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الكلية كلية طب حمورابي
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المرحلة 5
أستاذ المادة بشار صاحب خلف الشمري
6/7/2011 8:14:28 AM
giardia lamblia
giardia lamblia (also referred to as g. intestinalis and g. duodenalis) is a flagellated protozoan that infects the duodenum and small intestine. infection is more prevalent in children than in adults. giardia organisms are endemic in areas of the world with poor levels of sanitation. giardia is a particularly significant pathogen in people with malnutrition, certain immunodeficiencies, and cystic fibrosis.
giardia infects humans after ingestion of as few as 10–100 cysts. ingested cysts each produce two trophozoites in the duodenum. after excystation, trophozoites colonize the lumen of the duodenum and proximal jejunum, where they attach to the brush border of the intestinal epithelial cells and multiply by binary fission. as detached trophozoites pass down the intestinal tract, they encyst to form oval cysts. cysts are passed in stools of infected individuals and may remain viable in water for as long as 2 mo. their viability often is not affected by the usual concentrations of chlorine used to purify water for drinking.
epidemiology
the age-specific prevalence of giardiasis is high during childhood and begins to decline after adolescence. asymptomatic carriage may persist for several months. the major reservoir and vehicle for spread of giardia appears to be water contaminated with giardia cysts, but foodborne transmission occurs. giardia cysts are relatively resistant to chlorination and to ultraviolet light irradiation, boiling is effective for inactivating cysts.
humoral immunodeficiencies including common variable hypogammaglobulinemia and x-linked agammaglobulinemia predispose humans to chronic symptomatic giardia infection, suggesting the importance of humoral immunity in controlling giardiasis. there is a higher incidence of giardia infection in patients with cystic fibrosis, probably owing to local factors such as the increased amount of mucus, which may protect the organism against host factors in the duodenum. human milk contains glycoconjugates and secretory iga antibodies that may provide protection to nursing infants.
clinical manifestations
the incubation period of giardia infection usually is 1–2 wk but may be longer. children with g. lamblia may experience asymptomatic excretion of the organism, acute infectious diarrhea, or chronic diarrhea with persistent gastrointestinal tract signs and symptoms, including failure to thrive. most infections in both children and adults are asymptomatic.
symptomatic infections occur more frequently in children than in adults. most symptomatic patients usually have a limited period of acute diarrheal disease with or without low-grade fever, nausea, and anorexia in a small proportion an intermittent or more protracted course characterized by diarrhea, abdominal distention and cramps, bloating, malaise, flatulence, nausea, anorexia, and weight loss develops. initially, stools may be profuse and watery and later becomes greasy and foul smelling and may float. stools do not contain blood, mucus, or fecal leukocytes. varying degrees of malabsorption may occur. abnormal stool patterns may alternate with periods of constipation and normal bowel movements. malabsorption of sugars, fats, and fat-soluble vitamins has been well documented and may be responsible for substantial weight loss.
diagnosis
giardiasis should be considered in young children in child care or in any person who has had contact with an index case or a history of recent travel to an endemic area who has persistent diarrhea, intermittent diarrhea and constipation, malabsorption, crampy abdominal pain and bloating, or failure to thrive or weight loss.
a definitive diagnosis of giardiasis is established by documentation of trophozoites, cysts, or giardia antigens in stool specimens or duodenal fluid. several types of specimens from the gastrointestinal tract can be used to diagnose giardia infection.
for both trophozoites and cysts of giardia organisms, identification can be made on direct smears of stool specimens. stool specimens should be examined within 1hr of passage. trophozoites may be present in unformed stools as a result of rapid bowel transit they are not stable outside the gastrointestinal tract.
cysts are stable outside the gastrointestinal tract and are the infectious form. in patients in whom the diagnosis is suspected but in whom examination of stool specimens for giardia yields a negative result, aspiration or biopsy of the duodenum or upper jejunum should be performed. the biopsy can be used to make touch preparations and tissue sections for identification of giardia and other enteric pathogens, as well as to visualize changes in histologic features.
appropriately conducted direct examination of stool will establish the diagnosis in up to 70% of patients by a single examination, 85% by examination of a second stool specimen, and more than 90% by examination of three specimens. comparison of stool examination results with small bowel aspiration results in patients with diarrhea revealed that parasites were detected in 50% of stools of patients in whom a small bowel focus of infection was documented by aspiration. efforts to improve diagnostic testing include the use of polyclonal antisera or monoclonal antibodies against giardia organism–specific antigens in eia or immunofluorescent assays. polymerase chain reaction and gene probe–based detection systems specific for giardia have been used in environmental monitoring.
