Microbiology: Module 9 Flashcards

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Chapters 21, 22
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Septicemia, Bacteremia, Toxemia

  1. What?
    1. Septicemia: any microbial blood infection producing illness.
      1. Lymphangitis: infection and inflammation of lymphatic vessels is a sign of septicemia
    2. Bacteremia: septicemia caused by bacteria
    3. Toxemia: bacteria remain at infection site; release toxins into blood
  2. Signs/Symptoms?- fever, chills, nausea, vomiting, diarrhea, malaise
    1. Septic shock: systemic inflammation = extremely low blood pressure from dilation of vessels
    2. Osteomyelitis: inflammation of the bones (if bacteria invade bones)
    3. Toxemia symptoms: Exotoxin= cytotoxins, neurotoxins; Endotoxin: cause fever, disseminated intravascular coagulation, damaged leaky blood vessels and inflammation lead to low blood pressure = shock
  3. Diagnosis?- signs/symptoms (only ~50% patients have bacteria cultured from blood)


  1. What?- fever, extreme fatigue, malaise, difficulty breathing, and tachycardia (fast heart rate); Inflammation of endocardium (lining inside heart) and vegetations (bulky mass of platelets/clotting to bury bacteria, hiding them from immune system and drugs); embolus (pieces of vegetation/clot) may break off and block vessels
  2. Who?- many bacteria, opportunistic, microbiota; “viridans streptococci” (green pigment in blood culture)= 1/2 infections
  3. Diagnosis?- visualize vegetations via echocardiogram; culture bacteria from blood


  1. What?- fluctuating fever strikes every afternoon; chills, sweating, headache, myalgia, and weight loss
  2. Who?- Brucella : nonmotile, g(-), coccobacilli, no capsule; endotoxin causes some signs/symptoms; intracellular in uterine, placental, and phagocytic cells
  3. How?- contaminated dairy products, animal blood, urine, or placentas; invades through breaks in mucous membrane and travels via phagocytes
  4. Diagnosis?- serological (Ab) test;
  5. Treatment?- usually no treatment needed; attenuated vaccine for animals only


  1. What?- skin lesions, swollen lymph nodes @ infection site; then ascending lymphangitis; general manifestations can last months/years
  2. Who?- Francisella : small, nonmotile, obligate aerobe, g(-) coccobacillus, capsule blocks phagocytosis, endotoxin causes many symptoms; can survive phagocytosis by blocking fusion of lysosome to phagosome; has beta-lactamase
  3. How?- via tick bite or contact w/infected animals; small, can enter microabrasions; contact w/dead animals= highest risk
  4. Diagnosis?- difficult, general symptoms, serological test needed which can take weeks to get results
  5. Treatment?- Abx; vaccine for high risk people


  1. Bubonic plague: enlarged lymph nodes called buboes suddenly appear; then tissue death, subsequent gangrene (Clostridium) ; Pneumonic plague: bacterium inhaled or spreads to lungs from blood; develops rapidly (hours)
  2. Who?- Yersinia pestis : g(-) bacillus with capsule; virulence factors= adhesins, capsule, T3SS (antiphagocytic proteins block adaptive immune response)
  3. How?- bubonic: forms biofilm in flea esophagus, starving flea rapidly spreads; endemic in rodents, other mammals = amplifying hosts; contact w/flea feces and infected animals can spread; untreated = 50% fatal <week. Pneumonic: aerosols/ sputum spread, up to 100% fatal
  4. Diagnosis?- symptoms (can be nonspecific)
  5. Treatment?- Abx, rodent/flea control, good hygiene

Lyme Disease

  1. What?- three phases in untreated: bulls-eye rash, neurological symptoms (ie. meningitis), and severe arthritis (caused by immune response) that can last years; rarely fatal
  2. Who?- Borrelia - g(-) large spirochete; uses manganese instead of iron for metabolism, alters membrane proteins= evades defenses; dies=endotoxin
  3. How?- via deer tick, needs to be attached 36-48 hrs to infect w/enough bacteria; people moving to woodland areas and protected deer populations = infection rates going up
  4. Diagnosis?- signs/symptoms; bacterium rarely detected, serological for Ab needed
  5. Treatment?- early phase = Abx; late phase = difficult b/c immune system causing most symptoms

