Specific bacterias Flashcards
Streptococcus pyogenes
The name is derived from the Greek meaning pus(pyo)-forming(genes) chain(Strepto) of berries (coccus), because streptococcal cells tend to link together in chains of round cells (see image) and a number of infections caused by the bacteria, produce pus.
- Beta hemolytic
- Capsulated (hyaluronic acid - Important!)
- Group A Strep
- Gram positive
- Catalase negative
- Coagulase negative
- “M” protein in cell wall - Our own cells have similar molecules. When antibodies are formed, they can react with our own cells -> autoimmunity
- F-protein (fibronectin binding)
Exoenzymes:
1: hyaluronidase (,,spreading factor”)
2: DNase
3: streptokinase (cleaves plasminogen to plasmin promoting fibronolysis
Cause:
- Pharyngitis (“strep throat)
- Cellulitis
- Erysipelas
- Impetigo (localized skin infection)
- Poststreptococcal diseases: Rheumatic fever, Acute glomerulonephritis (GN) and Erythema nodosum
+ Strep. pyogenic exotoxins (SPE) can cause this 3 diseases:
1: Scarlet fever (“Strawbary tongue”, pharyngitis and diffuse rash in the face) - erythrogenic toxin -> erythrogen toxin, which can destroy the endothel cell of capillaries – red rash
2: Toxic shock-like syndrome
3: Necrotizing fascitis (life-threatening condition requiring surgery)
S. pyogenes can be cultured on blood agar plates. Under
ideal conditions, it has an incubation period of 1 to 3 days
Ignaz Semmelweis demonstrated that childbed fever (puerperal fever), caused by streptococcal infections, was transmitted to patients by doctor’s hands
Use Penicillin or macrolid (if the patient has penicillin allergy)
It is an infrequent, but usually pathogenic, part of the skin flora. It is the predominant species harboring the Lancefield group A antigen, and is often called group A streptococcus (GAS).
Erysipelas “red skin” aka “ignis sacer”, “holy fire”, and “St. Anthony’s fire” in some countries) is an acute infection typically with a skin rash, usually on any of the legs and toes, face, arms, and fingers. It is an infection of the upper dermis and superficial lymphatics, usually caused by beta-hemolytic group A Streptococcus bacteria on scratches or otherwise infected areas. Erysipelas is more superficial than cellulitis, and is typically more raised and demarcated.
Staphylococcus aureus
Mostly found in nose, nasopharynx in 5-10 % of the population
- Golden apperance on agar plate
- Gram positive (violet/blue)
- Facultative aerobe
- Catalase and coagulase positive
- Found in the nose, respiratory tract, and on the skin
- Beta hemolytic
- Mannitol fermentation: Agar plate turn yellow
- Protein A (!): Can bind to Fc region of antibodies and inhibit opsonization
- Selective cultivation method: 7.5% NaCl
- Adhesive proteins (collagene-, laminin-binding protein)
- Fibrinolysin -> lysis of fibrin
- DNase, hyalurinidase, phosphatase, lipase -> Invasivity in different tissues
- Toxic Shock Syndrome Toxin (TSST-1) septic stat , high fever, multi organ failer
- Leukocidin lysis of leukocytes
Can cause:
- Pneumoniae (most common cause of secondary bacterial pneumonia after viral infections!)
- Joint pain: Septic arthritis
- Abcesses
- Impetigo
- Acute bacterial endocarditis
- Endocarditis in IV-drug users (affect tricuspid valve in particular)
- Osteomyelitis
- Toxic shock syndrome (superantigen)
- Staph food poisoning (e.g. meats and dairy): Vomiting, diarrhea. Incubation period lasts one to six hours, with the illness itself lasting anywhere from thirty minutes to three days. Staphylococcus enterotoxin (SE) leads to diarrhoeae and vomiting, toxico-infection
- Scalded skin syndrome (epidermolytic exotoxins (exfoliatin) A and B, and cause detachment within the epidermal layer, by breaking down the desmosomes). Exfoliative toxin. These exotoxins are proteases that cleave desmoglein-1, which normally holds the granulosum and spinosum layers together.
