Download Viral and Parasitic Gastroenteritis - Mcst

‫‪Viral and Parasitic‬‬
‫‪Gastroenteritis‬‬
‫المهم كتبت عليه‬
‫الي مو مهم مكتوب‬
‫___فمعناتو معنانا ____الي ماعلق عليه فاضي‬
‫والي قرأه مكتوب‬
‫والون االحمر مهم‬
Viral Gastroenteritis
 Inflammation of the stomach and intestines caused by
viruses, which is also known as the stomach flu
 This highly contagious illness spreads through
 close contact with people who are infected
 contaminated food or water
 It can easily spread in close quarters
 childcare facilities
 Schools
 nursing homes
 cruise ships
 Viruses are responsible for up to ¾ of all infective
diarrhoeas
 Viral gastroenteritis is the second most common viral
illness after upper respiratory tract infection
 In developing countries, viral gastroenteritis is a major
killer of infants who are undernourished
 Rotaviruses are responsible for half a million deaths a
year
HEPATITIS
 Hepatitis is inflammation of the liver
 The disease can be caused by infections from parasites,
bacteria, or viruses
 Liver damage can also result from alcohol, drugs, or
poisonous mushrooms
 Hepatitis A, B, and C are clinically the most important
forms of viral liver disease
 Persons at risk of hepatitis B infection include
 1) individuals with multiple sex partners
 2) men who have sex with men
 3) sex contacts of infected persons
 4) injection drug users
 5) household contacts of chronically infected persons
 Death from chronic hepatitis B occurs in 15 to 25 percent
of chronically infected persons
reading
 Most hepatitis C infections result from illegal injection
drug use
 Transfusion-associated cases occurred prior to blood donor
screening
 now the incidence is less than 1 per 2 million transfused blood
units
 Fifty percent of those with hepatitis C go on to have
 chronic liver disease
 liver failure (cirrhosis)
 liver cancer
 Hepatitis C is the number one reason for receiving a liver
transplant in the United States
important
Classification of hepatitis viruses based on mode of transmission
Classification of major viral agents causing hepatitis
‫مو مره مهه‬
Hepatitis A Virus: Structure and Classification
 Virus classification
 Group: Group IV ((+)ssRNA)
 Family: Picornaviridae
 Genus: Hepatovirus
 Species: Hepatitis A virus
 Separate genus because of




differences with other enteroviruses
Naked icosahedral capsid
SS RNA (740 nucleotides)
Single serotype worldwide
Humans only reservoir
Electron micrograph of hepatitis A virions
‫جدا مهمه‬
Hepatitis A Virus Transmission
 Fecal-oral
 Close personal contact
 e.g., household contact, sex contact, child day care centers
 Contaminated food, water
 e.g., infected food handlers
 Blood exposure
 rare
Estimated prevalence of hepatitis A virus
‫ال‬
Hepatitis A: Pathogenesis
 Incubation 4 weeks (range 2-6 weeks)
 Oral cavity
GI tract
liver via blood
 Replicates in hepatocytes (little damage to cells)
released via bile to intestines 7-10 days prior to clinical
symptoms
 Liver damage and clinical syndrome result of immune
response and not direct effect of virus
Hepatitis A: Clinical Features
 An acute illness with
 discrete onset of symptoms

e.g. fatigue, abdominal pain, loss of appetite, nausea, vomiting
 Jaundice

elevated serum aminotransferase levels, dark urine, light stool
 Adults are usually more symptomatic
 Patients are infective while they are shedding the virus in the stool-
usually before the onset of symptoms
 Most cases resolve spontaneously in 2-4 weeks
 Complete recovery 99%
‫مو مهم‬
Hepatitis A - Diagnosis
 Detection of IgM antibody
 IgG positive 1-3 weeks later; suggests prior infection or
vaccination
‫مو مهم‬
Hepatitis A - Treatment
 Supportive: no specific role of antiviral therapy
 Lifelong immunity likely after infection or vaccination
PREVENTING HEPATITIS A
 Hygiene
 e.g., hand washing
 Sanitation
 e.g., clean water sources
 Hepatitis A vaccine
 pre-exposure
‫مو مرا مهم‬
HEPATITIS A VACCINES
 Inactivated vaccine
 Highly immunogenic
 97%-100% of children, adolescents, and adults have
protective levels of antibody within 1 month of receiving
first dose
 essentially 100% have protective levels after second dose
 Highly efficacious
 In published studies, 94%-100% of children protected
against clinical hepatitis A after equivalent of one dose
HEPATITIS A VACCINES
 1st dose at time 0
 2nd dose 6-12 months afterwards
POST-VACCINATION TESTING
 Not recommended
 High response rate among vaccinees
 Commercially available assay not sensitive enough to
detect lower (protective) levels of vaccine-induced
antibody
‫مو مرا مهمه‬
DURATION OF PROTECTION AFTER VACCINATION
 Protection begins 4 weeks after vaccine
 Persistence of antibody
 At least 5-8 years among adults and children
 Efficacy
 No cases in vaccinated children at 5-6 years
 Mathematical models of antibody decline suggest protective
antibody levels persist for at least 20 years
 Other mechanisms, such as cellular memory, may contribute
Hepatitis A Vaccine
 Pre-exposure Vaccination
 Persons at increased risk for infection