Mononucleosis (Kissing disease; Mono)

  1. What?- sever sore throat, fever; then swollen lymph nodes, fatigue, appetite loss. Immune system against infected B cells
  2. Who?- Epstein-Barr Virus (EBV, HHV-4): Nveloped dsDNA virus, icosahedral capsid; established latent infection replicating in nucleus; suppresses B-cell apoptosis; can lead to burkitt’s lymphoma and other cancers in certain parts of the world
  3. How?- via saliva; infects B cells which must be killed by cyto-T cells; majority of adults have Ab against EBV
  4. Diagnosis?- presence of large, lobed B-cells and neutropenia (neutrophil deficiency)
  5. Treatment?- relieve symptoms; too widespread to prevent

CMV Disease

  1. What?- most asymptomatic; in fetus, newborn, immunocompromised causes hepatomegaly, splenomegaly, jaundice, anemia; may be teratogen
  2. Who?- Cytomegalovirus (CMV): a herpesvirus, infects early in life and remains latent until immunocompromised
  3. How?- via bodily secretions: STD, in utero, transfusions; 50-100% adults
  4. Diagnosis?- signs (enlarged cells, etc)
  5. Treatment?- Fomivirsen (RNAi drug) stops spread; doesn’t cure

Yellow Fever

  1. What?- 3 stages: fever, headache, muscle aches; then remission period; then delirium, seizures, coma, hemorrhaging
  2. Who?- yellow fever virus (a flavivirus ): enveloped ssRNA(+), icosahedral capsid; Aedes mosquito vector; monkey reservoir
  3. How?- via Aedes bite; travels to liver to replicate; today in South America and Africa; hasn’t returned to US; 20% mortality rate
  4. Diagnosis?- detect viral Ag in blood
  5. Treatment?- supportive care, vaccine available, mosquito control

Dengue Fever

  1. What?- DF two stages: fever, edema, head and muscle pain; then fever returns and red rash. Dengue hemorrhagic fever (DHF): internal bleeding, shock, possibly death= severe hyperimmune response to second viral infection
  2. Who?- Dengue viruses 1, 2, 3, and 4 (flavivirus): enveloped ssRNA(+), icosahedral capsid
  3. How?- Aedes bite, infects monocytes, 1st infection mild, 2nd severe
  4. Diagnosis?- signs/symptoms of people who travel to endemic area; coming back in Florida and Texas
  5. Treatment?- control mosquitoes; vaccine would be bad if it can’t stop hemorrhagic fever once Ab recognize it

African Viral Hemorrhagic Fever

  1. What?- fever, fatigue, dizziness, muscle pain, exhaustion; then minor capillary hemorrhaging (petechiae); finally severe internal hemorrhaging, bleeding from orifices; death from shock, seizures, or kidney failure
  2. Who?- Ebolavirus and Marburgvirus : ssRNA(-), filamentous capsid; infected macrophages induce localized blood clotting, depletes clotting proteins = susceptible to massive bleeding
  3. How?- contact of bodily fluids of infected person; possible bat vector; no carrier state; mostly found in Africa
  4. Diagnosis?- symptoms and finding virus in blood
  5. Treatment?- fluid/electrolyte replacement; possible vaccines being studied


  1. What?- fevers, chills on 2-3 day cycle correlating to cell lysis; anemia, fatigue, weakness
  2. Who?- Plasmodium , 4 species, P. falciparum most severe, P. vivax also common; vector is Anopheles mosquito; Lifecycle; Virulence factors on guide if time available
  3. How?- P. falciparum most severe because adhesins making RBCs stick to capillary walls block blood flow = hemorrhaging and tissue death;
  4. Diagnosis?- Identify Plasmodium in blood
  5. Treatment?- species dependent, many resist chloroquine; heterogenous sickle cell trait = resistance; Duffy resists P. vivax