Methicillin-resistant Staphylococcus aureus - MRSA (!): Penicillin binding proteins 2A (PBP2A). Resistant to penicillin.
Use: β-lactam antibiotics with β-lactamase Inhibitors
eg.: amoxicillin + clavulanic acid ( or Vancomycin antibiotics in MRSA??”
Diagnostic steps:
- Sample should be taken: pus, wound secretion etc.
- Cultavation on blood agar typical colony morphology is seen (beta- hemolysis and golden pigmented colonies
- Catalase and Couagulase test on isolated colonies
- Antibiotic susceptibility testing - disk diffusion method
Extra:
“S. aureus produces various enzymes such as coagulase (bound and free coagulases) which clots plasma and coats the bacterial cell, probably to prevent phagocytosis. Hyaluronidase (also known as spreading factor) breaks down hyaluronic acid and helps in spreading it. S. aureus also produces deoxyribonuclease, which breaks down the DNA, lipase to digest lipids, staphylokinase to dissolve fibrin and aid in spread, and beta-lactamase for drug resistance.”
Two types of coagulase: Exocoagulase (free coagulase - detecting: coagulase tube test) and
Endocoagulase (bound coagulase on the bacterial surface - detecting: slide agglutination, latex-agglutination)
Staphylococcus epidermidis
“Enemy of orthopedics” - Infect artificial objects (e.g. joins and heart valves. Also in catheters (!)
- Part of normal flora
- Gram positive
- Produce white pigment without hemolysis
- Produce biofilm (extracellular material known as polysaccharide intercellular adhesin (PIA))
- Catalase and urease positive
- Coagulase negative
- Novobiocin sensitive (!) - important test to distinguish it from Staphylococcus saprophyticus, which is coagulase-negative, as well, but novobiocin-resistant.
- Facultative anaerobe
It is part of the normal human flora, typically the skin flora, and less commonly the mucosal flora. Although S. epidermidis is not usually pathogenic, patients with compromised immune systems are at risk of developing infection. These infections are generally hospital-acquired. S. epidermidis is a particular concern for people with catheters or other surgical implants because it is known to form biofilms that grow on these devices. Being part of the normal skin flora, S. epidermidis is a frequent contaminant of specimens sent to the diagnostic laboratory.
Antibiotics are largely ineffective in clearing biofilms. The most common treatment for these infections is to remove or replace the infected implant, though in all cases, prevention is ideal. The drug of choice is often VANCOMYCIN, to which rifampin or aminoglycoside can be added
Staphylococcus saprophyticus
- Novobiocin resistant
- Gram positive
- Catalase and urease positive
- Coagulase negative
- No hemolysis on blood ager
- White pigment?
Common cause of community-acquired urinary tract infections in sexually active females. In females 17–27 years old, it is the second-most common cause of community-acquired UTIs, after Escherichia coli. Sexual activity increases the risk of S. saprophyticus UTIs because bacteria are displaced from the normal flora of the vagina and perineum into the urethra (cystitist („honeymoon cystitis”))
S. saprophyticus can bind to the uroepithel and by the urease activity NH3 will irritate the mucosalayer
Enterococcus
Large genus of lactic acid bacteria
- Gram-positive
- Often occur in pairs (diplococci)
- Facultative anaerobic
- Can tolerate NaCl medium up to 6.5%
- No hemolysis
Two main types in the intestine of humans: E. faecalis (90–95% - Group D strep) and E. faecium (5–10%).
E. faecium
- bile resistant
- very resistant to vancomycin (VRE) - Have to use Linezolid and tigecycline
Can cause:
- Urinary tract infections
- Endocarditis
- Biliary tree infections
- Intestinal trauma /perforation -> sepsis, peritonitis
Use (lecture): cephalosporin and sulfonamid!
Th.: synergistic combination: ampicillin + gentamycin
Th: vancomycin increased level of resistance to glycopeptid : VRE: vancomycin resistant Enterococci
From a medical standpoint, an important feature of this genus is the high level of intrinsic antibiotic resistance. Some enterococci are intrinsically resistant to β-lactam-based antibiotics (penicillins, cephalosporins, carbapenems), as well as many aminoglycosides. In the last two decades, particularly virulent strains of Enterococcus that are resistant to vancomycin (vancomycin-resistant Enterococcus, or VRE) have emerged in nosocomial infections of hospitalized patients, especially in the US.
