Flashcards
Test 4
Cards in this deck (85)
- 1What are the characteristics of Mycobacterium?1. Small, aerobic bacilli
2. Facultative intracellular bacteria
3. Slow-growing
4. Contain unique cell wall structures that do not stain well with Gram stain and require Acid-Fast staining - 2What is the Acid Fast staining method?AKA Ziehl-Neelsen Method
1. Spread sputum sample on slide
2. Air dry and heat fix
3. Apply primary stain (Carbol fuchsin)
4. Heat sample until stain has dried
5. Decolorize with acid-alcohol
6. Apply counterstain (methylene blue) - 3What is the difference between Ziehl-Neelsen stains and Auramine-rhodamine stains?ZN = Fuchsia/blue
AR = Bright orange-yellow; not as specific as ZN staining, but much lower cost - 4What is the major component of mycobacteria membranes?Long-chain mycolic acids
Form a waxy coat - 5What diseases are caused bd by mycobacteria with a tuberculosis complex?M. tuberculosis, M. bovis, M. africanum, M. microti, and M. canetti
- 6What diseases are caused by by nontuberculous mycobacteria?Hansen's disease (leprosy) caused by M. leprae or M. lepromatosis
Buruli ulcer caused by M. ulcerans - 7What is tuberculosis?A disease caused by mycobacteria
1/3-1/2 of human population is latently infected
Transmitted through inhalation of aerosols - 8How do you detect tuberculosis?Hilar lymphadenopathy
Tuberculin skin test which detects exposure using purified protein derivative injected into the skin
- Stimulation of memory T cells causes local swelling if positive - 9What is the infectious dose of mycobacteria?~10 bacteria
- 10How does the immune system eradicate an active tuberculosis infection?Bacteria are "contained" within a granuloma
The bacteria remain viable, but are essentially quarantined - 11What is the difference between latent and primary TB?Latent (95% of patients) is asymptomatic infection
Primary (5% of patients) is active infection
-In the peripheral part of the lung tissue
-Patient is highly infectious
-Failure to control infection leads to miliary TB - 12What results from spontaneous healing in primary TB?Ghon complex (enlarged hilar lymph node + calcified peripheral lung lesion)
- 13What is reactivated (secondary) TB?Active infection after a latent infection
Often caused by immunocompromised status (i.e. HIV) when bacteria escape from the granuloma and establish a new, active infection of lung tissue - 14What is the QuantiFERON-TB Gold (QFT-G) Test?Blood samples are mixed with synthetic peptides representing ESAT-6 and CFP-10
If the patient is infected with TB, their white blood cells will release interferon-gamma in response to antigens - 15What is Lowenstein-Jensen medium used for?It is highly selective for Mycobacterium spp.
TB forms a brown, granular appearance - 16How is TB treated?Combination therapy: isoniazid, rifampicin, pyrazinamide, and ethambutol (2 mo.) then isoniazid and rifampicin (4 mo.)
Directly Observed Treatment, Short-course: direct observation by a healthcare worker to ensure patient completes treatment - 17What is leprosy?A chronic infection with Mycobacterium leprae that affects the cooler portions of the body leading to disfigurement, deformity, mutilations, and blindness
- 18What are some characteristics of M. leprae?Acid-fast (cell wall is rich in mycolic acids and glycolipids)
Obligate intracellular pathogen (cannot be grown on lab media)
95% of humans are naturally resistant
Endemic disease of US armadillos - 19How does M. leprae replicate?It replicates within macrophage/dendritic cells and Schwann cells causing nerve damage
- 20What is the difference between tuberculoid and lepromatous leprosy?Tuberculoid: strong cell-mediated immunity (Th1 response), macrophage killing, and few bacilli in skin smears
Lepromatous: weak cell-mediated immunity (Th2 response), strong humoral immunity, rapid bacterial proliferation, and many bacilli in skin smears - 21What are the signs/symptoms of leprosy?Skin lesions (plaques and macules), enlarged and tender peripheral nerves (causes muscle weakness, sensory deficits, and loss of sweating), and AFB in skin smears
Nerve damage is permanent - 22How do you treat leprosy?Tuberculoid: supervised monthly prescription of rifampin and dapsone daily for 6 months
