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Textbook of Pediatric Infectious Diseases (2 Volume Set): Medicine & Health Science Books @ maroc-evasion.info Principles and Practice of Pediatric Infectious Diseases: Expert Consult - Online "This book provides up-to-date information on infectious disease in children. New third edition of the best-selling resource aids in the diagnosis and treatment of more than of the most commonly seen pediatric infectious diseases.
Amoxicillin, erythromycin, clindamycin, doxycycline, and Image 1. Actinomyces have fastidious growth requirements. Staining of a crushed sulfur granule reveals branching bacilli. Image 1. Actinobacillus actinomycetemcomitans, one of the HACEK group of organisms, may accompany Actinomyces israelii and may cause endocarditis. As in this infant, most cases of actinomycosis are caused by Actinomyces israelii.
Blood cultures were repeatedly negative without clinical signs of endocarditis. Courtesy of Edgar O. Courtesy of Carol J. Baker, MD. Life- threatening disseminated infection, severe pneumonia, hepatitis, meningitis, and enceph- alitis occur occasionally, especially among young infants and immunocompromised hosts.
Ocular adenovirus infections can present as a follicular conjunctivitis or as epidemic keratoconjunctivitis.
In epidemic keratoconjunctivitis, there is an autoimmune infiltration of the cornea in addition to the fol- licular conjunctivitis. In both cases, ophthal- mologic illness frequently presents acutely in one eye followed by involvement of the other eye. In epidemic keratoconjunctivitis, corneal inflammation produces symptoms including light sensitivity and vision loss. Etiology Adenoviruses are double-stranded, nonenvel- oped DNA viruses; at least 51 distinct serotypes divided into 6 species A through F cause human infections.
Some adenovirus types are associated primarily with respiratory tract dis- ease, and others are associated primarily with gastroenteritis types 40 and Adenovirus type 14 is emerging as a type that can cause severe and sometimes fatal respiratory tract illness in patients of all ages, including healthy young adults, such as military recruits. Epidemiology Infection in infants and children can occur at any age. Adenoviruses causing respiratory tract infections usually are transmitted by respira- tory tract secretions through person-to-person contact, airborne droplets, and fomites, the latter because adenoviruses are stable in the environment.
The conjunctiva can provide a portal of entry. Community outbreaks of ade- novirus-associated pharyngoconjunctival fever have been attributed to water exposure from contaminated swimming pools and fomites, such as shared towels. Adeno- virus infections in transplant recipients can occur from donor tissues. Enteric strains of adenoviruses are transmitted by the fecal-oral route.
Adenoviruses causing respiratory and enteric infections circulate throughout the year. Enteric disease primarily affects children younger than 4 years. Adenovirus infections are most communicable during the first few days of an acute illness, but persistent and intermittent shedding for longer periods, even months, is common. Asymptomatic infections are common.
Reinfection can occur. Incubation Period Respiratory tract infection, 2 to 14 days; gastro- enteritis, 3 to 10 days.
Diagnostic Tests The preferred methods for diagnosis of adeno- virus infection include cell culture, antigen detection, and DNA detection. A pharyngeal or ocular isolate suggests recent infection, but a fecal isolate indicates either recent infection or pro- longed carriage.
Rapid detection of adenovirus antigens is possible in a variety of body fluids by commercial immunoassay techniques. These rapid assays can be useful for diagnosis of respiratory tract infections, ocular disease, and diarrheal disease. Enteric adenovirus types 40 and 41 usually cannot be isolated in stan- dard cell cultures.
Adenoviruses also can be identified by electron microscopic examination of respiratory tract or stool specimens, but this Polymerase chain reaction assays for adenovirus DNA rapidly are replacing other detection methods because of improved sensitivity and increasing commer- cial availability. Adenovirus typing is available from some reference and research laboratories. Treatment Treatment of adenovirus infection is supportive.
Image 2. Adenoviruses have a characteristic icosahedral structure. Adenoviruses are resistant to alcohol, detergents, and chlorhexidine and may contaminate ophthalmologic solutions and equipment. Lobar consolidation is unusual. Note interstitial mononuclear cell infiltration and hyaline membranes. Adenoviruses types 3 and 7 can cause necrotizing bronchitis and bronchiolitis. Disease is more severe in young children, the elderly , malnourished people, and pregnant women.