Streptococcus pneumoniae
S. pneumoniae is part of the normal upper respiratory tract flora, but, as with many natural flora, it can become pathogenic under the right conditions, like if the immune system of the host is suppressed
- Gram positive
- Alpha hemolytic
- Facultative anaerobic
- Capsulated (polysaccaride)
- IgA protease
- Bile soluble
- Lancet-shaped diplococci
Can cause
- “MOPS”
- Pnemonia: “Rust colored” sputum
- Otis Media
- Sinusitis
- Meningitis (!!! #1)
- Ulcus serpens corneae (eye infection)
Use: First choice are beta-lactams although penicillin resistance appeared by decreased affinity of PBP binding
Therapy: macrolid, fluoroquinolones. Sketchy: Macrolides or Ceftriaxone
S. pneumoniae can be differentiated from the viridans streptococci, some of which are also alpha-hemolytic, using an optochin test, as S. pneumoniae is optochin-sensitive. S. pneumoniae can also be distinguished based on its sensitivity to lysis by bile, the so-called “bile solubility test”. The encapsulated, Gram-positive coccoid bacteria have a distinctive morphology on Gram stain, lancet-shaped diplococci. They have a polysaccharide capsule that acts as a virulence factor for the organism
Viridans streptococci
“viridae” – Latin term for green
The organisms are most abundant in the mouth, and one member of the group, S. mutans, is the etiologic agent of dental caries in most cases and populations. S. sanguinis is also another potential cause. Others may be involved in other mouth or gingival infections as pericoronitis.
- Alpha hemolytic
- No capsule
- Optochin resistant (differentiate from Strep. pneumoniae)
- Bile resistant
- In general, pathogenicity is low.
- Can adhere to platelets (via dextrans)
Viridans streptococci have the unique ability to synthesize dextrans from glucose, which allows them to adhere to fibrin-platelet aggregates at damaged heart valves. This mechanism underlies their ability to cause subacute valvular heart disease following their introduction into the bloodstream (e.g., following dental extraction).
Bacillus anthracis
Bacillus anthracis is the etiologic agent of anthrax
- Gram positive
- Spore forming
- Capsule (poly-D-gamma-glutamic acid - a protein!!)
- Obligate aerob (need O2)
- No hemolysis
- Protective antigen (PA): pore formation on the membrane, toxins can enter the cell
Receive infections from:
- Zoonosis: infectious diseases of animals (usually vertebrates) that can naturally be transmitted to humans.
- Herbivore: an animal anatomically and physiologically adapted to eating plant materia
- Spore survives for decades
Exotoxin production:
1: Antrax edema factor - calmodulin-dependent adenylate cyclase, causes elevation of intracellular cAMP, and is responsible for the severe edema.
2: Antrax lethal factor - Protease of MAPK. Eesponsible for tissue necrosis
Four forms of human anthrax disease are recognized based on their portal of entry.
1: Cutaneous, the most common form (95%), causes a localized, inflammatory, black, necrotic lesion (eschar). Pustula maligna.
2: Inhalation, a rare but highly fatal form, is characterized by flu like symptoms, chest discomfort, diaphoresis, and body aches. Hemorrhagic pneumonia
3: Gastrointestinal, a rare but also fatal (causes death to 25%) type, results from ingestion of spores. Symptoms include: fever and chills, swelling of neck, painful swallowing, hoarseness, nausea and vomiting (especially bloody vomiting), diarrhea (bloody), flushing and red eyes, and swelling of abdomen.
