intro Etiology & Epidemiology Pathogenesis Clinical Manifestations Laboratory Findings Diagnosis complications Treatment Prognosis& Prevention
1) Invasive amebiasis is treated with a nitroimidazole such as metronidazole or tinidazole.
Tinidazole has similar efficacy to metronidazole, with shorter and simpler dosing, and is
🔹
better tolerated.
Adverse effects include nausea, abdominal discomfort, and a metallic taste that
disappears after completion of therapy.
Therapy with a nitroimidazole should be followed by treatment with a luminal agent, such
🔹
as paromomycin or iodoquinol or diloxanide furoate (can also be used in children > 2 yr).
note:
paromomycin is preferred but should not be given concurrently with metronidazole or
tinidazole, because diarrhea is a common side effect and may confuse the clinical picture.
🔹
Clinical presentations range from:
🔹 asymptomatic cyst passage (up to 10% risk to develop invasive disease within a year)
2) Asymptomatic intestinal infection with E. histolytica should be treated, preferably
with paromomycin or alternatively with either iodoquinol or diloxanide furoate.
🔷 Etiology
🔹
🔹
amebic colitis and amebic dysentery (see later),
ameboma (granulation tissue in colonic lumen mimicking colonic cancer in appearance), and
extraintestinal disease: usually involves the liver, but less common extraintestinal manifestations include amebic brain
3) For fulminant cases of amebic colitis, some experts suggest adding dehydroemetine
(1 mg/kg/ day subcutaneously or intramuscularly, never intravenously). Patients should be
Four morphologically identical but genetically distinct species of Entamoeba are known to hospitalized for monitoring& the drug should be discontinued if tachycardia, T-wave
abscess, pleuropulmonary disease, ulcerative skin, and genitourinary lesions.
🔹
infect humans:
🔷 🔶
History and Physical examination
Diagnosis of amebic colitis is made by:
depression, arrhythmia, or proteinuria develops.
🔹 Entamoeba dispar, the most prevalent species, does not cause symptomatic disease. 4) Broad-spectrum antibiotic therapy may be indicated in fulminant colitis to cover
Entamoeba moshkovskii, has increasingly been shown to cause diarrhea in infants and 🔹
▪️young children, 🔹pregnant women, 🔹 malnourished individuals, and 🔹 persons taking corticosteroids
Severe disease is more common in 1) Stool for E. histolytica antigen testing or PCR (has 95% sensitivity and
specificity).
possible spillage of intestinal bacteria into the peritoneum and translocation into the
🔹
children bloodstream.
invasive disease is more common in men (possibly due to an inhibitory effect of testosterone on innate immune 1) Uncomplicated amebic colitis: laboratory findings are 2) Microscopic examination of stool samples has a sensitivity of 60%. 5) Intestinal perforation and toxic megacolon are indications for surgery.
E. histolytica, the main pathogenic species and can become invasive in 4–10% of infected mechanisms in adult males).
E. histolytica Trophozoites are responsible for tissue often unremarkable. Sensitivity can be increased to 85–95% by examining three stools. Microscopy
🔹
patients. 6) In amebic liver abscess, image-guided aspiration of large lesions or left lobe abscesses
Complications
E. bangladeshi, studies are needed to ascertain its human pathogenicity.
•infection is usually acquired through the ingestion of parasite cysts.
invasion and destruction.
•Once trophozoites invade the intestinal mucosa, they 🔸 Amebic Colitis:
May occur within 2 wk of infection or may be delayed for months.
2) Amebic liver abscess: laboratory findings are a slight
leukocytosis, moderate anemia, high erythrocyte
cannot differentiate between E. histolytica and E. dispar unless phagocytosed
erythrocytes (specific for E. histolytica ) are seen. 1) Amebic colitis include: acute necrotizing
colitis, ameboma, toxic megacolon,
may be necessary if rupture is imminent or if the patient shows a poor clinical response 4-6
days after administration of amebicidal drugs.
Prognosis
Most infections evolve to either an asymptomatic carrier state or eradication.
multiply and spread laterally underneath the intestinal sedimentation rate, and elevations of hepatic enzyme 3) Endoscopy and biopsies of suspicious areas should be performed when stool 7) Chloroquine, which concentrates in the liver, may also be a useful adjunct to Extraintestinal infection carries about a 5% mortality rate.
Entamoeba species infect or colonize up to •Cysts are resistant to harsh environmental conditions, including chlorine concentrations
🔹
epithelium to produce the characteristic flask-shaped It affects all age-groups, but the incidence is strikingly common in children 1-5 yr of age. (particularly alkaline phosphatase) levels. sample results are negative and suspicion remains high. extraintestinal extension, or local perforation nitroimidazoles in the treatment of amebic liver abscess or in cases of treatment failure or Prevention
Amebiasis 10% of the world's population, particularly in commonly used in water purification, but can be killed by heating to 55°C (131°F).
•Cysts are also resistant to gastric acidity and digestive enzymes. ulcers. Onset is usually gradual, with colicky abdominal pains and frequent bowel movements (6-8/day). Stool examination for amebae is negative in more than 4) Various serum antibody (serologic) tests are available. Serologic tests results and peritonitis, chronic form of amebic colitis intolerance. 1) Exercising proper sanitation and hygiene.