Lepromatous: supervised monthly prescription of rifampin and dapsone PLUS clofazimine daily for 12-24 months - 23What is Mycobacterium ulcerans?A slow-growing, environmental pathogen that is the 3rd most common cause of mycobacterial disease in humans
Leads to the development of buruli ulcer but is rarely fatal - 24What mediates the buruli ulcer?Mycolactone TOXIN
Causes cell cycle arrest, apoptosis, and necrosis - 25What's the difference between yeastn yeasts and molds?Yeasts are budding single cells and molds are filamentous forms
Both are fungi! - 26Cryptococcus neoformansBudding yeast that is commonly found in guano-enriched soils and carried by pigeons
Transmitted by inhalation of infectious agent - 27What is the most common cause of meningitis in sub-saharan HIV patients?Cryptococcus neoformans
- 28What are the clinical presentations of Cryptococcus neoformans?Pulmonary infection with well-defined, non-calcified nodules on CXR
Causes pneumonia, tissue necrosis, and ACUTE MENINGITIS - 29How do you diagnose Cryptococcus neoformans in the lab?Only virulent strains grow at 37 degrees C
Expression of capsule is essential for virulence
Sabourand Agar, India Ink stain, H&E stain - 30What is Candida albicans?A dimorphic fungus that exists as a yeast or hyphae (at 37 degrees C)V
It has small, thin-walled, ovoid cells that reproduce by budding - 31What does the germ tube test indicate?Candida albicans
Fungal spores are mixed with human serum and germ tube formation can be seen under the microscope - 32Clinical presentations of Candida albicansMucocutaneous: oral thrush, diaper rash, etc.
Most cases respond to topical antifungals! - 33What is Histoplasma capsulatum?Dimorphic fungus
Switch from mycelium to yeast is necessary for virulence (opposite of C. albicans)
Promoted by bird and bat guano - 34What activities put you at a high risk for contracting Histoplasma capsulatum?Construction, renovation, exploring caves, tilling soil, cleaning up bird roosting sites
- 35What are the clinical presentations of Histoplasma capsulatum?Primary infection is pneumonia
Forms calcified nodules
Because of pulmonary calcified nodules and cavities, it is often confused with TB - 36What are protozoa?Single-celled, eukaryotic organisms whose major portals of entry are oral and skin.
The severity of the illness is directly related to the infectious dose and the number of repeated exposures - 37What differences are there in protozoan reproduction?In definitive hosts, reproduce sexually
In intermediate hosts, reproduce asexually - 38What are the stages of protozoans?Cyst: the inactive, non-motile, infective stage
Trophozoite: the motile vegetative stage which colonizes host tissues/cells - 39Excyst vs EncystIn protozoans...
Excyst -> cyst becomes a trophozoite
Encyst -> trophozoite becomes a cyst - 40What is the pathogenesis of parasites?Attach to specific host cells/tissues
Toxic metabolites are released on death
Tissue damage is due to invasion, destruction, and host responses - 41What is Entamoeba histolytica?A parasite that is passed through infective cysts which excyst into trophozoites
- 42How does Entamoeba histolytica?Consumed cysts excyst into trophozoites which move along the intestinal wall, eating RBCs, bacteria, protozoa, and human intestinal cells
Trophozoites invade colonic mucosa and cause erosions
The trophozoites encyst and the cysts are evacuated in the stool - 43What are the clinical presentations of Entamoeba histolysis?Abdominal pain, bloody/mucoid diarrhea, and flask-shaped ulcerations
Amebic liver abscess - "anchovy paste"
(can rupture into the abdomen, chest) - 44What is Giardia lamblia?Most common protozoan intestinal pathogen
Non-invasive
Beavers are reservoirs - 45What does Giardia lamblia look like under the microscope?Cover the epithelial surface resulting in a cobblestone-road like appearance which damages the intestine causing diarrhea
- 46Clinical presentations of Giardia lamblia?Diarrhea, gas, bloating, abdominal cramps, nausea, loss of appetite, weight loss
Irritable bowel syndrome (post-infection) - 47What is Plasmodium falciparum?Most virulent human malarial parasite (75% of cases)
- 48What are the clinical presentations of malaria?Headache, malaise, cough, myalgia, low grade fever (first 1-2 hours)
High fever, excessive sweating (2-6 hours)
Repeats every 48 hours
