gastrointestinal tract infection

71
GASTROINTESTINAL TRACT INFECTION SY. MIFTAHUL EL JANNAH

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Page 1: Gastrointestinal Tract Infection

GASTROINTESTINAL TRACT INFECTION

SY. MIFTAHUL EL JANNAH

Page 2: Gastrointestinal Tract Infection

Flora normal

• Enterobacteriaceae, kecuali Salmonella, Shigella, Yersinia, Vibrio dan Campylobacter

• Non dextrose fermenting Gram negative rods• Enterococci• Alpha hemolytic dan non hemolytic Streptococci• Diphtheroids• Sedikit S. aureus• Sedikit Yeast• Banyak anaerob

Page 3: Gastrointestinal Tract Infection

• Saat lahir usus steril, mo masuk bersama makanan, tdd Streptococcus asam

laktat dan Lactobacillus .

• For an infection to occur, the pathogen must be ingested in sufficient numbers or

possess attributes to elude the host defenses of the upper gastrointestinal tract and

reach the intestine

• Perkembangan pola makan merubah flora normal usus

• Asam lambung menjaga jumlah mo seminimal mungkin [103-105/g isi lambung]

• Seiring pH usus menjadi basa flora normal meningkat.

– Duodenum orang dewasa 108-1010 bakteri/g isi usus

– Jejunum dan ileum 105-108 bakteri/g

– Caecum dan kolon transversum 103-105 bakteri/g

– Kolon sigmoid dan rektum 1011 bakteri/g

Page 4: Gastrointestinal Tract Infection

Every day we swallow large numbers of microorganisms. Because of the body's defense mechanisms, however, they rarely succeed in surviving the passage to the intestine in sufficient numbers to cause infection.

Page 5: Gastrointestinal Tract Infection

Peran

• Sintesis vitamin K

• Konversi pigmen – pigmen empedu dan asam

– asam empedu

• Penyerapan zat-zat makanan dan hasil

pemecahannya

• Perlawanan terhadap mo patogen

Page 6: Gastrointestinal Tract Infection

Figure 22.1 As well as many colloquial expressions, several different clinical terms

are used to describe infections of the gastrointestinal tract. Diarrhea without

blood and pus is usually the result of enterotoxin production, whereas the

presence of blood and/or pus cells in the feces indicates an invasive infection with

mucosal destruction.

Page 7: Gastrointestinal Tract Infection

A wide range of microbial

pathogens is capable of

infecting the gastrointestinal

tract, and the important

bacterial and viral pathogens

They are acquired by the

fecal-oral route, from fecally

contaminated food, fluids or

fingers Many different

pathogens cause infections

of the gastrointestinal tract.

Some are found in both

humans and animals while

others are strictly human

parasites.

Page 8: Gastrointestinal Tract Infection

Infections of the

gastrointestinal tract can be

grouped into those that

remain localized in the gut and

those that invade beyond the

gut to cause infection in other

sites in the body. In order to

spread to a new host,

pathogens are excreted in

large numbers in the feces and

must survive in the

environment for long enough

to infect another person

directly or indirectly through

contaminated food or fluids.

Page 9: Gastrointestinal Tract Infection

The damaging effects resulting from infection of the gastrointestinal tract

Page 10: Gastrointestinal Tract Infection

Escherichia coli is a major cause of gastrointestinal infection, particularly in developing countries and in travelers. There is a range of pathogenic mechanisms within the species, resulting in more or less invasive disease. *Specialized tests are given in italics. (LT, heat-labile enterotoxin; ST, heat-stable enterotoxin.)

Page 11: Gastrointestinal Tract Infection

Bacterial causes of diarrhea • Escherichia coli

– This is one of the most versatile of all bacterial pathogens.

– Some strains are important members of the normal gut flora in

man and animals, whereas others possess virulence factors that

enable them to cause infections in the intestinal tract or at

other sites, particularly the urinary tract

– Strains that cause diarrheal disease do so by several distinct

pathogenic mechanisms and differ in their epidemiology

Page 12: Gastrointestinal Tract Infection

There are six distinct groups of E. coli with different pathogenetic mechanisms Initially

all diarrhea-associated Escherichia coli were termed enteropathogenic E. coli (EPEC).

