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Gastro Intestinal Tract

The gastro intestinal tract (GI tract) consists of the:

• mouth (oral cavity) • Oesophagus • stomach • small intestine • large intestine • rectum • anus

Introduction

• Ingestion of pathogens may cause many different infections• They may be confined to the gastro intestinal tract or start

spreading from there• A wide range of microbial pathogens is capable of infecting

the gastro intestinal tract• They are acquired by faecal – oral route, from faecaly

contaminated foods, fluids and finger• For an infection to occur

– Pathogen must be ingested in sufficient number– Or posses attributes to elude the host defences of the gastro intestinal

tract

Host Defences of The Gastro Intestinal Tract

• Saliva acts to flush away microbes that have tensiently settled on the mucosa.

• Lysozyme in saliva destroye bacteria.• Stomach acidity and proteolytic enzymes destroy or degrade

many infectious agents.• Bile secreted by the gallbladder is inhibitory to the growth of

many bacteria.• Normal peristalsis forces organisms to move along the GI

tract and to be excreted with fecal matter.• The mucosal layer protects epithelial cells.

Distribution of the Intestinal Micro flora

• Organisms in the stomach are usually transient, and their populations are kept low (103 to 106/g of contents) by acidity.

• The intestinal micro flora is a complex ecosystem containing over 400 bacterial species.

• Anaerobes(Bacteroides, anaerobic streptococci, and clostridia) outnumber facultative anaerobes(E coli).

• The flora is sparse in the stomach and upper intestine, but luxuriant in the lower bowel.

• Bacteria occur both in the lumen and attached to the mucosa, but do not normally penetrate the bowel wall .

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Metabolic Activities

• Intestinal bacteria are a crucial component of the enterohepatic circulation. (Enzyme : ß-glucuronidase, sulfatase, and various glycosidases,Metabolites : bilirubin, bile acids, cholesterol, estrogens, and metabolites of vitamin D. conjugated with glucouranic acid, sulfate, taurine & glycine)

• Antibiotics that suppress the flora can alter the fecal excretion and hence the blood levels of these compounds.

• The flora also plays a role in fiber digestion and synthesizes certain vitamins(Vitamin K).

The Intestinal Micro flora

• The intestinal micro flora may prevent infection by interfering with pathogens.

• Antimicrobial substances such as bacteriocins or short-chain fatty acids, which inhibit the growth of alien microorganisms.

• Antibiotics that upset the balance of the normal flora can favor both infection by exogenous pathogens and overgrowth by endogenous pathogens(Clostridium difficile).

• If the bowel wall is breached, enteric bacteria can escape into the peritoneum and cause peritonitis and abscesses.(The intestinal wall can be perforated by trauma (knife wounds & gunshot wounds), by disease (appendicitis, penetrating intestinal cancers), or by surgical procedures.)

Epidemiology

• Worldwide: 1 billion episodes; 3 million to 5 million deaths annually in children

• US: 1 to 2 episodes per year in children younger than 5 years; 300 to 400 deaths per year

Etiology• Bacteria:

- Common: Campylobacter jejuni, Shigella spp., Salmonella spp., E. Coli

- Less common: Yersinia enterocolitica, Bacillus cereus,C. Difficile

- Rare:Vibrio spp., Staphylococcus aureus, Clostridium perfringens, shigelloides, Aeromonas hydrophila

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Continued…

• Viruses:

-Rotavirus, calicivirus, astrovirus, enteric adenovirus (types 40 and 41)

• Immunocompromised hosts may be infected with cytomegalovirus (CMV), herpes simplex virus (HSV), Cryptosporidium ovale.

• Protozoans:– Entamoeba hisolytica– Giardia lamblia– Cryptosporidium parvum

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Enterotoxin-Mediated Diarrheal Diseases

• Several enterotoxin-producing bacteria cause diarrheal diseases

• The diarrheal disease caused by Vibrio cholerae and enterotoxigenic strains of E. coli has three main characteristics.– First, there is intestinal fluid loss that is related to the action of an

enterotoxin on the small bowel epithelial cells.– Second, the organism itself does not invade the mucosal surface;

rather, it colonizes the upper small bowel, adhering to the epithelial cells and elaborating the enterotoxin.

