Exam 4 Flashcards
mycoplasma: background
typical organism: commonly found
size: smallest cells ever discovered
morphology: pleomorphic; not just 1 shape
cell wall: no true cell wall; rigid cell wall (skeleton)
sterol: chemical; steroid; biologically strange
pleuropneumonia-like organisms (PPLO): old names
mycoplasma: culture
ascitic fluid or animal serum: does not grow on regular agar; grows on animal tissue (ascitic is tissue fluid)
*“fried egg” colonies: small colonies; shaped like egg
filterable: so small that they can pass through filters
contaminant: in hospitals/labs they are common issue with contamination
hosts: animals & plants (iffy)
specificity: very specific strains; if the bacteria is on a mouse, it won’t affect the person
mycoplasma: diseases of humans
nongonococcal urethritis: important; gonorrhea-like symptoms: not common
abscesses of brain: another disease of brain that can happen
pleural joint effusions: some cause joint disease
oral disease: another disease
pneumonia: big one; urethritis & pneumonia (important)
target age: 5-15 years
incubation: 1-3 weeks
symptoms: flu-like, *chest pain & bloody sputum
infection characteristics: most of the time seems like a cold or flu
asymptomatic: can be mild infection; just just don’t feel good; (not alarming)
symptomatic: can be neurological (afferent nervous system); patient can break out in skin lesions (most do not); ear infections
mortality: most people do not die
mycoplasma: diagnostic test
specimen: throat swab, sputum, urethral, more likely to take specimen if it is urethritis
culture: they can do this
serology: AB develops during infection
immune response: labs detect organism w/ immunological tests; immunofluorescent, CF
detection: some labs detect organism
mycoplasma: treatment
tetracycline and erythromycin: works on protein synthesis & ribosomes
penecillin, cephalosporin, and vancomycin: most strains are resistant to these; does not work because no cell wall
mycoplasma: epidemiology
transmission: inhalation; being too close (urethritis)
vaccine: none
immunity: person who had infection at a younger age should not have trouble with it again
rickettsia: background
morphology: rods and some cocci
giemsa’s stain: blue/purple stain; simple staining
macchiavello’s stain: complex stain; bacteria is stained red inside of blue cytoplasm (infected cells)
cell wall: similar to g -
culture: no agar; tissue culture or unhatched embryonated egg
tick is the main place that we get the disease
rickettsia: pathogenesis
endothelial cells of blood vessels: bacteria likes to grow here
lesions: on skin; unique
*typhus nodules: aggregation of WBC; found in brain or heart
phagocytosis: WBC tries to eat the bacteria, then the bacteria grows in WBC
rickettsia: clinical findings
flu-like symptoms; rash & enlargement of spleen and liver
typhus group
*epidemic typhus: worst form
*rickettsia prowazekii: causes typhus
symptoms: severe disease w/ prostation
mortality: up to 30%
*endemic typhus: mild; rarely fatal, problem at the end of WW2 in concentration camps
spotted fever group
*1 spotted fever: first form; produced from bacteria below
*rickettsia rickettsii: causes the disease
symptoms: rash; unique; shows up first on extremities
mortality: 60%
*2 rickettsial pox: second form; produced from bacteria below
*rickettsia akari: bacteria that causes the disease
symptoms: mild disease; rash
mites: how people get the disease
papule: pimple/sore produced from bite
black eschar: special name for papule/sore
scrub typhus
rickettsia tsutsugamuschi: causes the disease
black eschar from the mite bite
lymphadenopathy: swollen lymph nodes
lymphocytosis: high WBC count in bite area
Q fever
coxiella burnettii: causes the disease
symptoms: flu-like symptoms
hepatitis: caused by the bacteria
encephalopathy: brain degeneration
transmission: breathing in dried animal products (feces, urine, milk); farm animals and slaughterhouses; no bug
trench fever: background
very rare
rochalimaea quintana: causes the disease
symptoms: aches/pains, sweats, chills, and fever
european wars: WW1; low standard of living
trench fever: laboratory findings
isolation: inoculate blood into animals or chicken eggs
serological tests: CF, toxin neutralization (take AB & mix w/ germ and add to animal, if it does not get sick, it’s neutralized w AB)
weil-felix reaction: biological accident; cannot be grown on a petri plate; aby will bind into a protease (found in environment)
trench fever: treatment