4: Injection, symptoms are similar to those of cutaneous anthrax, but injection anthrax can spread throughout the body faster and can be harder to recognize and treat compared to cutaneous anthrax
Treatment: Penicillin for 3-5 days or doxycycline/ciprofloxacin as the second options
General: An endospore is a dormant, tough, and non-reproductive structure produced by certain bacteria from the Firmicute phylum. The name “endospore” is suggestive of a spore or seed-like form (endo means within), but it is not a true spore (i.e., not an offspring). It is a stripped-down, dormant form to which the bacterium can reduce itself. Endospore formation is usually triggered by a lack of nutrients, and usually occurs in gram-positive bacteria. In endospore formation, the bacterium divides within its cell wall. One side then engulfs the other. Endospores enable bacteria to lie dormant for extended periods, even centuries. Revival of spores millions of years old has been claimed.[3] When the environment becomes more favorable, the endospore can reactivate itself to the vegetative state. Most types of bacteria cannot change to the endospore form. Examples of bacteria that can form endospores include Bacillus and Clostridium.[4]
Antrax: The endospore is a dehydrated cell with thick walls and additional layers that form inside the cell membrane. It can remain inactive for many years, but if it comes into a favorable environment, it begins to grow again. It initially develops inside the rod-shaped form. Features such as the location within the rod, the size and shape of the endospore, and whether or not it causes the wall of the rod to bulge out are characteristic of particular species of Bacillus. Depending upon the species, the endospores are round, oval, or occasionally cylindrical. They are highly refractile and contain dipicolinic acid. Electron micrograph sections show they have a thin outer endospore coat, a thick spore cortex, and an inner spore membrane surrounding the endospore contents. The endospores resist heat, drying, and many disinfectants (including 95% ethanol).[3] Because of these attributes, B. anthracis endospores are extraordinarily well-suited to use (in powdered and aerosol form) as biological weapons. Such weaponization has been accomplished in the past by at least five state bioweapons programs—those of the United Kingdom, Japan, the United States, Russia, and Iraq—and has been attempted by several others
Bacillus cereus
- Gram-positive
- Rod
- Beta hemolytic bacterium
- Commonly found in soil and food
- Facultative anaerobes
- Spore forming
- No capsule, but have pili
Cause
- Diarrhea from meat, rice and vegetables
Diagnostics:
Lecithinase test for: Bacillus cereus (and Clostridium perfringens!). Lecithin: emulgeator (in egg yolk!). Lecithinase activity: breaks down lipoprotein to free fatty acid. Positivity: fat precipitates in the watery medium around colonies
It is the cause of “fried rice syndrome”, as the bacteria are classically contracted from fried rice dishes that have been sitting at room temperature for hours (such as at a buffet). Its virulence factors include cereolysin and phospholipase C.
B. cereus is responsible for a minority of foodborne illnesses (2–5%), causing severe nausea, vomiting, and diarrhea. Bacillus foodborne illnesses occur due to survival of the bacterial endospores when food is improperly cooked. Cooking temperatures less than or equal to 100 °C allow some B. cereus spores to survive. This problem is compounded when food is then improperly refrigerated, allowing the endospores to germinate. Cooked foods not meant for either immediate consumption or rapid cooling and refrigeration should be kept at temperatures below 10 °C or above 50 °C. Bacterial growth results in production of enterotoxins, one of which is highly resistant to heat and acids (pH levels between 2 and 11); ingestion leads to two types of illness, diarrheal and emetic (vomiting) syndrome.
Clostridium tetani
C. tetani produces a potent biological toxin, tetanospasmin, and is the causative agent of tetanus, a disease characterized by painful muscular spasms that can lead to respiratory failure and, in up to 10% of cases, death.
- Gram positive
- Obligate anaerobe
- Spore forming (soil and nails)
Tetanospasmin released in the wound is absorbed into the circulation and reaches the ends of motor neurons all over the body. Travel retrograd. Inhibit SNARE -> No vesicle release of GABA and Glycine (both are inhibitory) in Renshow cells in the spinal cord. This lack of inhibition cause hyperspasms in these muscles.
Characteristic features are risus sardonicus (a rigid smile), trismus (commonly known as “lock-jaw”), and opisthotonus (rigid, arched back).
