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147 Cards in this Set
- Front
- Back
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What is "meth mouth"?
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characterized by the following:
-xerostomia (dry mouth) -clenching/grinding of teeth -lack of oral hygiene -cravings for high-sugar food and beverages -teeth are often not salvageable |
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Describe the characteristics of S. mutans that contribute to plaque formation.
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-part of normal flora of oral cavity
-lactic acid fermentation decreases the pH -facultative/aerotolerant anaerobe -has glucosyltransferase (virulence factor) which converts sucrose-->glucan-->leads to adherence to tooth surface -initiation of dental caries |
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Describe the characteristics of Lactobacillus spp.
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-small part of normal oral flora
-lactic acid fermentation lowers oral pH -grows in low pH environ. -facultative/aerotolerant anaerobe or microaerophile -functions in the progression of caries |
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Describe the characteristics of Actinomyces viscosus in the oral cavity.
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-primary colonizer of dental plaque
-facultative/microaerophile, catalase + -role still unclear, but implicated in root surface caries |
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Describe the characteristics of Veillonella spp.
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-normal oral flora
-anaerobic -lactate-->weaker acids-->increases pH -has a possible anticarcinogenic role |
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Describe the relationship of diet with cavity formation.
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direct rltshp. btwn. caries and carb intake
-frequency of sugar intake seems to be more important than amount -sucrose: most cariogenic sugar, it is a substrate for lactic acid fermentation, used by S. mutans-->glucan-->adherence -low or non-cariogenic sugar subs include saccharin, sucralose (splenda), aspartame, xylitol |
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How can saliva help to prevent cary formation?
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it washes away food particles and unattached microbes
-buffering capacity to neutralize acids -large amounts of Ca and P ions lead to remineralization |
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How is a diagnosis of caries made?
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1)visual
-white spot on tooth enamel happens early and is first sign -fissure lesions often appear brown -root lesions appear leathery -cavitation viewed by eye or radiograph -quantitative light-induced fluorescence for early detection 2)tactile -use of probe to check surface texture (will be soft to probe) 3)quantification of cariogenic bacteria -mainly S. mutans and Lactobacillus |
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Briefly describe chronic gingivitis.
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-it is an inflammatory response limited to the marginal gingiva w/o bone loss or deep periodontal pockets
-usually reversible with tx with removal of plaque and calculus and good oral hygiene -found in kids and adults -common signs/sx are red,swollen gums, bleeding gums and halitosis -there is an increase in Actinomyces (+), Capnocytophaga (-)-obligate anaerobes |
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What is periodontitis?
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-progression of gingivitis to include loss of collagen attachment to the tooth and bone, loss of bone, and to deep periodontal pockets,
-cause of most tooth loss in adults |
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Describe the epidemiology and clinical signs and sx of chronic periodontitis
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-the prevalence/severity increases with age and this is not usually found in kids
-inflamed gums, gingival recession, bleeding pockets, tooth mobility/migration, bone loss around teeth, halitosis and unpleasant taste, usually no significant pain |
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What is the pathogenesis of chronic periodontitis?
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-spread of subgingival plaque causes pocket formation and enlargement-->anaerobic environment-->increased replication of anaerobic organisms
-inflammation below the pocket epithelium leads to destruction of CT and bone -several diff. microbes involved |
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Describe porphyromonas gingivalis and its role in periodontal disease.
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-part of normal flora but an opportunistic pathogen
-gram neg. coccobacilli -black pigmented anaerobe-requires hemin-->porphyrin pigment -cannot survive on metabolism of carbs -may require vit. K and peptides -virulence factors include fimbriae, hemagglutinins, hemolysins, proteases, polysaccharide capsule (K antigen), outer membrane vesicles |
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What are the bacteria of chronic periodontitis?
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Prevotella intermedia, tannerella forsythia (these 2 are similar to poryphromonas but do ferment carbs), capnocytophaga spp, porphyromonas gingivalis
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Describe capnocytophaga spp and its contribution to periodontitis.
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-part of normal flora
-gram neg bacilli, fusiform/spindle shaped -has gliding motility -facultative anaerobe -capnophilic -most associated with aggressive periodontitis |
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What is the tx for chronic periodontitis?
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-mechanical therapy-removal of plaque by scaling or planing
-surgical removal of inflamed tissue -replacement of lost teeth -oral hygiene improvements -antimicrobial agents (mouthwashes, abx) |
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Describe aggressive periodontitis.
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it is rare and may be inherited
-occurs in young ppl but rarely before puberty -more common in asians and W. africans -more common in females than males -cases often cluster in families -can be localized or generalized-localized form often begins with incisors or first molars -associated with bone loss around teeth -often does not present with bleeding, inflammation, or plaque accumulation -associated with immune deficiencies -tx is same as for chronic periodontitis |
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What type of bacteria are associated with aggressive periodontitis?
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some evidence for a specific association with aggregatibacter actinomycetemcomitans
-often isolated with actinomyces spp, gram - CB, capnophilic, microaerophile, tetracycline sensitive -colony morphology is not consistent |
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Describe acute necrotizing ulcerating Gingivitis (ANUG)--trench mouth.