tetracycline and chloramphenicol
sulfonamides: DO NOT use; makes it worse
epidemiology: arthopods
disease is spread by this
ticks and mites: helps spread
alimentary tract: where creatures are found
epidemiology: typhus
human lice
transmission: pooping and biting of lice
scratching: human scratches into head
parent to offspring transfer: baby gets it from mother
epidemiology: brill’s disease
typhus: relapse of old typhoid infection
lymph nodes: where disease hides
epidemiology: spotted fever
gotten from ticks
*passed transovarially: bacteria can be passed from mom
dog tick: people get infected; in the east
wood tick: people get infected; in the west
epidemiology: scrub typhus
germs are found in mites
reservoir: mites
parent to offspring transfer: baby gets bacteria from mother
epidemiology: Q fever
transmission:
humans:
epidemiology: trench fever
reservoir:
culture: blood agar w/ extra CO2
rickettsia: seasonal occurrence
lice:
ticks:
rickettsia: control
chemicals:
vegetation: cut vegetation (mow lawns), kill rodents
clothing: wear protective clothing
cleanliness:
pasteurization:
rickettsia: prevention
chlamydia: background
oligate intracelular parasites: cannot make a colony or grow by themselves on agar plate; grows in cells (g -)
ATP: most common chemical energy chlamydia can make its own
chlamydia: developmental cycle
*elementary body: form of organism that causes infection (very dense; similar to seeds or spores)
*reticulate body (initial body): EB wakes up in host cell & starts to function - divides & reproduces - makes big globin in vacuole (inclusion)
cycle time: 24-48 hours
chlamydia: structural items
peptidoglycan: no true peptidoglycan; sensitive to penicillin
toxin: some say it exists and kill mice; no big toxin
chlamydia: staining properties
elementary bodies: stains purple w/ giemsa (purple) & macchiavello’s (complex: chlamydia red any cytoplasm blue)
reticulate bodies: stains blue w/ giema
inclusions: stain purple (giemsa’s)
lugol’s iodine: same iodine as used in gram stain
chlamydia: culture
use unhatched baby chicken yolk sac and tissue culture
chlamydia: agents
antimicrobial heat and chemical (good disinfectants)
chlamydia: host-parasite relationship
subclinical infection: -
lifetime persistence: survive a long time in air-dried state
chlamydia psittaci: background
psittacosis or ornithosis (birds): name of disease (parrot fever)
glycogen: carbohydrate; inclusions of this do not contain glycogen
sulfonamide: resistant
pathogenesis: inhalation; dried bird poop
chlamydia psittaci: clinical findings
2 weeks after exposure it will show up in blood & sputum of person; lungs become patchy w/ inflammation; organs become large & congested (liver, spleen, heart, and kidneys)
flu-like: seems like never ending flu
incubation: 10 days w symptoms
symptoms: fever, sore throat, headache, *photophobia
mortality: 20%
chlamydia psittaci: laboratory diagnosis
specimen for culture: blood, sputum, lung tissue
serology: CF, measuring titer, responds good to high aby titer that lasts for months
chlamydia psittaci: treatment
tetracycline
aminoglycoside: resistant
chlamydia psittaci: epidemiology
risk groups: people with birds, chicken/poultry, farmers/packers
control: quarintine pet bird shipments; test for AB in birds
chlamydia pneumoniae (TWAR): pathogenesis
transmission: inhalation through air/breathing in a cough
bronchitis, sinusitis, and possible atherosclerosis: diseases caused
asymptomatic infections: mild infections
chlamydia pneumoniae (TWAR): epidemiology
300k per year in US; 1/2 of the population has aby against this
chlamydia pneumoniae (TWAR): diagnosis
CF & immunofluorescence
chlamydia pneumoniae (TWAR): treatment
tetracycline or erythromycin: not good responses in many patients
chlamydia trachomatis: background
glycogen: have these
sulfanomides: sensitive
chlamydia trachomatis: disease caused
trachoma
chlamydia trachomatis: clinical findings
eye disease
symptoms: scarring & blindness
conjunctiva and cornea: acute inflammation
incubation: 3-10 days
*panus: pathological development; extensions of vessels in eye into cornea of eye, causing blindness; local infection
chlamydia trachomatis: diagnosis
scraping; can be used directly or culture from it; aby or giemsa’s can be used
chlamydia trachomatis: treatment
sulfanomides, erythromycin, or tetracycline (relapses common)
chlamydia trachomatis: epidemiology
400 million active cases
20 million blind (major cause of blindness)