Vaccine - Toxoid
Clostridium botulinum
- Gram-positive,
- Obligate anaerobic
- Spore-forming (canned food and honney)
- Neurotoxin botulinum: However, C. botulinum tolerates traces of oxygen due to the enzyme superoxide dismutase, which is an important antioxidant defense in nearly all cells exposed to oxygen. C. botulinum is only able to produce the neurotoxin during sporulation, which can only happen in an anaerobic environment
The botulinum toxin can cause a severe flaccid paralytic disease in humans and other animals and is the most potent toxin known to mankind, natural or synthetic, with a lethal dose of 1.3–2.1 ng/kg in humans. The paralysis often have a descending paralysis. Inhibit SNARE formation
In infants. Often after eating honey. “Sloppy Baby Syndrome”.
Treatment: Give antitoxins
Staphylococcus haemolyticus and Staphylococcus hominis
Features
- Gram-positive
- White colonies weak or no hemolysis
- Novobiocin susceptible
- Belong to the normal flora of the skin, its largest populations are usually found at the axillae, perineum, and inguinal areas
- Nosocomial pathogen biofilm production on catheter, canuls, plastic devices, tubes of intubation
- Mucus layer damages help the invasion to the bloodstream bacteraemia and sepsis
- Coagulase negative staphylococci
- Catalase positive
- Non motile
- Non sporulating
- Facultatively anaerobic
The highly antibiotic-resistant phenotype and ability to form biofilms make S. haemolyticus a difficult pathogen to treat.
S. agalactiae
Beta haemolysis Group B strep Gram positive diagnostic antibiotic: bacitracin (R) CAMP test Lancfield group “B” Colonisation in the vagina
Clinical pictures: during pregnancy: abortion
during delivery the neonates can be infected: newborn pneumonia, ARDS, meningitis, sepsis
(Screening of pregnant women after the 35th week of gestation!)
#1 cause of meningitis in newborns neonatal sepsis
Use: ampicillin
Escherichia coli
gram-negative rod, facultatively anaerobic, fimbria
Glucose +, lactose +, indol+, urease -, H2S –
Maconci agar
Most E. coli strains are harmless, but some serotypes can cause serious food poisoning in their hosts, and are occasionally responsible for product recalls due to food contamination. The harmless strains are part of the normal flora of the gut, and can benefit their hosts by producing vitamin K2, and preventing colonization of the intestine with pathogenic bacteria. E. coli is expelled into the environment within fecal matter. The bacterium grows massively in fresh fecal matter under aerobic conditions for 3 days, but its numbers decline slowly afterwards
Under favorable conditions, it takes only 20 minutes to reproduce
“PATHI” - Er det her det er party???
There is one strain, E.coli #0157:H7, that produces the Shiga toxin (classified as a bioterrorism agent). This toxin causes premature destruction of the red blood cells, which then clog the body’s filtering system, the kidneys, causing hemolytic-uremic syndrome (HUS). This in turn causes strokes due to small clots of blood which lodge in capillaries in the brain. This causes the body parts controlled by this region of the brain not to work properly. In addition, this strain causes the buildup of fluid (since the kidneys do not work), leading to edema around the lungs and legs and arms. This increase in fluid buildup especially around the lungs impedes the functioning of the heart, causing an increase in blood pressure
Enterotoxigenic E.coli (ETEC):
- Traveler’s diarrhea and diarrhea in children in
developing countries.
- Transmission is via contaminated food or water.
- The disease is characterized by a watery diarrhea,
nausea, abdominal cramps and low-grade fever for
1-5 days.
- Enterotoxin
LT – is heat labile Increased cAMP alters the activity of sodium and chloride transporters producing an ion imbalance that results in fluid transport into the bowel.
ST – is heat stable, affects the cGMP system.