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-there are several predisposing factors such as poor oral hygiene, malnutrition, heavy smoking, emotional stress, recent infections
-signs/sx include red gums, inflamed, shiny, bleeding with ulcers, lesions are painful and covered by a pseudomembrane, halitosis, pt. may notice a metallic taste, usually no LN involvement, fever, or malaise |
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Describe the characteristics of Fusobacterium nucleatum and its role in ANUG.
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-part of normal flora
-obligate anaerobe, coaggregates with other bacteria -virulence factors include adhesins and endotoxin |
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Describe the characteristics of Treponema spp. and how it contributes to ANUG.
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includes T. vincentii, T. denticola
-obligate anaerobes -oral spirochetes can be grown in vitro in OTI medium -have periplasmic flagella for motility |
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Describe the microbes that contribute to ANUG.
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-microbes are anaerobic
-polymicrobial infection: fusospirochetal complex-oral spirochetes classified as treponema, but some sources list Borrelia as a potential cause -other organisms may be present such as bacteroides, prevotella, veillonella, and strep spp. |
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How is diagnosis of ANUG made?
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-fusobacteria presence
-spirochetes -leukocytes |
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What is noma?
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also called cancrum oris, gangrenous stomatitis
-extremely severe form of ANUG -happens in young children in developing countries -associated with severe malnourishment, recent infection usually viral or TB -the immune system is compromised-->lesion spreads-->tissue destruction and permanent disfigurement -abx and nutrition can stop disease progression but reconstructive surgery is required |
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What is Ludwig's angina?
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-signs and sx include swelling of the tissue at the front of the neck and fever
-caused by an endogenous infection with prevotella, porphyromonas, fusobacterium, anaerobic strep -usually spreads from dental or post-extraction infection -infection spreads B/L through sublingual or submandibular spaces -swelling of the glottis or tongue can lead to airway obstruction -tx includes making sure airway remains patent, abx tx, surgical drainage and removal of infection source |
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Describe a periodontal abscess.
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-signs/sx include red, swollen, and tender gingiva overlying the abscess
-continuous pain or pain with biting -infection often remains localized due to intermittent pus drainage through pocket or through alveolar bone -if left untreated leads to destruction of periodontal tissue and tooth loss -arises from a polymicrobial endogenous infection from subgingival plaque bacteria such as prevotella, poryphyromonas, fusobacterium, etc -tx: extraction of the tooth may be required, drainage of pus and irrigation of pocket with saline/mouthwash, abx in some cases |
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Describe cervicofacial actinomycosis.
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-not common
-associated with trauma or invasive oral procedures -signs/sx include submandibular region is most commonly affected, swelling, fibrosis often present around areas of swelling, pus is gritty/sand-like and contains visible, yellow granules -results from infection from endogenous flora, can be a mixed infection -actinomyces israelii is the most common culprit, anaerobic, granules are washed, ground and cultured on blood agar under anaerobic conditions at 37C -colonies have "molar tooth" morphology -areas of suppuration are surrounded by fibrosing granulation tissue tx:surgical drainage of abscess, long term abx |
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Describe oral candidiasis.
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-opportunistic
-primary oral candidiasis is pseudomembranous, erythematous, hyperplastic, candida associated lesions are multifactorial, anti-fungal therapy alone is not sufficient such as in denture induced stomatitis, etc -secondary oral candidiases are oral manifestations of systemic mucocutaneous candidiasis (not going to focus on this) |
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Describe the pathogenesis of oral candidiasis-thrush.
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the yeast cells adhere to fibronectin and/or extracellular matrix
-cells form pseudohyphae which can penetrate underlying tissues -diagnosis is made through clinical presentation, microscopic exam. of yeast, and germ tube test |
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Describe candida-associated denture stomatitis.
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-common in full time denture wearers or other orthodontic appliances
-erythema and edema of mucosa in contact with surface of upper denture, mucosa below the lower denture usually not involved -accumulation of plaque biofilms containing yeast and bacteria -contributing factors include poor hygiene, dentures that don't fit properly, iron and folate defic, DM, carb rich diet tx:antifungals |
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Describe herpes simplex virus.
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HSV1 (usually above waist) and HSV2 (usually below waist) can BOTH cause ORAL and genital lesions
-primary infection is asx , recurrences cause cold sores/fever blisters -linear dsDNA genome, large enveloped virus -envelope contains attachment proteins, fusion proteins, structural proteins, -persistent infections in neurons, lytic infections in epithelial cells/fibroblasts |
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Describe the epidemiology of HSV.
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very common infection, HSV 1 more prevalent
-primary infection usually occurs in children/adolescents -no seasonal incidence -humans are only reservoir -can be spread by contact with saliva, vesicular fluid, vaginal secretions |
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Describe the pathogenesis of HSV in primary infection.
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-virus replicates in mucoepithelial cells
-often asx -gingivostomatitis most often seen in children-lesions on oral mucosa, tongue, or gums,mild to severe fever, enlargement of LN, pain in mouth and throat, gingiva inflamed -pharyngotonsillitis seen in adolescents/adults with primary infection of oropharynx -lesions on tonsils -herpetic whitlow-finger lesion -infection of neuron and retrograde transport to trigeminal gangliaj -virus remains latent until reactivated-lifelong -virus travels to epithelium innervated by neuron and produces vesicular lesion, immune response limits spread and severity |
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Describe HSV reactivation.