🔹
resource-limited settings. •Amebae produce similar lytic lesions if they reach the Diarrhea is frequently associated with tenesmus. half of patients are positive in 70–80% of patients with invasive disease (colitis or liver abscess) at (less common). 8) To confirm cure, stool examination should be repeated every 2 wk following 2) Regular examination of food handlers and thorough investigation of
•The cysts germinate in the small intestine to form trophozoites. These actively motile Almost all stool is heme-positive, but most patients do not present with grossly bloody stools. 2) Amebic liver abscess may rupture into the
organisms colonize the lumen of the large intestine and may invade the mucosal lining. liver. Ultrasonography, CT, or MRI can localize and delineate presentation and in > 90% of patients after 7 days. completion of therapy until clear. diarrheal episodes may help identify the source of infection.
🔹
Constitutional symptoms and signs are characteristically absent. peritoneum, pleural cavity, skin, and
•Some transform to cysts and are passed out in the stool to infect other hosts. •These lesions are commonly called abscesses,
although they contain no granulocytes. Fever documented in only 1/3 of patients.Severe amebic colitis in infants and young children tends to be rapidly
the size of the abscess cavity.
The most common finding is a single abscess in the right 🔶 Differential diagnosis: pericardium.
3) No prophylactic drug or vaccine is available.
🔷 Epidemiology
progressive, with more frequent extraintestinal involvement and high mortality rates, particularly in tropical countries. hepatic lobe. 1) Amebic colitis: differentiated from colitis due to bacterial, mycobacterial, and
•Prevalence of infection with E. histolytica varies greatly by region and socioeconomic status.
•Food or drink contaminated with cysts and fecal-oral contact are the most common means
🔸
Amebic dysentery can result in dehydration and electrolyte disturbances.
Amebic Liver Abscess:
A serious manifestation of disseminated infection, is uncommon
viral pathogens, as well as noninfectious causes such as inflammatory bowel
disease.
2) Amebic liver abscess: differentiated from pyogenic liver abscess due to
of infection. •in children. Abscesses occur in < 1% of infected individuals (although diffuse liver enlargement has been associated with bacterial infection, hepatoma, and echinococcal cysts.
•Untreatedwater and soil contaminated by human feces used as fertilizer are important intestinal amebiasis), and may appear in patients with no clear history of intestinal disease and months to years after
sources of infection. Food handlers shedding amebic cysts play a role in spreading infection. exposure.
•In children, fever is the hallmark of amebic liver abscess and is frequently associated with abdominal pain, distention, and
enlargement and tenderness of the liver.
•Changes at the base of the right lung, such as elevation of the diaphragm and atelectasis or effusion, may also occur.
🔷 Etiology:
•Giardia infects humans after ingestion of as few as 10-100 cysts. After excystation,
trophozoites colonize the lumen of the duodenum and proximal jejunum, where they attach
to the brush border of the epithelial cells.
•As detached trophozoites pass down the intestinal tract, they encyst to form cysts.
Treatment
•Cysts are passed in stools of infected individuals and may remain viable in water for as long
🔷
as 2 months. Diagnosis 🔹
Asymptomatic excreters generally are not treated, except in specific instances such as:
🔹 outbreak control
Epidemiology: History and Physical examination prevention of household transmission by toddlers to pregnant women and patients with
🔹
Prognosis
Symptoms recur in some patients in whom reinfection cannot be
🔹
Giardia occurs world wide and is the most common intestinal parasite. Stool enzyme immunoassay (EIA) or direct fluorescent antibody tests for Giardia hypogammaglobulinemia,
Clinical Manifestations antigens have been tests of choice for giardiasis. documented and in whom an immune deficiency is not present, despite use of
Giardia infection usually occurs sporadically, but Giardia is a frequently identified etiologic situations requiring oral antibiotic treatment (Giardia may produce malabsorption of the
The incubation period of Giardia infection usually is 1-2 wk but may be longer. •Microscopy documentation of trophozoites or cysts in three stool specimens appropriate therapy.
agent of outbreaks associated with drinking water. antibiotic).
Protozoan Infection is high during childhood and begins to decline after adolescence. Asymptomatic
Children may experience asymptomatic excretion of the organism (most common), acute infectious diarrhea, or chronic
diarrhea with persistent gastrointestinal tract signs and symptoms, including failure to thrive and abdominal pain or
achieve a sensitivity of > 90%. •Symptomatic children with acute diarrhea in whom Giardia organisms are identified, and Several studies have demonstrated that variability in antimicrobial
🔹
carriage may persist for several months. •Aspiration or biopsy of the duodenum or upper jejunum should be considered in children who manifest failure to thrive or exhibit malabsorption or chronic diarrhea should susceptibility and resistant exists among strains of Giardia.
Diseases
Transmission of Giardia is common in certain high-risk groups, including children and
🔹
cramping.
Symptomatic infections occur more frequently in children than in adults. Most symptomatic patients usually have a
patients with chronic symptoms in whom giardiasis is suspected but in testing of receive therapy. Combined therapy may be useful for infection that persists after single-drug
🔹
Giardia duodenalis (also known as Giardia employees in childcare centers, consumers of contaminated water, travelers to certain areas stool specimens yields a negative result. In a fresh specimen, trophozoites usually therapy.
limited period of acute diarrheal disease with or without low-grade fever, nausea, and anorexia; in a small proportion of can be visualized by direct wet mount.
of the world, and persons exposed to certain animals. The major reservoir and vehicle for
Giardiasis lamblia or Giardia intestinalis) is a flagellated patients, an intermittent or more protracted course characterized by diarrhea, abdominal distention and cramps, bloating,
(Giardia duodenalis) protozoan that infects the duodenum and
spread of Giardia appears to be water contaminated with Giardia cysts, but food borne
transmission occurs. The seasonal peak in age-specific case reports coincides with the
malaise, flatulence, nausea, anorexia, and weight loss develops.