nongonococcal urethritis: background
VD: vinereal disease
symptoms: discharge from urethra, increased urinary frequency
incidence: 1/2 nongonococcal diseases are caused by chlamydia
pelvic inflammatory disease: occurs if left untreated
inclusion conjunctivitis
swimming pool conjunctivitis: nickname; self infection; from wiping eyes with towel with infected secretion on it
inclusion conjunctivitis of newborn
gets in babies eyes when born from mother’s secretion
inclusion conjunctivitis of newborn: diagnosis
scraping sample (urethra, cervix, vagina, conjunctiva), fluorescent aby test
inclusion conjunctivitis of newborn: treatment
tetracycline and erythromycin
inclusion conjunctivitis of newborn: control
dont be promiscuous; wear condoms
chlamydia: respiratory tract involvment
adult symptoms: gets in head, otitis, pharyngitis, & nasal obstruction
newborn symptoms: babies get this when born cough chlamydia in mouth
lymphogranuloma venereum (LGV)
VD: venereal disease; special strain
lymphogranuloma venereum (LGV): clinical findings
papule: starts out as pimple/sore on genetalia, anus, rectum; heals after a few days
regional lymph nodes: swell in area of papule; painful and large; burst and leak pus
other symptoms: flu like symptoms, skin rash, vomiting, blood, and anal discharge
advanced symptoms: elephantiasis (extreme swelling of rectum - cannot pop)
lymphogranuloma venereum (LGV): diagnosis
*frei test: injection into skin
lymphogranuloma venereum (LGV): treatment
sulfonamide and tetracycline
lymphogranuloma venereum (LGV): control
don’t be promiscuous; wear condoms
virology: background
structure: nucleic acid in center (capsid); subunits (little beads) are capsid meres, pipe is helical and hollow through the center, membrane bubble (envelope)
Propagation: growing viruses in lab; most common is tissue culture, we also use chicken eggs and animals
arboviruses: background
arthropod born: spread by ticks and mites
*robo viruses are spread by rodents
arboviruses: transmission
blood-sucking arthropods
arboviruses: arthropod vector
vector is non-human
transovarial transmission: from mom to baby arthropods
arboviruses: types of arboviruses
RNA, helical capsid, and envelope
arboviruses: 3 clinical syndromes
fever with or without rash:
encephalitis: highly fatal; made virus famous
hemorrhagic fever: severe and fatal
arboviruses: symptoms
flu-like (malaise, headache, upset stomach, vomiting), may or may not have rash
arboviruses: incidence
encephalitis: people get from mosquitoes when it is wet outside; in US there were 4k cases and 350 deaths
arboviruses: treatment
none
arboviruses: control
do not leave tires or buckets of water outside
hantavirus: background
deer mice; like to live in wood piles in the west
hantavirus: transmission
people go to wood piles and mice get scared and pee and so when the person touches the wood they also touch the pee unknowingly and may touch their face or inhale the bacteria
hantavirus: epidemiology
new mexico
hantavirus: pathogenesis
RT failure = death
ebola virus: background
endemic area: africa
lethality: highly fatal
helical virus
ebola virus: transmission
monkey to people; infected people to other people
ebola virus: clinical symptoms
flu-like: nausea, vomiting, diarrhea
possible rash
hemorrhage: severe; intestines and other sites
mortality: 90%
ebola virus: control
quarantine patients and sacrifice infected animals
picornavirus: background
pico means little; it is a little RNA virus
picornavirus: groups
enterovirus (intestine) and rhinovirus (respiratory or nose)
picornavirus: basic characteristics
small, RNA genome, and nonenveloped
poliovirus: background
enterovirus
poliomyelitis:
poliovirus: clinical findings (3 types)
abortive poliomyelitis: flu-like symptoms; patient gets over it
nonparalytic poliomyelitis: bad flu-like symptoms with aches and pains (stiffness and back pain); they have a complete recovery
paralytic poliomyelitis: made polio famous; paralysis from motor neuron damage; patient with either become crippled or die
poliovirus: immunity
iron lung; helps breathing
poliovirus: treatment
help with respiration; reduce pain (aspirin); correct hydration
poliovirus: control
live vaccine (works best); they put a drop of liquid on it and it is mutant virus, vaccine in general works good
rhinovirus group: culture
nose and throat
rhinovirus group: disease
common cold
rhinovirus group: treatment
aspirin, drink fluids, eat well, sleep
hepatitis viruses: background