– Third, the fecal effluent is watery and often voluminous, so that the diarrhea can result in clinical dehydration.

Cholera

• Cholera is a potentially epidemic and life-threatening secretory diarrhea

• characterized by numerous, voluminous watery stools, often accompanied by vomiting

• Stool volume can exceed 1 L/h, with daily fecal outputs of 15 to 20 L if the patient is kept hydrated.

• Cholera flourishes in communities with inadequate clean drinking water and sewage disposal

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Structure, Classification, and Antigenic Types

• Vibrios are Gram-negative, highly motile curved rods with a single polar flagellum.

• They tolerate alkaline media that kill most intestinal commensals, but they are sensitive to acid.

• Numerous free-living vibrios are known, some potentially pathogenic.

• Until 1992, cholera was caused by only two serotypes, Inaba (AC) and Ogawa (AB), and two biotypes, classical and El Tor, of toxigenic O group 1 V. cholerae.

• In 1992, cholera caused by serogroup O139 emerged in epidemic proportions in India and Bangladesh.

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Pathogenesis

• Vibrios are sensitive to acid, and most die in the stomach.• Surviving virulent organisms may adhere to and colonize the

small bowel, where they secrete the potent cholera enterotoxin (CT, also called “choleragen”).

• This toxin binds to the plasma membrane of intestinal epithelial cells and releases an enzymatically active subunit that causes a rise in cyclic adenosine 51-monophosphate (cAMP) production.

• The resulting high intracellular cAMP level causes massive secretion of electrolytes and water into the intestinal lumen.

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Host Defenses

• Gastric acid, mucus secretion, and intestinal motility are the prime nonspecific defenses against V cholerae.

• Breastfeeding in endemic areas is important in protecting infants from disease.

• Disease results in effective specific immunity, involving primarily secretary IgA, as well as IgG antibodies, against vibrios.

Epidemiology• Cholera is endemic or epidemic in areas with poor sanitation;

it occurs sporadically or as limited outbreaks in developed countries.

• Long-term convalescent carriers are rare.

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Diagnosis

• The diagnosis is suggested by strikingly severe, watery diarrhea.

• For rapid diagnosis, a wet mount of liquid stool is examined microscopically.

• Other methods are– the slide agglutination test of colonies with specific antiserum – fermentation tests (oxidase positive); and enrichment in peptone broth

followed by fluorescent antibody tests.– More recently the polymerase chain reaction (PCR) and additional

genetically-based rapid techniques have been recommended for use in specialized laboratories.

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Control

• Control by sanitation is effective but not feasible in endemic areas.

• A good vaccine has not yet been developed. A parenteral vaccine of whole killed bacteria has been used widely, but is relatively ineffective and is not generally recommended.

• Living attenuated genetically engineered mutants are promising, but such strains can cause limited diarrhea as a side effect.

• Antibiotic prophylaxis is feasible for small groups over short periods.

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Escherichia Coli in Diarrheal Disease

Clinical Manifestations• Escherichia coli is a common member of the normal flora of

the large intestine.• Depending on the virulence factors they possess, virulent

Escherichia coli strains cause either– noninflammatory diarrhea (watery diarrhea)– inflammatory diarrhea (dysentery with stools usually containing blood,

mucus, and leukocytes).

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Structure, Classification, and Antigenic Types

• These are Gram-negative bacilli of the family Enterobacteriaceae.

• Three groups of E coli are associated with diarrheal diseases.

• Strains producing enterotoxins are enterotoxigenic E coli (ETEC).– There are numerous types of enterotoxin. – Some of these toxins are cytotoxic, damaging the mucosal cells, – whereas others are merely cytotonic, inducing only the secretion of

water and electrolytes.

• A second group of E coli strains have invasion factors and cause tissue destruction and inflammation resembling the effects of Shigella(EIEC).

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Continued…….

• A third group of serotypes, called enteropathogenic E coli (EPEC), are associated with outbreaks of diarrhea in newborn nurseries, but produce no recognizable toxins or invasion factors.

Noninflammatory Diarrheas Caused by Enterotoxigenic Escherichia Coli

Clinical Manifestations– The diarrheal disease caused by ETEC is characterized by a rapid

onset of watery, non bloody diarrhea of considerable volume, accompanied by little or no fever

– Other common symptoms are abdominal pain, malaise, nausea, and vomiting.