•Stools initially may be profuse and watery and later become greasy and foul smelling and may float. Stools do not contain
•Biopsy of the small intestine should be considered in patients with characteristic
clinical symptoms, negative stool and duodenal fluid specimen findings, and one or 🔹
Prevention
Strict hand washing after any contact with feces. Individuals, especially
🔹
jejunum. summer recreational water season and may be a result of the extensive use of communal more of the following: children in diapers, should avoid swimming if they have diarrhea.
blood, mucus, or fecal leukocytes. Varying degrees of malabsorption may occur. Abnormal stool patterns may alternate abnormal radiographic findings (such as edema and segmentation in the small Individuals should also avoid swallowing recreational water and drinking
swimming venues by young children, the low infectious dose, and the extended periods of
with periods of constipation and normal bowel movements.
🔹
cyst shedding that can occur. In addition, Giardia cysts are relatively resistant to chlorination intestine); untreated water.
•Malabsorption of sugars, fats, and fat-soluble vitamins is well documented and may be responsible for substantial weight
🔹 🔹
and to ultraviolet light irradiation. an abnormal lactose tolerance test result; Travelers to endemic areas are advised to avoid uncooked foods.
loss. an absent secretory immunoglobulin A level; hypogammaglobulinemia; or Purification of drinking water can be achieved by a filter with a pore size of < 1
Boiling is effective for inactivating cysts.
Person-to-person spread also occurs, particularly in areas of low hygiene standards,
frequent fecal-oral contact, and crowding. Individual susceptibility, lack of toilet training,
🔹
•Giardia has been associated with iron deficiency in internationally adopted children.
Repeated Giardia infections correlate with growth stunting, decrease in cognitive function in children in endemic areas.
achlorhydria.
•Blood cell counts usually are normal. Giardiasis is not tissue invasive and is not
μm or by brisk boiling of water for at least 1 min. Treatment of water with
chlorine or iodine is less effective but may be used as an alternate method
crowding, and fecal contamination of the environment all predispose to transmission of associated with peripheral blood eosinophilia. when boiling or filtration is not possible.
🔹
enteropathogens, including Giardia, in childcare centers. •Iron deficiency should be considered in children with giardiasis
Humoral immunodeficiencies, including common variable immunodeficiency, selective Ig A
deficiencyand X-linked agammaglobulinemia, predispose humans to chronic symptomatic
Giardia infection, suggesting the importance of humoral immunity in controlling giardiasis.
🔹
Many individuals with AIDS have Giardia infection refractory to treatment.
Human milk contains glycoconjugates and secretory Ig A antibodies that may provide
protection to nursing infants against Giardia
Clinical Manifestations
The different forms of the disease are distinct in their causes, epidemiologic features, transmission, and geographic
🔹
distribution.
Localized Cutaneous Leishmaniasis: LCL (Oriental sore) is the most common form of leishmaniasis. can affect
individuals of any age, but children are the primary victims in many endemic regions.
The lesions typically begin as a small papule at the site of the sandfly bite, which enlarges to 1-3 cm in diameter and may
ulcerate over the course of several weeks to months.
The shallow ulcer is usually nontender and surrounded by a sharp, indurated, erythematous margin. There is no drainage
unless a bacterial superinfection develops.
•Regional lymphadenopathy and palpable subcutaneous nodules or lymphatic cords, the so-called sporotrichoid
appearance may occurIf lesions do not become secondarily infected, there are usually no complications aside from the 🔹
Treatment
🔹 Specific antileishmanial therapy is not routinely indicated for uncomplicated LCL
🔹
residual cutaneous scar. Lesions that are extensive, severely inflamed, or located where a scar would result in
Diffuse Cutaneous Leishmaniasis: DCL is a rare form of leishmaniasis manifests as large, nonulcerating macules, disability (near a joint) or cosmetic disfigurement (face or ear), that involve the lymphatics,
papules, nodules, or plaques that often involve large areas of skin and may resemble lepromatous leprosy. The face and
extremities are most often involved.
🔹 🔹
or that do not begin healing within 3-4 mo should be treated.
▪️ All patients with VL or ML should receive therapy.
🔹
Differential Diagnosis of VL (kala-azar)Malaria, typhoid fever, miliary The pentavalent antimony compounds (sodium stibogluconate [Pentostam] and
Disseminated Leishmaniasis: tuberculosis, schistosomiasis, brucellosis, amebic liver abscess, infectious meglumine antimoniate [Glucantime]) have been the mainstay of antileishmanial
🔷
In rare cases, parasites can spread (likely by the hematogenous route) in an immunocompetent host from a primary lesion mononucleosis, lymphoma, and leukemia
▪️
chemotherapy.