hepatitis: virus causes this
hepatitis viruses: pathogenesis
systemic disease (primarily liver)
hepatitis viruses: structure
DNA virus; contains envelope
hepatitis viruses: hepatitis virus agents
hepatitis A virus (HAV): short incubation hep (faster)
hepatitis B virus (HBV): serum hep; long incubation; type B
hepatitis C, D, etc viruses: less common
hepatitis viruses: clinical illness
jaundice, inflammation of the liver, flu-like symptoms, nausea, and vomiting
hepatitis viruses: transmission
HAV: fecal-oral route; people who make the food are infected and will contaminate
HBV: close contact; blood or intimate contact
Incubation: days-months
Non-A and Non-B hepatitis: C,D,E are basically the same as B
hepatitis viruses: HBSAG
hepatitis B surface antigen or australian antigen: discovered before virus; piece of virus found in serum of people with HBV and liver cancer patient
hepatitis viruses: prevention
vaccine
rabies: background
nature
acute: happens quickly
central nervous system: acute infection happens here
rabid animal: bite causes disease
rabies: rhabdovirus
envelope, RNA=hereditary material; shaped like a bullet
rabies: pathogenesis
grows in muscles, connective tissue, nervous tissue; grows in salivary glands
rabies: negri bodies
cytoplasmic inclusions; little bunches of viruses (negri)
rabies: clinical findings
nervousness, complaints of light and sound, person has trouble swallowing, coma, and dies
*vampire myth
rabies: vaccine
dead and alive (attenuated); illness is not common enough to vaccinate everyone
rabies: treatment
immune globulin
rabies: epidemiology
transmission: animal bites
control: quarantine or destroy infected
cases: in US over 7k cases; affects children
orthomyxoviruses: background
more than one virus; causes respiratory diesease
influenza: most important
myxo: affinity (attracted) from mucin
epidemics: what happens as a result of infection
types: A B C
The virus can stay alive for many weeks in the fridge
orthomyxoviruses: clinical findings
flu-like symptoms; chills, aches, pain, prostration
orthomyxoviruses: pathogenesis
airborne droplets: how it spreads; one person sneezes/coughs then someone breathes it in
inflammation and necrosis: inside person on linings of respiratory system on trachea and bronchial mucosa
orthomyxoviruses: structure
can grow in lab; pleomorphic spheres; organisms
hemagglutinin or neuraminidase: on surface of virus these are spikes, hema (blood
Neuraminidase (enzyme) responsibile for cutting through neuronic acid. Virus requires neuraminidase to facilitate the process of cutting through this surface
orthomyxoviruses: RNA
virus uses RNA for its gene and has 8 pieces
orthomyxoviruses: antigenic variation
evolves fast which is why people get it yearly
antigenic drift: 1) due to point mutations, change in one base to another (example g to c, a to t)
antigenic shift: 2) more drastic and significant; recombination/reassortment of RNA pieces, sex in viruses because the two different ones infuse, viruses infect same cell and trade RNA pieces
-these viruses can affect birds and pigs also
orthomyxoviruses: treatment
amantadine hydrochloride
orthomyxoviruses: vaccine
main weapon; only good for one year, wear mask
orthomyxoviruses: incidence
60k people die yearly (more than total amount for AIDS)
coronaviruses: background
gastroenteritis: flu-like disease where the gut gets infected, causing gastroenteritis, very common
paramyxovirus family and rubella virus: background
scarier than flu
paramyxovirus: background
RNA genome: has this along with helical and envelope
neuraminidase and hemagglutinin: they have this also; similar to other disease
syncytia: to infect cells (bubbles), the virus products are on the surface of these cells, syntica then fuses cells together, resulting in the formation of large bubbles with multiple nuclei
persistent infection: virus lasts a long time, making it not severe because it is slow
mumps: background
most famous paramyxovirus
mumps: pathogenesis
parotid glands: virus gets inhaled and goes from mouth to parotid glands
viremia: virus in blood
mumps: clinical features
localized; but can spread to testes, ovaries, pancrea, thyroid, and brain
salivary gland: enlargement of gland
aseptic meningitis: most dangerous condition; aseptic because there is no bacteria
mumps: orchitis
tests get congested and hemorrhage, in young men; exercising burns ATP, so their immune system cant find disease and causes relapse and causes sterility.