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-clinical presentation of lesions
-do a cell culture -Tzanck smear-exam. of cells at the base of the lesion, will see multinuc. giant cells, cowdry type A intranuclear inclusions -serology is not useful except in primary infections |
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What does coxsackie A cause?
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herpangina
hand-foot-mouth disease aseptic meningitis |
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Describe the characteristics of coxsackie A virus.
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-enterovirus, +ssRNA genome
-small, non-enveloped -infections are highest in the summer, seen mainly in kids at daycare, schools -infection milder in kids than adults -associated with areas of poor sanitation and crowding -humans are only reservoir -spread primarily by fecal/oral route, some by resp. -infects mucosa and lymph tissue but replication in secondary sites is responsible for sx |
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What is gastroenteritis?
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inflammation of the stomach and intestine
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What causes gastroenteritis?
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a wide range of organisms
-many result in no tissue inflammation -one of the most common diseases of humans -sx range from mild diarrhea to severe disease needing hospitalization -viral gastroenteritis is a frequent cause of mortality in kids in developing nations (esp. rotavirus) |
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What are the sx of gastroenteritis?
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nausea, diarrhea, vomiting, cramps, malaise, anorexia, myalgia, HA
-acute, watery diarrhea is the MAIN CLINICAL FEATURE -the clincal pres. of disease caused by viral agents is indistinguishable but epidemiology varies and gives clues to diagnosis |
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In the US, what causes most cases of gastroenteritis?
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viruses
-small inocula are required for disease -they replicate in sm. int. epithelial cells with overall mild tissue destruction -15-48 hr. incubation period and disease is short duration, 3-5 days -viruses may be shed at low levels for days-weeks after illness |
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What are the high risk groups for viral GI infection?
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hospital wards, daycare centers, nursing homes, immunosuppressed, travelers, military
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How is viral GI infection diagnosed?
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1)direct detection of virus in fecal samples by electron microscopy
2)rotavirus group A antigen (VP6 inner capsid protein) detection by enzyme linked immunosorbent assay or less sensitive latex agglut. procedures |
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What is the epidemiology of viral gastroenteritis?
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there are 2 chief settings for viral diseases
1)childhood diarrhea (2 yo and under) -occurs early in life, infection rates are similar in developed and third world countries implying that transmission is effective even in locations in which clean water and food are available 2)outbreaks -fecally contaminated food is common source (noroviruses), often raw shellfish -usually older kids and adults |
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Describe the structure of rotaviruses.
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-in the family reoviridae
-DsRNA genome , 11 segments -virus capsid contains its own RNA dependent RNA polymerase -they are fairly large virions -7 spp. groups of humans and animal rotaviruses based on VP6 antigens are known and designated A-G, most human disease caused by spp. groups A, B, C -the virion outer layer contains the key targets for neutralizing abs, VP4 (P protein) and VP7 (G protein) -US strains generally designated by G protein serotype with types G1-4 and G9 being most prevalent -only virus to date that has been proven to encode an enterotoxin! |
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Describe the epidemiology of rotavirus.
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most children have been infected by age 2 and problems with infection become minimal after that age
-initial infection after age of 3 mos. is most likely to result in severe disease with most severe cases falling btwn 3-36 mos of age -predictable, annual winter outbreaks peaking first in the South -most frequent cause of indentifiable infantile gastroenteritis -nosocomial outbreaks also well known for this virus |
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Describe the mechanism of rotavirus GI infection.
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infects sm. intestine villi enterocytes, disrupts osmotic function
-leads to a 5-7 day course of fever and vomiting |
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What 2 factors favor rotavirus persistence?
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1)constant source of susceptibles due to birth
2)antigenic variability facilitated by segmented genome shifts |
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Describe the rotavirus enterotoxin.
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NSP4 (nonstructural protein 4)
-stimulates secretion in the absence of histological alterations -triggers a Ca dependent signal transduction pthway in the intoxicated cell -mobilizes Ca from the ER, Chloride secretion is enhanced |
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What is the 2 receptor model for rotavirus intoxication?
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1)virion binds at cell surface receptor
2)NSP4 is produced in infected cell and released into intestinal lumen 3)NSP4 is bound at separate specific receptors on adjacent cells 4)secretory pthways are stimulated |
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What strengthens the rationale for rotavirus vaccines?
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the fact that further improvements in water and gen. hygiene are unlikely to decrease infections and the high level of rotavirus morbidity in the US
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Describe rotashield.
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-live atten. prep. of a reassortment virus for infants admin. at 2, 4, 6 mos of age
-after 800,000 kids received the vaccine a statistical link btwn. the vaccine and intestinal intussuception was made and rotashied was voluntarily removed from the market -decision is controversial -need to weigh risks with benefits |
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Describe rotarix.
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monovalent vaccine employing a live, attenuated human strain intended to provide protection against rotavirus strains G1, 3,4 9
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Describe Rotateq.
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live, oral vaccine contains 5 reassortment viruses from human and bovine strains.