Patients with noninvasive intestinal tract infection can be asymptomatic or can have nonspecific intestinal tract complaints. The mildest form of intestinal tract disease is nondysenteric colitis.
Progressive involvement of the colon can produce toxic megacolon, fulminant colitis, ulceration of the colon and perianal area and, rarely, perfora- tion. Colonic progression can occur at multiple sites and carries a high fatality rate. Amebomas can occur in any area of the colon but are more common in the cecum. Amebomas may be mistaken for colonic carcinoma. The liver is the most common extraintestinal site, and infection can spread from there to the pleural space, lungs, and pericardium.
Liver abscess can be acute, with fever, abdominal pain, tachypnea, liver tenderness, and hepatomegaly, or may be chronic, with weight loss, vague abdominal symptoms, and irritability. Rupture of a liver abscess into the abdomen or chest may lead to death. Infection also can spread from the colon to the genitourinary tract and the skin. Etiology The genus Entamoeba includes 6 species that live in the human intestine.
E histo- lytica, Entamoeba dispar, and Entamoeba moshkovskii. Groups at increased risk of infection in industrialized countries include immigrants from or long-term visitors to areas with endemic infection, institutionalized people, and men who have sex with men.
E histolytica is transmitted via amebic cysts by the fecal-oral route. Ingested cysts, which are unaffected by gastric acid, undergo excystation in the alka- line small intestine and produce trophozoites that infect the colon.
Infected patients excrete cysts intermittently, sometimes for years if untreated. Incubation Period Variable, ranging from a few days to months or years but commonly 2 to 4 weeks. Diagnostic Tests A presumptive diagnosis of intestinal tract infection depends on identifying trophozoites or cysts in stool specimens. Examination of Specimens of stool can be examined microscopically by wet mount within 30 minutes of collection or may be fixed in formalin or polyvinyl alcohol available in kits for concentration, permanent staining, and subsequent microscopic exami- nation.
Biopsy specimens and endoscopy scrapings not swabs can be examined using similar methods. Positive serologic tests persist even after adequate therapy. Ultrasonography, computed tomography, and magnetic resonance imaging can identify liver abscesses and other extraintestinal sites of infection. Aspirates from a liver abscess usually show neither trophozoites nor leukocytes. E dispar and E mosh- kovskii infections are considered to be non- pathogenic and do not require treatment.
Corticosteroids and antimotility drugs admin- istered to people with amebiasis can worsen symptoms and the disease process. The follow- ing regimens are recommended: Metronidazole is not effective. An alternate treatment for liver abscess is chloroquine administered con- comitantly with metronidazole or tinida- zole, followed by a therapeutic course of a luminal amebicide.
Percutaneous or surgical aspiration of large liver abscesses occasionally can be required when response to medical therapy is unsatis- factory.
In most cases of liver abscess, though, drainage is not required. Image 3. Trichrome stain. The ingested erythrocytes appear as dark inclusions. In these specimens, the parasite nuclei have the typical small, centrally located karyosome and thin, uniform peripheral chromatin. Courtesy of Centers for Disease Control and Prevention. The cysts are usually spherical and often have a halo B, C.
Mature cysts have 4 nuclei.
The nuclei have characteristically centrally located karyosomes and fine, uniformly distributed peripheral chromatin. The cysts in C, D, and E contain chromatoid bodies, with the one in D being particularly well demonstrated, with typically blunted ends. Here we see the site of tissue destruction, pre-debridement. Amebic liver abscesses are usually singular, large, and in the right lobe of the liver. Bacterial hepatic abscesses are more likely to be multiple.
Infection by Entamoeba histolytica occurs by ingestion of mature cysts 2 in fecally contaminated food, water, or hands. Excystation 3 occurs in the small intestine and trophozoites 4 are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts 5 , which are passed in the feces 1.
Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites can also be passed in diarrheal stools, but are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment.