mumps: control
vaccine
mumps: incidence
200k cases per year before vax, 3k after
rubeola (measles): pathogenesis
respiratory tract, rash (appears after 1-2 weeks), fever, coughing, red eyes, and runny nose
rubeola (measles): koplik’s spots
vesicles: similar to blister, but these bumps have clear liquid
buccal mucosa: vesicles break out in the lining of mouth and can become necrotic
rubeola (measles): immunity
do not usually get again
rubeola (measles): control
vaccine
rubella (german mealses): background
common name; 3 day measles
rubella (german mealses): pathogenesis
rash: starts on face and moves to lower trunk and extremities
rubella (german mealses): congenital rubella syndrome
if mother to be is infected; baby can also be
defects: heart, eyes, hearing, motor skills, brain
mental retardation: baby can be affected with this
rubella (german mealses): control
vaccinate mother to be
before vax 700k cases after vax 700
poxvirus family: background
family of viruses
rubella (german mealses): structure
complex
size: largest of viruses (very big on oil immersion, whale of viruses)
components: lipoprotein membrane, lateral bodies, core (look like dumbbells) double stranded DNA (has DNA) and enzymes
variola: background
small pox
variola: pathogenesis
respiratory tract: affected, along with mucous mebrance
viremia: can happen during infection
reticuloendothelial cells: WBC, likes to infect this
variola: clinical findings
fever and malaise: flu-like symptoms
papule to vesicle to pustule to crust: pimple-like on body; process
lesion locations: on face/mouth, less as you move away
variola: treatment
methisazone (marboran) works better for prevention; chance of dying 40% without treatment
variola: epidemiology
respiratory droplets: by contact or through air
reservoir: only in people
variola: vaccinia virus vaccination
first vax
multiple punctures: punture person with cow pus, then smallpox pus and they will have immunity to it because of cow pus
cross-protection: from cowpox to small pox
cowpox: background
hosts, Jenner: little girls that had cowpox from milking them because cows have blisters on their utters, which went to the girls hands, causing immunity to smallpox
largest smallpox cases in the wild was 1966, frozen sample in atlanta and moscow
adenovirus: structure
icosahedral symmetry: looks like satellite
DNA: the virus has DNA
pentons: looks like radio antenna, making it look like a satellite
hemagglutinin: on pentons and stick to RBC
adenovirus: pathogenesis
epithelial cells, likes to infect these as well as mucosa
adenovirus: clinical findings
cause several diseases
1) respiratory disease
symptoms: flu like
acute resp disease: in soilders bc they are close together
2) eye infection; more likely
swimming pool conjuctivitis: mild example
keratoconjuctivitis (shipyard eye): severe
3) GI disease; young people and infants
other disease: we dont know much about
Cystitis: bladder disease in children can be VD in adults and cervical lesions and urethritis
cervical lesions and urethritis: from VD
adenovirus: transmission
easily spread
herpesvirus family: background
DNA: type of virus
Icosahedral symmetry: in herpes
apparent or non apparent: apparent can be seen with eye; non-apparent means person is infected but you can’t visibly see it
vesicular eruption: in apparent infection (structures with fluid)
associated with skin and mucous membrane
types 1 and 2: two types the difference is some antigens
herpesvirus family: pathogenesis
primary infection: type 1 and 2; 1st time; person does not have any aby and in some individuals it is nonapparent (no evidence of virus)
recurrent infection: people who have latent infections and have antibodies
exposure to sunlight, fever, menstruation and stress wakes up the virus and causes it to be apparent
herpesvirus family: clinical findings
two groups
herpesvirus family: herpes type 1 infection
acute herpetic gingivostomatitis: includes a fever
eczema herpeticum: extensive spread outbreak of vesicles; on skin and includes a fever
keratoconjunctivitis: infection of the eye with herpes
encephalitis: most serious; brain infection; can kill people
herpes labialis: most common; commonly known as cold sores
herpesvirus family: herpes type 2 infection
genital herpes: outbreak in vesicles associated with reproductive organs; includes fever and local swelling of lymph nodes