-express human serotype proteins G 1-4 and P1A -3 doses starting at 6-12 wks at 4-10 week intervals -vaccine virus is shed in some pts -routine admin. of 3 doses recommended at 2,4, 6 months -rotavirus vaccines are working b/c the magnitude of the disease has been cut nearly in half |
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Describe the characteristics of the enteric adenoviruses.
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-dsDNA
-acid resistant capsid allows for gastric infections -causes endemic, severe diarrhea of infants -extended period 5-12 days of diarrhea fever, and vomiting caused by serotypes 40 and 41 mostly |
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How is adenovirus detected?
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immunoassay detection
-some molecular detection systems based on nucleic acids have also been developed -these viruses are fastidious and difficult to grow in culture |
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Describe the characteristics of caliciviruses.
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-2 genera that are pretty similar
1)sapporo-like viruses (classical or typical) 2)norwalk and SRSVs now known as noroviruses -non-enveloped, ssRNA genomes -epidemics of acute onset diarrhea and vomiting -typically mild and self-limited attacks of 24-48 hr duration -they are unculturable and very resistant to inactivation |
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Describe the epidemiology of caliciviruses.
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-produce disease in older children and adults in contrast to the other agents which principally affect young kids and infants
-classically associated with food (shellfish), but they are efficiently transmitted person to person and via contaminated surfaces and water as well as in food -immunity to reinfection is shortlived so multiple repeat infections possible |
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Describe astroviruses.
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ssRNA, star-shaped apparent on capsid by electron microscopy
-shed in large numbers in stool but seem less pathogenic than Norwalk viruses -probable infection of sm int -sporadic epidemiology, no seasonal link evident |
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Describe the epidemiology of Astroviruses.
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-sporadic, no seasonal link
-epidemic disease has been confirmed in young kids, peds wards, day cares and nursing homes -definitive diagnosis by electron microscopy |
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Describe the epidemiology of cholera.
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-acute diarrheal disease due to Vibrio cholerae infection
-disease is found worldwide, cause of massive human morbidity and mortality -causes periodic epidemics and pandemics -a frequent attendant of disasters (natural and human made) |
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What are the clinical manifestations of cholera?
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-it colonizes the sm. int. mucosa
-the colonized mucosa shows NO change in physical integrity -acute and massive watery diarrhea is the main feature, "rice water" stools -rapid depletion of fluids and electrolytes causes hypovolemic shock, met. acidosis and death -typically self-limiting and pts. recover if they can withstand the fluid loss -incubation period 1-5 days -massive volume watery diarrhea is cardinal sign (1L/hr) -mm. cramps, poor skin turgor, wrinkled skin over fingers, sunken eyes, missing pulse in extremities |
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Describe the characteristics of vibrio cholerae.
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gram neg. vibrio bacterium
-nonspore former -facultative anaerobe -motile, polar flagellum -classified by O antigens -2 serotypes are of concern: 1)serogroup O-1 2)serogroup O-139 |
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Describe cholera serogroup O-1.
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-classic epidemic cholera
-contains the epidemic associated biotypes "classic" and "el tor" -biotype El tor is now the dominant cause of O-1 serogroup caused cholera epidemics (it survives better in the environment) -both biotypes may be divided into additional epidemic associated serotypes: Inaba, Ogawa, Hikojima |
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Describe cholera serogroup O-139.
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-newly recognized cholera agent that appeared in 92 in India and has spread rapidly
-until this agent appeared all cholera was thought to be caused by serogroup O-1 -O-1 LPS synthesis genes were deleted and replaced with new genes in the O-139 strain -it can cause disease in ppl who have recovered from previous O-1 infection |
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What are the virulence factors of the cholera O-1 and O-139 strains?
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1)major pathogenic factor is the enterotoxin
-cholera toxin (or choleragen), product of phage encoded ctx AB genes, has A/B subunit structure -A is the active portion, enzyme that ADP ribosylates a GTP binding protein that regulates cAMP production -cAMP levels increase causing hypersecretion of water and electrolytes and severe diarrhea -B subunit is the binding portion 2)toxin coregulated pilus gene product-needed for attachment to host |
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What is CTX?
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a mobile genetic element
-a filamentous virus related to M13 -the cholera toxin genes are located on this DNA fragment called the CTX gene element, present on a chromosomal pathogenicity island -the CTX virus receptor is another virulence factor, the product of the tcp gene (toxin coregulated pilus), a proteins needed for V. cholerae attachment and colonization |
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What controls the expression of tcp and ctx genes in cholera?
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the toxR gene product, ToxR
-both genes are in effect environmentally regulated -they are expressed optimally in the sm. int. of the host -iron levels control expression, higher exp. when iron level is LOW -the ctx and tcp genes are examples of operons controlled by a 2 component signaling system -ToxR senses environment, activates the ctxAB operon to produce toxin and the tcp operon to produce the toxin coreg. pilus when appropriate -cells can take account of the total population levels to activate and deactivate genes accordingly |
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Describe the VPI pathogenicity island in cholera.
