Bacteria Cumulative

Question 1

Bacillus anthracis f

Answer 1

Gram positive spore forming rod commonly used as a biothreat weapon. Produces anthrax toxin: Edema factor which activates AC and leads to osmotic swell and Lethal factor which is a cytotoxic protein causes inflammation, macrophages activation, and cell death.

Can be cutaneous (ulcer with black eschar with raised edges due to edema factor), pulmonary caused by inhalation of the spores causing flu-like symptoms that leads to pulmonary hemorrhage and mediastinitis, and GI anthrax through ingestion of spores which is highly lethal

Also unique in that it is the only bacterium that produces a polypeptide capsule

Question 2

Bacteroides fragilis

Answer 2

Gram negative bacilli that populate the female genital tract that is rather antibiotic resistant (has beta lactamase) an has a capsular polysaccharide coat. Can lead to fever and localized pain, as well as abscesses.

Is an obligate anaerobe, thus metronidazole effective in treatment, treat for this if infection below the diaphragm

Question 3

Bartonella

Answer 3

Also known as the cause of cat scratch disease. Carried on insects and is one of the facultative intracellular pathgens (also is aerobic). Aside from cat scratch fever, which causes chronic lympahdenitis, it also causes trench fever.

Infections are often self limited

Question 4

Bordatella pertussis

Answer 4

Gram negative coccobaccilus which is the cause of whooping cough. Human is the only host and is passed via aerosols, then colonizes the ciliary respiratory epithelium

Another one of the classic toxin mediated bacteria, it produces pertussis toxin, which is an ADP-ribosylase that ribosylates the Gi protein, leading to an increase in cAMP and increasing secretions. Also produces AC, which requires host calmoldulin (so it’s only active in host), and Tracheal cytotoxin, which is a fragment of the cell wall and causes damage to the muco-ciliary ladder (loss of cilia)

Prevented by DTaP vaccine, and can only be treated during the early stages as late stages have very little bacteria

Question 5

Borrelia burgdorferi

Answer 5

Gram negative-like (lack LPS) helical shaped bacteria implicated in Lyme disease. Spread by Deer tickets (ixodes scapularis) very common to the northeast US. These are very want to cause systemic infection as they have endoflagella between their membranes. Will colonize arterial blood vessels, connective tissues (binds decorin protein on collagen), and skin

Are very unique to how many lipoproteins they possess (>100 predicted lipoporteins, more than any organism) and have a linear chromosomes with lots of linear and circular plasmids

Lyme disease progresses in stages 1) erythema migrans and a characteristic Bull’s eye rash around the tick bite, fever, chills 2) carditis, AV block, Bell’s palsy, and 3) Migratory polyarthritis and maybe subtle CNS effects (encephalopathy)

Can be problematic because they have few antigenic targets (outside of OspA) and can undergo antigenic variation

Treat with doxycylcine as soon as possible, ceftriaxone for more severe cases

Question 6

Brucella

Answer 6

Small, non-motile gram negative coccobacilli that are facultative intracellular pathogens that are harbored on cows, pigs, goats, and dogs. Causes brucellosis, which is a granulomatous infection that is often chronic and can have systemic manifestations

We generally encounter this pathogen via ingestion (usually unpasteurized dairy product) or contact with skin/mucus membrane and then grows within macrophages

Escapes the pathway leading to phagolysosome fusion and grows in a vacuole associated with the ER, accomplished by VirB gene that encodes a type IV secretion system which faciliates their growth in macrophages and is responsible for inhibiting lysosomal fusion

Key here is that they don’t impair macrophage ability to spread to the rest of the body, so will go through the RES and give rise to acute infection (undulent fever)

Treat with doxycycline and rifampin

Question 7

Campylobacter jejuni

Answer 7

Gram negative bacili (similar in structure to H. pylori) that is a commensal of animal GI tracts. It is bile salt resistant, microaerophilic, motile, and a slow grower. We encounter it by animal exposure or contaminated food. Has flagellae, as well as cytotoxins and enterotoxins though their mechanisms aren’t well understood

Causes Gastroenteric disease, and is associated with Guillain-Barre Syndrome as a post-infectious sequelae

Unique as they grow at high temperatures (grows in 42 degrees celcius)

Question 8

Chlamydia pneumoniae

Answer 8

An obligate intracellular pathogen (very difficult for us to culture) that infects the respiratory track epithelium (based off of tropism targets columnar ciliated cells). Encountered via aerosols of people coughing. From birds Produces atypical pneumonia.

