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systemic bacteriology, Lecture notes of Microbiology

covers lecture note on systemic bacteriology. includes short notes on each important bacteria which has oral manifestations

Typology: Lecture notes

2022/2023

Available from 09/06/2023

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SYSTEMIC BACTERIOLOGY
Staphylococci
General Characteristics:
Ubiquitous organisms, medically the most important group and cause major
problems in hospitals in compromised patients with debilitating diseases,
extensive surgery, immunosuppression, etc.,
May be part of the normal flora of carriers in the anterior nares, perineum, GIT,
skin, etc.
Physiology and structure:
Gram-positive cocci arranged in grape-like clusters, non-motile, non-sporing,
app Jim diameter.
Colonies are sharply defined, round, and convex, and grow readily on ordinary
media.
Aerobe and facultative anaerobe
On mar conkeys agar very small and pink colonies due to lactose
fermentation
Catalase positive, oxidase negative, ferment glucose and mannitol, producing
add but no gas.
Coagulase (‘clumping factor) positive
Protein A (useful for identification)
Capsule
Species-specific teichoic acid.
Epidemiology
Normal flora on human skin and mucosal surfaces.
Person-to-person spread through direct contact or exposure to contaminated
fomites.
Risk factors include the presence of a foreign body, previous surgical
procedures, and the use of antibiotics that suppress the normal microbial
flora.
Patients at risk for specific diseases include menstruating women (TSS),
infants (scalded skin syndrome), and children with poor oral hygiene
(impetigo) and intravascular catheters (bacteremia).
Clinical manifestations
Local or contiguous infections:
o Skin Folliculitis, boils, carbuncle, impetigo, furuncle
o Eye styes, conjunctivitis
pf3
pf4
pf5
pf8
pf9
pfa
pfd
pfe
pff
pf12
pf13
pf14
pf15
pf16
pf17
pf18
pf19
pf1a
pf1b
pf1c
pf1d
pf1e
pf1f

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SYSTEMIC BACTERIOLOGY

Staphylococci

General Characteristics:

  • Ubiquitous organisms, medically the most important group and cause major problems in hospitals in compromised patients with debilitating diseases, extensive surgery, immunosuppression, etc.,
  • May be part of the normal flora of carriers in the anterior nares, perineum, GIT, skin, etc. Physiology and structure:
  • Gram-positive cocci arranged in grape-like clusters, non-motile, non-sporing, app Jim diameter.
  • Colonies are sharply defined, round, and convex, and grow readily on ordinary media.
  • Aerobe and facultative anaerobe
  • On mar conkeys agar – very small and pink colonies due to lactose fermentation
  • Catalase positive, oxidase negative, ferment glucose and mannitol, producing add but no gas.
  • Coagulase (‘clumping factor) positive
  • Protein A (useful for identification)
  • Capsule
  • Species-specific teichoic acid. Epidemiology
  • Normal flora on human skin and mucosal surfaces.
  • Person-to-person spread through direct contact or exposure to contaminated fomites.
  • Risk factors include the presence of a foreign body, previous surgical procedures, and the use of antibiotics that suppress the normal microbial flora.
  • Patients at risk for specific diseases include menstruating women (TSS), infants (scalded skin syndrome), and children with poor oral hygiene (impetigo) and intravascular catheters (bacteremia). Clinical manifestations
  • Local or contiguous infections: o Skin – Folliculitis, boils, carbuncle, impetigo, furuncle o Eye – styes, conjunctivitis

o Lungs – pneumonia o Wounds – trauma or surgical sites (sp. Absomen) Disseminated infections:

