore affect not just HIV-infected infants but also HIV-exposed but uninfected infants who become infected by the pathogen via HIV-infected mothers or family members with coinfections. For these reasons, the updated guidelines for treating OIs in children consider treatment of infections among all children — both HIV-infected and uninfected — born to HIV-infected women.
Incidence of HIV infection is rising both among adolescents with perinatal infection who have survived into their teenage years and among youth with behaviorally acquired HIV infection. The adult OI guidelines are applicable to postpubertal adolescents, but younger prepubertal or pubertal adolescents may have differing drug pharmacokinetics and response to treatment, with management best served by the pediatric guidelines.
Updated Recommendations
Since the previous versions of these guidelines, major changes in the new recommendations are as follows:
Increased emphasis on the importance of antiretroviral therapy to prevent and treat OIs, particularly those OIs for which no specific treatment is available.
New evidence regarding diagnosis and management of immune reconstitution inflammatory syndromes.
New information concerning management of antiretroviral therapy in children with OIs, including potential drug–drug interactions.
New strategies for diagnosis of HIV infection and for presumptively ruling out HIV infection in infants that affect the need to start prophylaxis for the prevention of Pneumocystis jirovecii pneumonia in neonates. Prophylaxis against Pneumocystis carinii should be considered in all infants exposed to HIV.
Updated recommendations for immunizing HIV-exposed and HIV-infected children against hepatitis A, human papillomavirus, meningococcus, and rotavirus. Children with HIV infection and good immune function should be routinely vaccinated against varicella, measles-mumps-rubella, and human papillomavirus. To weigh potential risks and benefits of vaccination against rotavirus in an infant exposed to HIV infection, expert consultation may be needed.
New sections on aspergillosis; bartonella; human herpes viruses 6, 7, and 8; malaria; and progressive multifocal leukodystrophy. Children infected with HIV do not require routine prophylaxis against aspergillosis, coccidiomycosis, or cryptococcal disease.
New guidelines for discontinuing OI prophylaxis after immune reconstitution in children.
In addition, there are 6 tables with information concerning prevention and treatment of OIs in children and 2 figures depicting immunization recommendations for children aged 0 to 6 years and 7 to 18 years. The guidelines authors acknowledge that treatment of OIs is an evolving science and that therapeutic options and preferences may change on the basis of the availability of new agents or clinical data on existing agents. The recommendations in these guidelines will therefore be updated periodically and posted on the NIH AIDSinfo Web site.
Morb Mortal Wkly Rep. Published online August 26, 2009.
Clinical Context
The main cause of HIV infection among children is vertical transmission from their mother, and the current guidelines highlight that the mother and nuclear family unit continue to be a strong potential reservoir for OIs as these children grow. These OIs may also infect infants without HIV infection. Therefore, the authors of the current guidelines focus their recommendations regarding OI prevention and treatment to all children born to women with HIV infection.
The guidelines regarding OIs among children were last updated in 2004. The current revised recommendations were initially proposed by an expert panel at a meeting of the NIH in 2007 and were then endorsed by multiple governmental and physician specialty groups.
Study Highlights
The use of HAART among children can be useful to both prevent and treat OIs for which specific treatments are less effective, including infections such as cryptosporidiosis and microsporidiosis.
Immune reconstitution inflammatory syndrome (IRIS) can occur in children after the initiation of treatment of HIV infection. However, among adults, up to 30% of cases of IRIS may be present at 3 months after initiation of HAART. HAART should be continued in cases of IRIS, and nonsteroidal anti-inflammatory drugs should be added, along with close supervision, for adequate treatment of most moderate cases. Antibiotics are unnecessary in the treatment of IRIS.
The best timing to initiate HAART after an OI remains unclear and needs to be individualized to the patient's needs.
Vaccination against varicella and measles-mumps-rubella may be considered among HIV-infected children with age-specific CD4 levels of at least 15%.
Although vaccine immune response may be less than among immunocompetent peers, the human papillomavirus vaccine may be administered to girls with HIV infection.