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-stands for vibrio cholerae pathogenicity island
-it is a discrete region of the chromosome in which genes required for pathogenicity are clustered -the gene for the CTX virus receptor (tcp) is located on the VPI -the entire pathogenicity island, VPI, is the genome of another filamentous bacteriophage, VPI phage -the VPI virion coat is composed of the tcp gene subunit A gene product |
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Describe the sequential lysogenic conversions of cholera that lead to dangerous virulence.
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-a virus delivers pathogenic factors to the host (first lys. conversion event) that sets up the second lysogenic conversion event (the cholera toxin gene is delivered by CTX phage infection) by providing the receptor allowing that second virus infection to occur
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Describe the clinical manifestations of shigella.
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-facultative intracell. enteric bacilli causing an inflammatory disease of the large bowel
-inc. period 72 hrs -disease ranges from moderate diarrhea to severe dysentery -initial sx are fever, cramps, vomiting, watery diarrhea with progression to blood, mucous and PMNs in stools, cramps |
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Describe shigella.
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gram neg rod
-nonspore former -facultative anaerobe -nonmotile -lactose non-fermenter-enables to be distinguished from the normal flora bacterium E. coli |
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Describe the virulence factors of Shigella.
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1)enterotoxins-watery diarrhea that precedes dysentery
2)surface O antigen-in concert with other proteins introduced directly into the host cell by a type III secretion system, induces endocytosis into follicle-associated M intestinal cells of Peyer's patches by provoking ruffling and endocytosis (M cells binds antigens from the intestinal lumen and present to immune cells) -shigella will lyse phagosome and escape into the cytoplasm with cell to cell transmission to epithelial cells from basolateral side -results in inflammatory response drawing PMNs into region which further destabilizes tissues and enhances invasion 3)actin binding protein-promotes movement of microbe within and from cell to cell, adheres to actin and forces polymerization 4)shiga toxin -disruption of protein synthesis and damage to the int. epi., cleaves large ribosome subunit, may also activate macrophage apoptosis |
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How is diagnosis of Shigella made?
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-suspect shigellosis in any pt. with fever and diarrheal disease
-blood and mucus in feces plus an acute onset of disease 1)microscopic exam. of feces-PMNs and RBCs present, NOT seen in diarrhea caused by enterotoxins 2)culture-plate sample quickly, interfering spp. will overgrow shigella -blood tinged flecks of mucus are the ideal sample -does not ferment lactose which enables it to be distinguished from the normal flora bacterium E. coli 3)immunofluorescence techniques 4)sigmoidoscopic exam-shigellosis will show diffuse involvement of mucosa, multiple shallow ulcers amoebae infection will show focal patterns of ulcers |
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What is the tx for shigella?
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it is a self limiting disease
-requires fluid replacement, effective abx therapy may shorten course, eliminate carriers -the problem is that many shigella are MDR so must employ susceptibility testing |
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What are the complications of shigella?
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long term carrier state development is possible
1)Reiter's syndrome (urethritis, polyarthritis, inflamm. eye disease, skin lesions)-nonspecific acute inflamm. arthritis that ranges from slight to severe, strong assoc. with HLA B27 ppl 2)hemolytic uremic syndrome (HUS)-S. dysenteriae, type 1 infection (shiga toxin production), acute renal failure with poor prognosis 3)AI disease-plasmid encoded antigen reacts with host myosin |
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Describe the epidemiology of shigella.
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-humans are the sole reservoir for this agent
-person to person (fecal/oral) transmission primarily -food and water may sometimes be vehicles, ready to eat food touched by infected food workers -houseflies may play transmission role in tropics (no disease or replication in fly gut, primarily due to mechanical vectoring of fecal matter) -HIGHLY INFECTIOUS, LOW DOSE ORGANISM -often found in high numbers around toilets used by infected individuals -increased incidence in late summer -four spp (serological grps. A is most severe, D is least) -highest incidence in kids 1-4 yrs old |
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In the US, what species of shigella cause most cases?
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S. flexneri (gay males), S. sonnei (kids) (group B and D respectively)
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What is the single most important control measure for shigella?
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hand washing
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Describe the clincal manifestations of salmonella.
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-incubation of 12-48 hrs
-sudden onset of disease-fever, chills, cramps, diarrhea, vomiting -2-3 days duration in normal host -disease typically more severe in infants and elderly -also at greater risk are cancer pts., AIDS pts, diabetics, persons on abx therapy |
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Describe the characteristics of salmonella.
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gram neg rod
-nonspore former -facultative anaerobe -motile, lactose non-fermenter |
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What are the virulence factors of salmonella?
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1)enterotoxin
-invasion of mucosal cells may induce mucosal invasion genes, induction of cytoskeletal changes which causes host to engulf bacterium -this microbe can enter either M or intestinal epithelial cells -invasion genes are controlled by O2 status (active under anaerobic conditions) -infection pattern is distinct from shigella b/c salmonella don't leave the phagosome but simply tolerates all host attempts to kill it -has LPS-systemic disease sx leading to endotoxic shock -resistance to serum killing -acid resistance -phoPQ-controlled genes for phagocyte survival |
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How is diagnosis of salmonella made?