  • Through blood stream – osteomyelitis, polyarthritis, Ac. bacterial endocarditis, empyema, pneumonia, catheter-related bacteremia.
  • Toxin-associated infections – scalded skin syndrome, food poisoning, Toxic shock syndrome.
  • TSS – occurs in females using tampons, characterized by high fever with vomiting and diarrhea, the collapse of peripheral circulation, hypotensive shock, and scarlatiniform rash with desquamation of the skin.
  • Food poisoning, enterocolitis, and nosocomial infestations. Lab diagnosis:
  • Gram-positive, coagulase test & mannitol fermentation confirm the identification of S. aureus,
  • Grow rapidly when cultured on nonselective media. Treatment, Prevention & Control
  • Antibiotics of choice are oxacillin or vancomycin
  • The focus of infection must be identified and drained
  • Proper cleansing of wounds and use of disinfectant help prevent infections
  • Thorough hand washing a covering of exposed skin helps medical personnel prevent infection or spread to others. Streptococci General characteristics
  • Are a large group of bacteria, heterogenous, facultative anaerobes
  • Attach to epithelial surfaces via the lipoteichoic acid portion of fimbriae
  • Are classified into groups by serology Streptococci Morphological features:
  • Gram-positive cocci, arranged in long chains, non-motile, non-sporing, app.pm diameter, capsulated
  • Colonies are small, motile, semitransparent, grey to greyish white on blood agar
  • b-hemolytic, catalase.
  • Negative, P& R-positive; bacitracin-susceptible (important identification tests)
  • Group specific carbohydrate (A antigen) and type-specific antigen (m. protein) in cell wall
  • Produce streptolysin O and DNase B (antibodies against these antigens (ASO, anti-DNase B) are clinically important).
  • Capsulated; types are differentiated by swelling of the capsule in the presence of a specific antiserum (quelling reaction)
  • Aerobes and facultative anaerobes
  • Colonies usually are small, circular, raised, and smooth on blood agar; on prolonged intubation, autolysis occurs, and the center of the colony sinks (draughtsman appearance) due to the presence of an autolytic enzyme (amidase)
  • Catalase and oxidase negative
  • Large polysaccharide capsule
  • Teichoic acid is rich in choline that reacts with a serum protein (referred to as the C-reactive protein) this is a useful diagnostic test for systemic disease.
  • Bacteria are inhibited by optochin. Epidemiology
  • Most infections are caused by endogenous spread from the colonized nasopharynx or oropharynx.
  • Colonization is highest in young children.
  • Person-to-person spread through infectious droplets is rare.
  • Individuals with antecedent viral respiratory tract disease or other conditions that interfere with bacterial clearance from, the respiratory tract are at increased risk (or pulmonary disease.
  • Children and the elderly are at risk for meningitis.
  • People with hematologic disorders are at risk for fulminant sepsis. Clinical manifestations
  • Pneumonia – Lobar and Bronchopneumonia (one of the most common causes of community-acquired disease)
  • Meningitis (The most common cause of bacterial meningitis in most age groups)
  • Otitis media and septicemia Lab diagnosis: Confirmed by biochemical tests performed on a pure culture
  • Isolation of Pneumococci
  • Fermentation of insulin
  • Quellung reaction – Microscopy
  • Bile solubility test. Treatment, Prevention & Control
  • Penicillin is the drug of choice for susceptible strains.
  • Cephalosporins, erythromycin, chloramphenicol, or vancomycin are used for patients allergic to penicillin or for treatment of penicillin-resistant strains.
  • Immunization with 23-valent vaccines can prevent infection.