Severe disease: liver failure, shock, organ failure, coma, fatality - 49Why is Plasmodium falciparum so severe?It infects RBCs of ALL AGES
Creates knobs on infected RBCs which causes them to stick to endothelial cells and cause capillary obstruction
It has the shortest incubation period and has the most rapid erythrocytic cycle - 50What is the life cycle of the malaria parasitePro-Erythrocytic -> Erythrocytic -> Sporogenic
- 51What is the vector of the malaria parasite? How does it work?Female Anopheles mosquito
Sporogenic cycle begins and ends with the mosquito bite. The mosquito ingests human RBCs with haploid gametocytes that fuse to form diploid oocysts that divide and multiply in the mosquito. - 52What are the intermediate hosts of malaria?Humans
- 53What is the sporogenic cycle of malaria?1. After the mosquito ingests infected blood, the female and male gametocytes fuse to form zygote (diploid)
2. The zygote transitions to an oocyst and implants in the gut wall
3. The oocyst subdivides by meiosis into ~8,000 sporozoites (haploid)
4. The sporozoites migrate to salivary gland and cause transmission to new host upon feeding - 54What is the pro-erythrocyte stage of malaria?Human infection begins when a mosquito bites a human and injects a salivary anti-coagulant containing sporozoites. Those rapidly invade liver cells forming hepatic schizonts. The sporozoites replicate asexually to high levels, and then the schizont ruptures releasing merozoites which invade RBCs.
Vaccine inhibits pro-erythrocyte phase! - 55What is the erythrocyte (blood) stage of the malaria cycle?All forms of malaria infect RBCs, multiply to high numbers, and then rupture the RBC, releasing additional merozoites into the bloodstream
Released merozoites infect healthy RBCs, and some merozoites become haploid gametocytes - 56What morphological changes in RBCs are caused by P. falciparum?Knobs on the surface of infected RBCs that promote agglutination of RBCs and intracapillary sequestration
- 57How do you diagnose malaria?Stain blood with Giemsa stain
-Thick smears used for presence of parasites
-Thin smears used for species-level identification - 58How is malaria controlled?Insecticide treated bed nets, indoor residual spraying, control/eradication of mosquito population
- 59What is babesiosis?Intracellular parasite that looks like Plasmodium spp.
Reservoir: deer, cattle, and rodents
B. microti and B. divergens cause most human infection - 60What is the vector for babesiosis spp.?Ixodid (hard) ticks
- 61What are the symptoms of babesiosis?Malaise, fever, headache, and fatigue
- 62What are the general features of Clostridia spp.?Rod-shaped, some are motile, Gram-positive, form spores, and are obligate anaerobes
Many pathogenic species secrete toxins - 63What species types have the enzymes superoxide dismutase and catalase?Obligate aerobes and facultative aerobes
Obligate anaerobes DO NOT - 64Clostridium perfringensCharacteristics: Anaerobic, gram positive rod; non-motile, but grows rapidly; common in GI tract, ubiquitous in soil/water/sewage
Clinical implications: Intense abdominal cramps and diarrhea 8-22 hours after consumption, usually over within 24 hours; Gangrene (spores gain access through open wounds)
Pathology: results from temperature abuse of food; spores survive cooking, so comes from foods improperly stored; ALPHA TOXIN and perfringolysin O (enterotoxins)
Lab Diagnosis: NAGLER TEST used to demonstrate presence of alpha toxin using antitoxin
Treatment: remove dead tissue, large doses of anti-toxin, penicillin (gangrene) (STILL DEADLY) - 65Clostridium difficileCharacteristics: Gram-positive rod, motile via flagella, subterminal endospores, produces A&B toxin, opportunistic pathogen
Clinical implications: leading cause of hospital-acquired diarrhea,
Pathology: two exotoxins (TcdA, TcdB) cause watery secretions and damage to the mucosa which cause explosive diarrhea and/or life-threatening pseudomembranous colitis
Lab Diagnosis: PCR assays which test for the gene encoding toxin B, isolation of the organism from feces (selective medium, anaerobic conditions)
Treatment: Stop antibiotic therapy to allow normal flora to re-establish (diarrheal cases); vancomycin, metronidazole, fidaxomicin, fecal transplants (pseudomembranous colitis) - 66Clostridium botulinumCharacteristics: Gram-positive, endospore-forming (heat-resistant), anaerobic