🔹Mucosal Leishmaniasis: ML (espundia ) is an uncommon but serious manifestation of leishmanial infection resulting
to cause DL (defined as >10 lesions (usually in the hundreds) involving at least 2 noncontiguous areas of the skin). Sodium stibogluconate: the recommended regimen is 20 mg/kg/day intravenously (IV)
🔹
Etiology Pathogenesis or intramuscularly (IM) for 20 days (for LCL and DCL) or 28 days (for ML and VL). Prevention
Multiple species of Leishmania are known to cause human disease involving the skin & Cellular immune mechanisms determine resistance or
Diagnosis
Personal protective measures should include avoidance of exposure to the
🔹 🔹
from hematogenous spread of parasites to the nasal or oropharyngeal mucosa from a cutaneous infection. Approximately Laboratory Findings 1) Serologic Test Repeated courses may be necessary in patients with severe cutaneous lesions, ML, DCL, DL,
mucosal surfaces and the visceral reticuloendothelial organs. susceptibility to infection with Leishmania. or VL. An initial clinical response to therapy usually occurs in the 1st wk of therapy, but nocturnal sandflies and, when necessary, the use of insect repellent and
half of the patients have had active cutaneous lesions within the preceding 2 yr. Patients with cutaneous leishmaniasis or ML generally do Cutaneous or mucosal disease: serologic tests generally have low sensitivity
Leishmaniasis The leishmaniases are a diverse group of
🔷 Epidemiology
Factors influence the expression as either
🔹
subclinical infection or active disease are:
Nasal mucosal involvement (common): present with nasal congestion, discharge, and recurrent epistaxis. Oropharyngeal not have abnormal laboratory results unless the lesions are
🔹
and specificity and offer little for diagnosis. complete clinical healing (reepithelialization and scarring for LCL and ML, and regression of
🔹
permethrin-impregnated mosquito netting.
Control or elimination of infected reservoir hosts (e.g., seropositive domestic
🔹
and laryngeal involvement (less common) but associated with severe morbidity. VL (kala-azar): serologic testing by enzyme immunoassay, indirect fluorescence splenomegaly and normalization of cytopenias for VL) is usually not evident for weeks to a
diseases caused by intracellular protozoan secondarily infected with bacteria. ---------
🔶 🔹
Leishmaniases may occur sporadically throughout an endemic region or may occur in Host factors (genetic background, concomitant dogs) has had limited success.
(Leishmania) Marked soft tissue, cartilage, and even bone destruction occurs late in the course of disease and may lead to visible Laboratory findings in classic kala-azar include: Anemia assay, or direct agglutination is very useful because of the very high level of few months after completion of therapy.
parasites of the genus Leishmania. epidemic waves.
🔹
disease, nutritional status),
🔹 🔹
deformity of the nose or mouth, nasal septal perforation, and tracheal narrowing with airway obstruction. (hemoglobin, 5-8 mg/dL), thrombocytopenia, leukopenia antileishmanial antibodies. Adverse effects of antimony therapy are dose and duration dependent and Where anthroponotic transmission is thought to occur, as in south Asia,
🔸
Some 70 animal species including dogs and rodents, and humans, have been found as natural Parasite factors (virulence, size of the inoculum), and include: early recognition, diagnosis, and treatment of cases and vector control
Visceral Leishmaniasis: VL (kala-azar) typically affects children <5 yr old (L. infantum ) and older children and young (2,000-3,000 cells/μL), elevated hep 2) Demonstration of amastigotes in tissue specimens or isolation of the
🔸 🔹Currently, no effective vaccine is available
reservoir hosts of Leishmania parasites. possibly Vector -specific factors (vector genotype, fatigue, arthralgias and myalgias (50%) measures are essential for progress toward elimination.
adults (L. donovani ). organism by culture provide definitive diagnosis of leishmaniasis.In patients with VL,
🔸
Transmission may occur from animal to female sand fly (Phlebotomus) to human. immunomodulatory salivary constituents) abdominal discomfort (30%)
•After inoculation of the organism into the skin by the sandfly, the child may have a completely asymptomatic infection or smears or cultures of material from splenic, bone marrow, or lymph node aspirations
an oligosymptomatic illness or active kala-azar.
1. Children with asymptomatic infection are transiently seropositive.
are usually diagnostic. In experienced hands, splenic aspiration has a higher
diagnostic sensitivity, but it is rarely performed because of the risk for bleeding 🔸
🔸
elevated hepatic transaminase level (30–80%)
elevated amylase and lipase levels (almost 100%),
mild hematologic changes (slightly decreased leukocyte count, hemoglobin level, and
2. Children who are oligosymptomatic have mild constitutional symptoms (malaise, intermittent diarrhea, poor complications.
activity tolerance) and intermittent fever; most will have a mildly enlarged liver. In most of these children the illness will
resolve without therapy, but in approximately 25% it will evolve to active kala-azar within 2-8 mo. 🔸
platelet count) (10–30%), and
🔸 nonspecific T-wave changes on electrocardiography (30%).
sudden death from cardiac toxicity has rarely been reported with use of very high
3. kala-azar: the classic clinical features of high fever, marked splenomegaly, hepatomegaly, and severe cachexia typically
develop 3-6 mo after the onset of the illness. At the terminal stages, the hepatosplenomegaly is massive, there is gross doses of pentavalent antimony.
wasting, the pancytopenia is profound, and jaundice, edema, and ascites may be present. Anemia may be severe enough to Amphotericin B is very useful in the treatment of VL, ML or DL, and in some regions have
precipitate heart failure. replaced antimony as first-line therapy, especially in HIV-infected patients.
Bleeding episodes, especially epistaxis, are frequent. The late stage of the illness is often complicated by secondary
bacterial infections, which frequently are a cause of death. Death occurs in >90% of patients active kala-azar without
specific treatment and in 4–10% of treated patients.
•A younger age at the time of infection, HIV coinfection, and underlying malnutrition are risk factors for the development
and more rapid evolution of active VL.