Neisseria Gonorrhoeae

General characteristics

  • Is epidemic, with die highest incidence in sexually active age groups (15 – 25)
  • Is pyogenic Morphological Features
  • Gram-negative cocci (app 2Jim), occur characteristically in pairs (diplococci) with adjacent sides concave (bean shape)
  • Usually are intracellular
  • Capsulated, non-motile, strict aerobes, piliated
  • Colonies are small, round, convex, grey, and translucent on solid media; blood and chocolate agar are commonly used.
  • Thayer – Martin and Nezo York City media are selective media
  • Catalase and oxidase positive Epidemiology:
  • Humans are the only natural hosts
  • Asymptomatic carriage is the major reservoir
  • Transmission primarily by sexual contact
  • The disease is most common in blacks, people aged 15-24 years, (southeastern states), and people who have multiple sexual partners.
  • Higher risk of disseminated disease in patients with deficiencies in components of complement. Clinical manifestations
  • Urethritis; if complicated epididymitis, prostatitis (in males) and PID (in females) sterility.
  • Rectal infections
  • Bacteremia, arthritis
  • Pharyngitis
  • Disseminated infection.
  • Infant eye infection (ophthalmia neonatal) Lab diagnosis:
  • Gram stain of urethral specimens.
  • Culture is sensitive and specific but has been replaced with molecular probe techniques in many laboratories.

Clinical manifestations: Meningitis

  • Begins as mild pharyngitis
  • In the susceptible age group, disseminate to most tissues, resulting in fulminant meningococcemia with meningitis features.
  • Petechial eruptions with vasculitic purpura are the hall.
  • Water house – fridrichsen syndrome is a fulminating disease with hemorrhage, circulatory failure, and adrenal insufficiency.
  • Meningoencephalitis
  • Bacteremia, pneumonia, arthritis, urethritis. Lab diagnosis
  • Gram-negative diplococcus, identify by Gram stain of CSF and skin lesions.
  • Culture – Inoculate in nutrient broth or Thayer – martin chocolate agar & incubate in a candle jar Treatment, Prevention & Control
  • Breast-feeding infants have passive immunity (first 6 months).
  • Treatment is with penicillin (drug of choice), chloramphenicol, ceftriaxone, and cefotaxime.
  • Chemoprophylaxis for contacts is with rifampin or sulfadiazine (if the isolated organism is susceptible).
  • For immunoprophylaxis, vaccination is an adjunct to chemoprophylaxis; it is used only for serogroups A.
  • C, Y, and W135; no effective vaccine is available for serogroup B.

Corynebacterium

General Features

  • Causes disease primarily by elaboration of potent exotoxins.
  • The organism does not need to enter the bloodstream to produce systemic signs of disease.
  • Is a classic example of lysogenic conversion.
  • The tox gene that codes for die exotoxin is introduced into strains of C.
  • diphtheria by a lysogenic bacteriophage (fi-phage).
  • Is a component of the DTP vaccine.
  • Causes disease primarily in infants. Cellular morphology
  • Slender gram-positive rods that display pleomorphism
  • Some strains have club-shaped ends and some have intracellular polyphosphate granules known as metachromatic granules
  • Frequently remains attached after division, which gives them a Chinese letter pattern
  • Colonies – on serum broth – turbid and pellicle formation
  • Loejfler’s serum slope – very rapid growth; small, circular, white or creamy, and glistening
  • Tellurite blood agar – gray or black colonies
  • Facultative anaerobe. Toxin:
  • Complications and mortality rates are due to the systemic effects of exotoxin.
  • This 53,000 – Da protein is an example of the classic A-B exotoxin.
  • Production of exotoxin is the result of the tox + gene carried by a bacteriophage (/page)
  • Is a protein consisting of Fr – A – inhibits protein synthesis by binding to and inactivating elongation factors two Fr – B – responsible for toxin attachment to tissues and for transport of Fr – A into the cell. Primary effects of the toxin
  • Inhibits protein synthesis in the cardiac muscle causing structural and functional damage
  • Demyelination – can affect both peripheral and cranial nerves
  • Toxin synthesis is regulated by a chromosomally encoded element, diphtheria toxin repressor (DTxR) **Clinical manifestations
  1. Pharyngeal diphtheria:**
  • Acquired via the respiratory route; pharyngitis and tonsillitis are common pseudomembrane forms as the infection progresses composed of lymphocytes, plasma cells, cellular debris, fibrin, and bacteria greyish white and firmly adherent.
  • Cervical lymphadenitis – bull neck appearance
  • Complications associated with tissue damage principally at
  • Heart cardiac dysfunction, myocarditis, and circulatory collapse
  • Nervous system – motor defects result from demyelination; paralysis of throat muscles and polyneuritis 2. Cutaneous diphtheria
  • May present as a simple pustule or chronic non-healing necrotic ulcer.