Enterohemorrhagic E. coli (EHEC) - The symptoms start with a watery diarrhea that progresses to bloody diarrhea without pus and crampy abdominal pain with NO fever or a lowgrade fever. This may progress to hemolytic-uremic syndrome that is characterized by low platelet count,
hemolytic anemia, and kidney failure. The organism attaches via pili to the intestinal mucosa and liberates the shiga-like toxin (aka verotoxin). This is most often caused by serotypes O157:H7. Contaminated beef + milk
Cause:
UTI infections
Neonatal meningitis
Diagnostics:
1: Simple agar
2: Eosin-methylene blue medium (EM):
3: Lactose test: Purple colonies (lactose +)
Salmonella
Gram negative, facultative anaerobic rod Antigen structure: O antigens: very many variations (mozaic structure) H antigens: phase I and II Vi antigen (=capsule) sometimes
Biochemical properties:
H2S positive, glucose positive
Lactose negative, Urease negative, Indol negative
Glucose +, lactose -, H2S +, indol -, urease -
Adhesions – both fimbrial and non-fimbrial
Type III secretion systems and effector molecules
Involved in promoting entry into intestinal epithelial cells
Involved in the ability of Salmonella to survive inside
macrophages
Outer membrane proteins - involved in the ability of
Salmonella to survive inside macrophages
Flagella – help bacteria to move through intestinal mucous
Enterotoxin - may be involved in gastroenteritis
Iron capturing ability
Salmonella can cause:
1: Gastroenteritis (=salmonellosis) - From infected food (zoonosis). Bacterial multiplication trigger inflammation localized in the intestinal tract. Typically from S. enteritidis, S. typhimurium.
Incubation time: 14-48 hours
Chicken or pork meat and eggs from chicken and duck. Need 10^6 bacteria.
Diarrhea (can be bloody)
2: Abdominal typhus (=enteral fever) - Obligate human pathogen! From S. typhi, S. paratyphi A, B, C. Bacteria spread before active multiplication would trigger inflammation.
Fecal-oral infection
First 2 weeks: primary bacteremia
bacteria entering enteral macrophages (in Peyer’s patches)
delivered to mesenteral lymph nodes blood
asymptomatic phase
Multiplication in different organs (RES)
liver (Kupfer cells), gall bladder
Second bacteremia
with high number of bacteria!
Bacteria back to small intestine with bile
multiplication in Peyer’s patches
ulceration, perforation
Symtoms
Hepatosplenomegaly
Roseoles on chest & belly
Fever: gradually increasing to high levels („typhosus” head)
Blood laboratory values:
leukopenia
eosinophilia
lymphocytosis
Diagnostics
Specimen:
Stool: positive only from 2nd-3rd week
Urine: positive from 2nd week
Blood: haemoculture !!
Culture:
Eosin-methylene blue medium (EM): pink colonies (lactose -)
Brillant green or bismuth sulphite medium
Biochemical tests:
Glucose +, lactose -, H2S +, indol -, urease -
Serology:
O, H antigens
Gruber-Widal test
Culture: selective / differentiating media !!
1: Eosin-methylene blue medium (EM):
2: pink colonies (lactose -)
3: Brillant green medium
4: Bismuth-sulphite medium
5: Salmonella-Shigella agar
Serology:
1: O, H antigens (slide agglutination)
2: Kaufmann-White antigen scheme
Treatment:
1: Fluid replacement - usually enough
2: Antibiotics. Obligatory in severe cases (high fever, septicemia). Ampicillin, fluoroquinolons, 3rd gen. cephalosporins
Shigella
Shigella infection is typically by ingestion. Depending on the health of the host, fewer than 100 bacterial cells can be enough to cause an infection because it is acid stable (not killed in the stomach).
Features
- Gram-negative
- Facultative anaerobic
- Facultative intracellular
- No capsule (have O-antigen)
- Does not form spores
- Non-motile
- Green colonies on hektoin agar
- Acid stable (need few bacteria to infect the person)
- Closely related to Salmonella
- Use type 3 secretion
- Produce shiga toxin (inhibit 60S)
- Lactose negative
- H2S negative
- Urease negative
- Very low infective dose (10^2 bacteria)
When they meet M-cells in GI-tract, they are endocytoses, but they will leave before they are lysed in phagolysosomes.
Cause
- Gastroenteritis -> bloody diarrhea (Dysentery!)
- Shigellosis
- Shiga toxin inhibit 60S and protein synthesis (can result in hemolytic uremic syndrome and ulceration of large intestine)
Shigella diagnostics:
1: Native stool specimen - pus, mucus, blood
2: Culture: selective / differentiating media (!!)
2a: Eosin-methylene blue medium (EM): pink colonies (lactose negative)
2b: Salmonella-Shigella agar
2c: Deoxycholate citrate medium
3: Serology
4: Toxin detection - Serény test and On tissue culture
Treatment:
1: Antibiotics - to shorten the disease and to inhibit carriage ( Salmonella!)