•A small percentage of patients previously treated for VL develop diffuse skin lesions, a condition known as post–kala-azar
dermal leishmaniasis. The lesions are hypopigmented, erythematous, or nodular and usually involve the face and torso.
They may persist for several months or for many years.
by fatema okoff
1) Invasive amebiasis is treated with a nitroimidazole such as metronidazole or tinidazole.
Tinidazole has similar efficacy to metronidazole, with shorter and simpler dosing, and is
🔹
better tolerated.
Adverse effects include nausea, abdominal discomfort, and a metallic taste that
disappears after completion of therapy.
Therapy with a nitroimidazole should be followed by treatment with a luminal agent, such
🔹
as paromomycin or iodoquinol or diloxanide furoate (can also be used in children > 2 yr).
note:
paromomycin is preferred but should not be given concurrently with metronidazole or
tinidazole, because diarrhea is a common side effect and may confuse the clinical picture.
🔹
Clinical presentations range from:
🔹 asymptomatic cyst passage (up to 10% risk to develop invasive disease within a year)
2) Asymptomatic intestinal infection with E. histolytica should be treated, preferably
with paromomycin or alternatively with either iodoquinol or diloxanide furoate.
🔷 Etiology
🔹
🔹
amebic colitis and amebic dysentery (see later),
ameboma (granulation tissue in colonic lumen mimicking colonic cancer in appearance), and
extraintestinal disease: usually involves the liver, but less common extraintestinal manifestations include amebic brain
3) For fulminant cases of amebic colitis, some experts suggest adding dehydroemetine
(1 mg/kg/ day subcutaneously or intramuscularly, never intravenously). Patients should be
Four morphologically identical but genetically distinct species of Entamoeba are known to hospitalized for monitoring& the drug should be discontinued if tachycardia, T-wave
abscess, pleuropulmonary disease, ulcerative skin, and genitourinary lesions.
🔹
infect humans:
🔷 🔶
History and Physical examination
Diagnosis of amebic colitis is made by:
depression, arrhythmia, or proteinuria develops.
🔹 Entamoeba dispar, the most prevalent species, does not cause symptomatic disease. 4) Broad-spectrum antibiotic therapy may be indicated in fulminant colitis to cover
Entamoeba moshkovskii, has increasingly been shown to cause diarrhea in infants and 🔹
▪️young children, 🔹pregnant women, 🔹 malnourished individuals, and 🔹 persons taking corticosteroids
Severe disease is more common in 1) Stool for E. histolytica antigen testing or PCR (has 95% sensitivity and
specificity).
possible spillage of intestinal bacteria into the peritoneum and translocation into the
🔹
children bloodstream.
invasive disease is more common in men (possibly due to an inhibitory effect of testosterone on innate immune 1) Uncomplicated amebic colitis: laboratory findings are 2) Microscopic examination of stool samples has a sensitivity of 60%. 5) Intestinal perforation and toxic megacolon are indications for surgery.
E. histolytica, the main pathogenic species and can become invasive in 4–10% of infected mechanisms in adult males).
E. histolytica Trophozoites are responsible for tissue often unremarkable. Sensitivity can be increased to 85–95% by examining three stools. Microscopy
🔹
patients. 6) In amebic liver abscess, image-guided aspiration of large lesions or left lobe abscesses
Complications
E. bangladeshi, studies are needed to ascertain its human pathogenicity.
•infection is usually acquired through the ingestion of parasite cysts.
invasion and destruction.
•Once trophozoites invade the intestinal mucosa, they 🔸 Amebic Colitis:
May occur within 2 wk of infection or may be delayed for months.
2) Amebic liver abscess: laboratory findings are a slight
leukocytosis, moderate anemia, high erythrocyte
cannot differentiate between E. histolytica and E. dispar unless phagocytosed
erythrocytes (specific for E. histolytica ) are seen. 1) Amebic colitis include: acute necrotizing
colitis, ameboma, toxic megacolon,
may be necessary if rupture is imminent or if the patient shows a poor clinical response 4-6
days after administration of amebicidal drugs.
Prognosis
Most infections evolve to either an asymptomatic carrier state or eradication.
multiply and spread laterally underneath the intestinal sedimentation rate, and elevations of hepatic enzyme 3) Endoscopy and biopsies of suspicious areas should be performed when stool 7) Chloroquine, which concentrates in the liver, may also be a useful adjunct to Extraintestinal infection carries about a 5% mortality rate.
Entamoeba species infect or colonize up to •Cysts are resistant to harsh environmental conditions, including chlorine concentrations
🔹
epithelium to produce the characteristic flask-shaped It affects all age-groups, but the incidence is strikingly common in children 1-5 yr of age. (particularly alkaline phosphatase) levels. sample results are negative and suspicion remains high. extraintestinal extension, or local perforation nitroimidazoles in the treatment of amebic liver abscess or in cases of treatment failure or Prevention
Amebiasis 10% of the world's population, particularly in commonly used in water purification, but can be killed by heating to 55°C (131°F).
•Cysts are also resistant to gastric acidity and digestive enzymes. ulcers. Onset is usually gradual, with colicky abdominal pains and frequent bowel movements (6-8/day). Stool examination for amebae is negative in more than 4) Various serum antibody (serologic) tests are available. Serologic tests results and peritonitis, chronic form of amebic colitis intolerance. 1) Exercising proper sanitation and hygiene.