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culture-sample both food items and water, fecal matter, blood if fever is evident
-salmonellae do not ferment lactose which allows you to distinguish them from E. coli -use salmonella/shigella other selective agar-cells that cant ferment lactose have white colonies, others are bright red -fluorescent abs test -serological confirmation |
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What is the tx for salmonella?
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supportive for pt. in good health
-maintain fluid and electrolytes -abx not required in otherwise healthy pt if disease is not systemic -AIDS/immunocompromised pts. require more active intervention |
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Describe the epidemiology of salmonella.
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-primarily a disease of developed countries through improper handling of foods
-animal reservoirs and foods of animal origins are at issue primarily: eggs, beef, pigs, also dogs, cats, pet reptiles -in contrast to shigella, salmonella is a high dose microbe -usual route by contam. food or water (person to person rare but has happened) -infants more susceptible (6mos-5yrs) -infection increases in SUMMER AND FALL -convalescent carrier state recognized, up to a yr in infants |
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Describe the characteristics of systemic (endemic) mycoses.
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-dimorphic-have thermal dimorphic conversion, soil fungus
-resp. and granulomatous infections -potential to disseminate -geographically restricted |
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Describe the morphology of coccidioides immitis.
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dimpophic, spherule with endospores, arthroconidium
-normally found in soil, white, gray, or brown colony -powdery or wooly colony |
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What are the useful antigens for immunodiagnosis of coccy immitis?
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coccidioidin
spherulin -these are produced in the broth in which the mycelium grows |
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What are the clincal manifestations of coccidiodes immitis?
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also called "the great imitator"
-has pulmonary primary involvement -influenza like manifestations, fever, lympadenopathy, malaise, cough -may develop into diffuse pneumonia -possibly asx -most infections are self-limited -disseminated disease-more common in certain races and nationalities, higher prevalence during prego, problem in immunodeficient ppl, -erythema nodosum has a good prognosis b/c functional cell mediated immunity(allergic response-no organisms present, delayed HS to fungal antigens, develops 1 month after infection) |
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What groups of people are more likely to experience disseminated coccidiomycosis?
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american indians, asians, af. amer., and hispanics, prego(elevated levels of estradiol and progesterone enhance growth), immunodeficiency, chorioretinitis
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What is the epidemiology of Coccidioides immitis?
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southwestern USA
airborne (not communicable) soil dwelling (arthroconidia) lab exposure (arthroconidia) |
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How is identification of coccy made?
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-KOH for fresh samples
-PAS for fixed tissue -spherical form under microscope -culture-mold 25 degrees -be cautious of arthrospores -IgM/IgG to coccidioidin/spherulin |
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What is the tx for coccy?
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DOC is Fluconazole or amphotericin B
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Describe the morphology of histoplasma capsulatum.
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has microconidium, macroconidium-projections
-white or brown colony, cottony colony, slow growing up to 12 wks |
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What is the antigen in histoplasma that can be useful for diagnosis?
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histoplasmin
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Describe the clinical manifestations of histoplasmosis.
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influenza like to severe lung disease
-described as a reticuloendothelial disease -microconidia are inhaled and develop into yeast cells -cells may be phagocytosed and disseminated |
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What are the virulence factors of histoplasmosis?
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yeast releases urease to raise pH and interferes with phagolysosome killing activity of phagolysosome
host resistance: PMN expresses fungistatic activity, intracell. parasite (macrophage), functional cell-mediated immunity is essential |
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What is the epidemiology of histoplasmosis?
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ohio and mississippi river valleys
-not communicable -soil enriched with droppings, found in bat's intestine |
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How is ID of histoplasmosis made?
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can see intracellular yeast
-isolation from site of infections -can use serologic latex agglutination |
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What is the tx for histoplasmosis?
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DOC: intraconazole or amphotericin B
supportive therapy |
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Describe blastomyces dermatitidis.
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-dimorphic, broad based yeast
-pneumonia, cutaneous (granulomas), disseminated-likely acquired via dissemination from initial pulmonary infection -ohio and mississippi river valleys -soil dwelling -infective stage is microconidium -under microscope will see yeast DOC:amphotericin B, itraconazole, fluconazole |
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Describe paracoccidioides brasiliensis.
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yeasts-multiple buds
-pneumonia and disseminated disease -confined to central and south america, soil dwelling -DOC is itraconazole (2 yrs) -control is to avoid breathing when in peru |
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What are the morphological features of candida?
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-macroscopically appear creamy colonies
-microscopic budding yeast cells at 37 C -C. glabrata is the only spp. that forms only yeast cells ( not able to form pseudohyphae or hyphal structures) -other spp. form pseudohyphae-produced with budding cells fail to detach from one another -true hyphae such as germ tubes ( C. albicans, C. dubliniensis) formed in serum -form chlamydospore or chlamydoconidia which are thick walled, large spores that form in nutritionally deficient medium -from blastoconidia (budding cells) -can use fermentation and assimilation rxns like carb. fermentation, uptake of CHOs, N, and other elements to differentiate btwn. diff. spp. of candida |
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Describe the pathogenicity of candida.
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-not many virulence factors
-attachment, all spp. are capable of attachment, germ tube is more adhesive than yeast cell -has a protease, phospholipase, and heat shock proteins |
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What are the risk factors for candidiasis?
