Exam 3 – Microbiology Test Questions – Flashcards

Bordetella spp

Haemophilus influenzae

B.avium

B.bronchiseptica

B parapertussis

B. homesii

Bordetella pertussis

Coryza

birds

kennel cough-dogs

necrotic rhinitis-pigs

URT-humans

mild whooping cough

human

extremely small gran neg coccobacilli

strictly aerobic

obligate human pathogen-NO animal reservoir (unlike Salmonella enteridits)

Fastidious, slow growing-3 to 6 days for colonies of Border-Gengou agar

infects the URT-cilliated respiratory epithelium

elaborates powerful toxins which elicit most of the sx of the dx

pertussis means violent cough-assoc w/ whooping cough

DPT vaccine

1.culture bacteria from respiratory secretions (not always successful)-viable, but non culturable bacteria (VBNC) ex-can't use cotton swabs for sampling the throat b/c fatty acids in cotton kill the B pertussis bacteria

2. immunofluorescense assay on secretions-antibodies that recognize pertussis proteins

3. agglutination reaction on secretions-antibodies that recognize pertussis proteins

4.dx based on clinical dx-whoop-type coughing and lymphocytosis

worldwide problem-60 million cases, 600,000 deaths/yr

developed countries-dreamatic increase in cases with decreased vaccine use, rise of strains resistant to the vaccine

**Highly contagious-attack rates of 50-100%

transmission-aerosol droplets from coughing

females-higher attack rate, morbidity, mortality, don't know reason for this

age distrubution-recent shifts in age groups

prevaccine-predominately infected young children (1-3 years of age)

post vaccine-inc rate of infection in 2 groups (older children 5 to 14; young adults 18-25)

vaccines exert strong selective pressures on pathogens

selects for outgrowth of variants for which the vaccine doesn't evoke immune protection

vaccination has "pushed" bacterium into other age groups-fewer maternal antibodies remaining in older children, protection by vaccination in young children is not lifelong

binds to ciliated epithelium of URT

multiple adhesions

multiple toxins

pili-attachement to host cells

filamentous hemagglutinin-adherance to glycolipids-predominat in eukaryotic cells

capsule-antiphagocytic, adherence

pertacin-binds to host cells

pertussis toxin

adenylate cyclase toxin

lymphocytosis-promoting toxin

tracheal cytotoxin

dermonectrotic toxin

LPS (enterotoxin)

A1-B5 class of toxin (similar to CT)

B pentamer-binding to receptors on cells

A polypeptide-enzyme  which increases cAMP

may be the actual major virulence factor (as opposed to the pertussis toxin)

fragment of peptioglycan cell wall

destroys ciliated epithelial cell walls

diff from other toxins-struc component on cell wall-cleaves and destroys the cell wall

activates alternative complement pathway

fever

1. incubation stage

2. catarrhal or prodomal stage

3. paroxysmal stage

no overt symptoms

lasts 7 to 10 days

infected indiv is already infectious

lasts from 7 to 14 days

non specific sx-makes it east to mis dx

malaise, rhinorrhea, lacrimation, low grade fever, (cold of flu like)

dry cough develops, worse at night

paroxysmal coughing-tenacious mucus, series of repetitive coughs followed by a charac inspiratory "whoop" (cyanosis, convulsions, seizures)

px looks normal b/w paraoxysms w/ minimal fever

cillistatis-death of URT cilliated epithelial cells (tracheal cytotoxin), failure of respiratory escalator to move mucus from lungs to throat

lymphocytosis-neutrophil count in the tissues to 200,000 cells/ml

persistance-sx last 1-2 weeks, until ciliated cells redifferntiate from basal cells

erythromicin-doesn't alleviate sx bc cells are already dead

convalescene (3-4 weeks); lymphocytes dec gradually, cough subsides

upper respiratory tract

lower respiratory tract

middle ear

aerobic gram neg bacterium

coccobacillus or pleomorphic rods

obligate human pathogen

may be encapsulated or non encapsulated

required for growth-fastidious bacterium to culture, hemin, nicotinamide adenine dinucleotide (NAD)

chocolate agar-contains heat treated lysed erythrocytes

capsule-secreted polysacch "coat", antiphagocytic activity, resisits killin macrophages and polymorphonuclear neutrophils

pilus-rod like appendage, promotes attachment to target cells of URT or middle ear