  1. What?- most asymptomatic; poor immunity = fever, malaise, inflammation of lungs, liver, and heart; Contraction during pregnancy bad
  2. Who?- Toxoplasma gondii : cats definitive hosts; apicomplexan
  3. How?- ingest oocysts from contaminated food, cat fecal matter on hands; pseudocysts ingested from undercooked meat;
  4. Diagnosis?- detect in tissues
  5. Treatment?- only with immunocompromised and pregnant; sulfonamides

Chagas’ Disease

  1. What?- swelling, nonspecific symptoms; chronic manifestations many years after infection leading to heart failure
  2. Who?- Trypanosoma cruzi : endemic in south and central America; Triatoma is vector; circulates in bloods with intracellular stage in macrophages and heart muscle cells
  3. How?- Triatoma feces rubbed into bite; a leading cause of death in Latin America
  4. Diagnosis?- identify trypanosomes microscopically; xenodiagnosis (sterile bug takes blood meal, dissect bug a month later)
  5. Treatment?- can only treat early stage (only 1% develop early symptoms)


  1. What?- parasitic blood fluke (very common); transient dermatitis due to larval burrowing; eggs in other parts of body can calcify and cause renal failure, heart failure, bladder obstruction, death
  2. Who?- Schistosoma (blood fluke, 3 species): larvae from freshwater snails penetrate human skin, mature and breed in humans, eggs passed into environment via urine or feces, eggs hatch into a different larvae type that infects snails.
  3. How?- swim in ponds with infected snails; not in US
  4. Diagnosis?- identify spiny eggs in stool or urine sample;
  5. Treatment?- praziquantel drugs

Normal Microbiota of the respiratory system

Upper respiratory system only: Haemophilus , Veillonella , Staph. aureus , diphtheroids (harmless g(+) that resemble C. diphtheriae ), other g(-) cocci, and alpha-hemolytic streptococci including Strep. pneumoniae


Streptococcal Respiratory Diseases

  1. What?- sore throat, difficulty swallowing, can progress to scarlet or rheumatic fever
  2. Who?- group A strep- Strep. pyogenes : g(+) cocci, beta-hemolytic, many virulence factors; occurs when microbiota depleted, large inoculum introduced, or adaptive immunity impaired
  3. How?- respiratory droplets; often in winter or spring
  4. Diagnosis?- often confused with viral pharyngitis; streptococci in throat not diagnostic b/c normal part of pharynx microbiota; must verify species
  5. Treatment?- penicillin


  1. What?- sore throat, fever, oozing intracellular fluid thickens into thick pseudomembrane that can obstruct airways
  2. Who?- Corynebacterium diphtheriae : High G+C, pleomorphic; diphtheria toxin stops protein synthesis = cell death
  3. How?- respiratory droplets or skin contact with non-immunized (100,000s/yr to 2/yr today) or immunocompromised
  4. Diagnosis?- presence of pseudomembrane
  5. Treatment?- antitoxin and Abx; immunize!

Sinusitis and Otitis Media

  1. What?- sinusitis: pain and pressure in affected sinus (common in adults); otitis media: severe ear ache (common in kids)
  2. Who?- various microbiota (ie Strep. pneumoniae, Strep. pyogenes, Haemophilus, Moraxella, Staph. aureus)
  3. How?- bacteria in pharynx spread into sinuses via throat
  4. Diagnosis?- symptomatic
  5. Treatment?- penicillin; no prevention

Common Cold

  1. What?- sneezing, runny nose, congestion, malaise, sore throat, and cough; lasts ~week; usually no fever
  2. Who?- over 200+ strains; Rhinovirus most common cause: ssRNA+ naked polyhedral; attaches to ICAM-1 protein in nasal cavity cell cytoplasmic membranes; grows best at 33C and neutral pH; lytic; infected cells lose ciliary action, slough off, trigger inflammatory cytokines; stimulated nerves trigger mucus production and sneezing; localized inflammation = congestion
  3. How?- aerosols via sneezing/coughing, fomites, contact
  4. Diagnosis?- symptomatic
  5. Treatment?- symptom relief