Prior to infecting cells, is an Elementary Body that is compact infectious form that exists outside of the cell. This then attaches to the cell and induces phagocytosis, and then changes to Reticular Body (metabolically active). This activated form modifies the vesicular membrane by utilizing host ATP and forms inclusion bodies. When nutrients from the cell are exhausted, converts back to Elementary body and the host cell ruptures

C. pneumoniae is 5-15% of community acquired pneumonia, more readily seen in the eldery and younger people. Causes bronchitis, pharyngitis, pneumonia. Big thing here is that the antibody is not protective of subsequent infections.

Treatment: tetracycline, Macrolides

Question 9

Chlamydia trachomatis

Answer 9

Obligate intracellular pathogen that colonizes the epithelium of the urogenital tract (more readily in females) and passed via ocular secretions and sexual contact. Very often accompanies Neisseria gonorrhea

Prior to infecting cells, is an Elementary Body that is compact infectious form that exists outside of the cell. This then attaches to the cell and induces phagocytosis, and then changes to Reticular Body (metabolically active, replicative). This activated form modifies the vesicular membrane by utilizing host ATP and forms inclusion bodies. When nutrients from the cell are exhausted, converts back to Elementary body and the host cell ruptures

Transmitted via hand to eye contact.

C. thrachomatis has many different serotypes that dictate what kind of pathology will be observed. In developing world, it is the leading cause of blindess. In disease states, we’ll see cervitis, proctitis, prostatis, and urethritis in females, with the potential for infertility due to fallopian scarring), ectopic pregnancy, and chronic pelvic pain. Complications–> PID or, Reiters syndrome–> reactive arthritis, uviitis, urethritis (can’t see, can’t pee, and cant climb a tree)

In males, will cause epididymitis, proctitis, prostatitis, and uretherities

In infants, will present with mild pneumonia and purulent conjunctivitis

Treatment: Macrolides, tetracycline

Question 10

Clostridium botulinum

Answer 10

Gram positive sporulating rod often found in bad bottles of food, juice, and honey (honey’s the big one). In most cases, the bacteria never enters the body but rather we ingest the botulinum toxin. This causes flaccid paralysis by inhibiting ACh firing at NMJ (floppy baby syndrome). Treatment is the antitoxin

Question 11

Clostridium difficile

Answer 11

Gram positive sporulating rod that is often found in normal gut flora, but can become problematic in patients receiving antibiotic treatment, especially clindamycine

C. difficile produces two toxins. Toxin A, also known as enterotoxin, binds to the brush border of the gut. Toxin B, cytotoxin, causes cytoskeletal disruption via actin depolymerization, causing diarrhea and pseudomembranous colitis

Diagnosed by detecting the toxins in stool and PCR. Treat with metronidazol or oral vancomycin in severe cases.

Question 12

Clostridium perfringens

Answer 12

Gram positive sporulating rod that is generally found in soil and can get into wounds. Can also be ingested in food.

C. perfringens produces alpha toxin (a phospholipase) that can cause myonecrosis, or gas gangrene, and hemolysis in blood. When ingested in food, the bacteria releases enterotoxin, leading to food poisoning

Question 13

Clostridium tetani

Answer 13

Gram positive sporulating rod that is responsible for cause tetanus (lock jaw) via the tetanus toxin, which prevents the firing of inhibitory neurons controling muscles (GABA and glycine inhibition). Treated with the antitoxin.

Unlike clostridium botulinum, C. tetani spores tend to get into the body via inoculated puncture wounds, grow, and then release the toxin. Treatment is the antitoxin (possibly diazepam for the muscle spasms), and we also have a vaccine against it

Question 14

Corynebacterium diphtheria

Answer 14

Gram positive rod, similar to the clostridia genus due to its use of a potent toxin. Diphtheria toxin, encoded for on a beta-prophage, inhibits protein synthesis by binding to EF-2. Leads to diphtheria

Symptoms include pseumembranous pharyngitis (grayish-white membrane in the back of the mouth/throat), myocarditis, and lymphadenopathy. Almost never see it due to the vaccine

The big hallmark of the disease is Bull Neck, which is a byproduct of cervical lymphadenopathy and edema

Question 15

Enterococcus faecalis/faecium

Answer 15

Alpha/Gamma hemolytic groups of gram positive coccus catalase negative. Normal colonic flora that are penicillin resistant and can cause UTIs (in catheters), biliary tract infections, and subacute endocarditis following GI/GU procedures