neonatal herpes: infection in babies; mother has herpes and when the baby is born it gets infected from birth secretions; baby can get brain damage and can be fatal; baby may be brought into the world by c-section
miscellaneous: infected abrasions (wrestling), dentists did not wear gloves before aids
herpesvirus family: treatment
acyclovir and idoxuridine: most popular; treatments not cures; will help virus go back to sleep quicker
epstein-barr (EB) herpes virus: background
burkitt’s lymphoma and nasopharyngeal carcinoma: infection can develop into more serious problems
mononucleosis: common name for infection (mono)
fever that wont go away, malaise, enlargement of lymph nodes in spleen
varicella-zoster virus: background
type of herpes virus
varicella: official name of the herpes virus that causes the chicken pox
zoster: cause of shingles
they are actually the same virus
varicella-zoster virus: pathogenesis
varicella: infection of the respiratory tract
zoster: a flare up of the virus along the nerves that happens years
varicella-zoster virus: clinical findings
varicella: mainly seen in children and highly dangerous
patient group: children
symptoms: fever and outbreak of vesicles first on trunk, then face, limbs, and mouth
zoster:
patient group: seen in adults
symptoms: fever, pain, malaise, and vesicles break out on trunk, head, neck, and as the days go by the fluid will turn to pus and then will crust (scab)
varicella-zoster virus: treatment
acyclovir or vidiravin
the patient should not take immunosuppressant
varicella-zoster virus: vaccine
some people may have chicken pox or shingles vax to help it stay asleep; prevents disease
papilloma virus or papovirus: background
warts: dont kill people in the short run
structure: known as DNA viruses
transmission: person to person through direct contact and scratching
hand and plantar warts: warts on hands and feet (big and hard)
genital and perianal warts: other types of warts; warts associated with genitalia are smaller and soft; tend to grow back
cancer:
human immunodeficiency virus: background
acquired immune deficiency syndrome (AIDS): virus caused
structure: RNA virus; protein capsid and envelope
retrovirus: known as; genetic material is made of RNA and when infected it makes DNA and DNA is inserted into the host
antibody response: as time goes on the ability to give immune response decreases
incubation period: 6 months - 2 years
human immunodeficiency virus: inactivation
bleach, alcohol, lysol, hydrogen peroxide
human immunodeficiency virus: transmission
carrier: promiscuous people
body fluid: cuts, eyes, medical accidents
human immunodeficiency virus: pathogenesis
t-helper cells (main cell infected), B-cells (makes antibodies), macrophages (do a lot of killing to protect the body)
human immunodeficiency virus: initial symptoms
weakness and white patches on tounge (weight loss)
human immunodeficiency virus: aids-related complex
advanced stage; swollen glands, fever, sweats, diarrhea, and loss of weight
human immunodeficiency virus: complications
neoplasms: Kaposi’s sarcoma (shows as a development of dark purple areas on skin)
infection: pneumocytis, candida, and others
human immunodeficiency virus: diagnosis
ELISA, IF, RIA, Western blot *the best
human immunodeficiency virus: treatment
azidothymidine (AZT); invented as a cancer drug initially, dideoxyinosine (ddl), and saquinavir
human immunodeficiency virus: cancer
herpes, papilloma (both men and women can get cancer, but mostly women), hepatitis B, and HIV
spongiform encephalopathies of humans and animals: background
prions: cause the diseases called spongi because they have little bubbles like the sponge
nature: type of protein material
pathogenesis: cause degeneration of CNS;
pathology: get real close to someone
incubations: take a long time
immunology: no immunity
scrapie, mink, encephalopathy, kuru, mad cow disease, and creutzfeldt-jacob disease (CJD):
medical mycology: background
fungi: thousands of fungi; yeasts and molds (only about 100 cause disease)
mechanism of pathogenesis: main mechanism of causing fungi disease is hypersensitivity
hypersensitivity: basically an allergy
chronic granulomas: forms from disease; pimple filled with organism and pus (abscesses and necrosis)
medical mycology: structures of fungi
dimorphic fungi: 2 forms 1) filament like 2) yeast
conidia: asexual spores
chlamydospores (chlamydonidia): cells in the filament develop big thick walls