– Diarrhea and other symptoms cease spontaneously after 24 to 72 hours.

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Structure, Classification, and Antigenic Types

– ETEC organisms are Gram-negative, short rods not visibly different from E coli found in the normal flora of the human large intestine.

– Virulence-associated fimbriae are too small to be seen by light microscopy.

– Escherichia coli serotypes are specific O-group/H-antigen combinations.

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Pathogenesis

– Escherichia coli diarrheal disease is contracted orally by ingestion of food or water contaminated with a pathogenic strain shed by an infected person.

– The pathogenesis of ETEC diarrhea involves two steps: intestinal colonization, followed by elaboration of diarrheagenic enterotoxin(s)

– ST is actually a family of toxic peptides ranging from 18 to 50 amino acid residues in length.

– They can stimulate intestinal guanylate cyclase, the enzyme that converts GTP to cGMP.

– Increased intracellular cGMP inhibits intestinal fluid uptake, resulting in net fluid secretion.

– The E coli LTs are antigenic proteins whose mechanism of action is similar to that of Vibrio cholerae enterotoxin.

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Continued….

– This activates the adenylate cyclase, which produces excess intracellular cAMP, which leads to hypersecretion of water and electrolytes into the bowel lumen.

Host Defenses– As in any orally transmitted disease, the first line of defense against

ETEC diarrhea is gastric acidity.– Other nonspecific defenses are small-intestinal motility and a large

population of normal flora in the large intestine.– intestinal secretory immunoglobulin (IgA) directed against surface

antigens such as the CFAs and against LT appears to be the key to immunity from ETEC diarrhea.

– Human breast milk also contains nonimmunoglobulin factors (receptor-containing molecules) that can neutralize E coli toxins and CFAs.

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Diagnosis

– ETEC diarrhea is characterized by copious watery diarrhea with little or no fever.

– The diarrheal stool yields a virtually pure culture of E coli.– Since the disease is self-limiting, virulence testing of isolates and

serotyping is impractical except in an outbreak situation.– Confirmation is achieved by serotyping, serologic identification of a

specific CFA on isolates, demonstration of LT or ST production, and identification of genes encoding these virulence factors

• Control– Escherichia coli diarrheal disease is best controlled by preventing

transmission and by stressing the importance of breast-feeding of infants,

– The best treatment is oral fluid and electrolyte replacement (intravenous in severe cases).

Inflammatory Diarrheas Caused by Enteroinvasive, Cytotoxic, and Enteropathogenic Escherichia Coli

• Clinical Manifestation– Diarrhea caused by the enteroinvasive, cytotoxic, and

enteropathogenic (EPEC) strains of E coli ranges from very mild to severe.

– Illness is usually protracted and accompanied by fever.– Infection with a few serogroups (O157, O26) is characterized by

bloody diarrhea (hemorrhagic colitis).– Infection with the Shigella-like serogroups presents as bacillary

dysentery

• Structure, Classification, and Antigenic Types– The EPEC serogroups listed in Table 25-2 were the first E coli groups

to be recognized as causative agents of diarrhea in infants.

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Pathogenesis– Escherichia Coli strains belonging to the classic EPEC serogroups

(Table 25-2) bind intimately to the epithelial surface of the intestine,– The lesion caused by EPEC consists mainly of destruction of

microvilli.– Cell damage occurs in two steps.

• collectively termed attaching

• second is loss of microvilli which is the result of rearrangement of the host cell cytoskeleton.

– Loss of microvilli leads to malabsorption and osmotic diarrhea.– Diarrhea is persistent, often chronic, and accompanied by fever.– The E coli strains associated with hemorrhagic colitis

(enterohemorrhagic E coli, or EHEC) most notably O157:H7, produce relatively large amounts of the bacteriophage-mediated Shiga-like toxin.

– This toxin is called Vero toxin (VT), or Vero cytotoxin after its cytotoxic effect on cultured Vero cells.

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Continued..