Unlike the other Streptococcus (except Strep pneumo), these are diplococci

These are of particular interest because these bacteria Vancomycin-resistant entercocci, which are an important cause of nosocomial infection and can spread this resistance to other bacteria that are more virulent

Question 16

Francisella tularensis

Answer 16

Gram negative rod often found on wild rodents and rabits, very highly virulent. One of the facultative intracellular bacteria that is resistant to phagosome killing and is the cause of Tularemia

Acute, febrile illness high fever, chills, fatigue, headache, pharyngitis, sore joints, chest discomfort, dry cough, vomiting, abdominal pain, and diarrhea

Question 17

Group B Strep (Streptococcus agalactiae)

Answer 17

Gram positive coccus catalase negative beta hemolytic. Colonizes the vagina of females and is of particular concern in babies

Can cause pneumonia, meningitis, and sepsis in babies

Question 18

Haemophilus influenzae

Answer 18

Gram negative coccobacillus that can exist in encapsulated and nonencapsulated form spread via aerosols.

Exists as a facultative anaerobe

Pathogenesis is meadiated by LPS, pili for adherence, non-pilus adhesion, and Factors V and X. Also produces IgA protease

Causes Epiglottisis and meningitis (HIb serotype) as well as otitis media, pneumonia, conjuctivitis, and sinusitis (nontypeable strains)

Treat with amoxicillin +/- clavulanate for mucosal infections, ceftriaxone for meningitis, and rifampin prophylaxis for close contacts

Question 19

Helicobacter pylori

Answer 19

Gram negative curved (helical almost) and terminally flagellated that is catalase, oxidase, and urease positive (urease maintains higher pH in low pH stomach environment). Microaerophilic. Encounter is generally oral-oral contact, and transmission is either fecal-oral or gastric-oral.

Colonizes mucous layer lining the gastric mucosa and persists because of inability of host immune defenses to reach it.

Has adhesins, CagA virulence island (cytotoxin associated gene), LPS

Causes chronic gastritis, gastric cancer (CagA+ H. pylori) GERD (CagA+ protective), and Peptic ulcer disease

Can test using breath test, or ingestion of labeled urea test. Can confirm with upper GI endoscopy

Treat with amoxicillin (metronidazole if allergic to PCN), clarithromycine and a PPI

Question 20

How do we differentiate between Streptococcus and Staphylcoccus? Between the individual groups of Streptococcus? Between the two groups of Staphycoccus?

Answer 20

Streptococcus bacteria are catalase negative while staphylcoccus are catalase positive.

To differentiate between groups of Streptococcus, we use hemolysis plating. Group A (pyogenes) and Group B (agalactiae) Beta hemolytic, meaning they completely lyse RBCs. Enterococcus, Pneuomococcus, and Strep viridans are alpha hemolytic (don’t lyse), partial reduction of hemoglobin

The two groups of Staph, Staph aureus and not-Aureus (epidermidis) are differentiated by coagulase test. Aureus is positive, others are negative

Question 21

Klebsiella

Answer 21

Gram negative rod that is nonmotile and is encapsulate, lactose fermenter. Typically part of the normal flora but can produce very mucoid colonies due to its abundant polysaccharide capsules

Pathogenesis: Has elastase/proteases that cause local damage, exotoxin A (ADP-ribosylase) and Exotoxins S, T, and U (type III secretion), and LPS leading to sepsis.

Clinical presentation: Grows in the lungs, typically in immunocompromised or alcoholic patients, and causes necrosis, inflammation, and hemorrhage. Hallmark is the production of currant jelly sputum (blood+mucus)

Has an extended spectrum beta lactamase, typically treat with cephalosporins

Question 22

Legionella pneumophila

Answer 22

Gram negative baccili (can be pleiomorphic), very fastidious culturing, and is among the three most common causes of community acquired pneumonia. Encountered by aerosol generated form contaminated water systems. NO PERSON TO PERSON. Colonizes alveolar macrophages (dust cells)

Can be killed by PMNs but not by macrophages, it will live in these cells in the phagosome. It modifies the phagosome membrane, forming pores that allow for transfer of effector molecules that disrupt phagocyte trafficking and will associate with RER

Exists in two states:

1) Exponential phase: proliferative but not virulent
2) Post-exponential: Virulent but not proliferative

Causes vigorous immune response, leading to pneumonia. Infection can be controlled by cell-mediated immunity

Treat with macrolides (erythromycin/azithromycine) or fluoroquinolos (ciprofloxacin)

Question 23

Listeria monocytogenes

Answer 23

Gram positive rod, facultative aerobe. This is normally encountered by ingesting nonpasteurized milk, cold deli meats, or by vaginal transmission during birth.