In many cases, the trophozoites remain confined to the intestinal lumen A: In some patients the trophozoites invade the intestinal mucosa B: The invasive and noninvasive forms represent 2 separate species, respectively E histolytica and E dispar; however, not all persons infected with E histolytica will have invasive disease. These 2 species are morphologically indistinguishable. Transmission can also occur through fecal exposure during sexual contact in which case not only cysts, but also trophozoites, could prove infective.
Early symptoms include fever, headache, vomiting, and sometimes distur- bances of smell and taste, then progresses rap- idly to signs of meningoencephalitis including nuchal rigidity, lethargy, confusion, personal- ity changes, and altered level of consciousness. Seizures are common, and death generally occurs within a week of onset of symptoms. Granulomatous amebic encephalitis GAE caused by Acanthamoeba species and Balamu- thia mandrillaris has a more insidious onset and progression of manifestations occurring weeks to months after exposure.
Signs and symptoms include personality changes, sei- zures, headaches, nuchal rigidity, ataxia, cra- nial nerve palsies, hemiparesis, and other focal deficits.
Fever often is low grade and intermit- tent. Chronic granulomatous skin lesions pus- tules, nodules, ulcers may be present without central nervous system CNS involvement, particularly in patients with acquired immu- nodeficiency syndrome, and lesions on the midface may present for months before CNS involvement in immunocompetent hosts.
Characteristic signs include radial keratoneuritis and stromal ring infiltrate. Etiology Naegleria fowleri, Acanthamoeba species, and Balamuthia mandrillaris are free-living ame- bae that exist as motile, infectious trophozoites and environmentally hardy cysts. Epidemiology N fowleri is found in warm freshwater and moist soil. Most infections have been associ- ated with swimming in warm freshwater, such as ponds, lakes, and hot springs, but other sources have included tap water from geother- mal sources and contaminated and poorly chlorinated swimming pools.
Disease has been reported worldwide but is uncommon. The trophozoites of the parasite invade the brain directly from the nose along the olfactory nerves via the cribriform plate. In infections with N fowleri, trophozoites but not cysts can be visualized in sections of brain or in cerebrospinal fluid CSF. CNS infection attributable to Acanthamoeba occurs primarily in debilitated and immunocompro- mised people.
However, some patients infected with B mandrillaris have had no demonstrable underlying disease or disability. CNS infection by both amebae probably occurs by inhalation or direct contact with contaminated soil or water.
The primary foci of these infections most likely are skin or respiratory tract, fol- lowed by hematogenous spread to the brain.
Acanthamoeba keratitis occurs primarily in people who wear contact lenses, although it also has been associated with corneal trauma. Poor contact lens hygiene or disinfection prac- tices as well as swimming with contact lenses are risk factors. Acanthamoeba and Balamuthia GAE incubation periods are unknown but are thought to range from several weeks to months for CNS disease and within a few weeks for Acanthamoeba keratitis.
Diagnostic Tests In N fowleri infection, computed tomography scans of the head without contrast are unre- markable or show only cerebral edema; con- trast meningeal enhancement of the basilar cisterns and sulci may be found.
However, these changes are nonspecific.
N fowleri infection can be documented by microscopic demonstration of the motile trophozoites on a wet mount of centrifuged CSF. Smears of CSF should be stained with Giemsa, trichrome, or Wright stains to identify the trophozoites, if present; Gram stain is not useful. In GAE infections, CSF indices typically reveal a lymphocytic pleocytosis and an increased pro- tein concentration, with normal or low glucose concentrations.
N fowleri and Acanthamoeba species, but not Balamuthia species, can be cultured on special media; B mandrillaris can be grown using mammalian cell culture. Two survi- vors recovered after treatment with amphoteri- cin B in combination with an azole drug.
Early diagnosis and institution of high-dose drug therapy is thought to be important for optimiz- ing outcome. Effective treatment for infections caused by Acanthamoeba species and B man- drillaris has not been established.
Patients with keratitis should be evaluated by an ophthal- mologist. Early diagnosis and therapy are important for a good outcome. Note the typically large karyosome and the monopodial locomotion. Image 4. The amebae are very active and extend and retract pseudopods trichrome stain. From a patient who died of primary amebic meningoencephalitis in Virginia. B Brain histology: Fatal Naegleria fowleri meningoencephalitis, Italy.
