Viral and Parasitic Gastroenteritis

Viral and Parasitic Gastroenteritis
المهم كتبت عليه الي مو مهم مكتوب ___فمعناتو معنانا ____الي ماعلق عليه فاضي والي قرأه مكتوب والون الاحمر 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

Classification of major viral agents causing hepatitis
important Classification of hepatitis viruses based on mode of transmission Classification of major viral agents causing hepatitis

Hepatitis A Virus: Structure and Classification
مو مره مهه 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

Hepatitis A Virus Transmission
جدا مهمه 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

Hepatitis A: Pathogenesis
لا 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%

Hepatitis A - Diagnosis
مو مهم Detection of IgM antibody IgG positive 1-3 weeks later; suggests prior infection or vaccination

Hepatitis A - Treatment
مو مهم 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
مو مرا مهم 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

DURATION OF PROTECTION AFTER VACCINATION
مو مرا مهمه 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

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 Replicationمو مهم بس الاحمر
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

Global Patterns of Chronic HBV Infection
بس نسبة السعوديه 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
مهمه 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 Cirrhosis 6-15% in 5 years 20-23% in 5 years Hepatocellular carcinoma Liver failure Death Liver transplant Death

Outcome of Hepatitis B Virus Infection by Age at Infection
100 Symptomatic Infection Chronic Infection Birth 1-6 mos 7-12 mos 1-4 yrs Older Children and Adults 20 40 60 80 Chronic Infection (%) Symptomatic Infection (%)

HBV Modes of Transmission
مهمه Sexual Parenteral Perinatal

Concentration of HBV in Various Body Fluids
مهم Low/Not High Moderate Detectable semen serum vaginal fluid blood wound exudates saliva 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 الاحمر
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 Licensed in 1982
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

Hepatitis B Vaccine Safety
مو مهم 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
مو مرا مهم Routine infant Ages 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

Occupational Transmission of HCV
مهم 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

Chronic Hepatitis C Factors Promoting Progression or Severity
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
لا 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 Average 40 days Range days Case-fatality rate 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
لا 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

Infants who are breastfed also suffer milder disease manifestations
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 They commonly cause diseases such as
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
لا 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
لا 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

E. Treatment and prevention
لا 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

Caliciviruses (formerly known as Norwalk-like virus)
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 لا 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 Basic model: cyst → trophozoite → cyst
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

Clinical classification
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

Extraintestinal amoebiasis
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 Pus 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
Taenia saginata proglottid stained to show uterine branches. The pore on the side identifies T. saginata as a cyclophyllid cestode.

Viral and Parasitic Gastroenteritis

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