The hallmark of this disease is the hijacking of host actin polymerization, allowing for intracellular movement and spreading between cell membranes (avoiding humoral response). It escapes the phagolysosome with listeriolysin (LLO), which acts better at lower pH, and lyses the vacuolar membrane

All damage caused is due to the host response as there is no systemic exotoxin. Can cause granulomatosis infantiseptica, neonatal meningitis, and meningitis in immunocompromised patients. In most people, leads to self-limited gastroenteritis

Question 24

Mycobacterium leprae

Answer 24

Acid fast stained bacterium responsible for Hansen disease (leprosy), cannot be grown in vitro, and is transmitted human to human. Infects cool areas of the body. Intracellular bacteria- macrophages.

Hansen’s Disease comes in two forms: lepromatous and tuberculoid.
Tuberculoid: limited to a few hypoesthetic, hairless skin placques characterized by high cell-mediated immunity mediated largely by Th1
Lepromatous: Presents diffusely over the skin and is communicable, low cell mediated immunity. Good humoral response but doesn’t matter because it is an intracellular reaction. This can be lethal.

Treat with dapsone and rifampin if tuberculoid, clofazimine is added in cases of lepromatous form

Question 25

Mycobacterium tuberculosis

Answer 25

Acid fast stained (due to mycolic acids) bacterium that causes TB transmitted between humans via inhalation of droplets. These bacteria colonize the alveoli by taking up residence in alveolar macrophages. Spread to other sites by traveling in macrophages via blood and lymph. Oblgate aerobe.

The infection is typically contained by granuloma formation and follow cell mediated immunity- mediated via chord factor which activates macrophages. Sulfatides prevent phagolysosome fusion, allowing Mtb to live intracellularly.

If the containment is unstable, you get active TB disease with caseuous necrosis (tubercle) and hematogeous spread (miliary tuberculosis). Can seed anywhere in body and cause multi-organ failure.

The disease can be reactivated after being originally contained due to a number of factors (illness, malnutrition, stress, immunocompromised) via TNF inhibition.

Can test with PPD skin test (looks at T cell immunity not disease), which will screen positive with previous exposure or current infection, negative with no infection. More effective test is interfeuron gamma release assay to test for immune response using T cells.

Treatment- multiple drugs (RIPE- rifampin, isoniazid, pyrazinemide, ethambutol)

Question 26

Mycoplasma pneumoniae

Answer 26

Mycoplasma pneumoniae, causing atypical/walking pneumonia, is a pleiomorphic bacteria not seen on gram stain due to lack of a cell wall, and also has sterols that aid its membrane for stability (similar to humans, unique in that aspect), but are rather osmotically fragile

Encountered from respiratory droplets and can be moderately contagious as human is its only niche, colonizes the respiratory epithelium (no alveolar involvement). Adheres via P1 protein to respiratory cells

Leads to atypical, or “walking,” pneumonia which presents with headache, cough, and non-lobar patchy interstitial pattern.

Diagnosed with cold agglutinins
Not affected by cell wall antibiotics (treat with tetracycline, erythromycine, azithromycins (macrolides)

Question 27

Neisseria gonorrhoeae

Answer 27

Gram negative diplococci, non-maltose fermenter, and lacks a capsule. This bacteria lives in humans and is transmitted sexually (more frequenty male to female), or perinatally during delivery.

In women, it moves its way up the fallopian tubes and uses Pili and Opa proteins to form tight adhesions to mucosal cells (can make micro-colonies)

These bugs survive in host due to its ability to acquire iron (has receptors for human transferrin), resisting phagocytosis, and bind Human factor H, which inhibits complement

N. gonorrhoeae attaches to human cells and use Opa to facilitate their endocytosis and invasion. Also uses a LPS-like molecule, Lipooligosaccharide (LOS) that is cytotoxic to ciliated Fallopian tube epithelial cells. Will also take advantage of antigenic/phase variation

In women, causes Cervicitis, pelvic inflammatory disease, infertility, ectopic pregancy. In men, causes purulent urethral discharge and epididymitis. Disseminated Gonococal Infection leads to arthritis, rarely causing endocarditis and meningitis

Treat with ceftriaxone and azithromycin or doxycycline to treat possible chlamydial coinfection

Question 28

Neisseria meningitidis

Answer 28

Gram negative diplococci possessing a capsule and is a maltose fermenter. Transmitted by respiratory and oral secretions. Generally asymptomatic respiratory carriers but colonization can be caused by smoking or by an earlier virl infection. Found on the non-ciliated columnar epithelium of the nasopharynx.