radiographic contrast studies of the small intestine may show nonspecific findings such as irregular thickening of the mucosal folds. blood cell counts usually are normal. giardiasis is not associated with eosinophilia.
treatment
children with acute diarrhea in whom giardia organisms are identified should receive therapy. in addition, children who manifest failure to thrive or exhibit malabsorption or gastrointestinal tract symptoms such as chronic diarrhea should be treated.
asymptomatic excreters generally are not treated except in specific instances such as in outbreak control, for prevention of household transmission by toddlers to pregnant women and patients with hypogammaglobulinemia or cystic fibrosis.
metronidazole is the treatment most often prescribed in the united states for adults. furazolidone is less effective than metronidazole but is often prescribed in children because it is available in liquid form. furazolidone is the only drug approved by the u.s. food and drug administration for treatment of giardiasis. quinacrine is effective and inexpensive but is not available from any u.s. manufacturer. albendazole appears to be as effective as metronidazole with fewer adverse effects among children 2–12 yr of age and is effective against many helminths, making it useful for treatment when multiple intestinal parasites are identified or suspected.
paromomycin, a nonabsorbable aminoglycoside, is less effective than other agents but is recommended for treatment of pregnant women with giardiasis because of potential teratogenic effects of other agents. a combination of metronidazole and quinacrine has been used to treat refractory cases.
prognosis
several studies have demonstrated that variability in antimicrobial susceptibility exists among strains of giardia, and in some instances resistant strains have been demonstrated. combined therapy may benefit patients in whom infection persists after single-drug therapy, assuming reinfection has not occurred and the medication was taken as prescribed.
toxoplasmosis
vertical transmission of toxoplasma gondii occurs by transplacental transfer of the organism from the mother to the fetus after an acute maternal infection. fetal infection rarely can occur after reactivation of disease in an immunocompromised pregnant mother. transmission from an acutely infected mother to her fetus occurs in about 30% to 40% of cases, but the rate varies directly with gestational age. transmission rates and the timing of fetal infection correlate directly with placental blood flow the risk of infection increases throughout gestation to 90% or greater near term, and the time interval between maternal and fetal infection decreases.
the severity of fetal disease varies inversely with the gestational age at which maternal infection occurs. most infants have subclinical infection with no overt disease at birth however, specific ophthalmologic and cns evaluations may reveal abnormalities. the classic findings of hydrocephalus, chorioretinitis, and intra-cerebral calcifications suggest the diagnosis of congenital toxoplasmosis. affected infants tend to be sga, develop early-onset jaundice, have hepatosplenomegaly, and present with a generalized maculopapular rash. seizures are common, and skull films may reveal diffuse cortical calcifications in contrast to the peri-ventricular pattern observed with cmv. these infants are at increased risk for long-term neurologic and neurodevelopmental complications.
serologic tests are the primary means of diagnosis. igg-specific antibodies achieve a peak concentration 1 to 2 months after infection and remain positive indefinitely. for infants with seroconversion or a fourfold increase in igg titers, specific igm antibody determinations should be performed in patients to confirm disease. especially for congenital infections, measurement of iga and ige antibodies can be useful to confirm the disease. thorough ophthalmologic, auditory, and neurologic evaluations (head ct and csf examination) are indicated.
for symptomatic and asymptomatic congenital infection, initial therapy should include pyrimethamine (supplemented with folic acid) combined with sulfadiazine. duration of therapy is often prolonged even up to 1 year. optimal dosages of medications and duration of therapy should be determined in consultation with appropriate specialists.
rubella
with the widespread use of vaccination, congenital rubella is rare in developed countries. acquired in utero during early gestation, rubella can cause severe neonatal consequences. the occurrence of congenital defects approaches 85% if infection is acquired during the first 4 weeks of gestation close to 40% spontaneously abort or are stillborn. if infection occurs during weeks 13 to 16, 35% of infants can have abnormalities. infection after 4 months gestation does not seem to cause disease.
the most common characteristic abnormalities associated with congenital rubella include ophthalmologic (cataracts, retinopathy, and glaucoma), cardiac (pda and peripheral pulmonary artery stenosis), auditory (sensorineural hearing loss), and neurologic (behavioral disorders, meningoencephalitis, and mental retardation) conditions. additionally, infants can present with growth retardation, hepatosplenomegaly, early-onset jaundice, thrombocytopenia, radiolucent bone disease, and purpuric skin lesions ("blueberry muffin" appearance from dermal erythropoiesis).