There are no safety data regarding the application of the rotavirus vaccine to infants who are potentially immunocompromised, and the diagnosis of HIV infection in the infant may not even be established at the time of the first vaccination. Whether to provide vaccination against rotavirus among infants exposed to HIV may require consultation with an expert in infectious disease or immunology.
Bartenellosis may be prevented by the avoidance of body lice, cats, and cat fleas. Moderate cat-scratch disease among children with HIV infection typically does not respond to antibiotic therapy, and treatment is supportive.
Previous estimates have found that 1.1% of children with tuberculosis have a coinfection with HIV, a lower rate vs the adult population. Children with HIV infection should receive annual tuberculin skin tests. Treatment of active tuberculosis is similar among children with and without HIV, although the concurrent use of HAART can complicate tuberculosis treatment (particularly the use of rifamycins). The usual treatment period is 6 months.
Clarithromycin and azithromycin may be used to prevent M avium complex disease in children, but children with a sustained positive immune response to HAART for 3 months or longer may discontinue antibiotic prophylaxis against M avium complex.
Prophylaxis against aspergillosis and coccidiomycosis among children with HIV infection is not recommended. Voriconazole is the first-line therapy for active aspergillosis, and disseminated coccidiomycosis infection requires treatment with amphotericin B.
Children with HIV infection do not require routine testing for the cryptococcal antigen or prophylaxis against infection with cryptococcus.
Conversely, infants born to mothers with HIV infection should be considered for antibiotic prophylaxis against P carinii beginning at ages 4 to 6 weeks. Trimethoprim-sulfamethoxazole is the first-line agent for prophylaxis.
Children with HIV infection traveling to endemic areas of malaria infection should receive prophylactic antibiotics against malaria, and care must be taken to avoid significant interactions with HAART, if possible. Trimethoprim-sulfamethoxazole should not be used as prophylaxis against malaria.
Clinical Implications
The current study recommends routine vaccination against varicella, measles-mumps-rubella, and human papillomavirus among children with HIV infection and good immune function. However, vaccination against rotavirus may require consultation with an expert to weigh potential risks and benefits in an infant exposed to HIV infection.
Children with HIV infection do not require routine prophylaxis against aspergillosis, coccidiomycosis, or cryptococcus, but all infants exposed to HIV should be considered for prophylaxis against P carinii.
Medscape
News Author: Laurie Barclay, MDCME Author: Charles P. Vega, MD, FAAFP
September 8, 2009 — Children who either have been exposed to HIV or who are infected with HIV are at increased risk for certain opportunistic diseases, according to new recommendations published online August 26 in the Morbidity and Mortality Weekly Report.
The new guidelines were issued jointly by the US Centers for Disease Control and Prevention, the National Institutes of Health (NIH), the HIV Medicine Association of the Infectious Diseases Society of America, the Pediatric Infectious Diseases Society, and the American Academy of Pediatrics.
These guidelines update previous recommendations for clinicians and other healthcare practitioners providing medical care for HIV-exposed or HIV-infected children. Earlier guidelines were last published in 2002 and 2004, respectively.
"In the pre-antiretroviral era and before development of potent combination highly active antiretroviral treatment (HAART) regimens, opportunistic infections (OIs) were the primary cause of death in [HIV]-infected children," write Lynne M. Mofenson, MD, from the NIH in Bethesda, Maryland, and colleagues.
"Current HAART regimens suppress viral replication, provide significant immune reconstitution, and have resulted in a substantial and dramatic decrease in [AIDS]-related OIs and deaths in both adults and children.... Despite this progress, prevention and management of OIs remain critical components of care for HIV-infected children."
Development of Updated Guidelines
The Pediatric Opportunistic Infections Working Group, a panel of experts from the US government and academic institutions specializing in pediatric HIV infection and other infectious diseases, developed recommendations for the most effective strategies for diagnosis, prevention, and treatment of OIs.
For each OI, a pediatric specialist expert in that OI reviewed the literature for new information published since the previous guidelines were issued. In June 2007, revised recommendations were proposed at an NIH meeting, and the draft guidelines were revised further, reviewed and approved by the working group, and approved by the issuing organizations.