Spreads locally first and then to bloodstream, but minimal local inflammation. Will spread to the CNS (crosses BBB) and causes meningitis 50% of the time. Its damage is mediated by release of high doses of lipooligosaccharide (LOS) which leads to endotoxic shock and vascular shock

Virulence is dictated similarly to N. gonorrhoaea with Pili/Opa aiding adherence and entrance into host cells, iron acquisition, will avoid phagocytosis because of the capsule, has LOS, and has antigenic and phase variation.

Is preventable with vaccine (type B vaccine not widely available), and treated with ceftriaxone or penicillin G

Question 29

Pseudomonas aeruginosa

Answer 29

Gram negative rod, motile, capsulated, non-lactose fermenting, oxidase positive, catalase positive, strict aerobe. Has many means of avoiding treatment (efflux pumps, effective porins), so are sometimes difficult to treat. Most effective treatment is synergistic (piperacillin/tazobactam, cephalosporins, carbapenems)

Transmission is through “moist” sources as they are frequently found in water. Uses pili and polar flagella to colonize

Nasty bug because it has membrane degrading toxins (leukocidin which forms pores in cells and PLC which causes cell lysis). Has exotoxin A which inactivates EF-2, pyocyanin (generates reactive oxygen species), and delivers Exotoxins S, T, and U via Type III Sec system. Proteases to spread through infected tissue, LPS as well

Has capsule to avoid phagocytosis

Causes: pneumonia, sepsis, ecthyma gangrenosum (rapidly progressive necrotic cutaneous lesion typically seen in ICU patients), UTIs (nosocomial), osteomyelitis (IV drug users, diabetics at highest risk), otitis externa, and general skin infections, associated with burn victims

Question 30

Rickettsia rickettsiae

Answer 30

Coccobacillary, weakly gram negative, Obligate intracellular (need NAD and CoA from host) organism transmitted via arthopod vectors (dermacenter ticks) that colonize vascular endothelium. Unlike Coxiella brunetti, Rickettsia does not produce hardy spore-like extracelluar form

Rickettsia induce their uptake by vascular endothelial cells and escape their phagosomes via a phospholipase. It then takes advantage of host actin system for motility and spreading to other endothelial cells. During this process, some cells will be lysed by phospholipase and release free rickettsiae, which can cause very rapid systemic infection

Clinical: Rocky mountain spotted fever. Will observe eschars (piece of dead tissue of the skin), small hemorrhages, and sepsis syndrome. Will also observe vasculitis rash (palbable purpura), fever. Rash starts peripheral, and moves central.

Treat with doxycyclin empirically as testing won’t get back fast enough

Question 31

Salmonella enterica (Typhi and Typhimurium)

Answer 31

Gram negative rods that can disseminate hematogenously and have flagella (motile), encapsulated, facultative intracellular, acid labile

Typhi: Colonizes human macrophages and remain in phagosomes (prevent lysosomal fusion) and add bacterial proteins into the vacuole membrane that permits the acquisition of nutrients. Can also colonize gall bladder with a long-live asymptomatic carrier state. Is the cause of enteric fever (Typoid) which is a systemic infection with fever, abdominal symptoms, rose spots. Can cause intestinal hemorrage and perforation as well as focal infections (pericarditis, liver abscess, spleen abscess)

Typhimurium: Transmitted person to person but first encountered in contaminated food, colonizes the intestinal epithelium. Once in host, will deliver proteins via type III secretion. Will cause gastroenteritis, nausea, vomiting, fever, chills, headache, loose stools lacking blood/mucous, and an inflammatory cell response (dealt with by PMNs)

Question 32

Shigella

Answer 32

Gram negative, immotile, acid stabile, facultative intracellular
S. sonnei, flexneri, boydii, and dysenteriae (most virulent, produces shiga toxin) are gram negative rods found in the gut and are lactose non-fermenters, are fairly acid resistant. Lack flagella (unlike salmonella). Are intracellular invaders of the gut, encountered person to person via oral-fecal route

Has a large plasmid that encodes proteins that permit exploitation of intracellular environment

Shiga toxin inactivates 60s rRNA and blocks protein synthesis, and can cause hemolytic-ureminc syndrome (kidney failure, hemolysis, and thrombocytopenia) in the host (in S. dysenteriae)

Spread by using hemolysins to lyse the phagosome and use host actin to spread to adjacent cells, but rarely spreads beyond the mucosa