HAP protein-surface protein-promotes more intimate adhearance of baceterium to cells

endotoxins-LPS inflammatory, pyrogenic (fever), impairs cilliary func or URT cells

IgA1 proteases, destroys IgA, facillitates colonization of the mucosal surfaces

6 serotypes based on antigenic differnces in capsular polysaccharides

Serotype A, B, C...

most prominent disease causing strain in US in prior decades

VERY effective vaccine-worked well for a while

based on Sero B capsular polysacch

serotype B

NTHI

after widespread use of vaccine-most infections caused by unencapsulated strains

emerged as prominent cause of otitis media since the advent of the Hib vaccine

colonized the nasopharynx-many healthy children and adults

approx 8-10 mill cases/year in US

colonized LRT-adults with COPD

colonization early in life assoc w/ recurrent otitis media-middle ear infections

NTHI attaches to mucosa of throat using various adhesions

bacteria replicate in throat causing localized URT infections

throat-eutacian tube-nasopharynx-middle ear

replicated in middle ear-pure cultures of bacteria can be obtained from otic fluid

release of bacterial factors cause severe inflammatory response-acute pain, fever, potenial loss of hearing, usually not a lethal infection (meningitis)

another spp of haemophilus is correlated a higher probability of contacting a lethal disease

causitive agent for chancroid genital ulcer disease-breaks in skin

risk factor for aquisition of HIV, requires breaks in the skin to enter the body, infection was widespread in parts of Africa

contracting one pathogen may make you much more suseptible to infection by another pathogen or disease

hemophilus ducreyi-HIV

H. pylori-gastric carcinoma

Viral influenza (flu)-N. meningitis

pathogens evolve or adapt to take advantage of newly opened ecological niches w/in body

genus: mycobacterium

species: mycobacterium tuberculosis

mycobacterium avium-intracellulare (MAI complex)

mycobacterium leprae

1. tubercule bacilli-TB (M. tuberculosis)

2. MOTT of Atypicals-M avium-intracellulare

3. Leprae-leprosy or Hansen's disease (m. leprae)

have high lipid count

cell wall is a complex layered complex

peptidoglycan skeleton overlayed with layers of lipid

primary lipid-mycolic acid

lipid accounts for about 40% of dry weight of the cell

acid fastness

slow growth

resistance to disinfectant and strains

resistance to common antibacterial antibiotics

antigenicity-surface glycolipids

ziehl neelsen procedure-acid fast stain (carbol-fuchsin) is forced by heat or detergent into cell

Bacterium resists acid alcohol decolorization and retains red color of acid fast stain

not able to be stained by gram stain raegents

1. high lipid content

2. acid fast bacilli

3. slow growth rate

generation time-12-20 hours; 30 minute gen time for E. Coli

slow growth rate due to complex lipid-rich cell wall

acid fast bacilli (AFB)

non spore former

non motile

no capsule

obligate aerobe

simple growth medium-inorganic salts, asparagine, and glycerol

selective media, lowenstein 7H-10 or Middlebrook 7-11

colony appearance is extremely rough/dry colonies

1.immunity host

2. hypersensitivity host

3. infecting dose bacilli

brief-asymptomatic incident

chronic-progressive lung dx resulting in loss of almost all func lung tissue

close person to person contact

inhalation of infectious aerosols

1. primary TB-direct course (recent infection)

2. secondary TB (reactivation or reinfection)-activation of a latent infection, "new" direct course