travelers to intermediate and high HAV-endemic countries
MSM (Men who have sex with men)
Drug users
Persons who have clotting factor disorders
persons with chronic liver disease
 Communities with historically high rates of hepatitis A
-routine childhood vaccination
no
Hepatitis A Vaccine Immunogenicity, Side Effects
 Immunogenicity in children, adolescents, adults
 94-100% positive 1 month after dose 1
 99-100% positive after dose 2
 Most common side effects
 Sore injection site (50%), headache (15%), malaise (7%)
 No severe reactions known
 Safety in pregnancy unknown (risk likely is low)
 Currently licensed for aged 1 year and older
Hepatitis B ‫جدا مهم‬
Hepatitis B: Structure
 Member of the hepadnavirus group
 Virion(any particle of vurise) also referred to as
Dane particle
 42nm enveloped virus
 Core antigens located in the center (nucleocapsid)
Structure and Replication ‫مو مهم بس‬
‫االمحر‬
 Circular partially double stranded DNA of virus
 Initial replication to complete circular DNA with
subsequent transcription to make several mRNAs
some of which are translated into viral proteins
 One of the mRNAs is replicated with a reverse
transcriptase making the DNA that will eventually be
the core of the progeny virion
 Some DNA integrates into host genome causing
carrier state
 Virus stable and resist many stresses making them
more infectious
Hepatitis B Virus
TEM micrograph showing
hepatitis B viruses
The structure of hepatitis B virus
Prevalence of chronic infection with hepatitis B virus, 2006
‫مو مهم‬f
‫بس نسبة السعوديه‬
Global Patterns of Chronic HBV Infection
 High (>8%): 45% of global population


lifetime risk of infection >60%
early childhood infections common
 Intermediate (2%-7%): 43% of global population


lifetime risk of infection 20%-60%
infections occur in all age groups
 Low (<2%): 12% of global population


lifetime risk of infection <20%
most infections occur in adult risk groups
‫مهمه‬
Possible Outcomes of HBV Infection
Acute hepatitis B
infection
95% of infant3-5% of adult-acquired
acquired infections
infections
Chronic HBV infection
Chronic hepatitis
12-25% in 5 years
6-15% in 5 years
Cirrhosis
Hepatocellular
carcinoma
Death
20-23% in 5 years
Liver failure
Liver transplant
Death
Outcome of Hepatitis B Virus Infection by Age at Infection
Chronic Infection (%)
100
100
80
80
60
60
Chronic Infection
40
40
20
20
Symptomatic Infection
0
0
‫مهمه‬
HBV Modes of Transmission
 Sexual
 Parenteral
 Perinatal
‫مهم‬
Concentration of HBV in Various Body Fluids
High
blood
serum
wound exudates
Moderate
semen
vaginal fluid
saliva
Low/Not
Detectable
urine
feces
sweat
tears
breast milk
Hepatitis B Symptoms
 About 50%-60% of adults with HBV infection have no
signs or symptoms
 Those who do have symptoms might experience:
 Jaundice
 Fatigue
 Abdominal pain
 Loss of appetite
 Nausea, vomiting
 Joint pain
HBV Pathogenesis ‫مو مهم بس االمحر‬
 Virus enters hepatocytes via blood
 Immune response (cytotoxic T cell) to viral antigens expressed
on hepatocyte cell surface responsible for clinical syndrome
 5 % become chronic carriers (HBsAg> 6 months)
 Higher rate of hepatocellular in chronic carriers, especially
those who are “e” antigen positive
 Hepatitis B surface antibody likely confers lifelong immunity
 Hepatitis B Ab indicates low transmissibility
Elimination of HBV Transmission
 Prevent perinatal HBV transmission
 Routine vaccination of all infants
 Vaccination of children in high-risk groups
 Vaccination of adolescents
all children up through age 18
 Vaccination of adults in high-risk groups