o Morphology o Gram-negative bacilli, non-spore-forming, encapsulated, facultative anaerobes that ferment glucose. o Colonies – typical colonies are circular, convex, and glistening of mucoid. o The loss of capsules produces rough colonies that are flat, irregular, and granular. o Surface components & antigens of Enterobacteriaceae Flagella:

  • Composed of contractile fibrous proteins (flagellins)
  • Constitute tire H angitens (H = Hauch) (German) = Breath)
  • Preserved by formalin, destroyed by heat
  • Maximal in young cultures Fimbriae (pili):
  • Hair-like projections of protein on cell surface, promote adhesion
  • Develop in old (24 – 48 hr) broth cultures
  • Destroyed by heat, preserved by formalin
  • Six types are described, according to their ability to agglutinate red cells.
  • May interfere with H agglutination Capsule:
  • A thin layer of surface polysaccharide constitutes the K antigen (K = Kapseal (German) – capsule)
  • The formation is enhanced by sugar-containing media
  • Very prominent in klebsiella, in which as a loosely adherent slime layer, it creates mucoid colonies
  • May interfere with agglutination
  • Inhibits phagocytosis
  • May cross-react with capsular antigens of other bacteria Cell wall consists of two layers: 1. Outer layer: a complex of Lipopolysaccharide (LPS), protein, and lipids, which render Gram-negative cells less permeable to solutes
  • The side chains of repeating sugar units project from the outer LPS layer constituting the O antigen (O = Ohne (German) = without).
  • Associated with smooth colonies, resistance to killing by complement.
  • The absence of side chains is associated with rough colonies, auto- agglutination, nonvirulence, and killing by complement.
  • Core glycolipids form the basal layer to which side chains are attached (the enterobacterial common antigen)
  • Lipid A forms a layer between the lipopolysaccharide and a Phospholipid membrane.
  • Is the toxic moiety of ‘endotoxin”
  • Phospholipid membrane is similar in structure to the tire cell membrane (and therefore termed the ‘outer membrane’)
  • Proteins (outer membrane proteins, OMPs) are present in tire phospholipid membrane.
  • They include those responsible for solute transport (porins) and c-structural lipoproteins.
  • The inner layer of the cell wall consists of peptidoglycan maintaining cell rigidity. Exotoxins:
  • Enterotoxins: Produced by some strains of Esch. Colt & probably other Enterobacteriaceae.
  • Cytotoxins: Sh. dysenteriae and some strains of Esch. Coli. E.Coli
  • Physiology and structure
  • Gram - negative bacilli
  • facultative anaerobe
  • Fermenter
  • oxidase negative.
  • Oxidase negative.
  • The outer membrane makes tiny organisms susceptible to drying.
  • Lipo polysaccharide consists of outer somatic polysaccharide, core polysaccharide (common antigen), and lipid A (endotoxin).
  • Virulence factors
  • Capsule – suppresses phagocytosis
  • Endotoxin (LPS) – heat stable, composed of three components – Lipid A, the core polysaccharide, and the somatic O antigen, Lipid A moiety is responsible for most of the symptomatology.
  • Endotoxic shock – is initiated by endotoxin and consists of fever, leucopenia, hypoglycemia, hypotension and shock, DIC, and death from massive organ dysfunction.
  • Exotoxins – Heat – stable STa & STb, Hemolysin, Heat labile toxin LJ-1 & LJ- 1
  • Adhesion colonization factors – involved in surface interactions of bacteria and conjugation
  • Antimicrobial resistance – is fed on transferable plasmids.
  • Invasive capacity, Epidemiology
  • Most common aerobic, Gram-negative bacilli in the gastrointestinal tract.
  • Most infections are endogenous (patient’s normal microbial flora).

