viral and parasitic gastroenteritis n.
Skip this Video
Download Presentation
Viral and Parasitic Gastroenteritis

Loading in 2 Seconds...

play fullscreen
1 / 105

Viral and Parasitic Gastroenteritis - PowerPoint PPT Presentation

  • Uploaded on

Viral and Parasitic Gastroenteritis. 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

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about 'Viral and Parasitic Gastroenteritis' - armand

Download Now An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
viral gastroenteritis
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 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

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

Classification of hepatitis viruses based on mode of transmission

Classification of major viral agents causing hepatitis

hepatitis a virus structure and classification
Hepatitis A Virus: Structure and Classification
  • Virus classification
    • Group: Group IV ((+)ssRNA)
    • Family: Picornaviridae
    • Genus: Hepatovirus
    • Species: Hepatitis A virus
  • Separate genus because ofdifferences with other enteroviruses
  • Naked icosahedral capsid
  • SS RNA (740 nucleotides)
  • Single serotype worldwide
  • Humans only reservoir

Electron micrograph of hepatitis A virions

hepatitis a virus transmission
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
hepatitis a pathogenesis
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
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%
hepatitis a diagnosis
Hepatitis A - Diagnosis
  • Detection of IgM antibody
  • IgG positive 1-3 weeks later; suggests prior infection or vaccination
hepatitis a treatment
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
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 vaccines1
  • 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
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
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
hepatitis a vaccine immunogenicity side effects
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 structure
Hepatitis B: Structure
  • Member of the hepadnavirus group
  • Virionalso referred to as Dane particle
  • 42nm enveloped virus
  • Core antigens located in the center (nucleocapsid)
structure and replication
Structure and Replication
  • 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
Hepatitis B Virus

TEM micrograph showing hepatitis B viruses

The structure of hepatitis B virus

global patterns of chronic hbv infection
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
possible outcomes of hbv infection
Possible Outcomes of HBV Infection

Acute hepatitis B infection

95% of infant-acquired infections

3-5% of adult-acquired infections

Chronic HBV infection

Chronic hepatitis

12-25% in 5 years


20-23% in 5 years

6-15% in 5 years

Hepatocellular carcinoma

Liver failure

Liver transplant



outcome of hepatitis b virus infection by age at infection







Chronic Infection





Symptomatic Infection




1-4 yrs

1-6 mos

7-12 mos

Older Children

and Adults

Outcome of Hepatitis B Virus Infection by Age at Infection

Chronic Infection (%)

Symptomatic Infection (%)

hbv modes of transmission
HBV Modes of Transmission
  • Sexual
  • Parenteral
  • Perinatal
concentration of hbv in various body fluids









vaginal fluid


wound exudates




breast milk

Concentration of HBV in Various Body Fluids
hepatitis b symptoms
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
HBV Pathogenesis
  • 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
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
Hepatitis B Vaccine
  • 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
hepatitis b vaccine safety
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
hepatitis b vaccination
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 structure and classification
Hepatitis C Structure and Classification
  • Member of the flavivirusfamily
  • Enveloped single stranded RNA virus
  • Humans and chimpanzees only known reservoirs
  • 6 serotypes (genotypes) and multiple subtypes
    • based on high variability of envelope glycoproteins
occupational transmission of hcv
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
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
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
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
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
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
chronic hepatitis c factors promoting progression or severity
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
Hepatitis C: Diagnosis
    • usually positive within 2-5 months after infection
  • PCR
    • positive 1-2 weeks post infection
hepatitis d
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
Hepatitis D Virus Modes of Transmission
  • Percutaneous exposures
    • injecting drug use
  • Permucosalexposures
    • sex contact