Hepatitis B Vaccine
‫مهم‬
• Licensed in 1982
• 3 dose series, typical schedule 0, 1-2, 4-6 months
• 2 dose series (adult dose)
• Protection ~30-50% dose 1; 75% - 2; 96% - 3
• lower in older, immunosuppressive illnesses
•
e.g., HIV, chronic liver diseases, diabetes, obese, smokers
‫مو مهم‬
Hepatitis B Vaccine Safety
 Side effects rare
 Anaphylaxis estimated to occur in 1/600,000 doses
given
 No scientific data to link hepatitis B vaccine with
multiple sclerosis (MS), other autoimmune diseases,
autism
‫مو مرا مهم‬
Hepatitis B Vaccination
 Routine infant
 Ages 11-15 and through age 18
 Over 18 – high risk
 Occupational risk
 Hemodyalisis patients
 All STD clinic clients
 Multiple sex partners or prior STD
 Inmates in Correctional settings
 MSM
 IDU
 Institution for developmental disability
Hepatitis C Virus
Hepatitis C Structure and Classification
 Member of the flavivirus family
 Enveloped single stranded RNA virus
 Humans and chimpanzees only known reservoirs
 6 serotypes (genotypes) and multiple subtypes
 based on high variability of envelope glycoproteins
‫مهم‬
Occupational Transmission of HCV
 Inefficient by occupational exposures
 Average incidence 1.8% following needle stick from
HCV-positive source
 Case reports of transmission from blood splash to
eye
 Prevalence 1-2% among health care workers
Perinatal Transmission of HCV
 Transmission only from women HCV-RNA positive
at delivery
 Average rate of infection 6%
 Higher (17%) if woman co-infected with HIV
 No association with
 Delivery method
 Breastfeeding
 Infected infants do well
 Severe hepatitis is rare
Sexual Transmission of HCV
 Occurs, but efficiency is low
◦ Rare between long-term steady partners
◦ Factors that facilitate transmission between partners
unknown
 Accounts for 15-20% of acute and chronic
infections in the United States Partner studies
Household Transmission of HCV
 Rare but not absent
 Could occur through percutaneous/mucosal exposures
to blood
 Contaminated equipment used for home therapies
 Through sharing of contaminated personal material
(razors, toothbrushes)
Other Potential Exposures to Blood
 No or insufficient data showing increased risk
 intranasal cocaine use, tattooing, body piercing,
acupuncture, military service
Hepatitis C: Clinical Features
 Acute infection asymptomatic in over 80% of patients,
when present, acute illness usually mild
 Acute symptoms include jaundice, nausea, abdominal
pain, loss of appetite, dark urine
‫مهمه‬
Chronic Hepatitis C
Factors Promoting Progression or Severity
 Increased alcohol intake
 Age > 40 years at time of infection
 HIV co-infection
 Other
 Male gender
 Chronic HBV co-infection
Hepatitis C: Diagnosis
 ELISA
 usually positive within 2-5 months after infection
 PCR
 positive 1-2 weeks post infection
Hepatitis D
 Defective virus that requires co-infection with
hepatitis B for replication
 Enveloped with SS RNA genome
 Only antigen encoded in the delta antigen
Hepatitis D Virus Modes of Transmission
• Percutaneous exposures
• injecting drug use
• Permucosal exposures
• sex contact
Geographic Distribution of HDV Infection
Taiwan
Pacific Islands
HDV Prevalence
High
Intermediate
Low
Very Low
No Data
Hepatitis D
Pathogenesis
‫ال‬
 Pathogenesis
 Immune mediated
 Co-infection