Pneumococcal pneumonia

  1. lobar; 85% of pneumonia cases; short, rapid breathing; rust colored sputum; neutrophils in sputum
  2. Who?- Strep. pneumoniae : g(+); adhesins, capsule, and toxin pneumolysin (binds cholesterol in PM of ciliated cells, creates pores that lyses them; neutralizes lysosomes in phagocytes)
  3. How?- inhalation into (usually damaged) lungs; bacteria endocytosed by lung cells, replicate and lyse, damages lining which allows fluid from blood into alveoli, WBC attack bacteria causing inflammation and more fluid
  4. Diagnosis?- streptococci in sputum smears
  5. Treatment?- penicillin; vaccine given to kids

Primary Atypical (Mycoplasmal) Pneumonia

  1. pneumonia + mild symptoms including fever, malaise, sore throat, excessive sweating
  2. Who?- Mycoplasma : low G+C obligate aerobe, encapsulated, no cell wall, sterols in PM, small; adhesion protein allows attachment to base of cilia on epithelial cells
  3. How?- by nasal secretions
  4. Diagnosis?- difficult
  5. Treatment?- tetracycline or erythromycin

Klebsiella Pneumonia (Nosocomial Pneumonia)

  1. normal symptoms plus thick bloody sputum (destroys alveoli) and recurrent chills; often nosocomial
  2. Who?- Klebsiella : g(-) bacillus w/prominent capsule, endotoxin
  3. Diagnosis?- symptomatic and culture from sputum
  4. Treatment?- supportive; abx available but endotoxin creates severe and permanent damage to lungs, sometimes fatal.

Legionnaires’ Disease

  1. What?- pneumonia symptoms, pulmonary fxn rapidly decreases, 50% mortality if untreated
  2. Who?- Legionella : g(-), aerobic, pleomorphic; nutrient needy; intracellular parasite of freshwater protozoan phagosomes, protozoa release bacteria-filled vesicles that are inhaled by human host, into macrophages
  3. How?- survives in domestic water sources (showers, hot tubs, AC) kills human cells, causes tissue damage and inflammation, rarely spreads outside lungs
  4. Diagnosis?- fluorescent Ab staining, serological
  5. Treatment?- quinolone, macrolides; reduce bacteria in water


  1. What?- fever, cough, fatigue, chest pain, wheezing, coughing up blood, tubercles in lungs
  2. Who?- Mycobacterium tuberculosis : mycolic acid = slow growth and resistances, viable in aerosols for long time; replicate freely in macrophages. Primary tb: can develop tubercles (caseous necrosis in center). Secondary tb: reactivation by escaping tubercle. Disseminated tb: systemic infection (macrophages carry to other parts of body)
  3. How?- inhaled; alveolar macrophages endocytose; bacteria divide freely in macrophage; more macrophages come, get infected or sequester into tubercle; center macrophages die = caseous necrosis = stalemate; 10% people lose stalemate, often decades later = reactivation
  4. Diagnosis?- Tuberculin skin test, chest x-ray for tubercles,
  5. Treatment?- combo of drugs for months; resistant strains emerging, BCG vaccine sometimes available (effective?)


  1. What?- initially cold-like symptoms, then persistent powerful cough that fatigues, turning blue, ruptured eye vessels
  2. Who?- Bordetella : small, aerobic, nonmotile, g(-) coccobacillus; numerous virulence factors; bind cilia in trachea, stop ciliary elevator, invade neutrophils, survive in phagosomes, invade respiratory epithelial cells
  3. How?- highly contagious via airborne respiratory droplets, life threatening in children
  4. Diagnosis?- symptomatic
  5. Treatment?- supportive, prevent with DTaP vaccine

Inhalational Anthrax

  1. What?- initially resembles cold or flu, then severe coughing, lethargy, shock, and death
  2. Who?- Bacillus anthracis : g(+), endospore forming, hemolytic, aerobic; capsule and anthrax toxin kills human cells and edema
  3. How?- contact or inhalation of anthrax, most die
  4. Diagnosis?- identify in sputum
  5. Treatment?- aggressive abx; vaccine for select individuals