3.disseminated TB-extrapulmonary TB-non pulmonary infections

respiratory dx

infections restricted to lung or lower RT

1. inhalation bacilli

2. phagocytosis by avelor macrophages

3. growth of bacilli intraceullarly w/in macrophages (prescense of sulfatides)

4.exudative lesions or primary lesions

5.productive lesions

6.productive lesion expansion

7. caseous lesion

8. entry bacilli into bloodstream

prescnce of sulfatides

sulfatides func w/ inhibition of phagsome lysosome fusion; increases bacterial survival when phagocytosed

infected phagocytic cells burst releasing bacilli allowing further cycles of phagocytosis-lysosome mycobacterial replication and cell lysis

early part of infection

exudative lesions-charac by presence of poly morphonuclear leukocytes, fluid and inflammation

most bacilli growing intracellularly in macrophages

lesion may heal-reabsorption of inflammatory derived exudates

3 to 4 weeks after infections, host develops cellular immunity or allergy to the bacilli

large influx of mononuclear cells into lungs-formation of specific infection sites or tubercles

tubercle appears oas a granular nodule (granuloma)-host's mech for inhibiting bacillary multiplication

housed w/in tubercles are bacilli which can be reactivated

tubercles may harbor bacteria indefinitely

formation of tubercles or granulomas walls off lesions from healthy tissue

solid mass or nodule

central core-TB bacilli and enlarged macrophages

outer wall-fibroblasts, lymphocytes and neutrophils

neutrophils at lesion site release lysosomal enzymes that destroy tubercle (necrotic tissue), healthy tissue and some bacilli (allows lesion to expand)

caseation necrosis-semi solid coagulated mass (cheesy state) of host cells and bacilli

 can heal-calcification; infiltration of fibrous tissue and Ca deposits

or expansion of caseous lesion-resulting in cavities in lung after clearance of necrotic tissue

lesion epxansion involves portal vein

infectivity of other organs and tissues; bone marros, spleen, kidneys, and CNS

reactivation of bacilli from an "earlier" infection

reinfection of "new" bacilli from the environment

represents 2/3 of all "new" active cases of TB

residing w/in tubercle or "healed" primary lesions are dormant bacilli

bacilli reactive: dec immunological capabilities

1.elderly or young adults

2. immunosuppressive disease

3. chronic alcoholism

4. prolonged corticosteriod therapy

1. lung lesions-entry of bacilli into bloodstream

or

2. lymph sytem-possible infection of every organ

regional lymph nodes, kidneys, gential tract, CNS, long bones/weight bearing joints,

miliary TB-numerous small tubercles in body tissues-"millet seed" lesions

infection by TB bacillis, delayed hypersensitivity reac

intensity of hypersensitivy response; amount of mycobacterial antigen in the host

tuberculin Ag (mycobacterial Ag)

ability of macrophages to kill bacilli or inhibit growth-activated macrophages, killing/inhibition

T cell sensitivity-not life long

nursing home studies

immunocompetent elderly-one time Tuberculin (+)

may become non reactive-risk of contracting a primary infec

1. tuberculin testing-pos skin test reactivity

2.roentgenography-chest x rays (checking for tubercle or destroyed skin)

3. lab detection, microscopy, culture

inject 5 tuberculin units of PPD intradermally in forearm

measure size of induration (hardness) after 48 and 72 hours, degree of induration at site of injection is an indication of indiv present or past assoc w/ TB

tubercular infections-abnormal radiopaque patch

looking for tubercle or lung caberation

microscopy-clincial source of infecting bacilli, TB-sputum or lung secretions, disseminated TB-CSF, urine, joint material, or feces

direct identification of AFB-1.ziehl Neelson stain; 2. fluorescent acid-fast stain (smear eval-#AFB/field, culure-accurate species ID)

selective media-lowenstein Jensen or Middlebrook 7H10 or 7H11-prob 3 to 4 weeks colony detection, biochem tests-production of niacin, catalase, and nitrate reductase

nucleic acid probes-DNA probes

chromatographic analysis of cell wall lipids by HPLC (high performance liquid chromatography)