🔹
resource-limited settings. •Amebae produce similar lytic lesions if they reach the Diarrhea is frequently associated with tenesmus. half of patients are positive in 70–80% of patients with invasive disease (colitis or liver abscess) at (less common). 8) To confirm cure, stool examination should be repeated every 2 wk following 2) Regular examination of food handlers and thorough investigation of
•The cysts germinate in the small intestine to form trophozoites. These actively motile Almost all stool is heme-positive, but most patients do not present with grossly bloody stools. 2) Amebic liver abscess may rupture into the
organisms colonize the lumen of the large intestine and may invade the mucosal lining. liver. Ultrasonography, CT, or MRI can localize and delineate presentation and in > 90% of patients after 7 days. completion of therapy until clear. diarrheal episodes may help identify the source of infection.
🔹
Constitutional symptoms and signs are characteristically absent. peritoneum, pleural cavity, skin, and
•Some transform to cysts and are passed out in the stool to infect other hosts. •These lesions are commonly called abscesses,
although they contain no granulocytes. Fever documented in only 1/3 of patients.Severe amebic colitis in infants and young children tends to be rapidly
the size of the abscess cavity.
The most common finding is a single abscess in the right 🔶 Differential diagnosis: pericardium.
3) No prophylactic drug or vaccine is available.
🔷 Epidemiology
progressive, with more frequent extraintestinal involvement and high mortality rates, particularly in tropical countries. hepatic lobe. 1) Amebic colitis: differentiated from colitis due to bacterial, mycobacterial, and
•Prevalence of infection with E. histolytica varies greatly by region and socioeconomic status.
•Food or drink contaminated with cysts and fecal-oral contact are the most common means
🔸
Amebic dysentery can result in dehydration and electrolyte disturbances.
Amebic Liver Abscess:
A serious manifestation of disseminated infection, is uncommon
viral pathogens, as well as noninfectious causes such as inflammatory bowel
disease.
2) Amebic liver abscess: differentiated from pyogenic liver abscess due to
of infection. •in children. Abscesses occur in < 1% of infected individuals (although diffuse liver enlargement has been associated with bacterial infection, hepatoma, and echinococcal cysts.
•Untreatedwater and soil contaminated by human feces used as fertilizer are important intestinal amebiasis), and may appear in patients with no clear history of intestinal disease and months to years after
sources of infection. Food handlers shedding amebic cysts play a role in spreading infection. exposure.
•In children, fever is the hallmark of amebic liver abscess and is frequently associated with abdominal pain, distention, and
enlargement and tenderness of the liver.
•Changes at the base of the right lung, such as elevation of the diaphragm and atelectasis or effusion, may also occur.
🔷 Etiology:
•Giardia infects humans after ingestion of as few as 10-100 cysts. After excystation,
trophozoites colonize the lumen of the duodenum and proximal jejunum, where they attach
to the brush border of the epithelial cells.
•As detached trophozoites pass down the intestinal tract, they encyst to form cysts.
Treatment
•Cysts are passed in stools of infected individuals and may remain viable in water for as long
🔷
as 2 months. Diagnosis 🔹
Asymptomatic excreters generally are not treated, except in specific instances such as:
🔹 outbreak control
Epidemiology: History and Physical examination prevention of household transmission by toddlers to pregnant women and patients with
🔹
Prognosis
Symptoms recur in some patients in whom reinfection cannot be
🔹
Giardia occurs world wide and is the most common intestinal parasite. Stool enzyme immunoassay (EIA) or direct fluorescent antibody tests for Giardia hypogammaglobulinemia,
Clinical Manifestations antigens have been tests of choice for giardiasis. documented and in whom an immune deficiency is not present, despite use of
Giardia infection usually occurs sporadically, but Giardia is a frequently identified etiologic situations requiring oral antibiotic treatment (Giardia may produce malabsorption of the
The incubation period of Giardia infection usually is 1-2 wk but may be longer. •Microscopy documentation of trophozoites or cysts in three stool specimens appropriate therapy.
agent of outbreaks associated with drinking water. antibiotic).
Protozoan Infection is high during childhood and begins to decline after adolescence. Asymptomatic
Children may experience asymptomatic excretion of the organism (most common), acute infectious diarrhea, or chronic
diarrhea with persistent gastrointestinal tract signs and symptoms, including failure to thrive and abdominal pain or
achieve a sensitivity of > 90%. •Symptomatic children with acute diarrhea in whom Giardia organisms are identified, and Several studies have demonstrated that variability in antimicrobial
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carriage may persist for several months. •Aspiration or biopsy of the duodenum or upper jejunum should be considered in children who manifest failure to thrive or exhibit malabsorption or chronic diarrhea should susceptibility and resistant exists among strains of Giardia.
Diseases
Transmission of Giardia is common in certain high-risk groups, including children and
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cramping.
Symptomatic infections occur more frequently in children than in adults. Most symptomatic patients usually have a
patients with chronic symptoms in whom giardiasis is suspected but in testing of receive therapy. Combined therapy may be useful for infection that persists after single-drug
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Giardia duodenalis (also known as Giardia employees in childcare centers, consumers of contaminated water, travelers to certain areas stool specimens yields a negative result. In a fresh specimen, trophozoites usually therapy.
limited period of acute diarrheal disease with or without low-grade fever, nausea, and anorexia; in a small proportion of can be visualized by direct wet mount.
of the world, and persons exposed to certain animals. The major reservoir and vehicle for
Giardiasis lamblia or Giardia intestinalis) is a flagellated patients, an intermittent or more protracted course characterized by diarrhea, abdominal distention and cramps, bloating,
(Giardia duodenalis) protozoan that infects the duodenum and
spread of Giardia appears to be water contaminated with Giardia cysts, but food borne
transmission occurs. The seasonal peak in age-specific case reports coincides with the
malaise, flatulence, nausea, anorexia, and weight loss develops.