• Enteropathogenic E. coli (EPEC),

• enterotoxigenic E. coli (ETEC),

• enterohemorrhagic E. coli (EHEC) more important in developed

• enteroinvasive E. coli (EIEC),

• enteroaggregative E. coli (EAEC),

• and diffuse-aggregative E. coli (DAEC).

The diarrhea produced by E. coli varies from mild to severe, depending upon the strain

and the underlying health of the host.

EIEC and EHEC strains both cause bloody diarrhea

EPEC and ETEC are the most important contributors to global

incidence of diarrhea

Page 13: Gastrointestinal Tract Infection

Enteropathogenic E. coli (EPEC)

• Do not appear to make any toxins.

• They do produce bundle-forming pili (Bfp), intimin (an

adhesin) and an associated protein (translocated intimin

receptor, Tir). These virulence factors allow bacterial

attachment to epithelial cells of the small intestine, leading

to disruption of the microvillus (an 'attaching-effacing'

mechanism of action) leading to diarrhea.

Page 14: Gastrointestinal Tract Infection

Electron micrograph of enteropathogenic Escherichia coli adhering to the brush border of intestinal mucosal cells with localized destruction of microvilli. (Courtesy of S Knutton.)

Page 15: Gastrointestinal Tract Infection

The clinical features of bacterial diarrhea infection. It is difficult, if not impossible, to determine the likely cause of a diarrheal illness on the basis of clinical features alone, and laboratory investigations are essential to identify the pathogen.

Page 16: Gastrointestinal Tract Infection

Enterotoxigenic E. coli (ETEC)

• possess colonization factors (fimbrial

adhesins.

• ETEC diarrhea in children in developing

countries may be clinically indistinguishable

from cholera

Page 17: Gastrointestinal Tract Infection

• These bind the bacteria to specific receptors on the cell membrane of the

small intestine. These organisms produce powerful plasmid-associated

enterotoxins which are characterized as being either heat labile (LT) or heat

stable (ST):

– Heat-labile enterotoxin LT-I is very similar in structure and mode of action to

cholera toxin produced by V. cholerae, and infections with strains producing LT-I

can mimic cholera, particularly in young and malnourished children.

– Heat-stable enterotoxins (STs) in addition to or instead of LT. STs have a similar

but distinct mode of action to that of LT. STA activates guanylate cyclase activity,

causing an increase in cyclic guanosine monophosphate, which results in

increased fluid secretion. Immunoassays are commercially available for the

identification of ETEC.

Page 18: Gastrointestinal Tract Infection

Electron micrograph of enterotoxin Escherichia coli, showing pili necessary for adherence to mucosal epithelial cells. (Courtesy of S

Knutton.)

Page 19: Gastrointestinal Tract Infection

Enterohemorrhagic E. coli (EHEC)• Isolates produce a verotoxin

• The verotoxin (i.e. toxic to tissue cultures of 'vero'cells) is essentially identical to Shiga (Shigella)

toxin. After attachment to the mucosa of the large intestine (by the 'attaching-effacing'

mechanism also seen in EPEC) the produced toxin has a direct effect on intestinal epithelium,

resulting in diarrhea

• EHEC cause hemorrhagic colitis (HC) and hemolytic-uremic syndrome (HUS). In HC there is

destruction of the mucosa and consequent hemorrhage; this may be followed by HUS. Verotoxin

receptors have been identified on renal epithelium and may account for the kidney involvement.

While there are many serotypes of EHEC, the most common one in the USA is O157:H7.

• HUS is characterized by acute renal failure, anemia and thrombocytopenia, and there may be

neurologic complications HUS is the most common cause of acute renal failure in children in

the UK and USA.

Page 20: Gastrointestinal Tract Infection

Verotoxin-producing Escherichia coli infection, showing fibrin

'thrombi' in glomerular capillaries in hemolytic-uremic syndrome.

(Weigert stain.) (Courtesy of HR Powell.)

Page 21: Gastrointestinal Tract Infection

Enteroinvasive E. coli (EIEC) • Attach specifically to the mucosa of the large intestine

• Utilizing plasmid-associated genes, they invade the cells by endocytosis.