Clinical presentation: Will present with frequent defecation, and have mucous and blood. Diagnose with stool leukocytes

Question 33

Staphycoccus aureus

Answer 33

Gram positive coccus that groups in clusters (like grapes), catalase positive, coagulase positive, and is also Beta hemolytic. Commonly found in the nares

Very resistant bacteria for a number of reasons:
Produces Protein A, which binds to the Fc region of immunoglobulin preventing opsonization and complement activation. Coagulase helps build a fibrin capsule around the organism. Hemolysins which are toxins directly toxic to RBCs. Catalase helps prevent oxygen species from killing it. Penicillinase: beta-lactamase that can inhibit beta-lactam antibiotics.

Can penetrate with hyaluronidases, which attack connective tissue, fibrinolysin, which breaks down clots, and lipases which allow spread in fatty tissue. Essentially can cause inflammatory and toxin mediated disease

Staph aureus secretes three toxins:

1) Exfoliati: exfoliates skin and causes Scalded Skin Syndrome
2) Enterotoxins: cause vomiting and diarrhea (nonbloody), is also heat labile
3) Toxic shock syndrome toxin: superantigen that binds MHCII leading to polyclonal T cell activation, leading to fever, vomting, rash, desquamation, shock and end-organ failure (Staphylcoccal toxic shock syndrome). Can be associated with use of vaginal tampons or nasal packing

The big thing with S. aureus is that methicillin-resistant Staph aureus is a big deal in hospitals, often caused by mutation causing altered penicillin-binding protein

Question 34

Staphylcoccal epidermidis (not-aureus)

Answer 34

Gram positive coccus, coagulase negative that grow in clusters and are found in normal skin flora.

The big thing to remember with this bacteria is that it is very prone to infecting prosthetic devices and IV catheters by producing slime-like biofilm

Question 35

Streptococcus pneumoniae (Pneumococcus)

Answer 35

Gram positive diplococci catalase negative and are encapsulated (very important for virulence and resistance to phagocytosis), not virulent without the capsule. Also possess an IgA protease, which aids their survival at mucosal surfaces. Colonize the nasopharynx

Evokes a pyogenic response due to immune response caused by teichoic acid. Spread via respiratory aerosoles

Most common cause of meningitis, otitis media, pneumonia, and sinusitis

Question 36

Streptococcus pyogenes (Group A Strep = GAS)

Answer 36

Gram positive coccus, catalase negative, beta hemolytic and is pyogenic. Grow in chains. Human resevoir that may be carried in nasopharynx, skin, or GI asymptomatically

Has M protein, which aids in avoiding phagocytosis and is antigenitcally variable
Streptolysins S + O are the ones carrying out beta hemolysis
Pyrogenic exotoxins: superantigens that give rise to scarlet fever and toxic shock
Strepokinase: mediate rapid spread of infection

Causes three sets of diseases:

1) pyogenic: pharyngitis, cellulits, impetigo, erysipelas
2) toxigenic: scarlet fever, toxic shock-like syndrome, and necrotizing fasciitis
3) immunologic: rheumatic fever and glomerulonephritis caused by cross-reacting antibodies from infected host

Question 37

Streptococcus Viridans group

Answer 37

Nongroupable alpha hemolytic gram positive cocci of the streptococcus genus. These are normal oropharyngeal flora that can cause transient bacteriemia form dental procedures

Can cause fevers, night sweats, fatigue, and new-onset murmors (via damaging heart valves)

Question 38

Treponema pallidum

Answer 38

Gram-negative like (lacks LPS) spirochete (helical) that resides on HUMAN mucous membranes and small skin abrasions. It is spread sexually or cross placental (if the mother has it).

Similar to Borrelia burgdorferi, has few antigenic targets with no known toxins and takes advantage of lipoproteins to produce host response. Big this is that it is the cause of Syphylis

Primary: Genital Chancres due to damage of small vessels(painless), regional lymphadenopathy
Secondary: Invasion and systemic illness with flu like symptoms (Secondary = Systemic), maculopapular rash on hands/feet
Tertiary: Gummas (chronic granulomas), aortitis, neurosyphylis,
Congenital Acquired Syphylis: prematurity, diminished growth, facial tooth and bone deformities, deafness, and arthritis

Very effectively treated with penicillin, however it is difficult to reach high risk communities. Still no vaccine as there are too few antigenic targets.