infection with B at the same time (more severe)
 Superinfection

acquisition of Hep D in chronically Hep B
Hepatitis D - Clinical Features
 Coinfection
 severe acute diseaselow risk of chronic infection
 Superinfection
 usually develop chronic HDV infection
 high risk of severe chronic liver disease
Hepatitis E Virus
‫مو مرا مهم‬
TEM micrograph of hepatitis E virions.
Hepatitis E
 Non-enveloped single stranded RNA virus
 Resembles calicivirus or Norwalk agent
 Similar illness to Hep A except high mortality in
pregnant women
Hepatitis E - Epidemiologic Features
 Most outbreaks associated with fecally contaminated
drinking water
 Minimal person-to-person transmission
 U.S. cases usually have history of travel to HEV-
endemic areas
Hepatitis E - Clinical Features
• Incubation period
• Case-fatality rate
Average 40 days
Range 15-60 days
Overall, 1%-3%
Pregnant women, 15%-25%
• Illness severity
Increased with age
• Chronic sequelae
None identified
Prevention and Control Measures
for Travelers to HEV-Endemic Regions
• Avoid drinking water (and beverages with ice) of
unknown purity, uncooked shellfish, and uncooked
fruit/vegetables not peeled or prepared by traveler
Rotavirus
 Rotaviruses, found in many mammalian species
 Rotaviruses have a characteristic morphology that
distinguishes them from other reoviruses
A. Epidemiology
 Rotaviruses are divided into seven serogroups (A through G)
 Group A is the most important cause of outbreaks diseases in
humans
 Transmission of rotaviruses is via the fecal–oral route
 Seasonal incidence is associated with rotavirus infections
 January through March
 Infectious particles are relatively stable
 can survive for extended periods on various surfaces
 Account for about 50% of severe diarrhea in infants and young
children (up to age 2 years)
B. Clinical significance
‫ال‬
 Following ingestion, rotaviruses infect the epithelial cells of
the small intestine
 primarily the jejunum
 Rotaviruses are able to reach the small intestine because
they are resistant to the acid pH of the stomach
 The incubation period is usually 48 hours or less
 Infection can be subclinical or may result in symptoms
 ranging from mild diarrhea and vomiting to severe,
nonbloody, watery diarrhea with dehydration and loss of
electrolytes
 Although rotavirus infections are probably equally
widespread around the world
 the outcomes of infection vary significantly in different
regions
 malnutrition dramatically increases the severity of the
infection
 Infection results in some degree of lifelong immunity with
reinfected adults suffering a much milder illness
 Infants who are breastfed also suffer milder disease
manifestations
 In developing countries and areas where medical facilities
or personnel may be lacking, the mortality is significant
 An estimated 1 million deaths per year worldwide result from
rotavirus infection
C. Laboratory identification
 Severe diarrhea, dehydration, and electrolyte loss can
be due to a variety of causes
 definitive diagnosis cannot be made on clinical grounds
alone
 Identification can be made by detection of viral capsid
antigens in stool samples using ELISA
 An increase in the titer of antiviral antibody in a
patient’s serum can also be diagnostic
E. Treatment and prevention
 There is no specific antiviral drug appropriate for
treatment of rotavirus infections
 The most important clinical intervention is the rapid
and efficient replacement of fluids and electrolytes,
usually intravenously
 Prevention of rotavirus infections requires improved
sanitation measures
ADENOVIRIDAE ‫مهم‬
 Adenoviruses are
 Nonenveloped
 Icosahedral
 Double-stranded linear DNA
 They commonly cause diseases such as
 Respiratory tract infections
 Gastroenteritis
 Conjunctivitis
 Commonly infecting humans, other mammals, and
birds
 Over fifty serotypes of human adenoviruses are known
 most individuals have been infected by several different
types by adulthood
 Have not been associated with human malignancies
‫ال‬
A. Epidemiology and pathogenesis
 The site of the clinical syndrome is generally related to the
mode of transmission
 most adenoviruses are primarily agents of respiratory disease
 Most adenoviruses also replicate efficiently and
symptomatically in the intestine
 can be isolated from
 stool well after respiratory disease symptoms have ended
 from the stools of healthy persons
 Ocular infections are transmitted by
 direct inoculation of the eye by virus-contaminated hands
 ophthalmologic instruments
 children swim together
‫ال‬
B. Structure and replication
 The adenovirus capsid is composed of hexon
capsomers
 Replication of adenoviruses essentially follows the
general model for DNA viruses
 Attachment to a host cell receptor occurs via knobs on
the tips of the viral fibers
 The viral genome is then progressively uncoated while
it is transported to the nucleus
The structure of adenovirus
1 = penton capsomeres
2 = hexon capsomeres
3 = viral genome (linear dsDNA)
C. Clinical significance
 Adenoviruses all replicate well in epithelial cells
 The observed disease symptoms are related primarily to the
killing of these cells, and systemic infections are rare
 Most adenovirus infections are asymptomatic, but certain types
are more commonly associated with disease than others
 These diseases can be conveniently grouped into those affecting
the