Inside the cell they lyse the endocytic vacuole, multiply and spread to

adjacent cells, causing tissue destruction, inflammation, necrosis and

ulceration, resulting in blood and mucus in stools

Page 22: Gastrointestinal Tract Infection

Enteroaggregative E. coli (EAEC)

• Derive their name from their characteristic attachment pattern to tissue culture

cells .

• The pattern is an aggregative or 'stacked brick' formation. These organisms act in

the small intestine to cause persistent diarrhea especially in children in developing

countries.

• Their aggregative adherence ability is due to plasmid-associated fimbriae.

• EAEC also produce heat-labile toxins (an enterotoxin and a toxin related to E. coli

hemolysin) but their role in diarrheal disease is uncertain.

Page 23: Gastrointestinal Tract Infection

Diffuse-aggregative E. coli (DAEC) • Produce an alpha hemolysin and cytotoxic necrotizing factor 1

• They are also known as diffuse-adherent or cell-detaching E. coli.

• Their role in diarrheal disease, especially in young children, is incompletely

understood and somewhat controversial, with some studies reporting no

association.

Page 24: Gastrointestinal Tract Infection

• Specific tests are needed to identify strains of pathogenic E. coli :

• Because E. coli is a member of the normal gastrointestinal flora, specific tests are required to identify strains that may be responsible for diarrheal disease.

• Infections are more common in children and are also often travel-associated, and these factors should be considered when samples are received in the laboratory.

• It is important to note that specialized tests beyond routine stool cultures are required to identify specific diarrhea-associated E. coli types. Such tests are not ordinarily performed with uncomplicated diarrhea, which is usually self-limiting.

• Antibacterial therapy is not indicated for E. coli diarrhea

• Fluid replacement may be necessary, especially in young children. Treatment of HUS is urgent and may involve dialysis.

• Provision of a clean water supply and adequate systems for sewage disposal are fundamental to the prevention of diarrheal disease.

• Food and unpasteurized milk can be important vehicles of infection, especially for EIEC and EHEC, but there is no evidence of an animal or environmental reservoir.

Page 25: Gastrointestinal Tract Infection
Page 26: Gastrointestinal Tract Infection

Salmonella• Salmonellae common cause of food-associated diarrhea in many developed countries,

in some countries (e.g. the USA and UK) they have been relegated to second place by

Campylobacter.

• The most important of which, for human infection, is Salmonella enterica.

• All salmonellae except for Salmonella typhi and S. paratyphi are found in animals as well

as humans. There is a large animal reservoir of infection, which is transmitted to man via

contaminated food, especially poultry and dairy products.

• Waterborne infection is less frequent.

• Salmonella infection is also transmitted from person to person, and secondary spread can

therefore occur, for example within a family after one member has become infected after

consuming contaminated food

• Salmonellae are almost always acquired orally in food or drink that is contaminated

Page 27: Gastrointestinal Tract Infection

The recycling of salmonellae. With the exception of Salmonella typhi, salmonellae are widely distributed in animals, providing a constant source of infection for man. Excretion of large numbers of salmonellae from infected

individuals and carriers allows the organisms to be 'recycled'

Page 28: Gastrointestinal Tract Infection

MO lolos dari lambung multiplikasi dlm sal. Cerna menembus mukosa usus

di fagosit oleh makrofagkeluar dari SDPmenyebar, multiplikasi

duktus toraksikus aliran darah [bakteriaemia fase pertama/primer] pd hari ke-7 – 10

menginfeksi hepar, kandung empedu, limfe, ginjal dan sumsum tulangmultiplikasi dalam RES

aliran darah [jumlah semakin banyak, bakteriaemia fase kedua/sekunder],

melepaskan endotoksin [demam tinggi & gejala tifoid lainnya]

Bakteri dari kandung empedu

usus halus & jaringan limfoid

perdarahan

perforasi usus

Page 29: Gastrointestinal Tract Infection

The passage of salmonellae through the body. The vast majority of salmonellae cause infection localized to the gastrointestinal tract and do not invade beyond the gut mucosa. (cAMP, cyclic adenosine monophosphate.)