Question 39

Vibrio cholerae

Answer 39

Gram negative comma shape, also flagellated, oxidase positive found in water. Colonizes the small bowel epithelium, acid labile, oxidase positive

One of the classical toxin bacteria, as it produces cholera toxin, which permanently activates Gs, increasing cAMP levels and leading to increased secretions: rice-water stool, leading to hypovolemic shock

Doesn’t present with fever, inflammation, or stool in blood/leukocytes

Treat with fluid replacement and antibiotics

Question 40

What are considered the classical toxigenic bacteria?

Answer 40

Vibrio cholerae, which secretes cholera toxin in the intestines, leading to increase cAMP levels and leading to increased secretions leading to rice-water stool

Bordetella Pertusis, has two exotoxins and one endotoxin. Pertussis toxin and AC are secreted, causing an increase in cAMP leading to more respiratory secretions. The endotoxin, tracheal cytotoxin, which removes the cilia from the cells via innate immune stimulation

The clostridia have a bunch: Tetani causes rigid paralysis, botulinum causes flaccid paralysis, perfringens secretes alpha toxin which leads to necrotizing tissue, and difficle releases enterotoxin which leads to secretory diarrhea

Bacillus anthracis releases two exotoxins, edema factor (activates AC, leads to osmotic cell swell), and lethal factor (cytotoxic protein causing inflammation, macrophage activation, and cell death)

Corynebacterium diphtheriae secretes diphtheria toxin, which binds and inactivates EF-2 inhibiting protein synthesis of cells

Question 41

What are distinguishing factors of mycobacteria?

Answer 41

While phylogenitically gram positive bacteria, they have mycolic acid lipid coats, which are incredibly long lipid coats compared to other coats. Are aerobic cells and are incredibly fastidious

Question 42

What are the common themes of all Clostridia?

Answer 42

All Costridial species are gram positive rods that are obligate anarobes as well as spore formers. Many of the encounters, save C. difficile, is found in the soil

Question 43

What are the encapsulated organisms?

Answer 43

Pneumococcus, Haemaphilus influenzae, Klebsiella, and Neisseria meningitidis

The capsule allows them to avoid phagocytosis and avoid the complement response to some extend, allowing them to survive effectively survive in deep tissue. However, we can exploit this by designing vaccines toward the capsule via conjugation to other know proteins

Question 44

What are the general properties of Escherichia coli? Of the various subtypes (ETEC, EHEC, EPEC, EAEC, EIEC)

Answer 44

Gram negative rod that’s a facultative aerobe that colonizes the intestinal epithelium. Expresses H antigen (flagella), O antigen (LPS polysaccharide), and K antigen (capsular polysaccharide) which are used to serotype it. Undergoes gene exchange readily due to the presence of plasmids and contains pathogenicity islands inserted into the chromosome.

The major clinical presentation of E. Coli: neonatal meningitis (materal transmission, associated with the presence of the K1 capsule), opportunistic infection (pneumonia and bacteremia most important) and UTIs

Enterohemorrhagic E. Coli: The most severe of the E. colis, this auses effacement of enterocytes (loss of microvilli) and manipulate host actin to produce a pedestal for the bacterium to sit on. This also produces Shiga-like toxin, which can cause Hemolyic-Uremic syndrome as Shigella can. Also causes mild diarrhea and hemorrhagic colitis (afebrile, bloody diarrhea, few leukocytes in stool)

Enteroinvasive E. Coli: Like a less virulent shigella, invades into the intestinal mucosa and causes necrosis and inflammation. Clinical manifestation similar to shigella, simply lacking the HUS

Enteropathogenic E. Coli: Similar to EHEC, will form pedestal on cells, but lacks the toxin. Causes diarrhea with mucus but little to no blood, malaise, vomiting, fever, and childhood diarrhea

Enterotoxigenic E. Coli: Produces cholera-likke heat labile toxin and heat stable toxin (stimulates the secretion of Cl- and bicarb into the intestinal lumen), causes afebrile watery diarrhea. Coined as Traveler’s Diarrhea

Enteroaggregative E. Coli: Not much is known about these bacteria, but form a “stack brick” like colonization via aggressive adherence fimbriae, producing water diarrhea, vomiting, nausea, fever, and chills.

Question 45

What are the major extracellular gut microbes?

Answer 45

Enterohemorrhagic, Enteropathogenic, Enteroinvasive, and Enterotoxigenic E. Coli , Vibrio cholerae (cholera toxin), Campylobacter jejuni, Helicobacter pylori (in the stomach), and Clostridium difficile

These al resist acid and antimicrobial mechanisms of the gut (acid resistance correlates to LD because of how many make it through the stomach), resist mucous clearance and adhere to the epithelium, and compete with normal gut flora. Motility and adhesive pili are common features and generally transmit via fecal-oral route. Resistance is mediated by humoral response (secretory IgA)

Question 46

What are the major intracellular pathogens? What are the two different methods they adopt for intracellular habitation?