– The Shigella-like E coli strains are highly virulent;– oral exposure to a very small number of these invasive bacteria

causes severe illness.– The site of the infection is the colon, where adherence is rapidly

followed by invasion of the intestinal epithelial cells– An acute inflammatory response and tissue destruction produce

diarrhea with little fluid, much blood, and sheets of mucus containing polymorphonuclear cells.

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Host Defenses

– These defenses are frequently deficient or lacking in the infant and the elderly, which is consistent with the epidemiology of EPEC illness.

– Infection with these pathogens often excites an inflammatory cell response in the intestine, as is frequently reflected in the diarrheal symptoms.

• Diagnosis– Diagnosis is usually based on the symptomatology described above.– Escherichia Coli serotyping is useful in chronic cases and in

outbreaks, because identification of the agent and its antibiotic sensitivity pattern are valuable in these situations.

– Testing for specific EPEC virulence factors is usually impractical because it can be done only in reference and specialized research laboratories.

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Control

– Prevention and control are generally the same as for ETEC.– Intervention of the fecal-oral transmission cycle is most effective in

institutional situations.– Broad-spectrum antibiotics are recommended in chronic and/or life-

threatening cases.

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Salmonella

• Clinical Manifestations– Salmonellosis ranges clinically from the common Salmonella

gastroenteritis (diarrhea, abdominal cramps, and fever) to enteric fevers (including typhoid fever)

– The most common form of salmonellosis is a self-limited, uncomplicated gastroenteritis.

• Structure, Classification, and Antigenic Types– Salmonella species are Gram-negative, flagellated facultatively

anaerobic bacilli characterized by O, H, and Vi antigens.,– There are over 1800 known serovars which current classification

considers to be separate species.

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Host Defenses

– Both nonspecific and specific host defenses are active.– Non-specific defenses consist of gastric acidity, intestinal mucus,

intestinal motility (peristalsis), lactoferrin, and lysozyme.– Specific defenses consist of mucosal and systemic antibodies and

genetic resistance to invasion. Various factors affect susceptibility.

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Diagnosis

– Salmonellosis should be considered in any acute diarrheal or febrile illness without obvious cause.

– The diagnosis is confirmed by isolating the organisms from clinical specimens (stool or blood).

• Control– Salmonellae are difficult to eradicate from the environment.– General salmonellosis treatment measures include replacing fluid loss

by oral and intravenous routes, and controlling pain, nausea, and vomiting.

– Specific therapy consists of antibiotic administration.

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Shigellosis

• Clinical Manifestations– Symptoms of shigellosis include abdominal pain, watery diarrhea,

and/or dysentery (multiple scanty, bloody, mucoid stools).– Other signs may include abdominal tenderness, fever, vomiting,

dehydration, and convulsions.

• Structure, Classification, and Antigenic Types– Shigellae are Gram-negative, nonmotile, facultatively anaerobic, non-

spore-forming rods.– Shigella are differentiated from the closely related Escherichia coli on

the basis of pathogenicity, physiology (failure to ferment lactose or decarboxylate lysine) and serology.

– The genus is divided into four serogroups with multiple serotypes: A (S dysenteriae, 12 serotypes); B (S flexneri, 6 serotypes); C (S boydii, 18 serotypes); and D (S sonnei, 1 serotype).

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Pathogenesis

– Infection is initiated by ingestion of shigellae– An early symptom, diarrhea (possibly elicited by enterotoxins and/or

cytotoxin), may occur as the organisms pass through the small intestine.

– The hallmarks of shigellosis are bacterial invasion of the colonic epithelium and inflammatory colitis.

– These are interdependent processes amplified by local release of cytokines and by the infiltration of inflammatory elements.

• Host Defenses– Inflammation, copious mucus secretion, and regeneration of the

damaged colonic epithelium limit the spread of colitis and promote spontaneous recovery.

– The protective role of immune responses against the antigens is unclear.

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Diagnosis

– Shigellosis can be correctly diagnosed in most patients on the basis of fresh blood in the stool.

– Neutrophils in fecal smears is also a strongly suggestive sign.– Nonetheless, watery, mucoid diarrhea may be the only symptom of

many S sonnei infections, and any clinical diagnosis should be confirmed by cultivation of the etiologic agent from stools.

• Control– Prevention of fecal-oral transmission is the most effective control

strategy.– Severe dysentery is treated with ampicillin, trimethoprim-

sulfamethoxazole, or, in patients over 17 years old, a 4-fluorquinolone such as ciprofloxacin.

