Microbio Flashcards

1
Q

What are symptoms of schistosoma mansoni/japonicum? hematobium? How do you treat it?

A

Mansoni/japonicum = intestinal schistomiasis = liver hypertension = hepatosplenomegaly

Hematobium = urinary schistomiasis = hematuria + bladder inflammation + bladder calcifications

Diagnosis = eggs in either urine (hematobium) or stool (mansoni/japonicum) Treatment = praziquantel

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2
Q

What is taenia solium and taenia saginata? What kinds of symptoms do they cause in humans? What is human cystercosis?

A

Taenia solium = pork tapeworm Taenia saginata = beef tapeworm May be asymptomatic if the adult worm (definitive host) attaches in the intestines. Treat with praziquantel. If the egg/cyst (accidental host) forms in brain, causes neurocystercosis which can lead to deficits. Treat with surgery or albendazole. Definitive host = eating pork/beef infected with the tape worm Accidental host = eating something infected with proglottids from human infected (feces)

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3
Q

What are diphyllobothrum Latum? Sypmtoms? Treatment?

A

Fish tapeworm Fish tapeworm can grow up to 25m and has an affinity to B12. Symptoms include diarrhea, fatigue, B12 deficiency Treat with praziquantel

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4
Q

What are echinococcus?

A

Dog tapeworm which can form cysts (accidental host). Lifecycle = infect sheep viscera -> dog eats infected sheep -> human eat infected dog feces -> cyst forms If human were to eat infected sheep viscera, it would cause a definitive host infection -> dog tape worm infection and NOT cyst infection. The cyst typically forms in the liver and is asymptomatic initially. As it grows in size, may cause inflammation/calcifications to form. Needs to be surgically removed.

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5
Q

What is ascaris lumbarcoides?

A

Roundworm that infects humans. Mature into foot long worms that can be noticed in human stool. Causes Loeffler’s syndrome when the larvae of ascaris lumbarcoides infects lung tissue. May cause bowel obstruction (typically in kids) if they have ingested a large amount of eggs.

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6
Q

What is Trichuris Trichiura?

A

Whipworm

May cause the intestinal mucosa to be inflamed and lead to dysentery with very heavy infections

Treat with albendazol

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7
Q

What is Enterobius Vermicularis?

A

Pinworm Cause itching of the anus (typically in little kids) Itching caused by worms laying eggs on the anus Otherwise, non symptomatic. Diagnose with scotch tape test (use double sided scotch tape to catch pin worm eggs Treat with albendazole

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8
Q

What causes cystercicocis?

A

Taenia solium via accidental host infection (ingestion of eggs)

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9
Q

What are hookworms? What are some symptoms? How do they infect you?

A

Hookworms are worms that can infect humans by burrowing into the skin of the foot, traveling via circulation to the lungs and ultimately nest in the GI tract. Common in areas of poor sanitation since infection is from human feces.

Species: Ancylostoma duodenale

Symptoms include anemia, Loefflers syndrome, eosinophilia, inflammation Treat with albendazole

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10
Q

What is strongyloides stercoralis? Signs/symptoms?

A

Loeffler’s syndrome. Hyperinfection due to immune supression. Polymicrobial bacteremia. Unexplained eosinophilia.

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11
Q

What bacteria causes lyme disease?

A

Borellia Burgdorferi

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12
Q

What bacteria causes syphillis? What are the stages of syphillis?

A

Treponema Pallidum

Stage 1: Chancer sore on genitalia

Stage 2: Rash on hands and feet + lymphadenopathy

Stage 3: Diffuse systemic infection (many presentations)

Treat with penicillin

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13
Q

What is MacConkey’s agar used for?

A

Selective for gram negative bacteria and changes different colors based on lactose fermentation. Pink = lactose fermenting

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14
Q

Describe Mycobacterium tubercolosis?

A

Strict aerobe

Facultative Intracellular

TB is inhaled from aerosols coughed up by infected person -> bacteria take up residence in alveolar macrophage -> survive in phagosome by inhibiting fusion of lysosome with phagosome

Usually can be controlled by immune response

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15
Q

What are some risk factors for latent TB reactivation?

A

HIV infection, old age, alcohol use, drug use, immunosuppression etc.

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16
Q

Describe the histopathology of mycobacterium tuberculosis

A

Additional macrophages recruited to the site of infection

Macrophages morph into multinucleated giant cells

Lymphcytes recruited to site of infection -> lymphocytes surround macrophages

Fibrous tissue form arround macrophages and create granuloma. Macrophages release toxins trying to kill bacteria but end up damaging near by cells. This is called casseating necrosis. If the granuloma ruptures -> release of mycobacterium -> patient coughs -> spread of bacteria

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17
Q

What are clinical symptoms of TB?