Page 30: Gastrointestinal Tract Infection

• Salmonella diarrhea can be diagnosed by culture on selective media

• The organisms are not fastidious and can usually be isolated within 24 hours, although

small numbers may require enrichment in selenite broth before culture. Preliminary

identification can be made rapidly, but the complete result, including serotype, takes at

least 48 hours

• Fluid and electrolyte replacement may be needed for salmonella diarrhea

• Diarrhea is usually self-limiting and resolves without treatment. Unless there is

evidence of invasion and septicemia, antibiotics should be positively discouraged

because they do not reduce the symptoms or shorten the illness, and may prolong

excretion of salmonellae in the feces

• Salmonellae may be excreted in the feces for several weeks after a salmonella infection

Page 31: Gastrointestinal Tract Infection

Pengendalian• The large animal reservoir makes it impossible to eliminate the organisms, and preventive measures

must therefore be aimed at 'breaking the chain' between animal and man, and from person to person.

• Such measures include: maintaining adequate standards of public health (clean drinking water and

proper sewage disposal);

• Education programs on hygienic food preparation.

• Following an episode of salmonella diarrhea, an individual can continue to carry and excrete organisms

in the feces for several weeks. Although in the absence of symptoms the organisms will not be

dispersed so liberally into the environment, thorough handwashing before food handling is essential.

• People employed as food handlers are excluded from work until three specimens of feces have failed to

grow salmonella.

Page 32: Gastrointestinal Tract Infection

Campylobacter• Campylobacters are among the commonest causes of diarrhea

• Campylobacter spp. are curved or S-shaped Gram-negative rods

• They have long been known to cause diarrheal disease in animals, but are also

one of the most common causes of diarrhea in humans.

• The enterobacteria as they are microaerophilic and thermophilic (growing well

at 42°C); they do not therefore grow on the media used for isolating E. coli and

salmonellae.

• Several species of the genus Campylobacter are associated with human

disease, but Campylobacter jejuni is by far the most common. Helicobacter

pylori, previously classified as Campylobacter pylori, is an important cause of

gastritis and gastric ulcers

Page 33: Gastrointestinal Tract Infection

Campylobacter jejuni infection. Gram stain showing Gram-negative, S-shaped bacilli. (Courtesy of I

Farrell.)

Page 34: Gastrointestinal Tract Infection

• As with salmonellae, there is a large animal reservoir of campylobacter in cattle,

sheep, rodents, poultry and wild birds.

• Infections are acquired by consumption of contaminated food, especially poultry,

milk or water. Household pets such as dogs and cats can become infected and

provide a source for human infection, particularly for young children.

• Person to person spread by the fecal-oral route is rare, as is transmission from food

handlers.

• Campylobacter diarrhea is clinically similar to that caused by other bacteria such as

salmonella and shigella

• Pathology and histologic appearances of ulceration and inflamed bleeding mucosal

surfaces in the jejunum, ileum and colon are compatible with invasion of the bacteria

but the production of cytotoxins by C. jejuni has also been demonstrated. Invasion

and bacteremia are not uncommon, particularly in neonates and debilitated adults.

Page 35: Gastrointestinal Tract Infection

Inflammatory enteritis caused by Campylobacter jejuni, involving the entire mucosa, with flattened atrophic villi, necrotic debris in the crypts and thickening of the basement membrane. (Cresyl-fast violet stain.) (Courtesy of J Newman.)

Page 36: Gastrointestinal Tract Infection

• The clinical presentation is similar to that of diarrhea

caused by salmonellae and shigella, although the disease

may have a longer incubation period and a longer duration.

• Erythromycin is used for severe campylobacter diarrhea.

Erythromycin is the antibiotic of choice for cases of

diarrheal disease that are severe enough to warrant

treatment.

• Invasive infections may require treatment with an

additional antibiotic (e.g. quinolone, aminoglycoside, etc.).

Page 37: Gastrointestinal Tract Infection

Cholera• Cholera is an acute infection of the gastrointestinal tract

• Caused by the comma-shaped Gram-negative bacterium V.

cholerae. V. cholerae is a free-living inhabitant of fresh water, but

causes infection only in humans

• Cholera flourishes in communities with inadequate clean drinking

water and sewage disposal

• The 1990s have witnessed the seventh pandemic of cholera

spreading into Latin America. The disease remains endemic in

southeast Asia and parts of Africa and South America.