– Vaccines are not currently available, but some promising candidates are being developed.

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Camphylobacter

• Clinical Manifestations– Campylobacter species cause acute gastroenteritis with diarrhea,

abdominal pain, fever, nausea, and vomiting.

• Structure– Campylobacter species are Gram-negative, microaerophilic, non-

fermenting, motile rods with a single polar flagellum; they are oxidase-positive and grow optimally at 37° or 42°C.

• Classification and Antigenic Types– Campylobacter species have many serogroups, based on

lipopolysaccharide (O) and protein (H) antigens.– C jejuni possesses several common surface-exposed antigens,

including porin protein and flagellin.

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Pathogenesis

– The bacteria colonize the small and large intestines, causing inflammatory diarrhea with fever.

– Stools contain leukocytes and blood.– The role of toxins in pathogenesis is unclear.– C jejuni antigens that cross-react with one or more neural structures

may be responsible for triggering the Guillian-Barre syndrome.

• Host Defenses– Nonspecific defenses such as gastric acidity and intestinal transit time

are important.– Specific immunity, involving intestinal immunoglobulin (IgA) and

systemic antibodies, develops.– Persons deficient in humoral immunity develop severe and prolonged

illnesses.

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Diagnosis

• Control– Control depends on measures to prevent transmission from animal

reservoirs to humans.

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Other bacterial causes of Diarrhea

• Vibrio parahaemolyticus and Yersinia enterocolitica are food borne gram negative cause of diarrhea

• Clostridium perfringens and Bacillus cereus are spore forming gram positive causes of diarrhea

Viral Diarrhea• Over 3 million infants die of gastro entiritis each year, viruses

are the comenest causes• Rota virus• Replicating Rota virus cause diarrhea by damaging the

transport mechanism in the gut• They can be seen in fecal particles under electron

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Clinical Manifestations

– Rotaviruses induce a clinical illness characterized by vomiting, diarrhea, abdominal discomfort, fever, and dehydration

– It occurs primarily in infants and young children and may lead to hospitalization for rehydration therapy

– Although milder gastroenteric illnesses that do not require hospitalization are also common, most studies of clinical manifestations of rotavirus-induced gastroenteritis rely on data from hospitalized patients

– The duration of hospitalization ranges from 2 to 14 days with a mean of 4 days

– The highest attack rate is usually among infants and young children 6 to 24 months old, and the next highest in infants less than 6 months old

– Deaths from rotavirus gastroenteritis may occur from dehydration and electrolyte imbalance.

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Structure– Rotaviruses have a distinctive wheel-like shape – Complete particles have a double-layered capsid and measure about

70 nm in diameter– Within the inner capsid is the 37-nm core, which contains the RNA

genome– Morphologically, rotaviruses resemble the reoviruses, coltiviruses and

orbiviruses– The rotavirus genome contains 11 segments of double-stranded RNA

• Classification and Antigenic Types– Most human rotaviruses share a common group antigen and are

designated group A rotaviruses,– The non-group A viruses are divided into groups B, C, D, E, F, and G

on the basis of distinct group antigens– The group A rotaviruses are the most important agents of severe

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Host Defenses– The mechanism of immunity is not firmly established

– Serum antibody in volunteers was found to correlate with resistance to rotavirus-induced illness

– Serotype-specific immunity may be of importance in protecting against illness with individual serotypes, but this is still under investigation

• Diagnosis– Because the clinical manifestations of rotavirus gastroenteritis are not distinct

enough to permit a specific diagnosis, specimens must be examined in the laboratory

– Laboratory diagnosis of rotavirus infections requires identifying the virus in feces or rectal swab specimens

– When the number of specimens is limited, the most rapid method of rotavirus diagnosis in a hospital setting is by examination of a stool specimen by negative-stain electron microscopy

– Serologic evidence of rotavirus infection can be detected by various techniques, such as ELISA immunofluorescence, neutralization, and complement fixation

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Control

– The primary aim of treatment of rotavirus gastroenteritis is the replacement by the intravenous or oral route of fluids and electrolytes lost by vomiting or diarrhea