A

Fever, night sweats, weight loss, upper lobe pulmonary lesions

Pulmonary TB -> cavities or infiltrates are often seen in the apex of the lung

Extrapulmonary TB -> can occur in any organ (systemic infection)

Pott’s disease -> infection of the veterbrae

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18
Q

What are the treatments for mycobacterium tuberculosis?

A

Active infection = RIPE - Rifampin, Isoniazid, Pyrazinamide, Ethambutol

Prophylaxis - Rifampin + Isoniazid

Isolate the sick to prevent spread

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19
Q

Which bacteria causes Rocky Mountain spotted fever? What are the sigsn and symptoms associated with RMSF?

A

Rickettsia Rickettsii

Fever headache rash

Transmitted by tick bite

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20
Q

Which bacteria is associated with Q fever? Signs and symptoms? Common method of transmission?

A

Coxiella Burnetti causes Q fever.

Obligate intracellular

May also be transmitted by tick bite

The bacteria is common in some animals (i.e. cats, sheep etc.) and is particularly abundnat in the placenta of animals. Thus, when animals give birth, they may expose nearby humans to aerosolized droplets containing coxiella bacteria.

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21
Q

Which bacterria is typically associated with cat scratch disease? What are the signs and symptoms?

A

Bartonella Henselae

Leads to enlargement of lymph nodes near area where cat scratch occurred

Bartonella quintana -> transmitted by lice and typically is found in homeless individuals

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22
Q

What are the signs and symptoms of lyme disease? What bacteria is associated with lyme disease?

A

Erythema migrans (bullseye rash)

May lead to cardiac manifestation in stage 2 of infection (arrythmias)

Stage 3 -> migrating polyarrthritis of the joints

Bacteria -> borrelia burdorferi

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23
Q

What are the signs and symptoms of syphillis? What bacteria cause it? How do you treat it?

A

STD casued by treponema pallidum

Spirochete - gram negative

Three stages of syphillis:

1) Cankur sore (ulcerative lesion) on genitals
2) Rash on hands and feet
3) Tertiary syphillis manifests for patients who do not get treatment -> causes damage to brain, heart, eyes, liver, vessels etc.

Treat with penicillin

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24
Q

What are the signs and symptoms of leptospira interrogans?

A

Aerobic spriochete

Transmitted after exposure to water contaminated with animal urine with the bacteria in it

Symptoms: Initially - fever chills headaches

As bacteria disseminates in blood stream -> recurrence of sypmtoms + meningitis, conjunctivits, etc.

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25
Q

Answer the MCQ

Bonus: What are the mechanisms for the other drugs?

A

The answer is TMP-SMX (both inhibit metabolism of folate)

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26
Q

What is red man syndrome associated with?

A

Vancomycin infusion

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27
Q

What kind of allergy is associated with beta lactams? (i.e. penicillins, carbapenams, monobactams, cephalosporins?)

A

IgE mediated allergy

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28
Q

What allergy is associated with fluorquinalones (i.e. ciprofloxacin)

A

Tedinopathy (weakness of tendons such as achilles tendon)

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29
Q

What organism is associaed with chagas fever?

A

Trypanosoma cruzi - antigenic variation of surface glycoproteins

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30
Q

What structures are unique to Gram positive bacteria compared to Gram-negative bacteria and vice versa?

A

Gram-positive: a very thick peptidoglycan layer, teichoic lipoteichoic acid; Purple on gram stain

Gram-negative: outer membrane, periplasm, thin peptidoglycan layer, LPS (endotoxin); Pink on gram stain

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31
Q

What is the significance of having a second (outer) membrane in Gram-negative bacteria?

A

Periplasm is created; Very thin cell wall located in between two membranes; many antibiotics must penetrate two lipid layers instead of one if they are to be active; the outer membrane contains LPS, which leads to hypotension, shock, and multiorgan failure.

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32
Q

Which of the following allows some gram-negative bacteria to be serum-resistant?

A. lipid A;

B. teichoic acid;

C. peptidoglycan;

D. periplasm;

E. O-antigen

A

Long O-side chains are protective against complement-mediated lysis and cause the bacteria to be serum resistant.

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33
Q

What are the compoenents of LPS?

A

LPS is made of three parts:

1) Lipid A
2) Polysaccharide Core
3) O Antigen

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34
Q

What is the role of siderophores?

A

The amount of free iron in human serum, tissue fluids, and mucous secretions is far too low for bacterial growth, because most extracellular iron is tightly bound to the host proteins transferrin or lactoferrin. Many bacteria that colonize and infect humans have been shown to secrete low molecular weight molecules, siderophores, which remove iron from these host molecules and allow it to be taken up by the bacterial cells

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35
Q

What is the oxidase test testing for?

A

Certain bacteria (such as Pseudomonas aeruginosa and Neisseria spp., but not Escherichia coli) contain electron transport chains with a specific type of cytochrome, called cytochrome c. This cytochrome can be detected by using an “oxidase” test, which measures the ability of bacteria to oxidize and therefore change the color of N,N-dimethyl-p-phenylenediamine. Bacteria containing cytochrome c are said to be “oxidase positive.”