•Stools initially may be profuse and watery and later become greasy and foul smelling and may float. Stools do not contain
•Biopsy of the small intestine should be considered in patients with characteristic
clinical symptoms, negative stool and duodenal fluid specimen findings, and one or 🔹
Prevention
Strict hand washing after any contact with feces. Individuals, especially
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jejunum. summer recreational water season and may be a result of the extensive use of communal more of the following: children in diapers, should avoid swimming if they have diarrhea.
blood, mucus, or fecal leukocytes. Varying degrees of malabsorption may occur. Abnormal stool patterns may alternate abnormal radiographic findings (such as edema and segmentation in the small Individuals should also avoid swallowing recreational water and drinking
swimming venues by young children, the low infectious dose, and the extended periods of
with periods of constipation and normal bowel movements.
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cyst shedding that can occur. In addition, Giardia cysts are relatively resistant to chlorination intestine); untreated water.
•Malabsorption of sugars, fats, and fat-soluble vitamins is well documented and may be responsible for substantial weight
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and to ultraviolet light irradiation. an abnormal lactose tolerance test result; Travelers to endemic areas are advised to avoid uncooked foods.
loss. an absent secretory immunoglobulin A level; hypogammaglobulinemia; or Purification of drinking water can be achieved by a filter with a pore size of < 1
Boiling is effective for inactivating cysts.
Person-to-person spread also occurs, particularly in areas of low hygiene standards,
frequent fecal-oral contact, and crowding. Individual susceptibility, lack of toilet training,
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•Giardia has been associated with iron deficiency in internationally adopted children.
Repeated Giardia infections correlate with growth stunting, decrease in cognitive function in children in endemic areas.
achlorhydria.
•Blood cell counts usually are normal. Giardiasis is not tissue invasive and is not
μm or by brisk boiling of water for at least 1 min. Treatment of water with
chlorine or iodine is less effective but may be used as an alternate method
crowding, and fecal contamination of the environment all predispose to transmission of associated with peripheral blood eosinophilia. when boiling or filtration is not possible.
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enteropathogens, including Giardia, in childcare centers. •Iron deficiency should be considered in children with giardiasis
Humoral immunodeficiencies, including common variable immunodeficiency, selective Ig A
deficiencyand X-linked agammaglobulinemia, predispose humans to chronic symptomatic
Giardia infection, suggesting the importance of humoral immunity in controlling giardiasis.
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Many individuals with AIDS have Giardia infection refractory to treatment.
Human milk contains glycoconjugates and secretory Ig A antibodies that may provide
protection to nursing infants against Giardia
Clinical Manifestations
The different forms of the disease are distinct in their causes, epidemiologic features, transmission, and geographic
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distribution.
Localized Cutaneous Leishmaniasis: LCL (Oriental sore) is the most common form of leishmaniasis. can affect
individuals of any age, but children are the primary victims in many endemic regions.
The lesions typically begin as a small papule at the site of the sandfly bite, which enlarges to 1-3 cm in diameter and may
ulcerate over the course of several weeks to months.
The shallow ulcer is usually nontender and surrounded by a sharp, indurated, erythematous margin. There is no drainage
unless a bacterial superinfection develops.
•Regional lymphadenopathy and palpable subcutaneous nodules or lymphatic cords, the so-called sporotrichoid
appearance may occurIf lesions do not become secondarily infected, there are usually no complications aside from the 🔹
Treatment
🔹 Specific antileishmanial therapy is not routinely indicated for uncomplicated LCL
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residual cutaneous scar. Lesions that are extensive, severely inflamed, or located where a scar would result in
Diffuse Cutaneous Leishmaniasis: DCL is a rare form of leishmaniasis manifests as large, nonulcerating macules, disability (near a joint) or cosmetic disfigurement (face or ear), that involve the lymphatics,
papules, nodules, or plaques that often involve large areas of skin and may resemble lepromatous leprosy. The face and
extremities are most often involved.
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or that do not begin healing within 3-4 mo should be treated.
▪️ All patients with VL or ML should receive therapy.
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Differential Diagnosis of VL (kala-azar)Malaria, typhoid fever, miliary The pentavalent antimony compounds (sodium stibogluconate [Pentostam] and
Disseminated Leishmaniasis: tuberculosis, schistosomiasis, brucellosis, amebic liver abscess, infectious meglumine antimoniate [Glucantime]) have been the mainstay of antileishmanial
🔷
In rare cases, parasites can spread (likely by the hematogenous route) in an immunocompetent host from a primary lesion mononucleosis, lymphoma, and leukemia
▪️
chemotherapy.