Diagnosis

  • Organisms grow rapidly in most culture media.
  • Treatment, Prevention, and Control
  • Infections are controlled by the use of appropriate infection-control practices to reduce the risk of nosocomial infections.
  • Maintenance of high hygienic standards to reduce the risk of exposure to gastroenteritis strains.
  • Proper cooking of beef products to reduce the risk of EHEC infections.
  • Gastroenteritis is caused by different strains of Esch. Coli
  • septicemia and pyogenic - may cause wound infection, peritonitis, biliary tract infections, and neonatal meningitis

Salmonella

General characteristics

  • Most human disease results from salmonella typhi, salmonella enteritidis, salmonella typhimurium, salmonella paratyphi A, salmonella schottmiilleri, or salmonella choleraesuis.
  • Do not ferment lactose, but many species are Identified by the production of add, gas, and hydrogen sulfide from glucose Physiology and Structure:
  • Gram-negative bacilli,
  • Facultative anaerobe,
  • Oxidase-negative.
  • Lipo-polysaccharide consists of outer somatic polysaccharide, core polysaccharide (common antigen), and lipid A (endotoxin). Attributes of pathogenicity (virulence factors)
  • Possess an endotoxin causing diverse toxic manifestations, including fever, leukopenia, hemorrhage, hypotension, shock, and DIC.
  • May possess an exotoxin (enterotoxin)
  • Are aided by the anti-phagocytic activity of the capsule.
  • Can survive within macrophages by unknown means. Epidemiology
  1. Most infections are acquired by eating contaminated food products (poultry, eggs, and dairy products are the most common sources of infection).
  2. Direct fecal-oral spread in children.
  1. S, typhi, and S. paratyphi are strictly human pathogens (no alternative reservoir); these infections are passed from person to person; asymptomatic long-term colonization occurs commonly.
  2. Individuals at risk for infection include those who eat improperly cooked poultry or eggs, patients with reduced gastric add levels, and immuno- compromised patients.
  3. Infections occur worldwide, particularly in the warm months of the year. Clinical Diseases:
  • Enterocolitis: (Gastroenteritis or food poisoning)
  • Is currently the most common form of salmonella infection in the united states (approximately two million cases per year).
  • Occurs in multiple sources of contamination, including food, most commonly poultry and poultry products, human carries (particularly food handlers), exotic pets (turtles and snakes).
  • Is commonly caused by S.typhimurium and S.enteritidis, which usually require a high infecting dose with an 8- 48 hours incubation period.
  • Is a self-limiting illness manifested by fever, nausea, vomiting and diarrhea.
  • May have an increased carrier rate with antibiotic therapy.
  • Is usually characterised by the following pattern.
  • Ingestion of organisms in contaminated food.
  • Colonization of the ileum and cecum.
  • Penetration of epithelial cells in the mucosa and invasion, resulting in acute inflammation and ulceration.
  • Release of prostaglandin by enterotoxins, resulting in activation of adenyl cyclase and increased cyclic AMP.
  • Increased fluid secretion in the intestines. Septicemic (extraintestinal) disease:
  • Is an acute illness most often of nosocomial origin, with abrupt onset and early invasion of the bloodstream.
  • Is characterized by a precipitating incident that introduces bacteria (e.g., catheterization, contaminated IV fluids, abdominal or pelvic surgery), followed by a triad of chills, fever, and hypotension.
  • May cause local abscess, osteomyelitis, and endocarditis if the organisms are disseminated widely.
  • May be caused by many Salmonella species as well as other Enterobacteriaceae organisms.
  • Has a high mortality rate (30-50%), depending on the degree of preexisting debilitation. Enteric fevers:
  • Are produced mainly by S. typhi (typhoid fever) and a lesser degree by S. paratyphi and S.schottmulleri, all of which are strictly human pathogens.