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36
Q

What is the role of superoxide dismutase and catalase?

A

Although oxygen itself is only mildly toxic, it gives rise to two very reactive and toxic substances, hydrogen peroxide (H2O2) and superoxide anion (O2-). Superoxide is degraded by an enzyme called superoxide dismutase:

2O2- + 2H+ —> H2O2 + O2

Hydrogen peroxide may then be degraded to water and oxygen by an enzyme named catalase:

H2O2 + H2O2 —> 2H2O + O2

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37
Q

Define transformation, transduction, and conjugation

A

Transformation - Pieces of naked DNA, released into the environment by lysed bacterial cells, are taken up and incorporated into the chromosome of other bacterial cells.

Transduction - Bacteriophages (viruses that infect bacteria) act as vectors to introduce DNA from donor bacteria into recipient bacteria by infection

Conjugation - Cell-to-cell contact between two cells leads to the unidirectional transfer of genetic material from a donor to a recipient cell using sex pilus

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38
Q

What is a virulent phage?

A

These phage cause the host bacterium to lyse (“lytic infection”) as a consequence of the synthesis of many new virions within the infected cell.

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39
Q

What is a temperate phage?

A

These phage may cause either a lytic infection or a lysogenic infection, which is a quiescent infection in which the bacterium continues to grow and divide but passes the phage (now called a “prophage”) onto its progeny. Prophage DNA is often integrated into the host bacterium’s chromosome but may be induced to produce phage in a process similar to a lytic infection when the bacterium is stressed. Some temperate phages have acquired genes that are unrelated to phage processes but change the characteristics of the bacterium. Infection of a bacterium with such a phage may result in what is called “phage conversion”; the host bacterium acquires new properties, some of which may be important in virulence.

40
Q

Which of the following kinds of bacteria would NOT be expected to contain superoxide dismutase and catalase?

A. obligate aerobe;

B. obligate anaerobe;

C. facultative anaerobe;

D. aerotolerant anaerobe.

A

A. obligate aerobe;

B. obligate anaerobe;

C. facultative anaerobe;

D. aerotolerant anaerobe.

Obligate anaerobe -> can’t survive in oxygen rich setting -> does not have superoxide dismutase to get rid of oxygen radicals

41
Q

What are some features of staphylococci spp.?

A

Gram positive cocci that grow in grape like clusters

Key medically related staph: Staphylococcus aureus, S. epidermidis, and S. saprophyticus

42
Q

What are some key features of Staph epidermidis?

A

Gram positive cocci that grows normally on skin/nose.

Commonly infects prosthetic devices + IV catheters

Facultative anaerobe

Key test: Coagulase negative

43
Q

What are some key features of Staph aureus?

Signs and symptoms?

Toxins?

A

Gram + cocci - facultative organism

Beta hemolytic

Key distinguisher: Coagulase + and Catalase +

Appears gold on plates (hence name aureus)

Signs and symptoms:

  • Joint and bone infections -> septic arthritis
  • Rapid onset endocarditis (IV drug users + tricuspid valve)
  • Toxic shock syndrome
  • Staphylococcal food poisoning (common in mayo/custard/meats that have been left out) -> rapid onset vomitting
  • Scalded skin syndrome
  • Skin and soft tissue infections (abcesses + cellulitis)
  • pneumonia -> patchy infiltrate
  • S. aureus is a frequent cause of nosocomial infections

Toxins:

Main virulence factor: protein A

  • proteins A binds the FC portion of IgG, preventing complement activation and opsonization of bacteria

Toxic shock syndrome toxin 1 (TSST-1):

  • causes toxic shock syndrome without bacteremia. S. aureus may produce toxin at an isolated site such as infected wound (sutures) or during menstration.

Staphylococcal enterotoxins A-E, G-I:

  • Cause staphylococcal food poisoning and toxic shock syndrome.

Exfoliatin:

  • Causes scalded skin syndrome by disrupting junctions between endothelial cells
44
Q

What are superantigens and how do they function?

A

Super antigens are a class of antigens that cause massive immune response. Specifically, they cause a nonspecific activation of T-cells by binding nonspecifically to MHC2 + CD4+ T-cell receptors -> leading to massive cytokine release

Results in fever, shock, and organ failure

45
Q

What is hemolysin?

A

Hemolysin is a factor that causes the lysis of red blood cells when the bacteria are grown on blood agar plates.

46
Q

How is MRSA resistant to penicillin?

A

variant penicillin-binding protein called PBP2’ (encoded by the mecA gene) that does not bind other beta-lactam antibiotics

Thus, need to treat with vancomycin or linezolid

47
Q

Which streptococci are alpha hemolytic?

beta hemolytic?

