BACTERIA OF

DIGESTIVE INFECTION
DEPARTEMEN MIKROBIOLOGI FK UMSU

DR. RIZKA ARIANI, M.BIOMED

2019
STRUCTURE AND FUNCTION OF
THE DIGESTIVE SYSTEM
• The digestive system is essentially a tubelike structure,
the gastrointestinal (GI) tract or alimentary canal
• the mouth  pharynx (throat)  esophagus  stomach 
the small  large intestines
• accessory structures
• the teeth
• Tongue
• salivary glands
• Liver
• Gallbladder
• pancreas
NORMAL MICROBIOTA
OF THE DIGESTIVE SYSTEM
• Bacteria heavily populate most of the digestive system
• In the mouth, each milliliter of saliva can contain millions of bacteria
• Stomach and small intestine  less microorganism
• large intestine has enormous microbial populations  exceeding 100 billion bacteria
per gram of feces
BACTERIAL DISEASES OF
THE MOUTH
DENTAL CARIES (TOOTH DECAY)

• Teeth are hard and do not shed surface cells  masses of microorganisms and
their products to accumulate (dental plaque) are a type of biofilm  involved in
the formation of dental caries
• The most cariogenic (caries-causing) bacterium is Streptococcus mutans  a gram-
positive coccus that has important virulence characteristics
• The bacterial population of plaque may harbor over 400 bacterial species but is
predominantly streptococci and filamentous members of the genus Actinomyces
PERIODONTAL DISEASE

• Gingivitis
• Periodontitis
• Acute necrotizing ulcerative gingivitis or Vincent’s disease or trench mouth
GINGIVITIS

• infection is restricted to the gums or gingivae

• characterized by bleeding of the gums while the teeth are being brushed
• An assortment of streptococci, actinomycetes, and anaerobic gram-negative
bacteria predominate in these infections
PERIODONTITIS

• Chronic progression of gingivitis

• The gums are inflamed and bleed easily
• Sometimes pus forms in periodontal pockets surrounding the teeth
• The bone and tissue that support the teeth are destroyed  leading loss of the teeth

• Numerous bacteria of many different types, primarily Porphyromonas species

ACUTE NECROTIZING ULCERATIVE GINGIVITIS

• Other name : Vincent’s disease or trench mouth

• The disease causes enough pain to make normal chewing difficult
• Foul breath (halitosis) also accompanies the infection
• The bacteria usually associated with this condition is Prevotella intermedia
• Treatment with oxidizing agents, debridement, and the administration of
metronidazole or antibodies may be temporarily effective
 Foodborne
Disease

Food Food
Poisoning Infection
FOOD POISONING (FP)

• Food intoxication
• Merupakan penyakit yang disebabkan konsumsi makanan yang mengandung
toksin mikroba
• Mikroorganisme yang menghasilkan toksin tidak tumbuh pada sel host maupun
makanan yang terkontaminasi
• Penyebab penyakit  tertelannya toksin
STAPHYLOCOCCAL FOOD POISONING
1. STAPHYLOCOCCAL FOOD POISONING

• Disebabkan oleh : enterotoksin yang dihasilkan oleh bakteri gram positif

Staphylococcus aureus
• S. aureus menghasilkan enterotoksin yang stabil terhadap panas dan asam dari lambung
• Enterotoksin akan melalui lambung  usus halus  menyebabkan gejala klinis
• Enterotoksin staphylococcus  superantigen  berpotensi menyebabkan lethal
toxic shock syndrome
1. STAPHYLOCOCCAL FOOD POISONING

• Makanan yang biasa terkontaminasi adalah :

• Daging olahan
• Custard-filled pastries
• Salad kentang
• Es krim

• Kontaminasi makanan biasanya dikarenakan penyebaran dari karier dengan kolonisasi faringeal
yang asimptomatik  melalui bersin ataupun tangan terkontaminasi
• Makanan terkontaminasi  tidak berubah bentuk/warna dan juga rasa
• Memanaskan makanan hanya mematikan bakteri  tapi tidak menginaktivasi toksin yang stabil
0
terhadap panas (suhu 60 C)
1. STAPHYLOCOCCAL FOOD POISONING

• Onset penyakit cepat  inkubasi selama 4 jam

• Gejala yang timbul :
• Muntah
• Diare  air dan tidak berdarah
• Nyeri abdomen
• Mual
• Nyeri kepala
• Berkeringat
• Demam tidak ada