1) respiratory tract
2) eye
3) gastrointestinal (GI) tract
4) other tissues, including the urinary tract and heart
Gastrointestinal diseases
‫مهم‬
 Most human adenoviruses multiply in the GI tract and
can be found in stools
 generally asymptomatic infections
 Two serotypes have been associated specifically with
infantile gastroenteritis
 Adenovirus infections have been estimated to account
for 5 to 15 % of all viral diarrheal disease in children
D. Laboratory identification
 Isolation of virus for identification desirable in cases of
 epidemic disease
 nosocomial outbreak, especially in the nursery
 The virus is more commonly detected by direct test of
stool specimens by ELISA
‫ال‬
E. Treatment and prevention
 No antiviral agents are currently available
 Prevention of epidemic respiratory disease by
immunization has been used
 only for protection of the military population
 This vaccine contains live, unattenuated adenovirus
‫قراءة‬
Caliciviruses (formerly known as Norwalk-like virus)
 Norovirus replicates in the GI tract and is shed in the stool
 Infection is by
 fecal–oral route following ingestion of contaminated food or water
 person-to-person contact
 contact with contaminated surfaces
 Major cause of epidemic acute gastroenteritis
 It affects primarily adults and school-age children
 but not infants
 The clinical presentation is characterized by nausea, vomiting,
and diarrhea
 Symptoms last 24 to 48 hours, and the disease is self-
limited
 Radioimmunoassays and ELISA tests are available for
the detection of antiviral antibodies
 No specific antiviral treatment is available
 Careful attention to hand washing and measures to
prevent contamination of food and water supplies
should reduce the incidence of these infections
Gastrointestinal System Infection
Protozoa and Parasitic worm (Helminth)
Leishmania donovani Visceral leishmaniasis (kala-azar)
 In the visceral disease, the parasite initially infects macrophages,
which, in turn, migrate to the spleen, liver, and bone marrow,
where the parasite rapidly multiplies
 Symptoms include
 intermittent fevers
 weight loss
 spleen and liver enlarge
 jaundice may develop
 Mortality is nearly 100% within 2 years if the disease is untreated
 In some cases, complications resulting from secondary infection
and emaciation result in death
Leishmania donovani in bone marrow cell
Echinococcus granulosus (dog tapeworm)
 Infection produces large, hydatid cysts in liver, lung, and
brain
 Anaphylactic reaction to worm antigens can occur if the
cyst ruptures
 The disease follows ingestion of eggs in dog feces
 Sheep often serve as an intermediate host
 Echinococcosis is diagnosed by CT scan or biopsy of
infected tissue and is treated with albendazole and surgical
excision of intact cysts
E. granulosus scolex
E. granulosus life cycle
Schistosoma mansonin ‫مهمه‬
 The primary site of infection is the gastrointestinal tract
 Damage to the intestinal wall is caused by the host’s
inflammatory response to eggs deposited at that site
 The eggs also secrete proteolytic enzymes that further
damage the tissue
 Clinical presentation includes GI bleeding, diarrhea, and
liver damage
 Periportal fibrosis leads to portal hypertension and
massive splenomegaly
 The disease is transmitted by direct skin penetration
 This form of schistosomiasis is diagnosed by
identification of characteristic eggs in the stool
Schistosomes encopula
A Schistosoma mansoni egg with the
characteristic lateral spine
Entamoeba histolytica (Amebic dysentery)
 A world wide in distribution
 More often in tropical countries with poor sanitary
conditions
 A commensal protozoa when human has a normal
immune function
 Invading host tissues and causing amoebiasis when
human has a lower immune function
Morphology ‫ال‬
 Trophozoite
 No regular in shape, 20~60μm in size
 An active-moving trophozoite produce pseudopods
(organelle)
 A spherical central nucleus
 Peripheral chromatin
 Erythrophagocytosis
 Cyst
 Spherical in shape & 10~20μm in diameter. 1~4 nuclei
(similar to that of the trophozoite)
 Immature cyst (1 or 2 nuclei) has the glycogen vacuole &
chromatoid body
 No inclusions, disappear in mature cyst (4 nuclei)
 Infective stage
Entamoeba histolytica cyst
Life-cycle of Entamoeba histolytica
Life cycle
Hd,h
 Basic model: cyst → trophozoite → cyst
 Parasitic location: large intestine (common); intestinal
tissue or other tissues (occasional)
 Infective stage: mature cyst
 Trophozoite in diarrhea or pus; Cyst in formed feces
 Infection: by ingestion of mature cyst
‫ايوا‬
Clinical classification
 90% persons infected are carriers
 Intestinal amoebiasis
 Acute intestinal amoebiasis