microconidia: small pods
macroconidia: large pods
superficial mycoses: background
dematophytes:
trichophyton, microsporum, and epidermophyton: grow in keratinized tissue
pathogenic nature: like to eat keratin
tinea pedis (athlete’s foot): background
t.rubrum or e. floccosum: main species
symptoms: itching and inflammation, nails turn yellow, thick, and brittle (crumble easily)
dermatophytids: in some cases; rash; pt may have infection on toes, but still have rash on their legs (allergy); hard to treat
tinea corporis or tinea cruris (ringworm): background
t. mentagrophytes and m. audouini: main species
symptoms: development of papule (starts on skin), itchy, gets bigger as time goes by, turns into red ring and breaks up into different sections that form rings
tinea capitis (ringworm of scalp)
epidemiology: in children; or people with close contact
infection location: just above the hair root
kerion: cause bald spots
scutula: cup-like crust just above the hair on the skin
two infection types:
ectothrix infection: microsporum grows on surface of hair
endothrix infection: tricophyte grows inside of the hair (harder to treat)
treatment for dermatophytes
washing (2 times daily), miconazole cream, undecyclic acid, salicylic acid, benzoic acid, griseofulvin
control for dermatophytes
cleanliness
epidemiology for dermatophytes
contact (with cats and dogs), baber clippers, chairs, and especially showers and dressing rooms
men are infected for life worse in summer
subcutaenous mycoses: background
just under the skin
puncture: basic requirement for infection; must be damage into skin for the fungus to come in
lesions:
sporothrix schenckii: background
rose-growers disease
niche: lives on plants and wood
sporotrichosis: medical name
morphology: cigarette shaped gram positive; budding off
pathology: slowly develop abscesses along the lymphatic system
treatment:
selflimiting: disease can go away on its own
potassium iodide or amphotericin
B(most powerful and important): treatment
control: prevent trauma (punctures)
mycetoma: background
morphology:
petrielldium and actinomycetes:
pathogenesis:
trauma:
abscesses and draining sinuses:
deformity:
treatment:
sulfonamide and sulfone: will work as treatment
control: wear shoes and clean puncture wounds as soon as possible
systemic mycoses: background
etiology: soil-fungi
entry: inhalation; people dont really show symptoms
dimorphism: exists as a filament in nature; look like a yeast in patient
coccidioides immitis: background
coccidioidomycosis: name of disease
selflimited: can be self limiting, but also terrible
geography: SW US or Latin America (dry or deserts)
cell cycle:
endospore to spherule to endospore:
arthrospore: dried spores
acquisition:
symptoms:
fatal form:
lesions:
tuberculosis:
treatment: IV amphotericin B
epidemiology: in hot, dry weather
transmission: non-communicable; breathing in spore
blastomyces dermatitidis: background
blastomycosis: name of disease
morphology: dimorphic yeast in body; fuzzy at room temp on petri
lesions form in bones skin, acquisition: prostate, epididymis, and testes
treatment: amphotericin B and surgery
epidemiology: in nature this is common in animals like dogs, animals do not get disease from each other, rather nature; found in dirt & beaver dens *
histoplasma capsulatum: background
histoplasmosis: name of disease
morphology: dimorphic
acquisition: inhalation
pathogenesis: reticuloendothelial system; grows in WBC
symptoms: enlargement of lymph nodes, ulcers on nose and mouth as well as intestine
treatment: amphotericin B
epidemiology: common around the world
bird feces and bat guano: where it grows in nature
communicable: not communicable
candida albican: background
opportunistic mycoses
morphology: oval yeast
pseudomycelium and pseudohyphae: make these projection
germ tube test:
high risk groups: people on antibiotics, immunosuppressed, people with catheters, people taking steroids
pathogenesis: fungus likes to infect tissue and cause abscesses
infections:
thrust: in the mouth in babies and teenagers
vulvovaginitis: in the female genetalia
skin: infections of skin; moist places (folds: groin, armpit, between toes and fingers)
nails: may get infected
organs: in bad cases (lungs and kidneys)
chronic mucocutaneous candidiasis: babies may not have proper functioning T cells and the yeast will eat the baby up
not communicable
be clean and healthy to control
creptococcus neoformans