🔹Mucosal Leishmaniasis: ML (espundia ) is an uncommon but serious manifestation of leishmanial infection resulting
to cause DL (defined as >10 lesions (usually in the hundreds) involving at least 2 noncontiguous areas of the skin). Sodium stibogluconate: the recommended regimen is 20 mg/kg/day intravenously (IV)
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Etiology Pathogenesis or intramuscularly (IM) for 20 days (for LCL and DCL) or 28 days (for ML and VL). Prevention
Multiple species of Leishmania are known to cause human disease involving the skin & Cellular immune mechanisms determine resistance or
Diagnosis
Personal protective measures should include avoidance of exposure to the
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from hematogenous spread of parasites to the nasal or oropharyngeal mucosa from a cutaneous infection. Approximately Laboratory Findings 1) Serologic Test Repeated courses may be necessary in patients with severe cutaneous lesions, ML, DCL, DL,
mucosal surfaces and the visceral reticuloendothelial organs. susceptibility to infection with Leishmania. or VL. An initial clinical response to therapy usually occurs in the 1st wk of therapy, but nocturnal sandflies and, when necessary, the use of insect repellent and
half of the patients have had active cutaneous lesions within the preceding 2 yr. Patients with cutaneous leishmaniasis or ML generally do Cutaneous or mucosal disease: serologic tests generally have low sensitivity
Leishmaniasis The leishmaniases are a diverse group of
🔷 Epidemiology
Factors influence the expression as either
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subclinical infection or active disease are:
Nasal mucosal involvement (common): present with nasal congestion, discharge, and recurrent epistaxis. Oropharyngeal not have abnormal laboratory results unless the lesions are
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and specificity and offer little for diagnosis. complete clinical healing (reepithelialization and scarring for LCL and ML, and regression of
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permethrin-impregnated mosquito netting.
Control or elimination of infected reservoir hosts (e.g., seropositive domestic
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and laryngeal involvement (less common) but associated with severe morbidity. VL (kala-azar): serologic testing by enzyme immunoassay, indirect fluorescence splenomegaly and normalization of cytopenias for VL) is usually not evident for weeks to a
diseases caused by intracellular protozoan secondarily infected with bacteria. ---------
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Leishmaniases may occur sporadically throughout an endemic region or may occur in Host factors (genetic background, concomitant dogs) has had limited success.
(Leishmania) Marked soft tissue, cartilage, and even bone destruction occurs late in the course of disease and may lead to visible Laboratory findings in classic kala-azar include: Anemia assay, or direct agglutination is very useful because of the very high level of few months after completion of therapy.
parasites of the genus Leishmania. epidemic waves.
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disease, nutritional status),
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deformity of the nose or mouth, nasal septal perforation, and tracheal narrowing with airway obstruction. (hemoglobin, 5-8 mg/dL), thrombocytopenia, leukopenia antileishmanial antibodies. Adverse effects of antimony therapy are dose and duration dependent and Where anthroponotic transmission is thought to occur, as in south Asia,
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Some 70 animal species including dogs and rodents, and humans, have been found as natural Parasite factors (virulence, size of the inoculum), and include: early recognition, diagnosis, and treatment of cases and vector control
Visceral Leishmaniasis: VL (kala-azar) typically affects children <5 yr old (L. infantum ) and older children and young (2,000-3,000 cells/μL), elevated hep 2) Demonstration of amastigotes in tissue specimens or isolation of the
🔸 🔹Currently, no effective vaccine is available
reservoir hosts of Leishmania parasites. possibly Vector -specific factors (vector genotype, fatigue, arthralgias and myalgias (50%) measures are essential for progress toward elimination.
adults (L. donovani ). organism by culture provide definitive diagnosis of leishmaniasis.In patients with VL,
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Transmission may occur from animal to female sand fly (Phlebotomus) to human. immunomodulatory salivary constituents) abdominal discomfort (30%)
•After inoculation of the organism into the skin by the sandfly, the child may have a completely asymptomatic infection or smears or cultures of material from splenic, bone marrow, or lymph node aspirations
an oligosymptomatic illness or active kala-azar.
1. Children with asymptomatic infection are transiently seropositive.
are usually diagnostic. In experienced hands, splenic aspiration has a higher
diagnostic sensitivity, but it is rarely performed because of the risk for bleeding 🔸
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elevated hepatic transaminase level (30–80%)
elevated amylase and lipase levels (almost 100%),
mild hematologic changes (slightly decreased leukocyte count, hemoglobin level, and
2. Children who are oligosymptomatic have mild constitutional symptoms (malaise, intermittent diarrhea, poor complications.
activity tolerance) and intermittent fever; most will have a mildly enlarged liver. In most of these children the illness will
resolve without therapy, but in approximately 25% it will evolve to active kala-azar within 2-8 mo. 🔸
platelet count) (10–30%), and
🔸 nonspecific T-wave changes on electrocardiography (30%).
sudden death from cardiac toxicity has rarely been reported with use of very high
3. kala-azar: the classic clinical features of high fever, marked splenomegaly, hepatomegaly, and severe cachexia typically
develop 3-6 mo after the onset of the illness. At the terminal stages, the hepatosplenomegaly is massive, there is gross doses of pentavalent antimony.
wasting, the pancytopenia is profound, and jaundice, edema, and ascites may be present. Anemia may be severe enough to Amphotericin B is very useful in the treatment of VL, ML or DL, and in some regions have
precipitate heart failure. replaced antimony as first-line therapy, especially in HIV-infected patients.
Bleeding episodes, especially epistaxis, are frequent. The late stage of the illness is often complicated by secondary
bacterial infections, which frequently are a cause of death. Death occurs in >90% of patients active kala-azar without
specific treatment and in 4–10% of treated patients.
•A younger age at the time of infection, HIV coinfection, and underlying malnutrition are risk factors for the development
and more rapid evolution of active VL.
•A small percentage of patients previously treated for VL develop diffuse skin lesions, a condition known as post–kala-azar
dermal leishmaniasis. The lesions are hypopigmented, erythematous, or nodular and usually involve the face and torso.
They may persist for several months or for many years.
by fatema okoff