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pregnancy, elderly, infancy, burn, infection, AIDS, hematological disorders, diabetes, hypothyroidism, oral contraceptives, abx, steroid, chemo, catheter, and any other condition that results in immunosuppression
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Describe the clinical manifestations of candida.
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1)cutaneous and subcutaneous
-oral (thrush) occurs on gums, lips, mouth or palate -develops in most AIDS pts -forms whitish lesion comprised of epithelial cells, yeast, and pseudohypae -vaginal:prevalent in diabetics -onychomycosis:invasion of the nails and nail plates -dermatitis -diaper rash 2)systemic -caused by indwelling catheters, surgery, IV drug use to damage to skin or GI tract -cause transient infections in immunocompetent hosts and are usually resolved by immune system but are problematic in immunocompromised hosts -infections can develop anywhere including kidneys, heart, eyes,etc... 3)chronic mucocutaneous-typically are infections of the skin and mucus membranes -rare disease w/genetic backgrounds, onset early in childhood, associated with cellular immunodef. and endocrinopathies |
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How is the diagnosis of candidiasis made?
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-specimen sites (blood-systemic sites, CSF, materials from removed catheters, tissue samples stained with KOH)
-sputum not useful b/c candida is in normal flora -direct micro. exam, in gram stained samples will appear as large G+ cells -cells will have pseudohyphae, true hyphae, germ tubes, etc. -culture on saboraud's dextrose agar, chromagar, potato dextrose agar -serology is difficult b/c candida is found in normal flora, can use LAT , ELISA, beta-glucan |
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Describe the basics of cryptococcosis.
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-underlying cellular immunodeficiency prior to infection (AIDS, lymphoma)
-exogenous infections -cryp. neoformans is the most likely pathogen -cryp. gattii is a new emerging infection which is found in immunocompetent hosts though, it is fatal in most cases and found in pac. NW of the US -found in soil, bird droppings, -infection follows inhalation of dessicated yeast cells, usually starts as skin or pulmonary infection and then may progress to CNS which results in meningoencephalitis |
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Describe the morphology of cryptococcus neoformans.
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-microscopically appears as encapsulated yeast (with india ink)
-macro appears creamy, mucoid colonies -serotypes A-D, most freq. A, neoformans is serotype A, D |
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What are the pathogenicity factors of cryptococcus neoformans?
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1)capsule-evades phagocytosis
2)diphenol oxidase (laccase)-forms melanin from phenol containing substrates 3)ability to grow at 37C |
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What is the pathogenesis of cryptococcus?
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-infections initiated by inhalation of yeast cells
-pulmonary infection may be asx or mimic flu -can resolve w/o intervention -problematic in immune compromised ppl, results in systemic infections following multiplication of yeast cells -the yeast form prefers CSF which results in cryptococcal meningoencephalitis -fever, HA, stiff neck, increased CSF amount and pressure, low glucose, may present with lesions on tissue -all cases of meningoencephalitis are fatal -these diseases are not communicable !! |
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How is diagnosis of cryptococcus made?
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-samples from CSF, sputum, aspiration from skin lesion
-direct exam with india ink -culture SDA, PDA, birdseed agar in mixed infections, growth at 37C -growth on canavanine glycine bromothymol blue (CGB) medium-only way to diff. neoformans and gattii (gattii will appear blue on plate) -serology-detection of capsule antigen in CSF and serum by latex agglut. |
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Describe the clinical manifestations of Cryptococcus neoformans.
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1)pulmonary-asx/flu like/cavitation
2)disseminated-meningitis, cryptococcoma, skin lesions, other -C. gattii causes more extensive infections b/c much more virulent |
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Describe the basic characteristics of aspergillosis infection.
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-it is a powdery mold that produces many small conidia that aerosolize
-following inhalation severe allergic rxns can occur -usually asx in immunocompetent pts -in immunocompromised pts., conidia may germinate to produce hyphae that are capable of infiltrating tissues -most common spp. is A. fumigatus -found in air, soil -infects vascular tissue and pre-existing cavities -powdery mold colonies, have aerial hyphae with long conidiophores -under microscopy they are septate, hyaline hyphae with dichotomous branching), vesicule, and microconidia |
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What are the risk factors for aspergillus infection?
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1)immunosuppression, DM, exogenous infection by inhalation of spores
2)inhalation of spores by host HS rxns (allergy) 3)ingestion of products contaminated with aspergillus toxins (mycotoxicosis/hepatocellular and colon carcinoma) |
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Describe the pathogenicity factors of aspergillus.
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-hyphae, phospholipase
-alveolar macrophages are capable of engulfing and destroying conidia -in immunocompromised pts there is decreased phagocytosis so the conidia swell in the lung, germinate, form hyphal structures, can invade tissues, blood vessels, cavities, and may develop aspergilloma |
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What are the clinical manifestations of aspergillosis?