Geographic Distribution of HDV Infection


Pacific Islands

HDV Prevalence




Very Low

No Data

hepatitis d pathogenesis
Hepatitis DPathogenesis
  • 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
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
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
Hepatitis E - Epidemiologic Features
  • Most outbreaks associated with fecallycontaminated drinking water
  • Minimal person-to-person transmission
  • U.S. cases usually have history of travel to HEV-endemic areas
hepatitis e clinical features
Hepatitis E - Clinical Features
  • Incubation periodAverage 40 days

Range 15-60 days

  • Case-fatality rateOverall, 1%-3% Pregnant women, 15%-25%
  • Illness severityIncreased with age
  • Chronic sequelaeNone identified
prevention and control measures for travelers to hev endemic regions
Prevention and Control Measuresfor 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
  • Rotaviruses, found in many mammalian species
  • Rotaviruses have a characteristic morphology that distinguishes them from other reoviruses
a epidemiology
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
B. Clinical significance
  • 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
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
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
  • 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
a epidemiology and pathogenesis
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
b structure and replication
B. Structure and replication
  • The adenovirus capsid is composed of hexoncapsomers
  • 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 = hexoncapsomeres

3 = viral genome (linear dsDNA)

c clinical significance
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
Gastrointestinal diseases
  • 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
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
e treatment and prevention1
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, unattenuatedadenovirus
caliciviruses formerly known as norwalk like virus
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
leishmania donovani visceral leishmaniasis k ala azar
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
echinococcus granulosus dog tapeworm
Echinococcus granulosus (dog tapeworm)
  • Infection produces large, hydatidcysts 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
  • Echinococcosisis diagnosed by CT scan or biopsy of infected tissue and is treated with albendazoleand surgical excision of intact cysts

E. granulosus scolex

E. granulosus life cycle

schistosoma mansoni
Schistosoma mansoni
  • 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


A Schistosoma mansoni egg with the characteristic lateral spine

entamoeba histolytica amebic dysentery
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
  • Trophozoite
    • No regular in shape, 20~60μm in size
    • An active-moving trophozoiteproduce pseudopods (organelle)
    • A spherical central nucleus
    • Peripheral chromatin
    • Erythrophagocytosis


    • 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 & chromatoidbody
    • No inclusions, disappear in mature cyst (4 nuclei)
    • Infective stage

Entamoeba histolytica cyst

Life-cycle of Entamoeba histolytica

life cycle
Life cycle
  • Basic model: cyst → trophozoite → cyst
  • Parasitic location: large intestine (common); intestinal tissue or other tissues (occasional)
  • Infective stage: mature cyst
  • Trophozoitein diarrhea or pus; Cyst in formed feces
  • Infection: by ingestion of mature cyst
clinical classification
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

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
Laboratory diagnosis
  • Fecal examination
    • Wet mounts
      • Trophozoitesin diarrhea feces
    • Wet mounts stained with iodine
      • Cyst in formed feces
  • Pus examination
    • Trophozoitesin aspirate pus from abscesses
giardia lamblia giardiasis
Giardia lamblia(Giardiasis)
  • Giardiasis is the most commonly diagnosed parasitic intestinal disease in the United States
  • Ingested cysts form trophozoitesin 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

Giardia cell, SEM

Life cycle of Giardia lamblia

ascaris lumbricoides ascariasis roundworm disease
Ascaris lumbricoidesAscariasis(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 pyrantelpamoateor mebendazole

An adult female Ascaris worm.

Fertile egg in human faeces (detail)

ancylostoma duodenale hookworm disease
Ancylostomaduodenale(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 pyrantelpamoateor mebendazole
strongyloides stercoralis strongyloidiasis threadworm disease
StrongyloidesstercoralisStrongyloidiasis (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
trichuris trichiura trichuriasis whipworm disease
TrichuristrichiuraTrichuriasis (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
taenia saginata taeniasis
Taenia saginata (Taeniasis)
  • 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
  • Taeniasisis diagnosed by detection of proglottidsin the stool

Taenia saginata proglottid stained to show uterine branches. The pore on the side identifies T. saginata as a cyclophyllidcestode.