General characteristics:

  • Is a gram-negative, facultatively anaerobic, non-motile rod.
  • All Shigella species are pathogenic in small numbers for humans.
  • Have no known animal reservoir and are not found in soil or water unless contaminated with human fecal material.
  • Perpetuation of Shigella-induced disease is due largely to unrecognized clinical cases and convalescent and healthy carriers, less than 1% of whom are under the care of a physician.
  • The disease spreads through poor sanitation and is readily transmitted from person to person via food, fingers, feces, and flies.
  • All Shigella species ferment glucose with acid, but rarely with gas; only Shigella sonnei ferments lactose. Classification:
  • Is classified into four groups based on differences in somatic (O) antigens:
  • Group A: Shigella dysenteriae (rarely found in the united states, unless imported).
  • Group B: Shigella flexneri (common in the united states)
  • Group C: Shigella boydii (rarely found in the united states)
  • Group D: Shigella sonnei (the most common cause of shigellosis in the united states) Virulence attributes:
  • All Shigellae contain an endotoxic LPS.
  • destruction and ulceration.
  • Endotoxin and genes for adherence, invasion, and intracellular replication.
  • Permeability barrier of the outer membrane.
  • Organisms possess the capacity to multiply intracellularly, resulting in focal.
  • Exotoxin (Shiga toxin) is produced by S. dysenteriae; disrupts protein synthesis and produces endothelial damage.
  • Hemolytic colitis (HC) and hemolytic uremic syndrome (HUS) associated with Shigella, Epidemiology:
  • Humans are the only reservoir for these bacteria.
  • Disease spread person-to-person by fecal-oral route.
  • Patients at the highest risk for the disease are young children in daycare centers, nurseries, and custodial institutions; siblings and parents of these children; male homosexuals.
  • Relatively few organisms can produce disease (highly infectious).
  • Disease is worldwide with no seasonal incidence. Clinical disease:
  • Shigellosis (bacillary dysentery) is characterized by acute inflammation of the wall of the large intestine and terminal ilium; bloodstream invasion is rare.
  • Complications include necrosis of the mucous membrane, ulceration, and bleeding.
  • The disease is characterized by a sudden onset after a short incubation period (1-4 days), with abdominal pain, cramps, diarrhea, and fever.
  • Stools are liquid and scanty; after the first few bowel movements, they contain mucus, pus, and occasionally blood. Laboratory diagnosis:
  • Is made from stool culture of the organism into differential and selective media.
  • Cannot be made by using serology and blood culture.
  • Treatment, Prevention and Control.
  • Antibiotic therapy shortens the course of symptomatic disease and fecal shedding.
  • Empiric therapy can be initiated with fluoroquinolone or trimethoprim; or sulfamethoxazole.
  • Appropriate infection control measures should be instituted to prevent the spread of the organism, including hand washing and proper disposal of soiled linens.
  • Only Sdycnteriae infections require antibiotic therapy; however resistance to antibiotics has been developing,
  • Fluid replacement is the most important therapy.
  • Vaccines are under development,
  • Epidemiologic control by isolation of carriers, disinfection of excreta, and proper sewage disposal can be effective. General characteristics
  • Cholera is one of the most devastating diseases; the pandemic last for years; Prototype of enterotoxin-induced diarrhea.
  • A large and rather poorly characterized group of Gram-negative rods, mainly environmental, especially in marine and brackish waters.
  • Tolerate high salt concentrations (i.e. halophilic).
  • Curved rods, single polar flagellum. Oxidase positive, catalase positive. Fermentative
  • Species of medical interest
  • Vibrio cholera: Includes 72 serotypes, one of which (01) causes epidemic cholera
  • Vibrio parahaemolyticus: Causes gastroenteritis (from seafood)
  • Vibrio alginolyticus: Occasionally causes wound infection following wounds sustained in seawater