– In patients with severe dehydration and shock, intravenous rehydration is indicated for efficient replacement of fluid loss

– Virus-specific chemotherapy is not available– An attenuated monovalent bovine rotavirus strain (serotype 6) or an

attenuated monovalent rhesus rotavirus strain (serotype 3) has been administered orally to infants and young children as experimental vaccines. Their efficacy has been variable

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Continued……• Other viruses• Other viruses causing damage includes

– calici viruses – astro viruses– adeno viruses– parvo viruses– and corona viruses

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Food Poisoning• It is mainly caused by Staph. aureus enterotoxin and Cl.

botulinum toxin

• Exotoxins produced causes botulism– They are of three types food borne botulism, wound botulism and

infant botulism– They cause flaccid paralysis leading to muscle weakness and

respiratory arrest– Complete recovery may take months

• Five different entero toxins are produced by S.aureus– Thier mechanism of action is not understood– They affect the CNS and cause severe vomitting within 3-6 hrs– Diarrhea is not a feature, recovered within 24 hrs

Parasites and the Gastro Intestinal tract

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Protozoan infection

• Three species are of particular importance– Entamoeba hisolytica– Giardia lamblia– Cryptosporidium parvum

Entamoeba histolitica– Common in subtropical and trophical countries– Clinical manifestation vary from asymptomatic and severe diarrhea– They can be diagonised by the presence of characteristic 4 nucleated

cysts– They can be treated with Metronidazole

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Pathogenesis of E histolytica infection.

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Multiplication and life cycle of E histolytica.

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Control

– Preventive measures are limited to environmental and personal hygiene

– Effective drugs are available for liver abscess but intestinal infection is less successfully treated

– No single drug is completely effective in eradicating amebas from the gut, so reliance is often placed on combination therapy.

– Acute intestinal disease is best treated with metronidazole at a dose of 750 mg three times a day orally for 10 day

– children the dose is 40 mg/kg/day divided into three doses and given orally for 10 days.

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Giardia lamblia

– It is the first intestinal microorganism to be vieved under the microscope

– Giardia infection may be asymptomatic or it may cause disease ranging from a self-limiting diarrhea to a severe chronic syndrome.

– They can be treated with drugs including mepacrine hydrochloride, metronidazole and tinidazole

– The length of the incubation period, usually 1 to 3 weeks, depends at least partly on the number of cysts ingested.

– Signs and symptoms may include interference with the absorption of fat and fat-soluble vitamins, retarded growth, weight loss, or a celiac-disease-like syndrome

– Identification of Giardia in a specimen does not necessarily mean that this organism is responsible for the patient's symptoms. Giardia should be treated and eliminated when found, but other pathogens should be sought as well

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Giardia life cycle in humans

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Control

– Attention to personal hygiene is the key to preventing the spread of giardiasis

– Controlling the spread of Giardia in drinking water should be possible where community water treatment methods (e.g., disinfection and filtration) are available

– The drug of choice for treating Giardia infections is quinacrine hydrochloride

– This drug frequently causes dizziness, headache, and vomiting– Metronidazole and furazolidone also may be used

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Cryptosporidium parvum

• Is widely distributed in many animals

• Diarrhea ranges from moderate to severe

• Faecal examination is inadequate for identification

• Only immunocompromised patients need treatment

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Worm infections

• The most important worms clinically known as nematodes are– Ascaris lumbricoides and Trichuiris trichura, in which the infection

occurs by swallowing the eggs– Ancyclostoma duodenale and necator americanus, they infect by

active skin penetration by infective larvae– The pinworm or threadworm Enterobius vermicularis is the

commenest intestinal nematodes and least pathogenic

• Other intestinal worms include– Taenia saginata– Hymenolipis nata– Trichinella spiralis

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Life cycle of Ascaris lumbricoides

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Life cycle of Enterobius vermicularis.

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Diagnosis

– Diagnosis is made most often by identifying eggs in stool; occasionally, erratic adults emerge from body orifices.

• Control– Control is by sanitary disposal of feces and by education and

treatment– Mebendazole, the drug used, is effective against numerous intestinal

nematode infections and causes few side effects– Levamisole is also useful, as are pyrantel pamoate, piperazine citrate,

thiabendazole and albendazole

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