A

alpha - viridians, pneumoniae

partial hemolysis with greenish tint

beta - pyogenes, agalactiae

complete, clear hemolysis

48
Q

What are the clinical manifestations of strep pneumo?

A

Gram + diplococci

Catalase negative

Virulence factor: pneumolysin: degrades hemoglobin to a green pigment (therefore alpha hemolytic)

common cause of community acquired pneumonia

49
Q

What are the clinical manifestations of strep pyogenes?

A

Gram + cocci

Encapsulated -> made of hylauronic acid

catalase - and coagulase -

pyogenic (pus forming)

beta hemolytic

bacitracin sensitive

Diagnose: Anti-streptolysin-O titer, MALDI TOF, culture

Clinical manifestations:

  • Streptococcal pharyngitis
  • Scarlet fever -> Strawberry tongue + widespread face-sparing rash
  • Streptococcal toxic shock syndrome (STSS)
  • Skin and Soft Tissue Infections
    • Impetigo (pustular vesicle) -> honey crusted
    • cellulitis + erysiplas
  • Necrotizing fasciitis
    • skin becomes dusky and large blisters may form at surface
  • sequelae
    • Poststreptococcal glomerulonephritis -> 2 weeks after strep pharyngitis or supercial infection ->facial edema and cola colored urine
    • Acute rheumatic fever (JONES) -> only after pharyngitis

Virulence factor:

  • streptolysin S (oxygen stable) and streptolysin O (oxygen labile)
    • forms pores in the plasma membranes of human cells
    • repsonsible for beta hemolysis
  • M-protein -> molecular mimicry with myosin in heart -> endocarditis (mitral valve)
    • Fibrillar molecules that extend out beyond the surface of the bacterium; anchored in the peptidoglycan of the cell wall.
    • Used to serotype S. pyogenes.
    • Plays a role in preventing phagocytosis.
  • Streptococcal pyrogenic exotoxins (SPEs)
    • 3 major types (SPE A, SPE B, SPE C)
    • A and C are super antigens that may be responsible for scarlet fever
    • SPE B is protease which causes necrotizing fasciaitis
  • Streptokinase:
    • Causes lysis of fibrin clots by converting plasminogen to plasmin, which allows the bacteria to disseminate widely
  • C5a peptidase
    • cleaves C5a complement protein -> prevents activation of neutrophils /monocytes
50
Q

What does protein A do? Which bacteria uses it?

A

Protein A is found on staph aureus and it is a key mechanism it uses to avoid the immune system. Protein A binds to the FC portion of IgG, preventing immune system /complement activation/opsonization

51
Q

What is the role of c5a peptidase?

A

Strep pyogenes uses c5a petidase to cleave the complement protein c5a -> c5a responsible for recruiting phagocytes -> therefore no c5a -> no phagocytes

52
Q

How would you treat a strep pyogenes infection?

A
  • Strep pyogenes remains sensitive to pencillin
  • Cephalosporins and macrolides are recommended as alternatives, but resistance is increasing.
  • No vaccine is currently available.
53
Q

What are the signs/symptoms of trypanosoma cruzi infection

A

Sketchy -> Argentinian gas station

What: Parasite carried by kissing bug

Where: Commonly found in South america

How: Kissing bug bites you, and parasite is carried in its poop

LIfe cycle: Vector -> trypanomastigote

Bloodstream -> trypanomastigote

Intracellular (like in heart muscle) -> mastigote

Key symptoms: Megacolon, megaesophagus, Cardiomyopathy

54
Q

What are the signs and symptoms of aspergilosis?

A

Acute angle septated hyphae

Pneuomnia -> fungus balls in lungs of immunosuppressed

Treat with voriconazole

55
Q

Describe Listeria monocytogenes?

Vector of transmission

Signs and symptoms?

A

Sketchy = santa claus

Gram +

Catalase +

Facultative intracellular organism

Grows well at low temperatures

Foodborne transmission via unpasteurized milk products

  • Asymptomatic or influenza-like illness in pregnant women but can cause abortion, premature delivery, or bacteremia.
  • Neonatal disease. Early onset disease is acquired by transmission across the placenta from infected mother and is characterized by formation of disseminated abscesses and granulomas. Late onset disease acquire shortly after birth can cause meningitis.
  • Elderly or immunocompromised adults can develop meningitis.

Treat with : Ampicillin or Bactrim (TMP-SMX)

56
Q

Signs and symptoms of Corynebacterium diphtheriae?