Page 38: Gastrointestinal Tract Infection

Scanning electron micrograph of Vibrio cholerae showing comma-shaped rods with a single polar flagellum. ×13000. (Courtesy of DK

Banerjee.)

Page 39: Gastrointestinal Tract Infection

• Asymptomatic human carriers are believed to be a

major reservoir.

• The disease is spread via contaminated food; shellfish

grown in fresh and estuarine waters have also been

implicated. Direct person to person spread is thought

to be uncommon.

• V. cholerae serotypes are based on somatic (O)

antigens Serotype O1 is the most important and is

further divided into two biotypes: classical and El Tor.

Page 40: Gastrointestinal Tract Infection

Vibrio cholerae serotype O1, the cause of cholera, can be subdivided into different biotypes with different epidemiologic features, and into serosubgroups and phage types

for the purposes of investigating outbreaks of infection. Although V. cholerae is the most important pathogen of the genus, other species can also cause infections of both

the gastrointestinal tract and other sites.

Page 41: Gastrointestinal Tract Infection

• The severe watery non-bloody diarrhea is known as rice water stool

because of its appearance and can result in the loss of one liter of

fluid every hour.

• It is this fluid loss and the consequent electrolyte imbalance that

results in marked dehydration, metabolic acidosis (loss of

bicarbonate), hypokalemia (potassium loss) and hypovolemic shock

resulting in cardiac failure.

• Untreated, the mortality from cholera is 40-60%; rapidly instituted

fluid and electrolyte replacement reduces the mortality to less than

1%.

Page 42: Gastrointestinal Tract Infection

sekresi cairan isotonus dari dinding usus.

MO lolos dari barrier asam lambung

usus halus, bermultiplikasi dan membentuk eksotoksin disebut enterotoksin

bereaksi dengan reseptor pada membran sel epitel usus

mengaktifkan adenilat siklase, mengakibatkanMeningkatnya siklik adenosin monofosfat/cAMP

merangsang perubahan ATP menjadi ADP

ADP merangsang pengeluaran air dan elektrolit oleh dinding usus ke dalam rongga usus dan menahan penyerapan Na+ oleh dinding usus

Page 43: Gastrointestinal Tract Infection

The production of an enterotoxin is central to

the pathogenesis of cholera, but the

organisms must possess other virulence factors to allow them to reach the

small intestine and to adhere to the mucosal

cells.

Page 44: Gastrointestinal Tract Infection

Rice water stool in cholera. (Courtesy of AM Geddes.

Page 45: Gastrointestinal Tract Infection

SHIGELLA sp

• Infeksi peroral, terutama melalui makanan jenis sayuran, susu dan protein tinggi

• Dosis infeksi 103 kuman

• Berat ringannya tergantung spesies yang meninfeksi paling berat S. dysentriae, kemudian berturut-turut S. flexneri, S. boydii dan yang paling ringan S. sonnei.

Page 46: Gastrointestinal Tract Infection

MO melewati lambung

usus halus

kolon, ditangkap oleh epitel

multiplikasi, menyebabkan rusaknya sel epitelmenginfeksi jaringan sekitar

reaksi radang

nekrotik, pengelupasan epitel, perdarahan. [tidak pernah terjadi perforasi dan masuk ke organ dalam]

Page 47: Gastrointestinal Tract Infection

Shigella spp

Bentuk sel bakteriKoloni bakteri pada agar SSA

Page 48: Gastrointestinal Tract Infection

Shigellosis. Histology of the colon showing disrupted epithelium covered by pseudomembrane and interstitial infiltration. Mucin glands have discharged their

contents and the goblet cells are empty. (Colloidal iron stain.) (E, epithelium; I, interstitial infiltration; M, mucin in glands; P, pseudomembrane.) (Courtesy of RH

Gilman.)

Page 49: Gastrointestinal Tract Infection

Yersinia enterocolitica • member of the Enterobacteriaceae and is a cause of food-associated infection

especially among infants and particularly in colder parts of the world

• Y. enterocolitica is found in a variety of animal hosts including rodents, rabbits,

pigs, sheep, cattle, horses and domestic pets. Transmission to humans from

household dogs has been reported. The organism survives and multiplies, albeit

more slowly, at refrigeration temperatures (4°C) and has been implicated in

outbreaks of infection associated with contaminated milk as well as other foods.