• Penatalaksanaan :
• Anti diare
• Pain reliever  untuk nyeri abdomen
• Antibiotik tidak diindikasikan  tidak ada efek untuk enterotoksin
1. STAPHYLOCOCCAL FOOD POISONING

• Antibodi  protektif terhadap toksin  self limiting

• Imunitas hanya sementara  bisa terjadi infeksi kedua
• Pencegahan :
• Sanitasi yang baik
• Higienitas dalam produksi, persiapan dan penyimpanan makanan
CLOSTRIDIAL FOOD POISONING
2. CLOSTRIDIAL FOOD POISONING

• Penyebabnya bakteri anaerob pembentuk spora :

• Clostridium perfringens  sel bakteri harus termakan  memproduksi enterotoksin
• Clostridium botulinum  sel bakteri tidak harus termakan namun neurotoksin yang
tertelan menyebabkan penyakit

• Prosedur memasak dan pengemasan makanan kaleng  membunuh sel vegetatif

bakteri tetapi tidak membunuh endospora  endospora akan bergerminasi 
menghasilkan toksin
CLOSTRIDIUM PERFRINGENS FOOD POISONING

• Penyebab ketiga terbanyak di US

• Karakter klinis :
• Inkubasi cepat (8-12 jam)
• Gejala berupa :
• Keram perut
• Diare air
• Tidak ada demam, mual dan muntah
• Gejala hilang dalam 24 jam
8
• Makanan terkontaminasi oleh bakteri dalam jumlah banyak (>10 )  pada makanan tinggi protein (daging sapi, ikan dan unggas)
• C. perfringens bisa tumbuh secara cepat pada suhu ruangan  saat sporulasi dimulai  produksi enterotoksin berlangsung
CLOSTRIDIUM PERFRINGENS FOOD POISONING

• Enterotoksin merusak permeabilitaas epitelium usus halus  diare dan keram perut
• Enterotoksin  heat labile  pemanasan makanan yang cukup dapat merusak
0
toksin (suhu 75 C)
• Makanan yang telah dimasak sebaiknya disimpan di kulkas sesegera mungkin (suhu
yang rendah)  menghambat pertumbuhan dari C. perfringens
BOTULISM FOOD POISONING

• Penyebab keracunan yang berpotensi fatal

• Konsumsi makanan mengandung eksotoksin dari C. botulinum
• Endospora yang viabel pada makanan  bergerminasi  produksi toksin
• Tertelan toksin dalam jumlah sedikit  menyebabkan keracunan yang bahaya  penyakit parah
hingga kematian
• Toksin botulinum  neurotoksin  mengganggu sistem saraf otonom (pernapasan dan detak jantung)
0
• Toksin dapat dihancurkan dengan suhu panas (80 C selama 10 menit) dengan memasak makanan
• Biasanya makanan yang terkontaminasi  makanan dengan pengemasan kaleng yang kurang
baik, terutama makanan nonacidic seperti jagung dan kacang-kacangan
BOTULISM FOOD POISONING

• Pencegahan : atensi dan hati-hati dalam pengalengan dan praktik lain untuk preservasi makanan
• Pada bayi baru lahir hingga usia 2 bulan  karena mikroflora intestinal masih belum baik berkembang
 tidak dapat berkompetisi dengan C. botulinum  terjadi actual infection
• Keracunan jenis ini sangat bahaya  mortalitas tinggi pada pasien tidak diterapi
• Gejala :
• Paralisis lokal (gangguan penglihatan dan bicara)  18-24 jam setelah ingesti
• Terapi :
• Antitoksin botulinum jika terdiagnosis cepat
• Ventilasi mekanik jika ada paralisis pernapasan
• Toksin tidak terlalu tinggi  self limiting
BACILLUS CEREUS FOOD POISONING
B. CEREUS FOOD POISONING

• Gastroenteritis disebabkan bakteri ini dimediasi oleh dua jenis enterotoksin :

• Heat stable  enterotoksin resisten proteolisis  emetic form
• Heat labile  enterotoksin menimbulkan diarrheal form

• Patogenesis enterotoksin heat labile : stimulasi sistem adenylate cyclase–cyclic

adenosine monophosphate pada sel epitel intestinal  menyebabkan diare air
• Mekanisme heat stable  masih belum diketahui
FOOD INFECTION