  • Diagnosis?*
  • Treatment?*
  • Toxicity?*
A

aerobic Gram-positive bacilli

“club-shape” called the “coryneform”

**Despite immunization: C. diptheriae is maintained in human by asymptomatic carriage in immune humans.

Toxin: Diphtheria toxin (DT): A-B toxin -> ADP-ribosylating EF-2

Symtpoms:

  • Thick, grey adherent pseudomembrane ia a prominent indicator of diphtheria.
  • Cardiac arrthymia as toxin may enter circulation and damage heart tissue
  • skin infections following inoculation into abrasions or wounds

Culture:

  • Shows gram + bacteria that tend to lie in acute angles (chinese character)
  • Also grows on special medium called tellurite

Vaccine:

  • dTAP -> d = diphtheria and it is a toxoid vaccine

Treatment:

  • Horse antisera against DT
57
Q

What are examples of A-B toxins?

A

Diphtheria toxin - ADP riboslyates EF2 -> inhibits protein synthesis

Pertusis toxin - Increases levels of cAMP

Bacillis Anthracis - EF -> cutaneous anthrax LF -> lethal factor (pulmonary hemmorhage)

Tetanus toxin -> cleave snare proteins associated with glycine and GABA -> inhibits inhibitory neurotransmitter signaling

Botulinum toxin -> cleave snare proteins associated with Ach -> causes flaccid paralysis

58
Q

Which of the following is NOT a virulence factor of Listeria monocytogenes?

A. internalin;

B. ActA;

C. listeriolysin O;

D. edema factor

A

Which of the following is NOT a virulence factor of Listeria monocytogenes?

A. internalin; -> helps listeria enter cells

B. ActA; -> helps listeria move around cell and create protusions in the cell membrane

C. listeriolysin O; - lyses vacuoles where listeria is trapped in

D. edema factor

59
Q

Signs and symptoms of tetanus infection?

A

Gram + Anaerobe Rods (all clostridium)

Puncture wounds assocaited with tetanus spores

Symtpoms:

  • Lockjaw
  • Muscle spasms in response to minor stimuli
  • hypertension, tachycardia, arrhythmia, sweating and vasoconstriction

Diagnosis:

  • The diagnosis of tetanus is based upon consistent clinical findings.
  • Demonstration of tetanus toxin production is necessary for definitive identification of the organism.

Tetanus Toxin:

  • Tetanus toxin (also called tetanospasmin): An A-B toxin.
  • B chain mediates binding to cell receptors of inhibitory motor neurons in the spinal cord.
  • A chain a protease that cleaves proteins in the neuronal synapses resulting in blockade of the release of neurotransmitters.

Treatment:

  • Human tetanus immunoglobulin (IgG) is given to neutralize unbound tetanus toxin.
  • Boosters to tetanus toxin are given post tetani exposure
60
Q

Signs and symptoms of c. botulinum?

Toxin?

Diagnosis?

Treatment?

A

Gram + anaerobe bacilli

May be found in canned foods that were not properly treated or in honey (bees may carry it with pollen)

Spores, which are resistant to boiling, survive the canning process and subsequently germinate in the anaerobic environment of the sealed food container

Toxin:

  • Botulinum toxin, which is homologous to tetanus toxin, is also an A-B toxin and a protease
  • Toxin reaches cholinergic terminals at peripheral motor endplates, where it cleaves components of the neuroexocytosis apparatus. This blocks the release of acetylcholine and transmission of nerve impulses.

Symptoms:

  • Food-borne botulism: descending paralysis, diplopia, disarthria, dysphagia
  • Wound botulism: Occurs when a wound is contaminated with C. botulinum spores.
  • Infant botulism: C. botulinum colonizes the infant intestine, and toxin is produced and absorbed, leading to paralysis.

Treatment:

  • Treatment includes respiratory support and trivalent equine antitoxin.
61
Q

Signs and symptoms Actinomyces israelii?

A
  • Gram-positive bacilli anaerobic, nonspore-forming
  • Filamentous branching rod
  • Normal flora; found in the mouth, gastrointestinal tract, and female genital tract.
  • Key thing: Gram-stained sulfur granules

Determinants of Pathogenicity

  • Causes indolent, suppurative infections with fistulas and sulfur granules.
  • Once established, infected foci spread contiguously, often ignoring tissue planes.

Potentail Causes

  • Poor dentition or trauma leads to oral-cervicofacial disease

Diagnosis

  • Identification of the organism in Gram-stained sulfur granules
62
Q

Signs and symptoms of nocardia?

A

Sketchy -> Card game

Acid fast stain

Aerobic gram + filamentous branching rod

Catalase + -> CGD ( NADPH oxidase deficiency)

Urease +

Clincical manifestation:

  • Mainly infecting immunocompromised patients -> gluocorticoids, immunocompromised, HIV, elderly
  • Pulmonary: Pneumonia + cavitary lung abcess
  • CNS: Dissemination -> can form brain abscess
  • Cutaneous:

Treatment:

  • Trimethroprim/sulfamethoxazole and other sulfa drugs are the drugs of choice for Nocardia infections.
63
Q

Signs and symptoms of coxiella burnetti?