  • Vibrio: Occasionally causes septicemia after eating raw oysters
  • A potent enterotoxin is released and binds to ganglioside receptors on the mucosal cells.
  • After a lag period of 15-45 minutes, adenyl cyclase is activated and the camp concentration inside the intestinal cells increases.
  • Increased intracellular cAMP results in the excretion of electrolytes such as chloride and bicarbonate ions along with massive quantities of water. Symptomatology:
  • The major symptom of cholera is diarrhea.
  • The feces contain epithelial cells, mucus, and large numbers of V.cholerae.
  • The presentation can range from mild disease to severe life-threatening disease.
  • The disease is characterized by profuse watery diarrhea (rice water stools).
  • In severe cases, as much as one liter of fluid may be lost each hour.
  • The patient usually feels bloated and may have abdominal pain before the onset of diarrhea.
  • Death is caused by electrolyte abnormalities and massive fluid loss. Laboratory diagnosis:
  • V.Cholerae may be viewed directly in stool samples, particularly in dark-field microscopy.
  • Fluorescently labeled antibodies can be used in identifying the observed cells as V.cholerae.
  • Selective media for culture are based on the ability of vibrios to grow at an alkaline pH, and identification can be made by biochemical tests.
  • Treatment, Prevention, and Control
  • Intravenous administration of fluids and electrolytes is critical for recovery.
  • Oral administration of a solution containing glucose and electrolytes has been successful, but the patient must be capable of consuming the liquid by mouth.
  • Severely ill patients generally are too weak to ingest fluids.
  • Antibiotic therapy does not affect the disease once, the enterotoxin attaches to the intestinal cells, but can prevent later attacks by reducing the number of toxin-producing V.cholerae in the intestines,
  • Doxycycline (adults), trimethoprim-sulfamethoxazole (children), or furazolidone (pregnant women) is administered.
  • Improved hygiene is critical for control.
  • Immunization: with toxoids, live cells or attenuated cells provide only limited protection for approximately six months.
  • Vibrio parahaemolyticus is a marine vibrio that requires a relatively high salt concentration for growth. Epidemiology:
  • V.parahaemolyticus is distributed worldwide in marine environments and now is recognized as a common etiologic agent of acute enteritis associated with the consumption of improperly cooked seafood.
  • The bacterium accounts for about half of all of the above cases of food poisoning in Japan.
  • The best control measure is the consumption of only cooked seafood. Pathogenicity:
  • The enterotoxin of V. V.parahaemolyticus has not been characterized completely.
  • All strains, isolated from cases of gastroenteritis are capable of producing a heat-stable hemolysin that lyses human and rabbit erythrocytes.
  • The hemolysis has been designated kanawaga hemolysis, the enterotoxigenic strains are referred to as Kanawaga-positive V.parahaemolyticus. General characteristics
  • Pseudomonas Aeruginosa
  • Is a small, polarly flagellated, gram-negative rod with pilL
  • Is an aerobe and, unlike enterobacteria, is oxidase positive.
  • Nonfermenter.
  • Simple nutritional requirements.
  • Mucoid exopolysaccharide capsule
  • Is a small, polarly flagellated, gram-negative rod with pilL
  • Is an aerobe and, unlike enterobacteria, is oxidase positive.
  • Nonfermenter.
  • Simple nutritional requirements.
  • Mucoid exopolysaccharide capsule

Morphology

  • Slender, gram-negative bacillus, non-capsulated, non-sporing.
  • Colonies are smooth, large, translucent, and convex with a sweetish aromatic odor and a blue-green-pigmented surrounding colony.
  • Cytotoxin (leukocidin) – cytotoxic for eukaryotic membranes, (disrupts leukocyte function). Invasive factors include:
  • Pili, which attach to the damaged basement membrane of cells.
  • Phospholipase – Heat-labile hemolysin; mediates tissue damage
  • Collagenase and elastase – the destruction of elastin-containing tissues (blood vessels, lung tissue, skin) – collagen and complement factors.
  • Flagella, to promote motility.