detection of rubella-specific igm antibody usually indicates recent infection. additionally, measurement of rubella-specific igg over several months can be confirmatory. rubella virus can be isolated from blood, urine, csf, and throat swab specimens. infants with congenital rubella are chronically and persistently infected and tend to shed live virus in urine, stools, and respiratory secretions for 1 year. infants should be isolated while in the hospital and kept away from susceptible pregnant women when sent home.
cytomegalovirus
cmv is the most common congenital infection and the leading cause of sensorineural hearing loss, mental retardation, retinal disease, and cerebral palsy. congenital cmv occurs in about 0.5% to 1.5% of births. when primary infection occurs in mothers during a pregnancy, the virus is transmitted to the fetus in approximately 35% of cases. rates of cmv infection are three to seven times greater among infants born to adolescent mothers. the risk for transmission of cmv to the fetus is independent of gestational age at the time of maternal infection. the earlier in gestation that the primary maternal infection occurs, the more symptomatic the infant will be at birth. the most common sources of cmv for primary infections occurring in mothers during pregnancy are sexual contacts and contact with young children. it is well known that cmv can be transmitted to the fetus even when maternal infection occurred long before conception. this transmission can occur as the result of virus reactivation, chronic infection, or reinfection with a new strain.
more than 90% of infants who have congenital cmv infection exhibit no clinical evidence of disease at birth. approximately 10% of infected infants have symptoms at birth. findings include sga, microcephaly, thrombocytopenia, hepatosplenomegaly, hepatitis, intracranial calcifications, chorioretinitis, and hearing abnormalities. some infants can present with a blueberry muffin appearance as the result of dermal erythropoiesis. skull films may reveal periventricular calcifications. an additional 10% of infected infants may not present until later in infancy or early childhood, when they are found to have sensorineural hearing loss and developmental delays. mortality is 10% to 15% among symptomatic newborns. perinatal cmv infection acquired during birth or from mother s milk is not associated with newborn illness or cns sequelae.
congenital cmv infection is diagnosed by detection of virus in the urine or saliva. detection is often accomplished by traditional virus culture methods, but can take several weeks to obtain a result. rapid culture methods using centrifugation to enhance infectivity and monoclonal antibody to detect early antigens in infected tissue culture can give results in 24 hours. pcr also can be used to detect small amounts of cmv dna in the urine. detection of cmv within the first 3 weeks after birth is considered proof of congenital cmv infection.
there are no antiviral agents currently approved for the treatment of congenital cmv infection. trial studies in severely symptomatic newborns of the antiviral agent, ganciclovir, have shown a lack of progression of hearing loss.
herpes simplex virus
hsv-2 accounts for 90% of primary genital herpes. about 70% to 85% of neonatal herpes simplex infections are caused by hsv-2. most commonly, neonatal infections are acquired from the mother shortly before (ascending infection) or during passage through the birth canal at delivery. the incidence of neonatal hsv is estimated to range from 1 in 3000 to 20,000 live births. infants with hsv infections are more likely to be born prematurely (40% of affected infants are < 36 weeks gestation). the risk of infection at delivery in an infant born vaginally to a mother with primary genital herpes is about 33% to 50%. the risk to an infant born to a mother with a reactivated infection is less than 5%. more than 75% of infants who acquire hsv infection are born to mothers who have no previous history or clinical findings consistent with hsv infection.
most infants are normal at birth, and symptoms of infection develop at 5 to 10 days of life. symptoms of neonatal hsv infection include disseminated disease involving multiple organ systems, most notably the liver and lungs localized infection to the cns or localized infection to the skin, eyes, and mouth. symptoms may overlap, and in many cases of disseminated disease, skin lesions are a late finding. disseminated infection should be considered in any infant with symptoms of sepsis, liver dysfunction, and negative bacteriologic cultures. hsv infection also should be suspected in any neonate who presents with fever, irritability, abnormal csf findings, and seizures. initial symptoms can occur anytime between birth and 4 weeks of age, although disseminated disease usually occurs during the first week of life. hsv infections are often severe, and a delay in treatment can result in significant morbidity and mortality.
for the diagnosis of neonatal hsv infection, specimens for culture should be obtained from any skin vesicle, nasopharynx, eyes, urine, blood, csf, stool, or rectum. positive cultures obtained from these sites more than 48 hours after birth indicate intrapartum exposure. pcr is a sensitive method for detecting hsv dna in blood, urine, and csf.