A

Gram - obligate intracellular bacteria

Forms spore like structure and exist in animal droppings, dirt -> aerosolized

Also very high concentration in animal placenta

NO RASH

Symptoms

  • Q fever -> pneomonia, headache, fever
  • Hepatitis

Treatment:

  • Self limiting
64
Q

What are some features of Enterobacteriaceae?

What are some examples of Enterobacteriaceae?

A

Gram-negative facultative anaerobic bacilli and coccobacilli

e.g. Salmonella spp., Shigella spp., and Yersinia spp., E. Coli

65
Q

Describe Bordetella Pertussis

Signs and symptoms?

Stages?

Transmission?

Toxins?

Treatment?

A

Gram Negative coccobacilli

Whooping cough

Toxins:

  • Adenylate Cyclase Toxin: Edema factor
  • Trachael Toxin: Part of peptidoglycan which binds to trachea and cleaves cilliated epithelium
  • Peterussis Toxin: AB toxin which inhibits G protein inhitibtor -> increases cAMP levels
  • Dermonecrotic toxin: may be responsible for localized tissue destruction in infection.

Trasnsmission:

  • Cough during catarrhal (mucus) stage

Stages:

  • Stage 1: Incubation
  • Stage 2: Catarrhal
  • Stage 3: Paroxysmal (sudden worsening of disease)

Treatment:

  • Macrolides
66
Q

Describe SARS-COV2 ?

Signs and symptoms?

Treatment?

Diagnosis?

A

Enveloped (+)ssRNA virus

mutation limited by proofreading exoribonuclease

Spike Protein

Symtpoms:

  • Respiratory failure - typically occurs in the second week of illness (day 8-11)
  • Venous thrombosis/thromboembolism
  • Cardiac injury (myocarditis)
  • Neurologic complications (headache, dizziness, encephalopathy, seizure
  • Muscle injury (rhabdomyolysis)
  • Acute kidney injury

Diagnosis:

  • PCR: 70%-85% sensitivity (nasopharyngeal swabs); highly specific
  • Antigen: rapid, inexpensive, lower sensitivity than PCR
  • Serology: antibody appears about day 10 after symptom onset; most patients seroconvert within the first 3 weeks; estimated sensitivity 90% and specificity 99.8%

Treatment:

  • remdesivir
  • potential vaccine
67
Q

How do you treat tapeworms?

A

Praziquantel

68
Q

How do you treat roundworms?

A

Pinworm/Whipworm/Hookworm = Albendazole

Strongyloides = Ivermectin +/- albendazole

Treatment: W. bancrofti, B. malayi, L. loa: diethylcarbamazine (DEC); O. volvulus: ivermectin

For filariasis - also treat with doxycycline for intracellular Wolbachia (W. bancrofti, B. malayi, O. volvulus, but NOT Loa loa)

69
Q

Describe the lifecycle of Trichinella spiralis?

A

widespread in wild mammals, wild and domestic pigs; human acquires parasite through

consumption of meat containing trichinella cysts

variable, depend on presence of larvae in striated muscles and organs, and on the parasite load (<10 larvae/gram muscle, subclinical; 50 to 500, moderate symptoms; >1000, severe symptoms); most common symptoms are orbital edema, muscle pain, respiratory distress, headache and generalized weakness; myocardial and central nervous system involvement also produces signs and symptoms

70
Q

Describe Trichuris trichiura

Signs and symptoms?

Infection vector?

Treatment?

A
  1. Morphology: adult worm 35-50 mm (female); egg barrel-shaped with mucoid plug, 50 mm long
  2. Epidemiology: fecal-oral transmission; mostly in young children; Asia, Africa, Latin America
  3. Disease properties: symptoms of infection uncommon; heavy infection, protein calorie malnutrition, rectal prolapse, inflammatory diarrhea
  4. Diagnosis made by demonstration of eggs in feces
  5. Treatment: albendazole
71
Q

Describe entabmoeba histolytica

Signs and symptoms?

Diagnosis?

Treatment?

A

Transmission:

  • Ingestion of cysts in contaminated water

Signs and symptoms:

  • Liver abscess -> anchovy paste consistency
  • Flask shape ulcers on intestines -> bloody diarrhea

Diagnosis: Stool O/P looking for cysts

Treatment: Metronidazole

Luminal agents to remove cysts in intestines - paramycin

72
Q

What grows pink on MacConkey’s agar?

A

Gram negative lactose fermenting bacteria

E-coli

Klebsiella

Serratia

Enterobacter

73
Q

Signs and symptoms of Klebsiella Pneumonia?

A

Clinical manifestations:

  • Nosocomial Pneumonia/UTI
  • Pulmonary cavitation/lesion on CXR (similar to TB infection)
  • 3As
    • alcoholics -> commonly found in alcoholics
    • abscesses -> commonly forms abscesses
    • aspiration -> commonly causes infection through aspiration

Diagnosis:

  • Culture on MacConkey’s agar will grow pink since Klebsiella is gram negative and ferments lactose (like ecoli, serratia, enterobacter)
  • Urease +

Treatment:

  • Need to treat with carbapenam because most likely it is multidrug resistant
74
Q

Signs and symptoms of leptospira ?