Emerg Infect Dis. Fowleri produces an acute, and usually lethal, central nervous system disease called primary amebic meningoencephalitis. N fowleri has 3 stages: The trophozoites replicate by promitosis nuclear membrane remains intact 4. N fowleri is found in freshwater, soil, thermal discharges of power plants, heated swimming pools, hydrotherapy and medicinal pools, aquariums, and sewage.
Trophozoites can turn into temporary flagellated forms, which usually revert back to the trophozoite stage. Trophozoites infect humans or animals by entering the olfactory neuroepithelium 5 and reaching the brain. Acanthamoeba spp and B mandrillaris are opportunistic free-living amebae capable of causing granulomatous amebic encephalitis in individuals with compromised immune systems.
Acanthamoeba spp have been found in soil; fresh, brackish, and sea water; sewage; swimming pools; contact lens equipment; medicinal pools; dental treatment units; dialysis machines; heating, ventilating, and air-conditioning systems; mammalian cell cultures; vegetables; human nostrils and throats; and human and animal brain, skin, and lung tissues.
B mandrillaris, however, has not been isolated from the environment but has been isolated from autopsy specimens of infected humans and animals. Unlike N fowleri, Acanthamoeba and Balamuthia have only 2 stages: No flagellated stage exists as part of the life cycle. The trophozoites replicate by mitosis nuclear membrane does not remain intact 3.
The trophozoites are the infective forms and are believed to gain entry into the body through the lower respiratory tract or ulcerated or broken skin and invade the central nervous system by hematogenous dissemination 4. Acanthamoeba spp and B mandrillaris cysts and trophozoites are found in tissue.
Cutaneous anthrax begins as a pruritic papule or vesicle that enlarges and ulcerates in 1 to 2 days, with sub- sequent formation of a central black eschar. The lesion itself characteristically is painless, with surrounding edema, hyperemia, and painful regional lymphadenopathy.
Patients may have associated fever, lymphangitis, and extensive edema. Inhalational anthrax is a frequently lethal form of the disease and is a medical emergency. A nonspecific prodrome of fever, sweats, nonproductive cough, chest pain, headache, myalgia, malaise, and nausea and vomiting may occur initially, but illness pro- gresses to the fulminant phase 2 to 5 days later. In some cases, the illness is biphasic with a period of improvement between prodromal symptoms and overwhelming illness.
In addition, the liver and central nervous system CNS may be involved. Gastrointestinal tract disease can present as 2 clinical syndromes—intestinal or oropharyn- geal. Patients with the intestinal form have symptoms of nausea, anorexia, vomiting, and fever progressing to severe abdominal pain, massive ascites, hematemesis, bloody diarrhea, and submucosal intestinal hemorrhage. Oro- pharyngeal anthrax also may have dysphagia with posterior oropharyngeal necrotic ulcers, which may be associated with marked, often unilateral neck swelling, regional adenopathy, fever, and sepsis.
Hemorrhagic meningitis can result from hematogenous spread of the organ- ism after acquiring any form of disease and may develop without any other apparent clini- cal presentation. Etiology Bacillus anthracis is an aerobic, gram-positive, encapsulated, spore-forming, nonhemolytic, nonmotile rod.
B anthracis has 3 major viru- lence factors: The toxins are responsible for the significant mor- bidity and clinical manifestations of hemor- rhage, edema, and necrosis. Epidemiology Anthrax is a zoonotic disease most commonly affecting domestic and wild herbivores that occurs in many rural regions of the world. Natural infection of humans occurs through contact with infected animals or contaminated animal products, including carcasses, hides, hair, wool, meat, and bone meal.
Outbreaks of gas- trointestinal tract anthrax have occurred after ingestion of undercooked or raw meat from infected animals. Use of B anthracis in a biological attack would require immediate response and mobilization of public health resources.
These tests should be obtained before initiating antimicrobial therapy because previ- ous treatment with antimicrobial agents makes isolation by culture unlikely.