Clinical signs: flaccid paralysis; three forms (foodborne, infant, wound); nausea, vomiting, diarrhea, double vision, difficulty speaking; death comes from respiratory muscle paralysis
Pathology: disease is an intoxication by neurotoxins (A-H) (toxins are destroyed by boiling); botulism toxin blocks the release of ACh at the NMJ; can come from honey (infant), gravel/black-tar heroin (wound)
Lab Diagnosis: toxin activity tested in a mouse assay
Treatment: Repeated washing of the GI tract, administer antibodies against the toxin
EXTRA FACTS: used as a bioweapon in aerosolized form, used to eliminate wrinkles by inducing paralysis - 67Clostridium tetaniCharacteristics: Motile, Gram-positive rod with a terminal endospore (lollipop/tennis racquet appearance); vegetative cells are very oxygen-sensitive
Clinical signs: TETANUS; lockjaw, perspiration, drooling, back spasms, irregular heartbeat
Pathology: Spore enters skin through wounds, spore germinates (anaerobic conditions), tetanus neurotoxin is produced which blocks release of an inhibitory NT, and muscular contraction occurs with no relaxation
Lab Diagnosis: bacterium is rarely isolated, diagnosed by symptoms
Treatment: cleaning of wounds, passive immunization with anti-toxin, antibiotics (penicillin), immunization with toxoid (inactivated toxin) - 68What are the general features of Rickettsias spp.?Small, rod-shaped or coccobacilli, non-motile, Gram-negative (poorly), many transmitted by insects and ticks, and are obligate intracellular parasites
- 69Rickettsias rickettsiaeCharacteristics: Transmitted by ticks, causes ROCKY MOUNTAIN SPOTTED FEVER, most in men 40-60 years old
Clinical signs: fever, chills, headache, muscle pain, nausea, rash, joint pain, diarrhea
Pathology: Replication in endothelial cells, leakage of blood vessels
Diagnosis: culture not useful (use immunostaining)
Treatment: tetracyclines, chloramphenicol - 70Difference between Rickettsia and EhrlichiaRickettsia: Endothelium (host target cell), cytosol (cellular location)
Ehrlichia: Leukocytes (host target cell), cytoplasmic morulae (cellular location) - 71Ehrlicia chaffeensisCharacteristics: obligately intracellular, gram-negative cocci, grow as vacuole-bound Morulae, transmitted by LONE STAR TICK
Clinical signs: Causes monocytic ehrlichiosis, can be asymptomatic; fever, headache, muscle ache (sometimes rash)
Lab Diagnosis: low WBC count, immunofluorescence assay, PCR, isolation
Treatment: tetracyclines - 72Bartonella henselaeCharacteristics: Gram-negative bacilli, fastidious growth requirement (enriched blood agar, carbon dioxide, several weeks needed), facultative intracellular bacteria, causes CAT SCRATCH DISEASE
Clinical signs: cats usually asymptomatic; in humans, papule/pustule, regional adenopathy; in immunocompromised patients: bacillary angiomatosis (vascular proliferative disease), bacillary peliosis hepatitis (blood-filled cavities in the liver)
Pathology: transmitted to the cats from fleas (Ctenocephalides felis), more common in cats in warm climates
Diagnosis: history of cat contact, positive skin test response to antigen, histopathology of nodes
Treatment: azithromycin (most resolve without therapy) - 73General characteristics of SpirochetesGram-negative, motile (flagella beneath outer membrane), spiral-shaped, extracellular pathogens
- 74LeptospiraCharacteristics: genus of Spirochetes
Pathology: comes from water contaminated with rodent/animal urine, causes Leptospirosis
Rowers, tri-athletes at risk - 75Borrelia burgdorferiCharacteristics: cause Lyme disease
Clinical signs: BULLS EYE RASH (aka erythema migrans) (Stage 1), joint/muscle pain, irregular heartbeat, facial paralysis, conjunctivitis (stage 2); arthritis, immune disorder, advanced neurological disorders (stage 3)
Diagnosis: clinical signs, prevalence of ticks, culture from skin lesions, ELISA, Western blot, PCR
Treatment: tetracycline, erythromycin; some arthritis in later stages is treatment-resistant - 76Treponema pallidumCharacteristics: very difficult to grow in vitro (impossible to grow cell-free), humans are the only reservoir