In addition to covering the management of opportunistic diseases encountered in the United States (Pneumocystis pneumonia, Toxoplasma gondii, Mycobacterium avium complex, Coccidioides species, Cryptococcus neoformans, Histoplasma capsulatum, microsporidiosis, cytomegalovirus, invasive bacterial infections, bartonellosis, Candida [esophageal], and herpes simplex virus), the guidelines also discuss malaria — an OI that could be acquired during international travel.
For each OI, the report summarizes epidemiology, clinical presentation, and diagnosis in children. Main topics include preventing exposure to OIs, using chemoprophylaxis and/or vaccination to prevent infection, discontinuing primary prophylaxis after immune reconstitution, treating OIs, monitoring for adverse effects during treatment, managing treatment failure, preventing recurrence of OIs, and discontinuing secondary prophylaxis after immune reconstitution.
A working group of experts specializing in adult HIV and infectious disease prepared a separate report on the prevention and treatment of OIs in HIV-infected adults and postpubertal adolescents, titled "Guidelines for the Prevention and Treatment of Opportunistic Infections in HIV-Infected Adults and Adolescents."
Populations Affected by OIs
Because HIV-infected women coinfected with opportunistic pathogens may be more likely than women uninfected with HIV to transmit these OIs to their infants, an infected mother is an important pathway for OI transmission, as well as for HIV infection, among children. Furthermore, mothers and other family members coinfected with HIV and certain opportunistic pathogens may be more likely to transmit these infections horizontally to young children, increasing the probability that the child will primarily acquire these infections.
OIs may therefore affect not just HIV-infected infants but also HIV-exposed but uninfected infants who become infected by the pathogen via HIV-infected mothers or family members with coinfections. For these reasons, the updated guidelines for treating OIs in children consider treatment of infections among all children — both HIV-infected and uninfected — born to HIV-infected women.
Incidence of HIV infection is rising both among adolescents with perinatal infection who have survived into their teenage years and among youth with behaviorally acquired HIV infection. The adult OI guidelines are applicable to postpubertal adolescents, but younger prepubertal or pubertal adolescents may have differing drug pharmacokinetics and response to treatment, with management best served by the pediatric guidelines.
Updated Recommendations
Since the previous versions of these guidelines, major changes in the new recommendations are as follows:
Increased emphasis on the importance of antiretroviral therapy to prevent and treat OIs, particularly those OIs for which no specific treatment is available.
New evidence regarding diagnosis and management of immune reconstitution inflammatory syndromes.
New information concerning management of antiretroviral therapy in children with OIs, including potential drug–drug interactions.
New strategies for diagnosis of HIV infection and for presumptively ruling out HIV infection in infants that affect the need to start prophylaxis for the prevention of Pneumocystis jirovecii pneumonia in neonates. Prophylaxis against Pneumocystis carinii should be considered in all infants exposed to HIV.
Updated recommendations for immunizing HIV-exposed and HIV-infected children against hepatitis A, human papillomavirus, meningococcus, and rotavirus. Children with HIV infection and good immune function should be routinely vaccinated against varicella, measles-mumps-rubella, and human papillomavirus. To weigh potential risks and benefits of vaccination against rotavirus in an infant exposed to HIV infection, expert consultation may be needed.
New sections on aspergillosis; bartonella; human herpes viruses 6, 7, and 8; malaria; and progressive multifocal leukodystrophy. Children infected with HIV do not require routine prophylaxis against aspergillosis, coccidiomycosis, or cryptococcal disease.
New guidelines for discontinuing OI prophylaxis after immune reconstitution in children.
In addition, there are 6 tables with information concerning prevention and treatment of OIs in children and 2 figures depicting immunization recommendations for children aged 0 to 6 years and 7 to 18 years. The guidelines authors acknowledge that treatment of OIs is an evolving science and that therapeutic options and preferences may change on the basis of the availability of new agents or clinical data on existing agents. The recommendations in these guidelines will therefore be updated periodically and posted on the NIH AIDSinfo Web site.
Morb Mortal Wkly Rep. Published online August 26, 2009.