No con- trolled trials in humans have been performed to validate current treatment recommenda- tions for anthrax. For bioterrorism- associated cutaneous disease in adults or chil- dren, ciprofloxacin or doxycycline for children 8 years of age or older is recommended for initial treatment until antimicrobial suscepti- bility data are available.
Because of the risk of spore dormancy in mediastinal lymph nodes, the antimicrobial regimen should be continued for a total of 60 days to provide postexposure prophylaxis, in conjunction with administra- tion of vaccine. Meningitis treatment requires agents with known CNS penetration; meningeal involve- ment should be suspected in cases of inhala- tional anthrax or other systemic anthrax infections.
In addition, aggressive pleural fluid drainage is recommended if effusions exist and is recommended for treatment of all patients with inhalational anthrax. Image 5. Osteomyelitis Septic Arthritis Cutaneous Manifestatiions of Systemic Infections Bacteremia and Septic Shock Toxic Shock Syndrome Primary Immunodeficiency Diseases The Febrile Neutropenic Patient Infections in Pediatric Heart Transplantation Infections Related to Prosthetic or Artificial Devices Infections Related to Craniofacial Surgical Procedures Kawasaki Disease Staphylococcus aureus Infections Coagulase-Positive Staphylococci Coagulase-Negative Staphylococcal Infections Group B Streptococcal Infections Enterococcal and Viridans Streptococcal Infections Pneumococcal Infections Moraxella catarrhalis Diphtheria Bacillus Cereus and Other Bacillus Species Arcanobacterium haemolyticum Erysipelothrix rhusiopathiae Listeriosis Tuberculosis Leprosy and Buruli Ulcer: The Major Cutaneous Mycobacterioses Nocardia Citrobacter Extraintestinal Pathogenic Escherichia coli Diarrhea-Causing and Dysentery-Causing Escherichia coli Klebsiella Providencia Shigella Serratia Salmonella Plague Yersinia pestis Other Yersinia Species.
Miscellaneous Enterobacteriaceae Aeromonas Pasteurella multocida Cholera Vibrio parahaemolyticus Vibrio vulnificus Miscellaneous Non-Enterobacteriaceae Fermentative Bacilli Achromobacter Alcaligenes Eikenella corrodens Aggregatibacter species Brucellosis Klebsiella granulomatis Campylobacter jejuni Tularemia Haemophilus influenzae Helicobacter pylori Streptobacillus moniliformis Rat-Bite Fever Bartonella Infections Subsection 6 - Treponemataceae Relapsing Fever Leptospirosis Spirillum minus Rat-Bite Fever Syphilis Nonvenereal Treponematoses Subsection 7 - Anaerobic Bacteria Infant Botulism Actinomycosis Human Parvovirus B19 Human Polyomaviruses Herpes Simplex Viruses 1 and 2 Cytomegalovirus Epstein-Barr Virus Human Herpesviruses 6A, 6B, 7, and 8 Smallpox Variola Virus Enteroviruses, Parechoviruses, and Saffold Viruses Rhinoviruses Reoviruses Orbiviruses, Coltiviruses, and Seadornaviruses Alphaviruses a.
Western Equine Encephalitis c. Venezuelan Equine Encephalitis d. Chikungunya e. Other Alphaviral Infections Subsection 5 - Flaviviridae Louis Encephalitis b. West Nile Virus c.
Yellow Fever d. Japanese Encephalitis f. Murray Valley Encephalitis g. Tick-Borne Encephalitis h. Influenza Viruses Subsection 7 - Paramyxoviridae Parainfluenza Viruses Measles Virus Mumps Virus Respiratory Syncytial Virus Rabies Virus Subsection 9 - Arenaviridae and Filoviridae Lymphocytic Choriomeningitis Virus Filoviral Hemorrhagic Fever: Rift Valley Fever b.
Crimean-Congo Hemorrhagic Fever c. Phlebotomus Fever Sandfly Fever d. Chlamydia Infections Section 19 - Rickettsial Diseases Rickettsial and Ehrlichial Diseases. Section 20 - Mycoplasma Blastomycosis