Clinical signs: PRIMARY: lesion 2-10 days post infection (small, hard chancre at site), very infectious serous exudate forms in the center, regional lymph nodes may become enlarged, chancre erodes within 3-8 weeks; SECONDARY: 2-12 weeks after infection, widely disseminated bacteria causing rash, mucous patches/erosions in mouth, fever, headache, hair loss, joint pain, very infectious; lasts several weeks and then subsides; TERTIARY: occurs in less than half of untreated patients; 10-30 years after start of latent period, causes dementia, weakened aorta, necrotic areas, ataxia, ulcerating gumma, perforation of the palate; CONGENITAL: transmitted from mother to fetus, rash, multi-organ malformations, bone destruction, mental developmental problems
Pathology: transmitted through sexual contact or contact of infected regions (mucous membranes, open wounds) - 77Treponema pallidum (cont.)SYPHILIS
Diagnosis: prolonged staining (Giemsa) yields a pale pink appearance, non-treponemal tests (use cardiolipin as an antigen), RPR (rapid plasma reagin), VDRL (venereal disease research lab), complement fixation, FLUORESCENT TREPONEMAL ANTIBODY ABSORPTION TEST (fluorescence when positive)
Treatment: penicillins, tetracyclines - 78General characteristics of ChlamydiasObligate intracellular parasites, must be cultivated in lab animals or cell culture, Gram-negative coccobacilli, transmitted by interpersonal contact, do not require insects as vectors, DIMORPHIC/BIPHASIC life cycle
Diagnosis: isolation in cell culture; PCR MOST WIDELY USED, serological detection using fluorescent Abs
Treatment: ribosome inhibitors most effective (tetracycline, azithromycin) - 79Chlamydia-Chlamydophila developmental cycleElementary body = infectious form
Reticulate body = replicating form
EB binds to host cell, host cell takes up EB by phagocytosis, EB reorganizes to form RB, RB replicates by binary fission, asynchronized differentiation of RBs to EBs, then the EBs are released by either exocytosis or cell lysis - 80Chlamydia trachomatisCharacteristics: subdivided into different serovars, some of which are predominantly associated with one disease
Trachoma: leading cause of preventable blindness in the world, transmitted eye to hand to eye, children at greatest risk; causes tears, inflammation of conjunctiva, eyelid deformities, and eventually blindness
Inclusion Conjunctivitis: caused by serotypes D-K, common in infants, causes yellow discharge and swelling of eyelid, treated with erythrommycin
Non-gonococcal Urethritis: caused by D-K serotypes, most common bacterial STD in the US, women more likely to be asymptomatic, manifests as genital discharge, can cause epididymitis
Lymphogranuloma venereum: L serotypes, STD, rare in the US, more common in men, primary lesion is a tiny ulcer which then invades the lymph - 81Chlamydophila psittaciClinical signs: sudden headache/fever, non-productive cough, disorientation/delirium
Pathology: transmitted by contact/inhalation of infected bird droppings; rare in the US; pet shop owners, poultry workers at risk; SELDOM transmitted from person to person - 82Chlamydophila pneumoniaeCharacteristics: only one serotype, humans are the only known host, common cause of mild pneumonia
Clinical signs: can by asymptomatic, or mild cough and malaise
Pathology: transmitted person to person; correlation with atherosclerosis - 83General characteristics of Mycoplasmas and UreaplasmasExtracellular parasites, smallest free-living bacteria, lack peptidoglycan and other cell wall constituents, pleomorphic, some have terminal "tip" structures (look like fried egg)(M. pneumoniae, M. genitalium), BOUNDED BY A SINGLE MEMBRANE
- 84Mycoplasma pneumoniaeCharacteristics: extracellular pathogen (targets respiratory epithelial cells)
Clinical signs: causes ciliostasis (shedding of epithelial layer), impeding of upper resp. tract clearance, persistent cough, mild upper resp. disease
Pathology: transmission by aerosolized droplets, adheres via a specialized tip structure
Diagnosis: grows on serum-containing media, cold agglutination test (non-specific), serological and DNA based tests available
Treatment: ribosome inhibitors (tetracycline, erythromycin), NOT PENICILLINS - 85Ureaplasma urealyticumCharacteristics: a "mycoplasma" that produces urease enzyme (breaks down urea which causes inflammation)
Clinical implications: causes STD of human genital tract, causes NGUrethritis
Treatment: erythromycin and tetracycline