amoebic dysentery (bloody, mucus-containing diarrhea) +
lower abdominal discomfort + tenesmus
 Chronic intestinal amoebiasis

dyspepsia + weight loss + asthenia (common) / diarrhea
‫مهمه‬
 Extraintestinal amoebiasis
 Liver : amoebic hepatitis + amoebic liver abscess --- pain
in right-upper-quadrant + fever + marked tenderness of
liver
 Lung: amoebic pulmonary abscess --- pain in chest +
cough + fever

Sometimes, it can be carried to other organs
 Brain, skin
Laboratory diagnosis
 Fecal examination
 Wet mounts

Trophozoites in diarrhea feces
 Wet mounts stained with iodine

Cyst in formed feces
 Pus examination
 Trophozoites in aspirate pus from abscesses
Giardia lamblia (Giardiasis)
 Giardiasis is the most commonly diagnosed parasitic
intestinal disease in the United States
 Ingested cysts form trophozoites in the duodenum,
where they attach to the wall but do not invade
 Giardia infections are often clinically mild, although in
some individuals, massive infection may damage the
duodenal mucosa
 Because the Giardia parasite preferentially inhabits the
duodenum, fecal examination may be negative
 A commercial enzyme-linked immunosorbent assay to
measure Giardia antigen in fecal material has proven
useful
 Metronidazole is an effective treatment
 G. lamblia cysts are resistant to chlorine
concentrations used in most water treatment facilities
 So can effect in swemming pool
Giardia cell, SEM
Life cycle of Giardia lamblia
Ascaris lumbricoides
Ascariasis (roundworm disease)
 It is second only to pinworms as the most prevalent
multicellular parasite in the United States
 Approximately one third of the world’s population is
infected with this worm
 The disease is transmitted by ingestion of soil
containing the organism’s eggs
 Humans are the sole host
 Larvae grow in the intestine, causing abdominal
symptoms, including intestinal obstruction
 Roundworms may pass to the blood and through the
lungs
 Roundworm disease is diagnosed by detection of
characteristic eggs in the stool
 It is treated with pyrantel pamoate or mebendazole
An adult female Ascaris worm.
Fertile egg in human faeces (detail)
Ancylostoma duodenale (Hookworm disease)
 The worm attaches to the intestinal mucosa causing
 anorexia
 ulcer-like symptoms
 chronic intestinal blood loss, leading to anemia
 The disease is transmitted through direct skin penetration
by larvae found in soil
 Hookworm disease is diagnosed by identification of
characteristic eggs in the stool
 It is treated with pyrantel pamoate or mebendazole
Strongyloides stercoralis ‫قراءة‬
Strongyloidiasis (threadworm disease)
 It is relatively uncommon compared with infections by other intestinal
nematodes
 It is a relatively benign disease in healthy individuals but can progress
to a fatal outcome in immunocompromised patients because of
dissemination to the CNS or other deep organs in certain
immunocompromised Patients
 The disease is transmitted through direct skin penetration by larvae
found in soil
 Threadworm disease is diagnosed by identifying larvae in the stool
 It is treated with thiabendazole, albendazole or ivermectin
First stage larva (L1) of S. stercoralis
Trichuris trichiura ‫قراءة‬
Trichuriasis (whipworm disease)
 The infection is usually asymptomatic; however, abdominal
pain, diarrhea, flatulence, and rectal prolapse can occur
 The disease is transmitted by ingestion of soil containing
the organism’s eggs
 Whipworm disease is diagnosed by identifying
characteristic eggs in the stool
 It is treated with mebendazole
Egg of Trichuris vulpis
Taenia saginata (Taeniasis) ‫مهمه‬
 This form of the disease is caused by the larval form of Taenia
saginata (beef tapeworm)
 The organism primarily infects the intestines and does not
produce cysticerci
 Most infected individuals are asymptomatic
 The disease is transmitted by larvae in undercooked or raw beef
 Taeniasis is diagnosed by detection of proglottids in the stool
Taenia saginata proglottid stained to show
uterine branches. The pore on the side
identifies T. saginata as a cyclophyllid
cestode.