1. no hospitalization-past paitents were quarantied in sanatoriums

2.prolonged antibioitic therapy (6 to 24 months) chronic nature, tow months of isoniazid, rifampin, and pyrazinamide

four months daily or weekly doses of rifampin and isoniazid

combined anitbiotics to avoid drug resistance

inc period of therapy in px w/ HIV

many organisms are intracellular (hiding in macrophages)

rate of metab is slow

chemotherapeutic drug does not easily penetrate the fibrotic or caseous lesions

homeless, recent immigrants, drug addicts, AIDS px

nosocomial transmissions, AIDS px, w/ muilti drug resistant TB

highest case rate-non white males over 30, nonwhite females over 60

NYC-highest case rate, reporting 10% of all cases in US

1. family members of recently dx cases receive isoniazid chemoprophylaxis for 1 year

2. tuberculin skin testing screening-hospital workers

3. vaccination-attenuated bacille calmet guerin BCG, isolated from M bovis, immunize neg tuberculin reactors, vaccination of young children in countries w/ high rates TB, offers 20-80% protection for several years, not used in US since it induces a pos TB test

difficult, slow chronic dx diff to isolate people until months or years after infection,

px non compliance w/ therapy, immigrants, homeless, substance abuse, mental illness, or socioeconomic probs

mycobacteria other than tubercle bacilli

M avium-intracellulare complex (MAI)-two species diff to tell apart so its a "complex"

originally assoc w/ compromised pulmonary func (chronic bronchitis), clinically identical to pulmonary TB

risk groups-1990's AIDS px, terminal stages

transmission-ingestion of contaminated food or water

pathogenesis-mycobacteria multiply in lymph nodes-spread systemically, disseminated mycobacterial infection

organ involvement-die of mass organ failure from bacterial engorged organs, bacilli flood blood stream, bone marrow, bronchi, intestine, kidney, and liver

tx-antibiotic therapy-clarithrmycin, ethambutal, and rifabutin

prognosis-poor, mass bacilli impair organ func

**third most common cause of death in AIDS px

distinguising charac: strict intracellular parasite, not cultivated in vitro; no growth artificial media

cultivated in vivo-mouse foot pads or armidillos

very slow growth; generation time-12 days

person to person spread by inhalation or direct contact of lesions

1. inhalation of bacilli onto nasal mucosa

2. direct skin to skin contact (intact skin or penetrating wound) with respiratory secretions or wound exudates

entry-inhalation or skin contact

phagocytosed by macrophages

(4-12%) of infected indiv have weak macrophages-intraceullar survival

incubation is 2-5 years

infection-chronic progressive diease of skin and peripheral nerves that often leads to disfigurement

1.indeterminate or borderline leprosy

2.tuberculoid leprosy

3.lepromatous leprosy

intial sx-few hypopigmented areas of the skin plus a dermatitis

severe residual sx-damage to nerves that control muscles of hands and feet, subsequent wasting of muscles and loss of control-drop foot or claw hands

1.dependent on tx

2.dependent on immunological competence of indiv

most indiv recover spontaneosly

dev of either tuberculoid or lepromatous leprosy

tuberculoid leprosy

lepromatous leprosy

sx-1 to 3 shallow skin lesions, lesions are blanced, appear flat, contain few bacilli, localized areas of anesthesia (nerve damage), nerve damage as a result of inflammation that occurs during a cellular immune response to bacilli in the nerves (numbness or anesthesia) happens from local inflammation reaction

recovery is frequently self limiting

accountable for dx assoc disfiguration

degrees of disfigure; max resistance-disease affects superficial nerve endings and related skin areas or minimal resistance w/ organ involvement in eyes, testicles, and bones

early sx-small hypopigmented spotty lesions, numbness-hands and feet, loss of heat and cold sensibility, muscle weakness, chronic stuffy nose, thickened earlobes

