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Karteikarten von Brianne Schmiegelow, aktualisiert more than 1 year ago
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Erstellt von Brianne Schmiegelow
vor mehr als 8 Jahre
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| Frage | Antworten |
| What 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 |
| What 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) |
| What 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 |
| What is the major component of mycobacteria membranes? | Long-chain mycolic acids Form a waxy coat |
| What diseases are caused bd by mycobacteria with a tuberculosis complex? | M. tuberculosis, M. bovis, M. africanum, M. microti, and M. canetti |
| What diseases are caused by by nontuberculous mycobacteria? | Hansen's disease (leprosy) caused by M. leprae or M. lepromatosis Buruli ulcer caused by M. ulcerans |
| What is tuberculosis? | A disease caused by mycobacteria 1/3-1/2 of human population is latently infected Transmitted through inhalation of aerosols |
| How 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 |
| What is the infectious dose of mycobacteria? | ~10 bacteria |
| How does the immune system eradicate an active tuberculosis infection? | Bacteria are "contained" within a granuloma The bacteria remain viable, but are essentially quarantined |
| What 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 |
| What results from spontaneous healing in primary TB? | Ghon complex (enlarged hilar lymph node + calcified peripheral lung lesion) |
| What 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 |
| What 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 |
| What is Lowenstein-Jensen medium used for? | It is highly selective for Mycobacterium spp. TB forms a brown, granular appearance |
| How 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 |
| What is leprosy? | A chronic infection with Mycobacterium leprae that affects the cooler portions of the body leading to disfigurement, deformity, mutilations, and blindness |
| What 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 |
| How does M. leprae replicate? | It replicates within macrophage/dendritic cells and Schwann cells causing nerve damage |
| What 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 |
| What 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 |
| How 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 |
| What 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 |
| What mediates the buruli ulcer? | Mycolactone TOXIN Causes cell cycle arrest, apoptosis, and necrosis |
| What's the difference between yeastn yeasts and molds? | Yeasts are budding single cells and molds are filamentous forms Both are fungi! |
| Cryptococcus neoformans | Budding yeast that is commonly found in guano-enriched soils and carried by pigeons Transmitted by inhalation of infectious agent |
| What is the most common cause of meningitis in sub-saharan HIV patients? | Cryptococcus neoformans |
| What are the clinical presentations of Cryptococcus neoformans? | Pulmonary infection with well-defined, non-calcified nodules on CXR Causes pneumonia, tissue necrosis, and ACUTE MENINGITIS |
| How 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 |
| What 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 |
| What 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 |
| Clinical presentations of Candida albicans | Mucocutaneous: oral thrush, diaper rash, etc. Most cases respond to topical antifungals! |
| What is Histoplasma capsulatum? | Dimorphic fungus Switch from mycelium to yeast is necessary for virulence (opposite of C. albicans) Promoted by bird and bat guano |
| What activities put you at a high risk for contracting Histoplasma capsulatum? | Construction, renovation, exploring caves, tilling soil, cleaning up bird roosting sites |
| What 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 |
| What 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 |
| What differences are there in protozoan reproduction? | In definitive hosts, reproduce sexually In intermediate hosts, reproduce asexually |
| What are the stages of protozoans? | Cyst: the inactive, non-motile, infective stage Trophozoite: the motile vegetative stage which colonizes host tissues/cells |
| Excyst vs Encyst | In protozoans... Excyst -> cyst becomes a trophozoite Encyst -> trophozoite becomes a cyst |
| What 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 |
| What is Entamoeba histolytica? | A parasite that is passed through infective cysts which excyst into trophozoites |
| How 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 |
| What 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) |
| What is Giardia lamblia? | Most common protozoan intestinal pathogen Non-invasive Beavers are reservoirs |
| What 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 |
| Clinical presentations of Giardia lamblia? | Diarrhea, gas, bloating, abdominal cramps, nausea, loss of appetite, weight loss Irritable bowel syndrome (post-infection) |
| What is Plasmodium falciparum? | Most virulent human malarial parasite (75% of cases) |
| What 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 |
| Why 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 |
| What is the life cycle of the malaria parasite | Pro-Erythrocytic -> Erythrocytic -> Sporogenic |
| What 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. |
| What are the intermediate hosts of malaria? | Humans |
| What 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 |
| What 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! |
| What 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 |
| What morphological changes in RBCs are caused by P. falciparum? | Knobs on the surface of infected RBCs that promote agglutination of RBCs and intracapillary sequestration |
| How do you diagnose malaria? | Stain blood with Giemsa stain -Thick smears used for presence of parasites -Thin smears used for species-level identification |
| How is malaria controlled? | Insecticide treated bed nets, indoor residual spraying, control/eradication of mosquito population |
| What is babesiosis? | Intracellular parasite that looks like Plasmodium spp. Reservoir: deer, cattle, and rodents B. microti and B. divergens cause most human infection |
| What is the vector for babesiosis spp.? | Ixodid (hard) ticks |
| What are the symptoms of babesiosis? | Malaise, fever, headache, and fatigue |
| What 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 |
| What species types have the enzymes superoxide dismutase and catalase? | Obligate aerobes and facultative aerobes Obligate anaerobes DO NOT |
| Clostridium perfringens | Characteristics: 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) |
| Clostridium difficile | Characteristics: 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) |
| Clostridium botulinum | Characteristics: 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 |
| Clostridium tetani | Characteristics: 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) |
| What 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 |
| Rickettsias rickettsiae | Characteristics: 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 |
| Difference between Rickettsia and Ehrlichia | Rickettsia: Endothelium (host target cell), cytosol (cellular location) Ehrlichia: Leukocytes (host target cell), cytoplasmic morulae (cellular location) |
| Ehrlicia chaffeensis | Characteristics: 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 |
| Bartonella henselae | Characteristics: 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) |
| General characteristics of Spirochetes | Gram-negative, motile (flagella beneath outer membrane), spiral-shaped, extracellular pathogens |
| Leptospira | Characteristics: genus of Spirochetes Pathology: comes from water contaminated with rodent/animal urine, causes Leptospirosis Rowers, tri-athletes at risk |
| Borrelia burgdorferi | Characteristics: 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 |
| Treponema pallidum | Characteristics: 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) |
| Treponema 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 |
| General characteristics of Chlamydias | Obligate 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) |
| Chlamydia-Chlamydophila developmental cycle | Elementary 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 |
| Chlamydia trachomatis | Characteristics: 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 |
| Chlamydophila psittaci | Clinical 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 |
| Chlamydophila pneumoniae | Characteristics: 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 |
| General characteristics of Mycoplasmas and Ureaplasmas | Extracellular 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 |
| Mycoplasma pneumoniae | Characteristics: 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 |
| Ureaplasma urealyticum | Characteristics: 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 |
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