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1)allergic aspergillosis
-asthma -allergic bronchopulmonary aspergillosis 2)aspergilloma and extrapulmonary -aspergilloma (fungus ball in the lungs and paranasal sinuses) -conidia enter the preexisting cavity, germinate, and produce hyphae in cavity -otomycosis (external otitis) -onychomycosis -eye infections (conjunctival, corneal, intraocular) 3)invasive aspergillosis -fatal if untreated -pulmonary and disseminated 4)mycotoxicosis -some spp. produce aflatoxins which increase the severity of infections |
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How is the diagnosis of aspergillosis made?
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-samples of sputum, tissue samples, blood samples are rarely positive
-direct exam will see septate hyphae and conidia in sputum, intravascular hyphae in tissue -culture SDA (should grow at least 2 cultures) -serology-allergy detects IgE in serum, invasive infection (detection of galaktomanna antigen in serum via ELISA) |
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Describe the general characteristics of pneumocystis pneumonia (PCP).
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-greater incidence following AIDS epidemic
-does not cause disease in healthy ppl -caused by P. jiroveci (formerly known as P. carinii) -related to candida -no known natural reservoir |
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Describe the characteristics of P. jiroveci.
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-has 2 morphologically distinct forms
1)trophozoite-thin walled 2)cysts-thick walled, spherical, multinucleate, cysts can be stained with toluene blue, calcofluor white or silver stain -extracellular pathogen -the infectious form is the cysts, the bodies within the cysts are released and develop into trophozoites which then develop into another mature cyst |
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What are the symptoms of PCP?
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fever, non-productive cough, SOB, wt loss, night sweats, CXR shows diffuse B/L infiltrates
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What is the pathophysiology of PCP infection and who does it mostly occur in?
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-attacks the fibrous tissue of the lungs, thickening of alveoli, can result in hypoxia
-disease occurs when both cell. and humoral immunity are impaired, results from a defective clearing by alveolar macrophages |
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How is diagnosis of PCP made?
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-CXR-widespread pulmonary infiltrates
-ID of organism-lung biopsy tissue, sputum observed for organism, PCR based testing now in use -positive results are not a definitive diagnosis b/c this can be carried by healthy persons -THIS CANNOT BE CULTURED |
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What molecules are contained in the cell wall of fungi?
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chitin, beta glucan, and mannan
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What is thermal dimorphic conversion?
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refers to a property of many fungi that grow as a yeast at 37 C and a mold at 25 C
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What does yeast within a macrophage suggest?
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histoplasma capsulatum
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What yeast is always encapsulated?
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cryptococcus
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What is a hypha?
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a long strand or filament of cells
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What organism is associated with septate hyphae?
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aspergillus
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What organisms are associated with non-septate hyphae?
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rhizopus, mucor
-also often associated with pts. that have diabetes |
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What is a mycelium?
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a mat of hyphae
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What kind of fungi are asexual spores associated with?
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imperfect
sexual spores are associated with perfect fungi |
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What is a sporangium?
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-rhizopus and mucor fall into this category
-there are located on a sporangiophore which is a stalk that bears the sporangium -like a sac of spores |
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What is a conidium?
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-a cluster of spores being held up by a stalk like structure, no encased in a sac
-a conidiophore is a hypha branch that bears conidia -aspergillus and penicillium have these |
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What are arthroconidium?
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jointed arrangement of spores
-hypha fragmenting |
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What is a blastoconidium?
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just refers to a yeast cell that is budding
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What is a chlamydoconidium?
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swollen hypha
-these are like endospores in bacteria, they sustain the organism in environment under harsh conditions -don't really see this is tissue, seen in culture that has been growing for weeks on end |
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Compare/contrast micro and macroconidium.
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micro-unicellular, trichophyton
macro-multicellular, fusiform or banana shaped , microsporum Often associated with dermatophytes (ringworm) |
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What are the 4 types of mycoses infections?
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systemic
subcutaneous dermato- (such as ringworm) opportunistic NO TOXIGENIC VIRULENCE FACTORS ARE ASSOCIATED WITH A MYCOSIS (NO ENDO, EXOTOXINS) |
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What are the lab ID considerations in mycoses?
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-they are aerobes for the most part
-avoid inhaling the spores -yeasts grow rapidly -molds may require weeks to mature -safety cabinets for molds -you must submit suitable specimens to be grown |
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What are the common media for growing mycoses?
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1)sabouraud agar
2)potato dextrose agar -yeasts grow quickly but molds often require weeks to mature -yeasts are identified biochemically (molds by structure) -gram stain and chlorazol black (india ink and KOH) -use 10% KOH-direct observation -histological sections -latex agglutination, ELISA, nucleic acid detection |
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What are some of the antifungal targets?
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-cytoplasmic membrane sterols
-cell wall components -nucleic acid and protein synthesis -mitotic spindle formation |
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What does ketoconazole-itraconazole do?
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inhibits ergosterol synthesis
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What does amphotericin B do?
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used to treat systemic fungi
-targets ergosterol, causing membrane damage |
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What does Griseofluvin do?
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used to treat dermatophytes
-interferes with mitosis, targets microtubules |
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What do flucytosine do?
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interferes with DNA and protein synthesis
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What does terbinafine do?
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used to tx dermatophytes
-inhibits ergosterol synthesis-cell membrane target |
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What does caspofungin do?
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used to tx candida and aspergillus
-inhibits glucan synthesis, cell wall target |