later sx-diffuse to nodular lesions or lepromas (granulomatous thickenings w/ folds) result of massive intracellular overgrowth

lesion location-cooler parts of body, nose, ears, eyebrows, anterior third of eye, peripheral nerves at speicific sites, elbow wrist, ankle (optimum growth 30 deg) irreversible peripheral nerve damage-loss of feeling and permanent paralysis

secondary sx-trauma and mutilation to self-sensory loss-can't feel pain

untreated-death by kidney or respiratory failure

health pre disposing risk factor-inherited or acquired defect in cell mediated immunity

living conditions-long term household contact w/ leprotics, poor nutrition, crowded conditons, inadequate hygeine

prescence of skin lesions and nodules consistent w/ clinical dx

non culturable AFB in lesions (nasal discharges, tissue samples, and nodules)

neurological eval of extemetities-occurance of anasthesia, feather test

lepronin skin test-no aid in diag, lepromatous px-impaired cullular immune response and will not react

most indiv test pos to lepronin

combined antibiotic therapy-dapsone, rifampin, clofazimine, or ethinamide for a min of 2 years

pilot vaccine study-antileprosy studies in india; ICRC bacillus-vaccine is a killed leprosy bacilli from a human leproma

prevention w/ surveillance of high risk populations to discover early cases, chemoprophylaxis of healthy persons in close contact w/ leprotics, isolation of leprosy px

1/3 of worlds pop infected w/ TB bacillis

WHO declared TB global emergency

TB kills approx 2 mill people each year

each year there are 600,000 new cases of leprosy

organsims that lives on or in host org and gets its food from or at expense of host

often pathologcial but not always

toxoplasmosis

giardiasis

pinworms

crtosporidum diareha

trichomonas vaginitis

imported malaria

unnatural host to which the parasite may not be adopted for replication

unusal pathology

phylum sarcomastigophora

phylum apicomplexa

subphylum sarcodina

subphylum mastiogphora

under subphylum sarcodina

agents of amebiasis

worldwide distribution, many infected, many more carriers

confusion w/ morphologically similar but non invasive species E dispair

E histolytica specific antigen and PCR tests avail to distinguish the cysts from E dispar

2 stages

1.cyst stage passed out in fece, many parasites use this

2.trophozites stage passed in gut

fecal oral route of transmission

replicative stage:heat labile

**Pathogenic stage

about 20-30 million micron motile forms (ameboid)

No mitochondria, have mitosomes

phagocytosis of bacteria and red cells

secretion of various cytocidal agents

"amebapore" small peptides (77aa) that form a pore in cell membranes

trophozites differentiate into cysts (encystation)-formation of cysts

differentiation happens during passage through gut (changes in pH, cholesterol etc)

infectious cyst stage of the parasite can tolerate 55deg C, cholride levels of city water supply and normal levels of the gastric acid

large number of people infected (1-10%) carriers estimated

about 10 percent of infected individuals go on to get invasive pathology

fecal-oral spread, veneral transmission also seen

incidence in US when up as AIDS epidemic started

humans are main reservoir (millions of cysts can be passed in stools of infected indiv)

transmission by cysts

cyst wall disintegrates in distal small intestine and eight trophozoites are released per cyst

tropozites colonize large intestine

adhere to host cell through specific lectinss and secrete pore forming peptides that lyse cells

secrete various enzymes (proteases, collagenase)

induction of mucosal ulcers

acute inflammatory response, diareha, flatulence, and cramps,

chonic amebiassis can last for months for years (can have it for a while w/o even realizing what it is)

hepatic (liver) absess seen in about 5% of the cases-more common in adult males

absesses can extend into surrounding tissues, pneumonia, periontitis, chornic pericardial infection

in rare cases go to lungs and brain

stool examination of wet mouths to observe cysts and tropozites

enzyme linked immunoassays and PCR avail

tx diferent drugs avail to tx amebiassis depending on the stage and severity but generally good to tx