1a: TMP/SMX; fluoroquinolones, 3rd gen. cephalosporins
1b: resistance to ampicillin!
2: Supportive therapy: Fluid and electrolite replacement
(3: Vaccine is under development)
Shigella species generally invade the epithelial lining of the colon, causing severe inflammation and death of the cells lining the colon. This inflammation results in the diarrhea and even dysentery that are the hallmarks of Shigella infection. Shigella species invade the host through the M-cells interspersed in the gut epithelia of the small intestine, as they do not interact with the apical surface of epithelial cells, preferring the basolateral side. Shigella uses a type-III secretion system, which acts as a biological syringe to translocate toxic effector proteins to the target human cell. After invasion, Shigella cells multiply intracellularly and spread to neighboring epithelial cells, resulting in tissue destruction and characteristic pathology of shigellosis
S. dysenteriae strains produce the enterotoxin Shiga toxin, which is similar to the verotoxin (also called Shiga-like toxin) produced by Enterohemorrhagic E. coli. Both shiga toxin and verotoxin are associated with causing potentially-fatal hemolytic uremic syndrome.
Yersinia
Features:
- Gram negative
- Facultative anaerobic
- Capsulated
- Facultative intracellular
- Type of enterobacteriaceae
Two main types:
1: Y. Enterocolitica - Transmitted primary by puppy feaces to babies. Resistant to cold temperatures. Bipolar staining. Cause diarrhea. Important to note that it can mimic appendicitis. Cause the diease “yersiniosis”.
The portal of entry is the gastrointestinal tract. The organism is acquired usually by insufficiently cooked pork or contaminated water, meat, or milk. Acute Y. enterocolitica infections usually lead to mild self-limiting enterocolitis or terminal ileitis and adenitis in humans. Symptoms may include watery or bloody diarrhea and fever, resembling appendicitis or salmonellosis or shigellosis. After oral uptake, Yersinia species replicate in the terminal ileum and invade Peyer’s patches. From here they can disseminate further to mesenteric lymph nodes causing lymphadenopathy. This condition can be confused with appendicitis, so is called pseudoappendicitis. In immunosuppressed individuals, they can disseminate from the gut to liver and spleen and form abscesses
2: Y. Pestis - Cause Plague
3: Yersinia pseudotuberculosis
Diagnosis:
- Culture (contagiosity!),
- Gram or Giemsa staining (bipolar staining!)
Treatment: streptomycin, gentamicin (a.s.a.p.)
Prevention: inactivated vaccine (not too sufficient)
Klebsiella
Nosocomial infection (hospital acquired) Multidrug resistant Fermentate lactose Imobile Capsulated (polysaccaride) Jelly sputum Can mimic TB in lungs Urease positive In the family of Enterobacteriaceae Facultative anaerobic Gram negative rod
Glucose +, lactose +, urease +, indol -, H2S –
Diagnostics:
1: Capsule swelling test
2: Simple agar - very mucoid colonies (capsule)
3: Unpleasant, urine-like smell
4: Eosin-methylene blue medium
5: Lactose positive - Purple colonies
Occur in: ????? - Sketchy
- Abcesses
- Aspiration
- Alcoholics
Cause:
- Pneumonia
- UTI
urinary tract infection
cholecystitis, cholangitis
sinusitis, otitis media
Serratia
Nosocomial infection (hospital acquired) Multidrug resistant Fermentate lactose Mobile Endospore forming Facultative anaerobic Non-spore forming In the family of Enterobacteriaceae
- Form a red pigment
- Can be distinguished from other members of the Enterobacteriaceae family by their unique production of three enzymes: DNase, lipase, and gelatinase.
Cause:
- Pneumonia
- UTI
Enterobacter
Nosocomial infection (hospital acquired) Multidrug resistant Fermentate lactose Mobile Gram-negative Facultative anaerobic Non-spore forming In the family of Enterobacteriaceae Cause: - Pneumonia - UTI
Proteus spp.