A

Spirochete​

Clinical Manifestations

  • Commonly found in animals and humans are infected after swimming in water infected by animal urine
  • Initially -> flu like symptoms (fever, headache etc.)
  • Inflammation of eye with no pus
  • Leptospirosis -> also known as Weil’s disease
  • May eventually cause jaundice and kidney damage
75
Q

What is leshmaniasis? What is the vector for leshmania? What are signs and symptoms?

A

Transmission:

Caused by several species of the genus Leishmania; vector is the sandfly (phlebotamine)

Epidemiology:

a. Visceral disease in Africa, India, Brazil
b. Cutaneous disease throughout Latin America, Middle East
c. Mucocutaneous disease in Latin America

Signs and symptoms:

  1. Visceral (kala azar): parasites in macrophages of reticuloendothelial system -hepatosplenomegaly, pancytopenia (may be misdiagnosed as lymphoma)
  2. Cutaneous: chronic, non-healing ulcer with heaped-up margins
  3. Mucocutaneous: occurs months to years after cutaneous infection with L. braziliensis; mutilating disease of cartilage
76
Q

What are risk factors for strongyloides stercoralis?

A

Rhabdidiform larvae penetrate skin of host -> poor sanitation is risk factor

77
Q

Describe toxoplasmosis gondii infection? What are risk factors? What are signs and symptoms?

A

Transmission:

Cats required to complete the life cycle, while humans and other mammals ingest the cysts through contact with infected cat feces or consumption of infected un- or under-cooked meat (especially lamb and beef).

Signs and symptoms:

Tropism for the CNS and skeletal muscles

Immunocompetent -> Cervical lymphadenopathy

Immunocompromised -> CNS infection -> behavioral changes which promote further toxoplasmosis transmission

Treatment: Pyrimethamine + sulfadiazine or clindamycin or atovaquone; alternative: trimethoprim-sulfa

78
Q

Describe African Sleeping sickness? What is it caused by? What is the vector of transmission?

A

Caused by Trypanosoma brucei

Vector: Tsetse fly

Pathogenesis: Variant surface glycoproteins (VSGs) – shield the parasite (covers 90% of the surface coat) and prevent the host immune system from accessing the plasma membrane or any other invariant surface epitopes.

Clinical manifestations result from high level of parasitemia in blood (up to 1,000,000,000/ml) and CSF

(meningoencephalitis)

a. East African sleeping sickness caused by T. b. rhodesiense (acute disease)¾abrupt onset of fever, headache, occipital lymphadenopathy (Winterbottom’s sign)
b. West African sleeping sickness caused by T. b. gambiense (subacute, chronic meningoencephalitis) subtle personality changes -> somnolence -> coma ->death

79
Q

How does the HIV virus enter host cell?

A
  • Binding of gp120 protein to CD4 receptor
  • Co-receptor necessary for membrane fusion:
    • CCR5 (early, macrophage tropic)
    • CXCR4 (late, T-cell tropic or syncitia-inducing strains)
80
Q

What are potential antiretroviral targets?

A

Integrase

Reverse transcriptase

Protease enzyme -> prevents activation of virus

CCR 5

CXCR 4

81
Q

Describe Dengue virus

A

+ ssRNA enveloped virus carried by Aedes mosquito

Uncomplicated fever -> breakbone fever

Complicated -> dengue hemorrhagic fever

Breakbone fever -> feel like bones are breaking

Dengue hemorrhagic fever -> bruising, bleeding everywhere

82
Q

Describe EColi

Signs and symtpoms of EHEC?

ETEC?

A

Gram negative

Encapsulated, Catalase +

Pink on MacConkey’s Agar (due to lactose fermentation)

#1 cause of UTI

Causes sepsis via LPS (all gram -)

EHEC: (O157:H7 antigen)

  • Commonly transmitted via undercooked meat
  • Causes bloody diarrhea
  • Toxin is shiga like toxin -> inhibit 60S ribosomal subunit
  • Toxin causes damage to endothelial cells in the glomerulus of kidney

ETEC: (traveler’s diarrhea)

  • HL toxin -> heat labile toxin -> increases cAMP
  • HS toxin -> heat stabile toxin -> increases cGMP
  • Water diarrhea
83
Q

Describe Rhinovirus

What are the signs and symptoms?

A

+ ssRNA unenveloped

Acid Labile

Picornavirus

Optimal temperature for replication: 32°C (corresponds to the temperature found in the nose and large airways)

Rarely cause lower respiratory tract disease (replicates poorly at 37°C)

Pathogenesis

Rapid onset of infection; virus adheres to surface receptors within 15 minutes of entering the respiratory tract; binds to ICAM-1(inter-cellular adhesion molecule 1) receptors on respiratory epithelial cells which mediate cellular entry; infected cells release chemokines and cytokines which activate inflammatory mediators; results in upper respiratory epithelial cell lysis.