• Food infection terjadi akibat konsumsi makanan yang mengandung patogen dengan
jumlah banyak
• Patogen tersebut menyebabkan kolonisasi dan tumbuh di dalam tubuh host
 menyebabkan timbulnya penyakit
BACTERIAL PATHOGENS OF
THE DIGESTIVE SYSTEM
CAMPYLOBACTER JEJUNI
CAMPYLOBACTER JEJUNI

• the most common bacterial cause of gastroenteritis in the world

• Guillain-Barré syndrome, a reactive arthritis are complications of infection by C. jejuni
• usually results in a self-limited disease
• characterized by fever, abdominal cramping, and diarrhea
• The incubation period is 2 to 5 days
• Diarrhea is often preceded by a period of fever, malaise , myalgias, and abdominal pain
• Stools may have gross blood and pus present
• The diarrhea usually lasts 2 to 3 days, but abdominal discomfort may persist for several days
after resolution of the diarrhea
• The pathogen can be cultured from stool for several weeks after the illness
CAMPYLOBACTER JEJUNI

• Contaminated poultry is often the source of the infection  the organism is heat-
sensitive, thorough cooking of meat and poultry is effective in preventing human infection
• Other outbreaks have been traced to contaminated meat, water, and unpasteurized milk.

• There is prolonged fecal shedding of the organism but little person-to-

person transmission of the infection
• Macrolide antibiotic is preferred for prolonged disease
SALMONELLA SPECIES
SALMONELLA SPECIES

• Gastroenteritis and Food Poisoning

• Enteric Fever
GASTROENTERITIS AND FOOD POISONING

• Nontyphoidal Salmonella spp. can lead to gastroenteritis through the ingestion of

contaminated meat, poultry, eggs, dairy products, and aquaculture farmed fish and shellfish
• Symptoms usually start between 6 and 48 hours after ingestion of contaminated
foods and consist of nausea, vomiting, and diarrhea
• fever, headaches, and myalgias can be positive
• self-limited and resolves within a few days
ENTERIC FEVER

• Other name : typhoid fever

• commonly spread through fecally contaminated food or water
PATHOGENESIS

pathogen invades the small and large bowel wall

inflammatory response

Bacteria survive in the host immune cells (intracellular pathogens)

spreads throughout the body via the regional lymph nodes and bloodstream

it reaches the gall- bladder and Peyer’s patches in the colon

initiating the diarrheal stage of the illness

ENTERIC FEVER

potential
leading to
chronic colonization of transmission to
persistent shedding
gallbladder and biliary tree others (the classic
of the organism
Typhoid Mary case)
SHIGELLA SPECIES
SHIGELLA SPECIES

• diarrheal illness characterized by gross blood and pus

• There are four Shigella spp. Recognized
• S. sonnei (the most common in the United States)
• S. flexneri
• S. dysenteriae
• S. boydii
• incubation period of the disease can range from 1 to 7 days  most patients
develop symptoms within 12 to 50 hours after exposure
• fever, malaise, fatigue, and anorexia, a watery diarrhea with abdominal cramping then
develop gross blood and pus in the stool
PATHOGENESIS

• Invasion into the intestinal mucosa

• leads to ulceration and a marked inflammatory response
• the organism usually does not invade past the mucosa or disseminate into
the bloodstream
• The bacteria produce several toxins  shiga toxin  have cytotoxic, enterotoxic,
and neurotoxic effects
ESCHERICHIA COLI
ESCHERICHIA COLI

• Enterotoxigenic Escherichia coli (ETEC)

• Enteroinvasive Escherichia coli (EIEC)
• Enterohemorrhagic Escherichia coli (EHEC)

• Enteropathogenic Escherichia coli (EPEC)

• Enteroaggregative Escherichia coli (EAEC)
ENTEROTOXIGENIC ESCHERICHIA COLI (ETEC)

• heat-stable (ST) and heat-labile (LT)

• LT toxin is similar to V. cholerae toxin
• ST toxin binds to guanylate cyclase  increased intracellular cyclic guanosine
monophosphate (cGMP) levels and active efflux of water and electrolytes from the
intestinal cells  a watery diarrhea that lacks red blood cells and fecal leukocytes
• common cause of traveler’s diarrhea
ENTEROINVASIVE ESCHERICHIA COLI (EIEC)