“Swarming”
Lactose positive
Clostridium perfringens
Gram-positive, rod-shaped, anaerobic, spore-forming pathogenic bacterium of the genus Clostridium
Obligate anaerobic
Motor cycle accidents, deep wounds (combat)
Gas gangere (myonecrosis): alpha toxin, or lecithinase. Cleaves phospholipids in the plasma membrane.
Lecthinase cause hemolysis
Slow onset watery diarrhea caused by spore ingestion.
Diagnostics: Lecithinase test for: Clostridium perfringens (, and Bacillus cereus)
Treatment: IV penicillin G
Infections due to C. perfringens show evidence of tissue necrosis, bacteremia, emphysematous cholecystitis, and gas gangrene, which is also known as clostridial myonecrosis. The toxin involved in gas gangrene is known as α-toxin, which inserts into the plasma membrane of cells, producing gaps in the membrane that disrupt normal cellular function. C. perfringens can participate in polymicrobial anaerobic infections
Clostridium perfringens is the most common bacterial agent for gas gangrene, which is necrosis, putrefaction of tissues, and gas production. It is caused primarily by Clostridium perfringens alpha toxin. The gases form bubbles in muscle (crepitus) and the characteristic smell in decomposing tissue. After rapid and destructive local spread (which can take only hours), systemic spread of bacteria and bacterial toxins may cause death.
Corynebacterium diphtheriae
- Gram positive rod
- Neisser stain(!): Volutin granules become dark blue. Looks like matches
- Club shape
- V or Y formation
- Metachromatic granules
- Non-spore forming
Exotoxin
a and b subunit. a is the active part. b is the binding part. Cause ATP ribosylation of elongation factor 2 (EF-2) –> inhibit protein synthesis and cell death. Grayish exudate in the mucosa of the oropharynx.
In areas where diphtheria is endemic, C. diphtheriae in the nasopharyngeal passageways is common. Toxigenic strains in susceptible individuals can cause disease by multiplying and secreting diphtheria toxin into either skin or nasopharyngeal lesions. The diphtheritic lesion is often covered by a pseudomembrane composed of fibrin, bacteria, and inflammatory cells. Diphtheria toxin can be proteolytically cleaved into two fragments: an N-terminal fragment A (catalytic domain), and fragment B (transmembrane and receptor binding domain). Fragment A catalyzes the NAD+ -dependent ADP-ribosylation of elongation factor 2, thereby inhibiting protein synthesis in eukaryotic cells. Fragment B binds to the cell surface receptor and facilitates the delivery of fragment A to the cytosol.
diphtheria toxin which alters protein function in the host by inactivating the elongation factor EF-2. This causes pharyngitis and ‘pseudomembrane’ in the throat.
bacteria never enter the blood, only the toxin!!!!
- “Bulls neck” due to lymphadenopathy
- Myocarditis
- Liver and kidney problems
- Diphtheria
Diagnostics
0: Neisser staining
1: Löffler’s medium: a special substance used to grow diphtheria bacilli to confirm the diagnosis. Ivory colour. Clotted bovine serum, egg, heart extract, rapid growth, strong volutin granule formation. Ivory colour. Clotted bovine serum, egg, heart extract. Rapid growth, strong volutin granule formation
2: Clauberg medium: glycerin, blood, cystin and tellurite (selective!). The species reduce the tellurite to different extent grey – black colonies. Garlic smell.
3: Biochemical tests (catalase +, saccharose -)
4: Elek test for toxin production
5: Serology (antitoxin-titre)
Transmission:
- Respiratory droplets
Vaccine: toxoid (DiaPerTe) – booster at travel or occupational risk
Treatment: Antitoxins and macrolides
Proteus mirabilis
Proteus mirabilis is a Gram-negative, facultatively anaerobic, rod-shaped bacterium. It shows swarming motility and urease activity. P. mirabilis causes 90% of all Proteus infections in humans. It is widely distributed in soil and water
An alkaline urine sample is a possible sign of P. mirabilis. It can be diagnosed in the lab due to characteristic swarming motility, and inability to metabolize lactose (on a MacConkey agar plate, for example). Also P. mirabilis produces a very distinct fishy odor.
Biochemical tests: Urease +, H2S +, Lactose -