Answer 46

Listeria, Shigella, EIEC (enteroinvasic Escherichia coli), Rickettsia rickettsiae are intracellular pathogens that reside in the cytoplasm. To accomplish this, they must be able to invade host cells and lyse the endosome. They generally have actin-based motility that facilitate cell-to-cell spread (except for enteroinvasive E. coli). Normally dealt with by cell-mediated immunity

Salmonella, Mycobacterium tuberculosis, Chlamydiae, Legionella pneumophil and Brucella take advantage of host vacuoles and phagosomes. They often utilize Sec type III/IV to alter host physiology to prevent lysosome-phagosome fusion, making it a friendly niche. Some of these parasites can disseminate via the RES

Question 47

What are the major respiratory or nasopharyngeal pathogens?

Answer 47

Bordetella pertussis, Neisseria meningitidis, Strep pneumo, Haemophilus influenzae, Mycoplasma pneumoniae, Corynebacterium diptheriae are the major ones, however Pseudomonas aeruginosa, Staph, and strep can also be found there because they colonize many sites

Similar to gut microbes, these have to be able to adhere to epithelium and resist mucous clearance. Also, many have no significant environmental niche outside of humans, thus relying on human to human spread (Pertussis, H. influenzae, Strep pneumo, diptheria, and neisseria ). Lastly, resistance to humoral response based largely on IgA proteases (pneumococcus, H. influenzae, and Neisseria meningitidis)

Question 48

What are the only two shapes Gram Positive bacteria adopt (clinically)?

Answer 48

Gram positives can be divided into cocci or rods. The cocci are Staph and Strep whereas the rods are the clostridia, diphtheria, listeria, Bacillus anthracis

Question 49

What are the two pyogenic organisms?

Answer 49

Staphylcoccus aureus and the Streptococci (GAS, GBS, enterococcus, Viridans, Pneumococcus)

Pus is caused it suppurative diseases and is composed of dead neutrophils and bacteria

Question 50

What are the two types of Neisseria? What is their distinguishing structural/functional basis?

Answer 50

The two types of Nesseria are N. meningitidis and N. gonorrhoeae. These are the only Gram negative diplococci which we’ve discussed

Between the two, Gonococci are not maltose fermenters whereas meningitidis is, and meningitidis is encapsulated

Question 51

What is structurally unique about spirochetes? Functionally?

Answer 51

Spirochetes (Borrelia burgdoreferi and Treponema pallidum) are like Gram negative (stain this way) however structurally they lack LPS, thus why we classify them separately

Functionally, these are HIGHLY motile bacteria that are characterized by causing disease with a LOW BACTERIAL LOAD, triggering inflammation due to their lipoproteins

Often times will not be cleared in spite of vigorous immune resposes

Question 52

Which pathogens are extracellular pathogens that can be disseminated/invasive?

Answer 52

There are varying degrees of invasiveness, so we’ll categorize them as common, sometimes (most opportunistic), and rarely/never

Common: Treponema pallidum (syphylis), Borrelia burgdorferi (Lyme Disease, makes sense because does the same thing in the tick), and Listeria monocytogenes

Sometimes: Pseudomonas, N. meningitidis, pneumococcus, Haemophilus, S. aureus, GAS, campylobacter (C. fetus specifically), Clostridium perfringens

Rarely/never: Mycoplasma, Diptheria, Pertussis, EHEC, EPEC, ETEC, Vibrio cholerae, Helicobacter pylori, Clostridium difficile

Question 53

Yersinia pestis

Answer 53

THE BLACK PLAGUE. Gram negative coccobacillus that is often carried by fleas on rodents (can also be spread via aerosols)

Virulence factors: Type III secretion, complement resistance, iron acquisition, capsule, and the production of a protease with plasminogen activator activity that enhances its invasiveness and prevents accumulation of inflammatory cells around the foci of infection

Clinical presentation: Bubonic plague (grossly swollen lymph nodes or Bubos and full-blown gram - sepsis), Septicemic plague (sepsis without bubo formation), pneumonic plague (fulminant pneumonia and septicemia) Depends on the area of exposure for disease.

Used in biological warfare (AB resistant strains and increases to virulence)

Treatment with aminoglycosides, tetracyclines