parenteral acyclovir is the treatment of choice for neonatal hsv infections. acyclovir should be administered to all infants suspected to have infection or diagnosed with hsv. the most benign outcome with regard to morbidity and mortality is observed in infants with disease limited to the skin, eyes, and mouth.
congenital syphilis
congenital syphilis most commonly results from transplacental infection of the fetus, although the fetus can acquire infection by contact with a chancre at birth. additionally, hematogenous infection can occur throughout pregnancy. the longer the time elapsed between the mother s infection and pregnancy, the least likely she is to transmit the disease to the fetus.
intrauterine infection can result in stillbirth, hydropings fetalis, or prematurity. clinical symptoms vary but include hepatosplenomegaly, snuffles, lymphadenopathy, mucocutaneous lesions, osteochondritis, rash, hemolytic anemia, and thrombocytopenia. untreated infants, regardless of whether they manifest symptoms at birth, may develop late symptoms, which usually appear after 2 years of age and involve the cns, bones, joints, teeth, eyes, and skin. some manifestations of disease may not become apparent until many years after birth, such as interstitial keratitis, eighth cranial nerve deafness, hutchinson teeth, bowing of the skins, frontal bossing, mulberry molars, saddle nose, rhagades, and clutton joints. the combination of interstitial keratitis, eighth cranial nerve deafness, and hutchinson teeth is commonly referred to as the hutchinson triad.
many infants are asymptomatic at the time of diagnosis. if untreated, most infants develop symptoms within the first 5 weeks of life. the most striking lesions affect the mucocutaneous tissues and bones. early signs of infection may be poor feeding and snuffles (syphilitic rhinitis). snuffles are more severe and persistent than the common cold and are often bloody. a maculopapular desquamative rash develops over the palms and soles and around the mouth and anus. the rash may progress to become vesicular with bullae. severely ill infants may be born with hydropings and have profound anemia. severe consolidated pneumonia may be present at birth, and there may be laboratory findings consistent with a glomerulonephritis. csf evaluation may reveal a pleocytosis and elevated protein. more than 90% of symptomatic infants exhibit radiographic abnormalities of the long bones consistent with osteochondritis and perichondritis.
no newborn should be discharged from the hospital without knowledge or determination of the mother s serologic status for syphilis. all infants born to seropositive mothers require a careful examination and a quantitative nontreponemal syphilis test. dark-field examination of direct fluorescent antibody staining of organisms obtained by scraping a skin or mucous membrane lesion is the quickest and most direct method of diagnosis. more commonly, serologic testing is used. the nontreponemal reaginic antibody assays-the venereal disease research laboratory (vdrl) and the rapid plasma reagin-are helpful as indicators of disease. all infants born to seropositive mothers require a careful examination and a quantitative nontreponemal syphilis test. the test performed on the infant should be the same as that performed on the mother to enable comparison of results. an infant should be evaluated further if the maternal titer has increased fourfold, if the infant s titer is fourfold greater than the mother s titer, if the infant is symptomatic, or if the mother has inadequately treated syphilis. a mother infected later in pregnancy may deliver an infant who is incubating active disease. the mother and infant may have negative serologic testing at birth. when clinical or serologic tests suggest congenital syphilis, csf should be examined microscopically, and a csf vdrl test should be performed. an increased csf white blood cell count and protein concentration suggests neurosyphilis a positive csf vdrl is diagnostic.
parenteral penicillin is the preferred drug of choice for treatment of syphilis. penicillin g for 10 to 14 days is the only documented effective therapy for infants who have congenital syphilis and neurosyphilis. infants should have repeat nontreponemal antibody titers repeated at 3, 6, and 12 months to document falling titers. infants with neurosyphilis must be followed carefully with serologic testing and csf determinations every 6 months for at least 3 years or until csf findings are normal.
المادة المعروضة اعلاه هي مدخل الى المحاضرة المرفوعة بواسطة استاذ(ة) المادة . وقد تبدو لك غير متكاملة . حيث يضع استاذ المادة في بعض الاحيان فقط الجزء الاول من المحاضرة من اجل الاطلاع على ما ستقوم بتحميله لاحقا . في نظام التعليم الالكتروني نوفر هذه الخدمة لكي نبقيك على اطلاع حول محتوى الملف الذي ستقوم بتحميله .
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