• produce an infection similar to Shigella

• Patients usually develop a watery diarrhea similar to that produced by ETEC
• Some patients then progress to an invasive-type diarrheal syndrome, with
fever, abdominal cramping, and bloody stools
• Fecal leukocytes are abundant
ENTEROHEMORRHAGIC ESCHERICHIA
COLI (EHEC)
• starts as a watery diarrhea
• 1 or 2 days after  abdominal pain increases and stools become bloody
• disease is usually self-limited
• patients can develop hemolytic-uremic syndrome (HUS)  characterized by
hemolytic anemia, low platelet count, and kidney failure
• E. coli strain O157:H7 is among the principal causes of this syndrome
ENTEROPATHOGENIC ESCHERICHIA
COLI (EPEC)
• mechanism of diarrhea is not completely understood
• the organisms express various factors  facilitate their adherence to the intestinal
cells disruption and destruction of the brush border of the cells and other
intestinal cellderangements  reducing the absorptive capacity of the cells 
electrolyte abnormalities and diarrhea
• These organisms commonly affect children in nurseries and daycare centers.
• Patients often have low-grade fever, vomiting, and diarrhea
ENTEROAGGREGATIVE ESCHERICHIA
COLI (EAEC)
• The organism adhere to the intestinal surface but in a more clumped or
aggregative fashion
• organisms apparently first adhere to the intestinal wall via various adhesive molecules
 increase in the production of mucus  induce an inflammatory response by host
cyto-kine release
• These organisms are being increasingly recognized as a cause of traveler’s diarrhea
• Infections with these organisms can range from asymptomatic to a chronic
watery diarrhea.
VIBRIO SPECIES
VIBRIO SPECIES

• gram-negative rods, similar in appearance to Campylobacter

• They are usually found in water environ- ments and can contaminate fish and shellfish

• Species :
• Vibrio cholerae
• Vibrio parahaemolyticus
• Vibrio vulnificus
VIBRIO CHOLERAE

• causative agent of cholera

• organism creates enterotoxin that consists of two subunits : core A subunit surrounded
by five B subunits
• B subunits permit attachment to the small bowel mucosa;
• A subunit then enters the cell  increase in the amount of cyclic adenosine
monophosphate (cAMP  the cell secrete large amounts of water and electrolytes rice
water stools
• Many liters of stool can be produced daily  patients without adequate medical care are
at risk of death from dehydration
• Toxin mediated and non inflamatory stools are free of red and white blood cells
• Serogroups O1 and O139 have been implicated as causes of epidemic cholera
LISTERIOSIS
LISTERIOSIS

• Listeria monocytogenes
• Infeksi gastrointestinal dari makanan  bacteremia dan meningitis
• Makanan bisa terkontaminasi selama produksi maupun proses makanan
0
• Penyimpanan makanan di kulkas dengan suhu 4 C tidak bisa inaktivasi Listeria  psychotolerant
• Sel L. monocytogenes menghasilkan rantai asam lemak bercabang  menjada fungsi membran
sitoplasma pada suhu dingin
• Listeriosis terutama pada pasien immunocompromised
• Terapi :
• Penicillin
• Ampicillin
• Trimethoprim + Sulfa methoxazole
 Imunitas melawan L. monocytogenes : imunitas seluler dimediasi sel Th1

Pada pasien immunocompromised  diambil alih oleh sel fagosit intestinal  membentuk fagosom

Fagosom memicu produksi faktor virulen dari Listeria : listeriolysin O  melisis fagosom dan keluar dari sitoplasma

Bakteri bermultiplikasi dan menghasilkan faktor virulen mayor : ActA  mengiinduksi polimerisasi aktin sel host  aktin
membungkus sel bakteri dan berpindah ke membran sitoplasma

Kompleks tersebut membentuk filopods  kemudian difagosit  beredar di dalam darah

Bentuk filopod membantu L. monocytogenes untuk berpindah dari jaringan host tanpa tereksposure sistem imun :
antibodi, komplemen dan neutrofil
Sel bakteri tersebut keluar dari barrier intestinal dan dibawa
di sirkulasi lymph dan darah ke organ lain, contoh : hati

Kemudian bakteri akan bermultiplikasi sama seperti

di intestinal

Sel bakteri dapat juga menyeran sistem saraf pusat;

dimana bakteri tumbuh di sel neuron

Inflamasi dari meningens  meningitis

Listeriolysin O juga dapat menyebabkan infeksi kronis

pada beberapa jaringan
THANK YOU