  1. What?- sudden fever, pharyngitis, fatigue, congestion, cough
  2. Who?- Influenza virus A and B: ssRNA(-), enveloped, HA and NA glycoprotein spikes. NA hydrolyzes mucus to give access to cell surface; HA attaches to host epithelial cells and triggers endocytosis; symptoms are immune response to virus (cytokines and inflammation); damages lung epithelium, secondary bacterial infection possible (ie. Haemophilus )
  3. How?- inhalation or self-inoculation; complications most often in elderly, kids, weak immune system
  4. Diagnosis?- symptomatic with community outbreak
  5. Treatment?- supportive care; yearly multivalent vaccine

SARS (severe acute respiratory syndrome)

  1. What?- high fever, shortness of breath, difficulty breathing; 10% mortality
  2. Who?- a Coronavirus called SARS Virus: ssRNA(+), enveloped, helical capsid
  3. How?- via respiratory droplets
  4. Diagnosis?- via signs/symptoms
  5. Treatment?- supportive treatment

RSV (respiratory syncytial virus)

  1. What?- most common respiratory disease in newborns and young children; fever, runny nose, cyanosis (blue cast to skin), coughing, sometimes wheezing. Causes inflamed bronchioles (bronchiolitis) and pneumonia in infants, #1 respiratory killer of infants worldwide
  2. Who?- Respiratory Syncytial Virus : ssRNA(-), enveloped; causes syncytia to form in lungs, immune responses to RSV damages lungs
  3. How?- via close contact (kissing, touching), fomites, and sometimes respiratory droplets (less common)
  4. Diagnosis?- symptoms and immunoassay
  5. Treatment?- supportive care in young children; Ab against RSV and inhaled ribavirin in severe cases

Hantavirus Pulmonary Syndrome

  1. What?- cough, shock, and labored breathing; 4-10 days after infection 50% die
  2. Who?- Hantavirus : segmented (3 pieces) ssRNA(-), enveloped; invades blood capillary walls and lungs, then widespread inflammation and shock
  3. How?- inhalation of mouse excrement; not contagious by contact
  4. Diagnosis?- based on symptoms
  5. Treatment?- none; control rodents

Coccidioidomycosis (Valley Fever)

  1. What?- resembles pneumonia or TB, may become systemic
  2. Who?- Coccidioides : dimorphic soil Ascomycota fungus; grow as mycelial filaments and produce spores in soil
  3. How?- inhalation of conidia by mammals, converts to yeast form at body temp, germinate in alveoli into spherules with lots of spores; almost exclusive to southwestern US and northern Mexico
  4. Diagnosis?- presence of spherules in clinical specimens
  5. Treatment?- amphotericin B; masks reduce to conidia exposure

Histoplasmosis *** (Prof's fave)

  1. What?- most common fungal systemic disease in humans; asymptomatic in 95% of cases, otherwise coughing with bloody sputum or skin lesions, splenomegaly, hepatomegaly
  2. Who?- Histoplasma capsulatum : dimorphic soil ascomycete; in moist soils with bird or bat droppings; yeast form pathogenic at body temp
  3. How?- inhalation, then intracellular in alveolar macrophages, then spread systemically via blood/lymph; prevalent in eastern US
  4. Diagnosis?- identification from clinical samples
  5. Treatment?- no treatment needed in immunocompetent

Respiratory fungal pathogenesis

(1)Aerosolization of conidia; (2)Inhalation of conidia by host; (3)Travel into deep lung (alveoli); (4)Encounter innate immune cells

  1. Fungal cell wall components: alpha and beta-glucan, specific glycoproteins/polysaccharides
  2. Complement can bind wall; macrophage complement receptor 3 (CR3) recognizes complement and cell wall proteins
  3. Macrophage Dectin-1 recognizes beta-glucan
  4. Macrophage TLR-2 and -4 recognize glycoproteins and polysaccharides

(5) Conidia phagocytosed by macrophages; Two options: some degraded by macrophages/ other immune cells, some survive and replicate inside innate immune cells

(6) Dissemination to other organs: either degraded by cell-mediated response in 7-10 days OR overwhelm immune system=fungal sepsis