Clinical Context
The main cause of HIV infection among children is vertical transmission from their mother, and the current guidelines highlight that the mother and nuclear family unit continue to be a strong potential reservoir for OIs as these children grow. These OIs may also infect infants without HIV infection. Therefore, the authors of the current guidelines focus their recommendations regarding OI prevention and treatment to all children born to women with HIV infection.
The guidelines regarding OIs among children were last updated in 2004. The current revised recommendations were initially proposed by an expert panel at a meeting of the NIH in 2007 and were then endorsed by multiple governmental and physician specialty groups.
Study Highlights
The use of HAART among children can be useful to both prevent and treat OIs for which specific treatments are less effective, including infections such as cryptosporidiosis and microsporidiosis.
Immune reconstitution inflammatory syndrome (IRIS) can occur in children after the initiation of treatment of HIV infection. However, among adults, up to 30% of cases of IRIS may be present at 3 months after initiation of HAART. HAART should be continued in cases of IRIS, and nonsteroidal anti-inflammatory drugs should be added, along with close supervision, for adequate treatment of most moderate cases. Antibiotics are unnecessary in the treatment of IRIS.
The best timing to initiate HAART after an OI remains unclear and needs to be individualized to the patient's needs.
Vaccination against varicella and measles-mumps-rubella may be considered among HIV-infected children with age-specific CD4 levels of at least 15%.
Although vaccine immune response may be less than among immunocompetent peers, the human papillomavirus vaccine may be administered to girls with HIV infection.
There are no safety data regarding the application of the rotavirus vaccine to infants who are potentially immunocompromised, and the diagnosis of HIV infection in the infant may not even be established at the time of the first vaccination. Whether to provide vaccination against rotavirus among infants exposed to HIV may require consultation with an expert in infectious disease or immunology.
Bartenellosis may be prevented by the avoidance of body lice, cats, and cat fleas. Moderate cat-scratch disease among children with HIV infection typically does not respond to antibiotic therapy, and treatment is supportive.
Previous estimates have found that 1.1% of children with tuberculosis have a coinfection with HIV, a lower rate vs the adult population. Children with HIV infection should receive annual tuberculin skin tests. Treatment of active tuberculosis is similar among children with and without HIV, although the concurrent use of HAART can complicate tuberculosis treatment (particularly the use of rifamycins). The usual treatment period is 6 months.
Clarithromycin and azithromycin may be used to prevent M avium complex disease in children, but children with a sustained positive immune response to HAART for 3 months or longer may discontinue antibiotic prophylaxis against M avium complex.
Prophylaxis against aspergillosis and coccidiomycosis among children with HIV infection is not recommended. Voriconazole is the first-line therapy for active aspergillosis, and disseminated coccidiomycosis infection requires treatment with amphotericin B.
Children with HIV infection do not require routine testing for the cryptococcal antigen or prophylaxis against infection with cryptococcus.
Conversely, infants born to mothers with HIV infection should be considered for antibiotic prophylaxis against P carinii beginning at ages 4 to 6 weeks. Trimethoprim-sulfamethoxazole is the first-line agent for prophylaxis.
Children with HIV infection traveling to endemic areas of malaria infection should receive prophylactic antibiotics against malaria, and care must be taken to avoid significant interactions with HAART, if possible. Trimethoprim-sulfamethoxazole should not be used as prophylaxis against malaria.
Clinical Implications
The current study recommends routine vaccination against varicella, measles-mumps-rubella, and human papillomavirus among children with HIV infection and good immune function. However, vaccination against rotavirus may require consultation with an expert to weigh potential risks and benefits in an infant exposed to HIV infection.
Children with HIV infection do not require routine prophylaxis against aspergillosis, coccidiomycosis, or cryptococcus, but all infants exposed to HIV should be considered for prophylaxis against P carinii.
Medscape
Labels: children, guidlines, HAART, HIV, human papillomavirus, Immune reconstitution inflammatory syndrome, Infection, measles, meningococcus, mumps, rotavirus, rubella, trteatment, varicella
# posted by Pat O'Connor @ 3:03 AM