• The mechanism of pathogenesis is unknown, but the clinical features of the

disease result from invasion of the terminal ileum, necrosis in Peyer's patches and

an associated inflammation of the mesenteric lymph nodes

Page 50: Gastrointestinal Tract Infection

Yersinia enterocolitica infection of the ileum, showing superficial necrosis of the mucosa and

ulceration. (Courtesy of J Newman.)

Page 51: Gastrointestinal Tract Infection

CLOSTRIDIUM PERFRINGENS• Merupakan bakteri Gram positip yang membentuk endospora, anerob

obligat, menghasilkan enterotoksin yang tidak dihasilkan pada makanan

sebelum dikonsumsi, tetapi dihasilkan bila bakteri berkolonisasi di usus.

• Bakteri terdapat di tanah, usus manusia dan hewan, daging mentah,

unggas dan bahan pangan kering.

• Gejala timbul 8-24 jam setelah mengkonsumsi pangan yang tercemar

bentuk vegetatip bakteri dalam jumlah besar, berupa sakit perut, mual

dan diare jarang disertai muntah. Gejala dapat berlanjut selama 1-2

minggu [terutama pada anak-anak dan manula].

• Self limited

Page 52: Gastrointestinal Tract Infection

CLOSTRIDIUM PERFRINGENS

• Jenis makanan yang mudah terkontaminasi: saus

daging yang disimpan pada suhu yang menunjang

perkecambahan spora [30-370C]

• Belum ada pengobatan khusus

• Pencegahan: Tidak menyimpan makanan yang sudah

matang pada suhu kamar untuk jangka waktu yang

lama.

Page 53: Gastrointestinal Tract Infection

Gram stain of Clostridium perfringens.

Downloaded from: StudentConsult (on 20 October 2009 07:04 AM)© 2005 Elsevier

Page 54: Gastrointestinal Tract Infection

GAMBAR 2. Growth of Clostridium perfringens on sheep blood agar. Note the flat, spreading colonies and the hemolytic activity of the organism. A presumptive identification of C. perfringens can be made by detection of a zone of complete hemolysis (caused by the Ѳ;-toxin) and a wider zone of partial hemolysis (caused by the α;-toxin), combined with the

characteristic microscopic morphology.Downloaded from: StudentConsult (on 20 October 2009 07:04 AM)

© 2005 Elsevier

Page 55: Gastrointestinal Tract Infection

Distribution of Lethal Toxins in Clostridium perfringens Types A to E

Type Lethal ToxinsAlpha Beta Epsilon Iota

A + - - -B + + + -C + + - -D + - + -E + - - +

Page 56: Gastrointestinal Tract Infection

Clostridium perfringens is linked with two forms of food-associated infection. The common, enterotoxin-mediated infection (left) is usually acquired by eating meat or poultry that has been cooked enough to kill vegetative cells, but not spores. As the food cools, the spores germinate. If reheating before consumption is inadequate (as it often is in mass catering outlets), large numbers of organisms are ingested. The rare form associated with β-toxin-producing strains (right) causes a severe necrotizing disease.

Page 57: Gastrointestinal Tract Infection

Bacillus cereus

– Bakteri berbentuk batang. Gram positip, aerob,membentuk endospora yang tahan panas dan radiasi

– Keracunan

menelan bakteri atau bentuk sporanya bakteri bereproduksi dan menghasilkan toksin di dalam usus

mengkonsumsi pangan yang telah mengandung toksin

Page 58: Gastrointestinal Tract Infection

Bacillus cereus

Sel B. cereus dengan mikroskop elektron

Koloni di media agar darah

MIFTAHEL-2006

Page 59: Gastrointestinal Tract Infection

Bacillus cereus

Terdapat dua tope toksin: menyebabkan diare dan muntah/emesis

– Toksin penyebab diare, maka

gejala yang timbul berhubungan

dengan saluran bagian bawah,

berupa mual, nyeri perut seperti

kram, diare berair. Terjadi 8-16

jam setelah mengkonsumsi

pangan. Bakteri penghasil toksin

penyebab diare ini umumnya

mencemari sayuran dan daging.