  • Signs and symptoms:
  • Common cold
  • Cough, sneezing, rhinitis
  • Upper respiratory tract infection
84
Q

Describe HHV8

What are the signs and symptoms of HHV8?

A

dsDNA enveloped herpes family virus

associated with AIDs, immunosuppression, and kaposi sarcoma

Risk factors

  • Russian elderly men
  • HIV /AIDS
  • Endemic in africa

Signs and symptoms

  • Kaposi sarcoma -> causes lesions on mucus membranes, nose, extremeties, upper palate, and GI tract
  • Kaposi -> disregulation of VEGF -> causes uncontrolled angiogenesis
  • HHV8 can also infect Bcells and cause Primary effusionB cell lymphoma

Treatment:

if HIV positive, treat HIV -> reduces severity of kaposi

85
Q

Describe Norovirus

What are the signs and symptoms?

A

+ sense ssRNA unenveloped (fecal oral) virus

Calcivirus family

Highly contagious and highly stable. Not inactivated by alcohol or mild detergents (i.e. hand sanitizers).

Norovirus is the most common cause of acute gastroenteritis in the U.S.: 90% of epidemic non-bacterial gastroenteritis

Frequently causes large outbreaks within closed communities and in a variety of settings such as hospitals, nursing homes, schools, childcare centers, restaurants, cruise ships, and the military

Signs and Symptoms

Explosive Diarrhea

Gasteroenteritis

Diagnosis: PCR

Treatment: supportive

86
Q

Describe Rotavirus

What are signs and symptoms?

A

dsRNA

The virus is assembled as an unusual double-layered particle (DLP) in the cell cytosol. Outside cell, it becomes a TLP (triple layer particle).

Live attenuated viral vaccine available

Toxin:

NSP4 => promotes secretory diarrhea. The NSP4 protein has at least two functions. As an integral membrane protein, it is required for envelopment of the double-layered virus particle but then is removed concomitant with removal of the envelope and addition of the outer layer. A secreted fragment of NSP4 can bind to cell receptors that trigger the mobilization of intracellular calcium, stimulates anion movement across membranes, and causes fluid secretion into the intestinal lumen.

Treatment: Supportive

87
Q

Describe Parvovirus?

What are signs and symptoms?

A

non-enveloped - ssDNA

Slapped cheek disease (erythema infectiosum)

Common in kids and initially presents as flu like symptoms

88
Q

Describe parainfluenza virus

A

-ssRNA enveloped virus

PIV-1,PIV-2 = croup -inflammation of upper away leading to mucus buildup - distinct barking cough

PIV3 = bronchiolitis/pneumonia (worst)

PIV4 = mild infection/asymptomatic

89
Q
A
90
Q

How does a capsule help prevent complement activation?

A

Normally, C3b would bind and opsonize bacteria. However, capsule prevents that from happening -> decreasing amount of phagocytosis. Complement system therefore comes into play via classical pathway (via IgG/IgM)

“Capsules prevent desiccation in the environment and play a crucial role in the virulence of certain pathogens by preventing their engulfment by phagocytes. Capsules act primarily by preventing complement activation (via the alternate pathway) on the cell surface. The absence or a reduction in the amount of C3b bound to the bacterial cell surface reduces the ability of phagocytes to engulf these bacteria.”

Key encapsulated bacteria:

Streptococcus pneumoniae

Neisseria meningitidis

Haemophilus influenzae

91
Q

What is H antigen? O antigen? K antigen?

A

H antigen = flagella

O antigen = part of LPS

K antigen = Capsule

92
Q

Which ribosomal subunit is useful in identifying bacteria type?

A

Bacteria can be identified based on the16S rRNA gene sequence. Although the sequence of some regions of the 16S rRNA gene are common to all bacteria, others are unique to various bacterial genera and species. By using the polymerase chain reaction (PCR) with genus- or species-specific primers, it is now possible to identify bacteria in a very short period of time.

93
Q

How do most lymphocytes enter lymph nodes?

A

high endothelial venules

These venules are the primary site of entry of lymphocytes from other parts of the body. A lesser number of lymphocytes enter the node via the afferent lymphatic vessels.

94
Q

What are the determinants of pathogenicity for Nocardia?

A
  • Nocardia are able to neutralize oxidants, prevent phagosome acidification, and inhibit phagosome-lysosome fusion. Thus, while Nocardia lesions are extensively infiltrated with neutrophils, these cells are unable to efficiently kill the bacteria. Cell-mediated immunity is needed to control the infection.
  • Therefore, more commonly seen in individuals with deficient cell-mediated immunity (lymphoma, transplantation, AIDS).
95
Q
A