• Toksin penyebab muntah, gejala yang timbul akan lebih bersifat lebih parah dan akut dan berhubungan dengan saluran pencernaan bagian atas berupa mual dan muntah yang dimulai setelah 1-6 jam setelah mengkonsumsi pangan yang tercemar. Bakteri pengahasil toksin ini mudah mencemari pangan yang banyak mengandung pati /nasi yang didinginkan secara lambat dan disimpan pada suhu kamar dan tunas sayuran

Page 60: Gastrointestinal Tract Infection

Bacillus cereus

Pencegahan:

• Pengendalian suhu yang efektif untuk mencegah

pertunasan dan pertumbuhan spora

mengolah makanan dengan pemanasan bertekanan,

menggoreng, tidak menyimpan nasi pada suhu ruang

Page 61: Gastrointestinal Tract Infection

Bacillus cereus can cause two different forms of food-associated infection. Both involve toxins

Page 62: Gastrointestinal Tract Infection

• Rotaviruses

• These are morphologically characteristic viruses with a genome

consisting of 11 separate segments of double-stranded RNA.

Different rotaviruses infect the young of many mammals,

including children, kittens, puppies, calves, foals and piglets, but

it is thought that viruses from one host species occasionally

cross-infect another.

• There are at least two human serotypes. Replicating rotavirus

causes diarrhea by damaging transport mechanisms in the gut

Viral diarrhea

Page 63: Gastrointestinal Tract Infection

Rotavirus. The virus particles (65 nm in diameter) have a well-defined outer margin and capsules radiating from an inner core

to give the particle a wheel-like (hence 'rota') appearance. (Courtesy of JE Banatvala.)

Page 64: Gastrointestinal Tract Infection

• Replicating rotavirus causes diarrhea by damaging transport mechanisms in the

gut. The replicating virus damages transport mechanisms in the gut, and loss of

water, salt and glucose causes diarrhea

• The incubation period is 1 to 2 days. After virus replication in intestinal epithelial

cells there is an acute onset of vomiting, which is sometimes projectile, and

diarrhea which lasts from 4 to 7 days

• Infected cells in the intestine are destroyed, resulting in villous atrophy. The villi,

long finger- like projections, become flattened resulting in the loss of both the

surface area for absorption and the digestive enzymes, and raised osmotic

pressure in the gut lumen causes diarrhea.

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The mechanism of rotavirus diarrhea. Other viruses may have different mechanisms.

Page 66: Gastrointestinal Tract Infection

VIRUS POLIO• Didapat pada susu yang tidak dipasteurisasi

• Menimbulkan penyakit poliomielitis

• Virus masuk bersama susu multiplikasi di tonsil dan

kelenjar orofaring aliran limfe/limfogen menyebar

ke bercak peyer dalam dinding usus SSP serabut

motorik ke sumsum tulang belakang atau otak

• Virus dapat ditemukan dalam tonsil dan tinja

Page 67: Gastrointestinal Tract Infection

Virus polio

Morfologi selStruktur sel

Page 68: Gastrointestinal Tract Infection

VIRUS HEPATITIS A

• Jenis makanan: susu, sayuran , daging dan

kerang-kerangan dalam keadaan kurang

masak

• Sumber kontaminan: air, feses, penjamah

makanan yang carier virus hepatitis A

Page 69: Gastrointestinal Tract Infection

Virus Hepatitis

Bentuk sel

Struktur sel

Page 70: Gastrointestinal Tract Infection

FOOD POISONING • 'food poisoning' is restricted to the diseases caused by

toxins elaborated by contaminating bacteria in food

before it is consumed

• B. cereus

• Staph. aureus enterotoxin Eight different enterotoxins

are produced by different strains of Staph. aureus

• Cl. botulinum toxin

Page 71: Gastrointestinal Tract Infection

Staphylococcus aureus produces at least eight immunogically distinct enterotoxins, the most important of which are listed

here. Strains may produce one or more of the toxins simultaneously. Enterotoxin A is by far the most common in

food-associated disease.